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TELEGRAM RECALL 5

1-Homeless guy with bags going to police for shelter with 3 bags as he thinks someone wants to kill him because of the use of xrated cd(pornography). Management?

A full medical assessment

B admit for psychiatry assessment

C antipsychotic

D history from police ( I had this question in my exam but option D was not there..)

Consensus not refrence: initially complete history from patient and cares accompanying the patient thenFirst matabolic assessment,second psychiatric assessment.

2- alcoholic patient -now presented with alcoholic withdrawal symptoms-security cant control him-severe agitation-what u will give first :

1-I.M HALOPERIDOL (if psychotic features)

2-I.V THIAMINE

3-I.V MEDAZOLAM (no psychotic features)

(no options for..... DIAZEPAM...OR...LORAZEPAM)

در مورد alcohol withdrawal چيزى كه گايدلاين ميگه اينه :

- ديازپام خوراكى

- اگه همكارى نميكرد ديازپام رقيق شده يا ميدازولام IV

- اگه مريض خيلى آژيته بود و IV نميشد گرفت ميدازولام IM

- اگه مريض علائم سايكوتيك شديد هم داشت droperidol OR haloperidol IM (كه البته گفته بين اين دو هالوپريدول بهتره چون كمتر باعث كاهش seizure threshold ميشه)

alcohol withdrawal syndromes

|Syndrome | Clinical findings | Onset after last drink |

|Minor withdrawal |Tremulousness, mild anxiety, headache, |6 to 36 hours |

| |diaphoresis, palpitations, anorexia, GI upset; | |

| |Normal mental status | |

|Seizures |Single or brief flurry of generalized, |6 to 48 hours |

| |tonic-clonic seizures, short post-ictal period;| |

| |Status epilepticus rare | |

|Alcoholic hallucinosis |Visual, auditory, and/or tactile hallucinations|12 to 48 hours |

| |with intact orientation(sensorium rmains | |

| |normal, not delirious) and normal vital signs | |

|Delirium tremens |Delirium, agitation, tachycardia, hypertension,|48 to 96 hours |

| |fever, diaphoresis | |

3-Obese depressed middle age woman with signs of excessive hair growth. What to check:

tsh,

LFT,

testosterone,

cortisol in options

Cushing syndrome across but one up

4-27.Q about 65 yo your doc colleague who recently start to be forgetful and once been lost in place. What you must to do about it:

report to your top hospital managing office.

Talk to him.

Advice visit his gp.

Weird option about report him to appropriate board

across but one up

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5-which of the following is the best predictor value for prognosis a patient with systolic heart failure ?

1. jugular venous pressure

2.chest pain

3. prepheral edema

4.shortness of breath

5. Orthopnea

Prognosis of heart failure

The most frequently used factors for predicting survival in patients with systolic HF, many of which are direct or indirect measures of the severity of cardiac dysfunction, include:

• High New York Heart Association (NYHA) functional class ( table 2 below)

• Reduced left ventricular ejection fraction (LVEF) and reduced cardiac index (CI)

• Concomitant diastolic dysfunction, as established by a mitral flow velocity pattern on Doppler echocardiogram

• Reduced right ventricular function

• Low peak VO2 with maximal exercise and exercise hemodynamics

• Markers of reduced tissue perfusion including low mean arterial pressure, renal insufficiency (creatinine clearance 2 months of age. Apply to whole body from jawline down (include every flexure and area), leave overnight, then wash off. Wash clothing and linen after treatment and hang them in sun.

or

benzyl benzoate 25% emulsion left for 24 hours before washing off; repeat after 7 days .

ولی گال وزیکول نمیده اونای دیگه هم نمیخوره مولسکوم هم وزیکول نداره

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Various methods: liquid nitrogen …

45-50 y/o man having sex every night with hookers going to club, gambling, insomnia. Mx?

Mirtazapine

Depakine

Resperidone

Hypomania , risperidone

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46-35 years old woman with irregular menses came with 6weeks amenorrhea. fsh tsh oestradiol whitin nl levels.progestrone challenge test doesn't bleeding. whats the ioc?

pituitary mri

Vaginal sono (intrautrin scaring…)

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47- Interstate truck driver got insomnia with tremos, palpitation and wt loss for 3 months.next investigation?

1-TSH

2-Urinary drug sdreening

سئوال ٥٠ من همچنان معتقدم كه جواب گزينه ٢ هست .

تو آمدكس هم نوشتم :

احتمال اينكه يك راننده كاميون واسه بيدار موندن و رانندگى طولانى سراغ مصرف مواد بره خيلى بيشتره تا اينكه هايپرتيروئيد شده باشه . و اصولاً هر راننده كاميونى addict هست تا زمانى كه خلافش ثابت بشه .

دانيلا هم بعد كامنت من يك مقاله گذاشته كه خبر از ميزان بالاى مصرف مواد در رانندگان كاميون ميداد .

48- Young pt. travel by airplane had chest pain with dyspnea mild , no other symptoms hx of sickle cell triat what to do next ?

A) O2 by mask

B) hydration

C) blood transfusion

D) Intubation & O2

E) splenectomy

اون سئوالى كه ما جوابش رو ميزديم مسكن ، درد سينه نداشت و درد شديد پا داشت . من اون سئوال رو همچنان ميزنم مسكن ولى اين سئوال رو ميزنم اكسيژن (حتى اگه مسكن در گزينه ها باشه)

49-what is the most appropriate treatment in case of esophageal varise in addition to IV fluid blood.plt and plasma?

1.octerotide

2.Banding

3.TIPS

4.propranolol

5.Antibiotics

قدم اول هميشه درمان دارويى هست و مهمترين اقدام كنترل خونريزى. پس بلافاصله octerotide شروع ميكنيم

بعد از اين بايد هرچه زودتر اندوسكپى بشه براى band ligation يا sclerotherapy

یعنی اول مایعات و ترانسفیوژن بعد اکتروتید بعد انتی بیوتیک رو شروع میکنیم.آندوسکوپی و band ligationیا اسکلروتراپی اگر انجام مراحل فوق موفق نبود بالون مینه سوتا یا سوند بلاک مور.استفاده از TIPS درصورت موفق نبودن هیچ کدام از موارد فوق.TIPS را فقط در کسانی میتوان استفاده کرد که کاندید پیوند کبد هستند.

دكتر جان حق با شماست. من الان آپتوديت رو نگاه كردم و اونم نظرش مثل هاريسون هست. گفته احتمالاً ريسك عود خونريزى رو كم ميكنه اما نگفته چجورى. ضمناً اين رو هم نوشته:

A reasonable conclusion from these data is that patients with cirrhosis who present with upper GI bleeding (from varices or other causes) should be given prophylactic antibiotics, preferably before endoscopy (although effectiveness has also been demonstrated when given after endoscopy). The benefit to antibiotics is probably greater in patients with advanced liver disease (Child Pugh class B and C) [37] (table 1) but all patients with cirrhosis should be considered eligible.

