Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
129 Cards in this Set
- Front
- Back
|
HTN damages wht organs, what can this lead to
|
BV--> stroke, coronary disease
Kidney --> renal failure heart --> CHF Brain --> stroke |
|
|
what is the cause of HTN
|
Often its essential HTN, unknown cause. many factors contribute to it
1. Renal A constriction 2. Coarctation of aorta 3. Pheochromocytoma 4. Cushings 5. Primary Aldosteronism |
|
|
what is normal BP
PreHTN Stage 1 HTN Stage 2 HTN |
Normal: <120 <80
Pre: 120-139 or 80-89 Stage 1: 140-159 or 90-99 Stage 2: >160 or >100 |
|
|
what happens to renin when the kidneys arent being perfused
|
increased renin to increase ALDO and ANG II to increase blood volume (water retention)
|
|
|
hydrochlorothiazide
metolazone Indapamide Furosemide Triamterene Eplerenone |
Diuretics
THiazides: Na excretion. Hypokalemic alkalosis hydrochlorothiazide- thiazide metolazone- thiazide Indapamide- thiazide, dilator Loop: use in pts with renal insufficiency, CHF Furosemide- loop K SParring: used with thiazides, dont use with other K sparers like ACEi adn ARB Triamterene- K sparring Eplerenone- Aldosterone antagonist |
|
|
methyldopa
clonidine |
a 2 agonist
**stim presynaptic a2 in the medulla to DECERASE SNS **decrease BP by decreasing SNS (loose constriction) but also decreased renin |
|
|
mecamyllamine
trimethaphan |
ganglion blockers
|
|
|
guanethidine
reserpine |
adrenergic neuron blocking agents
|
|
|
phenelzine
|
MAO inhibitors
|
|
|
"-azosin"
prazosin doxazosin terezosin |
a1 blockers
**dilate veins and arteries **good for dx, tx of pheochromocytoma |
|
|
timolol
propranolol nadolol metoprolol Atenolol Nebivolol Acebutolol bisoprolol Pindolol Acebutolol penbutolol alprenolol oxprenolol labetalol carvedilol |
NON SPECIFIC B blocker
timolol propranolol nadolol B1 blocker, cardiospecific metoprolol Atenolol Nebivolol Acebutolol bisoprolol B blocker with Intrinsic sympathetic activity Pindolol Acebutolol penbutolol alprenolol oxprenolol Combined a/b blockers labetalol carvedilol |
|
|
Hydralazine
Sodium Nitroprusside |
dilators that use NO
|
|
|
minoxidil
diazoxide |
dilator that opens K channels
|
|
|
fenoldopam
|
dopamine 1 R stimulant
|
|
|
verapamil
dilttiazem nifedipine minodipine amlodipine nicardipine nisoldipine isradipine felodipine |
Ca channel blockers
|
|
|
what are hte 2 main categoires of drugs hat inhibit the RAS (rening angio system)
|
1. ACE inhibitors "-prils"
captopril enalapril 2. Angiotensin receptor blockers (ARB) "-artan" losartan candesarten eprosartan irbssartan Olmesartan Telmisarten valsartin |
|
|
captopril
enalapril losartan candesarten eprosartan irbssartan Olmesartan Telmisarten valsartin |
ACE inhibitior
ARB **both inhibit the renin angiotensin system |
|
|
whats aliskiren
|
renin inhibitor
|
|
|
what is the renin inhibitor
|
aliskiren
**when BF to kidney decreases renin is released. activated ANG II, ALDO released. retains water |
|
|
how is BP pressure controlled by baroreceptor reflex
|
1. Baro in carotid senses BP change
2. sends info to nucleus of the tractus solitaris 3. then to vasomotor center 4. to automatic ganglion 5. SNS nerve endings: a or b |
|
|
what drugs act on teh vasomotor center
|
methyldopa- a2 agonist
clonidine- a2 agonist guanabenz- guanfacine |
|
|
what drugs act at SNS nerve terminals
|
Guanethidine, Reserpine- adrenergic neruron blocking agents
Guanadrel |
|
|
what drugs act at the b receptors of the heart
|
Propranolol- b blockers
timilol nadolol B1 specific: metoprolol, atenolol, nebivolol acebutolol, bisoprolol |
|
|
what drugs act on the ANgiotensin R of vessels
|
