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315 Cards in this Set
- Front
- Back
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What is/are the postganglionic neurotransmitter(s) for the parasympathetic system?
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acetylcholine
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What is/are the preganglionic neurotransmitter(s) of the sympathetic system?
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acetylcholine
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What is/are the postganglionic neurotransmitter(s) of the sympathetic system?
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normally norepinephrine
can be acetylcholine can be epinephrine (adrenal gland) possibly ATP could be neuropeptide Y |
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Are sweat glands innervated by sympathetic or parasympathetic?
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sympathetic - release ACh like parasympathetic, but are defined by their origin point
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Where are nicotinic parasympathetic receptors found?
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on the postsynaptic surface of postganglionic nerve - they cause activation of postganglionic nerve
(this means they are at the first junction!) |
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Where are parasympathetic muscarinic receptors found?
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located on the end-organ
responds by activating phospholipase C or suppressing adenylyl cyclase activity (latter more important in heart) |
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What happens when ACh binds to a nicotinic receptor?
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allows Na+ to enter the cell, which causes depolarization
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What happens with ACh binds to a muscarinic receptor with a Gi subunit?
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acts on heptahelical receptor, acts on Gi (inhibitory) protein, decr adenylyl cyclase, decr cAMP, decr PKA -> reduce PKA and get more Ca++ entering the cell
Gi subunits are found in M2 muscarinics and alpha2 adrenergics |
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What happens with ACh binds to a muscarinic receptor with a Gq subunit?
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acts on heptahelical receptor (crosses membrane 7 times), acts on Gq protein, via PLC, via IP3 -> more Ca++ entering the cell
this causes constriction in smooth muscle cells that are not around endothelial cells (which would cause NO release and vasodilation with ACh) |
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Bethanecol works on what type of receptor?
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muscarinic
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Atropine blocks what type of receptor?
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muscarinic
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What are the five types of sympathetic receptors?
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nicotinic, alpha1, alpha2, beta1, beta2
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What are the characteristics of an alpha1 receptor?
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activated by norepi and epi
in vasculature heptahelical, couples to Gq, then PLC, IP3 +DAG -> increase Ca++ this causes coupling to myosin light chain kinase and contraction in smooth muscle alpha1 receptors cause vasoconstriction |
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What are the characteristics of a beta1 receptor?
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found on the heart
activated by norepi or epi heptihelical, couples to Gs protein, AC, cAMP, and PKA -> increase Ca++ and cause contraction |
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What are the characteristics of a beta2 receptor?
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activated by epinephrine (not norepi)
in vasculature heptihelical, couples to Gs protein, AC, cAMP, and PKA -> helps bronchodilate |
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What would you do to treat bradycardia?
Stimulate parasympathetics Inhibit parasympathetics Stimulate sympathetics Inhibit sympathetics |
Inhibit parasympathetics
resting HR without parasympathetics is about 100 bpm – so if HR is lower than 100, your parasympathetics are doing it use atropine to increase HR – block parasympathetics if HR is too low |
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What would you do to treat tachycardia?
Stimulate parasympathetics Inhibit parasympathetics Stimulate sympathetics Inhibit sympathetics |
inhibit sympathetics
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Where is ACh made and where is it stored?
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cytoplasm
vesicles choline + acetyl CoA --> acetylcholine + CoA |
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Black widow spider venom (latratoxin) promotes excessive release of what neurotransmitter?
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ACh
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What does botulinum toxin do?
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blocks ACh release
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How is ACh removed from the synaptic terminal?
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degraded by acetylcholinesterase
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When ACh is degraded and choline is taken up into the terminal, what drug blocks this reuptake process?
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hemicholinium
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If given parenterally, where does ACh act?
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parasympathetic end organs (muscarinic)
ganglia and adrenal medulla (nicotinic) CNS synapses (muscarinic) skeletal muscle (nicotinic) eccrine sweat glands and dilation of skeletal muscle vasculature (sympathetic-muscarinic) |
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What drug is the classic antagonist of muscarinic receptors?
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atropine - blocks parasympathetics
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Why isn't ACh a very useful drug?
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it is degraded quickly
also it is charged so it doesn't cross the GI and must be given parenterally |
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What will IV ACh do to blood pressure?
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lower it
activates muscarinic receptors to increase parasympathetics |
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What does Bethanechol do?
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it is a parasympathomimetic choline ester that selectively stimulates muscarinic receptors (with further selectivity for M3 receptors) without any effect on nicotinic receptors
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What does Pilocarpine do?
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it is a non-selective muscarinic receptor agonist in the parasympathetic nervous system, which acts therapeutically at the muscarinic acetylcholine receptor M3
useful in treating glaucoma and xerostomia (dry mouth) |
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Where is Muscarine from and what does it activate?
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from mushrooms
muscarinic agonist, so it stimulates parasympathetics |
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What are the muscarinic agonists?
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bethanechol
pilocarpine muscarine acetylcholine |
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What are the effects of anticholinesterases?
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bradycardia and vasodilation - parasympathetic stimulation because they increase acetylcholine concentrations outside the nerve
contract skeletal muscle (nicotinic) because they increase acetylcholine concentrations in the vicinity of the nicotinic receptor (at NMJ) can activate postganglionic nerve (nicotinic) by increasing acetylcholine concentrations in the synapse (less common) |
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What is the mechanism of action of edrophonium, an anticholinesterase?
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it binds to the active site
could use for PSVT because it is reversible |
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What is the CV use of anticholinesterases (such as physostigmine)?
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atropine intoxication
because atropine blocks muscarinics and hence parasympathetics, but anticholinesterases cause the ACh to hang around longer |
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What are symptoms of a cholinergic crisis?
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SLUDGEM: Salivation, Lacrimation, Urination, Defecation (or incontinence), Gastrointestinal distress, Emesis, Miosis
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What are drugs that can be given in a cholinergic crisis? (aka an OD of anticholinesterases)
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atropine - muscarinic receptor antagonist - reverses only muscarinic symptoms
pralidoxime for organophosphorous inhibitors |
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What are two anti-muscarinic drugs?
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atropine
scolopamine actions are to oppose parasympathetics, so they increase HR |
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How do you treat atropine toxicity?
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physostigmine
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Why would you use atropine for the CV system?
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bradycardia
AV block cholinergic crisis choline-ester toxicity hyperactive carotid sinus reflex |
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What will atropine do to hypotension caused by bradycardia?
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raise BP
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Which receptor are trimethaphan and hexamethonium antagonists of?
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nicotinic
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Which receptor are atropine and scopolamine antagonists of?
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muscarinic
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Bethanechol and Pilocarpine are agonists of what receptor?
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muscarinic
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Clonidine is an agonist and yohimbine is an antagonist of what receptor?
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alpha2 adrenergic
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Ephedrine works at what receptor?
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beta2 adrenergic
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What are the drugs that work on the nicotinic receptor?
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nicotine, ACh
trimethaphan (-), hexamethonium (-) |
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What are the drugs that work on the muscarinic receptor?
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muscarine, pilocarpine, ACh, bethanechol
atropine (-), scopolamine (-) |
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What are the drugs that work on the alpha1 adrenergic receptor?
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epi>=NE>>isoproterenol
dopamine, phenylephrine antagonists: phentolamine, phenoxybenzamine, prazosin, terazosin, doxazosin, labetalol, carvedilol |
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What are the drugs that work on the alpha2 adrenergic receptor?
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epi>=NE>>isoproterenol
clonidine, methyldopa, guanabenz phentolamine (-), phenoxybenzamine (-), yohimbine (-) |
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What are the drugs that work on the beta1 adrenergic receptor?
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isoproterenol>epi=NE
dopamine, dobutamine antagonists: propranolol, timolol, pindolol, labetalol, carvedilol, metoprolol, atenolol, esmolol |
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What are the drugs that work on the beta2 adrenergic receptor?
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isoproterenol>epi>>NE
ephedrine, pseudoepehrine, metaproterenol, terbutaline, albuterol, ritodrine, salmeterol antagonists: propranolol, timolol, pindolol, labetalol, carvedilol |
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The G protein pathways work through ELEVATED cAMP in which receptors?
