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Pharmacology Flashcards

1
Q

Types of drug administration

A

Systemic
- Enteral (GI tract: PO and PR-orally or rectally)
- Par-enteral (non-GI tract)
Local

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2
Q

Examples of parenteral drug administration (not via GI tract)

A
  • Intravenous
  • Intramuscular
  • Subcutaneous
  • Inhalers
  • Sublingual
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3
Q

Examples of local drug administration

A
  • Topical
  • Intranasal
  • Eye drops
  • Inhalation
  • Transdermal
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4
Q

What is pharmacodynamics?

A

Action of the drug on the body

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5
Q

What is pharmacokinetics?

A

Action of the body on the drug

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6
Q

What is an agonist?

A
  • Full affinity
  • Full efficacy
  • Mimics endogenous substance
    eg: Salbutamol is a beta 2 agonist
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7
Q

What is an antagonist?

A
  • Full affinity
  • No efficacy
  • Therefore decrease the activation of the receptor
  • Can be reversible or irreversible (if covalent bond forms)
    eg: propanolol is a beta blocker
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8
Q

Types of receptor ligands

A
  • Agonists (including partial)
  • Antagonists
  • Allosteric modulators
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9
Q

What is bioavailability?

A

How much of a drug reaches systemic circulation unaltered
- IV drugs have a 100% bioavailability as they go straight into systemic circulation

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10
Q

What does a competitive antagonist do?

A
  • Binds to the active site
  • Decreases efficacy reversibly
  • Affinity is unchanged
  • Ligand concentration is rate limiting
    eg: naloxone
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11
Q

What does a non-competitive antagonist do?

A
  • Binds away from the active site, changing its shape
  • Decreases efficacy irreversibly
  • Affinity is reduced
  • Ligand concentration is not the rate limiting step
    eg: ketamine
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12
Q

Ways drugs cross membranes

A
  • Passive diffusion
  • Facilitated diffusion
  • Active transport
  • Endocytosis
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13
Q

Factors of pharmacokinetics

A
  • Absorption
  • Distribution
  • Metabolism
  • Elimination
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14
Q

First pass metabolism

A
  • The gut and liver metabolise drugs given orally before reaching circulation
  • Phase 1 and 2 detoxification by the liver
  • Aims to slightly increase hydrophilicity
  • By microsomal enzymes, eg: CYP450
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15
Q

What does drug distribution depend on?

A
  • Blood flow to area
  • Permeability of capillaries
  • Protein binding (albumin=slower)
  • Lipochilicity/lipophobicity
  • Volume of distribution
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16
Q

What drugs can the kidney excrete?

A
  • Water soluble drugs
  • Not lipid soluble drugs
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17
Q

How does the liver metabolise drugs to help the kidney?

A
  • Phase 1: Mildly increases hydrophilicity via microsomal enzyme cytochrome p450
  • Phase 2: Majorly increases hydrophilicity by conjugation, making the drug polar, eg: acetylation, glucoronidation
  • Drug becomes water soluble
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18
Q

What are inducer drugs

A
  • Increase Cytochrome P450 activity and speed up metabolism of other drugs
  • May result in sub-therapeutic dose. less drug in blood.
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19
Q

What are inhibitor drugs?

A
  • Decrease Cytochrome P450 activity, reduce metabolism of other drugs
  • May result in toxicity
  • eg: erythromycin, grape juice
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20
Q

Examples of inducers

A

PCARBS

Phenytoin
Carbamazepine
Alcohol (chronic use)
Rifampicin
Barbiturates (St John’s Wort)
Sulfonylureas and smoking

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21
Q

Examples of inhibitors

A

ODEVICES

Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute use)
Sulphonamides and SSRIs

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22
Q

First order elimination of drugs

A
  • Catalysed by enzymes
  • Rate of metabolism directly proportional to drug concentration
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23
Q

Zero order elimination of drugs

A
  • Enzymes saturated by high drug doses
  • Rate of metabolism is constant
  • eg: ethanol, phenytoin
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24
Q