Losartan- ARB "-artan"
|
|
|
what are hte drugs that act on a R on vessels
|
prazosin a 1 blockers
"-azosin" doxazosin terazosin |
|
|
what drugs act on the SNS ganglion
|
trimethaphan- ganglion blockers
|
|
|
what drugs act on vascular SM
|
Hydralazine nitroprusside- - NO dilator
minoxidil, diazoxide- dilator, open K Verapamil, Diltiazem- Ca channel blocker Fenoldopam- dilator, D1 stimulant |
|
|
what drugs act on kidney tubules
|
Thiazides adn others
|
|
|
what drugs act on b R of the juxtaglomerular cells that release renin
|
Propranolol, other b blockers
|
|
|
why do HTN drugs fail
|
ppl dont take them
**ppl lower BP nad decerase the number of drugs needed by: loosing weight, no smoke, no salt, exercise |
|
|
there are SO many HTN drugs, can they be combined
|
sure thing
combining can decrease dose needed and decerase side effects |
|
|
any new HTN drugs must...
|
decrease BO by 10%, new drugs must be as effective as the old ones
|
|
|
shoudl we decrease pressure fast
|
nope, needs to be gradual
**also cant be too low. coronary perfusion pressure is the diastolic pressure and needs to be more than 90 |
|
|
in pts ikder than 50 what is more important, systolic or diastolic
|
systolic >140 is BAD
|
|
|
what is the first line drug for HTN
|
thiazides- hydrochlorothiazide
**if the person is DM, kidney disease, MI, heart failure, cerebrovascular disease. ADD a drug. ACEi, ARB, b blocker, Ca channel blocker **b blockers good for caucasian |
|
|
whats the polypill
|
combination pill for old folks
Statin b blocker ACE i Thiazide Diuretic asprin folic acid **reduce copays, drug companies do not like this |
|
|
what are the 4 major big classes of HTN tx
|
1. oral diuretics. thiazide, DOC for HTN
2. sympatholytics 3. direct vasodilators 4. Angiotensin inhibitor |
|
|
tell me about the use of thiazides for HTN
1. effectiveness 2. mech 3, side effects |
1. used as DOC, lower BP in 4-60% of peeps
2. decrease Na stores --> decrease blood volume. Long term will activate K channels --> decreased resistance. decreased Na content in SM 3. not common bc hte dose is lower to tx HTN than for diuresis. but... impotence, gout, hypokalemic alkalosis, increase renin. decreased glucose tolerance and increased lipids. **indapamide: also a dilator |
|
|
if a person is impotent, no longer tolerant to glucose, has increased lipids, hypokalemic alkalosis, and hyperurecemia and their BP is 120/80 what might they be taking
what was the short term and long term effect of getting such great BP |
thiazides
Long Term:decreased Na in SM cell --> decreased preipheral resistance SHort Term: decreased na leads to decreased blood volume to decrease BP **when thiazides are used for HTN there are less side effects when they are used as diuretics bc they are used in lower doses for HTN tx. but still impotence with lower dose |
|
|
thiazides are more effective in who
|
Aferican Americans (might have said caucasians, but its African Americans)
Old **impotence side effects |
|
|
ok so diuretics for HTN
1. Thiazide 2. Loop 3. K sparring |
1. THiazides: first choice, good in old blacks, low dose with dilators, ACEi or b blockers to counteract Na/Fluid retention. cheap. not good for sulfonamide allergies
2. Loop: severe cases only in pts with renal insufficiency or CHF 3. K sparring: in combination with thiazides/loops to decrease K loss. NOT used in combination with other K sparring drugs like ACEi adn ARB |
|
|
ok so thiazides are first line drugs for HTN, when might you not use them
|
its a sulfonamide so not used in ppl with allergies
|
|
|
K sparring diuretics shoudlnt be combined with what other HTN drugs, what are they combined with
