14. Renal Flashcards
Thiazides
act where
Cause what
Which is more potent v furosemide
Other affects
metabolic x4
Prox DCT
luminal NaCl Symport = secretion
Increased Na to distale drags potassium
activates RAAS
< potent than loop
Metab Reduce insulin secretion Rise chol ; TG Gout exacerb - red urate secr HyperCa
HypoCl HypoK Alkalosis
Red SVR - main exertion of hypotensive effects
0
0
Loop diuretic
inhibit what
NA K cl symporter
Amiloride inhibits what
Epithelial sodium channels
Inhibitors of vasopressin examples x2
cause what condition
Drugs which lead to nephrogenic diabetes insipidus such as lithium and demeclocycline.
Hartmanns contains & mmol
Osmolality
Sodium 131 mmol/l Chloride 111 mmol/l Potassium 5 mmol/l Calcium 2 mmol/l Lactate 29 mmol/l.
278 mosmol/kg,
Captopril
Mech- result
RBF?
SVR
Dry cough?
ACE inhibitors
Conversion Ag1->Ag2
Red aldosterone secretion,
Natriuresis.
RB flow is increased
Renal artery stenosis renal perfusion red
SVR red
The dry cough seen with ACE inhibitors is thought to be due to an accumulation of bradykinins.
Hypoklaemia
From
- insulin therapy
Cell membrane sodium-potassium = intracellular shift of potassium. - Nebulised salbutamol is a recognised treatment for hyperkalaemia.
- Prednisolone is capable of producing hypokalaemia due to excessive potassium excretion.
- conversely aldo antag - hyperk - Thiazide
5 Loops
Hyper
- Addison’s is associated with hyperkalaemia.
- Spironolactone is associated with potassium retention.
- ACEi
Mannitol
Osmotic diuretic Filtered at the glomerulus - not reabsorbed - creates an osmotic gradient - excreted - osmotic equivalent of water
Forced diuresis to treat drug overdoses
cerebral oedem
maintain a diuresis during surgery.
- Renal prostaglandins
= Renal arteriolar dilation
= tubular urine flow that is thought
protect against renal injury by reducing tubular obstruction by cellular debris. - free-radical scavenger
Reduces the harmful effects of free radicals during ischaemia-reperfusion injury.
- oxygen free radical scavenging properties,
-reduce the risk of an ischaemia-reperfusion injury.
Thiazides act where
Act where
On what
Thiazides, of which metolazone and bendroflumethiazide are examples, inhibit sodium reabsorption at the distal convoluted tubule.
Loop diuretics
Act where
Loop diuretics inhibit reabsorption from the ascending limb of the loop of Henle.
Spirinolactone
What is it
Acts where
Spironolactone is a synthetic steriod with an aldosterone-like structure which antagonises the effect of aldosterone on the distal convoluted tubule and collecting duct. It also has anti-androgen effects.
Mannitol is
acts where
Mannitol is an osmotic diuretic and works primarily on the proximal convoluted tubule but also has secondary effects on the descending loop of Henle and collecting ducts.
Bumetanide
Bumetanide is a loop diuretic
- plasma protein bound (>98%),
- cannot be freely filtered into the glomerulus, it is secreted into the tubular lumen by an organic acid transporter
- excreted unchanged.
It inhibits the Na+K+2Cl- co-transporter in the ascending loop of Henle, leading to an increased delivery of sodium and water to the distal convoluted tubule.
It is forty times more potent than furosemide.
Oxygen consumption in the nephron is decreased by loop diuretics and in the loop of Henle this may be reduced to basal levels.
Loop diuretics are associated with:
Hypokalaemia Hyponatraemia Hypomagnesaemia, and Metabolic alkalosis. They can also reduce ventricular preload by causing vasodilatation.
Thiazides
act @
causes
which also causes and may lead to
Also act at -
causing
s/e
mainly at the proximal part of the distal convoluted tubule to inhibit active resorption of sodium and chloride.
There is increased excretion of potassium and hydrogen ions (rather than inhibition of resorption) and a hypokalaemic alkalosis may develop.
They also act at the proximal tubule and cause weak inhibition of carbonic anhydrase, and have a direct vasodilatator action.
Side effects of thiazides are numerous and include:
Hypokalaemia
Hyponatraemia
Hyperuricaemia
Hypomagnesaemia
Hypercholesterolaemia (and high triglycerides) and rarely
Thrombocytopenia.
Hyperglycaemia occurs due to an enhancement of glycogenolysis and reduced insulin release.
Carbonic anhydrase
act where
do what
main use
inhibitors cause:
x6 common s/e
proximal convoluted tubule
Bicarbonate, sodium and potassium loss
are used mainly in the treatment of glaucoma.
Carbonic anhydrase inhibitors cause:
Metabolic acidosis
Hypokalaemia
Hyponatraemia
Renal calculi but not hypercalcaemia
Fatigue and paraesthesia of limbs
Stevens-Johnson’s syndrome.
Furosemide
Inhib what
where
binding to
Causes Increased what
Results in
Affect on oxygen in kidney?
Furosemide inhibits
Na+/K+/2Cl- co-transporter
in the ascending loop of Henle,
by binding to the chloride site.
This causes an increased delivery of sodium and water to the distal convoluted tubule,
where an exchange for hydrogen and potassium ions occurs.
The loss of water, sodium, chloride, hydrogen and potassium ions (as well as calcium and magnesium ions) then occurs. This may lead to hyponatraemia, hypokalaemia and hypochloraemic metabolic alkalosis.
Loop diuretics are generally used to treat oedema not hypertension.
Furosemide may reduce medullary oxygen requirements by diverting blood away from the juxtaglomerular area to the cortex, but this may have little impact on medullary hypoxia. There is no convincing evidence that this has renal protective effects.
K sparing diuretics
Potassium sparing diuretics such as amiloride and spironolactone are used in combination with other diuretics to counteract the loss of potassium. They are rarely used alone.
Mannitol
Mannitol is freely filtered by the glomerulus and is pharmacologically inert as it is neither excreted nor re-absorbed.
Hypokalaemia in asthma
4 meds/causes
Beta-2 adrenoreceptor agonists and epinephrine (adrenaline) cause a rise in intracellular potassium with resultant hypokalaemia.
Corticosteroids cause sodium and water retention and potassium loss.
A respiratory alkalosis (not hypercarbia) causes a compensatory shift of potassium into the cells.
Drugs that cause DI
/ Concetrating ability of kidneys
Li
Democycline
Gentamycin
Amphoter B
drugs removed by dialysis
methyldopa = 15% protein bound
somehwat water solublbe
removed well by diall
drugs not removed
furosemide
haloperiodl
nifedipine
all highly protein bound poorly removed
Dextrans
branch pollysach = bact modif sucrose
improve periph flow - reduce viscoity - adhere endothel + cell elements blood
cross match problems
impair plt activity
reduce level FVIII
S/E Rfail (tube obstrcut) anaphylactoid exn = x immunisations v bact anti a antogem formation rouleaux formation
not vte
Loop act where
whats the mechanism
what do they do to renal flow
mainly thick ascending loop
some action early distubule
inhib na and cl reab
increase flow
may cause a rise in lithim levels
Spinolactone
is there IV prep
metab
Canrenone
yes
Poatssium canrenoate
