chapter 4 Flashcards
increased hydrostatic pressure is from what disorders
2 categories
ones that impair venous return
localized: DVT
Systemic: congestive heart failure
what can cause reduced plasma osmotic pressure
loss of albumin
neprotic syndrome
cirrhosis
protein malnutrition
protein losing gastroenterophathy
when sodium and water are retained what happens to colloid osmotic pressure
diminished due to dilution
subcutaneous edema is in regions with what and distribution often influenced by what
-depending on position person is in called what
hydrostatic pressure, gravity
- legs when standing
- sacrum when recumbent
-dependednt edema
what kind of edema is characteristic of renal dysfunction
periorbital edema
describe the lungs in pulmonary edema
lungs are 2-3X normal weight and yield frothy, blood tinged fluid
-air, edema, and extravasated red cells
brain edema features
narrowed sulci and disteneded gyri
what would a peritoneal effusion caused by lymphatic blockage look like
-main cause
milky due to presence of lipids absorbed from gut
-from portal hypertension
systemic congestion and localized
systemic: cardiac failure
localized: isolated venous obstruction
both lead to edema
chronic passive congestion leads to
chronic hypoxia–> ischemia tissue injury and scarring
- hemorrhagic foci
- hemosiderinladen macrophages
reddish-blue, cyanosis
morphology of congested tissue
enlarged alveolar caps
alveolar septal edema
focal intralveolar hemorrhage
morphology of acute pulmonary congestion
from CHF
septa thickened and fibrotic
heart failure cells
morphology of chronic pulmonary congestion
central vein and sinusoids distended
centrolobular area hepatocytes necrotic
periportal hepatocytes may only develop fatty change
morph of acute hepatic congestion
centrilobular regions grossly red-brwon, slightly depressed
uncongested tan liver on outside part (nutmed liver)
chronic passive hepatic congestion
primary hemostasis
formation of primary platelet plug
secondary hemostasis
deposition of fibrin
TF exposed on surface of subendothelial cells (SM and fibroblasts)
- binds and activates factor VII
- leads to thrombin generation and fibrin
what acts to limit clotting to site of injury
T-PA
what is the last step in hemostasis
clot stabilization and resoprtion
-polymerized fibrin and platelet aggregates undergo contraction to form solid permanent plug
a granules of platelets have what selectin on their membrane
p selectin
what is contained inside alpha granules
factor 4 and 5, fibrinogen, vWF, TGF-B, PDGF
B or dense granules in platelts contain
calcium
ADP
Serotonin
epinephrine
what on the platelet binds to vWF
GP1b
deficient GP1b is what disease
bernard-soulier syndrome
bleeding disorder
what causes platelets to change shape
translocation of negatively charged phospholipids to platelet surface which bind calcium
how are platelets activated
thrombin cleaves PAR to activate it
ADP release gives rise to additional rounds of platelet activation called recruitment
deficiency of GpIIb/IIIa called
glanzmann thrombasthenia
what does GpIIb/IIIa usually do
connects platelets through fibrinogen linking
assembly of clotting cascade reaction complexes depsends on _____ binding ____ on what factors
calcium binding y-carboxylated lutamic acid on
2,7,9,10
enzyme that y-carboxylates these factors uses vitamin K
PTT what pathway and factors
intrinsic
8-12, II, V, firbrinogen
and negative cahgreged particle to active XII together with phospholipids and calcium
PT pathway and factors
II,V,VII,X and TF, phospholipids, and calcium added
deficiency of what factors leads to moderate to severe bleeding disorders
5,7,8,9,10
what factor deficiency leads to mild bleeding
XI
-lose ability of clot amplification from thrombin
what factor deficiency leads to people who don’t bleed and susceptible to what
XII and thrombosis
thrombin has a positive feedback that amplifies clotting on what factors
5,8,11
thrombin stabilizes the secondary hemostatic plug by activation what factor which covalently cross-links fibrin
13
thrombin on normal endothelium
anti-coagulant
clotting in vivo
1) TF activates VII to VIIa
2) TF and VIIa activate IX
3) IX and VIII activate X
4) X and V activate thrombin
5) thrombin converts fibrinogen to fibrin and also amplifies V,VIII,XI
clotting in lab intrinsic
1) neg charged surface glass beads activate 12
2) 11 activated
3) 9 activated
4) 8 and 9 activate 10
5) 10 and 5 activate thrombin
clotting in lab extrinsic
1) TF and VII activate X
2) X and Va activate thrombin
fibrinolysis limits size of clot and contributes to its later dissolution
-largely accopmlised by enzyme activity of
plasmin
-breaks down fibrin
elevation of D-dimers means what
marker of several thrombotic states
how is plasminogen converted to plasmin
by factor XII (no bleeding disease)
t-PA
t-PA
synthesized by endothelium and most active when bound to fibrin
what limits plasmin
a2 plamsmin inhibitor
platelet inhibitory effects of normal endothelium
PGI2
NO
ADPtase
thrombomodulin
inhibits thrombin
make it cleave and activate protein C which then inactivates factors Va and VIIIa
-requires protein S to work
-also vitamin K
antithrombin III
bind heparin like molecules on surface of endothelium and inhibit:
thrombin
factors: 9-12
tissue factor pathway inhibitor requires what and does what
needs protein S
binds and inhibits Tf/VIIa complexes
what are purpura
like petechiae but slightly larger
defects of 2ndary hemostasis what is cause and where is leed
defect coag factors
bleedis into soft tissue like muscle or jionts
hemarthrosis
generalized defects involving small vessels often presents with
can create what
palpable purpura and ecchymosies
-can create palpable mass of blood called hematoma
what is the virchow triad in thrombosis
abnormal blood flow
endothelial injury
hypercoagulability
injured endothelial cells secrete ____ which limits fibrinolysis and downregulates expression of t-PA
PAI
favors development of thrombi
factor V point mutaions
increases what
factor V leiden
increases DVT
factor V is resistant to cleavage by protein C
nucleotide change in 3’ UTR prothrombin gene
increases what
elevates prothrombin
3X increase in venous thrombosis
elevated homocystein
increases what and can also cause what
arterial and venous thrombosis
atheroslerosis
heparin induced thrombocytopenia syndrome
heparin and factor 4 bind and then go to platelet surface
Abs recognize this and bind
-activation, aggregation and consumption
-prothrombotic state
antiphospholipid Ab syndrome
anticardriolipin Ab
recurrent vascular thrombossis
throbocytopenia
recurrent fetal loss
presentaion of Antiphospholipid Ab syndrome
PMS bitch
pulmonary embolism
myocardial infarction
stroke
bowel infarction
arterial or cardiac thrombi begin where and what travel
turbulence or endothelial injury
retrograde travel
venous thrombi begin and goes
at stasis goes forward towards heart
lines of zahn description and indication
alternating red (RBCs) and tan (platelets and fibrin) indicates thrombus formed in flowing blood
mural thrombi occur where
in heart chambers or in aortic clumen
arterial thrombi location
coronary
cerebral
femoral
postmortem clots
gelatinous
dark red dependent portion
yellow chicken fat upper portion
fate of thrombus
PEDO
venous thrombi 2 types and can embolize where
superficial (rarely embolize)
DVT: large veins at or above knee, more often embolize to lung
arterial and cardiac thrombosis from what (2)
MI and atherosclerosis
vegetations from bacteria or fungi or previous damage can cause distrubed blood flow and induce formation of large thrombotic masses called
infective endocarditis
what occurs when emboli obstruct ___ or more of pulmonary circulation
60%
death, Right side heart failure
systemic thromboembolism are from
main spot it deposits
intracardiac mural thrombi
deposits in LE
fat and marrow embolism
after fracture of long bones pulmonary insufficency anemia neurologic symptoms thrombocytopenia
air embolism
decompression sickness
caisson disaease
amniotic fluid embolism
can cause death and 85% of time causes neurological damage to survivors
tear in placenta membrane or rupture of uterine veins
infarcts caused by venous thrombosis more likely in what organs
with single efferent vein
-testis and ovary
morphology of red infarct
-white
hemorrhagic
anemic
where do red infarcts occur
venous occlusions (testicular torsion)
loose spongy tissue (lungs)
dual circulating tissue (lungs and SI)
white infarcts occur
arterial occlusion ins solid organs with end artery supply like
heart, spleen, kidney
metabolic abnormalities in septic shock
increased insulin resistance
-imparired GLUT-4
hyperglycemia
- gluconeogenesis activated
- accute glucocorticoid product followed by adrenal insufficiency
adrenal necrosis due to intravascular dissemination is called
waterhouse-friederichsen syndrome
stages of shock
initial nonprogressive phase
-reflex compensatory mech activated, perfusion to vital organs maintained
progressive stage
-tissue hypoperfusion and lactic acidosis
irreversible stage
-cell survival not possible, lysosomal enzyme leak, organ failure
adrenal changes in shock
cortical cell lipid depletion
kidneys in shock
acute tubular necrosis
lungs in shock
if sepsis or trauma then diffuse alveolar damage
systemic intracvasuclar affect of shock
petechial hemorrhages
clinical consequence of hypovolemic and cardiogenic shock
hypotension, weak pulse, cool, clammy cyanotic skin
clinical consequence of septic shock
initial warm skin bc of vasodilation
