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1-Middle age man with HTN,DM was on warfarin,perindropil,metformin.1wk ago he started to take amiodarone,now present with right thigh swelling.On examination temp 37.9,tender,red thigh.his rt thigh is 4 cm bigger than left in circumference.whats your dx?

1.Hematoma

2.Cellulitis

Amiodarone cause increase warfarin serum level by stoping liver p450 enzyme. First measure then is stop warfarin and checking INR.

If the patient is diabetic then muscle infarction is a good DDX. Clinical manifestations of diabetic muscle infarction is an acute onset painful swelling of the thigh without history of trauma, could be mild to severe tender, patient can have mild fever. Us, CT, MRI are helpful.

2-a young girl who is on sertraline says she consume ecstasy for recreation. What’s your advise?

Ecstasy is contraindicated with sertraline

It can lead to irreversible psychosis

Sertraline and ecstasy are synergic

A variety of mechanisms can potentially increase the quantity or activity of serotonin: ↑production of serotonin due to ↑availability of precursors (L-tryptophan containing substances); ↓metabolism of serotonin (MAOIs, selegiline); ↑release of stored serotonin (amphetamine, cocaine, fenfluramine, MDMA, meperidine); reuptake inhibition (SSRIs, TCAs, SNRIs, NaSSAs, MDMA, dextromethorphan, meperidine, St. John's wort); direct stimulation of serotonin receptors (buspirone, LSD); unknown mechanisms (lithium)OXFORD

3-DM patient taking glimepride, metoprolol since 20 years, came with diabetic foot 1cm ulcer, ulcer was debridement now how will you manage?

Insulin

Continue same drugs

amoxicillin

MRI

Iv AB

Different questions different answers! (

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:

Adequate debridement, proper local wound care, relief of pressure on the ulcer by mechanical off-loading, and control of infection AB therapy (when present) are important components of therapy.

If the picture is a septic ulcer(foul smelling, purulent discharge, fever, lukocytosis, emphysema in graphy)no other investigation is needed and surgical debridement is required, but if there is a chronic ulcer or infection of the ulcer is doubtful MRI or bone scan would be helpful.

Here the diagnosis is made and the surgical debridment is done so the next measure would be AB therapy(if needed= usually in infected grade 1 and 2 and in all wounds grade3,4,5).

4-50 y/o pt with ulcer in dorsum of foot and red margin after debridement :

Rest and elevation

Oral antibiotics

IV antibiotics

Again: Adequate debridement, proper local wound care, relief of pressure on the ulcer by mechanical off-loading, and control of infection AB therapy (when present) are important components of therapy.

بين اينها كه خوب با حذف گزينه b و c به گزينه a ميرسيم .

ولى من همين سئوال رو ديدم با گزينه هاى كامل گذاشته بود يكى و مثلاً يك گزينه MRI هم داشت

درمورد اين سئوال بايد ديد توى سئوال اصلى چطور زخم رو توصيف كرده يا در عكس چى ميبينيم . اينكه گفته زخم حاشيه قرمز داره معادل سلوليت نيست ، يك زخم وريدى يا شريانى غيرعفونى هم حاشيه قرمز داره . لذا بايد ديد در سئوال اصلى چى اومده :

١- اگه زخم عفونى نباشه جواب ميشه a

٢- اگه عفونى باشه و mild-moderate باشه جواب ميشه b

٣- اگه عفونى باشه و severe جواب ميشه c

5-Woman who is diabetic and well controlled on Insulin and oral hypoglycaemic comes to you with an ulcer on the dorsum of her right fifth toe since 5 days. There yellowish purulent discharge from the ulcer. The lateral aspect of her leg till her ankle is inflamed, swollen and red. What will you do next?

A) IV Ticarcillin

B) Analgesics

C) MRI

D) Debridement of ulcer

E) angiography

اولاً كه ترشح موكوپرولنت نشانه عفونت شديد نيست . علائم عفونت شديد يعنى :

گانگرن ، سلوليت شديد ، علائم سيستميك ، استئوميليت و ....

بعد هم قدم اول كه دبريد هست هنوز انجام نشده اينجا

6-Old, diabetic lady has an erythematous, tender induration in Rt 5th toe on dorsum for 1wk. Her diabetes in control. Mx?

a) Amoxycilin/ clovulanate

b) Ticarcilin/ Clovulanate

c) MRI

Mild to moderate infection

Antibiotic therapy:

For mild to moderate infection with no evidence of osteomyelitis or septic arthritis: Amoxi/clave 875/125 bd or cephalexin 500 qid + metro 400mg bd

In pts who are sensitive to penicillins cipro500 bd + clinda450 tds.

For sever limb or life threatening-infections( systemic toxicity, septic shock, marked necrosis or gangrene, deep ulcer, presence of osteomyelitis or septic arthritis): piperacillin/tazobactam IV or ticarcillin/clavulanate IV

For pts sensitive to pc : cipro400mg bd IV + clinda900mg tds infusion.

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7-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

8-A middle aged man with long history of diabets present with pain and redness in leg. there was redness and venous discoloration around ankle?

1.duplex usg of leg

2.blood culture

3.angio

9--ureteric stone high in possition making pain.it is 2cm but doesnt block the passage of urine. what is mx?

1.lithothomy

2.some substance that dissolve the stone

3.ESWEL

4.Ureteroscopy with basket removal of stone.

این مطلب از آکسفورد بود، البته اینجا منظورش از ureteroscopy همراه با basketing نیست چون گفته عوارضش زیاده و از laser استفاده می کنن برای fragmentation, حالا اگه این گزینه واقعا همین basketing باشه من می زنم ESWL ولی اگه ureteroscopy خالی باشه اونو انتخاب می کنم چون بالای ۱ سانتی متر ارجحه

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Urinary tract calculi

Method:

Percutaneous nephrolithotomy (PCNL)

Rigid and flexible ureteroscopy (TUL)

Shock wave lithotripsy (ESWL)

• Percutaneous nephrolithotomy, which requires general anesthesia and hospitalization, is currently reserved for patients with the following clinical characteristics:

1) Large (>2 cm in diameter) or complex calculi (such as staghorn calculi)

2) Cystine stones (relatively resistant to shock wave lithotripsy)

3) Anatomic abnormalities, including horseshoe kidneys or UPJO

4) Stones within caliceal diverticula

• Ureteroscopy continues to be the treatment of choice for the majority of middle and distal ureteral stones, but also can be used to manage proximal ureteral and intrarenal calculi. In addition, ureteroscopic access is frequently useful for the management of ureteral calculi that have failed shock wave lithotripsy.

• Shock wave lithotripsy can be used to treat many renal calculi, but is not the ideal modality for the management of complex calculi, large or hard calculi, stones located in a caliceal diverticulum, or in patients with complex renal anatomy. Shock wave lithotripsy employs high energy shock waves produced by an electrical discharge or piezoelectric crystals, fragmenting the stone

• Medical therapy, for both prevention of new stone formation and facilitation of stone passage, should be considered in patients who undergo stone removal procedures

ureteral calculi

• Emergency therapy - In septic patients with obstructing stones, urgent decompression of the collecting system with either percutaneous drainage or ureteral stenting is indicated in combination with appropriate antimicrobial therapy . Definitive treatment of the stone should be delayed until sepsis is resolved. Additional indications for urgent decompression include bilateral obstruction with acute kidney injury and unilateral obstruction with acute kidney injury in a solitary kidney.

• Medical therapy - In a patient who has a newly diagnosed ureteral stone 5mm

- social

Uptodate : Non-contrast-enhanced helical computerized tomography is currently the preferred diagnostic test to establish the presence of nephrolithiasis.

The complete metabolic evaluation for nephrolithiasis consists of both blood and urine testing, including at least two 24-hour urine collections. In each 24-hour urine collection, the urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, and creatinine (to assess the completeness of the collection) should be measured. Also, urinary supersaturation should be calculated. Urine collections should not be performed if there is evidence of renal/ureteral obstruction or urinary tract infection from existing calculi.

ESWL:( Extracorporeal shock wave lithotripsy)

- diameter1-2cm

- distal urether

PCNL(percutaneous nephrolithotomy)

- diameter>2cm

open:

- staghorn

10.1-A lady presented with light headedness and palpitation she has similar episodes in last 3 months. On examination BP is 110/72 and pulse 74/min and after head tilt BP is 85/60 and pulse 98/min. treatment ?

⦁ Atropine

⦁ Pacemakers

⦁ Fluids

If it does not settled by supination then atropine

10.2-A lady in her 20s with lightheadedness (and ECG given – heart block 1st degree, I think). When you perform a table test – after head tilt for few minutes her pulse drops to 50 and BP

to 70/40. What is the management?

a. Pacemaker

b. Atropine

c. b-blocker

If it does not settled by supination then atropine

10.3 A guy with postural hypotension table tilt test was done and it was positive with his head above what can help in mx of this patient?

Fluid

Verapramil

Pacemaker

Digoxin

10.4 A young pt with repeated dizziness and fall when standing only. Head tilt test lowers BP to 70/50

What advise will you give?

fludrocortisone

increase salt and water intake

MEDSCAPE : The tilt-table test is a simple, noninvasive, and informative test first described in 1986 as a diagnostic tool for patients with syncope of unknown origin. In general, consider tilt-table testing for patients with the following issues:

• Hypotension (unexplained)

• Tachycardia when standing

• Pallor when upright

• Orthostatic palpitations

• Dizziness (unexplained)

• Lightheadedness

• History of frequent unexplained falls

• History of episodes of fainting or loss of consciousness

Technique : The tilt-table test involves placing a patient on a flat table with a foot support, then tilting the table upward for a period of time to observe changes in blood pressure and heart rate. The patient is initially positioned supine and horizontal on the table, then tilted by degrees to a completely vertical, upright position. During the study, blood pressure, heart rate, oxygen saturation, and cardiac rhythms are recorded and monitored for the end point of fainting, which indicates a positive tilt-test result.[7] The patient is also observed for signs and symptoms that would necessitate early termination of the study.

Results : A positive tilt-table test might be cardiac(decrese HR to less than 40 or asystole for 3s) or vasodepressor(HR does not fall more than 10% but BP falls grater than20-30) or mixed.

While testing if the patient was unstable(bp95th percentile while overweight is >85th percentile.

26-patient on venlafaxine well controlled start to develop pressure of speech, euphoria,… .what to do?

Add valproate

Add olanzapine

Add chlorpromazine

Answer : add olanzapine (bipolar disorder on antipedressants are likely to develop mania)

antidepressant medication is useful in moderate to severe depression (TABLE 19.1), or when depression has an anxiety disorder codiagnosis. 11 Antidepressant therapy should be avoided if bipolar disorder is suspected, and screening should be actively conducted for symptoms of past or previous mania.

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Management of acute mania This is a medical emergency requiring hospitalisation for protection of both family and patient. First line:

olanzapine 5 mg (o) nocte initially

or

risperidone 0.5–1 mg (o) nocte initially

Second line:

haloperidol or other first-generation

antipsychotic

Prophylaxis for recurrent bipolar disorder

(Over 90% will have a recurrence at some time: consider medication if two or more episodes of either mania or depression in the previous 4 years). Recommended prophylactic agents 5

lithium 125–500 mg (o) bd then adjusted

or

second-generation antipsychotic(quetiapine) agent( or (if depression prominent)

lamotrigine or carbamazine or sodium valproate

Management of bipolar depression

This is a difficult component to treat and antidepressants should not be used alone. Many mood-stabilising agents appear to have a bimodal (antidepressant and antimania) effect and can be

useful in the absence of classical antidepressants.

A recommended regimen is:

lithium, valproate, carbamazepine, quetiapine, lamotrigine or olanzapine

plus

an antidepressant (e.g. SSRI, SNRI or MAOI)

Antidepressants are usually withdrawn within 1–2 months because of a propensity to precipitate mania.

ECT is an effective treatment for bipolar depression while psychological therapies such as CBT and psychoeducation have proven efficacy. Bipolar I patients usually recover but proceed to have further episodes of depression or mania.

