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Final FA review > 2/23 > Flashcards

2/23 Flashcards

1
Q

Dyspnea on exertion

-why?

A

Failure or CO to inc. during exercise.

-dyspnea = SOB

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2
Q

Culture negative causes of endocarditis:

A 
HACEK organisms:
Hemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
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3
Q

2 most common culture neg. causes of endocarditis.

A

Coxiella burnetti

Bartonella

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4
Q

Tricuspid valve endocarditis:

-which bugs besides S. aureus?

A

Pseudomonas, and Candida.

*S. aureus most common

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5
Q

rheumatic fever.

-consequence of what?

A

-Group A strep pharyngitis!

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6
Q

Whats an Aschoff body?

A

-granuloma found in rheumatic fever.

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7
Q

What are Anitschkow cells?

A

-enlarged macrophages with ovoid, wavy, rod-like
nucleus.
-found in rheumatic fever.
-“caterpillar macrophages”

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8
Q

Fusion of aortic/mitral commissures.

-found in which disease?

A

-rheumatic heart diseaes (late sequela of rheumatic fever).

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9
Q

Rheumatic fever Sxs:

A 
FEVERSS
Fever 
Erythema marginatum
Valvular damage (vegetation and fibrosis) 
ESR 
Red-hot joints (migratory polyarthritis)
Subcutaneous nodules
St. Vitus’ dance (Sydenham chorea)
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10
Q

rheumatic fever: what are the early deaths due to?

A

myocarditis

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11
Q

SLE pericarditis: whats the fluid like?

A

serous, clear/yellow, protein rich w/few inflammatory cells.

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12
Q

Post MI pericarditis: whats the fluid like?

A

fibrinous, low protein count.

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13
Q

Acute pericarditis: more or less pain when leaning forward? During inspiration?

A
  • less pain leaning forward

- more pain on inspiration

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14
Q

Causes of fibrinous pericarditis:

A
  • Dressler syndrome
  • uremia (etiology is poorly understood)
  • radiation

*Presents with loud friction rub.

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15
Q

Causes of serous pericarditis:

A
  • viral pericarditis (often resolves spontaneously)

- noninfectious inflammatory diseases (e.g., rheumatoid arthritis, SLE).

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16
Q

Causes of Suppurative/purulent pericarditis:

A
  • bacterial infections (e.g., Pneumococcus, Streptococcus).

* Rare now with antibiotics.

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17
Q

ECG of cardiac tamponade?

A
  • low-voltage QRS

- electrical alternans (due to “swinging” movement of heart in large effusion - beat to beat alterations of QRS height).

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18
Q

Pulses paradoxus seen in which diseases?

A
  • cardiac tamponade
  • asthma
  • obstructive sleep apnea
  • pericarditis
  • croup.
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19
Q

What causes pulsus paradoxus?

A
  • when you breath in the right ventricle filled more so expands into pericardial space & also into LV space. LV usually displaces but now it can’t due to constriction of cardiac tamponade.
  • so LV is constricted, fills less. Less volume means less pressure (frank starling) so you get a drop in systolic BP on inspiration.
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20
Q

Tree bark appearance of syphillitic aorta due to what?

A

-irregular wrinkling of the tunica intima of the aorta.

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21
Q

Rhabdomyoma

  • most common primary cardiac tumor in who?
  • associated w/what disease?
  • where does it usually arise?
A
  • children
  • tuberous sclerosis
  • ventricle
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22
Q

Pyogenic granuloma

A
  • Polypoid capillary hemangioma that can ulcerate and bleed.
  • Associated with trauma and pregnancy.
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23
Q

Glomus tumor

A
  • Benign, painful, red-blue tumor under fingernails.
  • Arises from modified smooth muscle cells of glomus body.
  • glomus body = modified smooth muscle cells invovled in temp. regulation.
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24
Q

Angiosarcoma: associated w/what risk factors?

