Pharmacology Flashcards
Key side effects of methotrexate
Bone marrow suppression
and leukopenia and highly teratogenic
Gastro-intestinal disturbance
Folate deficiency - anaemia
Long term- Pulmonary fibrosis, Liver/renal/GI toxicity, Interstitial pneumonitis
Stomatitis – discontinue (sign of severe marrow depression)
Key side effects of Leflunomide
Hypertension and peripheral neuropathy
Key side effect of Sulfasalazine
Male infertility (reduces sperm count),Myelosuppression
Nausea
Rash
Oral ulcers
Key side effects of Hydroxychloroquine
Nightmares and reduced visual acuity and rash
Key side effects of biologics/ Anti-TNF medications
immunosuppression, Reactivation of TB or hepatitis B,Allergic reaction, reaction at infusion site
Key side effects of Rituximab (Anti-CD20 )
Night sweats and thrombocytopenia
Key side effects of steroids
Cushing Syndrome, Avascular necrosis, Addisons,Osteoporosis
Retardation of growth
Thin skin, easy bruising
Immunosuppression
Cataracts and glaucoma
Oedema
Suppression of HPA axis
Teratogenic
Emotional disturbance (including psychosis
Rise in BP
Obesity (truncal)
Increased hair growth (hirsutism)
Diabetes mellitus
Striae
neuronic to remember steroid effects
STEROIDS: Stomach ulcers, Thin skin, oEdema, Right and left heart failure, Osteoporosis, Infection (including Candida), Diabetes (commonly causes hyperglycaemia and uncommonly progresses to diabetes), and Cushing’s Syndrome.
Key side effects of cyclosporin
Gingival hypertrophy, hypertrichosis, nephrotoxicity
Key side effects of Tacrolimus
cardiomyopathy, peripheral neuropathy, diabetes
Key side effect of Anthracyclines (doxorubicin, daunorubicin)
cardiomyopathy
(MOA :prevention of the DNA double helix from being resealed)
Key side effects of Platinum agents (cisplatin, carboplatin)
peripheral neuropathy and sensorineural hearing loss, nephrotoxicity
(MOA: DNA-binding alkylating agents)
key side effects of Cyclophosphamides
haemmorhagic cystitis and transitional cell carcinoma of the bladder.
(MOA: alkylating agent)
Key side effect of tamoxifen
increases the risk of endometrial cancer and VTE
vaginal dryness, hot flushes ,weight gain, fatigue .
agranulocytosis and liver failure- rare
Key side effect of bleomycin
lung fibrosis
Key side effects of bisphosphonates
esophageal ulcer
atrial fibrillation, osteonecrosis of the jaw, atypical femoral stress fractures
Avoid in CKD because renally excreted
medications that can worsen MG
Beta-blockers, several antibiotics and antimalarials, Lithium and other drugs used in psychiatric disorders
Riluzole is used in the treatment for
Motor neuron disease
(antiglutamatergic drug which dampens motor nerve firing)
Drugs causing ototoxicity
Caused by aminoglycoside antibiotics (eg. gentamicin, vancomycin) and loop diuretics (eg. furosemide), most commonly.
treatment for Parkinson disease where there isn’t significant motor symptoms
MAO-B monoamine a oxidase inhibitors ,Monoamine Oxidase Type B (MAO-B) is an enzyme in our body that breaks down several chemicals in the brain, including dopamine. By giving a medication that blocks the effect of MAO-B, an MAO-B inhibitor), more dopamine is available to be used by the brain.
(Selegiline/Rosagiline)
COMT inhibitors MOA
Prolong effects of Levodopa by preventing it from breaking down, so given as adjuvant therapy
eg tolcapone and entacapone
physiological effects of Dopamine
Cognition
prevents lactation
emetic function (causes nausea)- example of an antagonist is Metoclopramide
inhibits gastric stimulation (anti-kinetic effect) – example of an antagonist is Domperidone
cardiac stimulation effects and peripheral vasoconstriction- dopamine is converted to norepinephrine/noradrenaline
CI/side effects of co-careldopa/co-beneldopa
CI: breast feeding and severe psychiatric illness
cautioned in endocrine disorders as well as severe pulmonary or cardiovascular diseases.
side effects: nausea, vomiting and anorexia. Disturbances in sleep,dizziness, syncope and arhythmias.
