Hemodynamic Disorders I Flashcards
edema
increased interstitial fluid
anasacara
edema with subQ tissue swelling
fluid in body cavity
hydro-
transudate
protein poor
exudate
protein rich
ascites
liver cirrhosis
-reduced albumin - reduced plasma osmotic pressure
nephrotic syndrome
glomeruli leaky - albumin loss
-lead to edema
sodium and water retention
can cause edema
-kidney disorders
CHF
renal hypoperfusion
-leads to edema
early - RAAS activated with increased ADH - restore renal perfusion
over time - retained fluid causes edema
subQ edema
influenced by gravity - dependent edema
-displaced - pitting edema
can signify underlying cardiac or renal pathology
pulmonary edema
left ventricular failure
hyperemia
active process
-artery dilation - increased blood flow
erythema
tissue turns red
response to hyperemia
congestion
passive process
-reduced outflow of blood from tissue
cyanotic
tissue is reddish blue
response to congestion
-deoxygenated Hg
acute pulmonary congestion
engorged capillaries with edema
chronic pulmonary congestion
septa thickened and fibrotic
-hemosiderin macrophages
heart failure cells
hemosiderin M0s - in chronic pulmonary congestion
acute hepatic congestion
central vein and sinusoids are distended
- centrilobular cells ischemic
- periorbial better oxygenated
chronic passive hepatic congestion
centrilobular red-brown and depressed - nutmeg liver
-hemosiderin M0s
centrilobular area of liver
likely to undergo necrosis
-at edge of blood supply
hemorrhage
extravasation of blood into extravasculature
hematoma
hemorrhage maintained in a tissue
petechiae
1-2mm hemorrhage in skin, mucous membrane, or serosa
purpura
> 3mm hemorrhages in skin, mucous membrane, or serosa
ecchymoses
> 1-2mm subQ hematoma
typical bruise
Hg (red-blue) > bilirubin (blue green) > hemosiderin (gold brown)
thrombosis
clot in intact vessels
site of vascular injury
vasoconstriction - due to endothelin
ECM promotes platelet adherence and activation
platelets aggregate to form plug
primary hemostasis
platelet aggregation forming hemostatic plug
tissue factor
factor III, or thromboplastin
-activates factor VII in extrinsic pathway of coagulation
thrombin
cleaves fibrinogen to fibrin
secondary hemostasis
fibrin and platelets
permanent plug
polymerized fibrin and platelet aggregates
t-PA
limit hemostatic plug at site of injury
antithrombosis of endothelium
adenosin diphosphatase, prostacyclin and NO - antiplatelet
heparin-like mlcs > antithrombin III, thrombomodulin - anticoagulant
t-Pa - fibrinolytic
thrombomodulin
binds thrombin and converts it to anticoagulant
- its ability to activate protein C
- inactivates factors Va and VIIIa
prothrombosis of endothelium
vWF - platelet binding
tissue factor - in response to TNF and IL-1 - extrinsic clotting
PAIs - antifibrinolytic
platelets
shed from megakaryocytes
alpha granules of platelets
P-selectin fibrinogen fibronectin factor V and VIII PF4 PDGF TGF-beta
delta granules of platelets
ADP ATP calcium histamine serotonin epinephrine
**important for coagulation and platelet aggregation
platelet adhesion
vWF > GpIb
bernard soulier syndrome
deficient GpIb
no platelet adhesion to vWF
bleeding disorder
TxA2
vasoconstrictor
also stimulates platelet aggregation
thrombin activity
1 - binds to PAR - activates platelet aggregation
2 - converts fibrinogen to fibrin
fibrinogen
binds to platelet GpIIb-IIIa receptor
-bridging interactions
glanzmann thrombasthenia
deficiency in GpIIb-IIIa receptor
-no fibrinogen bridging of platelets
clopidogrel
block ADP binding
block platelet aggregation
prostacyclin
PGI2
-vasodilator and inhibits platelet aggreagation
aspirin
irreversible COX inhibitor
-blocks synthesis TxA2
used to decreased chance of thrombosis
reactions of coagulation
surface of phospholipid
-held together by Ca2+
coumadin
anti-thrombotic agent
- inhibits binding of coagulation factors
- rxn that requires Vit K normally
blood coagulation converge on
factor V
intrinsic clotting pathway
factor XII
extrinsic clotting pathway
requires exogenous trigger
PT time
assays extrinsic pathway
factors VII, X, II, V, fibrinogen
add TF to citrated plasma
-add calcium - measure time to clot
PTT time
assays intrinsic pathway
factors XII, XI, IX, VIII, X, V, II, fibrinogen
negative charged particle (glass)
-time to clot measured
thrombin proinflammatory
through binding PARs
endogenous anticoagulants
antithrombins
protein C and S
TFPI
plasmin
breaks down fibrin
-releases fibrin split products
fibrinolytic cascade
t-PA
activates plasminogen to plasmin
virchows triad
lead to thrombus
1 - endothelial injury
2 - stasis or turbulent blood flow
3 - hypercoagubility of blood
thrombi in cardiac chambers
often due to endothelial injury
thrombophilia
hypercoagulability
leiden mutation
point mutation in factor V gene
-lead to hypercoagulabiltiy
resistant to cleavage by protein C
prothrombin gene mutation
hypercoagulability
homocystein
prothrombic effects
rare inherited causes of primary hypercoagulability
deficiency in antithrombin III, protein C, protein S
patients under age 50 with thrombosis
need to consider genetic causes
smoking and obesity
hypercoagulability
oral contraceptive
hypercoagulability
heparin induced thrombocytopenia syndrome
administration of unfractionated heparin
-antibodies for heparin and platelet complexes
results in thrombocytopenia
-also - prothrombotic state
antiphospholipid antibody syndrome
recurrent thrombosis
repeated miscarriage
valve vegetations
thrombocytopenia
antibodies to plasma proteins
-induce hypercoagulable state
false positive for syphilis**
secondary - to some other disorder
primary - no evidence of autoimmune disorder
growth of thrombi
toward heart
arterial - retrograde
venous - anterograde
lines of zahn
laminations in thrombi
-platelet/fibrin layers and red cell layers
show it was in flowing blood
-not postmortem
mural thrombi
in heart chambers or in aortic lumen
arterial thrombi
often occlusive
-coronary, cerebral, femoral arteries
phlebothrombosis
venous thrombi
-almost always occlusive
lots of red cells - red (stasis) thrombi
postmortem clots
gelatinous with dark red portion where red cells settled and yellow chicken fat upper portion
usually not attached to underlying wall
vegetations
thrombi on heart valves
libman sacks endocarditis
SLE vegetations
fate of thrombi
propagation
embolization
dissolution
organization and recanalization
venous thrombi
can embolize to lung
superficial venous thrombi
saphenous vein
-rarely embolize
deep venous thrombi
DVT
- popliteal, femoral, iliac veins
- can embolize to lung
trousseau syndrome
migratory thrombophlebitis
arterial thrombosis
often with atherosclerosis
DIC
disseminated intravascular coagulation
widespread fibrin thrombin in microcirculation
platelet and coagulation consumption
-can result in excessive bleeding catastrophe
