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Renal Drugs Flashcards

(59 cards)

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1
Q

volume dependence theory for essential hypertension

A

na retention

ECFV expansion

increased preload

increase CO

HTN!

  • low renin!!!

failure to autoregulate and vasodilate

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2
Q

nitroprusside

A

arterial and venous dilator

NO release followed by increase cGMP generation

IV – use in emergencies

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3
Q

side effect of selective alpha 1 blocker

A

orthostasis - take first dose in bed

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4
Q

aliskerin

A

renin inhibitor

inhibits renin to increase AII generation

don’t really know place in therapy yet

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5
Q

biotransformation

A

makes it easier for things to leave the body through the kidney

build up in CKD and can get symptomatic

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6
Q

propranolol

A

Non-selective Beta Blockers

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7
Q

K sparing diuretics adverse effects

A

hyperkalemia

gynecomastia (spiro)

triametere - kidney stones

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8
Q

renin profiling?

A

classify by renin level for essential htn

if high - beta blockers, ACEI, ARBs

if low - diuretics

not proven! urine monitor

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9
Q

IV contrast

A

known nephrotoxin!

can cause AKI

can lead to drug toxicity if can’t clear what they are taking

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10
Q

Carbonic Anhydrase inhibitors

A

Acetazolamide

Mountain Sickness Prophylaxis

Glaucoma (lowers intraocular pressure)

Proximal Tubule Diuretic – blocks countertransport of Na-H

Not used much for diuretic (only when HCO3 is high)

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11
Q

hydralazine

A

arterial dilator

direct effect on smooth muscle, safe in pregnancy

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12
Q

adverse effects of loop diuretics

A

increases Ca excretion

Hypokalemia

Metabolic Alkalosis

Hearing loss

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13
Q

losartan

A

ARB

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14
Q

non-selective alpha blocker

A

Blocks activation of receptors for vasoconstriction and NE release,

First line for treatment of HTN associated with cocaine – leads to reflex tachycardia

Do not use unless pheo, cocaine. If you gave a beta blocker to a patient with cocaine toxicity and hypertension, then you would knock out the beta effect which is in part vasodilatory and leave them with the unrestricted alpha effect of norepi if they are having cocaine or pheo.

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15
Q

Is toxin dialyzable?

A

low MW (fit through filter)

low protein binding (only free drug is filtered)

small Vd (only blood compartment is filtered)

low endogenous clearance (why bother if it will come out fast)

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16
Q

what does resistance dependent essential htn look like?

A

RAS

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17
Q

K sparing diuretics

A

**not used alone for HTN

all work distally

Triameterene, Amiloride block ENaC

Spiro is an aldo antagonist (lowers mortality in CHF)

good in CHF!

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18
Q

lithium overdose

A

very small, small Vd - dialysis!

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19
Q

Vaptans

A

conivaptal, tolvaptan

block ADH by binding it its recepotr

useful for hyponaturemia from CHF and cirrhosis

may be used to prevent cAMP generation in PKD

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20
Q

calcium channel blocker types

A

non-dihydropyridines (verapamil, diltiazen)

dihydropyridines (nifedipine)

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21
Q

thiazides

A

1 to treat HTN!!

block NCC on distal tubule

best for elderly, SBP - reduce U(Ca) - increase bone mineral density!!

distal action makes them less potent

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22
Q

adverse effects of non-dihydropyridines

A

constipation, negative inotrope, conduction delays

be careful if CHF, heart block, old people

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23
Q

hemodialysis

A

first created for overdose then instituted for CKD

Dialysis = stuff on one side of membrane that CAN’T MOVE through, and stuff that CAN MOVE through.

Based on diffusion, things move from one side of the membrane to the other.

Hemodialysis goes a little further.

Blood comes out of IV. Use a pump, stuff it into a machine full of fibers with hollow pores. Things will move to the other side based on their ability to move.

Would have concentration of 0 on the other side so things can move as fast as possible. Want a dialysate COUNTERCURRENT to FLUSH OUT THE OTHER SIDE OF THE MEMBRANE à if the concentration on the other side of the membrane is 0, things will move very quick!

Here’s another trick: b/c this is under pressure (like how kidney is under BP), there will be an ULTRAFILTRATE à H2O is forced to other side b/c of pressure and THINGS MOVE W/ WATER!

It’s a simple concept – things move across a membrane b/c they can and other things are stuck.

