diuretics Flashcards
Carbonic Anhydrase Inhibitors MOA
Inhibit formation of H+ and bicarb from H20 and CO2 via inhibition of CA and decrease resorption of NaHCO3
MOA of Loop diuretics
- Inhibit NaCl reabsorp TALOH
- Inhibit Na/K/2Cl transporter (lots of solutes in tubule; increase diuretic effect)renal prostaglandin prod via COX2 incr renal blood flow & inhibits Na reabsorption in the loop
Effects on blood flow thru vascular beds: relieve pul congestion prior to diuretic effect
*NOT shown to mortality
can cause you to loose magnesium and Ca
DTC
under the influence of parathyroid hormone
independent of Na
but if Na/Cl transport is blocked more Ca will be reabsorbeD?
18:mins
Early collecting tubule Na is reabsorbed under the presence of
aldosterone
Na and K is exchanged (not co transport) but you will see more K loss
ADH works where
collecting tubule
seen with decrease in serum Na
adenosine inhibitors
increase renal blood flow
Prostaglandins enhance the effect of what diuretics? how?
Role of 5 PG synthesized and with receptors in kidney poorly understood
PGE2 reduces Na reabsorption in TAL of Henle’s loop and ADH-mediated water transport in collecting tubule – enhance loop diuretics
if someone is on a loop diuretic what happens with protoglandins
increase production of prostaglandin (will be decreased under the presence of a Nonsteroidal anti-Inflammatory drug like indomethacin)
Made in distal tubule
Blunts sodium reabsorption
Vascular effects - decreases afferent tone and increases efferent tone leading to a increase in GFR
Natriuretic Peptides
MC: Acetazolamide (PO, ER, IV)
MC: Methazolamide (PO)
Carbonic Anhydrase Inhibitors(least important)
Carbonic Anhydrase Inhibitors MOA for glaucoma
Ciliary body secretes bicarbonate from blood into aqueous humor
Reduce formation of aqueous humor, thereby lowering IO pressure
Carbonic Anhydrase Inhibitors MOA for HTN
Works in PT
- increase excretion of HCO3, Na, K
- Decrease in H2O reabsorption- (increase rine vol & more alkaline)
all diuretics are eliminated
through the kidney
some like methazolamide is also metabolize din the liver
what are the main indications for carbonic anhydrase inhibitors
glaucoma
altitude sickness
used to be used to high BP
metabolic acidosis
why do we see hyperglycemia with carbonic anhydrase inhibitors
low potassium results in low absorption of glucose
also see reduced release of glucose
CNS symptoms with carbonic anhydrase inhibitors
- CNS (ie. drowsiness, malaise, HA, confusion, depression,irritable, nervous, excitement, dizzy) paresthesias: numbness, tingling of tongue, lips, anus) decrease electrolyte
o w/ high doses
what allergy do we worry about with carbonic anhydrase inhibitors
- Hypersensitivity (sulfas)
hematological concerns with carbonic anhydrase inhibitors
- Hematologic: anemia, leukopenia, thrombocytopenia (RARE)
this diabetic medication has diuretic properties.
SGLT2 - block Na & Glucose reabsorption.
increase prostaglandin production seen with can have what effect on edema
relieve edema even before you see diuretic effect
MOA of loop diuretics
Inhibit NaCl reabsorp Thick ascending loop of henley
Inhibit Na/K/2Cl transporter (lots of solutes in tubule; increase diuretic effect)
renal prostaglandin prod via COX2 increase renal blood flow & inhibits Na reabsorption in the loop
ADE of loop diuretics
- Hypo-K, metabolic alkalosis
- Hypo-Mg (check K and Mg)
- Increases UA levels (gout)
- Orthostatic hypotension
- Ca loss
Otic effects: Tinnitus, hearing impairment/loss - Hyperglycemia, glycosuria
- Hypersensitivity (sulfas)
- Electrolyte sx’s
- GI: N/V/D, anorexia, constipation
- Nervous, dizzy, lightheadedness, HA, paresthesias
- Hematologic: anemia, leukopenia, thrombocytopenia (rare)
DI with loop diuretics
- Digoxin-hypoK ír isk of toxicity
- Other diuretics: additive HoTN agents
- K+ loss drugs (amphloterocmin, corticosteroids)
- Erythro/AG Auditory tox
- Indomethacin –> dec. efficacy of loop diuretics
- Cholestyramine, colestipol ( absorption -bind to everything)
- Hypotension: additive effects
very significant DI seen with loop and thiazide seen with Indomethacin as a result of
prostaglandin production is inhibited by indomethacin
thiazide that has been studied the most
