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228 Cards in this Set

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Describe the relationship between resistance to blood flow and diameter of a blood vessel
resistance to flow is inversely proportional to the 4th power of the diameter (increase diameter -> increase flow -> decrease flow resistance)
what are the three main types of endothelial functions?
1. Barrier
2. Transport
3. Metabolic
what is the most common cause of ateriosclerosis?
atherosclerosis
what type of blood vessels does atherosclerosis effect?
large and medium sized arteries
why do atherosclerotic plaques like to form at the branch points of arteries?
these are sites of hemodynamic turbulence
atherosclerosis is a disease that primarily effects which layer of a blood vessel?
intima
describe the pathogenesis and components of atherosclerotic disease
- endothelial dysfunction
- lipid accumulation, smooth muscle proliferation in intima
- lipids cause cell injury, this attracts macrophages
- macrophages scavenge extracellular lipid and release growth factors
- eventual damage to endothelium causes platelets to adhere
what could causethe dysfunction (or damage) to the arterial endothelium seen in atherosclerosis? (6)
- hypercholesterolemia
- mechanical injury
- hypertension
- immune mechanisms
- toxins
- viruses
name the growth factors released by macrophages in the atherosclerotic process
(5)
FGF
TNF
IL-1
IFN
TGF-B
what are the two possible precursors to atherosclerosis (physical changes)
1. Fatty Streak
2. Intimal Cell Mass
what are the pros and cons of the "fatty streak" precursor hypothesis?
pro-composed of foamy macrophages
cons-seen in regions where atherosclerosis is not commonly found
What are the pros and cons of the "intimal cell mass" hypothesis?
pros - nodules of intimal smooth muscle at arterial branch points
cons - may only be age related change, no lipid deposition
what is the current prevalent thought explaining the pathogenic mechanism of atherosclerosis?
multifactorial process
name the 5 most common places atherosclerosis is found
1. abdominal aorta and iliacs
2. proximal coronary arteries
3. thoracic aorta, femoral, popliteal arteries
4. internal carotids
5. vertebral, basilar, middle cerebral arteries
name 7 possible complications of atherosclerosis
1. thrombosis (acute occlusion)
2. chronic stenosis (ischemia)
3. hemorrhage (into plaque)
4. aneurysm formation
5. ulceration (with atheroemboli)
5. calcification
what are the 4 most important risk factors in the development of atherosclerosis?
1. hyperlipidemia
2. hypertension
3. cigarette smoking
4. diabetes mellitus
what are the other 5 risk factors in the development of atherosclerosis?
1. age
2. sex (M>F)
3. genetics
4. diet
5. lifestyle (personality type, exercise habits)
name the 5 lipid types in order of size (large to small)
1. chylomicron
2. VLDL
3. IDL
4. LDL
5. HDL
what is inheritance pattern of type II familial hypercholesterolemia?
autosomal dominant
(mutation is on short arm of chromosome 19)
describe the mutation subsequent effects of type II familial hypercholesterolemia
mutation causes malfunctioning LDL receptor
(LDLs must be processed through a receptor independant pathway)
this leads to random cholesterol buildup
name some secondary causes of hyperlipoproteinemia
hypothyroidism
diabetes mellitus
nephrotic syndrome
renal failure
alcoholism
obstructive liver disease
pancreatitis
glycogen storage disease
porphyria
name 6 possible associations/complications of hypertension
atherosclerosis
angina
sudden cardiac death
aortic dissection
cerebral infarction
intracerebral hemorrhage
95% of hypertension is _____
5% of hypertension is ____
95% - essential (idiopathic)
5% - renal disease, endocrine related, other
3 modifiying factors of cardiac output
1. Blood volume
2. heart rate
3. contractility
3 modifying factors of TPR?
1. humoral factors (dilators, constrictors)
2. local factors (autoregulations)
3. neural factors (dilators, constrictors)
what are the blood pressures for the following?
