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BRS Year 2 > Pharmacology of CKD > Flashcards

Pharmacology of CKD Flashcards

1
Q

What is the action of mechanism of statins?

Give examples

A

Statins are a selective, competitive inhibitor of hydroxymethylglutaryl-CoA (HMG-CoA) reductase
This converts HMG-CoA to mevalonate in the cholesterol synthesis pathway in the liver.
By reducing hepatic cholesterol synthesis, an upregulation of LDL-receptors and increased hepatic uptake of LDL-cholesterol from the circulation occurs.
Drug examples: Simvastatin, atorvastatin



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2
Q

What is the target for statins?

A

hydroxymethylglutaryl-CoA (HMG-CoA) reductase

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3
Q

What are side effects of statins?

A

Muscle toxicity - likelihood increases with higher doses and in certain patients at increased risk of muscle toxicity.
Constipation or diarrhoea
Other gastrointestinal symptoms







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4
Q

What are statins useful for?

A

Decreasing LDL cholesterol

Effective at reducing the risk of adverse cardiac events in people

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5
Q

What should we ensure we do for patients on statins?

A

All patients should be regularly followed up to monitor for hyperkalemia and acute renal failure.

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6
Q

What interaction with statins should we be aware of?

A

Coadministration with potent CYP3A4 inhibitors (e.g. clarithromycin, erythromycin) may result in increased statin serum concentrations.

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7
Q

What is the mechanism of aspirin?

A

Irreversible inactivation of COX enzyme. Prevents oxidation of arachidonic acid to produce prostaglandins.

Reduction of thromboxane A2 in platelets reduces aggregation.

Reduction of PGE2

(i) at sensory pain neurons (reduces pain and sensation)
(ii) in the brain (decreases fever.)

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8
Q

What is the target for aspirin?

A

Cyclo-oxygenase (COX)

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9
Q

What are side efects of aspirin?

A

Dyspepsia
Haemorrhage
In the elderly, avoid doses >160mg daily (increased risk of bleeding) and co administer PPI if past history of peptic ulcer.

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10
Q

What is a downside of aspirin?

A

Blockade of COX1 in gastric mucosal cells reduces mucus/bicarbonate production which can expose the stomach lining to acid.

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11
Q

What can aspirin also be useful for?

A

most cost effective medicine for the prevention of secondary events of thrombosis.

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12
Q

What is the mechanism of trimethoprim?

A

Direct competitor of the enzyme dihydrofolate reductase. Inhibits the reduction of dihydrofolic acid to tetrahydrofolic acid (active form) – a necessary component for synthesising purines (A and G) required for DNA and protein production in bacteria

*in humans we get folate from diet so don’t need to synthesise folate

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13
Q

What is the target for trimethoprim?

A

Dihydrofolate reductase

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14
Q

Side effects of trimethoprim?

A

Diarrhoea

Skin reactions

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15
Q

What is trimethoprim often given alongside?

A

Often administered with sulfamethoxazole – known as co-trimoxazole (or TMP/SMX). In combination, they block two steps in bacterial biosynthesis of essential nucleic acids and proteins. This makes them bactericidal.
Individually they are bacteriostatic (stop replication but not kill them)

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16
Q

What do you need to monitor with administering trimethoprim?

A

Need to monitor blood counts with long term use or in those at risk of folate deficiency.
Also monitor serum electrolytes in patients at risk of developing hyperkalemia.

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17
Q

What is the mechanism of gentamicin?

A

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

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18
Q

What is the target for gentamicin?

A

30s ribosomal subunit

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19
Q

What are side effects of gentamicin?

A

Ototoxicity and nephrotoxicity

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20
Q

What is an important quality of gentamicin?

A

Gentamicin is an aminoglycoside antibiotic. Can pass through gram negative cell membrane in an oxygen dependent manner (why they are ineffective against anaerobic bacteria).

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21
Q

When and how would we administer gentamicin?

A

More likely to be administered intravenously (in hospital) for endocarditis, septicaemia, meningitis, pneumonia or surgical prophylaxis.

22
Q

What is the mechanism of calcium channel blockers and give examples?

A

Block L-type calcium channels – predominantly on vascular smooth muscle.
This results in a decrease in calcium influx, with downstream inhibition of myosin light chain kinase and prevention of cross-bridge formation.
The resultant vasodilation reduces peripheral resistance (Decreased BP)

Examples: amlodipine, felodipine

23
Q

What is the target of calcium channel blockers?

A

L-type calcium channel

24
Q

What are side effects of calcium channel blockers?

A

Ankle oedema- increased fluid leakage from capillaries into interstitial space)

Constipation

Palpitations

Flushing/Headaches

25
Q

Which channel blockers show a higher degree of vascular selectivity?

A

Dihydropyridine type calcium channel blockers (potent vasodilators with no effect on heart contractility e.g. amlodipine and felodipine)

26
Q

What is the mechanism of an ace inhibitors?

Give examples

A

Inhibit the angiotensin converting enzyme.
Prevent the conversion of angiotensin I to angiotensin II by ACE. (less vasoconstriction and Na and water reuptake so lower BP)
Examples: Ramipril, Lisinopril, Perindopril

27
Q

What is the target of ACEi’s?

A

Angiotensin converting enzyme

28
Q

What are side effects of ACE inhibitors?

A

Cough
Hypotension
Hyperkalaemia (care with K+ supplements or K+-sparing diuretics)
Foetal Injury (AVOID IN PREGNANT WOMEN)
Renal failure (in patients with renal artery stenosis)-
Urticaria/Angioedema



29
Q

What do most ACEi’s need for the therapeutic effect?

A

Most ACE inhibitors (not lisinopril) are pro-drugs. They require hepatic activation to generate the active metabolites required for therapeutic effects.

30
Q

What needs to be monitored in the administration of ACEi’s?

A

eGFR and serum potassium must be regularly monitored when prescribing ACE inhibitors.

31
Q

What is the mechanism of ARBS?

Give examples

A

These agents act as insurmountable (i.e. non-competitive) antagonists at AT1 receptor (found on kidneys and on the vasculature)
Example: Losartan, Irbesartan, Candesartan

32
Q

What is the target of an angiotensin receptor blocker?

A

Angiotensin receptor

33
Q

What are side effects of ARBs?

A

Hypotension
Hyperkalaemia (care with K+ supplements or K+-sparing diuretics)
Foetal Injury (AVOID IN PREGNANT WOMEN)
Renal failure (in patients with renal artery stenosis)-

34
Q

How do ARBs compare to ACEi’s?

A

Most trials indicate that angiotensin receptor blockers are not as effective anti-hypertensive agents as ACE inhibitors.

35
Q

What do losartan and candesartan require for a therapeutic effect?

A

Losartan and candesartan are pro-drugs. They require hepatic activation to generate the active metabolites required for therapeutic effects.

36
Q

What is the mechanism of Dapaglifozin?

A

Reversibly inhibits sodium-glucose co-transporter 2 (SGLT2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

37
Q

What is the target for Dapaglifozin?

A

SGLT2

The primary site of SGLT2 inhibitor action is the proximal convoluted tubule

38
Q

What are side effects of Dapaglifozin?

A

Uro-genital infections due to increased glucose load (5% of patients)

Slight decrease in bone formation



Can worsen diabetic ketoacidosis (stop immediately)

39
Q

What is the effect of SGLT2 inhibitors?

A

SGLT2 inhibitors cause weight loss and a reduction in BP

40
Q

Who are SGLT2 inhibitors less effective in and why?

A

SGLT2i action depends on normal renal function so they are less effective in patients with renal impairment

41
Q

What are the NICE guidelines in regarding to administering atorvastatin?

A

Offer atorvastatin if >10% risk of CVD within 10 years

42
Q

What should be offered to a patient with a BP >140/90?

A

AMBP (ambulatory blood pressure) OR HBPM (home blood pressure monitoring)

43
Q

If a patient has a BP from 135/85- 149/94 what should be done?

A 
Start treatment if theres is the following:
Target organ damage
CVD
Renal disease
Diabetes
>10% 10 yr CVD risk
44
Q

If a patient has a BP greater than 150/95 what should be done?

A

Start treatment

45
Q

What should be given for a patients older than 55 to treat hypertension?

A

Amlodipine

46
Q

How does target BP change for a patient with CKD?

A

Target should be lower e.g. 130/70

47
Q

How do we lower cardiovascular risk?

A

Lifestyle- smoking, salt, exercise

Atorvastatin for risk >10%

48
Q

What is proteinuria a marker of?

A

glomerular dysfunction AND damaging in its own right

49
Q

What interventions should be used to address proteinuria?

A

Angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB)

Sodium-glucose co-transporter-2 (SGLT-2) inhibitors (e.g. dapagliflozin)

Salt restriction (to normal recommended levels!)

50
Q

If an ACEi causes bp to be too low what should you do?

A

Stop it

51
Q

What you treat CKD with aspirin?

A

NICE guidelines in CKD:
Consider prescribing aspirin in people with a high risk of stroke or myocardial infarction

There is limited evidence of benefit even in people with multiple risk factors and there is a risk of harm

In general, we tend to avoid aspirin for primary prevention

52
Q

What drug can increase creatinine but not actually affect eGFR?

A

Trimethoprim inhibits the active renal tubular secretion of creatinine so the equation to calculate GFR is now invalid.

Trimethoprim breaks the link between creatinine and GFR

BRS Year 2 (110 decks)

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