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FPP Weeks 1 & 2 > Hemodynamic disorders and normal and abnormal hemostasis > Flashcards

Hemodynamic disorders and normal and abnormal hemostasis Flashcards

1
Q

What is maintained in normal fluid homeostasis?

A
  1. Vascular wall integrity
  2. Intravascular hydrostatic pressure
  3. Osmolarity
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2
Q

What is edema?

Where does it accumulate?

A

The accumulation of interstitial fluid in tissues

Subcutaneous tissues, body cavities (pleural cavity, pericardial cavity, peritoneal cavity)

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3
Q

What is anasarca?

A

Very severe generalized edema

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4
Q

What is the normal fluid balance?

A

2/3 intracellular
1/3 extracellular (interstitial)

with only 5% of extracellular fluid in vessels: blood plasma

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5
Q

What factors affect fluid balance?

A

Vascular hydrostatic pressure

Plasma colloid osmotic pressure (due to plasma proteins-albumin, globulin)

Lymphatic vessels pick up any residual

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6
Q

What causes edema?

A
  1. Increased hydrostatic pressure
  2. Decreased plasma osmotic pressure
  3. Lymphatic obstruction (lymphedema)
  4. Sodium (and water) retention
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7
Q

How does increased hydrostatic pressure occur?

A

Increased capillary pressure as a result of either venous obstruction or impaired venous return.

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8
Q

What are local examples of venous obstruction or impaired venous return? (leading to edema)

A

Deep vein thrombosis, mass lesion, lower extremity inactivity, cirrhosis

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9
Q

What is an example of a generalized venous obstruction or impaired venous return? (leading to edema)

A

Congestive heart failure.

Which also results in hypoperfusion of kidneys causing secondary hyperaldosteronism

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10
Q

What is another way that hydrostatic pressure can cause edema?

A

Arteriolar dilatation

as a result of Heat or Neurohumoral dysfunction (hypothalamic damage/malfunction)

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11
Q

How can edema occur from reduced plasma osmotic pressure?

A

Excessive loss of albumin leads to decreased intravascular volume and secondary hyperaldosteronism. (Albumin is the serum protein most responsible for maintaining colloid osmotic pressure)

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12
Q

What can cause albumin loss?

A

Nephrotic syndrome (protein-losing)

Protein-losing enteropathy (IBS, GI infections)

Malnutrition

Liver disease (reduced synth like cirrhosis)

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13
Q

How can lymphatic obstruction (lymphedema) cause edema?

A

Inflammatory

Neoplastic

Post-surgical/post radiation (removing lymphatic channels)

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14
Q

How does sodium (and water) retention occur?

A

Excessive salt intake w/ renal insufficiency
or
Acute reduction of renal function (like glomerulonephritis)

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15
Q

What causes subcutaneous edema?

A

Congestive heart failure and renal failure

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16
Q

What causes pulmonary edema?

A

Left ventricular failure

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17
Q

What causes edema of the brain?

A

Tumors cause focally

Viral infections cause diffusely

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18
Q

What is hyperemia?

A

An increase in blood volume within a tissue due to increased blood flow and arteriolar dilation.

An ACTIVE process.

Occurs at sites of inflammation

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19
Q

What is congestion?

A

An increase in blood volume within a tissue due to decreased/impaired outflow of venous blood.

A PASSIVE process

May occur systematically (liver and lung congestion due to heart failure) or locally (ex: obstruction of superior sagittal sinus of dura)

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20
Q

What are the two phases of clotting in normal hemostasis?

A

Primary and Secondary

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21
Q

What is important to the primary phase of clotting in normal hemostasis?

A
  1. Vasculature
  2. Blood flow
  3. Platelet count and function
  4. Extracellular matrix proteins
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22
Q

What is important to the secondary phase of clotting in normal hemostasis?

A
  1. Platelet plug

2. Coagulation factors

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23
Q

What are the important steps to primary hemostasis?

A
  1. Platelet adhesion
  2. Shape change
  3. Granule release
  4. Recruitment
  5. Aggregation
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24
Q

What are the important steps to secondary hemostasis?