1. Normal
2. Prehypertension
3. Stage 1 hypertension
4. Stage 2 hypertension
1. <120/80
2. 120-139/80-89
3. 140-159/90-99
4. >160/>100
name two renal associated causes of hypertension
1. chronic renal disease
2. renovascular disease
name two aortic problems known to cause hypertension
1. coarctation of the aorta
2. rigidity of the aorta
name a vessel change often caused by benign (chronic) hypertension
hyaline arteriosclerosis
(basement membrane thickening due to hyaline material in vessel walls)
what are the renal complications of hyaline arteriosclerosis?
may cause chronic renal insufficiency via arteriolar nephrosclerosis (aka. global glomerular sclerosis)
name a vessel change often seen in malignant (accelerated) hypertension
hyperplastic arteriolosclerosis
what does hyperplastic arteriosclerosis look like and what are the presenting symptoms?
it is a fibrinous necrosis where the arterioles look like onion skin. (this is a reaction to the high pressures)
patient would present with headache, blurred vision, malaise
what is Monckeberg's medial calcific sclerosis?
a degenerative calcification of the MEDIA of the artery. (intima not effected)
seen in elderly
what is fibromuscular dysplasia?
- irregular wavy thickening of medium sized arteries.
- renal and carotids most often affected
- women of reproductive age most often affected
- may also see alpha-1-antitrypsin deficiency
complications of fibromuscular dysplasia? (2)
1. renovascular HTN
2. arterial dissection
Fibromuscular dysplasia
What is this disorder?
hyperplastic arteriolosclerosis
what is this?
hyaline arteriolosclerosis
what is this?
name the four most common sites where atherosclerosis is found IN ORDER OF OCCURANCE
1. abdominal aorta
2. coronary artery
3. popliteal artery
4. carotid artery
name 6 possible complications of HTN
1. CHD
2. CHF
3. LVH
4. nephropathy
5. retinopathy
6. CVA
which portion of the blood pressure is responsible for most of the complications seen in HTN?
SYSTOLIC blood pressure
(pulse pressure is also partially responsible for CV events)
what is:
1. normal BP
2. Prehypertension
3. Stage 1 HTN
4. Stage 2 HTN
1. <120/<80
2. 120-139 / 80-89
3. 140-159 / 90-99
4. >160 / >100
the risk of what three events goes down when blood pressure is lowered?
1. Stroke (40%)
2. MI (25%)
3. Heart Failure (50%)
in which two conditions should we change our target (goal) BP from <140/90 to <130/90?
1. Diabetes Mellitus
2. Renal Impairment
describe short term control of BP when the BP is low
low BP = decreased stretch of vessel wall
decreased baroreceptor activity leads to decreased inhibition of vasomotor center
increased SNS discharge = vasoconstriction, increased CO
describe short term control of BP when the BP is high
high BP = increased stretch of vessel wall
baroreceptor stimulation inhibits SNS output
less SNS - vasodilation, decreased CO
what is most responsible for long term control of BP?
the kidney
(RAAS)
when RAAS is activated, what is the result?
Na+ and volume retention
increase in SNS activity
function of renin?
converts Angiotensinogen to AT1
function of ACE?
converts AT1 to AT2
(also breaks down bradykinin)
result when AT1 receptors are stimulated? (6)
1. vasoconstriction (coronary, renal, cerebral)
2. aldosterone release
3. direct Na+ retention
4. water retention (vasopressin release)
5. renin supression (negative feedback)
6. SNS activation
result when AT2 receptors are stimulated? (5)
1. CV protection
2. release of NO (vasodilation)
3. antidiuresis
4. antiproliferative
5. apoptosis
where are the four major mechanisms of action for antihypertensive drugs?
1. Volume depleters (diuretics)
2. Vasodilators
- direct and CCBs
3. Adrinergic inhibitors
4. RAAS inhibitors
three classes of diuretics used in treatment of HTN?
1. Thiazides
2. Loop
3. K+ sparing
what is the diuretic of choice in uncomplicated HTN?
HCTZ
which diuretic is used when more diuresis is required than can be obtained with HCTZ?
Loop (most often Furosemide)
when would K+ sparing diuretics be used?
