MS
MEDICAL SURGICAL
Abby Tabuena
Overview of the Structures & Functions of Nervous System
Central NS PNS ANS
Brain & spinal cord 31 spinal & cranial sympathetic NS
Parasypathatic NS
Somatic NS
C- 8
T- 12
L- 5
S- 5
C- 1
ANS (or adrenergic of parasympatholitic response)
SNS involved in fight or aggression response Effects of SNS (anti-cholinergic/adrenergic)
1. Dilate pupil – to aware of surroundings
Release of norepinephrine (adrenaline – cathecolamine) - medriasis
Adrenal medulla (potent vasoconstrictor) 2. Dry mouth
Increases body activities VS = Increase 3. BP & HR= increased
Except GIT – decrease GITmotility bronchioles dilated to take more oxygen
4. RR increased
* Why GIT is not increased = GIT is not important! 5. Constipation & urinary retention
Increase blood flow to skeletal muscles, brain & heart.
I. Adrenergic Agents – Epinephrine (adrenaline)
SE: SNS effect
II. PNS: Beta adrenergic blocking agents (opposite of adrenergic agents) (all end in –‘lol’)
- Blocks release of norepinephrine.
- Decrease body activities except GIT (diarrhea)
Ex. Propanolol, Metopanolol
SE:
B – broncho spasm (bronchoconstriction)
E – elicits a decrease in myocardial contraction
T – treats HPN
A – AV conduction slows down
Given to angina & MI – beta-blockers to rest heart
Anti HPN agents:
1. Beta blockers (-lol)
2. Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
3. Calcium antagonist
ex CALCIBLOC or NEFEDIPINE
Peripheral nervous system: cholinergic/ vagal or sympatholitic response Effect of PNS: (cholinergic)
- Involved in fly or withdrawal response 1. Meiosis – contraction of pupils
- Release of acetylcholine (ACTH) 2. Increase salivation
- Decrease all bodily activities except GIT (diarrhea) 3. BP & HR decreased
4. RR decrease – broncho constriction
I Cholinergic agents 5. Diarrhea – increased GI motility
ex 1. Mestinon 6. Urinary frequency
Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS
S/E- of anti-hpn drugs:
1. orthostatic hpn
2. transient headache & dizziness.
-Mgt. Rise slowly. Assist in ambulation.
CNS (brain & spinal cord)
I. Cells – A. neurons
Properties and characteristics
a. Excitability – ability of neuron to be affected in external environment.
b. Conductivity – ability of neuron to transmit a wave of excitation from one cell to another
c. Permanent cells – once destroyed, cant regenerate (ex. heart, retina, brain, osteocytes)
Regenerative capacity
A. Labile – once destroyed cant regenerate
- Epidermal cells, GIT cells, resp (lung cells). GUT
B. Stable – capable of regeneration BUT limited time only ex salivary gland, pancreas cells cell of liver, kidney cells
C. Permanent cells – retina, brain, heart, osteocytes can’t regenerate.
3.) Neuroglia – attached to neurons. Supports neurons. Where brain tumors are found.
Types:
1. Astrocyte
2. Oligodendria
Astrocytoma – 90 – 95% brain tumor from astrocyte. Most brain tumors are found at astrocyte.
Astrocyte – maintains integrity of blood brain barrier (BBB).
BBB – semi permeable / selective
-Toxic substance that destroys astrocyte & destroy BBB.
Toxins that can pass in BBB:
1. Ammonia-liver cirrhosis.
2. 2. Carbon Monoxide – seizure & parkinsons.
3. 3. Bilirubin- jaundice, hepatitis, kernicterus/hyperbilirubenia.
4. 4. Ketones –DM.
OLIGODENDRIA – Produces myelin sheath – wraps around a neuron – acts as insulator facilitates rapid nerve impulse transmission.
No myelin sheath – degenerates neurons
Damage to myelin sheath – demyellenating disorders
DEMYELLENATING DSE
1.)ALZHEIMER’S DISEASE– atrophy of brain tissue due to a deficiency of acetylcholine.
S&Sx:
A – amnesia – loss of memory
A – apraxia – unable to determine function & purpose of object
A – agnosia – unable to recognize familiar object
A – aphasia –
- Expressive – brocca’s aphasia – unable to speak
- Receptive – wernickes aphasia – unable to understand spoken words
Common to Alzheimer – receptive aphasia
Drug of choice – ARICEPT (taken at bedtime) & COGNEX.
Mgt: Supportive & palliative.
Microglia – stationary cells, engulfs bacteria, engulfs cellular debris.
II. Compositions of Cord & Spinal cord
80% - brain mass
10% - CSF
10% - blood
MONROE KELLY HYPOTHESIS: The skull is a closed vault. Any increase in one component will increase ICP.
Normal ICP: 0-15mmHg
Brain mass
1. Cerebrum – largest - Connects R & L cerebral hemisphere
- Corpus collusum
Rt cerebral hemisphere, Lt cerebral hemisphere
Function:
1. Sensory
2. Motor
3. Integrative
Lobes
1.) Frontal
a. Controls motor activity
b. Controls personality development
c. Where primitive reflexes are inhibited
d. Site of development of sense of umor
e. Brocca’s area – speech center
Damage - expressive aphasia
2.) Temporal –
a. Hearing
b. Short term memory
c. Wernickes area – gen interpretative or knowing Gnostic area
Damage – receptive aphasia
3.) Parietal lobe – appreciation & discrimation of sensory imp
- Pain, touch, pressure, heat & cold
4.) Occipital - vision
5.) Insula/island of reil/ Central lobe- controls visceral fx
Function: - activities of internal organ
6.) Rhinencephalon/ Limbec
- Smell, libido, long-term memory
Basal Ganglia – areas of gray matte located deep within a cerebral hemisphere
- Extra pyramidal tract
- Releases dopamine-
- Controls gross voluntary unit
Decrease dopamine – (Parkinson’s) pin rolling of extremities & Huntington’s Dse.
Decrease acetylcholine – Myasthenia Gravis & Alzheimer’s
Increased neurotransmitter = psychiatric disorder Increase dopamine – schizo
Increase acetylcholine – bipolar
MID BRAIN – relay station for sight & hearing
Controls size & reaction of pupil 2 – 3 mm
Controls hearing acuity
CN 3 – 4
Isocoria – normal size (equal)
Anisocoria – uneven size – damage to mid brain
PERRLA – normal reaction
DIENCEPHALON- between brain
Thalamus – acts as a relay station for sensation
Hypothalamus – (thermoregulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center, emotional responses, controls pituitary function.
BRAIN STEM- a. Pons – or pneumotaxic center – controls respiration
Cranial 5 – 8 CNS
MEDULLA OBLONGATA- controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
Vasomotor center, spinal decuissation termination, CN 9, 10, 11, 12
CEREBELLUM – lesser brain
- Controls posture, gait, balance, equilibrium
Cerebellar Tests:
a.) R – Romberg’s test- needs 2 RNs to assist
- Normal anatomical position 5 – 10 min
(+) Romberg’s test – (+) ataxia or unsteady gait or drunken like movement with loss of balance.
b.) Finger to nose test –
(+) To FTNT – dymetria – inability to stop a movement at a desired point
c.) Alternate pronation & supination
Palm up & down . (+) To alternate pronation & supination or damage to cerebellum – dymentrium
Composition of brain - based on Monroe Kellie Hypothesis
- Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP
Normal ICP – 0 – 15 mmHg
Foramen Magnum
C1 – atlas
C2 – axis
(+) Projectile vomiting = increase ICP
Observe for 24 - 48 hrs
CSF – cushions the brain, shock absorber
Obstruction of flow of CSF = increase ICP
Hydrocephalus – posteriorly due to closure of posterior fontanel
CVA – partial/ total obstruction of blood supply
INCREASED ICP – increase ICP is due to increase in 1 of the Intra Cranial components.
Predisposing factors:
1. Head injury
2. Tumor
3. Localized abscess
4. Hemorrhage (stroke)
5. Cerebral edema
6. Hydrocephalus
7. Inflammatory conditions - Meningitis, encephalitis
B. S&Sx change in VS = always late symptoms
Earliest Sx:
a.) Change or decrease LOC – Restlessness to confusion Wide pulse pressure: Increased ICP
- Disorientation to lethargy Narrow pp: Cardiac disorder, shock
- Stupor to coma
Late sign – change in V/S
1. BP increase (systolic increase, diastole- same)
2. Widening pulse pressure
Normal adult BP 120/80 120 – 80 = 40 (normal pulse pressure)
Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide)
3. RR is decreased (Cheyne-Stokes = bet period of apnea or hyperpnea with periods of apnea)
4. Temp increase
Increased ICP: Increase BP Shock – decrease BP –
Decrease HR Increase HR CUSHINGS EFFECT
Decrease RR Increase RR
Increase Temp Decrease temp
b.) Headache
Projectile vomiting
Papilledima (edema of optic disk – outer surface of retina)
Decorticate (abnormal flexion) = Damage to cortico spinal tract /
Decerebrate (abnormal extension) = Damage to upper brain stem-pons/
c.) Uncal herniation – unilateral dilation of pupil. (Bilateral dilation of pupil – tentorial herniation.)
d.) Possible seizure.
Nursing priority:
1.) Maintain patent a/w & adequate ventilation
a. Prevention of hypoxia – (decrease tissue oxygenation) & hypercarbia (increase in CO2 retention).
Hypoxia – cerebral edema - increase ICP
Hypoxia – inadequate tissue oxygenation
Late symptoms of hypoxia – B – bradycardia
E – extreme restlessness
D – dyspnea
C – cyanosis
Early symptoms – R – restlessness
A – agitation
T – tachycardia
Increase CO2 retention/ hypercarbia – cerebral vasodilatation = increase ICP
Most powerful respiratory stimulant increase in CO2
Hyperventilate decrease CO2 – excrete CO2
Respiratory Distress Syndrome (RDS) – decrease Oxygen
Suctioning – 10-15 seconds, max 15 seconds. Suction upon removal of suction cap.
Ambu bag – pump upon inspiration
c. Assist in mechanical ventilation
1. Maintain patent a/w
2. Monitor VS & I&O
3. Elevate head of bed 30 – 45 degrees angle neck in neutral position unless contra indicated to promote venous drainage
4. Limit fluid intake 1,200 – 1,500 ml/day
(FORCE FLUID means:Increase fluid intake/day – 2,000 – 3,000 ml/day)- not for inc ICP.
5. Prevent complications of immobility
6. Prevent increase ICP by:
a. Maintain quiet & comfy environment
b. Avoid use of restraints – lead to fractures
c. Siderails up
d. Instruct patient to avoid the ff:
-Valsalva maneuver or bearing down, avoid straining of stool
(give laxatives/ stool softener Dulcolax/ Duphalac)
- Excessive cough – antitussive
Dextrometorpham
-Excessive vomiting – anti emetic (Plasil – Phil only)/ Phenergan
- Lifting of heavy objects
- Bending & stooping
e. Avoid clustering of nursing activities
7. Administer meds as ordered:
1.) Osmotic diuretic – Mannitol./Osmitrol promotes cerebral diuresis by decompressing brain tissue
Nursing considerations: Mannitol
1. Monitor BP – SE of hypotension
2. Monitor I&O every hr. report if < 30cc out put
3. Administer via side drip
4. Regulate fast drip – to prevent formation of crystals or precipitate
2.) Loop diuretic - Lasix (Furosemide)
Nursing Mgt: Lasix
Same as Mannitol except
- Lasix is given via IV push (expect urine after 10-15mins) should be in the morning. If given at 7am. Pt will urinate at 7:15
Immediate effect of Lasix within 15 minutes. Max effect – 6 hrs due (7am – 1pm)
S/E of Lasix
Hypokalemia (normal K-3.5 – 5.5 meg/L)
S&Sx
1. Weakness & fatigue
2. Constipation
3. (+) “U” wave in ECG tracing
Nursing Mgt:
1. Administer K supplements – ex Kalium Durule, K chloride
Potassium Rich food:
ABC’s of K
Vegetables Fruits
A - asparagus A – apple
B – broccoli (highest) B – banana – green
C – carrots C – cantalope/ melon
O – orange (highest) –for digitalis toxicity also.
Vit A – squash, carrots yellow vegetables & fruits, spinach, chesa
Iron – raisins,
Food appropriate for toddler – spaghetti! Not milk – increase bronchial secretions
Don’t give grapes – may choke
S/E of Lasix:
1. Hypokalemia
2. Hypocalcemia (Normal level Ca = 8.5 – 11mg/100ml) or Tetany:
S&Sx
weakness
Paresthesia
(+) Trousseau sign – pathognomonic – or carpopedal spasm. Put bp cuff on arm=hand spasm.
(+) Chevostek’s sign
Arrhythmia
Laryngospasm
Administer – Ca gluconate – IV slowly
Ca gluconate toxicity: Sx – seizure – administer Mg SO4
Mg SO4 toxcicity– administer Ca gluconate
B – BP decrease
U – urine output decrease
R – RR decrease
P – patellar reflexes absent
3. Hyponatremia – Normal Na level = 135 – 145 meg/L
S/Sx – Hypotension
Signs of Dehydration: dry skin, poor skin turgor, gen body malaise.
Early signs – Adult: thirst and agitation / Child: tachycardia
Mgt: force fluid
Administer isotonic fluid sol
4.) Hyperglycemia – increase blood sugar level
P – polyuria
P – polyphagia
P – polydipsia
Nsg Mgt:
a. Monitor FBS (N=80 – 120 mg/dl)
5.) Hyperurecemia – increase serum uric acid. Tophi- urate crystals in joint.
Gouty arthritis kidney stones- renal colic (pain)
Cool moist skin
Sx joint pain & swelling usually at great toe.
Nsg Mgt of Gouty Arthritis
a.) Cheese (not sardines, anchovies, organ meat)
(Not good if pt taking MAO)
b.) Force fluid
c.) Administer meds – Allopurinol/ Zyloprim – inhibits synthesis of uric acid – drug of choice for gout
Colchicene – excretes uric acid. Acute gout drug of choice.
Kidney stones – renal colic (pain). Cool moist skin
Mgt:
1. Force fluid
2. Meds – narcotic analgesic
Morphine SO4
SE of Morphine SO4 toxicity
Respiratory depression (check RR 1st)
Antidote for morphine SO4 toxicity –Narcan (NALOXONE)
Naloxone toxicity – tremors
Increase ICP meds:
3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone)
4.) Mild analgesic – codeine SO4. For headache.
5.) Anti consultants – Dilantin (Phenytoin)
Question: Increase ICP what is the immediate nsg action?
a. Administer Mannitol as ordered
b. Elevate head 30 – 45 degrees
c. Restrict fluid
d. Avoid use of restraints
Nsg Priority – ABC & safety
Pt suffering from epiglotitis. What is nsg priority?
a. Administer steroids – least priority
b. Assist in ET – temp, a/w
c. Assist in tracheotomy – permanent (Answer)
d. Apply warm moist pack? Least priority
Rationale: Wont need to pass larynx due to larynx is inflamed. ET can’t pass. Need tracheostomy only-
Magic 2’s of drug monitoring
Drug N range Toxicity Classification Indication
D – digoxin .5 – 1.5 meq/L 2 cardiac glycosides CHF
L - lithium .6 – 1.2 meq/L 2 antimanic bipolar
A – aminophylline 10 – 19 mg/100ml 20 bronchodilator COPD
D – Dilantin 10 -19 mg/100 ml 20 anticonvulsant seizures
A – acetaminophen 10 – 30 mg/100ml 200 narcotic analgesic osteoarthritis
Digitalis – increase cardiac contraction = increase CO
Nursing Mgt
1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin)
Digitalis toxicity – antidote - Digivine
a. Anorexia -initial sx.
b. n/v GIT
c. Diarrhea
d. Confusion
e. Photophobia
f. Changes in color perception – yellow spots
(Ok to give to pts with renal failure. Digoxin is metabolized in liver not in kidney.)
L – lithium (lithane) decrease levels of norepinephrine, serotonine, acetylcholine
Antimanic agent
Lithium toxicity
S/Sx -
a. Anorexia
b. n/s
c. Diarrhea
d. Dehydration – force fluid, maintain Na intake 4 – 10g daily
e. Hypothyroidism
(CRETINISM– the only endocrine disorder that can lead to mental retardation)
A – aminophyline (theophylline) – dilates bronchioles.
Take bp before giving aminophylline.
S/Sx : Aminophylline toxicity:
1. Tachycardia
2. Hyperactivity – restlessness, agitation, tremors
Question: Avoid giving food with Aminophylline
a. Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI
b. Beer/ wine -
c. Hot chocolate & tea – caffeine – CNS stimulant tachycardia
d. Organ meat/ box cereals – anti parkinsonian
MAOI – antidepressant
m AR plan
n AR dil can lead to CVA or hypertensive crisis
p AR nate
3 – 4 weeks - before MAOI will take effect
Anti Parkinsonian agents – Vit B6 Pyridoxine reverses effect of Levodopa
D – dilatin (Phenytoin) – anti convulsant/seizure
Nursing Mgt:
1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate
- Do sandwich method
- Give NSS then Dilantin, then NSS!
2. Instruct the pt to avoid alcohol – bec alcohol + dilantin can lead to severe CNS depression
Dilantin toxicity:
S/Sx:
G – gingival hyperplasia – swollen gums
i. Oral hygiene – soft toothbrush
ii. Massage gums
H – hairy tongue
A - ataxia
N – nystagmus – abnormal movement of eyeballs
A – acetaminophen/ Tylenol – non-opoid analgesic & antipyretic – febrile pts
Acetaminophen toxicity :
1. Hepato toxicity
2. Monitor liver enzymes
SGPT (ALT) – Serum Glutamic Piruvate Tyranase
SGOT- Serum Glutamic Acetate Tyranase
3. Monitor BUN (10 – 20)
Crea (.8-1)
Acetaminophen toxicity can lead to hypoglycemia
T – tremors, Tachycardia
I – irritability
R – restlessness
E – extreme fatigue
D – depression (nightmares) , Diaphoresis
Antidote for acetaminophen toxicity – Acetylcesteine = causes outporing of secretions. Suction.
Prepare suctioning apparatus.
Question: The following are symptoms of hypoglycemia except:
a. Nightmares
b. Extreme thirst – hyperglycemia symptoms
c. Weakness d. Diaphoresis
PARKINSONS DSE (parkinsonism) - chronic, progressive disease of CNS char by degeneration of dopamine producing cells in substancia nigra at mid brain & basal ganglia
- Palliative, Supportive
Function of dopamine: controls gross voluntary motors.
Predisposing Factors:
1. Poisoning (lead & carbon monoxide). Antidote for lead = Calcium EDTA
2. Hypoxia
3. Arteriosclerosis
4. Encephalitis
High doses of the ff:
a. Reserpine (serpasil) anti HPN, SE – 1.) depression - suicidal 2.) breast cancer
b. Methyldopa (aldomet) - promote safety
c. Haloperidol (Haldol)- anti psychotic
d. Phenothiazide - anti psychotic
SE of anti psychotic drugs – Extra Pyramidal Symptom
Over meds of anti psychotic drugs – neuroleptic malignant syndrome char by tremors (severe)
S/Sx: Parkinsonism –
1. Pill rolling tremors of extremities – early sign
2. Bradykinesia – slow movement
3. Over fatigue
4. Rigidity (cogwheel type)
a. Stooped posture
b. Shuffling – most common
c. Propulsive gait
5. Mask like facial expression with decrease blinking eyes
6. Monotone speech
7. Difficulty rising from sitting position
8. Mood labilety – always depressed – suicide
Nsg priority: Promote safety
9. Increase salivation – drooling type
10. Autonomic signs:
- Increase sweating
- Increase lacrimation
- Seborrhea (increase sebaceous gland)
- Constipation
- Decrease sexual activity
Nsg Mgt
1. Anti parkinsonian agents
- Levodopa (L-Dopa), Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)
Mechanism of action
Increase levels of dopa – relieving tremors & bradykinesia
S/E of anti parkinsonian
- Anorexia
- n/v
- Confusion
- Orthostatic hypotension
- Hallucination
- Arrhythmia
Contraindication:
1. Narrow angled closure glaucoma
2. Pt taking MAOI (Parnate, Marplan, Nardil)
Nsg Mgt when giving anti-parkinsonian
1. Take with meals – to decrease GIT irritation
2. Inform pt – urine/ stool may be darkened
3. Instruct pt- don’t take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg
- Cause B6 reverses therapeutic effects of levodopa
Give INH (Isoniazide-Isonicotene acid hydrazide.) SE-Peripheral neuritis.
2. Anti cholinergic agents – relieves tremors
Artane mech – inhibits acetylcholine
Cogentin action , S/E - SNS
3. Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime
S/E: adult– drowsiness,– avoid driving & operating heavy equipt. Take at bedtime.
Child – hyperactivity CNS excitement for kids.
4.) Dopamine agonist
Bromotriptine Hcl (Parlodel) – respiratory depression. Monitor RR.
Nsg Mgt – Parkinson
1.) Maintain siderails
2.) Prevent complications of immobility
- Turn pt every 2h
Turn pt every 1 h – elderly
3.) Assist in passive ROM exercises to prevent contractures
4.) Maintain good nutrition
CHON – in am
CHON – in pm – to induce sleep – due Tryptopan – Amino Acid
5.) Increase fluid in take, high fiber diet to prevent constipation
6.) Assist in surgery – Sterotaxic Thalamotomy
Complications in sterotaxic thalmotomy- 1.) Subarachnoid hemorrhage 2.) aneurism 3.) encephalitis
MULTIPLE SCLEROSIS (MS)
Chronic intermittent disorder of CNS – white patches of demyelenation in brain & spinal cord.
