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268 Cards in this Set

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what are the 4 major types of herniation that occur in the brain?
subfalcine herniation
uncal herniation
herniation of cerebellar tonsils
Trans defect herniation
what is a common cause of brain herniation?
cerebral edema
may be caused by other conditions such as hematoma or tumor
very common cause of cerebral edema?
what is a subfalcine herniation/
occurs when the edema occur supratentorially in one hemi
the hemi that is expanding tries to escape toward the opposite hemi beneath the falx
get midline shift
what can happen in a subfalcine herniation of cinglate gyrus?
herniating cingulate gyrus can compress brr of ACA that supply one or both legs, producing weakness or sensory loss
what happens in an uncal herniation?
pushed in a downward fashion due to edema/mass effect so uncus is pushed across the tough edge of tentorium cerebelli into post fossa (very tough edge)
uncal herniation can press agianst what?
midbrain--lose respiration
what is Kernohan's notch and how does this occur?
indentation of contralateral tentorium that can be seen on contralateral side of midbrain opposite the lesion
occurs b/n edge of tentorium is close to midbrain and in herniation it indents the brainstem
what is a false-localizing sign?
Kernohan’s notch is a groove in the cerebral peduncle caused by this displacement of the brainstem against the incisura of the tentorium in some cases. The resulting ipsilateral hemiparesis is a false localising sign: since we are above the pyramidal decussation--same side as mass effect and herniation
called false localizing sign b/c neurological exam would localize the lesion on the opp side of the paralysis
what can happen in a transtentorial herniation?
when the medial aspect of temporal lobe is compressed against the free margin of tentorium cerebelli. with increasing displacment of the temporal lobe, CN3 is damaged and get dilation and impariement of eye mvmts on side of lesion. PcA compressed
contralateral cerebral peduncle is compressed resulting in hemiparesis ipsi to the side of the herniation: Kernohan's notch and false localizing sign
what is a tonsillar herniation?
displacement of cerebelum tonsils through foramen magnum: life threatening b/c caues brainstem compression and compromises vital resp and cardiac centers in medulla
waht are the clinical malformations of CNIII damage?
lateral deviation of eye (down and out), ptosis, pupillary dilation
progression of transtentorial herniation that compresses the brainstem can cause what?
hemorrhagic lesions in the midbrain and pons called Duret Hemorrhages b/c blood vssls are pulled and twisted and break to cuase hemorrhages
irreversible: seen at autopsy
if in midbrain: due to uncal herniation
describe contrecoup contusion
contusion: bruise on brain that occurs in response to a blow to surface of the brain
direct form of contusion = decelerating injury (fall or hit w/ crow bar): see damage at point of contact and oppostie to point of contact
sup orbital plate is a rough surface that damages brain (frontal lobes)
what are epidural hemorrhages?
caused by skull fx of the temporal bone which cross teh Middle cerebral artery. when the skull breaks the artery tears with it
blood accumulates b/n skull and dura
epidural space is a POTENTIAL space
lens shaped , grows quickly
what artery traverses through foramen spinosum?
middle meningeal artery: ruptured in epidural hematoma
fx of kids on playground : lose conscousness then they are fine:takes time to peel dura off "lucid interval"
subdural hemorrhages are produced by ?
torn bridging vv that conect the superficial vv on surface to the brain w/ superior sagital sinus
iff brain is bouncing around, tug on bridging vv or if brain is elderly it is pulled tighter increasing risk
is the epidural space or subdural more asily filled with blood
subdural: large space
epidrual is a potential space
what increases the change of subdural hemorrhage?
agin and degenerative brain disease
what is a subarachnoid hemorrhage?
blood accumulates in subarachnoid space usually from cortical vv and fills the sulcus so that the tops of the gyri can be sticking out of hemorrhage
*follows subarachnoid space even b/n 2 sulci
most cases of clinically significant SAH are associated with?
ruptured berry aneurysms, NOT trauma
what happens to our bone marrow with age? what can this lead to?
replaced with fat
bone fx can expose this fat to our blood circulation and fatty acids from this fat can cross the pulm capillaries and then coalesce to form small globuls of fat (fat emboli) that can get stuck in the capillaries of the brain especially at the jxn of gray and white matter
where do fat emboli like to go in brain?
jxn of gray and white matter that causs petechial hemorrhages w/n subcortical white matter
fatty acid cross pulm capillairies and coalesce to form fat emboli
how is the pattern of Wallerian degeneration different proximal to lesion? distal
proximal: axons cut off from cell body
distal/below lesion: axons for lateral CS tract, ALS, dorsal colums intact
what is GFAP?
glial fibrillary acidic protein: astrocyte specfic intermediate filament
uses to test to determine where tumor comes from
what does the astrocyte form during injury?
