eHypertension + diuretics

Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

ACE inhibitors - Ramipril - First line - ACE found on endothelial cells of 1. Vasodilation ● Dry cough – due to bradykinin - Pregnancy K+ sparing drugs
- Lisinopril Anti-hypertensives capillaries - mainly in lung 2. Reduction in the ADH release accumulation as well as - Renal failure – due to the post NSAIDS
- especially with - ACE converts angiotensin 1 - 2 3. Reduced aldosterone production vasodilation glomerular vasodilation Other anti-hypertensives
hypertension and type 2 - ACEi - inhibits ACE 4. Reduced cell growth and ● Hyperkalaemia - low aldosterone - - K sparring diuretics- hyperkalaemia
diabetes proliferation increased potassium
- ACTIONS OF ANGIOTENSIN 2 5. Reduce SNS activity- decrease CO( ● Renal failure
- heart failure w/ reduced STOPPED Beta 1 adrenoceptor),TPR(alpha ● Angioedema especially in
ejection fraction ( give with adrenoceptor) and venous return( blackpopulation
a bb) - some AngII still produced due to beta 1 adrenoceptor) and less renin ● hypotension
action of chymases secretion(B1 adrenoceptor on
*low dose initially since the Bp - bradykinin is a substrate for ACE - kidney)
is reduced suddenly, the vasodilation via NOS/NO
baroreceptor reflex can ACEi/ARB ↓ Diabetic nephropathy and
increase the SNS activity CKD with proteinuria by dilation of
and increase the renin efferent glomerular arteriole So called
secretion so that the preload “two pronged” approach ↓peripheral
increase which will vascular resistance →↓BP and dilation of
exacerbate the heart failure. efferent glomerular arteriole → reduced
intraglomerular pressure – good for type II
diabetes

Angiotensinogen receptor losartan Hypertension and heart failure - AT1 and AT2 receptors - AT! Target the AT1 receptor so more ● Renal failure - Renal artery stenosis K+ sparing drugs
Antagonist ( ARBS) Candesartan Use ARB instead of ACE Cardiovascular relation effective at inhibiting ● Hyperkalaemia- low aldosterone - - AKD NSAIDS
inhibitor if the patient cannot vasoconstriction increased potassium - pregnancy
tolerate the dry cough - no bradykinin effect - less effective Ag 2 can be produced from the ● hypotension
in patients with low renin chymase interaction without the
^ step 2 HF if intolerant of ACE -so ARBs are better (but ( less likely angioedema and dry cough -
ACEi more expensive) bradykinin)

Calcium channel blockers( Amlodipine Hypertension- Step 2 LTCCs allow inward Ca2+ flux into Blocking of the influx of the Ca into the SNS activation – tachycardia, Palpitations, Unstable angina, SIMVASTATIN - increased
LTCCs) cells – voltage operated calcium smooth muscle cells via the VOCC flushing, sweating and throbbing severe aortic stenosis effect
Dihydropyridine Highly protein bound Hypertension – Step 1 in the channel (VOCC) - releases channels (L-type ca channel)
and good oral African/Caribbean origin or the intracellular store of Ca2+ - Swollen ankles
bioavailability patient with >55 years old – contratcion Peripheral Vasodilation headache
Metabolised by the due to the low renin Oedema
liver - long half life hypertensive Expressed throughout the body -
- Targetting RAAS including vascular smooth muscle
- nifedipine not beneficial cells AND cardiac myocytes plus SA
- nimodipine ( Most common and AV node
selective for cerebral
vasculature)

Calcium channel blockers( Verapamil Arrhythmia CCBs target calcium initiated smooth Blocking of the influx of the Ca into the Constipations X Poor LV function (caution), Beta blocker- decrease SV
LTCCs) Angina muscle contraction (in hypertension) myocardial cells (smooth muscle type) Can worsen heart failure / heart block AV nodal conduction delay Other anti-hypertensives
Non-dihydropyridine – ( hypertension) - Due to the decreased CO Anti arrythmics
Phenylalkyamine - Acting on different sites on Depress SA node and slows AV
the alpha 1 subunit conduction, - inotrophy and - chonotrophy Bradycardia
- Prolongs action potential

Calcium channel blockers( Diltiazem Angina Blocking of the influx of the Ca into the Bradycardia Can worsen heart failure CY3A4 inhibitor - statins
LTCCs) Hypertension - mild to - Different selectivity for cells Mixed picture - Due to the decreased CO
Non-dihydropyridine – moderate vascular smooth muscles or
Benzothiazapines myocardium - both vasodilation, inotropic and
chronotropic effect
Diuretics Acetazolamide Glaucoma - Na/H exchanger - apical - h Decrease the Na reabsorption and the Acidosis ( H reabsorbed) Renal failure
carbonic anhydride inhibitors Altitude sickness into lumen bicarbonate reabsorption in the proximal Hypokalaemic metabolic acidosis ( loss of
- Bicarb transporter - tubule bicarb and upregulated Enac)
basolateral Renal stones
- Body compensates

Osmotic Diuretics Mannitol renal failure freely filtered and not reabsorbed Doesn’t have an effect on the channels hypernatraemia - water excretion not Renal failure
Drug poisoning only act to loss of water- work all the way associated with ions Not in heart failure - ECF VOLUME
Increased ICP/IOP along in the tubule EXPANSION - worsens
Increases ECF Dilution also hyponatraemia Pulmonary odema
Excessive use - dehydration
Reduce the intracellular volume

Diuretics furosemide Emergencies - very potent Reduces signs of volume overload - • hyponatraemia
loop diuretics • Severe oedema dyspnoea and peripheral oedema • Hypokalaemia
associated with congestive • Hypmagnasaemia
heart failure - 1st line, • Hypocalcaemia
nephrotic syndrome. • Hypovolaemia
• Treatment for Oliguric ARF. • Metabolic alkalosis
• Treatment of hypercalcemia • Postural hypotension
• Acute pulmonary oedema.
• Acute hyperkalaemia/ Acute
hypercalcemia.
• To x i c i t y of Br, F & I

Diuretics indapamide FIRST LINE ANTI BETTER FOR CCB in OEDEMA NCC in the distal tubule – decrease Na - Hypokalaemia renal failure 1. B blocker- hyperglycaemia
Thiazides / thiazide like Bendroflumethiazide HYPERTENSIVE ( step 2) reabsorption(Na/Cl) - Hyponatraemia Hypercalcemia 2. Steroids-hypokalaemia
- Hyperglycaemia ( esp w/ beta Hypokalaemia [Link] – lithium toxicity
Nephrotic syndrome Increase in k loss due to K coming back blockers) Hyponatremic [Link]-
to collecting duct via ROMK - Hyperlipidaemia Gout hyponatraemia
- Mild HF Increase the Ca reabsorption vasodilation - Hyperuricaemia ( gout ) +
- Hypercalciuria >excretion - NSAIDs
- osteoporosis - Hypercalcaemia - decreased - potassium sparing
excretion diuretics
- Arrhythmias
Activates the RAAs- acute kidney injury
Erectile dysfunction
Increase LDL and TG

Diuretics spironolactone Step 4 - resistant hypertension Aldosterone decrease = potassium Aldosterone receptor antagonist HYPERKALAEMIA Hyperkalaemia K+ sparing drugs
K+ sparing if potassium <4.5mmol/L increase Gynaecomastia Addisons Pregnancy
In HF - reduces sympathetic output ,
Step 2 in HF with reduced EF, - in some patients refractory reduce na and water retention
when symptoms contiune after hyperaldosteronism occurs due to
ACEi/bb excessive RAAS activity( aldosterone
escape)- despite ACEi/ARB
- spironolactone is give as an adjunct
to ACEI/ARB + DIURETIC -
significantly increases mortality
Alpha Blocker doxazosin Step 4 - resistant hypertension Relatively safe in renal disease SELECTIVE ANTAGONISM OF alpha 1 Postural hypertension- baroreceptor Postural hypotension Di-hydropyridines - oedema
if potassium >4.5mmol/L adrenoceptors in the smooth muscle reflex leading to dizziness
cell Headache and fatigue
BPH ( tamulosin) - act by - Reduce peripheral vascular Oedema
relaxing the smooth resistance Erectile dysfunction
muscle within the prostate and - Less renin produced
bladder neck

Beta blocker Bisoprolol - Hypertension- Step 4 Remember BLM For the hypertension- Bronchoconstriction Asthamatic and the COPD patient- Non - dihydropyridine -
Selective B1 ( ORAL) (Decrease the SNS activity - Block the Heart block non-selective verapamil and diltizem -
Atenolol- Heart failure - bisoprolol B2 - lung Nad in the In beta 1 adrenoceptor and Raynaud’s ( cold hands) CCBs - asystole
selective B1 alongside ACEi for heart B1 - heart reduce the CO, Less renin secretion) (Hyperglycaemia And the 2nd and 3rd degree heart
Propanolol- failure with reduced EF - step Hyperlipidaemia block - haemodynamic instability ( thiazide diuretics -
non-selective B1 2 - B1 - vasodilation For the heart failure-(Slower heart Hyperuricaemia) hyperglycaemia)
Sotalol- - B2 - bronchodilation rate, increase in the diastolic filling - Masks tachycardia induced by Hepatic failure
non – selective B1 AF – rate control period so increase in the CO so insulin induced hypoglycaemia
Metoprolol - IV In heart failure- reduces remodeling good for heart failure) - - Lethargy
and improves systolic function, b1 - Impotence
receptor - less renin