- Remission & exacerbation
- Common – women, 15 – 35 yo cause – unknown
Predisposing factor:
1. Slow growing virus
2. Autoimmune – (supportive & palliative treatment only)
Normal Resident Antibodies:
Ig G – can pass placenta – passive immunity. Short acting.
Ig A – body secretions – saliva, tears, colostrums, sweat
Ig M – acute inflammation
Ig E – allergic reactions
IgD – chronic inflammation
S & Sx of MS: (everything down)
1. Visual disturbances
a. Blurring of vision
b. Diplopia/ double vision
c. Scotomas (blind spots) – initial sx
2. Impaired sensation to touch, pain, pressure, heat, cold
a. Numbness
b. Tingling
c. Paresthesia
3. Mood swings – euphoria (sense of elation )
4. Impaired motor function:
a. Weakness
b. Spasiticity –“ tigas”
c. Paralysis –major problem
5. Impaired cerebellar function
Triad Sx of MS
I – intentional tremors
N – nystagmus – abnormal rotation of eyes Charcots triad
A – Ataxia
& Scanning speech
6. Urinary retention or incontinence
7. Constipation
8. Decrease sexual ability
Dx – MS
1. CSF analysis thru lumbar puncture
- Reveals increase CHON & IgG
2. MRI – reveals site & extent of demyelination
3. Lhermitte’s response is (+). Introduce electricity at the back. Theres spasm & paralysis at spinal cord.
Nsg Mgt MS
- Supportive mgt
1.) Meds
a. Acute exacerbation
ACTH – adenocorticotopic
Steroids – to reduce edema at the site of demyelination to prevent paralysis
Spinal Cord Injury
Administer drug to prevent paralysis due to edema
a. Give ACTH – steroids
b. Baclopen (Lioresol) or Dantrolene Na (Dantrene)
To decrease muscle spasticity
c. Interferone – to alter immune response
d. Immunosuppresants
2. Maintain siderails
3. Assist passive ROMexercises – promote proper body alignment
4. Prevent complications of immobility
5. Encourage fluid intake & increase fiber diet – to prevent constipation
6. Provide catheterization die urinary retention
7. Give diuretics
Urinary incontinence – give Prophantheline bromide (probanthene)
Antispasmodic anti cholinergic
8. Give stress reducing activity. Deep breathing exercises, biofeedback, yoga techniques.
9. Provide acid-ash diet – to acidify urine & prevent bacteria multiplication
Grape, Cranberry, Orange juice, Vit C
MYASTHENIA GRAVIS (MG) – disturbance in transmission of impulses from nerve to muscle cell at neuro muscular
junction.
Common in Women, 20 – 40 yo, unknown cause or idiopathic
Autoimmune – release of cholenesterase – enzyme
Cholinesterase destroys ACH (acetylcholine) = Decrease acetylcholine
Descending muscle weakness
(Ascending muscle weakness – Guillain Barre Syndrome)
Nsg priority:
1) a/w
2) aspiration
3) immobility
S/ Sx:
1. Ptosis – drooping of upper lid ( initial sign)
Check Palpebral fissure – opening of upper & lower lids = to know if (+) of MG.
2. Diplopia – double vision
3. Mask like facial expression
4. Dysphagia – risk for aspiration!
5. Weakening of laryngeal muscles – hoarseness of voice
6. Resp muscle weakness – lead respiratory arrest. Prepare at bedside tracheostomy set
7. Extreme muscle weakness during activity especially in the morning.
Dx test
1. Tensilon test (Edrophonium Hcl) – temporarily strengthens muscles for 5 – 10 mins. Short term- cholinergic. PNS effect.
Nsg Mgt
1. Maintain patent a/w & adequate vent by:
a.) Assist in mechanical vent – attach to ventilator
b.) Monitor pulmonary function test. Decrease vital lung capacity.
2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, 5/5, etc)
3. Siderails
4. Prevent complications of immobility. Adult-every 2 hrs. Elderly- every 1 hr.
5. NGT feeding
Administer meds –
a. Cholinergics or anticholinesterase agents
Mestinon (Pyridostigmine)
Neostignine (prostigmin) – Long term
- Increase acetylcholine
s/e – PNS
b. Corticosteroids – to suppress immune resp
Decadron (dexamethasone)
Monitor for 2 types of Crisis:
|Myastinic crisis |Cholinergic crisis |
|A cause – 1. Under medication |Cause: 1 over meds |
|2. Stress |S/Sx - PNS |
|3. Infection | |
|B S&Sx 1. Unable to see – Ptosis & diplopia | |
|2. Dysphagia- unable to swallow. | |
|3. Unable to breath | |
|C Mgt – adm cholinergic agents |Mgt. adm anti-cholinergic |
| |Atropine SO4 |
| |SNS – dry mouth |
7. Assist in surgical proc – thymectomy. Removal of thymus gland. Thymus secretes auto immune antibody.
8. Assist in plasmaparesis – filter blood
9. Prevent complication – respiratory arrest
Prepare tracheostomy set at bedside.
GBS – Guillain Barre Syndrome
- Disorder of CNS
- Bilateral symmetrical polyneuritis
- Ascending paralysis
Cause – unknown, idiopathic
- Auto immune
- r/t antecedent viral infection
- Immunizations
S&Sx
Initial :
1. Clumsiness
2. Ascending muscle weakness – lead to paralysis
3. Dysphagia
4. Decrease or diminished DTR (deep tendon reflexes)
- Paralysis
5. Alternate HPN to hypotension – lead to arrhythmia - complication
6. Autonomic changes – increase sweating, increase salivation.
Increase lacrimation
Constipation
Dx most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON (same with MS)
Nsg Mgt
1. Maintain patent a/w & adequate vent
a. Assist in mechanical vent
b. Monitor pulmonary function test
2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia
3. Siderails
4. Prevent compl – immobility
5. Assist in passive ROM exercises
6. Institute NGT feeding – due dysphagia
7. Adm meds (GBS) as ordered: – 1. Anti cholinergic – atropine SO4
2. Corticosteroids – to suppress immune response
3. Anti arrhythmic agents
a.) Lidocaine /Xylocaine –SE confusion = VTach
b.) Bretyllium
c.) Quinines/Quinidine – anti malarial agent. Give with meals.
- Toxic effect – cinchonism
Quinidine toxicity
S/E – anorexia, n/v, headache, vertigo, visual disturbances
8. Assist in plasmaparesis (MG. GBS)
9. Prevent comp – arrhythmias, respiratory arrest
Prepare tracheostomy set at bedside.
INFL CONDITONS OF BRAIN
Meninges – 3-fold membrane – cover brain & spinal cord
Fx:
Protection & support
Nourishment
Blood supply
3 layers
1. Duramater sub dural space
2. Arachmoid matter
3. Pia matter sub arachnoid space where CSF flows L3 & L4. Site for lumbar puncture.
MENINGITIS – inflammation of meningitis & spinal cord
Etiology – Meningococcus
Pneumococcus
Hemophilous influenza – child
Streptococcus – adult meningitis
MOT – direct transmission via droplet nuclei
S&Sx
- Stiff neck or nuchal rigidity (initial sign)
- Headache
- Projectile vomiting – due to increase ICP
- Photophobia
- Fever chills, anorexia
- Gen body malaise
- Wt loss
- Decorticate/decerebration – abnormal posturing
- Possible seizure
Sx of meningeal irritation – nuchal rigidity or stiffness
Opisthotonus- rigid arching of back
Pathognomonic sign – (+) Kernig’s & Brudzinski sign
Leg pain neck pain
Dx:
1. Lumbar puncture – lumbar/ spinal tap – use of hallow spinal needle – sub arachnoid space L3 & L4 or L4 & L5
Aspirate CSF for lumbar puncture.
Nsg Mgt for lumbar puncture – invasive
1. Consent / explain procedure to pt
- RN – dx procedure (lab)
- MD – operation procedure
2. Empty bladder, bowel – promote comfort
3. Arch back – to clearly visualize L3, L4
Nsg Ngt post lumbar
1. Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF
2. Force fluid
3. Check punctured site for drainage, discoloration & leakage to tissue
4. Assess for movement & sensation of extremeties
Result
1. CSF analysis: a. increase CHON & WBC Content of CSF: Chon, wbc, glucose
b. Decrease glucose
Confirms meningitis c. increase CSF opening pressure
N 50 – 160 mmHg
d. (+) Culture microorganism
2. Complete blood count CBC – reveals increase WBC
Mgt:
1. Adm meds
a.) Broad-spectrum antibiotic penicillin
S/E
1. GIT irritation – take with food
2. Hepatotoxicity, nephrotoxcicity
3. Allergic reaction
4. Super infection – alteration in normal bacterial flora
- N flora throat – streptococcus
- N flora intestine – e coli
Sx of superinfection of penicillin = diarrhea
b.) Antipyretic
c.) Mild analgesic
2. Strict resp isolation 24h after start of antibiotic therapy
A – Cushing’s synd – reverse isolation - due to increased corticosteroid in body.
B – Aplastic anemia – reverse isolation - due to bone marrow depression.
C – Cancer anytype – reverse isolation – immunocompromised.
D – Post liver transplant – reverse isolation – takes steroids lifetime.
E – Prolonged use steroids – reverse isolation
F – Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy
G – Asthma – not to be isolated
3. Comfy & dark room – due to photophobia & seizure
4. Prevent complications of immobility
5. Maintain F & E balance
6. Monitor vs, I&O , neuro check
7. Provide client health teaching & discharge plan
a. Nutrition – increase cal & CHO, CHON-for tissue repair. Small freq feeding
b. Prevent complication hydrocephalus, hearing loss or nerve deafness.
8. Prevent seizure.
Where to bring 2 yo post meningitis
- Audiologist due to damage to hearing- post repair myelomeningocele
- Urologist -Damage to sacral area – spina bifida – controls urination
9. Rehab for neurological deficit. Can lead to mental retardation or a delay in psychomotor development.
CEREBRO VASCULAR ACCIDENT – stroke, brain attack or cerebral thrombosis, apoplexy
- Partial or complete disruption in the brains blood supply
- 2 largest & common artery in stroke
Middle cerebral artery
Internal carotid artery
- Common to male – 2 – 3x high risk
Predisposing factor:
1. Thrombosis – clot (attached)
2. Embolism – dislodged clot – pulmo embolism
S/Sx: pulmo embolism
Sudden sharp chest pain
Unexplained dyspnea, SOB
Tachycardia, palpitations, diaphoresis & mild restlessness
S/Sx: cerebral embolism
Headache, disorientation, confusion & decrease in LOC
Femur fracture – complications: fat embolism – most feared complication w/in 24hrs
Yellow bone marrow – produces fat cells at meduallary cavity of long bone
Red bone marrow – provides WBC, platelets, RBC found at epiphisis
2.) Hemorrhage
3.) Compartment syndrome – compression of nerves/ arteries
Risk factors of CVA: HPN, DM, MI, artherosclerosis, valvular heart dse - Post heart surgery – mitral valve replacement
Lifestyle: 1. Smoking – nicotine – potent vasoconstrictor
2. Sedentary lifestyle
3. Hyperlipidemia – genetic
4. Prolonged use of oral contraceptives
- Macro pill – has large amt estrogen
- Mini pill – has large amt of progestin
- Promote lipolysis (breakdown of lipids/fats) – artherosclerosis – HPN - stroke
5. Type A personality
a. Deadline driven person
b. 2 – 5 things at the same time
c. Guilty when not dong anything
6. Diet – increase saturated fats
7. Emotional & physical stress
8. Obesity
S & Sx
1. TIA- warning signs of impending stroke attacks
- Headache (initial sx), dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or plegia (monoplegia – 1 extreme)
Increase ICP
2. Stroke in evolution – progression of S & Sx of stroke
3. Complete stroke – resolution of stroke
a.) Headache
b.) Cheyne-Stokes Resp
c.) Anorexia, n/v
d.) Dysphagia
e.) Increase BP
f.) (+) Kernig’s & Brudzinski – sx of hemorrhagic stroke
g.) Focal & neurological deficit
1. Phlegia
2. Dysarthria – inability to vocalize, articulate words
3. Aphasia
4. Agraphia diff writing
5. Alesia – diff reading
6. Homoninous hemianopsia – loss of half of field of vision
Left sided hemianopsia – approach Right side of pt – the unaffected side
Dx
1. CT Scan – reveals brain lesion
2. Cerebral arteriography – site & extent of mal occlusion
- Invasive procedure due to inject dye
- Allergy test
All – graphy – invasive due to iodine dye
Post
1. Force fluid – to excrete dye is nephrotoxic
2. Check peripheral pulses - distal
Nsg Mgt
1. Maintain patent a/w & adequate vent
- Assist mechanical ventilation
- Administer O2
2. Restrict fluids – prevent cerebral edema
3. Elevate head of bed 30-45 degrees angle. Avoid valsalva maneuver.
4. Monitor vs., I&O, neuro check
5. Prevent compl of immobility by:
a. Turn client q2h
Elderly q1h
- To prevent decubitus ulcer
- To prevent hypostatic pneumonia – after prolonged immobility.
b. Egg crate mattress or H2O bed
c. Sand bag or foot board- prevent foot drop
6. NGT feeding – if pt can’t swallow
7. Passive ROM exercise q4h
8. Alternative means of communication
- Non-verbal cues
- Magic slate. Not paper and pen. Tiring for pt.
- (+) To hemianopsia – approach on unaffected side
9. Meds
Osmotic diuretics – Mannitol
Loop diuretics – Lasix/ Furosemide
Corticosteroids – dextamethazone
Mild analgesic
Thrombolytic/ fibrolitic agents – tunaw clot. SE-Urticaria, pruritus-caused by foreign subs.
Streptokinase
Urokinase
Tissue plasminogen activating
Monitor bleeding time
Anticoagulants – Heparin & Coumadin” sabay”
Coumadin will take effect after 3 days
Heparin – monitor PTT partial thromboplastin time if prolonged – bleeding give Protamine SO4- antidote.
Coumadin –Long term. monitor PT prothrombin time if prolonged- bleeding give Vit K – Aquamephyton- antidote.
Antiplatelet – PASA – aspirin paraanemo aspirin, don’t give to dengue, ulcer, and unknown headache.
Health Teaching
1. Avoidance modifiable lifestyle
- Diet, smoking
2. Dietary modification
- Avoid caffeine, decrease Na & saturated fats
Complications:
Subarachnoid hemorrhage
Rehab for focal neurological deficit – physical therapy
1. Mental retardation
2. Delay in psychomotor development
CONVULSIVE Disorder (CONVULSIONS)- disorder of the CNS char. by paroxysmal seizures with or without loss of consciousness, abnormal motor activity, alteration in sensation & perception & change in behavior.
Can you outgrow febrile seizure? Difference between: Seizure- 1st convulsive attack
Febrile seizure Normal if < 5 yo Epilepsy – 2nd and with history of seizure
Pathologic if > 5 yo
Predisposing Factor
Head injury due birth trauma
Toxicity of carbon monoxide
Brain tumor
Genetics
Nutritional & metabolic deficit
Physical stress
Sudden withdrawal to anticonvulsants will bring about status epilepticus
Status epilepticus – drug of choice: Diazepam & glucose
S & Sx
I. Generalized Seizure –
a.) Grand mal / tonic clonic seizures
With or without aura – warning symptoms of impending seizure attack- Epigastric pain- associated with olfactory, tactile, visual, auditory sensory experience
- Epileptic cry – fall
- Loss of consciousness 3 – 5 min
- Tonic clonic contractions
- Direct symmetrical extension of extremities-TONIC. Contractions-CLONIC
- Post ictal sleep -state of lethargy or drowsiness - unresponding sleep after tonic clonic
b.) Petimal seizure – (same as daydreaming!) or absent seizure.
- Blank stare
- Decrease blinking eye
- Twitching of mouth
- Loss of consciousness – 5 – 10 secs (quick & short)
II. Localized/partial seizure
a. Jacksonian seizure or focal seizure – tingling/jerky movement of index finger/thumb & spreads to shoulder & 1 sideof the body with janksonian march
b. Psychomotor/ focal motor - seizure
-Automatism – stereotype repetitive & non-purposive behavior
- Clouding of consciousness – not in control with environment
- Mild hallucinatory sensory experience
HALLUCINATIONS
1. Auditory – schitzo – paranoid type
2. Visual – korsakoffs psychosis – chronic alcoholism
3. Tactile – addict – substance abuse
III. Status epilecticus – continuous, uninterrupted seizure activity, if untreated, lead to hyperprexia – coma – death
Seizure: inc electrical firing in brain=increased metabolic activity in brain=brain using glucose and O2=dec glucose, dec O2.
Tx:Diazepam (drug of choice), glucose
Dx-Convulsion- get health history!
1. CT scan – brain lesion
2. EEG electroencephalography
- Hyperactivity brain waves
Nsg Mgt
Priority – Airway & safety
1. Maintain patent a/w & promote safety
Before seizure:
1. Remove blunt/sharp objects
2. Loosen clothing
3. Avoid restraints
4. Maintain siderails
5. Turn head to side to prevent aspiration
6. Tongue guard or mouth piece to prevent biting of tongue-BEFORE SEIZURE ONLY! Can use spoon at home.
7. Avoid precipitating stimulus – bright glaring lights & noises
8. Administer meds
a. Dilantin (Phenytoin) –( toxicity level – 20 )
SE Ginguial hyperplasia
H-hairy tongue
A-ataxia
N-nystagmus
A-acetaminophen- febrile pt
Mix with NSS
- Don’t give alcohol – lead to CNS depression
b. (Tegretol) Carbamasene- given also to Trigeminal Neuralgia. SE: arrythmia
c. Phenobarbital (Luminal)- SE: hallucinations
2. Institute seizure & safety precaution. Post seizure: Administer O2. Suction apparatus ready at bedside
3. Monitor onset & duration
- Type of seizure
- Duration of post ictal sleep. The longer the duration of post ictal sleep, the higher chance of having status epilepticus!
4. Assist in surgical procedure. Cortical resection
5. Complications: Subarachnoid hemorrhage and encephalitis
Question: 1 yo grand mal – immediate nursing action = a/w & safety
a. Mouthpiece – 1 yr old – little teeth only
b. Adm o2 inhalation – post!
c. Give pillow – safety (answer)
d. Prepare suction
Neurological assessment:
1. Comprehensive neuro exam
2. GCS - Glasgow coma scale – obj measurement of LOC or quick neuro check
3 components of ECS
M – motor 6
V – verbal resp 5
E – eye opening 4
15
15 – 14 – conscious
13 – 11 – lethargy
10 – 8 – stupor
7 – coma
3 – deep coma – lowest score
Survey of mental status & speech (Comprehensice Neuro Exam)
1. LOC & test of memory
2. Levels of orientation
3. CN assessment
4. Motor assessment
5. Sensory assessment
6. Cerebral test – Romhberg, finger to nose
7. DTR
8. Autonomics
Levels of consciousness (LOC) –
1. Conscious (conscious) – awake – levels of wakefulness
2. Lethargy (lethargic) – drowsy, sleepy, obtunded
3. Stupor (stuporous) – awakened by vigorous stimulation
Pt has gen body weakness, decrease body reflex
4. Coma (Comatose) light – (+) all forms of painful stimulations
Deep – (-) to painful stimulation
Question: Describe a conscious pt ?
a. Alert – not all pt are alert & oriented to time & place
b. Coherent
c. Awake- answer
d. Aware
Different types of pain stimulation
- Don’t prick
1. Deep sternal stimulation/ pressure 3x– fist knuckle
With response – light coma
Without response – deep coma
2. Pressure on great toe – 3x
3. Orbital pressure – pressure on orbits only – below eye
4. Corneal reflex/ blinking reflex
Wisp of cotton – used to illicit blinking reflex among conscious patients
Instill 1-drop saline solution – unconscious pt if (-) response pt is in deep coma
5. Test of memory – considered educational background
a. Short term memory –
- What did you eat for breakfast?
Damage to temporal lobe – (+) antero grade amnesia
b. Long term memory
(+) Retrograde amnesia – damage to limbic system
6. Levels of orientation
Time Place Person
Graphesthesia- can identify numbers or letters written on palm with a blunt object.
Agraphesthesia – cant identify numbers or letters written on palm with a blunt object.
CN assessment:
I – Olfactory s
II – Optic s
III – Oculomotor m
IV – Trocheal m smallest CN
V – Trigeminal b largest CN
VI – Abducens m
VII – Facial b
VIII – Acustic/auditory s
IX – Glassopharyngeal b
X – Vagus b longest CN
XI– Spinal accessory m
XII – Hypoglossal m
I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee, bar soap, vinegar, cigarette tar
- Hyposmia – decrease sensitivity to smell
- Diposmia – distorted sense of smell
- Anosmia – absence of sense of smell
Either of 3 might indicate head injury – damage to cribriform plate of ethmoid bone where olfactory cells are located or indicate inflammation condition – sinusitis
II optic- test of visual acuity – Snellens chart – central or distance vision
Snellens E chart – used for illiterate chart
N 20/20 vision distance by w/c person can see letters- 20 ft
Numerator – distance to snellens chart
Denominator – distance the person can see the letters
OD – Rt eye 20/20 20/200 – blindness – cant read E – biggest
OS – left eye 20/20
OU – both eye 20/20
2. Test of peripheral vision/ visual field
a. Superiority
b. Bitemporally
c. Inferiorly
d. Nasally
Common Disorders – see page 85-87 for more info on glaucoma, etc.