|
ACEi, ARB: these are also K sparring
**good to combine them with K loosing diuretics like loop adn thiazides |
|
|
Angiotensin --> Angiotensin I --> angiotensin II
what enzyme stim, what drug |
ANG --> ANG I: stim by Renin. Aliskiren is a renin inhibitor
ANG I --> ANG II: stim by ACE (angiotensin converting enzyme) blocked by ACE inhibitors like captopril |
|
|
what do sympatholytic drugs do to baroreceptor reflex
|
activate baroreceptor reflex and cause Na retention
**Na retention is balanced by combining with a diuretic that will decrease Na |
|
|
the centrally acting sympatholytics are what
|
the a2 agonists. they inhibit NE release at medulla so there is less SNS tone
methydopa clonidine |
|
|
what is the action of clonidine and methydopa
|
a2 agonists for HTN
**decrease NT release via presynaptic **innhibit neurons via post synaptic **decrease BP by decreased renin and decrease vasoconstriciton |
|
|
both methyldopa and clonidine are a2 agonists. whats some diferentces in effectiveness and administration
|
clonidine more effective
methydopa is prodrug both are oral but clonidine can also be transdermal |
|
|
what are the side effects of mythydopa and clonidine
|
enter CNS- sedation, nausea, dizzy
clonodine: hypertensive crisis with sudden withdrawl Methydopa: hemolytic anemia with + coombs **a2 agonist |
|
|
what drus is associated with hemolytic anemia and a + coombs test
|
methydopa
a2 agonist |
|
|
what do clonidine nad methydopa interact with
|
they are a2 agonists, yohombine an a2 antagonist will interact
also TCA (tricyclic amines) |
|
|
what are hte ganglion blockers
|
mecamylamine- enters CNS, tourettes
trimetaphan **not used, too many side effects. block PNS and SNS |
|
|
what ar ehte adrenergic neuron blockers
|
guanethidine- inhibits exocytosis, replases NE in vesicles. if given IV can cause hypertensive crisis in pts with pheochromocytoma
reserpine- depletes NE in vesicles. interactions with MAOi **bind to NE containing secretory vesicles and inhibit release --> decrease SNS --> dilation --> decreased BP |
|
|
what is the adrenergic neuron blockers that interacts with MAOi
what is the adrenergic neuron blocker that inhibits exocytosis and can cause HTN crisis in pts with pheochromocytoma |
reserpine
guanethidine **both prevent NE release to decrease SNS, which means vasodilation and then decrease in BP |
|
|
what side effects are seen with:
guanethidine reserpine |
Guanathidine: postural hypotension, fluid retention, diarrhea, retrograde ejaculation
Reserpine: sedation, depression, stuffy nose, dry mouth, GI upset **these are adrenergic blockers, they prevent NE release |
|
|
what are my adrenergic 1 ANTAGONISTS
|
Azosin
prazosin terazosin doxazosin **block a1 so we get dilation of A and veins |
|
|
do azosins dilate veins arteries or both
|
BOTH
these are my a1 antagonists *bad bc they cause postural hypotension, renin increase to retain Na nad fluid, **good bc they dont affect plasma lipids |
|
|
what are phentolomine and phenoxybenzamine used for
|
non selective a blockers to dx/tx pheochromocytoma
|
|
|
what are hte goods and bads with a1 blockers (azosin)
|
BAD: postural hypotension, Na/Water retention bc renin increases,
Good: dont increase lipids |
|
|
what is the mechs of action for the olol's
|
B blockers
1. block b --> decreased HR, contraction force, CO 2. More effective in young whites, if your only going to use this it better be in a young white male |
|
|
what is best for old blacks
what is best for young whites |
diuretics
b blockers |
|
|
what is the unique thng about nebivolol
|
b blocker that also makes NO to dilate
