FS II-2 Thrombi, infarction, shock
Terms in this set (128)
What is hemostasis?
clotting in response to injury
What are the 3 components of homeostasis?
1) vascular wall (endothelial cells and underlying ECM)
3) coagulation cascade
What is the fibrinolytic phase of clotting associated with?
- anti-thrombotic events
- t-PA and thrombomodulin release
- trapped neutrophil
- trapped RBC
- polymerized fibrin
What is thrombosis?
the formation of a clotted mass within the NON-INTERUPPTED vascular system, it can vary in size and shape
Where can a thrombosis form?
in any area of vasculature
Does thrombosis indicate procoagulant or anticoagulant?
What is virchow's triad?
endothelial injury, abnormal blood flow, and hypercoagulability will lead to thrombosis
What can cause endothelial injury?
- turbulent blood flow as in scarred valves
- bacterial endotoxins
- cigarette smoke
endothelial injury leads to changes in ____-________ properties
_______ causes endothelial injury
endothelial injury causes _____ of stasis and leads to what types of events?
- pockets of stasis
- pro-thrombotic events
5 causes of abnormal blood flow
1) ulcerated atherosclerotic plaques
3) noncontractile heart muscles
4) hyperviscosity syndromes (viscous blood)
5) sickle cell anemia (buildup of blood)
genetic causes of hypercoagulability
1) factor 5 mutation causing it to always be active and always clotting
2) inability to stop clotting factors
3) inability to activate plasminogen (PAI mutations, plasminogen deficiency)
acquired causes of hypercoagulability
- stasis of blood flow
- pro-thrombotic events
- heart attack
- pregnancy and oral contraceptives
- hepatic dysfunction
What is disseminated intravascular coagulation?
- SECONDARY consequence to conditions
-like pregnancy complications (body forms microthrombi) and malignancy
- causes widespread thrombi in microcirculation
- leads to consumption coagulopathy
what is consumption coagulopathy?
using up coagulation in one place when it's needed elsewhere
Which thrombi have lines of Zahn?
arterial and cardiac
What are lines of Zahn?
form in arteries because of pulsing nature of flow, high thrombin and low blood captured, slowing of blood leads to capturing of blood
Where do arterial thrombi begin and where do they propagate?
begin at site of injury and retrograde
Are arterial thrombi occlusive or mural?
can be both
Where are 3 common sites of arterial thrombi?
coronary, cerebral, femoral
Arterial thrombi is the most common injury due to ________
look at pics
if you see histo with lumen filled with fibrin, it's what kind of clot?
Is cardiac thrombi occlusive or mural?
Two places cardiac thrombi can form
- heart valves
- over old infarcted cardiac tissue - weak and bulged so thrombus easily forms
Where do venous thrombi form?
in areas of blood stasis (immobilization)
Are venous thrombi occlusive or mural?
Venous thrombi contain more _____
erythrocytes - causes red or stasis thrombi
The venous thrombi have a point of ______
Venous thrombi grow towards _____
If the tail of the venous thrombi is not well attached, it leads to:
In which veins do venous thrombi form most commonly?
veins of lower extremities
What are 5 fates of the thrombus?
1) propagation - move to heart
2) obstruction - block blood flow
4) dissolution - must be quick though
5) organization and recanalization - increased blood flow
What's an emboli?
- any detached intravascular solid, liquid or gaseous mass carried to a site distant from point of origin
- 99% are dislodged thrombi
- blocks blood flow
80% of systemic thromboembolisms arise from:
mural cardiac thrombi
20% of systemic thromboembolisms arise from:
- thrombi on atherosclerotic lesions
- valve vegetations
- venous system
The damage produced by systemic thromboembolisms depends on:
1) caliber of occluded vessel (bigger vessel gets more damage)
2) collateral supply
3) vulnerability to anoxia (brain and heart are vulnerable)
Pulmonary thromboemoblism results from emboli formed where?
in deep leg veins
60-80% of pulmonary thromboembolisms are ____
What 3 things happen when more than 60% of pulmonary circulation is compromised?
1) sudden death
2) cor pulmonale
3) cardiovascular collapse
accumulation of pulmonary emboli lead to ______ _______
other sources of emboli
- fragments of plaques
- bacterial or parasitic aggregates
- gas (diving)
- fluid fat gets into blood
-amniotic fluid at birth
bone marrow emboli histo is rich in...
Infarction is ______ necrosis caused by:
ischemic necrosis caused by occlusion of arterial supply or venous drainage
99% of infarctions result from:
thrombotic or embolic events
infarct development is influenced by 4 things:
1) single or dual circulation
2) rate of occlusion development (suddenly is bad)
3) vulnerability to hypoxia
4) blood oxygen content
What is active disorder of perfusion?
What's a passive disorder of perfusion?
