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ESA 5 > Pharmo > Flashcards

Pharmo Flashcards

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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
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

ESA 5 (4 decks)

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