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ESA 5 > Pharmo > Flashcards

Pharmo Flashcards

1
Q

Yellow card

A

Black triangle = all
Established - serious
Paediatir= all

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2
Q

Legal requirements prescribing

A

Legible ink
2 ID
signed dated

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3
Q

Define slip, lapse, mistake, volation

A

Concentration
Memory
Knowledge
Intentional

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4
Q

First pass metb includes

A

Liver, gut wall and gut lumen

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5
Q

Describe protein binding of different drugs

A

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

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6
Q

What is Vd affected by?

A 
Receptor sites in tissues
Regional blood flow
Lipid solubility
Active transport
Disease
DDIs
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7
Q

CYP inducers

A 
Phenytoin
Carbamazepine
Barbiturates
Rifamipicin
Alocohol (chronic
St John's Wort
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8
Q

CYP inhibitors

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

Hepatic disease (opiates in cirrhosis)

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9
Q

When should you monitor drugs?

A

Long half life
Narrow TI
Risk of DDIS
0 order

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10
Q

What does BNF contain

A

Comprehensive list of all licensed drugs in the UK

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11
Q

Role of pharmacist in prescribing

A

No legal responsibility

Check prescriptions are correct

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12
Q

Pharmokinetics of Digoxin

A

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

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13
Q

How do you calculate Loading dose

A

Vd x [Drug at target}

Note that Vd = L or L/kg

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14
Q

How do you calculate the elimination rate constant?

A

=slope of the curve (k)

= clearance/Vd

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15
Q

Calculation of T1/2

A

Vd (kg)/Cl log0.5/k

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16
Q

T1/2 in children

A

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

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17
Q

Comptments and drugs

A

Equilibrium in each compartment.

Varies

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18
Q

Describe drug specificity and selectivity

A

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

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19
Q

DDI absorption example

A

Gastric emptying - metaclopramide. Affects Fe and tetracyline absorption

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20
Q

Types of ADRs

A

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

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21
Q

Preparations of testosterone?

A

Oral, IM, implant

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22
Q

Steroid hormones and distribution?

A

Steroid hormone binding globulin (not prog) and albumin

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23
Q

Use/ Actions of ostradiol

A 
Prevent HRT symptoms - hot flushes, support bone structure.
Anabolic
Na/H2O retention
Impair glucose tolerance
Increase coagubility
Improves mood and concentration
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24
Q

Side effects of oestradiol

A 
Water retention
N/V
Diabetes
Breast tenderness
Thromboembolism
Endometrial hyperplasia and cancer
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25
Q

Actions of prog

A 
Anabolic
Increase Bone density
Secretory to endometrium
Fluid retention
Mood changes
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26
Q

Side effects of Prof

A 
Water retention
Depression (PMS)
Irritability
Weight gain
Acne
N/V
Lack of conc
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27
Q

Actions/ Side effects of testosterone

A 
Male secondary sexual characteristics
Anabolic
Acne
voice change
Aggression
Metabolic adverse effect on lipids - increases LDL and decreases HDL
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28
Q

Preparations of COCP?

A

Monophasic

Triphasic

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29
Q

How does COCP work?

A

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

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30
Q

MEtabolism of COCP?

A

CYP

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31
Q

Absorption of COCP DDI?

A

Broad spec on flora

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32
Q

Some COCP ADRS

A 
Focal migranes (stroke)
Headache
Moodswing
Gall stones
Precipitate porphyria (skin sensitivity-dark urine-memntal disturb)
weight gain
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33
Q

Use of POP?

A

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

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34
Q

Formulation of HRT?

A

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

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35
Q

ADRs of HRT

A 
Breast cancer
Endometrial cancer
IHD
DVT
Uterine bleeding
Lipid profile
Thrombophilia
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36
Q

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

A

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

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37
Q

Affects of anti-progs

A

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

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38
Q

Effect of high LDL?

A

Pro atherogenic

Toxic to endothelial. enhance platelet aggregation.

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39
Q

Affect of obesity on lipid profile

A

Increases Cholesterol, Triglycerices and decreases HDL

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40
Q

Action of simvastatin/ atorvastatin

A

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.

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41
Q

ADR of simvastatin/ atorvastatin

A

LFTS (reversible)

Myopathy - CPK

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42
Q

Metab and elimination of Statins DDIS

A

CYP

OATP2 - fibrates and cyclosporin augment affect

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43
Q

Describe Benzafibrates action

A 
PPARalpha agonist.
More lipoprotein lipase
Reduce TG (espc Post prandial)
Not great LDL decrease
Increase LDL size
Increase HDL-C
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44
Q

ADRs Benzafibrates

A

Rhabdomolitis
Myopathy
LFTs

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45
Q

Nicotinic acid action

A

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

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46
Q

ADRS/ contraindications for Nicotinic acid

A 
Flushing, itching, headache
Hepatotoxicity
GI
Peptic ulcer
hyperglycaemia
CIs: Liver, PUD
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47
Q

Ezetimibe action and uses

A 
Cholesterol absorption. Circulates enterohepatically.
Lowers LDL (more hepatic receptors)
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48
Q

ADRs of Ezetimibe

A

Headache, abdo pain, diarrhoea

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49
Q

Give a statin?

