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622 Cards in this Set
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- 3rd side (hint)
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what type of cardiac condition are heart transplants for
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for ischemic heart disease and dilated cardiomyopathy
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how is success of cardiac transplant monitored
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Early diagnosis of graft rejection via endomyocardial biopsy
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cardiac transplants can be acutely or chronically graph rejected. which is described in the following
Interstitial lymphocytes Myocyte damage Treat with increased immunosuppression |
acute graph rejection
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cardiac transplants can be acutely or chronically graph rejected. which is described in the following
Diffuse coronary arterial intimal stenosis Caused by chronic low-level inflammation Causes silent infarction in denervated heart Causes CHF or sudden death |
chronic graph rejection
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cardiac transplants can be acutely or chronically graph rejected. which is described in the following
Interstitial lymphocytes and myocyte damage |
acute cardiac rejection
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cardiac transplants can be acutely or chronically graph rejected. which is described in the following
Interstitial lymphocytes and myocyte damage |
acute cardiac rejection
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cardiac transplants can be acutely or chronically graph rejected. which is described in the following
Marked arterial intimal stenosis |
chronic cardiac graph rejection
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Common Heart tumors are classified as either
a. Myxoma b. Lipoma c. Papillary fibroelastoma d. Rhabdomyoma which one is the following Most common primary heart tumor in adults 10% are associated with Carney complex Usually left atrium near foramen ovale |
a. Myxoma
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a. Myxoma
b. Lipoma c. Papillary fibroelastoma d. Rhabdomyoma Incidental valvular neoplasm Possibly just an organized thrombus Hair-like projections on valve surface Can embolize |
papillary fibroelastoma
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a. Myxoma
b. Lipoma c. Papillary fibroelastoma d. Rhabdomyoma Incidental valvular neoplasm Possibly just an organized thrombus Hair-like projections on valve surface Can embolize |
papillary fibroelastoma
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a. myxoma
b. lipoma c. papillary fibroelastoma d. rhabdomyoma Most common primary heart tumor in infants and children Gray myocardial mass protruding into ventricle Can obstruct valves or chamber “Spider cells” on microscopy |
rhabdomyoma
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“Spider cells” on microscopy, associated with most common primary heart tumor in infants and children. with which genetic disease is this associated
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tuberous sclerosis in Rhabdomyoma
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most common primary cardiac malignant tumor
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angiosarcoma
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Name the condition
Firm myocardium “Wax drip” atrial endocardial nodules deposits can be anywhere in heart |
Cardiac Amyloidosis
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A little FYI for you
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You like
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Most common lesion seen in atherosclerosis
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Hyaline arterolosclerosis
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AIDS pt, almost thought it was bacillary angioma so we could treat it, but its not... what is it and what is it caused by
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Kaposi's sarcoma
HHV8 |
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how much does this woman's heart weigh if it is normal
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around 300g
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Numerous epicardial granulomas in dilated cardiomyopathy. what 3 secondary causes could this be from
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1, sarcoidosis- this pic
2. anthracycline myocardial toxicity 3. iron overload |
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TL2
Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, or beta 2 or beta 3 or D1 or D2)) most vascular smooth muscle- contraction |
alpha 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, bet 2 or beta 3 or D1 or D2)
postsynaptic CNS adrenoceptors |
alpha 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3)
heart- increases force and rate of contractility |
beta 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, or beta 2 or beta 3, or D1 or D2)
respiratory, uterine and vascular smooth muscles- promotes smooth muscle relaxation |
beta 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3, or D1 or D2)
fat cells-activates lipolysis |
beta 3
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3, or D1 or D2)
smooth muscle- dilation in renal blood vessels |
D 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3 or D1 or D2)
nerve endings- modulates neurotransmitter release |
D2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3 or D1 or D2)
pupillary dilator muscle- contracts to dilate the muscle |
alpha 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3 or D1 or D2)
platelet aggregation |
alpha 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2 or beta 3 or D1 or D2)
skeletal muscle |
beta 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
skeletal muscle to promote potassium uptake |
beta 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
human liver- activate glycogenolysis |
beta 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
pilomotor smooth muscle to erect hair |
alpha 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
adrenergic and cholinergic nerve terminate to inhibit of transmitter release |
alpha 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
prostate contraction |
alpha 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
vascular smooth muscle contraction |
alpha 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
decrease in sympathetic outflow |
alpha 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
decrease in insulin release to inhibit lipolysis |
alpha 2
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
increase heart rate , increase heart contractility |
beta 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
increase renin release, increase lipolysis |
beta 1
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Name the type of autonomic receptor ( alpha 1, alpha 2, beta 1, beta 2, beta 3, D1 or D2)
vasodilator and bronchodilator |
beta 2
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which G-protein linked second messenger receptor decreases heart rate and contractility of atria
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M2- parasympathetic
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what are the sympathetic G-protein linked second messenger receptors
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alpha 1,2
beta 1,2,3 |
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what are the parasympathetic G-protein linked second messenger receptors
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M1,2,3
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Name the 5 classes of drugs used to treat hypertension
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1. diuretics
2. sympahtolplelegics- blockers of alpha/beta, nerve terminals, ganglia, or CNS sympathetic outflow 3. vasodilators- either Ca+2 blockers or others 4. angiotensin antagonists- ACE inhibitors or receptors blockers 5. renin inhibitors |
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80% of HTN is primary causes due to unknown factors. 20% of HTN cases are clearly defined and corrected. Name 4 examples of secondary factors of HTN
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pheochromocytoma
coarctation of aorta renal vascular disease adrenal cortical tumor |
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Definition:
primary autonomic mechanism for blood pressure homeostasis, involves sensory input from carotid sinus and aorta to the vasomotor center and output via the parasympathetic and sympathetic motor nerves |
baroreceptor reflex
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definition
vascular damage in heart, kidney, retina or brain |
end organ damage
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definition:
accelerated HTN causing rapid damage to vessels in end organs causing a medical emergency |
malignant HTN
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definition:
elevated BP (usually above pretreatment levels) resulting from loss of antihypertensive drug effect |
rebound HTN
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Definition:
tachycardia resulting from lowering of BP, mediated by baroreceptor reflex |
reflex tachycardia
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Name the class of antihypertensive drugs
drugs that lower blood pressure by decreasing the blood volume and probably by direct vascular effect |
diuretics
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Name the 2 diuretics most important for treating HTN
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1. thiazides- hydrocholothiazide - used for mild HTN
2. loop diuretics- furosemide- used for moderate to severe HTN |
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which of the diuretics has the following adverse effect:
hypokalemia, slight hyperlipidemia, hyperuricemia, hyperglycemia, lassitude, weakness, impotence |
hydrochlorothiazide
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what are the adverse effects of furosemide
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furosemide- diuretic- hypokalemia, hypovolemia and ototoxicity
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Name the antihypertensive drug and how it works in HTN:
act as an alpha 2 selective agonists a.clonidine b. reserpine c. propanolol d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide |
clonidine and methyldopa- cause a decrease in sympathetic flow by activation of alpha 2 receptor in CNS
both reduce BP by reducing cardiac output, decreasing vascular resistnace |
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Name the antihypertensive drug:
nicotinic blockers that act in the ganglia but has major compresatory response to salt retention and toxicities including blurred vision, constipation, urinary hesitancy, sexual dysfunction a. clonidine b. reserpine c. propanolol d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide |
trimethaphan- block parasympahtetics
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which class of antihypertensive drugs result in reduction of venous tone, heart rate, contractile force of the heart, reduced cardiac output, and decrease total peripheral resistance
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sympathoplegics
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Name the antihypertensive drug and how it works in HTN:
deplete the adrenergic nerve terminal of it NE stores to lower BP, but has toxicity of major depression a.clonidine b. reserpine c. propanolol d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide |
reserpine
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Name the antihypertensive drug and how it works in HTN:
act as an alpha 1 selective antagonists to reduce vascular resistance and venous return a. clonidine b. reserpine c. propanolol d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosin |
prazosin
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Name the antihypertensive drug and how it works in HTN:
act as an beta blocker to reduce cardiac output and decrease vascular resistance and angiotensin level a. clonidine b. reserpine c. propanolol d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapail |
propanolol
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name 2 nonselective alpha blockers and why they are of no use in chronic HTN
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phentolamine and phenoxybenzamine
no use bc excessive compensatory response especially tachycardia |
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Name the antihypertensive drug :
act as an vasodialator by releasing nitric oxide from endothelial cell but toxicites is tachycardia and drug induced lupus a. clonidine b. reserpine c. hydralazine d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapail |
hydralazine
side note: nitroprusside (short acting) but still also acts by releasing nitric oxide from drug or endothelium |
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Name the antihypertensive drug and how it works in HTN:
act as an calcium channel blocker to vasodilate and are suitable for chronic HTN a. clonidine b. reserpine c. captopril d. trimetaphan e. hydralazine f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapamil |
verapamil
side note: also diltiazem and nifedipine also work as calcium channel blockers to reduce influx of Ca+2 |
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Name the antihypertensive drug :
act as an vasodialator by opening potassium channels to hyperpolarize and relax smooth muscle cells. it also reduces insulin release a. clonidine b. reserpine c. hydralazine d. trimetaphan e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapail |
diazoxide
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Name the antihypertensive drug and the adverse events:
act as angiotensin-converting enzyme, kininase II to reduce blood levels of angiotensin II and aldosterone and increase endogenous vasodilator- bradykinin a. clonidine b. reserpine c. hydralazine d. captopril e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapail |
captopril- SAEs are cough and renal damage to the fetus
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Name the antihypertensive drug and the adverse events :
act as an angiotensin antagonists at the receptor to competitively inhibit angiotensin II at it AT1 receptor site a. clonidine b. reserpine c. hydralazine d. captopril e. losartan f. nitroprusside g. hydrochlorothiazide h. prazosine i. diazoxide j. verapail |
losartan- renal damage to fetus but less cough
aka angiotensin II receptor blocker ARBs |
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List the "stepped care" of drugs in a pt with HTN managment
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1. lifestyle changes- salt restriction an weight reduction
2. diuretics- either thiazide or loop 3. sympathoplegics- usually receptor blockers like propranolol or prazosin, clonidine (CNS action), reserpine (postganglionic neuron blocker) or 4. ACE inhibitor- captopril or losartan 5. vasodilator |
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Name the drug:
alpha 1 selective blocker (antagonists) cause less reflex tachycardia when reducing blood pressure a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
prazosin
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Name the drug:
alpha 2 selective blocker (antagonists). associated with cardiac sympathetic nerve endings a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
yohimbine
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Name the drug:
irreversible long acting irreversible alpha selective blocker (antagonists). Cause a reduction in vascular tone with a reduction of both arterial and venous pressures, but do cause barorecptor relex tachycardia due to drop in mean arterial pressure a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
phenoxybenzamine
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Name the drug:
short acting, reversible alpha non selective blocker (antagonists). Cause a reduction in vascular tone with a reduction of both arterial and venous pressures, but do cause barorecptor relex tachycardia due to drop in mean arterial pressure a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
phentolamine
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Name the drug:
best choice for use in pre-surgery of pt with pheochomocytoma due to severe HTN and hypovolemia a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
phenoxybenzamine
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what is the most important toxicites of alpha blockers
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extension of their alpha blocking effects... such as orthostatic hypotension, marked reflex tachycardia
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Name the drug:
have a more Beta 1 receptor antagonist selectivity so it can be advantageous when treating asthma a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
esmolol, metorpolol, acebutolol
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nonselective beta blocker used for HTN, angina pectoris, arrhythmia prophylaxis, hypertrophic cardiomyopathy, migraine prophylaxis, familial tremor
a. Yohimbine b. prazosin c. phenoxybenzamine d. phentolamine e. esmolol f. acebutolol g. propanolol h. timolol |
propranolol
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Name the drug and its mode of administration
beta blocker used to decrease the secretion of aqueous humor from the ciliary epithelium a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
timolol- given as topical drops
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Name the drug and its mode of administration
prostaglandin that increase aqueous flow in pt with glaucoma a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
latanoprost- topical drops
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Name the drug and its mode of administration
cholinomimetics that works by producing ciliary muscle contraction to open trabecular meshwork to increase outflow in pts with glaucoma a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
pilocarpine or physostigmine- topical of gel
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Name the drug and its mode of administration
nonselective alpha agonist, used in pts with glaucoma to increase outflow via uveoscleral veins a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
epinephrine- topical but obsolete also brimonidine
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Name the drug and its mode of administration
selective alpha 2 agonists used to decrease aqueous secretion in glaucoma pt a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
brimonidine also apraclonidine given as topical drops
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Name the drug and its mode of administration
diuretic given to pts with glaucoma to decrease the aqueous secretion due to lack of HCO3- a. acetazolamide b. brimonidine c. epinephrine d. pilocarpine e. latanoprost f. timolol |
acetazolamide given orally
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list the beta antagonist cardiovascular toxicites
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extension of their beta blocking activities which include bradycardia, AV block, and heart failure
pt with asthma have attacks |
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what is the mode of action of sympathomimetics and give examples of each
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1. directly active the adrenoreceptor- alpha agonists or beta agonists and dopamine agonists
2. indirectly act to increase concentration of catecholamines transmitter in the synapse such as amphetamines, cocaine, tricyclics and tyramines, MAOIs |
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what adrenoceptors are stimulated by epinephrine
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alpha 1 and 2 , beta 1 and 2