1. Glaucoma – Normal 12 – 21 mmHg pressure
- Increase IOP - Loss of peripheral vision – “tunnel vision”
2. Cataract – opacity of lens - Loss of central vision, “Blurring or hazy vision”
3. Retinal detachment – curtain veil – like vision & floaters
4. Macular degeneration – black spots
III, IV, VI – tested simultaneously
- Innervates the movementt of extrinsic ocular muscle
6 cardinal gaze EOM
Rt eye N left eye
IO SO O
S
LR MR E
SR
3 – 4 EOM
IV – sup oblique
VI – lateral rectus
Normal response – PERRLA (isocoria – equal pupil)
Anisocoria – unequal pupil
Oculomotor
1. Raising of eyelid – Ptosis
2. Controls pupil size 2 -3 cm or 1.5 – 2 mm
V – Trigeminal – Largest – consists of - ophthalmic, maxillary, mandibular
Sensory – controls sensation of the face, mucus membrane; teeth & cornea reflex
Unconscious – instill drop of saline solution
Motor – controls muscles of chewing/ muscles of mastication
Trigeminal neuralgia – diff chewing & swallowing – extreme food temp is not recommended
Question: Trigeminal neuralgia, RN should give
a. Hot milk, butter, raisins
b. Cereals
c. Gelatin, toast, potato – all correct but
d. Potato, salad, gelatin – salad easier to chew
VI Facial: Sensory – controls taste – ant 2/3 of tongue test cotton applicator put sugar.
-Put applicator with sugar to tip to tongue.
-Start of taste insensitivity: Age group – 40 yrs old
Motor- controls muscles of facial expression, smile frown, raise eyebrow
Damage – Bells palsy – facial paralysis
Cause – bells palsy pedia – R/T forcep delivery
Temporary only
Most evident clinical sign of facial symmetry: Nasolabial folds
VIII Acoustic/ vestibule cochlear (controls hearing) – controls balance (kenesthesia or position sense)
- Movement & orientation of body in space
- Organ of Corti – for hearing – true sense organ of hearing
Outer – tympanic membrane, pinna, oricle (impacted cerumen), cerumen
Middle – hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media
- Eustachean ear
Inner ear- meniere dse, sensory hearing loss (research parts! & dse)
Remove vestibule – meniere’s dse – disease inner ear
Archimedes law – buoyancy (pregnancy – fetus)
Daltons law – partial pressure of gases
Inertia – law of motion (dizziness, vertigo)
1.) Pt with multiple stab wound - chest
- Movement of air in & out of lungs is carried by what principle?
- Diffusion – Dalton’s law
2.) Pregnant – check up – ultrasound reveals fetus is carried by amniotic fluid
- Archimedes
3.) Severe vertigo due- Inertia
Test for acoustic nerve:
- Repeat words uttered
IX – Glossopharyngeal – controls taste – posterior 1/3 of tongue
X – Vagus – controls gag reflex
Test 9 – 10
Pt say ah – check uvula – should be midline
Damage cerebral hemisphere is L or R
Gag reflex – place tongue depression post part of tongue
▪ Don’t touch uvula
XI – Spinal Accessory - controls sternocleidomastoid (neck) & trapezius (shoulders and back)
- Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia
XII – Hypoglossal – controls movement of tongue – say “ah”. Assess tongue position=midline
L or R deviation
- Push tongue against cheek
- Short frenulum lingue –
Tongue tied – “bulol”
ENDOCRINE
Fx of endocrine – ductless gland
Main gland – Pituitary gland – located at base of brain of Stella Turcica
Master gland of body
Master clock of body
Anterior pituitary gland – adenohypophysis
Posterior pituitary gland – neurohypophysis
Posterior pituitary:
1.) Oxytocin – a.) Promotes uterine contraction preventing bleeding/ hemorrhage.
- Give after placental delivery to prevent uterine atony.
b.) Milk letdown reflex with help of prolactin.
2.) ADH – antidiuretic hormone – (vasopressin) -Prevents urination – conserve H2O
A. DIABETIS INSIPIDUS (DI- dalas ihi) – hyposecretion of ADH
Cause: idiopathic/ unknown
Predisposing factor:
1. Pituitary surgery
2. Trauma/ head injury
3. Tumor
4. Inflammation
* alcohol inhibits release of ADH
S & Sx:
1. Polyuria
2. Sx of dehydration (1st sx of dehydration in children-tachycardia)
- Excessive thirst (adult)
- Agitation
- Poor skin turgor
- Dry mucus membrane
3. Weakness & fatigue
4. Hypotension – if left untreated -
5. Hypovolemic shock
Anuria – late sign hypovolemic shock
Dx Proc:
1. Decrease urine specific gravity- concentrated urine
N= 1.015 – 1.035
2. Serum Na = increase (N=135 -145 meq/L) Hypernatremia
Mgt:
1. Force fluid 2,000 – 3,000ml/day
2. Administer IV fluid replacement as ordered
3. Monitor VS, I&O
4. Administer meds as ordered
a.) Pitresin (vasopressin) IM
5. Prevent complications
Most feared complication – Hypovolemic shock
B.) SIADH - Syndrome of Inappropriate Anti-Diuretic Hormone
- Increase ADH
- Idiopathic/ unknown
Predisposing factor
1. Head injury
2. Related to Bronchogenic cancer or lung caner-
Early Sign of Lung Ca - Cough –1. non productive 2. productive
3. Hyperplasia of Pit gland
Increase size of organ
S&Sx
1. Fluid retention
2. Increase BP – HPN
3. Edema
4. Wt gain
5. Danger of H2O intoxication –Complications: 1. cerebral edema – increase ICP – 2. seizure
Dx Proc:
1. Urine specific gravity increase – diluted urine
2. Hyponatremia – Decreased Na
Nsg Mgt:
1. Restrict fluid
2. Administer meds as ordered eg. Diuretics: Loop and Osmotic
3. Monitorstrictly V/S, I&O, neuro check – increase ICP
4. Weigh daily
5. Assess for presence edema
6. Provide meticulous skin care
7. Prevent complications – increase ICP & seizures activity
Anterior Pituitary Gland – adeno
1. Growth hormone (GH) (Somatotropic hormone)
Fx: Elongation of long bones
Decrease GH – dwarfism children
Increase GH – gigantism
Increase GH – acromegaly – adult
Puberty 9 yo – 21 yo
Epiphyseal plate closes at 21 yo
Square face
Square jaw
Drug of choice in acromegaly: Ocreotide (Sandostatin) SE dizziness
- Somatostatin Hormone – antagonizes the release of of GH
2. Melanocytes stimulating hormone - MSH
- Skin pigmentation
3. Prolactin/luteotrpic hormone/ lactogenic hormone - Promotes development of mammary gland
(Oxytocin-Initiates milk letdown reflex)
4. Adrenocorticotropic hormone – ACTH - Development & maturation of adrenal cortex
5. Luteinizing hormone – produces progesterone.
6. FSH- produces estrogen
PINEAL GLAND
1. Secretes Melatonin – inhibits lutenizing hormone (LH) secretion
THYROID GLAND (TG)
Question: Normal physical finding on TG:
a. With tenderness – thyroid never tender
b. With nodular consistency- answer
c. Marked asymmetry – only 1 TG
d. Palpable upon swallowing - Normal TG never palpable unless with goiter
TG hormones:
T3 T4 Thyrocalcitonin
- Triodothyronine -Tetraiodothyronine/ Tyroxine FX – antagonizes effects of parathormone
- 3 molecules of iodine - 4 molecules of iodine
Metabolic hormone
Increase metabolism brain –inc cerebration, inc v/s all v/s down, constipation
Hypo T3 T4 - lethargy & memory impairment –
Hyper T3 T4 - agitation, restlessness, and hallucination
7. Increase VS, increase motility
HYPOTHYROIDISM – all decreased except wt & menstruation, loss of appetite but with wt gain menorrhagia – increase in mens
HYPERTHYROIDISM - Increase appetite – wt loss, amenorrhea
SIMPLE GOITER – enlarged thyroid gland - iodine deficiency
Predisposing factors
1. Goiter belt area - Place far from sea – no iodine. Seafood’s rich in iodine
2. Mountainous area – increase intake of goitrogenic foods (US: Midwest, NE, Salt Lake)
Cabbage – has progoitrin – an anti thyroid agent with no iodine
Example: Turnips (singkamas), radish, peas, strawberries, potato, beans, kamote, cassava (root crops), all nuts.
3. Goitrogenic drugs:
Anti thyroid agents :(PTU) prephyl thiupil
Lithium carbonate, Aspirin PASA
Cobalt, Phenyl butasone
Endemic goiter – cause # 1
Sporadic goiter – caused by #2 & 3
S & Sx – enlarged TG
Mild restlessness
Mild dysphagia
Dx Proc.
1. Thyroid scan – reveals enlarged TG
2. Serum TSH – increase (confirmatory)
3. Serum T3, T4 – N or below N
Nsg Mgt:
1. Administer meds
a.) Iodine solution – Logol’s solution or saturated sol of K iodide SSKI
Nsg Mgt Lugol’s sol – violet color
1. use straw – prevent staining teeth
2. Prophylaxis 2 -3 drops Treatment – 5 to 6 drops
Use straw – to prevernt staining of teeth
1. Lugol’s sol., 2. tetracycline 3. nitrofurantin (macrodantin)-urinary anticeptic-pyelonephritis. 4. Iron solution.
B. Thyroid h / Agents
1. Levothyroxine (Synthroid)
2. Liothyronine (cytomel)
3. Thyroid extract
Nsg Mgt: for TH/agents
1. Monitor vs. – HR due tachycardia & palpitation
2. Take it early AM – SE insomnia
3. Monitor s/e
Tachycardia, palpitations
Signs of insomnia
Hyperthyroidism restlessness agitation
Heat intolerance
HPN
3. Encourage increase intake iodine – iodine is extracted from seaweeds (!)
Seafood- highest iodine content oysters, clams, crabs, lobster
Lowest iodine – shrimps
Iodized salt –easily destroyed by heat take it raw not cooked
4. Assist surgery- Sub total thyroidectomy-
Complication: 1. Tetany 2. laryngeal nerve damage 3.Hemorrhage-feeling of fullness at incision site.Check nape for wet blood. 4.Laryngeal spasm – DOB, SOB – trache set ready at bedside.
2.) HYPOTHYROIDISM – decrease secretion of T3, T4 – can lead to MI / Atherosclerosis
Adult – myxedema
Child- cretinism – only endocrine dis lead to mental retardation
Predisposing factor:
1. `Iatrogenic causes – caused by surgery
2. Atrophy of TG due to:
a. Irradiation
b. Trauma
c. Tumor, inflammation
3. Iodine def
4. Autoimmune – Hashimoto disease
S&Sx everything decreased except wt gain & mens increase)
Early signs – weakness and fatigue
Loss of appetite – increased lypolysis – breakdown of fats causing atherosclerosis = MI
Wt gain
Cold intolerance – myxedema - coma
Constipation
Late Sx – brittle hair/ nails
Non pitting edema due increase accumulation of mucopolysacharide in SQ tissue -Myxedema
Horseness voice
Decrease libido
Decrease VS – hypotension bradycardia, bradypnea, and hypothermia
Lethargy
Memory impairment leading to psychosis-forgetfulness
Menorrhagia
Dx:
1. Serum T3 T4 decrease
2. Serum cholesterol increase – can lead to MI
3. RA IU – radio iodine uptake – decrease
Nsg Mgt:
1. Monitor strictly V/S. I&O – to determine presence of myxedema coma!
Myxedema Coma - Severe form of hypothyroidism
Hypotension, hypoventilation, bradycardia, bradypnea, hyponatremia, hypoglycemia, hypothermia
Might lead to progressive stupor & coma
Impt mgt for Myxedema coma
1. Assist mech vent – priority a/w
2. Adm thyroid hormone
3. Adm IVF replacement – force fluid
Mgt myxedema coma
1. Monitor VS, I&O
2. Provide dietary intake low in calories – due to wt gain
3. Skin care due to dry skin
4. Comfortable & warm environment due to cold intolerance
5. Administer IVF replacements
6. Force fluid
7. Administer meds – take AM – SE insomia. Monitor HR.
Thyroid hormones
Levothyroxine(Synthroid), Liothyronine (cytomel)
Thyroid extracts
8. Health teaching & discharge plan
a. Avoidance precipitating factors leading to myxedema coma:
1. Exposure to cold environment
2. Stress 3. Infection
4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down
Complications:
9. Hypovolemic shock, myxedema coma
10. Hormonal replacement therapy - lifetime
11. Importance of follow up care
HYPERTHYROIDISM - Graves dse or thyrotoxicosis ( everything up except wt and mens)
-Increased T3 & T4
Predisposing factors:
1. Autoimmune disease – release of long acting thyroid stimulator (LATS)
Exopthalmos
Enopthalmos – severe dehydration depressed eye
2. Excessive iodine intake
3. Hyperplasia of TG
S&Sx:
1. Increase in appetite – hyperphagia – wt loss due to increase metabolism
2. Skin is moist - perspiration
3. Heat intolerance
4. Diarrhea – increase motility
5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia
6. CNS changes
8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations
7. Goiter
8. Exopthalmos – pathognomonic sx
9. Amenorrhea
Dx:
1. Serum T3 & T4 - increased
2. Radio iodine uptake – increase
3. Thyroid scan – reveals enlarged TG
Nsg Mgt:
1. Monitor VS & I & O – determine presence of thyroid storm or most feared complication: Thyrotoxicosis
2. Administer meds
a. Antithyroid agents
1. Prophylthiuracil (PTU)
2. Methymazole (Tapazole)
Most toxic s/e agranulocytosis- fever, sore throat, leukocytosis=inc wbc: check cbc and throat swab culture
Most feared complication : Thrombosis – stroke CVS
3. Diet – increase calorie – to correct wt loss
4. Skin care –
5. Comfy & cool environment
6. Maintain siderails- due agitation/restlessness
7. Provide bilateral eye patch – to prevent drying of eyes- exopthalmos
8. Assist in surgery – subtotal thyroidectomy
Nsg Mgt: pre-op
Adm Lugol’s solution (SSKI) K iodide
9. To decrease vascularity of TG
10. To prevent bleeding & hemorrhage
Mgt post op:
Complication: 1. Watch out for signs of thyroid storm or thyrotoxicosis
Triad signs of thyroidstorm;
a. Tachycardia /palpitation
b. Hyperthermia
c. Agitation
Nsg Mgt Thyroid Storm:
1. Monitor VS & neuro check
Agitated might decrease LOC
2. Antipyretic – fever
Tachycardia - ( blockers (-lol)
3. Siderails – agitated
Comp 2. Watch for inadvertent (accidental) removal of parathyroid gland
Secretes Para hormone
If removed, hypocalcemia - classic sign tetany – 1. .(+) Trousseau sign/ 2. Chvosteck’s sign
Nsg Mgt:
Adm calcium gluconate slowly – to prevent arrhythmia
Ca gluconate toxicity – antidote – MgSO4
3.Laryngeal (voice box) nerve damage (accidental)
Sx: hoarseness of voice
***Encourage pt to talk or speak post operatively asap to determine laryngeal nerve damage
Notify physician!
4. Signs of bleeding post subtotal thyroidectomy
- “Feeling of fullness” at incision site
Nsg mgt:
Check soiled dressing at nape area
5. Signs of laryngeal spasm
a. DOB
b. SOB
Prepare at bedside tracheostomy
6. Hormonal replacement therapy - lifetime
7. Importance of follow up care
(Liver cirrhosis – bedside scissor – if pt complaints of DOB)
(Cut cystachean tube to deflate balloon)
Parathyroid gland – pair of small nodules located behind the TG
11. Secrets parathyroid hormone – promotes Ca reabsorption
Thyrocalcitonin – antagonises secretion of parathyroid hormone
1. Hypoparthroidism – decrease of parathyroid hormone
2. Hyperparathroidsm
HYPOPARATHYROIDISM – decreased parathormone
Hypocalcemia Hyperphosphatemia
(Or tetany)
[If Ca decreases, phosphate increases]
A. Predisposing, factors:
1. Following subtotal thyroidectomy
2. Atrophy of parathyroid gland due to
a. Irradiation
b. Trauma
S&Sx:
1. Acute tetany
a. Tingling sensation
b. Paresthesia
c. Dysphagia
d. Laryngospasm
e. Bronchospasm
Pathognomonic Sign of tetany:
a. (+) Trousseau’s or carpopedial spasm
b. (+) Chvosteck’s sign
f. Seizure most feared complication
g. Arrhythmia
2. Chronic tetany
a. Loss of tooth enamel
b. Photophobia & cataract formation
c. GIT changes – anorexia, n/v, general body malaise
d. CNS changes – memory impairment, irritability
Dx:
1. Serum calcium – decrease (N 8.5 – 11 mg/100ml)
2. Serum phosphate increase (N 2.5 – 4.5 mg/100ml)
3. X-ray of long bone – decrease bone density
4. CT Scan – reveals degeneration of basal ganglia
Nsg Mgt:
1. Administration of meds:
a. Acute tetany –
Ca gluconate – IV, slowly
b. Chronic tetany
1. Oral Ca supplements
Ex. Ca gluconate
Ca carbonate
Ca lactate
Vit D (Cholecalceferol)
Drug diet sunlight
Cholecalceferol calcidiol calcitriol 7am – 9am
2. Phosphate binder
Alumminum DH gel (ampho gel)
SE constipation
Antacid
AAC MAD
Aluminum containing acids Mg containing antacids
Ex. Milk or magnesia
Aluminum OH gel Diarrhea
Constipation Maalox – magnesium & aluminum - Less s/e
2. Avoid precipitating stimulus such as bright lights & noise: photophobia leading to seizure
3. Diet – increase Ca & decrease phosphorus
- Don’t give milk – due to increase phosphorus
Good = anchovies – increase Ca, decrease phosphorus + inc uric acid. Tuna & green turnips- Inc Ca.
4. Bedside – tracheostomy set –due to laryngospasm
5. Encourage to breath with paper bag in order to produce mild respiratory acidosis – to promote increase ionized Ca levels
6. Most feared complication : Seizure & arrhythmia
7. Hormonal replacement therapy - lifetime
8. Important fallow up care
HYPERPARATHYROIDISM - increase parathormone. Complication: Renal failure
Hypercalcemia can lead to Hypophosphatemia
Bone dse - kidney stones
Mineralization
Leading to bone fracture
Ca – 99% bones
1% serum blood
Predisposing Factors:
1. Hyperplasia parathyroid gland (PTG)
2. Over compensation of PTG due to Vit D deficiency
Children – Rickets Vit D
Adults – Osteomalacia deficiency
Sippy’s diet – Vit D diet – not good for pt with ulcer
2 -4 cups of milk & butter
Karrel’s diet – Vit D diet – not good for pt with ulcer
6 cups of milk & whole cream
Food rich in CHON – eggnog – combination of egg & milk
S/Sx:
Bone fracture
1. Bone pain (especially at back), bone fracture
2. Kidney stone –
a. Renal colic
b. Cool moist skin
3. GIT changes – anorexia, n/v, ulcerations
4. CNS involvement– irritability, memory impairment
Dx Proc:
1. Serum Ca increase
2. Serum phosphorus decreases
3. X-ray long bones – reveals bone demineralization
Nsg Mgt: Kidney Stone
1. Force fluids – 2,000 – 3,000/day or 2-3L/day
2. Isotonic solution
3. Warm sitz bath – for comfort
4. Strain all urine with gauze pad
5. Acid ash diet – cranberry, plum, grapefruit, vit C, calamansi – to acidify urine
6. Adm meds
a. Narcotic analgesic – Morphine SO4, Demerol (Meperidine Hcl)
S/E – resp depression. Monitor RR)
Narcan/ Naloxone – antidote
Naloxone toxicity – tremors
7. Siderails
8. Assist in ambulation
9. Diet – low in Ca, increase phosphorus lean meat
10. Prevent complication
Most feared – renal failure
11. Assist surgical procedure – parathyroidectomy
12. Impt ff up care
13. Hormonal replacement- lifetime
ADRENAL GLAND
12. Atop of @ kidney
13. 2 parts
Adrenal cortex – outermost layer
Adrenal medulla - innermost layer
14. Secrets cathecolamines
a. Epinephrine / Norephinephrine – potent vasoconstrictor – adrenaline=Increase BP
Adrenal Medulla’s only disease:
PHEOCHROMOCYTOMA- presence of tumor at adrenal medulla
-increase nor/epinephrine
-with HPN and resistant to drugs
-drug of choice: beta blockers
-complication: HPN crisis = lead to stroke
-no valsalva maneuver
Adrenal Cortex –
1. Zona fasiculata – secrets glucocorticoids
Ex. Cortisol - Controls glucose metabolism (SUGAR)
2. Zona reticularis – secrets traces of glucocorticoids & androgenic hormones
M – testosterone
F – estrogen & progesterone
Fx – promotes development of secondary sexual characteristics
3. Zona glomerulosa - secretes mineralcortisone
Ex. Aldosterone
Fx: promotes Na & H2O reabsorption & excretion of potassium (SALT)
ADDISON’S DISEASE – Steroids-lifetime
Decreased adrenocortical hormones leading to:
a. Metabolic disturbances (sugar)
b. F&E imbalances- Na, H2O, K
c. Deficiency of neuromuscular function (salt & sex)
Predisposing Factors:
1. Atrophy of adrenal gland
2. Fungal infections
3. Tubercular infections
S/Sx:
1. Decrease sugar – Hypoglycemia – Decreased glucocorticoids - cortisol
T – tremors, tachycardia
I - irritability
R - restlessness
E – extreme fatigue
D – diaphoresis, depression
2. Decrease plasma cortisol
Decrease tolerance to stress – lead to Addisonian’s crisis
3. Decrease salt – Hyponatermia – Decreased mineralocorticoids - Aldosterone
Hypovolemia
a. Hypotension
b. Signs of dehydration – extreme thirst, agitation
c. Wt loss
4. Hyperkalemia
a. Irritability
b. Diarrhea
c. Arrhythmia
5. Decrease sexual urge or libido- Decreased Androgen
6. Loss of pubic and axillary hair
To Prevent STD Local – practice monogamous relationship
CGFNS/NCLEX – condom
7. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will stimulate pituitary gland to release melanocyte stimulating hormone.
Dx Proc:
1. FBS – decrease FBS (N 80 – 120 mg/dL)
2. Plasma cortisol – decreased
Serum Na – decreased (N 135 – 145 meg/L)
3. Serum K – increased (N 3.5 – 5.5 meg/L)
Nsg Mgt:
1. Monitor VS, I&O – to determine presence of Addisonian crisis
15. Complication of Addison’s dse : Addisonian crisis
16. Results the acute exacerbation of Addison’s dse characterized by :
Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia
17. Lead to progressive stupor & coma
Nsg Mgt Addisonian Crisis (Coma)
1. Assist in mechanical ventilation
2. Adm steroids
3. Force fluids
2. Administer meds
a.) Corticosteroids - (Decadron) or Dexamethazone
- Hydrocortisone (cortisone)- Prednisone
Nsg Mgt with Steroids
1. Adm 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.
2. Taper the dose (w/draw, gradually from drug) – sudden withdrawal can lead to addisonian crisis
3. Monitor S/E (Cushing’s syndrome S/Sx)
a. HPN
b. Hirsutism
c. Edema
d. Moon face & buffalo hump
e. Increase susceptibility to infection sue to steroids- reverse isolation
b.) Mineralocorticoids ex. Flourocortisone
3. Diet – increase calorie or CHO
Increase Na, Increase CHON, Decrease K
4. Force fluid
5. Administer isotonic fluid as ordered
6. Meticulous skin care – due to bronze like
7. HT & discharge planning
a) Avoid precipitating factors leading to Addisonian crisis
1. Sudden withdrawal crisis
2. Stress
3. Infection
b) Prevent complications
Addisonian crisis & Hypovolemic shock
8. Hormonal replacement therapy – lifetime
9. Important: follow up care
CUSHING’S SYNDROME – increase secretion of adrenocortical hormone
Predisposing Factors:
1. Hyperplasia of adrenal gland
2. Tubercular infection – milliary TB
S/Sx
1. Increase sugar – Hyperglycemia
3 P’s
1. Polyuria
2. Polydipsia – increase thirst
3. Polyphagia – increase appetite
Classic Sx of DM – 3 P’s & glycosuria + wt loss
2. Increase susceptibility to infection – due to increased corticosteroid
3. Hypernatrermia
a. HPN
b. Edema
c. Wt gain
d. Moon face
Buffalo hump
Obese trunk classic signs
Pendulous abdomen
Thin extremities
4. Hypokalemia
a. Weakness & fatigue
b. Constipation
c. ECG – (+) “U” wave
5. Hirsutism – increase sex
6. Acne & striae
7. Increase muscularity of female
Dx:
1. FBS – increase↑ (N: 80-120mg/dL)
2. Plasma cortisol increase
3. Na – increase (135-145 meq/L)
4. K- decrease (3.5-5.5 meq/L)
Nsg Mgt:
1. Monitor VS, I&O
2. Administer meds
a. K- sparing diuretics (Aldactone) Spironolactone
- promotes excretion of NA while conserving potassium
Not lasix due to S/E hypoK & Hyperglycemia!
3. Restrict Na
4. Provide Dietary intake – low in CHO, low in Na & fats
High in CHON & K
5. Weigh pt daily & assess presence of edema- measure abdominal girth- notify doc.
6. Reverse isolation
7. Skin care – due acne & striae
8. Prevent complication
- Most feared – arrhythmia & DM
(Endocrine disorder lead to MI – Hypothyroidism & DM)
9. Surgical bilateral Adrenolectomy
10. Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!
PANCREAS – behind the stomach, mixed gland – both endocrine and exocrine gland
Acinar cells (exocrine gland) Islets of Langerhans (endocrine gland ductless)
Secrete pancreatic juices at pancreatic ducts. ( cells
Aids in digestion (in stomach) secrets glucagon
Fxn: hyperglycemia (high glucose)
( Cells
Secrets insulin
Fxn: hypoglycemia
Delta Cells
Secrets somatostatin
Fxn: antagonizes growth hormone
3 disorders of the Pancreas
1. DM
2. Pancreatic Cancer
3. Pancreatitis
Overview only:
PANCREATITIS (check page 72)– acute inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to
Autodigestion – self-digestion
Cause: unknown/idiopathic
18. Or alcoholism
Pathognomonic sign- (+) Cullen’s sign - Ecchymosis of umbilicus (bluish color)- pasa
(+) Grey turner’s sign – ecchymosis of flank area
Both sx means hemorrhage
CHRONIC HEMORRHAGIC PANCREATITIS- “bangugot”
Predisposing factors - unknown
Risk factor:
1. History of hepatobiliary disorder
2. Alcohol
3. Drugs – thiazide diuretics, oral contraceptives, aspirin, penthan
4. Obesity
5. Hyperlipidemia
6. Hyperthyroidism
7. High intake of fatty food – saturated fats
DIABETES MELLITUS - metabolic disorder characterized by non utilization of CHO, CHON,& fat metabolism
Classification:
I. Type I DM (IDDM) – “Juvenile “ onset, common in children, non-obese “brittle dse”
-Insulin dependent diabetes mellitus
Incidence rate
1. 10% of population with DM have Type I
Predisposing Factor:
1. 90% hereditary – total destruction of pancreatic dells
2. Virus
3. Toxicity to carbon tetrachloride
4. Drugs – Steroids both cause hyperglycemia
Lasix - loop diuretics
S/Sx:
3 P’S + G
1.) Polyuria
2.) Poydipsia
3.) Polyphagia
4.) Glycosuria
5.) Weight loss
6.) Anorexia
7.) N/V
8.) Blurring of vision
9.) Increase susceptibility to infection
10.) Delayed/ poor wound healing
Mgt:
1. Insulin Therapy
Diet
Exercise
Complications – Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis (DKA) – due to increase fat catabolism or breakdown of fats
DKA –(+) fruity or acetone breath odor
Kassmaul’s respiration – rapid, shallow breathing
Diabetic coma (needs oxygen)
II. Type II DM – (NIDDM)
Adult/ maturity onset type – age 40 & above, obese
Incidence Rate
1. 90% of pop with DM have Type II
Mid 1980’s marked increase in type II because of increase proliferation of fast food chains!
Predisposing Factor:
1. Obesity – obese people lack insulin receptors binding site
2. Hereditary
S/Sx:
1. Asymptomatic
2. 3 P’s and 1G
Tx:
1. Oral Hypoglycemic Agents (OHA)
2. Diet
3. Exercise
Complication: HONKC
H – hyper
O – osmolar
N – non
K – ketotic
C – coma
III. GESTATIONAL DM – occurs during pregnancy & terminates upon delivery of child
Predisposing Factors:
1. Unknown/ idiopathic
2. Influence of maternal hormones
S/Sx :
Same as type II –
1. Asymptomatic
2. 3 P’s & 1G
Type of delivery – CS – due to large baby
Sx of hypoglycemia on infant
1. High pitched shrill cry
2. Poor sucking reflex
IV. DM ASSOCIATED WITH OTHER DISORDER
a. Pancreatic tumor
b. Cancer
c. Cushing’s syndrome
3 MAIN FOOD GROUPS
Anabolism Catabolism
1. CHON glucose glycogen
2. CHON amino acids nitrogen
3. Fats fatty acids free fatty acids (FFA) – Cholesterol & Ketones
Pancreas → glucose → ATP (Main fuel/energy of cell )
Reserve glucose – glycogen
Liver will undergo – glucogenesis – synthesis of glucagons
& Glycogenolysis – breakdown of glucagons
& Gluconeogenesis – formation of glucose form CHO sources – CHON & fats
Hyperglycemia – pancreas will not release insulin. Glucose can’t go to cell, stays at circulation causing hyperglycemia.
increase osmotic diuresis – glycosuria
Lead to cellular starvation
Lead to wt loss stimulates the appetite/ satiety center polyuria
(Hypothalamus)
Cellular dehydration
Polyphagia
Stimulates thirst center (hypothalamus)
Polydipsia
Increased CHON catabolism
Lead to (-) nitrogen balance
Tissue wasting (cachexia)
Increase fat catabolism
Free fatty acids
Cholesterol ketones DKA
Atherosclerosis coma
HPN death
MI stroke
DIABETIC KETOACIDOSIS (DKA)
- Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Coma.
- Ketones- a CNS depressant
Predisposing factor:
1. Stress – between stress and infection, stress causes DKA more.
2. Hyperglycemia
3. Infection
S/Sx: 3 P’s & 1G
1. Polyuria
2. Polydipsia
3. Polyphagia
4. Glycosuria
5. Wt loss
6. Anorexia, N/V
7. (+) Acetone breath odor- fruity odor pathognomonic DKA
8. Kussmaul's resp-rapid shallow respiration
9. CNS depression
10. Coma
Dx Proc:
1. FBS increase, Hct – increase (compensate due to dehydration)
N =BUN – 10 -20 mg/100ml --increased due to severe dehydration
Crea - .8 – 1 mg/100ml
Hct 42% (should be 3x high)-nto hgb
Nsg Mgt:
1. Can lead to coma – assist mechanical ventilation
2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3. Monitor VS, I&O, blood sugar levels
4. Administer meds as ordered:
a. Insulin therapy – IV push
Regular Acting Insulin – clear (2-4hrs, peak action)
b. To counteract acidosis – Na HCO3
c. Antibiotic to prevent infection
Insulin Therapy
A. Sources:
1. Animal source – beef/ pork-rarely used. Causes severe allergic reaction.
2. Human – has less antigenecity property
Cause less allergic reaction. Humulin
If kid is allergic to chicken – don’t give measles vaccine due it comes from chicken embryo.
3. Artificially compound
B. Types of Insulin
1. Rapid Acting Insulin - Ex. Regular acting I
2. Intermediate acting I - Ex. NPH (non-protamine Hagedorn I)
3. Long acting I - Ex. Ultra lente
Types of Insulin color & consistency onset peak duration
1. Rapid clear - 2-4h -
2. Intermediate cloudy - 6-12h -
3. Long acting cloudy - 12-24h -
Ex. 5am Hemoglucose test (HGT)
250 mg/dl
Adm 5 units of RA I
Peak 7-9am – monitor hypoglycemic reaction at this time- TIRED
Nsg Mgt: upon injection of insulin:
1.Administer insulin at room temp! – To prevent lipodystrophy = atrophy/ hypertrophy of SQ tissues
2. Insulin is only refrigerated once opened!
3. Gently roll vial bet palms. Avoid shaking to prevent formation of bubbles.
4. Use gauge 25 – 26needle – tuberculin syringe
5. Administer insulin at either 45(for skinny pt) or 90( (taba pt)depending on the client tissue deposit.
6. Don’t aspirate after injection
7. Rotate injection site to prevent lipodystrophy
8. Most accessible site – abdomen
9. When mixing 2 types of insulin, aspirate
1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration.
10. Monitor signs of complications:
a. Allergic reactions – lipodystrophy
b. Somogyi’s phenomenon – hypoglycemia followed by periods of hyperglycemia or rebound effect of insulin.
11. 1ml or cc of tuberculin = 100 units of insulin
- - 1 cc = 100 units
- - .5cc = 50 units
- - .1 cc = 10 units
6 units RA
Most Feared Complication of Type II DM
Hyper ↑ osmolarity = severe dehydration
Osmolar
Non - absence of lipolysis
Ketotic - no ketone formation
Coma – S/Sx: headache, restlessness, seizure, decrease LOC = coma
Nsg Mgt; - same as DKA except don’t give NaHCO3!
1.Can lead to coma – assist mechanical ventilation
2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3.Monitor VS, I&O, blood sugar levels
4.Administer meds
a. Insulin therapy – IV
b. Antibiotic to prevent infection
Tx:
O ral
H ypoglycemic
A gents
19. Stimulates pancreas to secrete insulin
Classifications of OHA
1. First generation Sulfonylurear
a. Chlorpropamide (diabenase)
b. Tolbutamide (orinase)
c. Tolazamide (tolinase)
2. 2nd generation sulfonylurear
a. Diabeta (Micronase)
b. Glipside (Glucotrol)
Nsg Mgt or OHA
1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia
2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction=CNS depression=coma) Antabuse-Disufram
Dx for DM
1. FBS – N 80 – 120 mg/dl = Increased for 3 consecutive times =confirms DM!!
+ 3 P’s & 1G
2. Oral glucose tolerance (OGTT) - Most sensitive test
3. Random blood sugar – increased
4. Alpha Glucosylated Hgb – elevated
Nsg Mgt;
1. Monitor for PEAK action of OHA & insulin
Notify Doc
2. Monitor VS, I&O, neurocheck, blood sugar levels.
3. Administer insulin & OHA therapy as ordered.
4. Monitor signs of hyper & hypoglycemia.
Pt DM –“ hinimatay”
20. You don’t know if hypo or hyperglycemia.
Give simple sugar
(Brain can tolerate high sugar, but brain can’t tolerate low sugar!)
Cold, clammy skin – hypo – Orange Juice or simple sugar / warm to touch – hyper – adm insulin
5. Provide nutritional intake of diabetic diet:
CHO – 50%
CHON – 30%
Fats – 20%
-Or offer alternative food products or beverage.
-Glass of orange juice.
6. Exercise – after meals when blood glucose is rising.
7. Monitor complications of DM
a. Atherosclerosis – HPN, MI, CVA
b. Microangiopathy – small blood vessels
Eyes – diabetic retinopathy , premature cataract & blindness
Kidneys – recurrent pyelonephritis & Renal Failure
(2 common causes of Renal Failure : DM & HPN)
c. Gangrene formation
d. Peripheral neuropathy
1. Diarrhea/ constipation
2. Sexual impotence
e. Shock due to cellular dehydration
8. Foot care mgt
a. Avoid waking barefooted
b. Cut toe nails straight
c. Apply lanolin lotion – prevent skin breakdown
d. Avoid wearing constrictive garments
9. Annual eye & kidney exam
10. Monitor urinalysis for presence of ketones
Blood or serum – more accurate
11. Assist in surgical wound debridement
12. Monitor signs or DKA & HONKC
13. Assist surgical procedure
BKA or above knee amputation
Overview: HEMATOLOGICAL SYSTEMS
I Blood
II Blood vessels
III Blood forming organs
1. Thymus – removed myasthenia gravis
2. Liver – largest gland
3. Lymph nodes
4. Lymphoid organs – payers patch
5. Bone marrow
6. Spleen – destroys RBC
Blood vessels
1. Veins –SVC, IVC, Jugular vein – blood towards the heart
2. Artery – carries blood away from the
21. Aorta, carotid
3. Capillaries
Blood 45% formed elements – 55% plasma – fluid portion of vlood. Yellow color.
Serum Plasma CHON’s (Produced in Liver)
1. Albumin- largest, most abundant plasma
Maintains osmotic pressure preventing edema
FXN: promotes skin integrity
2. Globulins – alpha – transports steroids Hormones & bilirubin
( - Transports iron & copper
Gamma – transport immunoglobulins or antibodies
3. Prothrombin – fibrinogen – clotting factor to prevent bleeding
Formed Elements:
1. RBC (erythrocytes) Spleen life span = 120 days
(N) 3 – 6 M/mm3
- Anucleated
- Biconcave discs
- Has molecules of Hgb (red cell pigment)
Transports & carries O2
SICKLE CELL ANEMIA –sickle shaped RBC. Should be round. Impaired circulation of RBC.
-immature cells=hemolysis of RBC=decreased hgb
3 Nsg priority
1. a/w – avoid deoxygenating activities
- High altitude is bad
2. Fluid deficit – promote hydration
3. Pain & comfort
Hgb ( hemoglobin)
F= 12 – 14 gms %
M = 14-16 gms %
Hct – 3x hgb 12 x 3 = 36
(hamatocrit) F 36 – 42% 14 x 3 = 42
M 42 – 48%
Average 42%
- Red cell percentage in whole red
Substances needed for maturation of RBC
a. Folic acid
b. Iron
c. Vit C
d. Vit B12 (cyanocobalamin)
e. Vit B6 (Pyridoxine)
f. Intrinsic factor
Pregnant: 1st trimester- Folic acid – prevent neural tube deficit
3rd tri – iron
Life span of rbc – 80 – 120 days. Destroyed at spleen.
WBC – leucocytes 5,000 – 10,000/mm3
|GRANULOCYTES |NON-GRANULOCYTES |
|1. Polymorphonuclearneutrophils |1. Monocytes (macrophage) - largest WBC |
|Most abundant 60-70% WBC |- involved in long term phagocytes |
|- fx – short term phagocytosis |- For chronic inflammation |
|For acute inflammation |- Other name macrophage |
| | |
|2. PM Basophils |Macrophage in CNS- microglia |
| |Macrophage in skin – Histiocytes |
|-Involved in Parasitic infection |Macrophage in lungs – alveolar macrophage |
|- Release of chem. Mediator for inflammation |Macrophage in Kidneys – Kupffer cells |
|Serotonin, histamine, prostaglandin, bradykinins | |
| |2. Lymphocytes |
|3. PM eosinophils |B Cell – L – bone marrow or bursa dependent |
|- Allergic reactions |T cell – dev’t of immunity- target site for HIV |
| |NK cell – natural killer cell |
| |Have both antiviral & anti-tumor properties |
| | |
| |3.Platelets (thrombocytes) |
| |N- 150,000 – 450, 000/ mm3 |
| |it promotes hemostasis – prevention of blood loss by activating clotting |
| |- Consists of immature or baby platelets known as megakaryocytes – target of virus – dengue |
| |- Normal lifespan 9 – 12 days |
Drug of choice for HIV Zidovudine (AZT or Retrovir)
Standard precaution for HIV gloves, gown, goggles & mask
Malaria – night biting mosquito
Dengue – day biting mosquito
Signs of platelet dis function:
a. Petecchiae
b. Ecchemosis/ bruises
c. Oozing or blood from venipuncture site
ANEMIA
Iron deficiency Anemia – chronic normocytic, hypocromic (pale), microcytic anemia due to inadequate absorption of iron leading to hypoxemic injury.
Incidence rate:
1. Common – developed country – due to high cereal intake
Due to accidents – common on adults
2. Common – tropical countries – blood sucking parasites
3. Women – 15 – 35yo – reproductive yrs
4. Common among the poor – poor nutritional intake
Suicide - common in teenager
Poisoning – common in children (aspirin)
Aspiration – common in infant
Accidents – common in adults
Choking – common in toddler
SIDS – common in infant in US
22. Common in tropical zone – Phil due blood sucks
Predisposing factor:
1. Chronic blood loss
a. Trauma
b. Mens
c. GIT bleeding:
i. Hematemesis-
ii. Melena – upper GIT – duodenal cancer
iii. Hematochezia – lower GIT – large intestine – fresh blood from rectum
2. Inadequate intake of food rich in iron
3. Inadequate absorption of iron – due to :
a. Chronic diarrhea
b. Malabsorption syndrome –celiac disease-gluten free diet. Food for celiac pts- sardines
c. High cereal intake with low animal CHON ingestion
d. Subtotal gastrectomy
4. Improper cooking of food
S/Sx:
1. Asymptomatic
2. Headache, dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor
3. Brittle hair, spoon shaped nails (KOILONYCHIA)=Dec O2=hypoxia=atrophy of epidermal cells
4. Atropic glossitis, dysphagia, stomatitis
5. Pica – abnormal craving for non edible food (caused by hypoxia=dec tissue perfusion=psychotic behavior)
Brittle hair, spoon shaped nail – atrophy of epidermal cells
N = capillary refill time < 2 secs
N = shape nails – biconcave shape, 180(
Atrophy of cells “Plummer Vinsons Syndrome” due to cerebral hypoxia
1. Atropic glossiti – inflammation of tongue due to atrophy of pharyngeal and tongue cells
2. Stomatitis – mouth sores
3. Dysphagia
Dx Proc:
1. RBC
2. Hgb
3. Reticulocyte
4. Hct
5. Iron
6. Ferritin
Nsg Mgt
1. Monitor signs of bleeding of all hema test including urine & stool
2. Complete bed rest – don’t overtire pt =weakness and fatigue=activity intolerance
3. Encourage – iron rich food
23. Raisins, legumes, egg yolk
4. Instruct the pt to avoid taking tea - impairs iron absorption
5. Administer meds
a. Oral iron preparation
Ferrous SO4
Fe gluconate
Fe Fumarate
Nsg Mgt oral iron meds:
1. Administer with meals – to lessen GIT irritation
2. If diluting in iron liquid prep –adm with straw
Straw
1. Lugol’s
2. Tetracycline
3. Oral iron
4. Macrodantine
3. Give Orange juice – for iron absorption
4. Monitor & inform pts S/E
a. Anorexia
b. n/v
c. Abdominal pain
d. Diarrhea or constipation
e. Melena
If pt can’t tolerate oral iron prep – administer parenteral iron prep example:
1. Iron dextran (IV, IM)
2. Sorbitex (IM)
Nsg Mgt parenteral iron prep
1. Administer of use Z tract method to prevent discomfort, discoloration leakage to tissues.
2. Don’t massage injection site. Ambulate to facilitate absorption.
3. Monitor S/E:
a. Pain at injury site
b. Localized abscess (“nana”)
c. Lymphadenopathy
d. Fever/ chills
e. Urticaria – itchiness
f. Hypotension – anaphylactic shock
Anaphylactic shock – give epinephrine
PERNICIOUS ANEMIA - megaloblastic, chronic anemia due to deficiency of intrinsic factor leading to
Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement.