GFAP: glial fibrillary acidic protein that the astrocytes send into their star-like processes to form a messwork: brain's method of scarring/like fibrosis except the GfAP is kept insie the astrocyte
how is GFAP diffent from fibrosis?
keptt inside astrocytes unlike in fibrosis hwen the collagen is made by the fibroblast and deposited outsdie the cell
what are gemistocytes?
when the astrocytes become so distended with GFAP during injurty and appear like gemstones
what is the brain's version of collagen?
what are the numerous resting macrophages scattered throughout neural tissue?
microglial cells
there are also macrophages from peripheral blood
what do microglial cells looke like when they aren't resting?
plump macrophages and can't be distinguised fro mthe ones that migrated into the area of damage from te blood
5 major categories of hypoxia?
hypoxic: drowning, high altitude
anemic: blood loss, CO inhalation
stagnant: CHF
Histotoxic: cyanide poisoning
Hypoglycemic: insulin shock
difference b/n hypoxia and ishemia?
ischemia: lack of blood flow
hypoxia: lack of oxygen, blood flow nl
what are the most vulnerable neurons to hypoxia? what do you call them?
Hippocampus (somner's sector)-one of the first areas to die therefore look for hypoxia
lamina 3, V
neurons in globus pallidus
what can happen in somner's sector?
death of neurons in hypoxia
loss of individual neurons
overt infarction: complete loss of blood supply to region for a sufficient period of time
what are the cortical levels that are damaged in laminar necrosis?
lamina III, V
see yellow discoloration
where are watershed areas? significance?
selectively vulnerable to hypoxia b/c hypoperfused: MCA/ACA
at the interface b/n the distributions of major cerebral arteries
what is a penumbra?
b/n the lethally damaged infarcted core and the normal brain lies the penumbra: area of constrained blod flow with partially preserved enery metabolism
w/o tx can progress to infarction
territory of MCA? ACA? PCA?
MCA: lateral
ACA: medial
PCA: occipital
what are lacunar infarcts?
small infarcts due to small vssl arteriosclerosis
basal ganglia ,pons
due to hypertension
what type of infarction can be caused by embolitc stroke?
hemorrhagic infarction bc dislodgement or dissolution of the embolus allows reperfusiton with leakage through vssls damaged by ischemia
most common cause of fatal intracerebral hemorrhage?
complication of hypertension: often located in the basal ganglia, thalamus, brainstem or cerebellum
type of hemorrhage usually caused by rupture of berry aneurysm?
SAH: cerebral aneurysm that arises at bifurcatoinss
80% Post communicatig A
waht must you do to evaluate a vascular malformtion?
for AVM do a cerebral angiogram with abnormal prolif of vssls
what is an AVM?
arteriovenous malfomation with artery going straight to a vein
may cause intracerebral hemorrhage
etiology and mxn of germinal matrix hemorrhages?
germinal matrix: area of developing brain that contains a collection of undiff neural and glial precursor cells that migrate out from the germinal matrix to other ares of the brain where tehy diff into mature cells
in area for stria terminals: b/n caudate and thalamus
hemorrhages occur during 13-34th week gestation
only have layer of endothelum and BM therefore can hemorrhage-dissect through this poorly suppoted tissue and lateral ventricle
occur with hypoxia and large swings in blood flow
etiology and mxn of periventricular leukomalacia?
watershed in neonate
necrosis or softening of the periventrcular white matter in the neonat due to ischmic damage associated with hypoxia conditions( resp distress, shock)
first to suffer in hypxia b/c watershed: hypoperfused
etiology and formation of kernicterus?
somtimes there is bleeding during labor and fetal blood enters through placenta, if mom's RBC Ag are different the mom's AB will destroy babys. the next child will have problems bc the mom' Ab cross placenta: hemolytic disease of newborn
RBC release hemoglobin--bilirubin, prematrue infant can't eliminate bilirubin and it crosses BBB and sticks to lipids (lipophilc)--get mito damage and severe CNS injurty=kernicterus
why no Kernicterus in adults?
Hb doesn't get past BBB b/c we have enzymes to conjugate bilirubin
explain the formation of tau
microtubule associated protein (MAP) that normally assits in the formation of MT
under certain circumstances it becomes abnomrally phosphorylated and aggregates w/n the cytoplasm to form a flame shaped structure w/n a pyramidal neuron
typical patient with Alzheimer diseaes?
over 65yrs old
dementia, perceptual deficits, aphasia
atrophic brai
gyri shrink, wide sucli because of loss of neurons in the cortex
*sparing of pre and post central gyri
what is fine in Alheimer's pts?
motor fxn bc no loss of neurons in pre or post central gyri
waht is a tangle?
seen in Alzheimer's pts
abnormal intracellular accumulations of phosphorylated Tau protein
**form inside the cell
what are plaques?
extracellular foci of beta amyloid
explain the formation of beta amyloid?
plaques are extracellular foci of beta amyoid
beta amyloid results from the beta pleated sheet formation of an abnormal cleavage prodcut of beta amyloid prucrusor protein
*transmembrane protein that if cleaved incorrectly forms beta sheet which then forms beta amyloid
tau makes?
intracellular tangles
Beta amyoid makes
extracelluar plaques b/c of incorrect cleavage
tau and plaques are problems in what disease?