Beta Blocker labetalol Gestational hypertension - for Use in pregnancy Decrease the SNS activity
hypertension Block the Nad in the In beta 1
adrenoceptor and reduce the CO,
Less renin secretion)
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Statin - ATORVAstatin- first Decreases LDL level HMG - Co A reductase - rate limiting Competitive inhibitor of HMG- Myalgia- diffuse muscle pain( increase in Renal impairement Grapefruit juice - inhibit
pass metabolism - Increases HDL level enzyme of mevalonate pathway to CoA reductase CPK) Liver impairement CYP3A4
active derivatives 24 Decrease Triglyceride levels cholestrol production from acetate Rhabdomylosis Pregnancy Amiodarone- myalgia
h half life - Need full lipid profile Upregulation of hepatic LDL GI disruption breastfeeding
HDL carrier of cholesterol away from receptors Nausea Take it at night cos the
Target- >40 % reduction in the circulation to liver for recycling. Increased clearance of circulating Headache cholesterol synthesis
SIMVAstatin - non- HDL-C at three months LDL takes place when the dietary
prodrug activated by Reduction in the total cholesterol Reduced CVS risk: Improved Increased liver enzymes intake is low.
first pass - half life is DOSE DEPENDANT causes the 15% reduction in the
2 hours - must be REDUCTION CHD mortality and 11% in total vascular endothelial function- NOCEBO EFFECT - when negative Amlodipine-increase the
taken 4 times a day Primary prevention – 20 mg mortality. Decrease endothelin, increased NO expectations of the patient regarding plasma level of statin
Atorvastatin once daily (vasodilation)
a treatment cause the treatment to
CYP3A4 expression (risk of 10 year CVD >10% LDL and the risk of atherosclerosis Stabilisation of atherosclerotic CY3A4 inhbitor-
is important using QRISK - cheap so cost • Accumulation of the LDL at the plaque – decrease in the SMC have a more negative effect than it -amiodarone
- can act as inducers benefit for prescribing for intima causes the oxidation by local proliferation and increase in collagen otherwise would have -diltiazem
and lower threshold - worth endothelial cell products (strengthen) -when off statins does muscle pain -macrolides
inhibitors(increase or benefit) • Oxidised LDL recruit monocytes Improved Haemostasis – decrease persist -increases plasma statin
decrease Secondary prevention( have • Monocytes causes the uptake of the plasma fibrinogen and platelet
in the plasma) had a major CV event)- 80 oxidised LDL via scavenger aggregation, increase fibrinolysis Maybe appropriate to
mg Atorvastatin receptors Anti- inflammatory- decrease withhold statin short-term
Rosuvastatin- has CKD - 20 Mg - lower • Foam cell formation proliferation of inflammatory cells whilst taking other agents
the best • Foam cell become necrotic – and into plaque, reduced CRP,
efficacy Long term effect of decreasing build up in the intima and the adhesion molecules and cytokines
Cerivastatin - mortality after the MI so you endothelial space Antioxidant- decrease superoxide
associated with the give to the patient after MI • Intima thickens and formation
renal failure and • smooth muscle proliferation
rhabdomylosis - Small NNT - 17-20 • Plaque builds up and rupture
forming the thrombus
• Fatty streak develops
Fatty streak are seen in the people
as young as 10- 20 year age group
as well.

Cholesterol - bile acids, steroid

hormones, membranes, vit D

Fibric acid derivatives( Fenofibrate – Hypertriglyceridaemia (with Decrease LDL – increase LDL receptor GI upset Photosensitivity Warfarin potentiation- risk of
Fibrates) albumin bound combination of diet) affinity for its receptor Cholelithiasis - gall stones Gall bladder disease Bleeding - increase
Hyperlipidaemia with low HDL Increase HDL Myositis- inflammation of the muscle anti-coagulation
levels but do not respond to Decrease Triglyceride( predominant Abnormal LFTs
the Nicotinic acid effect)
Co-prescribed with statin
Activation of the nuclear transcription
factor – PPAR alpha
Increase the expression of the gene
which causes the increase in
production of lipoprotein lipase –
increase clearance of triglycerides
Increase fatty acid uptake by the liver

Cholesterol absorption Ezetimibe- half life- Only used in conjunction with Secondary preventionn alreadyb Acts at the brush border of the small Headache Hepatic failure
inhibitors 22 hours the other drug had a CVd event - aiming for intestinal mucosa inhibiting NCPC1L1 Abdominal pain
No dose escalation - fixed 2.0mmol/L LDL cholesterol transporter Diarrhoea
dose at 10mg 10 mg SID 4.0mmol/L total cholesterol WHEN USED WIITH
Decreases LDL – hepatic LDL receptor STATINS - increased risk of
Statin and ezetimibe- - More serious - lower expression increases rhabdomyolosis + ciclosporin
 synergist action – targets No effect on the HDL and
benefit in CKD and Triglyceride
secondary CVD 40mg simvastatin + 10mg ezetimibe -
Prevention better both in long term Total cholesterol level decrease due to
-if statin not tolerated - or reduction of absorption of cholesterol by
only low dose tolerated Primary prevention aim for the gut - 50%
[Link]/L LDL and 5mmol/L total
cholesterol Prodrug- They only undergoes
Ezetimibe with fibrates or enterohepatic circulation so doesn’t
NA – familial pass the systemic circulation so less
Hypercholesterolaemia side-effect

PCSK9 inhibitors Alirocumab - Long term effects on -When LDL attaches to the LDL-R, No offsetting safety concerns + major
Evolocumab cholesterol lowering and receptor is internalised, adverse CV events
CVD risk unknown -LDL catabolised and receptor degraded
- Lifetime injections - or recycled in the cell of the liver - New drug - currently patented
expensive £100 per week -When the PCSK9 binds to the
- NICE recommend in primary receptors on the liver, it will promotes the
and secondary - degradation of the LDL receptors
RESISTANT FAMILIAL
HYPERCHOLESTEROLEM With inhibitor - more LDL receptors -
IA - high risk secondary more internalisation and degradation -
prevention removed from circulation
- PCSK9 inhibitors are
monoclonal
antibodies.

Non POM options Plant sterols Work with statin but not Some plant sterols have cholesterol Found in the legumes, grains –
ezitimibe ( compete in same lowering effects ( approx 0.7mmoll/L)
way ) structurally similar to cholesterol-
competing for the absorption

Fish oils
Fibre
Vitamin C/E

Alcohol- increase the HDL level

but increase the TG levels as well
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Oestrogen (sex steroid) Oestradiol Steroid hormone receptors - Synthetic oestrogen PK- Nausea and Vomiting
Ethinylestradiol - classic nuclear receptors- Oral and transdermal for the route of Water retention
effect through gene administration - absorbed from skin Sodium and water retention Breast tenderness
transcription - also have and mucous membrnaes + GI tract Raises HDL, lowers LDL Increase blood coagulability
membrane Decrease bone resorption VTE- venous thromboembolism
Metabolised in the liver and Mild anabolic Impaired glucose tolerance
- Therefore lag between excreted in the urine as the Impaired glucose tolerance Endometrial hyperplasia and cancer
receptor binding and effect as glucuronides and sulfates Increase blood coagulability Ovarian metaplasia and cancer
gene transcription must Breast hyperplasia and cancer
happen - Stimulates the growth of the
endometrium and breast OESTROGEN 9
All sex steroids are
synthesised from cholesterol - increase the production of
progesterone receptor

Progesterone (sex steroid) Levonorgestrel Synthetic progesterone PK- Secretory endometrium Fluid retention
Medroxyprogesteron Bound to the albumin and stored in Anabolic Acne
e acetate the adipose tissue Increase bone mineral density Nausea and vomiting
Norethisterone Metabolised in the liver and Mood changes PMS- premenstrual syndrome
Levonorgestrel excreted in the urine conjugated to Depression, irritability
the glucuronic acid Lack of concentration
Weight gain
Maintains pregnancy

- Stimulates the growth of the

endometrium and breast
- maintains the pregnancy and
inhibits the production of
oestrogen receptor

Testosterone (sex steroid) Stimulates the male characteristic, increase the HDL to LDL ratio ( Acne
hairy body, deep voice, anabolism, meaning less HDL compare to the Voice changes
Aggression LDL) so increase the risk of Increase aggression
atherosclerotic disease in males

Male secondary sexual characteristics

Anabolic

Combined Oral e.g. Ethinylestradiol Contraception Metabolised in liver by CYP450s Prevents the ovulation and reduces Venous Thromboembolism Smoking, obesity and hypertension All of them are enzyme
contraceptives pills (Synthetic oestrogen) Emergency contraception for the endometrial receptivity to increase inducing drugs-
and levonorgestrel( the levonorgestrel Soya protein- enhances oestrogenic inhibit implantation the risk of the VTE Anti- epileptics –
Synthetic effects - reduces its storage in carbamazepine or phenytoin
progesterone) adipose and muscle - therefore Thickens cervical mucus to inhibit – decrease the level of COCP
dependent on the reduces half life - 15 to 7 hours penetration of the sperm Antibiotics- rifampicin and
CYP450 rifabutin -
Decrease the levonorgestrel
level
Natural products- St John’s
Wort - by increasing the
production of hepatic
CYP450-
reduce the efficacy of the
COCP
HRT Oestradiol and Menopause - women with ROA – oral ,transdermal, BREAST CANCER - breast hyperplasia -
Medroxyprogesteron uterus implant, transvaginal, nasal short term use
e acetate
NOT FOR HEART DISEASE Increase risk of VTE
Increase risk of ischaemic heart
To prevent osteoporosis disease
To prevent symptoms such as
the hot flushes, sweats and Venous thromboembolism
dyspareunia (vaginal atrophy Increase the chance of having Stroke
due to lack of oestrogen) – oral only
Ovarian cancer
Beneficial effect on the lipid
profile (lowers LDL) but
doesn’t use just
to lower the CVS risk ( not if
patient obese etc)

