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BRS > pharmacology CKD > Flashcards

pharmacology CKD Flashcards

1
Q

What do you do for people under 135/85 mmHg bp?

A

Monitor at least every 5 years

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2
Q

When do you start drug treatment for people between 135/85 - 149/94 (stage 1) mmHg bp?

A

When they have any of these: target organ damage, CVD, renal disease, diabetes, 10 year CVD risk of 10% or more

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3
Q

what do you do for people with 150/95mmHg or more (stage 2 hypertension)?

A

start drug treatment

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4
Q

What are therapeutic objectives for someone with stage 2 hypertension and CKD?

A

Reduce hypertension to reduce CV risk & slow progression of CKD

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5
Q

For hypertension what treatment should you start if aged >55? What is the target bp and why, if they have CKD?

A
  • Amlodipine (L-type calcium channel blocker).

- Target bp is less than normal due to CKD eg 130/70

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6
Q

For CKD what treatment should be offered?

A

Blood pressure management to slow progression of CKD regardless of cause

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7
Q

For CV risk what treatment should be offered?

A

Lifestyle modification: smoking, salt, exercise.

-If CV risk >10% atorvastatin (13%-31% depending on ethnicity). Statins reduce cholesterol

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8
Q

What is proteinuria a marker of?

A

glomerular dysfunction (leaking)

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9
Q

For significant proteinuria (ACR>30) what could be given? What considerations?

A
  • ACE inhibitor or ARB. Or SGLT-2 inhibitor (dapaglifozin).
  • Salt restriction to normal recommended levels.
  • Stop amlodipine if ACE-inhibitor pushed blood pressure too low
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10
Q

Should you prescribe aspririn for CKD?

A

Consider in CKD in those with high risk of stoke or MI. but limited evidence of benefit even in those with many risk factors, and risk of harm. Generally avoid as primary prevention

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11
Q

What is the effect of trimethoprim on GFR ?

A

Invalidates GFR because inhibits active secretion of creatinine so equation is invalid (breaks link between creatinine and GFR)

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12
Q

How can ibuprofen and ACE inhibitors contribute to worsening GFR? What should be done to compensate?

A
  • Ibuprofen inhibits PG synthesis and reduces renal blood flow.
  • Ace inhibitors reduce perfusion pressure in glomerulus.
  • NSAIDS not good if kidney damage. Stop NSAIDS, use paracetamol instead.
  • Pause ACEi when acutely unwell.
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13
Q

What should we consider when prescribing drugs for someone with reduced renal function?

A
  1. might drug damage kidney and worsen kidney injury (ibuprofen)
  2. is drug eliminated by kidney so accumulates if kidney function impaired leading to side effects (eg. Morphine, metformin)
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14
Q

What are examples of statins?

A

Atorvastatin, simvastatin

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15
Q

What is mechanism of action of statins?

A

Competitive inhibitors of HMG-CoA reductase which is responsible for converting HMG-CoA to mevalonate in cholesterol synthesis. Statins reduce hepatic cholesterol synthesis, cause upregulation of LDL-receptors & increased hepatic uptake of LDL from circulation

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16
Q

What is drug target of statins?

A

HMG-CoA reductase

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17
Q

What are main side effects of statins?

A

Muscle toxicity (more likely with higher doses or in those with increased risk of muscle toxicity), constipation, diarrhoea, GI symptoms

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18
Q

What could potentially increase statin serum concentrations?

A

Co-administration with potent 3A4 inhibitors could increase statin serum concentrations

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19
Q

What is mechanism of aspirin?

A

Irreversibly inactivates COX enzyme, preventing conversion of arachidonic acid to produce prostaglandins. Reduction in thromboxane A2 in platelets reduces aggregation. Reduction of PGE2 at sensory pain neurones reduces pain and in brain decreases fever.

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20
Q

What is drug target of aspirin?

A

cyclo-oxygenase

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21
Q

What are side effects of aspirin?

A

Dyspepsia, haemorrhage.

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22
Q

What dose of aspirin should we avoid in elderly and why?

A

Avoid doses greater than 160mg daily because increased risk of bleeding

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23
Q

If history of peptic ulcer what could be do with aspirin?

A

co-administer PPI

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24
Q

How does aspirin contribute to peptic ulcer?

A

Blockade of COX1 in gastric mucosal cells reduces bicarbonate production exposing stomach lining to acid

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25
Q

What is mechanism of trimethoprim?

A

Direct competitor of enzyme dihydrofolate reductase, inhibiting reduction of dihydrofolic acid to tetrahydrofolic acid (active form), needed for synthesising purines required for DNA & protein production

26
Q

What is drug target of trimethoprim?

A

Dihydrofolate reductase

27
Q

What are side effects of trimethoprim?

A

diarrhoea, skin rxns

28
Q

What is trimethoprim often given in combination with and why?

A 
With sulfamethoxazole (co-trimoxazole). 
-They block 2 steps in bacterial biosynthesis of essential nucleic acids & proteins
29
Q

Why monitor blood counts in use of trimethoprim?

A
  • Monitor in long term use or those at risk of folate deficiency.
  • Monitor serum electrolytes In those at risk of hyperkalameia
30
Q

What is mechanism of gentamicin?

A

Binds to bacterial 30s ribosomal subunit disturbing translation of mRNA leading to formation of dysfunctional proteins

31
Q

What is drug target of gentamicin?

A

30s ribosomal subunit

32
Q

What are side effects of gentamicin?

A

ototoxicity & nephrotoxicity

33
Q

What is gentamicin ineffective against and why?

A

-Ineffective against anaerobic bacteria because is an aminoglycoside that can pass through gram negative cell membranes in an oxygen dependent manner

34
Q

What is gentamicin usually given for?

A

IV for endocarditis, septicaemia, surgical prophylaxis, meningitis, pneumonia

35
Q

What are calcium channel blocker examples?

A

Amlodipine, felodipine

36
Q

What is mechanism of calcium channel blockers?

A

Block L-type calcium channels mainly on vascular smooth muscle resulting in decrease in calcium influx with inhibition of myosin light chain kinase & prevention of cross bridge formation. Leads to vasodilation so reduces peripheral resistance

37
Q

What is drug target of calcium channel blockers?

A

L-type calcium channel

38
Q

What are side effects of calcium channel blockers?

A

Ankle oedema, constipation, palpitations, flushing/headaches

39
Q

Which calcium channel blockers has highest degree of vascular selectivity?

A

Dihydropyridine type calcium blockers

40
Q

What are examples of ACE inhibitors?

A

Ramipril, lisinopril, perindopril

41
Q

What is mechanism of ACE inhibitors?

A

Inhibit angiotensin converting enzyme (ACE) so prevents conversion of angI to angII by ACE

42
Q

What is drug target of ACE inhibitors?

A

Angiotensin converting enzyme

43
Q

What are side effects of ACE inhibitors?

A

Cough, hypotension, hyperkalaemia (care with K+ supplements & K sparing diuretics), foetal injury, renal failure in those with renal artery stenosis, urticaria/angioedema

44
Q

When is ACE inhibitor contraindicated?

A

pregnancy (foetal injury), severe renal artery stenosis

45
Q

What do most ΑCE inhibitors require for therapeutic effects?

A

Most (except lisinopril) are pro-drugs requiring hepatic activation to generate active metabolises for therapeutic effects

46
Q

What are examples of angiotensin receptor blockers?

A

losartan, irbesartan, candesartan

47
Q

What is mechanism of angiotensin receptor blockers?

A

Non-competitive antagonists at AT1 receptor on kidney and vasculature

48
Q

What is target of angiotensin receptor blocker?

A

Angiotensin receptor (AT1 receptor)

49
Q

what are side effects of angiotensin receptor blockers?

A

Hypotension, hyperkalaemia. Foetal injury, renal failure in those with renal artery stenosis

50
Q

Are angiotensin receptor blockers as effective as ACE-inhibitors?

A

no

51
Q

What do most ARBS require for therapeutic effect?

A

losartan & candesartan are pro-drugs requiring hepatic activation to generate metabolites for therapeutic effects

52
Q

What is mechanism of dapaglifozin? What type of drug is it?

A

SGLT-2 inhibitor. Reversibly inhibits sodium-glucose co-transporter 2 (SGLT2) in PCT to reduce glucose reabsorption/increase glucose excretion in urine

53
Q

What is drug target of dapaglifozin?

A

SGLT-2 at PCT

54
Q

What are side effects of dapaglifozin

A

-uro-genital infections (increased glucose load), slight decrease in bone formation, can worsen diabetic ketoacidosis (stop)

55
Q

What added benefits does dapaglifozin have?

A

Weight loss & reduction in BP

56
Q

What does dapaglifozin depend on and what are implications of this?

A

Depends on normal renal function so less effective in those with renal impairment

57
Q

What is mechanism of NSAIDs?

A

Inhibits COX enzyme that usually produces prostaglandins from arachidonic acid. Anti-inflammaotry, analgesic, antipyretic actions by inhibition of COX-2 and side effects due to inhibition of COX-1

58
Q

target of NSAIDS?

A

COX (cyclooxygenase)

59
Q

What are side effects of NSAIDs?

A

Gastric irritation, ulceration, bleeding, perforation, reduced creatinine clearance, possible nephritis, bronchoconstriction in susceptible (asthma contraindicated), skin, rashes, dizziness, hypertension, stroke, MI, chronic renal failure (analgesic abuse)

60
Q

What are uses of NSAIDs?

A

Analgesia moderate pain, antipyretics, anit-inflammatory for chronic imflammatory diseases, anti-aggregatory to inhibit platelet aggregation in those at risk of stroke/MI

BRS (81 decks)

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