Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular system > Chapter 3- Pathology > Flashcards

Chapter 3- Pathology Flashcards

1
Q

What are the 3 diff types of angina?

A
  1. Stable angina
  2. Unstable angina
  3. Prinzmetal (or variant) angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In what situations do stable angina arise?

A

Exertion

Emotional stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the main etiology of stable angina

A

Stable atherosclerotic plaque within the coronary arteries with > 70% stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Does stable angina represent reversible or irreversible myocardial injury?

A

Reversible injury

No necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the classic presentation of stable angina?

A
  1. Chest pain <20 minutes that radiates to the left arm or jaw (typically 5-10mins)
  2. Diaphoresis
  3. Shortness of breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the classic ECG finding in stable angina?

A

ST segment depression due to subendocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What relieves stable angina?

A

Rest

Nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Under what circumstances does unstable angina arise?

A

At rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the etiology of unstable angina?

A

Rupture of an atherosclerotic plaque—thrombosis—INCOMPLETE OCCLUSION of coronary artery. (Typically >90% occlusion of coronary artery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is the injury of unstable angina reversible or irreversible?

A 
Reversible injury to myocytes
No necrosis (Troponin levels are not elevated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the classic ECG finding in unstable angina?

A

ST segment depression due to subendocardial ischemia and/ or T wave inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What relieves unstable angina?

A

Nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a possible complication/sequelae of unstable angina?

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Under what circumstances does prinzmetal angina arise?

A

No predisposing circumstance

Episodic chest pain unrelated to exertion (occurs especially at night or early in the morning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes prinzmetal angina?

Give 4 exogenous drugs/ substances that can trigger vasospasm

Why do women who have had of variant angina often have a history of migraine headache?

What drug is useful in confirming the diagnosis of prinzmetal angina?

A
  1. Coronary artery vasospasm
  2. Cocaine, Triptan, tobacco, ergonovine (these agents induce vasoconstriction)
  3. Both migraine headache and prinzmetal angina are both associated with arterial vasospasms.
  4. Ergonovine triggers vasospasm in susceptible patient (used to induce uterine contraction and cessation of bleeding post partum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Is the injury sustained by prinzmetal angina reversible/irreversible?

A

If episode occurs for <20m= reversible injury w/ no necrosis

If episode >20 mins= reversible w/ necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the ECG finding in prinzmetal angina?

A

ST segment elevation due to transmural ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What relieves attack of prinzmetal angina?

A

Nitroglycerin

Ca channel blockers i.e diltiazem (to relieve vasospasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the single most common risk factor for developing Ischemic heart disease?

What causes ischemic heart disease?

A

Atherosclerosis

Compromised blood flow in the coronary vessels

  • decreased arterial perfusion
  • decreased venous drainage and build up of toxic metabolites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 4 types of Ischemic Heart Disease (ICH)

A
  1. Angina
  2. MI
  3. Sudden Cardiac Death
  4. Chronic Ischemic Heart Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is myocardial infarction

A

Necrosis of cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the etiologic processes involved in MI?

A

Rupture of atherosclerotic plaque
Subsequent thrombosis
COMPLETE OCCLUSION of coronary artery

Other causes include:
Coronary artery vasospasm (due to prinzmetal angina or cocaine)
Emboli
Vasculitis (of coronary arteries i.e Kawasaki disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the clinical presentation of MI?

A

Severe crushing chest pain >20mins
Radiates to the L. arm and jaw
Diaphoresis
Dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Does nitroglycerin relieve MI?

What is the most common cause of death in MI in the pre-hospital phase?

What is the most common cause of death from MI in the in-hospital phase?

A

NO

Ventricular fibrillation

Ventricular failure and subsequent cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which areas of the heart are most commonly affected my MI?

Which areas of the heart are generally spared?

A
  1. Left ventricle
  2. Right ventricle
    Both atria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 3 most commonly affected coronary arteries in MI in order of hierarchy

A
  1. Left Anterior Descending Artery (LAD) 45%
    • Infarction of anterior wall of the LV
    • Infarction of anterior septum of the LV
  2. Right Coronary Artery (RCA)
    • Infarction of Posterior wall of LV
    • Infarction of posterior septum
    • Infarction of papillary muscles of LV
  3. Left Circumflex Artery (LCX)
    • Infarction of lateral wall of LV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What form of cardiac mm necrosis is found at the initial stage of MI?

A

Subendocardial necrosis involving <50% of the wall thickness (Submyocardial infarction)

ST depression on ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What form of cardiac mm necrosis is found in continued or severe MI?

A

Transmural necrosis (Transmural infarction)

ST segment elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the most sensitive and specific marker (gold standard) for MI.

What does its levels RISE, PEAK, and NORMALIZE

A

Troponin I

Rise 2-4hrs after MI

Peak 24 hrs after MI

Return to normal: 7-10 days after MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which lab test is useful for detecting re-infarction that occurs days after MI? (3-10days)

  1. When does it RISE, PEANK and NORMALIZE?
  2. Why is CK-MB not as specific as Troponin?
  3. What is the function of CK-MB?
A

CK-MB (Creatine Kinase MB

Rise 4-6 hrs

Peak 24 hrs

Normalize- 72 hrs (3days)

Because it is produced by both cardiac and skeletal muscle

Transfers phosphate group from Creatine Kinase to ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the treatment for (Non-ST elevation MI)& Unstable angina?

