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FPP-MSS > Hemodynamic Disorders and Hemostasis > Flashcards

Hemodynamic Disorders and Hemostasis Flashcards

1
Q

What are three of the most frequent causes of morbidity and mortality that fit under this category?

A

Myocardial infarctions
Pulmonary embolism
Cerebral infarcts

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2
Q

What is a pathological example of vascular wall integrity failure?

A

Trama causing focal defect in vessel wall

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3
Q

What is a pathological example of intravascular hydrostatic pressure failure?

A

Congestive heart failure causes alveolar capillary congestions and eventually pulmonary edema

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4
Q

What is a pathological example of osmolarity failure?

A

Liver failure (cirrhosis) causes low total intravascular protein leading to edema

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5
Q

Where does edema generally go to?

A

Subcutaneous tissues

Body cavities

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6
Q

What two altered factors leads to edema?

A

Increased hydrostatic pressure

Decreased osmotic pressure

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7
Q

What can cause increased hydrostatic pressure?

A

Increased capillary pressure via venous obstruction OR impaired venous return

Arteriolar dilation – heat or neurohumoral dysfunction

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8
Q

What are some local examples of increased capillary pressure?

A

DVT, Mass lesion (obstructed venous outflow), lower extremity inactivity (long airplane rides), cirrhosis

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9
Q

What are some generalized examples of increased capillary pressure?

A

Congestive heart failure – increased hydrostatic pressure in alveolar capillaries due to left ventricular failure, pulmonary edema and eventually peripheral edema; hypo perfusion of kidneys causes secondary hyperaldosteronism

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10
Q

What can cause reduced plasma oncotic pressure?

A

Excessive loss of albumin – leads to decreased intravascular volume and secondary hyperaldosteronism

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11
Q

What can cause albumin loss?

A

Nephrotic syndrome (protein-losing)
Protein-losing enteropathy (IBS, GI infections, sprue)
Malnutrition
Liver Disease (reduced synthesis) – cirrhosis

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12
Q

What can cause lymphatic obstruction leading to lymphedema?

A

Inflammatory (infection)
Neoplastic cells
Post-surgical/post radiation

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13
Q

How does sodium and water retention cause edema and what are some examples?

A

Causes increased hydrostatic pressure (expanded intravascular vol) and decreased colloid osmotic pressure

Excessive salt intake with renal insufficiency
Acute reduction of renal function

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14
Q

Where are three places you can have edema?

A

Subcutaneous – CHF and renal failure
Pulmonary – LV failure
Edema of the brain - focally (tumors) and diffusely (viral infections)

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15
Q

What does hyperaldosteronism do?

A

Remember that aldosterone increases reabsorption of Na, increases secretion of K+, increases H20 retention which increases BP

This is because of kidney hypo perfusion so kidneys think they need to act to increase BP

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16
Q

What is hyperemia and how does it occur?

A

Increase in blood volume within a tissue

It’s due to an increase in blood flow and arteriolar dilation; occurs at sites of inflammation or in exercising skeletal muscles

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17
Q

What is congestion and how does it occur?

A

Increase in blood volume within a tissue

It’s due to decreased/impaired outflow of venous blood (passive)

This may occur systemically (liver and lung congestion d/t heart failure) or locally (obstruction of superior sagittal sinus of dura)

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18
Q

What is it called when you have chronic passive congestion of the liver?

A

Nutmeg liver – d/t centrilobular necrosis from prolonged passive congestion causing necrosis of hepatocytes

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19
Q

What are the 4 basic steps of primary hemostasis?

A
  1. Platelet adhesion
  2. Shape change
  3. Granule release
  4. Recruitment
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20
Q

What is secondary hemostasis?

A

When clotting factors and clotting cascade results in forming fibrin to seal the platelet plug.

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21
Q

What generates fibrin from fibrinogen??

A

Thrombin

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22
Q

What are the laboratory tests for Primary hemostasis?

A

Platelet count
Platelet function
vWillebrand studies

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23
Q

What are the laboratory tests for Secondary hemostasis?

A

Prothrombin time [PT} – extrinsic + common pathway
Activated partial thromboplastin time [aPTT] – intrinsic + common pathway
Fibrinogen activity

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24
Q

Scurvy

A

Vitamin C deficiency leads to vessel fragility

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25
Q

Thrombocytopenia

A

Too few platelets

26
Q

Hemophilia A

A

Factor 8 deficiency

27
Q

Hemophilia B

A

Factor 9 deficiency

28
Q

Vitamin K deficiency

A

Deficiency of factors 2, 7, 9, 10

29
Q

Disseminated intravascular coagulation (DIC)

A

factor and platelet consumption

30
Q

What is a hematoma?

A

Accumulation of blood within a tissue

31
Q

What are petechial hemorrhages? Purpura?

A

1-2mm hemorrhages into skin, mucous membranes or serial surfaces. Associated with low platelet counts, platelet dysfunction, loss of vascular wall support or local pressure

purpura: > 3mm hemorrhages associated with same disorders as petechiae

32
Q

What is ecchymoses?

A

> 1-2cm subcutaneous hematomas. Associated with trauma.

33
Q

What do Protein C and S do?