A

CVS risk tables in BNF

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50
Q

MoA metformin

A

Decrease insulin resistance and hepatic glucose production

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51
Q

Side effects metformin

A

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

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52
Q

MoA Gliclazide

A

Increase production
K/ATP channel antagonist
Increase Ca release

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53
Q

ADR sulphonylurea

A

Weight gain

Hypo

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54
Q

Pioglatizone Rosiglatizone MoA

A

PPAR receptor. Decrease FAs. Increased muscle and adipose sensitivity

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55
Q

Pioglatizone Rosiglatizone ADRs

A 
Bladder cancer
Fluid retention and CVS risk
Osteoporosis
No hypos
More LDL and HDL
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56
Q

Repaglinide, Nateglinide MoA

A

K/ATP antagonist

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57
Q

Repaglinide, Nateglinide ADRs

A

Hypo (lower risk)

No Weight gain

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58
Q

Repaglinide, Nateglinide pharmacokinetics

A

Short half life so taken before meals

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59
Q

DPP4 inhibits/ GLP1 analogue

A

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

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60
Q

GLP1/ DPP4 inhibitor ADRs

A

N/V
Diarrhoea
GORD
Injected so pain

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61
Q

SGLT2 inhibitor action

A

Blocks in PCT

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62
Q

SGLT2 ADRs

A

Polyurea
Polydipsia
Thrush
UTI

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63
Q

Acarbose/ a-glcosidase inhibitors ADRs

A

Flatulence

Diarrhoea

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64
Q

Criteria for treatment of Diab?

A

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

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65
Q

Physiological effects of Insulin

A 
Glucose uptake in liver, muscle, adipose
Glycogesis in liver
Lipogenesis in Adiposites
Proteogensis in Muscle cells
Inhibit gluconeogensis
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66
Q

Half live of insulin

A

5 mins

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67
Q

Best indulin regime

A

Long acting with rapid acting`

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68
Q

Types of insulins

A

Animal porcine and bovine

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69
Q

Short acting

A

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

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70
Q

Examples of short acting insulins

A

Actrapid, Humulin , Novorapid

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71
Q

Examples of longer acting insulins

A

Insulin Glargine

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72
Q

Rapid acting insulins

A

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

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73
Q

Intermediate acting inslins

A

Isophane intermediate actin (NPH)/ Humulin I.

Onset 1.5-3, peaks at 4-8. lasts 12-20.

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74
Q

Long acting basal analogue insulins

A

Slow onset 2-6hours, duration up to 24

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75
Q

Very long acting insulins

A

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

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76
Q

ADRs inslin

A

Hyper/hypos
Lipodystrophy
Painful injection site
Insulin allergy

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77
Q

Sources of insulin error

A

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

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78
Q

MoA orlistat

A

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

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79
Q

ADRs orlistat

A

Soft, fatty stools, risk of flatus, faecal incontinence

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80
Q

What is pharmacovigilance

A 
Process of identifying and then responding to safety issues about marketed drugs.
Ensure saftey
Minise risk
Optimise benefit
Withdrawral of drug results? (E)
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81
Q

Aims of pharmacovigilance

A

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

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82
Q

Why is pharmacovigilence needed?

A 
PAtients in trials are restricted
Limited duration of drugs
Specialists giving drugs in trials
Different monitoring
Not big enough sample
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83
Q

How are ADRs identified?

A

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

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84
Q

Advantages of spontaneous reporting

A 
Involves all
Everything included
IInexpensive
Continuous
Can generate ADR hypothesis
ID risk factors
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85
Q

Limitations of spontaneous reporting

A 
Undereporting
Delay in reorting
Misleading information given
No control group
Cant get incidence rate as no idea how many are treated
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86
Q

Controvosy in yellow card

A

Quality of patient reports?

Under reporting

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87
Q

Difference between pharmacogenetics vs genomics

A

Gene vs entire genome

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88
Q

Variability in ADRs. drugs

A

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

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89
Q

Variability in ACEi

A

Better for whites as they have a higher RAS activity

Older and afrocarribean = CCB

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90
Q

Issues surrounding pharmacogenetics

A

DNA database

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91
Q

Synthetic cortisol

A

Hydrocortisone

Prednisolone also a glucocorticoid

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92
Q

More potent than cortisol?

