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Pharmacology > Loop diuretics, thiazide and K+ sparing diuretics > Flashcards

Loop diuretics, thiazide and K+ sparing diuretics Flashcards

1
Q

loop of Henle - very permeable to

A

water, interstitium hyperosmotic – water is reabsorbed

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2
Q

TAL – impermeable to

A

water

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3
Q

TAL - reabsorbed

A

of sodium, potasium and chloride (co-transport)

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4
Q

how much sodium from the original filtrate is reabsorbed in the TAL

A

25%

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5
Q

what does TAL stand for

A

thick ascending limb

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6
Q

where are positive ions reabsorbed into

A

the blood

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7
Q

which pump is present in the ascending limb

A

Na+, K+, 2Cl-

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8
Q

how do loop diuretics work

A

Sodium is not reabsorbed into blood – don’t build up gradient – all the ions stay in the urine
Delivers hyperosmotic urine – ions stay inside the tubule

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9
Q

what drags the gradient

A

the sodium potassium ATPase - moves 3Na into the blood 2 K into epithelial cell -

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10
Q

what kind of diuretic is furosemide?

A

loop diuretic

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11
Q

what is the main action of the loop diuretic Furosemide?

A

inhibit Na+/K+/2Cl-

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12
Q

what does furosemide cause?

A

Cause 15-25% of filtered Na+ to be excreted – “Torrential urine production”

Result in increased osmotic pressure in filtrate delivered to distal tubule (decreases water reabsorption)

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13
Q

when is furosemide used/

A

Heart failure – chronic/or acute pulmonary oedema
Hypertension
Hepatic cirrhosis complicated by ascites
Nephrotic syndrome
Renal failure
Hypercalcaemia

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14
Q

what is hepatic cirrhosis?

A

high pressure in portal vein – get oedema in abdomen

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15
Q

nephrotic syndrome

A

filtration doesn’t work – get protein in the urine

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16
Q

what are the unwanted effects of furosemide? - directly related to the drugs renal action

A

Hypovolaemia/Hypotension – Excessive Na+ loss and diuresis
Hypokalaemia – K+ loss
Metabolic or “contraction” alkalosis – Increase plasma [HCO3-]

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17
Q

what are the unwanted effects of furosemide? - unrelated to the drugs renal action (rare)

A

dose-related hearing loss

allergic reactions: rashes, bone marrow depression

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18
Q

A 64-year old man with known congestive heart failure is admitted to the A&E with signs of acute pulmonary edema. He is immediately treated with oxygen by face-mask, morphine for respiratory distress, nitrates as vasodilators to reduce the pre-load as well as a bolus of diuretics intravenously to stimulate diuresis.

Which is the diuretic of choice to be used in this clinical condition?

A

furosemide

Pulmonary edema – water in the lungs

Furosemide – acts fast – gets liquid out lungs

Wouldn’t use mannitol – drags water from tissue – don’t want to keep water in alveroli – mannitol could stay in the alveoli too – keep water ther

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19
Q

where do thiazides act

A

on the sodium chloride cotransporter in the distal convoluted tubule (DCT)

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20
Q

what is absorbed in the DCT?

A

5% of sodium is reabsorbed

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21
Q

the DCT is impermeable to

A

water

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22
Q

what kind of pump is the sodium chloride pump that thiazides work on

A

atp ase

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23
Q

Na gets into the cell then into the blood, if the pump is blocked

A

can’t be reabsorbed into the cell

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24
Q

what kind of diuretic is hydrochlorothiazide

A

thiazide

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25
Q

how do thiazides work?

A

Block Na+/Cl- co-transporter

results in higher osmolarity of urine and decreased water reabsorption

26
Q

why is the effect of thiazides self limiting?

A

lower blood volume - refine secretin - angiotensin and aldosterone - limitation of the effect of thiazides (pleatueu)

27
Q

what are thiazides used for

A

Long term of diuretics
adjunct in congestive heart failure / hypertension

nephrogenic diabetes insipidus (“thiazide paradox”)

Variable oral absorption
10-20% for hydrochlorothiazide

28
Q

what are the unwanted effects of thiazides related to renal action

A

Hypokalaemia, metabolic alkalosis (as in Loop diuretics)
Hypocalciuria
Hypomagnesaemia
Hyponatraemia

29
Q

what are the rare unwanted effects of thiazides unrelated to renal action

A

Hyperuricaemia precipitating gout (thiazide competes with uric acid for tubular secretion)

Hyperglycaemia – impaired pancreatic release of insulin and diminished tissue utilization of glucose

Higher plasma cholesterol level

30
Q

what are the rare unwanted effects of thiazides unrelated to renal action

A

Hyperuricaemia precipitating gout (thiazide competes with uric acid for tubular secretion)

Hyperglycaemia – impaired pancreatic release of insulin and diminished tissue utilization of glucose

Higher plasma cholesterol level

31
Q

how much sodium is reabsorbed in the collecting duct

A

1-2%

32
Q

what is potassium exchanged with in the collecting duct

A

hydrogen

33
Q

what is the collecting duct activity dependent on?

