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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
Q

What are important laboratory screenings for primary hemostasis?

A
  1. Platelet count
  2. Platelet function (PFA-100 and platelet aggregation studies)
  3. vWillebrand studies (vW antigen and vW activity)
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26
Q

What are important laboratory screenings for secondary hemostasis? And what specifically do they test?

A
  1. Prothrombin time [PT]- Test extrinsic and common pathways
  2. Activated partial thromboplastin time [aPTT]- Test intrinsic and common pathways
  3. Fibrinogen activity
27
Q

What defects result in bleeding disorders?

A
  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
Q

What is scurvy?

A

Vitamin C deficiency leading to vessel fragility

29
Q

What is thrombocytopenia?

A

Too few platelets

30
Q

What is Glanzmann’s thrombasthenia?

A

An inherited defect within the platelet membrane

31
Q

What does Vitamin K deficiency/warfarin cause?

A

Deficiency of factors 2, 7, 9, 10

32
Q

What is disseminated intravascular coagulation (DIC)

A

Factor and Platelet consumption.

33
Q

What is hemorrhage?

A

Extravasation of blood from vessels.

Accumulating within a space

34
Q

What are common causes of hemorrhage?

A

Ruptured vessel (atherosclerosis, inflammation-vasculitis, aneurysm)

Peptic ulcer

Chronic congestion

Predisposition to hemorrhage with minimal trauma seen with decreased ability to clot

35
Q

What is a hematoma?

A

Accumulation of blood within a tissue

36
Q

What are petechial hemorrhages?

A

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
Q

What is purpura?

A

Greater than 3 mm hemorrhages.

Associated w same disorders as petechiae and w/ trauma, vaculitis, and vascular fragility

38
Q

What are ecchymoses?

A

Greater than 1-2 cm subcutaneous hematomas.

Associated with trauma and exacerbated by the other conditions (assoc with purpura and petechiae)

39
Q

What factors contribute to favor thrombosis?

A

Endothelial Injury
and
Abnormal Blood Flow

40
Q

What factors contribute to inhibiting thrombosis?

A

Antithrombin III

Protein C and S

Tissue factor pathway inhibitor

PGI2

41
Q

How do Protein C and S work?

A

Shut down Factor V and VIII

42
Q

How does Antithrombin III work?

A

As thrombin is generated, antithrombin III shuts it down.

43
Q

Hypercoagulability factors

A

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
Q

What is Factor 5 Leiden

A

Most common inherited predisposition to thrombosis

Changes the cleavage site for protein C.

Activated Protein C resistance

45
Q

Antiphospholipid antibodies?

A

Acquired autoantibodies against PL complexes

Assoc with arterial venous thromboses with high recurrence rates.

Inhibit clotting in vitro; promote clotting in vivo.

46
Q

What are the 2 types of lab testing for antiphospholipid antibodies?

A

Lupus anticoagulant (prolongation of clotting based tests)

and

Anti-cardiolipin antibodies (immunoassays for anti-cardiolipin)

47
Q

What is a thrombosis?

A

Formation of a blood clot within intact vessels

48
Q

Where does a thrombus begin?

A

At a site of endothelial injury, or turbulence of flow, or site of blood stasis

49
Q

What are the lines of zahn

A

Laminations apparent grossly or microscopically produced by alternating layers of platelets, fibrin, and RBCs

50
Q

What are the three primary abnormalities that lead to thrombus formation?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

51
Q

What is an embolus?

A

Detached intravascular mass carried by blood to site distant from origin.

52
Q

Types of emboli

A 
Thrombus (thromboembolism)
Fat-rupture of vascular sinusoids/venules
Air
Amniotic fluid
Tumor
53
Q

Sources of thromboemboli?

A

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
Q

What is a pulmonary embolism?

A

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
Q

What is infarction and what causes it?

A

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

56
Q

What are the two types of infarcts and what causes them?

A

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
Q

DIC

A

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
Q

What is the difference between a hematoma and a hemorrhagic infarct?

A

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

59
Q

What is shock

A

Systemic hypoperfusion caused by

  1. reduced cardiac output or
  2. decrease in effective circulating blood volume
60
Q

What are the 3 major types of shock

A
  1. Cardiogenic
  2. Hypovolemic
  3. Septic
61
Q

What are other types of shock

A

Neurogenic shock and Anaphylactic shock

62
Q

What are the stages of shock

A
  1. Nonprogressive phase
  2. Progressive phase
  3. Irreversible phase
63
Q

What distinguishes hypovolemic and cardiogenic shock vs. septic shock and what is similar in their clinical presentation?

A

Cool, clammy, and cyanotic skin vs. warm and flushed (initially)

They are all hyptension, tachycardic, tachypnea

64
Q

What causes septic shock most often?

A

Most often gram positive bacteria. Followed by gram negative bacteria and fungi.

FPP Weeks 1 & 2 (18 decks)

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