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Human Pathophyisology: Midterm > Lecture 3: CV Pathophysiology I > Flashcards

Lecture 3: CV Pathophysiology I Flashcards

1
Q

abnormally high hematocrit

A

polycythemia vera

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2
Q

What causes polycythemia vera?

A
  • overproduction of blood cell cursors by bone marrow

- genetic mutation

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3
Q

How is polycythemia vera treated? What are the complications?

A
  • regular phlebotomy

- increases risk of abnormal clotting, enlargement of spleen, and damage to bone marrow

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4
Q

fraction of blood volume that is erythrocytes (normal = 42-45%)

A

hematocrit

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5
Q

lower than normal hematocrit

A

anemia

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6
Q

What can cause anemia?

A
  • blood loss (heavy menstrual periods, hemorrhage, internal bleeding)
  • hemolysis (via infectious/autoimmune disease)
  • nutritional deficiencies (iron, vitamin B12)
  • defects in regulation of blood cell production
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7
Q

rupturing of red blood cells

A

hemolysis

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8
Q

too many white blood cells

A

leukemia

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9
Q

Why is leukemia damaging?

A
  • tends to go hand in hand with anemia

- immune defense does not function well; vulnerable to infection

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10
Q

too few white blood cells

A

AIDS, immune deficiency, chemotherapy

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11
Q

Why are low levels of leukocytes dangerous?

A

prone to infection

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12
Q

What happens during primary hemostasis?

A
  • vasoconstriction and formation of a platelet plug
  • tissue damage exposes collagen
  • platelets adhere to collagen via von Willebrand factor (vWF)
  • fibrinogen links aggregating platelets –> plug
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13
Q

released from platelets; causes vasoconstriction

A

thromboxane A2

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14
Q

What happens during secondary hemostasis?

A
  • transforms blood into a solid gel (clot/thrombus)
  • clot surrounds and reinforces platelet plug
  • blood solidifies at site of wound
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15
Q

How is the extrinsic pathway of hemostasis activated?

A
  • triggered by exposure of blood to sub-endothelial cells that produce tissue factor
  • some cells only produce tissue factor in response to damage
  • monocytes/macrophages produce tissue factor in response to inflammation
  • TF can also be found in circulating blood and endothelial cells even in the absence of damage
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16
Q

How is the intrinsic pathway of hemostasis activated?

A

activated by exposure to collagen

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17
Q

irreversibly binds to thrombin, preventing it from catalyzing the formation of fibrin

A

antithrombin

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18
Q

What about endothelial cells increases the effectiveness of antithrombin?

A

surface of endothelial cells contains heparin sulfate which enhances antithrombin 1000 fold

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19
Q

inactivates key acceleration factors in the coagulation pathway; second protein enhances the first

A

Protein C and Protein S

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20
Q

an endothelial receptor that binds thrombin and activates protein C

A

thrombomodulin

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21
Q

inactivates the complex of tissue factor

A

TFPI (Tissue Factor Protein Inhibitor)

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22
Q

What inhibits thrombin via negative feedback to limit clotting?

A

fibrin

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23
Q

a protein that cleaves the protein plasminogen to plasmin, which in turn enzymatically breaks down fibrin clots

A

tPA (tissue plasminogen activator)

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24
Q

inhibits platelet activation and aggravation; causes vasodilation

A

prostacyclin

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25
Q

inhibits platelet activation and causes vasodilation

A

nitric oxide

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26
Q

3 factors that help resolve blood clots:

A
  • tPA
  • prostacyclin
  • nitric oxide
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27
Q

Factors that inhibit clotting:

A
  • Antithrombin
  • Protein C/Protein S
  • Thrombomodulin
  • TFPI
  • Fibrin
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28
Q

rare genetic disorder; sex-linked; inability to produce vWF

A

hemophilia

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29
Q

lack of vWF, cannot form platelet plug

A

von Willebrand Disease

30
Q

when a piece of a thrombus breaks off and lodges in a blood vessel down stream

A

embolism

31
Q

thrombus associated with the rupture of an atherosclerotic plaque (ofter in coronary artery or brain) or atria fibrillation

A

arterial thrombosis

32
Q

thrombus that occurs in legs of a person who has been immobilized and leads to pulmonary embolism

A

venous (deep vein thrombosis)

33
Q

occurs in patients with heat stroke, sepsis, or other conditions that strongly activate the immune system

A

disseminated intravascular coagulation (DIC)

34
Q

an anti-clotting drug that interferes with the actions of vitamin K (necessary for certain clotting factors)

A

Coumadin (warfarin)