Treatment of bipolar disorders in pregnancy: First line medications — For pregnant patients with manic, hypomanic, or mixed episodes, we suggest first generation antipsychotics, which have been widely used during pregnancy. We prefer haloperidol , based upon its demonstrated efficacy in randomized trials. pregnant patients with manic, hypomanic, and mixed episodes often do not respond to or tolerate haloperidol .For these resistant patients, we suggest in order of preference risperidone , quetiapine , or olanzapine.

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28-Scenario of hyperkalemia pt present with confusion k 6.5,cr increas ur increase,next?

1.urgent hemodylasis

2. calcium resonium

3. 5% dextrose insulin 10 unit

اگه کلسیم گلوکونات تو گزینه ها نباشه بنظرم همون گزینه 3 یعنی دکستروز با انسولین جواب هست.

راجع به اين سوال براى خودم، جاى سوال داشت كه calcium resonium چيه، و اينو از يك گايدلاين uk براى درمان هيپركالمى پيدا كردم:

Calcium polystyrene sulphonate resin (Calcium Resonium®) enema 30g followed with 15g orally 4 times daily with regular lactulose will increase gut losses of potassium• When given rectally the calcium resonium must be retained for 9 hours followed by irrigation to remove resin from the colon to prevent faecal impaction. Bowel perforation can be a complication• The onset of action is slow (≥2 hours) and other measures should be employed in the interim to lower potassium levels. Do not add Calcium Resonium® to fruit juice which has a high potassium content• One gram of resin exchanges 1mmol/l Na for 1mmol/k

29-54 year male with pain in left iliac fossa & fever, history of blood in stools. what will u do?

a.USG

b.CT

c.Barium studies

d.colonoscopy

e.xray erect

Dx : Diverticolitis

DIAGNOSIS OF DIVERTICULITIS — The diagnosis of acute diverticulitis can often be made on the basis of the history and the physical examination. In the acute stage, it is helpful to perform further studies to confirm the diagnosis and to rule out other sources of acute abdominal signs.

Radiologic evaluation in the acute setting — Routine abdominal and chest radiographs are commonly performed in the patient with acute abdominal pain and are most useful in excluding other causes of pain, such as intestinal obstruction, rather than in making the diagnosis of diverticulitis.

CT scan — Computer tomographic (CT) scanning of the abdomen with IV and oral contrast is the diagnostic test of choice in patients suspected of having acute diverticulitis. It is useful for diagnosis, assessment of severity, therapeutic intervention, and quantification of resolution of the disease.

Contrast enema — Water-soluble contrast enema may be considered if CT is not available. Even if there is no evidence of perforation on physical examination, barium is absolutely contraindicated , as an unexpected perforation may still be present

30-Delusion in pregnancy,rx?

1.clozapin

2. lithium

3. carbamazepine

4 .sodium val

این با این استم که میشه کلوزاپین ولی سئوالات مشابهی داشتیم مثلا مریض بایپولار در حاملگی که روی یک SSRI بود و ما میخواستیم برای فاز مانیای مریض یک دارو اضافه بکنیم ، درسته که آنتی سایکوتیکها خیلی safe تر از لیتیوم یا ضدتشنجها هستن ولی گزینه های اون سئوال هم دقیقا مثل همین بود و به این دلیل که در گایدلاین وقتی درمورد درمان بایپولار حرف زده اسم تک تک آنتی سایکوتیکها رو آورده الا کلوزاپین ، لذا من فکر میکنم که کلوزاپین واسه این منظور در استرالیا approved نیست و لذا اون تست رو میزنم لیتیوم که داروی safe بعدی هست.

کلوزپین در حاملگی گروه B هست و لیتیوم گروه D پس کلوزپین جواب هست.

ليتيوم ميشه داد در حاملگى اما براى درمان bipolar. البته در رفرنسهاى استراليايى گويا انتخاب اوله اما در آپتوديت براى مواردى كه به خط اول و دوم درمان جواب نميدن نگه داشته شده

31-man 35 y old smoker complains chest discomfort in rest in the morning. ecg has st elevation in inf. lead. the symptom and ecg got normal without any drug.ex.test is mormal.in angiography right coronary artery spasm was seen.which one is not recomended?

1.TNG

2.Niphidipine

3.Aspirin

4.Prazosin

Coronary Artery Vasospasm

Symptoms typically occur at rest, syndrome of nonexertional chest pain with ST-segment elevation on electrocardiography. Transient ST-segment elevation on electrocardiography (ECG) is a characteristic finding in patients with variant angina. but it may only be present during symptomatic episodes and typically resolves completely within minutes. However, in more severe cases, ST elevation may be followed by T-wave inversions for hours to days. Treatment: Prinzmetal's angina typically responds to nitrates and calcium channel blockers. sublingual, topical, or intravenous (IV) nitrate therapy. Nitroglycerin administered by any route (intracoronary, IV, topical, or sublingual) effectively treats episodes of angina and myocardial ischemia within minutes, and long-acting nitrate preparations reduce the frequency of recurrent events. standard therapies, including antiplatelet or antithrombotic agents, statins, and beta blockers, may be administered. Once the diagnosis of coronary artery vasospasm is made, calcium channel blockade and long-acting nitrates may be used for long-term prophylaxis.

Concerns about specific drugs — Nonselective beta blockers, such as propranolol can exacerbate vasospasm and should be avoided. In addition, aspirin should be used with caution and at low doses, as it is an inhibitor of prostacyclin production at high doses. However, for patients with atherosclerotic cardiovascular disease, we give aspirin 75 to 81 mg daily.

Oral sumatriptan is used to treat acute migraine headache. However, its use has been associated with coronary vasospasm and myocardial infarction. We suggest avoiding all medications of the triptan class in patients with known or suspected coronary artery vasospasm.

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32-ECG Atrial fib, palpitation, HTN DM next inv?

A. Echo

B. TFT (probability of thyrotoxicosis)

C. LFT

33-80 year old lady, present with anaemia, she is a vegetarian, has exertional dyspnea for the past few months and now has chest tightness on climbing stairs. Most appropriate management?

A-Iron orally

B- Iron parenterally

C- Packed cell transfusion (symptomatic anemia HB38ºC) for ≥2 weeks without evidence of infection.

Drenching night sweats without evidence of infection.

Extreme fatigue (ie, ECOG Performance status 2 or worse; cannot work or unable to perform usual activities)

Corticosteroids are a key part of treatment, typically administered at oral doses equivalent to 1 to 1.5 mg/kg per day of prednisone . AIHA will often begin to improve within a few days, although delayed responses can be seen. After AIHA has improved, corticosteroids are typically tapered over a period of several weeks

Treatment of localized SLL — For patients with localized (stage I) SLL, we recommend treatment with involved-field radiation therapy alone rather than systemic chemotherapy. Patients with stage II or more advanced SLL are treated with chemotherapy regimens used for symptomatic CLL as discussed below.

38-A middle aged man coming to chest pain. ECG given showing inferior wall stemi tertiary

hospital is 300 km away from the ED. He was given morphine, oxygen . What is the next

management.

A -Repeat troponin 8 hrs after

B- IV Nitroglycerine

C -r TPA

D- PCI

اون سه تا زمانی که تو گایدلاین ذکر شده رو نگاه کن : در دیرترین حالت ماباید ظرف 2 ساعت PCI رو انجام بدیم ولی انتقال به مرکز ترشیاری جهت انجام اون بیش از 2 ساعت طول خواهد کشید لذا همونجا بهش TPA میدیم .

اینکه در گزینه ها نوشته PCI منظورش این نیست که اونجا داردن ، اتفاقا میخواد ببینه ما میدونیم اونجا PCI ندارن و جهت انجامش باید منتقل بشه به بیمارستان ترشیاری یا نه .

39-Man with ecg of STEMI with chest pain of 2 hrs duration in tertiary center , nitro aspirin amd morphin given wuts nxt ?

• PCI

• SC heparin

• TPA

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40- a 20 y/o aborigional man, alcoholic, smoker and a drug abuser visits ur clinic. He is in a state of delirium. What will be first investigation of choice?

Alcohol level in blood

Urine drug analysis

Alcohol breath test

Blood sugar

Urea and electrolytes

Answer : blood sugar

اين مريض بايد قند و الكترليتها توش چك بشه (الان گايدلاين رو هم ميذارم) و بين اين دوتا قند رو كه با يك گلوكومتر ميشه زود چك كرد اولين كار ميشه .

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41-an old man was found unconscious, after regaining conscious he said he is very cold, temp 34.2, BP 90/60 management?

Normal salin

Dopamine

Dextrose

Niloo & Leila : normal salin due to sepsis

این سوال به نطر میاد علت هایپوترمی محیطی باشه. اگر ورنیکه بخواد علت هایپوترمی در نطر گرفته شود با اینکه بیمار هوشیار هست و میگه سردش شده جور در نمیاد. فشار ۹ نزدیک به شوک هست بهتره سریع تر افزایش حجم داخل عروقی بشه

اين مطلب رو در پاسخ به اين شبه دوستان گذاشتم كه ميگفتن اين ميزان هيپوترمى نميتونه كاهش سطح هوشيارى بده . و اين نشون ميده كه دماسنج معمولى شايد نتونه دماى واقعى يك بيمار هايپوترم رو نشون بده .

اين رو هم محض كش دادن قضيه فرستادم !

ولى از اونجاييكه اگه هيپوترمى كاهش سطح هوشيارى مريض ناشى از افت قند باشه بعيده كه مريض خودش بدون دريافت قند هوشيار بشه لذا تقريباً اين علت منتفى هست و همون علل محيطى مطرح تر هست

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42-middle aged man develops cough and dyspnea. No history of smoking and occupational lung disease. On examination clubbing and inspiratory creptations on chest auscultation. Diagnosis?

Mesothelioma

Lung cancer

Sarcoidosis

Lung fibroids

mycoplasma

Common causes of clubbing due to pulmonary disfunction :

1-bronchogenic carcinoma

2-cystic fibrosis

3-bronchiectasis

4-diffuse fibrosing alveolitis

43-ulcerative colitis… whats best to come to Dx?

Sigmoidoscopy

Colonoscopy

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44- a 10 y/o football player presents with pain and limp at Rt knee. In regard to Osgood-Schlatter disease what will u advise?

It will resolve in 1-2 year

Stretch quadriceps & massage lump upward will resolve it

Complete bed rest

x-ray may be needed if no improvement

steroid injection

Answer : a

Management : Treatment is conservative as it is a self-limiting condition (6–18 months: average 12 months).

• If acute, use ice packs and analgesics.

• The main approach is to abstain from or modify active sports.

• Localised treatments such as electrotherapy are unnecessary.

• Corticosteroid injections should be avoided.

• Plaster cast immobilisation should also be avoided.

• Surgery may be used (rarely) if an irritating ossicle persists after ossification.

• Gentle quadriceps stretching.

• Graded return to full activity.

Prevention

• Promote awareness and early recognition of OSD.

• Program of stretching exercises for quadriceps mechanism in children in sport.

45-patient non compliant on dialysis came after 5 days last dialysis with dypnea and weakness what is you next action:

a-call dialysis unit

b-ABG

c- ecg

d- xray chest

ECG to role out electrolyte disturbances , especially hyperkalemia

46-pt on thyroxine, develop palpitation and irregular pulse asking treatment, on ecg- AF?

a)digoxin

b)pacemaker

c)stop thyroxine

d)metoprolol

In patients with clinical manifestations of thyroid storm, we begin immediate treatment with a beta blocker ( propranolol in a dose to achieve adequate control of heart rate, typically 60 to 80 mg orally every four to six hours), a thionamide, and glucocorticoids ( hydrocortisone , 100 mg intravenously every eight hours). One hour after a thionamide is given, we administer iodine (SSKI, five drops [20 drops/mL, 38 mg iodide/drop] orally every six hours, or Lugol's solution, 10 drops [20 drops/mL, 8 mg iodine/drop] every eight hours). (See 'Treatment' above.)

