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Mechanisms of Disease > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

What are the criteria for essential hypertension?

A
  1. Sustained pressure increase (systolic >140 and/or diastolic >90)
  2. Complex multigenetic disorder
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2
Q

What environmental factors can contribute to hypertension? (5)

A
  1. Obesity
  2. Stress
  3. Smoking
  4. Physical inactivity
  5. Heavy salt consumption
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3
Q

Blood pressure = ____.

A

Blood Pressure = Cardiac Output * Peripheral Resistance

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4
Q

What some primary regulators of blood pressure?

A
  1. Hormones
  2. Renal function
  3. Heart function
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5
Q

Name some humoral vasoconstrictors

A
  1. Angiotensin II
  2. Catecholamines
  3. Thromboxane
  4. Leukotrienes
  5. Endothelin
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6
Q

Name some humoral vasodilators

A
  1. Prostaglandins
  2. Kinins
  3. NO
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7
Q

α-adrenergic neural factors are ____

A

Vasoconstrictors

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8
Q

β-adrenergic neural factors are _____

A

Vasodilators

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9
Q

What type of arteriosclerosis is characterized by glassy eosinophilic protein deposits and narrow lumen of vessels

A

Hyaline arteriosclerosis

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10
Q

Hyaline arteriosclerosis is associated with ___ hypertension.

A

Benign hypertension

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11
Q

What type of arteriosclerosis is characterized by “onion-skinning,” where there is thickening of smooth muscle and basement membrane, but no collagen or connective tissue?

A

Hyperplastic arteriosclerosis

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12
Q

Hyperplastic arteriosclerosis is associated with _____ hypertension

A

Severe hypertension

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13
Q

What is atherosclerosis?

A

A type of arteriosclerosis characterized by formation of atheroma (aka atherosclerotic plaque)

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14
Q

Describe an atheroma

A
  • Collection of cholesterol crystals beneath the tunica intima in blood vessels that pushes into the lumen
  • Composed of a fibrous cap and a necrotic center
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15
Q

The vulnerability or stability of an atherosclerotic plaque is determined by what?

A

The thickness of the fibrous cap

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16
Q

What are foam cells?

A

Macrophages in atherosclerotic plaques that are attempting to digest lipids and failing to do so

(FC)

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17
Q

What are cholesterol clefts (CC)?

A
  • Cholesterol crystalizes out because there is so much of it
  • Occurs during staining/fixing
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18
Q

Explain the pathogenesis of atherosclerosis

A
  1. Endothelial cell dysfunction
  2. Formation of atherosclerotic plaque
  3. T cell-macrophage interaction
  4. Fracture of the plaque and thrombosis
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19
Q

Plaques initiate at sites where endothelium is _____.

A

Intact

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20
Q

What are the most important contributors to endothelial injury? (2)

A
  1. Hemodynamic disturbances (turbulence)
  2. Hypercholesterolemia
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21
Q

Where are apoproteins synthesized?

A

Liver

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22
Q

Are lipids or proteins less dense?

A

Lipids

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23
Q

What are the criteria for chronic hyperlipidemia?

A
  1. Damage to the tunica intima by LDL accumulation (macrophages attempt to remove)
  2. Impaired function of endothelial cells
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24
Q

Why do macrophage attempts at removal of LDL accumulation in the tunica intima damage endothelial cells?

A

Macrophages cannot digest oxidized LDLs, so they release ROS which in turn injures tissue and depletes NO

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25
Q

What is the difference between a fatty streak and a mature atheroma?

A

Mature atheromas have a fibrous cap

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26
Q

Cytokines released by macrophages during inflammatory reaction induce ______ and ______.

A
  • Smooth muscle cell proliferation
  • Extracellular matrix production
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27
Q

Normally leukocytes do not bind to endothelium, so why do they bind to dysfunctional endothelium in atherosclerosis?

A

Dysfunctional endothelial cells express adhesion molecules

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28
Q

Damaged endothelium provides a focal point for ______ and production of _____

A
  • Platelet binding and activation
  • Blood clots
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29
Q

Explain the pre-clinical phase of atherosclerosis

A

Normal artery → Fatty streak → Fibrofatty plaque → Advanced vulnerable plaque

  • Asymptomatic
  • Starts at a young age
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30
Q

Describe the clinical phase of atherosclerosis

A

Advanced vulnerable plaque can lead to:

  • Aneurysm and rupture
  • Occlusion by thrombus
  • Critical stenosis
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31
Q

What are the consequences of atherosclerosis? (3)

A
  1. Obstruction of blood flow
  2. Rupture of plaque (thrombosis)
  3. Weakening of underlying tunica media
32
Q

Myocardial infarction is responsible for ____ of deaths in the US

33
Q

______ is a group of diseases most commonly caused by atherosclerosis of coronary arteries.

A

Ischemic heart disease

34
Q

What is myocardial ischemia?

A

Lower perfusion of the heart than is needed; decreased blood flow with increased need

35
Q

Myocardial infarction is described as ______

A

Necrotic damage to the myocardium

36
Q

What biochemical changes occur in severe myocardial ischemia? (2)

A
  1. Increased lactate production
  2. Decreased ATP production
37
Q

How long is the reversible phase of myocardial ischemia before ischemic tissue becomes necrotic?

A

~30 minutes

38
Q

How long after MI is this image?

A

24 hours

Evidenced by coagulative necrosis (left)

39
Q

How long after MI is this image?

A

3-4 days

Evidenced by neutrophil infiltrate

40
Q

How long after MI is this image?

