Antihypertensives Pt. I Flashcards
Hypertension Background
• 46% of all Americans have BP ≥____
• 38% of Caucasians, 57% of ____
• >60% of all individuals over the age of ____
• Generally asymptomatic until end organ damage
• Only 50% of population getting treated and only 50% of these have BP under optimal control
• BP guidelines have changed ○ Used to be 140/90 ○ Now it's 130/80 - throws more people into the hypertensive group • More prevalent in AA • Side effects are an extension of their mechanism of action
130/80
AA
60
End Organ Consequences • Accelerated \_\_\_\_ • Renal damage especially \_\_\_\_ • Increased risk of bleeding \_\_\_\_ • Increased risk of aneurysm \_\_\_\_ • Increased risk of \_\_\_\_ (ventricular hypertrophy) • Increased risk of \_\_\_\_
• Untreated hypertension ○ Accelerated CAD § Angina pectoris > heart attacks • Renal damage ○ Proteinuria, reduce GMF (by measuring \_\_\_\_ [measure the amount in the blood, and based on weight/height]) • Bleeding stroke > brain damage • Congenital aneurysms are more likely to burst • Constant high BP puts heart on overload > pumping of heart begins to fail • Microbleeds can occur in eye > retinopathy (damages nerves and lose eyesight)
coronary artery disease diabetics strokes rupture aneurysm rupture retinopathy
creatine clearance
Risk factors
Unavoidable • \_\_\_\_ • Increased age • \_\_\_\_ • AfricanAmerican • \_\_\_\_
Modifiable • \_\_\_\_ • Obesity • \_\_\_\_ • Smoking • \_\_\_\_
• Nicotine stimulates nicotinic receptors in the ganglia > drive \_\_\_\_ nervous system • Exercise shown to reduce BP (not just stress, but also physiologic) ○ Cholesterol increases because the body increases \_\_\_\_ ○ Kidney function decreases
genetics male gender diabetes sodium intake alcohol intake exercise sympathetic LDL
Management
• MAP= CO x PVR
– CO ~ preload, heart rate, contraction force
– PVR ~ blood vessel diameter and stiffness
• So treatment strategies are:
– Slow/reduce ____ of the pump (the heart)
– Decrease ____ volume
– Open ____ (blood vessels)
– Decrease ____ activity to pump and pipes
• Manage high BP > lower renal arterial pressure • Drugs reduce CO ○ Reduce amount of blood pumped by heart • Slow/reduce force of heart - \_\_\_\_ • Dec plasma volume - \_\_\_\_ • Open pipes - \_\_\_\_ blocking agents (-azosin) • Decrease CNS activity ○ Problem: going to get CNS depressant effects (drowsy, lethargic)
force
plasma
pumps
CNS
beta blockers
diuretics
alpha1
• Centrally acting
○ Decrease sympathetic outflow
• Drugs are either ____ (decreases neurotransmitter release), or they deplete neurotransmitter (reduce activity at ganglionic sites; ____ - problem: the ganglia are the nerve cell bodies of the post ganglionic nerve fibers of both the sym and parasymp NS - can block sym, but can get side effects that blunt parasymp; powerful drugs, not on them for long periods of time - like in hospital to get the BP down really quickly [like ____ bursting in head]
• Deplete NT in periphery - adrenergic neuronal depleting agents
○ Work on nerves innervating BV or heart
§ Reduce amount of NE in nerve terms of symp system
• Work directly on receptors
○ Beta adrenergic blocking agents
§ Action not just on heart, but a ____ blunting effect; in the kidney (has beta receptors) and stimulation of the receptors enhances production of renin > stimulators of the RAT pathway > end product: ____ - vasoconstrictor, enhance secretion of aldosterone from adrenal cortex (water/sodium retention), stimulate NS centrally
Jacking up system can increase BP
alpha2 agonists
ganglionic blockers
vessel
CNS
angiotensin II
• At level of kidney: ____
• ACE inhibitors work on this sytem
○ Block conversion of ____ (10 to 8 AA)
○ All these drugs (ACE) end in -pril
○ Blocking ACE is a problem > development of drugs that block angio II receptors (-sartin)