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beta1 and beta2
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The G protein pathways work through decreased cAMP in which receptors?
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alpha2, muscarinic (type M2)
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How do the adrenergic amine drugs work?
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they reverse the direction of the axoplasmic catecholamine transporter, which releases NE from nerves
they are inactivated in the presence of cocaine or imipramine (which kill the axoplasmic pump) |
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Why should a person on MAOIs avoid beer, wine, and cheese?
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these foods contain tyramine, which is normally degraded by MAO in the intestine. tyramine displaces NE from vesicles, which can lead to greatly increase BP and a hypertensive crisis
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What is latratoxin?
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black widow spider venom - it promotes excessive release of ACh from post-ganglionic nerves
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How does clostridium botulinum toxin affect ACh?
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it blocks ACh release from the post-ganglionic nerve
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What is pilocarpine used for?
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to treat narrow angle galucoma and xerostoma (dry mouth)
it is muscarinic agonist - vagomimmetic |
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Which drug do you give for atropine toxicity?
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physostigmine - an anticholinesterase
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What is the drug of choice for a choline ester toxicity?
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atropine - it blocks parasympathetics at the muscarinic receptors
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What do you use atropine for?
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bradycardia, AV block, hyperactive carotid sinus reflex, choline ester toxicity
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Tyramine, amphetamine, ephedrine, and pseudoephrine are all types of what?
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adrenergic amines, which reverse the direction of the axoplasmic pump
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What are the direct and indirect effects of ephedrine (and pseudoephedrine) and what is it used for?
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indirect: release NE, which constricts and reduces mucosal congestion (alpha1 receptors)
direct: bronchodilates (beta2) found in cold medications |
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Cocaine and amphetamine work against each other via what mechanism?
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amphetamine pumps NE out of the cell via the axoplasmic pump, but cocaine poisons the axoplasmic pump
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What are the main actions at the beta1 receptors?
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increase HR, incr force, renin release in kidney
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What are the main actions at the beta2 receptors?
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bronchodilate
(this will decr TPR) |
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What are the main actions at the alpha2 receptors?
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inhibit NT release (negative feedback)
works by decreasing amount of cAMP |
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What are the main actions at the alpha1 receptors?
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contract vascular smooth muscle
works via PLC and IP3 |
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What are the main actions at the muscarinic receptors?
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decr HR, dilate vasculature (Ca++ influx in endothelial cells causes NOS + arginine -> NO), cause erection in sex organs (dilation)
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Metaproterenol, terbutaline, albuterol, ritodrine, and salmeterol all work at which receptor?
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B2 - they are B2 selective agonists and are used for bronchodilation
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What type of food must be avoided with pargyline?
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it is an MAOI so you should avoid foods high in tyramine like cheese, wine, and beer
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Why would you use dopamine in a patient with shock?
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it maintains renal perfusion in pts that are in shock
it vasoconstricts (alpha1) in high doses but vasodilates in low doses |
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What drug is better known as Sudafed and how does it work?
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pseudoephedrine - works indirectly on alpha1 (by releasing NE) to constrict and reduce mucosal congestion and works directly on beta1 to bronchodilate
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How do alpha blockers work?
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block alpha1 receptors to decrease both total peripheral resistance and blood pressure (also increases mucosal stuffiness, though)
nonselective also block alpha2 receptors to increase norepinephrine release from nerves (more tachycardia) |
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What are the three determinants of oxygen demand?
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intraventricular wall pressure (influenced by vent volume (preload and afterload, ejection fraction) and vent wall thickness(CHF))
heart rate ventricular contractility |
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What is the oxygen extraction across the myocardium?
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75% - this means that there are limited reserves for the delivery of oxygen in states of increased demand
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What are the determinants of oxygen delivery to the myocardium?
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total coronary blood flow, influenced by:
coronary vascular resistance aortic diastolic pressure duration of diastole diffusion (i.e. diabetes, atherosclerosis) O2 carrying capacity (anemia, exposed to CO) |
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What are the two types of angina?
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typical (set off by exercise or anxiety, when metabolic demand goes up)
variant - Prinzmetal's (coronary artery vasospasm) |
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What precipitates typical angina?
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decreased nutrient supply
increased metabolic demand |
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What are the therapeutic strategies for typical angina?
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increase nutrient supply (dilate coronary arterioles, treat atherosclerosis or diabetes, treat anemia)
decrease metabolic demand (slow HR, decr ventricular wall tension (afterload, preload)) |
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What is Prinzmetal's syndrome?
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variant angina, when the alpha adrenergic receptors are neurogenically activated and cause vasospasm
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What is the problem with Dipyridamole (Persantine) as an anti-anginal agent?
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it is a direct-acting vasodilator which favors arterial dilation over venous dilation, so it creates a "coronary steal phenomenon"
also, it increases the risk of Prinzmetal's |
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What agent would you use for a chemical stress test?
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Dipyridamole (Persantine)
arteriodilation > venodilation |
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Why does nitroglycerin work as an anti-anginal agent?
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venodilation > arteriodilation
redistribution of blood flow favors distribution the endocardium, which is the area of the heart that lacks blood the most because of the pressure there |
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Which anti-anginal agent causes Monday Disease and why?
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nitroglycerin, because you develop a tolerance to it and a dependence on it
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What are some adverse effects of taking nitroglycerin?
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orthostatic hypotension, vasodilation of meningeal vessels causing headaches, contraindicated in pts taking PDE5 inhibitors (viagra), tolerance and dependence may occur, high doses cause methemoglobinemia (esp in infants)
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Where are the nitrate/nitrite drugs eliminated?
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liver
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What are the Ca++ channel blockers with indications for angina?
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verapamil, nifedipine, nicardipine, amlodipine, diltiazem, bepridil
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Which Ca++ blockers are contraindicated in Prinzmetal's?
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the pines - nifedipine, nicardipine, amlodipine
they precipitate alpha vasostimulation |
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Precautions in using anti-anginal agents:
Verapamil plus __ can cause hypotension Nifedipine plus __ can cause hypotension |
alpha blockers
beta blockers (verapamil slows HR, a-blockers vasodilate) (nifedipine vasodilates, B-blockers vasodilate) |
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How does verapamil decrease angina?
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lowers HR (suppression of SA automaticity, suppression of AV conduction), negative inotropic, a little bit of vasodilation (tho cardiac blood flow stays the same)
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How do the pines (nifedipine, nicardipine, amlodipine) decrease angina?
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increase cardiac blood flow through vasodilation - do nothing for HR
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Which anti-anginal drugs cause venodilation?
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organonitrates
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Which anti-anginal drugs vasodilate and thus increase total coronary blood flow as their major mechanism?
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the pines (nifedipine, nicardipine, amlopidine)
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Which anti-anginal drugs decrease HR as their major mechanism?
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verapamil and B blockers
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Which is the longest acting "pine" of the anti-anginal drugs?
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amlopidine
peak plasma is 6-12 hours half life is 30-45 hours everything else is 30 min - 2 hours |
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Why are B-blockers not effective at treating Prinzmetal's?
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B's are blocked, but a's are unopposed, so there is still an increased risk of a-vasospasm
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What are the B-blockers used as anti-anginal agents?
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B: propranolol, timolol, nadolol, pindolol
B1: metoprolol, atenolol, acebutolol |
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Why is it good to use "pine" anti-anginal agents with propranolol (a non-selective B blocker)?
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pines cause a reflex increase in HR and AV conduction, which can be blocked by the direct effect of propranolol, which decreases HR and AV conduction
it is good to titrate the two to get the good effects of both and the bad effects of neither |
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What percent of cholesterol is synthesized endogenously and what percent is from dietary intake?
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67% made in the body
33% taken in through diet |
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What are the six strategies for treating high cholesterol?
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1. inhibit HMG-CoA reductase
2. inhibit cholesterol transport in intestines 3. prevent reabsorption of bile acids 4. inhibit HDL catabolism 5. increase synthesis of lipoprotein lipase 6. raise HDL levels by blocking cholesteryl ester transfer protein (CETP) - though this doesn't work yet |
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How do HMG-CoA reductase inhibitors work?
