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Flashcards in Pharmo Deck (392):
1

Yellow card

Black triangle = all
Established - serious
Paediatir= all

2

Legal requirements prescribing

Legible ink
2 ID
signed dated

3

Define slip, lapse, mistake, volation

Concentration
Memory
Knowledge
Intentional

4

First pass metb includes

Liver, gut wall and gut lumen

5

Describe protein binding of different drugs

Albumin = acidic drugs
Globulins = hormones
Lipoproteins = basic drugs
Acid glycoproteins = basic drugs

6

What is Vd affected by?

Receptor sites in tissues
Regional blood flow
Lipid solubility
Active transport
Disease
DDIs

7

CYP inducers

Phenytoin
Carbamazepine
Barbiturates
Rifamipicin
Alocohol (chronic
St John's Wort

8

CYP inhibitors

Omeprazole
Disulphram
Erythromycin/Macrolides
Valporate
Isoniazid
Cimetidine
Ethanol (acute)
Sulphonylureas
Grapefruit juiceCranberry
Antifungles

Hepatic disease (opiates in cirrhosis)

9

When should you monitor drugs?

Long half life
Narrow TI
Risk of DDIS
0 order

10

What does BNF contain

Comprehensive list of all licensed drugs in the UK

11

Role of pharmacist in prescribing

No legal responsibility
Check prescriptions are correct

12

Pharmokinetics of Digoxin

Long half life = 40hrs
Narrow Ti
builds up in renal failure
Large Vd

13

How do you calculate Loading dose

Vd x [Drug at target}
Note that Vd = L or L/kg

14

How do you calculate the elimination rate constant?

=slope of the curve (k)
= clearance/Vd

15

Calculation of T1/2

Vd (kg)/Cl log0.5/k

16

T1/2 in children

Higher as Vd is lower as more of their body is ECF

17

Comptments and drugs

Equilibrium in each compartment.
Varies

18

Describe drug specificity and selectivity

The more selective the less undesired effects elsewhere. Affinity for one receptor over another.
The more specific the more it can be used for a select organ. Specific basically means its so selective that no matter how much you give it wont work at another site

19

DDI absorption example

Gastric emptying - metaclopramide. Affects Fe and tetracyline absorption

20

Types of ADRs

A= augmented effect (dose)
B = Unpredicable off target
C = chronic
D = Delayed e.g. osteoporosis and steroids
E = End of treatment effects
Mild, moderate(additional treatment) or major

21

Preparations of testosterone?

Oral, IM, implant

22

Steroid hormones and distribution?

Steroid hormone binding globulin (not prog) and albumin

23

Use/ Actions of ostradiol

Prevent HRT symptoms - hot flushes, support bone structure.
Anabolic
Na/H2O retention
Impair glucose tolerance
Increase coagubility
Improves mood and concentration

24

Side effects of oestradiol

Water retention
N/V
Diabetes
Breast tenderness
Thromboembolism
Endometrial hyperplasia and cancer

25

Actions of prog

Anabolic
Increase Bone density
Secretory to endometrium
Fluid retention
Mood changes

26

Side effects of Prof

Water retention
Depression (PMS)
Irritability
Weight gain
Acne
N/V
Lack of conc

27

Actions/ Side effects of testosterone

Male secondary sexual characteristics
Anabolic
Acne
voice change
Aggression
Metabolic adverse effect on lipids - increases LDL and decreases HDL

28

Preparations of COCP?

Monophasic
Triphasic

29

How does COCP work?

Suppresses ovulation (inhibit LH and FSH), effect on mucus and endometrium

30

MEtabolism of COCP?

CYP

31

Absorption of COCP DDI?

Broad spec on flora

32

Some COCP ADRS

Focal migranes (stroke)
Headache
Moodswing
Gall stones
Precipitate porphyria (skin sensitivity-dark urine-memntal disturb)
weight gain

33

Use of POP?

Not as effective
Action on Cervical mucus and endometrium
Emergency contraception (72hrs) (120?)
Cu IUD - 5 days

34

Formulation of HRT?

Sequential or continuous
No shedding in continuous (Cx?)
Treat with lowest dose for shortest time

35

ADRs of HRT

Breast cancer
Endometrial cancer
IHD
DVT
Uterine bleeding
Lipid profile
Thrombophilia

36

Anti-oestrogens and action e.g. tamoxifen/ Clomiphene

Weak oestrogens - block receptors.
Induce ovulation by blocking oestrogen affect on put. More GnRH
Tamoxifen also acts at bone. Used in breast cancer.

Better for HRT as can reduce cancer risk, not be proliferative. But can increase hot flushes

37

Affects of anti-progs

Partial agonist again.
Sensitises uterus to prostaglandins (like increased O:P0)
Induction of labur
Terminaton of pregnancy

38

Effect of high LDL?

Pro atherogenic
Toxic to endothelial. enhance platelet aggregation.

39

Affect of obesity on lipid profile

Increases Cholesterol, Triglycerices and decreases HDL

40

Action of simvastatin/ atorvastatin

Inhibit HMGCoA reductase
Used in CVS risk and hypercholesterolaemia
Decrease VLDL and LDL.
Anti-inflammatory, plaque reduction, improved endothelial cell function, reduce thrombotic risk, slow neurodegeneration.

41

ADR of simvastatin/ atorvastatin

LFTS (reversible)
Myopathy - CPK

42

Metab and elimination of Statins DDIS

CYP
OATP2 - fibrates and cyclosporin augment affect

43

Describe Benzafibrates action

PPARalpha agonist.
More lipoprotein lipase
Reduce TG (espc Post prandial)
Not great LDL decrease
Increase LDL size
Increase HDL-C

44

ADRs Benzafibrates

Rhabdomolitis
Myopathy
LFTs

45

Nicotinic acid action

Reduces VLDL
Increase HDL (best C)
Inhibits lipoprotein synthesis.
Reduce coronary events

46

ADRS/ contraindications for Nicotinic acid

Flushing, itching, headache
Hepatotoxicity
GI
Peptic ulcer
hyperglycaemia
CIs: Liver, PUD

47

Ezetimibe action and uses

Cholesterol absorption. Circulates enterohepatically.
Lowers LDL (more hepatic receptors)

48

ADRs of Ezetimibe

Headache, abdo pain, diarrhoea

49

Give a statin?

