Medicine 2 Flashcards

1
Q

In a patient with ascending aortic dissection being prepared for surgery, increasing sob, bibasilar crackles that were not present on the initial evaluation - most likely cause of the new sxs is?

A

Acute aortic regurgitation- retrograde extension of intima tear can involve the aortic valve
- the dissection can also propagate into pericardial space n cause tamponade effect but in this case the presence of basilar crackles favors the dx AR than pericardial tamponade

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2
Q

In the evaluation of a patient with aortic dissection, when is transesophageal echo preferred to CT/MR angiography?

A

In patients with renal insufficiency (because of the contrast agents used)

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3
Q

Rx of acute decompensated heart failure

A
  • diuretics, oxygen
  • possibly vasodilator therapy ( nitroglycerin, nitroprusside)
  • early use of NONINVASIVE VENTILATION in pts with respiratory distress- rapid improvement n reduced need for mechanical ventilation
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4
Q

A 72 yr old man comes with chest pain for the past 6months that is brought on by exercise, lasts 2-3min n subsides with rest. He has HTN, hyperlipidemia, smoking hx. Echo shows LA dilation, mild concentric LV hypertrophy, calcified aortic valve with restricted opening, with estimated valve area of 1.6cm2
The most likely cause of his sxs is?

A

Coronary aa disease (CAD)
- AS is a common cause of angina and also syncope n HF. However, sxs do not typically occur until the stenosis becomes severe, usually <1cm2 valve area

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5
Q

An 84 yr old comes with sxs of CHF. Has hx of MI a year ago. BP is 144/82 PR- 98, cardiac catheterization would show

  • cardiac index
  • systemic vascular resistance
  • LVEDV
A

The pt has CHF due to LV systolic dysfunction (MI hx-ischemic CMP)

  • cardiac index-⬇️
  • systemic vascular resistance -⬆️
  • LVEDV-⬆️
  • as the cardiac contractility decreases the SVR is increased to maintain CO.
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6
Q

A relatively specific ECG finding for digitalis toxicity is?

A

Atrial tachycardia with AV block.

Due to increased ectopy n increased vagal tone

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7
Q

A 65 yr old woman comes with chest pain. Yesterday she was told she has early stage colon cancer. ECG reveals sinus tachycardia with deep symmetric T wave inversion in leads V2-V4. Coronary angiography shows no obstructive coronary aa disease. The most likely dx is?

A

Stress induced (takotsubo) CMP, AKA broken heart 💔 syndrome

  • usually in postmenopausal woman; physical or emotional stress; microvascular spasm with consequent ischemia n impaired contraction. The LV dysfunction is characteristically segmental- mid n apical hypokinesis n basilar hyperkinesis (balloon shape) on echo resembling an octopus trap (takotsubo in Japanese)
  • Rx is supportive, resolves on its own within several weeks
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8
Q

A 29 yr old had epistaxis 2 weeks back which required nasal packing. His BP was 170/110 and today, 180/112. He has occasional headache and fatigue. No other sxs or abnormal physical findings. ECG shows normal sinus rhythm, high voltage QRS complex, downsloping ST segment depression , T wave inversion in leads V5 n V6
Most likely Dx is?

A

Aortic coarctation
The ECG finding is consistent with LV hypertrophy which is not expected with essential hypertension under the age of 40. A cause of secondary hypertension should b sought.
- usually present with asymptomatic htn but can also have epistaxis, headache, lower extremity claudication

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9
Q

Pharmacologic stress test in angina - drugs used? Mechanism?

A

Adinosine, dipyramidol
- adinosine causes coronary vasodilation. There is a several fold augmentation of blood flow in non-obstructed coronary aas, blood flow in stenosed aa is also increased but to a much lesser extent➡️detectable reduction in radioactive isotope uptake in areas supplied by stenotic aas.(ischemic defect on myocardial perfusion imaging

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10
Q

A pt suddenly develops chest pain , diaphoresis, dizziness n becomes unresponsive shortly afterwards. His coworkers perform CPR n regains consciousness. In the ER, ECG shows normal sinus rhythm, ST elevation in leads V1-3. Mechanism of his syncopal episode?

A

Reentrant ventricular arrhythmia.

  • ventricular arrhythmias r common in the immediate post MI period
  • V. Fib is the commonest underlying arrhythmia for SCD post MI
  • onset of MI- arrhythmia occurring within 10min are called immediate/phase 1 ventricular arrhythmias. -reentry is the mechanism.
  • 10-60min- delayed or phase 1b- abnormal automaticity is the mechanism
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10
Q

A man is diagnosed to have a paroxysmal atrial fibrillation( with no structural abnormalities) and started on a drug therapy. 2 weeks later, on a treadmill test, heart rate is increased from 75 to 165 and QRS duration increases from 0.09 to 0.13
Which medications are most likely responsible?

