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PB+T > Hemodynamics > Flashcards

Hemodynamics Flashcards

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
Q

Leukocytes in coagulation

A
  • Adhere to platelets via P-selectins and contribute to inflammation
  • thrombin - induces leukocyte/monocyte adhesion and generates fibrin spilt products
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25
Q

Vitamin K

A

Cofactor in the binding of factors II, VII, IX and X

- warfarin inhibits these processes

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26
Q

Function of thrombin: 5

A 
Platelet activation
Endothelial activation 
Monocyte activation
Neutrophil adhesion
Lymphocyte activation
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27
Q

Anti-thrombin III: source, action and clinical significance

A

Source: binding of HLMs on endo cells
Action: inhibits activity of thrombin and factors IX,X,XI and XII
Clinical sig: heparin enhances activation

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28
Q

Protein C and S: source and action

A

Source: vitamin K dependent proteins
Action: inhibits activated factors V and VII

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29
Q

Tissue factor pathway inhibitor

A

Source: produced by endothelium
Action: inactivates tissue factor VIIa complexes

30
Q

TPA/PAI

A

TPA initiates degredation of fibrin: PAI inhibits TPA

31
Q

a2-antitrypsin

A

Indus free plasmin in the blood to keep it from degrading

32
Q

Alterations in normal bloodflow

A

Stasis and turbulence
Turbulence: atrial and cardiac thrombosis
- contributed to primarily by endo injury
Stasis: venous thrombosis

33
Q

Ulceration of atherosclerotic plaques

A
  • exposes sub endo collage -> thrombus formation

- results in turbulence

34
Q

Aneurysms: effect

A

Local stasis

35
Q

Acute MI

A

Stasis
Abnormal flow
Cardiac mural thrombi

36
Q

Hyperviscosity (polycythemia)

A

Increased resistance and stasis

37
Q

Sickle cell anemia

A

Vascular occlusion, stasis

38
Q

4 common genetic hyper coagulable states

A

Factor V Leiden mutation
mutated prothrombin gene
Mutant THFr gene
Increased clotting factors (7,9,11)

39
Q

Factor V Leiden mutation

A

COMMON, 2-15 Caucasians

  • individual’s with recurrent DVT’s
  • glu-> arg 506; factors resistant to Ca cleavage
  • hetero: 5x
  • homo: 50x
40
Q

Prothrombin gene mutation

A
  • Affects 1-2%
  • single 3’ mutation
  • increases prothrombin levels
  • 3x fold increased risk
41
Q

Young pt. presenting with thromboemboli

A

Must asses genetic susceptibility for clotting disorder

42
Q

DIC

A

Platelets aggregate in microcirculation consuming clotting factors,
Schistiocytes form from trauma in vasculature. Diffuse activation of fibrinolysin
- trt underlying disease to fix DIC

43
Q

Anti-phospholipid antibody syndrome

A

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
Q

Postmortem clots

A

Chicken fat, no lines of Zahn, and non-adherent

45
Q

Etiology: arterial thrombi

A

Ruptured atherosclerotic plaque, vasculitis, trauma

46
Q

Etiology: mural thrombi (cardiac)

A

Abnormal cardiac contractions or endocaridal injury

47
Q

Mural thrombi (aorta)

A

Ulcerated atherosclerotic plaque, aneurysmal dilation

48
Q

Vegetations

A

Infective endocarditis, sterile endocarditis, SLE

49
Q

PEs

A
  • 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
Q

Etiology of most Systemic thromboemboli

A

80% arise from intracardiac mural thrombi

  • 2/3 from left ventrical wall infarcts
  • 1/3 from left atrial dilation/fibrillation
51
Q

Fat/Marrow embolism

A

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
Q

Air emboli

A
  • from surgery or decompression

- trt: with slow decompression

53
Q

Amniotic fluid emboli: general

A

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
Q

Amniotic fluid emboli: clinical presentation

A

Sudden severe dyspnea, cyanosis, shock, neuroimpairment,

- if pt. survives; pulmonary edema, DIC

55
Q

Infarction

A

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
Q

Red infarcts

A

Venous occlusion,

- loose and dual circulation supplied tissue

57
Q

White infarcts

A

Arterial occlusion

- solid organs with single arterial supply

58
Q

Septic infarcts

A

Vegetation on cardiac valve embolizes

  • microbes seed tissue
  • abcess forms and occludes tissue
59
Q

Tissue vulnerability to ischemia

A
  • hypoxia sensitivity: brain (3-4 min), heart (20-30), fibroblasts (lots of hours)
  • O2 content: anemia, cyanosis
60
Q

Shock

A

Hypotension dude to either: decreased CO, or decreased blood volume
- impairs tissue perfusion and causes cellular hypoxia

61
Q

Shock types: 5

A

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
Q

Septic shock

A
  • 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
Q

Inflammation in septic shock

A
  • Activation of neutrophils, monos, and endos
  • TNF, interleukins (1,8 et al)
  • PGEs
  • activation of compliment
  • factor XII
  • immuneosuppression
64
Q

Immunosuppressive effect in septic shock

A

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
Q

Toxic shock

A

Very similar to septic shock, but mediated by superantigens

66
Q

Factors effected by thrombomodulin

A

Throne-thombomodulin-Seige breaker-APC-factors V and VIII

67
Q

Anti-thrombin III

A
  • Binds heparin like molecules

- inhibits factors IX,X,XI,XII (anti thrombin III has the biggest number in it; inhibits the biggest numbers)

68
Q

Activated Protein C (APC- siege breaker)

A
  • initiates proteolysis of factors Va and VIIIa (Harry V and henry VIII)
69
Q

Tissue factor pathway inhibitor

A

From endothelium; inactivates tissue factor-factor VIIa complex

70
Q

Lupus anticoagulant

A

Hypercoagulant state; aka anti-phospholipid antibody syndrome

71
Q

Alpha granules: components

A 
Fibrinogen
Fibronectin
vWf
P-selectins
PDGF 
TGF-B
72
Q

Dense granules: conponents

A 
ADP
Ca
ATP
Histamine
Serotonin
Epi

PB+T (20 decks)

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