Allosteric modulators

A
  • Increase/decrease normal ligand binding
  • eg: benzodiazepine
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25
Non-selective vs selective beta blockers
- Non-selective binds to every single beta adrenergic receptor (1 and 2) - CONTRAINDICATIONS - Selective binds only to a specific subtype of beta adrenergic receptor (eg: cardioselective) - Usually we just say more or less selective rather than categorising them in this way (eg: atenolol is a less selective B1 blocker)
26
Enzymes as drug targets
NSAIDS - Inhibit Cox-1 - Prevent arachidonic acid - Decrease prostaglandin production - Risk of GI bleeds due to ulcers as prostaglandins maintain stomach mucosa ACE inhibitors - Inhibit conversion of Angiotensin I -> II - Antihypertensive - Many side effects including hyperkalemia and dry cough
27
Transporters as drug targets
- Mostly ATP dependent - Proton pump inhibitors (eg: omeprazole) cause irreversible inhibition of H+, K+ and ATPase pumps, decreasing pH - Diuretics - Selective serotonin reuptake inhibitors - Tricyclic/tetracyclic antidepressants
28
How does local anaesthesia work
Blocks Na+ voltage gated channels
29
Specific vs selective drugs
- Specific - act on certain targets - Selective - act on subtype of target
30
Neurotransmitter in between synapses in cholinergic pharmacology
Always acetylcholine acting on nicotine
31
Ach binding at the nmj
- Autonomic sympathetic nervous system: Noradrenaline working on noradrenergic receptors - Autonomic parasympathetic nervous system: Muscarinic acetylcholine receptors - Somatic nervous system: Acetylcholinergic nicotinic receptors
32
Drugs at the neuromuscular junction
- Botolinum toxin (botox) - Curare (nAch-R antagonist) - Ach-ase inhibitors
33
How does botox work?
- Binds to presynaptic vesicles - Ach release inhibited - Paralysis
34
How do Ach-ase inhibitors work?
- Inhibit the breakdown of Ach - Increased concentration at the neuromuscular juntion
35
Overstimulation of Ach at the neurmuscular junction
Cholinergic crisis: Salivation Lacrimation Urination Defacation GI distress Emesis Anything that understimulates Ach does the opposite
36
Parasympathetic (Ach) responses
- Rest + digest - Pupil constricts - Lower heart rate - Bronchoconstritction - Increased GI motility and secretion - Detrusor muscle contracts - Penis points (erect)
37
Sympathetic (NAd) response
- Fight or flight - Pupil dilates - Increased heart rate - Bronchodilation - Decreased GI motility and secretion - Detrusor muscle relaxes - Penis shoots (ejaculation)
38
Adrenaline formation
Tyrosine -> DOPA -> Dopamine -> Noradrenaline -> Adrenaline
39
NAd alpha 1 and 2 receptors
- Vessels + sphincters - Agonism causes: - Vasoconstriction - Bladder contraction - Pupil dilation - (eg: tamsulosin alpha blocker for benign prostatic hyperplasia)
40
NAd beta 1 receptors
- Heart - Agonism causes increased force of heart contraction - Higher blood pressure - Renin release
41
NAd beta 2 receptors
- Lungs - Agonism causes bronchodilation
42
Agonism and antagonism in beta 2 receptors
Agonists: Short and long acting beta 2 agonists for asthma Antagonists: Non-selective beta blockers
43
Drug for community acquired pneumonia
Antibiotics such as amoxicillin/clarythromycin
44
Drug for HAP (hosp. aquired pneumonia)
Co-amoxiclav (3x daily, 500 or 125mg for 5 days)
45
What should you take with isoniazid
Pyramidine to prevent: - B6 deficiency - Siderobastic anaemia - Peripheral neuropathy
46
Drug for cellulitis
High dose oral antibiotic If MRSA, give vancomycin
47
Side effect of trimthoprim
Can cause birth defects in the first trimester of pregnancy
48
Drug for H.Pylori🧢
Clarythromycin Amoxicillin PPI For 7 days
49
Drug for gastroenteritis
- Campylobacter -> clarythromycin - Amoebiasis -> metronidazole and diloxanide - Giardiasis -> tinidazole
50
Drug for C.Difficile
- Vancomycin - 125mg - 4x a day - for 10 days
51
Drug for bacterial meningitis in community
Parenteral benzylpenicillin (IV or IM) and then refer to hospital urgently Dosage: - Children < 1: 300mg - Children 1-9: 600mg - Adults and children 10+: 1200mg
52
Drug for infective endocarditis
Antibiotics
53
Types of pain
- Acute (nociceptive) - Cancer - Neuropathic (nerve pain) - Chronic non-cancer (3+ months)
54
Possible categories for adverse drug reaction reporting:
Augmented - is the pain predictable/common? Bizarre - is there a chance of allergy? Chronic - has patient been using the drug for a long time? Delayed - has patient used drug in the past? End of use - is the patient withdrawing from the drug?
