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47 Cards in this Set
- Front
- Back
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diastole |
heart is relaxed and filled with blood (dia = going apart, like dialysis) |
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systole |
heart contracts, (sympathetic ns also starts with sy = has to do with increased contractility) |
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stroke volume |
volume of blood with each beat |
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cardiac output |
amount of blood pumped per minute (heart rate X stroke volume) |
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blood pressure |
-the cardiac output X peripheral resistance |
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sympathetic effects on heart rate |
beta 1 = increase contractility of heart beta 2 = relaxation of smooth muscles around blood vessels to heart/muscles, and bronchioles (b for bronchiole!) alpha 1 receptors : vasoconstriction of most blood vessels (contraction of smooth muscles) |
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muscarinic receptors on heart rate and blood pressure |
decrease contractility and heart rate, increase vasodilation (note from before, increase bronchiole contraction) |
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where are muscarinic receptors located? in the vascular system |
In the endothelium of the blood vessels. this endothelium also called the intima. |
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How do muscarinic receptors work in the blood vessels? |
-they relax them -they cause synthesis of nitrous oxide that relaxes the muscles |
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what is the pathway involved in renin angiotensin aldosterone system? |
angiotensinogen -- (renin)---> angiotensin I angiotensin I --- (Angiotensin converting enzyme ACE)--------------------> Angiotensin II Angiotensin II stimulates aldosterone release from the adrenal gland, which causes Na and water retention |
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how is renin activated? |
Renin is activated in response to low blood pressure = the baroreceptor reflex -it is the limiting step, as ACE is always present in the body -it is produced in the kidney (renal vessels) |
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how does angiotensin II increase blood pressure? (3 mechanisms) |
1. converts angiotensin I to angiotensin II to stimulate aldosterone= water retention 2. acts on blood vessels to create vasoconstriction 3. breaks down bradykinin, a vasodilator (recall released in immune response) |
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where are baroreceptors present (not for pharm but good to know for neuro)? |
-the carotid sinus (vagus nerve) and the aortic arch (glossopharyngeal nerve) |
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how are baroreceptors activated? |
-they sense distention in the aortic arch -low BP activates an inhibitory neuron to the vasomotor centre (which usually has sympathetic outflow raising BP) -they activate renin in response to low blood pressure which converts angiotensinogen --> angiotensin I (and then angiotensin II --> aldosterone --> retain fluid in kidneys) |
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what's the difference between essential and secondary hypertension? |
Essential = causes are diffuse or unclear, stuff like diet, genes, stress secondary = a known specific medical cause like tumours, renal artery blockage |
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What are the symptoms of hypertension |
-none -but it can kill you ("silent killer") |
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how are diuretics useful with hypertension and what else are they used for? |
-increase Na and H2O secretion -useful in MILD hypertension, or in more severe cases used with other drugs -also used for congestive heart failure (makes it easier to pump blood if there's less of it) |
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what are the side effects of diuretics? |
-loss of K+ because it is secreted with Na+. Important to take supplements -loss of K+ may cause arrhythmia |
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what are the two types of diuretics? |
thiazide diuretics (stop sodium and Cl reabsorption of the distal tubule, for mild-moderate hypertension) -loop diuretics: (act on loop of henle, stop sodium and chloride reabsorption, for severe hypertension) |
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alpha 2 agonists (ie clonidine) |
-used to treat hypertension -inhibits sympathetic nervous system in the brain -side effects = sedation and orthostatic hypotension |
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adrenergic neuron blocking agents (reserpine) |
-blocks ability of vesicles to store Norepinephrine side effects = sedation, depression, postural hypotension (so essentially it blocks norepinephrine) -less preferred than ACE inhibitors |
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Beta receptor blockers (non selective: propranolol, selective = metoprolol) |
bind to beta receptors and block the ability of the ligand to bind B1 is the receptor that causes heart contractility, and the main one of interest -used for hypertension and angina |
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alpha adrenergic blockers |
-block alpha 1 receptors that cause contraction of vascular muscles = vasodilation -side effect of orthostatic hypotension |
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ACE inhibitors |
-used for hypertension and congestive heart failure -inhibit synthesis of angiotensin II by inhibiting angiotensin converting enzyme (ACE) -lower blood pressure and blood volume (because more water excreted from urine from aldosterone) -causes coughs, rashes, orthostatic hypotension, fetal abnormalities -takes a while to work |
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which drugs cause orthostatic hypotension? |
