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RENAL > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Give examples of drugs which act on the kidney

A

Diuretics
Vasopressin (ADH) agonists/antagonists
SGLT2 inhibitors
Uricosuric drugs (promote uric acid excretion)

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2
Q

When does oedema occur?

A

When there is an imbalance between the rate of formation and absorption of interstitial fluid

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3
Q

What 4 forces are responsible for the constant water exchange between blood and the interstitium?

A

STARLING FORCES
Pc - hydrostatic pressure in capillary
Pi - hydrostatic pressure in interstitial fluid

Op - oncotic pressure of plasma
Oi - oncotic pressure of interstitial fluid

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4
Q

Changes in which of the 4 starling forces promotes Oedema?

A

Increased Hydrostatic Capillary pressure

Decreased Plasma Oncotic pressure

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5
Q

What diseases change the Hydrostatic capillary pressure and plasma oncotic pressure therefore leading to oedema?

A
  • nephrotic syndrome
  • congestive heart failure
  • hepatic cirrhosis with ascites
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6
Q

How does nephrotic syndrome contribute to oedema?

A
  • Increased production of interstitial fluid
  • Decreased blood vol and cardiac output
  • Activates RAAS
  • Salt and water retention
  • Increased Pc, Decreased Op
    => oedema
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7
Q

How does congestive heart failure cause oedema?

A 
Decreased cardiac output 
=> renal hypoperfusion 
=> activates RAAS
=> Water and Na retention 
=> blood volume and pressure increases
BUT Op decreases
=> pulmonary and peripheral oedema
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8
Q

How does Hepatic cirrhosis with Ascites contribute to oedema?

A
  • Increased pressure in the hepatic portal vein
  • decreased production of albumin
    => loss of fluid into the peritoneal cavity and oedema (ascites)

Activation of RAAS occurs in response

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9
Q

What subtype of diuretics work in the proximal convoluted tubule?

A

carbonic anhydrase inhibitors

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10
Q

Where do LOOP diuretics complete their action?

A

Thick ascending limb of the LOOP of Henle

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11
Q

What diuretics work in the early distal convoluted tubule?

A

Carbonic Anhydrase inhibitors

thiazides

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12
Q

Where in the nephron do potassium sparing diuretics act?

A

Collecting duct

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13
Q

Why must diuretics get into the filtrate in order to act?

A

site of action of most diuretics is the apical membrane of tubular cells

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14
Q

How do diuretics get into the filtrate?

A 
glomerular filtration (for drug not bound to large plasma protein)
secretion in prox. tubule via OATs/OCTs
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15
Q

What are OATs and OCTs?

A

organic anion transporters (OATs) – transport acidic drugs

organic cation transporters (OCTs) – transport basic drugs

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16
Q

How does secretion of a diuretic into the filtrat contribute to pharmacological selectivity?

A

secretion means concentration of diuretic in the filtrate is higher than that in blood

=> more likely to act on receptors in nephrons than elsewhere in the body

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17
Q

How do Organic anion transporters move from the interstitium into the lumen of the nephron?

A

Na/K ATPase regulates low intracellular Na
=> Na outside cell moves IN via conc. gradient
=> Na moves in on transporter which also brings in α-KG
=> α-KG exchanges back out of cell for an OAT
=> Then moved into lumen via PRIMARY ACTIVE transport

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18
Q

Give examples of drugs that use OATs?

A 
Diuretics (bumetanide, furosemide)
Simvastatin
Many penicillins
NSAIDs
Endogenous urate
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19
Q

Describe how OCTs travel from the interstitium to the tubule lumen?

A
  • Na/K ATPase regulates membrane potential
  • OC+ moves into cell due to negative membrane potential attraction
  • Move into lumen via antiport with H+
    OR primary active transport MDR1
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20
Q

What drugs are known to use OCTs?

A 
diuretics (amiloride, triamterene => potassium sparing)
atropine
metformin
morphine
procainamide
endogenous catecholamines
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21
Q

Describe the normal function of the Na/K/2Cl triple cotransporter

A

Na moves in via triple transporter and out via Na/K pump
Cl moves in via triple transporter and out via CIC-Kb/Barttin
K moves in via triple transporter and out via apical or basolateral K channels

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22
Q

Why is it important to have K channels on the apical membrane

A

So K moves back into lumen

=> can rebind to transporter

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23
Q

What creates the charge difference between the lumen (+ve) and interstitium (-ve)?

