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Path > CHF, Congenital Heart Disease, IHD, Cardiomyopathies, Myocarditis > Flashcards

CHF, Congenital Heart Disease, IHD, Cardiomyopathies, Myocarditis Flashcards

1
Q

CHF is…

A

the failure of the heart to pump an adequate amount of blood to supply the metabolic requirements of the organs

Comes from blood backing up (congesting) the liver, abdomen, lower extremities, and lungs

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2
Q

CHF may be due to pathologic conditions….

A

inside (directly related) or outside (peripheral problems like hypertension) to the heart

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3
Q

3 compensatory mechanisms for CHF

A
  1. Myocardial hypertrophy
  2. Ventricular dilation
  3. physiologic mechanisms (inc HR, intravascular volume, and catecholamines (E and NE), along with redistribution of BF,
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4
Q

What is myocardial hypertrophy

A
  • a compensatory mechanism for CHF
  • it’s a thickening of the heart muscle (myocardium) which results in a decrease in size of the chamber of the heart, including the left and right ventricles.
  • it helps initially, but the larger muscle fibers require more oxygen from the capillaries, which typically is not available
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5
Q

Etiology or the cause of CHF

A

ischemic heart disease
hypertension
myocarditis - inflammation of the heart (usually a virus)
cardiomyopathy - heart muscle damage
valvular disease - a damaged valve causes heart to work harder to keep blood flowing as it should

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6
Q

Manifestations of CHF are:

A
  1. Right ventricular failure - liver, lungs, feet, ankles
  2. Left ventricular failure - pulmonary edema
  3. left and/or right ventricular failure
  4. CHF due to left ventricular failure eventually leading to right ventricular failure
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7
Q

What does right ventricular failure look like and where does it occur?

A
  • congestion of the LIVER (a “nutmeg” pattern) and SPLEEN

- edema of the FEET and ANKLES

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8
Q

What does left ventricular failure cause?

A

pulmonary edema - abnormal buildup of fluid in the lungs

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9
Q

Left and/or right ventricular failure can cause..

A

cerebral hypoxia - not enough O2 to brain

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10
Q

What can cause congenital heart disease?

A

chromosomal anomalies or environmental factors

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11
Q

Congenital heart disease affects how many births in the US out of 1000?

A

6-8

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12
Q

Congenital heart disease is divided into:

A

cyanotic and noncyanotic forms

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13
Q

Examples of noncyanotic congenital heart disease:

A
  1. Atrial septal defect - doesnt allow shunting between atria
  2. Ventricular septal defect - doesnt allow shunting between Vs
  3. Patent/Open ductus arteriosus - this should (but doesnt) close within a few days of birth and connects the aorta to the pulmonary artery (bypasses the lungs)
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14
Q

Examples of cyanotic congenital heart disease

A

Tetralogy of Fallout (low O2 levels in blood):
1. ventricular septal defect (VSD) - hole between R/L Vs
2. narrowing of R ventricular outflow
3. overriding of the aorta over VSD
4. R ventricular hypertrophy - thickened wall of RV
Transposition of great arteries
-RV empties into aorta and LV into pulmonary artery

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15
Q

Ischemic heart Disease (IHD) is..

A

imbalance between the hearts blood supply and the hearts o2 demand (ischemia)

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16
Q

What’s the leading cause of death in the US?

A

Ischemic heart disease –> 500,000/year

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17
Q

Pathology of IHD

A
  1. narrowing of coronary arteries (usually at least 75%) by atherosclerosis –> gradual narrowing may lead to opening of collateral arteries (90% of IHD is due to coronary artery atherosclerosis)
  2. coronary artery thrombosis initiated by fissure in the fibrous cap of an atherosclerotic plaque
  3. increased myocardial oxygen demand (hypertension), diminished blood volume (hypotension/shock), reduced oxygenation (pneumonia, CHF), reduced oxygen carrying capacity (anemia)
18
Q

4 types of IHD

A
  1. Angina pectoris
  2. acute MI
  3. Chronic IHD with CHF
  4. Sudden cardiac death
19
Q

Describe stable angina

A

“chest pain” of several minutes duration usually associated with exercise or emotional stress and relieved by rest

-No myocardial necrosis occurs

20
Q

Describe unstable angina

A

episodes of chest pain become more frequent and the pain becomes more severe

-this usually precedes MI

21
Q

What causes acute myocardial infarction?

