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Pharm401 Exam 2: Misc Stuff I came up with to study
Terms in this set (69)
low central venous pressure
gives poor filling and low cardiac output
high central venous pressure
gives good filling and high cardiac output
When BP falls, the SNS is turned on. What does the SNS do to try to correct the low BP?
1. Increases cardiac output (Beta 1)
2. Increases resistance at arterioles (Alpha 1)
3. The arteries that feed the kidney also have Alpha 1 receptors. Resistance at these arterioles --> reduced glomerular filtration ----> increased central venous pressure ---> more cardiac filling ----> increased stroke volume ----> increased cardiac output ----> increased BP
4. JG cells on kidney directly stimulated by SNS (Beta 1)
What 2 signals doe the JG cells get from the SNS?
1. reduction in flow
2. direct stimulation from Beta 1 receptors
What do the JG cells do when there is low SNS activity?
1. decreased renin release
2. vasodilation, high blood flow
What do the JG cells do when there is high SNS activity?
1. increased renin release
2. vasoconstriction, low blood flow
How does renin influence BP?
Renin catalyzes angiotensinogen to convert into angiotensin I. Then, ACE catalyzes angiotensin I to convert into angiotensin II. Then, angiotensin II stimulates the secretion of Aldosterone, which holds onto sodium, and water follows sodium, fluid volume increase and blood pressure increases.
What are the 4 Types of Antihypertensive Drugs?
1. Diuretics -- get rid of sodium, followed by water
2. Sympatholytic - cut off SNS activity
3. Direct acting vasodilators -- dilates blood vessels directly
4. Renin-angiotensin inhibitors -- block RAAS system.
What 2 drugs have side effect or rebound hypertension?
Remember that these two drugs have different mechanisms for causing rebound hypertension!
How can withdrawl from Clonodine cause rebound hypertension?
Clonidine is a Sympatholytic drug and an Alpha 2 Agonist. It's job is to "turn off/decrease" the SNS.
With clonidine use, there is some receptor loss in the cell membrane due to over-stimulation. When we take away clonidine, there are fewer receptors left, so the the body is less able to decrease the SNS when it needs to and so blood pressure can increase to even higher levels than before clonidine therapy was started.
Eventually, the body cells will repopulate the receptors, so the best thing to do is to taper clonidine dose and add another hypertensive drug.
How can withdrawl from Propranolol cause rebound hypertension?
Propranolol is a Beta Blocker (Adrenergic Antagonist).
It blocks Beta receptors on the heart to lower BP.
With propranolol use, the Beta receptors are blocked, so these receptors are less likely to be normally desensitized to norepinephrine, so they are very sensitive to norepinephrine when propranolol is discontinued and these receptors are no longer blocked. Since the receptors are so sensitive to norepinephrine, they will work to increase blood pressure to even higher levels than before propranolol therapy was started.
What are the 2 rates that affect the heart?
1. automaticity - the rate at which the heart beats
2. conduction velocity -- the rate at which the heartbeat travels across the cardiac tissue
What is Torsade de Pointes? Why is it a problem? For what 2 drugs is this a side effect?
The over-lengthening of the Q-T interval since the action potential is lengthened too much. This happens with drugs that are K+ channel blockers.
This condition can lead to life-threatening arrhythmias.
Drugs with this side effect:
Quinidine -- NA+ blocker that is also K+ blocker
Sotalol - K+ channel blocker
To remember these two drugs, think of the fact that "Q" and "S" are both located in the "Q-T" interval :-)
Why is Propranolol a good "combo drug" to use when treating hypertension and angina? For example, why would it be good to give Propranolol with a nitroglycerine?
Propranolol is a Beta Blocker, so it blocks all beta receptors. Remember that Beta receptors are located not only on the heart but also on the JG cells in the kidneys.