Hormone replacement Menopasue women after Anabolic Endometrial hyperplasia and cancer Women with uterus
therapy- Synthetic Oestrogen Estradiol hysterectomy Raises HDL, lowers LDL Ovarian metaplasia and cancer
only Decreases bone resorption Breast cancer- long term use
Increase blood coaguability Venous Thromboembolism
Sodium and water retention Water retention
Impair glucose tolerance Impaired glucose tolerance
Breast tenderness
Nausea and vomiting

Finasteride Finasteride BPH Preventing enzyme which converts Sexual dysfunction

testosterone to DHT Erectile dysfunction
Decrease libido
Acting by shrinking the prostate
by means if androgen deprivation

Progesterone receptor Mifepristone Termination of pregnancy Sensitising the myometrium to Abdominal cramp
Antagonist prostaglandin-induced Dirrahoea
- RU486 contractions which causes the Infection
termination of the pregnancy Nausea
Vomittng
PID

Selective Estrogen Receptor Clomifene Treatment for infertility Acts as the partial agonist to Angioedema History of thromboembolism
modulator (SERM) anovulation compete with the oestrogen for the Alopecia
-Anti- oestrogens oestrogen receptor in the Abdominal distension1
hypothalamus binding which anxiety
causes the AP to produce the FSH - Abnormal uterine bleeding
creates an LH surge Hormone-dependent tumour

Selective Estrogen Receptor Tamoxifen Breast cancer- ER antagonist Prodrug- first pass metabolism in Endometrial cancer-ER agonist
modulator (SERM) - the liver Alopecia
Anti- oestrogens If the liver function is reduced, it Thrombosis and embolism
means that the active metabolite Fluid retention
will be decreased so need higher Anaemia
 dose to reach to the therapeutic
Action.
• In endometrium, acts as ER agonist
- Binding to the oestrogen
receptor in the breast causing
the cell cycle to arrest

Selective Estrogen Receptor Raloxifene Prophylaxis for the post- ER agonist and mimic the action of Leg cramps History of VTE
modulator (SERM) - Bone menopausal osteoporosis oestrogen in the bone Vasodilation
resorption inhibitors Prevent the risk of osteoporosis Peripheral oedema
Influenza

Selective Progesterone Ulipristal acetate Emergency contraception Delay or inhibit the ovulation Breast tenderness
receptor modulator with the Levonorgestrel Uterine fibroids Nausea and vomiting
partial progesterone Progestogen GI discomfort
antagonist Dizziness
Back pain

Bisphosphonates Alendronic acid Reduce bone turnover - PK - Control osteoclast activity Upper GI effects
OSTEOPOROSIS long half life - oesophagitis - stress important of
Prophylaxis and treatment Poor gut absorption remaining standing or sitting upright 30 mins
Absorption affected by food - must be after taking
Other diseases involving bone taken on empty stomach
e.g malignancy - pagets - hypocalcaemia - check vit D and calcium
levels prior to treatment
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Ultra-fast acting insulin Type 1 diabetes Get absorbed more quickly Hypoglycaemia
Aspart(FiASp) Beta cell failure Inject just before eating Hyperglycaemia
Insulin peaks about 30- 50 minutes Fine balance
Onset of action 10-15 mins Lipodystrophy- lipohypertrophy or
lipoatrophy
Painful injection- scarring
Rapid acting insulin Novorapid Rapid onset of action 5- 15 minutes Insulin allergies
Inject just before eating
Peaks ≈ 60 minutes
Last for 4 to 6 hours Contra - renal impairment
DDI - systemic steroids (cortisol) , other
hypoglycaemics
Short acting insulin Soluble insulin Start to work 30 to 60 minutes
Humulin S Inject at least 15- 30 minutes
Actrapid before the meal- several times a
day
Peaks≈2-3 hours
Duration ≈ 8-10 hours

Intermediate acting insulin Isophane insulin- Three times a day

Humulin I Slower onset 2-4 hours
nph Peaks 4- 8 hours
Duration up to 12- 20 hours

Long and very acting insulin Insulin Glargine Slow onset 2- 6 hours
Insulin D Duration up to 24 hours
egludec Very long up to 50 + hours

Biguanides Metformin- oral Type 2 diabetes – non- insulin Some gluconeogenic activity remains Decrease hepatic glucose GI upset - nausea, vomiting, diahorrea Drugs that impair renal
therapies and the life-style so risk of hypoglycemia reduced Production by inhibiting gluconeogenesis Excreted unchanged by kidneys function
Modification (Lactic acidosis – rare Impaired kidney function- CKD- - ACEi, diuretics, NSAIDs
1ST DRUG GIVEN - can be Suppresses appetite so limits weight Limits weight gain Vit B12 deficiency – rare GFR<30 ml/min
taken with others gain Nephrotoxic - loop and thiazide like
Weight gain Hypoglycaemia) Alcohol intoxication diuretics - increase glucose -
Hypoglycaemia – fears of Decrease CVS event reduce metformin action
patient

Sulphonylureas Gliclazide- oral Type 2 diabetes REQUIRE RESIDUAL PANCREATIC Stimulate the beta cell to release mild GI upset – nausea, vomiting, diarrhoea, hepatic and renal disease – caution, other hypoglycaemic agents
FUNCTION insulin hypoglycaemia (works at low [glucose]) those at risk of hypoglycaemia
Typically in combination with - ATP sensitive K channel blocker loop and thiazide like
others or if metformin Weight gain through anabolic effects - depolarises membrane diuretics ↑glucose so can
contraindicated of insulin - Ca2+ influx - insulin vesicles - insulin reduce SU action
secreted

Thiazolidinediones- rarely Pioglitazone - oral Type 2 diabetes t1/2 not related to duration of action – Increase insulin sensitivity in GI upset, fluid retention, fracture risk, heart failure because of fluid retention other hypoglycaemic agents
prescribed Rosiglitazone 6-8 weeks for benefit muscle and adipose tissue and bladder cancer
decrease hepatic glucose output
Weight gain because of fat cell PPAR gamma receptor agonists - gene
differentiation transcription

Glucagon- like Peptide 1 Exenatide – Type 2 diabetes Physiological effects of GLP-1: ↑glucose dependant synthesis of insulin GI upset, decreased appetite with weight Renal impairment other hypoglycaemic agents
Agonist parenteral – sc Pancreas: secretion from β-cells activate GLP-1 loss
Liraglutide ↑Insulin secretion (glucose receptor – resistant to degradation by
(incretin mimetics) dependent) DPP-4
↓Glucagon secretion
 ↑Insulin biosynthesis
Brain:
↓Food intake through increased
satiety
Liver:↓Glucose production
Muscle: ↑Glucose uptake
stomach:↓Gastric emptying

Subcutaneous injection
NICE suggest add-on if triple therapy
ineffective
Promote satiety – possible weight
loss?

Dipeptidyl peptidase- 4 Linagliptin Type 2 diabetes Supress appetite ~ weight neutral Prevent incretin degradation - ↑[plasma] GI upset, small pancreatitis risk (up to 1%) avoid in pregnancy, history of other hypoglycaemic agents,
inhibitors Sitagliptin incretin levels Glucose dependant so pancreatitis drugs ↑glucose can oppose
postprandial action do not stimulate gliptin action – thiazide like
insulin secretion at normal blood glucose and loop diuretics
– lower hypoglycaemic risk

Sodium- glucose co- dapagliflozin Type 1 and 2 diabetes Modest weight loss, hypoglycaemic ↓↓glucose absorption from tubular filtrate, UTI and genital infection, thirst and polyuria risk of DKA in TIDM, possible antihypertensive and other
transporter 2 inhibitors canagliflozin risk is low ↑urinary glucose excretion competitive hypotension hypoglycaemic agents
reversible inhibition of SGLT-2 in PCT
Session 6 Anti Arythmmics

Class 1B - fast Lidocaine - IV only Ventricular tachycardia - - ECG - increase in QRS in - Blocks Na+ channel and slows Abdominal upset Not used in atrial arrhythmias or AV
Mexiletine - oral only during ischaemia fast beating or ischemic - no conduction Less proarrhythmic junctional arrhythmia
Na channel blocker change in normal - Na channel blocker in the phase CNS effect : dizziness, drowsiness
Nerve block – blocking the 0
neuromuscular junction - Lidocaine works on open or - No change in the phase 0 in
inactive Na channel - found normal tissue
Not used in atrial arrhythmias in damaged myocardium - Decrease in the phase 0
or AV - Lidocaine dissociates conduction in fast beating or
junctional arrhythmia quickly - no effect on normal ischaemic tissue ( use
tissue dependant block)
- Blocks current after - Increase threshold of Na
depolarisation, but - Fast binding offset kinetics
dissociates before next AP

Class 1C - fast Flecainide - oral or iv ● Wide spectrum ● Increase in PR, ● Na channel blocker in the Proarrhythmia
( propafenone) ● AF- rhythm ● increase QRS, phase 0 Sudden death
Na channel blocker control(long- term) ● increase QT ● Very slow binding offset kinetics CNS and GI effect
● Supraventricular ● Decrease in phase 0 in normal
arrhythmias - tissue
fib/flutter ● Decrease in automaticity-
● Wolff- Parkinson increase in threshold of Na
white syndrome ● Increase APD and refractory
Period - esp in rapidly
depolarizing atrial tissue
K+ blocking effect

