Dyspnea and Cough (Tyler) DSA + Johnson Dyspnea Flashcards

1
Q

What is a cinical finding in chronic cough indicative of asthma?

A

episodic wheezing

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2
Q

What are alarm sx of cough?

A

fever

productive cough

progressive dyspnea

persistent wheezing

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3
Q

What are the most common sx of wegener’s

A

upper respiratory in 90% of pts

lower respiratory in 60%

renal involvement in 75%

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4
Q

What complication are wegener’s pts at high risk for?

A

venous thrombotic events

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5
Q

What lab tests are positive in wegener’s

A

>90% of ppl have positive c-ANCA/antiproteinase-3

10-25% have p-ANCA

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6
Q

What is the tx plan for Wegener’s?

A

induction of remission: prednisone + cyclophosphamide or rituximab w/ steroids

maintaining remission: azithioprine or methotrexate or rituximab

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7
Q

What is rituximab?

risks?

A

b-cell depleting Ab approved for tx of wegeners and microscopic polyangitis

both this and cyclophosphamide incr risk of infection

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8
Q

WHich drug used for treating wegeners should not be used in pts with kidney disfunction?

A

methotrexate

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9
Q

Prophylaxis for what infection should be done w/ cyclophosphamid tx?

A

pneumocystis jirovecii

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10
Q

What systems are mainly affected in churg-strauss?

A

small and medium vessels

skin and lung most common

can be heart, GI and peripheral nerves also

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11
Q

What are the clinical findings in Churg-Strauss?

A

marked peripheral eosinophilia

chest XR = transient opacities to pulmonary nodules

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12
Q

What is the treatment plan for Churg-Strauss?

A

corticosteroid taper over 3-6 mos and cyclophosphamide until complete remission

replace cyclophosphamide w/ methotrexate or azathioprine for maintenance

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13
Q

What are the 2 most frequently affected organs in sarcoidosis?

A

lung

liver

(followed by eyes, bone, skin, hear, and parotid gland)

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14
Q

What are 3 dangerous complications of myocardial sarcoidosis?

A

restrictive cardiomyopathy

cardiac dysrhythmias

conduction disturbances

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15
Q

What CBC measurement is elevated in sarcoidosis?

A

sed rate

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16
Q

What is the significance of elevated ACE levels in sarcoidosis?

A

commonly elevated, but neither sensitive nor specific enough to be of diagnostic value

17
Q

What are the radiograph stages of sarcoidosis?

A

I: hilar adenopathy alone

II: hilar adenopathy w/ parenchymal involvement

III: parenchymal involvement alone

IV: advanced fibrotic changes principally in upper lobes

18
Q

What is the general Tx of sarcoidosis?

A

corticosteriods

methotrexate, azathioprine, cyclosporine, or anti-TNF therapy with infliximab (used in steroid-intolerant pts or steroid-refractory dz)

19
Q

What is usually the most common sx of IPF?

A

progressive dyspnea

20
Q

What are the 2 FDA approved drugs for the use of IPF?

A

pirfenidone: antifibrotic w/out known MOA; tid and monitor LFTs
nintedanib: tyrosine kinase inh taken bid; diarrhea is major side efect

21
Q

What are the ACC/AHA stages of HF

A

A: at risk for HF, no structural Dz, no sx

B: structural heart disease, no sx

C: Structural dz + sx

D: refractory HF, needs biventricular pacemaker, LVAD, transplant; 1 yr mortality 50-60%

22
Q

What are the NYHA functional classifications of HF?

A

1: no limitation of phys activity, asymptomatic
2: slight limitation of PE, exertional sx, no sx at rest
3: marked limitations, less than ordinary activity causes sx, no sx at rest
4: unable to do PE w/out sx; SYMPTOMATIC AT REST

23
Q

What defines systolic HF?

A

EF < 40%, decr vent emptying so decr SV

S3 gallop

sx associated w/ hypoperfusion

24
Q

What characterizes diastolic HF?

A

normal EF

stiff ventricles, resistance to vent filling

SOB, DOE, pulmonary edema

25
Q

What characterizes high output HF?

A

EF reduced, but high CO

hyperthyroidism, pregnancy, anemia, beriberi, paget’s dz

26
Q

What characterizes low output HF?

A

seen in ischemic heart dz, HTN

dilated cardiomyopathy, valvular and pericardial dz

27
Q

What common drugs should be avoided in HF?

A

NSAIDS

inh COX 1 and 2 –> inh prostaglandin syn –> renal vasoconstriction –> makes fluid overload worse

28
Q

How do DIP and RB-ILD differ on CT?

A

DIP: peripheral or diffuse ground-glass opacities, reticular markings, sometimes small cysts

RB-ILD: bronchial wall thickening, centrilobular nodules, patchy ground-glass opacities

29
Q

In what lobes does IPF predominate?

A

lower lobes

(rarely upper)

30
Q

What does IPF look like on CT?

A

subpleural ground glass opacities + reticular patterns

(rare to see ground glass w/out reticular - usually leads to alt dx)

predominant to lower lobes