A

Class lC antiarrhythmics eg flacainide, propafenone.

  • occasionally used in Afib with structurally normal hearts.
  • they have the slowest rate of binding n dissociation from the sodium channel receptor. Under normal conditions these drugs do not cause any significant QRS or QT prolongation. But in faster heart rate the drugs have less time to dissociate ➡️higher number of blocked channels➡️progressive decrease in conduction n widening of QRS. This is known as use dependence.
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11
Q

Atrial fibrillation in Wolff-Parkinson-White syndrome is treated with?
Drugs contraindicated?

A
  • if unstable- cardioversion
    Stable- procainamide or ibutilide.
    -AV blocking agents such as b blockers, CCB, digoxin, adinosine r contraindicated as they may increase conduction through the accessory pathway
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12
Q

A 64 yr old man presents with sxs n signs of right heart failure. He had mitral valve repair surgery 12 yrs ago. A mid diastolic sound is heard on auscultation. X-ray- normal heart size, spotty calcification along the left heart border. Echocardiography- ejection fraction of 65%, mild mitral regurgitation. Dx?

A

Constrictive pericarditis

  • prior cardiac surgery, irradiation therapy, TB, malignancy, uremia are common antecedents.
  • rt heart failure, mid diastolic sound (pericardial knock), calcification on CXR r characteristic.
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13
Q

Sensitive Vs specific p/e n laboratory findings in CHF

A

Sensitive- BNP levels

Specific- clinical signs eg. Bilateral lung crackles, S3, ⬆️JVP…- their absence shouldn’t b used to rule out CHF

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14
Q

CHF, concentric LV hypertrophy with preserved injection fraction in the absence of hypertension hx, proteinuria, increased bleeding tendency…
Most likely cause is?

A

Amyloidosis

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15
Q

Carotid aa stenosis Mx

-what kind of intervention? Indications?

A

Carotid endarterectomy ( preferred over carotid aa stenting)
- indications
🚩symptomatic-70-99%stenosis
🚩asymptomatic-80-99% - as some evidences suggest. <80% are medically treated.
- all pts should be medically treated.

16
Q

A pt with inferior wall MI has holosystolic murmur at the apex.
What happens to the left ventricular filling pressure?

A

Increases!

- apical holosystolic murmur is indicative of MR which can develop as a complication of MI➡️increased LVEDV

17
Q

A 25 yr old woman comes with transient vision loss in the right eye. Past medical hx is unremarkable. BP-164/103, PR- 77 bruit below the right mandibular angle. Serum Cr-0.9, K-3.5
Plasma renin activity- high, plasma aldosterone concentration/plasma renin activity ratio-10
-most likely Dx?
- the best next step in the mx is?

A

-fibromuscular dysplasia- abnormal cell development in the arterial wall➡️vessel stenosis
Her Transient vision loss(amaurosis fugax), young age(usually 15-50), carotid bruit are suggestive.
- commonly involved vessels- renal, carotid, vertebral.
-renal aa involvement ➡️RAAS activation➡️hypertension. Aldosterone/renin~10 (<20) indicates secondary hyperaldoseronism.
-Dx- CT ANGIOGRAPHY of the abdomen, or duplex U/S

18
Q

In a pt with high output cardiac failure, the causes of heart failure is?

A

Decreased SVR leads to increased contractility n stroke volume to maintain CO➡️increased venous return➡️increased PRELOAD.
-widened pulse pressure, brisk carotid upstroke can b seen

19
Q

A pt with PAD, ankle brachial index of 1.1 in the rt, 0.65 in the left.
Next step in the mx?

A

<0.9 is consistent with PAD.
-A supervised graded exercise program is the most useful intervention
🚩low dose ASA n statin therapy- for those with ASCVD.
- surgical intervention is reserved for pts with limb threatening complications ( eg non healing ulcers), significant limitation in activities, failure to respond to initial Mx

20
Q

A pt comes with chest pain n ECG finding of ST segment depression n Twave inversion in leads V4-V6 after taking cocaine, indicating myocardial ischemia
The most appropriate next step is?

A

IV diazepam- reduce sympathetic outflow, ⬇️anxiety n agitation, decrease cardiac oxygen demand.

  • ASA, CCB, nitroglycerin r also effective in the initial mx. B-blockers should be avoided as they can cause unopposed alpha adrenergic stimulation.
  • Cardiac catheterization should b performed in pts with ST elevation MI or in those with persistent chest pain despite aggressive medical therapy
21
Q

Exertional dyspnea, pounding heart sensation, uncomfortable awareness of the heartbeat especially when lying on the left side, BP-150/45, PR-73
Most likely Dx?