A

Dexamethasone

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93
Q

Metabolic actions of glucocorticoids

A 
Glycogenolysis
Gluconeogenesis
Hyperglycaemia
Proteinolysis
Lipolysis (low/physiological)
Lipogenesis (high)
Redistricubution of fat centrally
Slight mineralocorticoid activity
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94
Q

Mineralocorticoid deficiency and example

A 
Fludrocortisone (a bit at GC)
Hyponatraemia
Dehydration
Hypotension
Hyperkalaemia
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95
Q

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

A 
GC     MC
HC equal
Pred more at GC
Dex and Bet +++GC no MC
Fludo --GC, +++MC
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96
Q

Pharmacokinetics of corticosteroids

A 
All have high bioav
All metabolised in liver 1 & 2
Glucoronidation in liver for stage 2
Clearance affected by age
Kidney can metabolise too
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97
Q

Steroid action on immune repsonse

A

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

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98
Q

MoA steroids

A

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

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99
Q

Some glucoorticoid ADRs

A 
Adrenal crisis - hypogly, shock/ hypotension/ hypokalaemia/ hyponatraemia/ dehydration
Inhbits osteoblast, ca absorption.
PUD
hypertension
DM
Catacts
Psychosis
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100
Q

Describe influenza A,B,C

A 
A = Multiple host species, most severe, various.
B = No animal reservoir, lower mortality
C = not clinically important
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101
Q

Amantadine and Rimantadine MoA

A

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

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102
Q

ADR amantadine and rimantadine

A

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

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103
Q

Give examples of neuroaminidase targetting drugs

A

Oseltamivir (Tamiflu) and Zanamivir

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104
Q

MoA of neuroaminidase targeting drugs

A

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

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105
Q

ADRs of neuroaminidase inhibitors

A

Vomiting, abdo pain, epistaxis.

Resp depression, bronchospasm

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106
Q

Folic acid antibitic examples and action

A

DNA synthesis

Trimethoprin and sulphonamides

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107
Q

What is an E test?

A

Sensitivity testing. Measures the minimum inhibitory concentration

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108
Q

What is the MIH?

A

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

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109
Q

What are breakpoints?

A 
Clinical testing data, wild type MIC, and antibiotic pharmacokinetics calulate breakponts.
Susceptibile
Intermediate
Resistnt.
Compare with MIC
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110
Q

Drug is effective when in microbiological terms?

A

Maximal concentration (Cmax) and MIC ratio.

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111
Q

MoA of antibiotics in terms of dependent killing

A

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

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112
Q

describe MDR, XDR PDR

A

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

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113
Q

ADR penicillin

A

Hypersensitivity, CNS

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114
Q

Cephalosportin ADR

A

Hypersensitity, C diff

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115
Q

Tetracylins ADr

A

N/V/D

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116
Q

Aminoglycosies ADR

A

Renal and ototoxicity

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117
Q

ADR Macrolides

A

N/V/D

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118
Q

ADR Cloramphenical and MoA

A

Broad spec, protein
BM
Liver toxicity

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119
Q

Glycopeptides

A

Renal, Bone marrow, ototoxoicity

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120
Q

Drugs that are monitored

A

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

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121
Q

Common DDIs for antibiotics

A

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

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122
Q

Digoxin ADRs

A

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

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123
Q

Describe RA

A

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

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124
Q

How is RA diagnosed

A 
Clinically
Morning stiffness
>3 joints (often hand)
Symmetrical
Rheumatoid nodules (ripe fruit)
Serum factor
X ray (only late stage)
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125
Q

Describe SLE/ Vasculitis

A

Necrosis of distal vessels
Skin rash
Granulomatosis with certain types

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126
Q

What are DMARDs

A

Disease modifying antirheumatic drugs

Lead to clinical improvement unlike NSAIDs.

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127
Q

Azathioprine MoA

A

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

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128
Q

Use of Azathioprine

A 
Transplants
SLE/ Vasc
Weak for RA
IBD
Bullous skin disease
Atropic dermatitis
Steroid sparing drug
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129
Q

ADRs Azathioprine

A

BM suppression
non hodgkin lymphoma
Infection
Hepatitis

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130
Q

Cacineurin inhibitors e.g. ciclosporin and Tacrolimys MoA

A

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

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131
Q

Cacineurin inhibitors e.g. ciclosporin and Tacrolimys ADRsa

A 
eGFR - nephrotoxic
BP - hypertension
Gingival hyperplasia
Hyperlipidaemia
N/V/D
CYP
Does not supress bone marrow
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132
Q

Uses of Cacineurin inhibitors e.g. ciclosporin and Tacrolimys

A

Transplants

Dermatis and psoriasis

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133
Q

Mycophenolate Mofetil (MMF) MoA

A

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

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134
Q

Uses Mycophenolate Mofetil (MMF)

A

Transplants
SLE
Monitor metabolite

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135
Q

Mycophenolate Mofetil (MMF) ADRs

A

N/V
Myelosuppression
Liver and kidney disease
Viral infection

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136
Q

Methotrexate MoA

A

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

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137
Q

Uses MTX

A

RA
Psoriasis
Crohns

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138
Q

Pharmokinetics MTX

A 
One a week
Long half life
Low bioavailability
Highly bound - NSAIDs
Renal excretion
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139
Q

ADRs MTX

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

Do baseline CXR, FBC, LFT, UE, Creatine

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140
Q

Sulphasalazine/ Masalazine MoA

A

Inhibit T cell proliferation and IL2

Inhibit neutrophil

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141
Q

Uses of sulphasalazine/ masalazine

A

RA
Chrons
UC

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142
Q

ADRs of sulphasalazine

A 
Safe in preg
Hepatits
Rash
ASprin reaction
N/V/ abdopain
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143
Q

AntiTNF e.g. infliximab MoA

A

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

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144
Q

USes infliximab

A

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

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145
Q

ADRs Infliximab

A

Viral infection

TB

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146
Q

Rituximab MoA

A

Targets CD20 B cells. Induces apoptosis.