Important side effects:
Involuntary movements, or dyskinesia,
postural hypotension and psychological effects which includes dementia, depression and schizophrenia-like syndrome with delusions and hallucinations
Levodopa interactions with other medications
risk of a hypertensive crisis when used with MAOI.
Risk of arrythmias with a general anaesthetic
with antihypertensives there is the increased risk of hypotension.
Why should you never stop Parkinson’s drug treatment abruptly?
Neuroleptic Malignant Syndrome
=sudden Depletion of dopamine in the hypothalamus/nigrostriatal pathway
Signs and symptoms: intense rigidity, causes fever, altered GCS- confusion
drug monitoring for sodium valproate
Monitor LFTs before and during first 6 months
Measure FBC before surgery to assess bleeding risk
Cautions for lamotrigine
Can exacerbate myoclonic seizures and Parkinson’s disease
Renal failure and hepatic failure (reduced dose) renally excreted
Alteplase Absolute contraindications for ischaemic stroke
Intracranial haemorrhage, neurosurgery/head trauma/stroke in past 3 months, uncontrolled hypertension, previous intracranial haemorrhage, known AV malformation/neoplasm/aneurysm, active internal bleeding, suspected endocarditis, bleeding diathesis, abnormal blood glucose
Alteplase Relative contraindications for ischaemic stroke
Minor/rapidly improving symptoms, seizure at stroke onset, severe stroke, major surgery or serious trauma in previous 2 weeks, previous GI/urinary tract haemorrhage in previous 3 weeks, recent lumbar puncture or arterial puncture at non-compressible site, post MI pericarditis which can turn hemorrhagic , pregnancy
Caution use of Atorvastatin in
Elderly patients
High alcohol intake or liver disease
Hypothyroidism (increases the risk of myositis with statins)
Patients at risk of muscle toxicity
Haemorrhagic stroke
Fibrates with statin increases rhabdomyolysis risk
Side effects Atorvastatin
GI disturbance
CNS effects – dizziness, headache, blurred vision
Colchicine (increased risk of rhabdomyolysis)
Hepatic effects
Muscle effects
Skin reactions
Hyperglycaemia
Weight change
Epistaxis
benzylpenicillin mainly effective against
aerobic gram-positive bacteria, with some activity against gram-negative cocci eg meningococcus and anaerobic organisms (no activity against gram-negative bacilli.)
Cephalosporins MOA
inhibit cell wall synthesis in a similar manner to penicillins but they are more resistant to hydrolysis by beta-lactamases.
succeeding generations having enhanced activity against gram-negative bacilli at the expense of gram-positive activity and increased ability to cross the blood-brain barrier
Adverse effects Cephalosporins
•Hypersensitivity
•GI disturbance
•Skin reactions
Cholestatic jaundice (clarythomycin and coamoxiclav can cause this too)
• interstitial nephritis
•Blood disorders
•Antibiotic associated colitis
chloramphenicol MOA
Inhibits protein synthesis in bacteria by binding reversibly to the 50S subunit of bacterial ribosomes.
Chloramphenicol adverse effects
Used ONLY in life-threatening conditions, because of its toxicity. Biggest unwanted effect is bone marrow toxicity (aplastic anaemia, reversible anaemia).
Can cause “grey baby” syndrome
Aciclovir MOA
inhibits synthesis of viral DNA. targets viral DNA polymerase terminating viral DNA synthesis and thus replication.
Most active against HSV.
NSAID Side effects
GI disturbance- due to inhibition of mucosal production of COX-1 generated prostaglandins.
Renal insufficiency
Salt/water retention
Hyponatraemia/hyperkalaemia
Cardiovascular effects
Hypersensitivity reactions
Headaches/dizziness
Skin reactions
COX 1 and COX 2 difference
COX 1 has a constitutive ‘housekeeping’ role, contributing to the regulation of homeostatic processes, such as renal and gastric blood flow, gastric cytoprotection and platelet aggregation.
COX 2 is expressed only after stimulation by an inflammatory process. The production of these prostaglandins contribute to the inflammatory/painful process, through vasodilation, increasing vascular permeability and sensitisation of nerve fibres to inflammatory mediators.
NSAIDS Contra-indications
GI bleeding/ulceration
Hypersensitivity reactions
Severe heart failure ( they cause water retention so NSAID would worsen this)
Severe renal impairment
Varicella zoster infection
Avoid 3rd trimester of pregnancy (inbhibits closure of ductus arteriosus)
NSAID cautions and contraindications neumonic
NSAID: No urine (i.e. renal failure), Systolic dysfunction (i.e. heart failure), Asthma, Indigestion (any cause), and Dyscrasia (clotting abnormality)
How does Allopurinol reduce the concentration of uric acid?
