Qbank 1st block Flashcards

1
Q

What are common etiologies of acute pericarditis?

A

Common etiologies include idiopathic causes, viral infections, autoimmune diseases (e.g., SLE, drug-induced lupus, RA), cardiac surgery or radiation, post-myocardial infarction, and uremia.

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2
Q

What are the clinical features of acute pericarditis?

A

Clinical features include pleuritic chest pain relieved by sitting up and leaning forward, and a triphasic friction rub.

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3
Q

What does the ECG show in acute pericarditis?

A

The ECG shows diffuse ST-segment elevations and PR-segment depressions.

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4
Q

What is the treatment for acute pericarditis?

A

Treatment includes NSAIDs +/- colchicine, glucocorticoids, and dialysis.

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5
Q

What is fibrinous pericarditis?

A

Fibrinous pericarditis is the most common subtype of acute pericarditis, characterized by fibrin-containing exudate within the pericardial sac.

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6
Q

What is the relationship between acute pericarditis and systemic lupus erythematosus?

A

This patient’s fibrinous pericarditis is likely due to untreated systemic lupus erythematosus.

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7
Q

What is the nature of chest pain in acute pericarditis?

A

The chest pain is sharp, may radiate to the shoulders or scapulae, worsens with inspiration or movement, and is alleviated by sitting up and leaning forward.

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8
Q

What is a triphasic friction rub?

A

A triphasic friction rub is a sound heard during cardiac auscultation throughout atrial systole, ventricular systole, and early ventricular diastole, resulting from fibrinous exudate.

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9
Q

What is acute myocarditis?

A

Inflammation of the myocardium often caused by infection, drugs, or autoimmune disease.

Common causes include coxsackie B virus, cocaine, and systemic lupus erythematosus (SLE).

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10
Q

What are some potential outcomes of myocarditis?

A

Arrhythmias, dilated cardiomyopathy, heart failure, sudden cardiac death.

Symptoms may vary from asymptomatic to severe.

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11
Q

What type of chest pain is associated with myocarditis?

A

Not pleuritic.

Echocardiography typically shows global cardiac enlargement.

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12
Q

What are common manifestations of arrhythmias?

A

Chest pain, palpitations, dyspnea, syncope.

Presentation can range from mild and asymptomatic to severe and life-threatening.

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13
Q

Is acute onset chest pain a typical manifestation of congestive heart failure?

A

No.

Patients more commonly present with chronic symptoms such as progressive dyspnea.

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14
Q

What does endocarditis refer to?

A

Inflammation of the cardiac valves, most often due to bacterial infection.

Risk factors include congenital heart defects, prosthetic heart valves, IV drug use.

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15
Q

What are typical presentations of endocarditis?

A

High fever, new murmur, vascular manifestations, immunologic phenomena.

Examples include petechiae, splinter hemorrhages, glomerulonephritis, Osler nodes.

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16
Q

What characterizes myocardial infarction?

A

Sudden-onset, severe substernal chest pain, often radiating to the shoulder or jaw.

Associated symptoms include nausea, pallor, and diaphoresis.

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17
Q

What is the typical presentation of pulmonary embolism?

A

Sudden-onset shortness of breath and pleuritic chest pain.

A triphasic pericardial friction rub suggests acute pericarditis.

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18
Q

What is the most common cardiovascular manifestation of SLE?

A

Acute fibrinous pericarditis.

It typically causes sharp pleuritic chest pain relieved by sitting up and leaning forward.

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19
Q

What is pathognomonic for acute fibrinous pericarditis?

A

Presence of a triphasic friction rub on cardiac auscultation.

This finding is highly indicative of acute fibrinous pericarditis.

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20
Q

What symptoms indicate a heart failure exacerbation?

A

Increased shortness of breath with minimal exertion, pleuritic chest pain, and peripheral edema.

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21
Q

What happens during an acute heart failure exacerbation?

A

The heart can no longer compensate and produce adequate forward flow, causing fluid backup into the pulmonary and venous circuits.

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22
Q

What physical exam findings suggest heart failure exacerbation?

A

Increased jugular venous distention, positive hepatojugular reflex, and pitting edema to the level of the knee bilaterally.

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23
Q

What does an R wave greater than 12 mm in lead aVL indicate?

A

It indicates left ventricular hypertrophy according to the Sokolow-Lyon Criteria.

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24
Q

What is the mechanism of action of milrinone?

A

Milrinone selectively inhibits phosphodiesterase-3, increasing levels of cAMP and cGMP.

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25
Q

What effects does increased cAMP have in the myocardium?

A

It results in increased protein kinase A activity and calcium availability in the sarcoplasmic reticulum, enhancing contractility.

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26
Q

What are the positive effects of milrinone?

A

Positive inotropic and chronotropic effects, increasing contractility.

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27
Q

What side effects may result from increased calcium due to milrinone?

A

Muscle cramps and potential chest pain.

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28
Q

What is the vasodilatory effect of milrinone?

A

Increased GMP concentrations result in vasodilation, which may cause headaches and dizziness.

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29
Q

In what clinical settings is milrinone beneficial?

A

In acute heart failure or pulmonary hypertension, especially in hospitalized patients.

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30
Q

What is cilostazol and its primary action?

A

Cilostazol is a phosphodiesterase-3 inhibitor that preferentially acts on vascular smooth muscle and platelets. It increases protein kinase A levels within blood vessels to prevent platelet activation.

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31
Q

How does cilostazol compare to milrinone?

A

Cilostazol has less effect on cardiac tissues compared to milrinone, which is more effective in increasing cardiac output.

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32
Q

What is the primary use of dipyridamole?

A

Dipyridamole is a non-selective phosphodiesterase and adenosine deaminase inhibitor, often prescribed with warfarin as an antiplatelet agent to prevent thromboembolic disease after mechanical valve replacement.

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33
Q

What are the vasodilatory properties of dipyridamole?

A

Due to its prostacyclin-dependent vasodilatory properties, dipyridamole may be used intravenously as a pharmacologic stress test agent.

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34
Q

What is dobutamine used for?

A

Dobutamine is a B1-adrenergic receptor agonist used in cardiogenic shock to increase contractility and cardiac output.

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35
Q

What is the indication for dobutamine?

A

Dobutamine is indicated for short-term use in patients in intensive-care settings.

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36
Q

What is midodrine and its primary action?

A

Midodrine is an a1-adrenergic receptor agonist prescribed for orthostatic hypotension, increasing peripheral vascular resistance.

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37
Q

What symptoms does midodrine improve?

A

Midodrine improves symptoms associated with orthostatic hypotension, such as dizziness, lightheadedness, and syncope.

38
Q

What is the key takeaway about milrinone?

A

Milrinone selectively inhibits phosphodiesterase-3, increasing cyclic adenosine monophosphate and cyclic guanosine monophosphate levels, leading to increased inotropy and chronotropy in the myocardium and vasodilation in vascular smooth muscle.

39
Q

What is one of the first signs of reversible cellular injury?

A

Cellular swelling due to decreased aerobic metabolism and ATP depletion.

40
Q

What role do Na+/K+-ATPase and Ca2+ pumps play in cells?

A

They maintain ion homeostasis by facilitating the efflux of Na+ and Ca2+ while promoting the influx of K+.

41
Q

What happens in the absence of Na+/K+-ATPase and Ca2+ pumps?

A

Na+ and Ca2+ accumulate intracellularly, causing an ion imbalance and leading to cellular swelling.

42
Q

What are myelin figures and what do they indicate?

A

Myelin figures are formed from calcium-induced phospholipase damage and indicate irreversible cellular damage leading to cell death.

43
Q

What contributes to cellular membrane instability during prolonged damage?

A

An influx of Ca2+ and activation of Ca2+-dependent degradative enzymes lead to irreversible cellular damage.

44
Q

What occurs during lysosomal rupture in irreversible cellular injury?

A

Lysosomal enzymes leak into the cellular matrix, causing indiscriminate degradation of cellular components, leading to necrosis.

45
Q

What happens to mitochondria in the early stages of cellular injury?

A

Mitochondria may experience swelling, which is reversible if the causative agent is removed promptly.

46
Q

What can continued damage to mitochondria lead to?

A

Membrane instability, leakage of pro-apoptotic enzymes, and disruption of essential functions, including the electron transport chain.

47
Q

What is the key takeaway regarding cellular swelling?

A

Swelling is an initial sign of reversible cell damage due to Na+/K+-ATPase and Ca2+ channel dysfunction secondary to ATP depletion.