A

tubular conc of sodium

34
Q

what is activity in the collecting duct regulated by?

A

aldosterone

35
Q

where is aldosterone secreted frm

A

the adrenal cortex

36
Q

what are aquaporins and where would you find them?

A

water channels that are in the wall of collecting duct

37
Q

how does vasopressin affect the number of aquaporins

A

decreases the number of aquaporins

ADH

38
Q

how does aldosterone affect the number of aquaporins

A

increases the number of aquaporins - helps the reabsorption of water and electrolytes

39
Q

what are the 2 classes od K+ sparing diuretics?

A

ENaC blocker and aldosterone antagonist

40
Q

examples of ENac blockers

A

triamterene and amiloride

41
Q

what is the action of ENas blockers

A

Directly block epithelial Na+ channel (ENaC) in distal tubule, collecting tubules and collecting ducts (limited diuretic efficacy)
Used in conjunction with loop and thiazide diuretics to maintain K+ balance

42
Q

what are the unwanted effects of ENaC blockers

A

Hyperkalaemia
Gastrointestinal disturbance (rare)
Idiosycratic reactions: rashes (rare)

43
Q

example of an aldosterone antagonist

A

spironolactone

44
Q

Actions of Aldosterone on Na+ reabsorption

A

Early phase: increasing opening of ENaC
Late phase: promotes DNA transcription
Increase synthesis of ENaC
Increase synthesis of Na+, K+- ATPase

45
Q

aldosterone antagonist uses

A 
in conjunction with loop and thiazide diuretics to maintain K+ balance
  adjunct therapy in heart failure
  hyperaldosteronism 
 primary (Conn’s syndrome)-rare
 secondary (due to hepatic chirrhosis)
46
Q

aldosterone antagonist unwanted effects

A

Hyperkalaemia (can be fatal if ACE inhibitor, angiotensin receptor antagonist or b-blocker are co-prescribed)
Gastrointestinal disturbance (common)
Menstrual disorders or testicular atrophy (acting on progesterone or androgen receptors

47
Q

what is hyperkalemia and what can it cause

A

high potassium – arthimia in the heart

48
Q

A 55-year old woman with known hypertension has been treated with furosemide and hydrochlorothiazide for peripheral edema. At a regular check-up the GP finds she still has ankle edema. Blood work shows K+ 2.8mEq/L.
What is the best recommendation:

A

add spironolactone

Potassium is a bit low
Want to decrease dieuretic effect – spironolcatone – gives potassium
Low potassium is dangerous

49
Q

A patient with congestive heart failure becomes refractory to a loop diuretic even if the normal doses where progressively increased 5-fold. Blood work shows K+ 4.0mEq/L.

What do you do next?

A

add spinonolactone

50
Q

angiotensin II

A

INCRESES:

  • sympathetic activity
  • tubular Na Cl reab, K excretion, and H2O retention
  • aldosterone secretion
  • arterial vasoconstriction - inc.BP
  • ADH secretion - collecting duct H2O absorption
51
Q

what does ACE do

A

converts angiotensin I to angiotensin II

52
Q

what do ACE inhibitors end in

A

-pril

53
Q

what does enalapril do/

A

inhibits the production of angiotensin II - used reduce oedema resulting in heartfaliure

54
Q

what can other kidney drugs do

A

alter pH of urine, alter excretion of organic molecules, used in renal faliure

55
Q

what would you use to treat cardiac decompression

A

Loop diuretics
Thiazides
K-sparing diuretics

Maintain [K+]o balance is particularly crucial as Low [K+]o is likely to increase toxicity of digitalis, thus is hazardous

56
Q

Hypertension

treat with

A

Thiazides
Loop diuretics

Maintain [K+]o balance is particularly crucial as
High [K+]o can be fatal if ACE inhibitor, angiotensin receptor antagonist or b-blocker are coprescribed

57
Q

Ascites treat with

A

Periodic administration of diuretics either eliminates the necessity for or reduces the interval between paracentesis
Contributes to the comfort of the patient
Conserves proteins, which otherwise will be lost when ascitic fluid is mechanically withdraw

Loop diuretics
Thiazides

58
Q

Chronic renal failure

A

Patient is more frequent subject to electrolyte imbalance
Diuretics are less effective in patients with primary renal disease
Higher doses of the thiazides may decrease the glomerular filtration rate

59
Q

acute renal failure

A

Diuretics are not recommended in incipient acute renal failure

60
Q

Nephrotic syndrome

A

Response to diuretics is often disappointing

Pharmacology (18 decks)

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