Name three.
they would be prescribed along with other diuretics to conserve K+
1. Amiloride
2. Spironolactone
3. Triamterene
MOA of thiazides?
block Na+ and Cl- reabsorption in distal convoluted tubule
(elimate 5-10% of filtered Na+, relatively weak)
Describe the actions of thiazides on the following ions:
1. K+
2. Ca++
3. Mg+
4. uric acid
1. K+ wasting
2. decreased excretion of Ca++
3. increased excretion of Mg+
4. decreased excretion of uric acid
MOA of loop diuretics?
reduce Na+ resorption from the ascending limb of the loop of Henle
(eliminates 20-25% of filtered Na+ -> more potent diuresis than HCTZ, but not as good as lowering BP)
compare the onset and duration of action of Loop vs Thiazide diuretics
onset - Loop diuretics fastest
duration of action - Thiazides longest
adverse effects of diuretics?
1. decreased serum ion concentrations of K+, Mg+, Na+
2. Hypovolemia
3. Hyperuricemia (watch in gout)
4. Hyperlipidemia
5. mild hyperglycemia (watch in DM)
6. hypercalcemia (thiazides)
MOA of K+ sparing diuretics?
inhibit reabsorption of Na+ is distal convoluted tubule and collecting duct. (Weak - <5% of filtered Na+)
**inhibit exchange of Na+ for K+ or H+; therefore reduce K excretion
differences in MOA between
1. spironolactone
2. triamterene, amiloride
1. competitive antagonist of aldosterone
2. block Na+ channel
what do alpha-1 receptors do?
mediate vasoconstriction
(Beta-2 mediate vasodilation)
effect of beta blockers on CV system?
1. HR
2. contractility
3. renin release
4. BP
5. AV conduction
1. decreased HR
2. decreased contractility
3. reduced renin release
4. reduced BP
5. reduced AV conduction
one adverse effect of beta blockers is unopposed a-adrinergic stimulation. what is the consequence of this?
vasoconstriction and ischemia
other adverse effects of beta blockers? (5)
1. bronchospasm
2. can mask hypoglycemia s/s
3. decrease in peripheral circulation
4. decrease in exercise tolerance
5. decrease in HDL
contraindications of beta blockers? (5)
1. asthma
2. cardiogenic shock
3. AV block
4. acute CHF
5. decreased HR
why must the abrupt withdrawal of beta blockers be avoided?
abrupt withdrawal causes a rebound increase in HR and contractility (could be disastrous)
therefore we must taper over 1-2 wks. whenever possible
name 3 alpha-1 blockers used in the treatment of HTN
1. doxazosin
2. prazosin
3. terazosin
blocking the alpha-1 receptors results in? (2)
1. reduction of arteriolar resistance
2. increase in venous capacitance
what is the "first dose phenomenon" in relation to a-1 blockers?
initial dose causes:
orthostatic hypotension
sudden syncope
two other adverse effects of a-1 blockers?
1. fluid retention
2. vertigo
besides lowering BP: 3 other benefits of a-1 blockers?
1. lower LDLs and TGs, raise HDL
2. may help Reynaud's (although CCBs preferred Tx)
3. reduction of urinary retention symptoms in BPH
name the 2 most commonly used centrally acting a-2 agonists in tx of HTN?
Clonidine
methyldopa
effect of centrally acting a-2 agonists on CO?
unchanged or mildly decreased
MOA of centrally acting a-2 agonists?
cross BBB

decrease SNS outflow

reduce catecholamine release

results in decrease of PVR and HR
methyldopa is a prodrug -what is it metabolized into?
MOA?
alpha-methylnorepinephrine

potent peripheral vasoconstrictor, but main action is in CNS: reduces CNS sympathetic output to periphery
MOA of reserpine?
inhibits peripheral NE, dopamine and serotonin uptake - results in vasodilation, decreased HR and contractility
adverse effects of reserpine?
bradycardia
possible CHF
increased gastric acid
two classes of CCBs?
non-dihydropyridines
dihydropyridines
name the two non-dihydropyridines
1. dilitazem
2. verapamil
name the two most commonly used dihydropyridines
1. amlodipine
2. nifedipine
describe the CCBs MOA as it relates to Ca++
CCBs block L type Ca++ channels
-this decreases entry of Ca++ into the cell (also decreases intracellular[Ca++] concentration)
on which type of muscle does Ca++ have the most effect on?
smooth muscle
effect of CCBs on arteries?
vasodilation
(decrease afterload on heart)
do CCBs decrease preload?