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Definition:
a dihydroxyphenylethylamine derivative such as norepinephrine or epinephrine |
catecholamine
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a drug that causes the dilation of the pupil,
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mydriatic
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a derivative of phenylisopropylamine- unlike catecholamines, this has oral activity a long have life and some CNS activity and indirected mode of action
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phenylisopropylamine like amphetamines and ephedrine
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name the type of adrenoceptor stimulated
most vascular smooth muscle- contraction to increase vascular resistance |
alpha 1
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name the type of adrenoceptor stimulated
adrenergic and cholinergic nerve terminals- inhibit transmitter release |
alpha 2
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name the type of adrenoceptor stimulated
heart- stimulates rate and force |
beta 1
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name the type of adrenoceptor stimulated
airways,uterine and vascular smooth muscle to relax |
beta 2
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name the type of adrenoceptor stimulated
fat cells stimulated for lipolysis |
beta 3
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name the type of adrenoceptor stimulated
renal and other splanchnic blood vessels to dilate which decrease resistance |
dopamine 1
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name the type of adrenoceptor stimulated
nerve terminals to inhibit adenylyl cyclase |
dopamine 2, alpha 2 and m2
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name the type of adrenoceptor stimulated
pupillary dilator muscle to contract leading to mydriasis |
alpha 1
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name the type of adrenoceptor stimulated
platelets stimulated to aggregate |
alpha 2
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name the type of adrenoceptor stimulated
juxtaglomerular cells stimulate to release renin |
beta 1
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name the type of adrenoceptor stimulated
human liver stimulated for glycogenolysis |
beta 2
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name the type of adrenoceptor stimulated
pilomotor smooth muscle contract to erect hair |
alpha 1
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name the type of adrenoceptor stimulated
fat cells stimulated to inhibit lipolysis |
alpha2
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name the type of adrenoceptor stimulated
pancreatic beta cell stimulated to release insulin |
beta 2
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name the type of adrenoceptor stimulated
pancreatic beta cells stimulated to inhibit insulin release |
alpha 2
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name the type of adrenoceptor stimulated
somatic motor neuron terminals of voluntary muscles cause tremor |
beta 2
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name the type of adrenoceptor stimulated
mediated primarily by trimeric coupling of Gq which when activated in turn activates phosphoinositide cascade to release IP3 and DAG from membrane lipid. Ca+2 is subsequently released from smooth muscle cells and enzymes are activated |
alpha 1
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name the type of adrenoceptor stimulated
receptor activation results in inhibition of adenylyl cyclase via coupling Gi protein |
alpha 2
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name the type of adrenoceptor stimulated
receptors stimulate adenylyl cyclase via the Gs protein which leads to increase in cAMP concentration in cell |
all beta receptors 1,2,3
also D1, H2, V2 |
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name the type of adrenoceptor stimulated
receptors activate adenylyl cyclase via Gs in neurons and vascular smooth muscle and they act via Gi and reduce synthesis of cAMP |
dopamine receptors
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t/f catecholamines enter the CNS effectively which is why are are used widely
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false- DO NOT enter the CNS effectively
there is an active pump that pumps excess catecholamines out of the CSF, bc peripheral catecholamines should stay peripherally and CNS catecholamines should stay centrally |
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what is the effect of phenylephrine on the smooth muscle of the pupillary dilator
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since is alpha agonist- it contracts producing mydriasis
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what is the effect on the smooth muscle of the bronchi in response to a beta 2 agonist
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relaxation- so good for reversing bronchospasm
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what types of adrenorecptors are located in the GI tract. and what will have when these receptors are stimulated
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both alpha and beta- activation of either will lead to relaxation of smooth muscle
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what types of adrenorecptors are located in the GU tract. and what will have when these receptors are stimulated
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alpha receptors in bladder trigone and sphincter area to mediate contaction
men have alpha 1 to mediate prostate smooth muscle contraction |
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name the type of adrenoreceptor and give a drug example
constrict skin and splanchnic blood vessels and increase peripheral vascular resistance and venous pressure. since the increase pressure can invoke a reflex bradycardia |
alpha 1 receptor agonists- phenylephrine
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name the type of adrenoreceptor and give a drug example
cause vasoconstriction when administered IV or topically (nasal spray) but when given orally they accumulate in CNS and reduce sympathetic outflow and blood pressure |
alpha 2 agonists- clonidine
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name the type of adrenoreceptor and give a drug example
cause significant reduction in arteriolar tone in the skeletal muscle vascular bed and can reduce peripheral vascular resistance and arterial blood pressure |
beta 2- albuterol
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t/f beta 1 agonist have little effect on vessels
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true
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what type of receptors are onthe heart
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beta 1 and 2
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what is the drug of choice for immediate treatment of anaphylactic shock
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epinephrine
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which type of drugs ( alpha1, alpha2, beta1, or beta2 agonist) should be used in the following situation:
an increase in blood flow is desired such as in acute cardiac heart failure |
beta 1
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which type of drugs ( alpha1, alpha2, beta1, or beta2 agonist) should be used in the following situation:
decrease in blood flow or increase in blood pressure is desired, such as spinal shock, local hemostatic and decongestant effects |
alpha 1 agonists
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which type of drugs ( alpha1, alpha2, beta1, or beta2 agonist) should be used in the following situation:
suppress premature labor |
beta 2 agonists
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which agonist receptor type has a toxicity that causes hypertension
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alpha 1 agonists
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which agonist receptor type has a toxicity that causes sinus tachycardia
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beta 1 agonists
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which agonist receptor type has a toxicity that causes skeletal muscle tremor
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beta 2 agonists
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Describe the baroreceptor reflex
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1st- carotid sinus and aortic arch sense increase arterial pressure
2nd- the receptors activate affect impulses to the vasomotor center in the medulla 3rd- the vasomotor center sends 2 signals via solitary tract fibers: 1. decreases sympathetic input to the heart and arterioles to vasodilate 2.signal to vagus to increase parasympathetic output to slow heart down so if give drug to produces increase bp then produce reflexive bradycardia and vice versa, if give drug that causes hypotension produce reflexive tachycardia |
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what is the initiating stimulus for the baroreceptor reflex
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change in blood pressure
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where are the receptor located that sense the increase in blood pressure
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carotid sinus at the bifurcation and aortic arch
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what events would occur in an elderly pt who suddenly stood up and experienced orthostatic hypotension
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1st decrease in stretch receptor in the aortic arch and carotid sinus are detected
2nd decrease in afferent impulse to the vasomotor center in the medulla 3rd. the vasomotor center sends out 2 signals 1. increase in sympathetic stimulation to the heart and pump harder and for arterioles to constrict 2. decrease in parasympathetic stimulation 4th increase in heart rate and cardiac output |
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how do we calculate mean blood pressure
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MAP = DP +.33 ( SP-DP)
MAP (mean arterial pressure) SP- systolic pressure DP- diastolic pressure SD-DP= pulse pressure MAP= CO X SVR CO cardiac output SVR systemic vascular resistance |
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An increase in vascular tone is caused by stimulation of which receptors?
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alpha 1
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How does alpha-1 stimulation most directly influence the BP response?
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Causes increase in diastolic BP
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An increase in systolic pressure and pulse pressure is caused by stimulation of which receptors? and results in what effect
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beta 1
1. increase in contractile force 2. increase in stroke volume 3. increase in cardiac output |
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Stimulation of which receptor
causes bradycardia in response to NE ? |
Reflex vagal stimulation of muscarinic (M2) receptors on the SA node causes bradycardia in response to the increase in mean BP caused by NE
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Epinephrine stimulates which receptors? How does stimulation of each receptor influence BP
|
alpha 1- increase diastolic pressure
alpha 2- none beta 1- increases systolic beta 2- vasodilator, increases pulse pressure which will decreases systolic bp |
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Phenylephrine stimulates what type of receptors
|
alpha 1
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How would bradycardia alter diastolic BP?
|
Bradycardia will increase the “runoff” time during diastole. This will allow diastolic BP to drop lower than it would at a higher HR, but will also allow increased ventricular filling time
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How will increased ventricular filling time (during bradycardia) alter systolic BP?
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Increased filling time may increase systolic pressure by stretching the heart muscle and increasing the inotropy (Frank-Starling Mechanism).
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The blood pressure effects of epinephrine are typically dose dependent. what are the effects of small doses vs large doses of epinephrine
|
small doses- exhibit more beta effect (isoproterenol)
large doses- exhibit more alpha effect (norepinephrine-like) |
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t/f a 15 minute infusion of norepinephrine induces a reflex tachycardia
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false- reflex bradycardia
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A 15 minute infusion of norepinephrine would have what immediate effect on the systolic and diastolic pressure
|
increase both pressures systolic and diastolic
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what is the effect of norepinephrine on the peripheral resistance after a 15 minute infusion of norepinephrine
|
NE contricts all blood vessels due to alpha1 ( but since doesn't have beta 2 effect) all blood vessels constricted which causes an increase in peripheral resistance
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what is the effect of low dose epinephrine on the chronotropy and inotropy after a 15 minute infusion
|
at low doses Epi has beta effect
Increase Chronotropy- heart rate increase inotropy- contraction of heart-contractility tachycardia, decreased diastolic BP (bc Beta 2), increased pulse pressure |
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what is the effect of high dose epinephrine on the chronotropy and inotropy after a 15 minute infusion
|
at high doses Epi has alpha effect
increased mean BP causing reflex bradycardia |
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Isoproterenol stimulates which receptors?
So what it the effects on Cardiovascular of i.v. Infusion of Isoproterenol |
beta more than alpha
so will increase contractility and heart rate due to the beta 1 stimulation but will also decrease peripheral resistance due to the beta 2 stimulation |
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what are the immediate effects on systolic and diastolic pressure after i.v. Infusion of Isoproterenol
|
systolic-no change or decrease
diastolic- decrease |
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what is the response of the vascular resistance skeletal muscle from
a. phenylephrine b. epinephrine c. isoproterenol |
since skeletal muscle has alpha and beta 2 receptors
a. phenylephrine (alpha agonist)- will increase skeletal tone b. epinephrine will increase or decrease depending on amount high does has more alpha effect, low does has more beta effect c. isoproterenol (beta agonist)- will decrease skeletal muscle tone |
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what is the response of the total peripheral resitance from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine will significantly increase TPR
b. epinephrine- will increase or decrease depending on amount high does has more alpha effect, low does has more beta effect c. isoproterenol- will decrease TPR |
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what is the response of the heart rate from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- decrease HR since this is an alpha agonist, will cause vasoconstriction which will produce a vagal response
b. epinephrine- will increase or decrease depending on amount high does has more alpha effect, low does has more beta effect c. isoproterenol- since it is a beta agonist will significantly increase the HR |
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what is the response of the heart's contractility from
a. phenylephrine b. epinephrine c. isoproterenol |
Heart rate is a beta 1 action
a. phenylephrine- alpha has no effect or slightly increase due to the vagal response slowing the heart down allowing more time for the ventricles to fill stimulating the stretch reflexes and thereby slightly increasing the contractility b. epinephrine- significantly increase the contractility c. isoproterenol- significantly increase the contractility |
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what is the response of the mean blood pressure from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- alpha so will increase the mean bp
b. epinephrine- slightly increase c. isoproterenol- beta so will decrease |
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what is the response of the diastolic blood pressure from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- increase the diastolic bp
b. epinephrine- either increase or decrease depending on dosing c. isoproterenol- beta 2 so decrease diastolic |
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what is the response of the systolic blood pressure from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- alpha will increase the systolic
b. epinephrine- increase systolic c. isoproterenol- beta has no effects on systolic |
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what is the response of the pulse pressure from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- is alpha agonist so has no effect on contractility or pulse pressure
b. epinephrine- has both beta and alpha effects but beta overtake and increases pulse pressure c. isoproterenol- beta 1 effects contractility to increase pulse pressure which is the difference in range between SP-DP |
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what is the response of the stoke volume and cardiac output from
a. phenylephrine b. epinephrine c. isoproterenol |
a. phenylephrine- alpha agonist which affects diastolic pressure so effects on stroke volume may vary but will decrease cardiac output due to bradycardial reflex
b. epinephrine- increase stoke volume and cardiac output c. isoproterenol- increase stroke volume and cardiac output |
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which of the alpha antagonists is an irreversible antagonist and has more alpha 1 affinity that alpha 2
|
phenoxybenzamine
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which of the alpha antagonists has higher affinity for alpha 1 receptors than alpha 2
|
prazosin
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which of the alpha antagonists has equal affinity for alpha 1 receptors and alpha 2
|
phentolamaine
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which drug for the adrenoreceptors is a mixed antagonists having equal beta 1 and beta 2 but this affintiy being greater than its alpha 1 and alpha 2
|
labetalol
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which of the beta antagonists has much greater affinity for beta 1 receptors than beta 2
|
metoprololol, acebutolol, esmolol, and the list goes on... olol
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which of the beta antagonists has equal affinity for beta 1 receptors and beta 2
|
propanolol, timolol
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which of the beta antagonists has much greater affinity for beta 2 receptors than beta 1
|
butoxamine
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t/f alpha adrenergic blockers have no effect on the action of isoproterenol
|
true- bc isoproterenol is a pure beta agonists
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can alpha adrenergic blockers reverse the vasoconstriction action of epinephrine
|
yes
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if a response to a bolus injection of a drug is rapid but short lived is it more likely and agonist or antagonists
|
agonists
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Propranolol belongs to
which class of drugs? |
non selective beta antagonists
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What causes a decrease in Heart Rate. when propranolol is administered to a pt?