What are some hemodynamic disorders?
hyperemia, congestion, hemorrhage, edema, hemostasis, thrombosis, embolism, infarction, shock
Hyperemia is what?
increase in blood volume within the tissue due to either inflammation or exercise
Is hyperemia passive or active? how?
active - arteriolar dilation and increased blood inflow
What color does tissue appear during hyperemia?
red - due to engorgement with oxygenated blood
Histology of hyperemia?
- dilated arterioles and capillaries
- engorged arterioles and capillaries
Congestion is what?
increase in blood volume within tissues as in cardiac failure or venous obstruction. The backup of venous return leads to peripheral edema and congestion
Is congestion passive or active? how?
passive - impaired outflow of VENOUS blood
What color does tissue appear in congested tissue?
cyanotic (blue-red) - accumulation of DEOXY hemoglobin
What's the difference between acute and chronic congestion?
- acute - increased volumes and pressure leads to edema
- chronic - congestion leads to low tissue perfusion and hypoxia. Has cell death, fibrosis, and hemorrhage due to the pressure
Passive liver congestion
- centrolobular venous (CLV) congestion --> necrosis (hypoxia) with sinusoidal congestion
- may be due to right-sided heart failure
- nutmeg liver results
review of blood flow through liver:
- hepatic triads gives blood to hepatic lobules (plentiful), goes to sinusoids and exits through central lobule vein where it's getting cleansed
- 3 vessels of hepatic triad: portal vein (large), hepatic artery, and bile duct
Histology of passive congestion of liver
- distended central vein and sinusoids due to BLOOD
- nutmeg appearance - red-brown, slightly depressed due to congestion
- tan areas - uncongested or fatty liver
- necrosis destroys central hepatocyte
- in chronic - more hepatic necrosis and hemorrhage due to congestion
Passive pulmonary congestion
- venous congestion (CHF)
- left-side heart failure --> increased pulmonary venous pressure due to congestion in lungs --> hyperemia --> congestive heart failure (CHF)
Acute pulmonary congestion is associated with CHF
- blood-engorged alveolar capillaries - you can't count the vessels, too engorged
- alveolar septal EDEMA leads to thickened walls
- intra-alveolar HEMORRHAGE (big red spot)
- HEART FAILURE CELLS = alveolar macrophages that eat up the RBC of hemorrhage
- FIBROSIS in alveolar septae
What is a hemorrhage?
an extravasation of blood from vessels. Can be internal (extravascular spaces) or external (nose bleed)
What conditions can cause hemorrhage?
lots of things - congestion, hemorrhagic diatheses (hemorrhaging without trauma, due to another disease), trauma (damage to capillaries or arteries), inflammation (destruction of BV), neoplastic erosion (tumors destroy BV), thrombocytopenia, coagulation deficiency
What volume and rate of loss of blood is associated with hemorrhage?
- rapid loss up to 20% of blood volume OR slow losses of larger amounts have NO AFFECT
- GREATER LOSSES --> hemorrhagic shock
what is hypovolemic?
hemorrhagic shock = decrease in volume of blood supply (hypo, vol)
What's an example of a site for hemorrhage?
brain versus other tissues
Hemorrhage can lead to iron deficiency anemia
if there is chronic or recurrent blood loss, anemia can result. For example, in peptic ulcer
Hemorrhage can lead to jaundice
extensive INTERNAL hemorrhage due to massive breakdown of RBC and hemoglobin leads to production of billirubin pigment
What are some clinical appearances of hemorrhage?
- palpable hemmorhage
- in soft tissue
- painful = muscle bruise
- fatal = brain
- pinpoint hemorrhage (1-2mm)
- in skin, mucous membranes, or serosal surfaces
- ruptured capillaries or arterioles
- occurs alongside thrombocytopenia, defective platelet function, or vasculitis
- slightly larger hemorrhages than petechiae (3-5mm)
- due to ruptured capillaries or arterioles
- occurs alongside trauma or vasculitis
- larger than purpura (1-2 cm)
- subcutaneous hematomas (bruises)
accumulation of interstitial fluid within tissues - transudate or exudate
What happens when extravascular fluid collects in body cavities? (NOT IN TISSUES, as in edema)
- in the pleura = hydrothorax
- in the peritoneium = Ascites
severe GENERALIZED edema of subcutaneous tissues and accumulation of fluid into cavities
What two opposing forces govern fluid movement between vascular and interstitial spaces?
1) vascular hydrostatic pressure = drives fluid out of vessels
2) osmotic pressure due to plasma = draws fluid back into vessels
What are edema conditions in regards to vessel fluid movement?
- increased hydrostatic pressure or decrease in osmotic pressure leads to increased fluid into interstitium
- there's a new equilibrium established due to increased extravascular water
- formation of transudate (non-inflammatory)
What are the 3 clinical causes of edema?
1) increased hydrostatic pressure
2) reduced plasma osmotic pressure (hypoproteinemia)
3) lymphatic obstruction (leads to lymphedema)
- also sodium and water retention
What causes increased hydrostatic pressure?
