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Mechanism of Disease > Exam 2: Cardiovascular Diseases > Flashcards

Exam 2: Cardiovascular Diseases Flashcards

1
Q

Causes of Hypertension:

Essential Hypertension

A

Sustained pressure increase (systolic over 140 and/or diastolic over 90)
Complex Multigenic disorder

Stress, obesity, smoking, inactivity, heavy salt consumption, genes whose products affect sodium reabsorption

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2
Q

Causes of Hypertension:

Secondary Hypertension

A

Renal Dysfunction
Endocrine Dysfunction
Cardiovascular Dysfunction
Neurologic Dysfunction

Parts of the body that participate in regulating blood volume

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3
Q

Hypertension

Hypertension

A

Regulation of Blood pressure through hormones, renal function, and heart function

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4
Q

Hypertension

Hyaline Arteriosclerosis

A

Protein deposits
Narrow lumen of vessels
Associated with benign hypertension
Leak of plasma proteins pas damaged endothelial cells
Glassy eosinophilic membrane

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5
Q

Hypertension

Hyperplastic Arteriosclerosis

A

Onion-skinning
smooth muscle and basemnt membrane overgrowing in response to the pressure increase
Associated with severe hypertension

PAS staining for basement membrane

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6
Q

Atherosclerosis

Characteristics of Atherosclerosis

A

Type of arteriosclerosis
Characterized by formation of atheromas
* atherosclerotic plaques
* lesion in tunia intima
* projecs into the lumen

Core is lipids w/ fibrous cap

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7
Q

Atherosclerosis

Pathogenesis of Atherosclerosis

A
  1. Endothelial cell dysfunction
  2. Formation of the atherosclerosis plaque
  3. T cells-macrophage interaction
  4. Fracture of the plaque and thrombosis
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8
Q

Pathogenesis of Atherosclerosis

  1. Endothelial Injury
A

Plaques initiate at sites where endothelium is intact
Results from endothelial dysfunction

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9
Q

Pathogenesis of Atherosclerosis

Most important contributors to Pathogenesis of Atherosclerosis step 1 are

A

Hemodynamic disturbancs
Hypercholesterolemia

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10
Q

Pathogensis: Atherosclerosis

Lipids are transported by…

A

apopproteins ( bind lipids)

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11
Q

Pathogensis: Atherosclerosis

Common abnormalities in Hypercholesterolemia

A

Sustained
Increased LDL levels
Decreased HDL levels
Presence of abnormal lipoproteins

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12
Q

Pathogensis: Atherosclerosis

Chronic Hyperlipidemia

A

Damage the intima by LDL accumulation
Atheroma begins to form as macrophages attempt to remove LDL
Directly affects endothelial functions

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13
Q

Pathogensis: Atherosclerosis

What causes oxidation of LDLs?

A

excess ROS

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14
Q

Pathogensis: Atherosclerosis

What happens to oxidized LDLs? What do they do?

A
  • Directly damage endothelial cells by attachment
  • Ingested by macrophages through specific receptor
  • Accumulate in phagocytes which then appear foamy
  • Stimulate cytokine, growth factor, and chemokine secretion to initiate immune response (monocyte recruitment)
  • Macrophages release ROS (injures tissue and depletes NO)
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15
Q

Pathogensis: Atherosclerosis

How does the fibrous cap of the atherosclerosis plaque form?

A

Cytokines released durign inflammatory reaction induce smooth muscle cell proliferation (which migrate to the endothelium) and ECM production to form fibrous cap

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16
Q

Pathogensis: Atherosclerosis

How are T cells involved in the Pathogensis of Atherosclerosis?

A
  • Dysfunctional endothelial cells express adhesion molecues
  • Bound leukocytes migrate into intima due to chemokines from macrophages
  • T lymphocytes induce chronic inflammation and release inflammatory cytokines
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17
Q

Pathogensis: Atherosclerosis

What causes thrombus formation?

