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Phase 2a > ICS - Pharmacology > Flashcards

ICS - Pharmacology Flashcards

1
Q

Which routes of drug administration are local?

A
  • Topical
  • Intranasal
  • Inhalation (can be systemic)
  • Transdermal (can be systemic)
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2
Q

Which routes of drug administration are systemic (enteral)?

A
  • Oral
  • Rectal
  • Sublingual/buccal
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3
Q

What does enteral drug administration mean?

A

Absorbed from gastrointestinal tract

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4
Q

Which routes of drug administration are systemic (parenteral)?

A
  • Intravenous
  • Intramuscular
  • Subcutaneous
  • Inhalation (can be local)
  • Transdermal (can be local)
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5
Q

Define first pass metabolism

A

Metabolism of a drug by the liver before being released into the systemic circulation - when drugs are administered orally

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6
Q

Define bioavailability

A

The proportion of drug given that enters the circulation and so can exert an effect on the body

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7
Q

Define agonist

A

Binds to a receptor to activate

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8
Q

Define antagonist

A

Binds to a receptor to prevent a reaction occurring

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9
Q

What is the difference between competitive and non-competitive antagonists?

A

Competitive antagonists bind directly to the active site of a receptor to prevent other things from binding whereas non-competitive antagonists bind to another part of the receptor (not the active site) to change the shape of the active site and prevent other things from binding

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10
Q

Define selectivity

A

The ability of a drug to discriminate between and only affect certain cell populations

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11
Q

Define specificity

A

The capacity of drug to trigger a response

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12
Q

What is the difference between endogenous and exogenous ligands?

A

Exogenous - originates outside body e.g. drugs
Endogenous - originates inside body e.g. hormones/neurotransmitters

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13
Q

Name 4 receptors that drugs target

A
  1. Ligand gated ion channels
  2. G protein coupled receptors
  3. Kinase linked receptors
  4. Cytosolic/nuclear receptors
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14
Q

What are ligand gated ion channels?

A

Membrane proteins that allow ions to pass through so that the cell undergoes a shift in electric charge distribution (e.g. nicotinic ACh receptor)

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15
Q

What are G protein coupled receptors?

A

Integral membrane proteins used to convert extracellular signals into intracellular responses (e.g. muscarinic and beta-2 adrenoceptor)

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16
Q

What are kinase linked receptors?

A

Enzymes that catalyse the transfer of phosphate groups between proteins (e.g. receptors for growth factors)

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17
Q

What are cytosolic/nuclear receptors?

A

Receptors that modify mRNA/protein synthesis (e.g. steroid receptors - steroids affect transcription)

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18
Q

Define affinity in drug action

A

How well a ligand binds to a receptor

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19
Q

Define efficacy in drug action

A

How well a ligand activates a receptor (how well it induces a conformation change)

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20
Q

Describe enzyme inhibitors

A

Molecules that bind to an enzyme and usually decreases its activity. There are reversible and irreversible inhibitors e.g. statins and ACE inhibitors

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21
Q

What are uniporters

A

Membrane transport proteins that transport individual molecules into a cell

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22
Q

What are symporters?

A

Membrane transport proteins that transport two molecules across a membrane in the same direction

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23
Q

What are antiporters?

A

Membrane transport proteins that transport two molecules across a membrane in different directions

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24
Q

What are ENaC inhibitors/blocking used for?

A

Problems relating to heart failure

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25
Q

What are ENaC inhibitors/blockers?

A

Epithelial sodium channel inhibitors. Decrease reabsorption of Na+ ions at the collecting ducts. Helps to prevent the loss of potassium and lower blood pressure

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26
Q

Give an example of an ENaC inhibitor/blockers

A

Amilioride

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27
Q

What are calcium channel blockers used for?

A

Lowering blood pressure

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28
Q

What are calcium channel blockers?

A

Prevent influx of calcium into smooth/cardiac muscle cells which causes vasodilation and decreased peripheral vascular resistance

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29
Q

Give 2 examples and 3 side effects of calcium channel blockers

A
  • Amlodipine (vasodilates and doesn’t decrease heart rate - non rate limiting)
  • Verapamil (vasodilates and decreases heart rate - rate limiting)
  • Constipation, dizziness, fatigue
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30
Q

What are sodium channel blockers used for?

A

Local anaesthetics, anticonvulsants etc.