What are the treatment for STEMI?

How is pain control achieved in unstable angina, STEMI & NSTEMI?

A
  1. Aspirin/(LMW)heparin, Clopidogrel- Limits thrombosis
  2. Supplemental 02- Minimizes ischemia
  3. Nitrates- Vasodilate coronary arteries
    - Decrease systemic venous resistance by venodilation—Reducing pre-load—Reducing cardiac work and 02 demand
  4. Beta blockers- Slows heart rate, decreasing 02 demand and risk for arrhythmia
  5. ACE inhibitors- Decreases LV dilation by
    I. Blocking vasoconstriction—decreasing preload
    II. Preventing Na $ H20 buildup–decreasing preload
    III. Decreases probability of LV dilation from increasing blood
    volume.
  6. Fibrinolysis or angioplasty-opens blocked vessel

STEMI
Percutaneous coronary intervention (preferred) or Fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What could most likely be complications of reperfusion after fibrinolysis or angioplasty?

How can reperfusion injury be demonstrated clinically?

A
  1. CONTRACTION BAND NECROSIS- Reperfusion, calcium influx—hyper-contractions of myofibrils.
  2. REPERFUSION INJURY- Generation of oxygen free radicals that further damage the myocytes after reperfusion.

By continued rise of cardiac enzymes despite better coronary blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q 
What are the changes that occur in < 4 hours after an MI?
In terms of-
1. Gross changes 
2. Microscopic changes 
3. Complications
A
  1. No gross change seen
  2. No microscopic change
  3. Cardiogenic shock (massive infarction)
    CHF
    Arrythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q 
What are the changes that occur in 4-24 hours after an MI?
In terms of-
1. Gross changes 
2. Microscopic changes 
    4-8 hours
    12-24 hours 
3. Complications
A
  1. Dark discoloration (dark mottling). Tetrazolium staining may identify infarction during this period w/ viable tissue red and infarcted tissue-red
  2. Coagulation necrosis (removal of nuclei from cells but cells maintain structural integrity)
    4-8 Hrs WAVY MYOFIBERS are seen (intact contacting fibers
    tugging on dead, non-contracture fibers)
    Edema separates myocardial cells
    12-24 Hrs- Contraction bands at borders of infarct due to
    reperfusion injury
  3. Arrythmias (hypoxia decreased ATP production which in turn impairs the Na-K-ATPase pump thus altering membrane potential.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the changes that occur in 1-3 days after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complication and it’s clinical presentation

A
  1. Yellow pallor (coz of the arrival of WBCs)
  2. Neutrophils present, dilated vessels (hyperemia) and extensive coagulation necrosis
  3. Fibrinolysis pericarditis (occurs only in transmural infarction)
    and presents with chest pain and friction rub.
    Fibrinolysis due to deposition of fibrin or inflammatory debris on the
    pericardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q 
What are the changes that occur in 4-7 days after an MI?
In terms of-
1. Gross changes 
2. Microscopic changes 
3. Complications
A
  1. Yellow pallor
  2. Macrophages (phagocytose dead necrotic debris leaving the heart in its weakest state and prone to rupture)
  3. Rupture of myocardial free wall (leads to cardiac tamponade)
    Rupture Inter-ventricular septum (leads to shunt)
    Rupture of papillary muscle (leads to valvular insufficiency or
    regurgitation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q 
What are the changes that occur in 1-3 weeks after an MI?
In terms of-
1. Gross changes 
2. Microscopic changes 
3. Complications
A
  1. Red border emerges as granulation tissue enters into the infarct
    Yellow infarct surrounded by hyperemic red borders.
  2. Granulation tissue (plump fibroblasts, collagen and blood vessels. Type I collagen

3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q 
What are the changes that occur in >1 month after an MI?
In terms of-
1. Gross changes 
2. Microscopic changes 
3. Complications
A
  1. White scar
  2. Fibrosis
  3. Aneurysm (due to weekend cardiac muscle which has been
    replaced by non-compliant scarred tissue)Mural thrombus (due to stasis of blood in areas of aneurysm)Dressler syndrome (autoimmune pericarditis that occurs 6-8 weeks post MI due to exposure of the immune system to pericardial antigens exposed from previous 4rm pericardial inflammation and can result in Fibrinous pericarditis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is SUDDEN CARDIAC DEATH?

A

Unexpected death due to cardiac disease that occur without symptoms or w/ symptoms occurring <1 hour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Most common etiology for Sudden cardiac death (SCD)?

What predisposes to SCD?

A

Acute ischemia—ventricular arrhythmia

Indeed 90% of patients have pre-existing atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are other less common causes of sudden cardiac death?

A

Mitral valve prolapse
Cardiomyopathy
Cocaine abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Chronic Ischemic Heart Disease?

What other heart condition can CIHD progress to?

A

Poor myocardial function due to chronic ischemic damage (WITH OR WITHOUT INFARCTION)

Progresses to CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is CHF?