49-football player has an injury while playing after that there was n effusion n he feel his leg is giving away n some other time his knee is locked dx?

1.ant.cruciate lig. injury

2.Med miniscal lig

3.med miniscal +lig.injury

4.patella fx

Effusion sign of ligament lesion + give away and locked knee signs of med. Mensci lesion

50-pt with RA is on many drugs.presents with fatigue on CBC all 3 cell line r reduced.reason?

1.Aspirin

2.Diclofenac

3.Hydroxychlorquin

• Hematologic: Aminoquinolines have been associated with rare hematologic reactions, including agranulocytosis, aplastic anemia, and thrombocytopenia; monitoring (CBC) is recommended in prolonged therapy. (خانوم غیاثوند خودمون

51- Psychotic pt admitted and fine but suddenly start behaving aggressively, and urine incontinence on antipsychotic and benzos:

relapse of psychosis,

uti,

benzotoxixicty,

antipsychotic toxicity

هم ميتونه عارضه bnz باشه هم فرم خفيفى از nms من اول با bnz موافق بودم اما بعداً بنظرم آمد دومى انتخاب بهترى هست. چون agitation با bnz شايع نيست.

Neuroleptic malignant syndrome — Neuroleptic malignant syndrome (NMS), a tetrad of clinical features (fever, rigidity, mental status changes, and autonomic instability), is associated with medications that block dopamine transmission. NMS is a rare but potentially life-threatening event that can be seen with all antipsychotic drugs with a reported incidence rate of less than one to three percent of patients taking these medications [ 22 ]. Treatment involves withdrawal of medication, and intensive management for cardiovascular support, control of hyperthermia, and fluid and electrolyte balance.

Anticholinergic effects — Anticholinergic side effects of antipsychotic drugs include dry mouth, urinary hesitancy, constipation, visual disturbance, and cognitive impairment. These effects tend to be worse in older patients.

NMS

One of antipsychotics side effects is urge incontinency.

Anticholinergics : bladder relaxants 38°C)

* Diaphoresis

* Pallor

* Dysphagia

* Dyspnea

* Tremor

* Incontinence

* Shuffling gait

* Psychomotor agitation

* Delirium progressing to lethargy, stupor, coma

Other general examination findings indicative of autonomic dysregulation include the following:

* Diaphoresis

* Sialorrhea

* Tachycardia

* Tachypnea, respiratory distress (31% of cases)

* Increased or labile blood pressure

* Hypoxemia (low pulse oximeter reading)

Now pay attention to BDZ’s side effects from murtagh page 510:

Monitor the following adverse effects:

• respiratory depression

• hypotension

• dystonic reactions, including choking

• neuroleptic malignant syndrome

52-a pt with heart failure on many drugs stop medication for 2 weeks now came with odema upto knee, chest was clear and with sinus tachycardia what to give?

1.digoxin (I think it’s the last choice in absence of AF)

2.metoprolol

JM P981: Digoxin

Digoxin was the mainstay of treatment of heart failure for decades prior to the use of ACE inhibitors. It was an effective agent but limited. The two indications for its current use are in patients with atrial fibrillation to control rapid ventricular rate and in patients with sinus rhythm not adequately controlled by the other agents above (ACEI,diuretics,BB,spirnolacton) Most patients are started on a low dose digoxin:

62.5–250 mcg (o) daily

52.1-another heart failure scenario pt on many medication and on digoxin .125 µg present with odema ,crepitation.first what to give

1.40 mg frusemide mane

2. 0.5 mg digoxin stat

3.metoprolol mane

4.all drugs together

On many medications!! Its important what medications?? Whats the dose of medications??

First: ACEI start low aim high then furesmide 40 up to 80 then BB then spirnolactone then dig.

Heart failure

JM P 981

Heart failure (unresponsive to first-line therapy)—stepwise strategy

ACE inhibitor

plus

Frusemide 40–80 mg (o) bd

plus

Spironolactone 12.5 (starting)—25 mg (o) daily

(monitor potassium and RFTs), if still congestion

plus

a selective beta blocker (if patient euvolaemic)

plus

digoxin (if not already taking it):loading dose: 0.5–0.75 mg (o) statim (depending on kidney function)

— then 0.5 mg (o) 4 hours later

— then 0.5 mg the following day

— then individualise maintenance

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54-Sudanese kid with high alkp and bilirubin is irritable and lethargic. High bilirubin, high alkp, low hb, asking for reason for his irritation?

a. ALL

b. Low 25 hydroxy-vitamin D

c. Low HB

d.hepatitis

e.malaria

يكى از دلايل rickets سوجذب هست كه ميتونه ناشى از مثلاً سلياك يا بيمارى شديد كبدى باشه! من در هرحال با كمبود ويتامين d موافقم.

RCH : Up to 90% of African-Australians in Melbourne will have low Vitamin D during the winter months. Low vitamin D is also seen in other refugee groups, especially people who have reduced sun exposure, including women who wear covering clothing

من كه گفتم اين بچه احتمالاً بيمارى كبدى داره و به همين علت هم آنمى داره و هم كمبود vit d. اما تنها علت irritability كمبود vit d هست

اصن يكى از اتيولوژى هاى ريكتز بيمارى شديد كبدى هست و مهم نيست پاتولوژى بيمارى چى باشه! از علل آنمى كمبود ويتامين d ميتونه باشه

Hepatic diseade(decrease vit-D(anemia

55- . walanderstrom macroglobunemia patient now has fever 39 cough dullness left base (pleural effusion) started on amoxclav n azithromycine now developed rash on chest. N rash was 100% papular heart and few vesicle. NO macules .

> > Amphotericin

> > Ganciclovir

> > Ceftriaxone

> > Prednisolone

55.1-Q about male around 45-47 yo with known waldenstrom's macroglobulinemia( ������) came with complains on fatigue, cough, fever( nothing special). Was given ampicillin and azytromycin. In next week day he developed skin rash ( guys, never ever in my life I saw smth like this, my apologises I'm sucks) Asking for investigation

1-rash biopsy

2- skin drug reaction

55.2- waldenstorm macroglobenemia patient came with rigors and fever and right lower lobar pneumonia or some infection like this admitted and started ampicillin and after minimal time generalised vesicular rash appeared asking management

prednisolone

immunoglobulin

cease ampicillin

Farzin: it represents both pemphigus and erythema molteforme ... pick skin Bx for Diagnosis and steroids for Rx. That's what I think is correct

يا راش در اثر افزايش پروتئين هاي خون هست كه بيشتر نزديك انگشتان و گوش و رگ هاي كوچيكه، شكل پورپوراس كه ممكنه دردناك باشه همراه با تب و درد استخوان

يا راش چيكن پاكس و زوناس كه اونم دردناك و خارش داره و درمان انتي وايرال ميكنيم

يا راش عفوني در اثر سلوليته كه همراه با تب و درد و تورم و قرمزي

و راش در اثر كموتراپي كه اونم دردناك و روي كف دست هست حالا اگه ماهيت راش و بهتر گفته بود ميشد تشخيص داد!