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competitive inhibitors of cholesterol synthesis at the rate-limiting step
induce LDL receptors more effective when taken at night because that's when cholesterol is made |
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What are the HMG-CoA reductase inhibitors?
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the statins
atorvastatin (lipitor), fluvastatin, simvastatin (zocor), lovastatin, pravastatin, rosuvostatin (crestor) |
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What are the adverse effects of the statins?
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liver toxicity (check ALT), myopathy, teratogenic, drug interactions with P450
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What does Ezetemibe (Zetia) do?
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it is a cholesterol absorption inhibitor
it reduces intestinal abroption by up to 50%, reduced LDLs, TGs, small increase in HDLs has a synergistic effect with statins (so it potentiates ADRs and are usually used in combo) |
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What do Cholestyramine and Colespitol do?
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It is a bile acid binding resin
binds bile acids in the intestine, increase production of LDL receptors, reduces plasma LDL, also increases HDL not absorbed, so there are few SEs, preferred tx in juveniles |
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What does Nicotinic Acid do?
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HDL catabolism inhibitor
inhibits clearance of HDL-ApoA1, elevates HDL in plasma, also small LDL decrease ADRs: flushing (via PGs), vomiting, diarrhea, gout, hyperglycemia in diabetics |
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What do Gemfibrozil, Clofibrate, and Fenofibrate (Tricor) do?
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lipoprotein lipase stimulants (fibrates)
in adipose tissue, incr lipoprotein lipase synthesis and incr clearance of TGs in liver, incr ApoA1 to incr HDL so . . . incr HDL, decr TG, LDL not affected (good for hypertriglyceridemia) |
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What are side effects of the fibrates (cholesterol drugs)?
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flu-like symptoms
GI problems |
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What does Torcetrapib do?
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it is a cholesterol ester transfer protein (CETP) inhibitor
huge HDL elevation, but also BP elevation, so doesn't incr survival these drugs don't actually work yet |
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During a normal inspiration, intrathoracic pressure falls by about __ as the diaphragm contracts and the chest wall expands.
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7 mmHg
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Because of __, venous return is increased more by inspiration than it is decreased by expiration.
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venous valves
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Heart rate in normal individuals also fluctuates in synchrony with the respiratory rate. This is called:
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normal sinus arrhythmia
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What is the net effect of inspiration on the cardiovascular system?
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transient increase in stroke volume and cardiac output
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Because of the inspiration-induced __ in intrathoracic pressure, the cardiopulmonary baroreceptors in the vascular and cardiac walls will be stretched and __ their firing rate which will __ arterial pressure.
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decrease
increase lower |
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What are some of the respiratory effects on the cardiovascular system?
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exercise - deep and rapid breathing contributes to venous return
yawning - decrease in intrathoracic pressure that increases venous return coughing - increase in intrathoracic pressure, reductions in cardiac output that could lead to fainting if prolonged valsalva maneuver |
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What is the Valsalva maneuver?
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forced expiration against a closed glottis
arterial pressure is abruptly elevated, which leads to a fall in venous return and a fall in BP, compensatory reflex increase in HR and peripheral vasoconstriction at the cessation of the maneuver, there is an abrupt fall in pressure, venous blood moves rapidly into the central venous pool, SV, CO, and arterial pressure increase rapidly, and reflex bradycardia occurs can be dangerous because this combination could rupture a vessel and cause a stroke |
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A person who stood upright without intermittent contraction of skeletal muscles in the legs would lose consciousness in how long?
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10-20 minutes
because of the decreased brain blood flow that would stem from diminshed central blood volume, SV, CO, and arterial pressure |
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What are the important effects of skeletal muscle contraction on venous return?
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compression of vessels expels venous blood and lymphatic fluid
the weight of the venous and lymphatic fluid columns is temporarily supported by the closed one-way valve leaflets |
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When standing, what does the primary disturbance signal to the cardiovascular center?
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htere is an increase in arterial and venous pressure in the lower extremities, which lessens the normal input from both arterial and cardiopulmonary baroreceptors, which are reflex adjustments to increase blood pressure
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HR and TPR are __ when a person stands than when the person is lying down.
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higher
they are not directly influenced by standing but are changed by compensatory responses |
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SV and CO are __ when a person stands than when the person is lying down.
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usually decreased below recumbant values during quiet standing despite the reflex adjustment that tend to increase them
reflex adjustments do not quite overcome the primary disturbance, so short term cardiovascular compensations never completely correct the initial disturbance |
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What are some of the effects of long-term bed rest?
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shift of fluid from lower extremities to upper parts of the body
distention of the head and neck veins, facial edema, nasal stuffiness, decreases in calf girth |
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What happens to a patient's blood volume after a few days on bed rest?
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the person becomes hypovolemic because their sympathetic drive is reduced
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How are the thin-walled caps in the feet able to withstand pressures greater than 100 mmHg in a standing individual without rupturing?
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caps have such a small radius, so the tension in the cap wall is modest despite very high internal pressures according to the law of Laplace
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Soldiers faint when standing at attention on a very hot day more often than on a cooler day. Why?
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fainting happens because of decr cerebral blood flow (below 60 mmHg)
on a hot day, temp reflexes override pressure reflexes to produce incr skin blood flow, so TPR is lower when standing on a hot day than on a cool one, and mean arterial pressure falls below 60 mmHg with less lowering of CO |
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For several days after an extended period of bed rest, pts often become dizzy when they stand upright quickly because of an exaggerated transient fall in arterial pressure. Why?
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pts tend to lose rather than retain fluid during extended best rest, so they end up with lower blood volumes
they are less able to cope with upright posture during the period required for blood volume to reach the value it had when periods of standing were part of the pt's normal routine |
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Vertical immersion to the neck in tepid water produces a diuresis in many people. What mechanisms account for this?
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pressure produced by water enhances reabsorption of fluid, compresses peripheral veins, reduces peripheral venous volume, and increases the volume of blood in the central venous pool
this stimulates cardiopulmonary mechanoreceptors and evokes diuresis by neural and hormonal pathways |
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How do cholestyramine and colestipol work?
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they bind bile acids in the intestine and increase production of LDL receptors (this reduces plasma LDL and increases HDL)
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Why do cholestryramine and colestipol have few side effects?
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they are not absorbed
they are the treatment of choice for juveniles they are the oldest and probably safest tx for hyperlipidemia |
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How does nicotinic acid work as a lipid lowering drug?
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it inhibits the clearance of HDL-ApoA-1, elevates HDL in the plasma, also has a small decr in LDLs, also reduces TGs
increases HDL more than any other drug |
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Why would you use nicotinic acid to lower lipid levels, and why would you not use it?
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it has a beneficial effect on all lipids, and the greatest increase in HDL of all the drugs
it has a lot of side effects: flushing, vomiting, diarrhea, flatulence, dyspepsia, hyperuricemia, gout, hyperglycemia in diabetics |
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How do the fibrates (gemfibrozil, clofibrate, fenofibrate) work to lower lipids?
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in adipose tissue, they incr lipoprotein lipase synthesis, and increase clearance of TGs
in liver, they incr ApoA1 to incr HDL so, decr TG, incr HDL, LDL not affected (good for high TGs) |
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Renin is secreted by the kidney and converts __ to __.
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antiotensinogen
angiotensin I |
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Where is angiotensinogen made and what substance stimulates its production?
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in the liver
angiotensin II (via pos feedback loop), glucocorticoids, estrogen |
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What are two functions of converting enzyme (dipeptdyl peptidase)?
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converts angio I -> angio II
degrades bradykinin |
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Renin is secreted by the juxtaglomerular cells of the kidney in response to these four conditions:
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decreased renal artery pressure
decr Na+ load to macula densa sympathetic nerve activation prostaglandins |
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Renin release is inhibited by:
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B blockers
atrial natiuretic peptide (ANP) incr renal artery pressure incr Na+ load to macula densa COX antagonists (decr prostaglandins) |
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What are the actions of angio II?