Beta Blockers do this:
1. Block SNS (Heart Beta receptors) from turning on to increase BP
2. Block Beta receptors on JG cells
Nitroglycerine is an angianginal agent that works by generating nitric oxide (NO), which relaxes smooth muscle and dilates blood vessels (including the great veins that feed the heart), so there is reduced preload, and a decrease in cardiac work. But, if you only give nitroglycerine, the resulting decreased BP will stimulate the JG cells on the kidneys to increase secretion of renin, which will catalyze conversion of angiotensinogen into angiotensin I, which will then convert into angiotensin II, which will stimulate increased vasoconstriction to increase BP. So, the body's own JG cells would counteract the effects of nitroglycerine.
However, if you give Propranolol too, since it is a Beta Blocker it will block the beta receptors on the JG cells so they will not be stimulated to increase renin secretion, so blood pressure will remain lower.
Remember that Propranolol has some side effects: Mainly Asthma but also can precipitate CHF!
What are the 3 shared side effects of the RAAS inhibiting drugs:
ACE Inhibitors (captopril), Angiotensin II Antagonists (losartan), and Renin Inhibitors (aliskiren)?
1. dry cough due to the inhibited destruction of bradykinin
2. renal failure due to interruption of homeostatic mechanism
3. Teratogen - should not be used during pregnancy due to severe fetal harm
In addition to the 3 shared side effects of the RAAS inhibiting drugs, what other side effects are specific to ACE Inhibitors (captopril)?
1. Angioedema (too much vasodilation = loss of airway possible)
2. first dose hypotension
3. hyperkalemia (too much K+)
In addition to the 3 shared side effects of the RAAS inhibiting drugs, what other side effect is specific to Angiotension II Antagonists (losartan)?
1. hyperkalemia (too much K+)
In addition to the the 3 shared side effects of the RAAS inhibiting drugs, what other side effect is specific to renin inhibitors (aliskiren)?
2. hyperkalemia is possible if DON'T have diarrhea side effect
Digoxin is a cardiac glycoside that is used to treat heart failure. How does it work to increase heart contractility?
Digoxin (cardiac glycosides) inhibits the Na-K pump. This pump normally acts to move Na out of the cell (up its concentration gradient) and K into the cell. There is another mechanism that allows Na back into the cell and "exchanges" Na for Ca, so Ca moves OUT of the cell. When Ca moves out, this decreases contractility. If we inhibit the Na-K pump, then Na builds up inside cell (since not being activity moved out), so other mechanism of Na-Ca exchange does not occur since Na will start leaving the cell there (down its gradient), so Ca will stay in cell and contractililty is maintained or increased.
By using Digoxin, you would have:
A. increased Calcium
B. Excretion of Sodium
C. Decrease release of Renin
D. Slow Repolarization
E. All of the above
F. None of the aove
E. All of the above
Digoxin acts to set of this series to reduce edema:
1. Na-K pump inhibited (slows down repolarization)
2. Calcium builds up in cell (lengthens Phase 4 and Phase ), so increases ventricle filling.
3. increases contractions
4. Increases BP
5. Decreases Renin
6. Decreases Angiotensin II
7. Decreases Aldosterone
8. Decreases Sodium (pee out sodium)
9. Decreases water (water follows, so digoxin has an INITIAL diuresis but is NOT a diuretic, so you would probably also use furosemide (thiazide) as diuretic with digoxin which can cause issues with lowering potassium level in body). Digoxin also decreases SNS activity (since increased cardiac output decreases SNS activity), which promotes urination as well.
10. Decreases edema
Which hypertension 2 drugs in particular tend to cause severe hypotension in first use?
1. Prazosin (Alpha 1 Antagonists)
2. Captopril (ACE Inhibitors)
Why is fluid retension a normal compensory part of lowering BP?
When BP drops, then the JG cells on the kidneys (which have Beta 1 receptors) sense the low BP and so stimulate the secretion of renin, which catalyzes angiotensinogen --> angiotensin I, then ACE catalyzes angiotensin I --> angiotensin II, which works on the renal medullla to secrete aldosterone, which holds onto sodium, and then water follows sodium, so fluid retention occurs.
What are Quinidine's side effects?
1. animuscarinic effects (bad)
2. afterpolarizations (caused by abnormal movemement of calcium) allow atrial arrhythmias to affect the ventricles due to effects at AV node.
3. Cinchonism (Tinitus)
4. Torsade de Points (long Q-T interval)
Which cardiac drugs need to be administered by IV? Why for each?
1. Lidocaine (first pass effect)
2. Nitroprusside (short half life)
Which antidysrrhythmic drug has a serious (often lethal over time) side effect of lung fibrosis (crystals left in the lungs)?
Which antidysrrhythmic drug should NOT be given to patients at severe risk of heart failure since this drug decreases heart contractility?
A deficiency in what electrolyte makes this Digoxin's side effects much worse?
Potassium (K+), since Digoxin competes with Potassium to inhibit the Sodium-Potassium pump. When there is less potassium (hyokalemia), then Digoxin does not have a lot of competition and can do a better job of inhibiting the Sodium-Potassium pump to such an extent that the heart actually stops working (digital toxicity).
What does activating heart Beta receptors do (drugs that are Beta Agonists)?
1. Increases CAMP
2. Increases Calcium
3. Increases myocardial contractility
What does blocking Alpha 1 receptors do (drugs that are Alpha Antagonists)?
1. Vessel dilation
2. Tissue perfusion (good!)
3. Decreases afterload (good since force of heart contraction will do more since less resistence to push through)
What heart failure drug is considered an Adrenergic Stimulant and acts both as a Beta Agonist and as an Alpha Antagonist? While this drug is good for heart failure treatment, what is it's big side effect?
side effect: tolerance, so it is usually only used once for extreme heart failure.
To remember this drug, think "D" for "dual acting", "B" for "beta agonist", and "A" for "alpha antagonist":
Which 2 cardiac drugs have serious first pass effects? Hint, you usually need to give these drugs by alternate means (IV, sublingual)
1. Nitroglycerin (give sublingual)
2. Lidocaine (give IV)
Which 2 cardiac drugs have the problem of tolerance as a side effect?
How do each of the following drug classes work to treat Angina?
2. Beta Blockers
3. Calcium Channel Blockers
Stable Angina: dilates VEINS (including great veins that fill the heart atria), so this decreases PRELOAD. Also decreases AFTERLOAD.
Variant Angina: increases oxygen supply by relaxing coronary vasospasms.
2. Beta Blockers
Stable Angina: decreases oxygen demand by decreasing heart rate and decreasing contractility. Decreases PRELOAD and AFTERLOAD.
Variant Angina: no effect
3. Calcium Channel Blockers
Stable Angina: decreases oxygen demand by dilating ARTERIES, decreasing heart rate, decreasing contractility, decreases AFTERLOAD (how much resistance the heart needs to pump through) also decreases PRELOAD.
Variant Angina: increases oxygen supply by relaxing coronary vasospasms.
How can you remember the difference between these two very similarly named drugs?:
1. Amiodarone -- "Ami" (think of name "Amy") gets along with everyone. So, she is a multi-class antiarrhythmic drug. We usually think of Amiodarone as Class III (K+channel blocker), but it also has properties of Class I, IV.
2. Amrinone -- "Amri" rhymes with "PDE". Amrinone is a PDE Inhibitor used to treat heart failure.
What antihypertensive drugs act on sympathetic nervous system (Sympatholics)?
What antihypertensive drugs act on blood vessels (vasodilators)?
Calcium Channel Blockers
What antihypertensive drugs act on RAAS?
What heart failure drugs increase cardiac efficiency by decreasing PRELOAD?
diuretics, vasodilators, Beta Blockers,ACE Inhibitors,
What heart failure drugs increase cardiac efficiency by decreasing AFTERLOAD?
vasodilators, Beta Blockers, ACE Inhibitors
What pump to Thiazide diuretics block?
Type III pump
What pump do High Ceiling (Loop) diuretics block?
Type II pump
How does the Type IV pump work
Type IV pump is like a school bus. The bus is the tubule and is carrying Na+ but is willing to let one Na+ off (reabsorbed) in exchange for either a K+ or a H+ (secretion).
What diuretics inhibit carbonic anhydrase at pump IV?
What diuretics compete with uric acid (and win) at the uric acid pumps?
Thiazides, High Ceiling (loop) diuretics
Digtitol toxicity (due to hypokalemia)
Lithium toxicity (due to low GFR)
Which two diuretics should be used in a patient with renal failure or renal insufficiency?
Indapamide (a thiazide that is metabolized in the liver)
Mannitol (osmotic diuretic since doesn't affect GFR).
What kind of diabetes insipidus can be treated by thiazide diuretics?
Nephro Diabetes Insipidus
In this condition, thiazide diurectcs actually help the person pee out LESS since the GFR is decreased.
How do high ceiling (loop) diuretics work?
Block Type II (Chloride) pump, so blocks active reabsorption of Cl- and passive reabsorption of Na+ at Pump II. Since Pump III is "lazy" and just does its normal job of Na+ reabsorption but no more, more Na+ will be presented to Pump IV, which will increase secretion of K+ and/or H+ at Pump IV (school bus, so you get hypokalemia and/or metabolic alkalosis.
Loop diuretic have NO EFFECT on carbonic anhydrase, so H+ levels stay the same.
Causes exccessive amounts of urine, can lead to hypovolemia and even shock.
Inhibit uric acid secretion at PCT, so hyperuricemia.
Loop diuretic SEs?
digoxin toxicity (due to hypokalemia)
ototoxicity (loss of hearing and tinnitus,or ringing in ears)
What intensifies hypokalemia and hyperglycemia?
What pump do Potassium-Sparing diuretics do?
Spironolactone is a competitive inhibitor of Aldosterone at Pumps III and IV. Spironolactone reduces Na+ reabsorption at these pumps.
Triamterene blocks Type IV pump, so it inhibits Na+ reabsorption at this pump.
Effect of Spironolactone depends on how much Aldosterone is in the blood.
What happens if a person takes both Spironolactone AND Captopril?
Captopril is an ACE Inhibitor, so it inhibits the formation of aldosterone by preventing the conversion of angiotensin I to angiotensin II. If there is less aldosterone in the blood, then spironolactone (an aldosterone inhibitor at Pumps III and IV) will not have as much effect, so body will have extreme hyperkalemia.
What is the osmotic drug we need to know?
Where does Mannitol work?
DCT and Collecting Duct
How does Mannitol work?
Increases osmotic pressure in the nephron tubule so that water stays in tubule and is peed out (since water goes from low to high osmotic pressure).
What is Mannitol used to treat?
Reduce intracranial pressure in brain injuries
Acute Renal Failure (most important use since you want patient to pee some but do not affect GFR).
Mannitol is only active until it is excreted, so only for short-term use.
NOT useful in mobilizaition of edema or CHF.
What two diuretics have NO EFFECT on GFR?
The other types of diuretics lower GFR.
What hormone makes the tubular membrane permeable to water to allow water reabsorption?
What turns OFF ADH?
What rapidly metabolizes ADH?
What is a synthetic ADH that actually has a longer duration of action than ADH and is resistant to peptidases?
What is Desmopressin used to treat?
Neurogenic Diabetes Insipidus (deficiency of ADH in brain)
What is Nephrogenic Diabetes Inspidus? What do you use to treat it?
Body has ADH but is INSENSITIVE to it.
Thiazide diuretics can be used to treat.
What is hyperuricemia?
High uric acid levels in the blood. Can cause Gout.
What drugs can be used to treat CHRONIC hyperuricemia?
1.Probenecid -- only for prevention! Blocks uric acid reabsorption pathway in PCT, so uric acid will stay in the tubule.
2.Sulfin-pyrazone (didn't talk about in class)
3. Allopurinol -- only for prevention! decreases circulating levels of uric acid. It's active metabolite is Alloxanthine, which has a longer half life than Allopurinol. Both forms of durg inhibit enzyme xanthine oxidase (which is required for synthesis or uric acid).
***DO NOT use Aspirin if suffer from gout!
What can be used for ACUTE attacks of hyperuricemia (gout)?
It disrupts mitosis, so blocks inflammatory response to crystals of uric acid.
blood in stool
acute renal failure
scant urine production
scant blood in urine
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