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CSIM2 > CPTP4.6-11 > Flashcards

CPTP4.6-11 Flashcards

1
Q

L-DOPA?

A
  1. Sinemet, Madopar. Replaces DA precursors. Given with DDI to prevent peripheral decarboxylation. Good for motor symptoms and ADLs compared to DA, and have fewer adverse effects, but more motor complications.
  2. Short term AEs: N&V, confusion/delusions, postural hypotension, sleep disorders (somnolence, insomnia, vivid dreams and nightmates).
  3. Long terrm: dyskinesias, response fluctuations (end-of-dose deterioration, unpredictable on/off switching). Dyskinesias occur in 100% of young patients after six years so may wish to hold off.
    Can manage motor complications with fractionated dose, adjunct treatments, DBS.
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2
Q

What do DDI do?

A

Reduce peripheral conversion of L-DOPA to DA; means get fewer side effects.

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3
Q

Dopamine agonists?

A

Bromocriptine, ropinirole, rotigotine, apomorphine. Act directly on D1/2 receptors in striatum. Used first line in young, fit patients. Less effective for motor symptoms than L-DOPA, and more adverse events, but fewer motor Cx.
Side effects: N&V, loss of appetite, postural hypotension, confusion, somnolence i.e. same as L-DOPA. Main is IMPULSE CONTROL DISORDERS; men (gambling and hypersexuality), F (shopping and eating). Usually settles on withdrawal but must be counselled!

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4
Q

MAOB inhibitors?

A

Rasagiline, selegiline. Irreversible inhibitors of MAO; means less breakdown of DA so more in cleft. Used first line in young, fit patients. Second line after L-DOPA in old/frail. Weak clinical effect but well tolerated (compared to L-DOPA and MAOI).
AEs: N&V, confusion, interact with SSRIs to give SEROTONIN SYNDROME.

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5
Q

Serotonin syndrome?

A

Agitation, confusion, tremor, myoclonus, bruxism, hyperreflexia, ANS dysfucntion, fever, vomiting, hyperpyrexia, rhabdomyolysis and coagulopathy. Ecstacy, MAOI and SSRI.

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6
Q

COMT inhibitors?

A

Entacapone. Prevents metabolism of L-DOPA to unwanted metabolites, and prevents DA degradation. Second line for both patient groups.
N&V, confusion, discoloured body fluids! INCREASE DYSKINESIAS.

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7
Q

Amantadine?

A 
Antiviral. Increases DA release, inhibits reuptake. Rarely used; can be used in late disease to treat dyskinesias. 
Causes confusion (bad in elderly), hallucinations, psychosis, livedo reticularis, ankle oedema.
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8
Q

Anticholinergics (PD)?

A

Block ACh action in striatum, decreasing relative excess of ACh in PD. Rarely used. Can exacerbate cognitive impairment, and get use anticholinergic side effects (xerostomia etc.)

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9
Q

Treatment algorithm for PD?

A
  1. Young onset, biologically fit, minimal comorbidities. Get DA or MAOI first, then L-DOPA or COMT inhibitor after. Avoid early L-DOPA because of likelihood of movement disorders, until it becomes essential.
  2. Old, frail, co-morbid. Get L-DOPA first. Then may move onto COMT/MAOI.
    If ever adding DA to L-DOPA, should reduce L-DOPA dose.
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10
Q

Treatments for various complications and non-motor features of PD?

A
  1. Peak-dose dyskinesias; reduce L-DOPA and give amantadine.
  2. Severe motor fluctuations despite optimal oral therapy; give apomorphine SC.
  3. Severe resistant tremor or severe motor fluctuations. Consider DBS.
    Non-motor; treat daytime sleepiness with modafinil, treat REM sleep disorder with clonazepam, treat orthostatic hypotension with med r/v and fludro.
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11
Q

Generalised and partial seizures?

A
  1. Generalised affects whole brain; include absence, myoclonic and generalised tonic-clonic.
  2. Partial has focal onset. Can be simple or complex depending on loss of consciousnss, or partial with secondary generalisation.
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12
Q

Indications for absence seizures?

A

Ethosuximide or valproate. Avoid carbamazepine, phenytoin.

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13
Q

Indications for generalised seizures?

A

Valproate. Can give lamotrigine or carbamazepine, but may exacerbate myoclonus. Avoid valproate in women of childbearing age/female children.

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14
Q

Treatment for myoclonus?

A

First line is valproate.

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15
Q

Drugs for partial seizures?

A

Lamotrigine or carbamazepine. Remember carbamazepine can auto-induce!

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16
Q

Sodium valproate?

A

Increases GABA concentration. First line for generalised seizures except absence. AEs include weight gain, parkinsonism, pancreatitis, teratogenicity (NTD, fetal valproate, lowers IQ). Caution in hepatic dysfunction (hepatically metabolised). CYP inhibitor. Highly PPB. No need to monitor.

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17
Q

General toxic effects of AEDs?

A

Ataxia, blurred vision, N&V, tremor, confusion. Also commonly get rash and several drug-drug interactions. SIADH common. Auto-induction with carbamazepine can give raised GGT etc.

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18
Q

Phenytoin?

A

As with carbamazepine, binds to Na+ channels. Used acutely after benzodiazepines in status. Gingival hyperplasia, rash, agranulocytosis. Needs monitoring. Interacts with OCP so need to tri-cycle. If give IV (status), can get hypotension and arrhythmias. Narrow TW. Highly PPB so free drug may cause toxicity. Monitoring: keep between 10 and 20, measure at any time. Do free drug if hypoalbuminaemic. Get cerebellar effects in toxicity. Acute toxicity is cerebellar, chronically get peripheral neuropathy, gingival hyperplasia, megaloblastic anaemia.

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19
Q

AEDs in utero?

A

Polytherapy is worse, and use lowest effective dose. Need extra folate and scans. Best is levetiracetam; worst is valproate and topiramate. (NTDs, fetal valproate, low IQ). But remember that several generalised seizures is also teratogenic! All AEDs are okay in breastfeeding.

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20
Q

Principles of AED management?

A

Start low, increase until have AEs or are seizure free. If no response, reconsider diagnosis and add new first-line drug, while tapering original. Then can start second line.

21
Q

AEDs and OCP?

A

Carbamazepine, phenytoin, topiramate and pheonbarbitone induce OCP so need to tri-cycle; lamotrigine levels are reduced by OCP. Avoid implanon, POP, patches. Can use depo or mirena. Will need to increase dose of emergency contraception.

22
Q

Which AEDs are highly PPB?

A

Carbamazepine, phenytoin, valproate.

23
Q

Monitoring AEDs?

A

Guide to dosing (especially phenytoin), check compliance, ?toxicity etc, pregnancy. May need to monitor carbamazepine and lamotrigine; not valproate.

24
Q

Which AEDs are primarily metabolised by liver?

A

Cytochrome P450: carba, phenytoin, partially valproate.
Hepatic glucuronidation:
lamotrigine, (valproate).

25
Q

Treating status epilepticus?

A
  1. ABC (O2, may need to intubate, monitor, IV access and bloods, BG, thiamine). Keep on AEDs.
  2. IV lorazepam 4mg. Can repeat x1 after 10-20 minutes. Or diazepam IV 10-20mg, max 40mg. Or midazolam. IV diazepam may cause thrombophlebitis.
  3. If not effective, can give phenytoin IV 15-18mg/kg in new patient, less if already on it.
    (Avoid status by treating serial seizures). If someone has a seizure, treat after 5 minutes. After 20, alert anaesthetist, after 30 do emergency intubation. 60-90 = ITU.
26
Q

Drugs causing parkinsonism?

A

APS (haloperidol/risperidone/quetiapine more likely to cause it than atypicals), metoclopramide, prochlorperazine, amiodarone, lithium. Essentially anti-emetics and neuroleptics. Cyclizine does. Domperidone okaY!

27
Q

Apomorphine?

A

Dopamine agonist; given SC for severe motor fluctuations; can cause skin nodules at injection site.

28
Q

Treating DTs?

A

Chlordiazepoxide, on symptom based score. Main problem is hyperarousal (hyperadrenergic state)therefore use benzo. Also give thiamine.

29
Q

Biguanides?

A

Metformin. Inhibit hepatic gluconeogenesis.
Good = weight neutral/loss, low cost, long track record.
Bad = GI AEs very common, lactic acidosis in renal impairment. Below 30?

30
Q

Sulfonylureas?

A

Gliclazide. Increase insulin secretion by binding to SUR receptor on beta cells; prevents K+ efflux so depolarise and release insulin. Low cost, track record long.
Get hypos and weight gain (more insulin).

31
Q

Thiazolidinediones?

A

Pioglitazone. Enhance lipogenesis, decrease lipolysis, decrease plasma FFAs (PPAR-gamma agonist).
Good = insulin sensitiser.
Bad = Fluid retention (in HF especially), weight gain (removes visceral fat but more extraabdominal), increased peripheral fracture rate.

32
Q

SGLT2 inhibitors?

A

-gliflozin. Prevents renal glucose reabsorption in PCT; get weight loss, but also UTIs.

33
Q

What are incretins?

A

Hormones secreted by intestinal cells in response to oral nutrients; help modulate glucose homeostasis and explain why oral glucose is better tolerated. Promotes satiety, increases insulin secretion etc. GLP-1. Cleaved by DPPIV

34
Q

DPP-IV inhibitors?

A

-gliptin. Inhibit DPP-IV so that GLP-1 half life is longer. Oral, no hypos, well tolerated, good at low GFR. But high cost.

35
Q

GLP-1 mimetics?

A

Exenatide. Resistant to DPP-IV, enhanced incretin efffects. No hypos and weight loss. Bad = SC, long term unknown, high cost. Pancreatitis.

36
Q

Insulin regimes?

A

Optimal T1 is basal-bolus (mimics normal physiology); can be on BD mix. NPH insulin aka isophane insulin is intermediate; can be given with rapid/soluble in mixes. T2 tend to use mixes, but need regular meal times, bad if exercise a lot. Insulin analogues can be rapid acting (novorapid, humalog) or long acting (glargine).

37
Q

Pros and cons of CSCI insulin?

A

Good = flexible, few hypos, less variability, low HbA1c. Bad = DKA risk, high cost.

38
Q

T2 management progression?

A

Lifestyle, monotherapy (metformin), dual (add gliclazide), triple (add pioglitazone, SGLT-2 or GLP-1 enhancer). Then can start on insulin, if not already.

39
Q

Statins?

A

Inhibit HMG-CoA reductase; stops conversion of HMG-Co-A to mevalonate. Enzyme more active at night. Less cholesterol syntheiss so less IC cholesterol, get more LDL endocytosed so serum non-HDL falls.
Indicated for primary and secondary prevention of stroke/CVD. Simvastatin has increased risk of myopathy in renal failure and hypothyroidism.
Get abnormal LFTs, rash, diabetes, myopathy (myalgia, raised CK)(especially simvastatin). Increased risk of rhabdo when given with fibrates.
Also accumulates with macrolides, ciclosporin, verapamil and diltiazem, amlodipine, amiodarone, azoles, protease inhibitors, grapefruit juice (inhibitors), and less with carbamazepine.

40
Q

Fibrates?

A

PPARalpha agonists. Lowers VLDL and LDL, increases HDL, stimulates LPL, increased ApoA1/2 synthesis. Side effects are myositis, hepatitis, pancreatitis. Used for high TG.

41
Q

Diagnosing DKA?

A

All three of: BG >11 or established diabetes, ketones >3 or urinary ++, ph<7.3 and/or HCO3- <15. Will have high anion gap.

42
Q

Managing DKA?

A

If SBP <90, give NaCl bolus. Once above 90, give 0.9% NaCl over an hour.
Start insulin (actrapid/humulin) 0.1unit/kg/hour with 0.9% NaCl.
If K+ >5.5 leave, 3.5-5.5 add 40mmol/L to solution, if under 3.5 need senior review.
Do hourly capillary glucose and ketones and venous gas at 60 mins, 120 mins then 2 hourly.
Aim for fall of ketones of >0.5mmol/L/hour OR bicarb rise by 3 and glucose fall by 3. Do not use urinary ketones.
Continue insulin until ketones <0.3 and pH>7.3. Can add glucose to it. If already on insulin, keep them on it.
Once recovered, give fast acting SC insulin with a meal then stop infusion 30 mins later.

43
Q

Treating hypoglycaemia?

A

See sweating, palpitations, drowsy, ataxic, nausea.
1. Conscious. Give 10-20g glucose (gel, sugar, lucozade).
2. Unconscious; give IV glucose 20% or IM glucagon.
After both, recheck levels; if <4 repeat, if >4 give oral carbs. Will likely feel very sick after glucagon.

44
Q

Diabetes in pregnancy?

A

Plan early, see MDT, extra folic acid, tight BG control (4-5.9 pre-meal, post meal <7.8). Women with T2DM will generally need insulin, if already on insulin then demands usually go up. Monthly HbA1c and ketonuria, on aspirin, extra scans, fundoscopy, continue insulin if established, warn of increased risk of hypos. Induce at 37 weeks. Sliding scale insulin/dextrose (GKI) (4-7) intrapartum with hourly BM, then afterwards previous levels of sensitivity return very quickly.

45
Q

Who has increased risk of hypos?

A

Pregnant, irregular lifestyle, very active, inject into areas of lipohypertrophy.

46
Q

Perioperative management of diabetes?

A

Aim for admission on day of surgery. Put early on list. Use VRII (sliding scale) if have to (i.e. if missing more than one meal); otherwise should be fine, unless BG gets above 12. VRII is 5% dextrose in 0.45% NaCl with 0.15% KCl. Monitor CBG at least hourly during and post op. In sedated patient aim for BG 6-10. Have insulin and glucose gel prescribed just in case. Try to minimise meals missed.

47
Q

Severe DKA?

A

pH<7.1, SBP<90, GCS<12, blood ketones >6, bicarb <5, sats <92%. May need ITU

48
Q

Ezetimibe?

A

Reduces absorption of cholesterol from gut. Secondary prevention along with statins

CSIM2 (21 decks)

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