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Pharm, Therapeutics, Toxic 8 Flashcards

1
Q

Drugs to avoid when BREASTFEEDING?

A
  • Abx: tetracycline, ciprofloxacin, chloramphenicol
  • psych: BZDs, lithium, clozapine
  • Aspirin
  • Amiodarone
  • Carbimazole
  • Cytotoxics
  • Methotrexate
  • Sulphonylureas
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2
Q

Drugs considered safe if breastfeeding?

A
  • Abx: penicillin, trimethoprim, cephalosporins
  • psych: TCAs, antipsychotics
  • asthma: salbutamol, theopyllines
  • endo: thyroxine, glucocorticoid (avoid high dose)
  • epilepsy: valproate, carbamazepine
  • CVS: warfarin, heparin, digoxin, beta-blockers, hydralazine
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3
Q

Breastfeeding C/Is?

A
  • drugs
  • viral infections
  • galactosaemia
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4
Q

Mechanism of Evolocumab and where is it used?

A
  • prevents PCSK9-mediated LDL receptor degradation by binding to PCSK9 and preventing circulating PCSK9 from binding to LDL-Rs on liver cell surface, therefore preventing their degradation
  • increasing liver LDLR results in ass reductions in serum LDL-cholesterol
  • use of evolocumab ass with reduced free PCSK9 (measure of target engagement)
  • dosage 140mg / 2 wks
  • specialist prescription, if LDL-C > 3.5 persistently
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5
Q

MoA of Fibrates

A
  • increase lipoprotein lipase activity via PPAR-alpha agonism
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6
Q

MoA of Ezetimibe

A
  • reduces intestinal absorption of cholesterol
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7
Q

Anaesthetic agent with features of:

  • rapid onset of anaesthesia
  • pain on IV injection
  • rapidly metabolised with little accumulation of metabolites
  • anti-emetic properties
  • moderate myocardial depression
  • widely used esp for maintaining sedation on ITU, total IV anaesthesia and for daycase surgery
A

PROPOFOL

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8
Q

Anaesthetic agent with features of:

  • extremely rapid onset so agent of choice for rapid sequence induction
  • marked myocardial depression may occur
  • metabolites build up quickly
  • unsuitable for maintenance infusion
  • little analgesic effects
A

SODIUM THIOPENTONE

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9
Q

Anaesthetic agent with features of:

  • mod-strong analgesic properties
  • may be used for induction of anaesthesia
  • produces little myocardial depression (so suitable agent if pt not haemodynamically stable)
  • may induce state of dissociative anaesthesia -> nightmares
  • can be used in neuropathoc pain porrly responsive to titrated opioids & oral adjuvant analgesics eg antidepressant/convulsant, esp when there is abnormal pain sensitivity eg allodynia, hyperalgesia, hyperpathia
A

KETAMINE

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10
Q

Anaesthetic agent with features of:

  • favourable cardiac safety profile with v little haemodynamic instability
  • no analgesic properties
  • unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal suppression
  • post-op vomiting common
A

ETOMIDATE

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11
Q

MoA of Ketamine?

A

NMDA-receptor antagonist

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12
Q

MoA of Gabapentin?

A

Modulates voltage-gated calcium channel

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13
Q

3 main features of serotonin syndrome?

A
  1. neuromuscular excitation (hyperreflexia, myoclonus, rigidity etc)
  2. ANS excitation e.g. hyperthermia
  3. altered mental state
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14
Q

Rx of serotonin syndrome:

  • 1st line?
  • if more severe?
A

IVI + BZD

- if more severe can use serotonin antagonist e.g. cyproheptadine & chlorpromazine

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15
Q

Examples of serotonin antagonists?

A

cyproheptadine & chlorpromazine

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16
Q

4 Drugs that can cause of serotonin syndrome?

A

MAO-inhibitors
SSRIs
ecstasy
amphetamines

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17
Q

Acute Rx of caustic/corrosive substance ingestion?

A

ABCDE - esp caution airway, look for peri-peal oedema

  • high dose IV PPI
  • urgent upper GI surgical referral if signs of perforation (e.g. surgical emphysema, CXR mediastinal widening)
  • AVOID neutralisation -> exothermic rxn -> further injury

If Sx -> urgent OGDto assess degree of ulceration (Zargar classification), if extensive injury on OGD consider urgent surgical exploration
If ASx -> observe & trial oral fluid

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18
Q

Acute & Chronic complications of caustic/corrosive substance ingestions?

A

Acute:

  • upper GI ulceration, perforation
  • upper airway injury & compromise
  • aspiration pneumonitis
  • infection
  • electrolyte disturbance e.g. hypocalcaemia in hydrofluoric acid ingestion

Chronic:

  • strictures, fistulae, gastric outlet obstruction
  • upper GI carcinoma (inc risk 1000-3000x)
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19
Q

Mechanism of action of Class Ia anti-arrthymics?

3 Examples?

A

Sodium channel blockers
- increases AP duration

quinidine
procainamide
disopyramide

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20
Q

Mechanism of action of Class Ib anti-arrthymics?

3 Examples?

A

Sodium channel blockers
- decreases AP duration

lidocaine
mexiletine
tocainide

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21
Q

Mechanism of action of Class Ic anti-arrthymics?

3 examples?

A

Sodium channel blockers
- no effect on AP duration

flecainide
encainide
propafenone

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22
Q

Mechanism of action of Class II anti-arrthymics?

examples?

A

Beta-blockers

propranolol
atenolol
bisoprolol
metoprolol

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23
Q

Mechanism of action of Class III anti-arrthymics?

examples?

A

Potassium channel blockers

amiodarone
sotalol
ibutilide
bretylium

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24
Q

Mechanism of action of Class IV anti-arrthymics?

examples?