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147
Q

Uses Rituximab

A

RA, especially with MTX

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148
Q

ADRs Rituximab

A

Hypergammaglobulinaemia

Hypersensitivity

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149
Q

Cyclophosphamide MoA

A

Alkylating - DNA cross links
BM supression
CYP
Kidney

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150
Q

Cyclophosphamide uses

A 
Lymphoma
Leukaemia
Sipus nephritis
Wegners granulomatosis
Polyarteritis nodosum
Vasculitis
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151
Q

Cyclophosphamide ASDRs

A

Haemorrhagic cystitis
Bladder cnacer, lymphoma, leukaemia
Hepatitis
Renal impairment

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152
Q

Pathophysiology asthma

A 
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
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153
Q

Basics of asthma treatment

A

Check compliance, technique

Eliminate triggers

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154
Q

Severe asthma criteria

A

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

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155
Q

Life threatening asthma

A

If severe plus

PEF

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156
Q

Near fatal asthma

A

PaCo2 >6 = mechanical ventilation

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157
Q

Treatment of acute asthma

A 
O2 high flow- sats >94
Nebulised salbutamol -continuous
Oral prednisolone 10-14 days
Nebulised ipratropium bromide 
Consider IV aminophyhlline (methylxanthine)
158
Q

Steps in asthma treatment

A

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
Q

SABA e.g. salbutamine tolbutaline action

A

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

160
Q

SABA ADRS

A

Adrenergic, tachycardia, palpitations, termor

161
Q

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

A

Better at preventing exacerbation

More potent

162
Q

Examples of inhaled cortico

A

Beclomethason, budesonide1

163
Q

Why CorticoS in asthma

A

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

164
Q

Leukotriene receptor antagonist e.g. montelukast MoA

A

Blocks action of cytokine to prevent inflam and mucus

165
Q

Montelukast effecacy?

A

Poor.

Only 15%

166
Q

ADRs montelukast

A

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

167
Q

Methylxanthines MoA e.g. theophylline

A

Antagonise adenosine receptor inhibit cAMP

168
Q

Methyxanthines ADRs

A 
Nausea
Headache
GORD
Arrythmias
Fits
DDIS- CYP
169
Q

Methyxanthines efficacy

A

Poor

Narrow TI

170
Q

LAMA e.g. ipotropoium bromide and tiotropium ADR

A

Urinary retention
Dry mouth
Glaucoma (esp neb)

171
Q

Anti IgE MoA

A

blocks IgE receptor so limits mast cell activation

172
Q

Efficacy IgE

A

Expensive buyt good at steroid sparing

173
Q

NSAIDs physiologic effects

A

Aalgesia
Anti-inflammatory
Anti-pyretic

174
Q

What are autocoids and what do they do?

A 
'Self-drugs' cause a local response in response to stimuli.
Bradykinin
Cytokines
NO
histamine
Leukotrienes
Neuropeptides
175
Q

What are Eicosanoids?

A

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
Q

What are COX and reactions they catalyse.

A 
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
Q

Describe COX1

A

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

178
Q

Half life of prostaglandins

179
Q

Describe COX2

A

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

180
Q

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

A 
Autocoids increase COX2
PGs bind to GPCRS (EP1-4 receptors)
Potent vasodilator
Pain modulation via:
Afferent sensation
Sensitisation of central nociception
Pyrexia
181
Q

Describe how prostaglandins cause vasodilation locally?

182
Q

Describe how prostaglandins cause pain via afferent sensation

A

(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
Q

Describe how prostaglandins can cause pain via sensitation of central nociception

A 
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
Q

Describe how prostaglandins can cause pyrexia

A

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
Q

Which COX inhibition reduces pain?

186
Q

How do NSAIDS inhibit COX

A

Competitive inhbition of COX hydrophobic channel.

Extent of COX1/2 varies.

187
Q

NSAIDs pharmokinetics

A

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

188
Q

ADRs of NSAIDS

A

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
Q

Describe COX2 specific drugs

A 
e.g. Celexib
Less ADRs
Increased CVS e.g. hypertension
Renal failure
Short term only
190
Q

DDIs of NSAIDS

A

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

191
Q

Describe Aspirin use and pharmacokinetics

A

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

192
Q

Describe all about paracetamol

A 
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
Q

MoA of Opioids

A 
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
Q

Describe enkephalin precursor receptor, MoA Pre, location

A 
Proenkephalin
DOR
(negative action on cAMP)
Decrease cAMP and Ca
Widely distributed
195
Q

Describe Dynorphin precursor receptor, MoA Pre, location

A

Prodynorphin
KOR
Ca2 direct channels (-ve)
Spinal cord

196
Q

Describe Endorphin precursor receptor, MoA Pre, location

A

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

197
Q

KOP agonist and results

A

Pentazocine

Dysphoria (confusion and disruption of thought)