Lewy bodies are problems in what disease?
waht is Pick's diese similar to?
but with accentuation of the frontal and temporal cortex instead of the association cortex
what would a Pick Disease pt present with?
inappropriate behavior b/c the personality component of frontal lobe is altered along with the temporal lobe
**Phineas Gage
**seere atrophy of the frontal and temporal lobes
who does parkinson's disease affect? how do the pts appear?
pts b/n 40-70
shuffling gait, rigidity, resting tremors, expressionless faces, bent posture, depression
what will you see pathologically in midbrains of Parkinson's pts?
loss of dopaminergeic neruons w/n the substantia nigra
Lewy bodies in the neuromelanin-laden neurons of the substantia nigra
describe typical pt with HD?
after 35yrs
each child 50% chance
chromosome 4
*chorea, involuntary muscle twitching
degeneration of caudate nucleus
hydrocephalus ex vacuo of lateral ventricles b/c they enlarge
typical pt with ALS
degenerative disease of the spinal cord
loss of motor neurons in ant horn
pts mm atrophy, including those of respiration...aspiration can result
what do ALS pts die of?
resp failure or pneumonia
need to know if they want to be intubated
loss of ant horn motor neurons throughout spinal cord..paralsis of mm including thos for respiration
what will you see grossly in spinal cord of pt with ALS?
total loss of alpha motor neurons in the anterior horn along with gliosis
lateral colums show loss of the lateral cortical spinal tract
*loss of AL's in ant horn
chromosome and gene for HD?
chrom 4
codes for protein: huntingtin
mxn of MS?
chronic demyalinating disease taht is remitting or relapsing
area of white matter undergo demyelination but if oligo involved are still ok can have remyelination
gliosis is left behind via GFAP
what is demyelinated in MS?
spinal cord--get motor problems
area of white matter
what is the most common area of demylination due to MS?
periventricular white matter
why would you order a GFAP stain?
GFAP: glial fibrillary acidic protein
Ab that identifies an intermediate filatment protein only found in astrocytes and helps to ID neoplasms of astrocytic origin
why would you order a cytokeratin stain?
identify adenocarcinomas
helpful in ID metastatic carcinomas
which brain tumor specifcally spreads throughout the CNS?
medulloblastomas--arise in teh core of the medulla of the cerebellum
very malignant
ofen metastizes to other areas of CNS via CSF
typical symptoms of pt with a schwannoma?
benigh lesion taht invlve the 8thCN
vertigo, hearing loss
occur at CP angle
where do epidymomas occur?
somewhere along the ependymal lining: inside ventricles
what is the survial for glioblastoma multiforme? what does it look like grossly?
very high grade malignant lesion
<1yr survival
ring enhancing lesion
often croses the corpus callosum from one hemi to the other..
butterfly lesion
where do medulloblastoms arise?
in the core or medulla of cerebellum
metastazie via CSF
is a meningioma bad? where do they areise?
benign lesion
arise in the meninges outside the brain or spinal cord
"psammoma bodies"-concentricaly laminated calcified structures
arise from arachnoid--stuck to dura
4 most common sources of metastatic cancer in the brain
or melanoma
microscopically what does a meningioma look like?
psammom bodies
microscopically what does a astrocytoma look like?
irreguar nuclei=slightly elongated
no pattern
microscopically what does a medulloblastoma look like?
small dark blue cells
which brain tumor is usualy seen in children?
medulloblastoma: very malignant, spread via CSF
what is the only form of bacterial meningitis that may occur in epidemics?
strep pneumo
CSF glucose level in bacterial meningitis? viral?
bacterial: low
viral: nomal glucose
explain how menigitis damages teh brain
bacteria multiply rapidly in cSF
cerebral edema occurs as a result of the vasogenic changes and bc of the cytotoxic effects of inflammatory mediators in the cellular exudate
decreased absorption of CNS by the arachnoid vili and obstruction of CSFflow
cerebral edma=increased intracranial P which can lead to herniation
also can lead to infarction b/c of decresed cerebral perfusoin
what will the CSF show if viral meningitis?
incrased number of inflammatory cells: lymphocytes
why do you have a decresa in glucose in bacterial meningitis?
bc of problems w/ a glucose transport system and b/c of a shift towrds anaerobic metabolism by the brain
common cause of chronic bacterial meningits?
common cause of fungal bacterial meningits?