A

Calcium channel blockers

verapamil
diltiazem

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25
Q

Therapeutic range of lithium?

when to take the sample?

A

0.4-1.0

12h post-dose

toxicity tends to occur > 1.5

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26
Q

When to take levels of ciclosporin?

A

Trough levels immediately before dose

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27
Q

When to take levels of digoxin?

A

At least 6hours post-dose

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28
Q

When to take levels of phenytoin if monitoring is required?

When would you consider monitoring phenytoin levels?

A

Trough levels immediately before dose

  • adjusted phenytoin dose
  • suspected toxicity
  • detection of non-adherence to prescribed meds
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29
Q

Taking Abx whilst on the COCP - do they reduce efficacy?

A

No extra precaution required for contraception

Except for Abx which are enzyme inducers i.e. rifampicin & rifaximin (& other enzyme inducers)

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30
Q

What are phase I reactions in drug metabolism?

A

Oxidation, reduction, hydrolysis

  • mainly by p450 enzymes, but also e.g. etoh dehydrogenase, xanthine oxidase
  • phase I products typically more active & potentially toxic
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31
Q

What are phase II reactions in drug metabolism?

A

Conjugation

- products typically inactive & excreted in urine/bile

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32
Q

What does zero-order kinetics describe in drug metabolism?

A

Metabolism that is independent of the concentration of reactant
- pathways become saturated -> constant amount of drug being eliminated per unit time

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33
Q

4 drugs which exhibit zero-order kinetics?

A

phenytoin
heparin
ETOH
salicylates - high-dose aspirin

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34
Q

What does acetylator status mean?

Which 5 drugs are affected by acetylator status?

A

50% UK population are deficient in hepatic N-acetyletransferase

  • isoniazid
  • procainamide
  • hydralazine
  • sulfasalazine
  • dapsone

‘slow acetylators’ are more likely to suffer hepatitixicity

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35
Q

What is meant by high first-pass metabolism?

Examples of drugs

A

Where a drug’s concentration is greatly reduced by hepatic metabolism before it reaches the systemic circulation, so much larger doses are needed orally than by other routes

aspirin
ISDN
GTN
propranolol
verapamil
lignocaine
isoprenaline
hydrocortisone
testosterone
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36
Q

What is mechanism of action of digoxin and it’s uses?

A
  1. decreases conduction through the AV node (slows ventricular rate in AF & flutter)
  2. +ive inotrope: inhibits Na/K ATPase pump, increasing force of cardiac muscle contraction (Sx relief in heart failure)
  3. stimulates the vagus nerve
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37
Q

Features of digoxin toxicity?

Rx?

A
  • generally unwell, lethargy, nausea & vomit, anorexia, confusion, yellow-green vision
  • arrhythmias e.g. AV block, bradycardia
  • gynaecomastia
  1. Correct arrhythmias
  2. Monitor K+
  3. Digibind if necessary

Likelihood of toxicity increases progressively when digoxin level rises, progressively, from 1.5-3

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38
Q 
Factors that precipitate digoxin toxicity?
pt factors
electrolytes/bloods
comorbidities
drugs
A

Pt: increasing age, hypothermia

Blds: low K, low Mg, high Na, high Ca, low albumin, acidosis

PMH/status: renal failure, myocardial ischaemia, hypothyroidism

Drugs: 
- amiodarone
- verapamil
- diltiazem
- spironolactone
- ciclosporin
- quinidine
& drugs which cause hypokalaemia etc
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39
Q

MoA of heparin?

LMWH?

unfractionated?

A

Activates antithrombin III

LMWH: increases action of antithrombin III on factor Xa

unfractionated heparin: forms a complex which inhibits thrombin & factors IXa, Xa, XIa, XIIa.

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40
Q

Difference between SC LMWH & unfractionated IV heparin:

duration?
monitoring?

A

LMWH has long duration of action, standard unfractionated is short

LMWH - anti-factor Xa if monitoring required

standard IV heparin - monitor APTT (this heparin is useful if high risk bleeding as can be monitored, and anticoag can be terminated rapidly)

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41
Q

4 Side-effects of heparin

A
  1. bleeding
  2. HIThrombocytopenia
  3. osteoporosis
  4. hyperkalaemia (inhibition of aldosterone secretion)

LMWH has lower risk of HIT & osteoporosis

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42
Q

Rx for heparin overdose

A

protamine sulphate (only partially reverses effects of lmwh)

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43
Q

How is heparin-induced thrombocytopenia mediated?
when does it usually develop?
what are 3 features?
Rx options?

A

Immune-mediated: Ab form against PF4 (platelet factor 4) & heparin complexes

  • > these Ab bind to these complexes on platelet surface
  • > induce platelet activation by cross-linking FcgammaIIA receptors
  • develops after 5-10days of Rx
  • pro-thrombotic
  • Rx options inc: alternative anticoagulants e.g. lepirudin & danaparoid
  1. > 50% reduction in platelets
  2. thrombosis
  3. skin allergy
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44
Q

What is acute intermittent porphyria?

How does it usually present?

A

Autosomal dominant condition caused by defect in porphobilinogen deaminase (haem biosynthesis affected)

  • abdo & neuropsych Sx in 20-40yrs olds, 5x more common in females
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45
Q

Drugs which may precipitate an attack of acute intermittent porphyria?

A
  • etoh, OCP
  • BZD, barbiturates
  • halothane, sulphonamides
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46
Q

4 commonest drug causes of urticaria?

A

aspirin
nsaids
penicillins
opiates

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47
Q

Drugs which are known to cause impaired glucose tolerance?

A
  • steroids
  • ciclosporin, tacrolimus
  • thiazides, furosemide (less common)
  • IFN-alpha
  • nicotinic acid
  • atypical antipsychotics e.g. olanzapine
  • beta-blockers - caution in diabetics as they can interfere with metabolic & autonomic responses to hypoglycaemia
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48
Q

Drugs that can cause photosensitivity?

A
  • thiazides
  • amiodarone
  • nsaids e.g. piroxicam
  • psoralens
  • sulfonylureas
  • tetracyclines, sulphonamides, ciprofloxacin
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49
Q

How do quinolones work? what is their MoA?

what are mechanisms of resistance?

A

Inhibit DNA synthesis and are bactericidal
- inhibit topoisomeras II (DNA gyrase) & IV

mechanisms of resistance: mutations to DNA gyrase, efflux pumps which reduce intracellular quinolone concentration

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50
Q

5 Adverse/side effects of quinolone?

A
  1. lower seizure threshold in epilepsy
  2. tendon damage/rupture (increased if pt on steroids; idiosyncratic)
  3. lengthen QT interval
  4. P450 enzyme Inhibitor!
  5. can provoke a haemolytic crisis in g6pd deficiency

quinolone generally avoided in children due to uncertain risk of cartilage damage

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51
Q

Why does carbon monoxide cause a left-shift of the o2 dissociation curve & tissue hypoxia?

What are the features?
What is Rx & indication?

A
  • has high affinity for Hb & myoglobin
  • headache 90%
  • nausea & vomiting; vertigo 50%
  • confusion 30%
  • subjective weakness 20%
  • severe: ‘pink’ skin & mucosa, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
Rx = 100% O2
Hyperbaric O2 are indicated if:
- LOC at any point
- neuro signs at any point
- myocardial ischaemia/arrhythmia
- pregnancy
CarboxyHb levels:
<3% non-smoker
<10% smokers
10-30% Sc: headache, vomiting
>30% severe toxicity
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52
Q

What is mechanism of action of Cyclosporin?

Indications?

Adverse effects? (‘increased’)

A

Calcineurin inhibitor immunosuppressant

Binds to form a complex with cyclophilin -> inhibits calcineurin -> inhibits activation of various transcription factors in T cells
- decreases T cell clonal proliferation by reducing IL-2 release

  • after organ Tx
  • RA, psoriasis (direct effect on keratinocytes, & modulates T cell function)
  • UC
  • pure red cell aplasia
  • nephrotoxic, hepatotoxic
  • fluid retention, HTN
  • hyperkalaemia, hyperlipidaemia, impaired glucose tolerance
  • tremor, gingival hyperplasia, hypertrichosis
  • increased susceptibility to severe infection
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53
Q

When to give Acetylcysteine in presumed paracetamol overdose?? (3)
How is it given?

A
  1. Staggered OD (taken over >1hr)
  2. Unknown/doubt in time of ingestion
  3. If plasma conc above the Rx line from 4hours (100) to 15h (15)

Give IV over 1hour to reduce number of adverse effects

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54
Q

King’s College criteria for Liver Tx in paracetamol-induced liver failure?

A 
arterial pH < 7.3, 24h after ingestion
or all of the following:
- PT > 100
- Cr > 300
- grade III/IV encephalopathy
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55
Q

Drug causes of thrombocytopenia?

A
  • NSAIDs, heparin
  • furosemide
  • penicillins, sulphonamides, rifampicin
  • carbamazepine, valproate
  • quinine
  • abciximab
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56
Q

Causes of low Mg?
Features?
Rx?

A
  • ETOH, diarrhoea
  • diuretics
  • low K, low Ca
  • TPM
  • conditions ass with diarrhoea e.g. IBD
  • metabolic disorders: Gitelmans, Bartters

Features:

  • tetany, paraesthesia
  • arrhythmias, seizures
  • decreased PTH secretion -> low Ca
  • ECG features similar to hypokalaemia
  • exacerbates digoxin toxicity

Rx:
> 0.4 oral 10-20mmol/d but diarrhoea common
< 0.4 IV e.g. 40mmol/24h

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57
Q

What is Trastuzumab?

Adverse effects?

A

Herceptin
= mAb directed against HER2/neu receptor

  1. flu-like sx & diarrhoea common
  2. Cardiotoxic: Echo monitoring done inc before Rx. More common when anthracyclines also used
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58
Q

Features of beta-blocker OD?
Rx?
If resistant?

A
  • bradycardia, hypotension, syncope, heart failure
  • Atropine if bradycardia
  • Glucagon if resistant (+ve inotrope & decreases renal vascular resistance)
  • Cardiac pacing if unresponsive to pharm Rx
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59
Q

Adrenaline:
what does it do physiologically?

Actions on alpha adrenergic receptors?
beta?

A
  • released by adrenal glands, acts on alpha 1/2 & beta 1/2 receptors
  • increases TPR & cardiac output
  • causes vasoconstriction in skin & kidneys -> narrow pulse pressure
  • it induces hyperglycemia, hyperlactatemia & hypokalaemia

Alpha:

  • inhibits pancreatic insulin secretion
  • stimulates glycogenolysis in lover & muscle
  • stimulates glycolysis in muscle

Beta:

  • stimulates pancreatic glucagon secretion
  • stimulates ACTH
  • stimulates lipolysis by adipose tissue
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60
Q

Rx of accidental injection of adrenaline?

A

Local infiltration of Phentolamine

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61
Q

P450 enzyme inducers?

A
  • phenytoin, carbamazepine
  • phenobarbitone
  • rifampicin
  • chronic etoh
  • griseofulvin
  • st Johns wort
  • smoking (affects CYP1A2)
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62
Q

P450 enzyme inhibitors?