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vasoconstrictor - incr BP
retains Na+, promotes aldosterone secretion inotropic on the heart central effects: thirst, ADH and ACTH release, sympathetic stimulation increases outflow of NE from nerves and adrenal medulla |
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What is the effect of ACE inhibitors on BP via bradykinin?
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converting enzyme degrades bradykinin, so when you block it, you have more bradykinin around, and bradykinin does its job and vasodilates more, which lowers BP
(also via blocking the production of angio II, it blocks vasoconstriction and the retention of Na+ which both would incr BP) |
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What are the two types of angio II receptor?
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type 1 - IP3 generated from PIP2 via PLC, which generates Ca++ causes actin myosin light chain kinase interaction, and constriction of smooth muscle
type 2 - appears to reduce BP |
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How does Losartan (Cozaar) work?
|
it is an angio II type 1 receptor antagonist - diminishes effects of the renin-angiotensin system
doesn't cause cough like ACE inhibitors avoid in pregnancy decr dose when used with thaizide it is less effective in blacks than whites, like the ACE inhibtors |
|
|
What are the ACE inhibitors?
|
captopril, enalapril, lisinopril, quinapril
|
|
|
How do ACE inhibitors work?
|
block conversion of angio1 to angio 2
antihypertensive, used in heart failure, post MI, diabetic nephropathy teratogenic other SEs: cough, proteinuria, rash, dysgeusia, hypotension, hyperkalemia, angioedema |
|
|
How does aliskirin work?
|
it is a renin inhibitor (blocks renin, reduces angio 1 and 2, reduces aldosterone, reduces BP)
approved for HTN, less effective in blacks than writes doesn't incr bradykinin like ACE inhibitors, so no cough side effect decr dose w thazide |
|
|
What are the arachidonic acid metabolites and what do they do to BP?
|
thromboxane A2 - vasoconstricts and aggregates platelets
PG E2 - vasodilation and pain sensitization (menstural pain - contracts uterus) leukotriene C4 and D4 - hypotension esp in anaphylaxis histamine - vasodilates (H1 and H2 receptors) bradykinin - vasodilator degraded by ACE |
|
|
Renin converts angiotensinogen to angiotensin I (blocked by __)
|
aliskerin
|
|
|
Angiotensin converting enzyme converts angiotensin I to angiotensin II (blocked by __ such as __)
|
ACE inhibitors
lisinopril |
|
|
Angiotensin II acts on __ (blocked by receptor antagonists such as __)
|
AT1 Receptors
losartan |
|
|
Six types of drugs used to treat CHF:
|
cardiac inotropes
diuretics balanced vasodilators (ACE inhibitors) aldosterone receptor antagonist (Spironolactone) ß blockers venodilators |
|
|
What type of mesoderm does the heart develop from?
|
splanchnic mesoderm
it develops rostral to the nervous system and it is the folding of the embryo that brings the heart in to the thorax |
|
|
Why is pain from the heart referred to the neck, arm, mandible, and ear?
|
visceral sensory nerve fibers run with the sympathetic nerves because there are neural crest cells that migrate into the outflow tract
(cardiopulmonary splanchnic nerves) |
|
|
Which of the following structures is NOT derived from neural crest ectoderm?
Adrenal medullary cells Cardiac muscle cells Celiac ganglion Cranial and dorsal root ganglion cells Melanocytes Smooth muscle cells of the aortico-pulmonary trunk Superior cervical ganglion |
cardiac muscle cells
|
|
|
What are the three venous systems in the developing embryo and what do they supply?
|
Vitelline veins - portal system, drain GI
Umbilical - drain placenta Cardinal - form the caval system (cardinal and caval start with C) |
|
|
Which of the following vessels is derived from the embryonic cardinal veins?
Azygous vein Gastro-omental veins Inferior mesenteric vein Sigmoid veins Splenic vein Superior rectal vein |
Azygous vein
(the cardinal veins form the caval system) |
|
|
What are the five components of the developing heart tube?
|
sinus venosus (vitelline, umbilical, and cardinal veins drain here)
primitive atrium primitive ventricle bulbus cordis truncus arteriosus the blood then flows into the aortic sac |
|
|
Blood returning to the developing heart from the developing gastrointestinal tract enters the:
Bulbus cordis Primitive atrium Primitive ventricle Sinus venosus Truncus arteriosus |
sinus venosus
|
|
|
As the heart tube develops, what direction does it bend?
If it bends the other way, what happens? |
to the right
and the sinus venosus, on the bottom, goes posteriorly if the heart tube bends to the left, the person will develop dextrocardia (with or without situs inversus) |
|
|
When the endocardial cushions fuse, what new structures do they form?
|
they grow out from the AV walls, fuse in the midline, and form the separation between the primitive ventricles and the primitive atria
In addition to dividing the AV canal into right and left channels, the endocardial cushions contribute to the tricuspid and mitral valves, the membranous portion of the interventricular septum, and the closure of the primary atrial septum. |
|
|
The endocardial cushions contribute to the development of all of the following heart structures EXCEPT the:
foramen ovale interatrial septum interventricular septum mitral valve tricuspid valve |
foramen ovale
|
|
|
What are the steps in the formation of the division of the primitive atrium?
|
before the primary septum fuses with the endocardial cushions and closes the primary foramen, a breakdown of the primary septum begins which forms the secondary foramen. the primary foramen then closes, and the secondary septum forms to the right of the primary septum. the secondary septum forms the foramen ovale, and the primary septum serves as a valve flap to close the foramen ovale after birth.
|
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|
Which of the following structures contributes to the formation of the secondary foramen?
Endocardial cushion Interventricular septum Primary septum Secondary septum Sinus venosus |
primary septum
|
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|
What happens in the fetal heart during partitioning of the bulbus cordis and truncus arteriosus?
|
the bulbar and truncal ridge tissue (from neural crest mesenchyme), which forms the aorticopulmonary septum, spirals and divides the bulbus cordis and truncus arteriosus into an asecnding aorta and pulmonary trunk
this results in the aorta taking origin from the left ventricle and the pulmonary trunk coming from the right ventricle |
|
|
The bulbar and truncal ridges are derived primarily from:
endocardial cushions neural crest mesenchyme sinus venosus somatic mesoderm splanchnic mesoderm |
neural crest mesenchyme
|
|
|
The aorticopulmonary septum is derived from the:
bulbar and truncal ridges endocardial cushions interatrial septum interventricular septum myoblasts |
bulbar and truncal ridges
|
|
|
What structures form the division of the primitive ventricles, and what are these structures formed by?
|
the muscular portion (bottom) is derived from myoblasts
the membranous portion (top) is formed by the endocardial cushions and their fusion with the aorticopulmonary septum |
|
|
Which of the following does NOT contribute to the formation of the interventricular septum?
Aorticopulmonary septum Bulbar ridges Endocardial cushions Myoblasts. Primary interatrial septum |
primary interatrial septum
|
|
|
Which arch forms the proximal part of the left pulmonary artery?
|
the left 6th aortic arch, proximal portion
(it is the left 6th aortic arch, distal portion, that forms the ductus arteriosus) |
|
|
What does the distal portion of the right 6th aortic arch form?
|
nothing - it degenerates
(it is the left 6th aortic arch, distal portion, that forms the ductus arteriosus) |
|
|
Which arch forms the proximal part of the right pulmonary artery?
|
the right 6th aortic arch, proximal part
|
|
|
Which aortic arch forms the ductus arteriosus?
|
the left 6th aortic arch, distal portion
|
|
|
What happens to the ductus arteriosus after birth?
|
its muscular walls constrict within 24-48 hours, and within a month it is just a fibrous ligament called the ligamentum arteriosum
|
|
|
The right 4th aortic arch contributes to the formation of the:
aortic arch aorticopulmonary septum ductus arteriosus primary interatrial septum subclavian artery |
subclavian artery
|
|
|
Which arch contributes to the aortic arch, and which contributes to the right subclavian artery?
|
left 4th aortic arch
right 4th aortic arch |
|
|
Where does the ductus venosus shunt blood?
|
from the left umbilical vein directly through the liver and into the IVC
|
|
|
Why do physicians give ibuprofen to babies whose ductus arterioses remain patent for longer than normal?
|
closure of the ductus arteriosus is mediated by bradykinin and prostaglandins - these vasodilate - if you can block them, you block vasodilation
|
|
|
Which of the following give rise to the ligamentum arteriosum?
