MMD Year 2 Drug List & Treatments (2)

8/12/2019 MMD Year 2 Drug List & Treatments (2)

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Drug Lists and Treatments for Year 2Cardio-Respiratory

Atrial FibrillationTreat underlying Cause

Drug Action Side-effectsHyperthyroidism Carbimazole inhibits

thyroperoxidase 1 Rashes/PruritisNeutropeniaAgranulocytosis 2

Propylthiouracil inhibitsthyroperoxidas e 1 inhibiting the enzyme5'-deiodinase 3

Agranulocytosi s2

Anti-arrhythmic drugsClass I4 Quinidine

Lidocaine

Na+ channel blocker

Class II28 PropranololAtenalolMetoprolol

Beta- blockers

Class III5 Amiodarone K+ channel blockerClass IV6 Verapamil Ca+ channel Blocker 7 Class V Digoxin

AdenosineNot Clear

Anticoagulants (to prevent stroke)Aspirin Blocks

thromboxaneA2 8 in

platelets

GI problems, ulcers

If aspirin allergy Clopidogrel inhibits P2Y 129

Warfarin Inhibits vitamin k 10 synthesis

HaemorrhageOsteoporosis

DVT and associated conditionsLMWH11

In case of renal failure Heparin 12 HIT syndrome 13 Warfarin Inhibits vitamin k

synthesisHaemorrhageOsteoporosis

COPDBronchodilators Salbutamol

AlbuterolShort acting B2agonist 14

Fine tremor on longterm use

SalmeterolFormoterol

Long acting B2 agonist

Ipratropium Short acting anti-cholinergic 15

Dry mouth andsedation

Tiotropium Long acting ant-chloinergic

Steroids 16 PrednisoneBeclomethasone

(inhaled)

Reduce inflammationof bronchial airway

Oxygen therapy


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AnginaSymptomatic Glyceryl trinitrate Turns into Nitric

Oxide 17 For unstable anginaimmediatey onadmission

AspirinHeparin

Already mentioned

Long term Aspirin as above As abovePropranololAtenalolMetoprolol

Beta-blockers

isosorbidemononitrate

Long acting nitrates 18

Nifedipineamlodipine

Ca2+ channel blocker

nicorandil K+ channel activators19

Simvastatin statins 20 reducecholesterol

Thalassemiasdesferrioxamine (IV) Iron chelation 21

HypertensionRamiprilCaptopril

ACE inhibitors 22

Incase ACE inhibitor

not tolerated

losartan Angiotensin receptor

blockersAmlodipineNifedipineVerapamil

Ca+ channel blocker

Bendroflumethiazidehydrochlorothiazide

Thiazide Diuretic 23 HypokalaemiaPostural HypertensionMetabolic Alkalosis

Maybe givenadditionally

Furosemide Loop diuretic 24 Hypokaleamia

SPironolactone Aldosterone 25 antagonist

Potassium sparing26

Hyperkalaemia

Amiloride ENaC blocker 27 HyperkalaemiaAtenololMetaprololpropranalol

Beta blockers 28

prazosin Alpha blocker 29

Lung cancerAdjuvant therpies 30 Erlotinib

Cisplatin


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Myocardial infarctionInitial Treatment

Morphine 31 Opioid analgesicOxygenGlyceryl Trinitrate Turns into Nitric OxideAspirin Blocks thromboxaneA2

in plateletsatenolol Betablockers

Only within first 12hours

streptokinase thrombolytic 32

Long term ManagementAspirin Blocks thromboxaneA2

in plateletsIf you cannot use

aspirin

Clopidogrel inhibits P2Y 12

simvastatin Statins reducecholesterol

Ramiprilcaptopril

ACE inhibitors

PropranololAtenalolMetaprolol

beta-blockers

Nicorandil K+ channel activator

Heart Failure

Ramiprilcaptopril

ACE inhibitors

If ACE inhibitors notpossible

Losartan Angiotensin II receptorblockers

Diuretics Frusemide Loop diureticshydrochlorothiazide Thiazide diureticSpironolactone Aldosterone antagonist

(potassium sparing)MetaprololBisoprolol

Beta blockers

Last resort Digoxin

To prevent clotting AspirinWarfarin

Anticoagulants

TuberculosisFirst two months Isoniazid

RifampicinPyrazinamideEthambutol

visual disturbancesnausea, vomiting or

diarrhoeadizzinessskin flushes

Following four months IsoniazidRifampicin

Fever , jaundice,pins and needles

depression or othermental disturbances


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Lower Respiratory Tract InfectionsBlind Therapy forsevere pneumonias