NO - CCBs don't really venodilate
which type of CCBs have greater coronary and peripheral vasodilation properties?
dihydropyridines
nifedipine
amlodipine
where do verapamil and diltiazem have their greatest effect?
on the heart
negative inotropes
decrease AV conduction
decrease HR
why is reflex tachycardia observed when dihydropyridines are used?
dihydropyridines vasodilate:
this reflexively activates the SNS, resulting in tachycardia
adverse effects of DHP CCBs?
1. flushing, diziness, headaches (due to vasodilation)
2. hypotension
3. pedal edema
adverse effects of non-DHP CCBs?
1. cardiotoxic effects (too low of HR, neg. inotropy; too much AV blockade)
2. constipation (verapamil)
besides HTN, what else can CCBs be prescribed for?
angina
Reynauds syndrome
African Americans
relation between mortality and CCBs?
increased mortality seen with short acting CCBs
MOA of ACEIs?
inhibit ACE
- reduces levels of AT2
- prevents inactivation of bradykinin (potent vasodilator)
- renin release is increased b/c of loss of feedback inhibition
why do ACEIs not completely block the effects of AT2?
peripheral enzymes are still converting AT1 to AT2
two ACEI side effects that bradykinin is responsible for?
1. cough
2. angioedema
three MAJOR indications for ACEI use?
1. HTN
2. CHF
3. diabetic renal disease
effect of ACEIs on serum [K+]?
increase serum [K+]
cautions/contraindications of ACEIs?
pregnancy (2nd/3rd trimester)
renal disease or failure
benefits of ARBs over ACEIs? (2)
1. ARBs inhibit RAAS more completely than ACEIs
2. ARBs don't increase bradykinin levels
MOA of ARBs?
block AT1 receptors leading to decreased BP.
No ACE activity
Both ACEIs and ARBs can be combined with what HTN therapy to have an additive effect?
HCTZ
Adverse reactions of ARBs? (4)
1. hyperkalemia
2. fetal renal toxicity
3. reduced renal function
4. rare angioedema (less than ACEIs)
K+ and Mg++ excretion is an effect of aldosterone that can cause?
arrythmias
effects of aldosterone? (6)
1. edema (due to Na+ and H2O retention)
2. endothelial fibrosis
3. increased blood clotting and platelet activation
4. cytokine activation resulting in vascular inflammation
5. LV dysfunction/hypertrophy/fibrosis
6. arrythmias
name of aldosterone receptor antagonist used to treat HTN?
spironolactone
MOA of spironolactone?
aldosterone receptor antagonist
- binds at aldosterone dependant Na+/K+ exchange site in distal convoluted tubule
- increases Na+ and H20 excretion, increases K+ reabsorption
WEAK DIURETIC
side effects of spironolactone? (4)
progestational and antiandrogenic side effects
1. gynecomastia
2. sexual dysfunction
3. irregular menses or amenorrhea
4. postmenopausal bleeding
name of drug that is a selective aldosterone blocker (SAB) that is better tolerated compared to spironolactone?
eplernone (INSPRA)
used for HTN, post MI heart failure
why is SAB better tolerated than spironolactone?
SAB has less affinity for androgen/progesterone receptors
which HTN drug is not a first line agent but may be used in resistant HTN?
Hydralazine
MOA of hydralazine?
direct acting arterioloar vasodilator, decreases PVR
(acetylated by liver)
adverse effects of hydralazine?
1. reflex sympathetic activity
2. Na+ retention (need for a diuretic)
3. DRUG INDUCED LUPUS (dose related)
4. peripheral neuritis (interferes with B6 metabolism)
Why is Monoxidil, a potent direct acting vasodilator useful in resistant HTN, seldom used?
many adverse effects
- hirsutism
- pulmonary fibrosis
- some cardiac myocyte damage
- marked Na+ and H20 retention
In multiple agent therapy of HTN: what drug is almost always one of the drugs used?