For patients with life-threatening thyroid storm admitted to an ICU, we suggest propylthiouracil (PTU) (200 mg orally every four hours) rather than methimazole as initial therapy ( Grade 2B ). PTU blocks T4 to T3 conversion and results in lower serum T3 levels for the first several days of treatment. However, for severe but not life-threatening hyperthyroidism, methimazole (20 mg every six hours) may be preferred because of its longer half life, lower risk of hepatic toxicity, and because it ultimately restores euthyroidism more quickly than PTU. Patients initially treated with PTU should be transitioned to methimazole before discharge from the hospital. (See 'Thionamides' above and "Pharmacology and toxicity of thionamides" .)

For patients with contraindications to thionamides who require urgent correction of hyperthyroidism, surgery is the treatment of choice. Patients who are to undergo surgery require preoperative treatment of thyrotoxicosis. We typically treat with beta blockers (if not contraindicated, propranolol 60 to 80 mg every four to six hours), glucocorticoids to inhibit conversion of T4 to T3 (eg, dexamethasone , 1 to 2 mg every six hours), and, in patients with Graves’ disease, iodine (SSKI, five drops [20 drops/mL, 38 mg iodide/drop] orally every six hours, or Lugol's solution, 10 drops [20 drops/mL, 8 mg iodine/drop] every eight hours). We continue treatment for up to five to seven days.

65-ECG of a patient with h/o CHF and hypothyroidism.He is on multiple drugs.She now presented with an episode of LOC.What will u do?

a)Reduce thyroxine

b)Give metaprolol

c)Give digoxin

d) DC cardioversion

( ECG was really bad and hard to guess )

مسلما ای اف بيشتر با هايپر همراه بوده اما تو مقالات خوندم که هايپو هم ميتونه از اين کارا بکنه

من فكر ميكنم اين مريض يك اپيزود كاهش سطح هوشيارى قبل مراجعه داشته و الان هوشيار هست و اين ديگه نيازى به شوك نداره و درمان دارويى كفايت ميكنه .

كم كردن لووتيروكسين هم بلافاصله اثر نداره لذا من فكر ميكنم بهتره يك دارو براى AF مريض شروع بشه و با توجه به اينكه مريض CHF هم داره به توصيه گايدلاين ديگوكسين ارجح هست به متوپرولول .

در درمان AF دو مرحله داریم یکی کنترل ریت ویکی نرمال کردن ریتم.در مرحله کنترل ریت از بتابلوکر وراپامیل و یا دیلتیازم ویا دیگوکسین.در مرحله کنترل ریتم اگر اختلال همودینامیک نداشت تا سه هفته بعد از INR بالای 1.8 که با ضد انعقاد داده ایم کاردیوورژن انجام میدهیم.اگر همودینامیک مشکل داشت بعد از شروع هپارین اکو ترانس ازوفاژیال میگیریم در صورت عدم مشاهده لخته در داخل دهلیز چپ کاردیورژن انجام میشود.داروهایی که برای کنترل ریتم داده میشود :آمیودارون .پروکایین آمید وایبوتیلید دیگوکسین برای کنترل ریت در CHF انتخابی است.

66- 13yr old girl came for abortion. she conceived 2months ago when she was raped.next step

A- Call child protection authority

B-Call sexual assault authority

C- Refer her to hospital for abortion

D- Call police

67-36yr female, sudden onset of left eye painless vision loss. which one mostly associated

Left carotid bruit

Pain in left temporal artery 

68-pts hear a poping sound in ear before that mild vertigo.nystagmus and then fall down.now have rt ear total SNHL .rt horner synd.and nystagmus what can cause?

1.basilar infarct

2.meningitis

3.acostic neuroma

4.acute labirantitis

Acute occlusion of the basilar artery

may cause brainstem or thalamic ischaemia or infarction. brainstem infarction results in rapid deterioration in level of consciousness and ultimately death.

the exact characteristics of which will depend on the site of occlusion:

sudden death/loss of consciousness

top of the basilar syndrome(This results in bilateral thalamic ischaemia due to occlusion of perforator vessels)

visual and oculomotor(3ed) deficits

behavioural abnormalities

somnolence, hallucinations and dreamlike behaviour

motor dysfunction is often absent

proximal and mid portions of the basilar artery (pons) can result in patients being 'locked in'

complete loss of movement (quadriparesis and lower cranial dysfunction)

preserved consciousness

preserved ocular movements (often only vertical gaze)

basilar artery thrombosis(Medscape):

• motor deficits(hemiparesisor tetraparesis or facial paresis)40-67%

• dysarthria and speech imparement 30-63%

• vertigo, nausea , vomiting 54-73%

• headache 40-42 %

• visual disturbances 21-33%

• altered consciousness17-33 %

Acoustic neuroma(Vestibular schwannoma)

Vestibular schwannomas (acoustic neuromas) account for 80 to 90 percent of cerebellopontine angle tumors (CPAs) in adults.

symptoms

Cochlear nerve ( Symptomatic cochlear nerve involvement occurred in 95 percent of patients [ 15 ]. The two major symptoms were hearing loss and tinnitus.

Vestibular nerve ( Involvement of the vestibular nerve occurred in 61 percent of patients [ 15 ]. Affected patients frequently acknowledged having unsteadiness while walking, which was typically mild to moderate in nature and frequently fluctuated in severity. True spinning vertigo was uncommon because these slow growing tumors cause gradual rather than acute asymmetries in vestibular function. In this setting, the central vestibular system can often compensate for the gradual loss of input from one side.

Trigeminal nerve ( Trigeminal nerve disturbances occurred in 17 percent of patients [ 15 ]. The most common symptoms were facial numbness (paresthesia), hypesthesia, and pain. The average duration of symptoms was 1.3 years; the symptoms usually occurred after hearing loss had been present for more than two years and vestibular symptoms for more than one year. (See "Trigeminal neuralgia" .)

Facial nerve (The facial nerve was involved in 6 percent of patients [ 15 ]. The primary symptoms were facial paresis and, less often, taste disturbances

Diagnosis(JM) is best clinched by high-resolution MRI. Audiometry and auditory evoked responses are also relevant investigations.

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اين سئوال يه مشكلى داره :

- در انفاركت بازيلار ما hearing loss نداريم .

- گزينه ديگرى كه به علائم ميخوره آكوستيك نوروما هست كه در اون ما سندرم هورنر نداريم !

اتفاقا شايع ترين علامت هاى اكوستيك نوروما تينيتوس و كاهش شنوايى هستن و بر اساس مد اسكيپ ورتايگو شيوع كمترى داره و بيشتر در تومورهاى كوچيك ديده ميشه

من با اكوستيك نوروما موافقم ولى! تنها دليلى هم كه دارم مداسكيپه كه گفته تومورهاى برين استم كه پره گانگليونيك نورون رو درگير ميكنن ميتونن هورنر بدن

Causes of vertigo :

1- with hearing loss

������������Meniere disease ➡️ old

������������Acoustic neuroma (Schwanoma)

������������Acute labyrintitis ➡️ young/inf

2- without hearing loss

������������Vestibular neuritis ➡️ young/inf

������������BPPV ➡️ old

������������PICA ➡️ old

69-37 years old lady with CIN-1 on PAP smear, her last smear was negative but 4 years back genital warts history what to do

A) do nothing

B) Colposcopy

C) Cone biopsy

D) hysterectomy

E) LEEP

Cervical intraepithelial neoplasia

Historically, mild, moderate, and severe dysplasia were the terms used to describe premalignant squamous cervical cellular changes. This nomenclature, although still in use, has generally been replaced by the term CIN, which is used to describe histologic changes (those detected with biopsy). CIN has three degrees of severity:

CIN 1 is considered a low grade lesion. It refers to mildly atypical cellular changes in the lower third of the epithelium (formerly called mild dysplasia). HPV viral cytopathic effect (koilocytotic atypia) is often present.

CIN 2 is considered a high grade lesion. It refers to moderately atypical cellular changes confined to the basal two-thirds of the epithelium (formerly called moderate dysplasia) with preservation of epithelial maturation.

CIN 3 is also considered a high grade lesion. It refers to severely atypical cellular changes encompassing greater than two-thirds of the epithelial thickness, and includes full-thickness lesions (formerly called severe dysplasia or carcinoma in situ).

[pic]

• In premenopausal women with low grade squamous intraepithelial lesions (LSIL) on cervical cytology, immediate colposcopy is the preferred method of evaluation, given the relatively high risk of underlying CIN 2,3 or more.

• In postmenopausal women with LSIL, options for further evaluation include: immediate colposcopy, repeat cytologic evaluation at 6 and 12 months, and HPV testing. In contrast to adolescents and premenopausal women, HPV testing can be useful for allowing many women to avoid colposcopy since the prevalence of HPV infection in this population is low. If HPV testing is negative for high oncogenic risk HPV types ( table 1 ), the patient should be followed with a repeat cytologic evaluation in 12 months.

• In pregnant women with LSIL, we perform colposcopy, but the procedure can be deferred until six weeks postpartum, when the cervix has returned to its nonpregnant status. Endocervical curettage is NOT performed in pregnancy.

[pic]

Low-grade squamous intraepithelial lesions (LSIL)

• A woman with a Pap test report of possible/definite LSIL should have a repeat Pap test in 12 months (Practice Point). If the repeat test at 12 months shows LSIL (definite or possible) the woman should be referred for colposcopy.

• A woman aged 30 years or more with a Pap test report of LSIL, without a history of negative smears in the preceding 2–3 years, should be offered either colposcopy or a repeat Pap smear at 6 months (Practice Point).

دوستان چيزى كه من در مورد HPV متوجه شدم رو بگم اينجا (البته تهش همين گفته شد اينجا ولى محض جمع بندى) :

ويروس HPV بيش از ١٠٠ نوع داره كه از نظر درگيرى به دو دسته اصلى پوستى و مخاطى تقسيم ميشه ، انواعى كه درگيرى پوستى ميدن احتمال خيلى كمى دارن كه به بدخيمى منجر بشن مثل همون سوش هايى كه باعث ايجاد كونديلوما (يا همون ژنيتال وارت) ميشن . ولى با اينحال احتمال بدخيمى در اونها صفر نيست و لذا اگر در خانمى ديديم ژنيتال وارت داره ولش نميكنيم به امون خدا و ازش يك PAP smear ميگيريم كه ببينيم اونجا خبرى هست يا نه و اگه خبرى نبود مثل يك فرد نرمال باهاش برخورد ميكنيم .

اونى كه توى مورتاگ نوشته كه HPV معادل است با LSIL ، اينجا از مريض پاپ گرفتن و در نمونه پاپ اسمير HPV تشخيص دادن (و در حقيقت چون اين از انواعى از HPV هست كه درگيرى مخاطى داده و پرخطر از نظر تبديل به بدخيمى محسوب ميشه لذا معادل LSIL درنظر گرفته شده).

70- 4year child has come with this ECG,Has complained of 4hours lightheadedness & palpitations. What’s next step of management:

A.Oral Digoxin

B.Immerse face in water

C.IV adenosine

D.IV sotalol

HR 200 and PR 20/MIN

[pic]

اين به احتمال زياد SVT with aberrancy هست . ولى مهم نيست چيه ، مهم اينه كه يك wide complex tachycardia هست (VT , SVT , WPW بودنش اصلاً مهم نيست فعلاً) و در اينجور موارد مثل يك VT با قضيه برخورد ميشه :

- اگه unstable بود D/C shock

- اگه stable بود آميودارون ، ليگنوكايين يا سوتالول

فقط يك تبصره داره داستان اونم اينكه در بچه ها اگه خواستيم درمان دارويى بكنيم اول يك دوز آدنوزين ميزنيم بعد ميريم سراغ داروهاى فوق

If narrow complex tachycardia (stable: vagus nerve stimulation

( unstable:

If widw complex tachycardia(unstable: defibrillation

(stable: amiodarone, lignocaine or sutalol

Unstable:1-chest pain 2-shortness of breath 3-altered level of consciousness 4-hypotension

71-

اينكه پتشى نداره و سابقه اى از علائم عفونى قبل داستان نميده به ضرر ITP هست .

اينكه اسپلنومگالى نداره به ضرر WVD هست .