Class 2 - slow Bisoprolol- oral ● AF- rate ● ECG- Increase in PR, Increase Action potential duration ● Bronchospasm -B2 agonist ● Don’t use in partial AV block ● Thiazide-
Propanolol - oral/iv control(short-term) ● decrease in HR and refractory period in AV node ● Hypotension or acute heart failure – hyperglycaemia
beta blocker Metoprolol- oral or IV ● Sinus and to slow AV conduction velocity ● Raynaud’s bradycardia ● CCB-verapamil-
catecholamine - Slows conduction at AV and ● Hyperglycaemia ● Asthmatic and COPD patient decrease the SV
Esmolol: iv only (very dependent sympathetic activity via B1 ● Hyperlipidaemia ● 2nd and 3rd degree heart
short acting T½, 9 tachycardia adrenoceptors ( SVT/Post ● Hyperuricaemia block
min) ● Converting re-entrant MI)
arrhythmia at AV
node

Class 3 - fast and slow Amiodarone – oral or Most arrhythmias ● ECG- increase in PR, Block the K channel ● Pulmonary fibrosis If it the patient has been
iv - half life 3 ● increase in QRS, - Can also act on the Na, Ca and ● Hepatic injury prescribed with the
K channel blocker MONTHS ● increase QT, also acts as the B blocker as ● Optic neuritis digoxin, may need to reduce
Central line ● Decrease in HR well ● Photosensitvity the dose as well
Has class 2 effect ● Thyroid disease as monitor warfarin more
So the refractory period increase and ● Increase LDL level closely
increase action potential
duration(APD) HITOPP

Increase in threshold
Decrease in the phase 4
Decrease in the speed of the AV
conduction

Class 3 – slow and fast Sotalol - although a Wide spectrum: ● ECG- increase in QT, Increase in the action potential Proarrhythmia,
K channel blcoker beta blocker - has supraventricular and ● Decrease HR duration and refractory period in fatigue,
some class 3 effects ventricular tachycardia atrial and ventricular tissue insomnia

Oral Slow AV conduction

Slow phase 4 (b-blocker)
Class 4- CCB- slow Verapamil- oral or iv Verapamil and diltiazem- AF – ● ECG- increase in PR, ● Block the Ca channel in the GI problem – constipation Partial AV block B blocker- decrease CO –
Diltiazem- oral rate ● Decrease in HR phase 2 lead to asystole
control ● Slow conduction through AV Not given in Hypotension, decrease in
Supraventricular tachycardia ● Refractory period in AV node CO or sick sinus
Angina ● Slope of phase 4 in SA to slow
HR – funny current

Adenosine - slow Adenosine - rapid IV Convert re-entrant - Acts on A1 receptors at AV node Abdominal discomfort
bolus supraventricular arrhythmias but has a very short half-life Arrhythmia
• Enhances K+ conductance – AV block
hyperpolarises cells of conducting tissue
(3 A’s
Decrease in the action potential A1 receptor)
duration
Causes the potassium current activation
in the SAN and AVN

Repolarisation occurs quickly- causes the

hyperpolarization-
causes the decrease in HR

Decrease in the Ca currents –

increase in the refractory in AV node

SLOWS AV CONDUCTION

Ivabradine Ivabradine – iv Reduce inappropriate sinus Blocks the funny current highly Flashing lights Avoid in pregnancy- teratogenicity
tachycardia expressed in sinus node
Reduce heart rate in heart Slow the sinus node but does not
failure affect blood pressure
and angina

Cardiac glycoside Digoxin AF – sinus rhythmn – rate ● Enhances the vagal activity Arrhythmias Loop and thiazide –
control- not the first line ● Increase the SV and reduces the Nausea and vomiting hypokalaemia
conductivity of the AV node and Hyperkalaemia
Heart failure in the sinus slow HR
rhythm patient ● Increase in K current – slow HR
● Decrease in Ca current –
increase
● Ca intracellularly – SV
● Increase in refractory period-
slow HR
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Session 6
antiplatelets/fibrinolytics

Antiplatelet -cyclooxygenase Aspirin Antiplatelet dose - baby • Absorbed by passive diffusion – COX-1 inhibitor and reduces Higher dose causes the bleeding time ● Reye’s syndrome – avoid caution - other antiplatelet

lox
inhibitor aspirin 75mg - LEARN hepatic hydrolysis to salicylic acid thromboxane A2 production from to prolong, causing the haemorrhagic <16 years and anticoagulants

I
High dose- analgesic arachidonic acid and inhibit the stroke and GI bleeding ● Hypersensitivity (additive/synergistic action)
Often co prescribed with other platelet aggregation – irreversible( ● 3rd trimester – premature
1. AF before considering antiplatelet agents not the receptor, the platelet hypersensitivity closure of ductus arteriosus COX-1 polymorphisms result

1
anticoags aggregating agent) in lack of efficacy in some
2. Secondary prevention of the Gastric protection required for long Inhibition last for the life span of the
stroke and the TIA (if others term use in at risk patients (proton platelet- 7 days
Glupses
are Contraindicated)
3. Secondary prevention of the
Acute coronary syndrome
pump inhibitor)
Higher does inhibit the endothelial PGI2
prostacyclin- analgesic function
linerbrain variation in
4. Post PCI and stent to damage u Cox i
serian should doesn'twork
reduce the ischaemic
complications

NSTEMI/STEMI - initial once

only 300 mg loading dose – notgiven vwere
chewable is best!
Acute ischaemic stroke children
initial 300 mg daily 2 weeks

(Secondary prevention of MI in
stable angina)

Anti-platelet Clopidogrel -need 1. Arterial thrombosis Ticagrelor acts reversibly at different Inhibit the binding of the ADP to # Bleeding! GI upset – dyspepsia and caution in high bleed risk patients clopidogrel requires CYPs for
loading dose 2. Reduces morbidity and site to clopidogrel and has active P2Y12 receptor causes the diarrhoea with renal and hepatic activation
ADP receptor antagonists Half-life- 7-8 hour mortality post-thromboembolic metabolites inhibition of the GP2b/3a rarely - thrombocytopenia impairment
Low onset of action stroke Receptors CYP inhibitors – omeprazole,
without the loading 3. Reduces secondary events • ticagrelor plus aspirin compared to - Independant of cox pathway ciprofloxacin, erythromycin,
dose post MI(take until 12 months clopidogrel plus aspirin Inhibit the activation of the GP2b some SSRIs ( ECOS)
post MI) with the addition of “….significantly reduced rate of death and 3a receptors – irreversible
Ticagrelor the aspirin from vascular causes….” at 12 Inhibitors need to consider use of other
Prasugrel 4. Secondary prevention in months PPIs with clopidogrel
- More rapid onset patient intolerant to aspirin • Faster onset of action, more GP2b and 3a receptors preventing
of action predictable - PLATO STUDY the fibrinogen binding ticagrelor can interact with
CYP inhibitors and inducers
Clopidogrel mono therapy
where aspirin is caution when co prescribed
contraindicated with other antiplatelet and
NSTEMI patients – 3 months anticoagulant agents or
STEMI patients - up to 4
weeks NSAIDs – increased
bleeding risk
Ischaemic stroke and TIA
long term secondary • clopidogrel needs stopping
prevention ~ 7 days prior to surgery in
most patients
• Prasugrel and ticagrelor
with aspirin in ACS patients
(undergoing PCI) for up to
12 months

Anti-platelets - Dipyridamole • Secondary prevention of dipyridamole inhibits cellular reuptake of Vomiting diarrhea Δ antiplatelets and
Phosphodiesterase inhibitors ORAL ischaemic stroke and TIAs adenosine → increased [adenosine] → dizziness anticoagulants, adenosine
• Adjunct for prophylaxis of inhibits platelet aggregation via adenosine
thromboembolism following (A2) receptors
valve replacement Stroke –
modified release Also acts as phosphodiesterase inhibitor
Arterial thrombosis which prevents cAMP degradation →
inhibit expression of GPIIb/IIIa

Antiplatelets- Glycoprotein 2 Abciximab Arterial thrombosis Target final common pathway – more Monoclonal Antibody irreversibly Bleeding risk- more than any other
b /3a inhibitors Ivi with bolus complete platelet aggregation blocks the GP2b and 3a receptors type of drug - dose adjustment for body
Half- life – 30 mins preventing the fibrinogen binding and von weight
>80% reduction in aggregation Willebrand factor (vWF) Thrombocytopenia – do the platelet
count
Administered i.v. Although half- life is 30 mins, slow Expensive drug
dissociation means the effect last
Specialist use in high risk for 12-36 hours post infusion.
percutaneous transluminal coronary
angioplasty patients with other drugs

fibrinolytics Streptokinase: Arterial thrombosis Streptokinase can only be used once Dissolve the fibrin meshwork of Bleeding Other antiplatelets and
Alteplase Short infusion – antigenic (not as antibodies develop the thrombus anticoagulants
Reteplase work in repetition) CVS effect- haemorrhage
Given until the PCI can be Alteplase in acute ischaemic stroke Bind to and activate the Haemorrhagic stroke
performed <4.5 hours from symptoms plasminogen to the plasmin. Heart failure
And depending on the severity Plasminogen dissolves the fibrin
of the symptoms • Following STEMI diagnosis acutely clot.
Maybe post MI? vs. primary PCI

Offer primary PCI if indicated, as

the preferred coronary reperfusion
strategy for people with acute
STEMI if:
- presentation is within 12
hours of onset of
symptoms and primary
PCI can be delivered
within 120 minutes of the
time when fibrinolysis
could have been given.
• ACEi should be offered to all
patients post MI once
haemodynamically stable

Anti-fibrinolytic Tranexamic acid menorrhagia Inhibit the activation of the fibrin

to the FDPs
IV or I.a
So the fibrin clot is not destroyed
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