HCTZ
a localized dilation of an artery is known as?
an aneurysm
where exactly in the blood vessel is the weakness that is seen in aneurysms?
in the media

can be a genetic or acquired weakness
name 5 etiologies of aneurysms
1. atherosclerosis
2. syphilis
3.mediastinal/retroperitoneal fibrosis
4. berry
5. mycotic
two shape types of aneurysms
1. fusiform
2. saccular
syphilitic aneurysms are most commonly seen in which population?
males 40-55 yrs
where are syphilitic aneurysms most commonly observed?
ascending aorta
(occasionally descending and abdominal)
describe the pathogenesis of a syphilitic aneurysm
1. T. pallidum casues obliterative endarteritis of the vasa vasorum
2. this leads to ischemia of media and adventitia
3. weakens aortic wall, get aneurysm
possible complications of syphilitic aneurysm?
aortic root dilation -> causes aortic regurgitation -> possible death from heart failure or rupture
- also: coronary ostial stenosis, severe aortic atherosclerosis and fibrosis ("tree bark")
5 risk factors for an atherosclerotic aneurysm?
1. hypertension
2. smoking
3. genetic factors (20% w/ first degree relative)
4. age (MC 6-9th decade)
5. sex (M>>F)
why is the abdominal aorta the most common location of atherosclerotic aneurysms?
no vasa vasorum below orfices of renal arteries
pathogenesis of an atherosclerotic aneurysm?
destruction and weakening of media by severe atherosclerosis. Increased collagenase, elastase activity in aneurysm
clinical manifestations of atherosclerotic abdominal aortic aneurysms?
**75% are asymptomatic**
- pulsatile mass w/ pain
- bruit
- rupture: severe pain (most often L flank), hypotension
in the case of an AAA - why is the lumen size of the aorta often not enlarged?
most of the dilation is due to a thrombus that has formed
mortality rate of a ruptured AAA?
90%
5 possible complications of atherosclerotic aneurysm?
1. rupture
2. aorto-enteric fistula
3. aorto-caval fistula
4. infection
5. embolization
where are Berry aneurysms most commonly found?
in the Circle of Willis
- most often in the bifurcations (Anterior commucnicating a. with anterior cerebral a.)
pathophysiology of Berry aneurysms?
**most are congenital**
high BP contributes
pathophysiology of mycotic aneurysm?
weakening of arterial wall secondary to an infection (usually occurs in patients with known sepsis)
is a dissecting aortic aneurysm a true or false aneurysm?
false aneurysm (just involves a tear in the intima)
risk factors for an aortic dissection?
1. hypertension (70%)
2. Marfans (defect in fibrillin)
3. Ehlers-Danlos (defect in collagen)
4. Pregnancy (increased plasma volume)
5. coarctation of aorta
6. aortic valve malformation
7. trauma
8. copper deficiency (causes defect in lysyl oxidase)
9. cystic medial degeneration
where is the most common location of an aortic dissection (within the blood vessel layers)
between outer 1/2 and inner 2/3 of aortic wall
presenting symptoms of aortic dissection:
1. severe, tearing chest pain radiating to back
2. +/- loss of pulses (due to pinched branch vessels)
3. +/- aortic insufficiency
fatality rate of aortic dissections if untreated?
90%
possible complications of a ruptured aortic dissection? (3)
1. cardiac tamponade
2. bleeding into pleural cavity, peritoneal cavity, mediastinum, retroperitoneum
3. double-barreled aorta:(bleeding back into true lumen)
list some situations that can lead to infective arteritis (5)
1. bacterial pneumonia
2. TB
3. intracardiac infection
4. septic microemboli
5. arterial trauma
possible complication of infective arteritis?
mycotic aneurysm
eitologic agents, diagnosis, management of infective arteritis?
same as IE
MC etiologic agents = staph, strep
MC cause of infective phlebitis?