CVS risk tables in BNF

50

MoA metformin

Decrease insulin resistance and hepatic glucose production

51

Side effects metformin

GI
Lactic acidosis (HRH)
Vit B 12 deficiency
No weight gain/hypos

52

MoA Gliclazide

Increase production
K/ATP channel antagonist
Increase Ca release

53

ADR sulphonylurea

Weight gain
Hypo

54

Pioglatizone Rosiglatizone MoA

PPAR receptor. Decrease FAs. Increased muscle and adipose sensitivity

55

Pioglatizone Rosiglatizone ADRs

Bladder cancer
Fluid retention and CVS risk
Osteoporosis
No hypos
More LDL and HDL

56

Repaglinide, Nateglinide MoA

K/ATP antagonist

57

Repaglinide, Nateglinide ADRs

Hypo (lower risk)
No Weight gain

58

Repaglinide, Nateglinide pharmacokinetics

Short half life so taken before meals

59

DPP4 inhibits/ GLP1 analogue

Integrinpathway
GLP released from distension of the stomach.
DPP4 breaks down GLP.
GLP increases insulin secretion and suppresses appetite
GLP1 agonist more effective

60

GLP1/ DPP4 inhibitor ADRs

N/V
Diarrhoea
GORD
Injected so pain

61

SGLT2 inhibitor action

Blocks in PCT

62

SGLT2 ADRs

Polyurea
Polydipsia
Thrush
UTI

63

Acarbose/ a-glcosidase inhibitors ADRs

Flatulence
Diarrhoea

64

Criteria for treatment of Diab?

over 7% = sulphonylureas
over 7.5 = TZD or 3rd drug
Insulin (titrated upwards)

65

Physiological effects of Insulin

Glucose uptake in liver, muscle, adipose
Glycogesis in liver
Lipogenesis in Adiposites
Proteogensis in Muscle cells
Inhibit gluconeogensis

66

Half live of insulin

5 mins

67

Best indulin regime

Long acting with rapid acting`

68

Types of insulins

Animal porcine and bovine

69

Short acting

30-60mins.
Given 15-30 preprandial
Peaks at 2 hours

70

Examples of short acting insulins

Actrapid, Humulin , Novorapid

71

Examples of longer acting insulins

Insulin Glargine

72

Rapid acting insulins

onset 5-15
Inject prandial
Peaks at 30-90
lasts 4-6

73

Intermediate acting inslins

Isophane intermediate actin (NPH)/ Humulin I.
Onset 1.5-3, peaks at 4-8. lasts 12-20.

74

Long acting basal analogue insulins

Slow onset 2-6hours, duration up to 24

75

Very long acting insulins

Fatty acid added so longer into blood stream. Lasts up to 50 hours (glargine)

76

ADRs inslin

Hyper/hypos
Lipodystrophy
Painful injection site
Insulin allergy

77

Sources of insulin error

Programme not written up
Name of insulin incorrect
Number/ dose unclear
Unit unclear

78

MoA orlistat

Gastric and pancreatic lipase inhibitor. FA conversion decreased by 30%. Needs to be combined with diet

79

ADRs orlistat

Soft, fatty stools, risk of flatus, faecal incontinence

80

What is pharmacovigilance

Process of identifying and then responding to safety issues about marketed drugs.
Ensure saftey
Minise risk
Optimise benefit
Withdrawral of drug results? (E)

81

Aims of pharmacovigilance

ID unrecognised safety hazards and quantify
Factors predisposing toxicity
Evidence for safety
False positive ADR

82

Why is pharmacovigilence needed?

PAtients in trials are restricted
Limited duration of drugs
Specialists giving drugs in trials
Different monitoring
Not big enough sample

83

How are ADRs identified?

Spontaneously reported to the MHRA - Medicines and healthcare products regulatory agency. through yellow card. (licencing responsibility. Can report to pharmacological company (post marketing surveillance).
Cohort or case control

84

Advantages of spontaneous reporting

Involves all
Everything included
IInexpensive
Continuous
Can generate ADR hypothesis
ID risk factors

85

Limitations of spontaneous reporting

Undereporting
Delay in reorting
Misleading information given
No control group
Cant get incidence rate as no idea how many are treated

86

Controvosy in yellow card

Quality of patient reports?
Under reporting

87

Difference between pharmacogenetics vs genomics

Gene vs entire genome

88

Variability in ADRs. drugs

Some toxic, some not
Some effective some non responders.
Particulary CYP

89

Variability in ACEi

Better for whites as they have a higher RAS activity
Older and afrocarribean = CCB

90

Issues surrounding pharmacogenetics

DNA database

91

Synthetic cortisol

Hydrocortisone
Prednisolone also a glucocorticoid

92

More potent than cortisol?

Dexamethasone

93

Metabolic actions of glucocorticoids

Glycogenolysis
Gluconeogenesis
Hyperglycaemia
Proteinolysis
Lipolysis (low/physiological)
Lipogenesis (high)
Redistricubution of fat centrally
Slight mineralocorticoid activity

94

Mineralocorticoid deficiency and example

Fludrocortisone (a bit at GC)
Hyponatraemia
Dehydration
Hypotension
Hyperkalaemia

95

Actions of hydrocortisone
Prednisolone
Dexamethasone, Betamethasone, fludrocortisone at GC and MC

GC MC
HC equal
Pred more at GC
Dex and Bet +++GC no MC
Fludo --GC, +++MC

96

Pharmacokinetics of corticosteroids

All have high bioav
All metabolised in liver 1 & 2
Glucoronidation in liver for stage 2
Clearance affected by age
Kidney can metabolise too

97

Steroid action on immune repsonse

Inhibit B, T, cytokines, cell adhesion molecules, phagocytes

98

MoA steroids

Steroid receptor (HSP dissociated)
Bind to hormone response element (HRE/ GRE) on DNA
Activates/ inhibits transcription = transactivation/ cis repression.
Transactivation = antiinflam
Cis repression = keratin, oesteo, POMC (side effects)
Trans repression (protein) = immune/ cytoknes
Some non genomic MoA via surface receptors

99

Some glucoorticoid ADRs

Adrenal crisis - hypogly, shock/ hypotension/ hypokalaemia/ hyponatraemia/ dehydration
Inhbits osteoblast, ca absorption.
PUD
hypertension
DM
Catacts
Psychosis

100

Describe influenza A,B,C

A = Multiple host species, most severe, various.
B = No animal reservoir, lower mortality
C = not clinically important

101

Amantadine and Rimantadine MoA

Block M2 channel and inhibit uncoating. Proton channel that allows A to enter.
Highly resistant

102

ADR amantadine and rimantadine

CNS nervousness, anxiety, agitation, insomnia think schitzo as similar to anticyclic

103

Give examples of neuroaminidase targetting drugs

Oseltamivir (Tamiflu) and Zanamivir

104

MoA of neuroaminidase targeting drugs

Neuroaminidase removes sialic acid bridges between virus particles so that particles can be exocytoses.
Blocking causes aggregation.
Earlier treatment the better.
High resistance - monitored by WHO

105

ADRs of neuroaminidase inhibitors

Vomiting, abdo pain, epistaxis.
Resp depression, bronchospasm

106

Folic acid antibitic examples and action

DNA synthesis
Trimethoprin and sulphonamides

107

What is an E test?