PenicillinErythromycin

Beta-Lactam 33 Macrolide 34

Legionella spp. (Do notrespond B-lactams)

Erythromycin+RifampicinOr Quinolone 35

Chlamydia Spp.,M. Pneumoniae (Do

not respond B-lactams)

ErythromycinOr Tetracycline 36 Or quinolone

LegionellaPneumophilia (severe)

ParenternalMacrolide+ Rifampicin

Abnormal HaemostasisFactor VIII deficiency(Haemophilia A)

Normal PT 37, NormalTT38

Long APTT39 Replace factor VIII

Haemophilia B (FactorIX Deficiency)

Normal PT, Normal TT Long APTT Replace factor IX

vW disease Normal PT, Normal TT Long APTT Replace VW factorHaemorrhagicDiesease Of newborn(lack of vit K)

Normal TT Long APTT, Long PT IV vitamin K

Liver Disease 40 Long APTT, PT, TTThrombocytopenia

Vit K, fresh frozenplasma (FFP)

Renal Disease41

Normal APTT, PT, TTNormal or slightly lowplatelets

Long Bleeding timeAbnormal plateletaggregration

Dialysis to removeuraemic productsPlatelet transfusion

Disseminatedintravascularcogulation 42

Long APTT, PT, TTLong bleeding timeRaised FDP 43 and D-dimer 44

Treat UnderlyingCause!FFP, Replace missingfactors and platelets

Massive transfusionsyndrome 45

long PT, APTTlong or normal TTLow plateletLow fibrinogen

FFP, Platelets

Blood TransfusionRecipient Donor

O- O+ A- A+ B- B+ AB- AB+O- O+ A- A+ B- B+ AB-

AB+


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Metabolism

HyperthyroidismMain Cause GravesDisease 46

Carbimazole inhibitsthyroperoxidase

Rashes/PruritisNeutropeniaAgranulocytosis

Propylthiouracil inhibitsthyroperoxidas e 1 inhibiting the enzyme5'-deiodinase

Agranulocytosi s2

HypothyroidismMain cause isHashimotos 47

Levothyroxine 48 T4 replacement palpitations,nervousness,headache, insomnia,swelling of the legs andankles, weight loss,and increased appetite

SteroidsAddisons Disease 49 Immune suppressant

Anti inflammatory 50

Suppression of response to injury and infectionSuppression of patients ability to synthesisecorticosteroidsOsteoporosis, growth inhibition, hyperglycaemiaOedema, and High BP

MicturitionFrequencyIncontinence

Oxybutynin Muscarinic Receptorantagonist 51

Standard anti-muscarinic effects 52

Overflow incontinence PrazosinFinasteride

Alpha receptorantagonistAnti testosterone 53

HypotensionErectile DysfunctionGynocomastia

Post-op urinaryretention 54

Bethanachol Muscarinic receptoragonist

Increased gut motility

DiureticsPulmonary embolism,chronic heart failureThick Ascending Loopof Henle (25%)

Frusemide Loop diureti c24 HypokalaemiaMet. AlkolosisHypovolaemia

Hypertension,Chronich Heart FailureDistal Tubule (10%)

bendroflumethiazide Thiazide diuretic s23

HypokalaemiaGout

Prevention of K+ lossCollecting tubule (3%)

Spironolactone K+ sparing aldosteroneAntagonis t 26

HyperkalaemiaMet. Acidosis

Intra-cranial and intra-ocular pressureProximal Tubule (5%)

Mannitol Osmotic Diuretic Increase in ECF


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Obesity/Metabolic SyndromeObesity Orlistat Inhibits pancreatic

enzyme lipaseSteatorrhea, oilyfaeces, flatulence

Sibutramine SNRI 55 Increase BP, dry mouthdizziness nausea

Rimonabant CB1 receptor blocker 56 Metabolic syndrome(treat underlyingissues, hypertensionand insulin resistance)

CaptoprilBendroflumethizideMetformin

ACE inhibitorThiazide diureticGluconeogensisinhibitor 57

DiabetesType I Actrapid insulin

Actraphane InsulinShort and long actinginsulin replacement

Type II Metformin Gluconeogenesisinhibitor (Biguanide)Glibenclamidegliclazide

Sulfonylurea 58

Glitazones Thiazolidinediones 59 Acarbose -glucosidase

inhibitors 60 Nategliniderepaglinide

Meglitinides 61

Endocrine Disorders

Prolactinoma62

Bromocriptine63

Dopamine agonistAcromegaly 64 Octriotide

LantriotideSomatostatinAnalogue 65

Bromocriptine Dopamine Agonist 66

GI InfectionsGiardia LambliaEntamoeba HistolyticaC. Difficile

Metronidazole

Severe salmonella/shigella/campylobacter

CiprofloxacinErythromycin

Acidosis/AlkalosisCondition Reason/ with example Mechanism CompensationRespiratory Acidosis Hypoventilation(COPD) CO2 retention Renal compensation