Xanthine oxidase inhibitor, reducing uric acid formation.
Cautioned use of infliximab in
•Malignancy
•Hepatitis B
•Pregnancy
•Tuberculosis
Interactions of methotrexate with other dugs
Trimethoprim/Co-trimoxazole (which is also a folic acid antagonist, severe bone marrow depression)
NSAIDs (toxicity)
Epidural anaesthesia
Injection or slow infusion via a cannula of an aqueous solution adjacent to the spinal column, but outside the dura mater, produces anaesthesia both above and below the site of injection after 15–30 min
Often used in combination with an opiate
Can be topped up , needs larger doses as it needs to diffuse into spinal cord
Spinal anaesthesia
Involves injection of an aqueous solution (1.5–2.5 mL) of local anaesthetic alone (often bupivacaine) or with an opioid into the lumbar subarachnoid space, usually between the third and fourth lumbar vertebrae
Quicker onset of action, lower dose needed
Unwanted effects local anaesthesia:
Local:irritation and inflammation, ischaemia from the use of vasoconstrictor agents
Systemic
Cardiovascular: myocardial depression, vasodilatation, hypotension, arrhythmias
CNS: agitation, confusion, tremors, convulsions, respiratory depression
Minimum Alveolar Concentration (MAC)
Minimum alveolar concentration at which 50% of the population will fail to respond to a single noxious stimuli
Measure of POTENCY,The lower the MAC the more potent the agent
Thiopental
(rarely used now)
Enhances activity at GABA A receptors
•Thiopental diffuses readily into the CNS due to its lipid solubility and predominantly un-ionised state
•Metabolism of thiopental occurs predominantly in the liver and up to 30% of the original dose may remain in the body at 24 h causing a ‘hangover’ effect
•zero-order kinetics- saturation related
Propofol
•
Enhances activity at GABA A receptors
Does not accumulate
replaced thiopental as an induction agent
•More rapid recovery and less hangover effect than occurs with thiopental
•Metabolism is by first order kinetics
Etomidate
•enhances activity at GABA A receptors
rapid onset of action after intravenous injection
•Its action is terminated by rapid metabolism in plasma and the liver by esterases
•Duration of action is about 6–10 min with minimal hangover
•Less effect on CVS so may be preferred in shocked patients
•Not used as a continuous infusion due to toxicity on adrenals and adrenocortical suppression
Ketamine
•Believed to act by blocking activation of the glutamate NMDA receptor, inhibit ACh nicotinic receptors, open 2 pore K channels
•‘dissociative anaesthesia’, in which there is a marked sensory loss and analgesia, as well as amnesia, without complete loss of consciousness
Depolarising Neuromuscular blocking drugs
Suxamethonium
Non-depolarising Neuromuscular blockers
•Atracurium
•Cisatracurium
•Mivacurium
•Pancuronium
•Rocuronium
•Vecuronium
Non-depolarising agents
MOA
Nerve impulse results in release of ach and drug
Drug binds to ach receptor but does not cause depolarisation
Calcium is not released from storage sarcoplasmic reticulum
Contraction does not occur, muscle therefore relaxes
Suxamethonium MOA
Nerve impulse results in release of ACh and drug
Drug binds to ach receptor causing depolarization
Drug stays on receptor causing repeated contractions
Calcium returns to storage and muscle isunreposnive to further contraction
A very prolonged paralysis occurs in about 1 in 2000–3000 individuals, who have a genetic deficiency of pseudocholinesterase
Neostigmine
the effect of a non-depolarising blocker can be reversed by intravenous injection of neostigmine, an anticholinesterase
An anti-muscarinic such as atropine or glycopyrrolate is given immediately before the neostigmine to prevent bradycardia or excessive salivation produced by stimulation of muscarinic receptors
Amiodarone
Class III anti-arrhythmic
•Prolongs cardiac action potential and delays refractory period
•Inhibits K+ channels involved in repolarisation
•Used to prevent myocardium going back into VF or VT
Side effects with amiodarone
Gastrointestinal disturbances
Corneal microdeposits
Hypothyroidism
Hyperthyroidism- high iodine content
Skin reactions – photosensitive skin rashes and blue-grey discolouration
Hepatotoxicity
Progressive pneumonitis and lung fibrosis
Proarrhythmic effects
Peripheral neuropathy/myopathy
Too much of it can cause bradycardia and heart blocks
Adenosine
has potent effects on the SA node inducing sinus bradycardia and slows impulse conduction through the AV node, with no effect on conduction in the ventricles. Therefore, it is useful in the emergency management of supraventricular tachycardia (SVT) for rapid conversion back to sinus rhythm
Adenosine Contra-indications
•Asthma/COPD (can trigger acute bronchospasm)
•Decompensated heart failure
•Long QT syndrome/AV block/sick sinus syndrome
•Severe hypotension
•Many cautions associated with cardiac disease
Adenosine side effects
Side effects are common but last less than 1 minute.
