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Phase 2a NEW > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

Physicochemical

A 
Drug reactions
Adsorption 
Precipitation
Chelation 
Neutralisation
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2
Q

Pharmacodynamics

A

drugs effect on the body

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3
Q

Pharmacokinetics

A

body.’s effect on drug

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4
Q

Treatment for paracetamol overdose

A

Activated charcoal - binds to paracetamol (adsorption) and then leaves the body like this

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5
Q

Treatment for opioid overdose

A

Naloxone

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6
Q

Pharmacodynamics pathways

A

Summation
Synergism
Antagonism
Potentiation

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7
Q

Pharmacokinetics pathways

A

ADME - Absorption, Distribution, Metabolism, Excretion

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8
Q

Drugs tend to be metabolised in

A

Liver
Kidneys
Lungs

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9
Q

Codeine

A

Metabolised into morphine

Codeine is essentially low-dose and slow-releasing morphine

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10
Q

Bioavailability

A

Comparison between how much oral drug vs IV drug makes it into the system (blood)
IV > Oral for bioavailability

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11
Q

Morphine side effects

A

Slows down gut motility and so level of adsorption (Para NS affected)

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12
Q

Acidity

A

Drug is split into 2 portions - ionised and unionised (tends to be equilibrium)
Unionised portion can coss through the phospholipid bilayer

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13
Q

Distribution - pathway of drug

A

Protein binding
Tissues
Effect sites

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14
Q

Volume distribution

A

Bigger VD = not much in blood

Lower VD = mostly in blood so more reaches effect site

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15
Q

Protein binding

A

How much drug can bind to protein

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16
Q

Metabolism

A

Morphine metabolised in Liver by CYP450 and then broken down into morphine-6-glucuronide (much more potent than morphine itself),

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17
Q

Anti-epileptic drug (acute epilepsy)

A

Phenytoin

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18
Q

Enzyme inhibition and induction

A

counter mechanisms of enzyme action

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19
Q

Warfarin

A

Warfarin inhibits vitK factors in coag cascade
it is highly protein bound and is affected by enzyme induction which causes it to have less of an effect.
Metronidazole inhibits this and so more warfarin is about in blood which can be toxic

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20
Q

AKI (acute kidney injury) -causing drugs

A

NSAIDs, ACEi, Furosemide, Gentamicin

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21
Q

Grapefruit juice

A

Interacts with warfarin by protein binding and CYP450 pathway

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22
Q

Excretion

A

Mostly extracted via kidney

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23
Q

Druggability

A

The ability of a protein target to bind small molecules ith high affinity
Also known as ligandability

