Essential Internal Med Diagnoses pt 2 Flashcards

1
Q

autoantibodies for ehrymatoid arthritis

A

Genetics: HLA-DR1/4

Antibodies: Rf, anti-CCP

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2
Q

is rheumatory arthritis an example of inflammatory or non-infl arthritis?

A

inflammatory. RA is characterizes by stiffness in the mornings/after rest, systemic symptoms, variable joint patterns.

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3
Q

osteoarthritis is progressive deterioration of __ ___ and surrounding joint structures caused by factors with secondary components of inflamation

A

deterioration of articular cartilagre. abnormalities in biomechanical forces –> proinflammatory cytokines –> degradation of proteoglycans by MMPS, –> fissuring, cartilage loss and subcondral bone thieckening.

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4
Q

T/f in osteoarthritis, activity makes the pain lesson (like in RA)

A

false. activity makes the pain worse, rest makes it better.

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5
Q

4 hallmark features of osteoarthritis on XRAY

A
  1. joint space narrowing
  2. osteophytes
  3. subchondral sclerosis
  4. bone cysts.
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6
Q

T/F people with anklysing spondylitis are positive for RF antibody (like in RA)

A

false. AS, psoriatic arthritis and reactive arthritis are examples of SERONEGATIVE arthropatheies in which they are negative for antibodies. they are assocaited with HLA-b27 though.

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7
Q

key seronegative arthropathy that has significant sacroiliitis and enthesitis

A

ankylosing spondylitis.

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8
Q

anchor drug for psoriatic arthritis

A

methotrexate

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9
Q

Sarcoidosis and amyloidosis are infiltrative disesase that can lead to ___ cardiomyopathies. What is the mechanism?

A

restrictive cardiomyopahties; impaired ventricular filling with preserved systolic function in a non-dilated, non-hypertrophied ventricle, seconary to factors that decreased myocardial compliance.

Mechanism: reduced ventricular compliance –> increased LVEDP –> increased pulmonary venous pressure + decreased CO.

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10
Q

Definition: idiopathic non-infectious granulomatous multi-system disease with lung involvedment in 90% of cases. Symptoms include chest symptoms like cough, dyspnea, chest pain, as well as skin changes like erythema nodosum, lupus pernio ,cardiac arrythmias, eveitis, arthralgia, peripheral lymphadenopathy, hepatosplenomegaly.

A

Sarcoidosis

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11
Q

Lofgren’s syndrome symptoms and disease association

A

LEAF: lymphadenopathy, erythema nodosum, arthralgias, fever –> sarcoidosis.

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12
Q

when do you not need to biopsy the lung in order to confirm sarcoidosis?

A

when the person has lofrgrens syndrome.

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13
Q

last stage of sarcoidosis key xray/ct findings.

A

pulmonary fibrosis /honey combing on xray

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14
Q

general treatments for sarcoidosis

A
  • stages 1 and II often resolve spontaneously
  • prednisone for other stages

NSAIDS if lofgrens.

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15
Q

classic ECG and physical exam findings of pericarditis, and key management strategies for it

A

ECG findings: diffuse ST elevation and PR depression.

PE: Audible friction rub, which is the movement of inflamed pericardial layers against each other.

treatment: high ASA, NSAIDS, colchicine to reduce recrrance.

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16
Q

Beck’s triad of pericardial effusion

A

low BP, elevated JVP, muffled heart sounds

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17
Q

key physical exam findings for pericardial effusions

A

Beck’s triad (low BP, elevated JVP, muffled heart sounds), tachycardia, pulsus paradoxus.

ECG is gold standard for detection– can lead to pericardial tamponade, which shows low voltage, sinus tachycardia and electrical alternans due to heart swing. –> emergency

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18
Q

etiology of aortic dissection

A

HTN (90% of cases), heritable disease (Marfans, EDS, Turner syndrome), aneurysm, iatrogenic (catheter/surgical), vasculitis, chronic syphilis infection, bicuspid AV

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19
Q

type A and B aortic dissection, and how they differ in management

A

A. proximal flap in the ascending aorta–> surgical management

B. Distal flap in the aorta–> IV beta blockers, vasodilators, stents.

complications of either type can lead to sudden death, cardiogenic shock, hemodynamic instability, pericardial effusion, pericardial tamponade, MI and aortic insufficiency.

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20
Q

note: be aware of the two key types of aortitis: giant cell and takayasu– plus patient profile.

A

Aortitis Definition: inflammatory diseases of the aorta Examples:
• Giant Cell Aortitis: 55+ F, often associated to temporal artertitis, can cause aneurysm/dissections
Takayasu’s Aortitis: young F, occlusive disorder of aortic branch vessels (pulseless disease), associated with eye problems
Management: steroids

21
Q

S3 sound is elicited by high ___ sided pressures of the heart

A

left sided presures

22
Q

elevated JVP, hepatomegaly, ascietes nad peripheral edema is due to ___ sided heart failure/elevated __sided pressuers

A

high right sided pressure.

23
Q

outline the neurohormonal compensatory mechanism in left heart failure

A

reduced cardiac output due to LHF–> back up of blood into L atrium –> back up in pulmonary circulation –> pulmonary edema –> reduced gas exchange and dyspnea .

this reduced CO –> reduced perfusion of renal artery –> RAAS and adrenergic activation –> renal salt and water retention –> more edema even though theres already pulmonary edema –> increased contractility and increased circulating volume –> increased cardiac outpupt –> organ perfusion –> increased afterload –> increaed LV workload, LV remodelling –> harmful

this is a good mechanism if it’s not chronic. but in LHF, it is.

leads to S3 and S4 sounds.

24
Q

exertional dyspnea, orthopnea, pulmonary edema (frothy, pink-tinged sputum), bibasilar rales, cough, nocturia, restlessness, confusion and S3/S4

these are symptoms of ___ sided heart failure

A

left heart failure

25
Q

right heart failure is aka __ ___

A

core pulmonale

26
Q

outline the mechanism of right heart failure

A

increaesd venosu pressure –> systolic volume overload –>increased RV worload –> RV hypertrophy –> decreased pumping ability.

27
Q

most common cause of right sided heart failure

A

left sided heart failure, pulmonary causes like emphysema, PE.

28
Q

location of aortic stenosis

A

right upper sternal boarder that radiates to carotids or apex.

29
Q

is aortic stenosis a systolic or diastolic murmur? Which shape? what additional sounds? what are it’s causes

A

aortic stenosis:

  • systolic murmur
  • systolic ejection murmur
  • PARVUS ET TARFUS/apical carotid delay. Soft S2 and s4 present.
  • causes: degenerative, rheumatic, biscuspid valve problems.
30
Q

location, shape, key findings and causes of pulmonic stenosis

A

left uppers ternal border, heard as a systolic ejection murmur.

  • characteristic of a right ventricular heave, would hear a right sided S4

contract to force blood into the left ventricle. If the left ventricle is noncompliant, and atrial contraction forces blood through the atrioventricular valves, a S4 is produced by the blood striking the left ventricle.

31
Q

radiation course, shape, associated findings and causes of mitral regurgitation

A

radiates from apex –> axilla

  • late systolic crescendo murmur
  • increases with valsalva
  • would see a dilated LV/LA, s3 sound.
32
Q

Corrigan’s pulse is indicative of what valve defect?

A

aoritc regurg in diastole

33
Q

__ sided murmurs will be louder on inspiration, and ___ sided murmurs will be louder on expiration.

A

Inspiration à R-sided murmurs will be LOUDER • Expirationà L-sided murmurs will be LOUDER

34
Q

how does valsalva change mitral valve prolapse sounds?

A

mitral valave prolapse will be a systolic murmur that gets LOUDER.

  • every valsalva maneuver decreases preload, causing all murmurs to be QUIETER, except with HOCM and MVP
35
Q

outline the mechanism of pathology of aortic stenosis

A

pressure overload because of fixed obstruction/narrowing–> increased systolic pressure –> increased mechanical stress –> ventricle works harder –> wall thickening –> concentric hypertrophy (bigger from muscle)

36
Q

how does aortic stenosis affect pulse pressure?

A

narrows pulse pressure.

37
Q

what additional heart sound is created by aortic stenosis

A
  1. systolic ejection murmur
  2. S4 because of non-compliant/stiff ventricle.
38
Q

Austin-flitn murmur and water hammer pulse is associated with what valvular condition

A

aortic regurgitation.

39
Q

1 cause of mitral stenosis

A

rheumatic heart disease

40
Q

symptoms, physical exam findings and management of mitral stenosis.

A
41
Q

Major Jone’s criteria for rheumatic fever

A

carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules.

42
Q

explain first degree heart block

A

not actually a block, just delayed PR interval >200ms. ALL P waves will conduct, just at a slower pace.

43
Q

Explain Type II A Wenckeback AVN block.

A

PR interval gradually lengthens before a P wave blocks and the cycle begins again.

44
Q

Explain Type IIB HP block

A

PR interval remains constant before a P wave blocks and the cycle begins again.

45
Q

explain type III Block

A

complete AV heart block. No p waves conduct to the ventricles. the atria and ventricles are not communicating and there is dissociation.

46
Q

Management of Afib

A
  1. anticoagulants with target INR 2-3, NOACS
  2. treat underlying cause
  3. rate control: beta blockers, CCB, digoxin.
  4. rhythm control: anti-arrhythmic (propafenone, amiodarone +/- cardioversion)
  5. ablation for uncontrolled rhythm
  6. pacemaker for uncontrolled rate.
47
Q
A

A flutter- regular ventricular rate.

48
Q
A

atrial fibrillation– abnormal ventricular response.