Glossary of BVI, WI
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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
- what is the most common cause of ateriosclerosis?
- 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?
- 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
- immune mechanisms
- name the growth factors released by macrophages in the atherosclerotic process
- 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)
- what are the 4 most important risk factors in the development of atherosclerosis?
- 1. hyperlipidemia
3. cigarette smoking
4. diabetes mellitus
- what are the other 5 risk factors in the development of atherosclerosis?
- 1. age
2. sex (M>F)
5. lifestyle (personality type, exercise habits)
- name the 5 lipid types in order of size (large to small)
- 1. chylomicron
- 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
obstructive liver disease
glycogen storage disease
- name 6 possible associations/complications of hypertension
sudden cardiac death
- 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 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?
3. Stage 1 hypertension
4. Stage 2 hypertension
- 1. <120/80
- 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
What is this disorder?
- Fibromuscular dysplasia
what is this?
- hyperplastic arteriolosclerosis
what is this?
- hyaline arteriolosclerosis
- 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
- 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
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
- 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)
- where are the four major mechanisms of action for antihypertensive drugs?
- 1. Volume depleters (diuretics)
- direct and CCBs
3. Adrinergic inhibitors
4. RAAS inhibitors
- three classes of diuretics used in treatment of HTN?
- 1. Thiazides
3. K+ sparing
- what is the diuretic of choice in uncomplicated HTN?
- 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?
- they would be prescribed along with other diuretics to conserve K+
- 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:
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+
3. Hyperuricemia (watch in gout)
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
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?
3. renin release
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
- 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:
- two other adverse effects of a-1 blockers?
- 1. fluid retention
- 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?
- 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?
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?
increased gastric acid
- two classes of CCBs?
- name the two non-dihydropyridines
- 1. dilitazem
- name the two most commonly used dihydropyridines
- 1. amlodipine
- 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?
(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?
- where do verapamil and diltiazem have their greatest effect?
- on the heart
decrease AV conduction
- 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)
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?
- 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
- three MAJOR indications for ACEI use?
- 1. HTN
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?
- 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?
- 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
- name of aldosterone receptor antagonist used to treat HTN?
- 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
- side effects of spironolactone? (4)
- progestational and antiandrogenic side effects
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?
- 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
- 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?
- 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
- two shape types of aneurysms
- 1. fusiform
- 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
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
- 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?
- 5 possible complications of atherosclerotic aneurysm?
- 1. rupture
2. aorto-enteric fistula
3. aorto-caval fistula
- 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
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?
- 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
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
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?
(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)
- most common colonizing bacteria in native valve IE?
- S. viridans
- 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
- bacteria types in a late prosthetic valve IE?
- Streptococcus, HACEK group
(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
- most common valve infected in general IE?
followed by aortic
- most common valve infected in IVDU IE?
followed by aortic
- side of heart infected in IVDU IE?
- MC infective organism in IVDU IE?
- S. aureus (often MRSA)
- two most common bacteria in nosocomial IE?
- S. aureus
- 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
- 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)
- 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 r
- 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
both have no capsule
- 7 virulence factors seen in all Strep?
- 1. extracellular dextran
3. liptechoic acids
4. M protein
5. compliment C5a peptidase
- 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)
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
- 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)
- 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
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
Which coronary is occluded?
- LAD - see hypertrophy and dilation as a result
- 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,
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
3. pulmonary HTN
4. chronic bronchitis
5. some congenital heart disease (L->R shunts)
- major risk factors for IHD? (4)
- minor risk factors for IHD? (7)
- 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?
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
5. sudden death
6. ventricular aneurysm
7. mural thrombus and embolization
- complication that is most common cause of death 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
what is this?
- coronary arterial dissection
How long after an AMI?
- 18-24 hrs
no nuclei, see beginnings of coagulative necrosis
type of MI?
- circumferential subendocardial MI
- Left main coronary occlusion
- Right main coronary artery
-posterior 1/2 of septum occluded
- Right main coronary artery
-posterior 1/2 of septum occluded
- 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
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)
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**
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