-ACE inhibitors (first dose), alpha adrenergic blockers, adrenergic neuron blockers, alpha 2 agonists, beta receptor blockers |
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angiotensin II receptor antagonists |
-blocks angiotensin II binding to receptors in the vascular smooth muscles -causes vasodilation -less potent but less side effects than ACE |
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calcium channel blockers (nifedipine, verapamil) |
-block calcium entry into smooth muscle cells, which relaxes arteries (decreased demands, more blood to heart) -block calcium entry into heart cells, which lowers contractility -used for angina, for hypertension, or for congestive heart failure |
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what are some OT precautions for vasodilators? |
-don't use heated modalities like whirlpool baths, will cause too much vasodilation and person could fall |
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beta blockers and exercise |
-they limit some exercise ability due to lowering heart contractility -unselective beta blockers may cause overheating ( you don't have to know that) |
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how to be careful of orthostatic hypotension |
-slow rising -ankle pumps (flexing and extending ankle before rising) -crossing one leg over the other when sitting before standing |
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cardiac drugs and fluid intake |
-get ppl to drink plenty of water as drugs increase fluid retention |
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reflex tachycardia |
-when heart rate rises as a result of lower bp -may happen in response to taking drugs, be aware of it |
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nitrates, ie nitroglycerin |
-turns into NO in the body (nitric oxide) -promotes cGMP that relaxes smooth muscles, especially in the veins -decreases blood pressure to treat hypertension -also used for angina and congestive heart failure |
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angina |
-chest pain when not enough oxygen gets into the heart -caused by atherosclerosis or vasospasm (constriction of arteries) -constriction of arteries = decreased oxygen and increased demand on the heart -pain caused by lactic acid build up -plaques caused by exertion and stress |
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How does the EKG change with angina? |
decreased ST (between ventricles contracting and atria relaxing) and T wave (atria relaxing) -arrhythmia |
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stable angina |
-plaque happens to narrow blood vessels formation: injury to endothelial layer, white blood cells enter and secrete factors that cause cells to proliferate -decreased oxygen supply to heart, and increased demands on heart from constriction |
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Unstable angina |
-there is already plaque -plaque ruptures (from stress, exercise) -clots form on the plaque = platelet buildup that makes it narrow more (clot is also called a thrombus) |
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variant angina |
-constricted blood vessels that aren't because of plaques -lack of oxygen supply |
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would you take nitrates (nitroglycerin) orally yes or no? why/why not? |
No, because the first pass metabolism takes up 90% of the drug. Tablets can be taken sublingually |
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how do cardiotonic drugs wok (ie digoxin) |
-increases contractility of the heart by inhibiting Na+/K+ pump -decreases excessive sympathetic stimulation -inhibits renin secretion (side action of Na+/K+ inhibition) -depresses AV node conduction (stops arrhythmia) -- does this by causing reflex stimulation of vagus nerve -decrease of PR (less electrical activity) |
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how does digoxin increase heart contractility? |
-inhibits the Na+/K+ ATPase pump -which increases the amount of Na in the cell (recall how usually there is mostly K+ in the cell) -increased calcium in the cell by Na-Ca exchange (to pump out Na +) -this causes calcium buildup in the heart muscle cells, which increases the strength of contraction (in contraction, intracellular Ca2+ activates Ca2+ release from the SR) |
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what's the net effect of digoxin changes on heart and vascular systems? |
-less arrhythmia (less electrical activity) -increased contractility of heart (from Na+/K+ pump inhibition) -decreased H2O retention (less renin) |
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side effects of digoxin |
-life threatening arrhythmias -anorexia, vomiting, visual disturbances, tachycardia (heart beating too fast), headache -important to be monitored (ie if person has liver troubles especially) |
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where is there edema when there is left side heart failure? |
-left atria/ventricles get blood from the lungs. Therefore fluid pools in the lungs. Causes difficulty breathing |
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where is edema when there is right side heart failure? |
the right heart gets blood from the vena cava/body systems. therefore there is ankle edema |
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what are the steps to norepinephrine transmission? |
1. tyrosine --> dopamine --> norepinephrine 2. packaged into vesicles 3. vesicles released when nerve fiber stimulated 4. norepinephrine binds to receptors and creates effects 5. reuptake |
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what are three mechanisms that terminate the effects of norepinephrine? |
1. uptake pump U1 brings NE back to neuron -then broken down by MAO in mitochondria 2. removing NE with uptake pump U2 in target cell, COMT (catechol-o-methyltransferase) degrades it 3. alpha 2 receptors in the presynaptic membrane inhibit further NE release |