(H+ loss/ HCO3- gain)Respiratory Alkalosis Hyperventilation

(anxiety/altitude)CO2 loss Renal compensation

(H+ gain/HCO3-loss)Metabolic Acidosis diarrhoea, keto-

acidosis, lactic acidosisGain of Acid/Loss ofbase

Respiratorycompensation (CO2loss/HCO3- falls)

Metabolic Alkalosis vomiting,

hypokaleamia,ingestion of HCO3-

Loss of Acid/Gain of

base

Respiratory

compensation (CO2retention/HCO3- rises)


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Brain and BehaviourParkinsons Disease

Levodopa 67 Dopamine pre-cursor on-off effect 68,dyskinesia 69,psychosis 70

Given with l-dopa BenserazideCarbidopa

PeripheralDecarboxylaseInhibitor 71

Rotigotine(transdermal patch)Bromocriptineapomorphine

Dopaminergic agonist Nausea/vomiting,hallucinations

Given with dopamineagonists

Domperidone Anti-emetic 72

entacapone COMT inhibitor 73 selegeline MAO-b inhibitor 74

Treatment for tremor benzatropine Anti-cholinergic 75 Anti-Muscarinic sideeffects 76

Used to reduce end -dose deterioration

amantadine Increases dopaminerelease from vesicle

Vit E supplements Anti-oxidantDeep brain stimulationof subthalamic nucleus

Pain!paracetamol 77 COX78 inhibitor but not

anti-inflammatoryAspirin Cox inhibitor,irreversibly blocksCOX1 and modifiesCOX2 activation

Peptic ulcers 79

ibuprofen,diclofenac 80, naproxen

NSAIDs- COX inhibition Peptic ulcers and GIproblems

In order of potency Tramadol, codeinemorphinefentanyl

opioids 81 Respiratorydepression, vomiting,addiction, constipation

TENS82

Heat padmassage

Gate control

mechanism83

Adjuvant therapies 84 AddictionSmoking NRT

Bupropion 85

Nicotine replacementtherapy,Anti-depressant

Alcohol Benzodiazepines(diazepam)

Modulate GABAergictransmission 86

Naltrexone Opioid antagonistBenzodiazepines Carbamezapine Anticonvulsant

Heroin Methadone Opioid agonist87

Naloxone Opioid antagonist 88


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EpilepsyPhenytoin 89 Carbamezapine 90 Sodium Valproate 91 Topiramate 92 Lamotrigine 93

Na+ channel blockers The first two can leadto pregnancy 94

Ethosuximade 95 Gabapentin 96

Calcium channelblocker

Clonazepam Benzodiazapene 97-GABAa receptor

Addiction

Phenobarbitone Barbiturates 98-GABAareceptor

Tiagabine GAT-1 99 inhibitorVigabatrin GABA transaminase 100

inhibitorLevetiracetam 101 SV2A blocker

Status Epilepticus(Emergency)

Diazepam (IV) Benzodiazapene

SchizophreniaChlopromazineFlupenthixolTriflouperazinehaloperidol 102

Typical neuroleptics 103 i.e. dopamine receptorantagonists

Anti-muscarinicTardive dyskinesia(long-term use,irreversible)

Clozaine

Olanzapinerisperidone

Atypical neuroleptic

i.e. D2 anatagonist and5-HT2

Less side effects

Depression 104 ImipramineAmitryptilineClomipramine

Try-cyclic anti-depressant 105

Postural hypotensionAnti-muscarinics

TranylcyprominePhenelzine

Irreversible non-selective MAO inhibitors

cheese effect 106

Moclobemide Reversible non-selectiveMAO inhibitor

Less chance ofcheese effect

Nausea, confusionFlouxetineCitalopramparoxetine

Selective serotoninreuptake inhibitor

nausea, headache,suicidal ideation 107

Venlafaxine Serotonin/noradrenalinere-uptake inhibitor

reboxitine Noradrenaline reuptakeinhibitors

Bipolar Disorder Lithium carbonate LithiumAnti-convulsants may beused

nausea, tremor,polyuria, fatigue

Severe depression Electro convulsiontherapy


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Alzheimers Disease /DementiaDonepezil Reversible

