CPTP4.18

Question 1

When do you treat stage 1 HTN?

Answer 1

Under 80, with: end organ damage, established CVD, DM, 10 year CVD risk >20%, renal disease. Treat stage 2 at any age.

Question 2

ACEI/ARB?

Answer 2

Inhibit ATI to ATII. First line in younger, non-African patients. Must check U&E. Can get first dose hypotension, interacts with NSAIDs, bad in renal artery stenosis. AEs also include cough, hypokalaemia, angioedema. Bad in pregnancy (cleft palate). ARB mitigate cough. Good in diabetic nephropathy. Young driven more by RAAS so ACE good.

Question 3

CCBs?

Answer 3

Block VGCC; relaxes vascular SM. First line >55. Safe in pregnancy. AEs inc. oedema, flushing, headache. Do not give verapamil and B-blocker together (profound hypotension).

Question 4

Thiazides (chlorthalidone, indapamide)?

Answer 4

Inhibit Na+ reabsorption in DCT. Bad in pregnancy (risk of olighydramnios. Slight risk of DM with B-blockers. AEs = low Na+/K+, dehydration. Bad in gout, renal failure. NB: thiazide-like preferable to bendoflumethiazide. Can be good in elderly as keep Ca2+ high.

Question 5

B-blockers HTN?

Answer 5

Indicated if young, intolerance to ACE/ARB. If have B-blocker and need second drug, give CCB not thiazide (DM). Not really safe in pregnancy (IUGR). AEs inc muscle cramps. Bad in asthma, COPD, heatr block. Be wary in heart failure. Can be good if have high levels of anxiety. Other AEs include cold extremities, bradycardia , bronchospasm, fatigue, intermittent claudication. Can also precipitate myasthenic crisis.

Question 6

HTN protocol?

Answer 6

Start on ACE/ARB or CCB according to age and ethnicity, then add the other one. Can progress to diuretic after (A+C+D); if K+ >4.5 then thiazide, if not spironolactone. If diuretic therapy not tolerated then try alpha or beta blocker.

Question 7

Alpha blockers in HTN?

Answer 7

Can give cleft palate in pregnancy. Indicated if diuretics not effective. Expensive. Good in LVH/F (better than B-blockers)

Question 8

Managing HTN in pregnancy?

Answer 8

ACE and ARB bad; associated with fetal BP/renal problems and skull defects. Aim for BP <150/100 if no complications, or <140/90 if there are. Methyldopa and nifedipine good; only labetolol if have concerns about preeclampsia.

Question 9

Statin doses in primary and secondary?

Answer 9

Primary 20mg atorvastatin, secondary 80mg.

Question 10

Resistant HTN?

Answer 10

Clinic BP >140/90 after step 3 treatment with optimal dosing (A + C + D)

Question 11

Managing acute heart failure?

Answer 11

Do not routinely give nitrates (if do, monitor BP closely) or opioids (indicated in severe, distressing SOB).
Give IV diuretics, usually as a bolus (furosemide). If already on diuretic, increase dose. Monitor renal function and body weight closely. Can combine loop and thiazide if resistant.
Only give vasopressors/inotropes if have potentially reversible cardiogenic shock (dobutamine).
Give O2 if hypoxic.
May need salt and fluid restriction.
Once stabilised, can start/continue B-blockers. Can also start ACE/ARB if have reduced LVEF.

Question 12

When are B-blockers bad in HF?

Answer 12

Shocked, HR <50, 2nd/3rd degree AV block.

Question 13

Treating chronic heart failure?

Answer 13

Give ACEI and B-blockers. If remain symptomatic on optimal therapy…

1. And moderate-severe, give aldosterone antagonist or hydralazine/nitrate (Afro-Caribbean).
2. Mild/mod give ARB.
3. Can give digoxin if still bad; symptomatic only (exercise tolerance, symptoms and fewer hospitalisations). Only for patients who remain symptomatic on ACE & B-blocker and one of the other three. Also good for concurrent AF.
4. Can give diuretics for symptoms. Loop acutely, thiazide chronically (if renal function okay).
5. Calcium channel blockers; avoid rate-limiting (-vely inotropic).

Question 14

Monitoring in chronic heart failure?

Answer 14

Function, fluid status, weight, U&Es, drugs, ECG.

Question 15

Spironolactone AEs?

Answer 15

Hyperkalaemia, gynaecomastia.

Question 16

Loop diuretics AEs?

Answer 16

Urinary frequency, hypokalaemia, volume depletion, renal impairment, gout, urinary retention.

Question 17

Digoxin toxicity?

Answer 17

N&V, abdominal pain, confusion, brady or tachy-arrhythmia, blurred or yellow/green vision. Reduce dose in renal impairment. Must monitor at least six hours after dose. Increased chance of toxicity if low magnesium or potassium, or raised calcium.

Question 18

Paracetamol?

Answer 18

Good first line. Reduces opiate requirements and enhances their quality. Very few contraindications. Max 4g daily. Fine in HEPATIC impairment, but can cause ALF.

Question 19

NSAIDs?

Answer 19

Reduces opiate requirement and improves quality, as with paracetamol. Inhibit COX. Contra in PUD, CVD (especially celecoxib and diclofenac), asthmatics with aspirin sensitivity, coagulation disorders. Caution in elderly and dehydrated, and with ACEI. Good for inflammatory arthritis.

Question 20

Codeine?

Answer 20

Weak opiate. First line step 2 WHO. Mild-moderate pain. Metabolism varies between people so some respond very poorly. All need laxatives (may get urinary retention). Can get toxicity. As liver is main site of metabolism, may be ineffective and cirrhosis and just contribute to HE. Avoid if EGFR <30.

Question 21

Tramadol?

Answer 21

Weak opiod. Most commonly used after bowel surgery as less constipating. Acts on opiod, 5-HT and adrenergic pathways. Can be used in chronic pain (less sedating). Not fully reversed by naloxone. Has multiple active metabolites.
Caution in renal/hepatic failure, raised ICP, severe resp. depression. Usual opiate toxidrome. Elderly particularly prone to AEs.
Can get serotonin syndrome with SSRIs.

Question 22

Morphine?

Answer 22

Less lipid soluble than diamorphine so crosses BBB less. Hepatically metabolised and renally excreted so caution in hepatic and renal impairment. No ceiling dose so titrate gradually. Do not exceed 50% increase a day, change from IR to MR when stable.

Question 23

Opiates in palliative?

Answer 23

CSCI preferred. Parenteral dose is 0.5x oral dose for morphine. Diamorphine is more soluble so may be preferred when morphine need exceeds 360mg. Patches are not suitable for acute pain or rapidly changing requirements. Starting CSCI; start 4 hours before next oral dose due (can still have PRNs).

Question 24

Reducing opioid side effects?

Answer 24

Rotation, opioid sparing agents (lidocaine/ketamine), exclude other causes of N&V (bowel obstruction) i.e. not really opioid toxicity.

Question 25

Managing opiate toxicity?

Answer 25

Give naloxone, then reduce opiate dose by 30-50%, check renal function, consider alternative.

Question 26

Minimising NSAID effects?

Answer 26

-coxib is more COX-2 selective. These, along with diclofenac and ibuprofen high dose are bad for CVD.
Worse for PUD are non-selective (diclofenac, naproxen, indamethacin). Also bad in 3rd TM preg, renal failure, hypovolaemia, HF, bone healing (osteoporosis). Do not use more than one oral NSAID at at time.

Question 27

Perioperative analgesia?

Answer 27

Afterwards, need regular e.g. co-codamol and PRN breakthrough (ideally via PCA). Always want non-opioid in there. Once mobilising, PCA/drip less appropriate. Often NBM in acute pain so IV morphine good.

Question 28

Pain and SOB EoL?

Answer 28

EGFR>30: morphine, 2.5mg, hourly.

<30 = alfentanil.

Question 29

Nausea and vomiting EoL?

Answer 29

EGFR>30: cyclizine, 8 hourly.

<30 = haloperidol, 4 hourly.

Question 30

Agitation EoL?

Answer 30

Midazolam SC 2.5mg every hour, regardless of renal function.

Question 31

Excess secretions EoL?

Answer 31

EGFR>30: hyoscine hydrobromide.

<30 = butylbromide (buscopan); less sedative.

Question 32

How does renal disease affect drug absorption?

Answer 32

Nephrotic syndrome increases pH and oedema so reduced bioavailibility.

Question 33

How does renal disease affect distribution?

Answer 33

Reduced protein binding, reduced serum albumin, displacement of drugs from proteins by accumulation of organic molecules = more free drug (larger apparent Vd)

Question 34

How does renal disease affect drug metabolism?

Answer 34

Most drugs that are renally excreted are not unchanged; they are actively metabolised. Renal failure retards the elimination of such metabolites. Get increased T1/2.

Question 35

How does renal disease affect elimination?

Answer 35

Depends on patient and drug. If drug is renally excreted, then excretion decreases as GFR decreases.

Question 36

Renal disease and pharmacodynamics?

Answer 36

Get toxicity if drugs accumulate, get increased sensitivity to some drugs, side effects are more poorly tolerated, some drugs are not effective e.g. loop diuretics and nitrofurantoin need to be filtered.

Question 37

Dose reduction in renal disease?

Answer 37

Use GFR as a basis, but if have narrow Tw then may need to measure drug levels. Reduce maintenance dose by increasing interval or reducing dose.

Question 38

Corrected dose calculation in renal disease?

Answer 38

Normal dose * (patients creatinine clearance/normal clearance). Remember to only multiply part of dose that is renally excreted!

Question 39

Oral morphine to S/C diamorphine? S/C morphine to S/C diamorpine?

Answer 39

Divide by 3. Other is divide by 2.

Question 40

Indications for corticosteroids in analgesia?

Answer 40

Raised ICP, nerve compression, liver capsule pain

Question 41

Amitriptyline?

Answer 41

Used for neuropathic pain. Acts on histamine, muscarininc and serotonergic receptors. Caution in arrhythmia, IHD. AEs are anticholinergic, sedation, dry mouth, hyponatraemia, urinary hesitancy.

Question 42

Gabapentin?

Answer 42

Neuropathic pain. Caution in absence seizures, psychosis and renal impairment. AEs are sedation, dizziness, ataxia. Needs 7 days titration. Good side effect profile.

Question 43

Pregabalin?

Answer 43

Neuropathic pain. Caution in CCF, renal impairment. AEs (as with gabapentin) are sedation, dizziness, ataxia. Quicker to act then gabapentin. Good side effect profile.