RESP PHARM SESSION 9 ASTHMA STEPS: ACUTE SEVERE STEPS: COPD MANAGEMENT: Acute exacerbation of COPD
1. Oxygen - high flow - aim to 1. Confirm diagnosis - prost 1. Nebulised salbutamol and/ or
Step 1 – don’t give – just use keep o2 94-98% bronchodilator obstructive ipratropium - if patient is
the B agonist 2. Nebulised salbutamol- spirometry hypercapnic - nebulising should be
Step 2- low dose ICS continuous if necessary - 2. Smoking cessation driven by air not oxygen
Step 3 a – add LABA (inhaled) oxygen driven 3. MRC dyspnea score 1. Oral steroids - can be less effective
and ICS 3. Oral prednisolone- a 4. Vaccination - flu + pneumococcal than in eosinophilic asthma due to
Step 3 b- if LABA not minimum of 5 days - give 5. Medications depending on reduced action of neutrophils
effective, stop LABA and paarenteral if not tolerated severity 2. Antibiotics- increase spectrum
increase dose of ICS to orally coverage with severity
medium or add LTRA 4. If not responding or LIFE 3. Review chronic treatment and
If LABA is effective, continue THREATENING- add action plan
LABA and increase ICS nebulised ipratropium
Step 4 – Increasing ICS up to bromide - SAMA
high dose 5. Consider IV aminophylline if
Step 5- Maintain high doser of life threatening/ near fatal
ICS and no success with above -
caution if taking oral
theophylline

ICA - inhaled corticosteroid beclomethasone Step 2 of the regular preventer Pass through plasma membrane, - Stops mucosal inflammation, Not many Pneumonia risk in COPD patients Few if taken correctly
Budesonide Therapy activates cytoplasmic receptors, widens airway, reduces mucus - If absorbed orally - candiadisis, at high doses
Anti-inflammatory effect fluticasone activated receptor then passes in to - Reduces symptoms, reduces hoarse voice - local
High dose ICS for the step 3 nucleus to modify transcription exacerbations, prevents death immunosuppression

Step 4 – high dose Rapid inactivation by hepatic - Prevent the Il 1 and 6 and TNF Beclomethasone absorbed thrugh gut
biotransformation following alpha and lungs
systemic absorption and only some - Also target the expression of Budesonide and fluticasone undergo
active and go to systemic anti-inflammatory products- Il 4 - the extensive first- pass metabolism
circulation increase - All the potential to produce the
- Inhibits arachidonic acid systemic side effects
- Poor oral bioavailability ,
lipophilic side chain added -
ihg affinity for GC receptor

SABA - b2 agonist Fast acting - ● ALL step of the ONLY USED AS REQUIRED - Agonist for b2 receptor - causes - Adrenergic: tachycardia(B1), - Beta blockers may
salbutamol asthma control bronchodilation - symtpom relief palpitations, tremor reduce effects
terbutaline ● Fast onset, short - Improves cilia function - mucus - Increase glycogenolysis and renin
duration cleaance - SVT
● If you have the CVD - tachycardia may provoke angina
asthmatic attack
- acute exacerbation
- Prevention of
bronchoconstriction prior to
exercise

LABA Salmeterol ● Add on therapy after Add on therapy with ICS - ONLY Reversal of the bronchoconstriction on CANNOT BE USED ALONE -
formoterol step 2 Can mask airway inflammation and the smooth muscle of the lungs USE WITH ICA
near fatal attacks
● Fast onset, long Prevention of bronchoconstriction
duration- formoterol during the exercise

● Slow onset, long Increase in cAMP by inhibiting the

duration-salmeterol phosphodiesterase

Used regularly, they reduce the

 asthma control

Inhibit the mast cell degranulation if you

use it intermittently

Will cause the mast cell degranulation if

you use it regularly

LABA and ICS Beclomethasone + Add on therapy after step ● Ease of use
formoterol - 2 ● Compliance increased- 1
symbicort versus 2 prescription to
worry about
● Cheaper than 2 individuals
inhalers
● Safety - LABA WITH ICS

LTRA ( leukotriiene receptor Montelukast LABA alternative in NICE Alternative to LABA in NICE LTC4 release by mast cell and - Headaches Used as an add on None reported
antagonist) Taken orally guidelines - useful in 15% of patients eosinophils can induce - Dry mouth
- most end up using LABA anyway bronchoconstriction, mucus - Gi problems
secretion and mucosal oedema, - hyperactivity
and promote inflammatory cell
recruitment
LRAs block the effect of cysteinyl
leukotrienes in the airways at the
CysLT1 receptor

LAMA tiotropium Step 4/5 of asthma – Anti- cholinergic – bind to M3 Glaucoma Generally ok for most people with
severe COPD Block the muscarinic effect – Dry mouth inhaled route
preventing the vagally mediated Urinary retention
Long acting so once daily bronchoconstriction Dry eyes
- Infrequent - anticholinergic effects

SAMA Ipratropium (ipratropium less selective for M3

bromide receptors compared to
tiotropium, M2 activity too

Methylxanthine Theophylline Step ¾ NARROW THERAPEUTIC INDEX Antagonise adenosine receptors NARROW THERAPEUTIC INDEX CYP450 inhibitors -
Good for aspirin induced Inhibit phosphodiesterase – Life threatening complications - increases
Aminophylline - IV asthma and poorly controlled increase cAMP – relaxation of arrythmias - must measure plasma concentration of
in LTAA - caution asthma smooth muscle airways conc theophyllines
when with theo Inhibits bronchoconstriction
GI session 10

Alginates and Antacids Gaviscon Peptic and duodenal ulcers Sodium alginate + magnesium Buffers stomach acids Magnesium salts - dishorrea Na+ and K+ containing preparations Can reduce absorption of
carbonate/ aluminium hydroxide Increase stomach content viscosity + Aluminium salts - constipation should be used with caution in renal many drugs so doses
reduce reflux failure should be separated (PPI
High [sucrose] in some inhibit the CYP2C9 or
preparations – hyperglycaemia in CYP2C19 which decrease
DM the metabolism of drugs)

Increased urine alkalinity

can increase aspirin
excretion

Proton pump inhibitors (PPI) Lansoprazole Peptic and duodenal ulcers Shortest effective duration at lowest Irreversibly inhibit the H+/K+ ATPase in GI disturbance – abdominal pain, Mask symptoms of Omeprazole CYP inhibitor –
Omeprazole effective dose gastric parietal cells constipation diarrhoea gastro-oesophageal cancer reduced clopidogrel action
GORD Final stage in the pathway – very
Esomeprazole Zollinger- Ellison syndrome • Often prescribed along side long significant reduction in acid secretion Headache, dizziness Osteoporosis – fracture risk PPIs can increase effects of
– short half life Helicobacter plyori eradication term NSAID or steroid Drowsiness/confusion warfarin and phenytoin -
– amoxicillin, clarithromicin monitor
and lansoprazole

H2 receptor antagonists Ranitidine Peptic and duodenal ulcers Other routes to pump inhibition mean Inhibition of H2 receptors – local # generally well tolerated - diarrhoea, Mask symptoms of Few common DDIs –
only partial reduction in acid histamine release contributes to proton headache gastro-oesophageal cancer, renal (reduced exposure to some
secretion pump activation impairment antivirals and protein kinase
inhibitors)
Current large scale recall on most
ranitidine containing products due to
possible carcinogenic contaminant -
lansoprazole typically first alternative
upon patient review

Aminosalicylates Mesalazine first line treatment in mesalazine has no role in Release of 5-aminosalicylic acid GI disturbance – nausea, dyspepsia are salicylates like aspirin – similar Enteric coated tablets may
ulcerative colitis (UC) rheumatoid arthritis Anti-inflammatory leukopenia - rare hypersensitivity break down quicker in
presence of PPI (because of
sulfasalazine has more side effects Topical action at the colon (enteric coated ↑pH)
so used infrequently for UC but sulfa tablets limit gastric breakdown)
group good for rheumatoid arthritis

Muscarinic receptor Hyoscine Anti - emetic Patch - good for who can’t take Competitive blockade of Side effects
antagonist hydrobromide People who can’t take tablets tablets muscarinic acetylcholine receptors • Sedation
Motion sickness – first line In the vestibular nuclei and the ctz • Memory problems
Bowel obstruction Agents acting on the vestibular nuclei which is in the medulla • Glaucoma
CTZ sits under the fourth ventricle • Dry mouth and constipation

H1 receptor antagonists Cyclizine Motion sickness - second after Agents acting on the vestibular In the vestibular nuclei Sedation Cyclizine- not used in the older ladies
HH fewer side effects - nuclei Inhibits the histaminergic signals Excitation and the
Cinnirazine- for CINNIRAZINE from the vestibular system to the Antimuscarinic – dry mouth, children
motion CTZ in the medulla constipation, urinary retention
sickness but need to Bowel pathology- first line Cardiac toxicity- long Qt interval
be active with or without
ondansetron- such as
Promethazine- the obstruction, GORD, IBS,
morning IBD,
sickness in the cancer
pregnancy

Levomepromazine
Diphenhydramine
Serotonin(5HT3) receptor Ondansetron motion sickness Acts on the visceral afferent in the 5HT produces by the ECF cell Side effects - uncommon
antagonist gut by(main effect) • Constipation
Granisetron Bowel pathology- first line- • Headache
Palonosetron such as Almost everyone – it’s often the Reduces the GI motility- • Elevated liver enzymes
5HT3- serotonin the obstruction, GORD, IBS, 1st line treatment peripheral
IBD, cancer along with the • Long QT syndrome
cyclizine 3rd line for hyperemesis Reduce the GI secretion-
gravidarum peripheral • Extra-pyramidal effects – dystonia,
Chemotherapy- after the parkinsonism
dexamethasone- second line Acts to inhibit the CTZ- centrally

