Diuretics

Front 1

Osmotics

Back 1

Mannitol
a sugar alcohol given IV, it increases the oncotic pressure thus trapping the water. It inhibits water reabsorption throughout the tubule.

uses:
- decreases intraocular pressure in glaucoma
- decreases intracranial pressure
- reopen kidney function: tex in rhabdomyolysis myoglobin will be released and trapped in tubules and damages it. mannitol increases the clearance

side effect: hypovolemia

Front 2

carbonic acid inhibitors

Back 2

Acetazolamide, Dorzolamide

We need CA in the proximal tubule so that H is made. Without the protons, Na cant enter. With CA inhibitors Na will build up in the lumen, water will follow, you will excrete it. also bicarbonate will be lost - metabolic acidosis.

uses: glaucoma, metabolic alkalosis, acute mountain sickness.

what is special: hypokalemia and acidosis together. (hypokalemia: when you get hypovolemia aldosterone will increase pga RAS, aldosterone cause Na reabsorption in expense of H and K)

side effects:
- bicarbonaturia, acidosis, hypokalemia, hyperchloremia, renal stones, sulfonamide hypersensitivity

Front 3

Loooooop diuretics

Back 3

Furosemide, Ethacrynic acid (no sulphur), Torsemide

inhibits Na/K/2Cl transporter: so you will get hypo-all ions. måla upp bilden är lättast, för normalt kommer K leak back out to cause positive charge in lumen, which is why Mg and Ca gets reabsorbed into blood.

uses:
- DOC in acute pulmonary edema (heart failure)
- Acute renal failure
- Edema
- HTN (they cause VD by increasing prostaglandins: so NSAIDs can cancel HTN effect of furosemide)
- anion overdose

Side effects: Sulfonamide hypersensitivity, hypo all ions, alkalosis, hyperuricemia (forusemide is a weak acid so it competes with urate to be secreted in proximal tubule), ototoxicity

drug interaction: aminoglycosides (it also causes ototoxicity: additive), Lithium, Digoxin (hypokalemia enhances digoxin toxicity: digoxin competes with K)

Front 4

Thiazides

Back 4

Hydrochlorothiazide, Indapamide, Metolazone

Inhibits Na/Cl symport in distal tubule. Here is where Ca enters via PTH. (PTH R: Gs: cAMP, PKA: phosphorylates the Ca channel). You get low Na inside the cell which helps getting the Ca into the blood causing hypercalcemia.

Uses:
- Nephrolithiasis (calcium stones)
- HTN
- Nephrogenic diabetes insipidus

side effects: Sulfonamide hypersensitivity, hypokalemia and alkalosis, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia

Drug interactions: Digoxin, also avoid this drug in DM patients (thiazides are also ATP-dependent K channel openers)

Front 5

K sparing agents

Back 5

Spironolactone, Eplerenone (blocks aldosterone R)
Amiloride, Triamferene (blocks Na channel)

Uses of spironolactone:
- hyperaldosterone states
- CHF: aldosterone is elevated in CHF pga RAS
- adjunct to K wasting agents: to correct the hypokalemia (it is itself K sparing)
- Antiandrogenic use: spironolactone is not very selective as a steroid receptor antagonist (gynecomastia in men, females may treat acne and hirsutism)

side effects: hyperkalemia and acidosis, antiandrogen

Amiloride and Triamferene
uses: adjunct to K wasting diuretics, lithium induced nephrogenic diabetes insipidus
side effects: hyperkalemia and acidosis

Note: Eplerenone is a selective aldosterone receptor blocker

Front 6

ADH agonists
ADH antagonists

Back 6

ADH agonists:
activates V2 receptors: Gs: insertion of aquaporin H2O channels into luminal membrane: this reduces urine volume. H2O gets reabsorbed into blood.
- Desmopressin

ADH antagonists
used in SIADH.
- Conivaptan: inhibits V2 receptor
- Lithium: inhibits ADH

Front 7

Summary af all Diuretics

Back 7

all increase urinary Na
All increase K except K sparing agents
only CA inhibitors increases HCO3
Loops increase Ca, Thiazide decrease Ca

Front 8

CA inhibitors: urine

Back 8

Na, K, HCO3

blood pH: acidosis

Front 9

Loops: urine

Back 9

Na, K, Ca, Mg, Cl

blood pH: alkalosis

Front 10

Thiazide: urine

Back 10

Na, K, Cl, (mindre Ca)

blood pH: alkalosis

Front 11

K sparing agents

Back 11

Na, K

blood pH: acidosis