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24
Q

Drug targets

A

Receptors
Enzymes
Transporters
Ion channels

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25
Receptors
Component of a cell that interacts with a specific ligand and initiates a chain of biochemical events leading to ligand observed effects Chemicals communicate via receptors
26
Ligands can be
Exogenous (drugs) | Endogenous (hormones, neurotransmitter)
27
Neurotransmitters
Acetylcholine | Serotonin
28
Hormones
Testosterone | Hydrocortisone
29
Autacoids (local)
Cytokines | Histamine
30
Receptor types
Ligand-gated ion channels (Nicotonic ACh receptor) G protein-coupled receptors (Beta-adrenoreceptors) Kinase-linked receptors (Growth factor receptors) Cytosolic/nuclear receptors (steroid receptors)
31
G protein-coupled receptors
One of the most common group of membrane receptors 7 membrane-spanning receptors Ligands include light energy, peptides, lipids, sugars and proteins G proteins (GTPases) act as molecular switches. (On when bound to GDP, off when bound to GTP) G proteins are guanine-nucleotide binding proteins which transmit signals from GPCRs
32
GPCR pathway
Ligand Receptor G protein Coupled receptor 2nd messenger
33
Kinase linked receptors
Transmembrane receptors activated when the binding of an extracellular ligand causes enzymatic activity on the intracellular side
34
Nuclear receptors
Work by modifying gene transcription Steroid hormones Tamoxifen (breast cancer) acts as a selective oestrogen receptor modular (SERM), or as a partial agonist of the oestrogen receptors
35
Chemical imbalances can lead to pathology
Allergy - increased histamine | Parkinson's - reduced dopamine
36
Receptor ligands
Agonist - Compound that binds to and activates receptor | Antagonist - Compound that reduces the effect of an agonist
37
Potency
EC50 - Conc that gives half the maximal response
38
Full agonists
Complete saturation
39
Partial agonists
Never reaches complete saturation
40
Efficacy/Intrinsic activity
Max response achievable from a dose
41
Potency vs efficacy
Drug may be potent but not efficacious and vice versa
42
Competitive antagonism
Antagonist reverses the effects of agonists
43
Non-competitive antagonist
Molecule binds to an allosteric (non-agonist) site on the receptor to prevent activation of a receptor
44
Cholinergic receptor types
Nicotinic (agonist), curare (antag) | Muscarinic (agonist), atropine (antag)
45
Histamine receptor types
``` All are GPCRs H1 - H2 - Contraction of ileum, acid secretion from parietal cells (agonist), Cimetidine (H2 antagonist) H3 - H4 ```
46
Affinity
How well a ligand binds to the receptor
47
Efficacy
How well a ligand activates a receptor
48
Antagonists
Have affinity but zero efficacy
49
Agonists
Have affinity and efficacy
50
Isoprenaline
Non-selective beta-adrenoreceptor agonist
51
Irreversible antagonist
BAAM
52
Receptor reserve
Where agonists need to activate only a small fraction of existing receptors to produce a maximal response, so spare receptors leftover (reserve)
53
Signal transduction (amplification)
Signaling cascade causes amplification of a signal and a response
54
Allosteric modulation
The ligand binds to site other than the active site of receptor and elicit a different response through a structural modification due to the binding at the allosteric site
55
Inverse agonism
When a drug binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist
56
Tolerance
Reduction in agonist effect over time | Continuous, repeated high concentrations
57
Desensitisation
Uncoupled protein is internalised and degraded
58
Salbutamol
B2-adrenoreceptor agonist
59
Streptokinase
Clot buster - degrades a clot | Enzyme which is a drug product
60
Statins
HMG-CoA reductase inhibitors Block the rate-limiting step in the cholesterol pathway A class of lipid-lowering medications that reduces the level of bad cholesterol Primary prevention of CV disease
61
ACEi
Increased blood pressure via the RAAS pathway Increases amount of salt and water retained by the body Inhibiting ACE reduces AT2 production and therefore causes this reduction in BP
62
Parkinson's disease - Symptoms
Hypokinesia Resting tremor Muscle rigidity Cognitive impairment
63
Parkinson's disease - Treatment
Substrate - L-DOPA is a precursor for dopamine biosynthesis which crosses the blood-brain barrier (BBB)
64
Drugs and ion transport
Passive - Symporters, channels | Active - ATP-ases