A
  • Damaged endothelium provides focal point for platelet binding and activation
  • Accumulation of platelets produces blood clot with contribution from inflammatory mediators
  • Clot breaks free
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18
Q

The tunica intima consists of:

A

Endothelium (simple squamous epithelium)
Supporting CT

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19
Q

Atherosclerosis

Atherosclerosis Progression

A

Normal Artery → Fatty streak → Fibrofatty Plaque → Advanced/Vulnerable Plaque →Aneurysm and Rupture/Occulusion by Thrombus/Critical Stenosis

Fatty streak can be bypassed and go straight to fibrofatty plaque (atheroma)

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20
Q

Atherosclerosis

What are the consequences of Atherosclerosis?

A

Obstruct blood flow
Rupture of plaque - thrombsis
Weaken underlying tunica media (aneurysm formation)
Coronary Artery Disease → MI

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21
Q

Myocardial Infarction is responsible for _ of deaths in US

A

1/4

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22
Q

Atherosclerosis

What are the clinical complications of atherosclerosis?

A

Occlusion results in infarct
* Myocardial Infarction
* Cerebral Infarction
* Peripheral vascular disease
Rupture results in hemorrhage
* Formation of thrombus
* Aortic aneurysm

Location of atherosclerotic plaque is crucial

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23
Q

Atherosclerosis

Thrombsis can produce…

A

distal occlusions and additional plaques

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24
Q

What is the path of blood flow through the heart?

A
  1. Blood from body
  2. Thru superior/inferior vena cava into right atrium
  3. Thru tricuspid valve into right ventricle
  4. Thru pulmonary arteries into the lungs
  5. Return from the lungs by pulmonary veins
  6. Thru left atrium
  7. Thru mitral valve into left ventricle
  8. Thru aortic valve into aorta and to the body
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25
Q

Myocardial Infarction

Ischemic Heart Disease

A

Group of diseases most commonly causes by atherosclerosis of cornary arteries

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26
Q

Myocardial Infarction

What is Ischemic Heart Diseases caused by?

A

Myocardial ischemia
* Lower perfusion than needed → Dcreased blood flow, Increased need

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27
Q

Myocardial Infarction

Lack of blood flow caused by ischemic heart disease affects:

A

Energy production
Nutrient availability
Waste Removal

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28
Q

Myocardial Infarction

Myocardial Infarction

A

type of Ischemic Heart Disease
Necrotic damage to the myocardium

Heart Attack

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29
Q

Myocardial Infarction

Can Severe Myocardial Infarction be stopped once it has started?

Can you prevent the damage?

A

Small window of time before cells die and damage is irreversible
Depends on ATP levels and accumulation of dangerous metabolites

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30
Q

Myocardial Infarction

Myocardial Infarction Pathology

A

24 hours: Coagulative Necrosis
3-4 days: Neutrophil infiltrate
7-10 days: Necrotic tissue being removed by macrophages
>2 weeks: Loose CT and vascularization (granulation tissue)
>Compensation: Scar tissue is healed - infarct

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31
Q

Myocardial Infarction

What is the effect of Reperfusion?

A

It impacts myocardiocyte function and surival

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32
Q

Myocardial Infarction

How does reperfusion work?

A

Temporary occlusion → flow is restored → reperfusion injury → salvage
* Flow restored
* Burst of ROS following resumption of oxygen-based energy production
* Some cells can cope and will recover → other will still undergo necrotis death

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33
Q

Myocardial Infarction

What is reperfusion injury?

A

Cells continue to dying for a period of time even though blood flow was restored

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34
Q

Myocardial Infarction: Reperfusion

What is Salvage in terms of reperfusion?

A

Degree to which you manage to stop myocardial infarction

i.e. 60% might be salvaged vs. losing 80-90%

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35
Q

Myocardial Infarction

How can timing of MI be assess clinically?

A

By measuring the protein release of necrotic cardiomyocytes
Increased levels of Troponin I, CK-MB, and Myoglobin

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36
Q

Cardiac Hypertrophy

What causes hypertrophy?