IV catheters (nosocomial)
1. MC etiologic agents in superficial veins? (2)
2. MC etiologic agents in pelvic and portal veins? (3)
3. MC etiologic agents in intracranial venous sinuses? (3)
1. S. aureus, Gram negative aerobic bacilli
2. Bacteroides, Streptococci, E. coli
3. H. influenzae, S. pneumoniae, S. aureus
Symptoms of infective phlebitis?
(pelvic, portal, intracranial)
pelvic - nausea, vomiting
portal - jaundice
intracranial - headache
What is the most common cause of myocarditis in the US?
infections, mainly viruses
name 5 bacteria known to cause myocarditis
1. Clamydiae
2. Rickettsiae
3. Corynebacterium diptheria
4. Neisseria meningitidis
5. Borrelia burgdorferi (Lyme)
what is a characteristic finding in lyme disease carditis?
bandlike collection of lymphoid cells in endocardium

(also see lymphocytes, plasma cells, macrophages in myocardium)
pericarditis is usually secondary - when it is primary what is the most common etiology?
viral
(also occasionally from TB)
MC bacterial cause of infective endocarditis?
Streptococcus viridans
(followed by Staph aureus)
most common bacteral cause of IE in IVDUs?
Staph aureus
bacteria seen causing IE in the presence of colon cancer?
Streptococcus bovis
differentiate between the symptoms seen in acute vs. subacute IE
acute - high fever, toxicity, death in a few days or weeks
subacute - low grade fever, night sweats, weight loss, weeks to months
1. acute IE most often caused by?
2. subacute IE?
1. S. aureus (MORE VIRULENT ORGANISM)
2. Streptococcus (LESS VIRULENT)
risk factors for native valve IE (3)
1. congenital heart disease
2. acquired abnormalities (RF, mitral valve prolapse, degenerative valve lesions)
3. idiopathic
most common colonizing bacteria in native valve IE?
S. viridans
(alpha hemolytic)
differentiate between the types of bacterial infection seen in early vs. late prosthetic valve IE
early (<60 days) - most often nosocomial
late (> 60 days) - most often community aquired
bacteria types in an early prosthetic valve IE? (2)
S. epidermidis
S. aureus
bacteria types in a late prosthetic valve IE?
Streptococcus, HACEK group
(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
most common valve infected in general IE?
mitral
followed by aortic
most common valve infected in IVDU IE?
tricuspid
followed by aortic
side of heart infected in IVDU IE?
right
MC infective organism in IVDU IE?
S. aureus (often MRSA)
two most common bacteria in nosocomial IE?
S. aureus
Enterococcus
four things always observed in the pathogenesis of IE?
1. altered endothelium OR valvular abnormalities (facilitates colonization)
2. Transient bacteremia
3. Bacterial adherence (formation of vegetation)
4. Host defenses (immune complexes and compliment cause peripheral effects
components of sterile vegitations? (2)
1. platelets
2. fibrin
three clinically important pathogens belonging to the Staph family?
1. S. aureus (very destructive)
2. S. epidermidis
3. S. saprophyticus (seen in UTIs)
**2 and 3 are coagulase negative: 1 is coag. (+)
8 virulence factors seen in Staph?
1. adherence
2. resistance to host defenses
3. toxins (alpha, beta, gamma)
4. Coagulase
5. Leukocidin
6. Staphylokinase
7. Proteases
8. Superantigens
regarding virulence factors of Staph:
1. mechamism of resistance to host defenses
2. function of beta toxin?
3. function of coagulase?
4. function of leukocidin
5. function of staphylokinase?
6. 2 examples of superantigens released by Staph
1. capsule, peptidoglycan
2. degrades sphingomyelin
3. converts fibrinogen to fibrin
4. damages host cell membrane
5. plasminogen activator
6. enterotoxin, TSST
are strep catalase + or -?
catalase negative
three ways to classify strep via hemolysis?
