Cardiovascular Diseases Flashcards
(75 cards)
1
Q
What are the criteria for essential hypertension?
A
- Sustained pressure increase (systolic >140 and/or diastolic >90)
- Complex multigenetic disorder
2
Q
What environmental factors can contribute to hypertension? (5)
A
- Obesity
- Stress
- Smoking
- Physical inactivity
- Heavy salt consumption
3
Q
Blood pressure = ____.
A
Blood Pressure = Cardiac Output * Peripheral Resistance
4
Q
What some primary regulators of blood pressure?
A
- Hormones
- Renal function
- Heart function
5
Q
Name some humoral vasoconstrictors
A
- Angiotensin II
- Catecholamines
- Thromboxane
- Leukotrienes
- Endothelin
6
Q
Name some humoral vasodilators
A
- Prostaglandins
- Kinins
- NO
7
Q
α-adrenergic neural factors are ____
A
Vasoconstrictors
8
Q
β-adrenergic neural factors are _____
A
Vasodilators
9
Q
What type of arteriosclerosis is characterized by glassy eosinophilic protein deposits and narrow lumen of vessels
A
Hyaline arteriosclerosis
10
Q
Hyaline arteriosclerosis is associated with ___ hypertension.
A
Benign hypertension
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
12
Q
Hyperplastic arteriosclerosis is associated with _____ hypertension
A
Severe hypertension
13
Q
What is atherosclerosis?
A
A type of arteriosclerosis characterized by formation of atheroma (aka atherosclerotic plaque)
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
15
Q
The vulnerability or stability of an atherosclerotic plaque is determined by what?
A
The thickness of the fibrous cap
16
Q
What are foam cells?
A
Macrophages in atherosclerotic plaques that are attempting to digest lipids and failing to do so
(FC)
17
Q
What are cholesterol clefts (CC)?
A
- Cholesterol crystalizes out because there is so much of it
- Occurs during staining/fixing
18
Q
Explain the pathogenesis of atherosclerosis
A
- Endothelial cell dysfunction
- Formation of atherosclerotic plaque
- T cell-macrophage interaction
- Fracture of the plaque and thrombosis
19
Q
Plaques initiate at sites where endothelium is _____.
A
Intact
20
Q
What are the most important contributors to endothelial injury? (2)
A
- Hemodynamic disturbances (turbulence)
- Hypercholesterolemia
21
Q
Where are apoproteins synthesized?
A
Liver
22
Q
Are lipids or proteins less dense?
A
Lipids
23
Q
What are the criteria for chronic hyperlipidemia?
A
- Damage to the tunica intima by LDL accumulation (macrophages attempt to remove)
- Impaired function of endothelial cells
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
25
What is the difference between a fatty streak and a mature atheroma?
Mature atheromas have a fibrous cap
26
Cytokines released by macrophages during inflammatory reaction induce ______ and \_\_\_\_\_\_.
* Smooth muscle cell proliferation
* Extracellular matrix production
27
Normally leukocytes do not bind to endothelium, so why do they bind to dysfunctional endothelium in atherosclerosis?
Dysfunctional endothelial cells express adhesion molecules
28
Damaged endothelium provides a focal point for ______ and production of \_\_\_\_\_
* Platelet binding and activation
* Blood clots
29
Explain the pre-clinical phase of atherosclerosis
Normal artery → Fatty streak → Fibrofatty plaque → Advanced vulnerable plaque
* Asymptomatic
* Starts at a young age
30
Describe the clinical phase of atherosclerosis
Advanced vulnerable plaque can lead to:
* Aneurysm and rupture
* Occlusion by thrombus
* Critical stenosis
31
What are the consequences of atherosclerosis? (3)
1. Obstruction of blood flow
2. Rupture of plaque (thrombosis)
3. Weakening of underlying tunica media
32
Myocardial infarction is responsible for ____ of deaths in the US
¼
33
\_\_\_\_\_\_ is a group of diseases most commonly caused by atherosclerosis of coronary arteries.
Ischemic heart disease
34
What is myocardial ischemia?
Lower perfusion of the heart than is needed; decreased blood flow with increased need
35
Myocardial infarction is described as \_\_\_\_\_\_
Necrotic damage to the myocardium
36
What biochemical changes occur in severe myocardial ischemia? (2)
1. Increased lactate production
2. Decreased ATP production
37
How long is the reversible phase of myocardial ischemia before ischemic tissue becomes necrotic?
~30 minutes
38
How long after MI is this image?
24 hours
Evidenced by coagulative necrosis (left)
39
How long after MI is this image?
3-4 days
Evidenced by neutrophil infiltrate
40
How long after MI is this image?
7-10 days
Evidenced by Necrotic tissue being removed by macrophages
41
How long after MI is this image?