در مورد راش امپيسيلين هم گفته دو نوع راش ميده يه نوع ماكولوپاپولر هست كه بعد ٤ روز معمولا اتفاق ميافته و بيشتر روي تنه و اكستنسور اندامهاس و بيشتر در خانمهاس

اكثرا در اثر عفونت مونو نوكلئوز و وايرال اينفكشن ها و لوكمي ايجاد ميشه، اين راش الرژيك نيست و درمان ادامه پيدا ميكنه و اگه دوباره امپيسيلين بديم اتفاق نميافته

يه راش ديگه يورتريكاله كه مطرح كننده الرژي به پنيسيلينه و ارتباطي با دوز نداره

من با تشخيص اول واكنش دارويى با قطع آمپى موافقم .

SUMMARY — Waldenström macroglobulinemia (WM) is a rare clinicopathologic entity demonstrating 10 percent or greater infiltration of the bone marrow by clonal lymphoplasmacytic cells and a monoclonal IgM gammopathy in the blood. Patients usually present in their seventh decade with symptoms related to the infiltration of the hematopoietic tissues or the effects of monoclonal IgM in the blood.

WM most commonly presents with pallor, oronasal bleeding, systemic complaints (eg, weakness, fatigue, weight loss, fever, night sweats) and organomegaly (eg, enlarged lymph nodes, spleen, and/or liver). In contrast to patients with multiple myeloma, involvement of the bone or kidneys is uncommon. (See 'Overview' above.)

An important presentation includes central nervous system signs and symptoms due to the hyperviscosity syndrome (eg, blurring or loss of vision, headache, ataxia, dementia, stroke, or coma). This may be severe enough to constitute a medical emergency, requiring urgent plasmapheresis. (

A classic finding in WM associated with hyperviscosity is the presence of dilated, segmented, and tortuous retinal veins, giving a "sausage link" appearance ( picture 1

Another major presentation is that of neurologic symptoms such as paresthesias and weakness. Other neurologic complaints may include cranial nerve palsies and sudden deafness. Patients with WM who are asymptomatic are considered to have smoldering WM (SWM).

The diagnosis of WM is made when the following two criteria are met (see 'Diagnosis' above):

Presence of an IgM monoclonal paraprotein on serum immunofixation.

Ten percent or more of the bone marrow biopsy sample must demonstrate infiltration by small lymphocytes that exhibit plasmacytoid or plasma cell differentiation (lymphoplasmacytic features or lymphoplasmacytic lymphoma) with an intertrabecular pattern. This infiltrate should express a typical immunophenotype (eg, surface IgM+, CD5+/-, CD10-, CD19+, CD20+, CD22+, CD23-, CD25+, CD27+, FMC7+, CD103-, CD138-).

The differential diagnosis includes other monoclonal gammopathies and lymphomas. Specifically, WM must be differentiated from IgM monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma, chronic lymphocytic leukemia, and mantle cell lymphoma.

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56-old recal with 2 year old boy with slighy mucopurulent discharge from penile prepuece…foreskin partially retracted…treatment ?

1- topical steroid

2- topical mupirocina

3- circumcision

4- cephalexin

Balanitis: Inflammation of the glans penis; it is usually associated with phimosis.

Balanoposthitis: inflammation of the glans penis and prepuce

Phimosis: constriction of the preputial orifice so that the prepuce cannot be retracted back over the

glans

Paraphimosis: retraction of phimotic foreskin, causing a painful swelling of the glans, severe cases may cause dry gangrene.

Balanitis

More severe inflammation of the glans penis +/- foreskin is often due to infection and is usually termed balanitis. It is common, affecting around 6% of uncircumcised and 3% of circumcised males.

Soaking in a warm bath with the foreskin retracted (if retractile and not too painful) will help with cleaning and urination may be easier in the bath. Topical hydrocortisone 1% cream or ointment may help in mild cases. Topical antibiotics creams are sometimes used but are of unproven efficacy.

Candida infection may be responsible in some infants. It is usually associated with more generalised napkin candidiasis and the presence of satellite lesions. Topical anti yeast creams (eg nystatin, clotrimazole, miconazole) will be helpful.

Bacterial infection

If there is significant cellulitis of the whole of the foreskin or the skin of the penile shaft then bacterial infection is likely and antibiotics should be given. Pain and swelling sometimes produce marked dysuria.

Streptococci (including Group A), staphylococci, and gram negative organism are most often responsible.

Swabbing the discharge is unhelpful because the normal foreskin is usually colonised with multiple organisms.

Most cases respond to oral antibiotics (eg Co-trimoxazole 4/20 mg/kg (max 160/800) 12 hourly or Amoxycillin 15 mg/kg (max 500 mg) 8hourly).

Analgesia is important, and sitting in a warm bath may ease dysuria.

Occasional cases require admission for parenteral antibiotics, and rarely urgent surgery (eg dorsal slit / circumcision) is indicated.Significant recurrent balanitis may be an indication for circumcision. Also, true phimosis may lead to recurrent balanitis and should be treated.

paraphemosis is due to retraction of foreskin in a pathologic phemosis

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56-A woman came with her 18 month old child anxious about pus surrounding the meatus and the foresking is partially retractable, what’s your next step ?

a. Circumcision

b. Betamethasone crem

c. Mipurocin cream

d. Oral phenoxymethyle penicillin

e. I.V benzathyne penicillin

57-30 yr old indigenous male with DM on insulin , smoker , drinks 12 standard drinks per day , BMI 32 he asked you otherthan regular insulin taking what to do for wt. reduction ?

1advice hem to do gastric by pass

2dec. Fat diet will dec. wt. rapidly

3severe exercise have no major rule in wt. reduction

4increase fiber diet reduce body wt.

5dec. alcohol & smoking will dec. wt

I saw it from previous discussions. They said like whenever you see something with aboriginals, its inform social and environmental issue. I couldn't find any reference though.

براى استراليا تعريف يك استاندارد درينك معادل ١٠ گرم الكل هست.