Arrhythmias, chest discomfort/pain, dizziness, dyspnoea, flushing, headache, hypotension, apprehension/impending doom, sweating, metallic taste, blurred vision, nausea/vomiting, cardiac arrest, apnoea, loss of consciousness
Atropine MOA
Muscarinic antagonist.
Blockade of muscarinic receptors reduces the inhibitory effect of the vagus nerve on the heart, increasing the rate of firing of the SA node and increasing conduction through the AV node.
Atropine side effects
Eyes (pupillary dilatation): blurred vision, mydriasis, angle closure glaucoma
GI tract (decreased motility/secretions/tone): constipation, abdominal distension, nausea, vomiting, dysphagia
CVS (increased HR, contractility, BP): tachycardia, palpitations, angina, hypertension, arrhythmias
Secretions (decreased sweat/salivary gland secretion): dry mouth, anhidrosis, thirst, increased body temperature
Urinary tract (decreased detrusor function and increased sphincter tone): urinary retention,
CNS: confusion, hallucination
Atropine contraindications
•GI: obstruction, paralytic ileus, pyloric stenosis, severe ulcerative colitis, toxic megacolon
•Urinary tract: bladder outflow obstruction, prostatic enlargement, retention
•Myasthenia gravis
Mirabegron
B3 adrenergic agonist, relaxes detrusor muscle, does not have anticholinergic effects, more expensive
Why is Aspirin not prescribed for children?:
Reyes syndrome
•Rare
•Usually occurs in children between 5 and 14 years of age
•Acute encephalopathy and fatty degeneration of the liver
•Usually follows viral illness, with rapid deterioration
•Overall mortality rate ~ 20%
Choice of Analgesia in Children ladder
- paracetamol
- paracetamol + NSAID eg ibuprofen
- Pareceamol NSAID +opiod (eg morphine)
Codeine use in children
restricted due to reports of morphine toxicity.
Codeine should only be used to relieve acute moderate pain in children >12 years and only if it cannot be relieved by other analgesic agents.
life-threatening adverse reactions have been identified in children with obstructive sleep apnoea who received codeine after tonsillectomy or adenoidectomy
Codeine not recommended for children with conditions that may compromise breathing (neuromuscular, cardiorespiratory, etc).
Gastric pH in children
Neutral at birth due to residual amniotic fluid. Continues to be neutral during neonatal period due to decreased gastric acid production. Adult values achieve around 2-3 years. This high pH means increased absorption of weak base drugs such as penicillins, resulting in lower doses needed whereas higher doses of acidic drugs will be required. Premature neonates have higher gastric pH due to immature gastric mucosa with reduced secretion of gastric acid.
Bile acid secretion neonates
decreased due to immaturity
Reducing fat absorption and therefore absorption of fat-soluble drugs such as diazepam.
Paracetamol metabolism in neonates
the predominant pathway is via sulphation.
In neonates CYP450 is immature so paracetamol is not metabolised via this route, resulting in less toxic metabolites and lower risk in overdose.
Vancomycin adverse effects
Nephrotoxicity
ototoxicity
Thrombophlebitis
Neutropenia
Thrombocytopenia
red man syndrome; occurs on rapid infusion of vancomycin
Moa:prevents bacteria making cell walls
Aminoglycoside MOA
Inhibit bacterial protein synthesis by binding to the 30S subunit of the ribosome irreversibly.
eg Gentamicin
Macrolides MOA
Inhibit bacterial protein synthesis by binding to the 50S subunit of the ribosome, preventing ribosomal translocation and therefore protein elongation eg Clarithromycin, Erythromycin, Azithromycin
Quinolones MOA
Inhibit bacterial DNA duplication through inhibition of topoisomerases, which interfere with DNA unwinding and therefore transcription and translation. eg Ciprofloxacin,
used mainly for Gram-negative infections
Quinolones side effects
GI upset
Prolonged QT interval
High risk of C. difficile
tendon damage (especially in patients > 60 and those with renal impairment or taking steroids)
Aortic aneurysm / dissection
Quinolones should also be used with caution in patients with epilepsy as they may lower the seizure threshold
Metronidazole MOA
inhibits bacterial DNA synthesis.specific antibiotic for anaerobic infections eg c difficile
Metronidazole Cautions/Contraindications
Alcohol must not be drunk while on metronidazole and for ~48 hours after the end of the course. Metronidazole interferes with alcohol metabolism leading to acetaldeyhyde accumulation and gives severe side effects as a result.
Use with caution in severe liver disease
Trimethoprim MOA
Inhibits bacterial folate synthesis through inhibition of dihydrofolate reductase.
Trimethoprim side effects
Commonly causes a skin rash
GI upset
Hypersensitivity is common and can be severe
Hyperkalaemia
Penicillin common side effects
GI upset, including antibiotic-associated C. difficile infection.
A degree of allergy to penicillin is very common, affecting up to 10% of the population.
Neurological toxicity (including convulsions and coma) can occur with very high-dose therapy or accumulation due to severe renal impairment.
Potential risks of SSRIs in pregnancy:
First-trimester use has a link with congenital heart defects
First-trimester use of paroxetine has a stronger link with congenital malformations
Third-trimester use has a link with persistent pulmonary hypertension in the neonate
Neonates can experience withdrawal symptoms, usually only mild
Metoclopramide
- a D2 receptor antagonist mainly used in the management of nausea.
- gastro-oesophageal reflux disease
- prokinetic action is useful in gastroparesis secondary to diabetic neuropathy
- often combined with analgesics for the treatment of migraine
Enzyme inducers: PC BRAS
Phenytoin
Carbamazepine
Barbiturates
Rifampicin
alcohol (chronic excess)
sulphonylureas.
Others: topiramate, St John’s Wort, and smoking.
Eg if someone takes st johns wort and warfarin, St John’s Wort is a P450 inducer so will reduce the concentration of warfarin, meaning the INR will decrease, increase warfarin metabolism and risk of clots.
Enzyme inhibitors: AO DEVICES
Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
ethanol (acute intoxication)
sulphonamides.
Others: grapefruit juice, amiodarone, and SSRIs (fluoxetine, sertraline).
eg these decrease warfarin metabolism and increase bleeding risk
Etodimate, propofol and thiopental MOA
enhance activity at GABA A receptors
what is zero order kinetics
constant amount (e.g. in grams / milligrams / micrograms) of drug is eliminated per unit of time (e.g. seconds / minutes). The metabolism is independent of the concentration of the reactant.
examples of zero kinetic drugs
Constantly aspiring to phone ethan
Constant ( zero order kinetics)
Aspirin (e.g. high-dose aspirin)
Phenytoin
Ethanol
Others: heparin, fluoxetine,omeprazole
Half life
Half life is the time taken to metabolise 50% of the drug
what is First order kinetics
drug elimination is proportional to the plasma concentration of drug
This means that the higher the drug concentration, the higher its elimination rate.the HALF-LIFE is constant
examples of first order kinetics
majority of drugs exhibiting ‘first-order’ elimination kinetics eg amitriptyline, ampicillin, apixaban, atenolol
Clinical features of lithium toxicity
coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
Polyuria
Visual disturbance
CNS disturbance including seizures, impaired co-ordination, dysarthria
arrythmias
coma
Rasburicase
Intravenous prophylaxis against gout during cancer chemotherapy
haemophilia A
deficiency in clotting factor VIII
HIV entry inhibitors
prevent HIV-1 from entering and infecting immune cells
maraviroc (binds to CCR5, preventing an interaction with gp41)
enfuvirtide (binds to gp41, also known as a ‘fusion inhibitor’)
factor IX
haemophilia B, also called christmas disease
Nucleoside analogue reverse transcriptase inhibitors (NRTI)
Acting as a chain-terminator to stop reverse transcription. examples: zidovudine (AZT), abacavir, emtricitabine
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Block the action of reverse transcriptase.transcriptase enzyme.examples: nevirapine, efavirenz
Protease inhibitors (PI)
These drugs inhibit HIV protease,
examples: indinavir, nelfinavir, ritonavir, saquinavir
Integrase inhibitors
block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell
examples: raltegravir, elvitegravir, dolutegravir
Drugs causing hyperkalaemia
Aldosterone inhibitors ( aldosterone normally promotes K secretion)
heparin (inhibits aldosterone secretion)
ACEi and ARB ( decrease aldosterone)
Potassium sparing diuretics ( drugs that cause diuresis without causing K loss)
Trimethoprim
Monitoring for statins
LFTs are checked before a statin is initiated, again within 3 months of initiation, and then 12 months after it was first prescribed.
