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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
# Myocardial Infarction Ischemic Heart Disease
Group of diseases most commonly causes by atherosclerosis of cornary arteries
26
# Myocardial Infarction What is Ischemic Heart Diseases caused by?
Myocardial ischemia * Lower perfusion than needed → Dcreased blood flow, Increased need
27
# Myocardial Infarction Lack of blood flow caused by ischemic heart disease affects:
Energy production Nutrient availability Waste Removal
28
# Myocardial Infarction Myocardial Infarction
type of Ischemic Heart Disease Necrotic damage to the myocardium | Heart Attack
29
# Myocardial Infarction Can Severe Myocardial Infarction be stopped once it has started? | Can you prevent the damage?
Small window of time before cells die and damage is irreversible Depends on ATP levels and accumulation of dangerous metabolites
30
# Myocardial Infarction Myocardial Infarction Pathology
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
31
# Myocardial Infarction What is the effect of Reperfusion?
It impacts myocardiocyte function and surival
32
# Myocardial Infarction How does reperfusion work?
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
33
# Myocardial Infarction What is reperfusion injury?
Cells continue to dying for a period of time even though blood flow was restored
34
# Myocardial Infarction: Reperfusion What is Salvage in terms of reperfusion?
Degree to which you manage to stop myocardial infarction | i.e. 60% might be salvaged vs. losing 80-90%
35
# Myocardial Infarction How can timing of MI be assess clinically?
By measuring the protein release of necrotic cardiomyocytes Increased levels of Troponin I, CK-MB, and Myoglobin
36
# Cardiac Hypertrophy What causes hypertrophy?
Increased workload * increased blood pressure * increased volume to move * damage to the wall Myocardiocytes become enlarged and add sarcomeres MI
37
# Cardiac Hypertrophy What are the consequences of cardiac hypertrophy?
* Increased heart size and mass * Increases protein synthesis * induction of immediate-early genes * Inductiton of fetal gene program * abnormal proteins * fibrosis * inadqueate vasculature
38
# Cardiac Hypertrophy Cardiac Dysfunction is characterized by...
Heart failure Arrhythimas Neurohumoral stimulation
39
# Conduction Disorders Bradycardia
< 60 bpm
40
# Conduction Disorders Tachycardia
> 100 bpm
41
# Conduction Disorders What are the mechanisms of Bradycardia?
Reduced SA node activity Blocked conduction
42
# Conduction Disorders Bradycardia: Reduced SA node activity | What is it? What causes it?
Contraction induced by slower pacemaker Multiple causes: * Age * Drugs * Sleep, fainting
43
# Conduction Disorders Bradycardia: Blocked Conduction | What causes it?
Similar causes to reduced SA node activity Linked to certain diseases | Signal not moving thru the heart
44
# Conduction Disorders Classifications of Tachycardia
Wide QRS Narrow QRS
45
# Conduction Disorders Tachycardia: Wide QRS
Ventricular supraventricular with conductance issue | More dangerous
46
# Conduction Disorders Tachycardia: Narrow QRS
Usually supraventricular (AV node or above) Include Atrial Fibrillation, Atrial flutter, Sinus Tachycardia
47
# Myocarditis Myocarditis
Inflammation due to infection of myocardium
48
# Myocarditis What causes Myocarditis?
US: viral infections are most common Non-infectious causes are autoimmune or drug hypersensitivity
49
# Myocarditis What are microscopic characteristics of Myocarditis?
Edema Interstitial inflammatory infiltrates Myocyte Injury
50
# Myocarditis What is the difference between MI and Myocarditis?
Type of immune cells present Infection occurs with edema
51
# Myocarditis Myocarditis Pathology
Different tissue responses depending on what is causing the Myocarditis. * Lymphocytic * Giant Cell * Hypersensitivity * Trypanosomes
52
# Carcinoid Syndrome Carcinoid Heart Disease
Cancer cells produce hormones that affect heart tissue - compromise function Fibrotic lesion Thickened endocardium
53
# Erythrocyte Disorders Anemia
Low Blood RBC levels
54
# Erythrocyte Disorders What causes anemia?
Can occur due to blood loss, hemolysis, or reduced erythropoiesis * Sickle Cell * Iron deficiency * Pernicious (aka megaloblastic)
55
# Erythrocyte Disorders What causes Iron Deficiency Anemia?
Most commonly due to bleeding * menstruation * GI Bleeds
56
# Erythrocyte Disorders Why is Iron Deficiency Anemia associated with pregnancy?
Fetus is taking iron to make blood
57
# Erythrocyte Disorders: Iron Deficiency Anemia What are sources of iron?
DIetary iron is absorbed in the intestines Iron is recycled from aged RBCs by macrophages
58
# Erythrocyte Disorders Iron Metabolism
59
# Erythrocyte Disorders What is the process of reduced Hb synthesis?
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
# Erythrocyte Disorders What are the clinical symptoms of reduced Hb synthesis?
Weakness Fatigue Malaise
61
# Erythrocyte Disorders What is Pernicious Anemia?
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
# Erythrocyte Disorders What is a characteristic of megaloblastic anemia?
Hypersegmented neutrophil seen in a peripheral blood smear
63
# Erythrocyte Disorders What is the pathogenesis of Megaloblastic Anemia?
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
# Erythrocyte Disorders What causes megaloblastic anemia/fundic cell damage?
Autoimmune attack on gastric mucoas * Loss of parietal cells (primary effect) * Antibodies that block (secondary effect)
65
# Erythrocyte Disorders: Megaloblastic Anemia What would cause loss of parietal cells?
Autoreactive T cells
66
# Erythrocyte Disorders: Megaloblastic Anemia How do antibodies block resulting in autoimmune attack on gastric mucosa?
Binding Intrinsic Factor Binding to receptor Proton Pump
67
# Platelet Disorders Thrombocytopenia
Platelet levels below normal
68
# Platelet Disorders What causes Thromocytopenia?
Decreased platelet production (Vitamin B12 deficiency/Hereditary) Decreased Survival (Immune-mediated/Thrombotic thrombocytopenic purpura)
69
# Platelet Disorders Drug-associated Immune Thrombocytopenia
Immune-mediated destruction of platelets
70
# Platelet Disorders: Drug-associated Immune Thrombocytopenia What drugs are associated with Drug-associated Immune Thrombocytopenia? How do they cause Drug-associated Immune Thrombocytopenia?