Sensitivity testing. Measures the minimum inhibitory concentration

108

What is the MIH?

The minimum concentration of antibiotic required to inhibt growth of a bacterium in vitro (mg/l). Antibiotic and isolate specific.

109

What are breakpoints?

Clinical testing data, wild type MIC, and antibiotic pharmacokinetics calulate breakponts.
Susceptibile
Intermediate
Resistnt.
Compare with MIC

110

Drug is effective when in microbiological terms?

Maximal concentration (Cmax) and MIC ratio.

111

MoA of antibiotics in terms of dependent killing

Time dependent killing - porlonged no at high conc e.g. beta lactams and glyco.
Concentration dependent killing e.g. aminoglycosides and quinolones

112

describe MDR, XDR PDR

MDR - Non-susceptibility to at least one agent in 3 or more categories
XDR NS to at least... in all but two or fewer
PDR
All microbial categories

113

ADR penicillin

Hypersensitivity, CNS

114

Cephalosportin ADR

Hypersensitity, C diff

115

Tetracylins ADr

N/V/D

116

Aminoglycosies ADR

Renal and ototoxicity

117

ADR Macrolides

N/V/D

118

ADR Cloramphenical and MoA

Broad spec, protein
BM
Liver toxicity

119

Glycopeptides

Renal, Bone marrow, ototoxoicity

120

Drugs that are monitored

Vancomysin and aminoglycosides.
Monitor FBC for clor
Renal and aud for gent

121

Common DDIs for antibiotics

Anticoag
Antiepileptics and carbapenems
Bisphosphonates (hypocal) and aminohlycosides
Digoxin in amino

122

Digoxin ADRs

blurred vision, confusion, drowsiness, dizziness, depression, psychosis, convulsions

123

Describe RA

Autoimmune
Common 1%
Initially localised to synovium
Inflammatory change and proliferation leading to destruction of cart and bone

124

How is RA diagnosed

Clinically
Morning stiffness
>3 joints (often hand)
Symmetrical
Rheumatoid nodules (ripe fruit)
Serum factor
X ray (only late stage)

125

Describe SLE/ Vasculitis

Necrosis of distal vessels
Skin rash
Granulomatosis with certain types

126

What are DMARDs

Disease modifying antirheumatic drugs
Lead to clinical improvement unlike NSAIDs.

127

Azathioprine MoA

Active metabolite = 6MP (Mercaptopurine)
Decreases DNA and RNA synthesis.
TMPT metabolises but varying rate. Low rates = myelosuppression

128

Use of Azathioprine

Transplants
SLE/ Vasc
Weak for RA
IBD
Bullous skin disease
Atropic dermatitis
Steroid sparing drug

129

ADRs Azathioprine

BM suppression
non hodgkin lymphoma
Infection
Hepatitis

130

Cacineurin inhibitors e.g. ciclosporin and Tacrolimys MoA

Against T helper cells and IL2
Cyclophilin protein/ TBP.
IL2 regulates WBCs

131

Cacineurin inhibitors e.g. ciclosporin and Tacrolimys ADRsa

eGFR - nephrotoxic
BP - hypertension
Gingival hyperplasia
Hyperlipidaemia
N/V/D
CYP
Does not supress bone marrow

132

Uses of Cacineurin inhibitors e.g. ciclosporin and Tacrolimys

Transplants
Dermatis and psoriasis

133

Mycophenolate Mofetil (MMF) MoA

Inhibits monophosphate dehydrogenase and therefore guanosine synthesis.
Inhibits B/T cell proliferation. but highly selective

134

Uses Mycophenolate Mofetil (MMF)

Transplants
SLE
Monitor metabolite

135

Mycophenolate Mofetil (MMF) ADRs

N/V
Myelosuppression
Liver and kidney disease
Viral infection

136

Methotrexate MoA

Inhibits dihydrofolate reductase and purine and thymidine synhesis (malignant only).
In RA - inhibits T cells, cell adhesion and adenosine

137

Uses MTX

RA
Psoriasis
Crohns

138

Pharmokinetics MTX

One a week
Long half life
Low bioavailability
Highly bound - NSAIDs
Renal excretion

139

ADRs MTX

Nausea
Mucositis
BM (give folic acid)
Hepatits/ cirrhosis
Pneumonitis
Tetratogen
Abortifacient

Do baseline CXR, FBC, LFT, UE, Creatine

140

Sulphasalazine/ Masalazine MoA

Inhibit T cell proliferation and IL2
Inhibit neutrophil

141

Uses of sulphasalazine/ masalazine

RA
Chrons
UC

142

ADRs of sulphasalazine

Safe in preg
Hepatits
Rash
ASprin reaction
N/V/ abdopain

143

AntiTNF e.g. infliximab MoA

Inhibits cytokine cascade- adhesion, recruitment, less angiogenesis, less joint destruction e.g. MMP

144

USes infliximab

Expensive so other DMARD must have been tried. Withdrawn if no effect in 6 months or any ADR.
RA
IBD

145

ADRs Infliximab

Viral infection
TB

146

Rituximab MoA

Targets CD20 B cells. Induces apoptosis.

147

Uses Rituximab

RA, especially with MTX

148

ADRs Rituximab

Hypergammaglobulinaemia
Hypersensitivity

149

Cyclophosphamide MoA

Alkylating - DNA cross links
BM supression
CYP
Kidney

150

Cyclophosphamide uses

Lymphoma
Leukaemia
Sipus nephritis
Wegners granulomatosis
Polyarteritis nodosum
Vasculitis

151

Cyclophosphamide ASDRs

Haemorrhagic cystitis
Bladder cnacer, lymphoma, leukaemia
Hepatitis
Renal impairment

152

Pathophysiology asthma

TH2 dirven inflammation
Airway remodelling
Bronchostriction
Mucosa oedema
Neutrophilic or eosinophilic
Mast cells-IgE and leukocytes
Bronchospasm and congestion due to epithelial damage, thickening of BM

153

Basics of asthma treatment

Check compliance, technique
Eliminate triggers

154

Severe asthma criteria

unable to comple sentences
HR >110
RR>25 PF 33-50% of best

155

Life threatening asthma

If severe plus
PEF

156

Near fatal asthma

PaCo2 >6 = mechanical ventilation

157

Treatment of acute asthma

O2 high flow- sats >94
Nebulised salbutamol -continuous
Oral prednisolone 10-14 days
Nebulised ipratropium bromide
Consider IV aminophyhlline (methylxanthine)

158

Steps in asthma treatment

1 inhaled SABA
2 Inhaled steroid (when SABA 3x or waking 1 or exacerbation with oral steroid in last 2 years)
3 LAba, ca add steroid, consider other drug (some people are unresponsive to ICS
4 Increase steroid to 2000mg a day, forth drug
5 oral steroid, other e.g. antiIGe, specialist care

159

SABA e.g. salbutamine tolbutaline action

SM
Inhibit mast cell degranulation
Increase cAMP, PKA, deacrease CA, more K currents.

