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COM - MOD 1 > Ch 4 - 5/9-5/11 Gallbraith > Flashcards

Ch 4 - 5/9-5/11 Gallbraith Flashcards

1
Q

Reduced plasma osmotic pressure is caused by what?

A

Albumin and liver disease decreases protein synthesis

Nephrotic syndrome leads to loss of proteins

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2
Q

How does sodium and water retention affect hydrostatic pressure and plasma osmotic pressure?

Result?

A

INC hydrostatic P
DEC osmotic P bc of dilution

Renal failure, can be caused by CHF

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3
Q

What can cause edema via lymphatic obstruction?

A

Trauma
Fibrosis
Tumor
Infection

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4
Q

How do you describe Transudative effusion?

A

Protein poor, serous, straw-colored

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5
Q

Characteristics of exudative effusion?

A

Protein rich, opaque, INC WBCs

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6
Q

Subcutaneous edema may signify what?

A

Cardiac or renal disease

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7
Q

What is a common characteristic of severe chronic renal disease?

CHF?

Liver disease?

A

Periorbital edema

Pulmonary edema

Ascites

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8
Q

Increased blood volume in tissue, either locally or systemically is called what?

Result of what?

A

Hyperemia

INC arterial blood delivery to a given location

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9
Q

Congestion is the result of what?

Causes what?

Chronic cases lead to what?

A

DEC blood outflow

INC hydrostatic pressure, leads to edema

Hypoxia and ischemia

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10
Q

Morphologically, what appearance do congested tissues take on?

A

Dusky, reddish-blue color (cyanosis) due to red cell stasis and deoxygenated hemoglobin

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11
Q

What is the 1st thing that happens in Hemostasis at the site of vascular injury?

What mediates this process?

A

Arteriolar constriction

Endothelin released from endothelium

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12
Q

Where do platelets come from?

A

Megakaryoctes from bone marrow

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13
Q

What do alpha-granules of platelets contain?

A

Fibrinogen
Factor V
vWF

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14
Q

What do delta-granules of platelets contain?

A

Calcium

ADP

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15
Q

Platelet adhesion occurs via what interaction?

What does this interaction cause?

A

GpIb - vWF

Activation

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16
Q

Activation of platelets induces what?

A

Shape change to increase surface area and increase negative charge at the surface
Degranulation
Release of TxA2

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17
Q

Platelets aggregate and link through what interaction?

A

Fibrinogen - GpIIb/IIIa

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18
Q

What induces conformational change to express the GpIIb-IIIa complex to be exposed?

A

ADP

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19
Q

What converts fibrinogen to fibrin?

What does this promote?

A

Thrombin

Further platelet activation, aggregation, contraction

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20
Q

What additional role does thrombin serve on endothelium?

A

Acts on normal endothelium to limit clot size

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21
Q

What is responsible for activating factors 9 and 10?

A

TF-7a

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22
Q

Thrombin feeds back and amplifies the coagulation cascade by activating what?

A

11, 8, 5

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23
Q

What does the PT measure?

What must you add?

A

Extrinsic pathway

TF, phospholipids, Ca

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24
Q

What does PTT measure?

What must you add?

A

Intrinsic

Negatively charged surface, phospholipids, Ca

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25
Q

What cleaves fibrin?

What is produced?

A

Plasmin

D-dimers

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26
Q

What does heparin activate?

What does this do?

A

antithrombin III

Inactivates thrombin, factors 9, 10, 11, 12

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27
Q

What does protein C do?

What does it require the help of?

A

Inactivates factors 5 and 8

Protein S

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28
Q

Defects of primary Hemostasis is associated with what?

Classic finding?

A

Mucosal cutaneous bleeding

Petechia (1-2mm) and purpura (4-10mm)

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29
Q

What can cause primary Hemostasis?

A

Renal failure leading to uremia and reduced platelet function

Thrombocytopenia

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30
Q

What is deficient in Glanzmann disease?

A

GpIIb-IIIa resulting in bleeding disorder bc platelets are impaired (primary Hemostasis)

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31
Q

What is Bernard-Soulier syndrome?

A

GpIb deficiency

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32
Q

What makes up Virchow triad?

A

Primary endothelial injury
Abnormal blood flow
Hypercoagulability

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33
Q

When does endothelial dysfunction result in a prothrombotic environment?

A

Chronic inflammation
HTN
Hyperlipidemia
Circulating toxins

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34
Q

In endothelial injury what are the Procoagulant effects?

What are the anti fibrinolytic effects?

A

DEC thrombomodulin
DEC protein C
DEC TF inhibitor

DEC t-PA

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35
Q

Turbulence normally occurs where?

Stasis?

A

Arteries and in the heart

Veins

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36
Q

What are clinical examples of altered blood flow?

A

Ulcerated atherosclerotic plaques
Aneurysms
Infarcted myocardial tissue
Prolonged immobilization (bed rest)

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37
Q

What is the defect in Factor 5 Leiden?

Most common among who?

A

Resistant to protein C

Caucasians 3-8%

38
Q

What is the 2nd most common inherited cause of hypercoagulability?

What gene?

A

Prothrombin gene mutation (INC prothrombin)

20210A

39
Q

Deficiency of what enzyme may result in a hypercoagulable state?

Results in what?

A

Cystathione B-sythase

Homocystein uri’s

40
Q

What are some examples of acquired hypercoagulability?

A 
Immobilization
MI or AFib
Trousseau's syndrome
Oral contraceptives and Hyperestrogenic state
Tissue injury
Smoking
HIT syndrome
Antiphospholipid Ab syndrome
41
Q

What is Trousseau’s syndrome?

A

Seen with malignant cancers (pancreatic, lung) where they reduce prothrombotic mucin

42
Q

What is HIT?

A

Abs that complex unfractionated heparin and platelet factor 4 activates the platelets and end up becoming consumed making CLOTS

43
Q

What is Antiphospholipid antibody syndrome?

What Ab levels may be elevated?

A

Recurrent vascular thrombosis, thrombocytopenia or recurrent fetal loss

Anticardiolipin Ab

44
Q

What are the clinical presentations with Antiphospholipid antibody syndrome?

A

PE
Stroke
MI
Bowel infarction

45
Q

What do lines of Zahn contain?

Indicates what?

A

Alternating red and tan regions regions (containing RBCs and platelets)

Thrombus formed in flowing blood

46
Q

Where are the common sites of arterial thrombi?

A

Coronary, cerebral, femoral arteries

47
Q

Where are the common sites of venous thrombi?

A

Veins of leg (superficial and deep)

Upper extremities

48
Q

Thrombi occurring in the heart or within the aorta are called what?

Occur when?

A

Mural thrombi

MI or AAA

49
Q

What happens in organization of thrombus?

A

Replaced by fibroblasts, smooth muscle and endothelial cells

50
Q

What happens in recanalization of thrombi?

A

New capillaries and small vessels grow through the structure

51
Q

What is the most common cause of increased hydrostatic pressure?

A

Impaired venous return

52
Q

What are the most common symptoms with defects of secondary Hemostasis?

Due to what?

A

Bleeding into joints (hemarthrosis) or soft tissue

Coagulation factor deficiencies (hereditary or acquired)

53
Q

What is characteristic of DIC?

A

Widespread microthrombi
Consumption of coagulation factors
Consumption of platelets

54
Q

What are some causes that may lead to DIC?

A

Sepsis
Childbirth problems
Massive trauma
Malignancy

55
Q

What do lab studies show in DIC?

A

Elevated PT and PTT
Low fibrinogen
INC D-diners
Thrombocytopenia

56
Q

What type of cells may be found in DIC?

A

Intravascular hemolysis - Schistocytes

57
Q

Vitamin K is essential for production of what?

Where is it found?

A

2, 7, 9, 10, Protein C, protein K

Leafy greens, synthesized by gut flora

58
Q

What kind of patients exhibit Vitamin K deficiency?

A

Pts receiving warfarin/Coumadin
Malnourished or prolonged parenteral nutrition
Prolonged Antibiotics

59
Q

Massive transfusion defined how?

What does it cause?

A

1.5 x blood volume in 24 hours

INC PT, PTT
DEC fibrinogen and platelets

60
Q

What is coagulation factor inhibitor?

What factor inhibition is most common?

A

Acquired Antibody resulting in impaired factor function

Factor 8 (Hemophilia A)

61
Q

A mixing study is used to determine what?

What will not correct if there is inhibitor present?

A

Whether abnormal clotting times are due to a decreased amount of factor (as in hemophilia) or due to presence of inhibitor

PTT

62
Q

Pulmonary Embolisms originate where?

A

DVTs in the leg (95%)

63
Q

What is a saddle embolus?

A

Straddles the pulmonary artery bifurcation

64
Q

Sudden death or right heart failure from PE may occur when?