What are the 2 classifications of CHF?

A

Right sided HF

Left sided HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give examples of causes of left sided HF

A 
Ischemia 
MI
Hypertension
Dilated cardiomyopathy 
Restrictive cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the clinical features of left sided HF?
1. In the lungs

What is the characteristic finding of alveolar cells associated with HF? It’s alias?

A
  1. Pulmonary congestion—pulmonary edema—Dyspnea, crackles, Orthopnea, Paroxysmal nocturnal dyspnea,

Congestion of small alveolar capillaries burst— intraalveolar hemorrhage— HEMOSIDERIN MACROPHAGES (HF CELLS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the relationship between CHF and the RAAS?

A 
Decreased forward perfusion--- activation of RAAS--- vasoconstriction by angiotensin II 
Aldosterone production (increase Na and fluid buildup)

Fluid buildup exacerbates the CHF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q
  1. What is the mainstay of treatment for CHF?
  2. What is the pneumonic of the drugs used in the treatment of CHF?
  3. What agents improve mortality in HF?
  4. African Americans have been shown to benefit from this medications
A
  1. ACE inhibitors
2. B-Sad (coz you have CHF) 
B-Blockers 
Spironolactone (K sparing diuretic)
ACE inhibitors, ARBs
Diuretics (Thiazides, furosemide), Digoxin
  1. B-Sa (B-blockers should only be used in the long term management of patients with HFrEF but not in decompensated HFrEF)
  2. H&N (Hydralazine & Nitrates)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the most common cause Right CHF?

What are other causes?

A
  1. Left sided HF

Other causes:

  • Left to right shunt
  • Chronic lung diseases (Cor pulmonale)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the clinical manifestations of Right sided CHF?

What are the clinical manifestations of Left sided HF?

A

Right sided
1. Jugular venous distention

  1. PAINFUL hepato-splenomegaly (nutmeg liver) due to distention of veins in liver. May progress to cardiac cirrhosis of liver.
  2. Dependent pitting edema (increased hydrostatic pressure)

Left sided

  1. Orthopnea
  2. Paroxysmal nocturnal dyspnea
  3. Pulmonary edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q
  1. What of these shunts presents with cyanosis shortly after birth?

R-L shunt?

L-R shunt?

  1. What weeks embryogenesis does congenital defect develop?
A
  1. R-L shunt

2. Week 3- Week 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the most common congenital heart defect?

What kind of shunt is seen here?

What is the consequence of a small shunt?

What is the consequence of a large shunt?

What is its murmur? And where can it be heard?

A
  1. VSD
  2. L-R shunt
  3. Small shunts are usually asymptomatic
  4. Large shunts can lead to eisenmenger syndrome
  5. Harsh holosystolic murmur heard at the left lower sternal border
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which congenital heart defect is associated with fetal alcohol syndrome?

A

VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the treatment?

A

Surgical closure

Small defects may close spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the most common type of ASD?

What type of shunt is seen here?

What is the type of ASD associated with Down syndrome?

A
  1. Ostium secundum (most commonly an isolated defect)
  2. L-R shunt
  3. Ostium primum (are often associated with other cardiac defects)
    Children with Down syndrome often have endocardial cushion defect (VSD, ASD, AV septal defect) and also have a low baseline HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the auscultatory clinical finding in ASD?

A
  1. Splitting of S2 (due to increased blood in right heart which delays closure of pulmonary valve)
  2. Loud S1 across the upper left sternal border
  • Increase L-R shunt increases volume of blood passing through the tricuspid valve over the mitral valve thereby keeping the tricuspid valve open for rapid RV filling throughout diastole so that at the onset of systole, the tricuspid valve snaps shut.
  • Simultaneous decreased flow across the mitral valve makes LV filling over before diastole is over and the mitral valve cusps float together prior to systolic closure.

Just imagine closing a door against resistance (of wind) compared to closing it with no resistance, of course slamming the door shut against resistance will create a loud noise.

  1. Systolic ejection murmur (due to increased blood flow along the pulmonary valve)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is an important complication of ASD? (L-R shunt)

A

Paradoxical embolus (and have an increased risk of stroke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q
  1. What disease is associated with a PDA?
  2. What kind if shunt is seen here?

3 What is the characteristic auscultatory finding in PDA.?

  1. What an anatomical site is auscultation best heard?
  2. Can PDA lead to eisenmenger syndrome? How?
A
  1. Congenital rubella
  2. L-R shunt
  3. Holosystolic ‘machine-like’ murmur
  4. Left infra clavicular region
  5. Yes, due to long standing L-R shunt. Resulting in lower extremity cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are manifestations of eisenmenger syndrome?

A

Reversal of L-R shunt to R-L shunt

Late cyanosis

Polycythemia

Clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q
  1. What is the pathology in transposition of the great arteries?
  2. Does this present with early cyanosis? How?
  3. What maternal disease is it associated with?
A
  1. Pulmonary artery arises from the LV
    Aorta arises from the RV
  2. Yes there is early cyanosis because the pulmonary and systemic circuits do not mix and this is incompatible with life.
  3. Maternal diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the management for transposition of great arteries?

What is the gross sequelae of the L and R ventricles?

