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

Lecture 3: CV Pathophysiology I Flashcards

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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
inhibits platelet activation and causes vasodilation
nitric oxide
26
3 factors that help resolve blood clots:
- tPA - prostacyclin - nitric oxide
27
Factors that inhibit clotting:
- Antithrombin - Protein C/Protein S - Thrombomodulin - TFPI - Fibrin
28
rare genetic disorder; sex-linked; inability to produce vWF
hemophilia
29
lack of vWF, cannot form platelet plug
von Willebrand Disease
30
when a piece of a thrombus breaks off and lodges in a blood vessel down stream
embolism
31
thrombus associated with the rupture of an atherosclerotic plaque (ofter in coronary artery or brain) or atria fibrillation
arterial thrombosis
32
thrombus that occurs in legs of a person who has been immobilized and leads to pulmonary embolism
venous (deep vein thrombosis)
33
occurs in patients with heat stroke, sepsis, or other conditions that strongly activate the immune system
disseminated intravascular coagulation (DIC)
34
an anti-clotting drug that interferes with the actions of vitamin K (necessary for certain clotting factors)
Coumadin (warfarin)
35
caused by blood pressure in the capliaries; favors filtration
capillary hydrostatic pressure
36
due to the osmotic force of proteins in the plasma, tending to draw fluid back into the capillary; favors reabsorption
capillary oncotic pressure
37
generally very low; can increase with swelling; favors absorption
tissue hydrostatic pressure
38
generally low; favors filtration
tissue oncotic pressure
39
non-permeating substances that create the osmotic pressure that favors reabsorption
colloids
40
the colloid osmotic pressure due to the presence of proteins in a solution
oncotic pressure
41
a disease of protein malnutrition
Kwashiorkor
42
What can alter fluid balance?
- 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
How does the lymphatic system resolve fluid imbalance due to inflammation?
returns leaked proteins to circulation; more permeable than tissue capillaries
44
How does the lymphatic system fight against infection?
lymph carries pathogens to lymph nodes where white blood cells can trap them
45
Which organs can temporarily withstand severe reductions in blood flow?
kidneys, skin, GI tract, liver
46
Which organs are most vulnerable to interruptions in blood flow?
brain, heart, skeletal muscle
47
Characteristics or arteries?
- low resistance | - highly elastic
48
Characteristics of arterioles?
- control TPR | - control blood flow to organs and tissues (vasodilation and constriction)
49
Characteristics of capillaries and venues?
- site of nutrient exchange - largest area - slowest flow - largest drop in BP
50
Characteristics of veins?
- low resistance - holds >60% of blood volume at rest - one-way valves - skeletal muscle pump
51
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
aneurysm
52
excessive pressure distends veins and damages valves; blood unable to return to heart and alternate pathways develop
varicose veins
53
heart valve does not close completely
valve insufficiency
54
valve does not open completely
valve stenosis
55
Characteristics of cardiac muscle?
- striated - gap junctions - longer action potentials due to prolonged opening of Ca+ channels (prevents summation of action potentials)
56
Why is the conduction through the AV node slower?
gives atria time to completely depolarize before the ventricles start to depolarize
57
cardiac muscle fibers that are specialized for rapid conduction of electrical impulse in the ventricle
Purkinje fibers
58
Name all the stages of an ECG wave.
P wave - atrial depolarization QRS complex - ventricular depolarization T wave - ventricular repolarization
59
only about half of the signal from SA node/atria is transmitted to the ventricles
partial AV block
60
none of the signal from SA node/atria is transmitted to ventricles; no synchrony --> ventricles beat slower than the atria
complete AV block
61
What are the complications of atrial fibrillation?
- decreased cardiac output | - increased risk of blood clot (arterial thrombosis)
62
Where do the abnormal signals of atrial fibrillation arise?
pulmonary vein
63
How can atrial fibrillation be treated?
- anti-arrythmics - anti-coagulants - ablation of a region of the pulmonary vein - surgical removal of the atrial appendage to prevent pooling of blood
64
What can cause changes in extracellular concentration of Na+, K+, or Ca+ that can interfere with cardiac rhythm?
- eating disorders (hypokalemia) - hyponaturemia (can results from overconsumption of water) - antidiuretic drugs (can lead to hyper or hypokalemia)
65
phase of ventricular contraction
systole
66
phase of ventricular relaxation
diastole
67
What causes the first heart sound -- "lub"?
closing of the AV valves (mitral and tricuspid)
68
What causes the second heart sound -- "dub"?
closing of the semilunar valves (aortic and pulmonic)
69
When do the heart sounds occur?
at the end of systole
70
What does a murmur during systole indicate?
insufficient AV valve or a stenotic semilunar valve
71
What does a murmur during diastole indicate?
insufficient semilunar valve or stenotic AV valve

Human Pathophyisology: Midterm (6 decks)

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