Aortic sac Left 4th aortic arch Left 6th aortic arch Right 4th aortic arch Right 6th aortic arch |
left 6th aortic arch
|
|
|
Which of the following is responsible for the formation of the medial umbilical ligaments?
Inferior epigastric arteries Superior vesical arteries Umbilical arteries Umbilical vein Urachus |
umbilical arteries
|
|
|
Which of the following is responsible for the formation of the ligamentum teres (round ligament of the liver)?
Inferior epigastric arteries Superior vesical arteries Umbilical arteries Umbilical vein Urachus |
umbilical vein
|
|
|
Congenital heart disease (CHD) is the most common cardiac condition in childhood. Which of the following answers or statements reflects the most frequent cause of CHD?
Chemical agents Chromosome defects Fetal distress Gene defects Maternal medications Rubella virus Unknown causes |
90% are unknown causes
9% are genetic 1% environmental |
|
|
What types of defects cause a left to right shunt (late cyanosis)?
|
atrial septal defect
ventricular septal defect patent ductus arteriosus |
|
|
What types of defects cause a right to left shunt (early cyanosis)?
|
tetralogy of Fallot
transposition of the great arteries (TGA) truncus arteriosus (presistent) |
|
|
What are 90% of the atrial septal defects caused by?
|
malformed (patent) foramen ovale
either excessive resorption of the primary septum or hypoplastic growth of the secondary septum, or both other 10% is from inadequate devt of primary septum (never reached endocardial cushion) and a high atrial septal defect from a sinus venosus defect |
|
|
What is the most common form of congenital heart disease?
|
interventricular septal defect (acyanotic L to R shunt)
90% of them involve the membranous portion 50% of them close spontaneously in kids |
|
|
Ventricular septal defects (VSDs) account for 40% of congenital heart defects. Which of the following is responsible for most forms of VSDs?
Abnormal formation of the endocardial cushions and aorticopulmonary septum Absence of the primary interatrial septum Atrophy of cardiac myoblasts Failure of the muscular septum to form Sinus venosus defect |
abnormal formation of the endocardial cushions and aorticopulmonary septum (membranous part of septum)
|
|
|
What are some consequences of maternal rubella during early pregnancy?
|
congenital heart defects (patent ductus arteriosus, pulmonary stenosis, ventricular septal defect), congenital cataracts, deafness
|
|
|
Which heart defect makes a machinery-like murmur?
|
patent ductus arteriosus (L to R acyanotic)
|
|
|
After birth, the ductus arteriosus usually closes. If the ductus remains patent, what clinical sign or symptom is most diagnostic of a patent ductus?
Congenital cataracts Cyanosis Deafness Infective endocarditis Machinery-like murmur Pulmonary hypertension |
machinery-like murmur
|
|
|
What are the four components of the Tetralogy of Fallot?
|
ventricular septal defect
pulmonary stenosis overriding (large) aorta right ventricular hypertrophy |
|
|
Which of the developmental consequences of the tetralogy of Fallot would be the last to occur?
Overriding aorta Pulmonary stenosis Right ventricular hypertrophy Ventricular septal defect |
right ventricular hypertrophy
|
|
|
Which of the following clinical signs would be most obvious on examination of a patient with tetralogy of Fallot?
Cyanosis Diffuse red rash Lack of a femoral pulse Pulmonary hypertension Sweaty palms |
cyanosis
|
|
|
What causes transposition of the great arteries?
|
failure of the normal spiraling of the aorticopulmonary septum
as a result, the aorta originates from the right ventricle and the pulmonary artery from the left ventricle |
|
|
Which of the following does not involve the bulbar and truncal ridges?
Atrial septal defect Common or persistent truncus Tetralogy of Fallot Transposition of the great arteries (TGA) |
atrial septal defect
|
|
|
A 13-year-old boy on physical examination reveals no femoral pulses, increased blood pressure in the upper extremities, and enlarged intercostal vessels. Which of the following abnormalities would be suspected?
Atrial septal defect Patent ductus arteriosus Postductal coarctation of the aorta Tetralogy of Fallot Transposition of the great arteries (TGA) Ventricular septal defect |
postductal coarctation of the aorta
|
|
|
Which of the following congenital defects would NOT be associated with “blue babies”?
Patent ductus arteriosus Tetralogy of Fallot Transposition of great vessels Truncus arteriosus (persistent or common trunk) |
Patent ductus arteriosus
|
|
|
Which of the following clinical signs and symptoms would NOT likely be present or occur with a postductal coarctation of the aorta?
Cyanosis in the toes Cyanosis shortly after birth Diminished and delayed femoral pulse Harsh systolic ejection murmur between the shoulder blades Higher blood pressure in the upper extremity than in the lower extremity Reduced dorsalis pedis pulse |
Cyanosis shortly after birth
|
|
|
What medication should NOT be given with diastolic dysfunction?
beta-blocker ACE inhibitor furosemide digoxin all can be used |
furosemide
|
|
|
Hepatomegaly can be a sign of:
acute pulmonary edema LAD occlusion right heart failure too much furosemide |
right heart failure
|
|
|
Enalopril is:
a preload reducer an inotropic agent a chronotropic agent an afterload reducer |
afterload reducer
|
|
|
What is the difference between pulmonary congestion and pulmonary edema?
|
pulmonary congestion is edema of the alveolar wall, which impairs gas exchange
pulmonary edema (more advanced that congestion) is fluid in the alveolar space, which replaces the air |
|
|
What is paroxysmal nocturnal dyspnea?
|
awakening with shortness of breath
cough with foamy sputum: alveolar fluid mixed with air brought up by mucociliary flow seen in left ventricular failure |
|
|
What is hemoptysis?
|
ruptured pulmonary capillaries mixes blood with alveolar fluid
you might cough up blood seen in left ventricular failure |
|
|
What would you see on an x-ray of someone in left ventricular failure?
|
diffuse haziness, scattered blotchy white areas with poorly defined edges, pleural effusion, incr pulmonary vasculature, enlarged L atrium
|
|
|
What is BNP and what does it do?
|
B-type (brain) natriuretic peptide
it enhances sodium excretion, which makes you excrete water made in ventricles, responds to volume and pressure overload, synthesized rapidly, good predictor of heart failure (>100 pg/L) |
|
|
What is cor pulmonale?
|
pulmonary disease that obliterates pulmonary capillary bed (like TB or emphysema)
it causes right ventricular failure |
|
|
If a patient had a distended liver or what is called "nutmeg liver", what is their primary disease?
|
right ventricular failure
nutmeg liver is due to atrophy of hepatic cells in center of lobule due to chronic passive congestion of the liver |
|
|
What is orthopnea?
|
dyspnea when supine
could be due to CHF, asthma, COPD |
|
|
What is trepopnea?
|
dyspnea when lying on the side
could be from CHF |
|
|
What is the definition of congestive heart failure?
|
a syndrome of dyspnea on exertion, edema of the lungs or extremities, and fluid retention resulting from cardiac dysfunction
|
|
|
What type of CHF would these conditions cause?
mitral stenosis, primary pulmonary hypertension, multiple pulmonary emboli, pulmonary valve stenosis, RV infarction |
right ventricular failure
|
|
|
Abdominal fullness, hepatomegaly, ascites, and leg edema are symptoms of what type of heart failure?
|
right sided ventricular failure
|
|
|
What are the chest x-ray findings in heart failure?
|
Cardiomegaly, pulmonary venous congestion, pleural effusions
|
|
|
What are some of the drugs that improve survival in CHF patients?
|
spironolactone (aldosterone antagonist)
carvedilol (decr catecholamines, selective B blocker) losartan (angio II receptor blocker) captopril, enalapril (ACE inhibitors) digoxin |
|
|
What are some of the drugs for CHF that do not increase survival?
|
diuretics (furosemide)
vasodilators (isosorbide dinitrate, nitroglycerine) |
|
|
What drugs are contraindicated in diastolic dysfunction?
|
diuretics and vasodilators
(patients do not tolerate a decrease in plasma volume or BP) |
|
|
What are the four characteristics you use to describe a heart murmur?
|
grade (1-6)
systolic vs. diastolic where heard best? (base or apex) does it radiate (carotids or axilla) |
|
|
What are the important characteristics of aortic stenosis?
|
Angina, syncope, dyspnea on exertion, early to mid-systolic, heard best over the base and tends to radiate to carotids
|
|
|
What are the characteristics of a mitral insufficiency?
|
Holosystolic, heard best at the apex and radiates to axilla
Pulmonary edema, acute shortness of breath, severe fatigue, atrial fibrillation |
|
|
What type of murmur is this?
Low pitched rumble Opening snap precedes murmur First heart sound accentuated Person presents with dyspnea with exertion and cough, hemoptysis |
mitral stenosis
|
|
|
What are the characteristics of an aortic insufficiency?
|
High pitched diastolic murmur heard best at base, may be asymptomatic for years or trauma may cause it, person might have exertional dyspnea first followed by orthopnea, PND, and diaphoresis, angina, and CHF
|
|
|
What are the characteristics of mitral valve prolapse?
|
Click-murmur syndrome (mid or late systolic click, followed by high pitched late systolic murmur), very common, mostly need to reassure people, or could do abx prophylaxis for dental procedures
|
|
|
What are the three types of arteriosclerosis?
|
atherosclerosis - inflammation of the intima, most important
Monckeberg's medical calcific sclerosis - on the outside, no ischemia or pathology arteriolosclerosis - due to HTN or diabetes, on small peripheral arteries |
|
|
What layer and what type of vessel does atherosclerosis affect?
|
the intima, in elastic (large) and medium sized muscular arteries
|
|
|
What are non-modifiable risk factors for atherosclerosis?
|
age
male gender family history genetic abnormalities |
|
|
What are modifiable risk factors for atherosclerosis?
|
hyperlimidemia
hypertension cigarette smoking diabetes |
|
|
What are some risk factors for atherosclerosis that are unlikely to be controllable but could be?
|
obesity
physical inactivity stress (type A personality) hyperhomocysteinemia post-menopausal estrogen reduction in women infx by Chlamydia pneumoniae |
|
|
What is a non-pharmacologic way to increase HDLs?
|
exercise
also, alcohol in moderation |
|
|
What is Type IV atherosclerosis?
|
atheroma - has a core of extracellular lipid
fat: foam cells, cholesterol crystals inflam cells: lymphs, macs necrosis, fibrosis, calcification, smooth muscle cells NEVER NEUTROPHILS! |
|
|
What is Type V atherosclerosis?
|
fibroatheroma - has a lipid core/fibrous layer (sometimes multiple), or mainly fibrotic or calcific
|
|
|
What is Type VI atherosclerosis?
|
complicated lesion - has a superimposed thrombus, a surface defect (due to atheroembolism, i.e. loss of part of the plaque), hemorrhage and/or calcification
|
|
|
What are some complications of atheromatous plaque?
|
luminal stenosis
ulceration, thrombosis, atheroembolism hemorrhage into a plaque wall weakening - aneurysm formation calcification - makes plaque brittle |
|
|
What are the three types of angina?
|
stable - >75% narrowed coronary artery, no myocardial necrosis
unstable - narrowed artery develops a mural, non-occlusive thrombus prinzmetal angina - vasospasm |
|
|
Where would an obstruction of the LAD (left anterior descending) lead to infarction?
|
anterior LV, apex, anterior 2/3 of interventricular septum
|
|
|
Where would an obstruction of the circumflex (from left coronary artery) artery lead to infarction?
|
small portion of lateral left ventricle
|
|
|
Where would an obstruction of the RCA (right coronary artery) lead to an infarction?
|
posterior LV wall, posterior 1/3 of interventricular septum
|
|
|
What is the timeline for macroscopic dating of an MI?
|
normal for 4-8 hours
8 hours: pale, edematous 36 hours: yellow with red edge 1 week: slight shrinkage 3 weeks: thinning 6-8 weeks: scarring 3 months: dense scar |
|
|
What type of necrosis comes from myocardial ischemia?
|
coagulation necrosis
contraction band necrosis or myocytolytic necrosis (due to partial ischemia or catecholamine excess) |
|
|
What is the timeline for microscopic dating of an MI?
|
4-12 hrs: beginning coagulative necrosis, edema
12-24 hrs: nuclear pyknosis, increased eosinophilia, CBs at edge, neutrophils at edge. 1-3 days: lost cross striations, nuclei. Neutrophils in center. 3-7 days: myocytes lost, neutrophils vanish, histiocytes appear. 7-10 days: advanced phagocytosis, early granulation tissue. 10-14 days: advanced granulation tissue. > 2 months: dense scar. |
|
|
What is the most common cause of death in the USA among individuals over the age of 45?
|
complications of atherosclerosis
(MI is about 25% of all deaths) |
|
|
What is the hypothesized mechanism of atherosclerotic plaque formation?
|
Platelets and monocytes adhere to injured sites, monocytes migrate into the intima. PDGF released from platelets attracts smooth muscle cells. Foam cells are derived from monocytes and smooth muscle cells. Extracellular lipid is derived both from death of foam cells and influx of serum cholesterol. The typical plaque thus has a soft base and a fibrous cap. Risk factors may have an additive effect.
|
|
|
female, 77 y/o, incompetent valve is likely to be:
acute infective endocarditis calcific aortic stenosis myxomatous degeneration of mitral valve mitral annular calcification rheumatic mitral stenosis |
mitral annular calcification
|
|
|
A patient with cancer of the left lung might present with all of the following symptoms except:
A.Hoarseness B. Dyspnea (shortness of breath) C. Hemoptysis (coughing blood) D. Leg swelling |
D. Leg swelling
|
|
|
Tension pneumothorax:
A. Is life-threatening. B. can be easily treated with a chest tube. C. Causes low blood pressure from pressure upon the heart. D. all of the above |
D. All of the above
|
|
|
What are the two set-point raising influences during physical exercise?
|
central command, which acts on the neural portion of the arterial baroreceptor system to incr mean arterial pressure
second set-point raising influence is from chemoreceptors and mechanoreceptors in the active skeletal muscles, which also incr sympathetic activity and mean arterial pressure |
|
|
What is one of the major primary disturbances during dynamic exercise?
|
the great decrease in TPR caused by vasodilator accumulation (but the arterial baroreceptor reflex still increases the sympathetics to increase mean arterial pressure)
|
|
|
What happens to cutaneous blood flow during exercise and why is this contradictory?
|
cutaneous blood flow increases during exercise despite an increase in sympathetic constriction because thermal reflexes can override pressure reflexes in the special case of skin blood flow control
|
|
|
Often cutaneous blood flow __ at the onset of exercise and then __ later during exercise as __.
|
decreases (bc of sympathetic constrictor activity)
increases body heat and temperature build up |
|
|
What are the two pumps that contribute to the cardiovascular response in dynamic exercise?
|
skeletal muscle pump from the legs
respiratory pump, which also promotes venous return during exercise |
|
|
How does the cardiovascular response to static exercise (isometric) differ from the response to dynamic exercise?
|
static exercise causes a compression of the vessels and a reduction in the blood flow, so TPR usually does not fall and may even increase
static exercise produces less of an increase in HR and CO and more of an incr in diastolic, systolic, and Pa than does dynamic exercise because of the higher afterload on the heart during static exercise, cardiac work is significantly higher than during dynamic exercise |
|
|
What are some cardiovascular alterations associated with conditioning?
|
incr in circulating blood volume, decr in HR, incr in SV, decr in arterial BP at rest
so during exercise, a trained person will be able to achieve a given workload and CO at a lower HR and higher SV |
|
|
Ventricular chamber enlargement often accompanies __ exercise whereas increases in myocardial mass and ventricular wall thickness are more pronounced with __.
|
dynamic exercise (endurance training)
static exercise (strength training) |
|
|
What is the normal resting HR and BP of a neonate? of a one-year-old?