|
|
|
what are the adverse effects of hte b blockers (-olol)
|
Heart/Lung (not for asthmatics)
GI CNS **increase TG, decrese **mask sx of hypoglycemia |
|
|
what adrenergics are bad for hte lipid profile
which adgrenergic wont really affect the lipid profile |
b blockers (increase TG, decrease HDL)
a2 antagonist: azosin |
|
|
ok so b blockers are best in young white males. who shoudl NOT get b blockers
|
1. Asthmatics
2. DM 2 (TG increase HDL decrease, mask hypoglycemia) 3. Heart Block 3. severe CHF |
|
|
who benefits most from b blockers (im not asking for young white ppl)
|
1. angina
2. after MI 3. migraine **not for use in: severe CHF, asthma, DM, heart block, really active, african. hypercholesterolemia, |
|
|
wht are the combined a/b blockers
when are they used what are side effects |
iabetalol
carvedilol **used in HTN emergencies May cause: orthostatic HTN, bronchospasm, liver damage |
|
|
when are labetalol and carvedilol used. what are their side effects
|
combined a/b blockers
Used in HTN emergency orthostatic HTN, bronchospasm, hepatotoxic |
|
|
what are the 2 oral dilators
what are the 3 IV dilators |
ORAL: used for chronic HTN
1. hydralazine minoxidil IV: used in emergencies 1. Sodium nitroprusside 2. diazoxide 3. fenoldopam |
|
|
what are the dilators that are specific for arteries
what does both |
1. hydralazine
2. minoxidil 3. diazoxide Nitroprusside does Arteries ADN veins |
|
|
are dilators in gemeral good for long term HTN tx
|
nope, they get reflex tachy adn increased renin release
**DONT USE ALONE (also dont really use b blockers alone unless in a young white person) |
|
|
hydralazine and minoxidil are used together with what?
|
these are dilators: dilators over time will cause tachy and increase renin (both are oral)
soo... used with: diuretics to resist water retention b blockers to prevent reflex tachy **not really used much any more for chronic tx |
|
|
what is the weird thing associated with minoxidil
|
oral dilator
**causes hypertrichosis. cardio effects when used topically for baldness |
|
|
what are adverse affects associated with dilators
|
reflex tachy
renin release --> fluid retention **increased CO (reflex tachy) so can induce angina and MI |
|
|
whats the risk of diuretics in pts with CAD
|
dilators cause reflex tachy so O2 demand in heart increases --> angina and MI
|
|
|
what are the dilators that act though NO
|
1. Hydralazine
2. Na Nitroprusside |
|
|
what are hte dilators that act through blocking K channels
|
1. Minoxidil
2. Diazoxide |
|
|
tell me about hydralazine
|
oral dilator that acts through NO
*dilates arteries only * not typically given as momotherapy: give with diuretics bc dilators increase renin. give with b blockers bc diuretics cause reflex tachy Combined with: isorbidide dinitrate its really good in the black populaiton **SLE in slow acetylators |
|
|
what dilator cab cause SLE in slow acetylators
|
hydralazine
**recall this is an arteriolodilator. **can be used with isosorbide dinitrate and its really good in blacks |
|
|
tell me about sodium nitroprusside
|
*dilator that acts through NO
Toxicic: CN accumulaiton, acidosis given IV and acts fast, effects go away fast after you stop |
|
|
what is the drug that acts fast and effects go away fast after you stop (given IV) and CN accumulaiton
|
cyanide
**Sodium Nitroprusside |
|
|
compare and contrast the dilators that act through NO
|
1. Hydralazine: SLE in slow acetylators. arteries only. used in severe HTN. ORal
2. Cyanide accumulaiton. dilates arteries AND veins. acts fast, effects leave fast. IV only. acidosis |
|
|
what are the 2 dilators that act thorugh K
