Essential Drugs Flashcards

1
Q

Azithromycin
What is it broadly
Class
MoA
Life threatening and QoL adverse reactions and SE
? important patient info

A

Antibiotic covering Gram + and Atypicals
Class: Macrolide
MoA: Binds to bacterial ribosome and inhibits protein synthesis -> cell growth
Adverse effects: GIT side effects (QoL)

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2
Q

Amoxicillin
What is it broadly
Class
MoA
Life threatening and QoL adverse reactions and SE
? important patient info

A

Beta lactam antibiotic
MOA: acts on cell wall of bacteria

Metabolism: liver
Excretion: renal (adjust according to GFR)

AE: Hypersensitivity (Beta lactam class effect): Type 1 so angioedema, anaphylaxis, bronchospasm, urticaria

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3
Q

Ceftriaxzone

A

3rd gen cephalosporin
Useful in bacterial infections and Meningitis (cross BBB good) for Gram pos and gram neg organisms
MoA - inhibit cell wall synthesis
Watch out for penicillin allergies
Adjust in renal impairment
Interaction: Anticoagulant (messes with Vitamin K metab.), NSAIDs (increases risk of bleeding)
AE: NEUROTOXIC, CNS (dizzy, headache), diarrhoea, SJS rarely

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3
Q

Metronidazole
MoA
Indications
Dose considerations
Adverse effects

A

Class: nitroimidazole derivative antibiotic
MOA: Toxic to DNA, forms highly reactive nitro
radical with anaerobic metabolism Fe:S proteins

Anaerobes
Bacterial vaginosis
C. diff
E. histolyca
G. lamblia

Metabolism: liver (dose adjust)
Excretion: bile, kidney

AE: disulfiram reaction with alcohol, metallic taste, neurotoxic, neutropaenia, INHIBITS WARFARIN METABOLISM

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4
Q

cloxacillin/flucoxacillin

A

Cloxacillin: resists beta-lactamase from staph
Flucloxacillin: better absorbed PO

Gram positive ONLY
skin and soft tissue infections

class: Beta-lactam antibiotic
Metabolism: liver
Excretion: kidney

AE: class effect of hypersensitivity

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5
Q

Azithromycin

A

Class: Macrolide
MOA: inhibits protein synthesis (50S ribosome)

Active against Gram +
H pylori, M. avium, chlamydia urtheritis/cervicitis
Allergic to penicillin: azithromycin is substitute

Metabolism: liver
Excretion: bile duct/kidney

AE: nausea, vomiting, diarrhoea

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6
Q

Doxycycline

A

Class: Tetracycline antibiotic
MOA: inhibit protein synthesis (30S subunit)

Acne, brucellosis, ricketssia
prophylaxis: P. falciparum malaria
Chlamydia (although azithromycin better)

Metabolism: not researched (hm)

AE: teeth discolouration, photosensitivity, n and v, AVOID IN PREG

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7
Q

Gentamicin

A

an Aminoglycoside covering most gram negative and gram positive Staphs
MoA - interferes with bacterial protein synthesis (binds to 30S ribosomal unit)
AEs - OTOTOXIC!; NEPHROTOXIC

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8
Q

amikacin (just brief overview)

A
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9
Q

Cotrimoxazole

A

Sulfonamide Derivative
MoA - both interfere with bacterial folic acid synthesis
its a nasty drug - minimal use outside of HIV (toxo, PCP, isospora) due to toxicity
AE’s - SJS, maculopapular rash, bone marrow suppression, diarrhoea
Electrolytes (inc. K; inc. Na; hypoglycaemia)

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10
Q

Vancomycin

A
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11
Q

Moxifloxacin

A
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12
Q

levofloxacin

A
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13
Q

ciprofloxacin

A
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14
Q

Warfarin

A
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15
Q

Unfractionated heparin

A

A unpredictable heparin but is forgivable
MoA - enhances action of ATT 3
Choice of drug in a pt with high risk of bleeding but not bleeding yet, because you can adjust quick and monitor them
Has antidote - protamine sulphate
Monitor important, monitor until PTT is normal range

