what percentage of sodium is reabsorbed?

where?

20-25% reabsorbed back to bloodstream (Loop H)

5-10 % reabsorbed in distal tubule.

3% in collecting duct 

Where does these take place?

1. Osmotic diuretics
2. CAI
3. Loop diuretics

1. Descending Loop of H and Proximal tubule
2. Proximal tubule 
3. Ascending loop of H

Where does these take place?

1. Thiazide diuretics
2. Potassium-sparing diuretics

1. Distal tubule
2. Distal tubule and collecting ducts

Carbonic Anhydrase Inhibitor drugs?

deriitives of?

which is used most commonly?

acetazolamide (Diamox)

methazolamide (Neptazane)

deriitives of sulfonamide antibiotics.

Most common--acetazolamide (Diamox)

• inhibits ion conc. in renal tubules==>sodium and water will be eliminated with the urine. (little sodium and water can be resorbed into the blood)

How does hydrogen ions effect urination?

What happens with it?

w/o it?

• "H" is needed for sodium and water to be reabsorbed back into the blood stream.

• needed to exchange sodium for hydrogen ions

• w/o "H"  sodium and water will b eliminated with urin

glaucoma, edema, and high-altitude sickness, epilepsy(rarely)

• open-angle glaucoma- to lower pressure
• edema- secondary from heart failure that has become resistant to other drugs.
• high-altitude sickness- prevents and treats symptoms. (headache, nausea, SOB, dizziness, drowsiness, and fatigue) 

• CAIs induce metabolic acidosis, which prevents seizure conitions
• CAIs induce respiratory acidosis as well. Both increase O2 during hypoxia

• metabolic acidosis- only benefical for prevention of seizures
• hypokalemia
• drowsiness
• anorexia
• parathesias (lack of sensitivity)
• hematuria (blood in urine)
• urticaria (hives)
• photosensitivity 
• melena (blood in stool)

• digitalis (digoxin) toxicity
• increase effects of: amphetamines, carbamaepine, cyclosporin, phenytonin, and quinidine

Loop Diuretic Drugs

• bumetanide (Bumex)
• furosemide (Lasix)
• torsemide (Demedex)

blocking sodium reabsorption

• increase prostaglandins in kidney-> dialation of blood vessels.
• decrease BP (botht he preload and central venous pressures, which are the filling pressures of the ventricles.

• potent diuretic- great loss of fluid loss
• dec. BP
• dec. pulmonary vascular resistance
• dec. systemic vasc. resistance
• dec. central venous pressure (atrium)
• dec. Lt. ventricle EDP
• K and Na depletion (why water follows)

• gets rid of Na and K
• manage liver or Renal disease
• controls Hypertension (manage edema 2ndary to Heart failure)
• helps excrete calcium in patients w/hypercalcemia

• last 2 hours
• their potent theri diuretic action continues even when creatinine clearance decreases below 25 mL/min (low GFR rate)

• Hypokalemia
• hyperuricemia (high uric acid levels)
• tinnitus (ringing of the ears)- autotoxicity
• hyperglycemia
• Nausea
• Vomiting
• thrombocytopenia,neutropenia
• blurred vison
• headache, vomiting, diarrhea

• when given w/Digoxin it increases the levels of toxicity b/c of Hypokalemia which is induced by diuretic.
• NSAIDS
• Sulfonylureas

• incre. GFR
• increase Renal plasma flow through kidney
•  Prevent kidney damage during ARF 
• glaucoma- reduces pressure for glaucoma

• treats early phases of ARF
• reduces ICP, and treat cerebral edema
• promotes excretion of toxic substances

• convulsions, thrombophlebitis, pumonary congestion
• headaches, chest pains
• tacycardia, blurred vision
• chills, fever

• when there is no urine present
• severe dehydration
• pulmonary congestion
• Cerebral hemorrhage (bleeding, stroke)

What route is Mannitol given by?

what kind of drug is it?

What is so special about Mannitol and how it is given? How should you store it?

• given IV with its own tubing and filter
• Can Not be stored in low temp because it can crystalize.
• used in neuro surgery. 

Potassium-Sparing Diuretic Drugs

which is more common? 

• amiloride (Midamor)
• spironalactone (Aldactone)--> more common
• triamterene (Dyrenium)
• spironalactone and triamterene BOTH are used for hyperaldosteronism, and for hypertension, and heartfailure

Potassium-Sparing Diuretics--> where?

action?

• where- collecting ducts and distal tubules
• interfere w/ Na and potassium exchange (Na is excreted and potassium retained.) 
• inhibit aldosterone receptor

prevents excretion of K (hold on to potassium)

premotes sodium and H2O excretion

What kind of Diuretic is Potassium-Sparing Diuretic. Weak or Strong?

What does this mean?

1. Spironolactone- gynecomastia in males (poliferation of breast). -post menopausal bleeding
2. triamterene- decrease folic acid=>formation of kidney stones and urinary cast

Thiazide diuretics

• hydrochlorothiazide (Esidrix, HyroDIURIL)
• chlorothiazide (Diuril)
• trichlormethiazide (Metahydrin)

• inhibits reabsortion of K, Cl, Na (its excreted)-K is not excreted as much
• dialate arteriols->decre. BP (b/c less periferal vascular resistance)
• decrease Na, H2O, and K.

shouldn't be used if creatinine clearance is <30-50 mL/min

normal=125 mL/min

metolazone (Zoroxaalyn) (Thiazide-like drug)----is effective even when creatinine is <10 mL/min

hypertension

edema

idiopathic hypercalceuria

diabetes insipidus (pee alot)

heart failure

adjuc. drug

adrenal heart failure-cirrosis and more

• BP, daily weight, I/O- Na, K, Cl(with thiazides) , diuretics given in the morning. K > 3 mEq/L- they dont need K supplement. eat potassium rich food (banana, dates, orage, broccoli, meat), drink enough H2O.
• dont eat liquorish with thiazide (b/c can cause hypokalemia 
• signs of hypokalemia- irregular pulse rate, muscle weakness, lethargy, constipation