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31
Q

What are sodium channel blockers?

A

Prevent influx of sodium into cells to slow depolarisation and so reduce conduction velocity

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32
Q

Give an example of sodium channel blockers

A

Lidocaine (local anaesthetic)

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33
Q

What are potassium channel blockers used for?

A

Treating arrhythmias and type II diabetes

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34
Q

What are potassium channel blockers?

A

Block ATP-dependent potassium channels so that they cannot open. This increases calcium influx and prolongs action potentials and also triggers insulin secretion in pancreatic beta cells

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35
Q

What are GABA inhibitors used for?

A

Sedatives (depress central nervous system)

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36
Q

What are GABA inhibitors?

A

Block neurotransmitter GABA from binding to GABA A receptors. Binds to GABA A receptors to cause prolonged opening of Cl- channel and increased influx of Cl- ions. This causes the action potential to decrease and inhibits activity

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37
Q

Give an example of GABA inhibitors

A

Barbiturates e.g. phenobarbital

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38
Q

What are sodium pump inhibitors used for?

A

Problems relating to irregular heartbeats (e.g. atrial fibrillation and atrial flutter)

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39
Q

What are sodium pump inhibitors?

A

A.k.a digitalis glycosides. Inhibit Na/K ATPase required for sodium pump (3Na+ out, 2K+ in) which increased intracellular Na+ and therefore intracellular Ca2+. This lengthens the cardiac action potential and so decreases heart rate

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40
Q

Give an example of sodium pump inhibitors

A

Digoxin

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41
Q

What are proton pump inhibitors used for?

A

Reducing gastric acid production (for heartburn/indigestion)

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42
Q

What are proton pump inhibitors?

A

Prevent exchange of K+ from intestinal lumen with cytoplasmic H+ in order to block gastric acid secretion

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43
Q

Give 2 examples and 5 side effects of proton pump inhibitors

A
  • Omeprazole, lanzoprazole
  • Headaches, dizziness, nausea, constipation/diarrhoea, abdominal pain
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44
Q

Define pharmacokinetics

A

Action of the body on a drug

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45
Q

Define pharmacodynamics

A

Action of a drug on the body

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46
Q

What are the 4 steps of pharmacokinetics?

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
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47
Q

What are 5 factors that affect absorption of a drug?

A
  • Motility
  • Acidity
  • Solubility
  • Complex formation
  • Direct action on enterocytes
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48
Q

What are 7 factors that affect distribution of a drug?

A
  • Blood flow
  • Capillary permeability
  • Protein binding
  • Volume of distribution
  • Size of molecules
  • How lipophilic/phobic a drug is
  • Blood brain barrier/blood testicle barrier
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49
Q

Describe metabolism of a drug (pharmacokinetics)

A
  • Lipid soluble drugs cannot be excreted by the kidney (liver metabolises them so they can be)
  • Liver makes drug hydrophilic and then polar
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50
Q

Describe the role of cytochrome p450 in drug metabolism

A

Enzymes that are involved in metabolism of drugs (making hydrophilic). They increase drug metabolism and are affected by inducers or inhibitors

51
Q

Give 5 things that act as inducers of cytochrome P450 (increase drug metabolism)

A
  1. Anti-epileptics
  2. St John’s Wort
  3. Chronic alcohol intake
  4. Smoking
  5. Avocado
52
Q

Give 5 things that act as inhibitors of cytochrome P450 (decrease drug metabolism)

A
  1. Antibiotics
  2. Anti-fungals
  3. SSRIs
  4. Acute alcohol intake
  5. Grapefruit juice
53
Q

Describe excretion of a drug

A

Usually via urine (others by liver in bile or faeces). Rate is pH dependent - weak acids (paracetamol/aspirin) clear faster when urine is alkalotic but weak bases (propanolol) clear faster when urine is acidic

54
Q

Define adverse drug reaction

A

A noxious and unintended response to a drug

55
Q

Give 3 reasons why drug interactions are more of a problem

A
  1. Ageing population
  2. Polypharmacy
  3. Increased use of OTC drugs
56
Q

How are adverse drug reactions classified?

A

ABCDE:
- Augmented
- Bizarre
- Continuing
- Delayed
- End-of-use

57
Q

How should adverse drug reactions be reported?

A

Yellow card scheme

58
Q

What are cholinergic receptors?