لیلا :تو شخص دیابتی گاستریک بای پس در BMI>35اندیکاسیون داره.افراد عادی باید BMI>40باشه

Management of obesity JM chapter: 78

For decreasing type 2 diabetes and insulin

Treatment is based on four major interventions:

1 reduction in energy intake

2 change in diet composition

3 increased physical activity

4 behavioural therapy

Goals:

1 no further weight gain

2 loss of 5–10% initial body weight

3 improve activity

Social support is essential for a successful weight  loss program. A better result is likely if close family members, especially the chief cook, are involved in the program, preferably striving for the same goals.

doctor–patient strategy

1 Promote realistic goals. Lose weight at the same rate that it was gained (i.e. slowly)—for example, 5–10 kg a year. A graph can be used for this purpose with an ‘exaggerated’ scale on

the vertical axis so that small variations appear highly significant and encouraging.

Promote the equation: Energy In  =  Energy Out  +  Energy Stored

The appropriate way to reduce the stored energy (fat) is either to reduce energy in (eat less) or increase energy out (exercise).

2 Dietary advice. Give advice on simple substitutions (e.g. fortified skim milk in place of whole milk, high-fibre wholemeal bread instead of white bread, and fruit and vegetables instead of biscuits and cakes as in-between

snacks

3 Counselling is simple and commonsense. It involves being supportive, interested and encouraging. A list of tips on coping is provided (see below ‘A practical plan’ for grade II and III obesity) and the patient advised to keep a food, exercise and behaviour diary.

احسان :اينا از redbook هست. در كل قسمت مربوط به overweight هيچ توصيه اى راجع به الكل نديدم. راجع به رژيم پر فيبر هم نديدم. اولين توصيه اش هم راجع به كاهش saturated fat هست. حالا هركى هرچى ميخواد بزنه. مطمئن باشيد اگه سيگار و كاهش مصرف الكل الويت داشت براى كاهش وزن، حتماً ميگفت

58-Parkinson with dementia started haloperidol for this confusion .two wk ago present by increase trmor and s/s of arkinson mx?

A. Inc haloperidol

B. Dec haloperidol

C. Inc ant arkinson drugs

D. Inc dose of levodopa

Because haloperidol cause parkinsonism like symptoms it increases tremor muscle rigidity hypokinesia so 1st step is to reduce its dose

Parkinson disease guideline

Nonpharmacological management

Nonpharmacological intervention is important at all stages of Parkinson’s disease. Studies suggest that various exercise modalities (including multidisciplinary rehabilitation, active music therapy, treadmill training, balance raining and ‘cued’ exercise training) are effective in improving functional outcomes for patients with Parkinson’s disease.

Pharmacological management

The commencement and initial choice of therapy must be individualized.

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Initial therapy

1 levodopa+benserazide 50+12.5 mg orally, 3 times daily, increasing to 100+25 mg 3 times daily over 1 to 2

weeks

OR

1 levodopa+carbidopa 50+12.5 mg orally, 3 times daily, increasing to 100+25 mg 3 times daily over 1 to 2 weeks

OR

1 pramipexole immediate-release 0.125 mg orally, 3 times daily, slowly titrating to effect, to a maximum of 1.5

mg 3 times daily or pramipexole extended-release 0.375 mg orally, once daily, slowly titrating to effect, to a

maximum of 4.5 mg once daily

OR

1 rotigotine 2 mg transdermally, daily, increasing by 2 mg every week until an effective dose is reached, to a

maximum of 8 mg daily.

Avoid metoclopramide and prochlorperazine in patients with Parkinson’s disease.

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59- Rh negative woman delivered an Rh negative boy, she is doing well. Coomb’s test result weak positive.What is the cause?

Rh related disease

ABO incompatibility

Genetic cause

ABO incompatibility

60-A labourer who is a heavy smoker find difficult to perform his duties and worried about his physical condition. On examination there is chest crackles, ankle edema, raised JVP, hepatomegaly and what is the cause most likely

a. COPD with cor-pulmonale

b. Congestive heart failure

c. SVC obstruction

d. budd chiari syndrome

last world: if we have LHF(pulmonary edema(pulmonary HTN(RHF

if we have cor-pulmonale: COPD/ILD/…(PAH(RHF

finally in both conditions we have right HF signs but in LHF we have pulmonary manifestation of pulmonary edema but in cor pulmonale there is pulmonary sysmptoms consistent with COPD …

COPD: symptoms: The three cardinal symptoms of COPD are dyspnea, chronic cough, and sputum

production and the most common early symptom is exertional dyspnea

signs: hyperinflation (eg, increased resonance to percussion), decreased breath sounds, wheezes,

crackles at the lung bases, and/or distant heart sounds [ 43 ]. Features of severe disease include

an increased anteroposterior diameter of the chest (“barrel-shaped” chest) and a depressed

diaphragm with limited movement based on chest percussion.

Cor pulmonale:

hepatic congestionmay lead to anorexia, right upper quadrant abdominal discomfort,

jaundice, peripheral edema, On auscultation of the lungs, wheezes and crackles may be

heard as signs of underlying lung disease, a systolic ejection murmur with sharp ejection

click over the region of the pulmonary artery may be heard in advanced disease along with

diastolic pulmonary regurgitation murmur, Hepatojugularreflux, pulsatile liver, systemic

venous congestion.

Right-sided failure

pitting peripheral edema, liver enlargement, high Jugular venous pressure, hepatojugular reflux,

peripheral edema or anasarca, Nocturia

Left-sided failure

Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing

respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood, Rales or

crackles, pulmonary edema, orthopnea

cardiogenic pulmonary edema

shortness of breath, profuse diaphoresis, dyspnea on exertion, orthopnea, and paroxysmal nocturnal

dyspnea. Pink, frothy sputum may be present. Auscultation of the lungs usually reveals fine, crepitant

rales, but rhonchi or wheezes may also be present. Rales are usually heard at the bases first; as the

condition worsens, they progress to the apices

differential diagnosis of COPD

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61-pregnant lady comes after taking care of her friends son who was later diagnosed as having EBV infection. She’s worried. What is your management?

-Ultrasound for hydrops

-Check serology for antibody titres

-Reassure

-Tell her to come if any symptoms arise

South Australian Perinatal Practice Guidelines

Epstein- Barr virus (glandular fever) in pregnancy: Early studies have reported that infants occasionally suffer damage due to maternal primary EBV infection just before conception or during pregnancy

طبق اين گايدلاين EBV در حاملگى با احتمال خيلى كم ميتونه خطرناك باشه ، و از طرفى اگه طرف علامتدار نشه ديگه احتمال انتقال خيلى كم ميشه . لذا بهترين كار اينه كه بگيم اگه علامتدار شد بياد چك كنيم سرولوژيش رو (كه آيا علائم مربوط به EBV هست يا نه) ، اگه علامتدار نشد ديگه احتمال انتقال به جنين صفر هست و اصلا كارى نياز نداره .