acetylcholinesteraseinhibitor 108

Nausea, diarrhoea,bradycardia, anorexia

Fewer side effects Rivastigmine Irreversibleacetylcholinesteraseinhibitor

Nausea, Vomiting

Tacrine acetylcholinesteraseinhibitor

Diarrhoea, vomiting,hepatotoxicity

Add-on Mementine NMDA receptorantagonist 109

Anxiety/ADHDDiazepamFlurezapamclobazam

Benzodiazapene-GABAa receptormodulator

Addiction, dependenceheadache(OD treat withFlumazenil 110 )

Buspirone Serotonin agonistFlouxetineCitalopramparoxetine

SSRI Nausea, headache

propranolol Beta blocker Hypotensionobsolete phenobarbitone Barbiturate-GABAa

receptor modulator

Migraine Paracetamolaspirin

NSAID mechanism 111

Severe head aches Sumatriptan Triptans 112

Huntingtons ChoreaTetrabenazineHaloperidol

Anti-dopaminergicagents 113

To treat depression Imipramineamitryptiline

Tricyclic antidepressants


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Human Development

Sub-fertilityclomiphine Eostregen inhibition 114

For PCOS115 metformin biguanide

Early delivery (IUGR)Before delivery glucocorticoids Enhances fetal lung

maturity andsurfactant

After delivery Artificial surfactant Allows for initialalveolar expansion

Birth AspyhxiaAdrenaline Induce surfactant

productionSodium bicarbonate Counteract acidaemiaHypoglycaemic Dextrose


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Locomotor

Muscular DystrophyPrednisoneDeflazacort

steroids 116 Cushings syndrome 117

PCT124118 Exon Skipping 119

Psoriatic ArthritisDiclofenac NSAIDs May worsen skin

problem, thereforemonitor

Methotrexate antimetabolite 120 Other DMARDS

For skin problems(ointments andcreams)

tar-baseddithranol-basedsteroid-basedvitamin D-likeointmentsvitamin A-like

Rheumatoid Arthritis esp. DMARDSAspirinDeclofenac

NSAIDs GI problems

Sulphasalazine 121

Methotrexate Anti-folateAzathioprine 122 Purine synthesisinhibitor

GoldSteroids Anti-inflammatory and

immune suppressantD-pencillamine 123 Reducing numbers of

T-lymphocytesInfliximab 124 Anti-TNFaEtanercept 125 Anti-TNFCyclosporine 126 Inhibits calcineurin

OsteoporosisEostregen progesterone

HRT127 Increased risk ofbreast/uterine cancersIncreased clotting

Alendronate Bisphosphonates 128 GI problems

For analgesics refer to pain under BB2 section.


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1 Thyroperoxidase liberates iodine for addition onto tyrosine residues on thyroglobulin for the production ofthyroxine (T4) or triiodothyronine (T3) (thyroid hormones).2 Agranulocytosis is an acute condition involving a severe and dangerous leukopenia, particularly ofneutrophils, causing a neutropenia in the circulating blood3 enzyme 5'-deiodinase converts T 4 to the active form T 3 in the periphery4 The class I antiarrhythmic agents interfere with the (Na+) channel. Class I agents are grouped by what effect

they have on the Na+ channel, and what effect they have on cardiac action potentials. Class 1 agents are calledMembrane Stabilizing agents. The 'stabilizing' is the word used to describe the decrease of excitogenicity ofthe plasma membrane which is brought about by these agents.5 Class III agents predominantly block the potassium channels, thereby prolonging repolarization. Theprolongation of the action potential duration and refractory period, combined with the maintenance of normalconduction velocity, prevent re-entrant arrhythmias.6 Calcium channel blockers work by blocking voltage-gated calcium channels (VGCCs) in cardiac muscle andblood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction. In the heart, adecrease in calcium available for each beat results in a decrease in cardiac contractility.7 Reduces contractility of the heart therefore workload8