A
  1. Creation of shunt after birth is required for survival as the pulmonary and systemic circuits do not mix.
  2. Admin of prostaglandin E to maintain PDA till definitive surgical repair is done.

Hypertrophy of RV
Atrophy of the LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the pathology behind truncus arteriosus?

Does this present with early cyanosis?

A

Failure of truncus arteriosus to divide into aorta and pulmonary artery.

Yes. Because deoxygenated blood from RV mixes with oxygenated blood before the great vessels separate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the pathology in tricuspid atresia?

What is the gross sequelae of the RV

Which congenital heart defect is tricuspid atresia associated with?

A
  1. Tricuspid valve fails to develop
  2. Hypo-plastic RV
  3. ASD with R-L shunt— EARLY CYANOSIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the pathology in coarctation of the aorta

What are the two forms of coarctation of the aorta?

A

Narrowing of the aorta

  1. Infantile form
  2. Adult form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Where is the coarctation in the infantile form of coarctation of the aorta?

How does this condition cause cyanosis in infants?

A
  1. Distal to the aortic arch (after the aortic arch) and proximal to the PDA (before the PDA).
    Infantile form is ass with a PDA
  2. Blood moving from the pulmonary artery shunts directly through the PDA into the (lower pressure) distal aorta (rather than going ahead to the lungs) due to the presence of the coarctation before the area of the PDA thus babies present with lower extremity cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which genetic syndrome is associated with Coarctation if the aorta?

A

Turner syndrome

66
Q

Where is the coarctation in the adult form of coarctation of the aorta?

What are the clinical findings present?

At which stage of life is this diseases classically discovered?

A
  1. Coarctation is found after the aortic arch (no PDA in adult form)
  2. HPN in the upper extremities due to increased blood surge through the arterial derivatives the aortic arch (R. Brachiocephalic A. Common carotid A. Left subclavian A.) as a result of the distal
    coarctation.
    Hypotension in the lower extremities with weak peripheral pulses.
  3. Adulthood
67
Q

What is the characteristic x-Ray finding in adult type coarctation of the aorta?

What valvular defect is (Adult type) coarctation of aorta associated with?

A
  1. NOTCHING OF RIBS ON THE X-RAY
    Due to the formation of collateral circulation across the intercostal arteries to compensate for HPN in these vessels.
    These engorged arteries impress upon the ribs cashing notching.
  2. Bicuspid aortic valve.
68
Q

How many chambers of the heart does dilated cardiomyopathy involve?

A

All 4 chambers

69
Q

Is dilated cardiomyopathy a systolic or diastolic dysfunction?

A

Systolic as the dilated casual muscles are weak and cannot pump effectively

70
Q

Give 3 complications of a dilated cardiomyopathy

A
  1. Mitral and tricuspid valve regurgitation
  2. Arrhythmias- stretching and dysfunction of conducting tissues
  3. Bi-ventricular CHF
71
Q

What is the most common cause of dilated cardiomyopathy?

A

Idiopathic

72
Q

What is the pattern of inheritance I’m dilated cardiomyopathy?

A

Autosomal dominant

73
Q

Give 5 causes of dilated cardiomyopathy

A
  1. Infection with coxsackie A/B (w/ dilated cardiomyopathy as a late complication)
  2. Alcohol- and it’s metabolites have a direct toxic effect on heart
  3. Doxorubicin- a chemotherapy
  4. Pregnant women in late pregnancy- soon after childbirth probably secondary to gestational HPN
  5. Genetic disorder (AD)
74
Q

What is the treatment for dilated cardiomyopathy?

A

Heart transplant

75
Q

How many chambers of the heart does hypertrophic myopathy affect ?

Name

A

Left ventricle

76
Q

What is the pattern of inheritance in hypertrophic cardiomyopathy?

What is the genetic defect?

A
  1. Autosomal dominant

2. Genetic mutations not sarcomere proteins (beta-myosin heavy chain mutation)

77
Q

What is a common complication of hypertrophic cardiomyopathy?

What is responsible for this complication?

A
  1. Sudden death (in young athletes)

2. Ventricular arrhythmias

78
Q

How is syncope induced by exercise associated with hypertrophic cardiomyopathy

A

Sub-aortic hypertrophy of the inter ventricular septum results in functional aortic stenosis.

79
Q

What is the biopsy finding in hypertrophic cardiomyopathy?

A

Myofibrils hypertrophy with disarray

80
Q

Is restrictive cardiomyopathy a systolic of diastolic cardiomyopathy?

Why?

A

Diastolic

Decreased compliance of ventricle reduces filling during diastole.

81
Q

Give causes of restrictive cardiomyopathy

A
  1. Amyloidosis- amyloid deposition
  2. Sarcoidosis- granulomas
  3. Hemochromatosis- excessive storage of iron in the tissues
  4. Endocardial fibro-elastosis (CHILDREN)
  5. Loeffler syndrome (eosinophilia–eosinophilic infiltrate–inflammation—fibrosis—restrictive cardiomyopathy
82
Q

What is a complication of restrictive cardiomyopathy?

A

CHF

83
Q

What is the characteristic ECG finding in restrictive cardiomyopathy?