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16
Q

Low molecular weight heparin

A
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17
Q

Aspirin

A

Class: NSAID, non-selective COX-inhibitor, salicylate

MOA: inhibits thromboxane and prostaglandin synthesis by inhibiting COX enzyme pathway IRREVERSIBLY
LOW DOSE- inhibits thromboxane synthesis only therefore useful in strokes, high dose inhibits both thromboxane and Prostaglandin synthesis (this makes low dose aspirin useful in stroke and MI over other NSAIDs
effectively: antiplatelet, anti-inflam, analgesic

Metabolism: liver
Excretion: kidney

AE: GIT ulcers (inhibits COX-1), BLEEDING
Hypersensitivity: multiple subtypes involving angioedema, urticaria, anaphylaxis, exacerbated respiratory disease, cutaneous disease

Chronic use: nephropathy

CI: malaria, heart failure, kidney failure, asthma

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18
Q

Clopidogrel

A

Drug class: Antiplatelet, antithrombotic
MOA: prevents aggregation of platelets (ADP binding to P2Y12 receptor)

Metabolism: liver, CYP450

AE: Bleeding
Hypersensitivity: angioedema, urticaria, macpap rash, DRESS
TTP

Contraindications: active bleeding, confirmed hypersensitivity, severe hepatic impairment

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19
Q

alteplase

A

Class: antithrombotic, tissue plasminogen activator
MOA: activates plasminogen to plasmin, leads to dissolution fibrin clot

Indications: fibrinolytic for acute MI, pulmonary embolism, ischaemic stroke

Metabolism: liver

AE: haemorrhage

CIs: hypersensitivity, gentamicin hypersensitivity, anticoagulant therapy, major surgery previous 3 mnths, HIGH RISK HAEMORRHAGE

drug interactions with coagulation inhibitors: ACE-i, heparin etc

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20
Q

contraindications to aspirin use

A
  1. known hypersensitivity
  2. asthma
  3. rhinitis
  4. nasal polyps
  5. children/teenagers: REYE’s syndrome
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21
Q

Furosemide

A

Loop diuretic
MoA: inhibits the Na, K, 2 x Cl transporter in the ascending loop

AE’s: OTOTOXICITY, dehydration, metabolic alkalosis, Electrolyte disturbances, sulfa group so Type 2 hypersensitivity

NB: CAN BE USED IN RENAL FAILURE, increase dose in fact, dont use in osteoporosis (causes hypocalcaemia)

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22
Q

Hydrocholothiazide

A

Thiazide diuretic
MoA: Inhibits the Na Cl pump in the DCT
AE’s - HYPERURICAEMIA AND GOUT, Electrolyte disturbances, hypercalcemia, in high dose = glucose intolerance

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23
Q

Enalapril
Class, MoA, CIs, AE, special considerations

A

ACE inhibitor
MoA - use brain im not typing it
CI’s - Renal artery stenosis, pregnancy, prev. angioedema, aortic stenosis
AE’s - Hyperkalaemia (decreases aldosterone therefore more K); Hypotension on first dose, drops GFR (watch renal fx and K)
Special considerations: Watch potassium closely, use K sparing diuretic carefully (spiro), watch for angioedema

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23
Q

Spironolactone

A

K sparing diuretic
MoA: Aldosterone antagonist, inhibits the NaK (K out, Na in) pump in the collecting duct
SE’s: HYPERKALAEMIA (especially when used with ACEi) [DO NOT give if K>5 or creat. >120]
Oestrogen things: Hirsutism, men boobies, sex. dysfunction

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24
Q

Carvedilol

A

Class: Beta blocker as well as alpha blocking activity
MoA: Non-selective beta and alpha blocking activity, slows HR, SV and CO, also causes vasodilation
life-threatening: WATCH for asthma!, anything that makes heart slow (AV block, long PR, HR <60), hypotension is CI

not essential - [Uses in CHF: dec. pulmonary capillary pressure, dec. HR, dec. systemic vascular resistance
Uses in HPT: reduces CO, dec. tachycardia (beta agonist induced and orthostatic), vasodiltion, decreased perpheriral resistance, decreased renal pressure and renin activity]