Coccidiodes, cyrptococcus
what is the difference b/n acte and chornic menigitis
acute: all over the brain
chronic: base of brain therefore see CN findings
how is a Tb meningitis diffrent from acute menigitis grossly?
acute: entire brain affected
chronic: rest of brain fine except base
what is the most common fungal infxn of the CNS?
cyrptococcus-occurs in debilitated pts, thick capsule
what are the most common cuass of severe chronic menigitis in US?
Tb and cryptococcus
clinical manifestation of Tb meningitis?
increased pressure, slightly decresed glucose, PPD +, sputum has acid fast bacilli
accumulates chiefly at teh base of the brain, obliterating the cisterns
usually has no sequale
the meningitis is usually almost always associated with infxn elsewhere in teh body: 80% of tuberculous leptomenigitis is associated with pulm Tb
3 types of neurosphyllis?
meningovascular syphillis, gerneral paresis, tabes dorsalis
what is meningovascular syphillis?
subactue or chronic meningitis
chronic inflam infiltrate
meningeal vssls infiltrated by lymphocytes and plasma cells
fibrous intimal prolif and thinning of media= Huebner arteritis
what is Huebner's arteritis and what is it associated with
infiltration of vssl by chronic inflam cells with fibrous obliteration of lumens leading to infarction
seen in sphyllis
what is general paresis?
invasion of brain parenchyma by spirchetes
brain shows marked atrophy, neuronal loss,gliosis
progressive mental and physical decline
waht is tabes dorsalis?
myelopathy thought to result from meningeal fibrosis and involvment of dorsal roots followed by degen of post colmns
3major s/x: pain, ataxia, urinary incontiaence
absent deep tendon relfexes b/c demylination of post columns
how does a cerbral abscess occur
almost always secondary to infxn elseehwere: lung abscess, empymea
symptoms relatd to mass effect: headache, vomiting, seizures
3 things that settle out in the interface b/n gray and white matter?
cerebral abscess
type of pt taht gets apergillis cerebritis?
cerbritis: filled with yellow pus that then leads to abscess
affects predime immunosuppressed ppl: transplant pts
type of pt taht gets cryptococcus meningtis/cerebritis
can occur in normal individuals ,but frequently occur in debilitated pts
type of pt that gets cysticercosis?
most common parastic disease of CNS
pt will be eating pork b/c of Taenia Solium or ingestion of ova from fecally contaminated water
asprgillis is seen in?
immunosuppresed pts
transplant pts
causes hemorrhagic ,necrotic lesions
virus associated with PML?
papova virus, almost always the JC virus
type of pt that gets PML?
HIV pts are predisposed to variety of opportunistic infxns taht can affect the CNS including PML and cMV
seen in other immunosuppresd situations but mostly AIDS
brain changes associated with PML?
widespread involvment of white matter, infected oligodendroglia that are enlarged
**multiple, nonenhancing white matter lesions w/o mass effect
visual deficits, personality changs, dementia, motor deficits
CMV inclusions look like? occur hwere?
periventricular area
owls eye
pathogenesis of polio?
tropism : selectively infects motor neurons (spinal cord, brainstem, cortex)
spreads to small intestine, CNS where it infects motor neurons in the spinal cord and brain stem and rarely the cerebral cortex
*see atrophy of anterior spinal nerves
who does subacute sclerosing panencephalitis occur in? what is the pathogensisi?
rare coniditon that occurs in children after acute episode of measles
perivacular inflammation with viral nucleocapsids
mesasles virus present in SSPE lacks the M protein that is necessary for assembling a virus at the cell surface therefore see inclusions w/ nuceli of infected neurons
opportunistic infxns that occur in the CNS of Aids pts?
toxoplasmosis: cat feces, get intracerebral mass lesions..abscesses
PML casused by JC
primary CNS lymphoma: well circumscribed
opportunisitc infxn hat occurs in the retina of AIDS pts?
brain tumor that occurs in AIDS pts?
CNS lymphoma
presents as single or multiple intracerebral masses
always high grade B cell lymphoma*
infiltrate of enlarged, atypical B cells in sheets and/or in a perivascular distribution
*bad prognosis
characteristics of prion disease pts?
rapidly progressive demeita, ataxia, dysarthria, frequent myoclonic jerks
changes that occur in PrPc that lead to prion disease?
exposure of the cellular prion protein PrPC to the abnormal prion protein PrPSC causes teh PrPC to convert to the disease producing PrPSC which is rich in beta pleated sheets
remarkable stable and highly resistant to normal methods of sterilizationg
what is the predominant cause of death in the US?
heart disease 30% (1/3 of all annual deaths)
which sex do we see an incrase in heart disease
females b/c more awarness
how have the death rates from heart diesae changed? what about the actual number of heart disease deaths? why?
declined by 25%
actual number of deaths declined 8%
b/c ability to Tx heart disese incresed
how do symptoms of heart disease differ in males vs females?
females: uneasy feeling in chest; not always pain, fatigue (very non specific)
males: dnt complain of fatigue
what are the 5 basic categories of cardiac disease?
