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
What effects does increased cAMP have in the myocardium?
It results in increased protein kinase A activity and calcium availability in the sarcoplasmic reticulum, enhancing contractility.
26
What are the positive effects of milrinone?
Positive inotropic and chronotropic effects, increasing contractility.
27
What side effects may result from increased calcium due to milrinone?
Muscle cramps and potential chest pain.
28
What is the vasodilatory effect of milrinone?
Increased GMP concentrations result in vasodilation, which may cause headaches and dizziness.
29
In what clinical settings is milrinone beneficial?
In acute heart failure or pulmonary hypertension, especially in hospitalized patients.
30
What is cilostazol and its primary action?
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.
31
How does cilostazol compare to milrinone?
Cilostazol has less effect on cardiac tissues compared to milrinone, which is more effective in increasing cardiac output.
32
What is the primary use of dipyridamole?
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.
33
What are the vasodilatory properties of dipyridamole?
Due to its prostacyclin-dependent vasodilatory properties, dipyridamole may be used intravenously as a pharmacologic stress test agent.
34
What is dobutamine used for?
Dobutamine is a B1-adrenergic receptor agonist used in cardiogenic shock to increase contractility and cardiac output.
35
What is the indication for dobutamine?
Dobutamine is indicated for short-term use in patients in intensive-care settings.
36
What is midodrine and its primary action?
Midodrine is an a1-adrenergic receptor agonist prescribed for orthostatic hypotension, increasing peripheral vascular resistance.
37
What symptoms does midodrine improve?
Midodrine improves symptoms associated with orthostatic hypotension, such as dizziness, lightheadedness, and syncope.
38
What is the key takeaway about milrinone?
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
What is one of the first signs of reversible cellular injury?
Cellular swelling due to decreased aerobic metabolism and ATP depletion.
40
What role do Na+/K+-ATPase and Ca2+ pumps play in cells?
They maintain ion homeostasis by facilitating the efflux of Na+ and Ca2+ while promoting the influx of K+.
41
What happens in the absence of Na+/K+-ATPase and Ca2+ pumps?
Na+ and Ca2+ accumulate intracellularly, causing an ion imbalance and leading to cellular swelling.
42
What are myelin figures and what do they indicate?
Myelin figures are formed from calcium-induced phospholipase damage and indicate irreversible cellular damage leading to cell death.
43
What contributes to cellular membrane instability during prolonged damage?
An influx of Ca2+ and activation of Ca2+-dependent degradative enzymes lead to irreversible cellular damage.
44
What occurs during lysosomal rupture in irreversible cellular injury?
Lysosomal enzymes leak into the cellular matrix, causing indiscriminate degradation of cellular components, leading to necrosis.
45
What happens to mitochondria in the early stages of cellular injury?
Mitochondria may experience swelling, which is reversible if the causative agent is removed promptly.
46
What can continued damage to mitochondria lead to?
Membrane instability, leakage of pro-apoptotic enzymes, and disruption of essential functions, including the electron transport chain.
47
What is the key takeaway regarding cellular swelling?
Swelling is an initial sign of reversible cell damage due to Na+/K+-ATPase and Ca2+ channel dysfunction secondary to ATP depletion.
48
common agent for viral pericarditis
cocxakie B
49
inhibidorbde la fosfodieeterasa 3 para insuficiencia cardiaca aguda
milridona
50
Side effects de milridona
dizINES , NAUSEA, MUSCLE CRAMPS
51
First sign of reversible cellullar injury
swelling
52
Recersible cellukar injury and swelling
decreased activity of ion pumps Na+,k+ atpasa
53
Right sided heart failure
leads II,III,AVF , RIGHT CORONARY ARTERY, PRELOAD DEPENDENT AVOID VASODILATORS
54
Miocardio gets highets perfusion
after de mitral valve opens during diastole
55
Local mediators to supply O2
adenosine y nitric oxide
56
Thiazide Diuretics
Hidroclotoriazide,clortalidone,clorotiazide,metolazone
57
Aórtic regurgitación
High lleft ventricular end Diastolic volume,high left ventricular pressure,high SV, low aortic diastolicpressure
58
Diastolic decrescendo murmur left lower sternal border
aortic regurgitation
59
Which maniobra aumneta los ruidos en el lado derecho cardiaco
deep inspiration
60
Water hammer pulse, head bobbing, disnea, bibasilar crackles
aortic regurgitation
61
Increase risk of aortic dissection
patiens w Marfan Syndrome
62
Clasification of Aortic regurgitation
standford A Y B
63
Standford A
ascending aorta y surgical managment
64
Standford B
descending aorta y medical managment Beta blocker 1st (esmolol) and then vasolitaror (nicardipina o nitriopursiato)
65
Complications of aortic disection
aortic rupture,aortic regurgitation, cardiac tamponade,isquemia
66
Cardiac tamponade
becks triad
67
Cardiac tamponade
becks triad
68
Cardiogenic shocks vs tamponade cardiac
pulmonary edema
69
Bronquiectasias,sinusitis y dextrocardia
kartagener sindrome
70
Hypertensive emergency
increase blood pressure >180/120,increase crestinite y signs of encefalophaty
71
Farmaco en hipertensive emergency
fenoldopam x renal protective properties
72
loud S1 w opening snap w diastolic rumbling murmur
mitral estenosis
73
Common manifestation of rheumathic heart disease
mitral estenosis
74
Infective enndocaridits cquse by
s aureus
75
Warty like vegetations
endocsrditis
76
Sindrome de marfan
trastorno del tejido conectivo, mutacion del gen de fibrilina 1
77
Marfan
aoritic regurgitation , volune overload, enlargment of left cavity, eccdntric hypertrophy
78
Watter hammer pulse head bobbing
aortic regurgitation
79
Two major diastolic murmurs
aortix regurgitation y mitral stenosis
80
You can think in right sided if
worsens w inspiration
81
Eccenctric hypertrophy
related w volume
82
Concenctric hypertrophy
pressure
83
Hypertrophic obstructive cardiomipathy
mutation of B heavy myosin chain and myosin binding protein c , systokic crescendo decresendo murur , present in young athlethes
84
Related w dilated irreversible cardiomiopaty
antraciclines (doxorubicin, daunorubicin )
85
Related w reversible cardiomioaty induced
trastuzumab (breast cancer treatment)
86
Septic shock
massive vasodilation, decrease pcwp , cvp , svr , compenssndo hay un infrease en cardiac index y venous o2 safuration
87
Machine like murmur
Patent ductus arteriosus
88
Derivation embriologica del ductus arteriosus
6to arch faringeo
89
Fish oil
decreased fatty acid dekivery to the liver
90
Stones,bonos,moans and psyquiatric overtones
Hypercalcemia secondary to thiazide diuretic use
91
Ekg findings en atrial fibrilation
Irregular RR , absent P waves , QRS estrecho