Cardiopathology Flashcards
1
Q
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])
A
multifactorial elastic dilated arteries arterial system
2
Q
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?
A
half living MI prevention diet warning signs
3
Q
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
A
common integrity vascular flow coronary, renal, cerebral large stuff blood flow
4
Q
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
A
fenestrations
SM
vaso vasorum
5
Q
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 \_\_\_\_
A
intima
media
bifurcations
fatty streak
oxygenation ostio curves prelesion nitus
6
Q
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
A
blood flow
childhood
fibrous
foam cells lymphocytes atheromas macrophages and T cells distend
7
Q
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
A
ostia
unaffected
paler
congo red
8
Q
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
A
chol chol scavengers media intima cyclic
9
Q
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
A
small and medium lipids and cholesterol SMC reversible necrotic debris diet prevention
10
Q
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
A
thrombi
hemodynamic stress
11
Q
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)
A
media trichrome LDL foam cells same chronic
12
Q
Foam Cells
• Foam cells in intima and medial layer > as progresses it forms a larger dense core ○ Presence in \_\_\_\_, and a major component of \_\_\_\_
A
fatty streak
atheroma
13
Q
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
A
lipid
lipid core
14
Q
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)
A
ulceration necrosis hemorrhage aneurysm overexertion thrombogenic elasticity Ca++ vaso vasorum
fat
saccular
fusiform/cylindrical
15
Q
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.
A
platelets
unaffected
lipid
16
Q
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 ____
A
bleed
necrosis
17
Q
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 \_\_\_\_
A
dystrophic calcification
crunchy
18
Q
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!
A
media
way around
elastic
crunchy
19
Q
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
A
important
vessel
lumen
MI
20
Q
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 ____
A
fibrous cap
emboli
thrombi
embolizing
21
Q
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 > ____
A
weakened
oxygenation
one
uniform
22
Q
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
A
aneurysm wall clot atheromas marfan's syndrome ECM
23
Q
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
A
genetic atherosclerotic abdominal aorta circle of willis syphilis vaso vasorum dissecting aneurysms
24
Q
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
A
hyperlipidemia age transgender estrogen male menopause modifiable endothelial disulfide ECM
25
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
```
26
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
27
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
```
28
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
29
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
```
30
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
```
31
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
```
32
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
```
33
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
```
34
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
35
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
```
36
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
```
37
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
```
38
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
```
39
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
40
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
41
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
```
42
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
```
43
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
```
44
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
45
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
```
46
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
47
```
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
48
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
```
49
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