|
neonate: 140 bpm, 60/35 mmHg
one-year-old: 120 bpm, 100/65 mmHg |
|
|
What are some of the age-dependent changes that occur in the heart?
|
decr in resting and max cardiac index
decr in max HR incr in contraction and relaxation time of the heart muscle incr in myocardial stiffness during diastole decr in number of functioning myocytes accumulation of pigment in myocardial cells |
|
|
What two things cause age-dependent increases in mean arterial pressure and pulse pressure?
|
decrease in arterial compliance
increase in TPR |
|
|
Why are arterial baroreceptor-induced responses to changes in BP blunted with age?
|
decr in afferent inputs because of an increase in arterial rigidity
and the total amount of NE contained in the sympathetic nerve endings of the myocardium decreases with age |
|
|
What are some of the protective effects of estrogen on the female heart?
|
lower arterial BP
greater aortic compliance improved ability to induce vasodilatory mechanisms these result in a lower cardiac afterload and lead to a lower left ventricular mass to body mass ratio |
|
|
What are the gender differences in cardiac electrical properties?
|
women have lower intrinsic HR and longer QT interval than men
they are at a greater risk of long-QT syndrome and torsades women are also twice as likely to have AV nodal re-entry tachycardias |
|
|
What is cardiogenic shock?
|
severely depressed myocardial functional ability
occurs whenever cardiac pumping ability is compromised (severe arrhythmia, abrupt valve disfunction, coronary occlusion, MI) |
|
|
What is hypovolemic shock?
|
accompanies hemorrhage (usually >20% blood volume), severe burns, diarrhea, vomiting - deplete body fluids and thus blood volume
a PE may evoke a shock that looks like hypovolemic shock (in that LV filling is compromised) |
|
|
What is anaphylactic shock?
|
severe allergic reaction, called an immediate hypersensitivity rxn
mediated by mechanisms (histamine, PGs, leukotrienes, bradykinin) that result in substantial peripheral vasodilation and increases microvascular permeability |
|
|
What is septic shock?
|
caused by vasodilator effects of infective agents, such as endotoxin, an LPS released from bacteria
these substances induce formation of nitric oxide synthase (called inducible NOS) which make large amounts of NO and vasodilate |
|
|
What is neurogenic shock?
|
produced by loss of vascular tone due to inhibition of the normal tonic activity of the sympathetic vasoconstrictor nerves
can occur with deep general anesthesia, reflex response to deep pain, or vasovagal syncope (mild form) |
|
|
What are some of the responses (compensatory mechanisms) to being in a shock state?
|
most look like what your body would do if it saw a drop in BP
greatly increased sympathetic activity (looks like pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction) the person might also be dizzy, confused, or lose consciousness additional compensatory mechanisms cause autotransfusion |
|
|
What are the compensatory mechanisms in shock that lead to "autotransfusion" of up to 1L of fluid?
|
breathing is rapid and shallow
release of renin (promotes angio2, which is a constrictor) - incr TPR adrenal medulla increases levels of epinephrine arteriolar constriction causes reduced capillary hydrostatic pressure, which causes a net shift of fluid into the vascular space glycogenolysis induced by NE and epi results in a release of glucose and a rise in extracellular osmolarity (via blood and interstital levels), which helps shift fluid from cellular space into extracellular (and intravascular) space |
|
|
Why do victims in hemorrhagic shock have a reduction in hematocrit?
|
there are several compensatory mechanisms in shock that lead to autotransfusion, which gets more fluid but not more blood cells into the blood
|
|
|
Which of the following would be helpful to hemorrhagic shock victims?
a. keep them on their feet b. warm them up c. give them fluids to drink d. maintain their BP with catecholamine-type drugs |
a. not helpful
b. not helpful if carried to extreme (cutaneous vasodilation adds to CV distress) c. helpful since fluid will rapidly be absorbed rapidly and incr circulating blood volume d. might be helpful as an initial emergency measure to prevent brain damage, but prolonged tx will promote the decompensatory mechanisms assoc with decr blood flow |
|
|
What happens to hematocrit during hypovolemic shock resulting from prolonged diarrhea?
|
increase - even though the compensatory response is autoransfusion, this amount of fluid is limited to 1L or less, so a substantial loss of fluid will raise hematocrit substantially
|
|
|
What happens to hematocrit during acute cardiogenic shock?
|
it may decrease because compensatory actions evoked may promote a fluid shift into the vascular space
however, wince CVP may also be elevated, cap hydrostatic pressures (and thus fluid shifts) are difficult to predict |
|
|
What happens to hematocrit during septic shock?
|
peripheral vasodilation may actually promote filtration of fluid (which would lead to incr hematocrit) but the low arterial and CVP may counteract the shift, so changes in hematocrit are difficult to predict
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What happens to hematocrit with chronic bleeding?
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chronic bleeding disorders are usually associated with low hematocrit and anemia bc RBC production may not keep pace with RBC loss whereas volume regulating mechanisms may be able to maintain a normal blood volume
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T/F
LV chamber enlargement with CHF increases the wall tension required to generate a given systolic pressure. |
true
the law of Laplace says that when the radius of a cylinder increases, the wall tension for a given internal pressure must also increase T = P x r |
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Why are diuretic drugs often helpful in treating pts in CHF?
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excessive fluid retention can induce decompensatory mechanisms that further compromise an already weakened heart
diuretic tx reduces fluid volume and the high venous pressures that are the cause of these problems (inadequate oxygenation of blood in lungs, cardiac dilation and incr metabolic needs, liver dysfunction due to congestion) |
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What is the potential danger of vigorous diuretic tx for a pt in CHF?
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if blood volume and CVP are reduced too far with diuretic tx, CO may fall to unacceptably low levels through the Frank-Starling law of the heart
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Why does renal artery stenosis produce HTN?
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bc of high resistance of the stenosis and pressure drop across it, flomerular capillary pressure and therefore GFR are lower than normal when arterial pressure is normal
a renal artery stenosis reduces urinary output caused by a given level of arterial pressure the renal fx curve is shifted to the right, and HTN follows |
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What are three potent vasoconstrictors that are released in shock?
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angiotensin 2
epinephrine ADH (vasopressin) – released whenever there is a signal to brain that the blood volume is low |
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Mitral valve prolapse
Infective endocarditis Noninfective endocarditis Mitral valve annular calcification Carcinoid syndrome/ pharmacologic agents Acute Rheumatic heart disease All of the above conditions can result in what type of valvular abnormality? |
an insufficiency
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What causes 99% of the cases of stenosis?
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chronic rheumatic heart disease (which fuses the free edges)
it can also be caused by a calcific aortic valve (senile or congenital) |
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What is the most common acquired valve abnormality in developed countries?
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Calcific aortic valve stenosis (Senile Type)
calcific nodules most prominent on aortic aspect and at base of valve cusps usually occurs in pts age 70-80-90, unlike congenital type which usually occurs in pts age 50-60 |
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What is a raphe in cardiovascular abnormalities?
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Fibrous attachment between cusp and aortic wall - site of incomplete separation
Inserts lower than commissures Seen sometimes in stenotic valves, esp congenitally bicuspid aortic valves (which are supposed to be tricuspid) |
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Which layers of the heart does acute rheumatic fever affect?
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Endocardium, myocardium, epicardium and cardiac valves = pancarditis
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In what disease are Aschoff bodies (fibrinoid necrosis surrounded by lymphocytes, plasma cells, and macrophages) and Anitschkow cells (caterpillar cells = macrophage with wavy nucleus) found?
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rheumatic fever heart disease
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What types of organisms cause infective endocarditis?
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staph aureus
strep viridans staph epidermitis HACEK oral flora (haemophilus, actinobacillus, cardiobacterum, eikenella, kingella) also fungi - aspergillus and candida |
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What are some clinical signs of infective endocarditis?
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fever, malaise, weight loss, flu-like symptoms
petechiae, subungal hemorrhages (splinter), and Roth spots in the eyes due to embolic disease |
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What are the 4 pathologic lesions that may cause thickened, hardened arteries (arteriosclerosis)?