A
  1. Tissue factor
  2. Phospholipid complex expression
  3. Thrombin activation
  4. Fibrin polymerization
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25
What are important laboratory screenings for primary hemostasis?
1. Platelet count 2. Platelet function (PFA-100 and platelet aggregation studies) 3. vWillebrand studies (vW antigen and vW activity)
26
What are important laboratory screenings for secondary hemostasis? And what specifically do they test?
1. Prothrombin time [PT]- Test extrinsic and common pathways 2. Activated partial thromboplastin time [aPTT]- Test intrinsic and common pathways 3. Fibrinogen activity
27
What defects result in bleeding disorders?
1. Vascular integrity 2. Platelet count and/or function 3. Von Willebrand factor deficiency or dysfunction 4. Clotting factor deficiencies/inhibition (Hemophilia A (factor 8) or Hemophilia B (factor 9)/liver disease/anticoagulants)
28
What is scurvy?
Vitamin C deficiency leading to vessel fragility
29
What is thrombocytopenia?
Too few platelets
30
What is Glanzmann's thrombasthenia?
An inherited defect within the platelet membrane
31
What does Vitamin K deficiency/warfarin cause?
Deficiency of factors 2, 7, 9, 10
32
What is disseminated intravascular coagulation (DIC)
Factor and Platelet consumption.
33
What is hemorrhage?
Extravasation of blood from vessels. Accumulating within a space
34
What are common causes of hemorrhage?
Ruptured vessel (atherosclerosis, inflammation-vasculitis, aneurysm) Peptic ulcer Chronic congestion Predisposition to hemorrhage with minimal trauma seen with decreased ability to clot
35
What is a hematoma?
Accumulation of blood within a tissue
36
What are petechial hemorrhages?
1-2 mm hemorrhages into skin, mucous membranes or serosal surfaces Associated with low platelet counts(thrombocytopenia), platelet dysfunction, loss of vascular wall support, or local pressure.
37
What is purpura?
Greater than 3 mm hemorrhages. Associated w same disorders as petechiae and w/ trauma, vaculitis, and vascular fragility
38
What are ecchymoses?
Greater than 1-2 cm subcutaneous hematomas. Associated with trauma and exacerbated by the other conditions (assoc with purpura and petechiae)
39
What factors contribute to favor thrombosis?
Endothelial Injury and Abnormal Blood Flow
40
What factors contribute to inhibiting thrombosis?
Antithrombin III Protein C and S Tissue factor pathway inhibitor PGI2
41
How do Protein C and S work?
Shut down Factor V and VIII
42
How does Antithrombin III work?
As thrombin is generated, antithrombin III shuts it down.
43
Hypercoagulability factors
Can be inherited or acquired. ``` Inherited: Factor 5 Leiden Protein C deficiency Protein S deficiency antithrombin III deficiency ``` Acquired: Malignancy Estrogens Antiphospholipid antibody syndrome
44
What is Factor 5 Leiden
Most common inherited predisposition to thrombosis Changes the cleavage site for protein C. Activated Protein C resistance
45
Antiphospholipid antibodies?
Acquired autoantibodies against PL complexes Assoc with arterial venous thromboses with high recurrence rates. Inhibit clotting in vitro; promote clotting in vivo.
46
What are the 2 types of lab testing for antiphospholipid antibodies?
Lupus anticoagulant (prolongation of clotting based tests) and Anti-cardiolipin antibodies (immunoassays for anti-cardiolipin)
47
What is a thrombosis?
Formation of a blood clot within intact vessels
48
Where does a thrombus begin?
At a site of endothelial injury, or turbulence of flow, or site of blood stasis
49
What are the lines of zahn
Laminations apparent grossly or microscopically produced by alternating layers of platelets, fibrin, and RBCs
50
What are the three primary abnormalities that lead to thrombus formation?
Endothelial injury Abnormal blood flow Hypercoagulability
51
What is an embolus?
Detached intravascular mass carried by blood to site distant from origin.
52
Types of emboli
``` Thrombus (thromboembolism) Fat-rupture of vascular sinusoids/venules Air Amniotic fluid Tumor ```
53
Sources of thromboemboli?
Vessels (deep vein thrombosis occurring in leg veins) Heart: atrial or ventricular walls or valve leaflets Atherosclerotic plaque-abdominal aorta, carotid artery Paradoxical embolism: travels through heart defect into systemic circulation (patent foramen ovale)
54
What is a pulmonary embolism?
Most common type of embolism Usual source is DVT Most are asymptomatic but serious consequences with saddle emboli (at bifurcation of pulmonary arteries) and multiple emboli.
55
What is infarction and what causes it?
Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of a particular tissue.
56
What are the two types of infarcts and what causes them?
Red infarct: hemorrhagic-occurs in loose tissues, dual circulation tissues, when flow is re-established, venous occlusions White infarct: anemic (no blood)- occurs in solid organs with end-arterial circulation. Like spleen or kidneys
57
DIC
Characterized by initial clotting (microangiopathy), resulting in organ ischemia, followed by bleeding tendencies. Consumptive coagulopathy: Widespread clotting leads to consumption of factors and platelets Clotting factors consumed = bleeding Platelets consumed = bleeding Associated with severe illnesses
58
What is the difference between a hematoma and a hemorrhagic infarct?
In a hemorrhagic infarct, blood is intermixed with necrotic tissue; in hematoma blood is collected and form a solid mass
59
What is shock
Systemic hypoperfusion caused by 1. reduced cardiac output or 2. decrease in effective circulating blood volume
60
What are the 3 major types of shock
1. Cardiogenic 2. Hypovolemic 3. Septic
61
What are other types of shock
Neurogenic shock and Anaphylactic shock
62
What are the stages of shock
1. Nonprogressive phase 2. Progressive phase 3. Irreversible phase
63
What distinguishes hypovolemic and cardiogenic shock vs. septic shock and what is similar in their clinical presentation?
Cool, clammy, and cyanotic skin vs. warm and flushed (initially) They are all hyptension, tachycardic, tachypnea
64
What causes septic shock most often?
Most often gram positive bacteria. Followed by gram negative bacteria and fungi.

FPP Weeks 1 & 2 (18 decks)

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