سرولوژى الان نه ها ، سرولوژى در صورت علامتدار شدن . يعنى گزينه D

62-An old man 72 years old came to ER with chest pain and shortness of breath. ECG and angiography done which revealed stenosis of Rt. Coronary 70% and left Coronary 30%.

Treatment?

A-Pace maker

B-Digoxin

C-Angioplasty for both coronaries

D-Angioplasty for Rt.coronary

E-Angioplasty for Lt.coronary

اندیکاسیون قطعی CABG تنگی left main هست(بالای پنجاه درصد).در موارد زیر هم CABG ترجیح داده میشه درگیری سه رگ در بیمار دیابتی .درگیری سه رگ با برون ده کمتر از 50.درگیری پروگزیمال LAD ویک رگ دیگر در دیابتی.درگیری پروگزیمال LAD و یگ رگ دیگر همراه با برون ده قلبی کمتر از50%

revascularization

• Among patients with stable angina, the goals of medical therapy or revascularization are to prolong life, decrease cardiac morbidity, and alleviate symptoms.

• Revascularization with either coronary artery bypass surgery (CABG) or percutaneous coronary intervention (PCI) is indicated the following groups of patients with stable angina pectoris:

1-Patients with activity-limiting symptoms despite optimal medical therapy

2-Active patients who prefer PCI for improved quality of life compared to medical therapy

3-Those with anatomy for which revascularization has a proven survival benefit:

A)significant left main coronary artery disease (greater than 50 percent luminal narrowing)

B)multivessel coronary artery disease (CAD) with a reduction left ventricular ejection fraction

C)large area of potentially ischemic myocardium.

• Available data suggest that most patients with one or two vessel disease are best managed with PCI, while

those with multivessel or left main disease associated with impaired left ventricular systolic function

(EFtriceps=>radial nerve=>posterior cord, middle trunk mainly C7(c6 has limited role too)

Elbow flexion=> brachialis: exclusively an elbow flexor=> musculocutaneous nerve=>lateral cord, upper

trunk C5 C6 also a little by proprioceptive branch of radial nerve

Biceps: main elbow flexor but also a supinator=> musculocutaneous nerve=>C567

brachioradialis: essentially as an elbow flexor,but also supinator and pronator=>radial

Flexion is controlled by segments C5 and 6 of the spinal cord, pronation and supination by C6, and extension by C7 and 8.

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69. A middle aged man with Rheumatoid arthritis presented with knee, ankle swelling and pain. Blood sent for full blood count and inflammatory mediators. Next step?

a. Intra-articular steroid

b. synovial fluid study for uric acid

c. blood culture and synovial fluid culture

if fever presents then aspirated synovial fluid should be evaluated for uric acid and gram stain/culture, if not only crystal study:

Synovial fluid analysis

Uptodate

INTRODUCTION — Synovial fluid analysis may be diagnostic in patients with bacterial infections or crystal-induced synovitis. The white cell count, differential count, cultures, Gram stain, and crystal search using polarized light microscopy are the most valuable studies. Noninflammatory fluids generally have fewer than 2000 white blood cells/mm 3 , with fewer than 75 percent polymorphonuclear leukocytes .

INDICATIONS

Suspected septic arthritis — The American College of Rheumatology (ACR) clinical guidelines committee suggests that unexplained inflammatory fluid, particularly in a febrile patient, be assumed to be infected until proven otherwise by appropriate culture. According to the ACR committee, synovial fluid analysis should be performed in the febrile patient with an acute flare of established arthritis (eg, rheumatoid arthritis, osteoarthritis) to rule out superimposed septic arthritis.

Unexplained joint, bursa, or tendon sheath swelling — When joint infection is thought to be unlikely, the main value of synovial fluid analysis is to permit classification into an inflammatory or noninflammatory category. Thus, synovial fluid analysis should be performed if joint or other (eg, bursa, tendon sheath) synovial fluid is readily obtainable and if the diagnosis is uncertain after history, physical examination, and standard laboratory tests.

Suspected crystal-induced arthritis — Synovial fluid analysis may be useful if sterile inflammation due to crystal disease is suspected, both in the acute setting and between attacks.

Acute arthritis — Synovial fluid analysis in a patient with acute monoarticular or oligoarticular arthritis may reveal crystals of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD). In combination with a negative Gram stain and bacterial cultures, a diagnosis of gout or pseudogout may be established.

70-An old patient with multiple drug history for various conditions posted for hip replacement surgery. Whats ur management post op?

a. Warfarin for 1 month (no other choice)

b. Warfarin for 3 months

c. Don’t give anything

d. LMWH for 1 week

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71-A 32 primi came at 28 weeks having contractions , her examination 3 weeks ago was pretty normal so as the baby too , u did a CTG , What is the best test to be done to reveal the problem of the baby and give a clue about early intervention to save it.

a. Fetal blood sampling

b. Mother serum for Ig anti D titration

c. B HCG

d. Ultrasound

e. Amniocentesis

در مورد این مریض چون گفته بهترین برای reveal the problem میتونه بررسی ریه های جنین باشه که برای این کار مایع آمنیون رو از نظر نسبت لیسیتین به اسفنگومیلین بررسی میکنیم.که اگر این نسبت کمتر از 2باشه کورتون میدیم.گزینه E

72-Female 24 yrs with 2nd ry amenorrheamen for 2 yrs all investigation normal Fsh ,LH , prolactin , TSH. Her U/S shows 3 -4 cysts ask dx :

1) Hypothyroidism

2) Pcos

3) Idiopathic hypothalamic dysfunction

4) Pitutary adenoma

هيچكدوم از اين گزينه ها همه آزمايشات نرمال ندارن و اين به علل مكانيكال بيشتر ميخوره بنظر من . شايد گزينه E كه نيست همچين چيزى باشه

Ayda: No it could be PCOs and the precise lab for its diagnosis is serum testosterone level, other findings is consistent with the Dx.

[pic]

73- A diabetic 65 year old woman noticed an uler on her foot for 7 days she came to hospital and u admitted her, surgical debridment was done and the ulcer is 1 cm and oosing a clear fluid , next best step ?

a. Oral amox. Clax + metronidazole

b. IV ticracillin + metronidazole

c. MRI

d. Dressing and checking the wound everyday

e. Wound toitel with povidone iodine

چون گفته ترشحات clear داره زخمش عفونی نیست که آنتی بیوتیک بدیم ویا MRI کنیم برا R/O. استومیلیت.پس پانسمان میکنیم هرروز چکش میکنیم.

