CardioPulm 3 Flashcards

1
Q

How does compliance differ from elasticity?

A

Compliance = change in volume per change in pressure. Inverse of elasticity. Increased in COPD.

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2
Q

Why do you have increased work of breathing in COPD?

A

You decreased alveolar elasticity in COPD&raquo_space; lung hyperinflation&raquo_space; increased TLC, FRC, residual volume, and diaphragmatic flattening. When diaphragm becomes flat it becomes harder to expand the thoracic cavity&raquo_space; ^ work of breathing.

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3
Q

What is empiric treatment for prolonged postnasal drip after URI?

A

Treat empirically with oral first gen antihistamine (chlorpheniramine) or combined antihistamine-decongestant (brompheniramine/pseudophedrine).

** Pt who don’t respond after 2-3 weeks should get further investigation (sinus imaging, PFT, high res CT)

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4
Q

What 3 meds are most likely to result in drug induced lupus?

A

Hydralazine, procainamide, isoniazid

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5
Q

What pharmacologic agent could be used in cases of persistent PAD despite aspirin and exercise?

A

Cilostazol: PDE inhibitor&raquo_space; ^ cAMP&raquo_space; inhibits platelet aggregation and causes peripheral vasodilation (in venous beds)

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6
Q

Ventricular aneurysms can be a post-MI complication for up to 3 months. How would this present on ECG and Echo?

A

ECG = persistent ST elevation after recent MI and deep Q waves in same leads.

Echo = thin, dyskinetic LV portion in area of MI.

Physical exam findings = progressive LV enlargement&raquo_space; HF, refractory angina, ventricular arrhythmia, mural thrombus, and mitral regurg (due to mitral annulus dilation)

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7
Q

Explain the pathophys behind situational (postmicturition) syncope?

A

^ Parasymp activity&raquo_space; profound bradycardia and varying degrees of AV block or asystole. Decreased symp output can also lead to vasodilation, hypotension, or syncope.

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8
Q

What is the underlying pathophys behind goodpasture’s syndrome?

A

autoantibodies to alpha 3 chain of type IV collagen found in alveolar and glomerular basement membranes. Can have IgG deposition along glomerular BM&raquo_space; nephritic range proteinuria and hematuria w/red cell casts.

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9
Q

What’s the MOA of adenosine in causing AV conduction delay?

A

Adenosine blocks L-type Ca2+ channels&raquo_space; decreased conduction velocity in AV node. This can lead to AV block and termination of AV re-entrant tachycardia.

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10
Q

What is Kussmaul’s sign an indication of?

A

Kussmaul’s sign = increase in JVD with inspiration. Indicates R ventricular filling defect.

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11
Q

What is the difference between bronchiectasis and chronic bronchitis?

A

Bronchiectasis = irreversible dilation and destruction of bronchi&raquo_space; chronic cough and impaired mucus clearance. Generally due to recurrent URI and chronic cough with daily mucous production.

Chronic Bronchitis = chronic productive cough for > 3mo in 2 successive years. Generally due to cigarette smoking.

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12
Q

What is the most likely cause of a murmur that is crescendo-decrescendo at L sternal border without carotid radiation?

A

HOCM - hypertrophic obstructive cardiomyopathy.

Typically in young Pt&raquo_space; IV septal hypertrophy. Common Sx = syncope, dyspnea, and chest pain

** Syncope typically due to outflow obstruction from hypertrophied myocardium but can also be due to arrhythmia, ischemia, or a ventricular baroreceptor response that causes vasodilation.

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13
Q

What diagnostic tests can you do to support a Dx of aspergillosis?

A

CT scan would show nodules with surrounding groundglass opacities (halo sign). Diagnostic tests would include serum biomarkers for cell wall components (galactomannan) and sputum/stain Cx. Bronchioalveolar lavage can also be used.

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14
Q

What is the Rx for invasive aspergillosis?

A

Voriconazole + echinocandin (caspofungin)&raquo_space; transition to oral voriconazole alone.

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15
Q

What initial pharmacologic treatment would you give for someone with hypertrophic cardiomyopathy?

A

Negative inotropic agents (BB, verapamil, disopyramide). BB prolong diastole (allow for greater filling) and decrease myocardial contractility which ultimately decrease the left ventricular outflow tract obstruction and would decrease sx of angina.

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16
Q

Why do you typically get arm pain with Pancoast/Superior Pulmonary sulcus tumors?

A

Tumor compression of brachial nerve&raquo_space; radiating arm pain and parasthesias, hand weakness, and referred shoulder pain (typically in ulnar distribution).

** can have horner invasion of sympathetic trunk&raquo_space; Horner syndrome (ptosis, miosis, anhidrosis). Can have hoarseness due to impingement on recurrent laryngeal nerve.

17
Q

An acute inferior STEMI would show up in leads:

A

II, III, and AVF

18
Q

What is the initial medical management of an acute aortic dissection?

A

IV BB. Because they lower HR and BP, and reduce LV contractility

19
Q

What imaging modality would you use to confirm a Dx of AAA?

A

Abdominal U/S

20
Q

What lung Dz would you suspect in a patient with progressive dyspnea, dry cough, and fine crackles in the absence of a smoking history? (** dec TLC, normal FEV1/FVC, and decreased diffusion capacity for CO2)

A

Idiopathic pulmonary fibrosis.

Can present with fine basilar crackles, end inspiratory squeaks, digital clubbing, and Loud P2/fixed split S2 due to pulmonary HTN.

21
Q

What test would you do to confirm a Dx of bronchiectasis?

A

Bronchiectasis = bronchial wall damage + airway dilation with recurrent infection, inflammation, and tissue damage.

Dx is with High Res CT. CXR isn’t diagnostic but can suggest linear atelectasis, dilated/thickened airways, and irregular peripheral opacities. Need CT to show bronchial wall thickening, lack of airway trapping, and bronchial dilation.

22
Q

If you had an acute anterolateral MI due to occlusion of LAD then you would have ST elevation in leads ___ and ST depression in leads ___-

A

elevation in I, aVL, and V2-V6

depression in II, III, aVF