1) impaired venous return - CHF (fluid in lungs), portal hypertension via liver cirrhosis, venous obstruction)
2) arteriolar dilation - heat or neurohumoral dysregulation
What causes reduced plasma osmotic pressure?
- renal disease = protein loss
- liver cirrhosis = reduced protein synth
What does lymphatic obstruction lead to?
What is sodium water retention and how does it lead to edema?
- high salt intake and low renal function
- increased renin-angiotensin-aldosterone secretion - this increases vasoconstriction and Na+ absorption --> high blood volume --> high cardiac output and high blood pressure/HP
the range of edema consequences are ______ to ______
annoying to rapidly fatal
What is characteristic of subcutaenous edema?
- underlying cardiac disease
- underlying renal disease
- can impair wound healing and clearance of infection
common examples of edema
- pulmonary edema - left ventricle failure, renal failure, can lead to death by interfering with breathing and being prone to infection
- brain edema --> compression --> ischemia life-threatening fo sho,
press skin and it doesn't come back to normal, this is a subcutaneous edema and indicated systemic disease.
Histo of edema
- dilated blood vessels
- space between interstitial tissues
- transudate (no cells) vs. exudate (you see cells)
Histo of pulmonary edema in lungs
- dilated capillaries
- thicker alveolar septa
- no inflammatory cells
- POTENTIAL TQ
What's an infarct?
an area of ischemic necrosis
What are infarcts caused by?
occlusion of vascular supply to tissue
most cardiovascular diseases are a result of
myocardial or cerebral infarct
Some causes of infarcts:
- arterial thrombus/emboli
- impinging the vessel
- torsion of vessel
What are 4 clinical effects of infarct? and what influences these effects?
1) no consequence
2) tissue necrosis
3) organ dysfunction
effected by vascular supply (single or dual), rate the occlusion develops, tissue vulnerability (brain), oxygen content of blood)
What's the difference between white and red infarct?
red has collateral blood from another supply and leads to hemorrhage while white only has 1 supply
single or dual?
what kind of tissue?
why is there hemorrhaging?
loose tissue where blood can collect (lung)
arterial and venous occlusions
ischemic coagulative necrosis
hemorrhaging due to bleeding into infarct from adjacent vessels
single or dual?
what kind of tissue?
solid organs that limits blood seepage from other organs, also tissue with end-arterial circulation (heart, kidney, brain)
What does the white infarct look like on gross anatomy?
- wedge shaped
- ISCHEMIC COAGULATIVE NECROSIS
- inflammation at margins due to fibrosis
white infarcts occur in ____ and ____. Red infarcts occur in _____.
renal and heart
Histology of renal infarct
- nucleus dies
- hypoxia --> kills cells and coagulative necrosis happens
- all pink globs, glomerulus is gone
Histology of myocardial infarct
- complete occlusion of coronary artery branch
- eosinophilia (pink)
- lose cell demarkation
- inflammation and cells
- intercalated disks (look like striped things)
when heart infarct scars:
fibrotic tissue and collagen present, not functional, results in congestive heart failure
What is the dual blood supply of lungs?
1) pulmonary arteries
2) bronchiole arteries
what's the most common cause of pulmonary infarct?
emboli in pulmonary artery, infarction will occur if bronchial arteries inadequately compensates
pulmonary infarct is often associated with ____
Pulmonary infarcts look ____
Histology of pulmonary infarct
- no nuclei
- eosinophilic (pink)
- dead septa, ischemic necrosis
- hemorrhage results
failure to profuse tissue
shock results in
- reduced cardiac output
- reduced circulating volume
- low perfusion
- reversible usually unless prolonged
- not just low BP
5 forms of shock
1) cardiogenic shock
2) hypovolemic shock
3) septic shock
4) anaphylactic shock
5) loss of vascular tone (neurogenic)
Shock is usually a _____ of lethal events
- what kind of damage
- results from low cardiac output due to pump failure due to infarction
- myocardiac damage due to infarction
- ventricular arrhythmia
- outflow obstruction by pulmonary embolism
- extrinsic compression leads to cardiac tamponade
- leads to
- results from low cardiac output due to loss of blood or plasma volume
- external fluid loss = diarrhea, urine, vomiting
- internal fluid loss = increased vasculature permeability
clinical manifestations of shock
- cardiovascular changes
- skin changes
what organ is really affected in shock?
causes of septic shock
microbial infection (septicemia) or local infection
septic shock results in:
decreased vascular tone (vasodilation and POOLING), cardiac output stays same or increases
mortality rate of septic shock
What three events lead to septic shock leading to multi-organ failure?
1) inflammatory mediators (coagulation)
2) endothelial activation or injury leading to thrombosis, vascular permeability, vasodilation, and DIC (high clotting)
3) metabolic abnormalities (leads to many effects)
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