Diabetic foot

if the diagnosis of diabetic foot is not made then:

The diagnosis of a diabetic foot infection is primarily based on suggestive clinical manifestations. The presence of two or more features of inflammation (erythema, warmth, tenderness, swelling, induration and purulent secretions) can establish the diagnosis. As many diabetic foot wounds are colonized by bacteria, the presence of microbial growth from a wound culture in the absence of supportive clinical findings is not sufficient to make the diagnosis of infection.

diagnosis of underlying osteomyelitis: The possibility of osteomyelitis should be considered in diabetic patients with foot wounds. The diagnosis of osteomyelitis is definitively made through isolation of bacteria from a sterilely obtained bone biopsy sample with histologic evidence of inflammation and osteonecrosis. However, bone biopsy is not always routinely available or practical. In such instances, the presumptive diagnosis is based on clinical and radiographic assessment. If bone is grossly visible, supportive radiographic findings may not be necessary. a conventional radiograph with consistent changes can be helpful in making the diagnosis of osteomyelitis and providing a baseline image useful for subsequent management decisions. If the radiograph is indeterminate or normal and the diagnosis remains uncertain, such patients should undergo magnetic resonance imaging (MRI), which is highly sensitive and specific for osteomyelitis and superior to radiographs, three-phase bone scans, and white blood cell scans.

Management:

A widely used classification of diabetic foot ulcers is that proposed by Wagner:

• Grade 0 – No ulcer in a high-risk foot

• Grade 1 – Superficial ulcer involving the full skin thickness but not underlying tissues

• Grade 2 – Deep ulcer, penetrating down to ligaments and muscle, but no bone involvement or abscess formation

• Grade 3 – Deep ulcer with cellulitis or abscess formation, often with osteomyelitis

• Grade 4 – Localized gangrene

• Grade 5 – Extensive gangrene involving the whole foot

GRADE 0 LESIONS— Counseling regarding preventive foot care should be given to any patient whose feet are at high risk, particularly patients with existing neuropathy. There are several measures that can markedly diminish ulcer formation, such as avoiding poorly fitting shoes, walking barefoot, and smoking, off load pressure and foot hygiene.

GRADE 1 AND 2 LESIONS

Extensive debridement, good local wound care, relief of pressure on the ulcer, and control of infection (when present) are believed to be important components of therapy for grade 1 and 2 foot ulcers

[pic][pic]

GRADE 3 LESIONS

Assessment for peripheral artery disease: Symptoms of claudication or extremity pain at rest, and physical findings of diminished or absent pulses, cool temperature, pallor on elevation, or dependent rubor should raise suspicion about the presence of peripheral artery disease. Noninvasive vascular studies including ankle-brachial index, pulse volume recordings and duplex ultrasonography should be obtained to confirm the diagnosis.

Assess for osteomyelitis: signs that suggest osteomyelitis are an ulcer size larger than 2 x 2 cm, unexplained elevation in the ESR, The diagnosis is clear if osteomyelitis is visible on plain radiographs, radionuclide bone imaging, magnetic resonance imaging and imaging with indium-labeled leukocytes are of great value.

debridement, infection control, local wound care, and relief of pressure. Surgical removal of infected bone may be necessary if the ulcer is not healing. A short period of hospitalization, with surgical debridement, including culture of material obtained from deep in the ulcer and bone biopsy, is often helpful in choosing antibiotic therapy .

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GRADE 4 AND 5 LESIONS — Patients with these more advanced lesions require urgent hospital admission and surgical consultation, and amputation may sometimes be required.

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74-6 year old child come with her parent, she has a short history of cough and anorexia, she has a fever 39, on examination you find lung sound is decreased in right site and there is dullness in the base of her lung. Treatment asked

a. Crystalline penicillin

b. Amoxyclav

c. Flucloxacillin

d. Azithromycin

pneumonia

JM P472

Community-acquired pneumonia

Antibiotic treatment

Mild pneumonia: amoxycillin/clavulanate 875/125 mg (o) 12 hourly for 7 days especially if S. pneumonia

isolated or suspected plus(especially if atypical pneumonia suspected) roxithromycin 300 mg (o) daily for

7 days

Moderately severe pneumonia

This requires hospitalisation

• Neonates

• Age over 65 years

• Coexisting illness

• High temperature: >38 ° C

• Clinical features of severe pneumonia

• Involvement of more than one lobe

• Inability to tolerate oral therapy

Benzylpenicillin 1.2 g IV 4–6 hourly for 7 days or Procaine penicillin 1.5 g IM daily (drugs of choice

for S. pneumoniae )or Ceftriaxone 1 g IV daily for 7 days (in penicillin-allergic patient)

• If atypical pneumonia use doxycycline, erythromycin or roxithromycin

severe pneumonia

azithromycin 500 mg IV daily (covers Mycoplasma, Chlamydia and Legionella) plus cefotaxime 1 g IV 8 hourly

or ceftriaxone 1 g IV daily.

[pic]

Pneumonia in children

• Mycoplasma are common in children over 5 years.

• S. pneumoniae is a cause in all age groups.

Treatment

Almost all those under 48 months should be admitted to hospital.

Mild (general guidelines only): amoxycillin (o) or roxithromycin (o)

Moderate: benzylpenicillin IV + roxithromycin (o)

Severe: flucloxacillin IV + gentamicin IV ± azithromycin (o)

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Guideline

In adults severe CAP has at least 2 of the following: (CORB scorring)

C = acute confusion

O = oxygen saturation 90% or less

R = respiratory rate 30 breaths or more per minute

B = systolic blood pressure less than 90 mm Hg or diastolic blood pressure 60 mm Hg or less

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75-a case of intoxicated patient with fever, visual hallcuniation, confused initial treat:

a-d5%

b- thiamain IV

c- antibiotics

D-oral diazepam loading.

این سئوال یا ممکنه مسمومیت با الکل باشه یا فرم خفیف انسفالوپاتی ورنیکه (البته ممکنه مسمومیت با خیلی داروهای دیگه هم باشه ولی از روی گزینه ها میشه فهمید که استم کامل سئوال حول محور یک بیمار الکلیک میگرده لذا بقیه مواد رو میذاریم کنار).

افتراق این دو گاهی اصلا راحت نیست همچنین دادن یک دوز گلوکز که میتونه در صورت هایپیوگلایسمیک بودن مریض ناشی از اوردوز الکل جونش رو نجات بده تاثیری در تسریع انسالوپاتی ورنیکه نداره (تزیق طولانی مدت گلوکز وریدی میتونه این کار رو بکنه) . لذا با تمام این تفاسیر به نظر من دادن دکستروز در این مریض ارجح هست.