A

Normal anticoagulants, vit K dependent, work to shut down clotting cascade to achieve balance

34
Q

What are the normal anti-coagulants?

A

Antithrombin III
Protein C and S
Tissue factor pathway inhibitor
PGI2

35
Q

What is the main inherited hypercoag example?

A

Factor 5 leiden – most common inherited predisposition to thrombosis
Single point mutation in FV (R506Q) G–>A (cleavage site for protein C)

36
Q

What is an example of an acquired hypercoag?

A

Acquired autoantibodies against phospholipid complexes.

Associated with arterial, venous thromboses and high recurrence rates.

37
Q

What are the two types of lab testing for antiphospholipid antibodies?

A

Lupus anticoagulant – prolonged clotting based tests

Anti-cardiolipin antibodies – immunoassays

38
Q

Define thrombosis.

A

Formation of a blood clot within intact vessels

39
Q

What are Lines of Zahn?

A

laminations apparent grossly or microscopically that are produced by alternation layers of platelets, fibrin and RBCs

40
Q

How can abnormal blood flow contribute to clotting/thrombus formation?

A

Turbulent blood flow causes endothelial cell injury leading to dysfunction and stasis. Stasis allows platelets and leukocytes to come into contact with walls of vessels – slows washout of clotting factors and impedes inflow of clotting factor inhibitors

41
Q

Where do venous thrombi most commonly occur?

A

Lower extremities, in association with stasis d/t immobilization/bed rest – reduces action of leg muscles and reduces venous return.

42
Q

What could happen with thrombi in the deep veins of the legs?

A

Could break off and travel to lungs – BAD

43
Q

Where do cardiac thrombi in the left atrium or left ventricle go?

A

Embolize to various organs

44
Q

Where do arterial thrombi go?

A

Obstruct critical blood flow resulting in infarcts (MI, stroke)

45
Q

Where do venous thrombi go?

A

Embolize to lungs from deep leg veins, local congestion/edema

46
Q

What are some of the risk factors to DVT?

A

Immobilization, CHF, pregnancy, obesity, tumor, trauma, surgery, burns

47
Q

What is an embolus?

A

Detached intravascular mass carried by blood to site distant from origin

48
Q

What are some different types of emboli?

A 
Thrombus 
Fat
Air
Amniotic fluid
Tumor
49
Q

If you have a thrombus in the right heart where may it travel?

A

Lungs

50
Q

If you have a thrombus in the left heart where may it travel?

A

systemic arterial circulation – lower legs, brain, intestines, kidneys, spleen, upper extremities

51
Q

What is a saddle emboli?

A

Usually from DVT, emboli at bifurcation of pulmonary arteries – serious

Travels from deep veins of leg –> right atrium –> right ventricle –> pulmonary arteries

52
Q

What is an infarction?

A

Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of a particular tissue

53
Q

What his a red infarct? Versus a white infarct?

A

Red: hemorrhagic, occurs in loose tissues where blood can collect

White: anemic, no blood, occurs in solid organs with end-arterial circulation (spleen, kidney)

54
Q

What is a septic infarct?

A

Necrosis with abscess formation (liquefactive necrosis with acute inflammation and suppuration)

55
Q

What is the different between hematoma and a hemorrhagic infarct?

A

In a hemorrhagic infarct, blood is intermixed with necrotic tissue; in a hematoma blood is collected and forms a solid mass

56
Q

What is disseminated intravascular coagulation?

A

Characterized by initial clotting, resulting in ischemia, followed by bleeding tendencies

Consumptive coagulopathy – widespread clotting leads to consumption of factors and platelets –> bleeding

Associated with sever illness

57
Q

What is shock and what causes it?

A

Systemic hypo perfusion caused by reduced cardiac output or decreased in effective circulation blood volume.

Hypotension –> impaired perfusion and cellular hypoxia –> tissue injury –> death

58
Q

What are the three major types of shock??

A

Cardiogenic: Failure of myocardial pump (MI, Cardiac tamponade)

Hypovolemic: Inadequate blood or plasma volume (hemorrhage, fluid loss)

Septic: Peripheral vasodilation, pooling of blood, endothelial activation of injury, leukocyte-induced damage (overwhelming microbial infection)

59
Q

What are the stages of shock?

A
  1. Non-progressive phase (initial): tachycardia, peripheral vasoconstriction, renal fluid ocnservation, perfusion of organs maintained
  2. Progressive phase: tissue hypoxia and lactic acidosis, lowering of tissue pH and blunting of vasomotor response, tissue hypo perfusion present
  3. Irreversible phase: cellular and organ injury present preventing survival, excessive production of lactic acid (anaerobic glycolysis)
60
Q

How will patients with hypovolemic and cardiogenic shock present versus patients with septic shock?

A

Hypovolemic and cardiogenic: hypotension, tachycardia, tachypnea – COOL, CLAMMY, CYANOTIC

Septic: hypotension, tachycardia, tachypnea – WARM AND FLUSHED

61
Q

What is the main cause of death in ICU’s?

A

Septic shock

Most often from gram positive bacteria (followed by gram negative bacteria and fungi)

FPP-MSS (17 decks)

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