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Hemodynamic Disorders and Hemostasis Flashcards

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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
Thrombocytopenia
Too few platelets
26
Hemophilia A
Factor 8 deficiency
27
Hemophilia B
Factor 9 deficiency
28
Vitamin K deficiency
Deficiency of factors 2, 7, 9, 10
29
Disseminated intravascular coagulation (DIC)
factor and platelet consumption
30
What is a hematoma?
Accumulation of blood within a tissue
31
What are petechial hemorrhages? Purpura?
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
What is ecchymoses?
>1-2cm subcutaneous hematomas. Associated with trauma.
33
What do Protein C and S do?
Normal anticoagulants, vit K dependent, work to shut down clotting cascade to achieve balance
34
What are the normal anti-coagulants?
Antithrombin III Protein C and S Tissue factor pathway inhibitor PGI2
35
What is the main inherited hypercoag example?
Factor 5 leiden -- most common inherited predisposition to thrombosis Single point mutation in FV (R506Q) G-->A (cleavage site for protein C)
36
What is an example of an acquired hypercoag?
Acquired autoantibodies against phospholipid complexes. Associated with arterial, venous thromboses and high recurrence rates.
37
What are the two types of lab testing for antiphospholipid antibodies?
Lupus anticoagulant -- prolonged clotting based tests | Anti-cardiolipin antibodies -- immunoassays
38
Define thrombosis.
Formation of a blood clot within intact vessels
39
What are Lines of Zahn?
laminations apparent grossly or microscopically that are produced by alternation layers of platelets, fibrin and RBCs
40
How can abnormal blood flow contribute to clotting/thrombus formation?
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
Where do venous thrombi most commonly occur?
Lower extremities, in association with stasis d/t immobilization/bed rest -- reduces action of leg muscles and reduces venous return.
42
What could happen with thrombi in the deep veins of the legs?
Could break off and travel to lungs -- BAD
43
Where do cardiac thrombi in the left atrium or left ventricle go?
Embolize to various organs
44
Where do arterial thrombi go?
Obstruct critical blood flow resulting in infarcts (MI, stroke)
45
Where do venous thrombi go?
Embolize to lungs from deep leg veins, local congestion/edema
46
What are some of the risk factors to DVT?
Immobilization, CHF, pregnancy, obesity, tumor, trauma, surgery, burns
47
What is an embolus?
Detached intravascular mass carried by blood to site distant from origin
48
What are some different types of emboli?
``` Thrombus Fat Air Amniotic fluid Tumor ```
49
If you have a thrombus in the right heart where may it travel?
Lungs
50
If you have a thrombus in the left heart where may it travel?
systemic arterial circulation -- lower legs, brain, intestines, kidneys, spleen, upper extremities
51
What is a saddle emboli?
Usually from DVT, emboli at bifurcation of pulmonary arteries -- serious Travels from deep veins of leg --> right atrium --> right ventricle --> pulmonary arteries
52
What is an infarction?
Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of a particular tissue
53
What his a red infarct? Versus a white infarct?
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
What is a septic infarct?
Necrosis with abscess formation (liquefactive necrosis with acute inflammation and suppuration)
55
What is the different between hematoma and a hemorrhagic infarct?
In a hemorrhagic infarct, blood is intermixed with necrotic tissue; in a hematoma blood is collected and forms a solid mass
56
What is disseminated intravascular coagulation?
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
What is shock and what causes it?
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
What are the three major types of shock??
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
What are the stages of shock?
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
How will patients with hypovolemic and cardiogenic shock present versus patients with septic shock?
Hypovolemic and cardiogenic: hypotension, tachycardia, tachypnea -- COOL, CLAMMY, CYANOTIC Septic: hypotension, tachycardia, tachypnea -- WARM AND FLUSHED
61
What is the main cause of death in ICU's?
Septic shock Most often from gram positive bacteria (followed by gram negative bacteria and fungi)

FPP-MSS (17 decks)

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