160

SABA ADRS

Adrenergic, tachycardia, palpitations, termor

161

Why use LABA e.g. formoterol, salmeterol (slightly lipophilic)

Better at preventing exacerbation
More potent

162

Examples of inhaled cortico

Beclomethason, budesonide1

163

Why CorticoS in asthma

Reduce exacerbations, ecrease eosinophils, imporve symptoms and function. Decrease inflam via transactivation and transrepression (cytokines)

164

Leukotriene receptor antagonist e.g. montelukast MoA

Blocks action of cytokine to prevent inflam and mucus

165

Montelukast effecacy?

Poor.
Only 15%

166

ADRs montelukast

Angioedema, dry mouth, arthralgia, fever, GI, rare

167

Methylxanthines MoA e.g. theophylline

Antagonise adenosine receptor inhibit cAMP

168

Methyxanthines ADRs

Nausea
Headache
GORD
Arrythmias
Fits
DDIS- CYP

169

Methyxanthines efficacy

Poor
Narrow TI

170

LAMA e.g. ipotropoium bromide and tiotropium ADR

Urinary retention
Dry mouth
Glaucoma (esp neb)

171

Anti IgE MoA

blocks IgE receptor so limits mast cell activation

172

Efficacy IgE

Expensive buyt good at steroid sparing

173

NSAIDs physiologic effects

Aalgesia
Anti-inflammatory
Anti-pyretic

174

What are autocoids and what do they do?

'Self-drugs' cause a local response in response to stimuli.
Bradykinin
Cytokines
NO
histamine
Leukotrienes
Neuropeptides

175

What are Eicosanoids?

20C phospholipid derivative.
Overlap with autocoids to ensure a robust inflamatory response. Localised release and short half lives allow fine control.
From arachidonic acid
Prostanoids and leukotrienes.
Prostanoids = prostaglandins (potent), prostacyclins and thromboxane

176

What are COX and reactions they catalyse.

Cyclo-oxygenase synthesis PGs.
Arachidonic acid to PGG
PGG to PGH
PGH to DEFI via PG enzymes
PGE most important in infalm
Types 1-4

177

Describe COX1

Isoform constitutionally expressed.
PG from COX1 in many places e.g. aid perfusion.
=ADRs

178

Half life of prostaglandins

10 mins

179

Describe COX2

Induced by injury
Expresses mediators e.g. bradykinin
Constitutionally expressed in parts of brain and kindey also.
Therapeutic effect of NSAIDs

180

How are prostaglandins produced in inflamation and how do they produce their effect

Autocoids increase COX2
PGs bind to GPCRS (EP1-4 receptors)
Potent vasodilator
Pain modulation via:
Afferent sensation
Sensitisation of central nociception
Pyrexia

181

Describe how prostaglandins cause vasodilation locally?

EP2

182

Describe how prostaglandins cause pain via afferent sensation

(EP2 binds to) EP1 receptor (Gq) causes peripheral nociception on C fibres resulting in sensitivity to bradykinin, inhibition of K channels and increased Na sensitivity (more APs)
Activates previously silent C fibres
Gq - increases Ca so more neurotransmittor release can = allodynia/hyperalgesia.

183

Describe how prostaglandins can cause pain via sensitation of central nociception

Increase cytokines from sustained nociception
Increased COX2
Increased EP2
Binds to Gs (EP2)
Increase in cAMP, PKA
Decrease in glycine receptor binding affinity
Increased pain/ sensitisation
Glycineric inhibition

184

Describe how prostaglandins can cause pyrexia

IL1 from macrophages from endotoxins tirggers PGE2 sythesis in the hypothalamus.
Triggers EP3 receptor (Gi)
Heat production and decrease heat loss.
Increase to assist bacterial killing.

185

Which COX inhibition reduces pain?

COX 2.

186

How do NSAIDS inhibit COX

Competitive inhbition of COX hydrophobic channel.
Extent of COX1/2 varies.

187

NSAIDs pharmokinetics

Heavilly bound.
Variable half lives
ibu=6
naprox=10

188

ADRs of NSAIDS

COX1
Stomach/GI = pain, heartburn, ulceration as PGE2 creates mucus, increases BF and reduces acid.
Renal in HRH or hypovol as PGE2, PGI2 maintain BF. Na, K, Cl, H2O retention.
Incresed bleeding time (asprin)
Hypersensitivity e.g. Stevens Johnson/ Mucositis
Bronchial asthma (CI = asthma_
Reyes syndrome - brain/ liver injury

189

Describe COX2 specific drugs

e.g. Celexib
Less ADRs
Increased CVS e.g. hypertension
Renal failure
Short term only

190

DDIs of NSAIDS

Extends opiate action
Reduces opiate ADR
Interact with each other
Hughly bound drugs e.g sulphonylyrea, warfarin and MTX

191

Describe Aspirin use and pharmacokinetics

Long term then risk
Irreversibly inhibit COX via acetylation
T1/2

192

Describe all about paracetamol

Low TI
No anti inflammatory action -
Anit pyretic
Good ADR profile in TI
Long term = hearing loss and affect metab
Unknown MoA
T1/2 = 2-4 hours
Caution in alchol compromised
OD in paed and elderly risk
Mainly phase II
When saturated = zero order
0-4 OD = activated charcoal

193

MoA of Opioids

Central effects (psychoactive)
Peripheral effects (gate theory) to counter pain as it is caused by physiological and psychological factors.
Inhibits substance P release from nerve nerminals

194

Describe enkephalin precursor receptor, MoA Pre, location

Proenkephalin
DOR
(negative action on cAMP)
Decrease cAMP and Ca
Widely distributed

195

Describe Dynorphin precursor receptor, MoA Pre, location

Prodynorphin
KOR
Ca2 direct channels (-ve)
Spinal cord

196

Describe Endorphin precursor receptor, MoA Pre, location

POMC
MOR
K outward flux and decreased (+ve)excitability
Brain

197

KOP agonist and results

Pentazocine
Dysphoria (confusion and disruption of thought)

