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Block 9; Week 1 & 2-M > Cardiovascular-Fung > Flashcards

Cardiovascular-Fung Flashcards

1
Q

How much does a female heart weigh? Male heart weight?

A

Female heart: 250-300 grams

Male heart: 300-350 grams

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2
Q

What is the vascular wall thickness of the right atrium & left atrium?

A

RA: 0.3-0.5 cm
LA: 1.3-1.5 cm

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3
Q

What are the 3 layers of cardiac tissue?

A

intima: endocardium w/ endocardial cells
media: cardiac myocytes w/ centrally located nuclei & striations
adventita: epicardium

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4
Q

What is the main distinguishing feature b/w cardiac muscle & skeletal muscle on histo?

A

cardiac: has intercalated discs & centrally located nuclei
skeletal: has peripherally located nuclei

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5
Q

What causes the striations in muscle?

A

myosin & actin
myosin-heavy chains
actin-light chains

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6
Q

Which valves have leaflets & chordae tendinae attached? Which side of the heart?

A

Tricuspid valve–right side
bicuspid valve-left side
the cuspids are the leaflets…

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7
Q

The chordae tendiae that attach to the tricuspid & bicuspid valves attach to what structure?

A

papillary muscles in the ventricular wall

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8
Q

T/F Semilunar valves have chordae tendinae which attach them to the ventricular wall of the heart.

A

False. Only the tricuspid & bicuspid valves.

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9
Q

Which are the semilunar valves?

A

aortic & pulmonic

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10
Q

Briefly describe the coronary arteries supplying the heart.

A

L has a short main branch & then divides into L circumflex & L anterior descending
R takes longer to branch

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11
Q

Where do the L & R coronary arteries pop off from?

A

the aorta!

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12
Q

What is the function of the endothelial cells in blood vessels?

A 
Maintain non-thrombogenic blood-tissue interface
Modulate vascular resistance
Metabolize hormones
Regulate inflammation
Regulate cell growth
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13
Q

What is the fcn of smooth muscle cells in blood vessels?

A 
Proliferate when stimulated
Synthesize
Collagen
Elastin
Proteoglycans
Growth factors
Cytokines
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14
Q

What is the ECM of blood vessels composed of?

A

elastin
collagen
glycosaminoglycan

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15
Q

Describe the structure of veins v. arteries.

A

arteries:
intima-endothelial lining
media-thick b/c they need to handle blood at high pressure-lots of smooth muscle!
adventitia-contains vaso vasorum to deliver nutrients to bv
veins:
same except media thinner

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16
Q

What are the main types of arteries?

A

Elastic artery–common carotid, aorta etc. Need recoil & resistance–lots of elastin
Muscular artery-radial artery etc. not as much elastin
Arteriole

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17
Q

Where does gas & nutrient exchange occur?

A

at the level of the capillaries…

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18
Q

Although muscular arteries have less elastin than elastic ones, they still have some in strategic places. Describe.

A

found in the internal & external elastic lamina

external elastic lamina separates the media from the adventitia

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19
Q

What is the vascular system besides the blood system?

A

the lymphatic system
uses skeletal muscle as its pump
includes lymph nodes
returns extra fluid to the cardiovascular system

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20
Q

How do veins get blood to move?

A

thru contraction of skeletal muscle

one-way valves prevent backflow

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21
Q

What are 6 mechanisms of dysfunction seen in cardiovascular disease?

A

Failure of the pump (heart)
Obstruction to flow
Regurgitant flow (regurgitant valve)
Shunted flow
Disorders of cardiac conduction (bundle branch blocks)
Rupture of the heart or a major blood vessel

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22
Q

What would be some ways to get failure of the pump?

A

MI

cardiac hypertrophy

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23
Q

What would be some ways to get obstruction of flow?

A

stenosis of a valve

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24
Q

What would be a way to get shunted flow?

A

congenital heart disease

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25
Q

How might you get a rupture of the heart or a major blood vessel?

A

aortic dissection

massive MI

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26
Q

What is the stereotypical response of cardiovascular disease?

A

intimal thickening after injury
smooth muscle cell recruitment to intima
macrophages & T cells get in there
deposition of matrix intima

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27
Q

What is the role of the kidney in HTN?

A

juxtaglomerular apparatus senses blood volume
if it senses it is too low–>will release renin
renin ultimately leads to increased BP via increased blood volume via increased sodium reabsorption

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28
Q

What exactly does renin do?

A

converts angiotensinogen to angiotensin I
in the lungs & other places w/ ACE, Ang I is converted to Ang II.
Ang II causes vasoconstriction.
Ang II also goes to the adrenal glands & causes the secretion of aldosterone.
THis prompts the reabsorption of sodium. Therefore, blood volume increases.