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24
Q

side effects of non selective beta blocker

Study These Flashcards
A

bronchodilation

25
beta blockers and HTN
not first line if no heart disease! does not prevent events
26
what htn drugs can you mix/not mix?
only ones you can't is ACEI + ARB
27
adverse effects of thiazides
Hypokalemia (Deliver Na to DT) Gout (increase in AII, Na reabsorption in PT, uric acid) Reabsorption of Ca Hyponaturemia Hyperglycemia (low insulin) Hyperlipidemia
28
what is Vd that is good for dialysis?
small Vd = more in blood compartment
29
pH and pKA of weak acids and bases
if pH \< pKa - all have H - HA, BH+ if pH \> pKa - no H - A- , B If pH \>\>\> pKa, mole will be CHARGED and TRAPPED in COMPARTMENTS! (basic pH à charged drug mole à can’t cross lipid membrane à drug will be trapped)
30
possible drug class for renal artery stenosis
ACEI, ARB high renin, ATII, aldo
31
PHASE I reaction
Phase 1 is taking LIPOPHILIC (simple long C molecules, big organic things) and ADDING POLAR SIDE GROUPS (electrophils – ketones, COOH, or nucleophiles, nitrogens and sulfars - do this to slightly INCREASE H2O SOLUBILITY + ADD SIDE GROUP that will allow something big to be ADDED TO THE END! Phase 1 à put something polar on molecule Phase 2 à conjugate something EXTREMELY POLAR to the first polar molecule that was added on in phase 1 to ENHANCE H2O SOLUBILITY
32
what does volume dependent HTN look like?
primary hyperaldo
33
loop diuretics
furosemide (lasix) short acting! good for edema (pulm) Blocks NKCC in TALH Increases Ca excretion Edema (pulm) HTN only in CKD CHF Nephrotic Syndrome Cirrhosis
34
PHASE II reaction
- big thing is PHASE 2 conjugation rxns aka adding a large residue to end of drug/biotransforming molecule (acetyl residues, glutathione residues, sulfyl residues) à these big side groups ENHANCE H2O SOLUBILITY SO IT CAN COME OUT OF THE KIDNEY Phase 1 à put something polar on molecule Phase 2 à conjugate something EXTREMELY POLAR to the first polar molecule that was added on in phase 1 to ENHANCE H2O SOLUBILITY
35
alpha 1 beta adrenergic blcoker
combined effect - less on cardiac output, HR
36
drug class for hyperaldo
diuretic, aldo-antagonist Na retention!
37
dihydropyridine side effects
edema from vasodilation, headache
38
causes of secondary hypertension
CKD hyperald RAS pheo
39
pH and charge of drugs
charged molecules do not cross bio membranes well (lipid - charges lik water)
40
which type of CCB are better for HTN?
dihydropyridines Better for HTN than non-dihydropyritines because more smooth muscle relaxation, less neg inotropy
41
possible drug class for pheochromocytoma
alpha and beta blockers elevated catecholamines
42
ACEI side effects
Kinin-induced cough Hyperkalemia
43
ARBs mechanism
Blocks 100% of ATII action, including non-ACE generated AII (more)
44
ACEI
captopril diminish generation of ATII from ATI increase kinins (vasodilation, inhibition of TGF-beta so decreased remodeling) The increase in bradykinin levels are helpful for remodeling and ARBs don’t have this effect. Decrease TGF-beta Do not use with ARB!
45
captopril
ACEI
46
Lithium + ibuprofen
lithium handled in PT like Na Na avid states increase lithium absorption and decrease elimination NSAID decresed GFR (impaired renal perfusion) - sodium avid (+ lithium avid!!)
47
Adverse effects of carbonic anhydrase inhibotrs
metabolic acidosis (lose HCO3) hypokalemia calcium phosphate kidney stones
48
non selective beta blocker
decreases renin, CO, periopheral resistance
49
alpha1selective adrenergic blockers
Blocks activation of receptor for vasoconstriction Relax sphincter in prostatic hypertrophy Lowers BP Not currently used for HTN because no cardiac benefit Has not been shown to decrease events
50
resistance dependence theory for essential hypertension
decreased renal BF, increased renin secretion, AII/aldo, HTN high renin!! looks like RAS
51
atenolol
Selective Beta-1 adrenergic Blockers
52
Bad rebound
drug has small alpha - leaves cells slowly! ongoing absorption from stomach level increases because still have pills in gut
53
selective beta1 beta blocker
Blocks chronotropic and inotropic effects, less effects on bronchial dilation and vascular dilation
54
treatment for phenobarbital OD
urinary alkalinization pKa = 7.3 - WA to human long half life! around forever
55
Canaglifozin
SGLUT2 blocker blocks Na/glucose cotransport in the PT - weight loss and decreases BP (adverse: high rate of DKA)
56
Good rebound
redistribution from intracellular stores increase amount in blood but good because it's coming from a place it wascausing harm NO clinical deterioration following HD opp for futher elimination!!
57
drug class for chronic kidney disease
diuretic low GFR, ECFV overload!
58
side effects of arterial dilators
hydralazine minoxidil Hair growth (rogaine) Vasodilation can lead to tachycardia so use with a beta blocker Edema so use with diuretic
59
Urine alkalinization
trap charged! drag molecules out of brain into urine ## Footnote Give bicarb à will force equillibrium reaction to create basic environment à drug will donate H+ and become charged à will trap drug in urineà guy wakes up. This guy has all sorts of problems to deal with, but is acutely medically improved by pH. This is about all things done by IV bicarb. Concept – Henderson Hasselback à change drug from one species to another environment that is BASIC to enhance its ability to have urinary elimination.

Renal 2 (4 decks)

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