1. alpha hemolytic (green)
2. beta hemolytic (clear)
3. gamma hemolytic (none)
give the species name(s) of:
1. group A strep
2. Group B strep
3. Group C strep
4. Group D strep
1. S. pyogenes
2. S. agalactiae
3. S. equi
4. Enterococcus (E. faecalis, E. faecium) AND Non-enterococcus (S. bovis)
two types of strains that are not Lancefield classified?
WHY are they not classified?
S. viridans
S. pneumoniae
both have no capsule
7 virulence factors seen in all Strep?
1. extracellular dextran
2. adhesin
3. liptechoic acids
4. M protein
5. compliment C5a peptidase
6. Capsule
7. toxins
regarding Strep virulence factors:
1. function of extracellular dextran?
2. function of lipotechoic acid?
3. function of M protein?
4. composition of capsule?
1. adherence
2. bind laminin
3. prevents phagocytosis
4. hyaluronic acid
6 toxins released by streptococci
1. streptolysin S (leukocidin)
2. streptolysin O (leukocidin)
3. Hyaluronidase (spreading factor, destroys CT)
4. streptokinases
5. proteases
6. pyrogenic exotixins (SPEs)
possible damage/complications from IE? (7)
1. vegetations can embolize
2. persistent bacteremia
3. circulating immune complexes
4. cytokine release
5. new or changing heart murmur
6. splenomegaly
7. fever
describe the circulating immune complexes (seen in infective endocarditis) that are deposited
1. Roth spots in retina
2. splinter hemorrhages
3. Osler's nodes (painful) on hands and feet
4. Janeway lesions (painless) on hands and feet
5. glomerulonephritis (with hematuria and RBC casts)
6. arthritis
7. petechiae
two major Duke's criteria for diagnosis of IE?
1. 2 positive blood cultures
2. endocardial involvement
minor Duke's criteria for diagnosis of IE? (6)
1. predisposing condition of IVDU
2. Fever >100.4
3. vascular phenomena
4. immunologic phenomena
5. echocardiogram
6. + blood culture
regarding Duke's criteria in diagnosis of IE: what would constitute a definite diagnosis?
1. pathology of vegetations
2. 2 major
3. 1 major, 3 minor
4. 5 minor
which abx. would be used in the treatment of staph induced IE?
beta lactam + gentamycin
which abx. would be used in the treatment of strep induced IE?
penicillin + aminoglycoside
which heart valve looks like a mercedes-benz sign?
Aortic valve
LAD - see hypertrophy and dilation as a result
Which coronary is occluded?
describe forward left sided heart failure
decreased contractility = decreased CO -> reduction in renal perfusion, systemic perfusion
describe backwards left sided heart failure
decreased compliance of LV places increased load on LA - LA dilates, pulmonary edema and pulmonary venous HTN common
MCC of R sided heart failure?
L sided heart failure
describe backwards R sided heart failure
decreased CO -> increased systemic venous pressures -> congestive hepatomegaly, splenomegaly,
peripheral edema,
fluid accumulation in pericardial, pleural and peritoneal spaces
myocardial adaptations to CHF? (6)
1. beta adrinergic stimulation
2. increased cytosolic [Ca++]
3. increased protein synthesis
4. cellular hypertrophy
5. change in protein isoforms (myosin) and oncogene expression
6. increased interstitial collagen formation
changes in blood volume in response to CHF? mechanism?
- increase in volume
- increase preload
- renal conservation of sodium and water
negative aspects of increasing peripheral vascular tone in response to CHF?
- increase afterload and decrease perfusion
4 common causes of heart failure?
1. ischemic heart disease (>80%)
2. hypertensive heart disease
3. valvular heart disease
4. primary myocardial diseases (cardiomyopathies, myocarditis)
in cor pulmonale:
1. look of R ventricle?
1. dilated R ventricle with hypertrophy
causes of cor pulmonale?