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senile (presentile) arteriolosclerosis
Monckeberg's sclerosis (medial calcification) hypertensive arteriolosclerosis atherosclerosis - the most important |
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What are some of the changes associated with senile arteriolosclerosis?
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intimal thickening (due to fibrosis)
medial muscle decreases collagen increases the internal elastic lamina becomes reduplicated and may develop gaps |
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What are some of the characteristics of Monckeberg's sclerosis?
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dystrophic calcification affected the medial layer (called medial calcific sclerosis)
does NOT produce ischemia because it doesn't involve the intima is age related |
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What are the two types of hypertensive ateriolosclerosis?
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hyaline arteriolosclerosis
hyperplastic arteriolosclerosis |
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What is the difference between hyaline arteriolosclerosis and hyperplastic arteriolosclerosis?
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hyaline is due to mild/moderate HTN and benign nephrosclerosis, arterioles show hyaline thickening induced by HTN or diabetes, leakage of plasma components
hyperplastic is caused by malignant HTN and malignant nephrosclerosis, small arteries show "onion skin" appearance or fibrinoid necrosis, may cause micro infarcts |
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What are the 4 pathologic lesions that may cause thickened, hardened arteries (arteriosclerosis)?
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senile (presentile) arteriolosclerosis
Monckeberg's sclerosis (medial calcification) hypertensive arteriolosclerosis atherosclerosis - the most important |
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What are some of the changes associated with senile arteriolosclerosis?
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intimal thickening (due to fibrosis)
medial muscle decreases collagen increases the internal elastic lamina becomes reduplicated and may develop gaps |
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What are some of the characteristics of Monckeberg's sclerosis?
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dystrophic calcification affected the medial layer (called medial calcific sclerosis)
does NOT produce ischemia because it doesn't involve the intima is age related |
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What are the two types of hypertensive ateriolosclerosis?
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hyaline arteriolosclerosis
hyperplastic arteriolosclerosis |
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What is the difference between hyaline arteriolosclerosis and hyperplastic arteriolosclerosis?
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hyaline is due to mild/moderate HTN and benign nephrosclerosis, arterioles show hyaline thickening induced by HTN or diabetes, leakage of plasma components
hyperplastic is caused by malignant HTN and malignant nephrosclerosis, small arteries show "onion skin" appearance or fibrinoid necrosis, may cause micro infarcts |
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What are the two ways you can classify an aneurysm?
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nature of the aneurysm (true or false)
shape (fusiform, saccular, dissecting, micro-aneurysm) |
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What is a false aneurysm?
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an aneurysm that is a pulsating (evacuated) peripherally organized hematoma - there is no remnant of the original artery in its wall (this would be a true aneurysm)
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What are three types of saccular aneurysms (in which only a portion of the circumference is weakened and connected by an ostium)?
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saccular aneurysm due to cystic medionecrosis - the commonest cause, associated with aging and HTN, also with Marfan syndrome
syphilitic aneurysm - usually at the proximal aorta because it targets vasa vasorum, it never leads to a dissecting aneurysm due to medial scarring Berry aneurysm in the circle of Willis - occurs at branch points, HTN facilitates devt, leads to SAH |
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What is the danger in even mild shock situations of not foregoing decompensatory mechanisms (when reduced arterial pressure leads to alterations that further reduce arterial pressure rather than correct it)?
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permanent renal or hepatic ischemic damage
often pts who have apparently recovered from shock die several days later because of renal failure and uremia |
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What is the definition of hypertension?
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persistent elevation of the systolic and diastolic blood pressure in the systemic arteries
140/90 mmHg isolated systolic HTN in the elderly is >160 mmHg systolic with diastolic less than 90 mmHg |
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What are the known causes of hypertension?
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primary HTN (93% of HTN) is idiopathic (though familial)
secondary is due to renal causes, endocrine causes, CV causes, neurologic causes, or can be drug induced |
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What are the types of renal parenchymal disease that lead to secondary HTN?
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glomerulonephritis (acute or chronic) - small vessel disease, finely granular kidney
chronic pyelonephritis - coarse scars polycystic renal disease - autosomal dominant, adult onset |
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What are some of the drugs that lead to drug induced HTN?
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birth control pill, cortisol, NSAIDS, nasal decongestants, cyclosporin, glycyrrhizic acid in licorice
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What are some of the effects of long standing HTN?
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left ventricular hypertrophy, LV failure, thrombi in heart, MI, dissecting aneurysm in aorta, berry aneurysm in circle of Willis, atherosclerosis, brain infarcts, brain emboli or dissection, lung edema due to LV failure, lung infarcts, terminal bronchopneumonia
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What are the four types of idiopathic cardiomyopathy?
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dilated ("congestive") cardiomyopathy (90%)
hypertrophic (with or without obstruction) cardiomyopathy (9%) restrictive cardiomyopathy arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVCM) |
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What is the following disease?
50% familial, autosomal dominant, b-myosin heavy chain mutation, myocytes in architechtual disarray, can cause sudden death in teens, diastolic dysfunction |
hypertrophic cardiomyopathy (9% of CM)
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What is the following disease?
30% familial, autosomal dominant, dystrophin mutation, myocytes get longer but not wider, can be assoc with Duchenne's MD and Becker MD, systolic contraction impairment |
dilated cardiomyopathy (90% of CM)
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What are the mechanisms through which ACE inhibitors help a patient in congestive heart failure?
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by decreasing the amount of angio2, they vasodilate (thereby improving cardiac pumping by afterload reduction)
by decreasing angio2 and stopping the pathway, aldosterone levels are reduced (which promotes fluid loss) they also prevent some of the inappropriate myocite and collagen growth that occurs with cardiac overload and failure |
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What are some of the altered diastolic properties in diastolic dysfunction heart failure?
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delayed myocyte relaxation (slow Ca++ removal)
inadequate ATP (to disconnect myofilament cross bridges) residual cross-bridge cycling during diastole (leaky SR and left over Ca++) increased myofibrillar passive stiffness (alterations in titin) decrease cardiac tissue passive compliance (remodeling, collagen cross-linking) |
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What are the systolic and diastolic values known as prehypertension?
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120-139 systolic
80-89 diastolic (140/90 is hypertension) |
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What are some reasons for increased TPR in HTN?
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decrease in density of microvessels
structural adaptations in the peripheral vascular bed increased activity of the vascular smooth muscle cells incr sensitivity and reactivity of the vascular SMCs to external constrictor stimuli diminished production and/or effect of vasodilator substances (NO) |
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Woman runner collapses at 19 mile of a marathon. Diaphoretic, pale, confused. BP 75/30, Pulse 144. RR 26. What type of shock?
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hypovolemic shock
give fluid to treat and to also distinguish between cardiogenic and hypo |
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60 year old black female three days post-op from routine laproscopic cholecystectomy. Pale, +JVD, DBP 50/0, Pulse is thready - 120, RR; rapid, shallow - 27. What type of shock?
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extracardiac shock
JVD caused by extracardiac or cardiogenic, probably this is caused by PE, she was probably immobile for a few days post-op fluids won't help her. could try thrombolytics but this is a hail mary |
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40 y/o male, substernal pressure "I feel like I'm going to die," pale, diaphoretic, mottled skin, wet crackles, BP 70/36, pulse 145, RR 26. What type of shock?
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cardiogenic shock
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74 y/o female, flushed, warm skin, rapid HR, no JVD, lungs clear, no leg edema, BP 80/40, P 145, RR 24. What type of shock?
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distributive shock
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25 y/o male in a MVA, neck pain, numbness in legs and arms, chest pain, breath sounds are equal and shallow, BP 60/0, P 160, RR 30. What type of shock?
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hypovolemic shock
trauma. give him volume |
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30 y/o w DM, fever of 101, nausea and vomiting, hasn't been able to eat for a couple of days, skin: cool, poor turgor and cap refill, dry mucous membranes, BP 90/70, P 120, RR 28, T 100. What type of shock?
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hypovolemic shock
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How do you treat a patient who comes in with leg claudication?
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the most serious risks are complications of atherosclerosis, so get them to change their risk factors such as smoking, cholesterol, lower BP
then you should reassure them that the claudication doesn't injure them and that they should begin an exercise program |