|
This patient must have had some
beta -1 sympathetic stimulation of the SA node that was blocked by propranolol. Normally, however , parasympathetic tone predominates in the heart |
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why would a heart rate reduced when Epi is given in the presence of propranolol
|
increasing blood pressure activates the baroreceptor reflex
Drugs that elevate BP cause reflex bradycardia as long as other drugs are not present to block the reflex arc. Before propranolol is administered, Epi causes a direct stimulation of the beta-1 receptors of the heart that is partially obtunded by the reflex vagal activity. When the beta-1 receptors are blocked by propranolol, the vasoconstrictor alpha action of Epi will produce a marked reflex bradycardia. This had been previously masked by the direct effects of beta-1 stimulation. |
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why is Captopril used to treat hypertension, CHF, and renal
syndromes like diabetic nephropathy and scleroderma |
Captopril is an is an ACE inhibitor it exerts its antihypertensive effects by blocking the formation of
angiotensin II (a potent vasoconstrictor) and is effective in reducing the afterload associated with CHF. It also reduces preload by reducing aldosterone secretion thus reducing salt and water retention. |
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ACE inhibitors also inhibit the degradation of which compound (a potent
vasodilator) The buildup causes which significant side effects that may cause life threatening upper airway obstruction. |
ACE inhibitors also inhibit the degradation of bradykinin (a potent vasodilator) The buildup of bradykinin causes significant side effects (e.g. cough & angioedema) The angioedema may cause life threatening upper airway obstruction. It involves edema of the face, mucous membranes, tongue, pharynx and larynx.
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which is an is an oral hypoglycemic agent used to treat type 2 diabetes
a. hydroclorothiazide b. glyburide c. Nifedipine d. verapamil |
glyburide
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which is a is a diuretic that causes hyperlipidemia, and impaired carbohydrate (glucose) tolerance
a. hydroclorothiazide b. glyburide c. Nifedipine d. verapamil |
hydroclorothiazide
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which drug is now considered the CCB ( calcium channel blocker ) of choice to use in patients with ischemic heart disease and hypertension in the presence of systolic dysfunction
|
Amlodipine
CCB-calcium channel blocker |
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pt brought to the ED is disoriented and complaining of a splitting headache and ringing in the ears. blood pressure is 190/120 mm Hg. Which drug is the best choice for immediate treatment?
labetalol metoprolol nicardipine phentolamine sodium nitroprusside |
sodium nitroprusside
Nitroprusside reduces preload and afterload by directly dilating arterioles and venules has a rapid onset of action and a short duration of action and is used in the ER to treat acute heart failure as well as acute hypertensive emergencies. It is metabolized to cyanide and then to the less toxic metabolite, thiocyanate |
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t/f Labetalol is a competitive agonist at both alpha and beta receptors
|
false- competitive ANTAGONIST at both alpha and beta receptors
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t/f Metoprolol is a competitive oral alpha-1 antagonist. Delayed onset of action.
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false- Metoprolol is a competitive oral BETA-1 antagonist. Delayed onset of action.
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t/f Nicardipine is a competitive oral CCB with a 20 minute onset of action. Delayed onset
|
true
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t/f Phentolamine is a non- competitive alpha-2 antagonist.
|
false- Phentolamine is a competitive alpha-1 antagonist.
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which drug a vasopressor that is administered parenterally for BP support during surgery or to terminate supraventricular tachycardia.
And also increases peripheral resistance by stimulating vascular alpha-1 receptors. |
Methoxamine
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which drug is a moderately selective beta-2 agonist widely used as a bronchodilator in managing exacerbations of asthma or other chronic obstructive airway diseases
|
Albuterol
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which drug is a nonselective alpha antagonist used in the diagnosis of pheochomocytoma, and the prevention of tissue necrosis after NE extravasation
|
Phentolamine
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which drug selectively stimulates beta-2 receptors and is used to treat bronchospasm or to delay premature labor
|
Terbutaline
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which drug can be to administer to prevent vasovagal syncope?
a. atropine b. clonidine c. nicotine c. prazosin d. propranolol |
atropine
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which drug is a selective alpha-2 agonist?
a. atropine b. clonidine c. nicotine c. prazosin d. propranolol |
clonidine
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which drug is a ganglionic stimulant?
a. atropine b. clonidine c. nicotine c. prazosin d. propranolol |
nicotine
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which drug is aan alpha-1 selective antagonist?
a. atropine b. clonidine c. nicotine c. prazosin d. propranolol |
prazosin
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which drug is a nonselective beta antagonist?
a. atropine b. clonidine c. nicotine c. prazosin d. propranolol |
propranolol
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why is Sildenfil is contraindicated in a patient taking nitroglycerin
|
because it potentiates the hypotensive effect of the nitrates which is done by inhibiting the breakdown of cyclic guanosine monophosphate (cGMP) by phosphodiesterase type 5, thereby elevating the level of cGMP
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|
t/f minoxidil is an indirect vasodilator
|
false- minoxidil is a DIRECT vasodilator
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what effects does Direct vasodilators such as hydralizine, minoxidil produce a on HR, stroke volume, and cardiac output.
|
Direct vasodilators produce a reflex sympathetic response leading to an increase in HR, stroke volume, and cardiac output.
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what effect does Minoxidil also causes on renin secretion
|
Minoxidil causes increase in renin secretion
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What are the signs of PCP intoxication? (FA p428)
|
belligerence, vertical and horizontal nystagmus, impulsiveness, psychomotor agitation, tachycardia, homocidality, delirium, fever
side note- withdrawal symptoms: anxiety, irritability, restlessness, anergia, disturbances of thought and sleep |
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What enzyme is deficient in alkaptonuria? What are the manifestations of alkaptonuria?
(FA p109) |
(aka ochronosis) defieciency in homogentisic acid oxidase in the degradative pathway of tyrosine. AR benign
Findings: dark connective tissue, pigmented sclera, urine turns black on standing may have debilitating arthralgias |
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Which type of E. coli causes the very common “Traveler’s diarrhea? (FA p15??)
|
ETEC,
E. coli, enterotoxigenic |
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Which fungal infection fits the following description? ( p155)
- causes diaper rash - opportunistic mold with septate hyphae that branch at a 45 degree angle - opportunistic mold with irregular nonseptate hyphae that branch at wide angles (>90 degrees) - dimorphic fungi common to SW US (San Joaquin Valley fever) - causes thrush in immunocompromised pts and vulvovaginitis in women - dimorphic fungi with broad-based budding yeast - known for causing pneumonia in AIDS pts start Bactrim prophylaxis when CD4 <200 - dimorphic fungi common to Mississippi and Ohio river valleys - causes a skin infection in those pricked by a thorn - yeast known for causing meningitis in AIDS pts |
- causes diaper rash - candida albicans
- opportunistic MOLD with septate hyphae that branch at a 45 degree angle -Aspirgillus fumigatus - opportunistic MOLD with irregular nonseptate hyphae that branch at wide angles (>90) Mucor and Rhizopus - dimorphic fungi common to SW US (San Joaquin Valley fever)- Coccidioidomycosis - causes thrush in immunocompromised pts and vulvovaginitis in women- candida albicans - dimorphic fungi with broad-based budding yeast- Blstomycosis - known for causing pneumonia in AIDS pts start Bactrim prophylaxis when CD4 <200 - Pneumoncystis jiroveci - dimorphic fungi common to Mississippi and Ohio river valleys- Histoplasmosis - causes a skin infection in those pricked by a thorn- Sporothrix chenckii - yeast known for causing meningitis in AIDS pts - Coccidioidomycosis |
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What is the cause of Chronic Granulomatous disease? What are the consequences of Chronic Granulomatous disease? (FA p204)
|
deficient in microbicidal activity of neutrophils owing to lack of NADPHOxidase activity.
Present with increase infections especially with S. aureus, E.Coli, and Aspergillus Confirm with nitroblue tetrrazolium dye |
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What are the two most common complications after an MI? (FA p263)
|
Most common- Cardiac arrthymia (important cause of death before reaching ED)
LV failure and pulmonary edema Cariogenic shock (after large infarcts- will increase mortality) Ventricular free wall rupture leading to cardiac tamponade, also papillary muscle weakness can lead to severe mitral valve regurgitation, also an interventricular septal rupture leading to VSD Aneurysm formation leads to decrease cardiac output so increase risk of arrythmia, embolus from mural thrombus Fibrinous pericarditis producing a friction rub 3-5 days post MI |
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What is Dressler’s syndrome? (FA p263)
|
autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI
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Where can you find nicotinic acetylcholine receptors in the body? (FA p231)
|
Nicotinic receptors are ligand gated Na/K channels
Being ionotropic receptors, nAChRs are directly linked to an ion channel Found on presynaptic channels in parasympathetic, sympathetics, presynaptic to adrenal medulla and directly to skeletal muscles (somatic) |
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What is the most common tumor of the appendix? (FA p291)
|
Carcinoid syndrome tumors (neuroendocrine cells) especially metastatic bowel tumors which secrete high levels of 5HT. Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right sided valvular disease.
Increase of 5HIAA in urine Treat with octreotide |
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Which antibiotic is known for causing the following side effect(s)?
