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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
What cleaves fibrin? What is produced?
Plasmin D-dimers
26
What does heparin activate? What does this do?
antithrombin III Inactivates thrombin, factors 9, 10, 11, 12
27
What does protein C do? What does it require the help of?
Inactivates factors 5 and 8 Protein S
28
Defects of primary Hemostasis is associated with what? Classic finding?
Mucosal cutaneous bleeding Petechia (1-2mm) and purpura (4-10mm)
29
What can cause primary Hemostasis?
Renal failure leading to uremia and reduced platelet function Thrombocytopenia
30
What is deficient in Glanzmann disease?
GpIIb-IIIa resulting in bleeding disorder bc platelets are impaired (primary Hemostasis)
31
What is Bernard-Soulier syndrome?
GpIb deficiency
32
What makes up Virchow triad?
Primary endothelial injury Abnormal blood flow Hypercoagulability
33
When does endothelial dysfunction result in a prothrombotic environment?
Chronic inflammation HTN Hyperlipidemia Circulating toxins
34
In endothelial injury what are the Procoagulant effects? What are the anti fibrinolytic effects?
DEC thrombomodulin DEC protein C DEC TF inhibitor DEC t-PA
35
Turbulence normally occurs where? Stasis?
Arteries and in the heart Veins
36
What are clinical examples of altered blood flow?
Ulcerated atherosclerotic plaques Aneurysms Infarcted myocardial tissue Prolonged immobilization (bed rest)
37
What is the defect in Factor 5 Leiden? Most common among who?
Resistant to protein C Caucasians 3-8%
38
What is the 2nd most common inherited cause of hypercoagulability? What gene?
Prothrombin gene mutation (INC prothrombin) 20210A
39
Deficiency of what enzyme may result in a hypercoagulable state? Results in what?
Cystathione B-sythase Homocystein uri's
40
What are some examples of acquired hypercoagulability?
``` Immobilization MI or AFib Trousseau's syndrome Oral contraceptives and Hyperestrogenic state Tissue injury Smoking HIT syndrome Antiphospholipid Ab syndrome ```
41
What is Trousseau's syndrome?
Seen with malignant cancers (pancreatic, lung) where they reduce prothrombotic mucin
42
What is HIT?
Abs that complex unfractionated heparin and platelet factor 4 activates the platelets and end up becoming consumed making CLOTS
43
What is Antiphospholipid antibody syndrome? What Ab levels may be elevated?
Recurrent vascular thrombosis, thrombocytopenia or recurrent fetal loss Anticardiolipin Ab
44
What are the clinical presentations with Antiphospholipid antibody syndrome?
PE Stroke MI Bowel infarction
45
What do lines of Zahn contain? Indicates what?
Alternating red and tan regions regions (containing RBCs and platelets) Thrombus formed in flowing blood
46
Where are the common sites of arterial thrombi?
Coronary, cerebral, femoral arteries
47
Where are the common sites of venous thrombi?
Veins of leg (superficial and deep) | Upper extremities
48
Thrombi occurring in the heart or within the aorta are called what? Occur when?
Mural thrombi MI or AAA
49
What happens in organization of thrombus?
Replaced by fibroblasts, smooth muscle and endothelial cells
50
What happens in recanalization of thrombi?
New capillaries and small vessels grow through the structure
51
What is the most common cause of increased hydrostatic pressure?
Impaired venous return
52
What are the most common symptoms with defects of secondary Hemostasis? Due to what?
Bleeding into joints (hemarthrosis) or soft tissue Coagulation factor deficiencies (hereditary or acquired)
53
What is characteristic of DIC?
Widespread microthrombi Consumption of coagulation factors Consumption of platelets
54
What are some causes that may lead to DIC?
Sepsis Childbirth problems Massive trauma Malignancy
55
What do lab studies show in DIC?
Elevated PT and PTT Low fibrinogen INC D-diners Thrombocytopenia
56
What type of cells may be found in DIC?
Intravascular hemolysis - Schistocytes
57
Vitamin K is essential for production of what? Where is it found?
2, 7, 9, 10, Protein C, protein K Leafy greens, synthesized by gut flora
58
What kind of patients exhibit Vitamin K deficiency?
Pts receiving warfarin/Coumadin Malnourished or prolonged parenteral nutrition Prolonged Antibiotics
59
Massive transfusion defined how? What does it cause?
1.5 x blood volume in 24 hours INC PT, PTT DEC fibrinogen and platelets
60
What is coagulation factor inhibitor? What factor inhibition is most common?