1. pulmonary embolus
2. emphysema
3. pulmonary HTN
4. chronic bronchitis
5. some congenital heart disease (L->R shunts)
major risk factors for IHD? (4)
smoking
DM
HTN
hypercholesterolemia
minor risk factors for IHD? (7)
obesity
age
male gender
family history
OCPs
sedentary lifestyle
personality
regarding critical stenosis:
___ reduction in blood flow?
___ reduction in area
___ reduction in diameter
90% reduction in blood flow
75% reduction in area
70% reduction in diameter
which type of plaques are at a higher risk of rupture?
lipid rich (soft) plaques
in an MI: the window period is?
reversible time (first 30 min)
- 1-2 min: loss of contractility
- 10 min: 50% depletion of ATP
- sarcoplasmic and mitochondrial swelling by EM
in an AMI: how long until irreversible myocardial damage occurs?
- mechanisms of irreversible damage?
20-40 minutes
- loss of membrane integrity (leakage on myoglobin, LDH, creatine kinase, potassium)
- chromatin clumping and disrupted sarcolemma
gross and microscopic pathology after an AMI?
1. 24h
2. 2-3d
3. 4-9d
4. 10-14d
5. 2-4 wk
6. >4 wk
1. G-> pale / M-> myocyte eosinophilia, contraction bands
2. G-> soft yellow tan / M-> neutrophils, nuclear diseintegration
3. G-> soft yellow tan / M-> inflammatory debris, macrophages
4. G-> yellow grey / granulation tissue, early collagen
5. firm, red-grey / scar formation
6. G-> firm, grey / mature scar
what is Dressler's syndrome?
autoimmune rxn. to pericardium 6-8 weeks after an MI
see - pericarditis, fever, joint pain, friction rub
some complications of AMI? (7)
1. cardiogenic shock
2. arrythmias
3. rupture
4. pericarditis
5. sudden death
6. ventricular aneurysm
7. mural thrombus and embolization
complication that is most common cause of death after an AMI?
arrythmias
when would rupture happen as a result of an AMI?
3 MC places of rupture?
most common 3rd-7th day
- free wall, septum, papillary muscle
coronary arterial dissection
what is this?
18-24 hrs
no nuclei, see beginnings of coagulative necrosis
How long after an AMI?
when would rupture happen as a result of an AMI?
3 MC places of rupture?
most common 3rd-7th day
- free wall, septum, papillary muscle
know
know
know
know
circumferential subendocardial MI
type of MI?
Left main coronary occlusion
HUGE MI!
occluded vessel?
Right main coronary artery
-posterior 1/2 of septum occluded
occluded vessel?
Right main coronary artery
-posterior 1/2 of septum occluded
occluded vessel?
Four common causes of Left Sided Heart Failure?
1. Ischemia (>80%)
2. Aortic or Mitral Valve disease
3. Systemic HTN
4. Myocardial disease
Five common effects of Left sided heart failure?
1. Dyspnea
2. Cough
3. Prerenal azotemia
4. Hypoxic encephalopathy
5. sodium overload and systemic dependent edema (hypoperfused kidneys)
Explain the mechanism behind Paroxysmal Nocturnal Dyspnea
patient lies down and fluid redistributes in the body, result is pulmonary edema
(total body hypoxia also contributor)
what causes the cough seen in left sided heart failure and what HF cause is it most commonly seen in?
cough results from left atrium pushing on bronchus
- most commonly seen in mitral valve disease
Two major common causes of Right sided heart failure?
1. Any disease interfering with lung ventilation (Emphysema, CF, etc.)
2. Left sided heart failure
what is the mechanism behind R sided HF due to pulmonary disease?
increased pulmonary vascular resistance due to fibrosis and/or the hypoxic vascular response
effects of R sided HF? (4)
1. Splanchnic congestion (hepatosplenomegaly, (+) hepatojugular reflex)
2. JVD
3. edema (from incr. venous hydrostatic pressure)
4. effusion (pleural)
which area of the left ventricle does the Left circumflex coronary artery supply?
lateral wall
which area of the left ventricle does the LAD supply?
anterior wall and apex
which area of the left ventricle does the R coronary artery supply?
posterior wall
in hypertensive heart disease most of the cardiac changes are due to increased cardiac work. Name three changes and the general result of these changes.
1. cardiomegaly
2. LV hypertrophy
3. cardiac myocyte hypertrophy
**leads to increased myocardial oxygen demand**