Hemodynamics Flashcards
1
Q
What is hemostasis?
A
blood clotting that prevents excess bleeding after blood vessel damage
2
Q
What is inappropriate clotting?
A
thrombosis
3
Q
What is migration of clots?
A
embolism
4
Q
What is hyperemia? Where is it often seen?
A
- active process, arteriolar dilation & increased blood inflow
- RED - oxygenated Hb
- sites of inflammation or active sk. m.
5
Q
What is congestion? When is it seen?
A
- passive process, impaired outflow of venous blood from a tissue
- blue/red (cyanosis) - deoxygenated Hb
- cardiac failure or isolated venous obstruction
6
Q
What does chronic congestion in the liver look like?
A
dark marks = nutmeg liver
necrosis / mush
7
Q
What is edema?
A
accumulation of interstitial fluid in tissues
8
Q
How much fluid in each compartment?
A
60% bw is water & 2/3 is intracellular
remaining is interstitial fluid
5% in blood plasma
9
Q
What is an effusion? examples?
A
extravascular fluid that collects in body cavities
- hydrothorax (pleural cavity)
–> CHF
- hydropericardium
- hydroperitoneum / ascites
–> severe liver dx
10
Q
What is anasarca?
A
severe, generalized edema due to fluid retention in tissues & cavities
–> weight gain & organ failure
11
Q
What can cause anasarca?
A
severe kidney dx, malnutrition
12
Q
What factors dictate fluid movement between vascular & interstitial spaces?
A
- colloid osmotic pressure (proteins)
- vascular hydrostatic pressure
13
Q
How to manipulate factors to increase fluid seeping out into interstitial space?
A
- increase hydrostatic pressure
- decrease colloid osmotic pressure
*capacity of lymphatic drainage is exceeded by fluid leakage
14
Q
What typically causes increased hydrostatic pressure?
A
- disorders impairing venous return
–> deep vein thrombosis, CHF
15
Q
What typically causes decreased plasma osmotic pressure?
A
- reduced plasma albumin from loss in circulation OR reduced synthesis
–> nephrotic syndrome (capillaries destroyed & albumin accumulation in urine/less in circulation)
–> severe liver dx (reduced synthesis)
–> malnutrition
16
Q
What can cause lymphatic obstruction & edema?
A
- inflammatory conditions (bacteria, etc)
- neoplastic conditions (cancer)
- congenital lymphedema
17
Q
What are the stages of lymphedema?
A
1: asymptomatic, abnormal flow, no fluid build up
2: swelling, accumulation of fluid, may reverse when elevated
3: permanent swelling, not relieved along with fibrosis of skin
4: lymphostatic elephantiasis, deformation of limb due to swelling & fibrosis
18
Q
What is hemorrhage?
A
extravasation of blood from vessels
19
Q
What causes hemorrhage?
A
- defective clot formation
- trauma
- atherosclerosis
- inflammatory
- neoplastic condition
- inherited/acquired defects
20
Q
List hemorrhage manifestations in order of increasing size.
A
- petechiae
- purpura
- ecchymoses
- hematoma
21
Q
What often causes petechiae?
A
- thrombocytopenia
- vitamin C deficiency
- infectious mononucleosis
- trauma: coughing
22
Q
What are the primary regulators of hemostasis?
A
endothelial cells
23
Q
4 basic steps of thrombus formation & dissolution?
A
- vasoconstriction
- platelet plug
- fibrin deposition
- clos stabilization & resorption
24
Q
Describe the vasoconstriction step of clot formation in detail.
A
- occurs immediately to reduce blood flow
- mediated by neurogenic reflex
- endothelial cells secrete endothelin
–> transient reflex allows platelet activation
25
What occurs during primary hemostasis?
- formation of platelet plug
- disruption of endothelium exposes BM collagen & VW factor
--> conformational change of platelet when interact/adhere with vW factor
--> release secretory granules to recruit more platelets & form a plug
26
What occurs during secondary hemostasis?
- activation of clotting factors & fibrin
- Tissue Factor is exposed & released: procoagulant glycoprotein on subendothelial cells
- clotting cascade started --> thrombin converts fibrinogen to fibrin (mesh)
- stabilizes clot & further activates platelets to aggregate
27
What occurs in clot resorption?
- Tissue plasminogen activator from endothelial cells expressed (t-PA)
--> limits clotting & resorbs clot (fibrinolysis)
- thrombomodulin blocks coagulation cascade as counter regulatory mechanism to only affect site of injury
28
What are platelets?
- disk-shaped, anucleate fragments of megakaryocytes
29
What mediates platelet adhesion?
vW factor
30
What are some congenital deficiencies that lead to bleeding disorders?
- vW factor deficiency (adhesion to wall affected)
--> gene mutation
--> less produced (severity differs)
- Glanzmann thrombasthenia
- Bernard-Soulier syndrome
31
What is the coagulation cascade?
- series of amplification enzymatic rxns leads to deposition of insoluble fibrin clot
- secondary hemostasis
32
What are the two coagulation cascade pathways?
- intrinsic: spontaneous, internal injury
- extrinsic: activated by external trauma
33
What activates intrinsic & extrinsic pathways?
intrinsic = damaged endothelial surface
extrinsic = tissue factor
34
What test evaluates intrinsic / extrinsic paths?
PT = extrinsic
PTT = intrinsic
35
What is the common path?
prothrombin --> thrombin
fibrinogen --> fibrin
36
Importance of vitamin K?
- regulation of coagulation / key role in synthesis of many factors
- synthesize protein C & S --> negative feedback regulation
37
What occurs with vitamin K deficiency?
- increased bruising & bleeding
38
What is Warfarin & what does it do?
- anticoagulant medication
- antagonist for vitamin K
--> inhibits clotting
39
What is the most important coagulation factor?
thrombin
39
What is the function of thrombin?
converts fibrinogen to fibrin
activates platelets
pro-inflammatory
anti-coagulation effects (prevent clotting after vascular repair)
40
What are the factors limiting coagulation?
- dilution of blood past site of injury
- negatively charged phospholipids required (do not bind - platelets)
- regulation by neighboring intact endothelium
- fibrinolytic cascade limits size of clot
--> plasmin activation
41
How does the endothelium limit coagulation?
- barrier to platelets interacting with vWF & collagen
- releases NO, prostacyclin, and adenosine diphosphate
- anticoagulant: factors inactivate thrombin
- fibrinolytic effects: make tPA
42
What is thrombosis? Examples?
- pathologic state of endothelial injury
- coronary artery dx, MI, HTN
- chronic injury (physical, infectious, abnormal blood flow, inflammatory mediators, toxins)
43
How does abnormal flow cause thrombosis?
- promote endothelial procoagulant activity
- stasis allows platelets & leukocytes to associate with endothelium
- stasis slows removal of activated clotting factors, impedes inflow of clotting factor inhibitors
44
What is hypercoagulability?
- abnormally high tendency for blood to clot
45
What is an important risk factor for venous thrombosis?
hypercoagulability
46
What are the primary/genetic hypercoagulable states?
- Factor V mutation
- prothrombin mutation
- increased levels of factor VIII, IX, or XI or fibrinogen
47
What are the secondary/acquired hypercoagulable states?
- prolonged bed rest / immobilization
- MI
- atrial fibrillation
- tissue injury (surgery, fracture, burn)
- cancer
- prosthetic cardiac valves
- disseminated intravascular coagulation
- heparin-induced thrombocytopenia -
- anti-phospholipid antibody syndrome
48
Where do thrombi develop?
- anywhere in cardiovascular system
--> arterial: sites of injury
--> cardiac mural: heart chambers/aorta
--> venous: sites of stasis
49
What are lines of Zahn?
- laminations observed grossly & microscopically in LIVING pt
- differentiates antemortem clots from postmortem clots
50
Describe arterial thrombi.
- typically rich in platelets
- often formed by endothelial injury
51
Describe venous thrombi.
contain high volume RBC
90% in legs / lower venous circulation
52
What are the fates of thrombi?
- propagation: enlarges
- embolization: dislodged & moved by circulatory system
- dissolution: activation of fibrinolytic factors
- organization & recanalization: older thrombi reorganized to facilitate some function
53
Venous thrombosis of superficial vs deep veins?
superficial:
- local congestion & swelling from impaired venous flow (varicose veins)
deep:
- deep venous thrombosis, larger veins
- may be asymptomatic 50%
- may embolize to lungs
**more serious
54
What are varicose veins?
- superficial venous thrombosis
- damaged valve
- twisted, large, & painful veins
55
What is a major cause of arterial & cardiac thrombosis? Why?
- atherosclerosis
- loss of endothelial integrity & abnormal flow
--> MI, ischemia to organs (brain, kidney, spleen)
56
Which organs have rich blood supply?
- brain, spleen, kidneys
57
What is DIC?
- disseminated intravascular coagulation
- widespread thrombosis within microcirculation
- consumption of platelets & clotting factors
- net result: excessive clotting & bleeding
58
DIC may occur from complications in?
obstetrics, injuries, cancer, etc.
59
Describe an embolism?
- solid, liquid, or gas mass carried by blood from point of origin to distant site
60
What is a common source of embolism?
thrombus
61
What are the types of embolism?
- pulmonary
- systemic thromboembolism
- fat
- amniotic fluid
- air
62
What is a pulmonary embolism?
- most common
- mostly from upper deep leg veins
- lodge in pulmonary artery / arterioles
- multiple can occur
- most small & progressively become organized
- large ones can cause sudden death
- multiple over time causes pulmonary HTN & right ventricular failure
63
What is systemic thrombocytopenia?
- arise from intracardiac mural thrombi (80%)
- can embolize to lower extremities most frequently + CNS, intestines, kidney & spleen
64
What is fat embolism?
- Injury to bone marrow causes release of fat globules into circulation
- rare clinical manifestations
- <10% pulmonary prob, neuro prob, anemia, thrombocytopenia, & petechial rash
65
What is amniotic fluid embolism?
- severe post-birth complication
- 80% mortality due to biochemical activation of coagulation system & immune system
- amniotic fluid enters into mothers circulation
66
What is air embolism?
- gas in circulation obstructs vascular flow
ex. decompression sickness in divers
67
What is an infarction?
- area of ischemic necrosis caused by occlusion of vascular supply to affected tissue
68
Common organs involved in complications of infarctions?
- brain & heart
69
Most infarction arise from what ?
- arterial thrombosis
- embolism
70
How to classify an infarction?
COLOR
- Red: contain hemorrhage
- White: arterial occlusion in solid organs
71
Where are red infarctions?
- venous occlusion
- loose tissue (lungs)
- tissue with dual circulation
- previously congested tissue
- reperfusion injury
72
Where are white infarctions?
- heart, liver, spleen
73
What is shock?
- state with diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion & leads to cellular hypoxia
74
What type of shock leads to irreversible tissue injury?
prolonged
75
What are the types of shock?
- cardiac
- septic
- hypovolemic
- anaphylactic
76
What are examples of cardiac shock?
- MI
- ventricular rupture
- arrhythmias
-cardiac tamponade
- pulmonary embolism
77
What is the principal pathogenic mechanism of cardiogenic shock?
- failure of myocardial PUMP from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
78
What are examples of hypovolemic shock?
- hemorrhage
- fluid loss
79
What is the principal pathogenic mechanism of hypovolemic shock?
inadequate blood or plasma volume
80
What are examples of septic shock?
- microbial infections
- gram - sepsis
- gram + septicemia
- fungal sepsis
- superantigens
81
What is the principal pathogenic mechanism of septic shock?
peripheral vasodilation & pooling of blood
endothelial activation
leukocyte induced damage
disseminated intravascular coagulation
activation of cytokine cascades
82
What causes anaphylactic shock ?
type 1 hypersensitivity