A

Increased workload
* increased blood pressure
* increased volume to move
* damage to the wall

Myocardiocytes become enlarged and add sarcomeres
MI

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37
Q

Cardiac Hypertrophy

What are the consequences of cardiac hypertrophy?

A
  • Increased heart size and mass
  • Increases protein synthesis
  • induction of immediate-early genes
  • Inductiton of fetal gene program
  • abnormal proteins
  • fibrosis
  • inadqueate vasculature
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38
Q

Cardiac Hypertrophy

Cardiac Dysfunction is characterized by…

A

Heart failure
Arrhythimas
Neurohumoral stimulation

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39
Q

Conduction Disorders

Bradycardia

A

< 60 bpm

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40
Q

Conduction Disorders

Tachycardia

A

> 100 bpm

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41
Q

Conduction Disorders

What are the mechanisms of Bradycardia?

A

Reduced SA node activity
Blocked conduction

42
Q

Conduction Disorders

Bradycardia: Reduced SA node activity

What is it? What causes it?

A

Contraction induced by slower pacemaker
Multiple causes:
* Age
* Drugs
* Sleep, fainting

43
Q

Conduction Disorders

Bradycardia: Blocked Conduction

What causes it?

A

Similar causes to reduced SA node activity
Linked to certain diseases

Signal not moving thru the heart

44
Q

Conduction Disorders

Classifications of Tachycardia

A

Wide QRS
Narrow QRS

45
Q

Conduction Disorders

Tachycardia: Wide QRS

A

Ventricular
supraventricular with conductance issue

More dangerous

46
Q

Conduction Disorders

Tachycardia: Narrow QRS

A

Usually supraventricular (AV node or above)
Include Atrial Fibrillation, Atrial flutter, Sinus Tachycardia

47
Q

Myocarditis

Myocarditis

A

Inflammation due to infection of myocardium

48
Q

Myocarditis

What causes Myocarditis?

A

US: viral infections are most common
Non-infectious causes are autoimmune or drug hypersensitivity

49
Q

Myocarditis

What are microscopic characteristics of Myocarditis?

A

Edema
Interstitial inflammatory infiltrates
Myocyte Injury

50
Q

Myocarditis

What is the difference between MI and Myocarditis?

A

Type of immune cells present
Infection occurs with edema

51
Q

Myocarditis

Myocarditis Pathology

A

Different tissue responses depending on what is causing the Myocarditis.
* Lymphocytic
* Giant Cell
* Hypersensitivity
* Trypanosomes

52
Q

Carcinoid Syndrome

Carcinoid Heart Disease

A

Cancer cells produce hormones that affect heart tissue - compromise function
Fibrotic lesion
Thickened endocardium

53
Q

Erythrocyte Disorders

Anemia

A

Low Blood RBC levels

54
Q

Erythrocyte Disorders

What causes anemia?

A

Can occur due to blood loss, hemolysis, or reduced erythropoiesis
* Sickle Cell
* Iron deficiency
* Pernicious (aka megaloblastic)

55
Q

Erythrocyte Disorders

What causes Iron Deficiency Anemia?

A

Most commonly due to bleeding
* menstruation
* GI Bleeds

56
Q

Erythrocyte Disorders

Why is Iron Deficiency Anemia associated with pregnancy?

A

Fetus is taking iron to make blood

57
Q

Erythrocyte Disorders: Iron Deficiency Anemia

What are sources of iron?

A

DIetary iron is absorbed in the intestines
Iron is recycled from aged RBCs by macrophages

58
Q

Erythrocyte Disorders

Iron Metabolism

59
Q

Erythrocyte Disorders

What is the process of reduced Hb synthesis?

A

RBCs have lower Hb content
Lower O2 levels induce Eryhtropoietin
Stimulates bone marrow - increased platelets
RBCs become microcytic
* smaller/varied size
* Hypochromic
* Varied shape

60
Q

Erythrocyte Disorders

What are the clinical symptoms of reduced Hb synthesis?

A

Weakness
Fatigue
Malaise

61
Q

Erythrocyte Disorders

What is Pernicious Anemia?

A

Vitamin B12 is required for thymidine synthesis which is required for DNA synthesis
Failure of DNA synthesis affects hematopoiesis
Megaloblastic - abnormally large blood cells and precursors

62
Q

Erythrocyte Disorders

What is a characteristic of megaloblastic anemia?

A

Hypersegmented neutrophil seen in a peripheral blood smear

63
Q

Erythrocyte Disorders

What is the pathogenesis of Megaloblastic Anemia?

A

Damage to fundic glands in stomach
* VItamin B12 absorption requires intrinsic factor
* Produced by parietal cells in glands

No Intrinsic factor → no vitamin B12 absorption → failure of thyamidine synthesis → failure of DNA synthesis → affects hematopoiesis → not making enough RBCs → Megaloblastic anemia

64
Q

Erythrocyte Disorders

What causes megaloblastic anemia/fundic cell damage?

A

Autoimmune attack on gastric mucoas
* Loss of parietal cells (primary effect)
* Antibodies that block (secondary effect)

65
Q

Erythrocyte Disorders: Megaloblastic Anemia

What would cause loss of parietal cells?

A

Autoreactive T cells

66
Q

Erythrocyte Disorders: Megaloblastic Anemia

How do antibodies block resulting in autoimmune attack on gastric mucosa?

A

Binding Intrinsic Factor
Binding to receptor
Proton Pump

67
Q

Platelet Disorders

Thrombocytopenia

A

Platelet levels below normal

68
Q

Platelet Disorders

What causes Thromocytopenia?

A

Decreased platelet production (Vitamin B12 deficiency/Hereditary)
Decreased Survival (Immune-mediated/Thrombotic thrombocytopenic purpura)

69
Q

Platelet Disorders

Drug-associated Immune Thrombocytopenia

A

Immune-mediated destruction of platelets

70
Q

Platelet Disorders: Drug-associated Immune Thrombocytopenia

What drugs are associated with Drug-associated Immune Thrombocytopenia? How do they cause Drug-associated Immune Thrombocytopenia?

A

Quinine, quinidine, vancomycin
* Bind platelet glycoproteins
* create antigens recognized by antibodies that mediate dstruction of platelets

71
Q

Platelet Disorders: Drug-associated Immune Thrombocytopenia

What effect does Heparin have on platelets?

A

Type I - direct aggregation of platelts
Type II - venous/arterial thrombosis

72
Q

Platelet Disorders: Drug-associated Immune Thrombocytopenia

Heparin-induced Thrombocytopenia

A

Aggregation produces thrombosis
Clots in large arteries

73
Q

Platelet Disorders: Heparin-induced Thrombocytopenia

What is the result of Heparin-Induced Thrombocytopenia?

A

Vascular insufficiency
Deep vein thrombosis
Emboli can cause fatal lung disease

74
Q

Platelet Disorders: Drug-associated Immune Thrombocytopenia

What effect does low MW heparin have on Heparin-Induced Thrombocytopenia?

A

Lowers the risk of aggregation produced thrombosis

75
Q

Platelet Disorders: Thrombotic Thrombocytopenic Purpura

What is Thrombotic Thrombocytopenic Purpura?

A

ADAMTS13 defificency causes abnormal vWF complexes that adhere to platelets

76
Q

Platelet Disorders: Thrombotic Thrombocytopenic Purpura

What are the effects of Thrombotic Thrombocytopenic Purpura?

A

Thrombtic clots in microcirculation
Accumulation of clots damages endothelium

77
Q

Platelet Disorders: Thrombotic Thrombocytopenic Purpura

What are the clinical symptoms of Thrombotic Thrombocytopenic Purpura?

A

Symptoms are episodic
Unknown factors contribute
Hemolytic anemia due to shear stress on RBCs

78
Q

Platelet Disorders: Thrombotic Thrombocytopenic Purpura

What is ADAMTS13?

A

Metalloprotease involved in formation of multimers that form the complexes in clot formation

79
Q

Leukocyte Disorders

Leukopenia

A

Lack of WBCs

80
Q

Leukocyte Disorders

What effect does agranulocytosis have?

A

Agranulocytosis is clinically relevant
Reduced neutrophil numbers that are clinically apparent
More susceptible to bacterial and fungal infections

81
Q

Leukocyte Disorders

What are the two mechanisms of Leukopenia?

A
  1. ineffective/inadequate granulopoiesis
  2. Increased removal/destruction of granulocytes from the blood

Not making enough and/or using too many

82
Q

Leukocyte Disorders

What are the types of Neutropenia?

A

Absolute neutropenia
Agranulocytosis (granulocyte deficiency)
Cyclic neutropenia

83
Q

Leukocyte Disorders

What can impair granulopoiesis?

A
  1. Suppression of hematopoietic stem cells (accompanied by anemia and thrombocytopenia)
  2. Defective precursors die in marrow (megaloblastic anemia)
  3. Rare congenital disorders (inherited defects prevent proper differentiation)
  4. Drug exposure
84
Q

Leukocyte Disorders

How do Chemotherapeutic agents affect granulopoiesis?

A

Alkylating agents and anti-metabolites
cause predictable, dose-dependent destruction of hematopoietic cells

85
Q

Leukocyte Disorders

What is the general effect of chemotherapeutic agents on granulopoiesis?

A

Anemia
Thrombocytopenia

86
Q

Leukocyte Disorders

What is the idoiocyncratic effect of drugs on granulopoiesis?

A

Toxic effect on precursors (Phenothiazines)
Ab-induced destruction of mature leukocytes (certian slfonamides)

87
Q

Leukocyte Disorders

How are neutrophils removed or overused immunologically?

A

Idiopathic
Associated with immune disease (SLE)
Drug exposure

88
Q

Leukocyte Disorders

How does splenomegaly result in neutrophil removal or overuse?

A

Increased sequestration
Anemia/thrombocytopenia

89
Q

Leukocyte Disorders

What would result in increased use/removal of neutrophils?

A

Overwhelimg bacterial, fungal, rickettsial infections

90
Q

Leukocyte Disorders

Cyclic Neutropenia

A

Every 3 weeks, for 3-5 days, neutrophil count drops near zero, then rebounds (very susceptible to infections)
Peripheral neutrophil/monocyte counts oscillate in opposite phases of same 3 week cycle

Rare

91
Q

Leukocyte Disorders

What does cyclic neutropenia provides insight to?

A

Mechanisms of normal neutrophil production and function

92
Q

Leukocyte Disorders

What is the genetic basis of Cyclic Neutropenia?

A

Classic case of childhood onset
Potentially autosomal dominant
Rare instances of spontaneous mutation in adults

93
Q

Leukocyte Disorders

What causes cyclic neutropenia?

A

Mutation in Neutrophil Elastase

94
Q

Leukocyte Disorders

What does the mutation in Neutrophil Elastase do?

A

Mutant is excessively inhibitory, which causes excessive troughs in production

Inhibits too much resulting in no neutrophils for 3-5 days

95
Q

Leukocyte Disorders

Where is Neutrophil elastase found?

A

In primary azurophilic granules of neutrophils and monocytes

96
Q

Leukocyte Disorders

What is the function of Neutrophil Elastase?

A

Inhibitory
Regulates production of neutrophils to prevent overproduction
Negative feedback

97
Q

Leukocyte Disorders

Neutrophil hematopoiesis

A

Requires 2 weeks to mature
survives peripherally for 12 hours
normally, large storage pool of precursors in marrow

98
Q

Leukocyte Disorders

How does neutrophil production normally occur?

Time wise

A

in waves
Negative feedback inhibits neutrophil production (Neutrophil elastase)
Sourse of oscillations in production

99
Q

Leukocyte Disorders

What is the purpose of neutrophil oscillations?

A

Time for maturation explains opposing cyclicity of the peripheral neutrophils and monocytes

100
Q

Leukocyte Disorders

How does neutrophil elastase cause inhibition of neutrophil production?

A

By inhibiting myeloblastic differentiation

Mechanism of Disease (11 decks)

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