A

60% of PA circulation is obstructed

65
Q

Where do systemic embolisms arise from?

A

80% from the heart (LV wall and LA dilation/fibrillation)

66
Q

What are the other sites of systemic thromboembolism?

A

Aortic aneurysms
Atherosclerotic plaques
Cardiac valves (vegetational)
Paradoxical emboli

67
Q

What is a paradoxical embolism?

A

Venous embolus that gains access to the systemic arterial circulation

68
Q

Where do the majority of systemic thromboembolism sludge?

A 
Lower extremities (75%)
Brain (10%)
69
Q

What causes fat and marrow embolism?

Where does it translocate?

A

Fractures of long bones

Venous sinuses and then travel to the lungs

70
Q

What is fat embolism syndrome?

Characterized by what?

A

Symptomatic fat and marrow embolisms

Pulmonary insufficiency, neurological symptoms, anemia, thrombocytopenia

71
Q

Air embolisms must be what size to produce a clinical effect?

How can they be introduced?

A

Greater than 100cc

Surgically (vascular, neurosurgical, laparoscopic)

72
Q

What is decompression sickness? Aka what?

A

Person experiences sudden decreases in atmospheric pressure (ascending from deep sea dive)
Nitrogen precipitates out of solution into the blood and tissues

Aka bends or chokes

73
Q

What is Caisson disease?

A

Persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis, most commonly in the femoral head, tibia, humerus

74
Q

What causes amniotic fluid embolism?

Can cause what serious condition?

A

Infusion of amniotic fluid/fetal tissue into maternal circulation via a tear in placental membrane or rupture of uterine veins

DIC

75
Q

What kind of cells are seen in an amniotic fluid embolism?

A

Squamous

76
Q

What is infarction?

Due to what?

A

Ischemic necrosis via occlusion of arterial supply or venous drainage

Arterial thrombosis or arterial embolism

77
Q

What is characteristic of a red infarct?

A

Tissue with a dual blood supply (LUNG)
Venous occlusion (torsion)
Previously congested tissue
Reperfused necrotic tissue after arterial occlusion

78
Q

What is characterisitc of a white infarct?

What organs?

A

Arterial occlusions in solid organs with end-arterial circulation

Spleen, kidney, heart

79
Q

When does a septic infarct occur?

What can it be converted to?

A

Infected cardiac valve vegetations embolize or when microbes seed necrotic tissue

Abscess w/greater inflammatory response

80
Q

What causes shock?

A

Diminished CO or reduced effective circulating blood volume -> cellular hypoxia

81
Q

What causes cardiogenic shock?

A

Low CO due to cardiac infarction, tamponade, arrhythmia

82
Q

What causes Hypovolemic shock?

A

Low CO due to low blood volume (hemorrhage from burns)

83
Q

What causes systemic inflammation?

Results in what?

A

Microbial infections, burns, trauma, pancreatitis

Hypoperfusion, cellular hypoxia

84
Q

What is the most common cause of death in US ICUs?

Mortality rate?

Causative organism?

A

Septic shock

20%

Gram positive bacteria

85
Q

What are the main characteristics of septic shock?

A

Vasodilation -> DEC BP
Increased permeability -> leakage and edema
Procoagulant state (INC thrombin), eventually DIC

86
Q

What metabolic disturbances can septic shock cause?

Inflammatory cytokines impair what?

A

Insulin resistance and hyperglycemia
Adrenal insufficiency and defect of glucocorticoids

GLUT4

87
Q

Cellular hypoxia and DEC ox-phos leads to what?

A

INC lactate production and lactic acidosis

88
Q

How does septic shock affect organs?

A

Systemic hypotension, edema, vascular leakage, stasis, thrombi

89
Q

What is the net effect/goal of reflex mechanisms during the Nonprogressive phase of shock?

A

Tachycardia, peripheral vasoconstriction, renal conservation of fluid

90
Q

What are the reflex compensatory mechanisms during Nonprogressive phase of shock?

A 
Baroreceptor reflex
Catecholamines release
ADH release
Symp stimulation
Activation of renin-angiotensin axis
91
Q

What characterizes the progressive phase of shock?

A

Tissue hypoperfusion, lactic acidosis, further vasodilation and peripheral pooling and stasis

92
Q

In cardiogenic/Hypovolemic shock, how does the patient present?

Septic shock?

A

Hypotension, tachypnea, weak, cool, clammy, cyanotic

Vasodilated, warm, flushed

COM - MOD 1 (7 decks)

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