48
Q

common agent for viral pericarditis

A

cocxakie B

49
Q

inhibidorbde la fosfodieeterasa 3 para insuficiencia cardiaca aguda

A

milridona

50
Q

Side effects de milridona

A

dizINES , NAUSEA, MUSCLE CRAMPS

51
Q

First sign of reversible cellullar injury

A

swelling

52
Q

Recersible cellukar injury and swelling

A

decreased activity of ion pumps Na+,k+ atpasa

53
Q

Right sided heart failure

A

leads II,III,AVF , RIGHT CORONARY ARTERY, PRELOAD DEPENDENT AVOID VASODILATORS

54
Q

Miocardio gets highets perfusion

A

after de mitral valve opens during diastole

55
Q

Local mediators to supply O2

A

adenosine y nitric oxide

56
Q

Thiazide Diuretics

A

Hidroclotoriazide,clortalidone,clorotiazide,metolazone

57
Q

Aórtic regurgitación

A

High lleft ventricular end Diastolic volume,high left ventricular pressure,high SV, low aortic diastolicpressure

58
Q

Diastolic decrescendo murmur left lower sternal border

A

aortic regurgitation

59
Q

Which maniobra aumneta los ruidos en el lado derecho cardiaco

A

deep inspiration

60
Q

Water hammer pulse, head bobbing, disnea, bibasilar crackles

A

aortic regurgitation

61
Q

Increase risk of aortic dissection

A

patiens w Marfan Syndrome

62
Q

Clasification of Aortic regurgitation

A

standford A Y B

63
Q

Standford A

A

ascending aorta y surgical managment

64
Q

Standford B

A

descending aorta y medical managment Beta blocker 1st (esmolol) and then vasolitaror (nicardipina o nitriopursiato)

65
Q

Complications of aortic disection

A

aortic rupture,aortic regurgitation, cardiac tamponade,isquemia

66
Q

Cardiac tamponade

A

becks triad

67
Q

Cardiac tamponade

A

becks triad

68
Q

Cardiogenic shocks vs tamponade cardiac

A

pulmonary edema

69
Q

Bronquiectasias,sinusitis y dextrocardia

A

kartagener sindrome

70
Q

Hypertensive emergency

A

increase blood pressure >180/120,increase crestinite y signs of encefalophaty

71
Q

Farmaco en hipertensive emergency

A

fenoldopam x renal protective properties

72
Q

loud S1 w opening snap w diastolic rumbling murmur

A

mitral estenosis

73
Q

Common manifestation of rheumathic heart disease

A

mitral estenosis

74
Q

Infective enndocaridits cquse by

A

s aureus

75
Q

Warty like vegetations

A

endocsrditis

76
Q

Sindrome de marfan

A

trastorno del tejido conectivo, mutacion del gen de fibrilina 1

77
Q

Marfan

A

aoritic regurgitation , volune overload, enlargment of left cavity, eccdntric hypertrophy

78
Q

Watter hammer pulse head bobbing

A

aortic regurgitation

79
Q

Two major diastolic murmurs

A

aortix regurgitation y mitral stenosis

80
Q

You can think in right sided if

A

worsens w inspiration

81
Q

Eccenctric hypertrophy

A

related w volume

82
Q

Concenctric hypertrophy

A

pressure

83
Q

Hypertrophic obstructive cardiomipathy

A

mutation of B heavy myosin chain and myosin binding protein c , systokic crescendo decresendo murur , present in young athlethes

84
Q

Related w dilated irreversible cardiomiopaty

A

antraciclines (doxorubicin, daunorubicin )

85
Q

Related w reversible cardiomioaty induced

A

trastuzumab (breast cancer treatment)

86
Q

Septic shock

A

massive vasodilation, decrease pcwp , cvp , svr , compenssndo hay un infrease en cardiac index y venous o2 safuration

87
Q

Machine like murmur

A

Patent ductus arteriosus

88
Q

Derivation embriologica del ductus arteriosus

A

6to arch faringeo

89
Q

Fish oil

A

decreased fatty acid dekivery to the liver

90
Q

Stones,bonos,moans and psyquiatric overtones

A

Hypercalcemia secondary to thiazide diuretic use

91
Q

Ekg findings en atrial fibrilation

A

Irregular RR , absent P waves , QRS estrecho