1. congenital heart disese: incid decreasd 31%
2. ischemic heart diseaes: incid decrased 25%
3. hypertensive heart disease
4. valvular heart disease
5. Non ischemic mycocardial diseae: 25% incresae in incidicence
what is the most common reason for transplant cardiomyopathy?
nonischmic (primary) myocardial disease
waht is cardiac reserve?
at rest CO 10-20% max output
cardiace rseerve: 5fold margin for increased output
how much cardiac fxn must be lost in heart disease pts before you see symptoms?
what are the 6 basic causes of cardiac disfxn?
1 pump failure: primary myocardiopathy
2 obstruction to blood flow: stenosis
3 regurgitant flow: insuff
4 disorders of cardiac condxn: atrial fib
5. disruption of continuity of the circulatory system: gunshot wound
6. aging: dilatation in chambers, change coronary vssls, chemical changes
what is the problem in cardiac failure?
inability to pump blood at a rate necesary for metabolizing tissues
when chronic = CHF
when most CHF pts present w/ symptoms they have developed what?
associated compensatory feature: cardiac hypertrophy (increase in heart size and wt)
CHF is characterized by either or both?
1. dimished CO (forward failure) due to either systolic disfxn or diastolic disfxn
2. damning of blood in the venous system (backward failure)
what is the diff b/n systolic disfxn and diastolic disfxn?
both can be the causes of diminised CO
systolic: progressive detioration of myocardial contractility
diastolic: iniability of chambers to relax to fill
diff b/n chronic and acute left sided heart failure?
chronic: slowly progressive degree of falure that occurs over time, can cause R heart failure
acute: rapidly progressive fatal corse, medical emergency with 50% mortality rate
what are some findings that you may see grossly in a leftsided heart failure?
cardiomegaly: hypertorphy, chamber dilatation
secondary enlargement of the L atrium
what chamber change is associated with ischemic heart disease? left sided valvular disease?
IHD: chamber dilatation
left sided valvular diseaes: LV hypertrophy
what lung pathology signifies prevous hemorrhage?
accumuatong of hemosiderin laden macrophages in the alveolar spaces (siderophores or heart failure cells): RBC follow fluid and they cant get out so the macrophages eat them and fill with hemosiderin
left sided heart failure can cause problems where
lung: widening of alveolar septa, heart failure cells (hemosiderin laden macrophages), edema in alveolar spaces
Kidney: renal hypopefusion which stimulates RAA
R sided heart failure is most commonly a consequence of ?
left sided heart failure: incrased pressure in pulm circulation increases the workload of the R ventricle
is isolated right sided failure common?
no..more commonly associated with left hart failure
termed cor pulmonale: in pts with lung disease
what other organ systems can be effected by right sided heart failure?
subcutaneous tissues: pitting edema with lower extremities most affected
liver and portal system: Congestive hepatomegaly
spleen: congestive splenomegaly
what is pitting edema?
extravasation and accumulation of interstitial fluid in the papillary dermis and subcut tissues: in R sided heart failure the indentation persits long after removal of the pressure * the greater the degree of right sided failure the more severe the edema
the higher the score (0-4) the worse the edema
with an increase in cardiac workload what is the adaptive response that it can cause?
increase in size or hypertrophy
what is the diff b/n pressure overload hypertrophy and volume overload hyprtrophy?
pressure overload: increase in the thickness of the ventrica wall subjected to the increased workload
volume overlowad: chamber dilation with increased ventricular diameter. Ventricular wall thickness normal
what are the characteristics of volume overload hypertrophy?
chamber dilation with increased ventricle diamter
ventricular wall thickness normal
overall cardiac muslce mass is increased bc the dilation has increased the overall size of the ventricular wall
is the chamber dilated in pressure hypertrophy?
no, only an increase in thickness
is the chamber dilated in volume hypertrophy?
yes, but the thickness is normal
increased cardiac mass
what would cuase a pressure overload hypertrophy in left side?
systemic hypertension, aortic stenosis
left ventricular wall is thickended w/o any increase in the size of ventricular chamber
what would indicate thickening of ventricular wall?
greater than 2 sonameters
what would cause pressure overload hypertrophy in right side?
cor pulmonale
waht is cardiac ischemia?
imbalance b/n the supply (perfusion) and demand of the heart for oxygenated blood
most common cause of IHD?
>90% of IHD, the cardiac ischemia is the result of redxn in coronary blood flow due to atherosclerotic coronary arterial obstruction
synonyms of IHD?
coronary artery disease (CAD)
coronary heart disease
what is the leading cause of death in US for both males and females?
is there a higher incidence of IHD in males or females?
in premen women IHD is uncommon
how has the death rate from IHD changed from 1963-2003?
fallen 50%
pathogenesis for IHD?
fixed atherosclerotic narrowing: dimished coronary artery perfusion
greater than 90% of IHD pts have what?
atherosclerosis in 1 or more of their major coronary arteries
how much obstruction is necessary to cause ischemia symptoms with exercise
75% or greater in major coronary to cause ischemia symtpoms
how much obstruction is necesary to cause ishemia when the individal is at rest?
