CARDIOLOGY Flashcards

1
Q

What is the most common early complication of myocardial infarction, occurring within 24-48 hours?

A

Cardiac arrhythmias (e.g., ventricular fibrillation, ventricular tachycardia).

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2
Q

What is cardiogenic shock, and when does it typically occur post-MI?

A

Severe decreased cardiac output and hypotension.

Occurs when more than 40% of the left ventricle is infarcted usually within the first few days post-MI.

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3
Q

When does ventricular free wall rupture typically occur after an MI, and what are the clinical signs?

A

A: Occurs 3-7 days post-MI. Clinical signs include cardiac tamponade, distant heart sounds, hypotension, and jugular venous distension.

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4
Q

A 59-year-old man is hospitalized after suffer- ing a severe myocardial infarction. He is ini- tially treated with nitrates, β-blockers, and aspi- rin, and subsequently undergoes cardiac catheterization with placement of two stents. Following the procedure he is hemodynami- cally stable without recurrence of chest pain. However, 5 days after admission his heart rate is 134/min, blood pressure is 72/35 mm Hg, and respiratory rate is 29/min. Physical exami- nation reveals distant heart sounds and an ele- vated jugular venous pressure. Which of the following complications is most likely causing this patient’s symptoms?
(A) Aneurysm formation
(B) Cardiac arrhythmia
(C) Fibrinous pericarditis
(D) Rupture of the papillary muscle (E) Rupture of the ventricular free wall

A

The most likely cause of this patient’s symptoms is ventricular free wall rupture, leading to cardiac tamponade—a serious complication that can occur 3 to 7 days after a myocardial infarction.

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5
Q

What is the key clinical finding in papillary muscle rupture, and when does it occur after an MI?

A
  • Acute mitral regurgitation
  • Pulmonary edema
  • New holosystolic murmur.

It occurs 2-7 days post-MI, commonly in inferior wall infarctions.

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6
Q

What clinical findings are associated with interventricular septal rupture, and when does it occur post-MI?

A
  • Heart failure
  • New holosystolic murmur at the left sternal border
  • Signs of a left-to-right shunt.

Typically occurs 3-7 days post-MI.

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7
Q

What is Dressler syndrome, and when does it occur?

A
  • Autoimmune pericarditis
  • Occurs 2-10 weeks post-MI
  • Pleuritic chest pain
  • Fever
  • Pericardial friction rub
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8
Q

What is a late complication of MI characterized by a bulging, dyskinetic area of the ventricular wall, and when does it occur?

A

A: Ventricular aneurysm, which develops weeks to months post-MI. It can lead to heart failure, arrhythmias, and thromboembolism.

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9
Q

When does acute pericarditis typically occur after MI, and what are the key symptoms?

A

A: Occurs 1-3 days post-MI, presenting with pleuritic chest pain and a pericardial friction rub.

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10
Q

What is a mural thrombus, and when is it most likely to form post-MI?

A

A: A mural thrombus is a thrombus that forms on the endocardium overlying an infarcted area, typically forming days to weeks post-MI. It can lead to systemic embolism.

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11
Q

What are the typical timeframes for complications of MI?

A

A:

First 24-48 hours: Arrhythmias.
1-3 days: Acute pericarditis.
3-7 days: Ventricular free wall rupture, papillary muscle rupture, septal rupture.
Weeks to months: Ventricular aneurysm, Dressler syndrome, mural thrombus.

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12
Q

A 68-year-old man presents to the emergency department with acute onset of chest pain, shortness of breath, and lightheadedness. He suffered an anterior myocardial infarction 5 days ago and was treated with thrombolytics. His current vital signs reveal a heart rate of 130/min, blood pressure of 75/40 mm Hg, and respiratory rate of 32/min. Jugular venous distension is noted on physical examination, and heart sounds are distant. Which of the following is the most likely cause of his current condition?

(A) Ventricular aneurysm formation
(B) Rupture of the ventricular free wall
(C) Rupture of the interventricular septum
(D) Papillary muscle rupture
(E) Dressler syndrome

A
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13
Q

A 72-year-old woman with a history of hypertension and hyperlipidemia presents with sudden-onset dyspnea and orthopnea 3 days after suffering a myocardial infarction. She has bilateral pulmonary crackles and a new holosystolic murmur heard at the apex. Echocardiography reveals severe mitral regurgitation. Which of the following is the most likely underlying cause of her condition?