D2 receptor antagonist Metacloperamide- • GORD Give in the mother who has just • Increases acetylcholine at muscarinic Galactorrhoea via prolactin release Don’t use if there is obstruction
use in the • Ileus -gut is paralysed- seen given birth because it improves receptors in the gut And if there is risk of perforation-
rescue for the in after the Lactation - domperidone • Promotes gastric emptying Extra- pyramidal effects- dystonia, because it is inflamed and the drug
chemotherapy the bowel operation and • ↑ tone at lower oesophageal sphincter Parkinsonism will increase the peristalsis
related emesis as severe so it closes
well as second infection, sepsis and trauma • ↑ tone and amplitude of gastric Caution of the side effects
line for the contractions
hyperemesis • ↓ tone of pylorus so it opens Sudden cardiac death- long QT and
graidum • Increases peristalsis VT (domperidone)
Domperidone

D2 receptor antagonist The zine’s: Antipsychotics Prochlorperazine in pregnancy Act on the CTZ Extra- pyramidal effects- dystonia
Chlorpromazine Motion sickness May also block the H1 and Parkinsonism
Haloperidol- Vertigo Muscarinic receptors(everything) Sedation
Chemotherapy Chemotherapy and palliation Hypotension
and pallative-
sedative action

Corticosteriods Dexamethasone Perioperative nausea and Acts on the CTZ Insomnia

vomiting May also have the properties on Increase in appetite
Methylprednisolone the D2 receptors antagonist Increase in the blood sugar
Chemotherapy- first line
Palliation

After meningitis, prevention of

the hearing loss

Second line for the bowel

pathology after the
ondansetron and cyclizine

People who have reduced

appetite due to the
chemotherapy

Cannabinoids- synthetic Nabilone Chemotherapy- use as the last Acts on the CTZ Dizziness
analogue of cannabis line drowsiness

Neurokinin 1 receptor Aprepitant Chemotherapy- with delayed Prevent the action of the substance Headache
antagonist emesis P at the CTZ in peripheral nerves Diarrhoea
Fosaprepitant Boost effects of 5H3 receptor Constipation
Netupitant Antagonist Stevens- Johnson syndrome

Anxiolytic and antidepressant

properties – anxiety and
depression
Nasogastric tube Vomiting Empty the stomach and
decompress it so no need to vomit
it
Use in the bowel obstruction –
cancer and IBD

Severe morning sickness – Morning sickness in In pregnancy, you give Rapid rise in the Bhcg stimulates
vomiting pregnancy promethazine(H1) or
Hyperemesis Gravidarum prochlorperazine(D2) the CTZ
Then add metaclopramide(D2) Typically in the first trimester
and Higher risk with the multiple
Then add ondansetron(5HT3) pregnancy

Opioid receptor agonist Loperamide ( gut Traveller’s diarrhoea Lopermide - gi peripheral effects Loperamide- specific to the mu Paralytic ileus
specific - first line) Diarrhoea receptors in the myenteric plexus Nausea and vomiting
Pain Codeine and morphine - peripheral Decrease tone of longitudinal and Sedation and addiction(codeine and
Codeine – converted and central effects circular smooth muscle morphine)
to morphine via Reduces the peristalsis but Constipation(opioid-induced
CYP2D6 increases segmental contractions constipation)
If the patient has the
less CYP2D6, it Decreases the colonic mass
means that there is movement by suppressing
less morphine in the gastrocolic reflex
plasma so need
higher dose. Codeine and morphine- mu and
delta receptors agonist
Morphine Uses when the patient is in pain

Osmotic laxatives Lactulose Constipation Increase the amount of water in the large
Macrogol bowel
Lactulose- hepatic - lactulose Draw fluid in
Movicol encephalopathy or retain the fluid they came in with -
cosmocol macrogol

Stimulant laxatives Docusate sodium Constipation Enhance gut motility and increase water
(glycerin)- Rectal Docusate sodium and electrolyte transfer into the lower gut
irritation and stimulant and stool softener
lubrication(+)
Senna Sodium Picosulfate
bisacodyl
Given orally or per
rectum

Bulk forming laxatives Isphagula husk Constipation Medicinal fibre- Stimulation through
methylcellulose increased faecal bulk, hydrophilic action
causing gut lumen water retention

Stool softeners Arachis oil Constipation Lubrication and break down of

Glycerol stool to aid passing
suppository Decrease surface tension of the
Docusate sodium Stool
Increase penetration of the fluid
into the stool
Session 11 Anti Coagulants For all heparins;

Parenteral anticoagulants – Unfractionated DVT/PE Heparin binding to the Bruising and bleeding Clotting disorders, renal impairment Other antithrombotic drugs,
UNFRACTIONATED Heparin AF Half- life for low dose- 30 min antithrombin(AT3) causes the Intracranial, at site of injection, GI, epistaxis (LMWH and fondaparinux) ACEi/ARB + spironolactone (
HEPARIN Higher dose- 2 hour conformational change and same below)
Inhibit the action of IV UHF for inpatient increase the activity Heptic and renal compromise
the coagulation Iv bolus then iv infusion IV infusion Antithrombin causes the inhibition Heparin induced thrombocytopenia -
See table on differences factors Fast onset Subcutaneous(s.c. for of the 2a and 10a ( but also the 9a, Autoimmune - 2-14 days after initiation of
Heparin normally prophylaxis) 11a.) heparin
produced in the mast Pregnancy To inhibit the 2a, heparin needs to (~1/100 – UFH vs. ~ 1/1000 LMWH)
cell and vascular Parenteral anticoagulants– simultaneously bind the (antibodies to heparin platelet factor 4
endothelium Prevention of VTE - poor GI absorption- large antithrombin and factor 2a. complex produced depletion of platelets but
preoperatively negatively charged molecules paradoxically can lead to thrombosis as
Heparin causes the Cancer related VTE Unfractionated heparin is Monitor the aPTT time when using more platelets activated by damaged
interaction of the large – bioavailability is the UFH endothelium)
antithrombin with the ACS Variable ( binds to endothelial
coagulation factor cells, plasma proteins) Hyperkalamia ( aldosterone inhibition)
1000 times
faster. Osteoporosis is rare- long-term ADR-
higher risk with the UHF- more in

pregnancy
Hpersensitivity rare

Parenteral anticoagulants – Dalteparin DVT/PE Almost always s.c. (enoxaparin i.v. in Do not inactivate thrombin (IIa) – not long Thrombocytopenia (less likely than
Low molecular weight Enoxaparin AF / ACS ACS) enough the UFH)
heparins (LMWH) • Bioavailability > Outpatient who need • Typically ~ 15 polysaccharides
90%, longer t1/2 ~ immediate heparinastion which are absorbed more uniformly • Inhibition of Xa specifically – by
2+h (unadjusted body (units/kg dosing) enhancing ATIII activity
weight)
Slow onset LMWH much more predictable in its
• More predictable dose response as action so normally requires little
Prevention of VTE - does not bind to endothelial cells, monitoring
preoperatively plasma proteins and macrophages –
Cancer related VTE it isn’t long enough

Pregnancy

Synthetic pentasaccharides Fondaparinux inhibits Xa by binding to ATIII Inhibition of the active clotting
– s.c., t1/2 18h
factor 10a

Heparin reversal protamine sulphate Cardiac arrest after the given i.v Protamine sulphate forms inactive renal
surgery complex with heparin
where they use a high dose of Much greater effect with UFH than
aspirin LMWH, no affect on fondaparinux dissociates heparin from ATIII,
irreversible binding amount given
guided by heparin dose
paradoxically can cause bleeding!?

Vitamin K antagonists - Warfarin Venous thromboembolism • Hepatic synthesis of clotting factors inhibit activation of vitamin K dependant Bleeding -Epistaxis and spontaneous Pregnancy -teratogenic in 1st Amiodarone, clopidogrel,
anti-coagulants half-life 36-48 hours PE prophylaxis and treatment 2, 7, 9 and 10 requires vitamin K as clotting factors retroperitoneal bleeding trimester and 3 rd trimester – brain quinolone and
CYP 2C9 inhibit the DVT and secondary cofactor for activation Inhibits conversion of vitamin K to active haemorrhage metronidazole – inhibition of
hepatic prevention reduced form – competitive inhibition of ANTIDOTE: DDI increase the effect of the CYP2C9
metabolism Superficial vein thrombosis • Delay in onset of action as VKOR (the Vit K epioxide reductase Give Vitamin K1 in excessive anticoagulation (bleeding) and some
Oral ≈ 100% Protein S and C deficiency circulating active clotting factors inhibition) bleeding, fresh frozen plasma and the decrease effects Cephalosporin- Reduce vit K
 bioavaliability present for several days - Must be Vitamin K antagonists prothrombin complex concentrate Drugs that decrease the effectiveness by eliminating
• Atrial fibrillation with high risk cleared and replaced with of warfarin (PC BRAS) gut bacteria
INR 2.5(+-0.5) of stroke (use CHA2DS2Vasc) non-carboxylated forms (inactive Ca is also a cofactor for those Delayed onset of action (48 hour) -so Phenytoin Warfarin and NSADIs-
DVT, PE and AF Cardioversion clotting factors) clotting factors-EDTA- calcium immediate heparin Carbamazepine increase the warfarin
chelating agent – to prevent the Need to consider amount of time needed Barbiturates
INR 3.5(+-0.5) • Heart valve replacement bio blood from clotting before surgery – surgery is Rifampicin in the blood – so meaning it is
Recurrent DVT or prosthetic and some Slow onset of action likely to PT is used as the INR- factor 7- prothrombotic Alcohol (chronic use) better at anti-
PE in patient mechanical require heparin cover (see later extrinsic pathway Highly protein bound so can have Sulphonylureas coagulating. So higher INR
currently receiving slides) if anticoagulation needed Activity varies individuals – race - increase Cp if you take another drug
anticoagulation • Generally used in longer immediately so monitoring INR is important Drugs that potentiate warfarin (O Warfarin and (barbiturates,
term anticoagulation You need to have the INR in range DEVICES) phenytonin, rifampicin,
compared to heparins however the higher the INR, the Omeprazole [Link]’s Wort) – decrease
better it is at anti-coagulating(clots Disulfiram the warfarin in the blood –
Bridging therapy with LMWH more slowly) . Too high INR can lead Erythromycin decrease the INR
often required when initiating to the risk of bleeding Valproate
or temporarily stopping Isoniazid Warfarin and cranberry juice-
warfarin (surgery, sickness…) Ciprofloxacin and Cimetidine decrease the
Ethanol (acutely) clearance of warfarin – so
Sulphonamide increase the risk of
haemorrhage

