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CSP1 > CSP2 > Flashcards

CSP2 Flashcards

1
Q

Locus of control

A

Expectancy that rewards are controlled by external forces or one’s own behaviour (internal vs. external)

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2
Q

Health belief model

A

action is a function of perceived likelihood of illness, seriousness, costs and benefits of action

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3
Q

Self efficacy

A

belief in ability to success, task specific

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4
Q

States of change

A 
Pre contemplation (happy with status quo)
Contemplation (think about change)
Preparation
Action
Maintenance or Relapse
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5
Q

What extent of obesity is associated with increased all cause mortality?

A

> 34

Not Grade 1 obesity 30-35

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6
Q

Basal metabolic rate for women

A

1200-1600 kCal per day

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7
Q

Total energy expenditure for most women

A

2000-2500

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8
Q

Strategies of behaviour modification

A 
Self monitoring
stimulus control
goal setting
cognitive restructuring
incentives
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9
Q

Successful slimming Recommendations

A

Diet and activity
400 kcal/day activity
Eat 5 times
Weigh 1 a week

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10
Q

Physical activity recommendation

A

30 minutes moderate activity on 5 or more days a week
Up to an hour/day to prevent obesity
Up to 90 minutes/day to maintain weight reduction

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11
Q

Who can have orlistat Rx (Xenical) - one you prescribe?

A
  • 12 years or older
  • BMI >30
  • BMI>37 with HTN, diabetes, dyslipidemia
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12
Q

Orlistat Rx (Xenical) dosage

A

120mg

With fat containing meals

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13
Q

Orlistat OTC (Alli) dosage - over the counter.

A

18 years
reduced calorie and low fat diet needed as well
60mg with fat containing meals
£12 per week

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14
Q

Orlistat effectiveness

A

Meta analysis shows weight change at 12 months compared to placebo

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15
Q

Side effects of orlistat

A
  • diarrhea
  • steatorrhea
  • minimised by maintaining strict low fat diet
  • reduce intake of fat soluble vitamins = multivitamins for 2 weeks
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16
Q

Atkins diet

A

Max 20g of carbs/day

Protein and fat

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17
Q

Appetite Suppressants

A 
Methylcellulose
Amphetamine derivatives
Sibutramine (SSRI derivative)
Rimonabant (cannabis antagonist)
GLP1 agonist = liraglutide, daily subcut injection, feel fuller and satisfied, reduces speed of stomach emptying, nausea and vomit, thyroid tumours, pancreatitis
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18
Q

Malabsoprtion inducers

A

Orlistat
Acarbose
SGLT2 inhibitors

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19
Q

Metabolic stimulants

A

Thyroxine

Beta-agonists

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20
Q

Gastric surgery

A

BMI 40 or above or 35 or above with comorbidities
Gastric Bypass = Roux en Y, restrictive and malabsoprtive (changed gut hormones)
LAP BAND = restrictive

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21
Q

Product licence

A

Marketing Authorisation

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22
Q

Off label

A

Use/route outside licensed indication

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23
Q

Liability

A

None to prescriber if

  • correct diagnosis
  • correct medicine choice
  • patient warned of potential adverse effects
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24
Q

MHRA

A

Medicines and Healthcare Products Regulatory Agency

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25
Q

Classification of Medicinal Products

A

General Sale List
Pharmacy Only medicines
Prescription Only medicines
Controlled Drugs

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26
Q

Prescription Only Medicines

A

To anyone except injections
Injections if purpose of saving life
Midwives, chiropodists, opticians, paramedics, practititoners direct

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27
Q

FP10s

A

GP prescriptions

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28
Q

FP14

A

Dentist prescriptions

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29
Q

FP10MDA-SS

A

Addict prescriptions

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30
Q

OM

A

On-in the morning:at night

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31
Q

PRN

A

When required

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32
Q

SOS

A

If neccessary

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33
Q

Black List

A

Indigestion remedies
Analgesics
Hypnotics & Anxiolytics
(not available on NHS)

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34
Q

Supplementary prescribing

A

Voluntary prescribing partnership
Between independent prescriber and supplementary prescriber
Agreed patient specific clinical management plan with patient agreement

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35
Q

BAN

A

British Approved Name

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36
Q

Most commonly implicated medications in adults

A

Antiplatelets
Diuretics
NSAIDs
Anticoagulants

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37
Q

NPSA

A

National Patient Safety Agency

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38
Q

Clinical Trial Positives

A

No confounding
No bias
Gives correlation

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39
Q

Define pharmacodynamics

A

Relationship between drug level and effect

‘what drug does to body’

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40
Q

Hysteresis

A

Relationship between drug concentrations and effect is not direct

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41
Q

Counter clockwise hysteresis

A 
Sensitisation of receptors
Delay of drug to site of effect
Agonist metabolite generation
Slow receptor kinetics
Time dependent protein binding
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42
Q