Acquired Antibody resulting in impaired factor function Factor 8 (Hemophilia A)
61
A mixing study is used to determine what? What will not correct if there is inhibitor present?
Whether abnormal clotting times are due to a decreased amount of factor (as in hemophilia) or due to presence of inhibitor PTT
62
Pulmonary Embolisms originate where?
DVTs in the leg (95%)
63
What is a saddle embolus?
Straddles the pulmonary artery bifurcation
64
Sudden death or right heart failure from PE may occur when?
60% of PA circulation is obstructed
65
Where do systemic embolisms arise from?
80% from the heart (LV wall and LA dilation/fibrillation)
66
What are the other sites of systemic thromboembolism?
Aortic aneurysms Atherosclerotic plaques Cardiac valves (vegetational) Paradoxical emboli
67
What is a paradoxical embolism?
Venous embolus that gains access to the systemic arterial circulation
68
Where do the majority of systemic thromboembolism sludge?
``` Lower extremities (75%) Brain (10%) ```
69
What causes fat and marrow embolism? Where does it translocate?
Fractures of long bones Venous sinuses and then travel to the lungs
70
What is fat embolism syndrome? Characterized by what?
Symptomatic fat and marrow embolisms Pulmonary insufficiency, neurological symptoms, anemia, thrombocytopenia
71
Air embolisms must be what size to produce a clinical effect? How can they be introduced?
Greater than 100cc Surgically (vascular, neurosurgical, laparoscopic)
72
What is decompression sickness? Aka what?
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
What is Caisson disease?
Persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis, most commonly in the femoral head, tibia, humerus
74
What causes amniotic fluid embolism? Can cause what serious condition?
Infusion of amniotic fluid/fetal tissue into maternal circulation via a tear in placental membrane or rupture of uterine veins DIC
75
What kind of cells are seen in an amniotic fluid embolism?
Squamous
76
What is infarction? Due to what?
Ischemic necrosis via occlusion of arterial supply or venous drainage Arterial thrombosis or arterial embolism
77
What is characteristic of a red infarct?
Tissue with a dual blood supply (LUNG) Venous occlusion (torsion) Previously congested tissue Reperfused necrotic tissue after arterial occlusion
78
What is characterisitc of a white infarct? What organs?
Arterial occlusions in solid organs with end-arterial circulation Spleen, kidney, heart
79
When does a septic infarct occur? What can it be converted to?
Infected cardiac valve vegetations embolize or when microbes seed necrotic tissue Abscess w/greater inflammatory response
80
What causes shock?
Diminished CO or reduced effective circulating blood volume -> cellular hypoxia
81
What causes cardiogenic shock?
Low CO due to cardiac infarction, tamponade, arrhythmia
82
What causes Hypovolemic shock?
Low CO due to low blood volume (hemorrhage from burns)
83
What causes systemic inflammation? Results in what?
Microbial infections, burns, trauma, pancreatitis Hypoperfusion, cellular hypoxia
84
What is the most common cause of death in US ICUs? Mortality rate? Causative organism?
Septic shock 20% Gram positive bacteria
85
What are the main characteristics of septic shock?
Vasodilation -> DEC BP Increased permeability -> leakage and edema Procoagulant state (INC thrombin), eventually DIC
86
What metabolic disturbances can septic shock cause? Inflammatory cytokines impair what?
Insulin resistance and hyperglycemia Adrenal insufficiency and defect of glucocorticoids GLUT4
87
Cellular hypoxia and DEC ox-phos leads to what?
INC lactate production and lactic acidosis
88
How does septic shock affect organs?
Systemic hypotension, edema, vascular leakage, stasis, thrombi
89
What is the net effect/goal of reflex mechanisms during the Nonprogressive phase of shock?
Tachycardia, peripheral vasoconstriction, renal conservation of fluid
90
What are the reflex compensatory mechanisms during Nonprogressive phase of shock?
``` Baroreceptor reflex Catecholamines release ADH release Symp stimulation Activation of renin-angiotensin axis ```
91
What characterizes the progressive phase of shock?
Tissue hypoperfusion, lactic acidosis, further vasodilation and peripheral pooling and stasis
92
In cardiogenic/Hypovolemic shock, how does the patient present? Septic shock?
Hypotension, tachypnea, weak, cool, clammy, cyanotic Vasodilated, warm, flushed

COM - MOD 1 (7 decks)

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