198

MOP agonist ad results

Morphine
N/V
Constipation
Drowsiness
Miosis
Resp depression
Hypotension

199

Opioid antagonist

Naloxone but t.5 = 1-1.5
Naltrexone is 4hpurs

200

Describe morphine kinetics

Lipophobic so not good at BBB
Metabolites also active
half life = 4 hours

201

Describe Diamorphine kinetics

=heroin
t.5 = 5 mins
polar so can cross BBB
Metablised to morphine
More in brain

202

Describe uses of opiods

Analgesic (particularly visceral)
Terminal illness
Morphine and clay/ Loperamide for diarrhoea
Methadone to maintain dependence
Tramadol = antidepressant as 5HT and NA

203

Fentanyl ADR not obvious

Puritis due to histamine release

204

Codeine use and kinetics

Mild analgesic
Oral
Metabolised to morphine
Some unaffected e.g. chinese as they lack CYP enzymes
Similar effect to tramadol

205

What are nociceptin and nocistatin

Nociceptin agonises ORL1 and nocistatin blocks
Gi so less cAMP

206

Describe schedule 2 and 5 controlled drugs

2 = storage, prescription and destruction conditions e.g. morphine and diamorphione
5= codeine- preparation regulations and keep invoice over the counter

207

Descrine caumarins MoA

Inhibit Vit K reduction so less active clotting factors II,VII,IX,X
Competitive inhibitor

208

Descriube caumarin ADRS

Tetratogenic
Bleeding (above 3.5)

209

DDIs Warfarin

CYP
Protein - NSAIDs, Sulphonylureas, MTX
Vit K from gut - cephalospoirn

210

Uses and kinetics warfarin

t=48hrs and slow offset
INR
DVT, valves, PE, AF

211

Heparin MoA

Deactivate thrombin and Xa and IXa.
Activates antithrombin III

212

Reversal of Heparin and warfarin

Protamine sulphate
Parenteral vit K

213

Kinetics of heparin

Poor absorption
Rapid onset and offset

214

ADRs heparin

Thrombocytopenia - autoimmune activated platelets
Osteoporosis
Bleed

215

Describe unfractionated

Large enough to bind with IIa, Xa too
Must monitor as variable kinetics/ behaviour via APTT
Non linear dose respose
Variable bio av
Action variable
Given IV (witha bolus)

216

Describe low molecule weight heparins

Only inhibits Xa (poorly ATIII)
Subcutaneous
No monitoring needed
Long t1/2
Oreducable

217

Describe Xa inhibitors e.g. Dabigatran

Selective Xa
Not really DDIs
Also get direct thrombin inhibitors

218

Explain dipyridamole

Phosphodiesterase inhibitor
more cAMP
inhibits thromboxane A2 production (like asmirip
Less aggregation.
Also positive inotrope and vasodilatory (flushes headaches) prevention of stroke.

219

Explain clopidogrel

ADP antagonist so blocks action at P2Y12 receptor, less Gi so more cAMP, less aggregation.
In ACS, PCI, used with asprin only 1 year after NSTEMI

220

How does alteplase work

=tPA
activates plasminogen
Works in presence of fibrin whereas streptokinase is general.
Better if earlier use
Bleeding brain and GI

221

Explain general types of anaesthetics

Regional
Local
Inhalational
IV general

222

Describe Guedel's signs of anaesthetic

1 - Norm tone, breathing and eye movement, slight analgesia
2 - excitement - possible aggretion, everything increased/ erratic
3 surgical anaesthesia - everything slightly to extremely relaxed
4 resp paralysis, flaccid with no breathing or eye movement

223

Describe the thalamo-cortical switch

Sudden anaesthesia above a certain anaesthetic conc

224

Loss of which functions with increasing concentrations

Memory
Consciousness
Movement
CVS/ REsp

225

What is the MAC

Minimum alveolar concentration at which 50% of patients fail to respond (move) to a surgical stimulus at 1atm.
[aleoli]=[spinal cord]

226

MAC-BAR

Autonomic loss of of carbiocascular response =1.5MAC

227

Induction and recovery affected by what properties

Solubility/ partition oefficients blood to gas/ oil to gas

228

What factors affect MAC

Age
Hyperthermia/ Hypo
Pregnancy
Alcoholism
Central stimulus
Opiods
NO (strongly reduces MAC)

229

Potential target sites of anaesthetics

Sensitise GABA e.g. propafol
Sensitise glycine
Inhibit Ach (not sedation bu analgesia and amnesia)
NMDA inhitors e.g. N2O and ket. Depress RF system

230

Fast and slow IV anaesthetics?

Fast= propafol
slow = ket

231

How is TIVA monitored

Total intravenous anaesthesia
Plasma conc for end point e.g. loss of eyelash of BUS (cortical activity)
Normally just used as bolus for induction in mixed anaesthesia

232

Local anaesthetic describe

Lipid soluble
pKa = dissociation constant
If lower then faster onset
Protein inding

233

Describe regional anaesthetic

Often a nerve block
A local anaesthetic or opioid

234

ADRs of anaesthetics

post opiod nausea and ovmiting PONV, hypotension, POCD (cog dys) for 1-2days
Local- systematic spread and CVS toxicity
Allergic
Fluranes - CS and resp depressin, arrhthmia, hypo, OCP, cough
NO2 - diffuse hypoxia
Propafol - CVS and resp depression

235

Classes of drugs used in anaesthetics

IV agents (induction)
Inhalational agents (maintainence
Anxiolytics/ hypnotics e,g, Benzos
Opiates (intraoperative analgesia_
NM blocking drugs
Antiemetics

236

Describe Carbonic anhydrase inhibitor use and ADRs and MoA

Reduces HCO3 production and absorption so less NA, Cl in PCT.
Glaucoma
Metabolic acidosis

237

Describe osmotic agent use and ADR

Cerebrala oedema
Dehydration

238

Loop diuretics ADR and use

Heart failure
Ca/Mg excretion
Ototoxicity
Myalgia
DDIs Digoxin and steroids

239

Thiazide/ thiazide like Use and ADRs

BP reducing
ED
Gout
Hypokalaemia
DDIs steroids, carbamazepine, digoxin

240

Aldosterone antagonists use and ADR

Liver disease, hypertension and HF.
Hyperkalaemia
Gynaecomastia

241

ADH antagonists e.g. demeclocycline/lithium moA

Reduces concentrating ability of CD

242

Amiloride vs spirono

Amiloride inhibits Nachannels in (ENAc)
Spirono = aldosterone receptor antagonist

243

HF drugs

Loop/ thiazide
Spirono
ACE inhib/ ARB (affective in year 1)
BBlockers
NOT Ca channel

244

Explain diuretic resistance

Non compliance
NSAIDS/ poor renal perfusion
High Na intake

245

Explain hypertension drugs

Thiazide, spirono
ACE inhibtors
CCB if over 65? or black
BBlockers (abit)