A

Receptors on the surface of cells that bind the neurotransmitter acetylcholine (ACh) (parasympathetic)

59
Q

What are adrenergic receptors?

A

Receptors on the surface of cells that bind the neurotransmitters catecholamines (adrenaline and noradrenaline) (sympathetic)

60
Q

Describe the cholinergic parasympathetic system

A
  1. Pre ganglionic neurons release ACh
  2. ACh binds to nicotinic receptors on post ganglionic neuron cell bodies
  3. Post ganglionic neurons release ACh
  4. ACh binds to muscarinic receptors on target organ cells
61
Q

Describe the adrenergic sympathetic system

A
  1. Pre ganglionic neurons release ACh
  2. ACh binds to nicotinic receptors on post ganglionic neuron cells body membranes
  3. Post ganglionic neurons release catecholamines (adrenaline/noradrenaline)
  4. Catecholamines bind and activate adrenergic receptors on target organ cell membranes
62
Q

What do direct-acting cholinergic agonists do?

A

Mimic/enhance the action of ACh at neuromuscular junctions e.g. carbachol constricts pupils

63
Q

What do indirect acting cholinergic agonists do (reversible)?

A

Inhibit enzyme AChE and so increases conc. of ACh at synapses e.g. donepezil for Alzheimer’s

64
Q

What is AChE?

A

Acetylcholinesterase - responsible for the breakdown of ACh

65
Q

What do cholinergic antagonists do?

A

A.k.a anticholinergic drugs inhibit the action of ACh

66
Q

What do nicotinic antagonists do?

A

Compete with ACh for binding to the nicotinic receptor e.g. curare relaxes skeletal muscles

67
Q

What do muscarinic antagonists do?

A

Compete with ACh for binding to the muscarinic receptor e.g. atropine treats bradycardia, diarrhoea and bladder spasms

68
Q

What is a cholinergic crisis?

A

Excessive accumulation of ACh leading to overstimulation of nicotinic and muscarinic receptors - usually due to inactivation/inhibition of AChE

69
Q

What are the main symptoms of a cholinergic criss?

A

SLUDGE:
- Salivation
- Lacrimation
- Urination
- Defecation
- Gastrointestinal distress
- Emesis (vomiting)

70
Q

What is the difference between alpha and beta adrenergic receptors?

A

Alpha receptors are involved in smooth muscle contraction and vasoconstriction whereas beta receptors are involved in smooth muscle relaxation and vasodilation

71
Q

What do alpha 1 adrenergic receptors cause?

A
  • Vasoconstriction
  • Increased peripheral resistance
  • Increased blood pressure
  • Mydriasis (dilated pupils)
  • Increased closure of internal sphincter of bladder
72
Q

What do alpha 2 adrenergic receptors cause?

A
  • Inhibition of noradrenaline release
  • Inhibition of ACh release
  • Inhibition of insulin release
73
Q

What do beta 1 adrenergic receptors cause?

A
  • Tachycardia
  • Increased lipolysis
  • Increased myocardial contractility
  • Increased release of renin
74
Q

What do beta 2 adrenergic receptors cause?

A
  • Vasodilation
  • Decreased peripheral resistance
  • Bronchodilation
  • Increased muscle and liver glycogenolysis
  • Increased release of glucagon
  • Relaxed uterine smooth muscle
75
Q

Give an example of an alpha-1 agonist and antagonist

A

Agonist - decongestant e.g. phenylephrine
Antagonist - tamsulosin

76
Q

Give an example of an alpha-2 agonist and antagonist

A

Agonist - vasodilator e.g. clonidine
Antagonist - yohimbine

77
Q

Give an example of a beta-1 agonist and antagonist

A

Agonist - inotrope e.g. dopamine
Antagonist - selective/non-selective beta-blockers

78
Q

Give an example of a beta-2 agonist and antagonist

A

Agonist - short/long acting beta agonists
Antagonist - non-selective beta blockers

79
Q

What are the 4 types of pain?

A
  1. Acute (<12 weeks)
  2. Chronic (>12 weeks)
  3. Nociceptive (damage to body tissue)
  4. Neuropathic (nerve related)
80
Q

Name the 5 areas of the brain involved with pain

A
  1. Insular cortex (degree of pain felt)
  2. Cingulate gyrus (pain sensation)
  3. Amgydala (emotional response)
  4. Primary motor response (pain location)
  5. Pre-frontal gyrus (pain awareness)
81
Q

Briefly describe the spinothalamic pathway

A
  • Unpleasant stimuli
  • Nociceptors stimulated by inflammatory mediators (e.g. bradykinin, cytokines, prostaglandins)
  • Signal travels in spinal cord
  • Decussates
  • Ascends to somatosensory cortex and projects to periaqueductal gray
82
Q

Describe pain inhibition - descending pathway

A
  • The descending pathway signals to inhibit the ascending pathway
  • Periaqueductal gray has increased opioid receptors and increased endogenous opioids (e.g. encephalin/dynorphine/morphine/endorphin)
  • These bind and inhibit neurotransmitter release to prevent signal transmission = analgesia
83
Q

Describe pain inhibition - gate control theory

A
  • Theory that non-painful input closes the nerve ‘gates’ to painful input
  • Excitatory responses are produced by small A-delta and C fibres
  • Inhibitory responses are produced by large A-beta fibres
  • Activation of large A-beta fibres can reduce and inhibit transmission of small A-delta and C fibres
84
Q

What are the 3 steps on the WHO analgesic ladder?

A

Step 1. Mild to moderate pain (non-opioids/NSAIDS)
Step 2. Moderate to severe pain (mild opioids with/without non-opioids)
Step 3. Severe pain (strong opioids with/without non-opioids)

85
Q

Which opioids are naturally occurring?

A

Morphine and codeine (from opium poppy)

86
Q

What is the main competitive opioid inhibitor?

A

Naloxone (treatment for opioid overdose)

87
Q

What is the difference between tolerance and dependance?

A

Tolerance occurs due to overstimulation of opioid receptors (causes desensitisation)
Dependence is a psychological state of craving euphoria

88
Q

Define therapeutic range

A

Dosage range or serum concentration of a drug usually expected to achieve the desired therapeutic effect without causing toxicity

89
Q

Describe normal paracetamol metabolism

A
  1. 95% is converted to non-toxic metabolites via phase II metabolism
  2. Conjugates with sulfate and glucuronide to be excreted via the urine
  3. 5% is oxidised via cytochrome P450 enzyme system
  4. Cytochromes P450 2E1 and 3A4 convert paracetamol into a highly reactive intermediate metabolite NAPQI
  5. NAPQI is detoxified by conjugation with glutathione to form non-toxic conjugates which are excreted via the urine
90
Q

Describe paracetamol overdose metabolism

A
  1. Phase II metabolism is overwhelmed
  2. More paracetamol is converted into NAPQI by cytochrome P450 enzyme system
  3. More conjugation with NAPQI depletes hepatocellular supply of glutathione
  4. Less glutathione means more NAPQI remains in the liver (hepatotoxicity)
  5. NAPQI reacts with cellular membrane molecules to result in hepatocyte damage/death and leads to acute liver necrosis
91
Q

What is the management of a paracetamol overdose if ingestion has occurred within 1 hour

A

Activated charcoal for doses of >150mg/kg

92
Q

What is the management of a paracetamol overdose if ingestion has occurred within 8 hours

A
  • Wait until 4 hours from ingestion the measure plasma levels
  • If results suggest acute liver injury, treat with IV N-acetylcysteine
93
Q

What are NSAIDs used for?

A

Relieving pain, reducing inflammation and bringing down high temperatures

94
Q

Describe the mechanism of action of non-selective NSAIDs

A
  • Enzyme cyclooxygenase (COX) converts arachidonic acid into thromboxanes (platelet adhesion), prostaglandins (vasodilation) and prostacyclins (vasodilation and inhibits platelet aggregation)
  • Non-selective NSAIDs reversibly inhibits both COX-1 and 2
95
Q

Give 3 examples and side effects of non-selective NSAIDs

A
  • Aspirin, ibuprofen and naproxen (majority of NSAIDs are non-selective)
  • GI upset, GI bleeding and renal impairment
96
Q

Describe the mechanism of action of COX2-selective NSAIDs

A
  • Same as non-selective NSAIDs but only affects COX-2
  • Doesn’t affect COX-1 therefore should provide anti-inflammatory relief without compromising gastric mucosa
97
Q

Describe COX-1

A

Constitutively expressed in the body. Plays a role in maintaining GI mucosa lining, kidney function and platelet aggregation

98
Q

Describe COX-2

A

Not constitutively expressed in the body. Inducibly expressed during an inflammatory response

99
Q

Give an example of a COX2-selective NSAID

A

Celecoxib

100
Q

What are ACE inhibitors used for?

