PB+T > Hemodynamics > Flashcards

Hemodynamics Flashcards

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0
Q

Deficiency in vW factor

A

Von Willebrand disease

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1
Q

Deficiency in Gp1b

A

Bernard Soulier syndrome

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2
Q

Deficiency of GpIIb-IIIa complex

A

Glanzmann thrombasthenia

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3
Q

Post-Mortem clot

A

Contains the lines of Zahn and is typically NOT attached to endothelial cell wall

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4
Q

Virchow’s triad: thrombus dev.

A

Stasis
Endothelial damage
Hypercoagulable state

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5
Q

Protection against thrombus formation

A
  • Endothelial cells themselves block contact with sub endo collagen from interacting with platelets.
  • PGI2
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6
Q

Heparin-like molecules

A

Activate antithrombin III

  • block thrombin and inhibits coag factors
  • produced by endothelial cells
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7
Q

TPA

A
  • converts plasminogen -> plasmin which cleaves fibrin, or serum fibrinogen
  • it destroys clotting factors
  • blocks platelet aggregation
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8
Q

Thrombomodulin

A
  • modulates thrombin to activate protein C which in turn inactivates factor V and VIII (important amplifying factors in the coag cascade)
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9
Q

Homocysteine in thrombosis

A

Increased levels -> damage endothelial cells

- this result from folate/B12 deficiency

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10
Q

Causes of increased hydrostatic pressure: 2 mechanisms and local vs. systemic

A 
Impaired venous return 
- DVT (local) 
- CHF (systemic) 
Arteriolar dilation 
- heat
- neurohumoral days regulation
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11
Q

Decrease in plasma oncotic pressure

A
  • Albumin loss: nephrotic disease

- low albumin: liver damage, malnutrition (often both occur)

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12
Q

Na retention

A

Causes both increased hydrostatic pressure and decreased colloid osmotic pressure - results from primary kidney disorder, hypoperfusion, CHF et al.

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13
Q

Lympedema: 4 causes

A

Chronic inflammation (fibrosis)
Radiation
Infection
Auxiliary lymphadenectomy < über testable

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14
Q

Anasarca: definition and common location

A

Generalized widespread edema with tissue swelling

- subQ, periorbital, lungs, brain

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15
Q

Hyperemia vs. congestion

A

Hyperemia: active shunting of blood to a specific area
Congestion: increase local blood volume due to decreased outflow (passive)

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16
Q

Morphology of hyperemia and congestion

A

Lungs: dusky red, (acutely) engorged caps, focal intralviolar hemorrhage (chronically) thick, fibrotic septa, hemosiderin laden macs. (Heart failure cells)
Liver: nutmeg liver, small punctuate hemorrhages

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17
Q

Hemorrhage classification: (by size)

A

Petechiae: 1-3 mm
Purpura: 3-10 mm
Ecchymoses: >10 mm
Hematoma: a big ecchymoses

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18
Q

Alpha granules

A 
Fibrinogen
Fibronectin
Factor V and VIII
Platelet factor 4 (binds heparin) 
PDGF
TGF-B
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19
Q

Dense granules

A 
ADP
ATP 
Ionized calcium
Histamine 
Serotonin
Epi
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20
Q

Activation of platelets

A
  • vWF cross ridges with the platelet GPTNS to collagen sub endothelial tissue
  • ionized Ca binds negatively charged surface GPTNS -> site for assembly of coagulation complexes
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21
Q

Events leading up to platelet plug (step 1)

A
  • Thrombin binds receptor on platelet surface
  • bound thrombin + ADP and TxA2 -> further aggregation
  • contraction of platelet cytoskeleton (irreversible process)
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22
Q

Fibrin functions

A

Activated by thrombin

  • crosslinks platelet plugin to a solid mesh work
  • binds GpIIa-IIIb between two platelets
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23
Q