Producing an inhibitory effect on platelet aggregation.9 is important in platelet aggregation and the cross-linking of platelets by fibrin10 Needed for activating clotting factors II, VII, IX and X, as well as the regulatory factors protein C, protein S,and protein Z11 No need for monitoring APTT, and can be given once daily rather than continuous IV12 Continous IV administration and monitoring of APTT13 Heparin induced thrombocytopenia14 Thereby causing smooth muscle relaxation, resulting in dilation of bronchial passages.15 It acts by blocking muscarinic receptors in the lung, inhibiting bronchoconstriction and mucus secretion.16 Potent anti-inflammatory drugs which work by transactivating and therefore upregulating lipocortinproduction. Lipocortin suppresses phopholipase A2 which prevents arachidonic acid formation thus stoppingdownstream active metabolites such as COX and LOX and platelet activating factor involved in inflammation.17

Nitric Oxide is a powerful vasodilator of blood vessels18 These widen the coronary arteries to improve blood flow to the heart. They are available as tablets orpatches19 These relax coronary arteries to increase blood flow. It works as selective vascular potassium channelactivator and therefore does not affect heart contractility20 They lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which is the rate-limiting enzyme ofthe mevalonate pathway of cholesterol synthesis. Inhibition of this enzyme in the liver results in decreasedcholesterol synthesis as well as increased synthesis of LDL receptors, resulting in an increased clearance of low-density lipoprotein (LDL) from the bloodstream.21 This is due to iron overload of constant blood transfusions2222 Prevents conversion of angiotensin I to angiotensin II, by inhibiting the enzyme angiotensin convertingenzyme, which is a powerful vasoconstrictor23 They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl- symporter. Thiazides also cause loss of potassium and an increase in serum uric acid.24 Loop diuretics act on the Na+-K+-2Cl- symporter (cotransporter) in the thick ascending limb of the loop ofHenle to inhibit sodium and chloride reabsorption.25 Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and thecollecting duct of the kidney nephron, it increases the permeability of the apical (luminal) membrane topotassium and sodium and activates the basolateral Na+/K+ pumps, stimulating ATP hydrolysis leading tophosphorylation of the pump and a conformational change in the pump exposes the Na+ ions to the outside.The phosphorylated form of the pump has a low affinity for Na+ ions, hence reabsorbing sodium (Na+) ionsand water into the blood, and secreting potassium (K+) ions into the urine. (Chlorine anions are alsoreabsorbed in conjunction with sodium cations to maintain the system's electrochemical balance.)Aldosterone stimulates H+ secretion by intercalated cells in the collecting duct, regulating plasma bicarbonate(HCO3) levels and its acid/base balance. Aldosterone may act on the central nervous system via the posterior pituitary gland to release vasopressin(ADH) which serves to conserve water by direct actions on renal tubular reabsorption


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26 Spironolactone inhibits the effect of aldosterone by competing for intracellular aldosterone receptors in thedistal tubule cells (it actually works on aldosterone receptors in the collecting duct). This increases theexcretion of water and sodium, while decreasing the excretion of potassium27 Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium

reabsorption in the distal convoluted tubules and collecting ducts in the kidneys28 Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect onresting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force ofcontraction, dilation of blood vessels and opening of bronchi, and also reduce tremor and breakdown ofglycogen.29 Reduce arteriolar resistance and increase venous capacitance causing reflex tachycardia.Depending onplasma concentration they may cause postural hypotension.Alpha-1 blockers may decrease LDL andtriglycerides and increase HDL. Also used in Benign Prostatic Hyperplasia 30 These are chemotherapy drugs given after surgical removal of the cancer, e.g. tamoxifen in breast cancer31 Morphines main effec t is binding to and activating the -opioid receptors in the central nervous system.Activation of the -opioid receptors is associated with analgesia, sedation, euphoria, physical dependence, andrespiratory depression.32

It belongs to a group of medications known as fibrinolytics, and works by activating plasminogen throughcleavage to produce plasmin. Plasmin is produced in the blood to break down the major constituent of bloodclots fibrin, therefore dissolving clots once they have fulfilled their purpose in stopping bleeding.33 -Lactam antibiotics are bactericidal, and act by inhibiting the synthesis of the peptidoglycan layer ofbacterial cell walls. The -lactam nucleus of the molecule irreversibly binds to (acylates) the Ser403 residue ofthe PBP active site. This irreversible inhibition of the PBPs prevents the final crosslinking (transpeptidation) ofthe nascent peptidoglycan layer, disrupting cell wall synthesis.34 The mechanism of action of the antibiotic macrolides is inhibition of bacterial protein biosynthesis bybinding reversibly to the subunit 50S of the bacterial ribosome, thereby inhibiting translocation of peptidyltRNA. This action is mainly bacteriostatic, but can also be bactericidal in high concentrations. Macrolides tendto accumulate within leukocytes, and are therefore actually transported into the site of infection.35 Quinolones inhibit the bacterial DNA gyrase or the topoisomerase IV enzyme, thereby inhibiting DNA

replication and transcription36 Tetracycline antibiotics inhibit protein synthesis by inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex. They do so mainly by binding to the 30S ribosomal subunit in the mRNA translationcomplex.37 The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalizedratio (INR) are measures of the extrinsic pathway of coagulation. They are used to determine the clottingtendency of blood, in the measure of warfarin dosage, liver damage, and vitamin K status. The reference rangefor prothrombin time is usually around 12 15 seconds; the normal range for the INR is 0.8 1.2. PT measuresfactors II, V, VII, X and fibrinogen.38 The Thrombin Time (TT), also known as the Thrombin Clotting Time (TCT), is a test of the time it takes for aclot to form, measuring the conversion of fibrinogen to fibrin. It is a coagulation assay which is usuallyperformed in order to detect for the therapeutic level of the anticoagulant Heparin. It is also sensitive indetecting the presence of a fibrinogen abnormality.39 The activated partial thromboplastin time (aPTT or APTT) is a performance indicator measuring the efficacyof both the "intrinsic" (now referred to as the contact activation pathway) and the common coagulationpathways.40 Liver disease leads to failure of production of coagulation factors, failure of vitamin K absorption or use,abnormal fibrinogen production41 Kidney disease leads to platelet defects due to uraemic retention products which leads to decreased plateletvessel wall interaction42 Widespread intravascular deposition of fibrin with consumption of coagulation factors and platelets, whichleads to complete depletion of clotting factors and platelets therefore more bleeding43 Fibrin degradation product (FDPs) are components of the blood produced by clot degeneration.44 D-dimer is a fibrin degradation product, a small protein fragment present in the blood after a blood clot isdegraded by fibrinolysis45 This is a transfusion of greater than 5litre in less than 24 hours, stored blood has very low coagulationfactors and platelets which leads to bleeding.


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46 Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor forthyroid-stimulating hormone (TSH). These antibodies cause hyperthyroidism because they bind to the TSHreceptor and chronically stimulate it.47 The underlying specifics of the immune system destruction of thyroid cells is not clearly understood. Various

autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors48 This is a precursor to tetraiodothyroxine (T4) which is then metabolised to the active form T3.49 Addison's disease (also known as chronic adrenal insufficiency, hypocortisolism or hypocorticism) is a rareendocrine disorder in which the adrenal gland does not produce enough steroid hormones (glucocorticoidsand often mineralocorticoids).50 Look at Dr. Burleighs lecture handout for steroids, e verything you need to know is there51 This acts on the parasympathetic division of the pelvic nerve which is involved in the muscle emptying thebladder, therefore when this is blocked less incontinence.52 dry mouth, difficulty in micturition, constipation, blurred vision, drowsiness and dizziness53 This is to treat benign prostatic hyperplasia which may be being fuelled by excess testosterone.54 This is usually due to the post op anaesthetic effects which are still working on the hypogastric nerves55 Sibutramine is a neurotransmitter reuptake inhibitor that reduces the reuptake of serotonin (by 53%),

norepinephrine (by 54%), and dopamine (by 16%), thereby increasing the levels of these substances in synapticclefts and helping enhance satiety; the serotonergic action, in particular, is thought to influence appetite.56 It has been developed from the knowledge that cannabis smokers often experience hunger, which is oftenreferred to as "the munchies". Therefore blocking the cannabinoid receptor will stop the hunger.57 Metformin improves hyperglycemia primarily through its suppression of hepatic glucose production (hepaticgluconeogenesis). Metformin activates AMP-activated protein kinase (AMPK), a liver enzyme that plays animportant role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats;activation of AMPK is required for metformin's inhibitory effect on the production of glucose by liver cells.58 Sulfonylureas bind to an ATP-dependent K+ (KATP) channel on the cell membrane of pancreatic beta cells.This inhibits a tonic, hyperpolarizing efflux of potassium, thus causing the electric potential over themembrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise inintracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore

increased secretion of (pro)insulin.59 These increase tissue insulin sensitivity by affecting gene expression60 Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digestcarbohydrates: Inhibition of these enzyme systems reduces the rate of digestion of carbohydrates. Lessglucose is absorbed because the carbohydrates are not broken down into glucose molecules61 Meglitinides which stimulate insulin release (nateglinide, repaglinide, and their analogs) quickly; they can betaken with food, unlike the sulfonylureas which must be taken prior to food (sometimes some hours before,depending on the drug)62 This is a prolactin secreting tumour of the pituitary gland63 Prolactin is under tonic inhibitory control vi dopamine from the hypothalamus hence dopamine agonistneeded to control prolactinoma64 Acromegaly is a disorder of excess growth hormone which is under control from two hormones,somatostatin (inhibitory) and growth hormone releasing hormone (GHRH), stimulatory65 Somatostatin inhibits the release of growth hormone66 This has weak inhibitory effect on growth hormone67 This is a precursor of dopamine which is turned into dopamine in the brain, dopamine cannot cross theblood-brain barrier hence the precursor form is given.68 This is a result of the long term effect of taking l- dopa described as dramatic fluctuations i n motorperformance, which are not always related with intake of l- dopa69 This is a loss of voluntary control of movement and split into chorea-like movements (hyperkinetic,purposeless dance-like movements) and dystonias(intense sustained muscle contraction)70 Up-regulation of dopamine is thought to be responsible for schizophrenic symptoms of delusions andhallucinations therefore over treatment in parkinsons can lead to these symptoms 71 L-dopa can be converted to dopamine in the periphery which can trigger the chemoreceptor trigger zoneleading to nausea and vomiting therefore a peripheral inhibitor of the conversion enzyme can prevent this.Also it can increase the amount of l-dopa that reaches the brain72 This is to prevent the vomiting side effect of dopamine agonists


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73 COMT is an enzyme which breaks down catecholamines including dopamine, therefore an inhibitor of thisenzyme would increase the dopamine availability74 This is the enzyme which breaks down dopamine after it has been released from the neuron thereforeinhibition would lead to increased amount of time that dopamine is available post-synaptically.75

This antagonises acetyl choline which decreases the imbalance between dopamine and acetyl choline.76 Dry mouth, blurred vision, constipation, urinary retention77 It inhibits COX which leads to its anti-pyretic and analgesic properties but it is broken down by peroxides ininflammatory lesions which is why it lacks anti-inflammatory properties. Also it modulates the endogenouscannabinoid system. One of the metabolites of paracetamol inhibits re-uptake of endogenous cannabinoidswhich are believed to be analgesic.78 Cox enzymes are needed to convert arachidonic acid into prostaglandins, prostacylin and thromboxane.Prostaglandins are involved in the inflammatory process which is why this produces and anti-inflammatoryeffect79 Cox 1 enzyme is needed to convert arachidonic acid into prostaglandin E2 which is important in maintainingthe lining of the stomach and aciditt, therefore blocking cox enzymes can lead to upper GI problems80 It is thought to have additional inhibition of lipoxygenase and phosphlipase a2 hence it is more potent anti-

inflammatory81 These act mainly through the -opioid receptor found mainly in the brain and spinal cord which causessupraspinal analgesia, it also responsible for its constipation and respiratory depressive effects82 Transcutaneous electrical nerve stimulation83 This theory postulates that innocuous stimuli activates inhibitory interneurons which prevent the firing ofthe nociceptors thus decreasing pain sensation84 Adjuvants are drugs which modify the effects of other drugs while giving very little if any effects themselves.IN pain they would typically involve anti-depressants, ant-convulsants, steroids, DMARDS, etc.85 This is dopamine and noradrenaline reuptake inhibitor and a nicotinic receptor antagonist.86 This is to prevent withdrawal symptoms of delirium tremens experienced.87 This is to provide relief of addiction whilst preventing physical damage done by heroin88 This is to ensure that if a patient seeks out the drug it does not provide as much relief as expected89

This has zero order kinetics. And should not be given for absent seizures (petit mal).90 Given for partial and tonic-clonic seizure91 Also blocks L-type calcium channels. It also decrease GABA metabolism and increases GABA synthesis92 Also has some calcium channel activity93 This also blocks calcium channels94 This is because they induce liver enzymes which can break down oral contraceptives95 Given in absent seizures. Blocks t-type calcium channels96 Its exact mechanism of action is unknown, but its therapeutic action on neuropathic pain is thought toinvolve voltage-gated N-type calcium ion channels. It is thought to bi nd to the 2 subunit (1 and 2) of thevoltage-dependent calcium channel in the central nervous system.97 Benzodiazapenes work by increasing the frequency of opening of GABAa receptors98 Barbiturates work by keeping the GABAa receptors open for longer99 GAT-1 is the channel which re-uptakes GABA therefore blocking this would increase the time GABA isavailable100 GABA transaminase is the enzyme which breaks down GABA (post synaptically) therefore blocking thisincrease the amount of GABA101 Levetiracetam binds to a synaptic vesicle protein, SV2A. This is believed to impede nerve conduction acrosssynapses.102 Can be given as depot i.e. slow release preparation to avoid non-compliance103 These also anatagonise muscarinic, histamine, and a2-adrenergic receptors104 Depression is thought to be due to lowering of monoamine (serotonin, noradrenaline) transmissiontherefore drug therapies are aimed primarily at increasing this either by stopping their re-uptake from thesynaptic clefts or blocking monoamine enzymes leading greater availability of the neurotransmitter.105 Fatal in overdose, therefore must not be given in suicidal cases. TCAs work by inhibiting the reuptake of themonoamine neurotransmitters serotonin and/or norepinephrine, leading to increased extracellular levels ofthese neurotransmitters and therefore enhanced neurotransmission. Many TCAs also have affinity as