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25
Q

Morphine

A

Class: opioid
MOA: mu-opioid receptor agonist

Metabolism: glucuronidation (UDP)
Excretion: urine

Histamine release: vasodilatation, itching, bronchoconstriction

AE: nausea & sedation (go away), constipation, resp depression (decrease brainstem responsiveness to CO2 and rhythmicity)

Caution: Hepatic and renal impairment, elderly, pregnancy near term, lactation, neonates, decreased pulmonary reserve (COPD and acute asthma)

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26
Q

Tramadol

A

Class: opioid (weak)
MOA: mu-receptor agonist, inhibit serotonin and noradrenaline reuptake

synergistic with paracetamol

Metabolism: Liver (CYP2D6)
Excretion: Renal

Drug interactions: carbamazapine induces its metabolism
predisposes to serotonin syndrome, be aware of giving with SSRIs, MAOIs

AEs: nausea, sedation, constipation, resp depression, less abuse potential however

CYP2D6 variants: slow metaboliser: poor analgesia but constipation
fast metaboliser: resp depression, coma and death

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27
Q

Codeine phosphate

A

Class: weak opioid
MOA: weak affinity for mu-opioid receptor (agonist)

Metabolism: liver CYP2D6
Excretion:

AE: morphine

CYP2D6 variants: slow metaboliser: poor analgesia but constipation
fast metaboliser: resp depression, coma and death

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28
Q

Paracetamol

A

class: acetaminophen is actual name, analgesic drug (not anti-inflam like NSAIDs), antipyretic

MOA: inhibits prostaglandin synthesis centrally (some COX inhibition peripherally)

Metabolism: liver
Excretion: renal

AEs: Hepatotoxicity (NAPQI metabolite is toxic!), nephropathy (also seen with aspirin and NSAIDs)

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29
Q

NSAIDs

A

Class: NSAIDs
MOA: inhibit COX-pathway, effectively preventing synthesis of prostaglandins from arachidonic acid
COX-1 selective: inhibit prostaglandins associated with gastric mucosal protection, platelet aggregation
COX-2 selective: inflam prostaglandins inhibited

Metabolism: liver
Excretion: kidney/bile

AE:
Bronchoconstriction: avoid in asthma
Fluid retention
Nephropathy and ARF
Bleeding
Hypersensitivity
Dyspepsia and peptic ulceration
Hepatotoxicity

CI: hypersensitivity, active peptic ulceration, Malaria

Caution: bleeding disorders, renal or hepatic impairment, heart failure, hypertension, asthma, history dyspepsia

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30
Q

Amitryptilline

A

Class: TCA antidepressant, also analgesic, anxiolytic, sedative

MOA:increases noradrenergic or serotonergic neurotransmission by blocking the norepinephrine or serotonin transporter (NET or SERT) at presynaptic terminals, antihistamine effect

good if have sleep and anxiety disorder

Metabolism: liver (including CYP3A4)
Excretion: kidney

AEs: fast, irregular heartbeat, DILI, dry mouth, blurred vision, weight gain, constipation

orthostatic hypotension, dizziness, sedation: alpha adrenergic blockade

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31
Q

Carbamazapine

A

Class: anticonvulsant
MOA: inhibits sodium channel firing

Indications: trigeminal neuralgia, Bipolar 1, epilepsy, post herpetic neuralgia

metabolism: CYP450 inducer and substrate
excretion: kidney

Beware: drug drug interactions (example treating neuropathic pain and on ARVs

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32
Q

COX-1 inhibitors vs COX-2 inhibitors

A

COX-1: gastric mucosal irritation
eg. indomethacin

COX-2: CVS side effects, but adding aspirin adds gastric mucosa problems

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33
Q

Lopinavir

A

ARV - protease inhibitor
PK: CYP450 inhibitor (ritonovir)
AE: Inc. in TAGs, inc. cholesterol, diarrhoea

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34
Q

Dolutegravir

A

ARV - InSTI
AE: Insomia
PK: It depends on CYP450 (conc. dec. by rif.)
Messes with renal tubular secretion of creat. - inc. creat. levels but GFR is not affected, so its not a problem
NB: HIGH genetic barrier to resistance

35
Q

Efavirenz

A

ARV - NNRTI
Low genetic barrier to resistance
SE’s: Neuropsych SEs, RASH AND HEPATOTOXICITY
PK: CYP450 metabolised - it is an INDUCER!

36
Q

Nevirapine

A

ARV - NNRTI
PK : CYP450 inducer!
AE: Rash and Hepatoxicity (WORSE than efavirenz)
Low genetic resistance barrier

37
Q

Tenofovir

A

ARV - NRTI
PK - CYP450 inducer or substrate
Renally excreted
NB: Interacts with other nephrotoxic drugs (Cyclosporins, aminogly.)
AE - NEPHROTOXICITY, OSTEOPAENIA
Special shiii: Also treatment for Hep B

38
Q

Fluconazole

A

Antifungal
MoA - inhibits fungal CPY450 and therefore STOPS FUNGAL CELL WALL SYN.
PK: Renally excreted - needs DOSE ADJUSTMENT
Inhibits CYP450!!!!
AE: Hepatotoxic, Neurotoxic

39
Q

Lamivudine

A

ARV - NRTI
PK - Renally elim. DOSE ADJUST
? interacts with sorbital
AE - FEW! : LACTIC ACIDOSIS (class effect)
In resistance: CRIPPLES VIRUS so we leave it in 2nd line even if resistance (M184V) developed

40
Q

Pyrazinamide

A

Anti-TB
MoA: Stops cell MEMBRANE synthesis
PK: Metabolised in liver (CI in severe hepatic failure)
AE: Arthralgia, Hyperuricaemia, ?Rash, HEPATOXIC
I REPEAT HEPATOXIC
Special Shiii : It kills PERSISTERS - good drug

41
Q

Amphoterrible B
whoops sorry Amphotericin B

A

Antifungal
MoA - Causes membrane leakage of cell content and consequent cell death
Prevent Mortality
PK - RENALLY METABOLISED!
AE - NEPHROTOXIC
Thrombophlebitis
Anaemia and LOW
HypoK, HypoMg

42
Q

Isoniazid

A

Anti-TB (And Ethionamide)
MoA - stops mycolic acid synthesis in cell wall (cell wall syn.)
PK: Liver metabolised, elim in kidney
AE: Neurotoxic, Hepatotoxic, Peripheral neuropathy, Hypersensitivity reaction (Rash, hepatitis)

43
Q

Ethambutol

A

Anti-TB
MoA - Bacteriostatic, inhibits cell wall synthesis
PK - renal elimination
AE - UVEITIS!!!! (cant give in < 8y/o)
Rash
Hyperuricaemia
peripheral neuropathy
NO DILI!

44
Q

Rifampicin

A

Class: Anti TB
MoA - Inhibit RNA polymerase

PK - potent CPY450 INDUCER! therefore lots of drug interactions

AE - Type 2 antibody mediated hypersens. reaction with haemolysis etc.

INTERSTITIAL NEPHRITIS: drug hypersensitivity reaction
Gives RED URINE
Also causes haem issues - anaemia, thrombocyto.
DILI!
flu syndrome
skin itching, rash

Special: It kills persisters in high dose

45
Q

Ethanol

A

Class: CNS depressent

MOA: enhances GABA, inhibits glutamate, enhances euphoria associated with opioids and endogenous cannabinoids

Toxicity: hypoglycaemia, hypothermia, metabolic acidosis, electrolyte disturbances, cardiac arrhythmias, aspiration, ototoxic and gastric irritation causes vomiting

Treat: reverse side effects, give thiamine if chronic alcohol abuse, haemodialysis if severe

Metabolism: saturable, in liver
distributes to all cells in body so affects ALL systems eg testicular atrophy, anovulation, immunosuppression, cardiomyopathy

Withdrawal symptoms: excitatory-increased BP, tachycardia, seizures, tremors, sweating