A

Reducing blood pressure

101
Q

Give 3 examples and 5 side effects of ACE inhibitors

A
  • Ramipril, lisinopril, enalapril
  • Dry cough, hyperkalemia, fatigue, dizziness, headaches
102
Q

What are diuretics used for?

A

Treatment of hypertension and oedema

103
Q

What are the 3 types of diuretics?

A

Loop diuretics, thiazide diuretics and spironolactone

104
Q

Describe loop diuretics

A
  • Act at ascending limb of loop of Henle
  • Reversibly inhibits Na/K/Cl cotransporter
  • Inhibits reabsorption of filtered Na+ and Cl- ions
  • Reduced hypertonicity of renal medulla
  • Water reabsorption at collecting ducts inhibited
105
Q

Give 2 examples and 5 side effects of loop diuretics

A
  • Bumetanide, furosemide
  • Dizziness, electrolyte imbalance, fatigue, headache, dehydration
106
Q

Describe thiazide diuretics

A
  • Blocks thiazide-sensitive Na-Cl symporter
  • Inhibits reabsorption of Na+ and Cl- ions at distal convoluted tubule
  • Reabsorption of water inhibited
107
Q

Give an example and 5 side effects of thiazide diuretics

A
  • Bendroflumethiazide
  • Hypocholoraemic alkalosis, diarrhoea, hyperglycaemia, hyperuricaemia, dehydration
108
Q

Describe spironolactone

A
  • Binds competitively to aldosterone receptor at aldosterone-dependent Na/K exchange site
  • Promotes excretion of Na+ and water and retention of K+
109
Q

Give 4 side effects and 2 severe effects of spironolactone

A
  • Drowsiness, dizziness, nausea, vomiting
  • Hyperkalaemia and anti-androgen effects (e.g. erectile dysfunction)
110
Q

What are beta blockers used for?

A

Reducing blood pressure

111
Q

Describe beta blockers

A
  • Block adrenergic receptors of sympathetic nervous system
  • Prevents catecholamines binding
  • Heart beats slower and with less force
112
Q

Give 2 examples and 3 side effects of beta blockers

A
  • Bisoprolol, propanolol
  • Dizziness, fatigue, nausea
113
Q

What are anti-bleeding drugs used for?

A

Prevents platelets from sticking together and forming blood clots

114
Q

What does aspirin do?

A
  • Irreversibly inhibits COX-1 and 2
  • Decreased thromboxane A2
  • Decreased platelet aggregation and increased bleeding time
115
Q

What do clopidogrel and ticlodipine do?

A
  • Liver metabolises them into active compounds
  • These compounds bind to ADP receptors on platelets to reduce platelet activation
116
Q

What does dipyridamole do?

A
  • Inhibits phosphodiesterase which inactivates cyclic AMP (cAMP)
  • Prostacyclin release stimulated and thromboxane A2 formation inhibited
  • Decreased platelet aggregation and vasodilation
117
Q

What are anti-coagulants used for?

A

Preventing blood clots

118
Q

What do apixaban and rivaroxaban do?

A
  • Inhibit factor Xa
  • Prevents prothrombin becoming thrombin
  • Prevents fibrinogen becoming fibrin
119
Q

What does heparin do?

A
  • Activates antithrombin
  • Decreases thrombin and factor Xa
  • prevents fibrinogen becoming fibrin
120
Q

What does warfarin do?

A
  • Anti-vitamin K
  • Decreased vitamin K dependent clotting factors (II - prothrombin, VII, IX, X)
121
Q

What is prothrombin time?

A

Time it takes for blood to clot

122
Q

What is international normalised ratio (INR)?

A

Calculation based on the results of a prothrombin time that is used to monitor individuals being treated with blood thinners

123
Q

What is the most important side effect of warfarin?

A

Teratogenic (abnormalities/problems for fetus/baby) - should not be given to pregnant women

124
Q

What are thrombolytics?

A
  • Drugs that break up and dissolve blood clots
  • Activate plasminogen
  • Forms plasmin
  • Plasmin is a proteolytic enzyme that breaks cross-links between fibrin molecules

Phase 2a (29 decks)

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