Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Therapeutics > Flashcards

Therapeutics Flashcards

1
Q

Should you stop a drug for chronic disease in pregnancy?

A

Usually better not to stop as disease may adversely affect the pregnancy e.g. epilepsy, DM, HTN

Less than 30 medicinal molecules are genuine human teratogens

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

How is absorption altered in pregnancy?

A

N + V –> increased gastric pH, reduced gastric emptying, increased gut transit time

Increased absorption from IM injections + inhalation due to increased bioavailability

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

Pharmocokinetics - 4 areas

A

Absorption, distribution, metabolism, elimination (ADME)

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

Pharmacokinetic changes in pregnancy

A

ADME picture is complicated but changes not clinically significant for most drugs. BEWARE drugs with narrow therapeutic index e.g. AEDs, enoxaparin - dosing may need to be altered

Drug effect may be delayed after oral doses but enhanced after IM injections

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

Teratogenicity

A

Potential for a drug to cause foetal malformations + affects the embryo 3-8wks after conception

3-8wks is period of highest risk as organs are formed

Pre-embryonic phase (days 0-14 after conception) = all or nothing effect = recovery or spontaneous loss

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

2nd and 3rd trimester of pregnancy

A

Can affect growth (IUGR) and functional development or have toxic effects on tissues

Adverse effects on neonate if given shortly before/during labour e.g. diazepam or pethidine

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

Do drugs cross the placenta?

A

Assume all drugs cross the placenta unless they have a high molecular weight e.g. heparins

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

1st trimester drugs

A

Avoid if possible! Only prescribe if expected benefit to mother outweighs risk to fetes e.g. AEDs

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

Drugs to avoid in 1st trimester

A

Androgens, cytotoxic drugs, lithium, quinolone abx, retinoids, sodium valproate, thalidomide, warfarin

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

Drugs to avoid in 2nd and 3rd trimester

A

ACEi + ARBs, aminoglycosides, NSAIDs + aspirin, opiates + bendodiazepines, sulphonamides, tetracyclines

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

Does adjustment in pregnancy

A

Maternal drug conc usually lower than non-pregnant when taking same dose. Foteal + placental metabolism also affects drug concn. Some drugs may need increasing e.g. lamotrigine or enoxaparin

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

Drugs when BF?

A

Drugs can be excreted in milk - greater risk if neonate/premature as immature excretory functions so drugs may accumulate.

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

What drug characteristics make them better for BF?

A

High MW e.g. insulin, heparin
High protein binding e.g. warfarin, NSAIDs
Low lipid solubility e.g. loratadine
Lower pH e.g. amoxicillin

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

Drugs to avoid during BF

A

Amiodarone, antithyroid drugs, benzodiazepines, lithium salts, radioactive iodine, statins, sulphonamides
AABILSS

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

Drug effects on lactation?

A

Drugs affecting DA activity cause main effect on lactation (through prolactin changes)
Early postpartum use of oestrogen may reduce milk vol - use progesterone contraception

Da agonists decrease milk production
Da antagonists promote lactation when inadequate

Some drugs may affect infant’s suckling reflex e.g. phenobarbital

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

Absorption in children

A

Oral - developmental changes in absorptive surfaces of gut, GI motility + intraluminal pH alter rate + extent
Absorption also affected by slower gastric emptying which takes 6-8m to reach adult levels
1st pass metabolism increased for some drugs

Percutaneous absorption increased the younger the pt due to thinner stratum corneum + increased skin hydration

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

Distribution in children

A

For water soluble drugs - higher doses per kg of bodyweight must be given to children than adults e.g. gentamicin (younger the child - greater their total body water as a % of weight)

For protein bound drugs - plasma proteins e.g. albumin reduced in neonates

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

Dosing in children

A

3 different ways:
Age - for low therapeutic index drugs
Weight - lots
Body surface area - for narrow therapeutic index drugs e.g. chemo

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

Drugs to avoid in children

A

IV chloramphenicol –> Grey baby syndrome (in neonates causing cyanosis, grey skin, reduced BP, CV collapse)

Aspirin –> Reye’s syndrome (mitochondrial damage leading to rash, vomiting + liver damage) <16yrs

Tetracycline –> growing teeth + bone so not given to <12yrs

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

First pass metabolism in elderly

A

In elderly - reduced hepatic BF - reduced 1st pass metabolism + greater drug effect. Significant increase in drug bioavailability e.g. nitrates, verapamil

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

Distribution of drugs in elderly

A

Increased body fat –> increased Vd of lipid soluble drugs so they accumulate e.g. diazepam

Decrease in total body water - decreased Vd for water soluble drugs so lower doses of water soluble drugs required e.g. digoxin

Reduced plasma protein conc –> reduction in plasma protein binding causes an increase in ‘free’ drug e.g. phenytoin so increased risk of toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Elimination of drugs in elderly

A

Really excreted drugs require does adjustment as renal elimination decreases e.g. digoxin, gentamicin, lithium salts, opiates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What problems do pharmacodynamic changes lead to in the elderly?

A
  • Changes in R sensitivity
  • Reduction in R no.
    –> increases sensitivity to several drugs e.g. decreased Da Rs leads to increased risk of EPS SEs
    Reduced baron function leads to increased hypoTN on antiHTI therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drugs to avoid in renal impairment

A

NSAIDs - cause nephrotoxicity (interstitial nephritis)

Vancomycin - renally eliminated

Gentamicin - both of above!

aminoglycosides, metformin, nitrofurantoin, potassium, lithium
MANPLN - metformin, aminoglycosides, nitrofurnatoin, potassium, lithium, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Causes of raised troponin apart from ACS

A

Sepsis
PE
CKD
CCF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3 features of opiate overdose

A

miosis
coma
respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Features of salicyclate overdose

A

N + V, tinnitus, deafness, sweating + hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Features of ecstasy/cocaine overdose

A

Mydriasis, hyperthermia, tachycardia, arrhythmia and agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Drink driving limit for alcohol

A

Blood - 80mg/100ml

Breath - 35mg/100ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Drugs to avoid in hepatic impairment

A

NWSSD - NSAIDs, warfarin, steroids, sedatives, diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Weight changes in AEDs

A

Valproate, gabapentin - weight gain

Topiramate - weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Drug OD treatments

A

Paracetemol - N-acetylcysteine - 3 bags over 21h
Stimulate OD - diazepam 10mg IV
Sedative (heroin) - Naloxone
Benzodiazepine - flumazenil
Ethylene glycol/methanol - fomepizole (or ethanol!)

bromocriptine - used in prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Classes of non-opioid analgesics

A

Paracetemol
NSAIDs
Antidepressants - amitryptline - SEs = dry mouth, constipation, reduced UO, cardiotoxicity
AEDs - gabapentin, pregabalin

34
Q

Side effects of morphine

A

Euphoria, constipation, respiratory depression, euphoria, low BP

35
Q

Classes of anti-psychotic drugs

A

Typical/1st gen = chlorpromazine, haloperidol - EPS side effects (D2 R antagonists) so due to reduced DA in nigro-striatal path

Atypical/2nd gen = clozapine, risperidone - act on serotonine, NA, and DA to avoid parkinson like effects - cause weight gain and blurred vision

36
Q

2 types of adverse drug reactions

A

Type A - ‘dose-dependent’ and predictable on the base of the pharmacology of the drug

Type B - bizarre - not predictable

37
Q

3 steps of the WHO pain ladder

A

Non-opioid analgesics e.g. paracetamol
Mild opoiod e.g. codeine
Strong opiod e.g. morphine

Can add NSAIDs at any stage

38
Q

Where is alcohol absorbed in the body?

A

Duodenum-jejunum = >80%
Rate of absorption is conc dependent + related to gastric emptying

W more affected by alcohol as have more fat + less h2o than men (alcohol is found in water component so they have less h2o so higher conc)

39
Q

Alcohol metabolism

A

Ethanol (ADH) –> acetylaldehyde (ALDH –> acetate

40
Q

How does alcohol effect the CNS?

A

GABA - potentiates (inhibitory)
NMDA - antagonises (excitatory)
Effects 5HT, opioid + DA NT (reward centres)

41
Q

Alcohol - drug interactions

A

CNS drugs e.g. tricyclic ADs, benzos, phenothiazines - increased drowsiness + sedation

AntiHTN drugs - enhanced hypotensive effect

Warfarin - affects anticoagulant control

Metronidazole/ketoconazole - inhibit aldehyde dehydrogenase causing accumulation of acetylaldehyde

42
Q

CAGE questionairre

A

C - cut down amount of drinking
A - annoyed by criticism
G - guilty feelings about drinking
E - eye opener in the morning

43
Q

What is delirium tremens?

A

Occurs 48-72h after withdrawal of alcohol
Chracacterised by agitation, confusion, paranoia, visual + auditory halluciantions

*tonic clonic seizures occur 24-48h

44
Q

What is pabrinex?

A

High potency vitamin B complex - contains high dose thiamine (B1), riboflavin (B2), B6, nicotinamide and vit c

45
Q

Principles of management of alcoholism

A

Recognition
ABCDE
Prevent/tx encepalopathy - thiamine + other Bs
Prevent/tx withdrawal - chlordiazepoxide

46
Q

Paracetemol OD likelihood in amounts

A

mg/kg
<75 - extremely unlikely
75 - 150 - rare
>150 - possible

47
Q

How does paracetemol cause toxicity?

A

Glutathione depletion

Direct oxidising and arylating effects

48
Q

Timings to antidote in paracetemol OD

A

8hr rule
Provided a pt is treated in 8hrs - not at risk of significant liver damage - worth waiting for plasma paracetamol conc if will be back before 8hrs

49
Q

What is a staggered OD?

A

If a pt takes paracetamol spread over <60mins = staggered

50
Q

Pharmacological tx of orthostatic hypotension

A

Fludrocortisone

Midodrine

51
Q

CHA₂DS₂-VASc

A

Score for AF stroke risk

  • Age
  • Sex
  • Congestive HF
  • HTN
  • Stroke/TIA/thromboembolism
  • Vascular disease
  • DM
52
Q

HAS-BLED

A

Score for major bleeding risk - estimates risk of bleeding for pts on anti-coag to assess risk benefit in AF care

  • HTN (uncontrolled or >160)
  • Renal disease
  • Liver disease
  • Stroke hx
  • Prior major bleeding or predisposition
  • Labile INR (unstable/high INRs)
  • Age (>65)
  • Medication usage predisposing to bleeding (aspirin, clopidogrel, NSAIDs)
  • Alcohol use (>8 drinks/wk)
53
Q

Treatment of acute severe asthma

A 
O2
Nebulised salbutamol
Prednisolone 40-50mg PO or hydrocortisone 100mg IV
if response poor..
Inhaled ipatropium 
IV Mg sulphate, aminophylline
54
Q

HTN definitions

A

Stage 1: clinic of 140/90 or ABPM 135/85
Stage 2: clinic of 160/100 or ABPM of 150/95
Severe: 180/110

55
Q

Anti HTN

A

Aged under 55 = ACEi (ARB if can’t tolerate)
>55 or Black-afro = CCB

Then add on the opposite so A + C
Then add on thiazide like diuretic A + C + D
For resistant HTN - consider another diurectic, alpha blocker (doxazosine) or b-blocker

56
Q

ACEi

A

e.g. ramipril, perindopril
SE: dry cough (BK)
Rare SE: angiodema, hyperkalemia

Check U+Es 1 wk after commencing
Contra-indications = pregnancy, BF

Also used: post-MI, HF, CKD

57
Q

ARB

A

e.g. losartan, candesaratan, valsartan

Do not cause cough
same contra-indications as ACE

Also used: HF, CKD

58
Q

CCB

A

Dihydropyridines e.g. amlodipine, felodipine
Main SEs: ankle oedema, acid reflux, gingival hyperplasia
Also used for: raynauds, angina

Non-dihydropyridines e.g. diltiazem (heart/BVs), verapamil (heart)
SEs: worsening HF, bradycardia, heart block
Also used for: tachyarrhytmias, angina, migraine, cluster headache

59
Q

Thiazide like diuretics

A

bendroflumethiazide
Blocks Na-Cl channels in DCT - Na and water loss

SEs: gout, ED, hypercalcaemia

60
Q

Loop diuretics

A

e.g. furosemide
block Na-K-Cl pump in thick ascending limb

SEs: electyolyte disturbance, polyuria, dehydration
used in: pulmonary oedema, CCF, nephortic syndrome, ascites

61
Q

K sparing diuretics

A

Aldosterone antagonists e.g. spironolactone . Low doses in HTN
Also used for: hyperaldosteronism, Conn’s
SEs: hyperkalemia, gynaecomastia, ED

62
Q

Beta blockers

A

reduced HR and force of contraction
reduce renin release

B1: increased cardiac rate + force
B2: vasodilation, bronchodilation, SM relaxation, hepatic glycogenolysis, muscle tremor

cardioselective (B1) = bisoprolol, metoprolol
non selective: propanolol

SEs: tiredness, bracycardia, bronchoconstriction, ED, hypoglycaemia

63
Q

Postural hypotension

A

> 20mmHg drop in SBP or >10mmHg drop in DBP on standing
Adrenal insuffiency, autonomic failure (DM, alcoholism, PD), drugs

Pharamcological management includes fludrocortisone or midodrine

64
Q

Why does HF lead to oedema?

A

Reduced renal BF –> activates RAAS –> Na and water retention –> oedema

65
Q

Treatment for HF with reduced EF (systolic)

A

ACE/ARBs - reduce preload + afterload
B-blockers - reduced symp overactivity
Aldosterone antagonists - reduce mortality
Diuretics - treat oedema - reduces preload
Digoxin - increases force of contraction - useful when HF caused by AF

66
Q

Treatment for HF with preserved EF

A

BP control

Symptomatic tx

67
Q

Categories of arrythmias

A

Fast/slow
Narrow complex/broad complex
Regular/irregular

68
Q

Treatment of SVT

A

Defib pads
Vagal manoeuvres
Carotid sinus massage
Adenosine 6mg IV
If ineffective: verapamil IV slow injection
DC cardioversion if haemodynamically unstable

69
Q

Atrial fibrillation

A

Paraoxysmal
Persistent
Permanent

Tx: anticoagulant and rate control OR rhythm control

Anti-coag: warfarin or DOACs
Rate: b-blockers, diltiazem, verapamil, digoxin
Rhythm: amiodarone, flecainide

70
Q

Digoxin

A

Inhibits Na/K ATPase in cardiac myocytes

SEs: N + V, diarrhoea, fatigue, arrhytmias, confusion

71
Q

Amiodarone

A

Prolongs AP duration + effective refractory period in all cardiac tissues

SEs: fibrosis, hepatitis, thyroid dysfucntion, photosensitivity, optic neuritis, orchitis

72
Q

Drugs that increase INR from warfarin interaction

A

Cranberry juice
Ciprofloxacin
Clarithromycin
Metronidazole

73
Q

Warfarin interaction - drugs that decrease INR

A

Dietary vit K
Rifampicin
Carbamazepine
St Johns wort

74
Q

Orlistat

A

Lipase inhibitor - prevents breakdown of dietary fats

SEs: abdo cramps, faecal urgency/incontinence, steatorrhoea

75
Q

Drugs to help obesity

A

Orlistat

In DM: GLP1 agonists, SGLT2 inhibitors

76
Q

Drugs for hyperlipidaemia

A

Statins - HMG CoA reductase inhibitor
Ezetimibe - inhibits intestinal absorption of cholesterol
Fibrates
PCSK9 inhibitors - monoclonal AB which binds to R for LDL cholesterol

77
Q

Main strategies for pharmacotherapy in angina

A

Slow HR and reduce metabolic demand
Improve blood supply (coronary vasodilatation)
Reduce preload
Reduce afterload

78
Q

Stable angina drugs

A 
Rate limiting drugs e.g. bblockers, verapamil, diltiazem
Nitrates e.g. isosorbide mononitrate
CCBs e.g. amlodipine
nicorandil 
ranolazine
79
Q

Antiplatelet agents

A

Aspirin
Clopidogrel (prodrug) - requires conversion by CYP450 - used for 1yr post MI but aspirin lifelong
Ticagrelor

80
Q

Secondary prevention following diagnosis of IHD

A 
Dual antiplatelet therapy - aspirin + clopidogrel
B blocker
ACEi 
Statin
Smoking cessation

Year 3 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions