I
PCM Spring Exam Material
I. Anemia
a. General Approaches to Anemia- Hematocrit < 41% in males, 200 mg/dl
ii. Plasma glucose of 126 mg/dl or higher after an overnight fast, documented on more than one occasion
iii. Ketonemia, ketonuria, or both
TYPE 2 DIABETES
i. Most patients are over 40 yo and obese
ii. Polyuria and polydipsia. Ketonuria and weight loss generally are uncommon at time of diagnosis. Candidal vaginitis in women may be an initial manifestation. Many patients have few or no symptoms
iii. Plasma glucose of 126 mg/dl or higher after an overnight fast on more than one occasion. After 75 g oral glucose, diagnostic values are 200 mg/dl or more 2 hrs after oral glucose.
iv. HTN, dyslipidemia, and atherosclerosis are often associated
b. Clinical Findings:
| |Type 1 Diabetes |Type 2 Diabetes |
|Polyuria and thirst |++ |+ |
|Weakness or fatigue |++ |+ |
|Polyphagia with weight loss |++ |- |
|Recurrent blurred vision |+ |++ |
|Vulvovaginitis or pruritus |+ |++ |
|Peripheral neuropathy |+ |++ |
|Nocturnal enuresis |++ |- |
|Often asymptomatic |- |++ |
c. Labs:
i. Urinalysis: Glucosuria, ketonuria
ii. Blood testing procedures: Glucose tolerance test, glycated hgb, serum fructosamine, self-monitoring of blood glucose, continuous glucose monitoring system, lipoprotein abnormalities in diabetes
d. DDx.: Hyperglycemia secondary to other causes (Cushing’s, CST, acromengaly, liver disease, muscle disorders…); Non-diabetic glycosuria
e. Goals of Treatment: Pt. ed, restore known metabolic derangements toward normal in order to prevent and delay progression of diabetic complications
f. Treatment: Pt. ed, diet, oral agents, insulin
X. Diseases of the Thyroid
a. Tests of Thyroid Function: TSH (most sensitive), free T4; thyroid radioactive iodine uptake and scan
b. Hypothyroidism and Myxedema
i. Essentials of Diagnosis
1. Weakness, fatigue, cold intolerance, constipation, weight change, depression, menorrhagia, hoarseness
2. Dry skin, bradycardia, delayed return of deep tendon reflexes
3. Anemia, hyponatremia
4. T4 and radioiodine uptake usually low
5. TSH elevated in primary hypothyroidism
ii. Clinical Findings:
1. Early: Fatigue, lethargy, weakness, arthralgias or myalgias, muscle cramps, cold intolerance, constipation, dry skin, HA, and menorrhagia PE: Thin, brittle nails, thinning of hair, and pallor, poor mucosa turgor, decreased return of deep tendon reflexes
2. Late: Slow speech, absence of sweating, constipation, peripheral edema, pallor, hoarseness, decreased sense of taste and smell, muscle cramps, aches and pains, dyspnea, weight changes, diminished auditory acuity PE: goiter, puffiness of face, carotenemic skin color, thinning of outer eyebrows, thickening of tongue, hard pitting edema, effusions
3. Labs: Free T4: normal to low; TSH: increased in primary, low or normal in pituitary insufficiency; Lipid panel (increased cholesterol), increased liver enzymes, CK…
iii. DDx: Unexplained heart failure, primary amyloidosis, pernicious anemia, depression
iv. Complications: Mostly cardiac (advanced CAD), megacolon, increased susceptibility to infection, organic psychoses, rarely causes infertility, miscarriage, can progress to myxedema coma
v. Treatment: Thyroid replacement therapy, usually T4; reassess T4 levels regularly
c. Hyperthyrodism
i. Essentials of Diagnosis
1. Sweating, weight loss or gain, anxiety, loose stools, heat intolerance, irritability, fatigue, weakness, menstrual irregularities
2. Tachycardia; warm, moist skin; stare; tremor
3. In Grave’s disease: goiter, ophthalmopathy
4. Suppressed TSH in primary hyperthyroidism; increased T4, free T4 and free T4 index
ii. General Considerations: Grave’s disease, Toxic adenomas, subacute thyroiditis, jodbasedow disease (iodine-induced hyperthyroidism), thyrotoxicosis factitia, struma ovarii, pituitary tumor, hashimoto’s thyroiditis, pregnancy and trophoblastic tumors, thyroid carcinoma, amiodarone-induced thyrotoxicosis
iii. Clinical Findings: SEE Essentials of Diagnosis; LABS: T4 an TSH levels, serum TSH receptor antibody, serum ANA and anti-dsDNA, sedimentation rate, thyroid radioactive iodine uptake and scan
iv. DDx: Anxiety, mania, acute psychiatric disorder, cardiac disease, hypermetabolism (pheochromocytoma), diabetes, Addison’s
v. Complications: Cardiac complication, periodic paralysis w/ exercise or heavy carb intake, hypercalcemia, osteoporosis, and nephrocalcinosis
vi. Treatment: Depends on cause
1. Graves: Propanol for sympathetic relief, thiouria drug, methimazole, propylthiouracil, iodinated contrast agents, radioactive iodine (destroys active thyroid tissue)- not to pregnant women
XI. Metabolic Bone Disease
a. Osteoporosis
i. Essentials of Diagnosis
1. Asymptomatic to severe backache from vertebral fractures
2. Spontaneous fractures often discovered incidentally on radiography; loss of height
3. Serum parathyroid hormone, 25(OH)D2, Ca, phosphorous, and alkaline phosphatase usually normal
4. Demineralization, esp. of spine, hip, and plevis
ii. Etiology
1. Hormonal deficiency: Estrogen, androgen
2. Hormonal Excess: Glucocorticoid, thyrotoxicosis, hyperparathyroidism
3. Immobilization, microgravity
4. Tobacco, Alcoholism
5. Malignancy, esp multiple myeloma
6. Meds: xs. Vit D, xs. Vit A, heparin therapy
7. Genetic: Aromatase deficiency, Type I collagen mutations, Osteogenesis imperfecta, idiopathic juvenile and adult osteoporosis, Ehlers-Danlos syndrome, Marfan’s syndrome, homocystinuria
8. Misc: Anorexia, protein-calorie malnutrition, vit. C deficiency, copper deficiency, liver disease, RA, uncontrolled DM, systemic mastocytosis
iii. Clinical Findings: Usually asymptomatic until fracture occurs; backache; loss of height; LABS: Serum Ca, phosphate and PTH are normal, test for thyrotoxicosis, hypogonadism, and vit. D deficiency; DEXA scan
iv. DDx.: See possible etiologies
v. Treatment: Sex hormones, biphosphonates (inhibit osteoclast-induced bone resorption), selective estrogen receptor modulators (SERMs), calcitonin, calcium and vit. D, teriparatide (analog of PTH)
vi. Prognosis: Good if interventions are started early
b. Osteomalacia
i. Essentials of Diagnosis
1. Painful proximal muscle weakness; bone pain and tenderness
2. Decreased bone density from diminished mineralization of osteoid
3. Lab abnormalities may include increases in alkaline phosphatase, decreased 25-hydroxy-vitamin D, or hypocalciumia, hypocalciuria, hypophosphatemia, secondary hyperparathyroidism
4. Classic radiologic features may be present
ii. General Considerations:Commonly caused by a deficiency in vit. D
iii. Etiology: Vit. D deficiency and resistance, deficient calcium intake, phosphate deficiency, aluminum toxicity, hypophosphatasia, fibrogenesis imperfecta ossium
iv. Clinical Findings: Depends on age and severity; ADULTS: asymptomatic at first followed by bone pain and muscle weakness, fractures may occur; CHILD: Ricketes
v. Diagnostic Tests: LABS: Serum calcium, albumin, phosphate, alkaline phosphatase, PTH, and 25-hydroxyvitamin D; DEXA
vi. DDx.: Osteoporosis (fairly neg. labs)
vii. Prevention and Treatment: Treat underlying cause; sunlight exposure and vit. D supplements, oral calcium
XII. Arthridities
a. Diagnosis and evaluation
i. Examination of the patient: Presence or absence of extra-articular manifestations: Is inflammation present? How many joints are involved? And What joints are affected?
1. Joint inflammation is manifested by redness, warmth, swelling, and morning stiffness of at least 30 min
b. Degenerative Joint Disease
i. Essentials of diagnosis
1. Commonly secondary to other articular disease
2. A degenerative disorder without systemic manifestations
3. Pain relieved by rest; morning stiffness brief; articular inflammation minimal
ii. General considerations: PRIMARY: Commonly affects some or all of the following: terminal interphalangeal joints, proximal interphalangeal joints, the metacarpophalangeal and carpometacarpal joints of the thumb, the hip, the knee, the metatarsophalangeal joint of the big toe, the cervical and lumber spine SECONDARY: Occurs in any joint as a sequela to articular injury (acute or chronic, metabolic or neurologic disease)
iii. Clinical findings S/S: Insidious onset; Initial: Articular stiffness < 15 min ( Pain on motion of the affected joint ( deformity, crepitus; joint effusion and inflammation are mild; LABS: none; IMAGE: Radiographs, joint aspiration
iv. DDx.: Usually not confused with other forms of arthritis
v. Prevention: Weight loss, HRT, maintaining normal vit. D level
vi. Treatment: Weight loss, NSAIDS, surgical measures if all else fails and is debilitating
vii. Prognosis: Better than RA, can be severe and debilitating
c. Crystal Deposition Arthritis (Gouty arthritis)
i. Essentials of diagnosis
1. Acute onset, typically nocturnal and usually monoarticular, often involving the 1st metatarsopharyngeal joint
2. Postinflammatory desquamation and pruritus
3. Hyperuricemia in most, ID of urate crystals in joint fluid or tophi is diagnostic
4. Dramatic therapeutic response to NSAIDs or colchicine
5. With chronicity, urate deposits in subcutaneous tissue, bone, cartilage, joints, and other tissue
ii. General considerations: Primary vs. secondary
iii. Clinical findings:
1. S/S: Sudden onset, frequently nocturnal, w/ or w/o obvious precipitation due to fluctuating serum urate levels; intense pain as the attack progresses; affected joint is swollen, tender; overlying skin is tense, warm, and dusky red; local desquamation and pruritis; tophi found in external ears, hands, feet, olecranon, and prepatellar bursas; fever is common
2. LABS: Serum uric acid is elevated (normal in 25%), CBC, sedimentation rate, aspiration of affected joint, tophus, x-ray
iv. DDx.: Cellulitis, acute pyogenic arthritis (exclude with bacteriologic studies), chronic RA, chronic lead intoxication
v. Treatment: ACUTE: NSAIDs (NO aspirin), corticosteroids, analgesics (for pain); BETWEEN ATTACKS: Diet (low purine diet (high purine: meats, yeasts, some vegetables), weight loss, decrease alcohol); low dose colchicines; allopurinol
vi. Prognosis:
d. Crystal Deposition Arthritis (Chondrocalcinosis and pseudogout)
XIII. Autoimmune Disease
a. Rheumatoid Arthritis
i. Essentials of Diagnosis
1. Prodromal systemic symptoms of malaise, fever, weight loss, and morning stiffness
2. Onset is usually insidious and in small joints; progression is centripetal and symmetric; deformities common
3. Radiographic findings: juxta-articular osteoporosis, joint erosions, and narrowing of the joint space
4. Rheumatic factor is usually present
5. Extra-articular manifestations: subcutaneous nodules, pleural effusions, pericarditis, lymphadenopathy, splenomegaly with leucopenia, and vasculitis
ii. Clinical Findings:
1. S/S: Prodromal symptoms: malaise, weight loss, and vague periarticular pain or stiffness; symmetric joint swelling with associated stiffness, warmth, tenderness, and pain; Stiffnes >30 min in morning (better throughout the day)
2. LABS: Rhematic factor, ANA, CBC; radiograph
iii. DDx.: Rheumatic fever, SLE, osteoarthritis, gout, septic arthritis
iv. Treatment: Education, physical and occupational therapy, systemic rest, articular rest, exercise, heat and cold, assistive devices, splints, weight loss; NSAIDS, TNF-α inhibitors, Methotrexate, CST
v. Course and Prognosis
b. Systemic Lupus Erythematosus
i. Essentials of Diagnosis
1. Occurs mainly in young women
2. Rash over areas exposed to sunlight
3. Joint symptoms in 90% of patients. Multiple system involvements
4. Depression of hemoglobin, WBC, and platelets
5. Serologic findings: ANA, anti-ds DNA ab, low serum complement levels
ii. Clinical Findings
1. S/S: Fever, anorexia, malaise, and weight loss. Skin lesions (butterfly rash), alopecia, joint symptoms; LABS: CBC, ANA, anti-ds DNA, complement levels
2. 4 of the following 11 criteria: Malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal disease, neurologic disease, hematologic disorders, immunologic abnormalities, positive ANA
iii. Treatment: Supportive care, rest, NSAIDs, CST
XIV. Headaches: Intensity, quality and site of pain
a. Tension HA:
i. S/S: Poor concentration, daily, tight in quality, exacerbated by emotional stress, fatigue, noise or glare. HA are generalized and may be most tense about the neck or back of the head
ii. Tx: NSAIDs, antimigrainous agents, relaxation techniques
b. Depression HA:
i. S/S: Worse than tension HA, arise in the morning, accompany depression
ii. Tx: Anti-depressants
c. Migraine:
i. S/S: Lateralized throbbing HA, can be generalized. Associated with anorexia, nausea, vomiting, photophobia, phonophobia, and blurring of vision. Usually have triggers, follow a prodrome and persist for hours
ii. Tx.: Avoid triggers, during attack rest in quiet, dark room, NSAID, or anti-migraine medication
d. Cluster HA:
i. S/S: Middle-aged men; severe uni-lateral periorbital pain occur daily for several weeks; accompanied by ipsilateral nasal congestion, rhinorrhea, lacrimination, redness of eye, and Horner’s syndrome; occur at night, awaken the patient, and last for < 2 hours; Spontaneous remission; have triggers
ii. Tx: Subcutaneous sumatriptan to treat current attack; Ergotamine tartrate as rectal suppository for prophylaxis therapy (also can use propranolol, lithium carbonate, prednisone)
e. Giant Cell (Temporal or cranial) Arteritis
i. S/S: Elderly; HA associated with myalgia, malaise, anorexia, weight loss; complication: loss of vision; exam reveals tenderness of scalp and over temporal arteries
ii. Tx: Biopsy, further tx in chapter 20
f. Posttraumatic HA
i. S/S: Appears within a day following injury; worsen over the ensuing week and then subside; described as a constant dull ache with superimposed thrombing; may be accompanied by nausea, ,vomiting, or scinitillating scotomas; disequilibirium, impaired memory, poor concentration, emotional instability; CT scan is normal
ii. Tx.: Encouragement and graduated rehab, HA may respond to NSAIDs
g. Cough HA
i. S/S: Last only a few minutes following coughing; GET A CT: rule out Arnold-chiari or some space occupying lesion
ii. Tx.: Sometimes clear after lumbar puncture, indomethacin may provide relief
h. HA due to intracranial mass lesions
i. S/S: Dependent of location; non-specific (mild-severe); may worsen with exertion or postural change; associated with nausea and vomiting; GET CT scan
i. HA due to other neurologic cause
XV. CVA
a. Transient Ischemic Attacks
i. Essentials of Diagnosis
1. Focal neurologic deficit of acute onset
2. Clinical deficit resolves completely within 24 hours
3. Risk factors for vascular disease often present
ii. General considerations: 30% of people with stroke have history of TIA; risk of stroke is highest in the one month following TIA
iii. Etiology: From embolization; Subclavian Steal Syndrome – transient vertebrobasilar ischemia, localized stenosis or occlusion of one subclavian artery proximal to the source of the vertebral artery
iv. Clinical Findings:
1. S/S: Vary between people, remain constant in an individual; abrupt onset followed by complete recovery;
a. Carotid artery: weakness and heaviness of contralateral arm, leg, or face; can also see numbness or paresthesias; slowness of movement, dysphagia, or monocular visual loss in eye contralateral to limbs affected; Exam: flaccid weakness, sensory changes, hyperreflexia, positive babinski response, dysphagia
b. Vertebrobasilar: Vertigo, ataxia, diplopia, dysarthria, dimness or blurring of vision, perioral numbness and paresthesias, and weakness or sensory complaints on one, both, or alternating sides of body
2. Imaging: CT scan, MR angiography
3. Labs: Assessment for HTN, heart disease, hematologic disorders, DM, hyperlipidemia, and peripheral vascular disease; CBC, fasting blood glucose and serum cholesterol and homocysteine determinations, serologic tests for syphilis, and ECG and CXR
v. DDx.: Focal seizures, classic migraine, focal neurologic deficits during periods of hypoglycemia in DM
vi. Treatment: Operative treatment if angiogram reveals focal high grade stenosis; stop smoking; anticoagulation therapy with Heparin followed by Warfarin; Treat underlying cause
b. Stroke
i. Essentials of diagnosis
1. Sudden onset of characteristic neurologic deficit
2. Patient often has history of HTN, DM, valvular heart disease, or atherosclerosis
3. Distinctive neurologic signs reflect the region of brain involved
ii. Lacunar infarction:
1. Small lesions that occur in the basal ganiglia, pons, cerebellum, anterior limb of internal capsule
2. Due to HTN; cause pure sensory deficit, ipsilateral ataxia with crural paresis, and dysarthria with clumisness of hand; CT
iii. Cerebral infarction: thrombotic or embolic occlusion
1. Clinical findings:
a. Carotid circulation
i. Opthalmic: Sudden, brief loss of vision in one eye
ii. ACA: Weakness and cortical sensory loss in contralateral leg; contralateral grasp reflex, paratonic rigidity, and abulia or frank confusion
iii. MCA: Contralateral hemiplegia, hemisensory loss, and homonymous hemianopia (eyes deviate toward side of lesion); global aphasia
b. Obstruction of vetebrobasilar circulation
i. PCA: Thalamic syndrome, spontaneous pain and hyperpathia; macular sparing hemianopia
ii. Veterbral artery: May be clinically silent; if both, or basilar: coma with pinpoint pupils, flaccid quadriplegia and sensory loss, and variable cranial nerve abnormalities
iii. Cerebellar arteries: Vertigo, nausea, vomiting, nystagmus, ipsilateral limb ataxia, and contralateral spinothalamic sensory loss in limbs
c. Imaging: CT scan in first 48 hours
d. Labs: CBC, sedimentation rate, blood glucose, serologic test for syphilis, ANA levels, lipid panel, ECG
2. Treatment: Thrombolytic therapy if within first 3 hours; anticoagulants, heparin followed by warfirin; Physical therapy
3. Prognosis
iv. Intracerebral hemorrhage
1. Clinical findings
a. S/S: Usually due to HTN; initial loss of consciousness; vomiting, HA; further signs depend on location
b. Imaging: CT scan without contrast
c. Labs: CBC, platelet count, bleeding time, PPT and aPPT, liver and renal function test; NO lumbar puncture
2. Treatment: Neurologic management is conservative and supportive;
v. Subarachnoid hemorrhage (often associated with aneurysm or AVM)
1. Essentials of Diagnosis:
a. Sudden severe HA
b. Signs of meningeal irritation usually present
c. Obtundation is common
d. Focal deficits frequently absent
2. Clinical findings
a. S/S: Sudden, very severe HA followed by nausea and vomiting; loss of consciousness; if consciousness is regained, confused and irritable, altered mental status; EXAM: Nuchal rigidity
b. Imaging: CT scan immediately
3. Treatment: Confined to bed, advised against exercise or straining, treated symptomatically for HA and anxiety, given laxatives and stool softeners; IF hyptertensive, slowly lower BP; Phenytoin to prevent seizures
vi. Intracranial Aneurysm
1. Clinical findings: Usually asymptomatic until they rupture, then present as subarachnoid hemorrhage; can have warning leak; SEE ABOVE FOR LABS AND IMAGING + angiography and lumbar puncture
2. Treatment: Surgical intervention to prevent further ruptures + treatment for subarachnoid hemorrhage
vii. Arteriovenous Malformations
1. Clinical findings
a. Supratentorial: Most are supratentorial; hemorrhage, recurrent seizures, HA, and focal deficits; generally bleed before the age of 40; cranial bruits (best heard over the ipsilateral eye or mastoid region)
b. Infratentorial: Clinically silent, may hemorrhage, cause hydrocephalus or lead to progressive and relapsing brain stem deficits
c. Imaging: CT scan, angiography, MRI
d. Labs: CSF examination
2. Treatment: Surgical intervention: either removal or emboliation
viii. Intracranial venous thrombosis
c. Spinal cord vascular disease
i. Essentials of diagnosis
1. Sudden onset of back or limb pain and neurologic deficit in limbs
2. Motor, sensory, or reflex changes in limbs depending on level of lesion
3. Imaging studies distinguish between infarcts and hematoma
ii. Infections of the spinal cord: Rare; only occurs in territory of anterior spinal artery; acute onset of flaccid, areflexive paraplegia ( spastic paraplegia with extensor plantar responses; dissociated sensory loss (preservation of vibration and position) Tx.: Symptomatic
iii. Epidural or subdural hemorrhage: Sudden severe back pain followed by acute comprehensive myelopathy
iv. Arteriovenous malformation of the spinal cord: Congenital; present with spinal subarachnoid hemorrhage or myeloradiculopathy; motor and sensory disturbances in legs or arms and to sphincter disorders; EXAM: upper, lower, or mixed motor deficit in legs, sensory deficits; IMAGING: Myelography, spinal arteriography; TRETMENT: ligation of vessels
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