A

Low voltage ECG & Diminished QRS amplitude.

84
Q

What is the causative organism of acute rheumatic fever?

A

Group A beta hemolytic strep

85
Q

How many weeks after a strep throat does acute rheumatic fever arise?

Which population?

A
  1. 2-3 weeks

2. Children

86
Q

What is the mechanism by which the immune system cross react with normal tissues in acute rheumatic fever?

Which specific antigen of the Group A beta hemolytic strep is responsible for this altered immune response

A

Molecular mimicry

Bacterial M protein (which resembles proteins in human tissue)

87
Q

What is the diagnostic criteria for Acute rheumatic fever?

A
  1. An evidence of past history of group A beta hemolytic strep infection (Elevated ASO, DNase beta titers)
  2. Minor criteria (non-specific: fever, elevated ESR)
  3. Major criteria (JONES CRITERIA)Migratory poly-arthritisPancarditis
    Endocarditis- Mitral valve more commonly involved
    Small vegetations along closure line- regurgitate
    MYOCARDITIS- most common cause of death during the
    acute phase
    Pericarditis- Friction rub, chest painSubcutaneous nodulesErythema marginatum (annular, non-pruritic rash with erythematous borders- trunk, limbs)Sydenham chorea (rapid, involuntary mm movement)
88
Q

What are the characteristic cells seen in the myocardial during acute rheumatic fever?

A

ASCHOFF BODIES which contains

-Foci of chronic inflammation
-Anitschkow cells (reactive HISTIOCYTE with slender, wavy nuclei:
“caterpillar nuclei”
-Giant cells
-Fibrinoid material

89
Q

What is the mechanism of myocytes damage in Chronic ischemic Heart Disease?

How does CIHD lead to dilated cardiomyopathy and CHF?

A

Repeated ischemic episodes leads to the replacement of contractile cardiac muscle into non-contractile fibrous tissue

The progressive replacement of cardiac tissues and buildup of fibrous tissue weakens the heart and makes it dilated. A dilated heart cannot pump effectively—CHF

90
Q

How does CIHD lead to stable angina

A

Repeated infarction—release of inflammatory factors—platelets aggregation—thrombosis of vessel lumen—fixed coronary stenosis

91
Q

Why do patients with CIHD show hibernating myocardium?

What are the Management goals for a hibernating myocardium?

A
  1. Hibernating myocardium has reduced contractile to due to poor perfusion but remains viable. May recover with revascularization. (Persistent myocardial dysfunction due to chronic ischemia)
  2. Reduce myocardial oxygen demand (beta blockers)
    Restore myocardial blood flow- coronary artery bypass grafting
92
Q

What is a stunned myocardium?

A

TRANSIENT myocardial dysfunction after blood flow is restored following short term ischemia.

Manifests as prolonged wall motion abnormalities days to weeks after short term ischemic attack. Resolves spontaneously

93
Q

How many days post-MI does acute Fibrinous pericarditis occur?

What are the 3 most commonly associated symptoms associated with pericarditis?

A

1-3 days post (transmural) infarct due to underlying myocardial inflammation

  1. Precordial pain that is relieved by leaning forwards and is exacerbated by leaning backwards
  2. Pericardial friction rub
  3. ST segment elevation and PR segment depression in ECG
94
Q

A complication of MI is ventricular aneurysm and ventricular pseudo-aneurysm.

Differentiate between the 2

A

Left ventricular pseudo-aneurysm is a complication of MI where myocardial rupture is contains within the pericardium or granulation tissue in contrast to a true ventricular aneurysm which aneurysm is contained within the walls of the myocardium.

95
Q

Give 4 sequelae of ventricular pseudo-aneurysm

How many days post MI are patents prone to pseudo-aneurysm formation and rupture?

A
  1. Rupture & hemorrhage
  2. Emboli formation
  3. Arrhythmias
  4. Cardiogenic shock

3-14 days (just memorize ;(

96
Q

How many weeks post STEMI does VENTRICULAR ANEURYSM develop?

A

2 weeks- months status-post large transmural MI w/ early infarct expansion

97
Q

What is the difference between infarct expansion and infarct extension?

A

Are 2 complications occurring in the early infarct period that can significant increase the functional infarct size.

INFARCT EXTENSION- Increasing the mass of necrotic tissue

INFARCT EXPANSION- thinning and dilating the infarcted zone (think of the necrotic tissue as a rubber band which expands to thin out and dilate the infarcted zone)

98
Q

Give 3 sequelae of ventricular aneurysm

A
  1. Arrhythmia (due to stretching and dysfunction of conducting tissues)
  2. Cardiogenic shock (due to progressive inability of the heart to pump efficiently and effectively)
  3. Thromboembolism (due to stasis of blood in site of aneurysm)
99
Q

What is the name of the paradoxic systolic out-bulging which can be palpated on the chest well in patients in ventricular aneurysm?

A

SYSTOLIC BULGE

100
Q

Are VENTRICULAR ANEURYSMS prone to rupture?

Why? Or Why not?

A

NO

Because they are lined by scar tissue.

101
Q

In What time frame does cardiac arrhythmias typically occur after MI?

