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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

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
A
stress
synergistic
HDL and LDL
LDL
HDL
HDL
high
HDL
26
Q

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
A

chornic

hemodynamic blood flow

27
Q

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)
A

permeability
adhesion
foam cells
adhesion

SMC
lipids

endothelial cells
macrophages

oxidation
fatty streaks
fibrous cap
hypersensitivity
antibodies
adaptive
28
Q

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
A

permeability
adhesiveness
coagulative activity
vasoactive

29
Q

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 \_\_\_\_
A
SMC
chemotactic
immunogenic
HDL
necrotic core
30
Q

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
A
phases
cytokines
metalloproteinases
autoimmunity
APC
31
Q

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
A
intima
LDL
foam cells
embryonic sources
atherogenicity
atheromas
32
Q

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
A
chronic
foam cells
SMC
fibrous cap
fatty streak
hypoxic
33
Q

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
A
gradual
angina pectoris
senile dementia
hypertension
intermittent claudication
sudden
rupture
renal artery
BP
oxugen
34
Q

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?
A
reversible
adeonsine
NG
typical or stable
unstable (crescendo)

exerted
spasm
regular
jaw

35
Q

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
A
ischemic
neural inputs
vagal
adrenergic agents
hypoxia
potassium
anywhere
misfire
36
Q

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
A
sustained or paroxysmal
palpitations
headedness
irregular
ventricular contraction
asytole
ventricular
37
Q

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
A
arterial
venous
thrombotic or embolic
vascular
occlusion
hypoxia
blood oxygen
collateral vessels
worse
38
Q

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
A
venous
dual
end-arterial
bacteria
abscess
coagulative
39
Q

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) [???]
A

arterial
reperfused
single

venous
reperfusion
dual

watershed
vaso vasorum

40
Q

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
A

watershed
contracted
coagulative

calcification
infarct
hypertension

41
Q

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
A
coagulative
coronary
partial
substernal
jaw
left
dyspnea
soreness
42
Q

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 ____
A
creatine kinase-MB
myoglobin
blood
seven
quickly
specific
43
Q

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 \_\_\_\_
A
0-1.5
coagualtive
wavy
8
vulnerability
44
Q

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 ____
A

neutrophil
anucleated
dead tissue
rupture

45
Q

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 > \_\_\_\_
A
macrophages
granulation tissue
elastic
functional
hypertrophy
CHF
46
Q

MI progression

• 10-14 days
• Granulation tissue 
– \_\_\_\_ tissue 
– \_\_\_\_
– (trichrome stain)
• Normal wound healing progression: granulation tissue
	○ BV, connective tissue (darker) > forms the \_\_\_\_ scar
A

connective
capillaries
collagenous

47
Q
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
A

2
cardiac
inflexible
distended

48
Q

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
A
arrhythmia
congestive heart failure
size and location
hypertrophy
breathing
49
Q

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
A
contractile
pericarditis
aneurysm
thrombi
occlusive
tightly

inflammation
emergency
larger