198
Q

MOP agonist ad results

A 
Morphine
N/V
Constipation
Drowsiness
Miosis
Resp depression
Hypotension
199
Q

Opioid antagonist

A

Naloxone but t.5 = 1-1.5

Naltrexone is 4hpurs

200
Q

Describe morphine kinetics

A

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

201
Q

Describe Diamorphine kinetics

A 
=heroin
t.5 = 5 mins
polar so can cross BBB
Metablised to morphine
More in brain
202
Q

Describe uses of opiods

A 
Analgesic (particularly visceral)
Terminal illness
Morphine and clay/ Loperamide for diarrhoea
Methadone to maintain dependence
Tramadol = antidepressant as 5HT and NA
203
Q

Fentanyl ADR not obvious

A

Puritis due to histamine release

204
Q

Codeine use and kinetics

A 
Mild analgesic
Oral
Metabolised to morphine
Some unaffected e.g. chinese as they lack CYP enzymes
Similar effect to tramadol
205
Q

What are nociceptin and nocistatin

A

Nociceptin agonises ORL1 and nocistatin blocks

Gi so less cAMP

206
Q

Describe schedule 2 and 5 controlled drugs

A 
2 = storage, prescription and destruction conditions e.g. morphine and diamorphione
5= codeine- preparation regulations and keep invoice over the counter
207
Q

Descrine caumarins MoA

A

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

208
Q

Descriube caumarin ADRS

A

Tetratogenic

Bleeding (above 3.5)

209
Q

DDIs Warfarin

A

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

210
Q

Uses and kinetics warfarin

A

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

211
Q

Heparin MoA

A

Deactivate thrombin and Xa and IXa.

Activates antithrombin III

212
Q

Reversal of Heparin and warfarin

A

Protamine sulphate

Parenteral vit K

213
Q

Kinetics of heparin

A

Poor absorption

Rapid onset and offset

214
Q

ADRs heparin

A

Thrombocytopenia - autoimmune activated platelets
Osteoporosis
Bleed

215
Q

Describe unfractionated

A 
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
Q

Describe low molecule weight heparins

A 
Only inhibits Xa (poorly ATIII)
Subcutaneous
No monitoring needed
Long t1/2
Oreducable
217
Q

Describe Xa inhibitors e.g. Dabigatran

A

Selective Xa
Not really DDIs
Also get direct thrombin inhibitors

218
Q

Explain dipyridamole

A

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

219
Q

Explain clopidogrel

A

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
Q

How does alteplase work

A 
=tPA
activates plasminogen
Works in presence of fibrin whereas streptokinase is general.
Better if earlier use
Bleeding brain and GI
221
Q

Explain general types of anaesthetics

A

Regional
Local
Inhalational
IV general

222
Q

Describe Guedel’s signs of anaesthetic

A

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
Q

Describe the thalamo-cortical switch

A

Sudden anaesthesia above a certain anaesthetic conc

224
Q

Loss of which functions with increasing concentrations

A

Memory
Consciousness
Movement
CVS/ REsp

225
Q

What is the MAC

A

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

226
Q

MAC-BAR

A

Autonomic loss of of carbiocascular response =1.5MAC

227
Q

Induction and recovery affected by what properties

A

Solubility/ partition oefficients blood to gas/ oil to gas

228
Q

What factors affect MAC

A 
Age
Hyperthermia/ Hypo
Pregnancy
Alcoholism
Central stimulus
Opiods
NO (strongly reduces MAC)
229
Q

Potential target sites of anaesthetics

A

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
Q

Fast and slow IV anaesthetics?

A 
Fast= propafol
slow = ket
231
Q

How is TIVA monitored

A

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
Q

Local anaesthetic describe

A

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

233
Q

Describe regional anaesthetic

A

Often a nerve block

A local anaesthetic or opioid

234
Q

ADRs of anaesthetics

A

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
Q

Classes of drugs used in anaesthetics

A 
IV agents (induction)
Inhalational agents (maintainence
Anxiolytics/ hypnotics e,g, Benzos
Opiates (intraoperative analgesia_
NM blocking drugs
Antiemetics
236
Q

Describe Carbonic anhydrase inhibitor use and ADRs and MoA

A

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

237
Q

Describe osmotic agent use and ADR

A

Cerebrala oedema

Dehydration

238
Q

Loop diuretics ADR and use

A 
Heart failure
Ca/Mg excretion
Ototoxicity
Myalgia
DDIs Digoxin and steroids
239
Q

Thiazide/ thiazide like Use and ADRs

A 
BP reducing
ED
Gout
Hypokalaemia
DDIs steroids, carbamazepine, digoxin
240
Q

Aldosterone antagonists use and ADR

A

Liver disease, hypertension and HF.
Hyperkalaemia
Gynaecomastia

241
Q

ADH antagonists e.g. demeclocycline/lithium moA

A

Reduces concentrating ability of CD

242
Q

Amiloride vs spirono

A

Amiloride inhibits Nachannels in (ENAc)

Spirono = aldosterone receptor antagonist

243
Q

HF drugs

A 
Loop/ thiazide
Spirono
ACE inhib/ ARB (affective in year 1)
BBlockers
NOT Ca channel
244
Q

Explain diuretic resistance

A

Non compliance
NSAIDS/ poor renal perfusion
High Na intake

245
Q

Explain hypertension drugs

A

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

246
Q

Decompensated liver disease drugs

A

Spirono
Loop
As kidneys retain sodium

247
Q

Nephrotoxic drugs

A 
ACE inhibitors
Aminoglycosides
Penicillins
Cyclosporin A
Metformin
NSAIDs
248
Q

Describe physiological control of BP

A 
RAAS
ADH (a bit but more osmotic)
Atrial naturetic peptide - stretch = dilation
Bradykinin
NO
Endothelin
249
Q

Describe the pathology of hypertension

A

Artheriosclerosis

Loss of compliance

250
Q

Aim for hypertension

251
Q

ADRs ACEi

A

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

252
Q

Examples of angiotension receptor blockers and receptor

A

Candesartan, lorsartan

AT1 to inhibt aldosterone and vasoconstriction

253
Q

Examples of CCBs

A

Amlodipine, verapamil, diltiazem

254
Q

CCB MoA

A

Vasodilate and decrease contractility some more than others

255
Q

ADRs CCBs

A

Symp activation
Gingival hyperplasia
Constipation
HF and bradycardia

256
Q

Alpha blockers example and action

A

Doxazosin

antagonise a1 so vasoconstriction

257
Q

Alpha blockers ADRs

A 
Postural hypo
Dizziness
Headache
Fatigue
Oedema
CI: UI
258
Q

BB ADRs

A 
Lethargy
Conc
Reduced exercise tolerance
Bradycardia
Raynauds
Imaired glucose tolerance
259
Q

Explain ventricular arrhyrhmias

A

Common,

Suddencause of death in people with no history

260
Q

Stages of AP in a myocyte`

A 
0 Na+
1 K+ Cl-
2 Ca++ K+
3 K+
4 K+
261
Q

Stages of AP in SAN

A 
4 = Naf
0 = Ca
3 = K
262
Q

Describe WPW syndrome

A

Wolf parkinson White = reentry throught the bundle of Kent

263
Q

Describe class 1

A

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
Q

ADRs class 1

A

Drowsiness
Dizziness
Proarrhythmic - ventricular response to atrial flutter

265
Q

Describe class 2 action

A

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

266
Q

Class 3 action

A

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

267
Q

Amioderone ADRs

A 
Pulmonary fibrosis
Hepatitis
Increased LDL
Thyroid
Warfarin and digoxin
268
Q

Sotalol moA and adrs

A

BB and III
Proarrhythic
fatigue
insomnia

269
Q

Class IV action

A

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

270
Q

ADRs class 4

A

AV block and aystole (with BB)
Hypotension
Gi

271
Q

Adenosine action

A

Enhances K conductance and hyperpolarises cell to prolong RP

C&G

272
Q

Adenosine ADR

A

Metallic taste
parasthesia
rash

273
Q

Drugs for AF

A

BB or CCB or Digoxin or amioderone

274
Q

Digoxin moA

A

Vagal activity so more refrac

275
Q

VT drugs?

276
Q

WPW?

277
Q

Re-entry SVT/ AV node?

A

Adenosine or B blocker or CCB.

Often re-entry at AV node

278
Q

Ectopic atrial tachy or sinus tachy?

279
Q

Flutter vs fibrillation

A

Prepared loop/ route vs random

280
Q

How are chemo agents discovered?

A

Screening
Chemical engineering
Molecular targetting
Serendipity e.g. platinum

281
Q

Types of cells in a tumour

A 
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
Q

What is the log kill ratio?

A

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

283
Q

Fractional cell kill hypothesis?

A

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

284
Q

Antimetabolite MoA

A

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

285
Q

Alkylating agents moA

A

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

286
Q

Intercalating agents moa

A

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
Q

Spindle poisons moa

A

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

288
Q

How does chemo resistance occur?

A 
Increase exit/ entry
Inactivation in cell
Enhanced repair
Multidrugresistant protein (MDRP)- removes 
Downreg of carriers
289
Q

Side effects of chemo

A 
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
Q

Dosing of chemo?

A

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

291
Q

Pharmokinetics of chemo

A

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

292
Q

Non chemo options?

A 
Hormones
Antibiotics
Angiogenesis
Gene expression
Signals ect.
293
Q

Define epilepsy

A

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

294
Q

Diagnosis of epilepsy

A

Evidence of recurrent seizures unprovoked or by identifyable caues

295
Q

Types of seizure

A

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
Q

How is status treated

A

IV benzo or phenytoin
NM blocking agent and ITU
Exclude hypoglycaemia

297
Q

Causes of epilepsy

A

2/3 idiopathic (age=RF)

Secondary = neurological condition, vascular disease, tumours

298
Q

Symptoms ad consequences of epilepsy

A 
Medico-social
Physical injury from fall
cognitive disease
Psychiatric disease
ADR to medication
Stigma/ loss of livlihood
Driving
299
Q

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

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

Sodium valporate

300
Q

Explain how enhancing GABA mediated inhibitio can work for epilepsy

A

Benzos
GABA receptor agonist
Increases Cl- and increases threshold

301
Q

VGSC blockers use epi

A

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

302
Q

Carbamezepine ADRs

A

Dizziness, drowsiness, ataxia, numbness tingling

GI, BP, rashes, neutropeia, hyponatraemia

Loads of DDIs

Tetratogenic

303
Q

Phenytoin ADRs

A

Tyes As - nystag and nervousness

Gingival hyperplasia/ stevens Johnson

304
Q

Lamotrigene ADRs

A 
Less frequent
N/V
Skin rash
DDIs
Not as tetratogenic
305
Q

Kinetics of VGSC blockers epilepsy

A

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

306
Q

Sodium valporate MoA

A

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

307
Q

ADRs of valporate

A

Ataxia
Weigh gain
Hepatotoxicity
DDIs

308
Q

Benzodiazepines ADRs

A 
Dependence withdrawral (seizure)
OD = resp and cns depression
Condision
Aggression
DDIs
309
Q 
First lie for primary generalised
Partial
Women
Status
Abscence
A 
VAlproate sodium
Carbamezepine
Lamotrigene (children)
Diazepam/ lorazepam
Cloazepam (short)
310
Q

OCP and antiepileptics

A

Carbamezepine and phenytoin interefere

311
Q

Additional supplements to pregnant epileptic women

A

Folate

Vit K in last trimester

312
Q

Briefly describe parkinsons and its symptoms

A 
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
Q

Diagnosis of parkinsons

A

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

314
Q

Other forms of parkinsonism

A

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

315
Q

Pathophysiology of parkinsons

A

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

316
Q

Management of parkinsons

A

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

317
Q

L Dopa MoA

A

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

318
Q

ADRs of L DOPA

A 
N/V/anorexia
Hyotension
Schitzo/ psychosis, delusions, pananoia
tachycardia
DDIs e.g MAO (hypotension)
Not absorbed as well with protein
319
Q

Kinetics of L dopa

A

Half life is 2 hours

Given orally so controlled release

320
Q

Examples of Dopamine receptor agonists

A

Apomorphine, bromocriptine, Ropinirole

321
Q

Use and ADRs of dopamine receptor agonists

A 
Motor treatment, less efficacy than L-Dopa
ADRs:
Impulse control disorders e.g. gambling,
hypersecuality,
increasing dosate
Sedation Hallucination
322
Q

Exaple of MAOI type B and effect

A

Selegiline
Smooth motor response
Neuroprotective

323
Q

COMT inhibitors examples and use

A

Entacapone - reduces peripheral breakdown of Dopa.

prolongs L dopa effect

324
Q

Examples of anticholinergics and use in parkinsons

A

procyclinide
Ach antagonises dopamine.
Treats tremor thats it

325
Q

Amatidine MoA and use

A

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

326
Q

Cause of MG

A

Autoantibody blockage of postsyn

327
Q

Symtoms of MG

A

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

328
Q

Exacerbating drugs of MG

A 
Aminoglycosides
BB, CCB, type 1
Succinylcholine
Mg
ACEi
329
Q

Management of MG

A 
Acetylocholinesterase inhibitors. 
Steroids
Azathioprine
IV IGs
Plasmapheresis to remove AChR
330
Q

Acetylcholinesterase ADRS

A 
Salivation
Sweating
Lacrimation
UI
Diarrhoea
GI upset
Emesis
331
Q

How is depression diagnosed?

A 
Tools e.g. PHQ 9
PAtient health questionnaire
2 of 3:
Low mood
Anhedonia (lack of pleasure)
Decreased energy
332
Q

Secondary symptoms of depression

A 
Decrased appetite
Sleep disturbance
Hopelessness
Reduced conc
Irritability
Self harm
Suicide
Reduced libido
Psychosis
333
Q

Pathophysiology of depression

A

Poorly understood

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

334
Q

Treatment of deression

A

Moderate - severe = SSRI and CBT

335
Q

Example of SSRIs

A

Citalopram
Sertraline
Fluoxetine

336
Q

Efficacy and ADRs of SSRIs

A 
Best, responably safe
Anorexia
ausea
Diarrhoea(normal in first 2 weeks)
Mania
Suicide - energyt and conc first
Withdraw slowly
337
Q

TCA example and MoA

A

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

338
Q

TCA ADRs

A 
Lowers seizure threshold
AND- accomodation, glands
CVS - tac, hypo, imair contractility
Constipation
OD= cardiac monitoring
339
Q

Example of SNRI

A

Non-selective monamine uptake inhibitors e.g. Venlafaxine

340
Q

Efficacy of DNRI and ADRs

A 
Not as well tolerated as SSRIs
Same ARDs
Sleep
BP 
Dry mouth
Hyponatraemia
Withdrawal syndrome
More mania
341
Q