Predisposing factor
1. Subtotal gastrectomy – removal stomach
2. Hereditary
3. Infl dse of ileum
4. Autoimmune
5. Strict vegetable diet
STOMACH
Parietal or ergentaffen Oxyntic cells
Fxn – produce intrinsic factor Fxn – secrets Hcl acid
For reabsorption of B12 Fx aids in digestion
For maturation of RBC
Diet high caloric or CHO to correct wt loss
S/Sx:
1. Headache dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor
2. GIT changes
a. Red – beefy tongue – PATHOGNOMONIC – mouth sores
b. Dyspepsia – indigestion
c. Wt loss
d. Jaundice
3. CNS –
Most dangerous anemia: pernicious due to neuroglogic involvement.
a. Tingling sensation
b. Paresthesia
c. (+) Romberg’s test
Ataxia
d. Psychosis
Dx:- Shilling’s test
Nsg Mgt – Pernicious anemia
1. Enforce CBR
2. Administer B12 injections at monthly intervals for lifetime as ordered. IM- dorsogluteal or ventrogluteal. Not given oral – due pt might have tolerance to drug
3. Diet – high calorie or CHO. Increase CHON, iron & Vit C
4. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged.
5. Avoid applying electric heating pads – can lead to burns
APLASTIC ANEMIA – stem cell disorder due to bone marrow depression leading to pancytopenia – all RBC are decreased
Decrease RBC decrease WBC decrease platelets
Anemia leukopenia thrombocytopenia
Increase WBC leukocytocys
Increase RBC polycythemia vera – complication stroke, CVA, thrombosis
Predisposing factors leading to Aplastic Anemia
1. Chemicals – Banzene & its derivatives
2. radiation
3. Immunologic injury
4. Drugs – cause bone marrow depression
a. Broad spectrum antibiotic - Chlorampenicol
- Sulfonamides – bactrim
b. Chemo therapeutic agents
Methotrexate – alkylating agents
Nitrogen mustard – anti metabolic
Vincristine – plant alkaloid
S/Sx:
1. Anemia:
a. Weakness & fatigue
b. Headache, dizziness, dyspnea
c. cold sensitivity, pallor
d. palpitations
2. Leucopenia – increase susceptibility to infection
3. Thrombocytopenia –
a. Peticchiae
b. Oozing ofblood from venipuncture site
c. ecchymosis
Dx:
1. CBC – pancytopenia
2. Bone marrow biopsy/ aspiration at post iliac crest – reveals fatty streaks in bone marrow
Nsg Mgt:
1. Removal of underlying cause
2. Blood transfusion as ordered
3. Complete bed rest
4. O2 inhalation
5. Reverse isolation due leukopenia
6. Monitor signs of infection
7. Avoid SQ, IM or any venipuncture site = HEPLOCK
8. Use electric razor when shaving to prevent bleeding
9. Administer meds
Immunosuppresants
Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days – 3 weeks to achieve max therapeutic effect of drug.
BLOOD TRANSFUSION:
Objectives:
1. To replace circulating blood volume
2. To increase O2 carrying capacity of blood
3. To combat infection if there’s decrease WBC
4. To prevent bleeding if there’s platelet deficiency
Nsg Mgt & principles in Blood Transfusion
1. Proper refrigeration
2. Proper typing & crossmatching
Type O – universal donor
AB – universal recipient
85% of people is RH (+)
3. Asceptically assemble all materials needed:
a. Filter set
b. Isotonic or PNSS or .9NaCl to prevent Hemolysis
Hypotonic sol – swell or burst
Hypertonic sol – will shrink or crenate
c. Needle gauge 18 - 19 or large bore needle to prevent hemolysis.
d. Instruct another RN to recheck the following .
Pts name, blood typing & cross typing expiration date, serial number.
e.) Check blood unit for presence of bubbles, cloudiness, dark in color & sediments – indicates bacterial contamination. Don’t dispose. Return to blood bank.
f.) Never warm blood products – may destroy vital factors in blood.
- Warming is done if with warming device – only in EMERGENCY! For multiple BT.
- Within 30 mins room temp only!
g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood deterioration.
h.) Avoid mixing or administering drug at BT line – leads to hemolysis
i.) Regulate BT 10 – 15 gtts/min KVO or 100cc/hr to prevent circulatory overload
j.) Monitor VS before, during & after BT especially q15 mins(local board) for 1st hour. NCLEX-q5min for 1st 15min.
- Majority of BT reaction occurs within 1h.
BT reactions S/Sx Hemolytic reaction:
H – hemolytic Reaction 1. Headache, dizziness, dyspnea, palpitation, lumbar/ sterna/ flank pain,
A – allergic Reaction hypotension, flushed skin , (red) port wine urine.
P – pyrogenic Reaction
C – circulatory overload
A – air embolism
T - thrombocytopenia
C – citrate intoxication – expired blood =hyperkalemia
H – hyperkalemia
Nsg Mgt: Hemolytic Reaction:
1. Stop BT
2. Notify Doc
3. Flush with plain NSS
4. Administer isotonic fluid sol – to prevent acute tubular necrosis & conteract shock
5. Send blood unit to blood bank for reexamination
6. Obtain urine & blood samples of pt & send to lab for reexamination
7. Monitor VS & Allergic Rxn
Allergic Reaction:
S/Sx
1. Fever/ chills
2. Urticaria/ pruritus
3. Dyspnea
4. Laryngospasm/ bronchospasm
5. Bronchial wheezing
Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antihistamine – diphenhydramine Hcl (Benadryl). Give bedtime.SE-Adult-drowsiness. Child-hyperactive
If (+) Hypotension – anaphylactic shock administer – epinephrine
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Adm. Antihistamine as ordered for AllergicRxn, if (+) to hypotension – indicates anaphylactic shock
24. administer epinephrine
9. Adm antipyretic & antibiotic for pyrogenic Rxn & TSB
Pyrogenic Reaction:
S/Sx
a. Fever/ chills d. tachycardia
b. Headache e. palpitations
c. Dyspnea f. diaphoresis
Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antipyretics, antibiotics
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Tepid sponge bath – offer hypothermic blanket
Circulatory Overload:
Sx
a. Dyspnea
b. Orthopnea
c. Rales or crackles
d. Exertional discomfort
Nsg Mgt:
1. Stop BT
2. Notify Doc. Don’t flush due pt has circulatory overload.
3. Administer diuretics
Priority cases:
Hemolytic Rxn – 1st due to hypotension – 1st priority – attend to destruction of Hgb – O2 brain damage
Allergic 3rd
Pyrogenic 4th
Circulatory 2nd
Hemolytic 2nd
Anaphylitic 1st priority
DIC – DISSEMINATED INTRAVASCULAR COAGULATION
25. Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a def of clotting factors (Prothrombin & Fibrinogen).
Predisposing factor:
1. Rapid BT
2. Massive trauma
3. Massive burns
4. Septicemia
5. Hemolytic reaction
6. Anaphylaxis
7. Neoplasia – growth of new tissue
8. Pregnancy
S/Sx
1. Petechiae – widespread & systemic (lungs, lower & upper trunk)
2. Ecchymosis – widespread
3. Oozing of blood from venipunctured site
4. Hemoptysis – cough blood
5. Hemorrhage
6. Oliguria – late sx
Dx Proc–
1. CBC – reveals decrease platelets
2. Stool for occult blood (+)
Specimen – stool
3. Opthalmoscopic exam – sub retinal hemorrhage
4. ABG analysis – metabolic acidosis
pH HCO3
R pH PCO2 respiratory alkalosis
O ph PCO2 respiratory acidosis
M ph HCO3 metabolic alkalosis
E ph HCO3 metabolic acidosis
Diarrhea – met acidosis
Vomitting – met alk
Pyloric stenosis – met alkalosis – vomiting
Ileostomy or intestinal tubing – met acidosis
Cushing’s – met alk
DM met acid
Chronic bronchitis – resp acid – with hypoxemia, cyanosis
Nsg Mgt DIC
1. Monitor signs of bleeding – hema test + urine, stool, GIT
2. Administer isotonic fluid solution to prevent shock.
3. Administer O2 inhalation
4. Administer meds
a. Vit K aquamephyton
b. Pitressin or vasopressin – to conserve water.
5. NGT – lavage
- Use iced saline lavage
6. Monitor NGT output
7. Provide heplock
8. Prevent complication: hypovolemic shock
Late signs of hypovolemic shock : anuria
Oncologic Nsg:
Oncology – study of neoplasia –new growth
Benign (tumor) Malignancy (cancer)
Diff - well differentiated poorly or undifferentiated
Encapulation – (+) (-)
Metastasis – (-) (+)
Prognosis – good poor
Therapeutic modality surgery 1. Chemotherapy plenty S/E
2. Radiation
3. Surgery most preferred treatment
4. Bone marrow transplant - Leukemia only
Predisposing factors: (carcinogenesis)
G – genetic factors
I – immunologic factors
V – viral factors
a. Human papiloma virus – causing warts
b. Epstein barr virus
E – environmental Factors 90%
a. Physical – irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma
b. Chemical factors –
- Food additives (nitrates
- Hydrocarbon vesicants, alkalies
- Drugs (stillbestrol)
- Uraehane
- Hormones
- Smoking
Male
3.) Prostate cancer - common 40 & above (middle age & above)
BPH – 50 & above
1.) Lung cancer
2.) Liver cancer
Female
1. Breast cancer – 40 yrs old & up – mammography 15 – 20 mins (SBE – 7 days after mens)
2. Cervical cancer – 90% multi sexual partners
5% early pregnancy
3. Ovarian cancer
Classes of cancer
Tissue typing
1. Carcinoma – arises from surface epithelium & glandular tissues
2. Sarcoma- from connective tissue or bones
3. Multiple myeloma – from bone marrow
Pathological fracture of ribs & back pain
4. Lymphoma – from lymph glands
5. Leukemia – from blood
Warning / Danger Sx of CA
C – change in bowel /bladder habits
A – a sore that doesn’t heal
U – unusual bleeding/ Discharge
T – thickening of lump – breast or elsewhere
I – indigestion? Dysphagia
O – obvious change in wart/ mole
N – nagging cough/ hoarseness
U – unexplained anemia A - anemia
S – sudden wt loss L – loss of wt
Therapeutic Modality:
1. Chemotherapy – use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells – GIT, bone marrow, and hair follicle.
Classification:
a. Alkylating agents –
b. Plant alkaloids – vincristine
c. Anti metabolites – nitrogen mustard
d. Hormones – DES
Steroids
e. Antineoplastic antibiotics
S/E & mgt
GIT - -Nausea & vomiting
Nsg Mgt:
1. Administer anti emetic 4 – 6h before start of chemo
Plasil
2. Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
26. Non irritating / non spicy
- Diarrhea
1. Administer anti diarrheal 4 – 6h before start of chemo
2. Monitor urine, I&O qh
- Stomatitis/ mouth sores
1. Oral care – offer ice chips/ popsickles
2. Inform pt – hair loss – temporary alopecia
Hair will grow back after 4 – 6 months post chemo.
-Bone marrow depression – anemia
1. Enforce CBR
2. O2 inhalation
3. Reverse isolation
4. Monitor signs of bleeding
Repro organ – sterility
1. Do sperm banking before start of chemo
Renal system – increase uric acid
1. Administer allopurinol/ xyloprin (gout)
27. Inhibits uric acid
28. Acute gout – colchicines
29. Increase secretion of uric acid
Neurological changes – peristalsis – paralytic ileus
Most feared complication ff any abdominal surgery
Vincristine – plant alkaloid causes peripheral neuropathy
2. Radiation therapy – involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill N rapidly producing cells.
Types of energy emitted
1. Alpha rays – rarely used – doesn’t penetrate skin tissues
2. Beta rays – internal radiation – more penetration
3. Gamma ray – external radiation – penetrates deeper underlying tissues
Methods of delivery
1. External radiation- involves electro magnetic waves
Ex. cobalt therapy
2. Internal radiation – injection/ implantation of radioisotopes proximal to CA site for a specific period of time.
2 types:
a.) Sealed implant – radioisotope with a container & doesn’t contaminate body fluid.
b.) Unsealed implant – radioisotope without a container & contaminates body fluid.
Ex. Phosphorus 32
3 Factors affecting exposure:
A.) Half life – time period required for half of radioisotopes to decay.
- At end of half life – less exposure
B.) Distance – the farther the distance – lesser exposure
C. ) Time – the shorter the time, the lesser exposure
D.) Shielding – rays can be shielded or blocked by using rubber gloves – ( & ( gamma – use thick lead on concrete.
S/E & Mgt:
a. Skin errythema, redness, sloughing
1. Assist in battling pt
2. Force fluid – 2,000 – 3,000 ml/day
3. Avoid lotion or talcum powder – skin irritation
4. Apply cornstarch or olive oil
b.) GIT –nausea / vomiting -
1. Administer antiemetic 4 – 6h before start of chemo - Plasil
2 Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
Non irritating / non spicy
Dysglusia – decrease taste sensitivity
-When atrophy papilla (taste buds) – 40 yo
Stomatitis
c.) Bone marrow depression
1. Enforce CBR
2. O2 inhalation
3. Reverse isolation
4. Monitor signs of bleeding
Overview of function & structure of the heart
HEART
- Muscular, pumping organ of the body
- Left mediastinum
- Weigh 300 – 400 grams
- Resembles a closed fist
- Covered by serous membrane – pericardium
Pericardium
Parietal layer Pericardial Visceral layer
Fluid – prevent
Friction rub
Layer
1. Epicardium – outermost
2. Myocardium – inner – responsible for pumping action/ most dangerous layer - cardiogenic shock
3. Endocardium – innermost layer
Chambers
1. Upper – collecting/ receiving chamber - Atria
2. Lower – pumping/ contracting chamber - Ventricles
Valves
1. Atrioventricular valves - Tricuspid & mitral valve
Closure of AV valves – gives rise to 1st heart sound or S1 or “lub”
2. Semi lunar valve
a. Pulmonic
b. Aortic
Closure of semilunar valve – gives rise to 2nd heart sound or S2 or “dub”
Extra heart Sound
S3 – ventricular Gallop – CHF
S4 – atrial gallop – MI, HPN
Heart conduction system
1. Sino atrial node (SA node) (or Keith-Flock node)
Loc – junction of SVC & Rt atrium
Fx- primary pace maker of heart
-Initiates electric impulse of 60 – 100 bpm
2. Atrioventicular node (AV node or Tawara node)
Loc – inter atrial septum
Delay of electric impulse to allow ventricular filling
3. Bundle of His – location interventricular septum
Rt main Bundle Branch
Lt main Bundle Branch
4. Purkenjie Fiber
Loc- walls of ventricles-- Ventricular contractions
SA node
Purkenjie Fibers
Bundle of His
Complete heart block – insertion of pacemaker at Bundle Branch
Metal – Pace Maker – change q3 – 5 yo
Prolonged PR – atrial fib T wave inversion – MI
ST segment depression – angina widening QRS – arrhythmia
ST – elev – MI
CAD – coronary artery dse or Ischemic Heart Dse (IHD)
Atherosclerosis – Myocrdial injury
Angina Pectoris – Myocardial ischemia
MI- myocardial necrosis
|ATHEROSCLEROSIS |ARTEROSCLEROSIS |
|- Hardening or artery due to fat/ lipid deposits at tunica intima. |- Narrowing or artery due to calcium & CHON deposits at tunica media. |
Artery – tunica adventitia – outer
- Tunica intima – innermost
- Tunica media – middle
ATHEROSCLEROSIS
Predisposing Factor
1. Sex – male
2. Black race
3. Hyperlipidemia
4. Smoking
5. HPN
6. DM
7. Oral contraceptive- prolonged use
8. Sedentary lifestyle
9. Obesity
10. Hypothyroidism
Signs & Symptoms
1. Chest pain
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis
Treatment
P – percutaneous
T – tansluminar
C – coronary
A – angioplasty
Obj:
1. To revascularize the myocardium
2. To prevent angina
3. Increase survival rate
PTCA – done to pt with single occluded vessel .
Multiple occluded vessels
C – coronary
A – arterial
B – bypass
A –and
G – graft surgery
Nsg Mgt Before CABAG
1. Deep breathing cough exercises
2. Use of incentive spirometer
3. Leg exercises
ANGINA PECTORIS- A clinical syndrome characterized by paroxysmal chest pain usually relieved by REST or NGT nitroglycerin, resulting fr temp myocardial ischemia.
Predisposing Factor:
1. sex – male
2. black raise
3. hyperlipidemia
4. smoking
5. HPN
6. DM
7. oral contraceptive prolonged
8. sedentary lifestyle
9. obesity
10.hypothyroidism
Precipitating factors
4 E’s
1. Excessive physical exertion
2. Exposure to cold environment - Vasoconstriction
3. Extreme emotional response
4. Excessive intake of food – saturated fats.
Signs & Symptoms
1. Initial symptoms – Levine’s sign – hand clutching of chest
2. Chest pain – sharp, stabbing excruciating pain. Location – substernal
-radiates back, shoulders, axilla, arms & jaw muscles
-relieve by rest or NGT
3. Dyspnea
4. Tachycardia
5. Palpitation
6.diaphoresis
Diagnosis
1.History taking & PE
2. ECG – ST segment depression
3. Stress test – treadmill = abnormal ECG
4. Serum cholesterol & uric acid - increase.
Nursing Management
1.) Enforce CBR
2.) Administer meds
NTG – small doses – venodilator
Large dose – vasodilator
1st dose NTG – give 3 – 5 min
2nd dose NTG – 3 – 5 min
3rd & last dose – 3 – 5 min
Still painful after 3rd dose – notify doc. MI!
55 yrs old with chest pain:
1st question to ask pt: what did you do before you had chest pain.
2nd question: does pain radiate? If radiate – heart in nature. If not radiate – pulmonary origin
Venodilator – veins of lower ext – increase venous pooling lead to decrease venous return.
Meds:
A. NTG- Nsg Mgt:
1. Keep in a dry place. Avoid moisture & heat, may inactivate the drug.
2. Monitor S/E:
orthostatic hypotension – dec bp
transient headache
dizziness
3. Rise slowly from sitting position
4. Assist in ambulation.
5. If giving NTG via patch:
i. avoid placing it near hairy areas-will dec drug absorption
ii. avoid rotating transdermal patches- will dec drug absorption
iii. avoid placing near microwave oven or during defibrillation-will burn pt due aluminum foil in patch
B. Beta blockers – propanolol
C. ACE inhibitors – captopril
D. Ca antagonist - nefedipine
3.) Administer O2 inhalation
4.) Semi-fowler
5.) Diet- Decrease Na and saturated fats
6.) Monitor VS, I&O, ECG
7.) HT: Discharge planning:
a. Avoid precipitating factors – 4 E’s
b. Prevent complications – MI
c. Take meds before physical exertion-to achieve maximum therapeutic effect of drug
d. Importance of follow-up care.