|
1. Minoxidil: opens K to stabilize the membrane. arteriodilator (no veins). hypertrichosis (hair growth)
2. Diazoxide: |
|
|
wht is rogaine
|
topical minoxidil
**its an arterodilator that acts through keeping K open to stabilize the membrane. it causes hypertrichomosis-- hair gorwth |
|
|
what is diazoxide
|
hyperpolarizes by activating ATP sensitive K channels --> SM relaxation --> dilation
inhibits insulin secretion. monitor for hyperglycemia, metabolic ketoacidosis. used in pts with insulinemia |
|
|
what are some of hte adverse reactions assoicated with diazoxide
|
dilator- activates ATP sensitive K channels to cause hyperpolarization so SM relaxes
Inhibits insulin release Na/Water retention (all dilators increase renin to do this) GI Hyperuricemia thrombocytopenia excess hari growth |
|
|
what is the D1 agonist
|
fenoldopam, dilator
t1/2 is 5 min reflex tachy, HA, flushing IV, liver matabolism |
|
|
whats fenoldopam
|
D1 agonist, dilator
*relax SM., *IV liver metabolism **reflex tachy, HA, glushing |
|
|
what are "dipines"
|
dihydropyridines, Ca channel blockers
Amlodipine Nifedipine**stongest dilator Nimodipine** most lipid soluble **gingival hyperplasia **reflex tachy |
|
|
what are the papaverine related Ca channel blockers
|
verapamil- stongest cardio effects. constipation
|
|
|
what are hte benzothiazepine related Ca channel blokcers
|
diltiazem
**dialtiazem is in btwn nifedipine (stong dilator) and verapamil (strongest cardio effects) |
|
|
how do Ca channel blockers work to decrease HTN
|
block slow (l) Ca channles to decrease intracellular Ca, decreased Ca --> relax SM to produce dilation --> decrease BP
|
|
|
are Ca channel blockers good to use alone
|
ya, esp in old blacks
|
|
|
what drugs have impotence as a side effect
|
diuretics
|
|
|
tell me some thing cool about the following Ca channel inhibitors
1. Dihydropryidines (nifedipine) 2. Verapamil 3. Diltiazem 4. Nimodipine |
1. strong dilator effect (reflex tachy)
2. constipation, stong cardio effects 3. in btwn nifedipine nad verapamil 4. most lipid soluble--> dilates in brain |
|
|
what Ca blockers cause reflex tachy wat ones dont
|
Reflex Tachy:
"dipines" bc they have a stong dilator effect NO Reflex Tachy: Verapamil and Diltiazem |
|
|
what drugs cause gingival hyperplasia
|
1. Dipines (ca channel blockers)
2. phenytoin 3. cyclosporine |
|
|
what are hte side effects associated with dipines
dihydropyridines: amlodipine, nifedipine, nimodipine |
reflex tachy (bc they do the most dilaiton of the Ca channel blockers)
vascular effects: flushing, dizzy, HA, peripheral edema gingival hyperplasia |
|
|
what Ca channle blocker is associated with constipation
|
verapamil
|
|
|
shoudl pts with L vent hypertrophy use Ca channel blockers as their only drug
|
nope
|
|
|
tell me the side effects of verapamil and dilttiazem
|
can cause bradycardia in pts with SA/AV node block
dont use in pts with block or CHF |
|
|
what are hte prils
whats the active, whats the pro |
ACE inhibitors
Active: captopril ProDrug: Captopril Enalapril and others... |
|
|
what is the thing about the metabolism/use of ACEi
|
they are all prodrugs that need to be convertived to active except for Captopril, its active
|
|
|
whats hte mech of action for the prils
|
ACE inhibitors
Angiotensin Converting Enzyme converts ANG I to ANG II. when this cant be done ANG II no longer works and BP is decreased |
|
|
whats active ANG I or II
|
II its activated by ACE
ANG II constricts so when its not working we get dilation, but NO reflex tachy with ACEi |
|
|
ok so ACE converts ANG I to II is this hte ony thing it does
|