35
Q

caused by blood pressure in the capliaries; favors filtration

A

capillary hydrostatic pressure

36
Q

due to the osmotic force of proteins in the plasma, tending to draw fluid back into the capillary; favors reabsorption

A

capillary oncotic pressure

37
Q

generally very low; can increase with swelling; favors absorption

A

tissue hydrostatic pressure

38
Q

generally low; favors filtration

A

tissue oncotic pressure

39
Q

non-permeating substances that create the osmotic pressure that favors reabsorption

A

colloids

40
Q

the colloid osmotic pressure due to the presence of proteins in a solution

A

oncotic pressure

41
Q

a disease of protein malnutrition

A

Kwashiorkor

42
Q

What can alter fluid balance?

A
  • Kwashiorkor
  • liver disease (decrease production of plasma protein)
  • inflammation –> vasodilation –> increased capillary hydrostatic pressure –> increase permeability –> causes proteins to leak out –> decreased plasma oncotic pressure
43
Q

How does the lymphatic system resolve fluid imbalance due to inflammation?

A

returns leaked proteins to circulation; more permeable than tissue capillaries

44
Q

How does the lymphatic system fight against infection?

A

lymph carries pathogens to lymph nodes where white blood cells can trap them

45
Q

Which organs can temporarily withstand severe reductions in blood flow?

A

kidneys, skin, GI tract, liver

46
Q

Which organs are most vulnerable to interruptions in blood flow?

A

brain, heart, skeletal muscle

47
Q

Characteristics or arteries?

A
  • low resistance

- highly elastic

48
Q

Characteristics of arterioles?

A
  • control TPR

- control blood flow to organs and tissues (vasodilation and constriction)

49
Q

Characteristics of capillaries and venues?

A
  • site of nutrient exchange
  • largest area
  • slowest flow
  • largest drop in BP
50
Q

Characteristics of veins?

A
  • low resistance
  • holds >60% of blood volume at rest
  • one-way valves
  • skeletal muscle pump
51
Q

a weakness in the wall of an artery that can progress to dissection ff the inner layer or the artery begins to tear; eventually will rupture

A

aneurysm

52
Q

excessive pressure distends veins and damages valves; blood unable to return to heart and alternate pathways develop

A

varicose veins

53
Q

heart valve does not close completely

A

valve insufficiency

54
Q

valve does not open completely

A

valve stenosis

55
Q

Characteristics of cardiac muscle?

A
  • striated
  • gap junctions
  • longer action potentials due to prolonged opening of Ca+ channels (prevents summation of action potentials)
56
Q

Why is the conduction through the AV node slower?

A

gives atria time to completely depolarize before the ventricles start to depolarize

57
Q

cardiac muscle fibers that are specialized for rapid conduction of electrical impulse in the ventricle

A

Purkinje fibers

58
Q

Name all the stages of an ECG wave.

A

P wave - atrial depolarization
QRS complex - ventricular depolarization
T wave - ventricular repolarization

59
Q

only about half of the signal from SA node/atria is transmitted to the ventricles

A

partial AV block

60
Q

none of the signal from SA node/atria is transmitted to ventricles; no synchrony –> ventricles beat slower than the atria

A

complete AV block

61
Q

What are the complications of atrial fibrillation?

A
  • decreased cardiac output

- increased risk of blood clot (arterial thrombosis)

62
Q

Where do the abnormal signals of atrial fibrillation arise?

A

pulmonary vein

63
Q

How can atrial fibrillation be treated?

A
  • anti-arrythmics
  • anti-coagulants
  • ablation of a region of the pulmonary vein
  • surgical removal of the atrial appendage to prevent pooling of blood
64
Q

What can cause changes in extracellular concentration of Na+, K+, or Ca+ that can interfere with cardiac rhythm?

A
  • eating disorders (hypokalemia)
  • hyponaturemia (can results from overconsumption of water)
  • antidiuretic drugs (can lead to hyper or hypokalemia)
65
Q

phase of ventricular contraction

A

systole

66
Q

phase of ventricular relaxation

A

diastole

67
Q

What causes the first heart sound – “lub”?

A

closing of the AV valves (mitral and tricuspid)

68
Q

What causes the second heart sound – “dub”?

A

closing of the semilunar valves (aortic and pulmonic)

69
Q

When do the heart sounds occur?

A

at the end of systole

70
Q

What does a murmur during systole indicate?

A

insufficient AV valve or a stenotic semilunar valve

71
Q

What does a murmur during diastole indicate?

A

insufficient semilunar valve or stenotic AV valve

Human Pathophyisology: Midterm (6 decks)

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