- Chlorthalidone**
Thiazide MOA
distal tubule co-transpoter sodium and chloride
- Inhibit NaCl resorpt (DCT)
increase prostaglandin too
chlorthalidone 1/2 life
40 hrs because 90% are bound to RBC
HYDROCHLOROTHIAZIDE 1/2 life
5.6-9 hrs
do not use if blood pressure is uncontrolled because very short half life
DOC: uncomplicated HTN
Thiazide Diuretic
DI with thiazide
all the same as loop diuretics in addition
Same as Loops
- Lithium thiazides lithium levels Li toxicity
- Ca2+ salts hyper-Ca from renal tubular reabsorption of Ca
Thiazides + loops used for severe renal dysfunction - Check K w/i 1st/2nd wk of tx
MOA of potassium sparing diuretics
Inhibit Na resorption in distal tubule
- Amil/Tria: inhibits Na flux thru ion channels of principal cell
- Spiron/epler: aldosterone antagonist
- Depends on prostaglandin production
K-sparing diuretics that act on Channels
- Tramterene
- Amiloride
K-sparing diuretics that Block Aldosterone
Block Aldosterone
- Spironolactone
- Eplerenone (more specific)
K-sparing diuretics Combo + HCTZ
Dyazide
- Maxzide
- Moduretic
- Aldactazide
used in the presence of -Oliguric renal failure (prevent anuria)
- Osmotic diuretics
- Mannitol (IV
Oliguric renal failure (prevent anuria)
- Decrease ICP prior to/during neurosurgery
- Decrease IOP acute angle-closure glaucoma
MOA of mannitol
Prevents normal resorpt of H20 via osmotic force (PCT, descending)
(large sugar molecule)
- ConivaptAN (po)
- TolvaptAN (IV)
drug class
ADH ANTagonist
AVP V1A &V2 antagonist - diuretic
- ConivaptAN (po)
- TolvaptAN (IV)
indications
- HTN, Ortho HoTN, hypoK, constipation, diarrhea, HA
-TolvaptAN warning
select liver damage
short term only
Demeclocycline
-Lithium
are both what types of drugs and what are their indications
Other ADH ANTagonists used to treat SIADH
- ConivaptAN (po)
- TolvaptAN (IV)
ADE
- Nephrogenic DI severe hypernatremia
dose adj in loop diuretics with renal failure
based on osmolairc volume
poor blood pressure control might be an issued with thiazides why?
short 1/2 life?
neprolithiasis might be useful to us
THIAZIDE
methazolamide drug class and where it acts
CAI
PCT
ADE of CAI
sulfa hypersensitivity
HYPERGLYCEMIA
metbaolic acidosis
drowsiness paresthesia
name all CAI
acetazolamide methalzolamide dorzolamide brinzolamide dichlorhenamide
dosage of acetazolamide
250mg 1-4x a day for glaucoma
250 mg -1g qd for altitude sickness
three major loop diuretics
furosemide
bumetanide
torsemide
inidcations for loop
Edema due to congestive heart failure, acute pulmonary edema, nephrotic syndrome, and hepatic cirrhosis
HF – used for control of fluid overload, not shown to reduce mortality, used for symptomatic relief
Hypertension – in patients with reduced renal function where thiazide diuretics may not be effective
Hypokalemic metabolic alkalosis
Mg+ loss (check K+ and Mg+)
Ca+ loss - may be compensated by reabsorption in distal tubule if dehydrated and
and increase Vit-D dependent reabsorption in gut
Increased uric acid levels - gout
are all sxs
loop diuretics
how would you treat HTN in a pt wiht reduced renal function
loop
NSAIDS can affect the function of what two diuretics
loop and thiazide
through PG
Cholestyramine can decrease absorption of
furosemide
increases urine volume
Diuretic
increases sodium excretion
naturuietic
increases solute free water excretion
aquaretic
high altitude sikness occurs over
> 9000 ft –> pulm edema
why due you have to be careful with salt and thiazides
more salt consumed the more K you will lose
which diuretics do you use in HF
fluid volume mngmt with thiazides but usually loop because renal function isn’t great
which diuretic would you primarily use for HTN
thiazides
CrCl>30
and not CKD 4 or 5
kidney disease what diuretic would you use
rentention of Na and water use thiazide or loop
what diuretic would you use with hepatic cirrohsis
low albumin causes activation of RAAS
spironalactone can be very effective
loop alone may be inefective
calcium kidney stones what diuretic would you use
thiazides (increases reabsorption)
hypercalcemia
loop blocks Ca reabsopriton
diabetes insipidus
thiazides reduce plasma volume
reduce plasma volume and GFR leads to greater Na water reabsorption and less fluid present in collecting tubule