90% or greater: only 10% of lumen remaining
what precipitates myocaridal ischmia (acute coronary syndromes)?
abrupt plaque change followed by thrombosis: rupture/fissuring, erosion/ulceration, hemorrhage into atheroma
*plaque is the underlyingcause
where must the acute plaque change occur to cause IHD?
doesn't have to occur in severely stenotic portions of arteries
2/3 of acute ruptures that lead to thromsos occur in vssl that are only 50% narrowed: plaque doesn't have to be in an area of a lot of build up
what are the 4 types of IHD?
stable angina
unstable angina
sudden death
what is uniqe about stable angina unlike other IHDs?
no plaque disruption
no plaque associated thrombus
what does increased C reactive protein indicate?
when eleveated has a predictive value for a risk of coronary heart disease b/c indicates chronic inflammation
role of vascoconsriction in IHD?
real,but not well defined role in actue conronary syndromes
4 distinct syndroms of IHD?
sudden cardiac death
angina pectoris
chronic IHD with heart failure
mxn of sudden cardiac death?
lethal arrythmia
how much stenosis is usually seen in pts with IHD sudden cardiac death?
>75% in one or more of the major coronary arteries near opening
who should you expect to see sudden cardiac death in?
youg: in pple with SCD under age 40
(sudden death in athletes, congenital structural abnormalities)
what IHD is characterized by paroxysmal and recrurent attakcs of substernal or precordial chest discomfort casued by transient MI that fall short of inducing the cellular necrosis taht defines infarction?
Angina pectoris
types of angina: stable, prinzmetal, unstable
what is the most common form of angina? what causes it?
stable angina
caused by redxn of coronary perfusin to a critical level by chronic stenosing coronary atherosclerosis
what provokes stable angina? how is ti relieved?
increaed cardiac demand: emotion, exercise
releived by rest or sublingual nitro
what form of angina occurs due to coronary artery spasm? waht relieves it?
Prinzmetal Angina
occurs at rest (at night)
relieved by vasodilators
**unrelated to physical activity
unstable or cresendo angina is caused by?
disruption of an atherosclertoci plaque with suprimposed thrombus
often the prodrome of MI
what is the death of cardiac muscle resulting from ischemia?
MI "heart attack"
most impt form of IHD
freq of MI rises with ___
increasing age
what risk factors acct for 50-60% of MI?
lipid risk factors: triglycerides, cholesterol
who is at greater risk for MI?
males but postmenopause female=men
40-45% under age 65
how has the incidince of IHD changed? how does this affecct incidenc of MI?
overall incidence of IHD declined 50%
decrase in MI
are most MIs transmural or subendocardial?
transmural: ischemic necrosis involves the full or nearly full thickness of the ventricular wall **involves full wall
what is the diff b/n transmural and subendocarial infarction?
transmural: full or near full thickness ventricular wall, acute plaque change
subendocardial: area of necrosis limited to the inner 1/3 of the ventricular wall or inner 1/2
waht 2 things cau cause subendothlial infarctions?
acute plaque change: plque disruption followed by coronary thrombus
prolonged and severe redxn in systemic BP as in shock
why is the subendocarium at risk for infarction?
the subendocarial zone is normaly the least well perfused region of the myocardium therefore most vulnerable to any redxn in coronary flow
in angina pectoris, is there death of cardiac muscle?
no, ischmia is less severe thn MI win which there can be death of cardiac tissue
what is the initial event in an MI?
sudden change in atheromatous plaque
then an immediate formation of inital platelet plug over plaque
what are the seq of events in an MI?
sudden disruption in plaque
platelets undergo adhesion, aggregation, activation and release of potent aggregators: thromboxane, 5HT
this stimulates vasospasm
extrinsic pathway of coagulation: larger and mor stable clot
w/n minutes thrombus eveloves to completely occlude the lumen
what percent of transmural pts have NO associated aterhosclerosis or acute atherosclertoc plaque change? in these pts what could be the c ause?
vasospasm: cocaine abuse
emboli: from left atrium associated with atrial fib leading to systemic embolization
when does myocardial necrosis begin after coronary occulsion? complete?
30 min after
complete 6 hrs after
how long is the window of opportunity to tx MI?
b/n the 30min it begins and 6 hrs later
predom mx of cell death in MI is due to what type of necrosis?
coagulation necrosis
irreversible injurty of ischemic myocytes occurs first where?
subendocardial zone
when does irreversible cell injurty occur in MI?
