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Haroon flashcards > Pharmacology > Flashcards

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
Q

Non-selective vs selective beta blockers

A
  • 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)
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26
Q

Enzymes as drug targets

A

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

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27
Q

Transporters as drug targets

A
  • 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
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28
Q

How does local anaesthesia work

A

Blocks Na+ voltage gated channels

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29
Q

Specific vs selective drugs

A
  • Specific - act on certain targets
  • Selective - act on subtype of target
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30
Q

Neurotransmitter in between synapses in cholinergic pharmacology

A

Always acetylcholine acting on nicotine

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31
Q

Ach binding at the nmj

A
  • Autonomic sympathetic nervous system: Noradrenaline working on noradrenergic receptors
  • Autonomic parasympathetic nervous system: Muscarinic acetylcholine receptors
  • Somatic nervous system: Acetylcholinergic nicotinic receptors
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32
Q

Drugs at the neuromuscular junction

A
  • Botolinum toxin (botox)
  • Curare (nAch-R antagonist)
  • Ach-ase inhibitors
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33
Q

How does botox work?

A
  • Binds to presynaptic vesicles
  • Ach release inhibited
  • Paralysis
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34
Q

How do Ach-ase inhibitors work?

A
  • Inhibit the breakdown of Ach
  • Increased concentration at the neuromuscular juntion
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35
Q

Overstimulation of Ach at the neurmuscular junction

A

Cholinergic crisis:
Salivation
Lacrimation
Urination
Defacation
GI distress
Emesis

Anything that understimulates Ach does the opposite

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36
Q

Parasympathetic (Ach) responses

A
  • Rest + digest
  • Pupil constricts
  • Lower heart rate
  • Bronchoconstritction
  • Increased GI motility and secretion
  • Detrusor muscle contracts
  • Penis points (erect)
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37
Q

Sympathetic (NAd) response

A
  • Fight or flight
  • Pupil dilates
  • Increased heart rate
  • Bronchodilation
  • Decreased GI motility and secretion
  • Detrusor muscle relaxes
  • Penis shoots (ejaculation)
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38
Q

Adrenaline formation

A

Tyrosine -> DOPA -> Dopamine -> Noradrenaline -> Adrenaline

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39
Q

NAd alpha 1 and 2 receptors

A
  • Vessels + sphincters
  • Agonism causes:
  • Vasoconstriction
  • Bladder contraction
  • Pupil dilation
  • (eg: tamsulosin alpha blocker for benign prostatic hyperplasia)
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40
Q

NAd beta 1 receptors

A
  • Heart
  • Agonism causes increased force of heart contraction
  • Higher blood pressure
  • Renin release
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41
Q

NAd beta 2 receptors

A
  • Lungs
  • Agonism causes bronchodilation
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42
Q

Agonism and antagonism in beta 2 receptors

A

Agonists: Short and long acting beta 2 agonists for asthma
Antagonists: Non-selective beta blockers

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43
Q

Drug for community acquired pneumonia

A

Antibiotics such as amoxicillin/clarythromycin

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44
Q

Drug for HAP (hosp. aquired pneumonia)

A

Co-amoxiclav (3x daily, 500 or 125mg for 5 days)

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45
Q

What should you take with isoniazid

A

Pyramidine to prevent:
- B6 deficiency
- Siderobastic anaemia
- Peripheral neuropathy

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46
Q

Drug for cellulitis

A

High dose oral antibiotic

If MRSA, give vancomycin

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47
Q

Side effect of trimthoprim

A

Can cause birth defects in the first trimester of pregnancy

48
Q

Drug for H.Pylori🧢

A

Clarythromycin
Amoxicillin
PPI

For 7 days

49
Q

Drug for gastroenteritis

A
  • Campylobacter -> clarythromycin
  • Amoebiasis -> metronidazole and diloxanide
  • Giardiasis -> tinidazole
50
Q

Drug for C.Difficile

A
  • Vancomycin
  • 125mg
  • 4x a day
  • for 10 days
51
Q

Drug for bacterial meningitis in community

A

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
Q

Drug for infective endocarditis

A

Antibiotics

53
Q

Types of pain

A
  • Acute (nociceptive)
  • Cancer
  • Neuropathic (nerve pain)
  • Chronic non-cancer (3+ months)
54
Q

Possible categories for adverse drug reaction reporting:

A

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
Q

Things that affect drug absorption

A
  • Acidity (eg: PPI), ionised drugs can’t cross phospholipid bilayer
  • Motility (eg: erythromycin)
  • Solubility
56
Q

Types of opioids

A
  • Naturally ocurring from the poppy - morphine + codeine
  • Modification - diamorphine (heroin), oxycodone, dihydrocodeine
  • Synthetic opioids - eg: pethidine
57
Q

What do opioids act on?

A
  • CNS + GI tract receptors
  • Resp centres of the brain (pontine)
58
Q

Side effects of opioids

A
  • Addiction
  • Constipation
  • Nausea and vomiting
  • Respiratory distress/depression
59
Q

Tolerance vs dependance

A
  • Tolerance - Physiological, body has gotten used to a certain amount of drug, desensitisation
  • Dependance - Physcological, craving euphora
60
Q

Treatment for opioid induced respiratory depression

A
  • Naloxone (competitive opioid inhibitor)
  • IV is fastest route
61
Q

Types of anticoagulants

A
  • Warfarin
  • Direct oral anticoagulation
  • Thrombolytics
  • LMWH (low molecular weight heparin)
  • Antiplatelets (aspirin, clopidogrel)
62
Q

What to give a patient bleeding on Warfarin?

A

Vitamin K

63
Q

How do NSAIDs decrease inflammation?

A

By inhibiting Cox2

64
Q

Side effects of ACE inhibitors

A
  • 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
Q

Side effects of PPIs

A

Prolonged use can increase fracture risk

66
Q

Dopamine agonists and antagonists

A
  • 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
Q

Where are DA (dopamine) receptors mostly found?

A

Nucleus accumbens in brain

68
Q

GABA

A
  • Main inhibitory CNS neurotransmitter
  • Agonists - benzodiazepines (eg: lorazepan and diazepan)
  • Anxiety, sleep disorders, alcohol withdrawal, status epilepticus,
69
Q

H1 and H2 antagonists

A
  • H1: For allergy (T1 IgE anaphylaxis), eg: loratidine
  • H2: 2nd line for GORD/high acid reflux after PPI, eg: ranitidine, cimetidine
70
Q

Glutamate

A

Main excitatory CNS neurotransmittor

71
Q

Drug factors that influence drug interactions

A
  • Solubility
  • Narrow therapeutic index:
72
Q

Factors that affect drug excretion

A
  • Acids cleared faster if urine is weakly basic
  • Bases clear faster if urine is weakly acidic
73
Q

Side effects of beta blockers

A
  • Low blood pressure
  • Slow HR
  • Symptoms of shock
74
Q

What can ankle swelling be caused by?

A

Calcium channel blockers (eg: amlodipine) OR heart failure

75
Q

Steroid side effects (glucocorticoids)

A

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
Q

Thiazides

A
  • eg: bendroflumethiazide and indapemide
  • Inhibits Na-Cl channel cotransporter in distal convoluted tubule
  • Increased Cl-, Na+ and water excreted
77
Q

Spironolactone

A
  • Inhibits ENaC channel in collecting duct (aldosterone antagonist)
  • Increased Na+ and water excreted
  • Increased K+ retention
78
Q

Mechanism of warfarin

A

Antivitamin K because in inhibits Vitamin K epoxide reductase

79
Q

Thrombolytics

A
  • “Clot buster”
  • eg: alteplase, activated tissue plasminogen, activates plasmin to degrade fibrin
80
Q

Additive/summative drug interaction

A

Total effect is the sum of the two drugs put together

81
Q

Synergy drug interaction

A

Taking the two drugs together increases the effect

82
Q

Antagonist drug interaction

A

Reduces the effect of the agonist

83
Q

Potentiation drug reaction

A

Effect of one drug is increased but the other one isn’t

84
Q

Where are most drugs metabolised and excreted?

A

Metabolised: liver
Excreted: kidneys

85
Q

Example of drug interaction that affects absorption

A
  • Morphine decreases motility in the GI system, decreasing absorption
86
Q

What happens if you add a drugs that is higher protein binding than the original drug?