nope its also called peptidyl dipeptidase and it kills bradykinin
when we have ACEi we have increased bradykinin. high bradykinin leads to coughing, angioedema and decreased HTN |
|
|
wht class of drugs is associated with an increase in bradykinin
|
ACEi
the ACE enzyme is also called peptidly dipeptidase and it destroys bradykinin so when we ahve ACEi we have increased bradykinin, this is good to decrease HTN but it also causes cough and angioedema |
|
|
do ACE inhibitors ("prils") affect the brain kidney or heart? what are the side effects
|
nope
mild side effects with no change in lipid panels **no reflex tachy bc it resets baro |
|
|
are ACEi used as monotherapy
|
ya, they are good and have few side effects, all can be given orally (as prodrug, need to be metabolized into active)
|
|
|
for ppl with DM renal disease, L vent hypertrophy what anti HTN drug is good
|
ACEi
**good in young/middle age whites. not so good in blacks |
|
|
are ace inhibitos (prils) good in blacks
|
not really better in young/middle age whites
good for: DM renal disease L vent hypertrphy |
|
|
what 2 anti HTN work really well together
|
diuretics and ACEi
ACEi decrease ALDO secretion so there is less Na reabs. the Na loss induced by diuretics is unopposed diuretics enhance hte anti HTN effec of ACEi **just be sure its not a K sparring diuretic bc --> hyperkalemia |
|
|
what are the pharmakokinetics of ACEi
|
oral
liver metabolism (good for ppl in renal failure) |
|
|
what are some adverse effects of ACE inhibitors (prils)
|
1. hypotension in hypovolumic pts
2. cough (bradykinin is increased and causes this as well as angioedema) 3. hyperkalemia bc no ALDO 4. renal failure 5. CI in pregnancy 6. rash 7. altered taste |
|
|
are ACEi good for preggos
|
nope
|
|
|
wht drug interactions are there with ACEi
|
K sparring diuretics. can get hyperkalemia
NSAIDS (decreased dilation, bradykinin --> PG) |
|
|
should you use K sparring diuretics with ACEi
|
nope, risk of hyperkalemia
|
|
|
what are the "sartans"
losartan valsartan |
Angiotensin R Blocker (ARB)
|
|
|
ARB block which ANG II R specifically
|
AT1. are in vascular SM and cause most of hte effects of ANG II
**DONT AFFECT bradykinin |
|
|
what affects bradykinin ACEi or ARB
|
ACEi
**ARB ("sartans") wont cause the cough and angioedema htat ACEi do |
|
|
whats more effective losartan or atenolol
|
losartan (ARB) *****
atenolol (b1 blocker) **less mortality, less side effects |
|
|
whats hte pahrmacokinetics of ARB (sartans)
|
oral
variable first pass liver metabolism **simliar to ACEi |
|
|
what are the adverse effects of hte ARB (sartans)
|
simiair to ACEi but NO cough or angioedema bc ARB dont increase bradykinin
*hypotension is hypovolumic pts *renal failure *no reflex tachy *CI in preggo *hyperkalemia maybe, dont use with K sparrring *rash |
|
|
losartan and valsartan are what
|
ARB,
|
|
|
what is the renin inhibitor
|
Aliskiren
*blocks ANG I formation **same as ACEi and ARB for effects on BP *wont affect bradykinin *CI in preg |
|
|
what blocks ANG I formation
|
renin inhibitor aliskiren
*simlar to ACEi and ARB *dont use when preggo *wont interfere with bradykinin (like ARB) |
|
|
if you are african american what are good drugs.what are bad
|
Good: duiretic, CCB
Bad: B blocker |
|
|
what HTN are good for DM
|
diuretic
ACEi ARB b blocker CCB |
|
|
1. what shouldnt a person with asthma be given?
2. what shouldnt a person over 65 be given 3. what ahsouldnt a blaxk person be given 4. what shouldnt a preggo get 5. what shoulnt your pt with angina get |
1. b blocker
2. centrally acting a2 3. b blocker 4. ACEi, ARB, Aliskiren 5. hydralazine |