A

K moving back into lumen

=> allows Ca and Mg to move paracellulary

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24
Q

What genetic diseases can affect the function of the triple co-transporter?

A

Mutation in transporter itself
CIC-Kb/Barttin mutation
K+ channel mutation

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25
Q

What does Bartter syndrome cause?

A

Na and H2O wasting

hypokalemia, alkalosis, and normal to low blood pressure

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26
Q

What are the main jobs of loop diuretics?

A
  • decrease hypertonicity of the medulla
  • prevent dilution of the filtrate in the thick ascending limb
  • increase the load of Na+ delivered to distal regions (=> lose K+)
  • increase excretion of Ca2+ and Mg2+
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27
Q

How soon after IV and oral administrations does furosemide tend to take effect?

A

IV - within 30 mins

Oral - within an hour

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28
Q

What are the contra-indications to a loop diuretic?

A

Severe hypovolaemia, or dehydration

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29
Q

What are the cautions with loop diuretics?

A

Severe hypokalaemia and/or hyponatraemia
hepatic encephalopathy
gout

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30
Q

What are the main adverse effects in loop diuretics?

A
  • hypokalaemia
  • metabolic alkalosis
  • hypocalcaemia, hypomagnesaemia
  • Hypovolaemia and hypotension
  • Hyperuricaemia
  • Dose-related loss of hearing
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31
Q

What mechanism do the thiazide diuretics block?

A

The Na/Cl co-transporter

32
Q

What site of the Na/Cl co-transporter do thiazide diuretics bind to?

33
Q

What site of the triple transporter do loop diuretics bind to?

34
Q

What are the main jobs of thiazide diuretics?

A
  • prevent the dilution of filtrate in the early distal tubule
  • increase the load of Na+ delivered to the collecting tubule
  • increase reabsorption of Ca2+
35
Q

Thiazides are becoming less commonly used for heart failure and hypertension. What drugs are beginning to be used more?

A

mild heart failure - loop agents

hypertension - indapamide or chlortalidione

36
Q

Why are thiazides thought to be useful in renal stone disease?

A

Reduced urinary excretion of Ca2+ discourages Ca2+ stone formation

37
Q

What are the contra-indications to thiazide diuretics?

A

Hypokalaemia

38
Q

What are the cautions with thiazide diuretics?

A

Hyponatraemia

gout

39
Q

What are the main differences in adverse effects between loop and thiazide diuretics?

A

Thiazide do NOT cause hypocalcaemia

They CAN, however, cause Erectile Dysfunction and impaired glucose tolerance in diabetes

40
Q

Describe how loop and thiazide diuretics cause loss of K+

A

Increased Na+ load caused by loop/thiazide
=> enhanced reabsorption of Na+
=> charge separation makes lumen more -ve
=> K+ moves across the lumenal membrane (enhanced secretion)
=> Secreted K+ ‘washed away’ by increased urinary flow in these areas of nephron
=> hypokalaemia

41
Q

What do potassium sparing diuretics Amiloride and Triamterene block?

A

Block the apical Na channel

=> decrease Na+ reabsorption

42
Q

What do Spironolactone and Eplerenone block?

A

Compete with aldosterone for binding to intracellular receptors

43
Q

What are spironolactone and eplerenon dependent on?

A

Aldosterone levels of Pt already

44
Q

What active form is spironolactone metabolised to?

45
Q

Triamterene is well absorbed from the G.I tract, absorption of amiloride is poor. TRUE/FALSE?

46
Q

Given alone, potassium sparing diuretics cause hyperkalaemia. TRUE/FALSE?

A

TRUE

They are usually used in combination with agents that cause potassium loss

47
Q

In what conditions are aldosterone antagonists used?

A
  • heart failure
  • primary hyperaldosteronism (Conn’s syndrome)
  • resistant essential hypertension
  • secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
48
Q

In what conditions are aldosterone antagonists contra-indicated?

A

Severe renal impairment
hyperkalaemia
Addison’s disease

49
Q

Give an example of an osmotic diuretic?

A

Mannitol

Must be given IV as extremely hydrophilic

50
Q

How do osmotic diuretics enter the filtrate?

A

via glomerular filtration, but are not reabsorbed

51
Q

Briefly explain how osmotic diuretics work?

A

osmotic diuretic in the filtrate increases osmolality
=> water is not reabsorbed
=> larger vol. of water dilutes the concentration of sodium in the filtrate
=> sodium is ALSO not reabsorbed
=> both Na and H2O are lost

52
Q

When are osmotic diuretics used?

A
  • acute hypovolaemic renal failure (maintain urine flow)

- acutely raised ICP/IOP (plasma osmolality extracts water from these compartments)

53
Q

What are the adverse effects of osmotic diuretics?

A
  • transient expansion of blood volume

- hyponatraemia

54
Q

When can an osmotic diuresis occur pathologically?

A

hyperglycaemia (Glucose remaining in the filtrate retains fluid)

Iodine contrast dyes
filtered at the glomerulus, but it not reabsorbed
=> creates osmotic load that takes water with it

55
Q

What can carbonic anhydrase inhibitors cause as a result of promoting electrolyte excretion?

A

alkaline* diuresis and metabolic acidosis

Due to excretion of HCO3- with Na+, K+ and H2O

56
Q

Carbonic anhydrase inhibitors are no longer used for their diuretic effect. TRUE/FALSE?

57
Q

What are carbonic anhydrase inhibitors used for?

A
  • glaucoma/ following eye surgery (Reduce IOP by suppressing formation of aqueous humour)
  • prophylaxis of altitude sickness
  • some forms of infantile epilepsy
58
Q

By alkalanising the urine with substances such as citrate salts, what can this help?

A
  • relief of dysuria
  • prevention of the crystallization of weak acids
    => decrease formation of uric acid stones
  • enhance the excretion of weak acids (e.g. salicylates such as Aspirin)
59
Q

What is the difference between Neurogenic and Nephrogenic Diabetes Insipidus?

A

Neurogenic DI – lack of vasopressin secreted from posterior pituitary.

Nephrogenic DI – inability of the nephron to respond to vasopressin.

60
Q

What drug is used to treat neurogenic DI and why?

A

Desmopressin* (synthetic analogue)

Has V2 receptor selectivity – avoids increase in blood pressure associated with V1 receptor activation

61
Q

There is no current pharmacological treatment for Nephrogenic DI. TRUE/FALSE?

62
Q

Give examples of substances which affect vasopressin RELEASE from pituitary.

A

ethanol inhibits secretion

nicotine enhances

63
Q

Give examples of substances that affect the ACTION of vasopressin on the kidney

A

Lithium
demeclocycline (antibiotic)
“vaptans”

64
Q

Why are the “vaptan” class of drugs known as aquaretics?

A

They cause H2O excretion without any loss of Na

65
Q

Where are the “vaptans” looking to be used?

A

Tx of heart failure

- most likely of value in hypervolaemic hyponatraemia (to reduce preload)

66
Q

What is tolvaptan currently used to treat?

A

Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)

-to correct the hyponatraemia

67
Q

Why do drugs only aim to inhibit SGLT2 and not also SGLT1?

A

SGLT1 also expressed in intestine

=> SGLT2 specific to kidney (responsible for 90% glucose reabsorption)

68
Q

Explain why the SGLT2 co-transporter has low affinity and high capacity, whilst the SGLT1 co-transporter has
high affinity and low capacity?

A

At level of SGLT2 glucose is plentiful => dont need high affinity.
However lots of it need removed from blood so you need the transporter to have a high capacity.

Further down at SGLT1 theres not a lot of glucose floating about
=> you need a high affinity, but a low capacity doesnt matter

69
Q

Inhibition of SGLT2 mimics what condition?

A

Familial Renal Glucosuria

70
Q

SGLT2 inhibitors treat independent of insulin in T2DM. TRUE/FALSE?

71
Q

What is relevant in the formation of prostaglandins?

A

formed from fatty acid arachidonic acid by the cyclo-oxygenase enzymes (COX1 and 2)

72
Q

Name the 2 major prostaglandins made by the kidney

A

PGE2 – medulla

PGI2 (prostacyclin) – glomeruli

73
Q

When are prostaglandins synthesised?

A

In response to:

  • ischaemia
  • mechanical trauma
  • angiotensin II
  • ADH
  • Bradykinin
74
Q

How do prostaglandins affect the GFR?

A

vasodilate the afferent arteriole

75
Q

How do NSAIDs precipitate renal failure

A
  • inhibit COX enzymes
    => Not forming prostaglandins
    => no vasodilation of afferent arteriole
    => decreased GFR
76
Q

What is the difference between uricosuric drugs and Allopurinol which is now widely used for gout prophylaxis?

A

Uricosuric drugs = block reabsorption of urate in proximal tubule => pee it out

Allopurinol = inhibits urate synthesis

RENAL (24 decks)

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