QRISK 2 calculator for patients up to and including 84 years of age.
Non hdl/ Ldl should improve by 40 %, reduction
Statin MOA
inhibit 3-hydroxy-3-methylglutaryl co-enzyme A (HMG CoA) reductase, an enzyme involved in cholesterol synthesis. Inhibition of HMG CoA reductase reduces low density lipoprotein cholesterol (LDL-C) levels by slowing down the production of cholesterol in the liver and increasing the liver’s ability to remove the LDL-C already in the blood
Desferrioxamine
indicated in:
Patients with serum iron level > 90umol/l or 60-90umol/l, who are symptomatic or have persistent iron on abdominal x-ray despite whole bowel irrigation or any patient with shock, coma or metabolic acidosis
CI statins
Do not prescribe atorvastatin to:
People with active liver disease, or unexplained persistent elevations of transaminases that are three or more times the upper limit of normal.
Women who are pregnant or breastfeeding.
Women of child-bearing potential not using appropriate contraception.
Key side effect of topiramate
weight loss
TB treatment
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
Causes of agranulocytosis
Associated with depleted levels of basophils and eosinophils.
Drug causes:
Carbamazepine
Carbimazole
Clozapine
h pylori treatment
Omeprazole (PPI) 20mg bd + Clarithromycin 500mg bd + Amoxicillin 1gram bd or Metronidazole
Warfarin anticoagulation reversal
Vitamin K1, start with this
Prothrombin complex concentrate can be used to reverse eg beriplex
(fresh frozen plasma)
Factor Xa inhibitors reversal
Andexanet alfa
Dabigatran (Direct thrombin inhibitor) reversal
Idarucizumab (monoclonal antibody fragment)
Digoxin MOA
Blocks NA/K ATPase
induces an increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility (positively inotropic) ,decreases heart rate ( negatively chronotropic)
reduces conduction at the atrioventricular (AV) node, preventing some impulses from being transmitted to the ventricles, thereby reducing the ventricular rate.
Antidysrhythmic drugs
Class I
Class II
Class III
Class IV
Class I – sodium channel blocker, lidocaine, is considered ‘membrane stabilising’.
Class II – are the B-blockers.
Class III – k channel blocker/ widen AP duration. amiodarone and sotolol. they act on both supraventricular and ventricular arrhythmias
Class IV – calcium channel blockers.
Thiazide and thiazide related diuretics MOA
inhibit sodium reabsorption (Na/cl cotransporter) at the beginning of the distal convoluted tubule.This prevents reabsorption of sodium and its osmotically associated water. Also causes vasodilation. The increased delivery of sodium to the distal tubule, where it can be exchanged for potassium, increases urinary potassium losses and may therefore cause hypokalaemia.
Thiazides reduce the clearance of uric acid, and raise the levels of uric acid in the blood.
HyperGLUC mnemonic for side effects of thiazides
→ hyperglycemia
→ Hyperlipidaemia
→ hyperuricemia
→ hypercalcemia
It can have HYPO effects in serum: including HYPOkalemia, HYPOnatremia and HYPOtension
dihydropyridines
selectively bind to Ca2+ channels in vascular smooth muscle in its inactivated state.
including amlodipine and nifedipine
non-dihydropyridine
more selective for the heart. reduce myocardial contractility.
bind in open state
Eg verapamil and diltiazem
Doxazosin, tamsulosin MOA
Alpha adrenoceptor blockers,blockade induces relaxation. α1-blockers therefore cause vasodilatation and a fall in blood pressure (BP), and reduced resistance to bladder outflow.
Monitoring of Azathioprine and methotrexate
Need to measure TMPT enzyme before starting treatment with azathioprine because some people are deficient which could result in toxic level. FBC and LFT every 3 months, U&E every 6 months ( 3 months for methotrexate)