CPTP4.18 Flashcards
(43 cards)
When do you treat stage 1 HTN?
Under 80, with: end organ damage, established CVD, DM, 10 year CVD risk >20%, renal disease. Treat stage 2 at any age.
ACEI/ARB?
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.
CCBs?
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).
Thiazides (chlorthalidone, indapamide)?
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.
B-blockers HTN?
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.
HTN protocol?
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.
Alpha blockers in HTN?
Can give cleft palate in pregnancy. Indicated if diuretics not effective. Expensive. Good in LVH/F (better than B-blockers)
Managing HTN in pregnancy?
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.
Statin doses in primary and secondary?
Primary 20mg atorvastatin, secondary 80mg.
Resistant HTN?
Clinic BP >140/90 after step 3 treatment with optimal dosing (A + C + D)
Managing acute heart failure?
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.
When are B-blockers bad in HF?
Shocked, HR <50, 2nd/3rd degree AV block.
Treating chronic heart failure?
Give ACEI and B-blockers. If remain symptomatic on optimal therapy…
- And moderate-severe, give aldosterone antagonist or hydralazine/nitrate (Afro-Caribbean).
- Mild/mod give ARB.
- 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.
- Can give diuretics for symptoms. Loop acutely, thiazide chronically (if renal function okay).
- Calcium channel blockers; avoid rate-limiting (-vely inotropic).
Monitoring in chronic heart failure?
Function, fluid status, weight, U&Es, drugs, ECG.
Spironolactone AEs?
Hyperkalaemia, gynaecomastia.
Loop diuretics AEs?
Urinary frequency, hypokalaemia, volume depletion, renal impairment, gout, urinary retention.
Digoxin toxicity?
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.
Paracetamol?
Good first line. Reduces opiate requirements and enhances their quality. Very few contraindications. Max 4g daily. Fine in HEPATIC impairment, but can cause ALF.
NSAIDs?
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.
Codeine?
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.
Tramadol?
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.
Morphine?
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.
Opiates in palliative?
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).
Reducing opioid side effects?
Rotation, opioid sparing agents (lidocaine/ketamine), exclude other causes of N&V (bowel obstruction) i.e. not really opioid toxicity.