55
Things that affect drug absorption
- Acidity (eg: PPI), ionised drugs can’t cross phospholipid bilayer - Motility (eg: erythromycin) - Solubility
56
Types of opioids
- Naturally ocurring from the poppy - morphine + codeine - Modification - diamorphine (heroin), oxycodone, dihydrocodeine - Synthetic opioids - eg: pethidine
57
What do opioids act on?
- CNS + GI tract receptors - Resp centres of the brain (pontine)
58
Side effects of opioids
- Addiction - Constipation - Nausea and vomiting - Respiratory distress/depression
59
Tolerance vs dependance
- Tolerance - Physiological, body has gotten used to a certain amount of drug, desensitisation - Dependance - Physcological, craving euphora
60
Treatment for opioid induced respiratory depression
- Naloxone (competitive opioid inhibitor) - IV is fastest route
61
Types of anticoagulants
- Warfarin - Direct oral anticoagulation - Thrombolytics - LMWH (low molecular weight heparin) - Antiplatelets (aspirin, clopidogrel)
62
What to give a patient bleeding on Warfarin?
Vitamin K
63
How do NSAIDs decrease inflammation?
By inhibiting Cox2
64
Side effects of ACE inhibitors
- High bradykinin accumulation in lungs causes dry cough (switch to ARB) - Dilutes afferent arteriole/glomerulus, can cause AKI (acute kidney injury) due to low GFR
65
Side effects of PPIs
Prolonged use can increase fracture risk
66
Dopamine agonists and antagonists
- Agonists, used in prolactinoma, acromegaly and early in Parkinson's - Antagonists often for nausea and vomiting (eg: metoclopramide, antiemetic) + for psychiatric disorders (eg: haloperidol)
67
Where are DA (dopamine) receptors mostly found?
Nucleus accumbens in brain
68
GABA
- Main inhibitory CNS neurotransmitter - Agonists - benzodiazepines (eg: lorazepan and diazepan) - Anxiety, sleep disorders, alcohol withdrawal, status epilepticus,
69
H1 and H2 antagonists
- H1: For allergy (T1 IgE anaphylaxis), eg: loratidine - H2: 2nd line for GORD/high acid reflux after PPI, eg: ranitidine, cimetidine
70
Glutamate
Main excitatory CNS neurotransmittor
71
Drug factors that influence drug interactions
- Solubility - Narrow therapeutic index:
72
Factors that affect drug excretion
- Acids cleared faster if urine is weakly basic - Bases clear faster if urine is weakly acidic
73
Side effects of beta blockers
- Low blood pressure - Slow HR - Symptoms of shock
74
What can ankle swelling be caused by?
Calcium channel blockers (eg: amlodipine) OR heart failure
75
Steroid side effects (glucocorticoids)
CUSHINGOID MAP Cataracts/glaucoma Ulcers Striae Hypertension Infection risk increase Necrosis of bone Growth restriction Osteoporosis ICP high DMT2 Myopathy Adipose hypertrophy Pancreatitis Sleep problems
76
Thiazides
- eg: bendroflumethiazide and indapemide - Inhibits Na-Cl channel cotransporter in distal convoluted tubule - Increased Cl-, Na+ and water excreted
77
Spironolactone
- Inhibits ENaC channel in collecting duct (aldosterone antagonist) - Increased Na+ and water excreted - Increased K+ retention
78
Mechanism of warfarin
Antivitamin K because in inhibits Vitamin K epoxide reductase
79
Thrombolytics
- "Clot buster" - eg: alteplase, activated tissue plasminogen, activates plasmin to degrade fibrin
80
Additive/summative drug interaction
Total effect is the sum of the two drugs put together
81
Synergy drug interaction
Taking the two drugs together increases the effect
82
Antagonist drug interaction
Reduces the effect of the agonist
83
Potentiation drug reaction
Effect of one drug is increased but the other one isn’t
84
Where are most drugs metabolised and excreted?
Metabolised: liver Excreted: kidneys
85
Example of drug interaction that affects absorption
- Morphine decreases motility in the GI system, decreasing absorption
86
What happens if you add a drugs that is higher protein binding than the original drug?
The original drug won’t work (competitive inhibition)
87
Morphine metabolism
- Metabolised into morphine-6-glucoronide by CYP450 - Cleared out by the kidney - Adding phenytoin makes the transfer more effective, causing a morphine overdose (enzyme induction)
88
What does metronidazole do?
- Decreases effect of CYP450 - Effect duration of morphine is longer as it’s being metabolised slower - This is enzyme inhibition
89
What is INR in pharmacology?
International normalised ratio - High INR = too much water or drug induced = enzyme inhibition
90