مضاف بر اينكه اگه بخواد كبوديهاى قبلى ناشى از WVD بوده باشه يعنى مريض دائم ميرفته تو در و ديوار كه هم سرش و هم باهاش كبود بوده كه اين منطقى نيست .

لذا منم فكر ميكنم همون گزينه b مناسبتر باشه .

والا هموفيلى كه اصلاً تو گزينه ها نيست .

بعدش اگه بخواد مارو به سمت هموفيلى ببره بايد اطلاعاتى از قبيل جنس مذكر به ما بده . و اينكه كلاً اين بچه از بدو تولد ناخوش احوال بوده و بخصوص علائم آنمى بصورت مزمن مثل رنگپريدگى ، خستگى زودرس ، تنگى نفس و امثالهم رو بده كه هيچى نداده .

72-which one can be phisiologic in a pregnant woman?

1.s3.

2.s4

3.dyastolic murmur

دیسترس .ارتوپنه. سوفل سیستولیک اجکشن و s3. میتونن فیزیولوژیک باشن

ولی PND و s4 .همیشه پاتولوژیک هستند.(هاریسون)

73-

[pic]

74-

young man after a quarrel had a fx of floor of eye.what is the most consistant symptom with that?

1.conjenital hge

2.cant open the mouth completely

3.loss of sensitive in skin around

4.reduce the visual acuity

[pic]

75-hypotonic child with open Anterior Fontanel what test to do?

1.TFT

2.usg cranial

75.1-mother come with 10 month old infant with increase head size from 25 percentile at birth to 75 percentile now and on examination child hypotonic with open anterior fontanelle what will you do next??

a.CT SACN head

b.check CMV infection

c..TSH

D.head ultrasound

e.rubella test

76-student with recurrent attack of abd . pain cramp and bloating 1week before exam RX

1.Antidepresant

2.smooth mascle relaxant

3.laxative

4.inc dietary fibr

5.dec.fat fibr

[pic]

77-35 yr women feel discomfort down below , condition developed after twice intercourse with new partner now condition resolve wn her partner go away last pap smear 18 ago was normal wt to do next

a- repeat pap

b- check chlamydia pcr in urine

c- cervical smear for HPV

اگه كلاميديا بود ، طرف بعد از رفتن شوهرش و عدم اينتركورس بايد همچنان علائمى ميداشت و علامت كلاميديا صرفاً ديسپارونى نيست .

chlamydia

• Risk factors for chlamydia infection include young age, multiple sex partners, inconsistent use of barrier contraceptives, and history of prior sexually transmitted infections.

• vaginal discharge, intermenstrual vaginal bleeding, and post-coital bleeding may be reported. Poorly differentiated abdominal pain or lower abdominal pain may indicate early upper genital tract involvement. O/E mucopurulent cervical discharge, cervical friability, and cervical edema may be seen. Chlamydial infection of the female urethra often accompanies cervicitis. Women with urethral infection complain of typical symptoms of a urinary tract infection, such as frequency and dysuria.

• Urinalysis reveals pyuria, but no organisms are seen on Gram stain or on routine culture.(sterile pyuria) Approximately 30 percent of women with chlamydia infection will develop pelvic inflammatory disease (PID) with upper genital tract involvement if left untreated. Women with PID may complain of lower abdominal pain, vaginal discharge, dysuria and constitutional symptoms, such as fever.

• The diagnosis of chlamydia is usually made with molecular methods, such as nucleic acid amplification (NAAT=PCR), which are highly sensitive and specific.

• Cervicitis may also be caused by Neisseria gonorrhea, trichomonas, bacterial vaginosis, or herpes simplex virus infection. (See 'Differential diagnosis' above.)

• TX : single dose azithromycin 1 g or Doxycycline 100 mg bd for 7 daysAdditional empiric therapy for gonorrhea should be based on a high suspicion of infection (eg, a positive Gram stain in men, a sexual partner recently diagnosed with gonorrhea). A single injection of ceftriaxone (250 mg) cures the majority of uncomplicated gonococcal urogenital, anorectal, and pharyngeal infections.

• chlamydia screening for 16 to 25 y/o female yearly by PCR is indicated if sexually active.

78-13 years old girl presented with intermitant abd.pain on ex. of urine culture ecoli 10 5 were identified how to treat?

1.oral nitroforantoin

2.parentral Gentamycin

3.oral cephalexin

4.oral ciprofluxacin

5.no treatment

انتخاب اول تريمتوپريم هست بعد سفالكسين و در درجه سوم كواموكسى كلاو يا نيتروفورانتوئين .

تو سئوال هندبوك اونها جزو گزينه ها نبودن كه نوبت به نيتروفورانتوئين رسيد .

79- A group of guys returned from camping in the forrest. After a week they were admitted to the ED with bruises on the skin, renal bleeding and shock. What is the most likely cause?

A.Giardia lamblia

B.Escherichia coli

C.Disseminated intravascular coagulation

D.Staphylococcus aureus...

E.Ross River fever

In my opinion its escherichia coli and manifestation of HUS

What are the Physical Signs and Laboratory Values on Admission to the Hospital with HUS?

Physical findings on admission to the hospital may include lethargy, abdominal tenderness, bruising (purpura), swelling, or dehydration. Features on admission that portend a severe or fatal outcome include coma, rectal prolapse, decreased or absent urine output (oligoanuria), or an elevated white blood cell count (WBC)—one greater than 20 x 10^9/l (i.e. greater than 20,000 per liter).

اين سئوال من فكر ميكنم HUS ناشى از E.Coli باشه و با گزينه b بيشتر موافقم .

علائم مريضها هم به DIC ميخوره هم به HUS ، و هر دو هم ميتونن بدنبال يك عفونت ايجاد شده باشن ، فقط فرقشون اينه كه مريض قبل يك HUS علائم گوارشى داشته بمدت ٢-٧ روز بعد HUS كرده ولى مريض اگه بدنبال يك عفونت بخواد DIC بكنه اول بايد sepsis كرده باشه ناشى از عفونت و متعاقباً DIC بكنه .

حالا احتمال اينكه اينها يك گاستروآنتريت داشتن و خيلى جديش نگرفتن كه بيان دكتر و بعد وخامت اوضاع و HUS مراجعه كردن بيشتره تا اينكه فرض رو بر اين بذاريم كه اينها اول سپسيس كردن و جديش نگرفتن (!!!) و بعد با DIC مراجعه كردن .

[pic]

[pic]

Thrombotic thrombocytopenic purpura

Thrombocytopenia

Microangiopathic hemolytic anemia

Neurologic symptoms and signs

Renal function abnormalities

Fever

Thrombocytopenia and microangiopathic hemolytic anemia, a form of nonimmune hemolysis(coombs neg) (defined by the presence of fragmented red cells [schistocytes] on the blood smear and a negative direct Coombs’ test [direct antiglobulin test]), are the clinical features of thrombotic microangiopathy (TMA), a specific histologic lesion of arterioles and capillaries .

Typical HUS — The name typical HUS is generally reserved for children. Typical HUS was first recognized in the 1980s, with the appearance of Shiga toxin-producing Escherichia coli (usually E. coli O157:H7) . This disorder, also called diarrhea-associated HUS, accounts for approximately 90 to 95 percent of HUS in children.

The term thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) describes acute syndromes with abnormalities in multiple organ systems

when these patients are initially evaluated, they can best be described by the comprehensive term TTP-HUS. An additional justification for the use of the term TTP-HUS is that the pathologic changes in patients described as having TTP or HUS are identical and the initial treatment of all adult patients is the same: plasma exchange

In some patients, neurologic abnormalities are dominant and acute renal failure is minimal or not present; these patients are considered by some to represent classical or "idiopathic" TTP, typically associated with severe ADAMTS13 deficiency.

In other patients, acute renal failure is dominant and neurologic abnormalities are minimal or absent; these patients are considered by some to represent HUS. However, some patients present with both severe neurologic abnormalities, such as seizures and coma, and acute renal failure, making this distinction difficult.

Some patients may have thrombocytopenia and microangiopathic hemolytic anemia with no neurologic or renal abnormalities. For example, over half of patients with severe ADAMTS13 deficiency have no or minimal neurologic or renal abnormalities

ETIOLOGY — Although many cases of TTP-HUS are idiopathic, a variety of underlying causes have been identified . Importantly, TTP-HUS is often a multi-factorial disease. TTP-HUS can occur (or recur) after pregnancy, infection, pancreatitis, and surgery . These and other acute stresses can trigger an initial or recurrent episode, perhaps due to the release of inflammatory cytokines or other prothrombotic mediators

Etiologic agents responsible for the TTP-HUS syndromes include Shiga toxin-producing bacteria; numerous drugs such as quinine (available over the counter in beverages such as tonic water and bitter lemon), antiplatelet agents, and chemotherapeutics; and factors related to malignancy, allogeneic hematopoietic cell transplant, cardiovascular surgery, and pregnancy. The common defect caused by these agents probably involves damage to vascular beds, although a shared molecular mechanism has not been established.

80- A five year old boy was brought by his mother because of pallor and tiredness. On examination there is splenomegaly. He has history of neonatal jaundice and also a history of gallstones. Reticulocytes 5%. What would you expect in the blood smear?

Atypical lymphocytosis

Sphere shaped red cell

Immature lymphocyte

Granulocytosis

Crescent shape blood red cell

Hereditary Spherocytosis(HS)

The diagnosis of hereditary spherocytosis (HS) is suspected in the presence of anemia, jaundice, and splenomegaly in a subject with a positive family history of hemolytic anemia. Gallstones of the pigment type, resulting from excess unconjugated bilirubin in bile, may be found in very young children, but the incidence of gallstones increases markedly with age. Routine blood counts reveal anemia and reticulocytosis, a low mean corpuscular volume (MCV↓), increased mean corpuscular hemoglobin concentration (MCHC↑), and an increased red cell distribution width (RDW↑). Spherocytes are prominent on the peripheral blood smear. Direct and indirect antiglobulin tests are negative.

The diagnosis of HS is confirmed in the presence of an abnormal screening test. The classic osmotic fragility test ( figure 1 ) has been supplanted by the more accurate eosin-5-maleimide binding test either alone or in combination with a second test, such as the acidified glycerol lysis time [ 33 ] or the cryohemolysis test.

81-Bamboo spine not responce to paracetamol, wt to do?

MTX

Hla27 testing

Physiotherapy

Indomethacin

In my opinion the answer is anti-TNF α

Pharmacological agents:

— NSAIDs (e.g. indomethacin 75–200 mg (o) or 100 mg rectally nocte daily or ketoprofen 100 mg rectally nocte to control pain, stiffness and synovitis)

— sulphasalazine (if NSAIDs ineffective)

— intra-articular corticosteroids for severe monoarthritis and intralesional corticosteroids for enthesopathyRefer for advice on above and especially for DMARD and bDMARD therapy.

Careful monitoring is required with NSAIDs and sulphasalazine.

• Systemic corticosteroids are not indicated.

• Immunosuppressants (low dose weekly methotrexate) and bDMARDs may be needed for severe intractable problems with psoriasis and reactive arthritis.

• These conditions should be managed in collaboration with a consultant.

• Although phenylbutazone is the most effective NSAID, its side effects (especially aplastic anaemia) are a major problem.

82-82y old lady had a hx of smoking 24pack a year, now 10kg wt loss, on physical ex only anorexia & left side supraclavicular LN, on chest and abdomen ct done nothing specific. What is the cause?

Ca lung

Ca stomach

Ca colon

Ca breast

Since gastric cancer can spread via lymphatics, the physical examination may reveal a left supraclavicular adenopathy (a Virchow's node ) which is the most common physical examination finding of metastatic disease, a periumbilical nodule (Sister Mary Joseph's node) or a left axillary node (Irish node).

Peritoneal spread can present with an enlarged ovary (Krukenberg's tumor ) or a mass in the cul-de-sac on rectal examination (Blumer's shelf ). However, there are patients with ovarian metastasis without other peritoneal disease.

Ascites can also be the first indication of peritoneal carcinomatosis.