20-40min in severly ischemic myocardium
what is the early feature in ishcemic necoris of myocardium?
start of ATP depletion w/n seconds
loss of contractility <2min
in an MI, where does the necrosis begin?
small zone in the myocardium beneath the endocardial surface in the center of the ischmic zone
use of TTC stain?
stain to highlight the area of necrosis that first becoms apparent after 2-3 hrs after the infarct
stain will be red where the enzymes are presereved..the enyzmes are depleted in the area of ischemic necrosis b/c they leak out therough the damaged cell membranes
LAD is involved in what percent of MI? Right coronary artery?
LAD: 40-50%-infarct involves ant wall of left ventricle
RC: 30-40%
time frame for reversible injury?
0-30 min
what time frame in eveoluatoin of MI would you not be able to tell if that person had an MI?
first 30min-4hr
what will the fibers of MI look like in thefirst 4-12hrs?
wavy fibers at the periphery of the infarct resulting from the forceful systolic tugs by the viable fibers
what must be done to repefuse the infarcted area?
goal of thereapy is to salvage the ischemic myocardium from potential infarction by restoration of tissue perfusion as quickly as possible by lysis, removal or bypass of occluding thrombus
waht is myocardial stunning?
associated with reperfusion injury: breif ischemia followd by reperfusion
may indcue cardiac failure
prolonged ischemic dysfxn
what is the time frame for reperfusion?
<20 min
wavefront of necrosis spreads from?
if occulsion extends >20 min wavefront of necrosis spreads how?
from subendo-subepi
reperfusion before 3-6hrs ischemica may exhibit stunning: viable but not fxnl
classic acute symptoms and signs of MI?
substernal chest pain with radiation down left arm
weak ,rapid pulse
sweating profusely: diaphoretic
dsypnea: due to impaired contractility and resultant pulm congestion
preferred biomarkers for myocardial damage?
cardic specific proteins: Troponin I and Troponin T: not normally detected in the circulation but after acute MI levels of both cardiac troponins rise at 2-4hrs and peak at 48hrs
the remain elevated 7-10 days after a acute event
for an acute MI measure what?
Troponin T and I b/c they peak at 48hrs after and stay up for 7-10 days
best alternative to troponin measurement?
cardiac creatine kinase: enzyme that is hghly concentrated in brain, myocarium, and skeletal muscle and has dimers M and B
what is the CK isoform MB? when does it rise?
CK-MB is principally from myocardium
rise w/n 2-4 hours of onset of MI, peaks at 24 hrs, retuns to noaraml at 72 hrs
why are troponins a better measure than CK-MB?
troponsin stay elevated for 7-10 days
CK-MB returns to nromal after 72 hrs and is not specific--can be elevated in skeletal muscle injury
absence of a change in the levels of CK and CK-MB during the first 2 days of chest pain and of troponin in the days follwoing indicates waht?
no dx of MI
what can C reactive protein serve as a marker for?
to predict the risk of myocardial infarct in pts with angina, and the risk of myocardial infarct in pts who recover from infarcts
what are the complications following an acute MI?
contractile disfxn
papillary muscle disfxn with mitral regurg
myocardial rupture
right ventricle infarction
infarct extension
mural thrombus
ventricular aneurysm
what is valvular stenosis?
failure of a valve to open completely, thereby impeding forward flow
is valvular stenosis an acute or chronic problem
almost alaways a chronic problem due to valve cusp abnormality
what is valve insuff?
failure of a valve to close completely allowing reversed flow
waht is teh diff b/c valvular stenosis and insuff?
stenosis: can't open
insuff: can't close
what is a pure vs mixed cardiac valve disfxn?
pure: when only stenosis or insuff is present
mixed: when both present in same value
most freq cause of aortic stenosis?
calcification of anatomically normal and congenitally bicuspid aortic valves
most freq cause of oartic insuff?
dilation of the aorta related to hypertension
most freq cause of mitral stenosis?
rheumatic heart disease
most freq cuase of mitral insuff?
myxomatous degeneration (mitral valve prolapse)
waht accts for 2/3 all valvular disease?
aquired stenoses of the aortic and mitral valves
what type of calcification is involved in valvular degeneration?
dystrophic calcification w/o signif lipid deposition or cellular prolif
most common of all valvular abnormaliite? asssoicated with?
calcific aortic stenosis
associated with advanced age
when do clinical features of calcific arotic stenosis occur?
8th (70s) or 9th (80s) decade
leads to CHF, angina
what happens to the left heart in calcific aortic stenosis?
pressure hypertrophy--left ven concentric hypertrophy
pathologic features of calcific aortic stenosis?
nodular masses of calcium heaped up w/n sinues of Valsalva
commissures not fused
no evidence of inflamm process
what percent of the pop has congenital bicuspid aortic valves?