A

7-10 days

Evidenced by Necrotic tissue being removed by macrophages

41
Q

How long after MI is this image?

A

>2 weeks

Evidenced by loose CT and vascularization (granulation tissue)

42
Q

Explain reperfusion injury

A
  • Burst of ROS following resumption of oxygen-based energy production
  • Some cells will cope and recover while others undergo necrotic cell death
43
Q

What are the clinical markers for MI?

A
  1. Troponin I
  2. Myocardial creatinine kinase (CK-MB)
  3. Myoglobin
44
Q

Why is myoglobin alone not a good marker for MI?

A

Myoglobin levels in the blood can go up with skeletal muscle damage too

45
Q

What are some possible causes of cardiac hypertrophy? (3)

A
  1. Increased workload
  2. Myocardiocytes add sarcomeres
  3. Myocardial infarct
46
Q

What are some possible causes of increased workload in the heart? (3)

A
  1. Increased blood pressure
  2. Increased blood volume to move
  3. Damage to heart walls
47
Q

Why can cardiac hypertrophy cause a new MI?

A

Cells get bigger, but no new cells are added, so no new vasculature forms to supply the larger tissue.

48
Q

Bradycardia is described as a heart rate of ______ and tachycardia is a heart rate of ______.

A
  1. <60 bpm
  2. >100 bpm
49
Q

What are the two mechanisms of bradycardia?

A
  1. Reduced SA node activity
  2. Blocked conduction
50
Q

What are the two classifications of tachycardia? Which is more severe (***)?

A
  1. Wide QRS***
  2. Narrow QRS
51
Q

What are subtypes of wide QRS tachycardia? (2)

A
  1. Ventricular
  2. Supraventricular with conductance issue
52
Q

What are the subtypes of narrow QRS tachycardia? (3)

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. Sinus tachycardia
53
Q

What are the potential causes of myocarditis? (3)

A
  1. Viral infections (enteroviruses)
  2. Autoimmune dysfunction
  3. Drug hypersensitivity
54
Q

What are the microscopic characteristics of myocarditis? (3)

A
  1. Edema
  2. Interstitial inflammatory infiltrates
  3. Myocyte injury
55
Q

What is carcinoid heart disease?

A
  • Secondary to hormone secretion by cancer cells
  • Characterized by fibrotic lesions and thickened endocardium
56
Q

Iron deficiency anemia is most commonly due to ______, especially from ______ (3)

A
  • Bleeding
  1. Menstruation
  2. GI bleeds
  3. Pregnancy
57
Q

What is pernicious anemia?

A
  • Lack of vitamin B12 (required for thymidine synthesis)
  • Causes hematopoiesis precursors to appear in the blood and hypersegmented neutrophils
58
Q

What is thrombocytopenia?

A

Low platelets

59
Q

Drug-associated immune thrombocytopenia can be induced by what drugs? (4)

A
  1. Quinine
  2. Quinidine
  3. Vancomycin
  4. Heparin
60
Q

How do quinine, quinidine, and vancomycin induce thrombocytopenia?

A
  • Bind platelet glycoproteins
  • Creat antigens recognized by antibodies
61
Q

How does heparin induce thrombocytopenia?

A

Type I: direct aggregation

Type II: venous/arterial thrombosis

62
Q

What are some potential consequences of clots in large arteries? (3)

A
  1. Vascular insufficiency
  2. Deep vein thrombosis
  3. Pulmonary embolism
63
Q

What is ADAMTS13?

A

A metalloprotease involved in blood clotting

Targets von Willebrand Factor (vWF)

64
Q

Thrombotic Thrombocytopenic Purpura (TTP) is the result of a ADAMTS13 deficiency, which causes _____

A

Abnormal vWF complexes that adhere to platelets, which cause thrombotic clots to form in microcirculation (red spots on the skin)

65
Q

TTP can cause _____ due to shear stress on RBCs

A

Hemolytic anemia

66
Q

What is agranulocytosis?

A

Lack of granular WBCs leading to increased susceptibility to bacterial and fungal infections

67
Q

What are the two mechanisms that could cause agranulocytosis?

A
  1. Ineffective/inadequate granulopoiesis
  2. Increased removal/destruction of granulocytes from the blood
68
Q

What is neutropenia?

A

Complete lack of neutrophils

69
Q

How can granulopoiesis be impaired (4)? Which is the most common (***)?

A
  1. Suppression of hematopoietic stem cells
  2. Defective precursors die in marrow (megaloblastic anemia)
  3. Rare congenital disorders
  4. Drug exposure***
70
Q

Granulopoiesis caused by suppression of hematopoietic stem cells can be accompanied by ____ and ____.

A
  • Anemia
  • Thrombocytopenia
71
Q

What drugs can impair granulopoiesis (3)? Which one is predictable and dose-dependent (***)

A
  1. Chemotherapeutic agents (anti-metabolites)***
  2. Phenothiazines (toxic to precursors)
  3. Sulfonamides (Ab-induced destruction)
72
Q

What is cyclic neutropenia?

A
  • Every 3 weeks for about 3-5 days neutrophil count drops to near zero then rebounds
  • Peripheral neutrophil/monocyte counts oscillate in opposite phases of same 3 week cycle
73
Q

Neutropenia can be caused by a mutation in ______, which is excessively _______

A
  • Neutrophil elastase
  • Inhibitory of myeloblastic differentiation
74
Q

Neutrophils can survive peripherally for _____

75
Q

What is the function of vasopressin?

A
  • Increase water reuptake by the kidneys
  • Constricts arterioles

Mechanisms of Disease (13 decks)

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