A

First few days

102
Q

What is the pathological series of events in MI

A
  1. Rupture of atherosclerotic plaque
  2. Thrombosis and occlusion of coronary artery
  3. Prolonged ischemia to cardiac tissues
  4. Infarction
103
Q

What are the common symptoms of Acute Coronary Syndrome?

A
  1. Retro-sternal pain
  2. Pain in the left arm/jaw
  3. Diaphoresis
  4. Nausea
  5. Vomiting
  6. Dyspnea
  7. Fatigue
104
Q

STEMI (ST Elevation MI)

  1. What are the ECG findings?
  2. Cardiac marker findings?
A
  1. Persistent ST segment elevation (>1mm in 2 contiguous limb leads and >2mm in 2 contiguous chest leads) or New LBBB (Left Bundle Branch Block)
  2. Increased Troponin (not required in the presence of persistent ST segment elevation)
105
Q

NSTEMI (Non-ST Elevation MI)

  1. What are the ECG findings?
  2. Cardiac marker findings?
A
  1. No ST segment elevation (ECG may be normal or show minor changes)
  2. Increased Troponin- indicating onset of 24 hrs
106
Q

Pathologic Q waves are indicative of what?

Give 4 requirements of a given Q wave to classify it as pathologic

A
  1. An old transmural infarct
  2. > 1mm (40ms) wide
    2mm deep
    Found in V1-V3
    25% of QRS complex
107
Q

Which other test apart from Troponin I and CK-MB can be used to diagnose MI

What is its advantage
What is its disadvantage?

A
  1. Serum myoglobulin
  2. Arises very quickly after an MI before Troponin and CK-MB
    Has a high negative predictive value if tested hours after an
    MI. (If serum myoglobulin is not elevated during this period,
    MI is unlikely)
  3. It has low specificity (but high sensitivity)
108
Q

What is the non-specific enzyme found in the liver, heart and skeletal muscle

A

AST (Aspartate transaminase)

109
Q

What are the 5 most common congenital anomalies presenting with R-L (5 Ts)

A
  1. Truncus arteriosus
  2. Transposition of the great arteries
  3. Tricuspid atresia (w/ RA-LA shunt)
  4. Tetralogy of fallot
  5. Total Anomalous Pulmonary Venous Return (TAPVR)
110
Q

What increases or decreases degree of shunting in patients with R-L shunt?

A

INCREASES SHUNT
1. Hypo ventilation

  1. Hypoxia
    These processes increased pulmonary artery resistance (due to decreased O2 leading to vasoconstriction of the P. Vessels)
  2. Crying

DECREASES SHUNT

  1. Hypotension
  2. Histamine release
  3. Sepsis
111
Q

What is the most common cyanotic congenital heart disease that presents in the neonatal period?

How does it present?

What is heard on auscultation?

What’s seen on X-ray?

What is the most common cyanotic congenital heart disease that presents after the neonatal period?

A
  1. Transposition of the great arteries
  2. Presents as cyanosis within the 24 hours and not relieved by supplemental oxygen
  3. Single S2 is heard on auscultation.
  4. Eggs on a strong appearance
  5. Tetralogy of fallot
112
Q
  1. What is Chronic Rheumatic Heart Disease?
  2. What is the general gross abnormality seen in CRHD?
  3. What is the gross valvular abnormality seen in ARHD?
  4. Which heart valve is most commonly involved in CRHD?
  5. Which valve is most commonly involved in heart disease due to wear and tear?
  6. What is the gross abnormality if the mitral valve is involved?
  7. What is the gross abnormality if the aortic valve is involved?
A
  1. VALVE SCARRING as a consequence of rheumatic fever
  2. Mitral stenosis with fish mouth appearance of the valves
  3. Mitral regurgitation
  4. Mitral valve
  5. Aortic valve
  6. Mitral stenosis+ thickening of the chordae tending and cusps
  7. Aortic stenosis as a result of fusion of the commissures.
113
Q

What is the major complication of CRHD?

A

Infectious endocarditis

114
Q

Give 2 causes of Aortic stenosis

What is a RF in the development of non-pathologic aortic stenosis?

A
  1. Normal wear and tear in aging population (>60y)
  2. CRHD

BICUSPIC aortic valve.

115
Q

What is the characteristic murmur heard in Aortic stenosis and why?

A
  1. Systolic ejection click + Crescendo-decrescendo murmur

Systolic click and a result of the extra force that the LV uses to push the “stiffened and stenotic” aortic valve open.

Crescendo-decrescendo: increases pressure as blood flows through the stenosed aortic valve followed by gradually decreased in pressure

116
Q

Give 3 complications of aortic stenosis

A
  1. Concentric LV hypertrophy
  2. Angina, syncope w/exercise
  3. Microangiopathic hemolytic anemia
117
Q

What is the treatment of aortic stenosis?

A

Valve replacement after the onset of complications

118
Q

Give 2 causes of aortic regurgitation

A
  1. Aortic root dilatation (syphilitic aneurysm, aortic dissection)
  2. Valve damage (infective endocarditis)- most common cause of isolated aortic root dilation
119
Q

What is the murmur heard in aortic regurgitation?

A

Early diastolic blowing murmur

120
Q

What are the clinical manifestations of aortic regurgitation?