(A) Rupture of the ventricular free wall
(B) Rupture of the papillary muscle
(C) Rupture of the interventricular septum
(D) Formation of a ventricular aneurysm
(E) Acute pericarditis

A
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14
Q

A 60-year-old man presents with new-onset shortness of breath 5 days after an inferior wall myocardial infarction. On physical examination, a loud holosystolic murmur is heard at the left lower sternal border, and there are signs of biventricular heart failure. Echocardiography reveals a significant left-to-right shunt. Which of the following is the most likely cause of this patient’s presentation?

(A) Ventricular free wall rupture
(B) Ventricular aneurysm formation
(C) Papillary muscle rupture
(D) Interventricular septal rupture
(E) Acute pericarditis

A
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15
Q

A 58-year-old man presents to the clinic with low-grade fever, pleuritic chest pain, and fatigue 4 weeks after suffering a myocardial infarction. On physical examination, there is a pericardial friction rub. ECG reveals diffuse ST-segment elevations. Which of the following is the most likely diagnosis?

(A) Papillary muscle rupture
(B) Acute pericarditis
(C) Dressler syndrome
(D) Ventricular free wall rupture
(E) Ventricular aneurysm

A
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16
Q

64-year-old man is brought to the clinic for evaluation of progressive dyspnea and fatigue 2 months after an anterior myocardial infarction. Physical examination reveals a displaced point of maximal impulse and a persistent S3 heart sound. An echocardiogram shows a dyskinetic bulge in the left ventricular wall with a large thrombus inside. Which of the following is the most likely diagnosis?

(A) Ventricular free wall rupture
(B) Ventricular aneurysm formation
(C) Interventricular septal rupture
(D) Mural thrombus formation
(E) Papillary muscle rupture

A
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17
Q

A 59-year-old man is admitted to the hospital after experiencing a myocardial infarction. On the third day of hospitalization, he reports sharp chest pain that worsens with deep inspiration and improves when sitting forward. A pericardial friction rub is heard on auscultation. ECG shows diffuse ST-segment elevations. Which of the following is the most likely diagnosis?

(A) Rupture of the ventricular free wall
(B) Papillary muscle rupture
(C) Ventricular aneurysm formation
(D) Acute pericarditis
(E) Mural thrombus formation

A
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18
Q

A 67-year-old woman presents to the emergency department with acute-onset right-sided weakness and difficulty speaking. She has a history of a large myocardial infarction 2 weeks ago. Her vital signs are stable, but a left ventricular thrombus is identified on echocardiography. Which of the following best describes the most likely complication she has experienced?

(A) Left-to-right shunt
(B) Pulmonary embolism
(C) Stroke due to systemic embolism
(D) Acute pericarditis
(E) Papillary muscle rupture

A
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19
Q

A 73-year-old man is admitted to the hospital after suffering a large anterior myocardial infarction. On the second day of hospitalization, he develops hypotension, cool extremities, and decreased urine output. A chest X-ray reveals pulmonary edema. Which of the following is the most likely cause of his symptoms?

(A) Ventricular aneurysm formation
(B) Cardiogenic shock
(C) Interventricular septal rupture
(D) Papillary muscle rupture
(E) Acute pericarditis

20
Q

Congenital heart disease: What are the causes of the right-to-left shunt?

A

The 5 T’s:
1. Truncus arteriosus (1 vessel) - Persistent truncus arteriosus

  1. Transposition (2 switched vessels) - D-transposition of great arteries
  2. Tricuspid atresia (3 = Tri)
  3. Tetralogy of Fallot (4 = Tetra)
  4. TAPVR (5 letters in the name) - Total anomalous pulmonary venous return
21
Q

What is the inheritance of Hypertrophic Cardiomyopathy?

A

Autosomal dominant with incomplete penetrance

22
Q

Mutation on Hypertrophic Cardiomyopathy:

A

Proteins of the cardiac sarcomere:
Myosin-binding protein C
Beta-myosin heavy chain

23
Q

Young person with systolic murmur at the left sternal border that increases in intensity during the strain phase of valsalva maneuver . What is the diagnosis?