§ On BV, in adrenal cortex
§ Similar effect to ACE inhibitors
§ Doesn’t do one, which may make them weaker but reduces potential side effects
• Alpha adrenergic antagonist
○ ____ - you want to block alpha 1 (blocking alpha 2 - increased NE release > makes heart start racing [____])
• Ca-channel blockers
○ Two classes: -pine (lodapine, nifedipine) - block Ca on ____ (vasodilation); virapapil block Ca channels in ____ > will vasodilate, but will also ____ the heart down
○ Implicated in the development of ____
• Vasodilators
○ Direct acting on ____
○ Some open ____ channels
○ Some enhance ____ pathway (vasodilators)
diuretics angio I to angio II vasodilate reflex tachycardia BV heart slow gingival hyperplasia BV K+ NO/cyclic GMP
Centrally Acting Antihypertensives 1
• Clonidine (Catapres®)
– ____
– decreases ____ sympathetic outflow to heart and blood vessels
• Decreased CO and PVR lowers BP
• Also useful in treating some excessive sympathetic nervous systems symptoms of ____ from CNS depressants
• Has some utility in management of ____ pain – sympathetically maintained pain
• Not used for hypertension anymore - too many \_\_\_\_ ○ Depresses CNS too much > people are too lethargic ○ Added on when \_\_\_\_ drugs and still not in an acceptable range • Not directly working on the organs, but slowing down things that come out of the CNS that innervate these organs • When people are withdrawing from CNS depressants (opposite of the activity of the drug): ○ Dampen down the symptoms • Utility in management of chronic pain: ○ Chronic oral facial pain - \_\_\_\_, sympathetically maintained pain § Abnormal crosstalk between symp and neurons that send pain signals to brain/spinal cord § May be due to nerve crushing injury, and they may try to reconnect resulting in abnormal connections
alpha2 adrenergic agonist
CNS
withdrawal
chronic
side effects
2/3
reflex sympathetic dystrophy
Centrally Acting Antihypertensives 2
• α-methyldopa (Aldomet®)
– Crosses ____and metabolized to α methyldopamine > ____
– α methylnorepinephrine a pure ____ agonist or so called “____”.
• Both clonidine and α methyldopa produce the following AEs: Sedation, ____ (apparently α 2 receptors on postganglionic parasympathetic neurons to salivary glands)
A-methyldopa
• False transmitter
• Not widely used > dampens the CNS
• Decreased ____ release in the CNS (like clonidine)
○ Dampens nerve activity going to the BV in the heart
• Xerostomia
○ Dampening symp, but it implies ____ is dominating
○ In salivary glands and the nerves that innervate > have a2 receptors > stimualted > decrease release of Ach to the glands
BBB alpha methylnorepinephrine a2 false transmitter xerostomia NT para
Ganglionic Blocking Agents
• Mecamylamine (Inversine®), Trimethaphan (Afronad®)
– Block ____ receptor on ganglia so some blockade of both ____ nervous systems
– Decrease PVR and CO
– Reserved for ____
– AEs typically reflect a blockade of the system that predominates in that organ:
• Severe ____, bradycardia on sympathetic side
• ____, constipation on parasympathetic side
• Block connection bt pregang and postgang nerve fibers ○ Hitting cell bodies on postgang nerve fiber ○ Hit symp and parasymp • Hit nerves that go to heart and to the BV ○ Decrease CO and PVR • Very powerful - only used in \_\_\_\_ ○ Not used long term > gets the BP rapidly down • AE: ○ On sympathetic side: § Blockade of the sympathetic nervous system - slow HR, dropping the BP too low ○ On parasympathetic side: § Salivary tissue, GI tissue > at rest predominates > on these drugs for a while > xerostomia and constipation ○ These are unpredictable
nicotinic N cholinergic sympathetic and parasympathetic hypertensive crisis hypotension xerostomia hospital settings
Adrenergic Neuronal Blocking Agents
• Guanethidine (Ismelin®) and Reserpine (Serpasil®).