A
  1. Hyper-dynamic circulation due to increased pulse pressure
    Increased systolic pressure (in the aorta and other blood vessels) as more blood is pumped per beat
    Decreased diastolic pressure(in the aorta) due to regurgitation of blood
  2. Bounding pulse (water hammer pulse)
  3. Quincke pulse (pulsating nail bed)
  4. Head bobbing
121
Q
  1. What is Mitral valve prolapse (MVP)?
  2. What causes MVP?
  3. In which genetic conditions is MVP likely to occur?
  4. Is this condition symptomatic or asymptomatic?
A
  1. Ballooning of the mitral valve into the LA during systole
  2. Myxoid degeneration of the valve which makes it floppy
  3. Ehler-Danlos syndrome, Marfan syndrome
  4. Asymptomatic
122
Q

What is the murmur heard in MVP?

Explain why thus murmur is heard

A

MID-SYSTOLIC CLICK followed by REGURGITATION MURMUR

Mid-systolic click due to sudden ballooning of the mitral valve into the LA in mid-systole as a result on increasing LV systolic pressure which the degenerated valve leaflet can no longer accommodate.

123
Q

Give 3 complications of MVP?

How common are these complications?

A
  1. Infective endocarditis
  2. Arrhythmias (due to stretching of the wall of the heart and disturbances in conducting tissues)
  3. Mitral regurgitation

Complications are rare

124
Q

What is mitral regurgitation?

Give causes of mitral regurgitation

A

Reflux of blood from the LV-LA during systole

  1. MVP- a usual predisposing factor
  2. LV dilatation
  3. Papillary rupture after MI
  4. Infective endocarditis
  5. ARHD
125
Q

What is the characteristic murmur of mitral regurgitation?

What increases the intensity of this murmur?

A
  1. Holosystolic “blowing” murmur
  2. Which increases with
    - squatting (increased systemic resistance therefore LV has to generate more force to eject blood thus increasing intensity of murmur)
    - Expiration (increased return to LA thus LV which increases systolic blood volume hence intensity of murmur)
126
Q

Give complications of mitral regurgitation

A

Left sided HF due to volume overload

127
Q

Give 2 differences between MVP and mitral regurgitation

A
  1. MVP is caused by ballooning of valve leaflet(s) into the LA during mid-systole as a complication of myxoid degeneration of the valve
    Mitral Regurgitation is caused by a reflux of blood from the LV-LA throughout systole
  2. The murmur of MVP is a mid-systolic click followed by a regurgitation murmur while the murmur of Mitral Regurgitation is a holosystolic (blowing) murmur
128
Q

What causes mitral stenosis?

A

Chronic Rheumatic Heart Disease

129
Q

What is the murmur of mitral stenosis?

What is responsible for its characteristic sound?

A

Opening snap followed by diastolic rumble

Opening snap is as a result of force generated by the LA to force blood through a stenosed mitral valve
Diastolic rumble is the sound heard from LV filling as blood squeezes through the stenosed mitral valve

130
Q

Give Complications of mitral stenosis due to LA dilatation and blood overload

A

Pulmonary congestion and alveolar hemorrhage

Pulmonary HPN and right-sided HF

LA dilatation–blood stasis–mural thrombi formation

Atrial fibrillation as a result of LA dilatation

131
Q

What is the most common cause of endocarditis?

Where is it commonly found?

A

Strep viridans

Mouth

132
Q

What type of endocarditis does does strep viridans cause?

Is this organism high virulence and low virulence?

What kinda of valves does this agent attach to?

Does it cause large or small vegetations in the valve?

A

Subacute endocarditis endocarditis-small vegetations that do not destroy the valve

Low virulence

Previously damaged valves (CHRD, MVP)

Small vegetations

133
Q

Why are previously damaged valves at risk for bacterial infection

A

Damage if valves released tissue factor and collagen which attracts platelets (forming thrombotic vegetations).

Transient bacteremia leads to trapping of bacteria in the vegetations

134
Q

What is the most common cause of endocarditis in IV drug users?

Is it a high virulence or low virulence organism?

A

Staph aureus

High virulence

135
Q

What valve is most commonly affected in endocarditis in IV drug users?

A

Tricuspid valve

136
Q

What kind of endocarditis is seen in IV drug users?

A

Acute endocarditis which damages the valve

137
Q

Which organism is associated with endocarditis of prosthetic valves?

Does it involve large or small vegetations?

A

Staphylococcus epidermidis

Large vegetations

138
Q

Give 2 organisms tart are responsible for endocarditis in patients with underlying colorectal (disease)cancer or ulcerative colitis

A
  1. Enterococcus faecalis

2. Strep bovis

139
Q

Which 5 organisms are associated with endocarditis of prosthetic valves?

A

HACEK organisms

Haemophilus
Actinobacillus
Cardiogaterium
Eikenella
Kingella
140
Q

Give 6 clinical manifestations of bacterial endocardial

A
  1. Fever
  2. Murmur
  3. Janeway lesions (painless erythematous lesions in palms and soles)
  4. Splinter hemorrhages (due to embolization of septic vegetations)
  5. Osler nodes (tender lesions on the fingers and toes)
  6. Anemia of Chronic inflammation
141
Q

What are the lab findings in endocarditis?