246

Decompensated liver disease drugs

Spirono
Loop
As kidneys retain sodium

247

Nephrotoxic drugs

ACE inhibitors
Aminoglycosides
Penicillins
Cyclosporin A
Metformin
NSAIDs

248

Describe physiological control of BP

RAAS
ADH (a bit but more osmotic)
Atrial naturetic peptide - stretch = dilation
Bradykinin
NO
Endothelin

249

Describe the pathology of hypertension

Artheriosclerosis
Loss of compliance

250

Aim for hypertension

BP

251

ADRs ACEi

Dry cough (not with angiotensin receptor blocker)
Real failure hyperkalaemia
Not to be used in preggers

252

Examples of angiotension receptor blockers and receptor

Candesartan, lorsartan
AT1 to inhibt aldosterone and vasoconstriction

253

Examples of CCBs

Amlodipine, verapamil, diltiazem

254

CCB MoA

Vasodilate and decrease contractility some more than others

255

ADRs CCBs

Symp activation
Gingival hyperplasia
Constipation
HF and bradycardia

256

Alpha blockers example and action

Doxazosin
antagonise a1 so vasoconstriction

257

Alpha blockers ADRs

Postural hypo
Dizziness
Headache
Fatigue
Oedema
CI: UI

258

BB ADRs

Lethargy
Conc
Reduced exercise tolerance
Bradycardia
Raynauds
Imaired glucose tolerance

259

Explain ventricular arrhyrhmias

Common,
Suddencause of death in people with no history

260

Stages of AP in a myocyte`

0 Na+
1 K+ Cl-
2 Ca++ K+
3 K+
4 K+

261

Stages of AP in SAN

4 = Naf
0 = Ca
3 = K

262

Describe WPW syndrome

Wolf parkinson White = reentry throught the bundle of Kent

263

Describe class 1

Na channell inhibitors
II= lidocaine- no change in phase O due to fast dissoc, decreased conduction
III = flecainide = phase 0 block, slowed conduction due to increased refractory beats

264

ADRs class 1

Drowsiness
Dizziness
Proarrhythmic - ventricular response to atrial flutter

265

Describe class 2 action

BB e.g. propanol, atenalol, bisoprolol and sotalol
Diminised phase 4 depolarisation so increase refrat in AV.
Conduction and generation

266

Class 3 action

Increased stage 3 and refractory period/ AP duration.
Prolonged repolarisation,
Conduction and generation

267

Amioderone ADRs

Pulmonary fibrosis
Hepatitis
Increased LDL
Thyroid
Warfarin and digoxin

268

Sotalol moA and adrs

BB and III
Proarrhythic
fatigue
insomnia

269

Class IV action

CCBs
Decrease inward Ca (conduction) and inotropy
Decreae slope of pacemaker potential at SA node
Conduction and generation

270

ADRs class 4

AV block and aystole (with BB)
Hypotension
Gi

271

Adenosine action

Enhances K conductance and hyperpolarises cell to prolong RP
C&G

272

Adenosine ADR

Metallic taste
parasthesia
rash

273

Drugs for AF

BB or CCB or Digoxin or amioderone

274

Digoxin moA

Vagal activity so more refrac

275

VT drugs?

BB

276

WPW?

Fleconide

277

Re-entry SVT/ AV node?

Adenosine or B blocker or CCB.
Often re-entry at AV node

278

Ectopic atrial tachy or sinus tachy?

BB or CCB

279

Flutter vs fibrillation

Prepared loop/ route vs random

280

How are chemo agents discovered?

Screening
Chemical engineering
Molecular targetting
Serendipity e.g. platinum

281

Types of cells in a tumour

A = Dividing cells with adequate blood supply
B = cells which are not actively dividing but are able to
C - no longer able to divide but contribute to bulk
Target A (low in prostate)

282

What is the log kill ratio?

109 cells before detectable
Kill ratioe.g. 99.9. until 10 cells left
Compartment model disagrees

283

Fractional cell kill hypothesis?

BM harder hit than cancer but better recovery so given in 2-4 week doses.

284

Antimetabolite MoA

MTX decreases folates- purine and thymidine
5Flurouracil inhibits thymidine
S phase only

285

Alkylating agents moA

Cross lnk DNA
Contain Cl- (DNA is positive/ nucleophillic)
Cl dissociates in cell leaving a postiive platinum ion/ molecule to bind

286

Intercalating agents moa

DNA transcription and dulication via topoisomerase II.
Anthracycline antibiotics e.. doxorubicin and daunorubici.
Intercalate between base pairs to prevent breaking/ re ligation during rapair and replication (topoisomerase II).
Generates free radicles

287

Spindle poisons moa

Stop mitosis
Inhibit microtubule polymerisation - vinva alkaloids e.g. vincristine
Inhibit microtubule depolymerisation e.g. taxanes e.g. paclitaxel

288

How does chemo resistance occur?

Increase exit/ entry
Inactivation in cell
Enhanced repair
Multidrugresistant protein (MDRP)- removes
Downreg of carriers

289

Side effects of chemo

Alopecia - scalp cooling
Mucositis and thrust
Pulmonary fibrosis
N/V
Cardiotoxicity
Lung toxiciy
Haematologyical tox
Diarrhoea
Local reaction
REnal failure
Myelosuppression
Myalgia
Neuropathy
Sterility
Phlebility
Gi perm

290

Dosing of chemo?

Performance score Who1-5 based on activity and co morbidities
clinical stage
pronostic factors

291

Pharmokinetics of chemo

Variable AD
E = liver and renal
DDIs
Monitor drug levels, organ damage and cancer

292

Non chemo options?

Hormones
Antibiotics
Angiogenesis
Gene expression
Signals ect.

293

Define epilepsy

Episodic discharge of abnormal high frequency electrical activity in the brain leading to seizure

294

Diagnosis of epilepsy

Evidence of recurrent seizures unprovoked or by identifyable caues

295

Types of seizure

General:
Tonic clonic/ grand mal = fit and loss of conscious
Absent/ petit mal = unconsoius often standing, no or little movement.