Clockwise hysteresis

A 
Tolerance of receptors
Feedback regulation
Time dependent protein binding
Antagonist metabolite generation
Disequilibrium between arterial and venous concentration
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43
Q

Drug targets

A

Enzymes
Ion channels
Ion carriers/transporters
Receptors

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44
Q

Affinity

A

How avidly drug binds to receptor
Low Kd = high affinity = low conc of ligand to bind half of receptors
- determined by strength of receptor-ligand interaction

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45
Q

Receptor Ligand Interaction

A

Electrostatic (common)
Hydrophillic
Covalent (least common)

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46
Q

Selectivity

A

Drugs ability to preferentially binding to certain receptors

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47
Q

Specificity

A

Number of different mechanisms involved In drug action

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48
Q

Potency

A

Conc. (EC50) or dose (ED50) of drug required to produce 50% of drugs maximal effect

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49
Q

Median inhibitory concentration

A

IC50

Concentration of an antagonist that reduces a specified response to 50% of the maximal possible effect

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50
Q

Efficacy

A

max effect (Emax) of a drug

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51
Q

Full agonist

A

Maximal response by occupying all or fraction of receptors

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52
Q

Partial agonist

A

Less than max response even when drug occupies all of receptors

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53
Q

Antagonist

A

Affinity but no efficacy

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54
Q

Inverse agonists

A

Agent which binds to same receptor as agonist but induces pharmacological response opposite to that agonist

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55
Q

Competitive antagonist

A

Reversibily binds to receptors as agonist but without activating receptor so competes for same binding site

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56
Q

Non comp antagonist

A

Reduces magnitude of max response attained by any amount of agonist

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57
Q

Allosteric modulator

A

Indirectly influences effects of an agonist

conformational change from binding to distinct site

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58
Q

Positive allosteric modulator

A

induces amplification of agonist

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59
Q

negative allosteric modulator

A

Reduces effects of agonist

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60
Q

Other antagonism types

A

Chemical
Physiologic
Pharmacokinetic

61
Q

biological therapies

A

Engineered macromolecule products like protein and nucleic acid based drugs
Antagonists
More specific and high potency/efficacy

62
Q

Pharmacokinetics

A

Description and prediction of time course of drugs in the body
Quantitative study of ADME

63
Q

Bioavailability

A

Fraction of unchanged drug that is absorbed intact and reaches the site of measurement

64
Q

Vd

A

Volume of distribution

= amount in body/conc in plasma

65
Q

Metabolism

A

Phase 1 = catabolic, P450 enzymes

Phase 2= anabollic

66
Q

Cytochrome P450

A

Haeme co-factor
In mitochondria and ER
activity varies

67
Q

First pass metabolism

A
  • before reaches site of measurement

- gut wall or liver

68
Q

Elimination pathways

A 
kidney
hepatoiliary
lungs
saliva
tears
sweat
other secretions
69
Q

1st order elimination

A

rate of elimination/metabolism proportionate to drug conc.

70
Q

0 order elimination

A

constant rate of drug eliminated/metabolised

71
Q

Half Life Rules

A

3.3 half lives to 90% steady state

5 half lives to <5% of initial conc.

72
Q

Clearance

A 
Total = renal + hepatic + other
Links drug conc. to rate of elimination
Volume per unit time
Clearance of organ = organ blood flow x extraction ratio of organ
total = (F x Dose)/AUC
73
Q

What do pre-contemplators need?

A

Information

74
Q

What do those wanting to change need?

A

Practical advice and guidance

75
Q

What do those trying and failing need?

A

Specialist treatment

76
Q

most to least intensive ways of changing behaviours

A

Specialist treatments - durg clinics, obesity treatments
Doctor advice
Health promotion

77
Q

ways of changing behaviours, in order of having largest population impact to smallest

A

health promotion
doctor advice
specialist treatment

78
Q

Obesity - strength of drive, effort required, target pop., efficacy of supportive meds

A

Strong strength
Substantial effort
target - well motivated, varied resources and barriers
Limited supportive meds

79
Q

Most valuable complication of obesity that by treating obesity would be economically effective?

A

DIABETES

80
Q

Define NEAT

A

non exercise activities - fidgeting

81
Q

Resting metabolic rate

A
  • increases with muscle mass
  • declines with age
  • declines during restriction of energy intake (diet)
82
Q

Approaches to changing behaviour

A

Behaviour
Diet
Medical

83
Q

Behaviour Modification Requirements

A

Goals - specific and realistic
Plan of action
Manageable slow changes

84
Q

Strategies of obesity behaviour modifications

A

Self Monitoring
Stimulus Control
Goal Setting - 5% weight loss over 6M, 1lb a week
Cognitive Restructuring

85
Q

Dietary Interventions

A

Quack cures
Fad diets
FAT AND SUGAR
About eating less not really about food groups

86
Q

Problem with fat

A

High calories but least satiating nutrient unlike protein

87
Q

Order of calorie content of food groups

A

Fat
Alcohol
Protein & Carbs
Fibre

88
Q

Who gets pharmacotherapy obesity treatment?

A
  • if BMI 27-29.9 + co-morbidities

- or higher BMI

89
Q

Who gets obesity surgery?

A
  • BMI 35-39.9 + co-morbidities

- >40

90
Q

New obesity drugs

A

Semaglutide
Lorcaserine
phentermine
Topiramate

91
Q

What does orlistat do?

A
  • blocks absorption from gut of 1/3 fat which is eaten
  • if too much eaten there is oily leakage, flatulence, diarrhoea
  • teaches people which foods contain fat = behavioural so then when stop taking tablets stopping eating fats should stay with you
92
Q

Reasons for initiation and maintenance of smoking?

A 
Initiation = social
Maintenance = pharmacological
93
Q

What is addiction a product of?

A

Person + drug + circumstances

94
Q

Peak Seeker

A
  • seeking for peak effect of smoking
    vs
    Heavy smoker - not very trough and peak life, don’t let it drop as get withdrawal/restless

Only a level of nicotine you can tolerate as it makes you sick

95
Q

Nicotine

A
  • stimulant
  • increases HR
  • stops boredom
  • immediate reward
  • neuroadaptation, dopaminergic, ACH receptor density
  • discomfort at low levels and high
  • illusion of positive effect as get rid of restlessness when don’t have it
  • other chemicals also play a role in smoke
  • nicotine hunger when conc deplete in brain or during other stress
  • nucleus accumbens
96
Q

Smoking risk vs benefit

A
  • higher stress until post quit
  • social, less bored, enjoy
  • weight loss
  • increased vigilance but lower performance
97
Q

How to assess a smoker’s dependence?

A
  • best = time to first cig in the morning (under half hour then dependent, serious if 5 mins)
  • CO in expired breaths
  • not how many cigs or types
98
Q

How long is smoking withdrawal?

A

4 weeks
Help is with these symptoms
IRRITABILITY
worse in heavier smokers
difficulty concentrating <2 weeks
LT urges to smokes but less and less frequent
Rarer = night time waking, constipation, mouth ulcers, RTI, gum bleeding, lower pain threshold, productive cough

99
Q

Average weight gain post smoking quitting

A

5-6kg

100
Q

Signs of smokers post quit

A 
HR drop
adrenaline and cortisol drop
tremor drop
increased skin temp.
decreased metabolism of caffeine and other drugs
101
Q

What effects smoke cessation success?

A

Heavy smokers
Depression
Urge to smoke

102
Q

Clinical advice smoking

A

Drugs for withdrawal
Reassurance and explain
Advise against early dieting regarding weight gain

103
Q

Adaptive Immunity Features

A
  • vast diversity of cell types
  • clonal expansion
  • danger of autoimmunity
  • B and T lymphocytes
104
Q

Innate Immunity Features

A
  • no autoimmunity
  • no clonal expansion
  • neutrophils/monocytes/eosinophils/mast cells
  • all cells of one kind
105
Q

B vs T lymphocytes

A

mature in bone marrow vs thymus
B have antibody as receptor
T only recognised when presented on cell surface

106
Q

Clonal deletion of B lymphocytes

A
  • in bone marrow
  • If an antigen engages with antibody
  • antibody expressed as IgM
  • if T dependent, in LN after activation during expansion and mutations
107
Q

Outer domain of HLA

A

2 alpha helices on beta pleated sheet

- antigen between helices

108
Q

HLA function

A 
present peptide antigens to T lymphocytes
Endogenous on class 1 to CD8 T lymph
Exogenous on class 2 to CD4
109
Q

MHC define

A
  • cluster of genes which encode molecules in antigen presentation
  • HLA region
110
Q

HLA define

A

Human Leukocyte Antigen

Genes and the molecules they encode

111
Q

Class I loci

A

HLA-A, B, C
Encoded at A, B, C locus
2 of each

112
Q

Class II loci

A

HLA-DP, DQ, DR alleles

2 of each

113
Q

Allele number

A

Number after locus letter
A*02:01:02:11
First pair = cross reactive group
Second pair = difference in amino acid sequence
Third pair = silent polymoprhisms in exons
Fourth pair = polymorph in introns

114
Q

What do APCs express

A

both class I and II

115
Q

Define haplotype

A

Team of alleles encoded on short section of 1 chromosome. Inherited from 1 parent and passed on intact if short enough otherwise crossovers

116
Q

Transplant terms

A 
Auto = given back to same person
Iso = between 2 identical twins
Allo = between 2 members of same species
Hetero/xeno = different species
117
Q

Kidney transplants

A

Allografts = antibody/T lymph rejection
AB against = ABO
T lymphocytes = HLA + peptide

118
Q

Types of rejection in kidney transplants

A

Hyperacute Rejection = mins to 4 days, complement
Acute = 5 days - 3 months, antibody, T lymphocyte
Chronic rejection = antibody or T lymphocyte, infection

119
Q

How to avoid rejection

A
  • do not if recipient has AB against donor HLA molecules
  • match donor and recipient for HLA alleles
  • use antirejection therapy
  • perform a cross match between donor cells and recip serum
  • screen all patients
  • avoid sensitisation = blood transfusion, pregnancy, previous graft
120
Q

Antirejection therapy

A
  • must be taken except if identical twin
  • prednisolone
  • azathioprime/mycophenolate
  • tacrolimus/ciclosporine
  • monoclonal ABs
121
Q

Bone Marrow Transplant

A

T lymphocyte mediated all
No need for cross matching of serum screening
Host vs graft disease & graft vs host

122
Q

How to prevent HvG and GvH

A

autografts use
in allografts T lymphocyte may be depleted
Antirejection therapy

123
Q

Type 1 hypersensitivity

A

IgE mediated
Histamine release from mast cells/basophils
Always allergic
Hayfever, asthma, anaphylactic shock

124
Q

Type 2 hypersensitivity

A

IgG & IgM mediated
Complement & phagocytosis
Autoimmune haemolytic anaemia, thrombocytopenia, myasthenia gravis, Goodpastures, pemphigus

125
Q

Type 3 hypersensitivity

A

Immune complexes
Autoimmune/allergic/antimicrobial
Extrinsic allergic alveolitis
Vasculitis, glomerulonephritis, arthritis

126
Q

Type 4 hypersensitivity

A 
Activated T lymphocytes 
Granulomas = CD4, macrophages
Without granuloma = CD8
Antimicrobial = TB, hep B, allergy, nickel sensitivity, coeliac
Autoimmune = sarcoid
127
Q

Type 5 hypersensitivity

A

ABs
Stimulate rather than destroying target
Graves

128
Q

HA B27

A

Ank Spon
RA
Colitic arthritis
Psoriatic Arthritis

129
Q

Cw6

A

Psoriasis

130
Q

DQ2 & DQ8

A

Coeliac disease

131
Q

DQ8 & DQ2

A

T1D

132
Q

DQ6

A

MS

133
Q

DR4

A

RA

134
Q

Eaton-Lambert Syndrome

A

Autoantibody to presynaptic Ca2+ in NMJ = weakness

Small cell lung cancer

135
Q

Auto-immune haemolytic anaemia

A

Autoantibodies to red cells
Destruction by complement system and phagocytes
Some AB act in warm and cold

136
Q

Causes of autoimmune haemolytic anaemia

A

Infections = syphilis, mycoplasma, EBv, virsus
Neoplasms = CLL, lymphoma
Autoimmune disease = SLE, RA, UC, PSS
Drugs = penicillin, methyl dopa

137
Q

Autoimmune thrombocytopenia

A 
Idiopathic thrombocytopenic purpura
SLE
CLL
Lymphoma
Drugs = AB, co-trimoxazole
138
Q

Coeliac disease

A
  • inflammatory disease
  • steatorrhoea, bloating, malabsorption
  • villous atrophy, deepened crypts, ulcers, lamina propria infiltrate, intra-epithelial lymphocytes
139
Q

Autoantibodies

A 
IgA Antibodies
Anti-transglutaminase antibodies
Anti endomysial antibodies
Anti reticulin antibodies
Anti Gliadin antibodies
140
Q

Gluten Coeliac

A

Alpha -gliadin - resistant to digestion in lumen of bowel

141
Q

Transglutaminase

A

tTG
enzyme
removes side chain amino group from glutamines converting them to glutamate
engaged when alpha gliadin leak into lamina propria and become deamidated
Bind to class II HLA
Activates T lymph which secrete cytokines = changes = villous atrophy, crypt enlargement

142
Q

HLA in coeliac

A

DQ2 and DQ8

143
Q

Role of IgA autoantibodies in coeliac?

A

Do not activate complement or opsonise for phagocytosis

May contribute by trapping antigen or block tTG action

144
Q

Coeliac RF

A

European
Females x 2
Severity varies
Infancy but often later

145
Q

Other coeliac features

A

dermatitis herpetiformis

146
Q

Other coeliac features

A

dermatitis herpetiformis

147
Q

IM contraindicated in who?

A

Haemophillia

148
Q

Max volume of IM vs subcut

A

5ml vs 2ml

CSP1 (20 decks)

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