A
    • blood cultures
  2. Anemia of chronic diseases ( low Hb, low Fe, reduced MCV, increased ferritin, increased TIBC, decreased iron saturation)
142
Q

What diagnostic modality is used toto diagnose lesions in valves?

A

Transesophageal echocardiogram

143
Q

Which disease is associated with Libman-Sacks endocarditis

Is it sterile or unsterile?

What valve does it commonly grow on? And what complication of the valve does it cause?

A

SLE

Sterile

Mitral valve (present on the surface and undersurface of they valve) and results in mitral regurgitation.

144
Q

What is non-bacterial thrombotic endocarditis (NBTE)

Which valve does it most commonly affect
what specific part of the valve
what valvular complication does it cause?

A

Sterile vegetations that arise due to a hypercoagulable state or adenocarcinoma.

Mitral valve
Along the lines of closures.
results in mitral regurgitation

145
Q

What is dilated cardiomyopathy?

Does this result in systolic or diastolic dysfunction?

What kind of CHF does it cause?

A

Dilation of all four chambers of the heart

Systolic dysfunction due to inability of the ventricles to pump.

Biventricular CHD

146
Q

What are the complications of dilated cardiomyopathy

A

Valvular regurgitation (due to stretching of the heart and thus the valves always from each other)

Arrhythmias (due to stretching and damage to the conduction tissues)

147
Q

What are the most common causes of dilated cardiomyopathy?

What is the mnemonic involved?

A
  1. Idiopathic
  2. Genetic (autosomal dominant)
  3. Alcohol (alcohol and it’s acetaldehyde metabolites directly affects the heart)
  4. Myocarditis (due to coxsackie A/B) characterized by lymphocytic infiltration in the myocardium. Dilated cardiomyopathy is a late complication. Presents wity chest pain, arrhythmia, sudden death, HF
  5. Doxorubicin
  6. Pregnancy (late pregnancy or months after childbirth)
ABCCCCDDE
Alcohol 
wet Beriberi
Chagas' disease 
Coxsackie A&amp;B 
peri-partum Cardiomyopathy

Doxorubicin, Daunorubicin
hEmochromatosis

148
Q

What is the treatment for dilated cardiomyopathy?

A

Heart transplant.

149
Q

What is hypertrophic cardiomyopathy?

A

Massive hypertrophy of the left ventricle which leads to its hypercontractility and non-compliance

150
Q

What causes hypertrophic cardiomyopathy?

What gene is affected in hypertrophic cardiomyopathy?

What are the proteins encoded by these mutated genes?

Is this a systolic or diastolic disease?

A

Usually due to genetic mutation in sarcomere proteins- AUTOSOMAL DOMINANT

Structural elements of myocardial sarcomeres

a. Beta-myosin heavy chain
b. Myosin-binding protein C

Diastolic disease (as the ventricles cannot fill during diastole)

151
Q

What disease is associated with sudden cardiac death in athletes?

Why?

A

Hypertrophic cardiomyopathy

Ventricular fibrillation secondary to hypertrophic cardiomyopathy

152
Q

What are the clinical features of hypertrophic cardiomyopathy?

A
  1. Decreased cardiac output
  2. Sudden cardiac death
  3. Syncope with exercise
153
Q

What causes aortic stenosis-like syndrome in hypertrophic cardiomyopathy?

What is the characteristic of the murmur?

Where is this murmur found?

A

Subaortic hypertrophy of the ventricular septum.

Harsh systolic ejection murmur accompanied by a palpable thrill

Found at the left lower sternal border.

154
Q

What does biopsy show in hypertrophic cardiomyopathy

A

Myofiber hypertrophy with disarray

155
Q

The most commonly associated gene in dilated cardiomyopathy is?

The most common mutation X-linked dilated cardiomyopathy is?

A

TTN which encodes protein TITIN

Dystrophin

156
Q

What are the clinical findings seen in dilated cardiomyopathy?

A
  1. Low pulse pressure (If the heart is dilated and not pumping properly, there will be very little difference between the systolic and diastolic pressure in the aorta)
  2. Systolic regurgitation murmur (dilated heart, valves drawn farther apart)
  3. S3 heart sound due to increased diastolic filling (of regurgitated blood from LA)
157
Q

What is the ultrasound findings of a dilated cardiomyopathy?

What is the x-Ray finding of a dilated cardiomyopathy?

A
  1. Global cardiac enlargement

2. Balloon appearance of the Heart

158
Q

What is takosubo cardiomyopathy?

A

Transient LV dysfunction as a result of increased catecholamines as a result of increased physical/emotional stress

159
Q

What is the characteristic echocardiogram result in takotsubo cardiomyopathy?

A

Apical ballooning of the LV

160
Q

What is the medical treatment for takotsubo cardiomyopathy?

A

ACE inhibitors
Diuretics
Beta blockers
Digoxin

161
Q

What is the value of the ejection fraction in hypertrophic cardiomyopathy?

A

Normal. (Both systolic and diastolic pressures are both reduced significantly)

Cardiovascular system (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions