Cardiopathology Flashcards
Arteriosclerosis
• Arteriolosclerosis
• Mönckebergmedial
calcific sclerosis
• Atherosclerosis,Arterial atherosclerosis
• Atherosclerosis
– ____ inflammatory disease of the arteries
• Progressive destruction and replacement of normal vessel structure
• Weaker and less ____ vessels
• Become permanently ____
• Atherosclerosis is one type of arteriosclerosis; there are three types: ○ Monckeberg medial calcific sclerosis ○ Atherosclerosis, arterial atherosclerosis - only occurs in the \_\_\_\_ (doesn't occur in capillaries or veins [unless you put the veins in the \_\_\_\_ for failing arteries])
multifactorial elastic dilated arteries arterial system
Atherosclerosis
• Uniquely human disease
• > ____of all deaths in the Western world
• Death due to atherosclerotic complications have decreased
– Change in ____ habits
– Improved treatment of ____ – ____ of recurrence
* Dogs don't get this disease unless on the same \_\_\_\_that people eat; not to the same extent as humans though * Treat MI to some extent; no \_\_\_\_ as to when it occurs * Rigorous medication and lifestyle changes that decrease risk of recurrence * Incoming: how to predict who's at risk?
half living MI prevention diet warning signs
Atherosclerosis
• Is the most ____ cause of arterial thrombosis
– Loss of endothelial ____
– Abnormal ____
• Occurs in medium sized arteries
– ____
• ____ Arteries
• RareinVeinsand Capillaries
* Arterial thrombosis > most common cause of MI * Endothelium is major player in coagulation cascade > lose integrity > high risk of AS * Hemodynamic stress > increase risk of endothelial injury * If occurs in capillary, immediately would be occlusive > but not enough \_\_\_\_ for it form there; why doesn't happen in veins > the \_\_\_\_ isn't that stressful
common integrity vascular flow coronary, renal, cerebral large stuff blood flow
Normal vasculature: intima
* Endothelial cells line lumen > some ECM with an internal elastic lamina; IEL has \_\_\_\_ that allows oxygenation of tunica media > made up of \_\_\_\_ cells (allows contractile ability; allows movement of blood) * The bottom half of media gets supplied by \_\_\_\_ (vessels) > brings oxygen in; adventitia has a lot of ECM and fibroblasts
fenestrations
SM
vaso vasorum
Atherosclerotic Lesions
• Begin in ____
• Progress to ____
• Occur in areas of hemodynamic stress
– ____, ostia, curves
• Changes in order of development – \_\_\_\_ – Fibrous (fibrofatty) plaque, Atheroma – Complicated plaque
• AS starts in intima and movement into media > formation of a true AS lesion; if only in intima it's of less concern, but once into media > affects \_\_\_\_ of vessel wall, integrity and elasticity of vessel wall • Most common site > hemodynamic stress > branching of vessels, at \_\_\_\_ (minor vessels branch off of bigger vessels), or \_\_\_\_ (structure of body) ○ Infants 3-7 > have prelesions; as long as teens following US diet you have some lesions; if they get bigger by time of adulthood they can cause problems ○ They begin at these sites, but they move away as they grow • Fatty streak > "\_\_\_\_" > protective response because you need to thicken things up to cushion blood to go down vessel at curves, etc; but also a \_\_\_\_
intima
media
bifurcations
fatty streak
oxygenation ostio curves prelesion nitus
Fatty streaks
- Linear, flat, yellow-white elevations on intimal surface that do not compromise ____
- Begin in early ____
- Precursors of ____ plaques (?)
• Contain – \_\_\_\_ – Extracellular fat and cholesterol – \_\_\_\_ • Also occur in areas not prone to atherosclerosis
• Can clinically observe them • Some areas of vasculature are resistant to forming \_\_\_\_ • Foam cells come from macrophages (trying to digest lipid) or SM cells ○ Filled with lipid and a tiny nucleus • Lymphocytes - both v • Do not change flow of blood, do not \_\_\_\_ vessel, they're present just under the endothelial cells
blood flow
childhood
fibrous
foam cells lymphocytes atheromas macrophages and T cells distend
Intercostal Artery, Fatty Streak
• Artery sliced longitudinally
• The little circles are ____ (tiny vessels coming off of major vessel)
• Little yellow lines connecting ostia, as blood is flowing there is turbulence right before ostia as it diverts into screen and some turb afterwards as well
○ The area above and below is largely ____ (paler area)
Renal Artery, Fatty Streak
• Presence of ostia and the yellow streaks before and after; ____ areas unaffected
• Can use lipophilic stain > \_\_\_\_ > areas right off ostia that pick up stain > primitive fatty streaks • Fatty streak ○ Endothelial cells on top; a tiny layer of EC lipid and foam cells (nuclei pushed to side and filled with lipid); some lymphocytes ○ Muscle middle layer unaffected
ostia
unaffected
paler
congo red
From Fatty Streak to Fibrous Plaque
• Risk site for atheroma > over time you have lipid > high \_\_\_\_ levels, or low levels of \_\_\_\_ > chol accumulate/LDL accum in fatty streaks > LDL are \_\_\_\_ > recruit macrophages and lymphocytes to site > produce mediators to recruit and other inflam molecules > accumulation of lipid > macro's from BS but all SM from the \_\_\_\_ > the SM cells divide > smooth muscle forming above the IEL, and elaborate the ECM (collagen deposition, etc.), become phagocytic and take in the lipid but they cannot metabolize lipid (LDL) > thickening of the \_\_\_\_ > protrude into BS > disrupt blood flow, mediators coming in disrupt endothelium and damage > \_\_\_\_ progression
chol chol scavengers media intima cyclic
Atheromatous, Fibrous, Lipid, or Fibrofatty Plaques, or Atheromas
- Grey-white, localized, firm protrusions
- Impede blood flow in ____ vessels
- Begins in intima but progresses to media
Consist of – \_\_\_\_ – Foam cells, necrotic debris – \_\_\_\_ derived collagen, elastin, proteoglycans • \_\_\_\_?
• Change the diameter of the lumen > initial reaction the vessel maintains shape and accommodate same amount of blood > eventually will not be able to • \_\_\_\_ > as you thicken intima > you do not have great oxygenation > some cells/tissue die • Collagen/other ECM proteins deposited from the SM cells • Reversible? ○ Able to intervene/return things back to normal ○ Can take atheroma and take it backwards > how can do without weakening the vessel wall? § Modifying \_\_\_\_ and preventing formation > focused on \_\_\_\_ efforts
small and medium lipids and cholesterol SMC reversible necrotic debris diet prevention
Mild Atheroma
• In the brain; fresh
• Yellowish spots are affected areas > look a little firmer > there are ostia coming off around it
○ Roll back > half of the vessel wall is occluded by atheroma > reduction in blood flow > increased risk of formation of ____ on top
§ Can have consider vessel involvement and the tissue is relatively unaffected at this stage
Fibrofatty Plaques
• This tissue is fixed
• Arrows are pointing at small atheromas; ostia nearby with areas of ____ > unlikely to have occluded the vessel
thrombi
hemodynamic stress
The Anatomy of Atherosclerotic Plaque
* Within an atheroma > progression to the \_\_\_\_ > fibrous cap (laying down of collagen, can see with \_\_\_\_ stain); and a lipid core (\_\_\_\_, cholesterol, \_\_\_\_, necrotic debris) * Amount of media is not the \_\_\_\_ on either side > usually completely comproised by lipid core * Strong blue > fibrous cap * C > lipid core; has cholesterol clefts; \_\_\_\_ inflammatory response occurring * Majority of media on bottom is compromised (when compared to top/left)
media trichrome LDL foam cells same chronic
Foam Cells
• Foam cells in intima and medial layer > as progresses it forms a larger dense core ○ Presence in \_\_\_\_, and a major component of \_\_\_\_
fatty streak
atheroma
Cholesterol Clefts
* When process tissue, the \_\_\_\_ is washed away > forms streaks in tissue * Can see some cells * This is part of the \_\_\_\_ in the center
lipid
lipid core
Complicated Plaque
• Fibrous plaque with one of the following complications:
– ____ of intimal surface
– Thrombosis or Occlusion
– Extensive ____
– Dystrophic calcification – Intimal \_\_\_\_ – Vessel distension/weakening – \_\_\_\_ – Embolic showers from ruptured plaque
• As long as atheroma isn't diminishing blood flow too much > you're going to be okay (unless \_\_\_\_) • Any time you take away endothelial layer (ulceration) > \_\_\_\_ surface (VWF, bring in clotting factors) • If thrombus gets too larger > leads to occlusion [???] • Extensive necrosis > large necrotic core > not only larger atheroma, but also because it decreases \_\_\_\_ and is at risk for calcification/rupture • Deposition of \_\_\_\_ > makes it less elastic (dystrophic); or you can have emboli forming from the necrotic core when the thrombus surface bursts • Intimal hemorrhage ○ When tissue is hypoxic, and occlude blood vessels > angiognesis of \_\_\_\_ > hemorrhage and then it can blow up the atheroma to occlude vessel • Aneurysm ○ Vessel wall is weakened and becomes less elastic > SM is being replaced with \_\_\_\_ and collagen > the vessel wall will distend (bulging - \_\_\_\_; or can be even - \_\_\_\_; and a dissecting aneurysm)
ulceration necrosis hemorrhage aneurysm overexertion thrombogenic elasticity Ca++ vaso vasorum
fat
saccular
fusiform/cylindrical
Ulcerated and Fibrofatty Plaques
• ____ adhering to atheroma > red
• Take cross section (blue) > regular atheromas, and some that are compromised by ulceration
• Red is ____ atheroma
Large Necrotic Core
• Media has been replaced by ____ and necrotic debris
Thickened Intima - Necrotic Core
• Thickening of intima > necrosis of underlying tissue
• Large thrombus on top (cut off in section)
• ECM underneath; then larger area of lipid debris, foam cells, etc.
platelets
unaffected
lipid
Hemorrhagic Plaque
• BV try to grow in, but then a ____ into the plaque
• Up top > fibrous cap
• Underneath > large area of hemorrhage into site and a lot of ____
bleed
necrosis
Dystrophic Calcification
• Calcium deposits seen in tissue section > stain purple
• Up top is normal; below it is firbous cap, and under the cap there is the SMC dividing, foam cells, lipid, etc (conjuncture, cannot see at this magnification)
• Green necrotic core > purple stain surrounding > ____
• All dark purple > calcified > if squeezed vessel it would feel \_\_\_\_
dystrophic calcification
crunchy
Monckeberg medial calcific sclerosis
• MMCS >looks different than dystrophic calcification > accum of purple deposits in \_\_\_\_ > all the \_\_\_\_, less \_\_\_\_ and feels \_\_\_\_ ○ Different presentation than last slide!
media
way around
elastic
crunchy
Thrombosed atheroma
* Most \_\_\_\_ thing that happens * Not really a normal part of \_\_\_\_ * Large amount of clefts and necrotic debris > so little \_\_\_\_ left > completely occluded vessel to a thrombus forming on top of a atheroma > most common cause of \_\_\_\_ * Different stain * Thrombus inside the lumen; on right you see large amount of lipid and debris > atheroma, and thrombus formed on top
important
vessel
lumen
MI
Ruptured Plaque
• ____ can rupture > what used to be in the space entered the BS > formation of ____
Thrombosed Ruptured Plaque
• When ruptured plaque > nidus for forming ____ on top > in order to prevent material from ____
fibrous cap
emboli
thrombi
embolizing
Aneurysm
- Saccular
- Cylindrical/fusiform
- Atherosclerotic (brown stuff) > compromised wall > and extend away from vessel wall > overlying atheroma is a thrombus
- Wasn’t occluding the vessel > you still lumen
- Aneurysm is a risk for rupture > ____ wall, less ____ (due to thrombus formation) > when burst > hemorrhage into cavity/death from blood loss
- Saccular > come off ____ side
- Fusiform > ____
weakened
oxygenation
one
uniform
Aortic Dissection
• Used to be called an aneurysm; but now mechanism and pathology is distinct from a regular ____
• Break in ____, allows vlood from lumen to flow into vessel wall:
○ Blood can ____ in wall (can see here)
○ When look at wall, cannot see normal wall > can hemorrhage and bleed out of the wall
○ Compromised lumen bc of ____
○ Can extend vessel wall so it can snap it shut [???]
• Important in ____ > very important in people who have dysfunction in ____ genes
aneurysm wall clot atheromas marfan's syndrome ECM
Aneurysm locations
• Causes may be ____, infectious, ____, etc
• Most common place > \_\_\_\_; most often due to AS • Berry (saccular) aneurysm > also likely caused by AS, but there are genetic predispositions > form in the \_\_\_\_ in the base of the brain ○ Supplies 20% of blood flow, limited amount of space • Aneurysm in aorta > \_\_\_\_ patients > occurs bc of damage to vessels that feed the aorta (\_\_\_\_; endoarteritis obliterans); also at risk for \_\_\_\_ and bleeding out
genetic atherosclerotic abdominal aorta circle of willis syphilis vaso vasorum dissecting aneurysms
MAJOR:
• Risk factors we can control > ____, hypertension
○ Treat with medicine, diet and exercise
• Genetics
• Aging
○ As you ____ you’re at greater risk of AS
• Gender
○ Do not effects of being ____; you would expect it to be the effects of the gender > ____
○ Having ____ hormones > greater risk of developing atheroma; once you go through ____ (women) after 5 years you have the same risks of men
• Obesity, diet > linked to hyperlipidemia; these are ____
○ Unclear how much obesity is linked to hyperlipidemia, hypertension
• Smoking > toxins get into blood > ____ cells are affected
• Homocysteine
○ Homocysteinemia
§ Cysteine important for forming ____ bonds; ECM needs them > homocysteines can degrade ____ > vessel walls more prone to atheroma formation
• Infections are not initial causes, but they are potential players and a risk factor
hyperlipidemia age transgender estrogen male menopause modifiable endothelial disulfide ECM
MINOR:
• ____ is linked to immune function; placebo effect is real (20% of injury is affected by you thinking about it)
• Occur in a \_\_\_\_ effect > have more than additive effect when more than one risk factor • X-axis > LDL-C, mg/dL (mmol/L) • Total cholesterol is made up of a mixture of \_\_\_\_ ○ Correlation: you can have low cholesterol, but have more risk because you have more \_\_\_\_ ○ LDL is the depositing cholesterol; \_\_\_\_ takes the cholesterol away from tissue (scavenging LDL) ○ Exercising boosts \_\_\_\_, taking drugs can change balance; having a \_\_\_\_ HDL to LDL ratio is better; modifications can be made to the \_\_\_\_ levels
stress synergistic HDL and LDL LDL HDL HDL high HDL
Pathogenesis of Atherosclerosis: Response to Injury Hypothesis
A ____ inflammatory response of the arterial wall initiated by some form of injury/insult to the endothelium
• Injury may be due to \_\_\_\_, or some of the stressors discussed above > creates a site where there can be a chronic progression which leads to formation of an atheroma
chornic
hemodynamic blood flow
Events of Pathogenesis
• Subtle but chronic endothelial injury/dysfunction
– Increased endothelial ____
– Increased leukocyte ____
- Monocyte adhesion and migration → ____
- Platelet ____ to denudation or adherent leukocytes
____ proliferation elaboration of ECM
Enhanced accumulation of ____
Factors involved in progression: ____, lipids, ____ and SMC
• Lipoproteins into vessel wall > \_\_\_\_ of lipoproteins ○ Can enter the tissue > become oxidized > a state where you begin the cycle ○ Oxidized LDL recruit monocytes (chemoattractant) > macrophages eat them, but they cannot metabolize > foam cells > formation of \_\_\_\_ • If occurs chronically > more lipid and high BP > platelets adhere > release of factors: bring in macro's, bring in SMC > creation of ECM > permanent change to tissue > creation of \_\_\_\_ > reduces perfusion of BV > creates a site for lipid accumulation and damage to the tissue • T cells are present; there is a question of \_\_\_\_ whether it's linked but never proven > people who have atheromas > have \_\_\_\_ to oxidized LDL (\_\_\_\_ immune response, not just innate)
permeability
adhesion
foam cells
adhesion
SMC
lipids
endothelial cells
macrophages
oxidation fatty streaks fibrous cap hypersensitivity antibodies adaptive
Role of Endothelial Cell
– Dysfunction
• ____ of normally less permeable arteries
• Increased ____ for platelets and leukocytes
• Increased ____
• Secrete ____ molecules, cytokines, growth factors
– Denudation and Injury
• Can change from resting to activated > site where platelets adhere and other cells can be recruited > increased coagulative activity
permeability
adhesiveness
coagulative activity
vasoactive
Role of Lipids - LDL
- Low density lipoprotein –LDL – Evidence from animals and genetics
- Lipids and Cholesterol accumulate in intima and are oxidized
Oxidized LDL is – Ingested by Macs and \_\_\_\_, but NOT metabolized – \_\_\_\_ for Macs – Induces endothelium to express adhesion molecules, cytokines, growth factors – Cytotoxic to endothelial cells and SMC – \_\_\_\_ • \_\_\_\_ can remove lipids from plaques
* HDL remove LDL and cholesterol * High levels of LDL will cause lipids to accumulate in intima and become oxidized * Can kill cells > formation of large \_\_\_\_
SMC chemotactic immunogenic HDL necrotic core
Role of Macrophage and T-Lymphocytes
- Involved in all ____ of atherogenesis
- Macrophage ®foam cells
- Secrete ____, chemokines, growth factors, and ____
- Macrophage present oxidized LDL to T-cell – ____?
- Activate endothelial cells to recruit more monocytes (M-CSF, MCP)
- Prelesion, postlesion, etc. > always present
- Macro’s are the ____ > can be the link of oxidized LDL to autoimmunity
phases cytokines metalloproteinases autoimmunity APC
Role of SMC
• Stimulated by Macrophage and T-cell products to – migrate into ____
– proliferate
– elaborate ECM –recruit more ____
• Form ____
• SMC from different segments of the arterial arbor are derived from distinct ____
– Account for difference in ____?
• SMC can migrate into intima > proliferate > and make ischemia ○ Deposits ECM > vessel stronger, chemoattractant, and a substrate for thrombogenesis • Some areas of vasculature never forms \_\_\_\_ > may be due to distinct SMC sources from embryo
intima LDL foam cells embryonic sources atherogenicity atheromas
Atherogenesis
* We discussed all this in words earlier * \_\_\_\_ injury occurs * Macrophages ingest lipid and form \_\_\_\_ * Accum of foam cells > recruit \_\_\_\_ > these will try to ingest lipid, but will also make ECM > make \_\_\_\_ ; will also proliferate and bring more SMC > leads to the cyclic event * Formation of foam cells, formation of \_\_\_\_ * Elaboration of collagen; thickening of intima > area is \_\_\_\_ > necrotic debris accumulate inside
chronic foam cells SMC fibrous cap fatty streak hypoxic
Consequences
• Ischemia –\_\_\_\_ – Myocardium – \_\_\_\_ – Cerebrum – \_\_\_\_ – Kidney - \_\_\_\_ – Leg muscle – \_\_\_\_
• Thrombosis or vessel obstruction – Infarction –\_\_\_\_ – MI, Stroke, etc • Hemorrhage –\_\_\_\_ – Stroke, aortic aneurysm
• Myocardial infarction > complete blockage of vessel; can get stroke in the brain • Can have enough AS > limited perfusion > ischemia ○ Heart: angina pectoris ○ Cerebrum: senile dementia ○ Kidney > important in kidney (\_\_\_\_): hypertension § If kidney thinks hypo perfused > immediately raises \_\_\_\_ ○ Increased demand of muscles > pain > intermittent claudication; not enough \_\_\_\_ to work them properly
gradual angina pectoris senile dementia hypertension intermittent claudication
sudden rupture renal artery BP oxugen
Angina Pectoris
• Intermittent chest pain caused by transient, ____ ischemia
– Pain due to ischemia induced release of ____, bradykinin, etc – Relieved by ____ or rest
– 3 Forms
• ____ Angina
• Prinzmetal or Variant Angina • ____ Angina
• Relieved by nitroglycerin (anything that will dilate vessels) • You're okay if you're just sitting, but not when you're exerted ○ Exertion induced chest pain • Typical/stable ○ \_\_\_\_ > take NG and you're fine • Prinzmetal/variant ○ Not due to AS; but due to a \_\_\_\_ of the vessel wall that leads to symptoms ○ Relieved by NG • Unstable (crescendo) ○ Chest pain when you're not exerting yourself; at \_\_\_\_ intervals ○ Not relieved by \_\_\_\_ ○ Suggests medical attention bc you're at high risk for MI • Pain radiating up to \_\_\_\_ and NG isn't helping?
reversible adeonsine NG typical or stable unstable (crescendo)
exerted
spasm
regular
jaw
Arrhythmias
- Abnormalities in myocardial contraction rate and rhythm
- ____ Injury is the most common cause
• Regulated by: – direct \_\_\_\_ (e.g., \_\_\_\_ stimulation) – \_\_\_\_ (e.g., epinephrine [adrenaline]) – \_\_\_\_ – \_\_\_\_ concentrations • Can originate \_\_\_\_ from the pacemaker nodes to individual myocytes
* Contractions can be too fast, too slow or at an inconsistent pace * Can occur at any node, or at individual myocytes misfiring (causing others to also \_\_\_\_) * Can be caused by heart being damaged > cannot beat properly
ischemic neural inputs vagal adrenergic agents hypoxia potassium anywhere misfire
Manifestations of Arrhythmias
• May be \_\_\_\_ (sporadic) – No noticeable change – \_\_\_\_ - Tachycardia (fast heart rate) – Syncope (loss of consciousness) – Light \_\_\_\_ – Bradycardia (slow heart rate) –\_\_\_\_ rhythm • Regular contraction • Dysfunctional \_\_\_\_ (ventricular fibrillation) • No electrical activity (\_\_\_\_)
* Can looked like nothing * \_\_\_\_ is worse than atrial
sustained or paroxysmal palpitations headedness irregular ventricular contraction asytole ventricular
Infarction
- Ischemic necrosis caused by occlusion of ____ supply or ____ drainage
- 99%result from ____ events
• Infarct development influenced by: – Nature of \_\_\_\_ supply – Rate of \_\_\_\_ development – Vulnerability of tissue to \_\_\_\_ – \_\_\_\_ content
• Coagulative necrosis • [???] • Ischemia > body responds by making vessels > forms \_\_\_\_ flow through angiogenesis ○ Being younger and having a heart attack is \_\_\_\_ than being older because they have formed additional vasculature
arterial venous thrombotic or embolic vascular occlusion hypoxia blood oxygen collateral vessels worse
Types of Infarcts
• Red
– ____ occlusion, loose tissue (lung), in tissue with ____ circulation, reperfusion
• White
– Solid, ____ organs
• Septic
– Presence of ____ (ie embolic bacterial vegetations from the heart)
– Lead to ____ formation
• Bland
* Bland > \_\_\_\_ necrosis, no infectious agent * Septic > bacteria, infectious agent
venous dual end-arterial bacteria abscess coagulative
White infarcts
____ insufficiency
not ____
____ blood supply
Red infarcts
____ insufficiency
____
____ blood supply
* White infarcts > all \_\_\_\_ tissues downstream of blockage are affected * Red infarcts > lung, \_\_\_\_, liver, testes, brain (red if you have reperfusion) [???]
arterial
reperfused
single
venous
reperfusion
dual
watershed
vaso vasorum
Red Infarcts
- Lung
• Spleen
• ____ appearance of an infarct because everything is occluded
• Kidney ○ Healed infarct, not just white but it's also \_\_\_\_ • \_\_\_\_ necrosis > can see structure, but no nuclei (all cells are dead); not enough time for inflam cell to enter and clean it up • Heart ○ Infarct on top of a lifetie of hypertension ○ White due to \_\_\_\_ (bottom left) ○ White due to \_\_\_\_ (there's a difference) § Due to \_\_\_\_ • Classic long-term hypertension heart > infarction
watershed
contracted
coagulative
calcification
infarct
hypertension
Myocardial Infarction
• ____ necrosis of myocardium after ____ artery occlusion
– full wall or ____ wall necrosis
- ____, crushing chest pain that radiates to neck, ____, ____ arm
- ____ is common
- Arrhythmia• Cannot distinguish from arm ____, or incredibly painful
○ Range of variation
coagulative coronary partial substernal jaw left dyspnea soreness
Markers of MI
- release of myocardial proteins into the blood
– ____
– cardiac troponins - T and I
– ____
– lactate dehydrogenase
(decreasing in specficity)• These things are usually not in the blood
• Highly specific
○ CKMB
○ Troponins
§ Above two stay in the ____, and can use as a predictor for how long ago you had the MI
§ It’ll be up for ____ days > useful in saying how long it’s been since you had the cardiac arrest
○ Myoglobin
§ Released quickly, but ____ goes away
○ Lactate dehydrogenase is not very ____
creatine kinase-MB myoglobin blood seven quickly specific
Myocardial Infarct Progression
• Reversibleinjury–____hr
• Irreversibleinjury
– ____ necrosis – ____ fibers
• 1 day old
• Within first hour: coagulative necrosis • Wavy fibers, few nuclei in myocytes > classic presentation of coag necrosis ○ 20 mins to 1.5 hour for myocyte to die ○ For neuron > it'll be \_\_\_\_ mins ○ Difference in \_\_\_\_
0-1.5 coagualtive wavy 8 vulnerability
MI Progression
- 2-3 days later
- ____ infiltrated
- ____ myocytes
- Influx of neutrophils > cleaning up myocytes
- Most dangerous time after heart attack > digesting ____ > heart still needs to beat > heart is at risk for ____
neutrophil
anucleated
dead tissue
rupture
MI progression
• 7-10days
• Phagocytic ____ have removed necrotic myocytes
• Macrophages try to clear up more debris, and recruit in wound-healing phenotypes > form \_\_\_\_ > scar tissue (strong not \_\_\_\_) > heart intact btu not nearly as \_\_\_\_ > remaining ventricular myocardium has to work harder > likely to \_\_\_\_ > risk for LV hypertrophy, less flexible > less elastic > \_\_\_\_
macrophages granulation tissue elastic functional hypertrophy CHF
MI progression
• 10-14 days • Granulation tissue – \_\_\_\_ tissue – \_\_\_\_ – (trichrome stain)
• Normal wound healing progression: granulation tissue ○ BV, connective tissue (darker) > forms the \_\_\_\_ scar
connective
capillaries
collagenous
Healed Infarct • \_\_\_\_ months • Collagen scar with few \_\_\_\_ cells • Trichrome stain
* Collagenous scar with myocytes left that are not \_\_\_\_ anymore; encased in collagen * Highly \_\_\_\_, not as functional as regular myocardium: inability to beat, tissue can be \_\_\_\_ (risk of aneu) and a risk for thrombus formation
2
cardiac
inflexible
distended
Complications of myocardial infarction
• \_\_\_\_ • most common cause of death in the first several hours following infarction. • Myocardial (pump) failure - can lead to \_\_\_\_ - shock - \_\_\_\_ of the lesion determine outcome • Myocardial Rupture
* [???] * Elastic part of heart replaced > \_\_\_\_ > point/limit to which it can occur > backing up of the blood > it will go into the lungs (CHF) > difficulty \_\_\_\_ > back up into the system if severe enough
arrhythmia congestive heart failure size and location hypertrophy breathing
Myocardial rupture
• Area of damage and now a physical hole where blood will hemorrhage
• Rupture of papillary muscle (on right)
Complications of MI • \_\_\_\_ dysfunction • Mural Thrombus • \_\_\_\_ • Ventricular aneurysm
• Contractile dysfunction ○ \_\_\_\_ • Mural thrombus ○ If heart isn't contracting > blood pools > risk for \_\_\_\_ > in heart, \_\_\_\_ thrombi is unlikely, but will form \_\_\_\_ attached thrombi > mural thrombi • Pericarditis ○ \_\_\_\_ around heart; medical \_\_\_\_ and treated as such • Ventricular aneurysm ○ The wall will distend > the ventricle is much \_\_\_\_, hold more blood, and area that will bode out > risk for rupture and poor contractility ○ Picture is vent aneurysm
contractile pericarditis aneurysm thrombi occlusive tightly
inflammation
emergency
larger