65
Protein ports
Uniporters - uses ATP to pull molcules in Symporters uses movement of a molecule to pull in another against conc grad Antiporters - one substance moves against its gradient after the other moves down
66
Na-K-Cl cotransporter (NKCC)
Example of a symporter Protein that transports Na, K and Cl into cells Functions in organs that secrete fluids
67
Epithelial sodium channel
Membrane-bound ion channel Causes reabsorption of Na+ ions at collecting ducts of kidneys nephrons Blocked by high-affinity diuretic amiloride (often used with thiazide) - Anti-hypertensive
68
Voltage-gated calcium channels
Found in the membrane of excitable cells (muscle, glial, cells, neurons, etc) At resting membrane potential, VDCCs are normally closed until activation resulting in depolarisation which then opens them Amlodipine is an angioselective CCB that lowers BP
69
Voltage-gated sodium channels
Conducts Na+ through plasma membrane | Lidocaine blocks transmission of action potentials
70
Voltage-gated potassium channels
Sulfonylurea lowers blood glucose levels by blocking potassium channels (Treatment of T2DM)
71
Receptor-mediated chloride channel
GABA-A receptor | Barbiturates increase the permeability of channel to chloride ions
72
Sodium-Potassium ATP-ase Pump
Digoxin - Inhibits this pump mainly in the myocardium | Mainly used for AF and heart failure
73
Proton pump (stomach)
Omeprazole (PPI - 1st in class) - Inhibits acid secretion (finitely irreversible)
74
Irreversible enzyme inhibitors
Organophosphates (irreversible inhibitors of cholinesterase)
75
Xenobiotics
Compounds foreign to an organism's normal biochemistry such as any drug or poison
76
Cytochrome P450
Membrane-associated proteins located in the inner membrane of mitochondria or in the endoplasmic reticulum of cells Major enzymes involved in drug metabolism Most drugs undergo inactivation by CYPs Many substances are bioactivated by CYPs to form their active compounds CYPs metabolise thousands of endogenous and exogenous chemicals
77
Naturally occurring opioids
From opium poppy
78
Naturally occuring opioids from opium poppy
Moprhine - strong | Codeine - weak
79
Chemically modified (simple)
Diamorphine Oxycodone Dihydrocodeine
80
Synthetic opioids
Fentanyl Pethidine Allentanil Remifentanil
81
Synthetic partial agonists
Buprenorhine
82
Synthetic partial antagonist
Naloxone
83
Bioavailability
First pass metabolism by liver | 50% of oral is metabloised by first pass
84
Routes of admin
IV fastest | Oral slowest
85
IV PCA
Patient-controlled analgesia
86
Opioid receptors are located in
Epidural/CSF
87
Transdermal patches for lipid-soluble drugs such as
Fentanyl
88
Opium contains
Morphine | Codeine
89
Controlled drugs legislation
Opioids class A drugs Secure storage 2 signatures required
90
Dihydrocodeine
1.5 times more potent than codeine
91
Oxycodone
1.5 times more potent than morphine
92
Opioid pharmacodynamics
Natural endorphins (endogenous morphine) and enkephalins GPCR - Via second messengers Inhibit release of pain transmitters at spinal cord and midbrain - and modulate pain perception
93
How opioids work
Descending inhibition of pain Part of fight or flight response Never designed for sustained activation Sustained activation leads to tolerance and addiction
94
Opioid receptors
MOP KOP DOP NOP
95
Kappa agonists cause
Depression instead of euphoria
96
All drugs currently used are
U agonists
97
Potency vs efficacy
Potency - strong or weak, how well drug binds to receptor (binding affinity Efficacy - Maximal response or not, Full or partial agonist
98
Opioid potency examples
Diamorphine (strongest) Morphine Pethadine (weakest)
99
Tolerance and dependence
Tolerance - down-regulation of receptors with prolonged use, need higher doses to achieve the same effect Dependence - psychological (craving, euphoria), physical Opioid withdrawal - lasts up to 72 hours
100
Side effects
``` Resp depression Sedation N and V Constipation Itching Immune suppression Endocrine effects ```
101
Opioid-induced resp depression
Call for help ABC IV Naloxone (titrate to effect), has a short half-life so wears off.
102
Opioids use in chronic non-cancer pain
Start to lose effectiveness quickly within weeks
103
Common opioids
Fentanyl | Tramadol
104
Pharmacogenetics
Codeine is a prodrug which needs to be metabolised by Cytochrome CYP2D6 to morphine to ork CYP2D6 activity varies in the population - codeine will have a reduced or absent affect in some of the population