MI – MYOCARDIAL INFARCTION – hear attack – terminal stage of CAD
- Characterized by necrosis & scarring due to permanent mal-occlusion
Types:
1. Trasmural MI – most dangerous MI – Mal-occlusion of both R&L coronary artery
2. Sub-endocardial MI – mal-occlusion of either R & L coronary artery
Most critical period upon dx of MI – 48 to 72h
- Majority of pt suffers from PVC premature ventricular contraction.
|Predisposing factors |Signs & symptoms |Diagnostic Exam |
|sex – male |1. chest pain – excruciating, vice like, visceral pain located |1. cardiac enzymes |
|black raise |substernal or precodial area (rare) |a.) CPK – MB – Creatinine Phosphokinase |
|hyperlipidemia |- radiates back, arm, shoulders, axilla, jaw & abd muscles. |b.) LDH – lactic acid dehydrogenase |
|smoking |- not usually relived by rest r NTG |c.) SGPT – (ALT) – Serum Glutanic Pyruvate Transaminase-|
|HPN |2. dyspnea |increased |
|DM |3. erthermia |d.) SGOT (AST) – Serum Glutamic Oxalo-acetic - increased|
|oral contraceptive prolonged |4. initial increase in BP |2. Troponin test – increase |
|sedentary lifestyle |5. mild restlessness & apprehensions |3. ECG tracing – ST segment increase, |
|obesity |6. occasional findings |widening or QRS complexes – means arrhythmia in MI |
|hypothyroidism |a.) split S1 & S2 |indicating PVC |
| |b.) pericardial friction rub |4. serum cholesterol & uric acid - increase |
| |c.) rales /crackles |5. CBC – increase WBC |
| |d.) S4 (atrial gallop) | |
Nursing Management
1. Narcotic analgesics – Morphine SO4 – to induce vasodilation & decrease levels of anxiety.
2. Administer O2 inhalation – low inflow (CHF-increase inflow)
3. Enforce CBR without BP
a.) Bedside commode
4. Avoid valsalva maneuver
5. Semi fowler
6. General liquid to soft diet – decrease Na, saturated fat, caffeine
7. Monitor VS, I&O & ECG tracings
8. Take 20 – 30 ml/week – wine, brandy/whisky to induce vasodilation.
9. Assist in surgical; CABAG
10. Provide pt HT
a.) Avoid modifiable risk factors
b.) Prevent complications:
1. Arrhythmias – PVC
2. Shock – cardiogenic shock. Late signs of cardiogenic shock in MI – oliguria
3. thrombophlebitis - deep vein
4. CHF – left sided
5. Dressler’s syndrome – post MI syndrome
-Resistant to medications
-Administer 150,000 – 450,000 units of streptokinase
c.) Strict compliance to meds
- Vasodilators
1. NTG
2. Isordil
- Antiarrythmic
1. Lydocaine blocks release of norepenephrine
2. Brithylium
- Beta-blockers – “lol”
1. Propanolol (inderal)
- ACE inhibitors - pril
1. Captopril – (enalapril)
- Ca – antagonist
1. Nifedipine
- Thrombolitics or fibrinolytics– to dissolve clots/ thrombus
S/E allergic reactions/ uticaria
1. Streptokinase
2. Urokinase
3. Tissue plasminogen adjusting factor
Monitor for bleeding:
- Anticoagulants
1. Heparin 2. Caumadin – delayed reaction 2 – 3 days
PTT PT
If prolonged bleeding prolonged bleeding
Antidote antidote Vit K
Protamine sulfate
- Anti platelet PASA (aspirin)
d.) Resume ADL – sex/ activity – 4 to 6 weeks
Post-cardiac rehab
1.)Sex as an appetizer rather then dessert –
Before meals not after, due after meals increase metabolism – heart is pumping hard after meals.
2.) Position – non-weight bearing position.
When to resume sex/ act: When pt can already use staircase, then he can resume sex.
e.) Diet – decrease Na, Saturated fats, and caffeine
f.) Follow up care.
CHF – CONGESTIVE HEART FAILURE - Inability of heart to pump blood towards systemic circulation.
- Backflow
1.) Left sided heart failure:
Predisposing factors:
1.) 90% mitral valve stenosis – due RHD, aging
RHD affects mitral valve – streptococcal infection
Dx: - Aso titer – anti streptolysine O > 300 total units
- Steroids
- Penicillin
- Aspirin
Complication: RS-CHF
Aging – degeneration / calcification of mitral valve
Ischemic heart disease
HPN, MI, Aortic stenosis
S/Sx
Pulmonary congestion/ Edema
1. Dyspnea
2. Orthopnea (Diff of breathing sitting pos – platypnea)
3. Paroxysmal nocturnal dysnea – PNO- nalulunod
4. Productive cough with blood tinged sputum
5. Frothy salivation (from lungs)
6. Cyanosis
7. Rales/ crackles – due to fluid
8. Bronchial wheezing
9. PMI – displaced lateral – due cardiomegaly
10. Pulsus alternons – weak-strong pulse
11. Anorexia & general body malaise
12. S3 – ventricular gallop
Dx
1. CXR – cardiomegaly
2. PAP – Pulmonary Arterial Pressure
PCWP – Pulmonary CapillaryWedge Pressure
PAP – measures pressure of R ventricle. Indicates cardiac status.
PCWP – measures end systolic/ diastolic pressure
PAP & PCWP:
Swan – ganz catheterization – cardiac catheterization is done at bedside at ICU
(Trachesostomy – bedside) - Done 5 – 20 mins – scalpel & trachesostomy set
CVP – indicates fluid or hydration status
Increase CVP – decrease flow rate of IV
Decrease CVP – increase flow rate of IV
3. Echocardiography – reveals enlarged heart chamber or cardiomayopathy
4. ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp acidosis
2.) Right sided HF
Predisposing factor
1. 90% - tricuspid stenosis
2. COPD
3. Pulmonary embolism
4. Pulmonic stenosis
5. Left sided heart failure
S/Sx
Venous congestion
- Neck or jugular vein distension
- Pitting edema
- Ascites
- Wt gain
- Hepatomegalo/ splenomegaly
- Jaundice
- Pruritus
- Esophageal varies
- Anorexia, gen body malaise
Diagnosis:
1. CXR – cardiomegaly
2. CVP – measures the pressure at R atrium
Normal: 4 to 10 cm of water
Increase CVP > 10 – hypervolemia
Decrease CVP < 4 – hypovolemia
Flat on bed – post of pt when giving CVP
Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular filling.
3. Echocardiography – enlarged heart chamber / cardiomyopathy
4.Liver enzyme
SGPT ( ALT)
SGOT AST
Nsg mgt: Increase force of myocardial contraction = increase CO
3 – 6L of CO
1. Administer meds:
Tx for LSHF: M – morphine SO4 to induce vasodilatation
A – aminophylline & decrease anxiety
D – digitalis (digoxin)
D - diuretics
O - oxygen
G - gases
a.) Cardiac glycosides
Increase myocardial = increase CO
Digoxin (Lanoxin). Antidote: digivine
Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure.
b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrs
c.) Bronchodilators: Aminophillin (Theophyllin). Avoid giving caffeine
d.) Narcotic analgesic: Morphine SO4 - induce vasodilaton & decrease anxiety
e.) Vasodilators – NTG
f.) Anti-arrythmics – Lidocaine
2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula
3. High fowlers
4. Restrict Na!
5. Provide meticulous skin care
6. Weigh pt daily. Assess for pitting edema.
Measure abdominal girth daily & notify MD
7. Monitor V/S, I&O, breath sounds
8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return
9. Diet – decrease salt, fats & caffeine
10. HT:
a) Complications :shock
Arrhythmia
Thrombophlebitis
MI
Cor Pulmonale – RT ventricular hypertrophy
b.) Dietary modifications
c.) Adherence to meds
PERIPHERAL MUSCULAR DISEASE
Arterial ulcers venous ulcer
1. Thromboangiitis Obliterans – male/ feet 1. Varicose veins
2. Reynauds – female/ hands 2. Thrombophlebitis
1.) Thromboangiitis obliterates/ BUERGER DISEASE- Acute inflammatory disorder affecting small to medium sized arteries & veins of lower extremities. Male/ feet
Predisposing factors:
- Male
- Smokers
S/Sx
1. Intermittent claudication – leg pain upon walking - Relieved by rest
2. Cold sensitivity & skin color changes
White bluish red
Pallor cyanosis rubor
3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis
4. Tropic changes
5. Ulcerations
6. Gangrene formation
Dx:
1. Oscillometry – decrease peripheral pulse volume.
2. Doppler UTZ – decrease blood flow to affected extremities.
3. Angiography – reveals site & extent of mal-occulsion.thrombophlebitis
4. ns shockcuff rotated clockwise q 15 mins = to promote decrease venouse return
5.
Nsg Mgt:
1. Encourage a slow progression of physical activity
a. Walk 3 -4 x / day
b. Out of bed 2 – 3 x a / day
2. Meds
a. Analgesic
b. Vasodilator
c. Anticoagulant
3. Foot care mgt like DM –
a. Avoid walking barefoot
b. Cut toe nails straight
c. Apply lanolin lotion – prevent skin breakdown
d. Avoid wearing constrictive garments
4. Avoid smoking & exposure to cold environment
5. Surgery: BKA (Below the knee amputation)
2.)REYNAUD’S PHENOMENON – acute episodes of arterial spasm affecting digits of hands & fingers
Predisposing factors:
1. Female, 40 yrs
2. Smoking
3. Collagen dse
a. SLE – pathognomonic sign – butterfly rash on face
Chipmunk face – bulimia nervosa
Cherry red skin – carbon monoxide poisoning
Spider angioma – liver cirrhosis
Caput medusae – leg & trunk umbilicus- Liver cirrhosis
Lion face – leprosy
b. Rheumatoid arthritis –
4. Direct hand trauma – piano playing, excessive typing, operating chainsaw
S/Sx:
1. Intermittent claudication - leg pain upon walking - Relieved by rest
2. Cold sensitivity
Nsg Mgt:
a. Analgesics
b. Vasodilators
c. Encourage to wear gloves especially when opening a refrigerator.
d. Avoid smoking & exposure to cold environment
VENOUS ULCERS
1. VARICOSITIES / Varicose veins - Abnormal dilation of veins – lower ext & trunk
- Due to:
a.) Incompetent valves leading to
b.) Increase venous pooling & stasis leading to
c.) Decrease venous return
Predisposing factors:
a. Hereditary
b. Congenital weakness of veins
c. Thrombophlebitis
d. Heart dse
e. Pregnancy
f. Obesity
g. Prolonged immobility - Prolonged standing
S/Sx:
1. Pain especially after prolonged standing
2. Dilated tortuous skin veins
3. Warm to touch
4. Heaviness in legs
Dx:
1. Venography
2. Trendelenberg’s test – vein distend quickly < 35 secs
Nsg Mgt:
1. Elevate legs above heart level – to promote venous return – 1 to 2 pillows
2. Measure circumference of leg muscles to determine if swollen.
3. Wear anti embolic or knee high stockings. Women – panty hose
4. Meds: Analgesics
5. Surgery: vein sweeping & ligation
Sclerotherapy – spider web varicosities
S/E thrombosis
THROMBOPHLEBITIS (deep vein thrombosis) - Inflammation of veins with thrombus formation
Predisposing factors:
1. Smoking
2. Obesity
3. Hyperlipedemia
4. Prolonged use of oral contraceptives
5. Chronic anemia
6. DM
7. MI
8. CHF
9. Postop complications
10. Post cannulation – insertion of various cardiac catheters
S/Sx:
1. Pain at affected extremities
2. Cyanosis
3. (+) Homan’s sign - Pain at leg muscles upon dorsiflexion of foot.
Dx:
1. Angiography
2. Doppler UTZ
Nsg Mgt:
1. Elevate legs above heart level.
2. Apply warm, moist packs to decrease lymphatic congestion.
3. Measure circumference of leg muscles to detect if swollen.
4. Use anti embolic stockings.
5. Meds: Analgesics.
Anticoagulant: Heparin
6. Complication:
Pulmonary Embolism:
- Sudden sharp chest pain
- Dyspnea
- Tachycardia
- Palpitation
- Diaphoresis
- Mild restlessness
OVERVIEW OF RESPIRATORY SYSTEM:
I. Upper respiratory tract:
Fx:
1. Filtering of air
2. Warming & moistening
3. Humidification
a. Nose – cartilage
- Parts: Rt nostril separated by septum
Lt nostril
- Consists of anastomosis of capillaries –
Kessel – Bach Plexus – site of epistaxis
b. Pharynx (throat) – muscular passageway for air& food
Branches:
1. Oropharynx
2. Nasopharynx
3. Layngopharynx
c. Larynx – voice box
Fx:
1. For phonation
2. Cough reflex
Glottis – opening
Opens to allow passage of air
Closes to allow passage of food
II. Lower Rt – Fx for gas exchange
a. Trachea – windpipe
- has cartillagenous rings
- site for permanent/ artificial a/w – tracheostomy
b. Bronchus – R & L main bronchus
c. Lungs – R – 3 lobes = 10 segments
L – 2 lobes – 8 segments
Post pneumonectomy - position affected side to promote expansion of lungs
Post segmental lobectomy – position unaffected side to promote drainage
Lungs – covered by pleural cavity, parietal lobe & visceral lobe
Alveoli – acinar cells
- site of gas exchange (O2 & CO2)
- diffusion: Daltons law of partial pressure of gases
Ventilation – movement of air in & out of lungs
Respiration – movement of air into cells
Type II cells of alveoli – secrets surfactant
Surfactant - decrease surface tension of alveoli
Lecithin & spinogometer
L/S ratio 2:1 – indicator of lung maturity
If 1:2 – adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness.
I. PNEUMONIA – inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates.
Etiologic agents:
1. Streptococcus pneumoniae (pnemococcal pneumonia)
2. Hemophilus pneumoniae(Bronchopneumonia)
3. Escherichia coli
4. Klebsiella P.
5. Diplococcus P.
High risk elderly & children below 5 yo
Predisposing factors:
1. Smoking
2. Air pollution
3. Immuno-compromised
a. AIDS – PLP
b. Bronchogenic CA - Non-productive to productive cough
4. Prolonged immobility – CVA- hypostatic pneumonia
5. Aspiration of food
6. Over fatigue
S/Sx:
1. Productive cough – pathognomonic: greenish to rusty sputum
2. Dyspnea with prolonged respiratory grunt
3. Fever, chills, anorexia, gen body malaise
4. Wt loss
5. Pleuritic friction rub
6. Rales/ crackles
7. Cyanosis
8. Abdominal distension leading to paralytic ileus
Sputum exam – could confirm presence of TB & pneumonia
Dx:
1. Sputum GSCS- gram staining & culture sensitivity - Reveals (+) cultured microorganism.
2. CXR – pulmo consolidation
3. CBC – increase WBC
Erythrocyte sedimentation rate
4. ABG – PO2 decrease
Nsg Mgt:
1. Enforce CBR
2. Strict respiratory isolation
3. Meds:
a. Broad spectrum antibiotics
Penicillin or tetracycline
Macrolides – ex azythromycin (zythromax)
b. Anti pyretics
c. Mucolytics or expectorants
4. Force fluids – 2 to 3 L/day
5. Institute pulmonary toilet-
a. Deep breathing exercise
b. Coughing exercise
c. Chest physiotherapy – cupping
d. Turning & reposition - Promote expectoration of secretions
6. Semi-fowler
7. Nebulize & suction
8. Comfy & humid environment
9. Diet: increase CHO or calories, CHON & vit C
10. Postural drainage - To drain secretions using gravity
Mgt for postural drainage:
a. Best done before meals or 2 – 4 hrs after meals to prevent Gastroesophageal Reflux
b. Monitor VS & breath sounds
Normal breath sound – bronchovesicular
c.) Deep breathing exercises
d.) Adm bronchodilators 15 – 30 min before procedure
e.) Stop if pt can’t tolerate procedure
f.) Provide oral care – it may alter taste sensation
g.) C/I – pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma)
Normal IOP – 12 – 21 mmHg
11. HT:
a.) Avoidance of precipitating factors
b.) Complication: Atelectacies & meningitis
c.) Compliance to meds
PULMONARY TUBERCULOSIS (KOCH DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB or tubercle bacilli or acid fast bacilli – gram (+) aerobic, motile & easily destroyed by heat or sunlight.
Predisposing factors:
1. Malnutrition
2. Overcrowding
3. Alcoholism
4. Ingestion of infected cattle (mycobacterium BOVIS)
5. Virulence
6. Over fatigue
S/Sx:
1. Productive cough – yellowish
2. Low fever
3. Night sweats
4. Dyspnea
5. Anorexia, general body malaise, wt loss
6. Chest/ back pain
7. Hempotysis
Diagnosis:
1. Skin test – mantoux test – infection of Purified CHON Derivative PPD
DOH – 8-10 mm induration
WHO – 10-14 mm induration
Result within 48 – 72h
(+) Mantoux test – previous exposure to tubercle bacilli
Mode of transmission – droplet infection
2. Sputum AFB – (+) to cultured microorganism
3. CXR – pulmonary infiltrate caseosis necrosis
4. CBC – increase WBC
Nursing Mgt:
1. CBR
2. Strict resp isolation
3. O2 inhalation
4. Semi fowler
5. Force fluid to liquefy secretions
6. DBCE
7. Nebulize & suction
8. Comfy & humid environment
9. Diet – increase CHO & calories, CHON, Vit, minerals
10. Short course chemotherapy
- Intensive phase
INH – isoniazide - give before meals for absorption
Rifampicin - given within 4 months, given simultaneously to prevent resistance
-S/E: peripheral neutitis – vit B6
Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.
PZA – Pyrazinamide – given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity
Standard regimen
1. Injection of streptomycin – aminoglycoside
Ex. Kanamycin, gentamycin, neomycin
S/E:
a. Ototoxicity – damage CN # 8 – tinnitus – hearing loss
b. Nephrotoxicicity – monitor BUN & Crea
HT:
a. Avoid pred factors
b. Complications:
1. Atelectasis
2. Miliary TB – spread of Tb to other system
c. Compliance to meds
- Religiously take meds
HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with histoplasma capsulatum transmitted to birds manure.
S/Sx: Same as pneumonia & PTB – like
1. Productive cough
2. Dyspnea
3. Chest & joint pains
4. Cyanosis
5. Anorexia, gen body malaise, wt loss
6. Hemoptysis
Dx:
1. Histoplasmin skin test = (+)
2. ABG – pO2 decrease
Nsg Mgt:
1. CBR
2. Meds:
a. Anti fungal agents
Amphotericin B (Fungizone)
S/E :
a. Nephrotoxcicity check BUN
b. Hypokalemia
b.)Corticosteroids
c.) Mucolytic/ or expectorants
3. O2 – force fluids
4. Nebulize, suction
5. Complications:
a.) Atelectasis
b.) Bronchiectasis COPD
6. Prevent spread of histoplasmosis:
a.) Spray breading places or kill the bird.
COPD – Chronic Obstructive Pulmonary Disease
1. Chronic bronchitis
2. Bronchial asthma
3. Bronchiectasis
4. Pulmonary emphysema – terminal stage
CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet mucus producing cells leading to narrowing of smaller airways.
Predisposing factors:
1. Smoking – all COPD types
2. Air pollution
S/Sx:
1. Prod cough
2. Dyspnea on exertion
3. Prolonged expiratory grunt
4. Scattered rales/ rhonchi
5. Cyanosis
6. Pulmo HPN – a.)Leading to peripheral edema
b.) Cor pulmonary – respiratory in origin
7. Anorexia, gen body malaise
Dx:
1. ABG
PO2 PCO2 Resp acidosis
Hypoxemia – causing cyanosis
Nsg Mgt:
(Same as emphysema)
2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity leading to narrowing of smaller airway.
Predisposing factor:
1. Extrinsic Asthma – called Atropic/ allergic asthma
a. Pallor
b. Dust
c. Gases
d. Smoke
e. Dander
f. Lints
2. Intrinsic Asthma-
Cause:
Herediatary
Drugs – aspirin, penicillin, ( blockers
Food additives – nitrites
Foods – seafood, chicken, eggs, chocolates, milk
Physical/ emotional stress
Sudden change of temp, humidity &air pressure
3. mixed type: combi of both ext & intr. Asthma
90% cause of asthma
S/Sx:
1. C – cough – non productive to productive
2. D – dyspnea
3. W – wheezing on expiration
4. Cyanosis
5. Mild apprehension & restlessness
6. Tachycardia & palpitation
7. Diaphoresis
Dx:
1. Pulmo function test – decrease lung capacity
2. ABG – PO2 decrease
Nsg Mgt:
1. CBR – all COPD
2. Meds-
a. Bronchodilator through inhalation or metered dose inhaled / pump. Give 1st before corticosteroids
b. Corticosteroids – due inflammatory. Given 10 min after adm bronchodilator
c.) Mucolytic/ expectorant
d.) Mucomist – at bedside put suction machine.
e.) Antihistamine
3. Force fluid
4. O2 – all COPD low inflow to prevent resp distress
5. Nebulize & suction
6. Semifowler – all COPD except emphysema due late stage
7. HT
a. Avoid pred factors
b. Complications:
- Status astmaticus- give epinephrine & bronchodilators
- Emphysema
c. Adherence to med
BRONCHIECTASIS – abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli.
Predisposing factors:
1. Recurrent upper & lower RI
2. Congenital anomalies
3. Tumors
4. Trauma
S/Sx:
1. Productive cough
2. Dyspnea
3. Anorexia, gen body malaise- all energy are used to increase respiration.
4. Cyanosis
5. Hemoptisis
Dx:
1. ABG – PO2 decrease
2. Bronchoscopy – direct visualization of bronchus using fiberscope.
Nsg Mgt: before bronchoscopy
1. Consent, explain procedure – MD/ lab explain RN
2. NPO
3. Monitor VS
Nsg Mgt after bronchoscopy
1. Feeding after return of gag reflex
2. Instruct client to avoid talking, smoking or coughing
3. Monitor signs of frank or gross bleeding
4. Monitor of laryngeal spasm
- DOB
- Prepare at bedside tracheostomy set
Mgt: same as emphysema except Surgery
Pneumonectomy – removal of affected lung
Segmental lobectomy – position of pt – unaffected side
PULMONARY EMPHYSEMA – irreversible terminal stage of COPD
- Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution of gases.
- Body will compensate over distension of thoracic cavity
- Barrel chest
Predisposing factor:
1. Smoking
2. Allergy
3. Air pollution
4. High risk – elderly
5. Hereditary - ( 1 anti trypsin to release elastase for recoil of alveoli.
S/Sx:
1. Productive cough
2. Dyspnea at rest – due terminal
3. Anorexia & gen body malaise
4. Rales/ rhonchi
5. Bronchial wheezing
6. Decrease tactile fremitus (should have vibration)– palpation – “99”. Decreased - with air or fluid
7. Resonance to hyperresonance – percussion
8. Decreased or diminished breath sounds
9. Pathognomonic: barrel chest – increase post/ anterior diameter of chest
10. Purse lip breathing – to eliminated PCO2
11. Flaring of alai nares
Diagnosis:
1. Pulmonary function test – decrease vital lung capacity
2. ABG –
a. Panlobular / centrolobular emphysema
pCO2 increase
pO2 decrease – hypoxema resp acidosis Blue bloaters
b. Panacinar/ Centracinar
pCO2 decrease
pO2 increase – hyperaxemia resp alkalosis Pink puffers
Nursing Mgt:
1. CBR
2. Meds –
a. Bronchodilators
b. Corticosteroids
c. Antimicrobial agents
d. Mucolytics/ expectorants
3. O2 – Low inflow
4. Force fluids
5. High fowlers
6. Neb & suction
7. Institute
P – posture
E – end
E – expiratory to prevent collapse of alveoli
P – pressure
8. HT
a. Avoid smoking
b. Prevent complications
1. Cor pulmonary – R ventricular hypertrophy
2. CO2 narcosis – lead to coma
3. Atelectasis
4. Pneumothorax – air in pleural space
9. Adherence to meds
RESTRICTIVE LUNG DISORDER
PNEUMOTHORAX – partial / or complete collapse of lungs due to entry or air in pleural space.
Types:
1. Spontaneous pneumothorax – entry of air in pleural space without obvious cause.
Eg. rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions
Eg. open pneumothorax – air enters pleural space through an opening in chest wall
-Stab/ gun shot wound
2. Tension Pneumothorax – air enters plural space with @ inspiration & can’t escape leading to over distension of thoracic cavity resulting to shifting of mediastinum content to unaffected side.
Eg. flail chest – “paradoxical breathing”
Predisposing factors:
1.Chest trauma
2.Inflammatory lung conditions
3.Tumor
S/Sx:
1. Sudden sharp chest pain
2. Dyspnea
3. Cyanosis
4. Diminished breath sound of affected lung
5. Cool moist skin
6. Mild restlessness/ apprehension
7. Resonance to hyper resonance
Diagnosis:
1. ABG – pO2 decrease –
2. CXR – confirms pneumothorax
Nursing Mgt:
1. Endotracheal intubation
2. Thoracenthesis
3. Meds – Morphine SO4
- Anti microbial agents
4. Assist in test tube thoracotomy
Nursing Mgt if pt is on CPT attached to H2O drainage
1. Maintain strict aseptic technique
2. DBE
3. At bedside
a. Petroleum gauze pad if dislodged Hemostan
b. If with air leakage – clamp
c. Extra bottle
4. Meds – Morphine SO4
Antimicrobial
5. Monitor & assess for oscillation fluctuations or bubbling
a. If (+) to intermittent bubbling means normal or intact
- H2O rises upon inspiration
- H2o goes down upon expiration
b.) If (+) to continuous, remittent bubbling
1. Check for air leakage
2. Clamp towards chest tube
3. Notify MD
c.) If (-) to bubbling
1. Check for loop, clots, and kink
2. Milk towards H2O seal
3. Indicates re-expansion of lungs
When will MD remove chest tube:
1. If (-) fluctuations
2. (+) Breath sounds
3. CXR – full expansion of lungs
Nursing Mgt of removal of chest tube
1. DBE
2. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space.
3. Apply vaselinated air occlusive dressing
- Maintain dressing dry & intact
GIT
I. Upper alimentary canal - function for digestion
a. Mouth
b. Pharynx (throat)
c. Esophagus
d. Stomach
e. 1st half of duodenum
II. Middle Alimentary canal – Function: for absorption
- Complete absorption – large intestine
a. 2nd half of duodenum
b. Jejunum
c. Ileum
d. 1st half of ascending colon
III. Lower Alimentary Canal – Function: elimination
a. 2nd half of ascending colon
b. Transverse
c. Descending colon
d. Sigmoid
e. Rectum
IV. Accessory Organ
a. Salivary gland
b. Verniform appendix
c. Liver
d. Pancreas – auto digestion
e. Gallbladder – storage of bile
I. Salivary Glands
1. Parotid – below & front of ear
2. Sublingual
3. Submaxillary
- Produces saliva – for mechanical digestion
- 1200 -1500 ml/day - saliva produced
PAROTITIS – “mumps” – inflammation of parotid gland
-Paramyxo virus
S/Sx:
1. Fever, chills anorexia, gen body malaise
2. Swelling of parotid gland
3. Dysphagia
4. Ear ache – otalgia
Mode of transmission: Direct transmission & droplet nuclei
Incubation period: 14 – 21 days
Period of communicability – 1 week before swelling & immediately when swelling begins.
Nursing Mgt:
1. CBR
2. Strict isolation
3. Meds: analgesic
Antipyretic
Antibiotics – to prevent 2( complications
4. Alternate warm & cold compress at affected part
5. Gen liquid to soft diet
6. Complications
Women – cervicitis, vaginitis, oophoritis
Both sexes – meningitis & encephalitis/ reason why antibiotics is needed
Men – orchitis might lead to sterility if it occur during / after puberty.
VERNIFORM APPENDIX – Rt iliac or Rt inguinal area
- Function – lymphatic organ – produces WBC during fetal life - ceases to function upon birth of baby
APENDICITIS – inflamation of verniform appendix
Predisposing factor:
1. Microbial infection
2. Feacalith – undigested food particles – tomato seeds, guava seeds
3. Intestinal obstruction
S/Sx:
1. Pathognomonic sign: (+) rebound tenderness
2. Low grade fever, anorexia, n/v
3. Diarrhea / & or constipation
4. Pain at Rt iliac region
5. Late sign due pain – tachycardia
Diagnosis:
1. CBC – mild leukocytosis – increase WBC
2. PE – (+) rebound tenderness (flex Rt leg, palpate Rt iliac area – rebound)
3. Urinalysis
Treatment: - appendectomy 24 – 45(
Nursing Mgt:
1. Consent
2. Routinary nursing measures:
a. Skin prep
b. NPO
c. Avoid enema – lead to rupture of appendix
3. Meds:
Antipyretic
Antibiotics
*Don’t give analgesic – will mask pain
- Presence of pain means appendix has not ruptured.
4. Avoid heat application – will rupture appendix.
5. Monitor VS, I&O bowel sound
Nursing Mgt: post op
1. If (+) to Pendrose drain – indicates rupture of appendix
Position- affected side to drain
2. Meds: analgesic due post op pain
Antibiotics, Antipyretics PRN
3. Monitor VS, I&O, bowel sound
4. Maintain patent IV line
5. Complications- peritonitis, septicemia
Liver – largest gland
- Occupies most of right hypochondriac region
- Color: scarlet red
- Covered by a fibrous capsule – Glisson’s capsule
- Functional unit – liver lobules
Function:
1. Produces bile
Bile – emulsifies fats
- Composed of H2O & bile salts
-Gives color to urine – urobilin
Stool – stircobilin
2. Detoxifies drugs
3. Promotes synthesis of vit A, D, E, K - fat soluble vitamins
Hypevitaminosis – vit D & K
Vit A – retinol
Def Vit A – night blindness
Vit D – cholecalciferon
- Helps calcium
- Rickets, osteoarthritis
4. It destroys excess estrogen hormone
5. For metabolism
A. CHO –
1. Glycogenesis – synthesis of glycogens
2. Glycogenolysis – breakdown of glycogen
3. Gluconeogenesis – formation of glucose from CHO sources
B. CHON-
1. Promotes synthesis of albumin & globulin
Cirrhosis – decrease albumin
Albumin – maintains osmotic pressure, prevents edema
2. Promotes synthesis of prothrombin & fibrinogen
3. Promotes conversion of ammonia to urea.
Ammonia like breath – fetor hepaticus
C. FATS – promotes synthesis of cholesterol to neutral fats – called triglycerides
LIVER CIRRHOSIS - lost of architectural design of liver leading to fat necrosis & scarring
Early sign – hepatic encephalopathy
1. Asterixis – flapping hand tremors
Late signs – headache, restlessness, disorientation, decrease LOC – hepatic coma.
Nursing priority – assist in mechanical ventilation
Predisposing factor:
Decrease Laennac’s cirrhosis – caused by alcoholism
1. Chronic alcoholism
2. Malnutrition – decreaseVit B, thiamin - main cause
3. Virus –
4. Toxicity- eg. Carbon tetrachloride
5. Use of hepatotoxic agents
S/Sx:
Early signs:
a. Weakness, fatigue
b. Anorexia, n/v
c. Stomatitis
d. Urine – tea color
Stool – clay color
e. Amenorrhea
f. Decrease sexual urge
g. Loss of pubic, axilla hair
h. Hepatomegaly
i. Jaundice
j. Pruritus or urticaria
2. Late signs
a.) Hematological changes – all blood cells decrease
Leukopenia- decrease
Thrombocytopenia- decrease
Anemia- decrease
b.) Endocrine changes
Spider angiomas, Gynecomastia
Caput medusate, Palmar errythema
c.) GIT changes
Ascitis, bleeding esophageal varices – due to portal HPN
d.) Neurological changes:
Hepatic encephalopathy - ammonia (cerebral toxin)
Late signs: Early signs:
Headache asterexis
Fetor hepaticus (flapping hand tremors)
Confusion
Restlessness
Decrease LOC
Hepatic coma
Diagnosis:
1. Liver enzymes- increase
SGPT (ALT)
SGOT (AST)
2. Serum cholesterol & ammonia increase
3. Indirect bilirubin increase
4. CBC - pancytopenia
5. PTT – prolonged
6. Hepatic ultrasonogram – fat necrosis of liver lobules
Nursing Mgt
1. CBR
2. Restrict Na!
3. Monitor VS, I&O
4. With pt daily & assess pitting edema
5. Measure abdominal girth daily – notify MD
6. Meticulous skin care
7. Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHON
Well balanced diet
8. Complications:
a. Ascites – fluid in peritoneal cavity
Nursing Mgt:
1. Meds: Loop diuretics – 10 – 15 min effect
2. Assist in abdominal paracentesis - aspiration of fluid
- Void before paracentesis to prevent accidental puncture of bladder as trochar is inserted
b. Bleeding esophageal varices
- Dilation of esophageal veins
1. Meds: Vit K
Pitrisin or Vasopresin (IM)
2. NGT decompression- lavage
- Give before lavage – ice or cold saline solution
- Monitor NGT output
3. Assist in mechanical decompression
- Insertion of sengstaken-blackemore tube
- 3 lumen typed catheter
- Scissors at bedside to deflate balloon.
c. Hepatic encephalopathy –
1. Assist in mechanical ventilation – due coma
2. Monitor VS, neuro check
3. Siderails – due restless
4. Meds – Laxatives – to excrete ammonia
HEPATITIS- jaundice (icteric sclera)
Bilirubin
Kernicterus/ hyperbilirubinia
Irreversible brain damage
Pancreas – mixed gland (exocrine & endocrine gland)
PANCREATITIS – acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion.
Bleeding of pancreas - Cullen’s sign at umbilicus
Predisposing factors:
1. Chronic alcoholism
2. Hepatobilary disease
3. Obesity
4. Hyperlipidemia
5. Hyperparathyroidism
6. Drugs – Thiazide diuretics, pills Pentamidine HCL (Pentam)
7. Diet – increase saturated fats
S/Sx:
1. Severe Lt epigastric pain – radiates from back &flank area
- Aggravated by eating, with DOB
2. N/V
3. Tachycardia
4. Palpitation due to pain
5. Dyspepsia – indigestion
6. Decrease bowel sounds
7. (+) Cullen’s sign - ecchymosis of umbilicus hemorrhage
8. (+) Grey Turner’s spots – ecchymosis of flank area
9. Hypocalcemia
Diagnosis:
1. Serum amylase & lipase – increase
2. Urine lipase – increase
3. Serum Ca – decrease
Nursing Mgt:
1. Meds
a.) Narcotic analgesic - Meperidine Hcl (Demerol)
Don’t give Morphine SO4 –will cause spasm of sphincter.
b.) Smooth muscle relaxant/ anti cholinergic
- Ex. Papavarine Hcl
Prophantheline Bromide (Profanthene)
c.) Vasodilator – NTG
d.) Antacid – Maalox
e.) H2 receptor antagonist - Ranitidin (Zantac) to decrease pancreatic stimulation
f.) Ca – gluconate
2. Withold food & fluid – aggravates pain
3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation
Complications of TPN
1. Infection
2. Embolism
3. Hyperglycemia
4. Institute stress mgt tech
a.) DBE
b.) Biofeedback
5. Comfy position - Knee chest or fetal like position
6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON
7. Complications: Chronic hemorrhagic pancreatitis
GALLBLADDER – storage of bile – made up of cholesterol.
CHOLECYSTITIS/ CHOLELITHIASIS – inflammation of gallbladder with gallstone formation.
Predisposing factor:
1. High risk – women 40 years old
2. Post menopausal women – undergoing estrogen therapy
3. Obesity
4. Sedentary lifestyle
5. Hyperlipidemia
6. Neoplasm
S/Sx:
1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night
2. Fatty intolerance
3. Anorexia, n/v
4. Jaundice
5. Pruritus
6. Easy bruising
7. Tea colored urine
8. Steatorrhea
Diagnosis:
1. Oral cholecystogram (or gallbladder series)- confirms presence of stones
Nursing Mgt:
1. Meds – a.) Narcotic analgesic - Meperdipine Hcl – Demerol
b.) Anti cholinergic - Atropine SO4
c.) Anti emetic
Phenergan – Phenothiazide with anti emetic properties
2. Diet – increase CHO, moderate CHON, decrease fats
3. Meticulous skin care
4. Surgery: Cholecystectomy
Nursing Mgt post cholecystectomy
-Maintain patency of T-tube intact & prevent infection
Stomach – widest section of alimentary canal
- J shaped structures
1. Anthrum
2. Pylorus
3. Fundus
Valves
1. 1.cardiac sphincter
2. Pyloric sphincter
Cells
1. Chief/ Zymogenic cells – secrets
a. Gastric amylase - digest CHO
b. Gastric lipase – digest fats
c. Pepsin – CHON
d. Rennin – digests milk products
2. Parietal / Argentaffin / oxyntic cells
Function:
a. Produces intrinsic factor – promotes reabsorption of vit B12 cyanocobalamin – promotes maturation of RBC
b. Secrets Hcl acid – aids in digestion
3. Endocrine cells - Secrets gastrin – increase Hcl acid secretion
Function of the stomach
1.Mechanical
2.Chem. Digestion
3.Storage of food
-CHO, CHON- stored 1 -2 hrs. Fats – stored 2 – 3 hrs
PEPTIC ULCER DISEASE – (PUD) – excoriation / erosion of submucosa & mucosal lining due to:
a. Hypercecretion of acid – pepsin
b. Decrease resistance to mucosal barrier
Incidence Rate:
1. Men – 40 – 55 yrs old
2. Aggressive persons
Predisposing factors:
1. Hereditary
2. Emotional
3. Smoking – vasoconstriction – GIT ischemia
4. Alcoholism – stimulates release of histamine = Parietal cell release Hcl acid = ulceration
5. Caffeine – tea, soda, chocolate
6. Irregular diet
7. Rapid eating
8. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen
Indomethacin - S/E corneal cloudiness. Needs annual eye check up.
9. Gastrin producing tumor or gastrinoma – Zollinger Ellisons sign
10. Microbial invasion – helicobacter pylori. Metromidazole (Flagyl)
Types of ulcers
Ascending to severity
1. Acute – affects submucosal lining
2. Chronic – affects underlying tissue – heals & forms a scar
According to location
1. Stress ulcer
2. Gastric ulcer
3. Duodenal ulcer – most common
Stress ulcers – common among eritically ill clients
2 types
1.Curing’s ulcer – cause: trauma & birth
hypovolemia
GIT schemia
Decrease resistance of mucosal barriers to Hcl acid
Ulcerations
2.Cushing’s ulcer – cause – stroke/CVA/ head injury
Increase vagal stimulation
Hyperacidity
Ulcerations
GASTRIC ULCER DUODENAL ULCER
|SITE |Intrum or lesser curvature |Duodenal bulb |
|PAIN |-30 min – 1 hr after eating |-2-3 hrs after eating |
| |- epigastrium |- mid epigastrium |
| |- gaseous & burning |- cramping & burning |
| |- not usually relieved by food & antacid |- usually relieved by food & antacid |
| | |- 12 MN – 3am pain |
|HYPERSECRETION |Normal gastric acid secretion |Increased gastric acid secretion |
|VOMITING |common |Not common |
|HEMORRHAGE |hematemeis |Melena |
|WT |Wt loss |Wt gain |
|COMPLICATIONS |a. stomach cause |a. perforation |
| |b. hemorrhage | |
|HIGH RISK |60 years old |20 years old |
Diagnosis:
1. Endoscopic exam
2. Stool from occult blood
3. Gastric analysis – N – gastric
Increase – duodenal
4. GI series – confirms presence of ulceration
Nursing Mgt:
1. Diet – bland, non irritating, non spicy
2. Avoid caffeine & milk/ milk products
Increase gastric acid secretion
3. Administer meds
a. Antacids
AAC
Aluminum containing antacids Magnesium containing antacids
Ex. aluminum OH gel ex. milk of magnesia
(Ampho-gel) S/E diarrhea
S/E constipation
Maalox (fever S/E)
b. H2 receptor antagonist
Ex
1. Ranitidine (Zantac)
2. Cimetidine (Tagamet)
3. Tamotidine (Pepcid)
- Avoid smoking – decrease effectiveness of drug
Nursing Mgt:
1. Administer antacid & H2 receptor antagonist – 1hr apart
-Cemetidine decrease antacid absorption & vise versa
c. Cytoprotective agents
Ex
1. Sucralfate (Carafate) - Provides a paste like subs that coats mucosal lining of stomach
2. Cytotec
d.) Sedatives/ Tranquilizers - Valium, lithium
e.)Anticholinergics
1. Atropine SO4
2. Prophantheline Bromide (Profanthene)
(Pt has history of hpn crisis With peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na.
4. Surgery: subtotal gastrectomy - Partial removal of stomach
|Billroth I (Gastroduodenostomy) |Billroth II (Gastrojejunostomy) |
|-Removal of ½ of stomach & anastomoses of gastric stump to the duodenum. |- removal of ½ -3/4 of stomach & duodenal bulb & anastomostoses of gastric stump to |
| |jejunum. |
Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first.
Nursing Mgt:
1. Monitor NGT output
a. Immediately post op should be bright red
b. Within 36- 42h – output is yellow green
c. After 42h – output is dark red
2. Administer meds:
a. Analgesic
b. Antibiotic
c. Antiemetics
3. Maintain patent IV line
4. VS, I&O & bowel sounds
5. Complications:
a. Hemorrhage – hypovolemic shock
Late signs – anuria
b. Peritonitis
c. Paralytic ileus – most feared
d. Hypokalemia
e. Thromobphlebitis
f. Pernicious anemia
7.)Dumping syndrome – common complication – rapid gastric emptying of hypertonic food solutions – CHYME leading to hypovolemia.
Sx of Dumping syndrome:
1. Dizziness
2. Diaphoresis
3. Diarrhea
4. Palpitations
Nursing mgt:
1. Avoid fluids in chilled solutions
2. Small frequent feeding s-6 equally divided feedings
3. Diet – decrease CHO, moderate fats & CHON
4. Flat on bed 15 -30 minutes after q feeding
BURNS – direct tissue injury caused by thermal, electric, chemical & smoke inhaled (TECS)
Nursing Priority – infection (all kinds of burns)
Head burn-priority- a/w
2nd priority for 1st & 2nd ( - pain
2nd priority for 3rd ( - F&E
Thermal- direct contact – flames, hot grease, sunburn.
Electric, – wires
Chem. – direct contact – corrosive materials acids
Smoke – gas / fume inhalation
Stages:
1. Emergent phase – Removal of pt from cause of burn. Determine source or loc or burn
2. Shock phase – 48 - 72(. Characterized by shifting of fluids from intravascular to interstitial space
=Hypovolemia
S/Sx:
- BP decrease
- Urine output
- HR increase
- Hct increase
- Serum Na decrease
- Serum K increase
- Met acidosis
3. Diuretic/ Fluid remobilization phase - 3 to 5 days. Return of fluid from interstitial to intravascular space
4. Recovery/ convalescent phase – complete diuresis. Wound healing starts immediately after tissue injury.
Class:
I. Partial Burn
1. 1st degree – superficial burns
- Affects epidermis
- Cause: thermal burn
- Painful
- Redness (erythema) & blanching upon pressure with no fluid filled vesicles
2. 2nd degree – deep burns
- Affects epidermis & dermis
- Cause –chem. burns
- very painful
- Erythema & fluid filled vesicles (blisters)
II Full thickness Burns
1. Third & 4th degrees burn
- Affects all layers of skin, muscles, bones
- Cause – electrical
- Less painful
- Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue.