Types of receptors
- Ligand-gated ion channels - nicotinic ACh receptors - G protein coupled receptors (most common) - beta-adrenoreceptors - Kinase-linked receptors - for growth factors - Cystolic/nuclear receptors - steroid hormones
91
What is a receptor?
A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects
92
Exogenous vs endogenous ligands
Exogenous - drugs Endogenous -hormones, neurotransmitters etc
93
Codeine
- Needs to be converted to morphine to work - 10% of people don’t have cytochrome CYP2D6 that converts it - 10% of people have too much of the enzyme - Don’t give it to kids or breastfeeding mothers
94
Oral bioavailibility of opioids
- 50% - 5mg diamorphine = 10mg morphine = 100mg pethidine - Give double amount of oral morphine compared to IM
95
Opioid withdrawal
- Starts within 24 hours - Lasts about 72 hours
96
Patient risk factors for adverse drug reactions
- Gender (F>M) - Elderly - Neonates - Polypharmacy - Genetic predisposition - Hypersensitivity - Hepatic/renal impairments - Adherance problems
97
Drug risk factors for adverse drug reactions
- Steep dose-response curve - Low therapeutic index - Commonly causes ADRs
98
Augmented ARD
- Extension of primary effect (eg: bradycardia and propanolol, hypoglycaemia and insulin) - Secondary effect (eg: bronchospasm with propanolol) - High morbidity, low mortality - Excludes drug abuse and overdose
99
Bizzare ARD
- Not predictable or related to pharmacology - Not dose dependant - Can't be readily reversed - Can be allergy or hypersensitivity - Low morbidity, high mortality
100
Continuous ARD
- Uncommon - Related to cumulative dose - Time related - eg: steroids and osteoporosis, analgeis nephropathy, colonic dysfunction due to laxatives
101
Delayed ARD
- Usually dose related - Shows itself some time after use of drug
102
Ending of drug use ARD
- Uncommon - Occurs soon after drug withdrawn - eg: opiate withdrawal, adrenocortical insufficiency due to glucocorticoud withdrawal, withdrawal seizures when anticonvulsants are stopped
103
Failure ARDs
- Common - Dose related - Often caused by drug interactions - eg: oral contraceptive pill, warfarin
104
Affinity vs efficacy vs potency
- Affinity - how well a ligand binds to its receptor - Efficacy - how well a ligand successfully activates its receptor - Potency - relative strength of the drug, how well it causes a response in the body
105
What is the EC50?
The dose required to pertain 50% of a response
106
What is a therapeutic range?
- Upper and lower bounds of safe doses of a drug. - Narrower range = need more care in dispensing
107
Treatment for cardiogenic shock
- Dobutamine - Increases force and rate of cardiac contraction
108
When to give opioids?
- In chronic severe pain relief - Mostly cancer pain
109
Risk factors for morphine metabolism
- Elderly - Not eating or drinking - Reduced kidney function - Do renal profile to assess metabolic function before prescribing
110
What is the mechanism of action for erythromycin?
Inhibits protein syntesis by binding to ribosomal 50s subunit
111
Mechanism of ACh release
- Action potential arrives at presynaptic terminal - ACh is release into synapse and binds to postsynaptic receptor - Broken down by AChesterase into acetate and choline - Choline reuptaken by presynaptic terminal - Binds with Acetyl CoA to form new ACh
112
What are the three classes of enzyme inhibitors?
- Reversible - Irreversible - Partially reversible
113
Side effects of acetylcholinesterase inhibitors
- Nausea - Diarrhoea - Dizziness - Bradycardia - Insomnia - Headaches - Muscle cramps (link to parasympathetic activation)
114
Mechanism of aspirin
- Irreversibly inhibits Cox-2 - Prevents the breakdown of arachidonic acid into prostaglandin H2 (non-selective for Cox-1 and Cox-2)
115
Furosemide
- Loop diuretic - Inhibits Na-K-Cl channels in ascending loop of Henlé - Increases ion and water excretion and inhibits their absorption in PCT
116
Drugs for TB (ripe) and their side effects
Rifampicin - 6 months - red urine and tears, hep, drug interactions Isoniazid - 6 months - hep, peripheral neuropathy Pyramizinamide - 2 months - hep, arthralgia, rash Ethambutol - 2 months - optic neuritis Give first 2 for 12 months if in CNS
117
What to report on an MHRA yellow card
- All suspected reactions to herbal medicines and black triangle drugs - All serious suspected reactions for established drugs, vaccines, contrast media and drug interactions

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