- SE: teeth discoloration (FA p182) - SE: tendonitis (FA p184) - SE: red man syndrome (FA p185) - SE: gray baby syndrome (FA p182) - SE: cartilage damage in children (FA p184) - SE: nephrotoxicity (esp. with cephalosporins), ototoxicity (esp. with loop diuretics) p181) - SE: pseudomembranous colitis (FA p182), |
- SE: teeth discoloration Tetracycline
- SE: tendonitis FluoroquinoBONES - SE: red man syndrome- Rifampin - SE: gray baby syndrome- Chloramphenicol - SE: cartilage damage in children-FluoroquinoBONES - SE: nephrotoxicity (esp. with cephalosporins), ototoxicity (esp. with loop diuretics) - Aminoglycosides - SE: pseudomembranous colitis- clindamycin |
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Describe the steps involved in the pupillary light reflex. (FA p400)
|
light in retina send a signal via CN2 to pretectal nuclei in the midbrain to activate bilateral Edinger-Westphal nuclei, pupils contract bilaterally (consensual reflex)
Result: illumination of 1 eye result in bilateral pupillary constriction Marcus-Gunn pupil- afferent pupillary defect due to optic nerve defect or retinal detachment. there is a decrease in pupillary constriction when light is shone in affected eye |
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Which diuretic is used to lower intracranial pressure? What are the contraindications to the
use of this diuretic? (FA p451) |
mannitol
contraindicated in pt with anuria or CHF |
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What are the common causes of eosinophilia? (FA p327)
|
NAACP
Neoplastic Asthma Allergic process Collagen vascular disease Parasites |
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Chapter 8 of Note Packet
On EKG a right atrial enlargement will be seen where especially in the limb leads |
On P wave- great than 2.5 mm
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On EKG a left atrial enlargement will be seen where
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negative deflection of P wave > 1mm in V1
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On EKG a right atrial enlargement and a left atrial enlargement will be seen where
|
Right atrial enlargement- p wave on limb 2 greater than 2.5mm
left atrial enlargement- negative p wave deflection in V1 >1mm |
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On EKG a right ventricular hypertrophy will be seen where
|
r wave is great than s wave in V1
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|
On EKG a left ventricular hypertrophy will be seen where
|
S wave in V1 + R wave in V5-6 greater than 35mm
is often associated with left axis deviation |
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name the chamber enlargement
p wave on lead 2 greater than 2.5 mm |
right atrial enlargement
|
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|
name the chamber enlargement
negative deflection of p wave in V1 and greater than 1mm |
left atrial enlargement
|
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|
name the chamber enlargement
p wave on lead 2 greater than 2.5 mm and negative deflection of p wave in V1 and greater than 1mm |
both left and right atrial enlargement
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|
name the chamber enlargement
R wave greater than S wave in V1 and right axis deviation |
right ventricular hypertrophy
|
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|
name the chamber enlargement
S wave in V1 + R wave in V5-6 is greater than 35 mm and ST and T wave inversion in V5-6 |
left ventricular hypertrophy
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what is meant by the pressure difference drives the flow of blood in CV
|
the pressure difference in the aorta (around 120) , the pressure at the right atria 0mmHg, blood moves forward to areas of lower pressure
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flow velocity is =
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flow/ cross sectional area
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when cross sectional area is increased in a vessel what happens to velocity of flow
|
decrease
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which faster flow velocity, vena cava or systemic capillaries
|
vena cava
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when cross sectional area is decreased in a vessel what happens to the velocity of flow
|
increases
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if resistance increase what will happen to flow
|
flow will decrease
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if resistance decreases, what will happen to flow
|
flow will increase
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|
which vessels are called the resistance vessels
|
arterioles- bc change flow through the capillary beds through either increasing or decreasing resistance
|
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|
what is bernouli principle
|
total energy=potential energy + kinetic energy
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what keeps blood vessels open and not collapsing
|
the lateral pressure from the static blood keeps the blood vessels open
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|
describe the flow of fluid in a vessel
|
parabolic ( greatest velocity in center) and laminar (Laminar flow, sometimes known as streamline flow, occurs when a fluid flows in parallel layers, with no disruption between the layers)
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t/f some frictional resistant between laminas exist which is called turbulence
|
false- called viscosity
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what makes the blood more viscous
|
red blood cells
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what is the effect of polycythemia on viscosity
|
increase in RBCs creates a more viscous blood which will increase frictional resistance which will make flow harder so the heart must pump harder to generate a hight pressure to maintain the same amount of blood flow
|
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|
what is Poiseuille's law
|
ΔP is the pressure drop= 8 X viscosity X length/ pi X pressure differnce X radius^4
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|
t/f flow is proportionally related to viscosity
|
false- flow is INVERSELY proportionally related to viscosity
|
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|
t/f flow is proportionally realated to the radius^4
|
false- inversely
change in pressure= 8 nl / pi r^4 |
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t/f resistance in series is additive
|
true
|
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|
circulatory flow to our organs is arranged in (parallel or series)
|
parallel
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|
t/f in small blood vessels the RBCs are pulled to the fastest lamina (on the outside) and the plasma is pulled toward the center
|
false- RBCs pulled toward the fastest lamina which is in the center. the plasma is pulled toward the outside, the slower lamina
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|
what will happen if a blood vessel is exposed to high viscous drag (high velocity and high viscosity)
|
a tear in the intimal layer, dissecting aneurysm
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t/f flow is inversely proportional to length
|
false- inversely related
change in pressure= 8 nl / pi r^4 |
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|
what is the hydraulic resistance equation
|
8nl / pi r^4
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t/f maximum contraction stops flow in all small vessels
|
false- max contraction stops flow in arterioles but does not stop flow in other arterial vessels
|
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|
t/f large arteries are high resistance blood vessels
|
false- large arteries are low resistance blood vessels
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|
arterial volume = cardiac output - peripheral runoff
what is peripheral run off |
the volume of blood that leaves the arterial system into the periphery
|
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t/f the key to controlling peripheral run off is compliance
|
false- key is total peripheral resistance
|
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|
how much time does the heart spend in diastole vs systole
|
2/3 time in diastole
1/3 time in systole |
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MAP - RAP= CO X TPR
what is the effect of beta blocker on HR, SV, CO what is the effect of Ca+ antagonists on TPR |
beta blocker on decrease HR, decrease SV, decrease CO
the effect of Ca+ antagonists is decrease TPR |
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what is compliance and what is it due to in the vessels
|
change in volume / change in pressure
due to large elastic component in large arteries |
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what is more compliant, arteries or veins
|
veins about 20X more compliant
veins are a volume buffer arteries are a pressure buffer |
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|
which one is a volume buffer , which one is a pressure buffer
arteries or veins |
veins are a volume buffer
arteries are a pressure buffer |
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if the diastolic pressure drops due to loss of compliance, what will happen to the pulse pressure
|
increase
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|
what are Karotkoff sounds
|
the sounds heard on stethoscope when slowly begin to release pressure from BP cuff, due to the turbulent flow when the blood is first able to pass through the arteries
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|
when laminar flow resumes after release pressure from BP what pressure is this (systolic or diastolic)
|
diastolic, can not hear laminar flow
|
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in the mean arterial pressure equation, how do we convert units of mmHg*min/liter from dyn*s/cm5
|
MAP - RAP= CO X TPR
multiple by 80 TPR=80 X (MAP-RAP) / CO |
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t/f veins work to smooth pressure differences
|
false- arteries
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t/f compliance is due to the smooth muscle and diameter
|
false- due to large elastic component and collagen
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around what age do the arteries begin to harden and what is the effect on diastolic flow
|
60 yrs
decreases diastolic flow |
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t/f hardening of the arteries always shows an increase in pulse pressure
|
true
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how can an organ control its blood flow to match its metabolic need
|
control the resistance by altering the diameter of the arterioles, metarterioles and precapillaries sphincters
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t/f like other muscle types (cardiac, skeletal) smooth muscle is fully relaxed in the resting state in order to allow for a consistent basal tone
|
false- smooth muscle NOT fully relaxed in the resting state, it allows either contraction or relaxation from the resting state.
can maintain its resting state with very low expenditure of energy |
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|
definition:
a mechanism by which blood flow is kept relatively constant despite changes in perfusion pressure |
autoregulation
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Chapter 10 CV
how can an organ control how much blood it needs for its metabolic processes |
alter diameter or arterioles, metarterioles, and precapillary sphincters to change resistance to flow
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what is the myogenic mechanism in the auto regulation pathway of peripheral ciruclation
|
vascular smooth muscle in blood vessel contracts in response to stretch and relaxes with a reduction in tension.
this is an intrinsic property of smooth muscle, this will occur if the endothelium is intact or not |
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t/f most metabolic waste are vasoconstrictors
|
false- vasodilators, when meetabolic waste increases resistance decreases and blood flow is increase to get rid of the waste. but will not see this effect in a vessel that is not directly attached to an organ
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|
name the vasodilators the endothelial cells produce
|
nitric oxide, EDCF, prostacyclin
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name the vasoconstrictors the endothelial cells produce
|
endothelin, endoperioxidase and thromboxanes
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Describe the mechanism of action for an agonist that works through the production of nitric oxide to have its effect
|
1st agonist binds to endothelial cells
2nd. binding of agonist stimulates release of nitric oxide synthase 3rd nitric oxide synthase catalyzes production of NO from l-arginine 4th NO diffuses through endothelial cell wall and stimulates guanylate cyclase in smooth muscle to produce cGMP and GTP 5th cGMP is a smooth muscle relaxer resulting in vasodilation |
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areas in the medulla influence the CV activity. Where is the pressor region located and what does it do to the CV. Where is the depressor region located
|
pressor region produces vasoconstriction, accelerates the heart rate and enhances cardiac contractility. innervates veins, arteries, arterioles and the heart by releasing NE overall to increase MAP
depressor region inhibits the pressor region and acts through direct spinal inhibition |
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t/f blood vessels of the skeletal muscle and skin receive parasympathetic input
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false- DO NOT receive parasympathetic input
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the adrenal medulla is stimulated in the "fight or flight" response. what types of hormones will it release and in what proportions
|
Epi- 85%
NE- 15% |
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what will the kidney release in response to reduced blood volume or pressure. and what does this enzyme do
|
renin- catalyzes the conversion of angiotensinogen to angiotensin 1
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what converts angiotensin 1 to angiotensin 2. what is the function of angiotensin 2
|
angiotensin converting enzyme
angiotensin 2 is an powerful vasoconstrictor |
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t/f the baroreceptor reflex senses chronic changes in blood pressure
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false- senses acute changes
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which waste product build up may cause vasodilation when in contact with a metabolically active tissue
|
CO, lactate, H+, K+, adenonsine
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why does the extrinsic regulation by sympathetic stimulation affect the veins, arteries and arterioles but not the venules or capillaries
|
no smooth muscle in the venules or capillaries
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name a tumor of the adrenal medulla that greatly increase the release of NE and Epi
|
pheochromocytoma
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what is the effect of the chemoreceptors in the carotid and medulla being stimulated. to what compounds are they sensitive to
|
sensitive to CO2 , low O2, and pH changes in the blood
carotid chemoreceptors- increase firing with low O2 or high CO2 or low ph Medullary chemoreceptors- respond to high CO2 or low pH both increase sympathetic output to increase vasocontriction and increase cardiac output |
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Chapter 11
why is the resistance blood vessels of the microcirculation the arteriole. give 4 reasons |
1. thick smooth muscle layer
2. endothelial lining 3. precapillary sphincters which may close or open depending on metabolic need 4 diameter small |
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do capillaries have smooth muscle
|
no- walls are a single endothelial cell thick to allow for adequate diffusion
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how does lipid solubility effect permeability
which compounds have the highest lipid solubility |
increase solubility increase permeability
CO2 and O2 |
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what type of capillary permeability is present in the liver
|
discontinuous to allow for higher permeability to promote exchange of solutes
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what type of capillary permeability is present in the kidney and intestines
|
fenestration
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what type of force is needed to push substances through through pores in order to leave the capillaries
|
hydrostatic pressure
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capillary beds have predominately which type of adrenergic receptors on their sphincters to dilate or reduce resistanec
|
beta- adrenergic
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how does hydrostatic pressure change as you travel the length of hte capilary
|
pressure highest in the arteriole end and lowest at the venule end
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increase in hydrostatic pressure can lead to increased filtration, but it can also lead to what other negative effect
|
edema in the surrounding tissue
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what is the osmotic pressure mainly due to
|
albumin
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which contributes more to the osmotic pressure in the capillaries, and by how much
albumin or globulins |
albumin - 65%
globulins- 15% |
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what is the Frank Starling theory
|
Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice-versa.
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what is the Starling equation for net fluid across capillaries
|
fluid mvt= K (filtration forces- reabsorption forces)
=K ( hydrostatic pressure +pi interstitial fluid) - ( pi capillary + Pressure Interstitial Fluid) |
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a decrease in pi capillary can be caused by which situation
|
protein malnutrition
liver disease so there is a decrease in protein synthesis kidney diseases result in in protein loss throughout the urine |
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what can cause an increase in pi interstitial fluid
|
release of protein in damaged tissue
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blood flow through the coronary arteries is greatest during which phase of the cardiac cycle (systole or diastole)
|
diastole- the recoil of the aorta pushes blood back again the aortic valve, pushing blood into the coronary arteries
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what does the right coronary artery supply
|
right atrium
right ventricle poster left ventricle SA node (55%) AV node (95%) |
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what does the left coronary artery supply
|
left atrium
anterior/ lateral left ventricle SA node (45%) IV septum bundle branches |
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what influences the perfusion pressure of the coronary arteries
|
aortic pressure and direction of flow
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what is systolic crunch
|
when ventricles contract during systoles they squeeze the arteries traveling through the muscle providing increased resistance to blood flow
this systolic crunch is greatest near the endocardial surface |
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where do a majority of the MI being in the heart
|
endocardial region
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systolic crunch has the biggest effect in which ventricle and why
|
in left ventricle bc more muscle and generates greater preesure
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t/f flow through the left coronary artery is reduced during diastole
|
false- flow through the left coronary artery is reduces during systole
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how much time is spent in diastole vs systole
|
diastole- 2/3
systole 1/3 |
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what is the most important factor in determining coronary blood flow
|
myocardial O2 requirement
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what is the adenosine hypothesis
|
need O2 to convert ADP to ATP, so if O2 low then ADP is converted to AMP which is broken down to adenosine which is lipid permeability. Adenosine is a vasodilator so this will increase the coronary blood flow
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capillaries are arranged (parallel or perpendicular) to the surface of the skin
|
perpendicular like a radiator
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t/f there is a low density of capillaries since the skin is not very metabolically active
|
true
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what is responsible for the heat transfer to the skin
|
venous plexus
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t/f neural regulation outweighs any metabolic needs of the skin
|
true
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sweat glands are innervated by sympathetic cholinergic fibers which release Ach. what is the result of the stimulation to the sweat gland
|
production of bradykinin which is a potent vasodilator
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t/f neural input to the vasculature in the brain overrides the metabolic need of the brain
|
false- the metabolic demand overrides the neural input
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The BBB exist at the choroid plexus and at the capillaries. Where are some exceptions
|
hypothalamus pineal gland and area postrema
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what organs comprise the splanchinic circulation
|
GI tract, liver, spleen, and pancreas
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what is the purpose of liver sinusoids
|
filter the blood and remove bacteria with the reticuloendothelial cells aka Kupffer cells
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|
describe the blood flow to the liver
|
1. hepatic artery supplies about 1/4 of blood (oxygenated)
2. hepatic portal vein supplies about 3/4 of blood (unoxygenated) but since the liver is very efficient at extracting out O2 no problem |
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in utero circulation how is 80% of the O2 saturated blood brought in to fetus
|
though umbilical vein
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half of the blood that enters the umbilical vein bypasses the liver. how
|
uses the ductus venousus
the other half of blood does go to the liver |
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how is blood shunted from the IVC to the left atrium in the fetus
|
through the foramen ovale
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t/f the ventricles in the fetus operate in series
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false- operate in parallel
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only 1/10 of the blood in the RV in a fetus travels to the lungs. where do the rest go
|
passes through the ductus arteriosus to the aorta
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|
what circulatory changes are seen at birth
|
umbilical vein constricts
ductus venousus closes |
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|
what activates the respiratory center of a newborn
|
asphyxia, the lungs fill with air so that pulmonary vascular resistance decreases dramatically
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|
why is blood flow reversed in the ductus arteriosus after birth
|
decreased pulmonary vessel resistance and increases total peripheral resistance which causes a constriction
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|
an increase in TPR shifts the cardiac function curve which way
|
clockwise so there is less cardiac output
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a decrease in TPR shifts the cardiac function curve which way
|
counterclockwise- resulting in more cardiac output
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|
Chapter 15
What is the pace of the SA node |
60-100 beat per mintue
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what is the normal beats per minute of the AV node
|
40-60
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what is the pace of the His Bundle
|
30-40
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What is the pace of the Purkinje Fibers
|
20-30
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|
What are the normal paces of the major conduction pathways
|
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|
|
FYI
|
FYI
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|
Right Bundle Branch Block.