A
  • sun exposed areas
  • radiation
  • arsenic
  • PVC (liver)
  • chronic lymphedema (skin)
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25
Q

Will kaposi sarcoma blanch?

A

-no

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26
Q

Does a negative biopsy exclude Temporal arteritis?

A
  • no.

- lesions are segmental.

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27
Q

Two most common signs of Temporal arteritis?

-what can it lead to?

A
  • Unilateral headache, jaw claudication

- irreversible blindness due to ophthalmic art. occlusion.

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28
Q

Temporal arteritis

-associated w/what disorder?

A

-polymyalgia rheumatica

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29
Q

Takayasu arteritis Sxs:

A
  • “Pulseless disease” (weak upper extremity pulses)
  • fever
  • night sweats
  • arthritis
  • myalgias
  • skin nodules
  • ocular disturbances.
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30
Q

Temporal & Takayasu arteritis:

  • what type of inflammation?
  • inc or dec. ESR?
A
  • granulomatous

- inc. ESR

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31
Q

Can calcific aortic stenosis lead to outflow obstruction?

A
  • yes.

- aortic stenosis murmur.

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32
Q

During systole, where is contraction force the strongest?

A

-endocardium. Hence its the most susceptible to ischemia.

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33
Q

What receptors modulate coronary flow?

A
  • alphta 1

- beta 2

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34
Q

Osler node: type 3 HSR or septic emboli?

A

-type 3 HSR

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35
Q

Janeway lesion: type 3 HSR or sepetic emboli?

A

-septic emboli

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36
Q

Which cells synthesize the fibrous cap of an atheroma?

A
  • smooth muscle cell

- special SMCs that can produce collagen.

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37
Q

What lung problem can cause pulsus paradoxus?

A

-severe obstructive lung disease

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38
Q

What drugs prevent eosinophil degranulation?

A

-corticosteroids.

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39
Q

Clinical definition of myopathy

A

-muscle pain w/serum CK 10x normal.

40
Q

Bile acid sequesterants and statins

-any interaction?

A

-take them 4 hours apart b/c the sequesterants may dec. absorption of the statin.

41
Q

Essential HTN

  • first line med?
  • what about if they have CHF or diabetes?
A
  • hydrochlorothiazide

- If they have CHF or DM, give ACE inhibitor.

42
Q

Beta blocker overdose

-treatment?

A

-glucagon

43
Q

Fatty streak

-will an atheroma form there?

A

-fatty streaks often occur in regions not particularly prone to atheroma formation. So answer is not necessarily.

44
Q

Whats the most common cause of aortic stenosis?

A

Senile calcific aortic valve degeneration.

45
Q

Acute onset heart failure in setting of recent viral infection:

A

Dilated cardiomyopathy.

46
Q

Polyarteritis nodosa:

-Sxs

A
  • nonspecifics
  • abdominal pain, melena
  • HTN, neuro dysfunction
  • cutaneous eruptions, levido reticularis
  • renal damage (immune complexes)
  • leukocytosis (neutros)

-lesions of varying stage

47
Q

Polyarteritis nodosa:

-Tx

A

cyclophosphamide

48
Q

Kawasaki disease

-Sxs?

A
  • Fever, cervical lymphadenitis, conjunctival injection, changes in lips/oral mucosa (“strawberry tongue” D ), hand-foot erythema, desquamating rash.
  • coronary artery aneurysm, thrombosis => rupture, MI.
49
Q

How does Kawasaki present?

A

acute febrile illness

  • fever may persist after tylenol.
  • only condition where you give a child w/fever aspirin.
50
Q

What is the only circumstance where you give a feverish child aspirin?

A

Kawasaki disease.

-otherwise you dont to prevent reye syndrome

51
Q

Wegerners

-what kind of inflammation?

A

-granulomatous and necrotizing vasculitis.

52
Q

c-anca

-other names?

A
  • PR3-ANCA

- anti-proteinase 3

53
Q

Wegeners:

-Sxs:

A
  • Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
  • Lower respiratory tract: hemoptysis, cough, dyspnea.
  • Renal: hematuria, red cell casts.
54
Q

microscopic polyangitis vs wegeners

A

compared to Wegener’s. MP has:

  • no nasopharyngeal involvement.
  • no granulomas.
  • P-ANCA
55
Q

p-anca

-other names?

A
  • anti-myeloperoxidase

- MPO-anca

56
Q

What are ANCAs?

A

-ANCA (Abs) can directly bind to leukocytes (neutros etc.) and stimulate them to release their granules which contain ROS and proteolytic enzymes.

57
Q

Churg Strauss

A

Asthma, sinusitis, palpable purpura

  • peripheral neuropathy (e.g., wrist/foot drop).
  • Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis).
58
Q

What kind of inflammation is Churg Strauss?

A

-Granulomatous, necrotizing vasculitis with eosinophilia

59
Q

Henoch-Schönlein purpura

-Sxs:

A

NAPA

  • nephritis
  • arthralgia/arthritis
  • palpable purpura
  • abdominal pain
60
Q

Can you use beta-blockers in cardiogenic shock?

Can you use beta-blockers in vaso-spastic disease?

A
  • no, they’re contraindicated.

- no, they’re contraindicated.

61
Q

non-dihydropyridines

  • name some
  • uses?
A
  • verapamil, diltiazem.
  • cardiac Ca channel blockers.
  • the dihydropyridines are selective only for vascular smooth muscle.
62
Q

dihydropyridines

  • name some
  • uses?
A
  • Amlodipine, nimodipine, nifedipine
  • “dipine”
  • vascular smooth muscle
  • lack cardiac depressant effects
63
Q

Nimodipine

  • use?
  • differs from other dihydropyridines
A

-subarachnoid hemorrhage (prevents cerebral vasospasm)

64
Q

Calcium channel blockers

-side effects

A
  • Cardiac depression, AV block, peripheral edema, flushing, dizziness
  • hyperprolactinemia
  • constipation
65
Q

What is first-line therapy for hypertension in pregnancy?

A

Hydralazine w/methyldopa

66
Q

Hydralazine

  • mechanism?
  • potential side effect?
A
  • inc. cGMP => relax smooth muscle.
  • arterioles > venules.
  • drug induced SLE, esp in slow acetylators.
  • Its binds strongly to plasma proteins, so thats why it can cause sle-like syndrome and it can be used in pregnant women for HTN.
67
Q

Hydralazine & peripheral neuritis

A

-Can cause B6 deficiency.

68
Q

Hypertensive emergencies: commonly used drugs:

A

nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.

69
Q

Fenoldopam

A

D1 agonist

  • HTN emergency, esp in pts w/renal insufficiency.
  • coronary, peripheral, renal, and splanchnic vasodilation.
  • dec. BP
  • inc. natriuresis.
70
Q

Minoxidil & diazoxide

  • mech?
  • use?
A
  • open K channels => hyperpolarization of smooth muscle.
  • results in arterial vasodilation.
  • used for HTN emergencies.

*minoxidil can be used for baldness.

71
Q

endothelial cell M3 receptor

A
  • non innervated receptors
  • M3: Gq = cause release of NO
  • you know its muscarinic so you know its gonna be dilatory and not constriction.
72
Q

isosorbide dinitrate

A

-its like nitroglycerin but for chronic use.

73
Q

Statins: side effects

A
  • hepatotoxicity

- rhabdo (esp if given w/fibrates or niacin).

74
Q

Niacin

-mechanism

A
  • dec. lipolysis (inhibiting adenylate cyclase)

- dec. VLDL synth (blocks apoB-100 gene expression)

75
Q

Niacin tox:

A

-flushing (give aspirin)
-hyperuricemia
-hyperglycemia (acanthosis nigricans)
-

76
Q

Bile acid resins

  • name them
  • side effects
A
  • cholestyramine, colestipol, colesevelam
  • bad taste, GI discomfort, dec. absorption of ADEK, cholesterol gallstones.
  • Drugs that inc. hepatic chol. synthesis can lead to chol. gallstones. Like bile acid resins & fibrates.
77
Q

What can leads to cholesterol gallstones

-as far as content of bile

A
  • low bile salts.

- high cholesterol.

78
Q

Cholesterol absorption blocker

  • name it
  • where does it work
A
  • ezetimibe

- small intestine brush border

79
Q

Fibrates

  • mech
  • side effects
A
  • inc LPL which inc. TG clearance from blood.
  • activates PPAR-alpha to induce HDL synth.
  • may get fatter since ur storing more TGs via LPL.
  • myositis (esp w/statins)
  • hepatotoxicity, cholesterol gallstones (esp w/bile acid resin use).
80
Q

Which two drugs used together will lead to cholesterol gallstones?

A

fibrates & bile acid resins.

81
Q

PPAR-alpha

-how does it work?

A

If you activate this you bypass insulin and just turn on insulin-related genes.
-hence the inc in LPL function due to fibrates which activate PPAR-alpha.

82
Q

Which nerve does digoxin stimulate?

A

vagus n.

83
Q

Cardiac glycosides

  • basic mechanism?
  • uses?
A
  • By blocking Na/K ATPase (competing w/K) you dec the gradient of Na. This inhibits the Na/Ca exchanger the pumps Ca out. So more Ca in myoctes = inc. inotropy.
  • Stimulates vagus: Only squirts ACh at nodal tissue, which slows down nodal conduction. This dec. HR.
  • so you’ve inc. inotropy and dec. HR!

-can be used for CHF & afib.

84
Q

ECG changes due to cardiac glycosides

A
  • Dec. AV nodal conduction = inc. PR interval.
  • Speeds electrical impulse through atrial myocardium, so P wave would be narrowed.
  • Speeds impulse conduction velocity through ventricles, so QRS complex would be narrowed.
85
Q

Digoxin

  • notable side effects
  • how is it excreted?
A
  • intracell. Na inc = you’re loading cations! Cell can hit threshold potential easier! Leads to Arrythmias.
  • cholinergic, blurry yellow vision.
  • ECG—ST scooping, T-wave inversion, arrhythmia, AV block.
  • Excreted renally, so renal failure can lead to toxicity.
86
Q

Which drugs can cause digoxin tox?

A

VAQ

  • verapamil, amiodarone, quinidine.
  • they dec. digoxin clearance.
87
Q

diuretics & digoxin

-what should you watch out for?

A

-diuretics can cause hypokalemia which can cause digoxin toxicity.

88
Q

digoxin & hyperkalemia

A
  • indicates a poor prognosis.
  • digoxin competes w/K at the Na/K ATPase. So it blocks K from coming into cell. Causes hyperkalemia and dec. intracellular K.
89
Q

antidote to digoxin tox

A
  • normal potassium (it will probably be too high)
  • Mg
  • anti-digoxin Fab fragments
  • cardiac pacer
90
Q

How does beta-1 stim. inc. inotropy?

A

beta1 = Gs = inc. cAMP = inc PKA activity = phosphorylates Ca channel = Ca influx = muscle contraction.

91
Q

autonomic inn. of heart

A
  • Beta receptors: nodal tissue and ventricular tissue,

- Muscarinic innervation only on nodal tissue.

92
Q

How do fibrates and bile-acid-resins lead to chol. gallstones?

A

they inc. cholesterol content of bile.

93
Q

Central venous pressure = measure of what?

A

pressure in RA

94
Q

Do pt’s w/cor pulmonale have inc or dec renin/aldo?

A

inc renin/aldo

  • ANP/BNP is in effective but just lowers the already increased renin/aldo. So net effect is still inc. renin/aldo.
  • whenever there is fluid backup you’re gonna have low blood pressure. Think about where the baroreceptors are: aortic arch, carotid artery, etc.
95
Q

where are baroreceptors located?

A

In arteries! Not veins!

Final FA review (52 decks)

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