– Causes slow depletion of ____ from postganglionic adrenergic nerve terminal
– Guanethidine competes for NE ____
– Reserpine blocks NE ____ into vesicles
– Drugs will decrease PVR and CO
– Reserpine enters ____ readily and depletes NE there also increasing risk of depression
– Both drugs cause lots of ____ and stomach cramping and diarrhea
– Theoretically up-regulate ____
• These drugs are working at nerve terminals that innervate BV and cardiac tissue ○ Slowly deplete NT: § Slow leaking out § Competition for the NE for getting into the vesicles □ If NE is synthesized and cannot get into the vesicles in the nerve terminal > it cannot be spit out during an AP • Guanethidine - totally excluded from \_\_\_\_; reserpine readily gets in ○ Tragic discovery: reserpine was used for high BP, and 10-15% would get very depressed on these drugs; drugs were created afterwards to create drugs that bumped on NE; the discovery of depression • Depleting NT at the BV > profound vasodilatory effect > \_\_\_\_ • Make the PNS predominate > stomach cramping and diarrhea • Body compensates > upregulates alpha and beta receptors ○ Cautionary: increasing \_\_\_\_ in locals for dentistry can add to this problem
norepinephrine reuptake entry CNS orthostatic hypotension alpha and beta receptors
CNS
postural hypotension
epi
Some Drugs Affecting BV
VASODILATORS • Alpha antagonists ○ Alpha1 selective - ends in \_\_\_\_ • Ca++ blocking agents ○ Two ways to cause vasodilation: § Block positive from \_\_\_\_ § \_\_\_\_ positive ions going out ○ Pure vasodilator (dihydropyridines): end in pine ○ The other two also slow the \_\_\_\_ down (diltiazem and verapamil) • K+ agents ○ Open them (\_\_\_\_) ○ Not widely used; used in emergencies ○ Major AE of minoxidil: used as an ointment (rhogaine) Taking pills for BP > \_\_\_\_
-azosin going in accelerate heart agonist hypertrichosis
Some Drugs Affecting BV
VASODILATORS
• Activator of NO/cyclic GMP system
○ NO enhances ____ and increase production of cGMP > vasodilation
○ NG mainly used in an acute ____
• Angiotensin II antagonists
○ End in ____
○ Not just vasodilators > blcok ang II receptors throughout the body
§ Not as powerful as other agents > well ____
§ Reduce aldosterone secretion from adrenal cortext > less ____ retention
§ Blunting peripherally of the symp
guanylate cyclase angina attack -sartan tolerated water/sodium
Non-Selective α Adrenergic Blockers
• Phentolamine (Regitine®, Oraverse®), phenoxybenzamine (Dibenzyline®)
• High incidence of ____ and reflex tachycardia (α 1, α 2 blockade)
• Phentolamine still used for ____, ____ diagnosis and most recently in small dose accelerating soft tissue local ____
• Block both alpha1 and alpha2 > lower BP • On first doses > postural hypotension because they vasodilate ○ Body turns on reflex mechanisms and speeds up the heart > reflex tachycardia; more likely to happen to these because they block alpha2; release of NE at the heart at b1 receptors > begins to drive the heart in addition to the response of vasodilation • Phentolamine is the active ingredient in oraverse ○ Doesn't use in local anesthetic overdose; just make the lip/tongue numbness go away quicker ○ Have to inject it in area with the local • Pheochromocytoma ○ [???] ○ Cure: \_\_\_\_ remove it ○ Phentolamine given IV in the diagnosis; if reverse the BP surge then they do imaging studies in order to confirm that there is a pheo there
postural hypotension hypertensive crisis pheochromocytoma anesthetic recovery surgically
Quality of Life Issues Associated with Prolonged Lip and Tongue Numbness • In adults/teenagers - difficulty \_\_\_\_ And everyone’s favorite: Speaking Drinking/Eating Drooling
• Opposing epi > making the local distribute quicker > \_\_\_\_ up the vessels ○ Lidocaine by itself would only last \_\_\_\_ mins for the tongue; with epi you now have pulpal anesthesia of \_\_\_\_ minutes
smiling
opens
5-10
60-90
In Pediatric Dental Patients Also:
Lip, Tongue and Cheek ____
biting/mutilation
Time to return of normal sensation in lower lip
• Very ____ - never made an impact on the market
expensive
Selective α1 Blockers
• Prazosin (Minipres®), Doxazosin (Cardura®), Terazosin (Hytrin®)
– All decrease PVR which lowers BP
– Also useful as adjuncts in treating ____
– Postural hypotension/ ____ can occur
– “____” by blocking α1 receptors and leaving β1 and β2 open for epi.