what will this look like on EKG |
1. rabbit ears on V1
2. wide S wave on 1 and V6 3 long QRS 4. St and T wave inversion in V1-2 |
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|
what type of block is this
|
Right bundle branch block
1. rabbit ears on V1 2. wide S wave on 1 and V6 3. long QRS 4. ST and T wave inversion on V1-2 |
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Left Bundle branch block.
describe the type of finding on EKG |
Wide S-wave in V1 & wide, large R-wave in I & V6
QRS > 0.12 sec ST & T-wave polarity opposite major QRS polarity |
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|
Name the type of block
Wide S-wave in V1 & wide, large R-wave in I & V6 QRS > 0.12 sec ST & T-wave polarity opposite major QRS polarity |
Left bundle branch block
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|
Name the type of block
|
left bundle branch block
Wide S-wave in V1 & wide, large R-wave in I & V6 QRS > 0.12 sec ST & T-wave polarity opposite major QRS polarity |
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|
Describe the findings on EKG
|
Left axis deviation > - 400 (more negative)
+/- Small Q-wave in lead I rS complex in lead III |
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|
list the type of findings on the EKG
|
QRS axis > 120
Small Q-wave in lead III |
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|
a primary AV block will have what finding on EKG
|
prolonged PR interval
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|
FYI
|
FYI
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|
Mobits 2
|
Mobitz2
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|
Name the type of AV block
|
Mobitz 2
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|
Name the type of AV block
|
3rd AV block
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|
Name the 3 types of premature complexes (systoles)
|
1. Premature Atrial Complexes
(PAC) 2. Premature Junctional Complexes (PJC) 3. Premature Ventricular Complexes (PVC) |
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|
name the type of premature complex
|
Premature Atrial Contraction
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|
which class of drug will affect Phase 0 of the AP
|
Class 1 are Na+ channel blockers
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|
which class of drug will affect Phase 0 of the AP
|
Class 1 are Na+ channel blockers
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|
Class 2 Antidysrhythmics drugs affect which phase of the cardiac AP
|
these are Beta blockers so decrease phase 4 in slow response tissue such as AV node which will increase ERP
decrease Ca+2 influx |
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|
where do class 3 antidysrhythmics work
|
K+ channels blockers so work at phase 2 and 3
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|
where do class 4 antidysrhytmics work on the slow AP of the heart
|
Ca+2 channels blockers so work on Phase 0
|
|
|
Name 3 examples of class 1A Antidysrhythmics
Whase phase of the AP do they work on |
Quinidine, Procainamide
Blocks Na+ channels Phase 0 of myocardium (fast-response tissue) conduction velocity of depolarization K+ channel blockade (Phase 2) of slow-response tissue (particularly SA node) threshold potential slope of Phase 4 ERP of fast-response tissue |
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|
which class of antidysrhythmics will lengthen the QT interval
|
class 1A
quinidine, procainamide |
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|
which class of antidysrhythmics will shorted the QT interval
and give examples |
class 1B
lidocaine and phenytoin |
|
|
what effect on the AP does Class 1C have the QT interval
|
no effect on QT, Na+2 blocker
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|
which drug will have this effect on a pt
|
torsade de pointe
quinidine class 1A antidysthythmics, blocks Na+2 channels to lengthen QT interval |
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|
Torsades de pointe
how is the drug that causes this SAE eliminated from body |
quinidine-Class IA Antidysrhythmics
80% hepatic 20% renal |
Blocks Na+ channels
Phase 0 of myocardium (fast-response tissue) conduction velocity of depolarization K+ channel blockade (Phase 2) of slow-response tissue (particularly SA node) threshold potential slope of Phase 4 |
|
|
the most common AE of quinidine is GI upset and cinchonism. what is cinchonism and what other serious AE can it cause
|
cinchonism- HA, dizziness and tinnitus
torsades de pointes |
|
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|
what is quinidine indicated for
|
A fib and flutter in order to get back to sinus rhythm
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|
how is procainamide different from quinidine since they are both class 1 A antidysrthymics
|
procainamide is
1. Less antimuscarinic (anticholinergic) 2. More SA/AV nodal depression 3. Ganglionic blocker 4. Less QTc prolongation |
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|
|
what are the SAE of procainamide
|
1 More cardiac depression so can Precipitate CHF
2. Hypotension 3. Drug-induced SLE |
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|
Name the class of antidysrhythmics
1. Na+ channel blockade Prolongs ERP but shortens QT 2. Effects diseased/ischemic myocardium 3. Blocks K+ channels in ischemic myocardium |
class 1 B
lidocaine phenytoin |
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|
what are the class 1B antidysrhythmics indicated for
|
ventricular dysrhymias
|
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|
|
name the class of antidysrhythmics
Potent Na+ channel blockade Prolongs ERP but not QT Slows conduction of myocardium Increases ERP but shortens RRP |
class 1C
|
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|
|
name 2 class 1C antidysrhythmics
|
flecainide and propanfenone
|
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|
|
name the class of antidysrhythmics
Reduces slow channel currents Decreases Ca++ influx during Phase 0- repolarization, especially in AV node Slows the heart rate: Slows the rate of automaticity by decreasing Na+ influx during Phase 4 |
class 2 beta blockers
|
|
|
|
name 3 class 2 antidysrhythmics
|
beta blockers
propanolol, esmolol, metoprolol decrease Slope of Phase 4 automaticity Slow-response tissue (AV node) ↑ ERP decrease Ca++ influx through Ca++ channels |
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|
|
what are the adverse effects of class 2 antidysrhythmics
|
beta blocker AEs
Cardiac (beta1 effects) SA nodal block (bradycardia) AV nodal block Hypotension Heart failure Bronchospasm (beta2 effects) |
|
|
|
what are the indications of class 2 antidysrhythmics
|
Atrial dysrhythmias-AV nodal blockade
Ventricular dysrhythmias- Particularly catecholamine-induced rhythms |
|
|
|
what are the cardiac effects of class 3 antidysrhythmics and give 2 examples
|
K+ channel blockade-Prolongs ERP
Agents: Sotalol and Amiodarone |
|
|
which antidysrhythmics was probably given to produce this AE and what is the mechanism of action to prolong the QT interval and PR interval.
How long is the half life |
Amiodarone: K+ channel blockade- Prolongs ERP
T1/2 53 days |
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|
what are the indications for the class 3 antidysrhythmics
|
ventricular dysrththmias
|
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|
|
What is ibutalide indicated for
|
converting atrial flutter or fibrillation to normal sinus rhythm
|
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|
|
what are the cardiac effects of class 4 antidysrhythmics
|
Ca+ channel blockers
decreases Slope of Phase 0 in SA & AV nodes Effective in prolonging ERP Especially of AV node Depresses myocardium Effects Phase 2 of APD Slow-response tissue (AV node) ↑ ERP |
|
|
|
name 2 examples from class 4 antidysrhythmics and their indication
|
Verapamil
Diltiazem Atrial dysrhythmias |
|
|
|
what is the cardiac effects of adenosine
|
Inhibits AV & SA node conduction- AV node > SA node
Inhibits cAMP-mediated Ca++ influx Enhances K+ conductance increases AV nodal ERP |
|
|
|
what is the drug of choice for supraventricular tachycardia
|
adenosine
|
|
|
|
what is the mechanism of action for digoxin
|
Mechanisms of action:
Positive inotrope Negative chronotrope Inhibits Na+ - K+ - ATPase Increased Na+ & Ca++ within cell |
|
|
|
which antidysrhythmic has the following effects
Slows AV nodal conduction Increases vagal response Prolongs ERP of AV node |
digoxin
|
|
|
|
what are the 2 indications for digoxin
|
atrial arrhythmias to slow conduction through AV node
and CHF to increase contractility |
|
|
|
Magnesium is indicated for which cardiac condition
|
torsades de pointes and digoxin toxicity
|
|
|
|
list the drugs in each class:
name the drugs in each class of antidysrhythmic Class 1 Class2 Class 3 Class 4 Miscellaneous |
Class I
IA – quinidine, procainamide IB – lidocaine IC – flecainide, propafenone Class II Propranolol, metoprolol Class III Amiodarone, sotalol Class IV Verapamil, diltiazem Miscellaneous Adenosine, digoxin |
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically unstable with hypotension: sBP< 90 mmHg
|
Drug of choice: atropine
|
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically unstable with SVT/Atrial Tachycardia
|
Synchronized electrical cardioversion
|
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically stable with hypotension: sBP< 90 mmHg
|
don't treat
|
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically stable with SVT/Atrial Tachycardia
|
adenosine
|
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically stable with Atrial flutter/ A Fib and unstable with ventricular rate > 150
|
Synchronized electrical cardioversion
|
|
|
|
what is the Dysrhythmias Treatment of choice in a pt that is clinically stable with Atrial flutter/ A Fib and stable with ventricular rate (control heart rate < 100 BPM)
|
Ca+2 blocker ditiazem
|
|
|
|
what is the difference in treatment of choice in pt with ventricular dysrhythmias for the following situation
1. VT (pulse present)- If unstable (hypotension) - 2. VT (pulse present)-If stable 3. VT (pulseless)/ VF |
1. VT (pulse present)- If unstable (hypotension) - synchronized electrical cardioversion
2. VT (pulse present)-If stable – amiodarone, lidocaine, procainamide 3. VT (pulseless)/ VF Electrical defibrillation |
|
|
|
what is the difference between cardoversion and defibrillation
|
Cardioversion
Delivery of energy synchronized to the QRS Avoids R on T phenomenon (delivery during RRP) Avoids precipitating ventricular dysrhythmias with delivery of energy Defibrillation Electrical energy delivered randomly during the cardiac cycle |
|
|
|
what is mitral annular calcification and in what population does this most often occur .
|
degenerative calcification of mitral valve ring.
occurs in older women or pt wih myxomatous mitral valve ( mitral valve prolapse) or elevated LV pressure can predispose to infective endocarditis |
|
|
|
a midsystolic click is heart in which type of valvular deficiency
|
mitral valve prolapse
|
|
|
what caused this dilated cardiomyopathy.
what causes the death in these pt |
Sarcoidosis
causes CHF, thromboemboli, and arrythmias |
|
|
|
Chapter 18 of Notes
which virus is associated with polyateritis nodosa |
hepatitis B
|
|
|
|
Cryoglobulinemia is associated with which viral infection
|
hepatitis C
|
|
|
|
what are the 2 staining patterns of ANCA and which vasculitis are associated with these 2 types of ANCA stains
|
c-ANCA ( antibodies ot proteinase3): Wegner's granulomatous
p-ANCA ( antiboies to myeloperoxidase): polyateritis nodosa and microscopic polyangitis |
|
|
|
ANCA-mediated vasculitis shows attack on cytoplasmic antigens in neutrophils or enzymes in primary or azurophilic granules in neutrophils. What is the end result
|
End result increased vascular permeability, weakened walls with bleeding or aneurysm formation, intimal proliferation with thrombosis- all of which cause local ischemia
|
|
|
|
what is the classical physical sign for hypersensitivity angiitis
|
palpable purpura
|
|
|
name 7 causes for this palpable purpura
|
1. Serum sickness
2. Infectious diseases - viral or bacterial 3. Neoplasms 4. Connective tissue diseases (SLE) 5. Drug reactions 6. HS Purpura, 7. Cryoglobulinemia |
|
|
|
Name the condition, the vector and the classic triad
incubation period of one to two weeks after a tick bite. Initial symptoms may include: fever, nausea, emesis, severe headache, muscle pain, lack of appetite Later signs and symptoms include: maculopapular rash, petechial rash, abdominal pain, joint pain |
Rocky Mountain Spotted Fever
R. rickettsii classic triad of findings for this disease are fever, cenetripetal rash, and history of tick bit |
|
|
Name the condition, the vector and the classic triad
incubation period of one to two weeks after a tick bite. Initial symptoms may include: fever, nausea, emesis, severe headache, muscle pain, lack of appetite Later signs and symptoms include: maculopapular rash, petechial rash, abdominal pain, joint pain |
Rocky Mountain Spotted Fever
R. rickettsii classic triad of findings for this disease are fever, cnetripetal rash, and history of tick bit |
|
|
|
name 6 drugs than can cause palpable purpura
|
drug induced vasculitis:
1. Allopurinol, 2. gold, 3. thiazides, 4. sulfonamides, 5. phenytoin, 6. PCN |
|
|
Name the condition
In which population is this predominately seen is this deadly Which Igs are elevated Classic triad of purpura, arthritis and abdominal pain (80% of patients), usually occurs after URI, immunization |
Henoch-Schonlein Purpura
Children and young adults most common Self-limited, 6-16 weeks- may have relapsing renal disease (glomerulonephritis) IgA elevated- deposits and complement found on vessel wall, mild leukocytosis. |
|
|
Name the condition:
How is the different from HS purpura immune complexes containing IgG and IgM which precipitate out of serum at cool temperatures |
Cryoglobulinemia: Recurrent episodes of palpable purpura, Hepatoslpenomegaly (HSM), lymphadenopathy and polyarthralgias
HS purpura usually on buttocks and legs |
|
|
what is the condition:
recurrent oral ulcers but what other 2 findings must also be present what are the major complicaiotns |
Bechet's sydrome: with Apthous (ulcers)
plus 2 of the following: recurrent genital ulceration, eye lesions, skin lesions, pathergy test* Blindness may complicate, treat empirically,usually abates by itself |
|
|
|
Bechet's syndroms may complicate several disease states (CLASH)
|
Cryoglobulinemia, Leukemia, Arthritis, Sjogren’s Syndrome, and Hepatitis B
|
|
|
what is the pathogenesis of this PAN kidney (polyarteritis nodosa)
|
Polymorphonuclear neutrophils invade all layers of vessel wall and perivascular areas
Intimal proliferation and wall degeneration result (a transmural process) Necrosis causes lumen obstruction, thrombosis, infarction of distal tissues, and sometimes hemorrhage Lesions segmental, tend to occur at bifurcations of vessels |
|
|
Kidneys are most commonly affected organs with p-ANCA titers positive in some patients
what other organs are commonly affected. which size vessels are attacked |
Polyarteritis nodosa
Main effects through renal, CV, GI, nervous system,and cutaneous vessel involvement Affects medium and small muscular arteries with a necrotizing vasculitis, with segmental aneurysm formation |
|
|
Livedo reticularis.