A

AR

22
Q

Syncope associated with specific triggers eg. Micturation, defecation, cough is due to?

A

Alteration of autonomic response and can lead to CARDIOINHIBITORY, Vasodepressor or mixed response.
- Dx is situational syncope (eg postmicturational syncope), a form of vasovagal syncope

22
Q

Pulseless electrical activity is managed with?

A

PEA is managed with uninterrupted CPR along with vasopressor therapy to maintain adequate cerebral n coronary perfusion ( asystole is managed similarly)

  • potential reversible causes should be investigated
  • pulseless ventricular tachycardia, despite being a non perfusing rhythm, does require defibrillation
23
Q

A man comes to the ER after being involved in a motor vehicle accident. He has pain in the left lower extremity n groin . VS r with in normal limits. Iv lines r secured n Foley catheter is placed. 30min later the pt develops difficulty breathing. BP is80/50, pR-120, erythematous rash n wheals over the chest n abdomen
The most likely cause of his deterioration is?

A
Anaphylactic shock (most likely latex allergy)- from gloves, Foley catheters...
-fat embolism doesn’t occur until at least 12-24 hours following injury n this patient’s rash is urticaria not petechial
24
Q

Sudden cardiac death in a patient with prior MI complicated by LV systolic dysfunction ejection fraction

A

Ventricular arrhythmias- usually ventricular tachycardia degenerating to ventricular fibrillation.
- if ejection fraction remains below 30 despite optimal therapy (post MI medications), placement of implantable cardioverter-defibrilator (ICD) is indicated

26
Q

A pt diagnosed with metastatic breast cancer comes with nausea, anorexia, fatigue. Orthostatic hypotension, dry oral mucosa, lower extremity edema. Na-130, k-5, Cr-1.2, glucose -70
What test is necessary to confirm the dx?

A

Cosyntropin stimulation test➡️failure of cortisol levels to raise following cosyntropin administration is diagnostic
- metastatic breast ca to the adrenals- primary adrenal insufficiency.

28
Q

Pharmacologic Rx of acute pericarditis (viral or idiopathic)

A

NSAIDs in combination with colchicine

29
Q

Dobutamine can be used in decompensated systolic dysfunction. How does it affect the LV end systolic volume(LVESV)?

A

⬆️contractility ➡️forward ejection of a higher volume of blood➡️DECREASE in LVESV

30
Q

A 78yr old hypertensive pt comes with generalized body swelling, raised JVP with prominent V waves. A holosystolic murmur is heard at the left lower sternal border. The murmur is due to?
A) dilation of tricuspid valve annulus
B) flailing of a tricuspid valve leaflet

A

Dilation of tricuspid valve annulus (restrict closure of the valve leaflets)-Indicating a secondary (functional) cause of TR- usually results from RV enlargement
this patient likely has decompensated LV failure due to HHD➡️secondary RV overload
- flailing of the valve leaflet- can occur secondary to chordae tendineae in TR myxomatous degeneration, an example of primary TR ( far less common than secondary TR)

34
Q

A 60yr old woman presents with SOB, systolic murmur at the sternal border increasing with inspiration, wheezes and bibasilar crackles, peripheral edema. Echo shows dilated LV with ejection fraction of 30% and a mildly dilated RV. Pulmonary aa systolic pressure is estimated at 55mm Hg (<25 is normal). The best initial Rx for this patient’s pulmonary hypertension is?

A

This patient’s sxs including SOB, TR… and echocardiographic findings r suggestive of PH. But it’s a secondary PH (secondary to LV systolic dysfunction as indicated by low ejection fraction) than idiopathic PH. The mx of PH in this case includes:- loop diuretics and ACEI/ARBS often with beta blockers.
- endothelin receptor antagonists like bosentan have no place in here; they are for primary PH

35
Q

A 62 yr old comes with worsening SOB, dry cough. She was recently treated with chemotherapy n radiation therapy after mastectomy. BP is 160/100, PR is 130, RR is 30, heart sounds are heard, neck veins r distended. Bilateral crackles r heard on the chest. She’s most likely to benefit from which of the ff interventions?
A) dobutamine B) noninvasive ventilation
C) pericardiocentesis

A

Noninvasive ventilation

  • she is having acute decompensated heart failure from LVsystolic dysfunction due to the cardiotoxic effects of chemoradiation therapy.
  • early use of noninvasive ventilation in pts with hypoxemia n RD provides rapid improvement n reduces the need for mechanical ventilation
  • pericardial tamponade is not the case here because she has hypertension (instead of hypo) and heart sounds are not muffled