4. Infarction Flashcards
Infarction
• Infarct: area of ____ necrosis caused by occlusion of vascular supply to tissue
• Infarction: process by which infarcts occur
• Classification:
– ____ (hemorrhagic) vs white (anemic)
– ____ (septic) or bland
• Important cause of illness
– 40% of all deaths in US consequence of CVD; most of these due to myocardial or ____ infarct
• Causes of infarcts (mostly arterial):
– ____ thrombus and embolism
– Complication of ____
– Less common causes:
• Extrinsic compression of a vessel (e.g., ____)
• Edema in a confined space
• Blood vessel twisting (e.g., ____, bowel volvulus)
– Venous blockade (e.g., thrombus)
• May cause infarct, more commonly ____; ____ channels restore venous outflow and arterial inflow
ischemic
red
infected
cerebral
arterial atherosclerosis tumor testicular torsion congestion bypass
• Clinical consequences of an infarct: – Inconsequential – Tissue necrosis – Organ dysfunction – Death • Note: Partial occlusion (e.g., \_\_\_\_) – leads to ischemia and typically results in \_\_\_\_ and occasionally \_\_\_\_ – Ischemic necrosis of extremities problem in \_\_\_\_ population (gangrene)
• Clinical consequece of infarction influenced by: – Vascular supply • \_\_\_\_: kidney, spleen, heart • \_\_\_\_: lungs, liver – Rate occlusion develops • Slowly developing occlusions leads to development of \_\_\_\_ blood supply – Tissue vulnerability to hypoxia • \_\_\_\_>\_\_\_\_>\_\_\_\_ – \_\_\_\_ content of blood (normal individual vs anemic or cyanotic pt)
• Results in ischemia, and ultimately coagulative necrosis • Infarcts occur from \_\_\_\_ occlusion • Ischemic necrosis of extremities - diabetic • Vascular supply ○ Some organs are endoarterial - single blood supply § More susceptible to infarction than dual supply ○ Dual supply • Rate of occlusion ○ Rapid occlusion > rapid anoxia > immediate death § No chance for collateral development ○ Slowly develops > ischemia develops and collateral BV develop > important for myocardial infarcts • \_\_\_\_ can survive low O2 over longer periods • If patient is already compromised (\_\_\_\_, Hb problems) > patient more susceptible to ischemic event
stenosis
atrophy
necrosis
diabetic
single dual collateral neurons myocardium fibroblasts oxygen
total
fibroblasts
anemia
Classification of infarcts
• White (anemic, pale) infarcts
– Arterial occlusions in ____ organs
– Tissue with ____ circulation (heart, kidney, brain)
– Tissue ____ limits seepage of blood from adjoining vascular beds
– ____ necrosis
It occurs in tissues that because of its density, there is limited seepage of blood from adjacent blood vessels. Without that seepage, adjoining vascular beds cannot provide any blood supply. So this infarcted tissue is not
going to be perfused by seepage of blood from the adjacent vessels that are still receiving blood. The tissue will die as a result of coagulative necrosis, which is the result of the drop in ____ and denaturation of ____ enzymes. There is no-or-limited autolysis and no heterolysis, which usually occurs because of inflammation, but there is no ____ because no blood supply.
solid
end-arterial
density
coagulative
pH
proteolytic
inflammation
White infarcts (continued):
– Tend to be ____-shaped with occluded vessel at ____ and periphery of organ forming ____
– Lateral margins ____—blood flow from adjacent vessels
– Margins may be hemorrhagic (acute) and eventually hyperemic (inflammation)
– Main histologic finding: ____ necrosis
– Inflammation at the margins; why?
– Fate of infarct: repair—____
– Complications: ____ infarction: microbes seed necrotic tissue
– Exceptions: Brain infarct leads to ____ necrosis– ____
wedge apex base irregular ischemic (coagulative) scar septic liquefactive abscess
Classification of infarcts
• Red (hemorrhagic) infarcts
– Tissue with ____ blood supply (e.g., lung, liver)
– ____ tissue where blood can collect in infarcted zone (e.g. lung)
– Arterial or venous occlusion
– ____ necrosis
– Hemorrhage due to bleeding into infarct from ____ vessels
• Tissue with dual blood supply
• Tissue with extensive ____ circulation
dual "loose" ischemic coagulative adjacent collateral
Examples of infarcts • White infarcts: – \_\_\_\_ – \_\_\_\_ • Red infarcts: – \_\_\_\_
renal
heart
pulmonary
- Kidneys connected to bladder via ____
- ____ artery that enters each kidney, perfusing the cortex and medulla
- Functional unit = ____ (glomeruli, tubules)
ureters
renal
nephron
Renal Infarct: Coagulative necrosis
• Morphological changes:
• Gross:
• ____/firm, tissue retains ____ outline
• Microscopic:
• cell architecture ____; reveal structure of living tissue but lacks clear ____
• Lacks cell boundaries
– ____
• nucleus
– ____
– karyorrhexis
– ____
• Fate: necrotic tissue removed by ____
* TR: normal live kidney * BR: eosinophilic (lost mRNA that normally take up hematoxylin), retains its basic cell architecture, cannot find cell borders, and no nuclei (all \_\_\_\_)
pale basic remains definition eosinophilia pyknosis karyolysis phagocytes karyolysis
- R: no ____, no nuclei, ____
- Fate of infract > removed by ____
- Dead tissue is one of the most potent inducers of ____ reaction (occuring in adjacent tissue that is being perfused)
cell borders
eosinophilia
phagocytes
inflam
• TL: left side, ____ necrosis: pale, eosino, no nuclei; right side: ____ zone, would see BV, nucleated cells (phagocytes: PMNs, macro’s) that are surrounding infarcted tissue > ____
• BL: presence of inflammatory cells, top-left: eosinophilic
• Cannot repair/resolve until you remove the ____
○ Kidney with limited ____ ability > healing is by scar (____ cells)
○ Reduced in ____
○ Remodeling of structure bc of tensile strength of collagen that distorts it > ____ phenotype
coag necrosis hyperemic heterolysis etiology proliferative stable function bread-and-butter
Myocardial infarct
• Complete occlusion of major branch of ____ artery
• Gross: initially ____
* Firm and pale appearance * Remaining live tissue becomes \_\_\_\_
coronary
pale
hypertrophic
Myocardial infarction • Complete occlusion of major branch of coronary artery • Histopath: – \_\_\_\_ – Loss of structure: • Nuclei • \_\_\_\_ disks • Cell demarcation • Inflammatory infil
* TR: normal histology, presence of intercalated disks allow the smooth muscles to work as one unit * BR: middle of infarct; eosino, some intercalated disks but they're \_\_\_\_ down; limited number of nuclei * Will ultimately become \_\_\_\_
eosinohpilia
intercalated
breaking
phagocytosed
- L: dead myocardial cells, with inflam cells interdispersed that are degrading/digesting the ____ cells
- Will resolve/heal with a thin ____ tissue
myocardial
connective/scar
- Once dead tissue is removed, ____ will occur
- R: thin white band on right is a thin ____ tissue layer, chalky (____ calcification); this part of the heart will ____ out
fibrosis
connective
dystrophic
blow
- Who is more likely to survive a MI > ____ will be more likely to survive (65 > 45)
- Coronary artery will form sudden occlusion, and the blood supply downstream is blocked (45); no ____ circulation formation
- In the 65 y.o, developing artherosclerosis for longer, as development there is a gradual decrease in perfusion > the BV respond by developing ____ > allow the blood to bypass the blockade and provide downstream circulation > these channels develop further, so once total occlusion of major vessel occurs, there will still be ____ to that tissue (____)
older collateral collaterals BF compromised