Direct acting oral Apixaban Different DOACs are indicated Oral administration, standard dosing Direct Xa # Bleeding dabigatran contraindicated in low Δ Less frequent interactions
anticoagulants (DOAC) edoxaban in many presentations where and little to no direct monitoring Inhibit both free Xa and that bound creatinine clearance (<30 mL/min) than warfarin but affected by
rivaroxaban vitamin K antagonists required with ATIII, do not directly effect Caution and dose adjustments particularly in CYP inhibitors and inducers
(warfarin) used to be the only thrombin (IIa) - hepatic metabolism and GI bleed risk groups Little information on use in pregnancy [plasma] reduced by
option excreted partly by kidneys and breastfeeding – avoid carbamazepine, phenytoin
Lower intracranial bleed risk compared to and barbiturates [plasma]
warfarin
increased by macrolides

Direct acting oral dabigatran Direct IIa others are at very low creatinine
anticoagulants (DOAC) Selective direct competitive thrombin clearance (<15 mL/min)
inhibitor, both circulating and thrombus
bound IIa
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Antibiotics - beta lactam Beta lactams Flucloxacillin: Individual sensitivity testing often Interfere with synthesis of bacterial cell
Penicillin: Staph Aureus – skin abscess required - particularly in secondary wall peptidoglycan
Phenoxymethylpenici Staph Epidermidis – prosthetic care - Binds to penicillin binding protein
llin ( penicillin V) Infections preventing transpeptidation
Amoxicillin, CEFELAXIN enzyme
Flucloxacillin( beta Pencillin V- strep mainly Clinical applications: Septicaemia -
lactamase resistant ), Strep Pyogenes- bacterial Pneumonia Meningitis Biliary tract Active against both gram positive
Co- amoxiclav ( pharyngitis/tonsilits infections UTIs (especially in and negative bacteria
clavulanic acid + pregnancy or in patients Gram stain will tell whether it will
amoxicllin - beta Amoxicillin unresponsive to other drugs) work or not
lactamase inhibitor) Strep pneumoniae – mild Sinusitis
pneumoniae
Cephalosporins; Haemophilius influenza –
ceftriaxone pneumonia or common cold
CEFALEXIN
Carbapenems- Ceftriaxone good activity in
meropenem the csf
Can cause [Link] – dirrahoea

Vancomycin- gram positive

Antibiotics Tetracyclines: Doxycycline – gram pos – Individual sensitivity testing often Affect protein synthesis Gentamicin- nephrotoxic and ototoxic Tetracyclines shouldnt be ghiven to Macrolides inhibits CYP3A4
Doxycycline ( oral penicillin allergy required - particularly in secondary children, <12 years, pregnant and
only) Doxycycline- mild pneumoniae care Tetracyclines - affect tRNA binding to breastfeeding women - causes teeth
– if penicillin allergy ribosome - taken up by susceptible staining
Macrolides: And moderate pneumoniae Nitrofurantoin- 50% of orally taken is organisms - bacteriostatic
Clarithromycin Plasmodium excreted in urine in unchanged form -
Erythromycin Chlamydia trachomatis concentrates in urine - especially Macrolides - inhibit bacterial protein
Azithromycin useful for urinary tract infections synthesis by effecting ribosomal
translocation - bactericidal/bacteriostatic
Aminoglycoside; Clarithromycin-
Gentamicin Legionella pneumophila – Nitrofurans - bacterial cell - nitrofuran
atypical reductase converts into active form -
Nitrofurans respiratory pathogens attack ribosomes and dna proteins +
Nitrofurantoin - Also similar to inhibit citric acid cycle
penicillin - used after

Gentamicin- gram neg

Antibiotics Quniolones: Gram neg Individual sensitivity testing often Nucleic acid synthesis inhibitor Tenditinis +/- rupture
ciprofloxacin required - particularly in secondary Aortic dissection
Pseudomonas aeruginosa care Inhibit topoisomerase - a bacterial dna CNS effects - convulsions
Complicated UTIs gyrase - prevent DNA supercoil that
gonorrhea allows transcription and replication

Antibiotics trimethoprim UTI Nucleic acid synthesis inhibitor - folate Teratogenic in pregnancy
acid antagonist

- Reversible inhibitor of
dihydrofolate reductase - needed
for making nucleic acids and
proteins - bacteriostatic and
bactericidal
Antibiotics Metronidazole [Link] – profused Metronidazole - CYP2C9 inhibitor Nucleic acid synthesis inhibitor Has a disulfiram like action so
dirrahoea- hospital acquired - avoid alcohol when using
associated withthe antibiotics Thought that protozoa and anaerobes
usage – sporulating metabolise it

Trichomonas vaginalis

Antivirals Aciclovir EBV- HSV has two serotypes: DNA polymerase inhibitor

herpes simplex - genital 1- mouth/lip/eye infections Activated in infected cells - viral enzyme
herpes - do not prescribe topical antiviral - thymidine kinase more effective at
available OTC phsophorylating - thus activating
Varicella zoster - NICE - no oral antivirals for herpes
labialis in healthy patients
- consider clinical judgment - may be
more lenient with
immunocompromised patients

2 - genital infection
1st episode - oral aciclovir within 5
days of start of episode - topical not
recommended limited evidence
Recurrent episodes - episodic
antiviral treatment - less than 6 a
year:
800mg tds for 2 days or 200mg 5x for
5 days

Suppressive antiviral treatment - if

attack more frequent that 6 time per
year - causing psychological distress
- or affecting scoial life

400mg BD or 200mg QDS

Dosage incraese if recurrences still
occur
Stop after a year - assesses
recurrence
Type of Drug Name of Drug Disease Contextual Info MOA Side effects Contraindications Drug - Drug
interactions

Dopamine - LEVADOPA CO-careldopa - IPD - first line Dont use dopamine as it cannot LDOPA -crosses BBB by active transport Adv- Low side effects such as N&V , Pyridoxine (vitamin B6)
sinemet cross BBB Converted into dopamine by hypotension, Psychosis, Tachycardia increases peripheral
- used in combination (levadopa/carbidopa) dopaminergic neurons in SN - efficacy Highly efficacious breakdown of L-DOPA
with a peripheral T1/2 2 hours - affected by presence of the neurones =
DOPA decarboxylase CO-beneldopa - • short dose interval Formulations of L-DOPA motor fluctuations Disadvantages include MAOIs risk hypertensive
inhibitor madopar • fluctuations in blood levels • Reduced dose required - needs enzyme conversion crisis - at high dose
(levodopa/benserazid and symptoms • Reduced side effects • Oral administration - in the long term loss of efficacy,
e) • (physiologically dopamine is • Increased L-DOPA reaching brain • Absorbed by active transport catatonia development, motor complications (Many antipsychotic drugs
produced tonically) • In competition with amino acids (NB such as wearing off, dyskinesias, Dystonia, block dopamine receptors
• 90% inactivated in intestinal wall high protein meals) freezing and parkinsonism is a side
• Tablet formulations • monoamine oxidase & DOPA effect (newer, ‘atypical’
only – Standard decarboxylase antipsychotics less so))
dosage – variable • 9% converted to dopamine in
strengths – peripheral tissues
Controlled release • DOPA decarboxylase
preparations (CR) –
Dispersible Madopar
(not soluble)

Dopamine receptor agonists • Non Ergot Add on therapy for the IPD or Dopamine receptor agonists Adv- direct acting, less motor
-Ropinirole first line complications, possible
Pramipexole De nevo – doesn’t have to use Neuroprotection
-patch Rotigotine - dopamine
used in dysphagia Disadv- less efficacy than the LDOPA
Impulse control disorder –
Apomorphine- (pathological gambling,
subcutaneous hypersexuality, compulsive shopping, desire
patient with the to increase dose, punding)
severe motor More psychiratric - dose limiting
fluctuations Expensive

Side effects-
Sedation
Hallucinations
Confusion
Nausea
Hypotension

Monoamine oxidase B Rasagiline Can be used alone Monoamine oxidase B

inhibitors Selegiline Prolong the action of the Metabolises
L-dopa dopamine so by inhibiting it, it will
Smooths out motor response increase the dopamine
Maybe neuroprotective

Catechol-O- methyl Entacapone – No therapeutic effect alone Add diagrams Prolong motor response of L-dopa
Transferase(COMT) doesn’t cross Prevents symptoms of wearing off
inhibitors BBB Can use combination tablets – - Prevents breakdown of LDOPA
COMT inhibitor , L-DOPA and to 3-O-methyldopa - competes
Opicapone - also peripheral dopa with LDOPA for AT into CNS
does not cross decarboxylase
inhibitor- Stavelo
anticholinergics • Trihexyphenidydyl Minor role in treatment of PD Some effect on tremor but causes Acetyl Choline may have antagonistic Adv- treat tremor, not acting via
• Orphenadrine problelms effects to dopamine- reduce ACh levels dopamine systems
• Procyclidine
Disadvantages- no effect on
bradykinesia