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antagonists at the 1 -adrenergic, 2 -adrenergic, 5-HT2, and D2 receptors, and as agonists at the 5-HT1A andsigma receptors thus causing the side-effects106 This is hypertensive crisis which is due to the presence of tyramine residues found mostly in cheesesamongst other foods. This is due mainly to MAOa interaction with tyramine which displaces noradrenaline and

adrenaline from synaptic vesicles which leads to hypertension107 The drug is safe in overdose108 Acetylcholinesterase is the enzyme which breaks down ACh post-synaptically therefore inhibiting it willincrease the post-synaptic availability of ACh109 This is based on the idea that alzheimers is based on a slow atypical increased release of glutamate.Therefore blocking this has shown slower rates of cognitive decline in of patients.110 It reverses the effects of benzodiazepines by competitive inhibition at the benzodiazepine binding site onthe GABAa receptor.111 Needs no further discussion112 This is a selective 5-HT1d and 5-HT1b agonist which vasoconstricts cerebral arteries, cerebral arteryvasodilation is thought to be a cause of headaches/migraines113 These drugs are given to control symptoms, huntingtons is due t o neurodegenration of indirect pathway in

the basal ganglia therefore drugs are given to tame the direct pathway 114 This prevents normal receptor recycling and causes an effective reduction in hypothalamic estrogenreceptor number. Since estrogen can no longer effectively feedback on the hypothalamus, GnRH secretionbecomes more pulsatile, which results in increased pituitary gonadotropin (FSH, LH) release. Increasedgonadotropin levels cause growth of the ovarian follicle, followed by follicular rupture, otherwise known asovulation.115 This is polycystic ovarian syndrome which leads to subfertility, it happens in fat people mainly due to insulinresistance116 Mechanism in muscular dystrophy is unclear but generally slows down progression of disease.117 These are with all steroids, truncal obesity, osteoporosis, skin thinning, classic moon face118 This treatment basically replaces the opposite mRNAs to any stop codons and therefore prevents theirreading in cell machinery to try and stop any preliminary stop codons in the gene119119

This treatment skips over entire mutated exons that are in duchenne and demotes the disease tobeckers dystrophy120 that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction, has beenshown to work for both skin and joint problems.121 reducing the synthesis of inflammatory mediators known as eicosanoids and inflammatory cytokines122 Azathioprine is a purine synthesis inhibitor, inhibiting the proliferation of cells, especially leukocytes.123 It works by reducing numbers of T-lymphocytes, inhibiting macrophage function, decreasing IL-1,decreasing rheumatoid factor, and preventing collagen from cross-linking.124 Infliximab neutralizes the biological activity of TNF by binding with high affinity to the soluble (free floatingin the blood) and transmembrane (located on the outer membranes of T cells and similar immune cells) formsof TNF and inhibits or prevents the effective binding of TNF with its receptors. Biological activities that areattributed to TNF include: induction of proinflammatory cytokines such as interleukin (IL) 1 and IL 6,enhancement of leukocyte movement or migration from the blood vessels into the tissues by increasing thepermeability of endothelial layer of blood vessels; and increasing the release of adhesion molecules.125 It reduces the effect of naturally present TNF, and hence is a TNF inhibitor. Etanercept mimics the inhibitoryeffects of naturally occurring soluble TNF receptors,126 This complex of cyclosporin and cyclophilin inhibits calcineurin, which, under normal circumstances, isresponsible for activating the transcription of interleukin 2.127 Oestrogen inhibits osteoclast activity and therefore a protective effect on bones.128 The bisphosphonates inhibit osteoclast activity and increase bone mass

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MMD Year 2 Drug List & Treatments (2)