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29
Q

What happens if you get volume overload & your BP is too high?

A

get atrial natriuretic peptide released from the heart.
This causes the excretion of sodium & water.
also causes vasodilation.

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30
Q

What is considered a normal BP?

A

less than 120/80

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31
Q

What is considered pre-HTN?

A

over 120/80

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32
Q

What is considered HTN?

A

over 140/90

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33
Q

What is considered malignant HTN?

A

200/120 & above

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34
Q

What is essential HTN?

A

HTN w/ a primary identifiable cause.

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35
Q

What are some genetic causes of essential HTN?

A

gene defects of aldosterone metabolism

defects of sodium reabsorption

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36
Q

What are some polymorphisms that can cause essential HTN?

A

at the loci of…
angiotensin
angiotensin receptor
RAAS

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37
Q

What are some vascular causes of essential HTN?

A

vasoconstriction

structural changes

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38
Q

What are some environmental factors that can cause essential HTN?

A 
Diet
Stress
Obesity
Smoking
Physical inactivity
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39
Q

What is secondary hypertension?

A

HTN that is secondary to some disease process

Happens only 5-10% of the time

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40
Q

What are some renal causes of secondary HTN?

A 
Acute glomerulonephritis
Chronic renal disease
Polycystic disease
Renal artery stenosis
Renal vasculitis
Renin-producing tumors
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41
Q

What are some endocrine causes of secondary HTN?

A 
Adrenocortical dysfunction
Exogenous hormones
Pheochromocytoma
Acromegaly
Hypothyroidism
Hyperthyroidism
Pregnancy-induced
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42
Q

What are some cardiovascular causes of secondary HTN?

A 
Coarctation of aorta
Polyarteritis nodosa
Increased intravascular volume
Increased cardiac output
Rigidity of aorta
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43
Q

What are some neurologic causes of secondary HTN?

A

Psychogenic
Increased intracranial pressure
Sleep apnea
Acute stress

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44
Q

When would you see hyaline arteriolosclerosis? What would you see?

A

benign essential HTN
see: Eosinophilic deposition around the arterioles in the kidney. Kidney would look blown up. Kidney would have a rough outer surface b/c of the hyaline arteriosclerosis.

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45
Q

When would you see hyperplastic arteriolosclerosis? What would you see?

A

malignant HTN
proliferation of the smooth muscle cells around the arterioles of the kidney.
more smooth muscle cells in the media
see hemorrhages along the outside of the kidney

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46
Q

What is an atheroma? What are its 3 main parts?

A

raised lesions w/ a soft, yellow core of lipid covered with a fibrous cap

  1. media
  2. necrotic center
  3. fibrous cap
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47
Q

What are 3 negative consequences of atheromas in the lumen of a blood vessel?

A
  1. obstruct blood flow-stenosis
  2. rupture & cause vessel thrombosis
  3. lead to aneurysm formation
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48
Q

What is found in the necrotic center of an atheroma?

A

cell debris
cholesterol crystals
foam cells
calcium

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49
Q

What is found in the center of a fibrous cap?

A 
smooth muscle cells
macrophages
foam cells
lymphocytes
collagen
elastin
proteoglycans
neovascularization
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50
Q

What are some constitutional risk factors for the development of atherosclerosis?

A
  1. age
  2. genetics
  3. gender
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51
Q

What are some modifiable risk factors for the development of atherosclerosis?

A
  1. Hyperlipidemia
  2. HTN
  3. Cigarette Smoking
  4. Diabetes
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52
Q

What are some other risk factors for the development of atherosclerosis?

A 
Inflammation
Hyperhomocystinemia
Metabolic syndrome
Lipoprotein a
Hemostatic factors
Sedentary life style
Type A personality
Obesity
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53
Q

What is the response to injury hypothesis for atherosclerosis?

A

atherosclerosis is a chronic inflammatory and healing response to arterial wall and endothelial injury

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54
Q

What are some of the pathological events leading to atherosclerosis?

A 
Endothelial injury
Lipoprotein accumulation
monocyte adhesion
Formation of foam cells
platelet adhesion
smooth muscle cell recruitment
smooth muscle cell proliferation & ECM production
lipid accumulation
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55
Q

SO…the first step in atherosclerosis is endothelial injury. What are some possible causes of injury?

A

Mechanical denudation
Immune complex deposition
Irradiation
Chemicals

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56
Q

What are some possible causes of endothelial dysfunction?