Partial/ focal:
Simple = conscious
Complex
Can lead to secondary gene. one area (symptos depend on area)
Often with aura

Status >5mins or 2 back to back without any recovery in between. Convulsive or non convulsive may lead to SUDEP

296

How is status treated

IV benzo or phenytoin
NM blocking agent and ITU
Exclude hypoglycaemia

297

Causes of epilepsy

2/3 idiopathic (age=RF)
Secondary = neurological condition, vascular disease, tumours

298

Symptoms ad consequences of epilepsy

Medico-social
Physical injury from fall
cognitive disease
Psychiatric disease
ADR to medication
Stigma/ loss of livlihood
Driving

299

Explain how votage gated sodium channel blockers work and list the types for epi

Carbamezepine
Phenytoin
Lamotrigine
Inactive so reduce chance of abnormal firing.
prolongs inactivation stae and detatches

Sodium valporate

300

Explain how enhancing GABA mediated inhibitio can work for epilepsy

Benzos
GABA receptor agonist
Increases Cl- and increases threshold

301

VGSC blockers use epi

Carbamazepine general, partial not absence
Phenytoin the same
Lamotrigene all 3
Valporate all 3

302

Carbamezepine ADRs

Dizziness, drowsiness, ataxia, numbness tingling

GI, BP, rashes, neutropeia, hyponatraemia

Loads of DDIs

Tetratogenic

303

Phenytoin ADRs

Tyes As - nystag and nervousness
Gingival hyperplasia/ stevens Johnson

304

Lamotrigene ADRs

Less frequent
N/V
Skin rash
DDIs
Not as tetratogenic

305

Kinetics of VGSC blockers epilepsy

C- linear PK but inducable (monitor)
P-NON linear half (monitor
E- Lear PK
Sodium valporate - Linear

306

Sodium valporate MoA

Inhib of inactivating enzymes of GABA
Stimulates synthesis of GABA
Weak Ca channel blocker
VGSC blocker

307

ADRs of valporate

Ataxia
Weigh gain
Hepatotoxicity
DDIs

308

Benzodiazepines ADRs

Dependence withdrawral (seizure)
OD = resp and cns depression
Condision
Aggression
DDIs

309

First lie for primary generalised
Partial
Women
Status
Abscence

VAlproate sodium
Carbamezepine
Lamotrigene (children)
Diazepam/ lorazepam
Cloazepam (short)

310

OCP and antiepileptics

Carbamezepine and phenytoin interefere

311

Additional supplements to pregnant epileptic women

Folate
Vit K in last trimester

312

Briefly describe parkinsons and its symptoms

Idiopathic
Neurodegenerative
Progressive
Motor and non-motor
Tremor
Rigidity
Ataxia
Resting tremor
Slurring speech
Pain
Mood changes
Bradykinesia
Urinar symptoms
Sleep disorder
Swallowing difficulties

313

Diagnosis of parkinsons

Clinically
Exclude other forms of parkinsoniasm
Response to treatment - normal neuro imaging

314

Other forms of parkinsonism

Multi system atrophy
Vascilar parkinsonism
Drug induced (antipsychotics)
Corticobasal degeneration

315

Pathophysiology of parkinsons

Loss of dopaminergic neurones in rthe substantia nigra so less inhibition of the neostriatum
More Ach in neostriatum

316

Management of parkinsons

Drugs
Symptomatic
Surgery e.g. lesions if ADR if ADR with L Dopa

317

L Dopa MoA

Active transport across BBB
Given with peripheral DOPA decarboxylase inhibitor to reduce systemic effects.
Loss of efficacy over time

318

ADRs of L DOPA

N/V/anorexia
Hyotension
Schitzo/ psychosis, delusions, pananoia
tachycardia
DDIs e.g MAO (hypotension)
Not absorbed as well with protein

319

Kinetics of L dopa

Half life is 2 hours
Given orally so controlled release

320

Examples of Dopamine receptor agonists

Apomorphine, bromocriptine, Ropinirole

321

Use and ADRs of dopamine receptor agonists

Motor treatment, less efficacy than L-Dopa
ADRs:
Impulse control disorders e.g. gambling,
hypersecuality,
increasing dosate
Sedation Hallucination

322

Exaple of MAOI type B and effect

Selegiline
Smooth motor response
Neuroprotective

323

COMT inhibitors examples and use

Entacapone - reduces peripheral breakdown of Dopa.
prolongs L dopa effect

324

Examples of anticholinergics and use in parkinsons

procyclinide
Ach antagonises dopamine.
Treats tremor thats it

325

Amatidine MoA and use

Unceartain but promotes dopamine release.
Anticholinergic
NMDA inhibition
Tremor, few side effects

326

Cause of MG

Autoantibody blockage of postsyn

327

Symtoms of MG

Fluctuating, fatigueable weakness of skeletal muscles
Extraocular common
Bulbar involvement - dysphagia, dysphonia, dysarthria
Myasthenic criss
Overtreatment = cholinergic crisis

328

Exacerbating drugs of MG

Aminoglycosides
BB, CCB, type 1
Succinylcholine
Mg
ACEi

329

Management of MG

Acetylocholinesterase inhibitors.
Steroids
Azathioprine
IV IGs
Plasmapheresis to remove AChR

330

Acetylcholinesterase ADRS

Salivation
Sweating
Lacrimation
UI
Diarrhoea
GI upset
Emesis

331

How is depression diagnosed?

Tools e.g. PHQ 9
PAtient health questionnaire
2 of 3:
Low mood
Anhedonia (lack of pleasure)
Decreased energy

332

Secondary symptoms of depression

Decrased appetite
Sleep disturbance
Hopelessness
Reduced conc
Irritability
Self harm
Suicide
Reduced libido
Psychosis

333

Pathophysiology of depression

Poorly understood
Monoamine deficiency - 5HT and Na or binding sites but can be normal

334

Treatment of deression

Moderate - severe = SSRI and CBT

335

Example of SSRIs

Citalopram
Sertraline
Fluoxetine

336

Efficacy and ADRs of SSRIs

Best, responably safe
Anorexia
ausea
Diarrhoea(normal in first 2 weeks)
Mania
Suicide - energyt and conc first
Withdraw slowly

337

TCA example and MoA

Imipramine
Lofepramine
Inhibits Na uptake, muscurinic blockade and alpha 1 so sympthaolytic and mimetic

338

TCA ADRs

Lowers seizure threshold
AND- accomodation, glands
CVS - tac, hypo, imair contractility
Constipation
OD= cardiac monitoring

339

Example of SNRI

Non-selective monamine uptake inhibitors e.g. Venlafaxine

340

Efficacy of DNRI and ADRs

Not as well tolerated as SSRIs
Same ARDs
Sleep
BP
Dry mouth
Hyponatraemia
Withdrawal syndrome
More mania

341

Describe paranoid schizophrenia

Psychoses (other causes include depression, mania, delerium, depression)
Psychosis = lack of context with reality
Halucinations
Delusions
Unusual speech (thought)
Behavioural changes
Lack of insight
Negative symptoms include:
apathy
asociality
Social neglect

342

What are delusions

A fixed false blief that is out of keeping with someones culture or religious beliefs

343

Schitzophrenia increases risks of

Early death 20 years
substance abuse
Suicide

344

Pathophysiology of schitzophrenia

Dopamine excess (not negative)
5HT excess/ glutamate excess possible

345

Describe the dopamine pathways in the brain

Nigrostriatal - motor/ extrapyradimal (results in tardive dyskinesia)
MEsocortical - enhanced negative and cognitive
Tuberinfundibular - hyperprolactinamia