– Decrease symptoms of ____
– Tamsulosin (Flomax®) selective for blocking ____ receptor on prostate, urethra and bladder neck. Not use to treat hypertension.
• All end in \_\_\_\_ • Treatment of CHF ○ A weak heart pumping through tight BV > make things even worse > more heart damage • \_\_\_\_ reflex tachycardia than the non-selective alpha blockers • Stimulates a1, b1 and b2 - wad of epi to someone on a1 blcoking agent ○ Vasoconstrictive effects of epi is block because the drug has higher \_\_\_\_ for the receptors ○ B1 and B2 is still open for epi > pure stimulation > increased HR, and b2 vessels would open up § Increase HR and a lowering of BP ○ Doesn't normally happen at the doses that we use • Doesn't shrink prostrate ○ [???] ○ Relieve the symptoms of being unable to pee ○ Treating high BP or enlarged prostate > side effects > so developed tamsulosin > only blocks the specific subtype alpha receptor on urethra, bladder neck and prostate > relaxes the \_\_\_\_ and other tissues nearby but it doesn't open up the BV
CHF reflex tachycardia epinephrine reversal phenomena benign prostate hypertrophy -asozin less affinity prostate
Other Direct-Acting Vasodilators 1
• Hydralazine (Apresoline®), Sodium Nitroprusside, Nitroglycerin (Nitrostat®)
– Either directly increase the activity of ____ or increase nitric oxide concentrations
– All decrease PVR. Very powerful. Reserved for ____.
– Postural hypotension/____ are strong possibilities
– Slow acetylators of hydralazine have increased risk of a ____ (rash, joint pain)
• Used for hypertensive crisis • Give off NO when processed, or directly stimulate cGMP • NG - purely used \_\_\_\_ for acute angina attack ○ Some pill formulations/bandage formulations > dermal delivery ○ For acute - quickest via \_\_\_\_ • Hydralazine - genetics involved in their AE ○ Two types who process drugs differently: § Slow \_\_\_\_ □ People have increase risk of a lupus-like syndrome (not true Lupus) § Fast metabolizer
guanylate cyclase hypertensive crisis reflex tachycardia lupus-like syndrome sublingually sublingual metabolizers
Other Direct-Acting Vasodilators 2
• Minoxidil (Loniten®), Diazoxide (Hyperstat®)
– Both are ____ on blood vessels
– End result is decrease PVR. Again very powerful. Diazoxide still used for ____.
– Both likely to cause orthostatic hypotension and ____
– Minoxidil’s side effect of hypertrichosis lead to the development of an ointment marketed as (Rogaine®) to treat ____
• Which antihypertensive either causes hypertrichosis?
