PHARMACOLOGY Flashcards

1
Q

Antidotes?

Benzos
Anticholinergics
TCA
Ethylene glycol
Aspirin
Digoxin
Dabigatran
Oragnophosphate
Fe
Lead
CCB
BB
Methemoglobinemia
MTX

A

Flumanezil
Physostigmine
Na bicarb
Ethanol
Bicarb, dialysis
Digibind
Idracizumab
Atropine
Desferrozamine
DMSA
Ca, atropine
Insulin dex, adrenaline
Methylene blue
Na bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Can’t use activated charcoal for poisonings in?

A

Acids, alkali, metals, alcohols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Digoxin poisoning: clinical and ECG findings?

A

Digoxin causes cardiovascular toxicity and hyperkalaemia, but onset is delayed by hours while the drug is being distributed into the myocardium and other tissues.

ECG: slow AF/ AV block/ bradyarrhythmia, VT/VF, PAT, reverse tick ST depression, hyperkalemia

Clin: GI/CNS SE’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Digoxin poisoning treatment?

A

Fluids
Electrolyte
WH other cardiac meds: BB/CCB, hyperkalemic agents, anything that could worsen it
Digibind if unstable/ hyperkalemic/ arrest/ end organ dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antidepressant poisoning for all classes? Manifestations and management.

A

Mirtazipine: CV/CNS - relatively safe

MAOIB: ACh/ sympathomimetic - can be lethal

SSRI: sympathomimetic/ACh/CV

SNRI: sympathomimetic/ACh/CV

TCA: significant lethality; ACh + CV

Tx:
- TCA: bicarb if acidosis
- activated charchoal
- benzos for seizures
- cardiac monitoring
- fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

OHA’s/ insulin poisoning management?

  • Insulin
  • Metformin
  • Sulfonylureas
A

Insulin: replace electrolytes, IV glucose

Metformin: dialysis if pH < 7.0/ lactate > 20, Na bicarb, charchol

Sulphonylureas: Glucose, octreotide, activated charcoal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Antipsychotic overdose symptoms and management?

A

Symptoms
- CV: tachy, hypotension, QTc prolongation
- CNS: depression, seizures
- Anticholinergic SE’s

Treatment
- Activated charcoal
- GI decontamination
- Norad if hypotensive
- IVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is paracetamol normally metabolised? What changes with toxicity?

A

Normal
- glucorinidated 95%
- CYP450 and Glutathione detoxified 5%

Toxicity
- Glurodinate sufulated saturated –> goes down CYP450 pathway
- Glutathione used up –> produces NAPQI which is toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What increases risk of hepatotoxicity in paracetamol overdose?

A

HIV
Malnourished
Liver enzyme inducer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to decide when to stop NAC?

A

ALT decreasing
INR normalised
paracetamol conc low
clinically well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of low and high clearance drugs (from liver)?

A

Low clearance
- Benzos
- Anticonvulsants
- NSAIDs

High clearance
- Antipsychotics
- Antidepressants
- Narcotics
- BB
- CCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

High clearance drugs depend on __
Low clearance drugs depend on __

A

High –> blood flow
Low –> enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the difference between potency and efficacy?

A

Efficacy: maximum effect
Potency: concentration at which 50% effect achieved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens if you give full agonist and partial agonist together? (methadone and buprenorphine)

A

Partial agonist starts being an ANTAGONIST –> full effect goes down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens if you give agonist and competitive antagonist?

A

Efficacy same, potency decr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens in tachyplaxis? Examples? Draw graph.

A

Receptors getting used to drug

Cocaine, BB, nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens in anticlockwise hysteresis?

A

Desitrbuting to site of action; drug has incr effect over time

Dig, warfarin,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Abx killing types? State the drug
1) Time above MIC
2) Peak conc, MIC
3) AUC/MIC

A

1) Beta lactams
2) Aminoglycosides
3) Vanc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Formula for Vd?

A

Amount of drug in body/ amount of drug in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does food increase/decrease bioavailability

A

Fast absorption of food: more in body
Slow absorption of food: less in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Formula for loading dose?

A

LD = Vd x Plasmaconc

22
Q

Does giving a larger loading dose mean you will get to steady state quicker?

A

Only if
- dosing interval same as half life
- loading dose is double
Then immediately achieves steady state

If not 4-5 half lives

23
Q

Maintenance dose formula?

A

Cpss x Cl

24
Q

Most drugs are zero order or first order kinetics?

A

First order

25
Q

Hepatic Cl formula?

A

Hep Cl = ER x BF

26
Q

Which drugs need to be reduced in liver impairment?

High or low clearance? Examples?

A

Low clearance
- benzos
- anti epileptics
- NSAIDs

27
Q

Clearance determines?

A

Dose rate

28
Q

Clearance formula?

A

IV
- Cl = dose / AUC

PO
- Cl = dose x F / AUC

29
Q

Half life determines the?

A

dosing rate/interval

30
Q

Dose rate formula?

A

Plasma steady state x clearance

31
Q

What can you use urinary alkalisation for?

A

MTX
Aspirin

32
Q

What can you use hemodilaysis for?

A

metformin
lithium
salicylates
toxic alcohols

33
Q

What can prognosticate digoxin poisoning?

A

Degree of hyperK reflects degree of toxicity + predicts risk of death (not cause of death)

34
Q

Indications to start NAC?

A

○ Above line at 4 hours

○ Signs of hepatotoxicity: liver tenderness, GI symptoms, elevated ALT/AST on presentation

○ Liver failure even without a paracetamol history

○ Suspected ingestion > 7.5g and PCT concentration unavailable

○ Unknown time of ingestion and
§ Concentration PCT > 10
Evidence of liver injury

35
Q

When to stop NAC?

A

Limit duration to 3 days
- If ALT elevated/ serum con detectable can continue
- Stop when conc undetectable/ ALT decreasing normal, INR < 2.0

36
Q

Opioid receptor types:

A

Mu
Kappa
Delta

37
Q

Opioid effect on hormones?

A

Large doses –> inhibit GABA and cause a burst of DA neuron activity
Inhibits pituitary hormone release
Reduces thyrotropin
Increased GH
Resp depression
Reduces gut motility
Methdone can prolong QT interval

38
Q

Opioids withdrawal treatment?

A

Buprenorphine
DIazepam

39
Q

Options for opioid dependence?

A

Methadone
Buprenorphine
Naltrexone

40
Q

Smoking cessation options

A

NRT
Vernicicline: Nicotine partial agonist (SE: CVD)
Antidepressants: notriptyilline, buproprion

41
Q

How is alcohol broken down in liver?

A

Ethanol –> alcohol dehydrogenase –> Acetyldehyde

Acetyldehyde –> Acetyl dehydrogenase –> acetate

Acetate –> CO2 water

When too much bring produced –> acetyl coA –> FA’s

Too much alcohol –> CYP2E1 overwhelmed –> produced ROS

42
Q

Acute and chronic complications of alcohol excess?

A

ACUTE
- Wernicke’s: confusion, ataxia, ophthalmoplegia
- hypoglycemia
- NMDA surpassed, increased GABA
- DA release
- disturbed sleep

CHRONIC
- neuropathy
- cerebellar degeneration
- korsakoff’s: retro/anterograde amnesia, confabulation
- absorption: esp thiamine
- cognition + brain atrophy

43
Q

Alcohol withdrawal timing?

A

early: 6 hrs - 2 days
late: delirium terms up to 4 days

44
Q

Which substances cause withdrawal seizures?

A

ONLY BENZOS AND ALCOHOL CAUSES WITHDRAWAL SEIZURES

45
Q

Giving thiamine in alcohol withdrawal helps with what?

A

ocular palsies: most quickly
confusion/ataxia more slowly: may be residual defects

46
Q

Options for alcohol dependence?

A

Naltrexone:
□ Blocks opioid receptors –> decreases DA

Acamprosate:
□ inhibits NMDA receptor –> decreases symptoms of withdrawal

Disulfiram:
□ Raises acetyldehyde concentration –> aldehyde reaction

Topiramate/ gabapentin/ ondansetron/

47
Q

CO poisoning: what increases risk of long term complications?

A
  • Cardio/cerebrovascular disease
    • Sustained LOC
    • Neuro abnormalities after waking from coma
      • Exposure > 15 hours
48
Q

Complications of CO poisoning?

A
  • Delayed neuropsych syndrome
    ○ Cognitive deficit
    ○ Personality changes
    ○ Movement disorders
    ○ Focal deficit
    Can last 240 days post exposure
49
Q

CO poisoning treatment?

A
  • HFNP for atleast 6 hours initially
    • IVF if hypotensive
    • Ionotropic/circulatory support if concerns of myocardial depression
      ○ ECG monitoring
50
Q

Salicylate poisoning causes?

A
  • Aspirin
    • Wintergreen oil (essential oil) –> methyl salicylate
    • Choline salicylate (analgesic gel, including for teething)
      Salicylic acid: teething gels, skin peeling gels
51
Q

Salicylic acid treatment?

A
  • Decontamination with activated charcoal
    • Urinary alkalinisation
52
Q

What can’t you use activated charcoal for?

A

Cannot be used for acids, alkali, alcohols, ions/metals E.G. LITHIUM