Assessment findings
Rule of nines
Head & neck = 9%
Ant chest = 18%
Post chest = 18%
@ Arm 9+9 = 18%
@ leg 18+18 = 18%
Genitalia/ perineum= 1%
Total 100%
Nursing Mgt
1. Meds
a.) Tetanus toxoid- burn surface area is source of anaerobic growth – Claustridium tetany
Tetany
Tetanolysin tetanospasmin
Hemolysis muscle spasm
b.) Morphine SO4
c.) Systemic antibiotics
1. Ampicillin
2. Cephalosporin
3. Tetracyclin
4. Topical antibiotic :
1. Silver Sulfadiazene (silvadene)
2. Sulfamylon
3. Silver nitrate
4. Povidone iodine (betadine)
2. Administer isotonic fluid sol & CHON replacements
3. Strict aseptic technique
4. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange
5. If (+) to burns on head, neck, face - Assist in intubation
6. Assist in hydrotherapy
7. Assist in surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement
8. Complications:
a.) Infection
b.) Shock
c.) Paralytic ileus - due to hypovolemia & hypokalemia
d.) Curling’s ulcer – H2 receptor antagonist
e.) Septicemia blood poisoning
f.) Surgery: skin grafting
GUT – genito-urinary tract
Function:
1. Promote excretion of nitrogenous waste products
2. Maintain F&E & acid base balance
1. Kidneys – pair of bean shaped organ
- Retro peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s capsule.
Parts:
1. Renal pelvis – pyenophritis – infl
2. Cortex
3. Medulla
Nephrones – basic living unit
Glomerulus – filters blood going to kidneys
Function of kidneys:
1. Urine formation
2. Regulation of BP
Urine formation – 25% of total CO (Cardiac Output) is received by kidneys
1. Filtration
2. Tubular Reabsorption
3. Tubular Secretion
Filtration – Normal GFR/ min is 125 ml of blood
Tubular reabsorption – 124ml of ultra infiltrates (H2O & electrolytes is for reabsorption)
Tubular secretion – 1 ml is excreted in urine
Regulation of BP:
Predisposing factor:
Ex CS – hypovolemia – decrease BP going to kidneys
Activation of RAAS
Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus
Angiotensin I mild vasoconstrictor
Angiotensin II vasoconstrictor
Adrenal cortex increase CO increase PR
Aldosterone
Increase BP
Increase Na &
H2O reabsorption
Hypervolemia
Ureters – 25 – 35 cm long, passageway of urine to bladder
Bladder – loc behind symphisis pubis. Muscular & elastic tissue that is distensible
- Function – reservoir or urine
1200 – 1800 ml – Normal adult can hold
200 – 500 ml – needed to initiate micturition reflex
Color – amber
Odor – aromatic
Consistency – clear or slightly turbid
pH – 4.5 – 8
Specific gravity – 1.015 – 1.030
WBC/ RBC – (-)
Albumin – (-)
E coli – (-)
Mucus thread – few
Amorphous urate (-)
Urethra – extends to external surface of body. Passage of urine, seminal & vaginal fluids.
- Women 3 – 5 cm or 1 to 1 ½ “
- Male – 20cm or 8”
UTI
CYSTITIS – inflammation of bladder
Predisposing factors:
1. Microbial invasion – E. coli
2. High risk – women
3. Obstruction
4. Urinary retention
5. Increase estrogen levels
6. Sexual intercourse
S/Sx:
1. Pain – flank area
2. Urinary frequency & urgency
3. Burning upon urination
4. Dysuria & hematuria
5. Fever, chills, anorexia, gen body malaise
Diagnosis:
1. Urine culture & sensitivity - (+) to E. coli
Nursing Mgt:
1. Force fluid – 2000 ml
2. Warm sitz bath – to promote comfort
3. Monitor & assess for gross hematuria
4. Acid ash diet – cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication
5. Meds: systemic antibiotics
Ampicillin
Cephalosporin
Sulfonamides – cotrimaxazole (Bactrim)
- Gantrism (ganthanol)
Urinary antiseptics – Mitropurantoin (Macrodantin)
Urinary analgesic- Pyridum
6. Ht
a.) Importance of Hydration
b.) Void after sex
c.) Female – avoids cleaning back & front
Bubble bath, Tissue paper, Powder, perfume
d.) Complications:
Pyelonephritis
PYELONEPHRITIS – acute/ chronic infl of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess formation.
- Lead to Renal Failure
Predisposing factor:
1. Microbial invasion
a. E. Coli
b. Streptococcus
2. Urinary retention /obstruction
3. Pregnancy
4. DM
5. Exposure to renal toxins
S/Sx:
Acute pyelonephritis
a. Costovertibral angle pain, tenderness
b. Fever, anorexia, gen body malaise
c. Urinary frequency, urgency
d. Nocturia, dsyuria, hematuria
e. Burning on urination
Chronic Pyelonephritis
a. Fatigue, wt loss
b. Polyuuria, polydypsia
c. HPN
Diagnosis:
1. Urine culture & sensitivity – (+) E. coli & streptococcus
2. Urinalysis
Increase WBC, CHON & pus cells
3. Cystoscopic exam – urinary obstruction
Nursing Mgt:
1. Provide CBR – acute phase
2. Force fluid
3. Acid ash diet
4. Meds:
a. Urinary antiseptic – nitrofurantoin (macrodantin)
SE: peripheral neuropathy
GI irritation
Hemolytic anemia
Staining of teeth
b. Urinary analgesic – Peridium
5. Complication- Renal Failure
NEPHROLITHIASIS/ UROLITHIASIS- formation of stones at urinary tract
- calcium , oxalate, uric acid
milk cabbage anchovies
cranberries organ meat
nuts tea nuts
chocolates sardines
Predisposing factors:
1. Diet – increase Ca & oxalate
2. Hereditary – gout
3. Obesity
4. Sedentary lifestyle
5. Hyperparathyroidism
S/Sx:
1. Renal colic
2. Cool moist skin (shock)
3. Burning upon urination
4. Hematuria
5. Anorexia, n/v
Diagnosis:
1. IVP – intravenous pyelography. Reveals location of stone
2. KUB – reveals location of stone
3. Cytoscopic exam- urinary obstruction
4. Stone analysis – composition & type of stone
5. Urinalysis – increase EBC, increase CHON
Nursing Mgt:
1.Force fluid
2.Strain urine using gauze pad
3.Warm sitz bath – for comfort
4.Alternate warm compress at flank area
5. a.) Narcotic analgesic- Morphine SO4
b.) Allopurinol (Zyeoprim)
c.) Patent IV line
d.) Diet – if + Ca stones – acid ash diet
If + oxalate stone – alkaline ash diet - (Ex milk/ milk products)
If + uric acid stones – decrease organ meat / anchovies sardines
6. Surgery
a. Nephectomy – removal of affected kidney
Litholapoxy – removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones
b. Extracorporeal shock wave lithotripsy
- Non - invasive
- Dissolve stones by shock wave
7. Complications: Renal Failure
BENIGN PROSTATIC HYPERTROPHY - enlarged prostate gland leading to
a. Hydro ureters – dilation of ureters
b. Hydronephrosis – dilation of renal pelvis
c. Kidney stones
d. Renal failure
Predisposing factor:
1. High risk – 50 years old & above
60 – 70 – (3 to 4 x at risk)
2. Influence of male hormone
S/Sx:
1.Decrease force of urinary stream
2.Dysuria
3.Hematuria
4.Burning upon urination
5.Terminal bubbling
6.Backache
7.Sciatica
Diagnosis:
1. Digital rectal exam – enlarged prostate gland
2. KUB – urinary obstruction
3. Cystoscopic exam – obstruction
4. Urinalysis – increase WBC, CHON
Nursing Mgt:
1. Prostatic message – promotes evacuation of prostatic fluid
2. Limit fluid intake
3. Provide catheterization
4. Meds:
a. Terazozine (hytrin) - Relaxes bladder sphincter
b. Fenasteride (Proscar) - Atrophy of Prostate Gland
5. Surgery: Prostatectomy – TURP- Transurethral resection of Prostate- No incision
-Assist in cystoclysis or continuous bladder irrigation.
Nursing mgt:
c. Monitor symptoms of infection
d. Monitor symptoms gross/ flank bleeding. Normal bleeding within 24h.
3. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention
ACUTE RENAL FAILURE – sudden immobility of kidneys to excrete nitrogenous waste products & maintain F&E balance due to a decrease in GFR. (N 125 ml/min)
Predisposing factor:
Pre renal cause- decrease blood flow
Causes:
1. Septic shock
2. Hypovolemia
3. Hypotension decrease flow to kidneys
4. CHF
5. Hemorrhage
6. Dehydration
Intra-renal cause – involves renal pathology= kidney problem
1. Acute tubular necrosis-
2. Pyelonephritis
3. HPN
4. Acute GN
Post renal cause – involves mechanical obstruction
1. Stricture
2. Urolithiasis
3. BPH
CHRONIC RF – irreversible loss of kidney function
Predisposing factors:
1. DM
2. HPN
3. Recurrent UTI/ nephritis
4. Exposure to renal toxins
Stages of CRF
1. Diminished Reserve Volume – asymptomatic
Normal BUN & Crea, GFR < 10 – 30%
2. Renal Insufficiency
3. End Stage Renal disease
S/Sx:
|1.) Urinary System |2.) Metabolic disturbances |
|a.) polyuria |a.) azotemia (increase BUN & Crea) |
|b.) nocturia |b.) hyperglycemia |
|c.) hematuria |c.) hyperinulinemia |
|d.) Dysuria | |
|e.) oliguria | |
|3.) CNS |4.) GIT |
|a.) headache |a.) n/v |
|b.) lethargy |b.) stomatitis |
|c.) disorientation |c.) uremic breath |
|d.) restlessness |d.) diarrhea/ constipation |
|e.) memory impairment | |
|5.) Respiratory |6.) hematological |
|a.) Kassmaul’s resp |a.) Normocytic anemia |
|b.) decrease cough reflex |bleeding tendencies |
|7.) Fluid & Electrolytes |8.) Integumentary |
|a.) hyperkalemia |a.) itchiness/ pruritus |
|b.) hypernatermia |b.) uremic frost |
|c.) hypermagnesemia | |
|d.) hyperposphatemia | |
|e.) hypocalcemia | |
|f.) met acidosis | |
Nursing Mgt:
1. Enforce CBR
2. Monitor VS, I&O
3. Meticulous skin care. Uremic frost – assist in bathing pt
4. Meds:
a.) Na HCO3 – due Hyperkalemia
b.) Kagexelate enema
c.) Anti HPN – hydralazine
d.) Vit & minerals
e.) Phosphate binder
(Amphogel) Al OH gel - S/E constipation
f.) Decrease Ca – Ca gluconate
5. Assist in hemodialysis
1. Consent/ explain procedure
2. Obtain baseline data & monitor VS, I&O, wt, blood exam
3. Strict aseptic technique
4. Monitor for signs of complications:
B – bleeding
E – embolism
D – disequilibrium syndrome
S – septicemia
S – shock – decrease in tissue perfusion
Disequilibrium syndrome – from rapid removal of urea & nitrogenous waste prod leading to:
a. n/v
b. HPN
c. Leg cramps
d. Disorientation
e. Paresthesia
5. Avoid BP taking, blood extraction, IV, at side of shunt or fistula. Can lead to compression of fistula.
6. Maintain patency of shunt by:
i. Palpate for thrills & auscultate for bruits if (+) patent shunt!
ii. Bedside- bulldog clip
- If with accidental removal of fistula to prevent embolism.
- Infersole (diastole) – common dialisate used
7. Complication
- Peritonitis
- Shock
8. Assist in surgery:
Renal transplantation : Complication – rejection. Reverse isolation
EYES
External parts
1. Orbital cavity – made up of connective tissue protects eye form trauma.
2. EOM – extrinsic ocular muscles – involuntary muscles of eye needed for gazing movement.
3. Eyelashes/ eyebrows – esthetic purposes
4. Eyelids – palpebral fissure – opening upper & lower lid. Protects eye from direct sunlight
Meibomean gland – secrets a lubricating fluid inside eyelid
a. Stye/ sty or Hordeolum- inflamed Meibomean gland
5. Conjunctiva
6. Lacrimal apparatus – tears
Process of grieving
a. Denial
b. Anger
c. Bargaining
d. Depression
e. Acceptance
2. Intrinsic coat
I. sclerotic coat – outer most
a.) Sclera – white. Occupies ¾ post of eye. Refracts light rays
b.) Canal of schlera – site of aqueous humor drainage
c.) Cornea – transparent structure of eye
II/ Uveal tract – nutritive care
Uveitis – infl of uveal tract
Consist of:
a.) Iris – colored muscular ring of eye
2 muscles of iris:
1. Circular smooth muscle fiber - Constricts the pupil
2.radial smooth muscle fiber - Dilates the pupil
2 chambers of the eye
1. Anterior
a.) Vitereous Humor – maintains spherical shape of the eye
b.) Aqueous Humor – maintains intrinsic ocular pressure
Normal IOP= 12-21 mmHg
II. Retina (innermost layer)
i. Optic discs or blind spot – nerve fibers only
No auto receptors
cones (daylight/ colored vision) rods – night twilight vision
phototopic vision “scotopic vision” = vit A deficiency – rods insufficient
ii. Maculla lutea – yellow spot center of retina
iii. Fovea centralis – area with highest visual acuity oracute vision
Physiology of vision
4 Physiological processes for vision to occur:
1. Refraction of light rays – bending of light rays
2. Accommodation of lens
3. Constriction & dilation of pupils
4. Convergence of eyes
Unit of measurements of refraction – diopters
Normal eye refraction – emmetropia
ERROR of refraction
1. Myopia – near sightedness – Treatment: biconcave lens
2. Hyperopia/ or farsightedness – Treatment: biconvex lens
3. Astigmatisim – distorted vision – Treatment: cylindrical
4. Prebyopia – “old slight” – inelasticity of lens due to aging – Treatment: bifocal lens or double vista
Accommodation of lenses – based on thelmholtz theory of accommodation
Near vision = far vision=
Ciliary muscle contracts= ciliary muscle dilates / relaxes=
Lens bulges lens is flat
Convergence of the eye:
Error:
1. Exotropia – 1 eye normal
2. Esophoria – corrected by corrective eye surgery
3. Strabismus- squint eye
4. Amblyopia – prolong squinting
GLAUCOMA – increase IOP – if untreated, atrophy of optic nerve disc – blindness
Predisposing factors:
1. High risk group – 40 & above
2. HPN
3. DM
4. Hereditary
5. Obesity
6. Recent eye trauma, infl, surgery
Type:
1. Chronic – (open angle G.) – most common type
Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema
2. Acute (close angle G.) – Most dangerous type
Forward displacement of iris to cornea leading to blindness.
3. Chronic (closed – angle) - Precipitated by acute attack
S/Sx:
1. Loss of peripheral vision – tunnel vision
2. Halos around lights
3. Headache
4. n/v
5. Steamy cornea
6. Eye discomfort
7. If untreated – gradual loss of central vision – blindness
Diagnosis:
1. Tonometry – increase IOP >12- 21 mmHg
2. Perimetry – decrease peripheral vision
3. Gonioscopy – abstruction in anterior chamber
Nursing mgt:
1. Enforce CBR
2. Maintain siderails
3. Administer meds
a. Miotics – lifetime - contracts ciliary muscles & constricts pupil. Ex Pilocarpine Na (Carbachol)
b. Epinephrine eye drops – decrease secretion of aqueous humor
c. Carbonic anhydrase inhibitors. Ex. acetapolamide (Diamox)
- Promotes increase out flow of aquaeous humor
d.) Temoptics (Timolol maleate)- Increase outflow of aquaous humor
4. Surgery:
Invasive:
a. Trabeculectomy – eyetrephining – removal of trabelar meshwork of canal or schlera to drain aqueous humor
b. Peripheral Iridectomy – portion of iris is excised to drain aqueous humor
Non-invasive:
Trabeculoctomy (eye laser surgery)
Nursing Mgt pre op- all types surgery
1. Apply eye patch on unaffected eye to force weaker eye to become stronger.
Nursing Mgt post op – all types of surgery
1. Position unaffected/ unoperated side - to prevent tension on suture line.
2. Avoid valsalva maneuver
3. Monitor symptoms of IOP
a. Headache
b. n/v
c. Eye discomfort
d. Tachycardia
4. Eye patch – both eyes - post op
CATARACT – partial/ complete opacity of lens
Predisposing factor:
1. 90-95% - aging (degenerative/ senile cataract)
2. Congenital
3. Prolonged exposure to UV rays
4. DM-
S/Sx:
1. Loss of central vision - “Hazy or blurring of vision”
2. Painless
3. Milky white appearance at center of pupil
4. Decrease perception of colors
Diagnosis: Opthalmoscopic exam – (+) opacity of lens
Nsg Mgt:
1. Reorient pt to environment – due opacity
2. Siderails
3. Meds – a.) Mydriatics – dilate pupil – not lifetime
Ex. Mydriacyl
c. Cyslopegics – paralyzes ciliary muscle. Ex. Cyclogye
4. Surgery
E – extra
C - capsular
C – cataract partial removal of lens
L - lens
E – extraction
I - intra
C - capsular
C – cataract total removal of lens & surrounding capsules
L - lens
E – extraction
Nursing Mgt:
1.Position unaffected/ unoperated side - to prevent tension on suture line.
2.Avoid valsalva maneuver
3.Monitor symptoms of IOP
a. Headache
b. n/v
c. Eye discomfort
d. Tachycardia
4.Eye patch – both eyes - post op
RETINAL DETACHMENT- separation of 2 layers of retina
Predisposing factors:
1. Severe myopia – nearsightedness
2. Diabetic Retinopathy
3. Trauma
4. Following lens extraction
5. HPN
S/Sx:
1. “Curtain –veil” like vision
2. Flashes of lights
3. Floaters
4. Gradual decrease in central vision
5. Headache
Diagnosis- opthaloscopic exam
Nursing Mgt:
1. Siderails (all visual disease)
2. Surgery:
a. Cryosurgery
b. Scleral buckling
EAR –
1. Hearing
2. Balance (Kinesthesia or position sense)
Parts:
1. Outer-
a. Pinna/ auricle – protects ear from direct trauma
b. Ext. auditory meatus – has ceruminous gland. Cerumen
c. Tympanic membrane – transmits sound waves to middle ear
Disorders of outer ear
Entry of insects – put flashlight to give route of exit
Foreign objects – beans (bring to MD)
H2O - drain
2. Middle ear
a.) Ear osssicle
1. Hammer -malleus
2. Anvil -Incus for bone conduction disorder conductive hearing loss
3. Stirrups -stapes
b. Eustachian tube - Opens to allow equalization of pressure on both ears
- Yawn, chew, and swallow
Children – straight, wide, short
b. Otitis media
Adult – long, narrow & slanted
c. Muscles
1. Stapedius
2. Tensor tympani
3. Inner ear
a. Bony labyrinth – for balance, vestibule
Utricle & succule
Otolithe or ear stone – has Ca carbonate
Movement of head = Righting reflex = Kinesthesia
b. Membranous Labyrinth
1. Cochlea – ( function for hearing) has organ of corti
2. Endolymph & perilymph – for static equilibrium
3. Mastoid air cells – air filled spaces in temporal bone in skull
Complications of Mastoditis – meningitis
Types of hearing loss:
1. Conductive hearing loss – transmission hearing loss
Causes:
a. Impacted cerumen – tinnitus & conduction hearing loss- assist in ear irrigaton
b. Immobility of stapes – OTOSCLEROSIS
c. Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes
d. Stapes can’t transmit sound waves
Surgery
Stapedectomy – removal of stapes, spongy bone & implantation of graft/ ear prosthesis
Predisposing factor:
1. Familiar tendency
2. Ear trauma & surgery
S/Sx:
1. Tinnitus
2. Conductive hearing loss
Diagnosis:
1. Audiometry – various sound stimulates (+) conductive hearing loss
2. Weber’s test – Normal AC> BC
result BC > AC
Stapedectomy
Nursing Mgt post op
1. Position pt unaffected side
2. DBE
No coughing & blowing of nose
- Night lead to removal of graft
3. Meds:
a. Analgesic
b. Antiemetic
c. Antimotion sickness agent. Ex. meclesine Hcl (Bonamine)
4. Assess – motor function – facial nerve - (Smile, frown, raise eyebrow)
5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap
SENSORY NEURAL HEARING LOSS/ NERVE DEAFNESS
Cause:
1. Tumor on cocheal
2. Loud noises (gun shot)
3. Presbycusis – bilateral progressive hearing loss especially at high frequencies – elderly
Face elderly to promote lip reading
4. Meniere’s disease – endolymphatic hydrops
e. Inner ear disease char by dilation of endo – lympathic system leading to increase volume of endolin
Predisposing factor of MENIERE’S DISEASE
Smoking
Hyperlipidemia
30 years old
Obesity – (+) chosesteatoma
Allergy
Ear trauma & infection
S/Sx:
1. TRIAD symptoms of Meniere’s disease
a. Tinnitus
b. Vertigo
c. Sensory neural hearing loss
2. Nystagmus
3. n/v
4. Mild apprehension, anxiety
5. Tachycardia
6. Palpitations
7. Diaphoresis
Diagnosis:
1. Audiometry – (+) sensory hearing loss
Nursing mgt:
1. Comfy & darkened environment
2. Siderails
3. Emetic basin
4. Meds:
a. Diuretics –to remove endolymph
b. Vasodilator
c. Antihistamine
d. Antiemetic
e. Antimotion sickness agent
f. Sedatives/ tranquilizers
5. Restrict Na
6. Limit fluid intake
7. Avoid smoking
8. Surgery – endolymphatic sac decompression- Shunt
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AV
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