Hemodynamics Flashcards
artery or vein? label the layers from outer-most to inner-most
artery
what is the tunica intima consisted of?
ENDOTHELIUM
basement membrane
internal elastic lamina
what is the tunica media consisted of?
SMOOTH MUSCLE
collagen, reticular, elastin fibers
external elastic lamina
what is the tunica adventitia consisted of?
CT
lymphatic vessels
artery or vein? ID layers
vein
define edema
abnormal accumulation of fluid in interstitium and body cavities
list the four main causes of edema
- increased microvascular permeability (leaky vessel)
- increased vascular hydrostatic pressure
- decreased intravascular osmotic pressure
- decreased lymphatic drainage
ID the pathologies and describe colors
list the two main causes of non-inflammatory edema
hepatic failure
heart failure
how does hepatic failure cause edema?
reduced albumin production - decreased oncotic pressure
portal hypertension aka blocked blood from stomach/intestines to the liver - increased hydrostatic presssure
how does heart failure (dec CO) cause edema?
define hyperemia. is it an active or passive process?
arteriolar dilation causing a local increase in volume of blood
active process
list ways in which hyperemia occurs
inflammation
physical activity
increased blood flow to GI after food
physiologic mechanism to dissipate heat
define congestion. is it active or passive?
passive
impaired/decreased outflow of blood
list ways in which congestion occurs
CHF
local venous obstruction
organ displacement
ID hyperemia or congestion
hyperemia - specifically erythema
ID hyperemia or congestion
congestion
ID hyperemia or congestion
CHRONIC congestion
define erythrophagocytosis
macrophages that contain whole RBCs
define hemosiderin-laden macrophages
brown, iron containing from breakdown of RBC
heart failure cells
define hemostasis
PHYSIOLOGICAL response to vascular damage and stops bleeding
define thrombosis
PATHOLOGIC activation of hemostatic process to induce clot
what is virchow’s triad?
factors that contribute to hemostasis and thrombosis
1. endothelial injury !!!
2. change in blood flow
3. blood hypercoaguability
describe the hemostatic process (4 steps)
- primary hemostasis - vasoconstriction and platelet grouping to form a plug
- secondary hemostasis - coagulation to form fibrin mesh
- fibrinolysis - remove platelet/fibrin plug
- tissue/vascular repair
what is von willebrand factor? how does it aid in hemostatic process?
protein that helps blood clot
primary hemostasis
what is tissue factor? how does it aid in hemostatic process?
initiates extrinsic path of coagulation cascade
secondary hemostasis
describe the intrinsic coagulation cascade
factors 12 11, 9, 8 -> common path, factor 10 -> (prothrombin to thrombin factor 2) -> fibrinogen (1) -> fibrin clot
describe the extrinsic coagulation cascade
tissue factor 3 -> factor 7 -> common path, factor 10 -> (prothrombin to thrombin factor 3) -> fibrinogen -> fibrin clot
list the vitamin k dependent coag factors
factors 2, 7, 9, 10
define fibrinolysis
prevents blood clots from forming pathogenic condition
describe the role of plasmin in the fibrinolytic system
digests fibrin clots and releases fibrin degradation products
inhibits additional fibrin formation
what’s the most important/potent coagulation inhibitor?
antithrombin 3 - made by endothelium and hepatocytes
list the three hemorrhage descriptive terms
petechia
ecchymosis
suffusive
define petechia
pinpoint hemorrhage
minor vascular damage
define ecchymosis
more extensive vascular damage than petechia
define suffusive
larger, contiguous area of tissue hemorrhage damage
paintbrush
ID hemorrhage type
ID hemorrhage type
ID hemorrhage type(s)
- petechia
- ecchymosis
ID hemorrhage type
what does hemorrhage significance depend on?
amount, location, rate
exsanguination is __% of blood loss volume
40%
in which organs is it worst to have hemorrhage?
brain and heart - very little room to expand
define thrombus
group of platelets, fibrin in injured blood vessel
physiologic vs persistent thrombus
physiologic - normal, rapidly resolves after healing
persistent - forms on wall of injured vessel (thromboembolism)
list major determinants of thrombosis
VIRCHOWS TRIAD
*** alterations of endothelium to cause increased production of pro-coag substances
describe cardiac and large arterial thrombi
due to endothelial damage
dull
firmly attached to vessel wall, red/grey with lamellated appearance due to rapid flow
alternating white platelets/fibrin
ID this pathology
cardiac/large arterial thrombi
describe venous thrombus
due to areas of slow blood flow/stasis
dark red, gelatinous since large amount of erythrocytes loosely
occlusive
ID pathology
venous thrombus
list the four types of thrombus resolution
full resolution - return to normal structure/function
granulation after debris removal - incorporated into vessel wall
recanalization - invasion/growth of endothelial blood channels in vessel, causing permenant narrowing
embolus - thromboemboli lodged in smaller sized vessels
ID the types of thrombus resolution
L - full resolution
embolus
granulation
recanalized
where do venous emboli typically lodge?
pulmonary circulation
causes R sided HF or infarcts
where do arterial thromboemboli lodge?
in the tissue that depends on it
ex: saddle thrombus
what two main things could occur due to occlusion of a vessel?
hypoxia
infarct
what’s occurring here?
infarct
define acute red infarct
red, often swollen or slightly raised
cause: hemorrhage
define subacute pale infarct
pale
cause: necrosis > swell > forces blood out of infarcted region
define chronic infarct
pale, shrunken, firm, fibrosis
describe the concept of disseminated intravascular coagulation (DIC)
endothelial damage > thrombosis > too much clotting and usage of factors > ischemia in one organ/area > lack of clotting factors in rest of body so too much bleeding in other areas