Name the disease usually associated with this. In which population does this disease usually present what are the signs and symptoms |
polyarteritis nodosa
Occurs at any age, peaks in the 40s-50s Men outnumber women by 2.5 to 1 Signs and symptoms of fever, weight loss, abdominal and musculoskeletal pain |
|
|
Polyarteritis nodules.
which parts of the body are not involved |
Pulmonary arteries NOT involved, bronchial artery uncommonly involved
Venules NOT involved |
|
|
|
t/f 70% of patients with PAN eventually have cardiac involvement
|
true
|
|
|
|
what is the treatment for pt with Polyarteritis nodosa
|
Combination of prednisone in high doses and cyclophosphamide
|
|
|
|
what is the difference between PAN and microscopic polyangiits
|
microscopic polangiits: A necrotizing vasculitis, affects venules, capillaries and arterioles, but small and medium sized arteries may also be affected
in microscopic polangiits: Pulmonary capillaritis and glomerulo- nephritis present unlike classic PAN |
|
|
|
name the condition:
Hypereosinophilia, “allergic” rhinitis and asthma with vasculitis Systemic necrotizing vasculitis of medium and small arteries develops with tissue infiltration of eosinophils Evolves over years Rhinitis precedes development of asthma |
CHURG-STRAUSS SYNDROME
|
|
|
|
how is CHURG-STRAUSS SYNDROME diagnosed?
what are the symptoms of CHURG-STRAUSS SYNDROME. what do people with CHURG-STRAUSS SYNDROME die of what type of ANCA do pts have |
Diagnosis by biopsy
Eosinophilia of > 1,000 cells /uL in 80% Symptoms of fever, malaise weight loss, severe asthma attacks and pulmonary infiltrates Heart involved in 62% and cause of death in 23% Positive p-ANCA titers may be seen |
|
|
|
name the condition:
C-ANCA A necrotizing GRANULOMATOUS vasculitis of small and medium vessels renal, upper and lower respiratory tracts. May affect other organ systems Ages 15-75, peaks in 30s-40s, rare before adolescence, rare in blacks Male to female ratio 1 to 1 |
WEGENER’S GRANULOMATOSIS
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name the condition:
describe the symptoms |
Wegners
Usual presentation upper respiratory tract Nasal ulcers, rhinorrhea, sinus pain Ocular inflammation in >50% Lung involvement in most- X-rays show nodules, infiltrates or cavities Kidney- glomerulonephritis with protein and blood loss with casts Skin- varies with purpura and nodules |
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name the condition
A necrotizing GRANULOMATOUS vasculitis of small and medium vessels often mistaken on CXR for Tb |
wegners nodules from wegners granulomatous
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Wegners
how it is diagnosed which antibodies present what is the treatment which other vasculitis has the same treatment how do people die from wegners |
Diagnosis by biopsy- lung tissue best
C-ANCA antibodies present Renal disease in 77% if left untreated, accounts for most of the associated mortality Like PAN, use cyclophosphamide* and steroids |
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name the condition
Febrile, multisystem disease of children Erythema of pharynx, lips and palms Desquamation of finger tips Nonsuppurative cervical adenopathy |
KAWASAKI DISEASE
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name the condition
#1 cause acquired heart disease in US children |
kawasaki disease
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in this kid with Kawasaki, what is the pathogenesis and what may kill him
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Mononuclear cell infiltration
Beadlike aneurysm formation with thrombosis auto-immune process Association with a strain of S.aureus 2.8% develop fatal complications: aneurysm of right coronary (ruptured with pericardial tamponade) |
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name the condition and in what population this is most common in
Headache- 77%- classic presentation of fever, anemia, high ESR (>50) and headache in an elderly patient Jaw claudication present in up to 51% |
Giant cells arteritis
50 years of age and over usually women, Scandanavians |
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Pt with Giant Cell arteritis
what is the pathogenesis |
Temporal artery most often involved
A panarteritis with inflammatory mononuclear infiltrates in the vessel wall with frequent giant cell formation T cells predominate Involvement of multiple medium and large sized arteries may go undetected, such as this branch of temporal, opthalmic |
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what is the treatment for the pt with Giant cell arteritis
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immediate prednisone at high doses
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name the condition
PE reveals tender muscles without weakness or atrophy Inflammation (synovitis) of the knees occurs ESR elevated, rheumatoid factor ABSENT Associated with GCA in 20- 40% of patients |
POLYMYALGIA RHEUMATICA
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what is the diagnostic criteria for polymyalgia rheumatica
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Over 50 years of age
Aching/am stiffness in 2 of 3 : neck, shoulder girdle, pelvic girdle ESR greater than 40 mm/h Symptoms present for more than 1 month Absence of other disease |
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name the condition:
Inflammatory and stenotic disease of large and medium sized arteries Aortic arch and branches Most often in adolescent girls Vasa vasorum often involved |
TAKAYASU’S ARTERITIS
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name the condition and treatment
Symptoms of ischemia in sites supplied by involved vessels Also see fever, weight loss, malaise, night sweats, anorexia and arthralgias Death usually from CHF or CVA Suspect in young woman with onset of absent pulses, BP discrepancy, and arterial bruits |
takayasu
high dose prednisone with surgical repair/angioplasty |
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name the condition and treatment
Symptoms of ischemia in sites supplied by involved vessels Also see fever, weight loss, malaise, night sweats, anorexia and arthralgias Death usually from CHF or CVA Suspect in young woman with onset of absent pulses, BP discrepancy, and arterial bruits |
takayasu
high dose prednisone with surgical repair/angioplasty |
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90% of acute pericarditis is caused by what
what is considered acute |
viral or idiopathic
less than 6 weeks |
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list 4 different forms of pericardial disease
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1. Acute Pericarditis *
2. Pericardial Effusion * 3. Pericardial Effusion with Cardiac Tamponade * 4. Constrictive Pericarditis |
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acute pericarditis presents with chest pain. how is this chest pain different from MI
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Chest pain localized to retrosternal and left precordial regions and frequently radiates to trapezius ridge and neck
Pleuritic in nature Aggravated by deep inspiration and coughing or recumbency Relieved by sitting up and leaning forward |
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acute pericarditis may present with pericardial friction rub. what does this sound like
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High pitch/Scratchy/Leathery to-and-fro sound. May have 3 components.
Inconstant: May disappear/reappear in few hours Best heard in expiration with the patient in sitting position. |
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what does acute pericarditis look like on EKG
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ECG: ST-segment elevation/PR-segment depression
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what is the treatment for acute pericarditis
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Bed rest
Non--steroidal anti-inflammtory agents-Aspirin 650 mg x 6hrly Ketorolac IV: For pain relief |
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what are the characteristic difference of pericarditis vs. MI in the following areas
1. character of pain 2. change with respiration 3. change with position 4. duration 5. response to nitroglycerin 6. st segment elevation 7. pr segment depression |
differential
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name the condition
what are the 4 most common causes what is Ewart's sign |
Pericardial effusion "water bottle heart"
Common causes: Viral or Idiopathic, Neoplasms, Infections - (Tuberculosis, bacterial), Uremia Ewart’s sign: Patch of dullness on percussion and bronchial breathing on auscultation, between the vertebral column and the scapula, caused by compression of left lung base by pericardial fluid |
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how much fluid is required to cause a cardiac tamponade
what are the common etiologies |
Fluid necessary to cause P. Tamponade:
200 – 2000 ml (depends upon the rate of accumulation) Etiologies: Neoplasm Uremia Idiopathic or viral pericarditis |
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list 4 features of this cardiac tamponade
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Dyspnea, orthopnea and fatigue
Tachycardia Decreased systolic blood pressure with narrow pulse pressure Pulsus Paradox |
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what is the Beck's triangle in a cardiac tamponade
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1. Decreased arterial pressure
2. Increased venous pressure 3. Quiet heart/Distant Heart Sounds |
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what is pulsus peradoxus that is caused in a cardiac tamponade and list the differential diagnosis
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An exaggeration of the normal variation (decline with inspiration) in the systolic pressure during inspiration.
Is an abnormally large inspiratory decline in arterial systolic pressure (>10 mmHg). What is the paradox?: On auscultation heart beat will be present but radial pulse will not be palpable (in inspiration) because of very low stroke volume at that time Differential: Obstructive airway disease Pulmonary embolism Constrictive pericarditis Cardiogenic shock Restrictive cardiomyopathy |
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what is pulsus peradoxus that is caused in a cardiac tamponade and list the differential diagnosis
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An exaggeration of the normal variation (decline with inspiration) in the systolic pressure during inspiration.