Describe paranoid schizophrenia

A 
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
Q

What are delusions

A

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

343
Q

Schitzophrenia increases risks of

A

Early death 20 years
substance abuse
Suicide

344
Q

Pathophysiology of schitzophrenia

A 
Dopamine excess (not negative)
5HT excess/ glutamate excess possible
345
Q

Describe the dopamine pathways in the brain

A

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

346
Q

Describe MOa and examples of typical antipsychotics

A 
Haloperidol
Chlorpromazine
Dpamine blockage
Anticholinergic
Alpha-adrenergic
347
Q

Uses and adrs of typical antipsychotics

A 
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
Q

Examples and Moa atypical antipsychotics

A 
Olanzepine
Risperidone
Quetiapine
Clazapine.
Same same but less side effects.
Defined as less likely to cause parkinsonism but not neccessarily better
349
Q

ADRs atypical antipsychotics

A 
Agranulocytosis
Immunesuppression
Weight gain (saity)
Diabetes
Prolactin
Sedation
350
Q

Anxiety symtoms

A 
Fear
Avoidance
Light headedness
SOB
Hot/Cold
Nausea
Palpitations
Numbness
ins and needles
GABA?5HT?NA??
351
Q

Treatment of anxiety

A

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

352
Q

What is bipolar disorder

A

Mania and depression, hypomania (mild)for prolonged periods

353
Q

Symptoms of mania

A 
Overactivity
Poor conc
Poor sleep
Rapid speech
Poor judgement e.g. addiction/ spending
Sexually disinhibited
Psychotic symptoms- hallucinations, grandiose, delusions
354
Q

Treatment of bipolar

A

Lithium
VGSC anti epileptics
Antipsychotics

355
Q

Lithium Moa and efficacy

A

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
Q

ADRs of lithium

A 
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
Q

Examples and effect of acetylcholinesterase inhibitors in Altzeimers

A

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

358
Q

ADRs of AChesterase inhibitors in alt

A 
N/V/D
Difficulty sleepine
muscle crams
anorexia
Gi bleed
359
Q

NMDA antagonist example and ARDS and use

A 
Moderate/ sever dementia
Well tolerated
Hypertension
Dyspnoea
Headache 
Dizziness 
Drowsiness
e.g. memantine
360
Q

Explain stomach acid secretion

A

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

361
Q

PPI kinetics

A

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
Q

H2 receptor antagonist

A

Short t1/2
BD dosage
Gyneacomastia
Cheap

363
Q

Alginates

A

Gaviscon

Viscous layer over exposed layer

364
Q

PPI ADRs

A

Diarrhoea, gastrinomas, TB, C diff, oesteoporosis

365
Q

GORD treatment

A

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

366
Q

Treatment of PUD

A 
H pylori (lansoprazole
Stop NSAID
367
Q

How does H pylori cause disease?

A

Produce lipopolysaccharides and peptides to stimulate chemotaxis and inflammation

368
Q

Neurogenic control of guy

A

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

369
Q

Causes and lifestyle factors for constipation

A

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

370
Q

Bulk laxatives example and MoA

A

Ispaghula husk

Fibre, days to work

371
Q

Bulk Adrs

A

Flatulence,
Abdo pain
CI: obstrction

372
Q

irritant moa and examples

A

Senna

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

373
Q

Irritant ADRS

A 
Colonic atony (constipation)
Hyokalaemia
374
Q

Lectulose moa

A

Osmotic agent, dissachoride broken down into lactose/ monomers.

375
Q

Lectulose ADRs

A

Distention
Abdopain
Nausea
Diarrhea

376
Q

Macrogols e.g. movical moa

A

Osmotic
Prevents dehydration
CI obstruction

377
Q

Glycerol Supps moa

A

Softner

Safe not effectie

378
Q

MAcrogols adrs

A

Bloating dia

CI: obstruction

379
Q

Glycerol suppos ADRs

A

Anal irritation, burning, dia, gas, nausea

380
Q

Phosphate enema moa

A

Osmotic, quickly and severe

381
Q

Phosphate enema adrs

A

dehydration, cramps, gas

382
Q

Mechanism of emesis

A

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
Q

Hyoscine MoA and ADRs

A

Anti muscurinic
Symp effects
used in motion sickness and short lived

384
Q

Mebeverine moa

A

Antimuscurinic used in GI spasms and IBS.

385
Q

Cyclizine MoA and ADRs

A

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

386
Q

Metoclopramide

A 
D2 antagonist
Anti cholinergic blocks vagal afferent 5HT
ADRs
Extrapyradimal
Prolactin
387
Q

Domperidone moa and adr

A

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

388
Q

Ondansetron moa adrs

A 
5HT antagonist
Vagal stimulation blocked
Post op/chemo
adrs:
headache
flushing
constipation
389
Q

Diarrhoea causes and treatmetn

A 
Overflow
Drugs treat symptoms not cause
Fluid and electrolytes
Anti-motility
bulk forming
Fluid absorbents
390
Q

Loperamide moa and Adrs

A

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
Q

Bulk forming moa in dia

A

Increase water absorption

392
Q

Fluid absorbents example and ise

A

Kaolin - absorbs more flid

ESA 5 (4 decks)

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