105
Metabolism of morphine
Morphine is mebtaolised to Moprhine 6 glucuronide which is more potent than morphine and is renally excreted In renal failure it will build up and may cause resp depression
106
Tramadol
``` Weak opioid agonist Slightly stronger than codeine It is a Prodrug Interacts with SSRIs, take care when prescribing to patients on antidepressants Controlled drug ```
107
Summary
Oral bioavilability is 50% for oral morphine Titrate the dose to suit patient Potentil for resp depression POtential for addiciton - be careful for starting strong opioids for chronic backache Dont issue repat prescription without seeing patient
108
Blood pressure control
Raise it in shock | Lower it in hptn
109
Heart rate control
Speed up bradycardias | Slow down tachycardias
110
A drug to lower bp will
lower heart rate
111
Nicotine and curare
Nicotine activates neuromuscular junction | Curare opposed this activation
112
Vagal nerve stimulation
slows the heart
113
NS
Somatic - skeletal muscle Autonomic - involuntary Enteric - gut
114
PNS
Sympathetic | Parasympathetic
115
Sympathetic NS
Release noradrenaline which activates adrenergic receptors (alpha and beta)
116
Parasympathetic NS
Release ACh which acts on muscarinic receptors
117
Sympa vs Para NS
Both NS first release ACh but then para fibres then release Noradrenaline whereas sympa fibres releases ACh
118
Muscarinic receptors
M1-5 GPCRs G proteins can activate second messengers M1 - Brain M2 - Heart (activation slows the heart) M3 - Glandular and smooth muscle (bronchoconstriction) M4/5 - CNS
119
Atropine
For life-threatening bradycardias and cardiac arrest
120
Muscarinic agonists
Pilocarpine - stimulates salivation (sjogrens syndrome),
121
Muscarinic antagonists
Atropine | Hyoscine
122
Hyoscine
Palliative care for drying secretions
123
Bronchoconstriction treatment
Ipratropium bromide - short acting | Tiotropium - long acting
124
Overactive bladder treatment
Solifenacin (anticholinergic)
125
ACh
Major transmitter innervating skeletal muscle
126
Anti-cholinergic side effects
Confusion Constipation Drying of mouth
127
Catecholamines
Noradrenaline - management of shock in ICU Adrenaline - Anaphylaxis management Dopamine
128
Signaling pathway
Receptor Cell G protein
129
Signaling receptors
Alpha 1 and 2 Beta 1, 2 and 3 Beta 2 is the only receptor where Adrenaline dominates over NAd
130
Alpha agonists
Septic shock treatment | Alpha 1 activation causes vasoconstriction
131
Alpha 2
Clonidine - Alpha 2 agonist (lowers BP)
132
Alpha 1 blockers
Blok alpha 1 to lower BP Tamsulosin - treats prostatic hypertrophy Doxazosin - Lowers BP Alpha 2 blockers arent useful so dont learn them
133
Beta agonists
Beta 2 activation, muscle relaxation in asthma | However beta agonists cause tachycardia and affect glucose metabolism in liver (increases glcuose production)
134
Beta blockers
Propanolol - blocks Beta 1 and 2, slows HR, reduces tremor, may cause wheeze Atenolol -Beta 1 selective, main effects on heart
135
Beta 1 and 2
Beta 1 mainly affects heart | Beta 2 mainly affects lungs
136
Uses of beta blockers
``` Angina MI prevention High BP Arrhythmias Heart failure ```
137
Beta blockers - side effects
Bronchoconstriction Bradycardia Hypoglycaemia Cardiac depression
138
hYPERSENSITIVTY
iMMEDIATE aCUTE DELAYED
139
Antibodies
IgM - made at start of infection | IgE - allergies
140
Type 1 reactions
Acute anaphylaxis Hay fever Asthma
141
Atopy
An inherited tendency to exaggerated IgE response to antigen | Hay fever, eczema, asthma
142
Skin prick test
Check for allergic responses
143
Histamine
Drives allergic responsesT
144
Histamine
Drives allergic responses
145
Atopy diagnosis
Skin prick test | RAST test
146
Hay fever treatment
Antihistamines | Steroids
147
Anaphylaxis treatment
``` Adrenaline Fluids Bronchodilators Steroids Anti-histamines ```
148
Goodpastures syndrome
Autoantibodies formed - Type 2 reaction - Ig bound to surface antigens Lung and kidney problems (pulmonary haemorrhage and glomeruloneprhtis (renal inflamamtion)) Treatment - remove anitbodies
149
Mycoplasma pneumonia
Causes pneumonia Type 2 reaction Causes haemolytic anaemia
150
Type 3 diseases
Endocarditis | Alveolitis
151
Type 4 reactions
Formation of granulomas | Slow process
152
Adverse drug reaction
Has to be noxious and unintended
153
Side effect
An unintended effect of a drug that can be beneficial | Tend to be minor and predictable