A

The original drug won’t work (competitive inhibition)

87
Q

Morphine metabolism

A
  • 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
Q

What does metronidazole do?

A
  • Decreases effect of CYP450
  • Effect duration of morphine is longer as it’s being metabolised slower
  • This is enzyme inhibition
89
Q

What is INR in pharmacology?

A

International normalised ratio
- High INR = too much water or drug induced = enzyme inhibition

90
Q

Types of receptors

A
  • 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
Q

What is a receptor?

A

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
Q

Exogenous vs endogenous ligands

A

Exogenous - drugs
Endogenous -hormones, neurotransmitters etc

93
Q

Codeine

A
  • 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
Q

Oral bioavailibility of opioids

A
  • 50%
  • 5mg diamorphine = 10mg morphine = 100mg pethidine
  • Give double amount of oral morphine compared to IM
95
Q

Opioid withdrawal

A
  • Starts within 24 hours
  • Lasts about 72 hours
96
Q

Patient risk factors for adverse drug reactions

A
  • Gender (F>M)
  • Elderly
  • Neonates
  • Polypharmacy
  • Genetic predisposition
  • Hypersensitivity
  • Hepatic/renal impairments
  • Adherance problems
97
Q

Drug risk factors for adverse drug reactions

A
  • Steep dose-response curve
  • Low therapeutic index
  • Commonly causes ADRs
98
Q

Augmented ARD

A
  • 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
Q

Bizzare ARD

A
  • Not predictable or related to pharmacology
  • Not dose dependant
  • Can’t be readily reversed
  • Can be allergy or hypersensitivity
  • Low morbidity, high mortality
100
Q

Continuous ARD

A
  • Uncommon
  • Related to cumulative dose
  • Time related
  • eg: steroids and osteoporosis, analgeis nephropathy, colonic dysfunction due to laxatives
101
Q

Delayed ARD

A
  • Usually dose related
  • Shows itself some time after use of drug
102
Q

Ending of drug use ARD

A
  • Uncommon
  • Occurs soon after drug withdrawn
  • eg: opiate withdrawal, adrenocortical insufficiency due to glucocorticoud withdrawal, withdrawal seizures when anticonvulsants are stopped
103
Q

Failure ARDs

A
  • Common
  • Dose related
  • Often caused by drug interactions
  • eg: oral contraceptive pill, warfarin
104
Q

Affinity vs efficacy vs potency

A
  • 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
Q

What is the EC50?

A

The dose required to pertain 50% of a response

106
Q

What is a therapeutic range?

A
  • Upper and lower bounds of safe doses of a drug.
  • Narrower range = need more care in dispensing
107
Q

Treatment for cardiogenic shock

A
  • Dobutamine
  • Increases force and rate of cardiac contraction
108
Q

When to give opioids?

A
  • In chronic severe pain relief
  • Mostly cancer pain
109
Q

Risk factors for morphine metabolism

A
  • Elderly
  • Not eating or drinking
  • Reduced kidney function
  • Do renal profile to assess metabolic function before prescribing
110
Q

What is the mechanism of action for erythromycin?

A

Inhibits protein syntesis by binding to ribosomal 50s subunit

111
Q

Mechanism of ACh release

A
  • 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
Q

What are the three classes of enzyme inhibitors?

A
  • Reversible
  • Irreversible
  • Partially reversible
113
Q

Side effects of acetylcholinesterase inhibitors

A
  • Nausea
  • Diarrhoea
  • Dizziness
  • Bradycardia
  • Insomnia
  • Headaches
  • Muscle cramps

(link to parasympathetic activation)

114
Q

Mechanism of aspirin

A
  • Irreversibly inhibits Cox-2
  • Prevents the breakdown of arachidonic acid into prostaglandin H2

(non-selective for Cox-1 and Cox-2)

115
Q

Furosemide

A
  • Loop diuretic
  • Inhibits Na-K-Cl channels in ascending loop of Henlé
  • Increases ion and water excretion and inhibits their absorption in PCT
116
Q

Drugs for TB (ripe) and their side effects

A

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
Q

What to report on an MHRA yellow card

A
  • All suspected reactions to herbal medicines and black triangle drugs
  • All serious suspected reactions for established drugs, vaccines, contrast media and drug interactions

Haroon flashcards (10 decks)

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