346

Describe MOa and examples of typical antipsychotics

Haloperidol
Chlorpromazine
Dpamine blockage
Anticholinergic
Alpha-adrenergic

347

Uses and adrs of typical antipsychotics

Uses - haloperidol in emergencies
Can be iven depot
ADRs include sedation
Parkinsonism
Dystonia
Akathisia (restlessness)
Tardive dys
Neuroleptic malignant syndrome (rigidity)
Hyperthermia
CPK
Autonomic
Decreased BP
Postural hypotension
weight gain
Gyaenocomastia
pigmentation
OD: CNS and CVS sidden death

348

Examples and Moa atypical antipsychotics

Olanzepine
Risperidone
Quetiapine
Clazapine.
Same same but less side effects.
Defined as less likely to cause parkinsonism but not neccessarily better

349

ADRs atypical antipsychotics

Agranulocytosis
Immunesuppression
Weight gain (saity)
Diabetes
Prolactin
Sedation

350

Anxiety symtoms

Fear
Avoidance
Light headedness
SOB
Hot/Cold
Nausea
Palpitations
Numbness
ins and needles
GABA?5HT?NA??

351

Treatment of anxiety

CBT first line
Anxiolytics and antipsychotics in crises/ really severe
SSRI/NI first if stage 3/4

352

What is bipolar disorder

Mania and depression, hypomania (mild)for prolonged periods

353

Symptoms of mania

Overactivity
Poor conc
Poor sleep
Rapid speech
Poor judgement e.g. addiction/ spending
Sexually disinhibited
Psychotic symptoms- hallucinations, grandiose, delusions

354

Treatment of bipolar

Lithium
VGSC anti epileptics
Antipsychotics

355

Lithium Moa and efficacy

Increases 5HT
Reduces certain other neurotransmittor effects
Best for lowering suicide in bipolar but only after 1 year
Good stabilser
Augments antideprresants in unipolar depression

356

ADRs of lithium

Nephrotoxic
Hypothyroid
Hair loss
memory
Thurst
Polyuria
Tremor
Drowsiness
Weight gain

OD: dysarthria
cognitive impairment
give anticonvulsants and increas fluids/ dyalise.

monitor 3 months
NSAIDS increase

357

Examples and effect of acetylcholinesterase inhibitors in Altzeimers

Prolongs progresion by one year. Increases arousal, memory, attention and mood (not if severe)
e.g. Donepezil and galantamine

358

ADRs of AChesterase inhibitors in alt

N/V/D
Difficulty sleepine
muscle crams
anorexia
Gi bleed

359

NMDA antagonist example and ARDS and use

Moderate/ sever dementia
Well tolerated
Hypertension
Dyspnoea
Headache
Dizziness
Drowsiness
e.g. memantine

360

Explain stomach acid secretion

HKATPase exchanger on apical
Becomes phiosphorylated as part of ccle which is stimulated by luminal K
Found in tubulovesicles (canalioicular membrane precursor)

361

PPI kinetics

Acid activated pro drug
Accumulate selectively in acid space
Only bind to active pumps so delayed action (2-3 days)
Restoration from de novo synthesis (covalent binding)

362

H2 receptor antagonist

Short t1/2
BD dosage
Gyneacomastia
Cheap

363

Alginates

Gaviscon
Viscous layer over exposed layer

364

PPI ADRs

Diarrhoea, gastrinomas, TB, C diff, oesteoporosis

365

GORD treatment

Step up or step down
symtoms vs healing
Not bothered about H pylori

366

Treatment of PUD

H pylori (lansoprazole
Stop NSAID

367

How does H pylori cause disease?

Produce lipopolysaccharides and peptides to stimulate chemotaxis and inflammation

368

Neurogenic control of guy

Intrinsic -local enteric system
Extrinic:
instestino=intestinal -one segment distensioncauses intenstinal inhibition
Anointestinal reflex - distension of anus inhibits gut
Gastrocolic and duodenal colic

369

Causes and lifestyle factors for constipation

Medical cause e.g. DM, dehydration, preg, cancer, obstruction, drugs
Increase fluids
Exercise

370

Bulk laxatives example and MoA

Ispaghula husk
Fibre, days to work

371

Bulk Adrs

Flatulence,
Abdo pain
CI: obstrction

372

irritant moa and examples

Senna
stimulates gut motility - water and electroyte retentiona dn peristalsis -rapid. used if soft faeces

373

Irritant ADRS

Colonic atony (constipation)
Hyokalaemia

374

Lectulose moa

Osmotic agent, dissachoride broken down into lactose/ monomers.

375

Lectulose ADRs

Distention
Abdopain
Nausea
Diarrhea

376

Macrogols e.g. movical moa

Osmotic
Prevents dehydration
CI obstruction

377

Glycerol Supps moa

Softner
Safe not effectie

378

MAcrogols adrs

Bloating dia
CI: obstruction

379

Glycerol suppos ADRs

Anal irritation, burning, dia, gas, nausea

380

Phosphate enema moa

Osmotic, quickly and severe

381

Phosphate enema adrs

dehydration, cramps, gas

382

Mechanism of emesis

pyloric sphincter closes
Cadia and oesophagus relac
Contraction of abdominal wall and diaphragm
Glottis closes with elevation of soft palate
Ach, H1, 5HT in medullary centre
Postrema = part of medullar on the floor of the fifth ventricle (dopamine)

383

Hyoscine MoA and ADRs

Anti muscurinic
Symp effects
used in motion sickness and short lived

384

Mebeverine moa

Antimuscurinic used in GI spasms and IBS.

385

Cyclizine MoA and ADRs

H1 antagonist
Anti musc
Used in acute N/V
QT prolongation sedative

386

Metoclopramide

D2 antagonist
Anti cholinergic blocks vagal afferent 5HT
ADRs
Extrapyradimal
Prolactin

387

Domperidone moa and adr

D2 antagonist, increase gastic empyting and in acute n/v. adrs prolactin and dystonia

388

Ondansetron moa adrs

5HT antagonist
Vagal stimulation blocked
Post op/chemo
adrs:
headache
flushing
constipation

389

Diarrhoea causes and treatmetn

Overflow
Drugs treat symptoms not cause
Fluid and electrolytes
Anti-motility
bulk forming
Fluid absorbents

390

Loperamide moa and Adrs

immodium
opiate analue
reduce motility and increase anal tone and sensory defecation reflex, good for chronic
CI; IBD = toxic megacolon,
abdo pain, constipation, sleepiness, vomiting and dry mouth

391

Bulk forming moa in dia

Increase water absorption

392

Fluid absorbents example and ise

Kaolin - absorbs more flid