A 
Hemodynamic disturbances
Hypercholesterolemia
Hypertension
Smoking
Infectious agents
Homocysteine
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57
Q

What are hemodynamic disturbances? How do they contribute to the formation of endothelial dysfunction and atherosclerosis?

A

principle of plaques being deposited at areas of disturbed blood flow, like branch points and ostia of exiting vessels
ALSO the posterior wall of the abdominal aorta

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58
Q

What is a protective hemodynamic factor against atherosclerosis?

A

non-turbulent laminar flow

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59
Q

What are the dominant lipids found in plaques?

A

cholesterols & cholesterol esters

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60
Q

What are 2 conditions that predispose to hyperlipidemia, and therefore increased risk of atherosclerosis?

A

diabetes type II

hypothyroidism

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61
Q

HOw do lipids lead to atherosclerosis?

A
  1. lipids increase oxygen free radical formation–which decrease NO & the ability of a bv to vasodilate.
  2. oxygen free radicals make LDL oxidized. THis is eaten by macrophages=foam cells.
  3. Oxidized LDL increases release of growth factors, cytokines, chemokines–more monocytes!
  4. Oxidized LDL causes endothelial dysfunction (also bad for smooth muscle cells).
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62
Q

What does it take to convert a fatty streak into a mature atheroma?

A

smooth muscle cell proliferation & extracellular matrix synthesis.
promoted by chemokines & growth factors

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63
Q

What are 4 serious possible consequences of atherosclerosis?

A
  1. MI
  2. Cerebral infarction
  3. aortic aneurysm
  4. peripheral vascular disease
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64
Q

HOw can atherosclerosis lead to an aortic aneurysm?

A

with the atheroma formation, increased distance is created b/w the lumen where the nutrients are & the media…necrosis ensues with time
the medial wall gets thinner
rupture becomes possible-aneurysm formation.
called cystic medial degeneration

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65
Q

T/F Females’ estrogen levels are protective for a time against atherosclerosis.

A

True. The process is delayed longer. More common in men, therefore.

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66
Q

How does peripheral vascular disease from atherosclerosis present?

A

patients will get pain when they walk b/c their legs don’t get enough oxygen

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67
Q

When has atherosclerosis accomplished stenosis of a blood vessel?

A

Critical stenosis when the blood vessel is 70% occluded from the atheroma.

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68
Q

What are some possible negative consequences that result from chronic decreased perfusion ?

A

Bowel ischemia
Chronic Ischemic Heart Disease
Ischemic encephalopathy
Intermittent claudication

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69
Q

What is an acute plaque change?

A

Rupture or fissure exposing highly thombogenic plaque contents
Erosion or ulceration exposing the thrombogenic subendothelial basement membrane to blood
Hemorrhage into the atheroma

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70
Q

What is the process of atherosclerosis at the preclinical stage? What age group does this usu occur in?

A

usu younger people

  1. normal artery
  2. fatty streak
  3. fibrofatty plaque
  4. advanced/vulnerable plaque
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71
Q

In which step of atherosclerosis formation does the organization of a thrombus & calcification occur?

A

b/w fibrofatty plaque & advanced vulnerable plaque

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72
Q

What are some possible outcomes at the clinical stage once you have an advanced vulnerable plaque? Which age group does this occur in?

A
  1. Aneurysm & Rupture
  2. Occlusion by Thrombus
  3. Critical STenosis
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73
Q

What is ischemic heart disease? What is it also known as?

A

syndromes involving myocardial ischemia

aka coronary artery disease

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74
Q

What is myocardial ischemia?

A

Myocardial ischemia is an imbalance between the supply and demand of the heart for oxygenated blood

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75
Q

What are some things that can cause ischemic heart disease?

A

> 90% blockage of coronary arteries with plaque
coronary emboli
blockage of coronary arteries
severe hypotension

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76
Q

What are some of the symptoms of IHD?

A

Tachycardia
Myocardial hypertrophy
Hypoxemia

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77
Q

What are some acute coronary syndromes that fall within ischemic heart disease?

A

Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death

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78
Q

What is angina pectoris? WHat are its 3 variants?

A

Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis
Variants:
Stable
Prinzmetal
Unstable

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79
Q

What is stable angina? What provokes & alleviates the symptoms?

A

Caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
Physical activity, emotional excitement or increased cardiac workload
Relieved by rest or vasodilators

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80
Q

What is prinzmetal angina? What provokes and alleviates those symptoms?

A

Caused by coronary artery spasm unrelated to physical activity, heart rate or BP
Relieved by vasodilators and calcium channel blockers
COCAINE ABUSE

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81
Q

WHat is unstable angina? What can it indicate?

A

Pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest
Seen in artery occlusion of 90% or greater

Warning of impending acute MI

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82
Q

What is unstable angina caused by?

A

Acute plaque change with superimposed thrombosis/embolism

Vasospasm

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83
Q

What is an MI?

A

Death of cardiac muscle due to prolonged severe ischemia

84
Q

What is the sequence like leading up to an MI ?

A

Acute change of an atheromatous plaque exposes very thrombogenic contents
Platelets adhere to the exposed plaque and degranulate and initiate vasospasm
Tissue factor activates the coagulation cascade adding to the bulk of the thrombus
Thrombus completely occludes the lumen of the vessel

85
Q

10% of MIs are caused w/o the typical coronary vascular pathology. What are some of these causes?

A 
vasospasm-cocaine, platelet aggregation
emboli
Vasculitis
Sickle cell disease
Amyloid deposition
Vascular dissection
Severe hypotension (shock)
86
Q

What are some sources of emboli that can cause MI?

A

Atrial fibrillation of left atrium
Vegetations from infective endocarditis
Left sided mural thrombus
Paradoxical right sided emboli

87
Q

WHat is reversible injury with MIs?

A

Reversible injury is ischemia lasting no more than 20-30 minutes
Cessation of aerobic metabolism within seconds
Loss of contractility within 60 seconds

88
Q

What is irreversible injury with MIs?

A

Prolonged severe ischemia leads to myocyte necrosis

Necrosis is complete within 6 hours of onset

89
Q

The morphologic features of an MI depend on which factors?

A

Location and severity of the atherosclerosis
Size of the vascular bed perfused by the obstructed vessel
Duration of the occlusion
Oxygen demands of the affected myocardium
Extent of collateral circulation
Heart rate, cardiac rhythm and O2 saturation

90
Q

What is the direction of myocardial ischemia?

A

inside outward!

starts in the endocardium

91
Q

What are 2 types of infarctions?

A

Transmural

Subendocardial

92
Q

What is a transmural infarction? What would the EKG show?

A

Necrosis involves the full thickness
Associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
ST elevation infarcts

93
Q

What is a subendocardial infarct? What would the EKG show?

A

Necrosis limited to the inner 1/3-1/2 of the ventricular wall
Due to any reduction in coronary flow: plaque disruption with lysed thrombus, global hypotension
Non-ST elevation infarcts

94
Q

WHich part of the heart does the LAD supply?

A

Apex
Anterior wall of LV
Anterior 2/3 of ventricular septum

95
Q

Which part of the heart does the right coronary artery supply?

A

Posterior 1/3 of septum (dominant)
RV free wall
Posterobasal wall of LV

96
Q

Which part of the heart does the Left Circumflex artery supply?

A

LV myocardium

97
Q

WHat are the clinical features seen in ischemic heart disease?

A

Rapid, weak pulse
Diaphoresis
Dyspnea
Asymptomatic sometimes

98
Q

Myoglobin
When do you see the rise in levels?
Peak of levels?
Other info?

A

Rise: 0-2 hours; first biomarker to rise
Peak: 6-8 hrs
found in skeletal & cardiac muscle, so not specific

99
Q 
CK-MB
When do you see the rise in levels?
Peak of levels?
Sensitive, specific?
Other info?
A 
Rises w/i 2-4 hours
Peak: 24 hours
sensitive, but not specific
CK-MB is also found in skeletal muscle
there is also CK-MM & CK-BB
100
Q

Where are CK-MM & CK-BB found?

A

CK-MM: cardiac & skeletal muscle

CK-BB: brain & lung

101
Q 
Troponin I & T
When do you see the rise in levels?
Peak of levels?
Sensitive, specific?
Other info?
A 
Rise: 2-4 hours
Peak: 48 hours
last to show up, but also longest lasting
most sensitive & specific
Levels persist for 7-10 days
102
Q

WHat is the medical treatment for an MI, ischemic heart disease?

A 
Aspirin
Heparin
Oxygen
Nitrates
Beta-adrenergic inhibitors
ACE inhibitors
Reperfusion
103
Q

WHat is involved in reperfusion? What are some different ways to do that?

A 
Rescues ischemic myocardium and limits infarct size
Thrombolysis 
Angioplasty
Stent placement
Coronary artery bypass graft (CABG)
104
Q

What are some limitations to reperfusion?

A

Rapidity of alleviating the obstruction

Extent of the correction and the underlying causal lesion

105
Q

What are some adverse complications of reperfusion?

A

Arrhythmias
Myocardial hemorrhage with contraction bands
Irreversible cell damage superimposed on the original injury (reperfusion injury)
Microvascular injury
Prolonged ischemic dysfunction (myocardial stunning)

106
Q

What are some complications involved in MI?

A 
Contractile dysfunction
Arrhythmias
Myocardial rupture
Pericarditis
Right ventricular infarction
Infarct extension
Infarct expansion
Mural thrombus
Ventricular aneurysm
Papillary muscle dysfunction
Progressive late heart failure
107
Q

What is ischemic cardiomyopathy ?

A

Progressive heart failure as a consequence of ischemic myocardial damage

Appears due to function decompensation of hypertrophied noninfarcted myocardium

108
Q

What are 2 types of arrhythmia that can result from MI? Where do these arrhythmias usu originate?

A

Asystole
Ventricular fibrillation
**Arrhythmia normally occurs at a site distant from the conduction system
Adjacent to scars of previous myocardial infarction

109
Q

What are some nonatherosclerotic conditions that can cause sudden cardiac death?

A 
Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis 
Cardiomyopathies
Pulmonary hypertension
Drug abuse (cocaine, meth)
Hereditary or acquired cardiac arrhythmias 
Long QT
Short QT
WPW
Sick sinus syndrome
Catecholamine polymorphic VT
Systemic metabolic and hemodynamic alterations
Catecholamines
110
Q

What is heart failure?

A

Heart is unable to pump blood sufficiently to meet the demands of the tissue
Heart can only pump blood sufficiently at elevated filling pressures

111
Q

What are some causes of heart failure?

A

Chronic or acute valve disease
Long standing hypertension
Ischemic heart disease with myocardial infarction
Fluid overload

112
Q

What are the 2 types of heart failure?

A

Forward Failure

Backward Failure

113
Q

What is forward failure?

A

decreased cardiac output and tissue perfusion

Left sided heart failure

114
Q

What is backward failure?

A

pooling of blood in the venous system (pulmonary and/or peripheral edema). Liver congestion
Right sided heart failure

115
Q

What are some adaptive mechanisms to deal with heart failure?

A 
Frank Starling mechanism: the more stretch by fluid, the greater contractility
Ventricular Remodeling-hypertrophy
Neurohormonal mechanisms: 
NE-HR increases
RAAS-BV & BP increases
ANP-decreases BP
116
Q

What is hypertrophy really? What are the changes involved for the myocytes?

A 
Increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size
Myocytes increase:
Protein synthesis to increase sarcomeres
Mitochondria to gain more energy
Nuclear size increases due to ploidy
117
Q

What is pressure overload hypertrophy?

A

Concentric increase in the wall thickness crazy hypertrophied LV. Usu still a normal chamber size.

Cardiac weight is increased
Sarcomeres increase in parallel to the long axes of cells

118
Q

What is volume overload hypertrophy?

A

Get dilation of the ventricle. Larger chamber. Ventricular wall thickness probably hasn’t really increased.

Cardiac weight is increased
Sarcomeres increase in series with existing cells
Ventricle wall thickness may be increased, normal or less than normal

119
Q

Why does hypertrophy eventually fail as a compensatory mechanism?

A

Eventually fails b/c there is no increase in capillaries to supply the new muscle. Do increase sarcomeres & nuclei.

120
Q

What are other reasons that hypertrophy eventually fails?

A

Change in myocardial metabolism
Alteration in intracellular handing of calcium ions
Apoptosis of myocytes
Reprogramming of gene expression

121
Q

What are the 2 types of left sided heart failure?

A

Systolic failure-Insufficient cardiac output (pump failure)

diastolic failure-Stiff ventricle that cannot expand and increase its output

122
Q

What are some causes of left sided heart failure?

A

Ischemic heart disease
Hypertension
Aortic and valvular diseases
Myocardial diseases

123
Q

What are the main problems with left sided heart failure that give rise to its main symptoms?

A

Congestion of pulmonary circulation
Stasis of blood in left chambers
Hypoperfusion of tissues

124
Q

What are the main symptoms of left sided heart failure?

A 
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
125
Q

What is another name for right sided heart failure? What are its 2 main causes?

A

Cor Pulmonale
Caused by:
Left sided heart failure
Pulmonary HTN

126
Q

What are possible causes of Pulmonary HTN that could lead to right sided heart failure?

A

Parenchymal disease of the lung
Pulmonary vasculature disorders
Pulmonary thromboembolism
Hypoxic conditions

127
Q

WHat are the symptoms of right sided heart failure?

A 
Systemic and venous congestion
Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites 
Abnormal mental function
Renal failure
128
Q

What are the medical treatments for heart failure?

A

Diuretics
Renin-angiotensin-aldosterone blockers (ACE inhibitors)
β-blockers (lower adrenergic tone)

129
Q

What is hypertensive heart disease?

A

Results from sustained increased hypertension that causes pressure overload and ventricular hypertrophy

Classified as
Left-sided (systemic) HHD
Right-side (cor pulmonale) HHD

130
Q

What is the diagnostic criteria for systemic hypertensive heart disease?

A

Left ventricular hypertrophy without any other cardiovascular pathology
History or pathologic evidence of hypertension

131
Q

What is the diagnostic criteria for pulmonary hypertensive heart disease?

A

Characterized by right ventricular hypertrophy and dilation

Can be acute (pulmonary embolism) or chronic

132
Q

What are some forms of valvular heart disease?

A 
Mitral Stenosis
Mitral Regurgitation
Mitral annular calcification
mitral valve prolapse
Aortic stenosis
aortic reguritation
Calcific aortic stenosis
Calcific stenosis of congenitally bicuspid aortic valve
Rheumatic fever
Acute Rheumatic heart disease
Chronic Rheumatic heart disease
Infective Endocarditis
Non-infective endocarditis: Nonbacterial thrombotic endocarditis, Libman Sacks Endocarditis
Carcinoid Heart Disease
133
Q

What is stenosis? What does it lead to?

A

Failure of a valve to open completely, which impedes flow

Leads to pressure overload

134
Q

What is insufficiency/regurgitation?

A

Failure of a valve to close completely, allowing reversed flow
Leads to volume overload
Functional regurgitation

135
Q

Rheumatic heart disease can lead to which forms of valvular heart disease?

A

mitral stenosis
mitral regurgitation
aortic stenosis
aortic regurgitation

136
Q

Infective endocarditis can lead to which forms of valvular heart disease?

A

mitral regurgitation

aortic regurgitation

137
Q

What can calcification of a valve lead to in terms of valvular heart disease?

A

mitral regurgitation

aortic stenosis

138
Q

What can messing with the chordae tendinae or papillary muscles lead to?

A

mitral regurgitation

139
Q

What are some other things that can cause mitral regurgitation?

A

drugs

LVH

140
Q

Aside from rheumatic heart disease & infective endocarditis, what else can cause aortic regurgitation?

A 
Marfan syndrome
Syphilis
Ankylosing spondilitis
Rheumatoid arthritis
degenerative aortic dilation
141
Q

Calcific aortic stenosis is another form of valvular heart disease. What causes it? When does it present? What are the complications of it?

A

caused by normal wear & tear
presents in 7th-9th decades of life
complications: LVH, pressure overload

142
Q

What is the mechanism involved in creating calcific aortic stenosis?

A

Valves have “osteoblast like cells” that cause the deposition of calcium. Ca++ is made inside the fibroelastic tissue of the valve.

143
Q

What is calcific stenosis of congenitally bicuspid aortic valve? When does it present?

A

form of valvular heart disease

Most frequent congenital cardiovascular malformation
Due to normal wear and tear
Presents in the fifth to seventh decades of life

144
Q

What is mitral annular calcification? What can that lead to?

A

Calcifications in the peripheral fibrous ring of the mitral valve
Does not affect valvular function or become clinically important
Rare complications:
Regurgitation
Stenosis
Arrhythmias and sudden cardiac death

145
Q

What is mitral valve prolapse? What does it look like on histo?

A

Mitral valve leaflets are floppy and prolapse into the left atrium during systole
Histologic change is myxomatous degeneration by an unknown mechanism

146
Q

What might be a physical exam finding in a patient with mitral valve prolapse? What are some rare complications of this?

A

Most patients are asymptomatic and associated with a midsystolic click

Rare complications:
Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias
147
Q

What is rheumatic fever? What is a frequent consequence of it?

A

Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis
Acute rheumatic carditis is a frequent consequence

148
Q

What are some important clinical features of rheumatic fever?

A 
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
149
Q

What is a special histo feature of rheumatic fever? Where is it found?

A

Aschoff bodies-include lymphocytes, plasma cells, Anitschkow cells.
Aschoff looks like granulomatous reaction. Surrounds a blood vessel. Inflammatory reaction—macrophages w/ prominent nucleoli—bodies.
found in any layer of the heart (pancarditis)

150
Q

Aside from aschoff bodies, what are other distinguishing features of acute rheumatic disease?

A

Vegetations with underlying fibrinoid necrosis

MacCallum plaques within the left atrium

151
Q

T/F Aschoff bodies are an important distinguishing feature of chronic rheumatic disease.

A

F. This form of rheumatic disease does not include aschoff bodies.

152
Q

What is chronic rheumatic disease?

A

A deforming fibrotic valvular disease
Only cause of mitral stenosis
Other valves can be involved

153
Q

What does the mitral valve look like in a patient with chronic rheumatic disease?

A

Leaflet thickening
Commissural fusion and shortening
Thickening and fusion of tendinous cords

154
Q

Another form of valvular heart disease is endocarditis. What is thiS? What are the 2 major forms?

A

Serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe
Vegetations composed of thrombotic debris and organisms
Acute or subacute forms

155
Q

What is acute endocarditis?

A

Previously NORMAL heart valve by a highly virulent organism
Necrotizing, ulcerative, destructive lesions
Difficult to cure with antibiotics

156
Q

What is subacute endocarditis?

A

Insidious infections of deformed valves by organisms of lower virulence
Less destructive lesion
Cures produced with antibiotics

157
Q

What is an organism that can infect native but deformed valves, producing ____ endocarditis?

A

strep viridans

subacute endocarditis

158
Q

What is an organism that can infect healthy valves, producing ____ endocarditis?

A

staph aureus

acute endocarditis

159
Q

What is an organism that can infect prosthetic heart valves? Other organisms that can infect valves in general?

A

staph epidermis (coagulase -)

Other:
HACEK
Enterococci
Gram negative bacilli
Fungi
160
Q

What does HACEK stand for?

A

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

161
Q

Why can it be a challenged to cure endocarditis with antibiotics?

A

b/c heart valves are not very vascular, for the delivery of antibiotics

162
Q

Non infective endocarditis is caused by which 2 conditions?

A

Non-infected (sterile) vegetations caused by:
Non-bacterial thrombotic endocarditis
Libman-Sacks endocarditis (SLE)

163
Q

What is nonbacterial thrombotic endocarditis?

A

Previously referred as marantic endocarditis
Characterized by deposition of small sterile thrombi on the leaflets of cardiac valves
Vegetations are thrombi that do not invade or elicit an inflammatory reaction
May be the source of systemic thrombi

164
Q

Which patients experience nonthrombotic endocarditis?

A

cancer (mucinous adenocarcinoma), sepsis or hypercoagulable state

165
Q

What is Libman-Sacks disease?

A

occurs in patients with SLE
patients have vegetations

Get Intense valvulitis with fibrinoid necrosis of the valve

166
Q

Where are the vegetations located in Libman-Sacks disease?

A

mitral and tricuspid valves
Valvular endocardium
Chords
Mural endocardium of the atria

167
Q

What do the vegetations look like on histo in Libman-Sacks disease?

A

Vegetations composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies

168
Q

What are 2 types of artificial heart valves? What are possible complications of this?

A

mechanical, tissue
complications:

Thromboembolism
Infective endocarditis with ring abscess
Structural deterioration

169
Q

What’s the deal with carcinoid heart disease?

A

carcinoid tumors can often occur in the GI tract
if they occur outside the portal system & dump into the IVC they will go into the RA & plaques will form on the tricuspid & pulmonary valves
Note: these plaques are endocardial fibrous thickenings

170
Q

What are primary & secondary cardiomyopathies?

A

primary: disorder confined to heart muscle, 3 subtypes
secondary: myocardial involvement in a multiorgan disorder

171
Q

What are the 3 subtypes of primary cardiomyopathies?

A

dilated
hypertrophic
restrictive

172
Q

What is dilated cardiomyopathy?

A

Characterized by progressive cardiac dilation and contractile dysfunction

173
Q

What is hypertrophic cardiomyopathy?

A

Characterized by myocardial hypertrophy, poorly compliant LV myocardium leading to abnormal diastolic filling and intermittent ventricular outflow obstruction

174
Q

What is restrictive cardiomyopathy?

A

Characterized by primary decreased ventricular compliance resulting in impaired filling during diastole

175
Q

What is the leading cause of unexplained LVH?

A

hypertrophic cardiomyopathy

176
Q

What is the mechanism of impairment for the the following:

dilated, hypertrophic, restrictive cardiomyopathy?

A

dilated: contractility (systole)

hypertrophic & restrictive: compliance (diastole)

177
Q

What are some possible causes of dilated cardiomyopathy?

A 
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
178
Q

What are some possible causes of hypertrophic & restrictive cardiomyopathy?

A

hypertrophic;
genetics

restrictive:
Idiopathic
Amyloidosis
Radiation induced
Fibrosis
179
Q

What is Arrhythmogenic right ventricular cardiomyopathy? What cause it?

A

Disease is related to defective cell adhesion proteins in the desmosomes that link adjacent myocytes
Aut Dom
thin RV wall: loss of myocytes, fatty infiltration, fibrosis
Right ventricular failure
Various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)

180
Q

What is myocarditis?

A

Infectious or inflammatory processes that cause myocardial injury

181
Q

What are some different types of myocarditis?

A

Infectious
Immune-mediated
Sarcoidosis
Giant Cell Myocarditis

182
Q

What are some infectious agents that can cause infectious myocarditis?

A 
Viruses
Bacteria
Fungus
Protozoa 
Helminths
183
Q

What are some viruses that can cause infectious myocarditis?

A

Coxsackie A/B, Enterovirus, HIV, CMV

184
Q

What are some bacteria that can cause infectious myocarditis?

A

Chlamydia, Neisseria, Borrelia, Rickettsia

185
Q

What are some causes of immune mediated myocarditis?

A 
Post-viral
Poststreptococcal
SLE
Drug hypersensitivity
Methyldopa
Sulfonamides
Transplant rejection
186
Q

What is pericardial disease? How much fluid should usu be in the pericardial sac?

A

this is when extra fluid gets stuck in the pericardial space

should only be 20-30 mL normally…w/ thin clear straw colored fluid

187
Q

With chronic pressure how much fluid can get stuck in there? With rapid effusion?

A

Chronic: up to 500 mL!
Rapid: 200-300 mL

188
Q

What do the following mean?
pericardial effusion
hemopericardium
purulent pericarditis

A

pericardial effusion: distended by serous fluid

hemo: distended by blood
purulent: pus

189
Q

What are some different forms of acute pericarditis?

A 
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
190
Q

What are some different forms of chronic pericarditis?

A

Adhesive pericarditis

Constrictive pericarditis

191
Q

What does serous acute pericarditis look like?

A

Produced by non-infectious inflammatory diseases

Mild lymphocytic infiltrate in the epipericardial fat

192
Q

What does fibrinous/serofibrinous pericarditis look like?

A

Most frequent type with a loud pericardial friction rub

Composed of serous fluid mixed with fibrinous exudate

193
Q

What is fibrinous/serofibrinous pericarditis associated with?

A

Associated with acute MI, postinfarction syndrome, uremia, chest radiation, RF, SLE, trauma

194
Q

What causes acute purulent pericarditis?

A 
Caused by invasion of microbes into the pericardial space by
Direct extension
Seeding from the blood
Lymphatic extension
Introduction during cardiotomy
195
Q

What are possible end results of acute purulent pericarditis?

A

Acute inflammatory reaction that can produce a mediastinopericarditis
Organization and scarring usual outcome with constrictive pericarditis

196
Q

What causes acute pericarditis-hemmorhagic? What is it?

A

Blood with a fibrinous or suppurative effusion
Most commonly caused by a metastatic malignant neoplasm
Also found in TB and bacterial infections and post-cardiac surgery

197
Q

What’s the deal with acute pericarditis-caseous?

A

Rare
Almost always due to TB by direct spread, but sometimes fungus
Leads to a disabling, fibrocalcific, chronic constrictive pericarditis

198
Q

What is adhesive mediastinopericarditis? What category does it fall into?

A

Follow infectious pericarditis, cardiac surgery, radiation
Pericardial sac is obliterated and pericardium adheres to surrounding structures
**falls into the category of chronic pericarditis

199
Q

What is constrictive pericarditis? How do the heart sounds present?

A

Heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
Mimic restrictive cardiomyopathy
Heart sounds are muffled or distant

200
Q

Give 4 cardiac tumors.

A

myxoma
rhabdomyoma
lipoma
papillary fibroelastoma

201
Q

What is a myxoma?

A

Most common primary tumor in adults
BENIGN

Most often in the atria, but can arise in any chamber
10% associated with Carney complex

202
Q

Which chromosomal abnormalities can cause a myxoma? Which cell type do they originate from?

A

Arise from primitive multipotent mesenchymal cells

chromosomes 12 & 17

203
Q

What pop are rhabdomyomas common in? Also called? Associated with what?

A

Most frequent primary tumor in children
Associated with tuberous sclerosis
Considered hamartomas

204
Q

T/F Rhabdomyomas are the most common primary tumor in adults.

A

FALSE
in children…
myxoma is most common primary in adult

205
Q

Is a lipoma benign or malignant? Which tissue is it found in?

A

Benign tumor of mature adipose tissue

206
Q

Where are lipomas most often located?

A

Most often located in the LV, RA or atrial septum

207
Q

What’s the deal with a papillary fibroelastoma?

A

Benign neoplasm often discovered at autopsy

Resemble Lambl excrescences

Block 9; Week 1 & 2-M (10 decks)

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