A palpable liver mass can indicate metastases, although metastatic disease to the liver is often multifocal or diffuse. Liver involvement is often, but not always, associated with an elevation in the serum alkaline phosphatase concentration. Jaundice or clinical evidence of liver failure is seen in the preterminal stages of metastatic disease

83-a patient present with symptom of dysuria and hematuria. she has a history of weight loss from a few month with malaise. on U/E RBC and pus cells present. your diagnose?

1.RCC

2.Renal tuberclusis

3.bladder carcinoma

Isolated pyuria  

Uptodate:

Assuming no contamination with vaginal secretions, pyuria alone is usually indicative of urinary tract infection (including tuberculosis, in which conventional bacterial cultures may be negative). Sterile pyuria may also suggest an asymptomatic kidney stone or some form of tubulointerstitial disease, such as analgesic nephropathy.

NEJM:

• A recently (within preceding two weeks) treated urinary tract infection (UTI) or inadequately treated UTI.

• UTI with 'fastidious' organism (an organism that grows only in specially fortified artificial culture media under specific culture conditions) - eg, Neisseria gonorrhoeae.

• Renal tract tuberculosis.[2]

• Chlamydial urethritis.

• False negative culture due to contamination with antiseptic.

• Contamination of the sample with vaginal leukocytes.

• Interstitial nephritis: sarcoidosis (lymphocytes not neutrophils).

• Urinary tract stones.

• Renal papillary necrosis: diabetes, sickle cell disease, analgesic nephropathy.

• Urinary tract neoplasm, including renal cancer and bladder cancer.

• Polycystic kidneys.

• Interstitial cystitis.

• Prostatitis.

• Kawasaki disease.[3]

• Other reported associations include appendicitis and systemic lupus erythematosus

In RCC, there can be hamaturia, but no pus cell and mean age at diagnosis is 55 yrs.

Genitourinary and adrenal disease — TB of the urinary tract may present with hematuria, proteinuria, and "sterile" pyuria. In the kidney the disease frequently localizes to the renal papillae, and characteristic distortion of the collecting system tract may be seen radiographically. Flank pain, hydronephrosis, and cystitis indicate more severe disease, and spread to the genitalia may occur. Diagnosis is established by culture of the organism from the urine; acid-fast microscopy generally is not performed on urine samples because of the normal presence of nonpathogenic, nontuberculous mycobacteria in many individuals. Focal scarring of the kidneys and the collecting system may occur even after successful treatment.

INTRODUCTION — Tuberculosis can lead to two major forms of renal disease: direct infection of the kidney and lower urinary tract; and secondary amyloidosis. Other causes include nephrotoxicity induced by antimicrobial agents and hyponatremia due to the syndrome of inappropriate ADH secretion induced by pulmonary involvement or miliary disease.

Diagnosis — The diagnosis of genitourinary tuberculosis may be suspected from the symptoms, urinary findings, a possible past history of tuberculosis, and a positive tuberculin skin test . The urine is classically sterile by routine culture, but some patients have concurrent bacteriuria. Thus, a positive culture does not exclude the presence of urinary tuberculosis in the appropriate clinical setting.

Confirmation of the diagnosis requires the demonstration of tubercle bacilli in the urine, although the constellation of dysuria, sterile pyuria, hematuria, and the characteristic IVP findings are highly suggestive of urinary tract tuberculosis. The finding of acid-fast organisms in the urine sediment with a Ziehl-Neelsen stain or fluorescent dye techniques is not pathognomonic for this disorder, since nonpathogenic mycobacteria may occasionally be present; furthermore, false negative results commonly occur .

Thus, urine culture is the gold standard for establishing the diagnosis. Three to six first morning midstream specimens should be sent to maximize the likelihood of a positive result; false negative results may occur if the patient is receiving antituberculous therapy or broad spectrum antibiotics which may inhibit mycobacterial growth because of the high urinary concentrations obtained . Bacilli are shed into the urine intermittently; as a result, only 30 to 40 percent of single specimens are positive in patients with active disease

TREATMENT — The approach to treatment of renal tuberculosis is generally the same as that for pulmonary tuberculosis.

84-A young lady with H/O rhinorrhea,low grade feve,photophobia with some neck stiffness.

LP-protein,glucose both are normal,

rbc-200,

lymphocyte-3oo,

neutrophil -20

whats your management?

1.iv ceftriaxone

2.iv acyclovir (indicated in encephalitis not viral meningitis)

3.analgesia and observation

Meningitis jm p290

The classic triad is: headache, photophobia, neck stiffness. [pic]

Treatment of viral meningitis: Organise hospitalisation where treatment will be supportive. Suspected herpes simplex encephalitis should be treated with IV aciclovir immediately.

preferred imaging: MRI

[pic]

85-55 y male on clopidrogrel with h/o drug eluting stent insertion 1w earlier came to you for the evaluation of uncomplicated varicocele operation which will take place a few weeks later.next:

1.postpone surgery for12 month and then do it

2.continue clopidrogrel until day of surgery

3.give ffp and do surgery now

4.discontinue clopidrogrel and do surgery

Handbook p 480

Indications for the use of the anti-platelet agent clopidogrel include the treatment of acute coronary syndrome and stroke and the prevention of myocardial infarction, • stroke, and stent occlusion. For patients with stents, particularly drug-eluting stents, continuous therapy with clopidogrel is essential, particularly in the first two years after insertion of the stent. In the case in question, whilst stopping the anti-platelet drug for the duration of the surgery might increase the risk of myocardial occlusion, the risk would not be as major as when using the drug for possible stent blockage. If this patient had a coronary artery stent in situ and surgery was essential, it is likely that surgery would proceed in the presence of the anticoagulants. In this case, however, with no history given of previous stent insertion, it would be reasonable to stop the anticoagulants now in preparation for surgery a week later (B is correct). The effect of the aspirin and clopidogrel should be suitably diminished within one week of stopping the agents and platelet transfusion would be unnecessary. Obviously, for a more acute surgical emergency with a high risk of haemorrhage. platelet transfusion might be considered. Vitamin K and protamine have no effect on platelet function.

دو مدل استنت داريم كه جلوى هركدوم مدت زمان لازم درمان ضدپلاكت رو نوشتم :

Drug eluting = 1 year

Bare metal = 1 month (3 not 1m)

و اگه عمل اورژانسى نباشه بايد تا اتمام دوره درمانى عمل به تعويق بيوفته .

- آسپيرين ، كلوپيدوگرل و ديپيريدامول ضدپلاكت هستن و بايد درصورت نياز عمل در حضور انها انجام بشه

- وارفارين ضدفاكتورهاى انعقادى هست و درصورت عمل خیلی اورژانسى بايد ffp داد خیلی اورژانس نبود یه ویتامین کا میدیم و بعد از یه کوچولو استراحت عمل میکنیم اگرم اصلا اورژانس نبود يكهفته قبل عمل قطع ميكنيم ، وقتى INR به ٢ رسيد هپارين شروع ميكنيم شش ساعت قبل عمل هپارين رو هم قطع ميكنيم .

86-old recall with pregnant with genital herpes, wot to diagnose latency?

Pcr,

igm now,

biopsy from ulcer

IgG

86.1-Pregnant with genital herpes,what test to identify it is new or recurrent infection??

A.get a swab of wart for culture

B.sample of wart for pcr

C.review her serology status in week

D.send a sample for serology now

E.Igm

Primary genital infection — Primary genital infection refers to the first occurrence of HSV infection. These patients do not have preexisting antibodies to either HSV-1 or HSV-2. Type-specific antibodies to HSV generally develop within the first 12 weeks after infection and persist indefinitely [2].

If a new HSV infection is clinically suspected during pregnancy, laboratory confirmation is required. Ideally active lesions are still present at the time of presentation and a swab for viral PCR can be collected as well as type-specific serology. PCR positivity for a HSV type for which IgG is negative suggests a primary genital HSV infection. Regardless of whether there is PCR confirmation, serial serology should be obtained to confirm seroconversion. C/S in indicated if active lesion present or rupture of membrane less than 4 hours.

[pic]

87-pt with spasticity of lower limb. Tingling and numbness in upper limb. Dx

A- Guiilian barre

B- Cord compression

C- Syringomyilia

Syringomylia involve cervical special cord(damaged lateral horn and compress motor track)

Handbook p 487

کورد کامپرشن، مثلا به دلیل هرنی دیسک گردنی، علایمش پارستزی دستها و اسپاستیسیتی در پاها

(Upper Motor Neuron Lesion)

هست.

سیرنگومیلی این طور که نوشته بیشتر باعث از بین رفتن حس درد و حرارت میشه. ضمنا در مورد علایم موتورش، این جور که نوشته باعث فلج شل میشه نه اسپاستیک

syringomylia

Definition: is a generic term referring to a disorder in which a cyst or cavity forms within the spinal cord. This cyst, called a syrinx, can expand and elongate over time, destroying the spinal cord.

Symptoms: pain, paralysis, weakness,[1] and stiffness in the back, shoulders, and extremities. Syringomyelia may also cause a loss of the ability to feel extremes of hot or cold, especially in the hands. The disorder generally leads to a cape-like loss of pain and temperature sensation along the back and arms. Each patient experiences a different combination of symptoms.

88-A pregnant lady with clear feature of delusion presents to you.manage :

A-Clozapine

B-Li

C-Valproate

D-Carbamazepine

E-Clonazepam

89-a young girl 15 y collapsed at exercise.her father had HOCM.after ecg and echo find no abnormality next step?

1.holter

2.stress echo

3.repeat echo after 3 years

Ambulatory ECG monitoring (holter) — Ambulatory ECG monitoring should be performed for 24 to 48 hours in all patients diagnosed with HCM (based on clinical and imaging findings) as part of the risk assessment for ventricular arrhythmias and risk for sudden death. In addition, in patients with palpitations in whom the etiology is uncertain or if there is suspicion for atrial fibrillation/flutter, ambulatory monitoring should also be considered.

Exercise testing — We proceed with exercise stress testing in all patients with known or suspected HCM (based on clinical and imaging findings) as part of the risk stratification (ie, abnormal BP response to exercise) and for the assessment of LV outflow tract (LVOT) gradient. Exercise treadmill testing is the preferred method of stress, rather than using a pharmacologic stress agent

90-pic of varicocele. Pt has scrotal swelling which subsides with lying down.what is the most imp inv.

ct abd

xray

us groin

هندبوك در پاسخ سئوال ٣.١٥٣ نوشته كه هر مريضى كه با درد يا تورم بيضه مراجعه ميكنه بايد سونو بشه و فقط در دو حالت نياز به سونو نيست :

Obvious inguino-scrotal hernia

Suspected torsion

اين رو هم من تهش اضافه كنم داخل پرانتز كه :

١- هيدروسل در پيرها اغلب خوش خيم هست ولى در جوانها بعلت احتمال بدخيمى بيضه بايد حتماً بررسى بيشتر بشه.

٢- واريكوسل برعكس ، يعنى در پيرها نياز به بررسى از نظر RC داره .

91- patient has rheumatoid arthritis had history of DVT. Now he came with black fingers.what is the inv

ANCA??

Anticardiolipin

ANA

Anti ds DNA

Two major types of questions:

1-with a history of DVT or repeated abortions suspicious of antiphospholipid synd ( anticardiolipin

2-with no previous history suspicious of vasculitis or RA ( ANCA

antiphospholipid syndrome

INTRODUCTION — The antiphospholipid syndrome (APS) is defined by two major components :

The occurrence of at least one clinical feature: vascular event or pregnancy morbidity

The presence of at least one type of autoantibody known as an antiphospholipid antibody (aPL) on two separate occasions at least 12 weeks apart

APS occurs as a primary condition or in the setting of an underlying systemic autoimmune disease, particularly systemic lupus erythematosus (SLE).

CLINICAL MANIFESTATIONS — APS is characterized by venous or arterial thromboses, morbidity occurring in the setting of pregnancy, and/or aPL-related clinical manifestations that are not part of the APS classification criteria, such as livedo reticularis, thrombocytopenia, cardiac valve disease, or aPL-nephropathy

Deep vein thrombosis — 32 percent

Thrombocytopenia — 22 percent

Livedo reticularis — 20 percent

Stroke — 13 percent

Superficial thrombophlebitis — 9 percent

Pulmonary embolism — 9 percent

Fetal loss — 8 percent

Transient ischemic attack — 7 percent

Hemolytic anemia — 7 percent

In rare patients, APS results in multiorgan failure because of multiple blood vessel occlusions, a condition referred to as “catastrophic antiphospholipid syndrome” ].