A

necrosis of cardiac muscle caused by ischemia

-usually follows unstable angina

22
Q

Clinical presentation of MI

A 
chest pain
shortness of breath
nausea/vomitting
diaphoresis - non-stop sweating
low-grade fever
23
Q

What kind of test is done in regards to MI?

What does the test look at?

A

EKG

Test looks to see if there is elevation of serum enzymes (CREATINE KINASE) and TROPONIN derived from necrotic myocytes

24
Q

Describe the pathology of MI

A 
coagulation occurs (few hours)
neutrophil infiltration (few days)
granulation tissue (1 week)
scar formation (weeks-months)
25
Q

What are some treatments done to mediate MI and what do you need to be worried about from the treatments?

A

Placement of stents to open the coronary arteries clogged by the atherosclerotic plaques
Coronary artery by-pass grafts
Clot-busting drugs such as tissue plasminogen activator (TPA)

Reperfusion injury is a risk of these treatments (tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of oxygen

26
Q

What is reperfusion injury and when could it occur?

A

a risk of these treatments (tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of oxygen

when treating MI

27
Q

List complications that can come from MI (7)

A 
arrhythmia and sudden death
CHF/shock
mural thrombus/emboli
myocardial rupture
mitral valve regurgitation
ventricular aneurysm
chronic ischemic heart disease
28
Q

what condition is it when you have progressive cardiac decompensation following acute MI? It can also be secondary to smaller ischemic events, with an eventual mechanical pump

A

chronic IHD with CHF

29
Q

T of F: sudden cardiac death may occur in individuals with or without a previous history of IHD?

A

True

30
Q

Describe sudden cardiac death

A

sudden onset of ischemia-induced cardiac arrythmia (improper beating of the heart) with or without myocardial necrosis/infarction

31
Q

What kind of classification of cardiomyopathy is described when the heart is involved as part of a multi-system disorder?

A

Secondary cardiomyopathy

32
Q

What kind of classification of cardiomyopathy is described when the disease is solely or predominately confined to the heart muscle?

A

Primary cardiomyopathy

33
Q

3 morphologic patterns of cardiomyopathy

A

dilated - all 4 heart chambers
hypertrophic
restrictive

34
Q

How can dilated cardiomyopathy come about?

A
  • primary or secondarily
  • genetic (20-50% of cases)
  • or acquired
35
Q

What is associated with dilated cardiomyopathy?

A

poor ventricular contractility (systolic dysfunction)

36
Q

How can hypertrophic cardiomyopathy come about?

A 
primarily
genetic (inherited as autosomal dominant with variable expression)
37
Q

What is hypertrophic cardiomyopathy?

A

a disorder of sarcomeric proteins (myosin, myosin binding protein C, troponin T)

38
Q

What occurs during spontaneous myocardial hypertrophy?

A

This is under the hypertrophic cardiomyopathy

asymmetric hypertrophy is greater in the interventricular septum than the left ventricular free wall and oftern obstructs the LV outflow tract

39
Q

What is restrictive cardiomyopathy?

A

a decrease in ventricular compliance (wall is stiffer), resulting in impaired ventricular filling during diastole

40
Q

What is the most common cause of myocarditis (inflammation involving the myocardium) in the US?

A

viral infection
(it can also be caused by bacteria, fungus, and parasites)

-non-infectious causes include toxins, hypersensitivity reactions and auto-immune disorders

41
Q

Pathology of myocarditis? List a common cause of myocarditis and then what this can cause

A
  • viral infection produces a lymphocytic infiltrate with foci of necrosis
  • pyogenic bacteria causes abscesses
  • parasites infect individual myocytes or are in interstitial areas with surrounding inflammatory cells
  • hypersensitivity (usually to drugs) causes a perivascular inflammatory infiltrate with many eosinophils

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