Delirium tremens

[pic]

alcohol withdrawal syndromes

|Syndrome | Clinical findings | Onset after last drink |

|Minor withdrawal |Tremulousness, mild anxiety, headache, |6 to 36 hours |

| |diaphoresis, palpitations, anorexia, GI upset; | |

| |Normal mental status | |

|Seizures |Single or brief flurry of generalized, |6 to 48 hours |

| |tonic-clonic seizures, short post-ictal period;| |

| |Status epilepticus rare | |

|Alcoholic hallucinosis |Visual, auditory, and/or tactile hallucinations|12 to 48 hours |

| |with intact orientation(sensorium rmains | |

| |normal, not delirious) and normal vital signs | |

|Delirium tremens |Delirium, agitation, tachycardia, hypertension,|48 to 96 hours |

| |fever, diaphoresis | |

JM P: 209

Treatment of Delirium tremens

• Hospitalisation

• Correct fluid and electrolyte imbalance with IV therapy

• Treat any systemic infection

• Thiamine (vitamin B1 300 mg IM or IV daily for 3–5 days, then thiamine 300 mg (o) daily

• Diazepam 5 mg by slow IV injection (over several minutes) every half hour until symptoms subside or diazepam

20 mg (o) every 2 hours (up to max. 100 mg daily) until symptoms subside. This dose is usually required for 2–3

days, then should be gradually reduced till finished.

If psychotic features (e.g. hallucinations and delusions)

• add haloperidol 1.5–5 mg (o) bd, titrated to clinical response

Other types of delirium:

[pic]

76-A 58yr old man returned from Thailand after 2 weeks holiday with his wife. Now presents with fever, malaise, pain in the right upper quadrant. His lab findings were given with a big list of all the FBE, LFTs, etc. Almost all his LFTs raised. GGT was very high. Whats the diagnosis?

a. Hepatitis A (could be but raised ggt is against)

b. Cholangitis (possible)

c. Liver abscess

d. Acute pancreatitis

e. Cholecystitis (non-obstructive) ( jaundice abscent

76.1- Man coming back after endemic area with severe jaundice fever ,tender liver and enlarge 5cm

Very high alt ast ggt alp

a hepatitis A (possible)

b hepatitis B (possible)

c malaria

d mononucleosis

the same stem, all in all if there is a obstructive scenario(pale stool, dark urine) more prone to gall stone or cholangitis and if not more incline to hepatic disorders

Acute cholangitis

This is due to bacterial infection of the bile ducts secondary to abnormalities of the bile duct, especially gallstones in the common duct. Other causes are neoplasms and biliary strictures.

Charcot triad (present in 70%) is shown in the diagnosis box.

DxT: fever  ( often   with   rigor )  +   upper abdominal pain + jaundice  = acute cholangitis

Acute cholecyctitis

Patients with acute cholecystitis are usually ill appearing, febrile, and tachycardic, and lie still on the examining table because cholecystitis is associated with true local parietal peritoneal inflammation that is aggravated by movement. Abdominal examination usually demonstrates voluntary and involuntary guarding.

Elicitation of "Murphy's sign" may be a useful diagnostic maneuver. While palpating the area of the gallbladder fossa just beneath the liver edge, the patient is asked to inspire deeply, causing the gallbladder to descend toward the examining fingers. Patients with acute cholecystitis commonly experience increased discomfort and may have an associated inspiratory arrest. In one study, using cholescintigraphy as the gold standard, the sensitivity and specificity of a positive Murphy's sign were 97 and 48 percent, respectively [ 18 ]. The sensitivity of Murphy's sign may be diminished in the elderly

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76- A young patient with asthma history complains of intermittent dysphagia on esomeprazole 40mg for a few months, now asking management?

a. Change to pantoprazole

b. Increase dose of esomeprazole

c. Fluticasone

سلام این مریص می تونه ازوفاژیت ایوزینوفیلی باشه چون شیوعش بالا رفته در افراد حساس به انتی ژن خاص به وجود میاد و برای همین نکته گفته اسم داره

درمان کنترل علایم اول ppi که تو این مریص جواب نداده در مرحله بعد حذف برخی موادعذایی و یا گلوکوکورتیکویید های موصعی بلعیدنی مثل فلوتیکازون یا بودزونید ..و کورتن سیستمیک برای بیماران شدید که به درمانهای موصعی مقاوم هستند

77-Child if any body cough in the home he goes and take a shower rx parents tried all measure without any benefits

Fluoxetine…… 6y

Paroxetine

Fluvoxamine…… 8y

درمان OCD اطفال سرترالين و فلووكسامين هست .

آذین: فلووكسامين برای افسردگی اطفال چویس نیست ولی برای ocd در اطفال چویس هست

Pediatrics ocd

Treatment:

In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory that most SSRIs are not suitable for use by persons younger than 18 years for treatment of "depressive illness." After review, this agency decided that the risks to pediatric patients outweigh the benefits of treatment with SSRIs, except fluoxetine (Prozac), which appears to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.

Currently, evidence does not support an increased risk of suicide in obsessive-compulsive disorder (OCD) or other anxiety disorders treated with SSRIs. Clinicians are advised to use SSRIs when indicated while watching the child closely for suicidal ideation and advising parents to carefully assess the child for suicidal thoughts, plans, and actions.

78-The patient you are about to see, known that he is always making problem with the doctors, misbehave and shouting at them. What you will do?

Refuse to see him

Ask him to go to another hospital

Ask other colleague to see him

See him in the presence of the police

See him in the presence of other health staff.

79-50 year old woman come with the complaint of hot flush, she was on cyclical HRT from 5 years ago when she had a hot flush and her FSH was elevated. 3 month ago she stoped her HRT because of fear of breast cancer, mamo and PAP done all was normal , treatment was asked

A. Testosterone patch

B. COC

C. Continues HRT

با توجه به اينكه بيش از دو سال از منوپوزش ميگذره بهتره از continuous HRT استفاده كنه .

البته گزينه B معلوم نيست منظورش چيه دقيقاً چون در HRT هم فرم cyclical و هم فرم continuous از COC استفاده ميشه .

[pic]

Every one is with C here but I think we cant continue HRT more than 5 yr even if all evaluations are normal. I’d rather with clonidine or SSRI here.

80-If you have third nerve palsy, which feature will tell u that it is not due to diabetic neuropathy?

a. Ptosis

b. Intact pupil reflex

c. Impaired down and out gaze

d. Enophthalmos

[pic]

[pic]

[pic]

3rd nerve:

1-30% lid elevation ( 70% sympathetic nerve system) (closing the eye lid: 7th )

2-pupil reflex ( in Rt eye : Rt optic nerve is afferent & Lt oculomotor nerve is efferent)

3-eye movements: the down and out eye(3rd nerve palsy) sunset eyes(↑ICP->3rd N compression)

[pic]

Note: cause parasympathetic fibers run with 3rd nerve aiming to innervate ciliary muscles(pupil contriction)in traumatic complete 3rd N palsy we have mydriasis but its not present in pure 3rd N palsy(ischemic)

87-All of the following constituent of human milk confer immunity against gastroenteritis except :

A.IgA

B.IGg

C.Macrophages

D.Lactoferrin

E.T lymphocytes

88-A female paient had a long operation in lithotomy position , which muscle could be affected ?

a. Flexor hallucis longus

b. Flexor hallucis brevis

c. Extensor hallucis longus

common proneal nerve

89-A sheep farmer with h/o anaemia, weight loss, fatigue, RUQ pain, jaundice comes to ur clinic with fever, itching, shortness of breath. Asking for causative organism?

Echinococcus granulosus

Coxilla burnetii

Brucella melitensis

Saccharopolyspor

Leila: hydatid can cause all except fever, one reason for fever in hydatid cyct could be allergic reactions(pt has pruritis here)

90-. A mother brings her two year old child who has genital warts. The mother had CIN 1 lesion 3 years ago. What could be a possible cause for the warts in the child now:

A. Swimming in the river

B. Sexual abuse

C. Acquired during birth through infected birth canal

Somayeh: read the last paragraph

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91- Middle aged man who is hypertensive and just treated for his helicobacter pylori with triple therapy. Now comes with urine protein and haematuria with 3-4renal cysts seen on USG. Diagnosis?

a. PKD

b. IgA Nephropathy

c. Nephrotic syndrome

d. Acute Interstitial Nephritis

اگه PKD باشه بايد زياد پيشرفت كرده باشه كه به CRF رسيده و پروتئينورى داده . اين احتمالش وجود داره ولى اينكه بگيم عارضه PPI هست من فكر ميكنم تشخيص بهتريه .

AIN due to drug…

92-meningitis scenerio,lymphocyte high, neutrophils 10,RBCs 200 ,protein and glucose are normal, what is your management:

1.analgesic and observe

2. do MRI

3. ceftriaxone

4. IV acyclovir.(…encephalitis)

Predominant cell in viral meningitis is lymphocytes and pr and glucose can be normal. Treatment is conservative.

1. is correct

93- Engineer man in coal mine present with nocturnal cough,pt heavy smoker,on ex everything normal chest clear and normal cxr,wt todo next

1.endoscopy

2.ct chest

3.repeat cxr after 6 month

4.MRI

Challenging question…

A few tips:

Chronic cough

•Cough that has been present longer than three weeks is either subacute (three to eight weeks) or chronic (more than eight weeks).

•Timing

Nocturnal cough → asthma, left ventricular failure, postnasal drip, chronic bronchitis, whooping cough

Waking cough → bronchiectasis, chronic bronchitis, G O R D

• three most common causes of chronic cough (Harrison): PND, Asthma, GERD

•steps: empirical therapy for GERD (PPI) and PND(antihistamins+/-coamoxiclave), evaluation for asthma

حالا ديگه انتخاب با خودتون اندوسكوپي كه اصلا تشخيصي نيست برا گرد، سي تي هم كه چست نرمال بوده و كاهش وزن نداشته و ... چست تكرار كنيم كه چي بشه؟ ام ار اي هم كه فك كنم يارو گزينه پر كرده ديگه.

با اين تفاسير اگه مثل آدم بخوان اطلاعات رو امتحان كنن من گزينه هايي مثل پي اچ متري يا درمان تجربي گرد يا ترشح پشت حلق رو ميزنم، اگه نه واقعا همين باشه سوْال مثلا با شك به ... ميزنم سي تي. نميدونم والا يه چي بوده مثلا تو چست ديده نشده مثلا تو سي تي ببينيم.

94-Which of the following is the best predictor value for prognosis a pt with systolic heart failure?

Jugular venous pressure

Chest pain

Peripheral edema

Shortness of breath

Orthopnea

در مورد این سوال باید به دنبال گزینه ای بریم که کمترین EF باعثش بشه که اون نشون دهنده پروگنوزه واینجا ارتوپنه هست که هاریسون هم اینوگفته

However, relying on only a univariate predictor such as the LVEF to estimate survival is not very sensitive in the individual patient. As mentioned above, large trials have demonstrated that patients with NYHA class II or III HF have a worse prognosis than those who are asymptomatic. Despite the difference in outcome, the difference in mean LVEF between asymptomatic and symptomatic patients in these trials was small: 28 to 31 percent in asymptomatic patients [8,17] versus 25 percent in patients with moderate symptoms [9].

به عبارت ديگه يك بيمار با ef ٢٠٪ ولى آسيپتوماتيك، در مقايسه با بيمار ديگه اى با ef ٣٠٪ ولى فانكشن كلاس ٣، پروگنوز بهترى داره.

اونى كه بيشتر نشون دهنده بدتر بودن فانكشن كلاس بيمار باشه.

eart Failure Survival Score — The Heart Failure Survival Score (HFSS) is another prospectively validated model, developed in and for patients with advanced HF (NYHA class III or IV) ( table 1 ) [ 27 ]. This score was derived from a multivariable analysis of 268 ambulatory patients referred for consideration of cardiac transplantation and validated in 199 similar patients. The predictors of survival in the HFSS include:

Presence or absence of coronary artery disease

Resting heart rate

LVEF

Mean arterial blood pressure

Presence or absence of an intraventricular conduction delay on ECG

Serum sodium

Peak VO2

SUMMARY — Patients with HF often have one or more of the above univariate predictors of decreased survival despite maximal medical therapy. Routine evaluation to estimate severity should include determination of NYHA class; and echocardiography to measure LVEF, assess diastolic and right ventricular function, and identify other abnormalities such as regional wall motion abnormalities; and measurement of the plasma sodium and creatinine concentrations.

The most frequently used factors for predicting survival in patients with systolic HF, many of which are direct or indirect measures of the severity of cardiac dysfunction, include:

High New York Heart Association (NYHA) functional class ( table 2 )

Reduced left ventricular ejection fraction (LVEF) and reduced cardiac index (CI)

Concomitant diastolic dysfunction, as established by a mitral flow velocity pattern on Doppler echocardiogram

Reduced right ventricular function

Low peak VO2 with maximal exercise and exercise hemodynamics

Markers of reduced tissue perfusion including low mean arterial pressure, renal insufficiency (creatinine clearance ................
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