\>2 weeks
Evidenced by loose CT and vascularization (granulation tissue)
42
Explain reperfusion injury
* Burst of ROS following resumption of oxygen-based energy production
* Some cells will cope and recover while others undergo necrotic cell death
43
What are the clinical markers for MI?
1. Troponin I
2. Myocardial creatinine kinase (CK-MB)
3. Myoglobin
44
Why is myoglobin alone not a good marker for MI?
Myoglobin levels in the blood can go up with skeletal muscle damage too
45
What are some possible causes of cardiac hypertrophy? (3)
1. Increased workload
2. Myocardiocytes add sarcomeres
3. Myocardial infarct
46
What are some possible causes of increased workload in the heart? (3)
1. Increased blood pressure
2. Increased blood volume to move
3. Damage to heart walls
47
Why can cardiac hypertrophy cause a new MI?
Cells get bigger, but no new cells are added, so no new vasculature forms to supply the larger tissue.
48
Bradycardia is described as a heart rate of ______ and tachycardia is a heart rate of \_\_\_\_\_\_.
1. \<60 bpm
2. \>100 bpm
49
What are the two mechanisms of bradycardia?
1. Reduced SA node activity
2. Blocked conduction
50
What are the two classifications of tachycardia? Which is more severe (\*\*\*)?
1. Wide QRS\*\*\*
2. Narrow QRS
51
What are subtypes of wide QRS tachycardia? (2)
1. Ventricular
2. Supraventricular with conductance issue
52
What are the subtypes of narrow QRS tachycardia? (3)
1. Atrial fibrillation
2. Atrial flutter
3. Sinus tachycardia
53
What are the potential causes of myocarditis? (3)
1. Viral infections (enteroviruses)
2. Autoimmune dysfunction
3. Drug hypersensitivity
54
What are the microscopic characteristics of myocarditis? (3)
1. Edema
2. Interstitial inflammatory infiltrates
3. Myocyte injury
55
What is carcinoid heart disease?
* Secondary to hormone secretion by cancer cells
* Characterized by fibrotic lesions and thickened endocardium
56
Iron deficiency anemia is most commonly due to \_\_\_\_\_\_, especially from ______ (3)
* Bleeding
1. Menstruation
2. GI bleeds
3. Pregnancy
57
What is pernicious anemia?
* Lack of vitamin B12 (required for thymidine synthesis)
* Causes hematopoiesis precursors to appear in the blood and hypersegmented neutrophils
58
What is thrombocytopenia?
Low platelets
59
Drug-associated immune thrombocytopenia can be induced by what drugs? (4)
1. Quinine
2. Quinidine
3. Vancomycin
4. Heparin
60
How do quinine, quinidine, and vancomycin induce thrombocytopenia?
* Bind platelet glycoproteins
* Creat antigens recognized by antibodies
61
How does heparin induce thrombocytopenia?
Type I: direct aggregation
Type II: venous/arterial thrombosis
62
What are some potential consequences of clots in large arteries? (3)
1. Vascular insufficiency
2. Deep vein thrombosis
3. Pulmonary embolism
63
What is ADAMTS13?
A metalloprotease involved in blood clotting
Targets von Willebrand Factor (vWF)
64
Thrombotic Thrombocytopenic Purpura (TTP) is the result of a ADAMTS13 deficiency, which causes \_\_\_\_\_
Abnormal vWF complexes that adhere to platelets, which cause thrombotic clots to form in microcirculation (red spots on the skin)
65
TTP can cause _____ due to shear stress on RBCs
Hemolytic anemia
66
What is agranulocytosis?
Lack of granular WBCs leading to increased susceptibility to bacterial and fungal infections
67
What are the two mechanisms that could cause agranulocytosis?
1. Ineffective/inadequate granulopoiesis
2. Increased removal/destruction of granulocytes from the blood
68
What is neutropenia?
Complete lack of neutrophils
69
How can granulopoiesis be impaired (4)? Which is the most common (\*\*\*)?
1. Suppression of hematopoietic stem cells
2. Defective precursors die in marrow (megaloblastic anemia)
3. Rare congenital disorders
4. Drug exposure\*\*\*
70
Granulopoiesis caused by suppression of hematopoietic stem cells can be accompanied by ____ and \_\_\_\_.
* Anemia
* Thrombocytopenia
71
What drugs can impair granulopoiesis (3)? Which one is predictable and dose-dependent (\*\*\*)
1. Chemotherapeutic agents (anti-metabolites)\*\*\*
2. Phenothiazines (toxic to precursors)
3. Sulfonamides (Ab-induced destruction)
72
What is cyclic neutropenia?
* 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
Neutropenia can be caused by a mutation in \_\_\_\_\_\_, which is excessively \_\_\_\_\_\_\_
* Neutrophil elastase
* Inhibitory of myeloblastic differentiation
74
Neutrophils can survive peripherally for \_\_\_\_\_
12 hours
75
What is the function of vasopressin?
* Increase water reuptake by the kidneys
* Constricts arterioles