GpIIa-IIIb

A

Serves as fibronectin receptor crosslinking them into a solid mesh

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24
Leukocytes in coagulation
- Adhere to platelets via P-selectins and contribute to inflammation - thrombin - induces leukocyte/monocyte adhesion and generates fibrin spilt products
25
Vitamin K
Cofactor in the binding of factors II, VII, IX and X | - warfarin inhibits these processes
26
Function of thrombin: 5
``` Platelet activation Endothelial activation Monocyte activation Neutrophil adhesion Lymphocyte activation ```
27
Anti-thrombin III: source, action and clinical significance
Source: binding of HLMs on endo cells Action: inhibits activity of thrombin and factors IX,X,XI and XII Clinical sig: heparin enhances activation
28
Protein C and S: source and action
Source: vitamin K dependent proteins Action: inhibits activated factors V and VII
29
Tissue factor pathway inhibitor
Source: produced by endothelium Action: inactivates tissue factor VIIa complexes
30
TPA/PAI
TPA initiates degredation of fibrin: PAI inhibits TPA
31
a2-antitrypsin
Indus free plasmin in the blood to keep it from degrading
32
Alterations in normal bloodflow
Stasis and turbulence Turbulence: atrial and cardiac thrombosis - contributed to primarily by endo injury Stasis: venous thrombosis
33
Ulceration of atherosclerotic plaques
- exposes sub endo collage -> thrombus formation | - results in turbulence
34
Aneurysms: effect
Local stasis
35
Acute MI
Stasis Abnormal flow Cardiac mural thrombi
36
Hyperviscosity (polycythemia)
Increased resistance and stasis
37
Sickle cell anemia
Vascular occlusion, stasis
38
4 common genetic hyper coagulable states
Factor V Leiden mutation mutated prothrombin gene Mutant THFr gene Increased clotting factors (7,9,11)
39
Factor V Leiden mutation
COMMON, 2-15 Caucasians - individual's with recurrent DVT's - glu-> arg 506; factors resistant to Ca cleavage - hetero: 5x - homo: 50x
40
Prothrombin gene mutation
- Affects 1-2% - single 3' mutation - increases prothrombin levels - 3x fold increased risk
41
Young pt. presenting with thromboemboli
Must asses genetic susceptibility for clotting disorder
42
DIC
Platelets aggregate in microcirculation consuming clotting factors, Schistiocytes form from trauma in vasculature. Diffuse activation of fibrinolysin - trt underlying disease to fix DIC
43
Anti-phospholipid antibody syndrome
Cause: Abs form to epitopes on plasma proteins unveiled by phoslips. Effect: hypercoagulable state - false positive test for syphilis Clinical manifestations: recurrent thrombosis, recurrent miscarriages, cardiac valve vegetations, tcytopenia, PE, pulmonary HTN
44
Postmortem clots
Chicken fat, no lines of Zahn, and non-adherent
45
Etiology: arterial thrombi
Ruptured atherosclerotic plaque, vasculitis, trauma
46
Etiology: mural thrombi (cardiac)
Abnormal cardiac contractions or endocaridal injury
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Mural thrombi (aorta)
Ulcerated atherosclerotic plaque, aneurysmal dilation
48
Vegetations
Infective endocarditis, sterile endocarditis, SLE
49
PEs
- Generally silent due to small size and collateral circulation. Become organized Medium emboli - pulmonary hemorrhage from vascular rupture - infarction of left sided heart failure Large/saddle - dead.
50
Etiology of most Systemic thromboemboli
80% arise from intracardiac mural thrombi - 2/3 from left ventrical wall infarcts - 1/3 from left atrial dilation/fibrillation
51
Fat/Marrow embolism
Fracture of long bones, tissue trauma Histologically: looks like a bone marrow section - results in free fatty acid toxicity, platelet activation, and granulocyte recruitment
52
Air emboli
- from surgery or decompression | - trt: with slow decompression
53
Amniotic fluid emboli: general
Tear in placental membrane, or rupture of uterine veins - infusion of amniotic fluid, fetal tissue into maternal tissue - diffuse alviolar damage - pulmonary edema - fibrin thrombi in vascular beds
54
Amniotic fluid emboli: clinical presentation
Sudden severe dyspnea, cyanosis, shock, neuroimpairment, | - if pt. survives; pulmonary edema, DIC
55
Infarction
Occlusion resulting in ischemia - 40% of deaths in US resultant from CVD, most due to MI, cerebral infarction - morbidity includes gangrene - result is coagulative necrosis: except in brain -> liquifactive
56
Red infarcts
Venous occlusion, | - loose and dual circulation supplied tissue
57
White infarcts
Arterial occlusion | - solid organs with single arterial supply
58
Septic infarcts
Vegetation on cardiac valve embolizes - microbes seed tissue - abcess forms and occludes tissue
59
Tissue vulnerability to ischemia
- hypoxia sensitivity: brain (3-4 min), heart (20-30), fibroblasts (lots of hours) - O2 content: anemia, cyanosis
60
Shock
Hypotension dude to either: decreased CO, or decreased blood volume - impairs tissue perfusion and causes cellular hypoxia
61
Shock types: 5
anaphylactic: systemic vasodilation and increased vasc. Perm. neurogenic: loss of vascular tone -> periph. Pooling septic: inflammation, metabolic abnormalities, immune suppression organ dysfunction hypovolemic: Cardiogenic: Toxic: superantigen mediated
62
Septic shock
- Inflammation compliment IL-16/8, NO, PAF -> systemic response: antiinflammatory signals (IL-1r inhibitor, IL-10) - endo act - metabolic abnormalities - immune suppression - organ dysfunction
63
Inflammation in septic shock
- Activation of neutrophils, monos, and endos - TNF, interleukins (1,8 et al) - PGEs - activation of compliment - factor XII - immuneosuppression
64
Immunosuppressive effect in septic shock
The hyper state of infection results in a swing away from TH1 inflammatory cells to TH2 anti-inflammatory/immune response - anti-inflammatory cytokines, IL-10, apoptosis et al.
65
Toxic shock
Very similar to septic shock, but mediated by superantigens
66
Factors effected by thrombomodulin
Throne-thombomodulin-Seige breaker-APC-factors V and VIII
67
Anti-thrombin III
- Binds heparin like molecules | - inhibits factors IX,X,XI,XII (anti thrombin III has the biggest number in it; inhibits the biggest numbers)
68
Activated Protein C (APC- siege breaker)
- initiates proteolysis of factors Va and VIIIa (Harry V and henry VIII)
69
Tissue factor pathway inhibitor
From endothelium; inactivates tissue factor-factor VIIa complex
70
Lupus anticoagulant
Hypercoagulant state; aka anti-phospholipid antibody syndrome
71
Alpha granules: components
``` Fibrinogen Fibronectin vWf P-selectins PDGF TGF-B ```
72
Dense granules: conponents
``` ADP Ca ATP Histamine Serotonin Epi ```
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