A

Hypertrofic Cardiomyopathy

24
Q

Young person with systolic murmur at the left sternal border that increases in intensity during maneuvers that decrease left ventricular blood volume . What is the diagnosis?

A

Hypertrofic Cardiomyopathy

25
Q

Young person with systolic murmur at the left sternal border that increases in intensity during standing . What is the diagnosis?

A

Hypertrofic Cardiomyopathy

26
Q

Maneuvers that increase LV volume:

A
  • Squatting
  • Supine leg raise
  • Handgrip
27
Q

Maneuvers that decrease LV volume:

A
  • Standing
  • Strain phase of valsalva
28
Q

Antiarritmicos que prolongam o intervalo QT:

A

Classe Ia: Bloqueiam canais de sódio e potássio, prolongando o potencial de ação.
Quinidina
Procainamida
Disopiramida

Classe III: Bloqueiam canais de potássio, prolongando a repolarização.
Amiodarona (embora prolongue o QT, raramente causa Torsades de Pointes)
Sotalol
Dofetilida
Ibutilida

29
Q

Principal classe de drogas que alarga o QRS

A

Antiarrítmicos da Classe I

Observação: O efeito “use dependence” é mais evidente na Classe IC, tornando o alargamento do QRS mais pronunciado durante o exercício.

30
Q

Hand grip
- Parametro que altera
- Sopro que aumenta
- Sopro que diminui

A
  • Aumenta a pós carga do VE
  • Insuficiência aórtica, Insuficiencia mitral e defeito do septo ventricular (aumento da pressão aórtica e ventricular esquerda)
  • Prolapso de válvula mitral e cardiomiopatia hipertrófica (aumento do volume de sangue no VE), estenose aórtica
31
Q

22q11.2 deletion cardiovascular association:

A

DiGeorge Syndrome - Tetrallogy of Fallot
Truncus arteriousus
Transposition of the great arteries

32
Q

Fibrilin 1-mutation cardiovascular associations:

A

Marfan Syndrome -
Cystic medial necrosis (dyssecting aortic aneurysm & aortic valve regurgitation)
Mytral valve prolapse

33
Q

Frataxin mutation cardiovascular associations:

A

Friedreich ataxia -
Hypertrophic cardiomiopaty

34
Q

Sex chromosome monosomy:

A

Turner sydrome (45,X) -
Bicuspid aortic valve
Coarctation of the aorta

35
Q

Mecanismo de ação da adenosina

A

Aumenta a condutância de potássio, hiperpolariza a membrana e reduz a entrada de cálcio

36
Q

Drogas com risco de torsades de pointes.

A

Sotalol
Ibutilida

(bloqueadores dos canais de cálcio)

37
Q

Drogas que atuam na fase 0 da despolarização miocárdica

A

Procainamida
Flecainida
Lidocaina

38
Q

Drogas que atuam na fase 2 da despolarização miocárdica

A

Verapamil
Diltiazem

39
Q

Mecanismos de ação dos beta-bloqueadores na cardiomiopatia hipertrófica

A
  • Aumenta o tempo de diastole, aumentando o volume diastólico final
  • Diminui a contratilidade diminuindo a quantidade de sangue ejetado (aumenta o volume sistólico final)
40
Q

Maiores fatores de risco para AAA?

A
  • > 65 anos
  • Tabagismo
  • Sexo masculino
41
Q

Mecanismo de ação das estatinas:

A

Inibe a HMG - Coa redutase, diminuindo a síntese de colesterol hepático e aumentando a expressão de receptores hepáticos de LDL.

42
Q

Manifestações da Granulomatose com poliangeite

A

Trato respiratório superior: sinusite/otite e deformiade nasal em sela

Trato respiratório inferior: nódulos e cavitações

Renal: Glomerulonefrite rapidamente progressiva

Pele: livedo reticular e úlceras

43
Q

Biópsia na GPA

A

Arterite necrotizante com inflamação granulomatosa

44
Q

Biópsia na PAN

A

Inflamação transmural segmentar de vasos de artérias musculares de médio tamanho com necrose fibrinoide

45
Q

Biópsia em Churg-Strauss

A

Granulomas necrotizantes com predominancia de eosinofilos

46
Q

Sopro holossistólico no apex com irradiação para axila

A

Regurgitação mitral

47
Q

Cilostazol action mechasnismo: