Brainscape's Knowledge GenomeTM

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


See full index

MRCP I > Pharma > Flashcards

Pharma Flashcards

1
Q

Phase I reactions:

A

oxidation, reduction, and hydrolysis. Mainly performed by the P450 enzymes but some drugs are metabolised by specific enzymes, for example alcohol dehydrogenase and
xanthine oxidase. Products of phase I reactions are typically more active and potentially toxic

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

Phase II reactions:

A

conjugation. Products are typically inactive and excreted in urine or bile.
Glucuronyl, acetyl, methyl, sulphate and other groups are typically involved.
* The majority of phase I and phase II reactions take place in the liver.

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

First-Pass Metabolism

A

concentration of a drug is greatly ↓ before it reaches the systemic circulation due to hepatic metabolism. As a consequence much larger doses are need orally than if given by other routes. This effect is seen in many drugs, including:
* Aspirin
* Isosorbide dinitrate
* Glyceryl trinitrate
* Lignocaine
* Propranolol
* V erapamil

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

Zero-Order Kinetics

A

describes metabolism which is independent of the concentration of the reactant. This is due to metabolic pathways becoming saturated resulting in a constant amount of drug being eliminated per unit time. This explains why people may fail a breathalyser test in the morning if they have been drinking the night before
Drugs exhibiting zero-order kinetics * Phenytoin
* Salicylates * Heparin
* Ethanol

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

Drugs exhibiting zero-order kinetics *

A

Phenytoin
* Salicylates * Heparin
* Ethanol

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

Drugs affected by acetylator status:

A
  • Isoniazid
  • Procainamide * Hydralazine * Dapsone
  • Sulfasalazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

P-450 Dependent Drugs WEPTD:

A
  • Warfarin
  • Estrogen
  • Phenytoin
  • Theophylline
  • Digoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

P450 inhibtors: (causing low metabolism of WEPTD → Toxicity)

A

Acute alcohol intake
* Allopurinol
* Amiodarone
* Cimetidine, omeprazole
* Dapsone
* Imidazoles: ketoconazole, fluconazole
* INH
* Macrolides (Azithro-Clarithro-Erythro mycins)
* Quinolones (ciprofloxacin)
* Quinupristin
* Sodium valproate
* Spironolactones
* SSRIs: fluoxetine, sertraline
* Grapefruit juice (potent inhibitor of the cytochrome P450 enzyme CYP3A4)
* Protease inhibitors (ndinavir, nelfinavir, ritonavir, saquinavir)

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

P450 inducers:

A
  • Antiepileptics: phenytoin, carbamazepine (note that valporate is an inhibitor)
  • Barbiturates
  • Chronic alcohol intake
  • Griseofulvin
  • Quinidine
  • Rifampicin
  • Smoking (affects CYP1A2, reason why smokers require more aminophylline)
  • St John’s Wort
  • Sulfa drugs
  • Tetracycline
  • Nevirapine (NNRTI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Drugs that can be cleared with Hemodialysis

A

Barbiturate
* Lithium
* Alcohol (inc methanol, ethylene glycol)
* Salicylates
* Theophyllines (charcoal hemoperfusion is
preferable)

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

Drugs which cannot be cleared with HD include

A

Tricyclics
* Benzodiazepines (diazepam,midazolam,alprazolam)
* Dextropropoxyphene (co-proxamol)
* Digoxin, β-blockers

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

Drugs to avoid in Renal Failure

A
  • Antibiotics: tetracycline, nitrofurantoin
  • NSAIDS
  • Lithium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Drugs likely to accumulate in renal failure - need dose adjustment

A

Most antibiotics including penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
* Digoxin, atenolol
* Methotrexate
* Sulphonylureas
* Furosemide
* Opioids

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

Drugs relatively safe in renal failure - use in normal dose

A

Antibiotics: erythromycin, rifampicin
* Diazepam
* W arfarin

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

Drug Induced Impaired Glucose Tolerance

A

Thiazides, furosemide (less common)
* Steroids
* Tacrolimus, cyclosporin
* Interferon-α
* Nicotinic acid (vitamin B3)
β-blockers cause a slight impairment of glucose tolerance. They should also be used with caution in
diabetics as they can interfere with the metabolic and autonomic responses to hypoglycemia

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

drugs Hepatocellular Picture

A
  • Alcohol
  • Amiodarone
  • Anti-tuberculosis: isoniazid,
    rifampicin, pyrazinamide
  • Halothane
  • MAOIs
  • Methyldopa
  • Paracetamol
  • Sodium valproate, phenytoin
  • Statins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

drugs Cholestasis (+/- Hepatitis)

A

Anabolic steroids, testosterones
* Antibiotics: flucloxacillin, co-amoxiclav,
erythromycin*, nitrofurantoin
* Fibrates
* Oral contraceptive pill
* Phenothiazines:
prochlorperazine
* Rarely: nifedipine
* Sulphonylureas

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

drugs Liver Cirrhosis

A

Amiodarone * Methotrexate * Methyldopa

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

Drugs Causing Visual Disturbance:

A

Cataracts
* Steroids
Corneal opacities
* Amiodarone * Indomethacin
Optic neuritis
* Ethambutol
* Amiodarone
* Metronidazole
Retinopathy
* Chloroquine, quinine Blue tinge in vision:
* Sildinafil Yellow-green tinge:
* Digoxin

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

Drugs Causing Gingival hyperplasia

A
  • Phenytoin
  • Cyclosporin
  • Calcium channel blockers (especially nifedipine)
    Other causes of gingival hyperplasia include
  • Acute myeloid leukemia (myelomonocytic and monocytic types)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Drugs Causing Urticaria:

A
  • Aspirin
  • Penicillins * NSAIDs
  • Opiates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Drugs Causing Acute Intermittent Porphyria (AIP)

A
  • Alcohol
  • Barbiturates
  • Benzodiazepines
  • Halothane
  • Oral contraceptive pill
  • Sulphonamides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute Intermittent Porphyria (AIP) safe drugs

A
  • Paracetamol * Aspirin
  • Codeine
  • Morphine
  • Chlorpromazine * β-blockers
  • Penicillin
  • Metformin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drug Induced Thrombocytopenia (probable immune mediated)

A
  • Heparin
  • Abciximab
  • NSAIDs; ASA
  • Diuretics: furosemide
  • Quinine
  • Antibiotics: penicillins, sulphonamides, rifampicin
  • Anticonvulsants: carbamazepine, valproate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Drug Induced Pancytopenia:

A
  • Cytotoxics
  • Antibiotics: trimethoprim, chloramphenicol
  • Anti-rheumatoid: gold (sodium aurothiomalate), penicillamine
  • Carbimazole*
  • Anti-epileptics: carbamazepine
  • Sulphonylureas: tolbutamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Drug Induced Photosensitivity:

A
  • Thiazides
  • Tetracyclines, sulphonamides, ciprofloxacin
  • Amiodarone
  • NSAIDs e.g. Piroxicam
  • Psoralens
  • Sulphonylureas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nicotine replacement therapy

A

Adverse effects nausea &
include vomiting, flu-like
headaches
and
symptoms
* Nice recommend offering a
combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge or nasal spray) to people who show a high level of dependence on nicotine or who have found single forms of NRT inadequate in the past

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

Nicotinic receptor partial agonist Varenicline

A
  • Should be started 1 week before the patien target date to stop
  • The recommended course of is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)
  • Has been shown in studies to
    be more effective than bupropion
  • Nausea is the most common adverse effect. Other include headache, insomnia, abnormal dreams
  • V arenicline should be used with caution in patients with a history of depression or self-harm.
  • Contraindicated in pregnancy and breast feeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist Bupropion

A
  • Should be started 1 to 2 weeks before target date.
  • Small risk of seizures (1: 1,000)
  • Bupropion should not be prescribed to individuals with epilepsy or other conditions
    that lower the seizure threshold, such as alcohol or benzodiazepine withdrawal, anorexia nervosa, bulimia, or active brain tumors. It should be avoided in individuals who are also taking MAOIs. When switching from MAOIs to bupropion, it is important to include a washout period of 2 weeks. Also pregnancy and breastfeeding are contraindications.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Salicylate Overdose:

A

mixed respiratory alkalosis and metabolic acidosis
sweaty, confused patient
pulmonary edema suggests severe poisoning and
is an indication for hemodialysis

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

Indications for hemodialysis in salicylate overdose

A
  • Serum concentration > 700mg/L
  • Metabolic acidosis resistant to treatment
  • Acute renal failure
  • Pulmonary edema
  • Seizures
  • Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Paracetamol Overdose:

A

Management:
* Start N-acetyl cysteine immediately
* Naloxone if there is hypoxia or respiratory depression

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

King’s College Hospital criteria for liver transplantation (paracetamol liver failure) Arterial pH < 7.3, 24 hours after ingestion OR all of the following:

A
  • Prothrombin time > 100 seconds
  • Creatinine > 300 μmol/l
  • Grade III or IV encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

The following patients are at ↑ risk of developing hepatotoxicity following a paracetamol overdose:

A
  • Chronic alcohol excess
  • Patients on p450 enzyme inducers (rifampicin, phenytoin, carbamazepine)
  • anorexia nervosa: ↓ glutathione stores
  • HI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Digoxin Toxicity:

A

Actions
* ↓ conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
* ↑ the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump

Features
* Generally unwell, lethargy, nausea & vomiting, confusion,
* Arrhythmias (e.g. AV block, bradycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Precipitating factors Digoxin Toxicity:

A
  • Classically: Hypokalemia*
  • Myocardial ischemia
  • Hypomagnesemia, acidosis (Hypo pH), Hypercalcemia, Hypernatremia
  • Hypoalbuminemia
  • Hypothermia
  • Hypothyroidism
  • Drugs: amiodarone, quinidine, verapamil, spironolactone (compete for
    secretion in distal convoluted tubule therefore ↓ excretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Digoxin Toxicity: management

A

Management
* Digibind
* Correct arrhythmias
* Monitor K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Indications for administration of Digoxin specific Fab Fragment are:

A
  • Hemodynamic instability
  • Life-threatening arrhythmias
  • Serum potassium >5 mmol/l in acute toxicity
  • Plasma digoxin level >13nmol/l
  • Ingestion of more than 10 mg digoxin in adults and 4 mg in children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Cyanide

A

Presentation
* ‘Classical’ features: BRICK-RED SKIN, smell of bitter almonds
* Acute: hypoxia, hypotension, headache, confusion
* Chronic: ataxia, peripheral neuropathy, dermatitis
Management
* Supportive measures: 100% oxygen
* Definitive: IV dicobalt edetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Ethylene glycol toxicity management -

A

fomepizole. Also ethanol / hemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Ethylene glycol - Features of toxicity are divided into 3 stages:

A

Features of toxicity are divided into 3 stages:
* Stage 1: symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness
* Stage 2: metabolic acidosis with high anion gap and high osmolar gap. Also tachycardia,
hypertension
* Stage 3: acute renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Cocaine heart

A
  • Myocardial infarction
  • Both tachycardia and bradycardia may occur
  • Hypertension
  • QRS widening and QT prolongation
  • Aortic dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cocaine neuro impact

A

Neurological effects
* Seizures
* Hypertonia
* Hyperreflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Ecstasy overdose features

A

Clinical features
* Neurological: agitation, anxiety, confusion, ataxia
* Cardiovascular: tachycardia, hypertension
* Water intoxication
* Hyperthermia
* Rhabdomyolysis
* Hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Ecstasy treatment

A

Management
* Supportive
* Dantrolene may be used for hyperthermia if simple measures fail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mercury Poisoning:
Features

A
  • Paraesthesia
  • Visual field defects
  • Hearing loss
  • Irritability
  • Renal tubular acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

chelation therapy for acute inorganic mercury poisoning

A

2,3-dimercapto-1- propanesulfonic acid (DMPS), D- penicillamine (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning.

no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Lead Poisoning features

A

abdominal pain and neurological signs
Features
* Abdominal pain
* Peripheral neuropathy (mainly motor)
* Fatigue
* Constipation
* Blue lines on gum margin (only 20% of adult patients, very rare in children)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Lead Poisoning investigations

A

Microcytic anemia
* Blood film shows red cell
abnormalities including basophilic stippling and clover- leaf morphology
* Raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to differentiate from acute intermittent porphyria
* Urinary coproporphyrin is also ↑ (urinary porphobilinogen and uroporphyrin levels are normal to slightly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Lead Poisoning Management

A

Dimercaptosuccinic acid (DMSA)
* D-penicillamine
* EDT A (EthyleneDiamineTetraAcetic acid)
* Dimercapro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Carbon Monoxide

A

Confusion, pyrexia and pink mucosae are typical features of carbon monoxide poisoning

Management
* 100% oxygen
* Hyperbaric oxyge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Indications for hyperbaric oxygen

A
  • Loss of consciousness at any point
  • Neurological signs other than headache
  • Myocardial ischemia or arrhythmia * Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Oculogyric Crisis features

A

dystonic reaction to certain drugs or medical conditions
Features (extra pyramidal)
* Restlessness, agitation
* Involuntary upward deviation of the eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Causes- Oculogyric Crisis

A

Phenothiazines
* Haloperidol
* Metoclopramide
* Postencephalitic Parkinson’ s disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Oculogyric Crisis

A

Treatment
* Procyclidine * Benztropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Contraindicated in pregnancy antibiotics

A

Tetracyclines
* Aminoglycosides
* Sulphonamides
* Trimethoprim
* Quinolones: the BNF advises to avoid due
to arthropathy in some animal studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

drugs CI in preggo

A

ACE inhibitors, ARBs
* Statins
* W arfarin
* Sulfonylureas
* Retinoids (including topical)
* Cytotoxic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Breastfeeding Contraindications:

A

Antibiotics: ciprofloxacin, tetracycline, chloramphenicol, sulphonamides
* Psychiatric drugs: lithium, benzodiazepines, clozapine
* Aspirin
* Carbimazole
* Sulphonylureas
* Cytotoxic drugs
* Amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

safe in breastfeeding

A

Antibiotics: penicillins, cephalosporins, trimethoprim
* Endocrine: glucocorticoids (avoid high doses), levothyroxine*
* Epilepsy: sodium valproate, carbamazepine
* Asthma: salbutamol, theophyllines
* Psychiatric drugs: tricyclic antidepressants,
antipsychotics**
* Hypertension: β-blockers, hydralazine,
methyldopa
* Anticoagulants: warfarin, heparin
* Digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Standard Heparin mOA and monitoring

A

Activates antithrombin III forms a complex that inhibits Xa, IXa, XIa and XIIa

Activated partial thromboplastin Anti-Factor Xa (although routine time (APTT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

LMWH) MOA

A

Activates antithrombin III forms a complex that inhibits Xa,

monitored with Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Heparin-induced thrombocytopaenia (HIT)

A
  • Immune mediated - antibodies form which cause the activation of platelets
  • Usually does not develop until after 5-10 days of treatment
  • Despite being associated with low platelets HIT is actually a prothrombotic condition
  • Features include a greater than 50% reduction in platelets, thrombosis and skin allergy
  • Treatment options include alternative anticoagulants such as lepirudin and danaparoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

drenaline induced ischemia

A

phentolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Phenytoin monitoring

A

Trough levels immediately before dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Cyclosporin monitoring

A

Trough levels immediately before dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Digoxin monitoring

A

Digoxin
* At least 6 hrs post-dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Lithium range

A

Lithium
* Range = 0.4 - 1.0 mmol/l
* Take 12 hrs post-dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Botulinum Toxin (‘Botox’) indications

A
  • Blepharospasm
  • Hemifacial spasm
  • Focal spasticity including cerebral palsy patients, hand and wrist disability associated with
    stroke
  • Spasmodic torticollis
  • Severe hyperhidrosis of the axillae
  • Achalasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Isotretinoin adverse effects

A

dverse effects
* Teratogenicity: ♀s MUST be using two forms of contraception (e.g. COCP and condoms)
* Dry skin, eyes and lips: the most common side-effect of isotretinoin
* Low mood, depression
* Raised triglycerides
* Hair thinning
* Nose bleeds (caused by dryness of the nasal mucosa)
* Benign intracranial hypertension: isotretinoin treatment should not be combined with
tetracyclines for this reason

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Conversion between opioids

A

Oral codeine Oral morphine Divide by 10
Oral tramadol Oral morphine Divide by 5
Oral morphine Oral oxycodone Divide by 2

Oral morphine
To
Subcutaneous diamorphine Divide by 3
Oral oxycodone
Subcutaneous diamorphine Divide by 1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Hydrocortisone Equivalence

A

1mg prednisolone = 4mg hydrocortisone
* 1mg dexamethasone = 7mg prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Chemotherapy Side effects

A
  • Anxiety
  • Age less than 50 years old
  • Concurrent use of opioids
  • The type of chemotherapy used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

metoclopramide in cancer

A

For patients at low-risk of symptoms then drugs such as metoclopramide may be used first-line. For high-risk patients then 5HT3 receptor antagonists such as ondansetron are often effective, especially if combined with dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Doxazosin

A

α-1 adrenoceptor antagonist used in the treatment of hypertension and benign
prostatic hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Lithium MOA

A

Mechanism of action - not fully understood, two theories:
* Interferes with inositol triphosphate formation
* Interferes with cAMP formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Lithium Adverse effects

A

Adverse effects
* Nausea/vomiting, diarrhea
* Fine tremor
* Polyuria
* Thyroid enlargement, may lead to hypothyroidism
* ECG: T wave flattening/inversion
* W eight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Monitoring of patients on lithium therapy

A

Inadequate monitoring of patients taking lithium is common - NICE and the National Patient
Safety Agency (NPSA) have issued guidance to try and address this. As a result it is often an
exam hot topic
* Lithium blood level should ‘normally’ be checked every 3 months. Levels should be taken 12
hours post-dose
* Thyroid and renal function should be checked every 6 months
* Patients should be issued with an information booklet, alert card and record book

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

lithium tax precipitated by

A

precipitated by dehydration, renal failure, diuretics
(Especially bendroflumethiazide) or ACE inhibitors and ARBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

lithium tox features

A

Features of toxicity
* Coarse tremor (a fine tremor is seen in therapeutic levels)
* Acute confusion
* Seizure
* Coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

lithium tox treatment

A

anagement
* Mild-moderate toxicity may respond to volume resuscitation with normal saline
* Hemodialysis may be needed in severe toxicity
* Sodium bicarbonate is sometimes used but there is limited evidence to support this. By
increasing the alkalinity of the urine it promotes lithium excretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Tricyclic Overdose Features of severe poisoning include:

A

Features of severe poisoning include:
* Arrhythmias
* Seizures
* Metabolic acidosis
* Coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Tricyclic Overdose ECG changes include:

A
  • Sinus tachycardia
  • Widening of QRS
  • Prolongation of QT interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

phenytoin se chronic

A

Chronic
* Common: gingival hyperplasia, hirsuitism, coarsening of facial features
* Megaloblastic anemia (secondary to altered folate metabolism)
* Peripheral neuropathy
* Enhanced vitamin D metabolism causing osteomalacia
* Lymphadenopathy
* Dyskinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Sodium Valproate MOA

A

management epilepsy and is first line therapy for generalised
seizures. It works by increasing GABA activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Sodium Valproate Adverse effects

A

Adverse effects
* Gastrointestinal: nausea
* ↑ appetite and weight gain
* Alopecia: regrowth may be curly (note that phenytoin → hirsutism while valporate → alopecia)
* Ataxia
* Tremor
* Hepatitis (also with phenytoin)
* Pancreatitis
* Teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Anticholinesterase Effects overdsose Features

A

Features can be predicted by the accumulation of acetylcholine (mnemonic = SLUD)
* Salivation
* Lacrimation
* Urination
* Defecation
* Cardiovascular: hypotension, bradycardia
* Also: small pupils, muscle fasciculation

87
Q

Anticholinesterase OD managment

A

Management
* Atropine
* The role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear
benefit

88
Q

St John’s Wort

A
  • Shown to be as effective as tricyclic antidepressants in the treatment of mild-moderate
    depression
  • Mechanism: thought to be similar to SSRIS (although noradrenaline uptake inhibition has also
    been demonstrated)
  • NICE advise ‘may be of benefit in mild or moderate depression, but its use should not be
    prescribed or advised because of uncertainty about appropriate doses, variation in the nature of preparations, and potential serious interactions with other drugs’
    Adverse effects
  • Profile in trials similar to placebo
  • Can cause serotonin syndrome
  • Inducer of P450 system, therefore ↓ levels of drugs such as warfarin, Cyclosporin. The
    effectiveness of the combined oral contraceptive pill may also be ↓
89
Q

Non-selective monoamine oxidase inhibitors

A
  • E.g. tranylcypromine, phenelzine
  • Used in the treatment of depression and other psychiatric disorder
  • Not used frequently due to side-effects
90
Q

Adverse effects of non-selective monoamine oxidase inhibitors

A

Hypertensive crisis: MAOIs reacting with tyramine containing foods e.g. Cheese, pickled
herring, Bovril, oxo, marmite, broad beans, liver, wine.
* Anticholinergic effects

91
Q

Serotonin Receptors Agonists

A
  • Sumatriptan is a 5-HT1D receptor agonist which is used in the acute treatment of migraine
  • Ergotamine is a partial agonist of 5-HT1 receptors
92
Q

Serotonin Receptors Antagonists

A
  • Pizotifen is a 5-HT2 receptor antagonist used in the prophylaxis of migraine attacks.
  • Methysergide is another antagonist of the 5-HT2 receptor but is rarely used due to the risk of
    retroperitoneal fibrosis
  • Cyproheptadine is a 5-HT2 receptor antagonist which is used to control diarrhea in patients with carcinoid syndrome
  • Olanzapine is 5-HT2 antagonist and D2 dopamin receptor blocker, it’s an atypical antipsychotic
  • Ondansetron and Granisetron are 5-HT3 receptor antagonist and is used as an antiemetic… They
    cause conistipation, dizziness and headache.
93
Q

Triptans

A

are specific 5-HT1 agonists used in the acute treatment of migraine. They are generally used second line when standard analgesics such as paracetamol and ibuprofen are ineffective

94
Q

Prescribing points Triptans:

A
  • Should be taken as soon as possible after the onset of headache, rather than at onset of aura
  • Oral, orodispersible, nasal spray and subcutaneous injections are available
    Adverse effects
  • ‘Triptan sensations’ - tingling, heat, tightness (e.g. Throat and chest), heaviness, pressure
    Contraindications
  • Patients with a history of, or significant risk factors for ischemic heart disease or cerebrovascular disease
95
Q

Dopamine Receptor Agonists:

A

Indications
* Parkinson’s disease
* Prolactinoma/galactorrhoea
* Cyclical breast disease
* Acromegaly
Adverse effects
* Nausea/vomiting
* Postural hypotension
* Hallucinations
* Daytime somnolence

96
Q

Benzodiazepines

A

enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). They therefore are used for a variety of purposes:
* Sedation
* Hypnotic
* Anxiolytic
* Anticonvulsant
* Muscle relaxant

97
Q

The BNF gives advice on how to withdraw a benzodiazepine. The dose should be withdrawn in steps of about 1/8 (range 1/10 to 1/4) of the daily dose every fortnight. A suggested protocol for patients experiencing difficulty is given:

A
  • Switch patients to the equivalent dose of diazepam
  • Reduce dose of diazepam every 2-3 weeks in steps of 2 or 2.5 mg
  • Time needed for withdrawal can vary from 1 month to 1 year or more
98
Q

Amiodarone

A

class III antiarrhythmic agent used in the treatment of both atrial and ventricular tachycardias.

ain mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I-a effect)

99
Q

The use of amiodarone is limited by a number of factors

A
  • Long half-life (20-100 days)
  • Should ideally be given into central veins (causes thrombophlebitis)
  • Has proarrhythmic effects due to lengthening of the QT interval
  • Interacts with drugs commonly used concurrently e.g. ↓ metabolism of warfarin = P450 inhibtor
  • Numerous long-term adverse effects (see below)
100
Q

Monitoring of patients taking amiodarone

A

TFT, LFT, U&E, CXR prior to treatment. U&E to check hypokalemia
* TFT, LFT every 6 months

101
Q

Adverse effects of amiodarone use

A
  • Thyroid dysfunction
  • Corneal deposits
  • Pulmonary fibrosis/pneumonitis
  • Liver fibrosis/hepatitis
  • Peripheral neuropathy, myopathy
  • Photosensitivity
  • ‘Slate-grey’ appearance
102
Q

Amiodarone-induced hypothyroidism (AIH)

A

The pathophysiology of amiodarone-induced hypothyroidism (AIH) is thought to be due to the high iodine content of amiodarone causing a Wolff-Chaikoff effect (an autoregulatory phenomenon where thyroxine formation is inhibited due to high levels of circulating iodide)

103
Q

Flecainide moa

A

Vaughan Williams class I-c antiarrhythmic. It slows conduction of the action potential by acting as a potent sodium channel blocker. This may be reflected by widening of the QRS complex and prolongation of the PR interval

104
Q

Flecainide and MI

A

lecainide was actually shown to ↑ mortality post myocardial infarction and is therefore contraindicated in this situation.

105
Q

Flecainide indications

A

Indications
* Atrial fibrillation
* SVT associated with accessory pathway e.g. Wolf-Parkinson-White syndrome

Adverse effects
* Negatively inotropic
* Bradycardia
* Proarrhythmic
* Oral paraesthesia
* Visual disturbance

106
Q

Statins Moa

A

inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol
synthesis → Statins: ↓ cholesterol synthesis.

107
Q

Statins Adverse effects

A

Myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, ♀, low BMI and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
* Liver impairment: 2008 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

108
Q

Statins (HMG CoA reductase inhibitors) AE

A

Myositis, pruritus, cholestasis

109
Q

Nicotinic Acid

A

reatment of patients with hyperlipidemia, although its use is limited by side-effects. As well as lowering cholesterol and triglyceride concentrations it also raises HDL levels
Adverse effects
* Flushing
* Impaired glucose tolerance
Myositis

110
Q

β-blocker overdose management

A

: atropine + glucagon

Glucagon has a positive inotropic action on the heart and ↓ renal vascular resistance. It is therefore
useful in patients with β-blocker cardiotoxicity

Hemodialysis is not effective in β-blocker overdose

111
Q

β-Blocker Cardiotoxicity Features

A

Bradycardia
* Hypotension
* Heart failure
* Syncope

112
Q

Furosemide moa

A

inhibiting chloride absorption in the ascending loop of Henle. The name of Lasix is derived from lasts six (hours) referring to its duration of action.

113
Q

Furosemide AE

A

Adverse effects
* Hyponatremia
* Hypokalemia
* Hypocalcaemia
* Hypochloraemic alkalosis (Hyper pH)
* Ototoxicity
* Renal impairment (from dehydration + direct toxic effect)
* Hyperglycaemia (less common than thiazides)
* Gout

114
Q

Bendroflumethiazide MOA

A

thiazide diuretic which works by inhibiting sodium absorption at the beginning of the distal convoluted tubule (DCT)

mechanism of Hypokalemia:
* ↑ sodium reaching the collecting ducts
* Activation of the renin-angiotensin-aldosterone

115
Q

Bendroflumethiazide Common adverse effects

A
  • Dehydration
  • Postural hypotension
  • Hyponatremia, Hypokalemia, Hypercalcemia
  • Gout
  • Impaired glucose tolerance, Hyperglycaemia
  • Impotence
116
Q

Spironolactone

A

aldosterone antagonist which acts act in the distal convoluted tubule

117
Q

Spironolactone Adverse effects

A
  • Hyperkalemia * Gynaecomastia
118
Q

Adenosine:

A

Adenosine
* Dipyridamole enhances effect
* Aminophylline ↓ effect

Causes transient heart block in the AV node
* Agonist of the A1 receptor which inhibits adenylyl cyclase thus reducing cAMP and causing
hyperpolarization by increasing outward potassium flux
* Adenosine has a very short half-life of about 8-10 seconds

119
Q

Adverse effects Adenosine:

A

Chest pain
* Bronchospasm
* Can enhance conduction down accessory pathways, resulting in ↑ ventricular rate (e.g. WPW)

120
Q

Calcium channel blockers SE

A

side-effects: headache, flushing, ankle edema

121
Q

Dihydropyridines (e.g. nifedipine, amlodipine)

A

Effects peripheral circulation i.e. Used for hypertension, raynaud’s
* May bring on angina due to sympathetic reflex following vasodilation
* Side-effects: headache, flushing, ankle edema

122
Q

Verapamil, Diltiazem

A
  • Contraindications: heart failure, heart block, on β-blockers
  • Side-effects: headache, constipation, heart block
123
Q

Aspirin MOA

A

works by blocking the action of both cyclooxygenase-1 and 2.
Hypotension, bradycardia, heart failure, ankle swelling
Ca Channel Blocker
Indications & Notes SE / CI

Verapamil
Angina, hypertension, arrhythmias Highly negatively inotropic
Should not be given with beta-blockers as may cause heart block
Heart constipation, hypotension, bradycardia
failure,
Diltiazem
Nifedipine, amlodipine, felodipine (dihydropyridines)
Hypertension, angina, Raynaud’s Flushing, headache, ankle swelling
Affects the peripheral vascular smooth muscle more than the myocardium and therefore do result in worsening of heart failure (but not amlodepine)
Cyclooxygenase is responsible for prostaglandin, prostacyclin and thromboxane synthesis. The blocking of thromboxane A2 formation in platelets reduces the ability of platelets to aggregate which has lead to the widespread use of low-dose aspirin in cardiovascular disease. All patients with established cardiovascular disease should take aspirin if there is no contraindication.

124
Q

ho should receive aspirin according to the current guidelines

A

All people with established cardiovascular disease (stroke, TIA, IHD, peripheral arterial disease)
* All people aged 50 years and over with a 10-year cardiovascular risk = 20%
* All people with diabetes mellitus (type 1 or 2) who are = 50 years old or who have: diabetes >
10 years, taking treatment for hypertension or evidence of target organ damage
* All people with target organ damage from hypertension

125
Q

Who should receive aspirin according to the current guidelines?

A

All people with established cardiovascular disease (stroke, TIA, IHD, peripheral arterial disease)
* All people aged 50 years and over with a 10-year cardiovascular risk = 20%
* All people with diabetes mellitus (type 1 or 2) who are = 50 years old or who have: diabetes >
10 years, taking treatment for hypertension or evidence of target organ damage
* All people with target organ damage from hypertension

126
Q

Angiotensin-converting enzyme (ACE) inhibitors Moa

A

Mechanism of action:
* Inhibit the conversion angiotensin I to angiotensin II

127
Q

ace SE

A

Side-effects:
* Cough: occurs in around 15% of patients and may occur up to a year after starting treatment. Thought to be due to increased bradykinin levels
* Angioedema: may occur up to a year after starting treatment
* Hyperkalaemia
st
* 1 -dose hypotension: more common in patients taking diuretics

128
Q

Cautions and contraindications ACEi

A

Pregnancy and breastfeeding - avoid
* Renovascular disease - significant renal impairment may occur in patients who have
undiagnosed bilateral renal artery stenosis
* Aortic stenosis - may result in hypotension
* Patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) -
signficantly increases the risk of hypotension
* Hereditary of idiopathic angioedema

129
Q

ACEi Monitoring

A

Urea and electrolytes should be checked before treatment is initiated and after increasing dose
* A rise in the creatinine and potassium may be expected after starting ACE inhibitors. Acceptable increases are an increase in serum creatinine, up to 50% from baseline or up to 265
μmol/l (whichever is smaller) and an increase in potassium up to 5.5 mmol/l.

130
Q

Acute Gout

A

Colchium alkaloids
*colchicine

NSAIDS
*indoethacine *Naproxen *Phenylbutazone *Ibuprofen

131
Q

Chronic Gout

A

Uricosuric
*probenecid
*sulfinpyazone

Xanthine Oxidase Inhibitor
*allopurinol

132
Q

Allopurinol

A

is used in the prevention of gout. It works by inhibiting xanthine oxidase which is responsible for the oxidation of 6-mercaptopurine to 6-thiouric acid

133
Q

Initiating allopurinol prophylaxis - see indications

A
  • Allopurinol should not be started until 2 weeks after an acute attack has settled
  • Initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of
    < 300 μmol/l
  • NSAID or colchicine cover should be used when starting allopurinol
134
Q

Indications for allopurinol

A

Recurrent attacks - the British Society for Rheumatology recommend ‘In uncomplicated gout
uric acid lowering drug therapy should be started if a second attack, or further attacks occur
within 1 year’
* Tophi
* Renal disease
* Uric acid renal stones
* Prophylaxis if on cytotoxics or diuretics
* Patients with Lesch-Nyhan syndrome often take allopurinol for life

135
Q

Interactions
Azathioprine

A
  • Metabolised to active compound 6-mercaptopurine
  • Xanthine oxidase is responsible for the oxidation of 6-mercaptopurine to 6-thiouric acid
  • Allopurinol can therefore lead to high levels of 6-mercaptopurine
  • A much ↓ dose (e.g. 25%) must therefore be used if the combination cannot be avoided
136
Q

Interactions
Cyclophosphamide

A

Allopurinol ↓ renal clearance, therefore may cause marrow toxicity

137
Q

Hormone Replacement Therapy (HRT) indications

A

Indications
* Vasomotor symptoms such as flushing, insomnia and headaches
* Premature menopause: should be continued until the age of 50 years
* Osteoporosis: but should only be used as second-line treatment

138
Q

Hormone Replacement Therapy (HRT) SE

A

Side-effects
* Nausea
* Breast tenderness
* Fluid retention and weight gain

139
Q

HRT SE

A

Side-effects
* Nausea
* Breast tenderness
* Fluid retention and weight gain

140
Q

HRT Potential complications HRT

A

↑ Risk of breast cancer: ↑ by the addition of a progestogen
* ↑ Risk of venous thromboembolism: ↑ by the addition of a progestogen
* ↓ Risk of endometrial cancer: ↓ by the addition of a progestogen but not eliminated completely.
The BNF states that the additional risk is eliminated if a progestogen is given continuously

141
Q

Combined OCP: HRT

A

↑ Risk of breast cancer
↑ Risk of DVT
↓ Risk of endometrial ca.

142
Q

Combined Oral Contraceptive Pill:Examples of UKMEC 3 conditions include

A

Examples of UKMEC 3 conditions include
* More than 35 years old and smoking less than 15 cigarettes/day
* BMI 35-39 kg/m2
* Migraine without aura and more than 35 years old
* Family history of thromboembolic disease in first degree relatives < 45 years
* Controlled hypertension
* Breast feeding 6 weeks - 6 months postpartum

143
Q

Combined Oral Contraceptive Pill:
Examples of UKMEC 4 conditions include

A
  • More than 35 years old and smoking more than 15 cigarettes/day
  • BMI > 40 kg/ m2
  • Migraine with aura
  • History of thromboembolic disease or thombogenic mutation
  • History of stroke or ischemic heart disease
  • Uncontrolled hypertension
  • Breast cancer
  • Major surgery with prolonged immobilisation
144
Q

Tamoxifen

A

is a selective estrogen receptor modulator (SERM) which acts as an estrogen receptor antagonist and partial agonist. It is used in the management of estrogen receptor positive breast cancer

145
Q

Tamoxifen AE

A

Adverse effects
* Hot flushes
* Menstrual disturbance: vaginal bleeding, amenorrhoea
* V enous thromboembolism
* Endometrial cancer
* Alopecia
* Cataracts

146
Q

Raloxifene

A

is a pure estrogen receptor antagonist, and carries a lower risk of endometrial cancer

147
Q

Warfarin

A

is an oral anticoagulant which inhibits the reduction of vitamin K to its active hydroquinone form, which in turn acts as a cofactor in the formation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C

148
Q

Dentistry in warfarinised patients

A

chheck INR 72 hours before procedure, proceed if INR < 4.0

149
Q

Factors that may potentiate warfarin

A
  • Liver disease
  • P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
  • Cranberry juice
  • Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
  • Inhibit platelet function: NSAIDs
150
Q

Side-effects warfarin

A

Hemorrhage
* Teratogenic
* Skin necrosis: when warfarin is first started biosynthesis of protein C is ↓. This results in a
temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis

151
Q

Warfarin overdose: Major bleeding

A

Stop warfarin
Vitamin K 5mg IV
Prothrombin complex concentrate - if not available then FFP*

152
Q

Warfarin overdose:INR > 8.0
No bleeding or minor bleeding

A

Stop warfarin, restart when INR < 5.0
If risk factors for bleeding then give vitamin K 0.5mg IV or 5mg PO. Risk factors include:
* Age > 70 years
* First year of warfarin therapy
* History of gastrointestinal bleeding
* Hypertension
* Alcohol excess
Dose can be repeated after 24 hours if INR still high

153
Q

INR 6.0 - 8.0
No bleeding or minor bleeding

A

Stop warfarin, restart when INR < 5.0

154
Q

Acyclovir

A

Acyclovir is phosphorylated by thymidine kinase which in turn inhibits the viral DNA polymerase

155
Q

Ribavirin

A
  • Effective against a range of DNA and RNA viruses
  • Interferes with the capping of viral mRNA
156
Q

Interferons

A

Inhibit synthesis of mRNA, translation of viral proteins, viral assembly and release

157
Q

Amantadine

A
  • Used to treat influenza
  • Inhibits uncoating of virus in cell
158
Q

Nucleoside Analogue Reverse Transcriptase Inhibitors (NRTI)

A

Examples: zidovudine (AZT), didanosine, lamivudine, stavudine, zalcitabine

159
Q

Protease inhibitors (PI)

A

Inhibits a protease needed to make virus able to survive outside the cell * Examples: indinavir, nelfinavir, ritonavir, saquinavir

160
Q

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI)

A

(NNRTI)
examples: nevirapine, efavirenz

161
Q

HIV: anti-retrovirals - P450 interaction

A
  • nevirapine (NNRTI): induces P450
  • protease inhibitors: inhibits P450
162
Q

General NRTI side-effects:

A

peripheral neuropathy
* Zidovudine: anemia, myopathy, black nails
* Didanosine: pancreatitis

163
Q

Protease inhibitors (PI) SE

A

Examples: indinavir, nelfinavir, ritonavir, saquinavir
* Side-effects: diabetes, hyperlipidemia, buffalo hump, central obesity, p450 enzyme inhibition
* Indinavir: renal stones, asymptomatic hyperbilirubinemia
* Ritonavir: a potent inhibitor of the p450 system
HIV: anti-retrovirals - P450 interaction
* nevirapine (NNRTI): induces P450
* protease inhibitors: inhibits P450

164
Q

Cyclosporin moa

A

immunosuppressant which ↓ clonal proliferation of T cells by reducing IL-2 release. It acts by binding to cyclophilin forming a complex which inhibits calcineurin, a phosphotase that activates various transcription factors in T cells

165
Q

Cyclosporin + tacrolimus

A

inhibit calcineurin thus decreasing IL-2

166
Q

Adverse effects of Cyclosporin

A
  • Nephrotoxicity
  • Hepatotoxicity
  • Fluid retention
  • Tremor
  • Hypertension
  • Hyperkalemia
  • Hypertrichosis
  • Hyperplasia of gum
  • Impaired glucose tolerance, hyperglycemia.
167
Q

Tacrolimus

A

Tacrolimus is a macrolide antibiotic and is used as an immunosuppressant to prevent transplant rejection. It has a very similar action to Cyclosporin; the action of tacrolimus differs in that it binds to a protein called FKBP rather than cyclophilin
Tacrolimus is more potent than Cyclosporin and hence the incidence of organ rejection is less. However, nephrotoxicity and impaired glucose tolerance is more common

168
Q

Azathioprine

A

metabolised to the active compound mercaptopurine, purine synthesis inhibitor, inhibiting the proliferation of cells, especially leukocytes/lymphocytes.

autoimmune diseases, or in combination with other immunosuppressants in organ transplantation. Caution should be exercised when it is used in conjunction with purine analogues such as allopurinol, you may give only 25% of the usual dose of azathioprine. Thiopurine methyltransferase (TPMT) deficiency is present in about 1 in 200 people and predisposes to azathioprine related pancytopaenia. A thiopurine methyltransferase (TPMT) test may be needed to look for individuals prone to azathioprine toxicity

169
Q

Azathioprine SE

A
  • Bone marrow depression
  • Nausea/vomiting
  • Pancreatitis
170
Q

Methotrexate

A

antimetabolite which inhibits dihydrofolate reductase, an enzyme essential for the synthesis of purines and pyrimidines

171
Q

Methotrexate - Adverse effects

A

Adverse effects
* Mucositis
* Myelosuppression * Pneumonitis
* Liver cirrhosis

172
Q

Prescribing methotrexate

A
  • Methotrexate is a drug with a high potential for patient harm. It is therefore important that you are familiar with guidelines relating to its use
  • Methotrexate is taken weekly, rather than daily
  • FBC, U&E and LFTs need to be regularly monitored. The Committee on Safety of Medicines
    recommend ‘FBC and renal and LFTs before starting treatment and repeated weekly until
    therapy stabilised, thereafter patients should be monitored every 2-3 months’
  • Folic acid 5mg once weekly should be coprescribed, taken more than 24 hours after
    methotrexate dose
  • The starting dose of methotrexate is 7.5 mg weekly
  • Only one strength of methotrexate tablet should be prescribed (usually 2.5 mg)
  • Avoid prescribing trimethoprim or cotrimoxazole concurrently - increases risk of marrow
    aplasia
173
Q

Mycophenolate mofetil

A

nhibits inosine monophosphate dehydrogenase

174
Q

Methotrexate

A

antimetabolite which inhibits dihydrofolate reductase

175
Q

Rituximab: se

A

Side effects:
* Flu-like illness
* ↓BP during fever
* Tumor side pain

176
Q

Finasteride

A

an inhibitor of 5-α-reductase, an enzyme which metabolises testosterone into dihydrotestosterone. Its indications are:
* Benign prostatic hyperplasia
* ♂-pattern baldness

177
Q

Finasteride se

A

Adverse effects:
* Impotence
* ↓ libid
* Ejaculation disorders
* Gynaecomastia and breast tenderness
Finasteride causes ↓ levels of serum prostate specific antigen

178
Q

Bisphosphonates

A

analogues of pyrophosphate, a molecule which ↓ demineralisation in bone.
They inhibit osteoclasts by reducing recruitment and promoting apoptosis

179
Q

Bisphosphonates SE

A

Adverse effects
* Esophageal reactions: oesophagitis, esophageal ulcers (especially alendronate)
* Osteonecrosis of the jaw
* MHRA has warned about an increased risk of atypical stress fractures of the proximal femoral
shaft in patients taking alendronate

180
Q

Sildenafil

A

a phosphodiesterase type V inhibitor used in the treatment of impotence

181
Q

Viagra - contraindicated by

A

nitrates and nicorandil

Nicorandil has a nitrate component as well as being a potassium channel activator The BNF recommends avoiding α-blockers for 4 hours after sildenafil

182
Q

Sildenafil CI

A

Contraindications
* Patients taking nitrates and related drugs such as nicorandil
* Hypotension
* Recent stroke or myocardial infarction
* Non-arteritic anterior ischemic optic neuropathy

183
Q

Adverse effects Sildenafil

A
  • Visual disturbances e.g. Blue discoloration, non-arteritic anterior ischemic neuropathy
  • Nasal congestion
  • Flushing
  • Gastrointestinal side-effects
184
Q

Octreotide:

A

Overview
* Long-acting analogue of somatostatin
* Somatostatin is release from D cells of pancreas and inhibits the release of growth hormone
Uses
* Acute treatment of variceal hemorrhage
* Acromegaly
* Carcinoid syndrome
* Prevent complications following pancreatic surgery
* VIPomas

185
Q

Octreotide:

A

Adverse effects
* Gallstones (secondary to biliary stasis)

186
Q

Theophylline,

A

The main use of
theophyllines in clinical medicine is as a bronchodilator in the management of asthma and COPD
The exact mechanism of action has yet to be discovered. One theory suggests theophyllines may be a non-specific inhibitor of phosphodiesterase resulting in ↑ cAMP. Other proposed mechanisms include antagonism of adenosine and prostaglandin inhibition

187
Q

Theophylline poisoning features:

A

Acidosis, Hypokalemia
* V omiting
* Tachycardia, arrhythmias
* Seizures

188
Q

Theophylline poisoning Management

A

Activated charcoal
* Charcoal hemoperfusion is preferable to hemodialysis

189
Q

Alcohol Withdrawal Mechanism

A
  • Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
  • Alcohol withdrawal is thought to lead to the opposite (↓ inhibitory GABA and ↑ NMDA glutamate transmission)
190
Q

Alcohol Withdrawal features

A

Features
* Symptoms start at 6-12 hours
* Peak incidence of seizures at 36 hours
* Peak incidence of delirium tremens is at 72 hours
Management
* Benzodiazepines
* Carbamazepine also effective in treatment of alcohol withdrawal
* Phenytoin is said not to be as effective in the treatment of alcohol withdrawal seizures

191
Q

Proton Pump Inhibitors (PPI)

A

group of drugs which profoundly ↓ acid secretion in
the stomach. They irreversibly block the hydrogen/potassium adenosine triphosphatase enzyme system
(the H+/K+ ATPase) of the gastric parietal cell. Examples include omeprazole and lansoprazole.

192
Q

Aminosalicylates:

A

5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis

193
Q

Sulphasalazine

A

A combination of sulphapyridine (a sulphonamide) and 5-ASA
* Many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz
body anemia
* Other side-effects are common to 5-ASA drugs (see mesalazine)

194
Q

Mesalazine

A
  • A delayed release form of 5-ASA
  • Sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
  • Mesalazine is still however associated with side-effects such as GI upset, diarrhea, headache,
    agranulocytosis, pancreatitis*, interstitial nephritis
195
Q

Immunoglobulins: Therapeutics
The Department of Health issued guidelines on the use of intravenous immunoglobulins in May 2008
Uses

A
  • Primary and secondary immunodeficiency
  • Idiopathic thrombocytopenic purpura (ITP)
  • Myasthenia gravis
  • Guillain-Barre syndrome
  • Kawasaki disease
  • Toxic epidermal necrolysis (TEN)
  • Pneumonitis induced by CMV following transplantation
  • Low serum IgG levels following hematopoietic stem cell transplant for malignancy
  • Dermatomyositis
  • Chronic inflammatory demyelinating polyradiculopathy
196
Q

Inhibit cell wall formation

A

*Penicillins
* Cephalosporins * Isoniazid
* V ancomycin

197
Q

Inhibit protein synthesis

A

*aminoglycosides (cause misreading of mRNA)
* chloramphenicol *macrolides (e.g.
erythromycin)
* tetracyclines *fusidic acid
* (Quin/Dalfo)pristin * Linezolid

198
Q

Inhibit DNA synthesis

A

*quinolones (e.g. ciprofloxacin)
* metronidazole
* sulphonamides * trimethoprim

199
Q

inhibit RNA synthesis

A

rifampicin

200
Q

Bactericidal antibiotics

A
  • Penicillins
  • Cephalosporins
  • Isoniazid
  • Aminoglycosides
  • Quinupristin+Dalfopristin (combination)
  • Metronidazole
  • Quinolones: ciprofloxacin, levofluxacin
  • Rifampicin
  • Nitrofurantoin → Damages bacterial DNA
201
Q

Bacteriostatic antibiotics

A
  • Chloramphenicol
  • Macrolides
  • Tetracyclines
  • Fusidic acid
  • Quinupristin
  • Dalfopristin
  • Linezolid
  • Sulphonamides
  • Trimethoprim
202
Q

Erythromycin

A

1st macrolide used clinically. Newer examples include clarithromycin and azithromycin. Erythromycin may potentially interact with amiodarone, warfarin and simvastatin
Macrolides act by inhibiting bacterial protein synthesis. If pushed to give an answer they are bacteriostatic in nature, but in reality this depends on the dose and type of organism being treated.

203
Q

Erythromycin is used in gastroparesis as i

A

it has prokinetic properties, Promotes gastric emptying

204
Q

Adverse effects of erythromycin

A
  • GI side-effects are common
  • Cholestatic jaundice: risk may be ↓ if erythromycin stearate is used
  • P450 inhibitor
205
Q

Quinolone’s

A

group of antibiotics which work by inhibiting DNA synthesis and are bactericidal in nature. Examples include:
* Ciprofloxacin * Levofloxacin

206
Q

Adverse effects Quinolone’s

A
  • Lower seizure threshold in patients with epilepsy
  • Tendon damage (including rupture) - the risk is ↑ in patients also taking steroids. Achilles
    tendon ruptures. Tendon damage is a well documented complication of quinolone therapy. It appears to be an idiosyncratic reaction, with the actual median duration of treatment being 8 days before problems occur
207
Q

Quinupristin & Dalfopristin Antibiotics

A

Overview
* Injectable streptogrammin antibiotic
* Combination of group A and group B streptogrammin
* Inhibits bacterial protein synthesis by blocking tRNA complexes binding to the ribosome
Spectrum
* Most Gram positive bacteria
* Exception: Enterococcus faecalis

208
Q

Quinupristin & Dalfopristin Antibiotics AE

A

Adverse effects
* Thrombophlebitis (give via a central line)
* Arthralgia
* P450 inhibitor

209
Q

Linezolid

A

type of oxazolidonone antibiotic which has been introduced in recent years. It inhibits bacterial protein synthesis by stopping formation of the 70s initiation complex and is bacteriostatic nature

210
Q

Linezolid adverse effects

A

Adverse effects
* Thrombocytopenia (reversible on stopping)
* Monoamine oxidase inhibitor: avoid tyramine containing foods

211
Q

Sulfonamides

A

Antibacterial sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthetase (DHPS), an enzyme involved in folate synthesis.

212
Q

Co-trimoxazole:

A

: sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections.

213
Q

Diethylcarbamazine:

A

MRCP I (21 decks)

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