Is an abnormally large inspiratory decline in arterial systolic pressure (>10 mmHg). What is the paradox?: On auscultation heart beat will be present but radial pulse will not be palpable (in inspiration) because of very low stroke volume at that time Differential: Obstructive airway disease Pulmonary embolism Constrictive pericarditis Cardiogenic shock Restrictive cardiomyopathy |
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describe the pt with constrictive pericarditis vs. pt with restrictive
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difference
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what is the treatment for pt with streptococcal A URI
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PCN or erthromycin for 10 days
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what is the treatment of pt with acute rheumatic fever who develops congestive heart failure
who develops arthritis |
digoxin, diuretics for CHF
salicylates for arthritis and bed rest |
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what is the most common cause of mitral valve stenosis
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rheumatic valvular disease from chronic rheumatic fever
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what is the pathology of symptomatic mitral stensois
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THICKENED MITRAL CUSPS
+/- CALCIFIC DEPOSITS FUSION OF VALVE COMMISSURES SHORTENING OF CHORDAE WITH FUSION “FISH MOUTH” OR FUNNEL ORIFICE |
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what is the main symptom of mitral stenosis
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1. dyspnea-bc reduced compliance of the lung
2. pulmonary edema- during emotional stress infection, fever, or PREGNANCY 3. A fib |
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Describe the arterial pulse findings, the jugular pressure findings and palpitation on PE
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aterial pulse normal or dimished
jugular pressure prominent a wave palpitation- inconspicuous LV |
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list 3 findings on auscultation
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mitral valve stenosis
1. accentuated S1 2. opening snap 3. diastolic murmur |
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name 2 other causes of degenerative mitral insufficiency
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1. mitral valve prolapse
2. marfan 3. calcification of MV annulus (from MI) |
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list 3 causes of inflammatory causes for mitral valve insufficiency
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1. rheumatic heart disease
2. SLE 3. scleroderma |
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name 4 causes of structural causes for mitral valve insufficiency
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1. ruptured chrodae tendinae
2. ruptured papillary 3. dilated mitral valve annulus 4. paravalvular prosthetic leak |
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describe the pathophysiology of mitral valve insufficiency
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1. impedance to ventricular emptying is reduced- LV decompresses into lA
2. volume of regurgitated flow- volume overload |
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what can be heard on auscultation
on physical exam, what can bring out the sound of a mitral valve prolapse |
1. holosystolic murmur- from apex to axilla and systolic ejection murmur from ischemic MR
2. use the valsalva to prolong the murmur and bring it closer to S1 |
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list 4 etiologies of aortic stenosis
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1. hypertrophic cardiomyopathy
2. supravalvular 3. congenital 4 acquired |
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list 5 possible causes of this pt acquired aortic stenosis producing the dilated aorta
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1. rheumatic heart disease- producing the fish mouth
2. degenerative- old people getting Ca+2 deposits 3. atherosclerosis 4. calcific due to Paget's disease 5. rheumatoid |
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Senile aortic stenosis
describe the pulse of this pt on PE |
pusus parvus and tardus in carotid-
slow-rising pulse and anacrotic pulse, is a sign where, upon palpation, the pulse is weak/small (parvus), and late (tardus) relative to its usually expected character. With respect to aortic stenosis, "typical findings include a narrow pulse pressure, LVH, a harsh late-peaking systolic murmur heard best at the right second intercostal space with radiation to the carotid arteries, and a delayed slow-rising carotid upstroke (pulsus parvus et tardus). |
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what is the pathophysiology of this pt with aortic stenosis
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increased afterload leads to increase LV wall stress so the LV compensates by hypertrophy. later there is a loss in contractility of LV and develops left heart failure
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why could a pt with aortic stenosis have a normal cxr unlike this pt who has a dilated aortic root
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chest x-ray may be normal bc the hypertrophy of the LV is CONCENTRIC (central) from pressure overload not eccentric like in mitral regurg or in aortic insuffiency
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what is the pathophysiology of mitral insufficiency vs aortic insufficiency
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CONTRAST TO MITRAL INSUFFICIENCY
AI: EJECTING BLOOD INTO HIGH AFTERLOAD (AORTA) MI: EJECTING BLOOD INTO LOW AFTERLOAD (LEFT ATRIUM) |
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list 4 causes for aortic insufficiency
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mostly males
2/3 from rheumatic heart fever 2. infective endocarditis 3. aortic root dilation- marfans 4. syphilis or ankylosing spondylitis |
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describe the palpation, murmurs and physical signs of a pt with aortic insufficiency
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1. arterial jack hammer pulse, widening pulse pressure
2. diastolic high pitched murmur blow, loud systolic aortic ejection, austin flint murmur 3. pt bobs head or jars body |
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what is the treatment of pt with aortic insufficiency
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if in CHF- give digoxin, diuretics to reduce afterload
also can give nitroprusside |
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what is an Austin Flint murmur
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a mid-diastolic[citation needed] or presystolic murmur[1] low-pitched rumbling murmur which is best heard at the cardiac apex.[2] It is associated with severe aortic regurgitation
The blood jets from the aortic regurgitation strike the anterior leaflet of the mitral valve, which often results in premature closure of the mitral leaflets. This can be mistaken for mitral stenosis. |
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Chapter 22
what are 5 the leading risk from developing HTN |
renal failure, CHF, stroke, CAS, retinopathy
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According to the JNC, what are the classification of BP for adults
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normal- 120/80 check every 2 yrs
prehypertensive- 120-139/ 80-89 check every year stage 1- 140-159/ 90-99 confirm in 2 months stage 2- >160/ >100 refer or treat immediately |
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t/f HTN more common in whites than African Americans
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false- HTN more common in AA than whites
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what are the CV risk factors for HTN (9)
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1. Age: men older than 55, women older than 65
2. diabetes mellitus 3. elevated LDL or low HDL 4. estimated GFR < 60ml/min 5. family hx of premature CVD 6. mircroalbuminuria 7. obesity BMI>30kg/m2 8. decreased physical activity 9.tobacco used |
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what are the end target organs damaged in HTN
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heart, brain, CKD, peripheral arteries, retinopathy
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what 4 regulators monitor peripheral resistance
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1. direct innervation- alpha 1 and beta 2
2. local regulators- low pH(dialtor), increase O2 (vasodilator), adeonsine (dilator), PGs (decrease), EDRP (decrease), endothelina (constrictor) 3. blood viscosity- Hematocrit (increases TPR) 4. Circulating regulators- angiotensin 2 (increases TPR), catecholamine (increase TPR) |
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what is the effect of thirst on blood volume
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increase in thirst increases blood volume
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what effects so the kidneys have on blood volume :aldosterone, antidiuretic hormone, sympathetic nervous system, atrial natriuetic peptide
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aldosterone (increase renal retension)
antidiuretic hormone, sympathetic nervous system, atrial natriuetic petptide |
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how are stroke volume, cardiac output and heart rate related
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CO=HR X SV
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how is blood pressure, cardiac output, and peripheral resistance related
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BP= CO X PVR
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where is renin produced and when is renin released, and what does it do
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produced by smooth muscle cells of juxtaglomerulus of afferent arterioles in the kidney.
JGA release renin in response to decrease renal perfusion pressure, decreased Na+ concentration and beta adrenergic stimulation enzyme needed for angiotensinogen to angiotensin 1 |
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what coverts angiotensin 1 to angiotensin 2 and where does this conversion take place
|
angiotensin converting enzyme, takes place in the lungs
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what is the role of angiotensin 2, and what is the effect on BP
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regulate Na+ uptake and acts as vasoCONSTRICTOR and stimulates the adrenal cortex to produce aldosterone
Angiotensin 2 vasoconstrictor so will increase BP |
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what is the effect of aldosterone, and what is its effect on BP
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aldosterone acts on the renal tubles to promote reabsorption of Na and H2O which will increase plasma volume through this reabsorption which will increase cardiac output
aldosterone increase H20 reabsorption so will increase BP |
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t/f endothelin is a vasodilator
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false- vasoconstrictor
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t/f nitric oxide is a vasoconstrictor
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false- vasodilator
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List 7 secondary causes of HTN
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1. renal parenchymal disease- diagnose based on elevated BUN/creatinine and decreased creatinine clearance and abnormal urine analysis
2. renovascular disease- severe HTN, abdominal bruits, your women or old men, use angiography and plama renal vein assay 3. Pheochromocytoma 4. Cushing- high cortisol, moonfacies, truncal obesity, proximal muscle weakness, hirsutism- test with morning plasma cortisol after suppression with dexamethasone 5. hyperaldosteronism- induces HTN and K wasting 6. hyper hypotheyroidism 7. coartation of arota 8. meds- nasal decongestants, NSAIDS, OCP |
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Chapter 23
t/f internal mammary is often affected by atheromas |
false- rarely affected
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t/f homocysteine promotes thombosis
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true
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t/f tobacco use promotes thrombosis and elevates fibrinogen
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true
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t/f plaques with a thick fibrous cap are small lipid core are more likely to rupture
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false- think fibrous cap. large lipid core and high macrophage content more likely to rupture
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which drugs are used to reduce cardiac events and total mortality in pt with high cholesterol and LDL
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HMG CoA reductase- like simvastatin
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what is peripheral artery disease and how does it present
|
most commonly associated with atherosclerosis
most often affects legs, presents with claudication, leg or calf pain when walking and relived by rest progressive obstruction leads to ischemic pain at rest in the foot or toes and is worst at night |
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what population is at highest risk for peripheral artery disease
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60-70 year old who smoke, have HTN, hypercholesterolemia and diabetes
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what physical finding on exam point to peripheral arterial disease
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intermittent claudication, distally decreases pulses, bruits, hair loss, shiny skin, deceased temp, cyanosis or pallor
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what is the ankle/ brachial index in pts with peripheral artery disease
|
normally- ratio of ankle to brachial artery pressure is >1
PAD or occlusive disease- ration is <1 indicating ischemia |
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what are the implications of an ankle/ brachial index of .78
|
VERY BAD!!! 30% 5 year risk of MI, ischemic stroke and vascular death,
developing ischemic ulcers with gangrene high, fungal infections more common, necrosis look for no hair and shiny lower extremities |
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Which risk factors are targeted in pt with peripheral artery disease and how are they managed
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1. smoking- stop
2. diabetes mellitus- insulin 3. HTN- aspirin + dipyridamole 4. hyperlipidemia- 5. have pt exercise |
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when is percutaneous tranluminal angiolasty recommend in a pt with peripheral artery disease
|
when the claudication interferes with work or is persistent with rest or there is tissue loss
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what is the site of most aortic aneurysm
|
below the renal arteries so its painless, but when it does rupture causes sudden ripping or tearing back pain
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what are 2 main populations at higher risk for thoracic aortic aneurysms
|
atherosclerosis pt and Marfan's pt
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what is Takayasu's arteritis
|
pulselss disease, especially in Japanese females, aortic panarteritis leading to eventual lumen obliteration, localized aneurysms
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tertiary syphilis is associate with which CV condition
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aortic arteritis- especially in aortic root leading to "eggshell calcification" which cause ascending aneurysm, valvular disease or coronary artery ostial stensosis
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what s a paradoxical emboli
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emboli that arise in the venous system and pass though a right to left intracardiac shunt
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what are the 5Ps of an thrombosis
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Pulselessness
Pain Pallor Paraesthesia Paralysis |
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what are the treatments for a thrombus
|
anticoagulant
surgical thomboembolectomy or bypass thrombolytics |
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name the condition:
AKA thromboangiitis obliterance occlusive peripheral vascular disease of small and medium sized arteries and vein male smokers under 30yrs triad: claudication, Raynaud's phenomenon, superficial thrombophlebitis |
Buerger's disease -
remember Goljan talking about the male who put his finger up his nose and lost the finger!!! from Raynauds' phenomenon- distal ulcers and gangrene of fingertips |
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which conditions are associated with Raynauds disease vs Raynaud's phenomenon
|
Disease- vasospasm of small arteries and arterioles, exaggerated reflex sympathetic with cold, Blue, White, Red. women with normal pulses
Phenomenon- Scleroderma, arterial occlusive disease, pulmonary HTN, frost bite, drugs (ergot, beta antagonists, chemo) |
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which artery is most commonly affected by a peripheral aneurysm
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popliteal artery
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what type of heart failure will a AV fistula cause (low output or high output)
|
high output
increase of blood flow over fistula so skin warm, but decrease of blood over distal tissue so skin cool |
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when would a surgeon create an AV fistula
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for hemodialysis
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describe Virchow's triad for venous thrombosis
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1. stasis
2. vascular damage 3. hypercoagulability |
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t/f D dimers are decreased with DVTs
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false- increased with clot formation
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what is the treatment for a DVT
|
anticoagulant initially with IV heparin, then warfarin for 3-6 months
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what is the difference between primary and secondary lymphedema
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primary- inherited disorder
secondary- due to damage, obstruction of normal lymphatic channels. this causes infection, neoplasm, treat with compression hose and elevation Filariasis most common worldwide- remember the pic of the HUGGGGEEEE swollen leg that hall rolls, while the other leg is super skinny |
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at what age does the AHA recommend screening for cholesterol levles
|
at age 20 and then every 5 years afterwards
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what is the desired range for cholesterol and how can HDL help in the equation to figure out a perons' risk for coronary heart disease
|
LDL= total cholesterol - HDL - TGs/5
desired range is under 200mg/dl for LDL and HDL over 60 if have HDL over 60 than can subtract 1 risk factor from pts bc high HDL is protective ACHILD CHD risk factors Age Cigarettes HTN Infarct Low LDL Diabetes |
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what is considered a high cholesterol level
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greater than 340mg/dl
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if a pt has a 300 mg/dl total cholesterol, HDL of 40 mg/dl, and TGs of 450 mg/dl. what is the LDL and is this peroson's classification
|
CAN NOT USE THIS EQUATION BC TGS TOOOO HIGH. HAVE TO BE UNDER 400, SO LETS SAY TGS 350
LDL= total- HDL- TGs/5 300- 40- 350/5= 190mg/dl at the desirable level |
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what are the risk factors for coronary heart disease
|
ACHILD
Age Cigarettes HTN Infarct Low LDL Diabetes |
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what is hard CHD
|
Hard CHD= myocardial infarction + coronary death
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|
what are the most effective drugs in lowering the LDL and total cholesterol levels and how do they work
|
statins. working by inhibiting HMG CoA reductase the Rate limiting step in cholesterol synthesis
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what are the first drugs of choice for elevated LDLs and TGs. give 3 examples
|
statins- atorvastatin- Lipitor, rosuvastatin- Crestor and simvastatin- Zocor
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Describe the AE of rosuvastatin in the Asian population
|
serious myopathy and myalgias due to increase serum levels
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what type of monitoring should be done in pts taking higher than normal does of statins
|
liver function test- looking for symptomatic hepatitis, will be increased ATL levels
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|
what is the current proposed mechanism of benefits of using statins
|
statins stabalize plaque, decrease inflammation, and rever endothelial disfunction (decrease serum CRP)
may inhibit macrophage proliferation may decrease thrombus formation by increasing tissue metalloproteinase inhibitors |
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Which drugs increase the risk of mypathies with statin use
|
gemfibrozil- CYP3A4 Inhibitor and niacin
lovastatin and simvastatin undergo extensive 1st pass metabolism |
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when are statins contraindicate
|
1. pregancy- bc fetus needs cholesterol
2. active liver disease 3. persistent elevation of aminotransferase |
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how do bile acid binding resins work
|
resins bind to bile acids in intestines and increase fecal excretion which increases hepatic bile acid production from cholesterol stores. then hepatic LDL receptors stimulated to increase in number thus lowering serum LDL
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when are bile acid binding resins indicated and give 2 example
|
when there is an elevated LDL level with normal TGs.
cholestryramine and colesevelam |
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bile acid binding resins are usually combined with which 2 drugs
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statins- gemfibrozil and niacin
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what is the major AE with bile acid binding resins
|
constipation, dyspepsia,
so can give colesevelam to decrease the GI effects |
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which drug inhibits VDLD sysnthesis and release of fatty acids from adipose tissue and increases lipoprotien lipase activity
|
niacin
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which drug more than any other drug increase HDL levels, decreases LDL and reduces TGs
|
niacin
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what are the adverse effects of niacin (5)
|
flushing, puritis, elevated glucose, hyperurecemia, pepitc ulcer disease
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how can the AE's of niacin be minimized
|
cutaneous flushing and pruritis can be decreased by pre-treating with aspirin, taking niacin with meals and using the lowest dose possible
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when is niacin contraindicated
|
active liver disease and peptic ulcer disease
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|
name 3 fibrates and their mechanism of action
|
gemfibrozil, fnofibrate, clofibrate.
increase lipoprotein lipase activity, decrease TG levels, may inhibit LDL secretion, used in combination with resins and niacin |
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what is the major AE of fibrates
|
choleslithiasis- especially gembirozile which increases the lithogenisity of bile and encourages gallstone to form
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when are fibrate contraindicated
|
gallbladder disease, severe liver disease, kidney dysfunction
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|
ezetimibe is a new class of fibrate. how and where does it work
|
selective inhibitor of dietary and biliary cholesterol absorption to increase expression of hepatic LDL receptors
acts at brush border ezyme system of SI, converted to active glucuronide form in liver |
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when is exetimibe contraindicated
|
moderate to severe liver disease and in children under 10
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|
what is the effect of estrogen on LDL
|
lowers LDL, lowers lipoprotein, lowers fibrinogen
but raises HDL and TGs NOT recommended for prevention of CAD |
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|
what are omega 3- polyunsaturated fatty acids indicated for and what is the mechanism of action
|
treatement of elevated TGs
omacor- prescription version reduces hepatic production of TG and VLDL |
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|
name the adrenoreceptor type
nerve endings- modulates transmitter release |
dopamine 2
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name the adrenoreceptor type
most vascular smooth muscle- leading to contaction |
alpha 1
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name the adrenoreceptor type
platelet aggregation |
alpha 2
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name the adrenoreceptor type
fat cells leading to inhibition of lipolysis |
alpha 2
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name the adrenoreceptor type
heart- increasing force and contractility |
beta 1
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name the adrenoreceptor type
vascular smooth muscle relaxation |
beta 2
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name the adrenoreceptor type
liver - activates glycogenlysis |
beta 2
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name the adrenoreceptor type
dilates renal smooth muscle in vessels |
dopamin 1
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name the adrenoreceptor type
contraction of pupillary dilator muscle |
alpha 1 to dilate pupil
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name the adrenoreceptor type
adrenergic an cholinergic nerve terminals- inhibit transmitter release |
alpha 2
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name the adrenoreceptor type
prostate contraction |
alpha 1
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Chapter 27
name 3 K+ sparring drugs and where do they work in the kidney |
spironolactone, amiloride, and triamterren- inhibit the ability of adrenal hormone aldosterone to stimulate Na+ reabsorption in the distal tubule and promote K+ retention rather than K+loss
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what are the SAE of spironolactone
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gynecomastia and impotence bc structurally similar to progesterone
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t/f the first line of drug in CHF are loop diuretics
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true
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what is the mechanism of action of the class 1a antiarrhythmics
Give 3 examples |
block Na+ fast channels to lengthen the ADP and QT
Quinide, procainamide, disopyramide |
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what is the mechanism of action of the class 1b antiarrhythmics
Give 3 examples |
lidocaine, mesiletine, tacos
block Na+ channels decreases ADP and shortens QT |
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what is the mechanism of action of the class 1c antiarrhythmics
Give 2 examples |
blocks Na+ channles but no change in APD
flecainide and propafenone |
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what is the mechanism of action of the class 2 antiarrhythmics
Give 1 examples |
beta blockers, block catecholamines effects
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what is the mechanism of action of the class 3 antiarrhythmics
Give 3 examples |
blocks K+ current to lenghten the APD
amiodarone, sotolol, ibutilide |
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what is the mechanism of action of the class 4 antiarrhythmics
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blocks inward flow of Ca+2 especially at the AV node
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which antiarrhythimics may cause SLE symptoms
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HIPP
hydralazine, isoniazide, procainamide, phenytoin |
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phenytoin is which class of antiarrhythmic and when is it used
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class 1b, given as DOC for digoxin induced atrial and ventricular arrhythmias
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name 2 examples of calcium channel blockers
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verapamile and diltiazem
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what is used to treat torsades de pointe
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magnesium
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what are the AE of ACE inhibitors
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1. sudden drop in BP on first dose
2. renal failure 3. dry cough 4. dizziness hypotension, 5. hyperkalemia, 6. agranulocytosis, neutropenia (captropril), 7. angioedema |
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what is the major SAE of ARBs
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renal failure
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what is the effect of hydralizine
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vasodilator, to decrease PVR
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what would you not give a pt with HTN and asthma
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not Beta blocker
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what is a good choice of med for pt with HTN and diabetes
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ACEi, to benefit from renal disease
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what determines myocardial supply and demand
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HR, contractility, preload and afterload
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t/f 95% of MI are secondary to atherosclerosis and thrombus
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true
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what is acute coronary syndrome
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when O2 demand is greater than supply leading to ischemia, and if ischemia last for a long time leads to infarction
ACS is an umbrella term for other conditions: unstable angina, NSTEMI, STEMI |
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ADP and TXA are (agonist or antagonist) for platelet formation
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agonist
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what is hirudin and where does it work
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leech spit, works to inhibit thrombin
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after occlusion of vessel, local mediator produce vasospasm. what is the effect on CNS, Sympathetic NS and alpha sympathetic
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CNS + SUmp NS inputs cause increase in beta receptors
unopposed alpha sympathetic stimulation causes more spasms |
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what causes the re-perfusion injury
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Ca+2, O2 and neutrophils in about 6 hrs cause injury. neutrophils occlude lumen, so decrease blood flow and procude chemoattractant and O2 free radicles
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what are the typical symptoms of acute coronary syndrome
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crushing, heaviness, substernal radiation to anterior chest, neck and arms
visceral pain but not specific diaphoresis and dyspnea nausea and vomiting |
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what is the Levin's sign in acute coronary syndrome
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the sanford and son rxn :-)
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if during an ACS there is pulmonary edema, what till be 2 findings
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dyspnea and pink frothy sputum
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in acute coronary syndrome, what happens to the Na/K ATPase activity and the way in which cells repolarize
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decrease in Na/K ATPase activity which delays the phase 3 repolarization.
ischemic cells re polarize in the opposite way of normal cells |
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what do Q waves mean on ECG
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mean dead myocardium
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On ECG, on which leads would we look for an Anterior, lateral, inferior, or posterior MI
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anterior- V1-V4 LAD
lateral- lead 1, aVL, V5-6 LCX inferior- 2,3, aVF RCA or LAD posterior- depressed V13 RCA |
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what is V-fib treated with
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shock em, rapid defibrillation
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what is Dressler's syndrome
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autoimmune pericarditis, could be associated with long term anticoagulant, in days to 6 weeks post infarction
presents with fever and pericardial chest pain |
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where do thiazides work in the kidneys
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distal convoluted tubules
Na/Cl symport inbibitors |
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t/f the major side effect of hyrocholothiazide is hyperkalemia
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false- HYPOkalemia, hypercalcemia, hyperlipidemia,hyperurecemia
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t/f furosemide s work at the loop of Henle
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true- loop diuretic blocks Na/K/2CL symporter
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where do Potassium sparing diuretics work in the kidney
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acts the distal convoluted tubule and collecting duct to inhibit ENac channel
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where does aldosterone work in the kidney
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collecting duct, to increase Na reabsorption, increase K and H excretion
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t/f spironolactone can cause hypokalemia and gynecomastia
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false- HYPERkalemai
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Captopril is which class of drug and what are the AE
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ACE inhibitor (pril)
cough, HYPERkalemai, angioedema high dose captopril0 neutropenia, impaired taste,proteinureia |
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what is the effect of angiotensin 2 on the myocytes, cardiocyte, and fibroblast
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increase IP3 adn Ca+2, and protein kinase C to constrict cells and promote cell growth
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what is the effect of angiotensin 2 on the glomeruli
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constrict efferent arterioles and enlarge glomerular pores to promote microalbuminureia and proteinuria
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what is the effect of angiotensin 2 on the sympathetic nerve endings
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enhances NE release
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what is the effect of angiotensin 2 on the juxtaglomerular apparatus
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inhibit renin release to relive increased intraglomerular pressure
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what is the effect of angiotensin 2 on the adrenal cortex
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synthesizes aldosterone to increase the Na retention and kaliuresis
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what is the effect of angiotensin 2 on the fibrinolytic system
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increase plaminogen activator inhibitor1- to impair fibrinolysis
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what is the effect of angiotensin 2 on the on the peripheral resistance system
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direct vasoconstriction
enhancement of peripheral noradrengeric neurotransmitter increase CNS sympathetic discharge release of catecholamines from the adrenal medulla all this to say= rapid pressor response |
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what is the effect of angiotensin 2 on the renal function
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1. increase Na+2 reabsorption
2. release aldosterone from adrenal cortex 3. renal vasoconstriction, Increase NE from neurotransmitter in kidney and increase sympathetic tone |
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what is the effect of angiotensin 2 on the CV
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increase afterload and increase wall tension
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give 1 example of an angiotensin 2 receptor blocker
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losartan
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what is the mechanism of action for calcium channel blockers at the arterioles and on the heart
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1. at the arterioles produce vasorelaxation by blocking the Ca+2 entry into the arteriolar smooth muscle to inhibit excitation
2. has a negative inotropic and chronotropic effects by blocking the Ca+2 entry into the arteriolar smooth muscle to inhibit excitation |
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name 3 Ca+2 channel blockers
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Diltiazem, amlodipine, verapamil
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of the Ca+2 channel blockers, which one has the best effect on decrease HR and cardiac contractility
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verapamil
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of the Ca+2 channel blockers, which one increases peripheral vasodilation and coronary blood flow the most
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dihydropyridine such as amlodipine and Nifedipine
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of the Ca+2 channel blockers, which one has NO effect on the SA/AV node conduciton
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ihydropyridine such as amlodipine and Nifedipine
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what are the AE of Ca+ channel blockers
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facial flushing, HA, constipation, non pitting ankle edema
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Prazosin and Terasozine are which type of adrenergic drugs and what is their mechanism of action on the CV system
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alpha 1 blockers- inhibit vasoconstriction, so reduce peripheral resistance and reduce preload
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Clonidine and methyldopa are which type of adrenergic drugs and what is their mechanism of action on the CV system
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alpha 2 agonists, diminish the CNS sympathetic outflow and activate alpha 2 receptors to decrease NE and Epi in synapse
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name 3 drugs that active the NO/ guanlate cyclase pathway
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hydralazine, nitroprusside, nitroglycerin
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Name 2 drugs that act on K+ channel as activators on the vascular smooth to cause peripheral vasodilation
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minoxidinile (rogain) and diazoxide
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which drug is an adrenergic neuron terminal inhibitor that binds to catecholamine storage vesicles in the peripheral and central nervous system rendering them unable to store or release NE and Epi
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reserpine
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Chapter 30
t/f endocarditis is a disease caused by microbial infection of the epicardial lining of the heart |
false- endocarditis is a disease caused by microbial infection of the ENDOTHELIAL lining of the heart
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what is the characteristic legion of endocarditis
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vegetations on the heart valve
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which organism usually cause subacute bacterial endocarditis and what is the time frame for this disease
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low virulence organism such as Strept Viridans
evolves over weeks or months |
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which organism usually cause acute bacterial endocarditis and what is the time frame for this disease
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high virulence organisms Staph aureus
occurs over days to weeks |
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what is native valve endocarditis
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infection of a previously normal heart valve or one damaged by congenital or acquired disease
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what is the difference between early and late prosthetic valve endocarditis
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early infection of the prosthetic valve happens within the first 2 month
late infection of the prosthetic valve happens after the first 2 month |
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what is the difference between infectious and noninfectious endocarditis
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noninfectious- refers to STERILE vegations, lesions are thrombotic rather than inflammatory
such as in marantic endocarditis in terminal malignancy infectious is inflammatory with infectious vegetations |
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which drugs can be given as a prophylaxis for subacute bacterial endocarditis
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2 grams amoxicillin or PCN or ampicillin
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which valve is more likely to be infected in a pt with endocarditis who uses IV drugs and with which organism
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tricuspid valve, Staph aureus
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what is the most common organism causing endocarditis after cardiac surgery
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Staph epidermidis
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what is the most common organism causing endocarditis while pt is in the hospital
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Staph, Candida and gram negative bacilli
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what is the probable organism causing endocarditis in pt with colon cancer
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strept bovis
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what is the term for sterile vegetation that develops in pt with SLE
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libman sacks endocarditis-non infective
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marantic endocarditis is associate with with diseases
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cancer, uremia and chronic wasting diseases
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t/f the left side of the heart is more commonly involved in valvular damage in routine cases
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true
acute bacterial and IV drug users endocarditis usually have tricuspid valves involved |
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what is the gold standard for endocarditis
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cardiac ultrasound
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in which cases is surgery eminent for pt with endocarditis
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1. if heart failure develops bc of the valvular damage and have to replace valve
2. if emboli occur 3. renal failure immune complex glomerunephritis but will need hemodialysis 4. if fungal |
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what is the most common procedure (82%) that can cause an incident of transient bacteremia and lead to endocarditis
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dental extraction, and even brushing of teeth
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