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(pharm) pharmacology of CKD Flashcards

1
Q

what are four commonly prescribed drugs for CKD?

A

statins

aspirin

trimethoprim (usually in the form on co-trimoxazole)

gentamicin

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2
Q

what are statins?

A

selective, competitive HMG-CoA reductase inhibitors

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3
Q

name statins that are commonly prescribed to treat CKD

A

atorvastatin

simvastatin

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4
Q

explain the primary mechanism of action of statins

A

selective, competitive inhibitor of HMG-CoA reductase

usually converts HMG-CoA to mevalonate in the cholesterol synthesis pathway

so when HMG-CoA reductase is inhibited = reduced hepatic cholesterol synthesis

less cholesterol in the liver so upregulation of LDL receptors and therefore increase hepatic uptake of LDL cholesterol from circulation

= reducing serum LDL cholesterol levels and therefore also cardiovascular risk

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5
Q

what is the drug target for statins?

A

hydroxymethylglutaryl-CoA (HMG-CoA) reductase

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6
Q

what are the main side effects of statins?

A

muscle toxicity

constipation/diarrhoea

other gastrointestinal symptoms

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7
Q

what do statins inhibit and what is the impact of this?

A

statins inhibit HMG-CoA reductase and therefore the conversion of HMG-CoA to mevalonate

= so there will be reduced hepatic cholesterol synthesis

= an upregulation of LDL receptors and increased hepatic uptake of LDL cholesterol from circulation

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8
Q

what is HMG-CoA reductase and what does it normally do?

A

hydroxymethylglutaryl-CoA (HMG-CoA) reductase

enzymes that catalyses the conversion of HMG-CoA to mevalonate in the cholesterol synthesis pathway

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9
Q

how is cholesterol synthesis reduced as a result of statin administration?

A

statins inhibit HMG-CoA reductase so less HMG-CoA is converted into mevalonate, hindering the cholesterol synthesis pathway

= less hepatic cholesterol synthesis

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10
Q

what is the impact of reducing hepatic cholesterol synthesis?

A

by reducing hepatic cholesterol synthesis, LDL receptors are upregulated so there is increased LDL cholesterol uptake from the circulation into the liver

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11
Q

why is it important to reduce hepatic cholesterol synthesis?

A

to stimulate the upregulation of LDL receptors

= to then increase LDL cholesterol uptake from the circulation into the liver

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12
Q

why are higher doses of statins dangerous?

A

the likelihood of muscle toxicity occuring as a side effect increases at higher doses

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13
Q

when is there an increased risk of muscle toxicity with statins?

A

at higher doses of statins

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14
Q

why are statins prescribed for chronic kidney disease patients?

A

patients with CKD have an increased cardiovascular risk

= statins will reduce serum cholesterol, thereby reducing the risk of strokes and MIs

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15
Q

why are patients with CKD at a higher risk of cardiovascular events?

A

in renal dysfunction, the endocrine system works harder to regulate blood pressure + increased blood supply to the kidneys

= your heart has to pump harder, which can lead to heart disease

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16
Q

why do patients taking statins have to be followed up?

A

should be regularly followed up to monitor for hyperkalaemia and acute renal failure

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17
Q

what can increase statin serum concentrations and why?

A

coadministration with potent 3A4 inhibitors may result in increased statin serum concentrations

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18
Q

explain the mechanism of action of aspirin

A

irreversible inactivation of COX enzyme = prevents oxidation of arachidonic acid to produce prostaglandins

  • reduction of thromboxane A2 in platelets reduces platelet aggregation
  • reduction of PGE2 at sensory pain neurones reduces pain and sensation and in the brain decreases fever
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19
Q

what does aspirin prevent?

A

prevents the oxidation of arachidonic acid to produce prostaglandins
(as a result of COX-2 inhibition)

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20
Q

the production of which substances in downregulated due to aspirin administration?

A

prostaglandins including thromboxane A2 and PGE2

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21
Q

how does aspirin affect platelets?

A

platelets aggregate less as there is less thromboxane A2 prostaglandin

(due to inhibition of COX-2 enzyme by aspirin)

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22
Q

how does aspirin affect PGE2 and what are the implications of this?

A

aspirin reduces PGE2 prostaglandin synthesis due to COX-2 inhibition

= less PGE2 at sensory pain neurones results in reduced pain and sensation

= less PGE2 in the brain decreases fever

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23
Q

what does PGE2 reduction at sensory pain neurones cause?

A

reduced pain and sensation

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24
Q

what does PGE2 reduction in the brain cause?

A

decreases fever

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25
what is the drug target for aspirin?
COX enzyme
26
what are the side effects of aspirin?
dyspepsia haemorrhage (increased risk of peptic ulcers)
27
what must you ensure when prescribing aspirin to the elderly?
avoid doses greater than 160mg daily (any higher = increased risk in bleeding)
28
what is the maximum dose of aspirin that can be prescribed for the elderly and why?
maximum 160mg daily = any higher is associated with an increased risk in bleeding
29
what must you ensure when prescribing aspirin to patients with a history of peptic ulcers and WHY?
ensure you co-administer PPIs = as aspirin increases the risk of peptic ulcer fomration
30
what is low-dose aspirin particularly good at preventing?
most cost-effective medicine for the prevention of secondary events of thrombosis
31
explain how aspirin overuse can lead to peptic ulcers
blockade of COX1 in gastric mucosal cells reduces mucus/bicarbonate production + reduced prostaglandin production (due to COX-2 inhibition) = can expose the stomach lining to acid
32
explain the mechanism of action of trimethoprim
direct competitor of the enzyme dihydrofolate reductase = inhibits the reduction of dihydrofolic acid to tetrahydrofolic acid (active form) = so less tetrahydrofolate available for synthesising purines required for DNA and protein production
33
what is the drug target for trimethoprim?
dihydrofolate reductase enzyme
34
what are the side effects of trimethoprim?
diarrhoea | skin reactions
35
what is trimethoprim often administered with?
often administered with sulfamethoxazole – known as co-trimoxazole
36
what is co-trimoxazole?
trimethoprim + sulfamethoxazole = co-trimoxazole = block two steps in bacterial biosynthesis of essential nucleic acids and proteins
37
explain the mechanism of action of co-trimoxazole
in combination, trimethoprim AND sulfamethoxazole block two steps in bacterial biosynthesis of essential nucleic acids and proteins
38
what does co-trimoxazole block?
two steps in bacterial biosynthesis of essential nucleic acids and proteins
39
when and how must trimethoprim use be monitored?
long term use = monitor blood count folate-deficient patients = monitor blood count patients at risk of hyperkalemia = measure serum electrolytes
40
what does trimethoprim inhibit?
inhibits the reduction of dihydrofolate to tetrahydrofolate (active form) = latter is required to synthesis purines for DNA and protein synthesis
41
how does dihydrofolate compare to tetrahydrofolate?
tetrahydrofolate is the active form, made form the reduction of dihydrofolate by dihydrofolate reductase
42
what is tetrahydrofolic acid important?
a necessary component for synthesising purines required for DNA and protein production
43
how does dihydrofolate compare to tetrahydrofolate?
tetrahydrofolate is the active form, made from the reduction of dihydrofolate by dihydrofolate reductase
44
what is the mechanism of action of gentamicin?
binds to the bacterial 30s ribosomal subunit disturbing the translation of mRNA leading to the formation of dysfunctional proteins
45
what is the drug target for gentamicin?
bacterial 30s ribosomal subunit
46
what are the side effects of gentamicin?
ototoxicity and nephrotoxicity
47
what does gentamicin bind to?
bacterial 30s ribosomal subunit
48
what does gentamicin prevent?
prevents the translation of mRNA leading to the formation of dysfunctional proteins
49
define ototoxicity
ear poisoning which results from exposure to drugs or chemicals that damage the inner ear, often impairing hearing and balance
50
define nephrotoxicity
rapid deterioration in the kidney function due to toxic effect of medications and chemicals
51
what kind of antibiotic is gentamicin?
aminoglycoside antibiotic
52
how does gentamicin interact with gram-negative bacteria?
can pass through gram-negative cell membrane in an oxygen-dependent manner
53
why is gentamicin ineffective against anaerobic bacteria?
gentamicin can only pass through the (gram-negative) cell membranes in an oxygen dependent manner = ineffective w bacteria that do not rely on oxygen (anaerobic bacteria)
54
how is gentamicin likely to be administered?
more likely to be administered intravenously (in hospital)
55
what is gentamicin likely to be administered for in a hospital setting?
or endocarditis, septicaemia, meningitis, pneumonia or surgical prophylaxis
56
what other medications can be given for CKD?
calcium channel blokcers (amlodipine, felodipine) ACE inhibitors (ramipril, lisinopril, perindopril) angiotensin receptor blockers (losartan, irbesartan, candesartan) daptaglifozin NSAIDs (ibuprofen, naproxen, diclofenac)
57
how is eGFR calculated?
calculated in ml/min using an online calculator
58
what are the therapeutic objectives for a patient with: 1) stage 2 hypertension? 2) chronic kidney disease?
1) reduce the hypertension to reduce cardiovascular risk | 2) tighter control of hypertension to slow progression of CKD
59
why is it the aim to reduce hypertension in patients who have it?
to reduce cardiovascular risk
60
how is the progression of CKD slowed?
tighter control of blood pressure
61
what are the two most common causes of CKD?
diabetes and hypertension
62
explain how CKD is linked to hypertension
persistent hypertension narrows, damages and hardens the arteries = impairs the ability of renal arteries and vessels to filter the blood efficiently
63
what treatment is best recommended for a patient with stage 2 hypertension?
initiate drug treatment depending on age & ethnicity
64
what treatment is best recommended for a patient with chronic kidney disease?
tighter blood pressure control | to slow progression of CKD
65
how is cardiovascular risk managed in patients w CKD?
1) conservative measures (e.g. lifestyle changes to do w diet, smoking, weight loss) 2) atorvastatin if CVR is high enough (to reduce cholesterol levels)
66
in patients that have significant proteinuria, what treatments can be initiated?
1) ACEi or ARBs 2) SGLT2 inhibitors (e.g. daptaglifozin) 3) salt restriction (to normal recommended levels) = drugs/interventions that improve proteinuria
67
what is proteinuria a mark of?
glomerular dysfunction
68
in hypertensive patients, when can the antihypertensive drug of choice sometimes be stopped?
if the drug reduces the BP too low and causes hypotension
69
would you consider treating a patient w CKD with aspirin?
- considered only in patients at a high risk of MI or stroke but overall = in general, aspirin is avoided for primary prevention
70
the use of trimethoprim invalidates GFR calculators why is this?
trimethoprim inhibits tubular creatinine secretion = rapid yet reversible increase in serum creatinine (independent of any changes in GFR - i.e. increase caused by something other than low GFR) = translates into a falsely low estimated GFR when creatinine-based equations are used
71
what is the link between GFR and creatinine?
as the GFR decreases, the creatinine concentration increases
72
how does ibuprofen affect GFR levels?
causes GFR to worsen/reduce = due to 1) inhibition of (vasodilatory) prostaglandin synthesis = reduced renal blood flow 2) reduced creatinine clearance (more remains within the plasma)
73
how do ACE inhibitors affect GFR?
as ACE inhibitors reduce glomerular perfusion pressure = GFR falls (exacerbated by sepsis)
74
when prescribing for a patient with reduced renal function, what two things MUST you consider?
1) might the drug damage the kidney? = and possibly worsen the AKI (e.g. ibuprofen) 2) is the drug eliminated by the kidney? = and will it accumulate in the blood and cause side effects (e.g. metformin, morphine) (damage, eliminate)

brs (phase 1b) (71 decks)

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