Side effects- confusions, drowsiness,

SLUDGE

Amantidine Dyskinesia - doesn't work on poorly effective NMDA receptor inhibition Few side effects - hallucinations
any other motor symptoms

Little effect on tremor

surgery Carried out stereotactically Highly selected cases Better to do deep brain stimulation of
- Dopamine responsive subthalamic nucleus
All entered into controlled - Significant side effects with
trails LDOPA Compared to destructive lesions of
- No psychiatric illness thlamus for tremor, globus pallidus for
dyskinesias

• Acetylcholinesterase Pyridostigmine - oral Myasthenia gravis - Drugs affecting mg - excerbates: – Enhance neuromuscular transmission – Excess dose can cause depolarising block
inhibitors auto-immune condition - • Aminoglycosides – Skeletal and smooth muscle – cholinergic crisis
Neostigmine – oral antibodies to Ach recptor on • Beta-blockers, CCBs, quinidine, • Prevents breakdown of ACh in NMJ – Muscarinic side effects - treat with air way
and IV preparations post synpatic membrane procainamide • ACh more likely to engage with support, resp support, IVIG,plasmapharesis
(ITU) • Chloroquine, penicillamine remaining receptors
• Quicker action, • Succinylcholine - Improves muscle power - take • Antimuscarinic side effect –
duration up to 4 Fluctuating, fatiguable, • Magnesium before food - 40 mins to help – miosis and the SSLUDGE syndrome:
hours weakness skeletal muscle – • ACE inhibitors dysphagia » Salivation,
• Significant Extraocular muscles – » Sweating,
antimuscarinic side commonest presentation • Acute exacerbation – Myasthenic • Onset 30min; peak 60-120min; duration » Lacrimation
effect – Bulbar involvement – crisis ( resp failure, weakness, 3-6hr » Urinary incontinence
dysphagia, dysphonia, swallowing) • Dose interval and timing crucial » Diarrhea,
dysarthria » GI upset and hypermotility
– Limb weakness – proximal • Overtreatment – Cholinergic crisis - » Emesis)
symmetric stop pyridostigmine - IV anti
– Respiratory muscle muscarinic
involvement - (crises)

= MG

Myasthenia - actual • Corticosteroids

– Decrease immune response
• Steroid sparing
– Azathioprine
• IV immunoglobulin
Acute decline or crisis – 60% will
respond after 7-10 days
• Plasmapheresis
– Removes AChR antibodies and
short-term improvement
Platinum compounds Cisplatin Chemotherapy Ototoxicity Forms platinated interstrand or Mucositis – GIT epithelial damage;
Alkylating agents Nephrotoxicity intrastrand adducts leading to worst in oropharynx; sore
inhibition of DNA synthesis throat/mouth, diarrhoea, GI bleeding
Mechanisms of resistance: Bulky and more effective at
Pump on cancer cell membrane inhibiting DNA synthesis Skin toxicity –
causes Adducting the section of DNA Local:
decreased entry or increased exit of which is bound to cancer-causing irritation and thrombophlebitis of
agent chemicals veins, extravasation ( vein popped,
Inactivation of the agent in the cell’s medication travels around skin - emergency)
nucleus General:
Bleomycin
Alkylation causes enhanced dna • Hyperkeratosis
lesion repair- • Hyperpigmentation
and neutralises it • Ulcerated pressure sores
Busulphan, doxorubicin,
cyclophosphamide, actinomycin D
Alkylating agents Cyclophosphamide Chemotherapy CYCLOPHOSPHAMIDE giving alkylating agent which will • Hyperpigmentation
- Alopecia
- Hyperpigmentation cause : Nausea and vomiting- CTZ trigger zone
- Arrhythmia - Base mispairing Acute phase: 4-12 hours
- cardiomyopathy - Ds or ss break Delayed onset: 2-5 days later
- Pulmonary fibrosis - Ligand formation Chronic phase: may persist up to 14 Days
- Hemorrhagic cystitis All mechanisms prevent DNA
replication Alopecia – hair thins within 2-3 weeks
Ds break = necrosis or apoptosis = - May be total
cell death - May re-grow during therapy
- Marked with vinca alkaloids ( doxorubicin
ANti metabolite - dna Methotrexate - once Chemotherapy myelosuppression Competitive reversible and cyclophosphamide) Penicillin - Methotrexate
synthesis weekly Dihydrofolate reducatase Helped with scalp cooling NSAIDS – Methotrexate-
half-life 60 hours Inhibitors - no tetrahydrofolate - stops hepatotoxicity and
folate cycle Lung toxicity leukopenia rheumatoid
Capecitabine Inhibits the synthesis of the DNA, Pulmonary fibrosis: bleomycin ( arthritis
RNA and proteins beware concurrent radiotherapy) St John’s wort - Capecitabine
mitomycin C, cyclophosphamide, Grapefruit juice- Capecitabine
melphalan, chlorambucil -causes
pulmonary fibrosis
Anti metabolite 5 – fluorouracil Chemotherapy myelosuppression Inhibits thymidylate synthase(TS) Warfarin DDI – increase the
directly so prevents conversion of Cardiotoxicity: level of 5
pyrimidines to DNA. TS is also cardiomyopathy: flurouracil
needed for the folate cycle so folate • doxorubicin, high dose cyclophosphamide
cycle is inhibited which prevents arrhythmia:
formation of purines which are • cyclophosphamide, etoposide
also needed for the production of
DNA. Haemotological toxicity: different
agents affect the different lineage if
the cells – neutrophils or platelets
Spindle poisons Vincristine - Vinca Chemotherapy VINCRISTINE Interrupt mitosis at spindle Neutropenic sepsis, thrombocytopenia, Vincristine and itraconazole
alkaloids - Alopecia assembly checkpoint. anaemia (antifungal) –
Taxanes- Paclitaxel - Peripheral neuropathy Spindle fibres are needed to pull Neuropathy
strands of DNA to opposite poles Mucositis
of the cell so a nuclear membrane Nausea and vomiting For bleomycin , you cannot
can form around them and a Diarrhoea give the patient
cytoplasm can divide between Cystitis oxygen because it can
them respectively. Spindle Alopecia worsen the pulmonary
microtubules must depolymerise to Pulmonary fibrosis fibrosis.
pull dna strands apart from Renal failure
 metaphase plate. Myelosuppression
Cardiotoxicity
Vinca alkaloids- Microtubule Sterility
assembly inhibitors by preventing spindle Myalgia
formation- inhibit Neuropathy
polymerisation phlebitis
Paclitaxel- microtubule
depolymerisation inhibitors- stimulate
polymerisation but inhibit
depolymerisation

anaesthetics

Local anasthetics Bupivacaine Local Anaesthetic The other is call the esterase They are the amide anaesthetic Use of amides – longer acting and more
Dentistry anaesthetics and they will not be charged stable
Obstretics before they enter the cell. After Onset determined by the pKa
Regional surgery they have entered the cell Ester- shorter acting
Post- op (wound pain) membrane and they have become
Chronic pain management charged and they will block the Na Give the adrenaline because they will cause
channel. The Na channel will be vasoconstriction – to have longer effect and
blocked so the Na outside the cell duration of the pain blocking as well as can
will not be able to come through. decrease the dose of the anaesthetic.
And the action potential will not be
produced. Lipid soluble so increase in the potency

Local anasthetics Lidocaine Local anaesthetic

Dentistry
Obstretics
Regional surgery
Post- op (wound pain)
Chronic pain management

Local anasthetics Ropivacaine Local anaesthetic

Dentistry
Obstretics
Regional surgery
Post- op (wound pain)
Chronic pain management
 - Tiredness CONGEN MALFORMATIONS Warfarin
- Drowsiness Worst - valporate Alcohol
- Nausea and vomiting Best - levetiracetam/ lamotrigrine COCP
- Mood changes and suicidal Antibiotics
ideation
- Osteoporis

Benzodiazepines IV loarezpam Status epilepticus ca n increase dose but cant take GABAa Agonists Cvs collapse
Rectal diazepam back remember Increase Cl- conductance - less likely to Airway issues
Buccal or intranasal Anxiolytic fire AP
midazolam Sleep aids Work best when membrane positive - in a
Alcohol withdrawal seizure
No firing neurones - no seziure

Anti epileptic Carbamazepine - Seizures - CYP INDUCER Na channel blocker Dizziness, Fatigue , Ataxia, Diplopia COCP
Chronic pain and bipolar Causes Na channels to remain in Antibiotics
disorders an inactive state suicidal thoughts
Prevent axons from firing joint pain
repeatedly bone marrow failure

SJS

Anti epileptic Phenytoin Status epilepticus - 3rd line Zero order kinetics - careful with Na channel blocker Bone marrow suppression COCP
dose adjusting Causes Na channels to remain in Hypotension Antibiotics
an inactive state Arrhythmias - iv use
CYP INDUCER Prevent axons from firing
repeatedly SJS

Anti epileptic Sodium valproate 1at line for generalised CYP INHIBITOR GABAa and Na blocking effect Liver failure Any women of child bearing age - Other AEDS - will increase
epilepsy Pancreatitis teratogenic them
Lethargy

Anti epileptic lamotrigine Focal epilepsy Na channel blocking and may some ca
efect
When valproate is
contraindicated

Anti epileptic Levetiracetam Safe in pregnagcy Synaptic vesicle glycoprotein binder -

stops the release into synaose and
reduces neuronal activty