46
Q

Methamphetamines

A

Drug class: stimulant

MOA: indirect acting sympathomimetic, increases dopamine, serotonin and noradrenaline

euphoria, but less intense than cocaine & lasts longer
paranoia, hyperthermia, tachycardia, hyperytension, palpitations, loss of appetite, anxiety, insomnia

very lipophilic and can cross BBB

eg: methylphenidate, ephedrine

Metabolism: liver-CYP2D6

Withdrawal symptoms: sedation, depressed mood, overeating

AEs: Hallucinations, anorexia, hyperthermia (serotonin)

47
Q

Cocaine

A

Class: stimulant

MOA: inhibits dopamine reuptake, prolongs action of dopamine within synapse

Effects: euphoria, tachycardia, palpitations, insomnia, decreased appetite, local vasoconstriction

Adverse effects: risk of intracranial haem, ischaemic stroke, MI, arrhythmia, seizures

withdrawal symptoms: mild

48
Q

Cannabis

A

Drug class: cannabinoid

MOA: acts on cannabinoid receptors, decrease dopamine inhibition

Leads to: euphoria, relaxation
daily use assoc. with anxiety attacks, hallucinations and psychosis
relieves N &V associated with chemo, appetite stimulant

abrupt cessation: restless, irritable, agitation, insomnia, cramps

Treat with benzos

Metabolism: liver (CYP450)

49
Q

Heroin

A

Class: opioid

MOA: mu-agonist, inhibit GABA neurons, leads to euphoria, pupillary miosis, conjunctival injection, decreased resp rate and bradycardia, absent bowel sounds. Pulm oedema, aspiration pneumonia, rhabdomyolysis in OD

Greater availability and higher potency than morphine
short-acting

TOLERANCE

Withdrawal: nausea, vom, diarrhoea
Insomnia, myalgia (u receptors, u agonists relieve this), sweating, mydriasis, lacrimation, rhinorrhoea, agitation
tachycardia, raised BP (NE affects)

50
Q

Benzodiazepines

A
51
Q

Sulfonylurea

A

Class: Sulfonylurea
all the gli……….
Glimepiride: preferred in elderly
Glibenclamide: avoid in elderly

MOA: relies upon residual Beta cell function in pancreas. Promotes insulin secretion from these cells & stimulates their growth, enhances beta cell sensitivity to glucose, reduces GLUCAGON release

Metabolism: liver, CYP450
Excretion: renal (beware low GFR)

AEs: Hypoglycaemia (esp if old, renal impairment, irreg meals), weight gain

CI: severe hepatic impairment, pregnancy, avoid if renal impairment eGFR less than 60

52
Q

Medical management alcohol withdrawal

A

benzos
anticonvulsants (except phenytoin) eg. carbamazapine
beta blockers
clonidine (alpha 2 agonist)

disulfiram: build up of acetaldehyde which makes you feel crap

Naltrexone (as seen with opioid withdrawal and dependence)

53
Q

Medical management alcohol withdrawal

A

benzos
anticonvulsants (except phenytoin) eg. carbamazapine
beta blockers
clonidine (alpha 2 agonist)

disulfiram: build up of acetaldehyde which makes you feel crap

Naltrexone (as seen with opioid withdrawal and dependence)

54
Q

4 drugs contraindicated for malaria

A
  1. Mannitol
  2. Corticosteroids
  3. Heparin
  4. Aspirin/NSAIDs (renal impairment)
55
Q

Quinine

A

Class: antimalarial
MOA: prevents nucleic acid synthesis, protein synthesis and glycolysis in P. falciparum

ONLY IF IV ARTESUNATE UNAVAILABLE
Loading dose very NB, over 4 hrs, IV
then 10mg/kg slow infusion over 8 hrs

Metabolism: liver
Excretion: needs to be dose adjusted in renal failure (adjust maintenance dose, not loading dose) NB

AE: hypoglycaemia, arrhythmias

Not ideal drug: 3 times a day, metallic taste

56
Q

Artesunate

A

Class: antimalarial
MOA: blocks asexual forms malaria parasite

First line
Does not need to be dose adjusted in renal and hepatic impairment (unlike quinine)
Give 3 doses 12 hrs apart before starting oral therapy

Metabolism: liver (CYP2A6-beware amiodarone, isoniazid)

AE: delayed haemolysis (1 week plus, non immune patients eg. non-endemic areas, children, hyperparasitaemia)

57
Q

artemether lumefantrine

A

Class: antimalarial

Prevents asexual parasite AND sexual gametocyte stages that can infect mosquito

oral, twice a day for 3 days, dose adjust according to weight
Maximise absorption: fat
better tolerated, 3 days only instead of 7 for quinine

fist line for uncomplicated malaria

Metabolism: CYP450, beware rifampicin and efavirenz

CI: allergic, less than 5kg (usually iv anyway because vulnerable), severe malaria (at least 3 doses IV before transitioning to oral AL), pregnant in 1st trimester

58
Q

P.ovale and P. vivax

A

Latent phase, need to add Primaquine (everyday for 14 days, NOT IN PREGNANCY)

59
Q

malaria prophylaxis

A

Mefloquine (weekly). Start at least one week before entering a malaria area, take once
weekly while there and for four weeks after leaving the malaria area, OR

Doxycycline (daily). Start one day before entering a malaria area, take daily while there and
for four weeks after leaving the malaria area, OR

Atovaquone-proguanil (daily). Start one to two days before entering malaria area, take daily
while there and for seven days after leaving the area.

60
Q

contraindications to mefloquine

A

epilepsy
psych
arrhythmias
infant less than 5kg

61
Q

contraindications to doxycycline

A

Pregnancy. Children
under eight
years of age.
Caution in travellers
with myasthenia
gravis.

62
Q

contraindications for atovaquone-proguanil

A

renal impairment
pregnancy; lack of data though

63
Q

how to treat status epilepticus

A
  1. Benzo
    IV: diazepam, clonazepam, lorazepam
    Buccal: Loraz, midaz
    IM: loraz, clonaz
    PR: diaz

Then IV infusion phenytoin/ phenobarb in kids
Still not working: intubate and give thiopental(barb)/propofol infusion

BUT NB: phenobarb and thiopental are barbs and INDUCE metabolism of phenytoin so infusion of phenytoin may become subtherapeutic

64
Q

Carbamazapine

A

Class: anticonvulsant

MOA: enhances GABA, prolongs inactivation Na channels
Autoinduces itself after 2 weeks at maximal induction

PK: potent inducer CYP450
Metabolism: CYP450 in liver

AEs: BM suppression: aplastic anaemia, agran
Hypersensitivity
Cerebellar symptoms: ataxia, vertigo

Induces metabolism of tramadol?

65
Q

which 3 anticonvulsant drugs have similar structure and are cross-reactive with risk of hypersens reaction

A

Phenos and carbamazapine

66
Q

Phenobarb

A

Class: Barbiturate, anticonvulsant
MOA: enhances action of GABA

metabolism: liver, also potent inducer CYP450, induces metabolism of phenytoin

AE: hyperactivity in kids, sedation (goes away), systemic hypersensitivity

67
Q

diabetogenic drugs

A
  1. Glucocorticoids
  2. Thiazide diuretics
  3. Atypical antipsychotics
  4. ARVs (Protease inhibitors)
  5. I need to check this but tacrolimus?
68
Q

Intermediate acting insulin

A

Protophane or Humulin N

once or twice dly/ usually @ night not after 10pm
takes 2-4 hrs to work, lasts 16-24 hrs

69
Q

short acting insulin

A

actrapid
works within 30 min, take 30 min before meal
stops working after 2-4 hrs

70
Q

Biphasic insulin

A

Mix short acting and intermediate acting insulin diff proportions eg. 30/70

Given twice daily. First dose before breakfast, second after supper

covers mealtime and basal insulin requirements
ACTRAPHANE

71
Q

what is preferred insulin regimen

A

Basal bolus

mimics normal insulin secretion in beta cells

Combo: pre-meal short acting insulin (bolus) that you give before each meal (30 min)

plus

long-acting insulin used/or intermediate?: protophane/Humulin N
at BEDTIME no later than 10pm

50:50 ratio

72
Q

initial total daily insulin dose

A

0.6 units/kg body weight

73
Q

Insulin

A

Class: hormone, protein so needs to be given subcut as degraded in GIT if given orally

MOA: increases glucose entry into cell, stimulates lipogenesis, protein synthesis, glycogenesis and glycolysis, basically prevents hyperglycaemia and increases glucose storage, utilisation

Secreted by Beta cells in pancreas

Metabolised in KIDNEY

AE: weight gain, accumulation of fat at drug IM site, HYPOGLYCAEMIA

74
Q

Metformin

A

Class: Biguanide

MOA: reduces hepatic gluconeogenesis & glycogen metabolism, also reduces beta oxidation
does not really enhance lipogenesis, raises HDL

Metabolism; it actually isnt metabolised in liver so liver safe!
Excretion: excreted unchanged in urine-NB GFR needs to be monitored

AE: GIT, LACTIC ACIDOSIS (inhibits conversion lactate to glucose), reduced B12 absorption
NO WEIGHT GAIN, HYPOGLYCAEMIA
Does not effect insulin secretion

CI: eGFR below 30, raised creatinine, CCF

75
Q

which antimalarial drug is only used for prophylaxis and not treatment?

A

Mefloquine (neuropsych)

76
Q

rapid acting insulin

A

Novolog, apidra, Humalog

77
Q

prescribing tips in renal failure

A

beware ace-inhibitors and spironolactone because they can cause hyperK+

Other drugs affected by renal failure:
Erythropoietin-renal failure and anaemia
Activated Vit D

78
Q

prescribing tips hepatic failure

A

beware propanolol: drug with extensive first pass metabolism

rather chose drugs that are metabolised via conjugation instead of CYP450

79
Q

which drugs to avoid in elderly

A

be aware: GFR slows down and so does hepatic metabolism (opposite of pregnancy)

  1. anticonvulsants
  2. hypnotics
  3. morphine
  4. NSAIDs
  5. Warfarin
80
Q

examples of arbs

A

losartan
anything sartan basically

remember know benefits of bradykinin such as renal vasodilation

81
Q

which drugs cause anterograde amnesia

A

any drugs that help you to relax

eg. diazepam, midazolam
alcohol

82
Q

how does phenytoin toxicity present

A

SEIZURES

ataxia, nystagmus, slurred speech

83
Q

unfractionated heparin

A

Class: anticoagulant
MOA: increases activity antithrombin 3

shorter half-life, quick to switch on and off
PROs: has antidote (protamine sulphate), quick to start/stop, have to monitor PTT so can pick up on bleeding quick

beware concurrent use of NSAIDs, anticoagulants

monitor internal coag pathway: aPTT

84
Q

low molecular weight heparin

A

Class: anticoagulant

MOA: increase activity antithrombin 3, inhibits Factor 10A AND 2A (thrombin)

No need for monitoring, longer half life so danger if there’s a bleed, no antidote

renal clearance, do not give if end stage renal disease

AE: bleeding

CI: heparin induced thrombocytopaenia

85
Q

Warfarin

A

class; anticoagulant

MOA; competes with Vit K, inhibits factors 2,7,9,10
Also inhibits Protein c, s and z: hypercoag state in first few days as these are body’s natural anticoagulants

First inhibits natural anticoagulants then acts on coagulants
Takes 48-72 hrs to work because natural clotting factors in blood need time to be destroyed. Therefore need to give heparin. Warfarin skin necrosis NB (warfarin destroys protein s and c resulting in formation tiny clots in vessels)

Antidote: fast: FFP, PCC, slow: Vit K

monitor external coag pathway (INR)

Highly protein bound

CI: do not give with alcohol, pregnant, recent intracranial haemorrhage, cirrhosis (liver unable to synthesise albumin and clotting factors so more predisposed to bleeding), known coagulation defects

86
Q

adverse effects heparin

A

NB just to remember that heparins do not thrombolyse, they just prevent further formation if clot

Bleeding
Osteoporosis
Alopecia
Thrombosis

Heparin induced thrombocyopaenia