K channel openers
hypertensive crisis
reflex tachycardia
male patterned baldness
Calcium Channel Blockers • Nifedipine (Procardia®), Amlodipine (Norvasc®), Felodipine (Plendil®) – Dihyropyridines just block \_\_\_\_ on BV – So primary effect is \_\_\_\_ – Also used in tx of \_\_\_\_ and CHF
• Verapamil (Calan®), Diltiazem (Cardizem®) – Block Ca channels on ____
– So decrease cardiac output also besides PVR
– Same uses as above plus certain ____
• Both groups can cause postural hypotension and ____
• The bottom two act similarly to \_\_\_\_ • Angina - not enough oxygen getting to the heart > chest pain > exercise, emotional stress ○ Opening up the BV > decrease cardiac workload; and the ones that also slow heart (V and D) > decrease \_\_\_\_ demand • Good for CHF > because they vasodilate ○ Slow the heart > counterintuitive > beneficial • Phenytoin and cyclosporine also cause postural hypotension and gingival hyperplasia • Good for \_\_\_\_ arrhytmias ○ -pine drugs aren't use because they only vasodilate
Ca channel vasodilation angina heart and BV arrhythmia gingival hyperplasia
beta blockers
myocardial oxygen
tachy
Actions of ACE Inhibitors and ARBs
• Subtypes of angiotensin II receptors (AT1 and AT2) ○ These drugs: § Indirectly > decrease synth of angiotensin II > blocking \_\_\_\_ receptors • Angiotensinogen > renin released from juxtglomerula appartu > converts to \_\_\_\_ (10 AA peptide - prodrug) > ACE (kinase 2) converts it into \_\_\_\_ (8 AA - active) ○ By blocking ACE doesn't mean you're wiping out all the angiotensin II in the body; there are other \_\_\_\_ still making it ○ ACE inhibitors prevent conversion of A1 to A2 § ACE normally inactivates \_\_\_\_ (pain mechanism; stimulate free nerve endings; natural vasodilator) § ACE inhibitors also blocks break down of bradykinin > more \_\_\_\_ § In about 20% of individuals > increase bradykinin in the resp tree > \_\_\_\_ that doesn't go away; the users have to discontinue the drug § Increase in bradykinin sometimes causes \_\_\_\_: swollen face and neck □ Resembles an \_\_\_\_ reaction, but not truly; due to bradykinin Can cut off the airway
angio II
angio I
angio II
chemicals
bradykinin vasodilation dry, itchy cough angioedema anaphylactic
Actions of ACE Inhibitors and ARBs
• Stimulating ATI causes: ○ \_\_\_\_ ○ Aldosterone secretion § Increase \_\_\_\_ retention ○ Stimulates the sympathetic § Blunting with drugs ○ \_\_\_\_ secretion § Hormone that causes vasoconstriction ○ Some interest in blocking angiogenesis
○ Subtype-2 does some of the opposite things • Difference between -sartins - just block the receptors; they do not get involved with anything in the above ○ Don't see an \_\_\_\_ cough, and they're not implicated in \_\_\_\_ (the ones that are are the -prils)
vasoconstriction water and sodium vasopressin itchy dry angioedema
Angiotensin Converting Enzyme (ACE) Inhibitors
• Captopril (Catapres®), Enalopril (Vasotec®), Lisinopril (Prinivil®), Benzopril (Lotensin®)
– All block conversion of angiotensin 1 to angiotensin 2 leading to decreased ____ release from adrenal cortex, ____, and some CNS blunting of sympathetic stimulation to heart and blood vessel. So decrease CO and PVR.
– May have added benefits in ____
– All block bradykinin breakdown causing additional ____ but also dry cough in 20% of individuals, rash and rare cases of angioedema.
• Benefits in diabetics ○ Place on an ACE > better blood sugar control > NOT \_\_\_\_ ○ On prediabetics with hypertension > didn't go on to develop full-blown \_\_\_\_ • Don't see a lot of \_\_\_\_ - not as powerful a vasodilator as the others (alpha 1 blockers, etc.)
aldosterone
vasodilation
diabetics
vasodilation
cured
diabetes
postural hypotension
Angiotensin Receptor Blockers
• Losartan (Cozaar®), Valsartan (Diovan®), Ibresartan (Avapro®), Candesartan (Atacand®)
• Same actions as ACE Inhibitors except no ____effects (dry cough, rash, angioedema).