Quinine, quinidine, vancomycin * Bind platelet glycoproteins * create antigens recognized by antibodies that mediate dstruction of platelets
71
# Platelet Disorders: Drug-associated Immune Thrombocytopenia What effect does Heparin have on platelets?
Type I - direct aggregation of platelts Type II - venous/arterial thrombosis
72
# Platelet Disorders: Drug-associated Immune Thrombocytopenia Heparin-induced Thrombocytopenia
Aggregation produces thrombosis Clots in large arteries
73
# Platelet Disorders: Heparin-induced Thrombocytopenia What is the result of Heparin-Induced Thrombocytopenia?
Vascular insufficiency Deep vein thrombosis Emboli can cause fatal lung disease
74
# Platelet Disorders: Drug-associated Immune Thrombocytopenia What effect does low MW heparin have on Heparin-Induced Thrombocytopenia?
Lowers the risk of aggregation produced thrombosis
75
# Platelet Disorders: Thrombotic Thrombocytopenic Purpura What is Thrombotic Thrombocytopenic Purpura?
ADAMTS13 defificency causes abnormal vWF complexes that adhere to platelets
76
# Platelet Disorders: Thrombotic Thrombocytopenic Purpura What are the effects of Thrombotic Thrombocytopenic Purpura?
Thrombtic clots in microcirculation Accumulation of clots damages endothelium
77
# Platelet Disorders: Thrombotic Thrombocytopenic Purpura What are the clinical symptoms of Thrombotic Thrombocytopenic Purpura?
Symptoms are episodic Unknown factors contribute Hemolytic anemia due to shear stress on RBCs
78
# Platelet Disorders: Thrombotic Thrombocytopenic Purpura What is ADAMTS13?
Metalloprotease involved in formation of multimers that form the complexes in clot formation
79
# Leukocyte Disorders Leukopenia
Lack of WBCs
80
# Leukocyte Disorders What effect does agranulocytosis have?
Agranulocytosis is clinically relevant Reduced neutrophil numbers that are clinically apparent More susceptible to bacterial and fungal infections
81
# Leukocyte Disorders What are the two mechanisms of Leukopenia?
1. ineffective/inadequate granulopoiesis 2. Increased removal/destruction of granulocytes from the blood | Not making enough and/or using too many
82
# Leukocyte Disorders What are the types of Neutropenia?
Absolute neutropenia Agranulocytosis (granulocyte deficiency) Cyclic neutropenia
83
# Leukocyte Disorders What can impair granulopoiesis?
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
# Leukocyte Disorders How do Chemotherapeutic agents affect granulopoiesis?
Alkylating agents and anti-metabolites cause predictable, dose-dependent destruction of hematopoietic cells
85
# Leukocyte Disorders What is the general effect of chemotherapeutic agents on granulopoiesis?
Anemia Thrombocytopenia
86
# Leukocyte Disorders What is the idoiocyncratic effect of drugs on granulopoiesis?
Toxic effect on precursors (Phenothiazines) Ab-induced destruction of mature leukocytes (certian slfonamides)
87
# Leukocyte Disorders How are neutrophils removed or overused immunologically?
Idiopathic Associated with immune disease (SLE) Drug exposure
88
# Leukocyte Disorders How does splenomegaly result in neutrophil removal or overuse?
Increased sequestration Anemia/thrombocytopenia
89
# Leukocyte Disorders What would result in increased use/removal of neutrophils?
Overwhelimg bacterial, fungal, rickettsial infections
90
# Leukocyte Disorders Cyclic Neutropenia
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
# Leukocyte Disorders What does cyclic neutropenia provides insight to?
Mechanisms of normal neutrophil production and function
92
# Leukocyte Disorders What is the genetic basis of Cyclic Neutropenia?
Classic case of childhood onset Potentially autosomal dominant Rare instances of spontaneous mutation in adults
93
# Leukocyte Disorders What causes cyclic neutropenia?
Mutation in Neutrophil Elastase
94
# Leukocyte Disorders What does the mutation in Neutrophil Elastase do?
Mutant is excessively inhibitory, which causes excessive troughs in production | Inhibits too much resulting in no neutrophils for 3-5 days
95
# Leukocyte Disorders Where is Neutrophil elastase found?
In primary azurophilic granules of neutrophils and monocytes
96
# Leukocyte Disorders What is the function of Neutrophil Elastase?
Inhibitory Regulates production of neutrophils to prevent overproduction Negative feedback
97
# Leukocyte Disorders Neutrophil hematopoiesis
Requires 2 weeks to mature survives peripherally for 12 hours normally, large storage pool of precursors in marrow
98
# Leukocyte Disorders How does neutrophil production normally occur? | Time wise
in waves Negative feedback inhibits neutrophil production (Neutrophil elastase) Sourse of oscillations in production
99
# Leukocyte Disorders What is the purpose of neutrophil oscillations?
Time for maturation explains opposing cyclicity of the peripheral neutrophils and monocytes
100
# Leukocyte Disorders How does neutrophil elastase cause inhibition of neutrophil production?
By inhibiting myeloblastic differentiation

Mechanism of Disease (11 decks)

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