In addition to those already mentioned above, other possible aPL-related clinical manifestations include migraine headache, Raynaud phenomenon, pulmonary hypertension, avascular necrosis, cutaneous ulcers that resemble pyoderma gangrenosum, adrenal insufficiency due to hemorrhagic infarction, and cognitive deficits . For some of these clinical entities, the true relationship between the occurrence of the condition and the presence of aPL is not clear.

In 31 percent of cases, the cutaneous lesions were evident at presentation. The following frequency of lesions was observed :

Livedo reticularis — 26 percent

Digital necrosis — 8 percent

Splinter hemorrhages — 5 percent

Superficial venous thrombosis — 5 percent

Post-phlebitic ulcers — 5 percent

Circumscribed cutaneous necrosis — 4 percent

Thrombocytopenic purpura — 4 percent

Pseudovasculitis — 3 percent

Extensive cutaneous necrosis — 2 percent

Anetoderma — 2 percent

Primary APS versus APS with SLE — Some data suggest that the clinical manifestations of primary APS and APS associated with SLE are similar. In contrast, a subsequent study of 122 patients noted that the frequencies of arterial thrombosis, venous thrombosis, and fetal loss were greater in patients with APS and SLE than in those with primary APS

aPL are directed against serum proteins bound to anionic phospholipids and may be detected by:

Lupus anticoagulant tests

Anticardiolipin antibody ELISA

Anti-ß2 glycoprotein-I ELISA

Autoimmune and rheumatic diseases — The most frequent rheumatic disease associated with aPL is SLE. aPL occur in a substantial proportion of patients with SLE

approximately 50 percent of patients with an LA have SLE.

Both LAs and aCL have also been found in patients with a variety of other autoimmune and rheumatic diseases (eg, scleroderma, psoriatic arthritis) but, in the absence of clinical events associated with the APS, their significance is not clear

92-female pregnant come for antenatal care all ex normal admit that her husband hit her a lot of times when he drink alchohol and he take care that not make any bruise in her body what the action?

rm police

2.arrange couple meeting

3.make escape plan with her

4.talk with her husband alone

5.urgent admision??

Do I have to report a suspected crime? no

Australian jurisdiction except New South Wales has a general statutory requirement that doctors report a suspected crime, although they may be required to report specific offences such as child abuse or domestic violence or neglect.

Do I have to report suspected domestic violence?

In Tasmania the Family Violence Act 2004 requires health professionals to report suspected cases of family violence to a police officer as soon as practicable, where the violence involved the use of a weapon, sexual violence or physical violence. In other jurisdictions, health organisations have policies that require reporting of criminal offences or other conduct to the police or another agency. For example, NSW Health domestic violence policies require the reporting of suspected domestic violence to the police.

(Another table jm p 1011)

93-homeless guy with bags going to police for shelter with 3 bags as he thinks some ppl want to kill him cause of the use of x rated cd(pornographies).

1.full medical assessment

2. admission for psychiatric work up

3. antipsychotics

4. admit him

5.history frm police

First matabolic assessment,second psychiatric assessment. I have no idea

94-pt coming first time for ocp,hx with unilaterla headache with photophobia,advice?

a) cocp contraindictd

b) ct

c) can take ocp

[pic]

[pic]

[pic]

95-

Asymptomatic bacteriuria (concentration greater than 10*8 colony-forming units/L) does not need treatment except: pregnancy, urinary tract stones , patient who wants to undergo an urological procedures)

حالا اگه كمتر از اين باشه ولى مريض علامت داشته باشه درمان ميخواد

96-fight in pub Swelling over left parietal. Vitals unstable. Left pupil dilated. Left c.n. lesion mentioned.(no ct was there)

a. burrhole rt parietal

b. burrhole left parietal

c. ct (first doing ct then if indicated burrhole)

A recently fixed dilated pupil with corresponding imaging evidence of an expanding heamatom is considered an indication for emergency targeted burr hole placement . if the symptoms are concurrent with CT then the answer is Lt burrhole otherwise we should performe more diagnostic imaging.

این در واقع سوراخهایی هست که با دریل معمولا و گاهی حتی با سوزن و .... در جمجمه ایجاد میکنند برای خروج هماتوم ساب دورال و احیانا اپی دورال، اسم دیگه اینکار هم تریفینوتومی هست.

در وضعیت عادی که سی تی و جراح اعصاب و اتاق عمل و قیر و قیف و بقیه امکانات ردیف باشه که بیمار میره اتاق عمل و طبق سی تی تصمیم گیری میشه

معمولا تو اپی دورال ، کرانیوتومی انجام میشه و تو ساب دورال برهول زده میشه

اما در وضعیت های خاص یعنی نبود امکانات و اورژانس بودن شرایط :

مثلا در این بیمار گفته مردمک یکطرفه دیلاته

این یعنی بیمار داره دچار هرنی مغزی میشه

و شما زمان برای اعزام و .... ندارید

بعد گفته سی تی هم ندارد پس باید از روی علایم تصمیم بگیرید که محل احتمالی خونریزی کجاست

بر اساس اینکه فکر میکنیم خونریزی سمت راست هست یا چپ جمجمه، هفت نقطه را به ترتیب سوراخ میکنند تا خون خارج شود، اگر خارج نشد میرن سراغ سمت مقابل

یک وقتهایی هم سی تی داریم ولی جراح نداریم که بر اساس محل خونریزی در سی تی، محل سوراخ ها را انتخاب میکنیم،

97-man had marked anxiety. Isolated, poor hygiene, leave school, nevere work. what will help u to reach dx

A- eccentric attair(schizotypal personality disorder(جادوگر یا فالگیر...

B- perplexity

C- depressed affect

D- auditory hallucination( prodrome of schizopherenia

98-کلسيم بيشتر از 7.5 و يا علايم در حد پارستزی بعد از عمل پاراتيرويئدکتومی رو کلسیم اورال ميديم ديگه? @

پارستزى دور لب و گزگز ، اينها tetanic equivalent محسوب ميشن و بايد IV داد .

خود عدد هيپوكلسمى به تنهايى در غياب علائم ملاك تصميم گيرى نيست و در قدم بعد بايد كلسيم يونيزه چك بشه .

[pic]

Uptodate:

• Patients with hypocalcemia who are severely symptomatic (carpopedal spasm, tetany, seizures, decreased cardiac function, or prolonged QT interval) require rapid correction of calcium levels with IV calcium therapy. We also suggest IV calcium therapy in asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (1.9 mmol/L)

• Intravenous calcium is NOT warranted as initial therapy for asymptomatic hypocalcemia in patients with impaired renal function in whom correction of hyperphosphatemia and of low circulating 1,25-dihyroxyvitamin D are usually the primary goals.

• For those with milder symptoms of neuromuscular irritability (paresthesias) and corrected serum calcium concentrations greater than 7.5 mg/dL (1.9 mmol/L), initial treatment with oral calcium supplementation is sufficient. If symptoms do not improve with oral supplementation, intravenous calcium infusion is required.

• To effectively treat hypocalcemia in patients with concurrent magnesium deficiency, hypomagnesemia should be corrected first.

98-یه سوالی هست در رکال ها که داروی فشار خون در تنگی دوطرفه شریان کلیوی چی هست؟

renal artery stenosis

uptodate

Unilateral renal artery stenosis

Introduction: Renal artery stenosis is a relatively common finding in older patients with hypertension. However, renal artery stenosis is the primary cause of hypertension (ie, renovascular hypertension) only in certain settings. Atherosclerosis, which primarily affects patients (particularly men) over the age of 45 years and usually involves the aortic orifice or the proximal main renal artery. This disorder is particularly common in patients with diffuse atherosclerosis.

Etiology — There are two major causes of unilateral renal artery stenosis: Atherosclerosis, Fibromuscular dysplasia

Diagnostic clues: An acute elevation in serum creatinine of at least 30 percent after administration of angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB). Angiotensin II constricts both the afferent and efferent arterioles, but preferentially increases efferent resistance.

Diagnosis: duplex Doppler, computed tomography and MRA

TREATMENT

Medical therapy (essentially all patients)

Percutaneous angioplasty with or without stent placement

Surgical revascularization or, in some cases, resection of a "pressor" kidney

Medical therapy — The availability of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) has markedly improved the ability to control the blood pressure in patients with renovascular disease . If goal blood pressure is not reached with angiotensin inhibition alone, other antihypertensive drugs, such as a thiazide diuretic (preferably chlorthalidone ), a long-acting calcium channel blocker, an aldosterone antagonist, or a beta blocker, should be added as necessary.

Bilateral renal artery stenosis

Medical therapy — Bilateral renal ischemia induces activation of the renin-angiotensin-aldosterone system and promotes sodium retention with resultant volume expansion; both of these factors contribute to the ensuing rise in BP. As a result, the combination of a diuretic and an angiotensin converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) can control the hypertension in most patients, and is likely to be more effective than other antihypertensive agents. The major problem with this regimen is a hemodynamically-mediated decline in glomerular filtration rate (GFR) as detected clinically by a rise in serum creatinine. Lowering the systemic BP will tend to reduce the intraglomerular pressure below normal because of the stenotic lesion. Blocking angiotensin II formation with an ACE inhibitor or ARB will blunt this autoregulatory response and tend to reduce the GFR. This effect is more pronounced with diuretic-induced volume depletion, since the hypovolemia-induced increase in angiotensin II levels makes maintenance of the GFR more angiotensin II-dependent. The net effect is a rise in the serum creatinine concentration in most patients with severe bilateral renovascular disease [ 8 ] and some of those with less severe disease. However, these observations do not mean that ACE inhibitors or ARBs are contraindicated in this disorder as long as the patient is carefully monitored. The decline in GFR is small in most patients, with a large increase in the serum creatinine concentration occurring in less than 5 to 10 percent of cases. Furthermore, renal function can be improved in many patients by discontinuing the diuretic [ 9 ] and in most cases by discontinuing the ACE inhibitor or ARB .

Total recall group: ACEI are contraindicated in bilateral renal artery stenosis

99-70 year old male patient on warfarin came with abdominal pain, INR: 5.7, CT given

Similar picture (bladder haematoma)

a. Suprapubic catheterization

b. Bladder decompression

c. Inject vit K

d. Laparoscopy

e. Surgical exploration

نباید bladder تخلیه بشه چون اثر فشاریش داره یه کم جلوی خونریزی رو می گیره

به طور خلاصه : اگر خونريزى اكتيو و شديد داشته باشيم ٢ گزينه داريم:

١-اف اف پى ٢-فاكتور ريكامبيننت هفت و كنسانتره پروترومبين. گزينه ٢ گرونتره ولى خطر انتقال عفونت و واكنش هاى ناشى از اف اف پى و ترالى نداره و نياز به هماهنگى گروه خونى هم نداره. حالا در هر دو گزينه ويتامين كى به صورت آى وى ١٠ ميليگرم هم بايد بديم

Warfarin

INR9, stable = Hold w, vit k 5-10 mg po

INR>1.5, bleeding or surgery = Hold w, vit k 10 mg IV, FFP 3-4 u

100-young lady in her 3rd trimester in her pregnancy coming to ED with severe lower abdominal pain. she is not able to walk. in Urine ex. protein+++RBC+++

1.UTI ??

2.symphisis pubis sepration

3.abrubtion

Pubic symphysis separation — Peripartum pubic symphysis separation (pubic diastasis, symphysiolysis, osteitis pubis) is uncommon, but not rare; inconsistent definitions and sporadic reporting prevent an accurate estimate of incidence. Purported risk factors include fetal macrosomia, precipitous labor or rapid second stage of labor, intense uterine contractions, previous pelvic pathology or trauma to the pelvic ring, multiparity, and forceps delivery .Standard treatment of pubic symphysis separation is conservative: bedrest in the lateral decubitus position, pelvic support with a brace or girdle, ambulation with a walker or crutches, and a graded exercise protocol

[pic]

101- وقتی ريفامپيسين ميديم به ديابتی انسولينی آيا بايد انسولين رو زياد کنيم يا نه؟

[pic]

102-pregnant lady with unilatral renal artrey stenosis and htn tx?

a -ACEI

b-Methyldopa ??

c-b blacker??