1% with the 2 cusps freq not equal in size larger cusp has a raphe (seam)
what are aortic bicuspid valves more susceptible to ?
progressive degenertive calcification; develop significant calcification earlier
when do ppl with calcific stenosis of congenitally bicuspid aortic valves develop s/s?
earlier than nl aortic stenosis (8and 9th)
occur in 6th and 7th decades
in who does mitral annular calcification occur in?
women over 60
individuals with myematous mitral valves
pts with elevaed left vent P-hypertension
do mitral annular calcfications affect valve fuxn?
what is the cuase of discovery of mital annular calcificatoin/
large calcium deposits are detected by ultrasound or radiography for other reasons
who does mitral valve prolapse affect?
3% of adults in US: young women
what is the problem in myxomatous degeneration of mitral valve?
one or both mitral valve leaflets are floppy and prolapse into the left atrium during systole
what are the primary changes in mitral valve prolapse?
intercordal balooning of mitral valve leaflets
leaflets are enlarged, thick, rubbery
20-40% invovlement of tricuspid valve
what do you call foca inflammatory lesions w/n the heart of someone with rheumatic fever?
aschoff bodies
what are teh 5 fidings in Acute Rheumatic fever?
erythemia marginatum
subcutaneous nodule
what is used to diagnosis actue rheumatic fever/
jones criteria: evidence prior group A strp infxn plus either 2 major system findings, or 1 majr system fidning plus fever or elevaed c-reactive protein
actue RF is due to
sequelae of group A strep infxn
occurs 10 days-6 weeks after clinical episode of sore throat
only 1% pts die during primary episode
how has the incidence of acute RF changed in us?
declined dramatically: 0.3-1cases/year b/c of Tx
how has the incidence of rheumati valvular heart disease changed?
dropped 25% b/c of the decrease in actue RF
when does rhumatic valvular heart diseaes occur?
years or even decades after the episode of ARF
what valvles does RHD affect?
mitral and aortic valves, uncommonly the tricuspid, only rarly the pulmonic valve
99% of mitral stenosis is caused by
what are the key morphilogical features of acute rheumatic heart disease?
myocardial aschoff bodies
fibrinous pericarditis
what are the anatomical changes of the mitral valve in chronic RHD?
leaflet thickening
commissureal fusion and shortening
thickening and fusion of the tendionsou cords
what are ashcoff bodies?
inflam lesions in heart of acute RF
swollen eosinophilc collagen surrounded by lymphocytes
what is uniqe about the vasculurization in rheumatic valve?
neovascularization: nl avascular
see vssls=RHD
is infective endocarditis good or bad?
very serious ..colonization or invasion of the heart valves by a microbe leading to formation of bulky, friable vegetations
most causes of infective endocarditis are due to ?
in what diseae do you see bulky friable vegetations, destrxn of valves, risk of systemic microemboli?
infective endocarditis
how is acute bacterial endocarditis different from subacute in terms of time?
acute: rapidly progressive
subacute: insidious onset: weeks-months
what bacterial org is responsible for acute bacterial endocarditis?
S aurus: high virulent bacteria
what bacterial org is responsible fro subactue bacterial endocarditis?
S viridans: low virulence bacteria
describe recovery/tx of acute vs subactue bacterial endocarditis?
acute: even with aggressive antibiotic therapy 50% pts die in days or weeks of onset of symptoms
subacute: most pts recovr w/ antibiotic therapy
waht is the most consistent sign of infective endocarditis?
what disease is charactrized by deposition of small (1-5mm) single or multiple thrombi along the line of closure of the valve leaflets or cusps
nonbacterial thrombotic endocarditis: may fragment and produce systemic emboli which produce obstruction in coronary arateries or brain vasculature
was is contained in the valvular lesions of nonbacterial thrombotic endocarditis?
no microorg bc the valvular lesions are sterile
major risk factor for nonbactrial thrombotic endocarditis?
hypercoag state
compare vegetations in RHD, IE, NBTE, Libman Sachs
RHD: row of small warty vegetations alog the lines of closure of leaflets
IE: large irregular masses o the valve cusps than can extend onth chorda
NBTE: small, bland vegetations attached at the line of closure
LSE: small vegetations on either side or both of leaflets
are libman sachs vegetatiosn infective?
no they are small sterile vegetations that occur on mtiral and tricuspid valves
who is at risk for libman sachs disease?
SLE pts with lupus anticoagulant
carcinoid heart diseae is caused by?
carcinoid tumors produing high levels of circulating serotonin
what can carcinoid syndrome result in?
fibrous intimal thickening of the endocardial surfaces of the right side of the heart: R ventricle, tricuspid and pulmonic valves
the intimal thickening of right side of heart casued by carcinoid syndrome is composed of waht?
smooth muscle prolif
increased acid mucopolysach matrix
*no elastin fibers
**see intimal thickenin
if you want a prosthetic valve instead of a bioligcal valve waht must you need to take?
what is the major failure mode of bioprosthes?
structural deterioration calcification and/or tearing causing secondary regurgitaton