• Will decrease PVR and CO
• Very well ____ drugs. Much less postural hypotension than other vasodilators
• Both ACEIs and ARBs used in ____
• All end in \_\_\_\_; all directly block the angio 2 receptors ○ Do all the same things as ACE inhibitors, except don't inhibit the bradykinin breakdown > no angioedema and no dry cough • Both ACEIs and ARBs used in CHF ○ Have some vasodilation effects, and by blocking aldosterone you get less \_\_\_\_ (in CHF you retain those); and they slow the heart down a little bit
bradykinin tolerated CHF -sartan water and sodium
Beta Adrenergic Blocking Agents 1
• ____: Propranolol (Inderal®), Nadolol (Corgard®), Timolol (Blocadren®)
• ____ : Labetalol (Normodyne®), Carvedilol (Coreg®)
• ____: Metoprolol (Lopressor®), Atenolol (Tenormin)
• All decrease ____, decrease ____ release by kidney and somewhat blunt ____ outflow
• Three types of beta blockers (-olol) ○ Non-selective (b1 and b2) § Problem: if you block b2 you'll get \_\_\_\_ which is an issue for asthmatics ○ Non-selective (with a1 blocking activity) § Used in the treatment of \_\_\_\_ ○ Cardioselective (b1 only) • Decrease renin release ○ Some blunting of the RAT system • Early on in therapy > \_\_\_\_ > blunting sympathetic activity • Most likely to casue postural hypotension: the ones that also block \_\_\_\_
non-selective non-selective with alpha1 blocking activity cardioselective (b1 only) CO renin sympathetic
vasoconstriction
dizziness and being tired
alpha1
Beta Adrenergic Blocking Agents 2
• Other indications include ____, cardiac arrhythmias, ____ (nonselective), and CHF (nonselective with ____).
• AEs: ____ with non- selective, worsening of intermittent ____ with non-selective, postural ____ (with nonselective with α blockade), bradycardia, sedation.
•____ interaction with nonselective
• Intermittent claudication ○ People try to walk across parking lot and they get \_\_\_\_ in legs > because of poor blood flow in their legs > plaques, and carry less oxygen ○ The BV in legs are mainly \_\_\_\_ > block B2 > casue they to constrict ○ Usually have clogged up \_\_\_\_ also > signal to look at these too! • Sedation - cross the \_\_\_\_ • Look similar to local anesthetic • Epi interaction with nonselective > icnreased BP with \_\_\_\_
angina migraines alpha bronchoconstriction claudication hypotension epinephrine
cramping B2 coronaries BBB tachycardia
- 1:50,000 = 1 gram/50,000 ml = 1000 mg/50,000 ml = 0.02 mg/ml x 1.7 ml/carpule = ____ mg/carpule
- 1:100,000 = 1 gram/100,000 ml = 1000 mg/100,000 ml = 0.01 mg/ml x 1.7 ml/carpule = ____ mg/carp
- 1:200,000 = 1 gram/200,000 ml = 1000 mg/200,000 ml = 0.005 mg/ml x 1.7 ml/carpule =____ mg/carp
MRD in 150 lb adult = ____ mg (____ cartridges of 1:100,000)
0.034
0.017
0.0085
0.20
11
Epinephrine Receptor Actions
Alpha – 1 Adrenergic
____ skin and mucous membranes
Beta – 1 Adrenergic
Increased ____
Increased ____
Beta –2 Adrenergic
____
____ skeletal muscle and internal organs
vasoconstriction heart rate contraction force bronchodilation vasodilation
Epi/Propranolol Hypertensive Interaction
Alpha – 1 Adrenergic
Vasoconstriction skin and mucous membranes
• Propranolol ○ \_\_\_\_ is blocked ○ \_\_\_\_ is blocked • Don't use epi, just use locals • If need hemostasis - use two cartridges (.034mg of epi) • [???] • Knock out A1 with \_\_\_\_ - other is left unopposed > increased HR but a drop in BP ○ \_\_\_\_
B1
B2
azosin
epinephrine reversal phenomenon
Epi/Metoprolol Hypertensive Interaction
NO ____
B1
Diurtetics Sites of Action
• Wherever sodium goes \_\_\_\_ goes • Diuretics block the reabsorption of sodium and water > keep them in the \_\_\_\_ • As far as BP is concerned > the drugs that are used: ○ Hit the loop of the henle (\_\_\_\_ diuretics) § More action is occurring here than in the distal tubule > more \_\_\_\_ drug (not more \_\_\_\_) § Enhance excretion of K+ > low blood K+ > \_\_\_\_ ○ Distal tubule (\_\_\_\_ diuretics) ○ \_\_\_\_ sparing diuretics > block aldosterone, or a Na+ channel > \_\_\_\_ diuretic effect, but they keep K+ in the body § Combined with loops/thiazides to prevent potassium loss ○ \_\_\_\_ inhibitors § Acetazolamide > prevent high altitude sickness > when go into high altitude and not used to it you begin to hyperventilate > blowing off \_\_\_\_ > blood becomes alkaline because you build up sodium bicarb □ This drug blocks the reabsorption of sodium bicarb; get a very \_\_\_\_ □ Also used in \_\_\_\_ > a lot of bicarb in the ocular chamber
water kidney tubules loop powerful potent cardiac arrhytmias
distal
K+
weak
carbonic anhydrase
CO2
alkaline urine
glaucoma
Diuretics 1 • Thiazides: Chlorothiazide (Diuril®), Hydrochlorothiazide (Hydrodiuril®) – Main use is \_\_\_\_. Low \_\_\_\_ effect. – Decrease sodium and water reabsorption in \_\_\_\_. Some \_\_\_\_ lost also. Initially decreases in blood volume but over time this returns to \_\_\_\_.
• Loop diuretics: Furosemide (Lasix®), Ethacrynic Acid (Edecrin®)
– Main use is ____
– Much more ____. ____ ceiling effect.
• AEs of both:____, dehydration, ____, increased uric acid in blood
• Thiazides ○ Work in distal tubule ○ Low ceiling § Don’t diurese as much as loops ○ Keeps water and sodium in distal tubule > lower \_\_\_\_ volume > lower BP ○ Initially see a decrease in plasma volume > overtime it \_\_\_\_ > must be doing something else! • Good in CHF > reduce H2O and Na+; get the water out of the \_\_\_\_ • Loops ○ More powerful ○ Mainly used for CHF • Hypokalemia - low blood K+ • Increased uric acid in blood > compete with uric acid secretion in the renal tubule; so uric acid isn't secreted as readily > can end up with \_\_\_\_ and uric acid crystals
hypertension ceiling distal tubule potassium normal
congestive heart failure powerful high xerostomia hypokalemia
plasma
regulates
lungs
gout
Diuretics 2
• Potassium sparing diuretics
– Spiranolactone (Aldactone®): ____. Aldosterone cause Na and H2O retention and K excretion.
– Triamterene (Dyrenium®) : ____ in distal tubule of kidney
– Weaker than other diuretics. Mainly combined with thiazides and loops to decrease ____ loss.
Hersh says aldosterone causes ____ “retention”.**
- If you block aldosterone, you get sodium and water ____,
and potassium ____.
- Weaker diuretics. Typically add on drugs. Occasionally used alone on patients with ____ (blood potassium is too low).
aldosterone antagonist
Na channel blocker
K loss
Na and H2O
excretion
secretion
hypokalemia
Some Clinical Considerations
• Additive CNS depressant effects when opioids or benzodiazepines prescribed with centrally-acting ____.
• Xerostomia most likely with ____ and centrally-acting α2 agonists
• Postural hypotension must likely with ____, Ca channel blockers, ____ enhancers, K channel activators, ____ blockers
• Don’t push epinephrine dose in patient on ____
• NSAID (ibuprofen, naproxen) therapy for more than 5 day may blunt antihypertensive effects of ____, ACE inhibitors and ____
- Xerostomia because you’re peeing so much, dehydrated.
- Centrally acting a-2 agonists- neurons have a-2 receptors.
- Remember the epinephrine reversal phenomenon is with the ____ blockers.
- Last bullet point- why? Because in the kidneys, prostaglandins are the
good guys – increase renal blood flow and ultimately increase the secretion of sodium and water. Its been shown in people on NSAID
therapy for more than 5 days, can blunt some of the antihypertensive effects of various drugs. Makes sense because you get ____ so your BP goes up. Doesn’t mean you can’t give NSAIDs on BP meds, it means keep the course short
a2 agonis diuretics a1 . blockers NO/cGMP adrenergic neuronal nonselective B blockers beta blockers diuretics
a1
water and sodium retention