از اونجايي كه متيل دوپا تو تنگي شريان كليه تاثيري نداره ، تو اين شرايط حاملگي و تنگي شريان كليه بتابلاكر ميديم

Medscape:

Restrict conservative treatment in patients with an established diagnosis of ischemic renal disease (IRD) to those with absolute contraindications to surgery or angioplasty or to patients who are likely to succumb due to other comorbid conditions before advancing to end-stage renal disease because of IRD. Clinicians must rely on pharmacologic agents (eg, combination of calcium channel blockers to control blood pressure and optimize renal perfusion), accepting the high probability of deterioration in renal function and shortened survival.

تنگی یک طرفه شریان کلیه--->ACEI

تنگی دوطرفه شریان کلیه--->ACEI کنتراندیکه-آنژیوپلاستی

102.1 old patient with DM and unilateral renal artery stenosis, Rx

Methyldopa

ACEi

Thiazide

Metoprolol

Answer: ACEI

102.2 old patient with DM and bilateral renal artery stenosis?

Methyldopa

ACEI

Thiazide

Metoprolol

Answer: Thiazide

103-a final year student/intern comes to u and tells u he is schizophrenic and currently on olnazipine but he still cant concentrate completely,what next

a)in the dose of olanazpine

b)ask him to see his psychiatrist immediately

c)excclude him from clinical rounds

4)inform university

Amedex : B

Me:D

[pic]

104-A 52 year old alcoholic man, presents with ankle oedema, distended abdomen, urine protein ++, blood + bp high, with past history of MI? Whats the diagnosis

A CHF

B Ac nephritis

C Renal Artery stenosis

D Nephrotic Syndrome

E Liver cirrhosis

Amedex: A is more relevant due to MI history and HTN

105-a 50 year old man present with hypertension with asthma and reflux nephropathy .lab inv were given.there was high urea,high creatinine and proteiuria 900 mg/day.what is the choice of anti HTN?

1.amlodipine

2.losartan

3.perindropil(a long acting ACEi)

4.indapamide

5.BB

بخاطر داستان كليه ش بهتره ACEI يا ARB بگيره ولى چون از عوارض شايع ACEI سرفه هست و مريض آسم هم داره بهتره از ARB استفاده بشه .

In my opinion BB is contraindicated in asthma, ARB or ACEI are relatively contraindicated in CRF(leads to incretion of BUN, Cr), its good to choose a CCB . but its ok if we start with ARB and tight control of renal function.not to mention cough due to increased bradychinin in lung from ACEi use has nothing to do with asthma.

106-A boy developed fever, proteinuria and hematuria 3 weeks after URTI. What is the most important indicator for admission?

a. Gross hematuria

b. Proteinuria +++

c. Fever 39 degrees C

d. Oedema

e. Headache and hypertension

IgA nephropathy versus PSGN

Patients with IgA nephropathy, which is the most common cause in primary glomerulonephritis in many developed countries, often have one or recurrent episodes of gross hematuria, usually occurring one to three days after a URI due to either viral or bacterial infections.

Poststreptococcal glomerulonephritis (PSGN) is induced by pharyngeal or skin infection with specific nephritogenic strains of group A, beta-hemolytic streptococci. PSGN and IgA nephropathy can be distinguished by renal biopsy, but biopsy usually is not be performed if the clinical history is highly suggestive of PSGN and resolution begins within one to two weeks and usually not performed in IgA nephropathy for hematuria in the absence of findings suggestive of a worse prognosis such as proteinuria above 1000 mg/day or an elevated serum creatinine.

The latent period from the onset of infection to the detection of hematuria is between one and three weeks with group A, beta-hemolytic streptococcal (GAS) pharyngitis (and between three and six weeks following streptococcal skin infection) compared with less than five days in IgA nephropathy after a bacterial or viral URI.

Throat culture and laboratory tests for GAS (eg, streptozyme test) should be positive in PSGN following a URI but usually not in IgA nephropathy. Recurrent episodes of gross hematuria are common in IgA nephropathy but rare in PSGN since only certain streptococcal strains can cause renal disease and there is long-term persistence of antibodies against nephritis-associated streptococcal antigen, a leading candidate for the causative antigen .

IgA nephropathy is typically a chronic disease and persistent microscopic hematuria is common after resolution of the URI. In contrast, PSGN gradually resolves after the infection has cleared. In children, a diuresis typically begins within one week, the serum creatinine returns to the previous baseline by three to four weeks, and hematuria resolves within three to six months

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107-A young female sex worker present for normal check-up and on lab test you found she has

gonorrhoea. Besides treating her, what next will you do?

A. Trace contacts of her past one year

B. Ask her to avoid sex

C. Trace contacts of her for past 6 months and treat them

D. Inform health department

In most cases, contact tracing can be undertaken by the index patient (patient referral), with health care provider assistance as an alternative option (provider referral). This needn’t be a complex or time-consuming exercise – generally it simply involves a discussion between health care provider and the patient.

Broadly, there are two different methods used to advise contacts: patient referral and provider referral.

Patient referral:

The index patient personally notifies his or her contact.

The health care provider provides the information to be imparted by the index patient to the partner.

Advantages

Individuals usually prefer to notify contacts personally

Quicker and easier

Disadvantages

Less confidentiality

Patients may not actually contact partners

Provider referral:

The health care provider directly advises the contact or uses another agency (for example, sexual health service, public health unit or health department contact tracer) to ensure that contacts are notified.

The health care provider must have the explicit approval of the index patient.

Advantages

Higher level of confidentiality for the index patient

Method of choice when an individual fears a violent reaction, and for certain situations and conditions (for example, pulmonary TB, transfusion-related infections, when contact will involve sex workers or person with intellectual disability)

May be appropriate for serious infections such as HIV where rigorous case finding is warranted

Disadvantages

More time- and resource-intensive

Sex workers with STIs may be reluctant to disclose the identity of clients. It should be borne in mind that protected sex is practised almost universally within the sex industry. Provider referral may be the preferred contact tracing strategy.



اگه كامل بخونيد مطلب رو توضيح داده كه provider referral اينجا يعنى چى. دليل اينكه همه اينها رو نوشتم توضيح دادن همين بود. اين در provider referral خود درمان كننده، با contact ها تماس ميگيره و بهشون اطلاع ميده يا اينكه اين كار رو از طريق another agency انجام ميده. ضمن اينكه گفته provider referral روش ترجيحى هست و ممكنه درمانگر از روش patient referral هم استفاده كنه! در واقع انتخاب استراتژى tracing با خودتونه. مهم اينه كه بايد trace كنيد!

Provider referral doesn't mean exactly "health department". Health provider is the clinician who provides caring. Acc to ALL guidelines including the redbook notes, it's the clinician duty to trace the contacts via a appropriate strategy.

Yes it's possible to use other agencies but it is not an obligation and is solely based on clinician decision wether to inform contacts in person or inform them via other agencies.

Next step: contact tracing

Second step: notifying (as far as I can remember the notification is not immediate)

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108-pt with low folic acid, howell-jolly body, stomatitis, normal bowel, weight loss, inv?

Small bowel Bx

Colon

Vit B12

Niloo: Howell–Jolly bodies are seen with markedly decreased splenic function. Common causes include asplenia (post-splenectomy), trauma to the spleen, and autosplenectomy caused by sickle cell anemia. Other causes are radiation therapy involving the spleen, such as that used to treat Hodgkin lymphoma. Howell–Jolly bodies are also seen in: severe hemolytic anemia, megaloblastic anemia, hereditary spherocytosis, heterotaxy with asplenia and myelodysplastic syndrome (MDS).

Ayda: Howel jolly bodies:sickle cell(hyposplenism).celiac.IBD.myeloprolifrative

Mohamad: coeliac can cause autosplenectomy …

Answer : a

109-pt on SSRI for 1 year after 6 months from SSRI she developed DM what investigation?

RFT

LFT

CBC

Abdominal CT

Amedex: may be A no direct relation but may be we have to check BUN , Cr before starting glucose lowering agents.

گرچه در رفرنس ها چیزی پیدا نکردم، بعضی از مقالات گفتند که انتی دپرسانت ها من جمله SSRI ها ممکنه به طور غیر مستقیم (افزایش وزن) یا مستقیم (افزایش مقاومت به انسولین) باعث دیابت بشن.

اما هرچی فکر میکنم ارتباطی با آزمایشاتی که تو گزینه‌ها ذکر شده و دیابت تازه تشخیص داده شده پیدا نمیکنم

فقط شاید renal function test یه کم مرتبط باشه...

من تو آپتوديت فقط يه قسمتى پيدا كردم كه گفته بود در يك تحقيق نشون دادن كه بعد از ٢ سال مصرف پاروكستين ريسك ديابت ٢ برابر شده بود. علتش رو هم ربط داده بودن به افزايش وزن...

فکر میکنم Renal function, چون امکان داره رو زمینه دیابتی که تازه کشف شده بیمار از قبل کاهش GFR هم داشته باشه، که برای تجویز بعضی SSRI ها مشکل ایجاد می کنه.

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110-woman is challenged with coc but does not get withdrawal bleeding which organ is affected?

Ovary

Uterus

Pituitary

Hypothalamus

Fallopian tubes

Answer: B

111- 17 y.o. girl with primary amenorrhea. Breast development is Tanner 4, although she has axillary and pubic hair of adult type. Shortest girl of class. O/e no palpable masses in the abdomen, vaginal examination is not performed. She is short (like 140 cm?).

a. Mullerian dysgenesis

b. Ovarian dysgenesis

c. Pitutary tumor

d. PCO

puberty

keyvan:-Adrenarche (pubic and axillary hair growth) is caused by adrenal androges specilly DHEA

-Thelarche (breast developement) is mainly as a result of ovarian estradiol

-Primary amenorrhea common causes include : ovary(43%), hypothalamus(27%), uterus such as mullerian agenesis(19%)

According to above statements :

-Hypothalamic amenorrhea > no adrenarche & no thelarche

-Mulerrian agenesis amenorrhea > intact adrenarche & thelarche

-Ovarian amenorrhea > intact adrenarche but impared thelarche

Me : (T(A(M)

Adrenarche: CRH > ACTH > adrenal gland > DHEA > pubarche

Thelache: GnRH > FSH,LH > ovary > estrogen > breast

Menarche: GnRH> FHH,LH> ovary> estrogen&progesterone> uterus

Mullerian agenesis: missing uterus and variable degrees of vaginal hypoplasia

Nl hormone levels

Nl thelarche

Nl adrenarche

No menarche

Gonadal dysgenesis : ovarian dysgenesis/hypogonadotropic hypogonadism/Turner

Elevated FSH,LH, No ovarian estrogens

Nl adrenarche

No thelarche

No menarche

Hypothalamic hypogonadism: functional hypothalamic amenorrhea

CRH↓ GnRH↓ ACTH↓ FSH,LH↓ …

No thelarche

No adrenarche

No menarche

Pituitary tumors / congenital GnRH deficiency / hyperprolactinemia

Nl CRH Nl ACTH ↓GnRH

Nl adrenarche

No menarche

No thelarche

112-4 yr child easily bruising , petechial, 5 cervical rubbery LN, no splenomegaly, plt 5×109 other blood value normal.Mx?

Cytotoxic drugs

Prednisolone

IVIg

PLT transfusion

پلاكت نرمال طبق معيار استراليايى اينه :

١٥٠ الى ٤٠٠ ضرب در ١٠ به توان ٩ در ليتر

(در صفحه ١٤٤ مورتاگ هست)

اين مريض به ITP نميخوره چون هم هيستورى از شروع علائم با يك عفونت نميده و هم لنفادنوپاتى توى ITP معمولاً نداريم .

اين يا ALL هست يا لنفوم ، كه البته ruberry LN كركتريستيك لنفوم هست ، لنفوم تشخيص اولشه .