154
PDE5 inhibitors
Improve urinary flow
155
Adverse drug reactions
``` Toxic effects (beyond therapeutic range) Collateral effects (therapeutic range) Hypersusceptibility effects (below therapeutic range) ```
156
Toxic effects
Nephrotoxicity with high doses of aminoglycosides such as gentamicin Dysarthria and ataxia with lithium toxicity Cerebellar signs and symptoms with xs phenytoin Tend to occur if drug doses are too high or renal/hepatic issues
157
Collateral effects
Standard therapeutic doses Beta-blockers cause bronchoconstriction Broad-spectrum antibiotics cause C difficile
158
Hypersusceptibility reactions
Subtherapeutic effects | Anaphylaxis and penicillin
159
Severity of ADRs
Mild - nausea, drowsiness, itching rash | Severe - Resp depression, neutropenia, haemorrhage, anaphylaxis
160
Time independent reactions
Occur at any time during treatment | INR increase when erythromycin administered with warfarin
161
Time-dependent reactions
Rapid reactions - red man syndrome due to histamine release with rapid administration of vancomycin First dose reactions - Hypotension and ACEi Early reactions - Nitrate induced headache Intermediate reactions - delayed immunological reactions such as stevens-johnson syndrome with carbamazepine Late reactions - adverse reactions of long term steroids
162
Rawlins Thompson classification of ADRs
Type A - Predictable, dose dependent, common Type B - Bizzare, not predictable, not dose depedent Type C - Chronic, osteporosis and steroids Type D - Delayed, maligancies after immunosuppression Type E - End of treatment, occur after abrupt drug withdrawal - opiate withdrawal syndrome Type F - Failure of therapy
163
DoTS - ADRs classification
Dose relatedness Timing Patient susceptibility
164
Risk factors for ADRs
Patient risk - F>M, Elderly and neonates, polypharmacy, genetic predisposition, hypersensitivity/allergy, hepatic/renal impairment Drug risk - Low therapeutic index, a steep dose-response curve Prescriber risks
165
Causes of ADRs
Pharmaceutical variation Receptor abnormality - malignant hyperthermia with general anesthetics Abnormal biological system unmasked by drug - primaquine induced haemolysis Abnormalities in drug metabolism Immunological Drug-induced interaction Multifactorial - many reasons
166
Type A - Augmented, predictable
Extension of primary effects - bradycardia and propanolol
167
Type B - Bizzare, not predictable
Allergy | Hypersensitivity
168
Idiosyncrasy
Inherent abnormal response to a drug | Rare but serious
169
Types of allergic reaction
Type 1 - Immediate anaphylactic - IgE Type 2 - Cytoxic antibody - IgG, IgM Type 3 Type 4 - Delayed hypersensitivty - contact dermatitis
170
Type C - Continuous
Steroids and osteoporosis Analgesic nephropathy Steroids and Iatrogenic Cushing's syndrome Colonic dysfunction due to laxatives
171
Type D - Delayed
Teratogensis - drugs taken in the first trimester
172
Type E - Ending of drug use
Withdrawal
173
ADR suspicion
New drug Dosage increase Drug is stopped
174
Most commons drugs with ADRs
``` Antibiotics Anti-neoplastics NSAIDs CNS drugs Hypoglycaemics Cardiovascular drugs ```
175
Most common systems affected
``` GI Renal Haemmorhagic Endocrine Dermatological ```
176
Common ADRs
``` Confusion Nausea Balance problems Diarrhea Constipation Hypotension ```
177
Black triangle indicates a medicine
Undergoing additional monitoring
178
Serious reactions
Fatal Life-threatening Disabling Results in hospitalisation or prolongs it
179
Allergic reactions to drugs
Interaction of drug/metabolite/non-drug element with patient and disease Subsequent re-exposure Exposure may not be medical - penicillin in dairy products`
180
Intolerance is not same as
Allergy
181
Drug hypersensitivity
Immediate - anaphylaxis | Delayed - rahes, hepatitis, cytopenis
182
Anaphylaxis can be
Immunological | Non-immunological
183
Anaphylaxis is mediated by
IgE
184
Type 1 hypersesnivity
Acute anaphylaxis Prior exposure to antigen/drug IgE antibodies formed and attach to agents and activate the release of histamine, prostaglandins etc
185
Anaphyaxlsis
``` Rapid onset Vasodilaiton Increased vascular permability Bronchoconstriciton Urticaria Angeo-oedema ```
186
Type 2 reactions
Antibody-dependent cytotoxicity | Drug or metabolite combines with protein
187
Type 3 reactions
Antigen-antibody complexes and activate complement | Vasculitis
188
Type 4 reactions
Lymphocyte mediated Contact dermatitis Stevens-Johnson syndrome
189
Non-immune anaphylaxis
Due to direct mast cell dragranulation | No prior exposure
190
Anaphylaxis main features
Exposure to the drug, immediate rapid onset Rash Swelling (lips, face, oedema, central cyanosis) Wheeze/SOB Hypotension (anaphylactic shock) Cardiac arrest
191
Shock
Lack of body organ perfusion | Leads to loss of consciousness
192
Management of anaphylaxis
``` ABC Stop drug if infusion Adrenaline IM/Epipen High flow Oxygen IV fluids IV Antihistamine IV Hydrocortisone IV Adrenaline for Anaphylactic shock ```
193
Adrenaline
Vasoconstriction Stimulation of B1 adrenoreceptors Reduces oedema and bronchoconstriction
194
Risk factors for hypersensitivity
Medicine factors - proteins or macromolecules | Host factors - F>M, HIV, Pred drug reaction, uncontrolled asthma
195
ABC
ATP Binding Cassette | Carrier mediated transport
196
SLC
Soluble carrier OAT1 is an example - organic anion transporter, found in kidney and secretes penicillin and uric acid Probenecid blocks it leading to uric acid excretion
197
Pinocytosis
Carrier mediated entry into the cytoplasm
198
Amphotericin
Antifungal
199
Drug absorption in gut
Drug needs to be lipid-soluble to be absorbed into gut
200
Drug formulation
Some formulated to dissolve slowly (modified release) or have an enteric coating that is resistant to stomach acidity - Aspirin has an EC
201
First pass metabolism - Barriers
Intestinal lumen Intestinal wall Liver Lungs
202
Intestinal lumen
Digestive enzymes
203
Intestinal wall
Cellular enzymes - MAO | Efflux transporters - P-gp which limits absorption by transporting drug back into gut lumen
204
Liver
Major site of drug metabolism
205
Transcutaenous
Transdermal patches - Fentanyl patches
206
Thiopental
Rapid anaesthetic because of initial high brain conc, but is short-lived as continued muscle uptake lowers blood conc and indirectly the brain conc
207
Protein binding
Commonest reversible binding occurs with plasma protein albumin
208
Lipid soluble drugs
Pass easily through BBB
209
CYP450
Membrane bound isoenzyme Present in smooth endoplasmic reticulum Largely in livet tissue Cimetidine and grapefruit induce/inhibit CYP450 Smoking and alcohol increase drug metabolism rapidly which can lead to consequences
210
Phase 1 reaction
Breaking drug down | Introduction of a functional group
211
Phase 2 reaction
Building drug up with functional active chemical groups (such as methyl group)
212
Excretion
Fluids - urine, bile, sweat, breast milk Solids - faeces, hair Gases - expired air (volatiles)
213
Total urine excretion determined by
Glomerular filtration Tubular secretion Reabsorption
214
Ethanol enzyme system
Alcohol dehydrogenase
215
Ciprofloxacin
UTI drug
216
Lipid vs water-soluble drugs
Lipid soluble faster than water-soluble drugs
217
Opiates
Analgesia | Codeine, tramadol
218
Depressants
Sedation | Benzodiazepines, gabapentinoids, alcohol
219
Stimulants
Increase alertness | Amphetamines, cocaine, caffeine, ecstasy/MDMA
220
Cannabinoids
Relaxation, euphoria | Cannabis, spice
221
Hallucinogens
Altered sensory perceptions | LSD, magic mushrooms
222
Anaesthetic
Anaesthesia, sedative | Ketamine, NOX
223
New psychoactive substances
Legal high | Tend to be used in clubs
224
Substance use disorder (addiction)
Compulsive use of a substance despite harmful consequences
225
Alcohol units guidelines
14 units per week spread over 3 days or more
226
Alcohol specific deaths by condtition
Alcoholic liver disease Alcoholic cardiomyopathy Alcohol induced acute pancreatitis
227
Alcohol withdrawal
``` Tremors Agitation Tachycardia Hptn Seizures Hallucination - visual/tactile ```
228
Alcohol and pregnancy
Foetal alcohol syndrome - Pre/postnatal growth retardation, Craniofacial abnormalities
229
Psychosocial effects of excessive alcohol consumption
Interpersonal relationships - violence, rape, depression/anxiety Work problems Poverty Driving incidents/offences
230
Alcohol-use disorders - Primary prevention
Pricing - Make less affordable (MUP - minimum unit pricing) Availability - Licensing Marketing - Limit exposure to young children Campaigns - Drinkaware
231
Alcohol-use disorders - Screening
Clinical interview as part of routine exam in patients who are pregnant, smoking, health problems that are likely alcohol-induced FAST - Fast alcohol screening test

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