A
  • ciprofloxacin, erythromycin
  • simetidine, omeprazole
  • isoniazid
  • amiodarone
  • allopurinol
  • ketoconazole, fluconazole
  • fluoxetine, sertraline
  • valproate
  • acute etoh
  • ritonavir
  • quinupristin
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63
Q

Serotonin 5-HT receptor agonist examples

A

Sumatriptan 5-HT1D agonist (acute migraine Rx)

Ergotamine partial 5-HT1 agonist

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64
Q

Serotonin 5-HT receptor antagonist examples

A 
Pizotifen = 5HT-2 antagonist (migraine prophylaxis)
Cyproheptadine = 5HT-2 antagonist (diarrhoea in carcinoid syndrome)
Ondansetron = 5HT-3 antagonist (anti-emetic)
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65
Q

Acid-base balance in salicylate OD?

A

Mixed resp alkalosis & metabolic acidosis

  • early stimulation of resp centre -> rest alkalosis
  • direct acid + acute renal failure -> acidosis
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66
Q

Features of salicylate OD?

A
  • lethargy, sweating, fever
  • nausea, vomiting
  • tinnitus
  • hyperventilation
  • hypo & hyperglycaemia
  • seizures, coma
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67
Q

Rx of salicylate OD?

What are the indications for haemodialysis?

A
  • ABCDE, charcoal
  • Urinary alkalisation with IV sodium bicarbonate (enhances urine elimination of aspirin)

HD indications:

  • serum conc > 700
  • resistant metabolic acidosis
  • acute renal failure
  • pulmonary oedema
  • seizures, coma
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68
Q

Features of tricyclic OD:
early?
severe?
ECG changes?

A

Early (anticholinergic):

  • dry mouth
  • agitation, sinus tachycardia
  • blurred vision, dilated pupils

Severe (esp amitriptyline, dosulepin):
- arrhythmias, seizures, metabolic acidosis, coma

ECG:

  • sinus tachycardia
  • QRS widening (>100 ass with inc risk seizures, >160 ass with ventricular arrhythmias)
  • prolongation of QT interval
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69
Q

Rx of tricyclic OD?

A
  • IV Bicarbonate to correct acidosis is 1st line* It may reduce seizure & arrhythmia risk
  • IV lipid emulsion can be used to bind free drug & reduce toxicity
  • class Ia Ic & III anti-arrhythmics are C/I
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70
Q

Rifampicin:
MoA?
side-effects?

A
  • inhibits bacterial DNA dependent RNA poymerase, preventing transcription of DNA -> mRNA
  • flu-like Sx, orange secretions
  • hepatitis, enzyme inducer
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71
Q

Isoniazid:
MoA?
side-effects?

A
  • inhibits mycelia acid synthesis
  • peripheral neuropathy (give pyridoxine/vit B6)
  • hepatitis, agranulocytosis
  • enzyme inhibitor
  • psychosis
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72
Q

Pyrazinamide:
MoA?
side-effects?

A
  • converted by pyrazinamidase into pyrazinoic acid -> inhibits fatty acid synthase I
  • hyperuricaemia -> gout
  • arthralgia, myalgia
  • hepatitis
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73
Q

Ethambutol:
MoA?
side-effects?

A
  • inhibits enzyme arabinosyl transferase which polymerises arabinose into arabinan
  • optic neuritis (check acuity before & during Rx)
  • rash
  • dose adjustment required in renal impairment
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74
Q

Features of stages of toxicity of ethylene glycol/antifreeze?

Rx?

A
  1. Sx similar to xs etoh: confusion, slurred speech, dizziness
  2. tachycardia, hypotension, metabolic acidosis with raised anion gap & high osmolar gap
  3. acute renal failure

FOMEPIZOLE (etoh dehydrogenase inhibitor)
HD if refractory

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75
Q

Which Abx inhibit cell wall formation?

A

peptidoglycan X-linking: penicillins, cephalosporins, carbopenems
peptidoglycan synthesis: glycopeptides e.g. vancomycin

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76
Q

Which Abx inhibit protein synthesis?

A

50S subunit: macrolides, chloramphenicol, clindamycin, linezolid, streptogrammins

30S subunit: aminoglycosides, tetracyclines

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77
Q

Which Abx inhibit DNA synthesis?

A

quinolones

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78
Q

Which Abx damages DNA?

A

metronidazole

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79
Q

Which Abx inhibit folic acid formation?

A

sulphonamides

trimethoprim

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80
Q

Which Abx inhibits RNA synthesis?

A

rifampicin

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81
Q

Why does cyanide lead to poisoning?

What are the features?

Rx?

A
  • from reversible inhibition of cellular oxidising enzymes (cytochrome c oxidase) leading to cessation of mitochondrial electron transfer chain -> cells can’t make ATP -> histotoxic hypoxia

classical: brick-red skin, smell of bitter almonds
acute: hypoxia, hypotension, headache, confusion
chronic: ataxia, peripheral neuropathy, dermatitis

  • high lactate, metabolic acidosis

100% O2
IV Hydroxocobalamin
can also use combo from: amyl nitrite inh, sodium nitrite iv, sodium thiosulfate iv

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82
Q

GHB can cause what life-threatening feature?

A

Resp depression, esp when taken with e.g. etch

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83
Q

Rx of motion sickness

A

Hyoscine (most effective but side-effects)

> Cyclizine > promethazine

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84
Q

Features of an oculogyric crisis (acute dystonia)?

Causes?

Rx?

A
  • restlessness, agitation
  • involuntary upward deviation of the eyes
  • phenothiazines
  • haloperidol
  • metoclopramide
  • post encephalitic Parkinson’s disease

Rx = IV antimuscarinic
Benztropine / Procyclidine

85
Q

Half-life of digoxin?

A

36-48hours

86
Q

What are the features of lithium toxicity?

What are the usual precipitants?

What is the Rx?

A
  • coarse tremor
  • hyperreflexia
  • acute confusion, seizure, coma
  • dehydration, renal failure, diuretics esp bender, ACE-I, NSAIDs, metronidazole

Mild-mod: volume resuscitation
Severe: HD
sodium bicarb sometimes used but limited evidence (?increasing urine alkalinity to promote excretion)

87
Q

Clinical features of ecstasy poisoning?

Rx?

A
  • hyperthermia
  • hyponatraemia
  • rhabdomyolysis
  • neuro: agitation, anxiety, confusion, ataxia
  • CVS: tachycardia, HTN

Rx: supportive
Dantrolene for hyperthermia if needed

88
Q

Drug causes of urinary retention?

A
  • TCAs
  • anticholinergics
  • NSAIDs
  • opioids
  • disopyramide
89
Q

Which drugs need to be avoided in renal failure?

A

Abx: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin

90
Q

Drugs which are likely to accumulate in CKD and need dose adjustment?

A 
Most Abx inc: penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
digoxin
atenolol
MTX
sulfonylureas
furosemide
opioids
91
Q

IV Immunoglobulin - how it it formed?

uses?

A
  • formed from large pool of donors e.g. 5000… IgG molecules with a subclass distribution similar to that of normal blood, with a half-life of 3 weeks
  • 1ry, 2ry immunodeficiency, ITP, myasthenia, GBS, Kawasaki, TEN, CMV pneumonitis, dermatomyositis etc
92
Q

How are monoclonal Ab made?

What is the main limitation and how is it overcome?

A

Somatic cell hybridisation: fusion of myeloma cells with spleen cells from a mouse that’s been immunised with the desired Ag -> resulting fused cells = hybridoma
-> acts as a factory for producing further mAbs

  • main limitation is that mouse Abs are immunogenic -> formation of HAMAs: human anti-mouse Ab
  • overcome by combining the variable region from mouse Ab with constant region from human Ab
93
Q

monoclonal Ab used in RA & Crohn’s that is anti-TNF

A

Infliximab

94
Q

monoclonal Ab used in RA & non-Hodgkin’s lymphoma that is anti-CD20

95
Q

monoclonal Ab used in metastatic colorectal ca and head & neck ca that is an EGFR antagonist

96
Q

monoclonal Ab used in metastatic breast cancer that is anti-HER2/neu

A

Trastuzumab/herceptin

97
Q

monoclonal Ab used in CLL that is anti-CD52

A

Alemtuzumab

98
Q

monoclonal Ab used in prevention of ischaemic events in pts undergoing PCI that is a glycoprotein IIb/IIIa receptor antagonist

99
Q

monoclonal Ab used in prevention of organ rejection that is anti-CD3

100
Q

PD-1 (programmed cell death) inhibitor example?
PD-1 receptors are found on the surface of T cells. T cell is alerted to a cancer cell -» cancer cell can express PD-L1 protein = ligand which binds to & deactivates the T cell receptor
Therefore = mechanism cancer cells use to evade the immune system & disable T cells
The PD-1 inhibitors are antibodies which block this receptor, leaving the T cells to remain active and alert other immune cells e.g. macrophages to the cancer cells.

101
Q

mAb used in colorectal cancer that is a VEGF inhibitor?

A

Bevacizumab

102
Q

Absolute C/I to cOCP?

A 
>35y.o. smoking >15cigs/day
migraine with aura
Hx of thromboembolic disease/thrombogenic mutation
Hx of stroke/IHD
breastfeeeding <6wks post-partum
uncontrolled HTN
current breast ca
major surgery with prolonged immobilisation
103
Q

Adrenoceptors are all G-protein coupled receptors.

Alpha-1 receptor stimulation leads to what & how?

A
  • activates phospholipase C -> IP3 -> DAG*
  • vasoconstriction
  • GI smooth muscle relaxation
  • salivary secretion
  • hepatic glycogenolysis
104
Q

Alpha-2 receptor stimulation leads to what?

A
  • inhibits adenylate cyclase*
  • mainly presynaptic: inhibition of transmitter release (inc NA, Ach from autonomic nerves)
  • inhibits insulin
  • platelet aggregation
105
Q

Beta adrenoceptors stimulate adenylate cyclase.

What does Beta-1 receptor stimulation lead to?

A
  • mainly located in the heart -> increases HR & force
106
Q

What does Beta-2 receptor stimulation lead to?

A
  • vasodilation
  • bronchodilation
  • GI smooth muscle relaxation
107
Q

What does Beta-3 receptor stimulation lead to?

108
Q

MoA of cocaine?

A

Cocaine blocks uptake of dopamine, noradrenaline & serotonin

109
Q 
Adverse effects of cocaine:
cardio?
neuro?
psych?
others esp if abdo pain?
A

CVS:

  • tachy/bradycardia, HTN
  • MI, aortic dissection
  • QRS widening & LQTS

Neuro:

  • hypertonia, hyperreflexia
  • mydriasis, seizures

Psych:
- agitation, psychosis, hallucinations

Other:

  1. ischaemic colitis
  2. hyperthermia
  3. metabolic acidosis
  4. rhabdomyolysis
110
Q

What to suspect if abdo pain/rectal bleeding in suspected cocaine abuse?

What will happen to acid-base balance?

A

Ischaemic colitis

Metabolic acidosis

111
Q 
Rx of cocaine toxicity:
1st line?
for chest pain?
for MI?
for HTN?
A

1st: Benzos
chest pain: BZDs + GTN
MI: 1ry PCI
HTN: BZDs + sodium nitroprusside

112
Q

Gross MoA of Teicoplanin?

A

Inhibits bacterial cell wall formation
(similar to vancomycin i.e. a glycopeptide that inhibits peptidoglycan synthesis, but has much longer duration of action)
- give OD after loading dose

113
Q

Rx for severe salicylate poisoning?

114
Q

Rx options for paracetamol OD

A
  • activated charcoal if ingested <1hr ago
  • NAC
  • liver Tx
115
Q

Rx for benzodiazepine OD

A

Flumazenil

116
Q

Rx for TCAs OD

A

IV bicarbonate

117
Q

Rx options for lithium toxicity

A
  • volume resuscitation
  • HD if severe
  • sodium bicarb but limited evidence
118
Q

Rx options for warfarin toxicity

A
  • vitamin K

- prothrombin complex concentrate

119
Q

Rx for heparin toxicity

A

protamine sulphate

120
Q

Rx for beta-blocker toxicity

A
  • atropine if bradycardia

- IV glucagon if resistant

121
Q

Rx for ethylene glycol or methanol poisoning

A
  • Fomepizole

- HD if refractory

122
Q

Rx for organophosphate insecticide poisoning

A
  • Atropine

- (pralidoxime role unclear)

123
Q

Rx for iron toxicity

A

Desferrioxamine = chelator

124
Q

Rx for Lead poisoning

A

Dimercaprol

Calcium edetate

125
Q

Rx for cyanide poisoning

A

Hydroxocobalamin

or combo of: amyl nitrite,, sodium nitrie, sodium thiosulfate

126
Q

MoA of Tacrolimus (similar to cyclophosphamide)?

A
  • decreases IL-2 release by inhibiting calcineurin
  • binds to and forms complex with FKBP, that activates T cell transcription factors to inhibit calcineurin
  • reducing IL-2 release decreases T cell clonal proliferation
  • more potent than ciclosporin therefore lower incidence or organ rejection
  • nephrotoxicity & impaired glucose tolerance more common
127
Q

MoA of Octreotide?
Adverse effect?

Uses?

A
  • long -acting somatostatin analogue
  • (somatostatin released from D cells of pancreas, inhibiting release of GH, glucagon & insulin)
  • can cause gallstones 2ry to biliary stasis due to inhibition of hepatic bile secretion & gallbladder emptying
  • acute Rx of vatical haemorrhage
  • acromegaly
  • caricnoid syndrome
  • VIPomas
  • refractory diarrhoea
  • prevent complications post-pancreatic surgery
128
Q

4 indications for dopamine receptor agonists?

Examples of drugs?

Adverse effects?

A
  1. PD
  2. prolactinoma/galactorrhoea
  3. cyclical breast disease
  4. acromegaly

e.g. bromocriptine, ropinirole, cabergoline, apomorphine

  • nausea & vomiting
  • postural hypotension
  • hallucinations
  • daytime somnolence
  • ergot-derived DA agonists: fibrosis
129
Q

Adverse effect of ergot-derived Dopamine receptor agonists?

What monitoring is required before/during Rx?

A
  • Fibrosis: cardiac, pulmonary, retroperitoneal

- ESR, Cr, CXR

130
Q

Drugs that can be cleared by heamodialysis: BLAST?

A 
Barbiturate
Lithium
Alcohol, methanol, ethylene glycol
Salicylates
Theophyllines (charcoal haemoperfusion is preferable)
131
Q

3 actions of metformin?

A
  1. increases insulin sensitivity
  2. decreases hepatic gluconeogenesis
  3. may reduce GI absorption of carbs
132
Q

What does organophosphate insecticide poisoning lead to?

What are the features (SLUDC)?

Rx?

A

Inhibition of acetylcholinesterase

Salivation
Lacrimation
Urination
Defecation/diarrhoea
Cardio: low HR low BP
also small pupils, muscle fasciculation

Rx = Atropine

133
Q

Example of a beta-1 agonist?

A

Dobutamine

134
Q

Example of a alpha-1 agonist?

A

Phenylephrine

135
Q

Example of a alpha-2 agonist?

136
Q

What is the target of Rituximab?

137
Q

What is the target of Infliximab?

138
Q

What is the target of Cetuximab?

A

EpidermalGFR

139
Q

What is the target of Alemtuzumab?

140
Q

What is the target of Abciximab?

A

glycoprotein IIb/IIIa receptor

141
Q

What is the target of OKT3

142
Q

MoA of Flecainide?

Indications?

When is it C/I?

Adverse effects?

A 
class 1c anti-arhythmic: Sodium channel (Nav1.5) blocker that slows conduction of the action potential
-> widening QRS, PR interval prolongation
  1. AF
  2. SVT with accessory pathway e.g. WPW

C/I post-MI (increased mortality)

  • negative inotrope
  • bradycardia
  • proarrhythmic
  • oral paraesthesia
  • visual disturbances
143
Q

MoA of Finasteride?
Indications?
Adverse effects?

A

5 alpha-reductase inhibitor (which normally metabolises testosterone -> DHT)

  1. BPH
  2. Male pattern baldness
  • impotence, decreased libido, ejaculation disorders
  • gynaecomastia, breast tenderness
  • also lowers PSA
144
Q

How does Aspirin work?

Currently, what is it 1st line for?

What 3 drugs does it potentiate?

A

Cox-1 & 2 inhibitor

  • Cox is responsible for the synthesis of prostaglandin, prostacyclin & thromboxane
  • blocking thromboxane A2 formation in platelets reduces platelet aggregation

1st line in IHD

Potentiates

  1. oral hypoglycaemics
  2. warfarin
  3. steroids
145
Q

Teratogenic effects of ACE-I?

A

renal dysgenesis

craniofacial abnormalities

146
Q

Teratogenic effects of alcohol?

A

craniofacial abnormalities

147
Q

Teratogenic effects of aminoglycosides?

A

ototoxicity

148
Q

Teratogenic effects of carbamazepine?

A

neural tube defects

craniofacial abnormalities

149
Q

Teratogenic effects of chloramphenicol?

A

‘grey baby’ syndrome

150
Q

Teratogenic effects of cocaine?

A

intrauterine growth retardation

preterm labour

151
Q

Teratogenic effects of diethylstilbestrol?

A

vaginal clear cell adenocarcinoma

152
Q

Teratogenic effects of smoking?

A

preterm labour

intrauterine growth retardation

153
Q

Teratogenic effects of tetracyclines?

A

discoloured teeth

154
Q

Teratogenic effects of thalidomide?

A

limb reduction defects

155
Q

Teratogenic effects of valproate?

A

neural tube defects

craniofacial abnormalities

156
Q

Teratogenic effects of warfarin?

A

craniofacial abnormalities

157
Q

Teratogenic effects of maternal DM?

A 
macrosomia
neural tube defects
polyhydramnios
preterm labour
caudal regression syndrome
158
Q

What drugs can cause corneal opacities?

A

amiodarone

indomethacin

159
Q

What drugs can cause optic neuritis?

A

ethambutol
amiodarone
metronidazole
vigabatrin

160
Q

What drugs can cause retinopathy?

A

chloroquine

quinine

161
Q

What drug can cause blue discolouration of vision & non-arteritis anterior ischaemic neuropathy?

A

sildenafil

162
Q

Metabolic pathways in paracetamol OD

what is mechanism of action of NAC?

A

NAC is a glutathione precursor, which replenishes hepatic glutathione

  • Liver normally conjugates paracetamol with glucuronic acid/sulphate
  • In OD conjugation system is saturated -> leading to oxidation by p450 mixed function oxidases -> producing toxic metabolite
  • Glutathione conjugates with the toxin forming non-toxic mercapturic acid
  • but then glutathione runs out, the toxin forms covalent bonds with cell proteins -> denaturing -> cell death
  • this occurs in hepatocytes & renal tubules -> can cause a DELAYED NEPHROTOXICITY
163
Q

Drug most contra-indicated in G6pd deficiency due to risk of haemolysis?

A

Quinolones

164
Q

Management of accidental injection of adrenaline?

A

local infiltration of phentolamine

165
Q

MoA of statins for hyperlipidaemia?

Adverse effects?

A

HMB CoA reductase inhibitors

  • myositis (esp when prescribed with vibrates)
  • deranged LFTs
166
Q

MoA of Ezetimibe? for hyperlipidaemia?

Adverse effects?

A

Decreases cholesterol absorption in the small bowel

- headache

167
Q

MoA of Nicotinic acid for hyperlipidaemia?

Adverse effects?

A

Decreases hepatic VLDL secretion

- flushing, myositis

168
Q

MoA of Fibrates for hyperlipidaemia?

Adverse effects?

A

PPAR-alpha agonist so it increases lipoprotein lipase expression

  • myositis, pruritis, cholestasis
  • esp muscle toxic when prescribed with statins
169
Q

MoA of Cholestyramine for hyperlipidaemia?

Adverse effects?

A

Decreases bile acid reabsorption in small bowel -> up regulating the amount of cholesterol that is converted to bile acid
- GI side-effects

170
Q

Alpha-1 blocker used in Rx of HTN & BPH?

171
Q

Alpha-1A blocker - acts mainly on urogenital tract?

A

Tamsulosin

172
Q

Example of a alpha-2 blocker?

173
Q

Example of a non-selective alpha-blocker?

A

Phenoxybenzamine (previously used in peripheral arterial disease)

174
Q

Examples of mixed alpha & beta blockers?

A

carvedilol, labetalol

175
Q

4 Drugs which may exacerbate heart failure?

A
  1. NSAIDs(except low-dose aspirin) (fluid retention)
  2. glucocorticoids (fluid retention)
  3. pioglitazone (fluid retention)
  4. Verapamil (negative inotrope)
  5. class 1 antiarrhythmics & esp Flecainide (negative inotrope & proarrhythmic)
176
Q

MoA of sildenafil?
C/I?
Side-effects?

A

= phosphodiesterase V inhibitor

C/I:

  • hypotension
  • recent stroke/MI (wait 6m)
  • nitrates/nicorandil etc

Side-effects:

  • visual: blue discolouration, non-arteritis anterior ischaemic neuropathy
  • nasal congestion, flushing, headache
  • GI side-effects
  • avoid alpha-blockers 4h after dose
177
Q

Target of nivolumab in melanoma?

Target of ipilimumab?

A

PD-1 (inhibitor)
CTLA-4 (inhibitor)
- hypophysitis & hypothyroid with prolonged Rx

178
Q

Abx known to be harmful in pregnancy

Others?

A
  • tetracyclines, aminoglycosides, sulphonamides, trimethoprim, quinolones
  • ACE-I, A2RBs, statins, warfarin, retinoids, sulfonylureas, cytotoxics
179
Q

MoA of metformin?

A

Activates AMP-activated protein kinase (AMPK) = major cellular regulator of lipid & glucose metabolism
-> promotes glucose uptake, fatty acid oxidation & insulin sensitivity. And inhibits gluconeogenesis

180
Q

Why does XS etoh lead to polyuria?
What causes nausea with hangovers?
Tremors?

A

etoh inhibits ADH secretion
- it blocks channels in the neurohypophyseal nerve terminal, reducing calcium-dependent secretion of ADH

Nausea ass with hangovers is mainly due to vagal stimulation to the vomiting centre

Tremors due to increased glutamate production by neurones to compensate for previous etoh inhibition

181
Q

MoA of macrolides?

mechanism of resistance?

adverse effects?

A

Protein synthesis inhibitors by blocking translocation - they are bacteriostatic but it’d depends on dose & type of organism

Resistance: by post-transcriptional methylation of 23S bacterial ribosomal RNA

X GI side-effects common
X cholestatic jaundice
X p450 inhibitor
X STOP statins

182
Q

Drugs that can cause agranulocytosis?

5As

A

Antithyroid drugs - carbimazole, propylthiouracil
Antipsychotics - atypical e.g. Clozapine
Antiepileptics - carbamazepine
Abx - penicillin, chloramphenicol, co-trimoxazole
Antidepressant - mirtazapine
Cytotoxics - MTX

183
Q

When can allopurinol be used as gout prophylaxis in someone who hasn’t had gout before?

A

If on cytotoxic or diuretics

e.g. if on CHOP for non-Hodgkin’s lymphoma (hyperuricaemia, tumour lysis syndrome)

184
Q

6 medical indications for botulinum toxin?

A
  • blepharospasm
  • hemifacial spasm
  • focal spasticity inc CP, hand & wrist disability post-stroke
  • spasmodic torticollis
  • severe hyperhidrosis of axillae
  • achalasia
185
Q

How does amiodarone induce hypothyroidism?

Can it be continued?

A

Due to high iodine content causing Wolff-Chaikoff effect: auto regulatory phenomenon there thyroxine formation is inhibited due to high levels of circulating iodide

  • can be continued if needed
186
Q

What are the causes of amiodarone-induced thyrotoxicosis?
Rx?
Can amiodarone be continued?

A

Type 1: XS iodine-induced thyroid hormone synthesis

  • goitre
  • Rx with carbimazole/potassium perchlorate

Type 2: amiodarone-related destructive thyroiditis

  • no goitre
  • Rx with corticosteroids

Stop amiodarone

187
Q

Effects of excessive Ach?

dumbels

A 
Diarrhoea
Urination
Miosis/muscle weakness
Bradycardia/bronchorrhea
Emesis
Lacrimation
Salivation/sweating
188
Q

Side-effects of beta-blockers?

A

fatigue
cold peripheries
sleep disturbances
bronchospasm

189
Q

Drugs that cause lung fibrosis?

A

amiodarone
cytotoxics: busulphan, bleomycin
anti-rheumatoids: MTX, sulfasalazine, gold
nitrofurantoin
ergot-derives DA agonists: bromocriptine, cabergoline, pergolide

190
Q

Examples of sulfonylureas

A 
gliclazide
chlorpropamide (long-acting
191
Q

side effects of sulfonylureas?

A

hypoglycaemic episodes
increased appetite & weight gain
SIADH
cholestatic liver dysfunction

192
Q

Reduced GCS + poorly reactive pupils + complaining of poor vision + metabolic acidosis + raised anion gap???

A

Methanol poisoning

193
Q

Which anti-TB drug needs dose adjusting in renal impairment?

A

ethambutol

194
Q

St Johns wort for depression:

  • ?mechanism
  • ?efficacy
  • ?adverse effects
  • prescribing?
A
  • may be similar to SSRIs
  • may be as effective as TCAs in mild-mod depression
  • similar adverse effect profile to placebo BUT CAN CAUSE SEROTONIN SYNDROME
  • P450 INDUCER - so decreases levels of warfarin, cyclosporin, OCP
195
Q

Causes of low magnesium?

A
  • diuretics eg furosemide
  • etoh, diarrhoea
  • TPN
  • low K, low Cl
  • Crohns, UC
  • Gitelmans, Bartters
196
Q

Features of low magnesium?

A
  • paraesthesia, tetany, arrhythmias, seizures
  • decreased PTH secretion -> hypocalcaemia
  • ECG features similar to hypokalaemia
  • exacerbates digoxin toxicity
197
Q

Rx of low magnesium?

A

<0.4 IV eg 40mmol over 24h

>0.4 oral 10-20mmol/24h but can cause diarrhoea

198
Q

Allopurinol:

  • how/when to start to for prophylaxis of gout?
  • indications?
  • adverse effects?
  • which 2 drugs does it interact with?
A
  • 2 wks after acute attack has settle, with said/colchicine cover, on 100mg OD then dose titrating up aiming for serum uric acid <300
  • rec gout attacks, top, renal disease, uric acid renal stones, prophylaxis when on cytotoxic/diuretics
  • Derm: SCAR, DRESS, Steven-Johnsons

Azathioprine - use much lower doses of it with Allopurinol, if cannot be avoided

Cyclophosphamide - allopurinol reduces renal clearance, so may cause marrow toxicity

199
Q

What acid-base imbalance does benzodiazepine OD cause?

A

Resp acidosis (resp depression)

200
Q

MoA of dobutamine?

A

beta-1 agonist

201
Q

What Abx is contra-indicated in g6pd deficiency because it can precipitate a haemolytic crisis?

A

Ciprofloxacin/quinolones

202
Q

Rx of cyanide poisoning?

A

100% O2

IV Hydroxocobalamin

203
Q

what is the origin of the constant/variable region in monoclonal antibodies?

A
  • variable region from mouse Ab

- constant region from human Ab

204
Q

Which Abx inhibit protein synthesis via reversible inhibition of the 50S subunit?

A
  • macrolides
  • chloramphenicol
  • clindamycin
  • linezolid
  • streptogrammins
205
Q

Which Abx inhibit protein synthesis via inhibition of the 30S subunit?

A
  • tetracyclines

- aminoglycosides

206
Q

Which lipid-lowering drugs can cause myositis?

Which dual combo Rx is at high risk?

A
  • statin
  • FIBRATE
  • nicotinic acid
  • caution co-prescribing statin & fibrate
207
Q

Anticholinesterase inhibitors eg organophosphates lead to accumulation of acetylcholine
- what are the features?

A 
Salivation, Small pupils
Lacrimation
Urination
Defecation/Diarrhoea
CVS: hypotension, bradycardia
Muscle fasciculation
208
Q

Cardiotoxicity with Trastuzumab is more common when which drugs have been used?

A

Anthracyclines

EXAM (21 decks)

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