اگه پلاكت بالاى ١٠ بود كموتراپى ميخواست يعنى a ولى حالا كه ٥ هست بايد پلاكت تزريق بشه بعد كه اومد بالا كموتراپى بشه .

(ترشولد تزريق پلاكت وقتى است كه زير ١٠ رسيده باشه)

113-placenta previa 26 wks gestation, 10 ml bleeding before, now present with 50 ml bleeding, next most important?

Usg

Cross match

Oxytocin

Amniotomy

The first episode of significant bleeding usually occurs in the patient’s home and is usually not heavy. The patient should be admitted to hospital and no vaginal examination made, as this may start torrential bleeding. In hospital the patient’s vital signs are checked, the amount of blood loss assessed and blood cross-matched.(Llewellyn)

Placenta previa

Uptodate:

Placenta previa should be suspected in any woman beyond 20 weeks of gestation who presents with painless vaginal bleeding before digital vaginal examination is performed because palpation of the placenta can cause severe hemorrhage.

Previous placenta previa, previous cesarean deliveries, and multiple gestation are major risk factors for placenta previa.

The characteristic clinical presentation is painless vaginal bleeding, which occurs in 70 to 80 percent of cases. An additional 10 to 20 percent of women present with both uterine contractions and bleeding, which is similar to the presentation of abruptio placenta. In approximately one-third of affected pregnancies, the initial bleeding episode occurs prior to 30 weeks of gestation.

Some conditions that may be associated with placenta previa include placenta accreta, malpresentation, preterm labor or premature rupture of the membranes, vasa previa and velamentous insertion of the umbilical cord.

The diagnosis of placenta previa is based upon identification of placental tissue covering or proximate to the internal cervical os on transvaginal ultrasound examination.

Management:

Asymptomatic previa

• In pregnancies with asymptomatic placenta previa, we monitor placental position with ultrasound examination as an outpatient and counsel these patients to avoid excess physical activity and to call their provider promptly if bleeding or labor occurs. We perform cesarean delivery at 36 to 37 weeks.

Acute management of bleeding previa

• An actively bleeding placenta previa is a potential obstetrical emergency. Women with active bleeding are hospitalized for close maternal and fetal monitoring and supportive care. Indications for emergency cesarean delivery include refractory life threatening maternal hemorrhage, nonreassuring fetal status, and significant vaginal bleeding after 34 weeks of gestation.

Conservative management after an acute bleed

• These women should be able to return to the hospital quickly if rebleeding occurs and should not have additional pregnancy complications.

• We recommend a course of antenatal corticosteroid therapy for symptomatic patients between 23 and 34 weeks of gestation. We also recommend anti-D immune globulin for symptomatic Rh(D)-negative women to prevent possible alloimmunization. Readministration of anti-D immune globulin is not necessary if delivery or rebleeding occurs within three weeks, unless a large fetomaternal hemorrhage is detected.

• Vaginal delivery may be attempted when the placental edge is >10 mm from the internal os because the risk of hemorrhage during labor is much lower.

114-post menopausal by 4 y yellowish green vaginal discharge no sexual intercourse. Cause?

Candidia

Chlamydia

Endometrial cancer

Cervicitis

114.1- Postmenoupausal lady (5-6 yrs ) with green brown vaginal discharge sexual life with husband asking dx

Chlaymydia

Endomet ca

Candida

114.2 Post menopausal since 4 years with yellowish green vaginal discharge , no sexual intercourse . what is the cause ?

a.chlymedia

b.Endometrial cancer

c. cervisitis

d. atrophic vaginitis

Vaginal discharge is made by the skin cells of the vagina and cervix under the influence of the female hormone, estrogen. Women who are menopausal normally have minimal vaginal discharge as a result of lower levels of estrogen.

In women who are premenopausal, it is normal to have about one-half to one teaspoon (2 to 5 mL) of white or clear, thick, mucus-like, and mostly odorless vaginal discharge every day. However, the amount and consistency of the discharge varies from one woman to another.

Atrophic vaginitis

CLINICAL MANIFESTATIONS:

Vaginal dryness

Vaginal burning or irritation

Decreased vaginal lubrication during sexual activity

Dyspareunia, including vulvar or vaginal pain (at the introitus or within the vagina)

Vulvar or vaginal bleeding (eg, postcoital bleeding, fissures)

Vaginal discharge (leukorrhea or yellow and malodorous)

Pelvic pressure or a vaginal bulge

Urinary tract symptoms (eg, urinary frequency, dysuria, urethral discomfort, hematuria)

Endometrial cancer

CLINICAL PRESENTATION:

Abnormal uterine bleeding:

• Postmenopausal women – Any bleeding, including spotting or staining. Three to 20 percent of women with postmenopausal bleeding are found to have endometrial carcinoma and another 5 to 15 percent have endometrial hyperplasia

• Age 45 to menopause – Any abnormal uterine bleeding, including intermenstrual bleeding in women who are ovulatory, frequent (interval between the onset of bleeding episodes is less than 21 days), heavy (total volume of >80 mL), or prolonged (longer than seven days). In addition, endometrial neoplasia should be suspected in women with prolonged periods of amenorrhea (six or more months) in women with anovulation. Among cases of endometrial carcinoma, 19 percent occur in women aged 45 to 54 years compared with 6 percent in those aged 35 to 44 years.

• Younger than 45 years – Abnormal uterine bleeding that is persistent, occurs in the setting of a history of unopposed estrogen exposure (obesity, chronic anovulation) or failed medical management of the bleeding, or in women at high risk of endometrial cancer (eg, Lynch syndrome).

Cervical cytology findings:

• Adenocarcinoma – Adenocarcinoma is sometimes seen on cervical cytology. Since the malignant cells may arise from either the cervix or endometrium, further evaluation with cervical and endometrial biopsy is required.

• Atypical glandular cells – Atypical glandular cells detected by cervical cytology should be investigated with an endometrial (and endocervical) biopsy to determine whether an endometrial neoplasm is the cause.

• Endometrial cells – The presence of endometrial cells on cervical cytology is reported in the results in women ≥40 years of age. The appearance of normal endometrial cells on cytology in asymptomatic premenopausal women is rarely associated with pathology and no further work-up is required [ 13 ]. Symptomatic or high risk women still require evaluation as appropriate.

There is no sign like vaginal discharge for endometrial cancer, esp if its not blood stained

Vaginal cancer

Clinical manifestation: The majority of patients with vaginal carcinoma present with vaginal bleeding, either postmenopausal or postcoital. Other symptoms include a watery, blood-tinged, or malodorous vaginal discharge, vaginal mass, urinary symptoms (eg, frequency, dysuria, hematuria), or gastrointestinal complaints (eg, tenesmus, constipation, melena). Pelvic pain from extension of disease beyond the vagina is present in 5 percent of patients. However, as many as 20 percent of women are asymptomatic at time of diagnosis. These vaginal cancers may be detected as a result of cytological screening for cervical cancer.

Acute cervisitis

ETIOLOGY:

Infection — Chlamydia trachomatis and Neisseria gonorrhoeae are the most common organisms identified.

Herpes simplex virus (HSV) and Trichomonas vaginalis account for a few cases. Tuberculosis, Mycoplasma genitalium, Bacterial vaginosis(gardnella) and streptococci (group A) have also been implicated as causative agents of acute cervicitis. Bacterial vaginosis is unlikely to be a cause of isolated cervicitis, without concurrent vaginal findings.

Noninfectious causes — Noninfectious cervicitis is usually caused by mechanical or chemical irritation. Sources of mechanical irritation include trauma from surgical instruments or foreign objects (eg, pessary, diaphragm, tampon, cervical cap, string from intrauterine contraception). Chemical irritation can be caused by exposure to latex, vaginal douches, or contraceptive creams. Radiation therapy and systemic inflammatory disease (Behçet's syndrome) are other noninfectious sources of cervicitis.

Signs and symptoms — A significant proportion of women with cervicitis are asymptomatic.

All women have:

Purulent or mucopurulent vaginal discharge and/or

Intermenstrual or postcoital bleeding

Some women also have one or more of the following:

Dysuria, urinary frequency

Dyspareunia

Vulvovaginal irritation

In conclusion I think sometimes we have to read the authors minf through popular statements like:

…4 to 5 years passed from menopause > cancer

...post coital bleeding > cancer

…yellowish green discharge> infection

115-55 yr main with inability in abduction n external rotation of his rtshoulder,all movements r painful.Next appropriate initial step?

Regular paracetamol

MRI

Apply sling

JM p704: rotator cuff tendonopathy

Treatment

Systematic reviews to date have a lack of sufficient information to provide conclusive evidence-based recommendations for treatment. NSAIDs might provide some relief from pain while corticosteroid

injections and physiotherapy could improve range of movement. Experienced therapists believe that

peritendon and subacromial corticosteroid injections are efficacious in selected patients.

• Rest during the acute painful phase

• Analgesics and NSAIDs (up to 4 weeks)

• Peritendon or subacromial injection (if no tears on ultrasound)

• Physiotherapy—an active program including scapular stabilising exercises and rotator cuff strengthening

116-cause of ca 14.8 , ph normal, esr high , pth normal, ;diagnosis:

cancer

-renal failure

-1ry hyperparathyroid

Primary hyperpara:

PTH: high

Ca: high

Secondary hyperpara(CRF):

PTH: high

Ca: normal/low

Cancer: (PTHrp)

PTH: normal

Ca: high (↑↑↑)

117-Adolescent lady 16y old presents with amenorrhea,she is dedicated ballet dancer and BMI 16, on exm breast buds tanner one...what next?

Send to adolescent health center

Reassure

Abdominal US

Check FSH , LH

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118- a man who was smoker and drinks alcohol was having complaint weakness on walking. On further inquiry there was history of intermittent claudication from back thigh to legs bilateral. Distance was decreased to 200m as compared to previous distance. Right ABI 0.8 left 0.9 On examination after exercise weak dorsiflexion.

What ix u will do

a. mri lumbosacral spine

b. Doppler veinous for DVT

c. arterial Doppler lower limbs

d. angiography lower limb arteries

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در بیماری که

نارسایی شریانی داشته باشد هنگام راه رفتن علامت غالب درد است مانند( سندرم لریش) و تمام اندام دردناک است در ضمن در این بیمار ضعف در مسیر عصب سیاتیک میباشد وبا فعالیت به علت افزایش فشار به نخاع اختلال در ریشه s1 که همان ضعف دورسی فلکشن هست به وجود می اید به همچنین ABI در حد قابل قبول علیرغم اختلاف هر دو اندام میباشدبنابرین mri بهترین گزینه هست

119-case of mild proteniura + what to do first:

repeat urine dipstick

-do after walk

-protin/cr ratio

-biposy.

يا اندازه گيرى Pr/Cr ratio يا اندازه گيرى پروتئين ٢٤ ساعته .

119.1 same question asking what to do to reach diagnosis? Same options.

biopsy

proteinuria

>Isolated proteinuria is defined as proteinuria without hematuria or a reduction in glomerular filtration rate (GFR).

>The normal daily protein excretion (including all proteins) is less than 150 mg (usually 40 to 80 mg). The normal

rate of albumin excretion is less than 20 mg/day.

>The gold standard for measurement of protein excretion is a 24-hour urine collection but its cumbersome and

incorrect collection. Most commonly, the urine protein-to-creatinine ratio (UPCR) in a spot first- or second-

morning urine sample after avoiding exercise is used to estimate 24-hour proteinuria and to follow the effects of

treatment in patients with proteinuric kidney diseases.

>Consider transient or orthostatic proteinuria in patients with isolated proteinuria.

Orthostatic (also referred to as postural) proteinuria is defined as elevated protein excretion (in children >4

mg/m 2 per hour and in adults >50 mg over eight hours). while in the upright position and normal protein

excretion while in a supine or recumbent position. The standard way to make the diagnosis of orthostatic

proteinuria is to measure the protein to creatinine ratio (Pr/Cr) of urine samples collected in the recumbent

position as a first morning void and in the upright position. The normal value for urine Pr/Cr ratio is ................
................

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