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MY PHASE 2A MEDICINE > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacokinetics?

A

What the body does to a drug

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2
Q

What are the four actions of drugs in the body?

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

What are mechanisms of absorption? (4)

A
  1. Active transport
  2. Diffusion
  3. Facilitated diffusion
  4. Endocytosis
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4
Q

What are the variables of absorption? (4)

A
  1. pH
  2. Vascularity (e.g. shock reduces SC absorption)
  3. Surface area
  4. Contact time (e.g. with food = slower gastric emptying)
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5
Q

What is the definition of bioavailability?

A

Rate and extent to which an administered drug reaches the systemic circulation (e.g. IV = 100%)

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6
Q

What is first pass effect?

A

A phenomenon of drug metabolism whereby the concentration of a drug is greatly reduced before it reaches the systemic circulation. First have to pass

  • Intestinal lumen
  • Intestinal wall
  • Liver
  • Lungs
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7
Q

Where are microsomal enzymes located? Give an example.

A

SER e.g. cytochrome p450

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8
Q

What is the role of microsomal enzymes in a) phase 1 rxns and b) phase 2 rxns?

A

Phase I reactions – biotransform substances

Phase II – glucuronidation

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9
Q

Where are non- microsomal enzymes located? Give an example.

A

Cytoplasm and mitochondria e.g. conjugases/esterases/alcohol dehydrogenase

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10
Q

What is the purpose of phase 1 metabolism?

A

polarise lipophilic drugs, reduction / oxidation / hydrolysis

catalysed by cytochrome P450 system

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11
Q

What is the purpose of phase 2 metabolism?

A

conjugation, e.g. glucuronic acid, polarisation of drugs to be excreted by renal or biliary systems

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12
Q

What is first order metabolism?

A

catalysed by enzymes, rate of metabolism directly proportional to drug concentration

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13
Q

What is zero order metabolism?

A

enzymes saturated by high drug doses, rate of metabolism is constant, e.g. ethanol, phenytoin

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14
Q

What is pharmacodynamics?

A
  • What the drug does to the body

- Its effect on cellular receptors via signal transduction

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15
Q

Are microsomal enzymes seen more in phase 1 or phase 2 reactions?

A

Phase 1.

Non- microsomal = phase 2

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16
Q

Which cranial nerves are parasympathetic?

A

CN 3, 7 , 9 , 10

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17
Q

What neurotransmitter do
a) parasympathetic
b) sympathetic
post- SYNAPTIC nerves release?

A

BOTH release acetylcholine

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18
Q

What kind of receptor does acetylcholine act on?

A

NICOTINIC receptor

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19
Q

What neurotransmitter do
a) parasympathetic
b) sympathetic
post-GANGLIONIC nerves release and what do they act on?

A

a) acetylcholine -> muscarinic receptor

b) noradrenaline -> alpha/beta adrenoreceptors

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20
Q

What is the principal neurotransmitter in the body?

A

Acetylcholine

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21
Q

What receptor does Ach interact with in the somatic nervous system?

A

Post-synaptic nicotinic receptors at the neuromuscular junction.

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22
Q

Give examples of adverse muscarinic agonist effects.

A
  1. Diarrhoea.
  2. Urination.
  3. Miosis.
  4. Brachycardia.
  5. Emesis (vomiting).
  6. Lacrimation.
  7. Salivation.
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23
Q

Give 2 examples of Ach action in the CNS.

A
  1. Motion sickness; Ach stimulates the vomiting centre in the brain.
  2. Ach leads to increase dopamine re-uptake and so can worsen the symptoms of Parkinson’s.
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24
Q

Briefly describe catecholamine synthesis.

A

Tyrosine -> L-DOPA -> Dopamine -> Noradrenaline -> Adrenaline.

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25
Q

What is the function of α1 activation?

A
  1. Vasoconstriction (raise blood pressure)

2. Increased closure of internal sphincter of the bladder

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26
Q

What is the primary function of α2?

A

α2 is responsible for pre-synaptic inhibition; it inhibits NAd release.

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27
Q

Give an example of an alpha 1 agonist/antagonist

A 
agonist = phenylephrine (nasal decongestant)
antagonist = Tamsulosin ( treat BPH)
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28
Q

What would an α1 adrenergic antagonist do?

A
  1. Vasodilation.

2. Relaxation of bladder neck = reduced resistance to bladder outflow.

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29
Q

What are the primary functions of β1?

A
  1. Increased cardiac effects e.g. force, rate and conduction.
  2. Increased renin secretion.
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30
Q

What would a β1 adrenergic antagonist do?

A
  1. Reduce CO.

2. Reduce renin secretion.

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31
Q

Give an example of a beta 1 agonist and their use

A

epinephrine/dopamine (inotropes) e.g. in septic shock

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32
Q

Give an example of a beta 2 agonist and their use

A

SABA/LABA e.g. in asthma

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33
Q

What diseases could an β1 adrenergic antagonist be used in the treatment of? Give an example of a drug

A

Hypertension, angina and arrhythmia

e.g. selective/non-selective beta blockers ( atenolol=just B1, propanolol B1/2 so may cause wheeze)

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34
Q

How do beta blockers lower blood pressure?

A

By reduction in cardiac output and gradual

reduction in central sympathetic outflow activity

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35
Q

What is the action of an INOTROPIC drug?

A

Affects the force of cardiac contraction

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36
Q

What is the action of a CHRONOTROPIC drug?

A

Affects the heart rate

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37
Q

Is propanolol positively or negatively inotropic?

A

negatively inotropic

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38
Q

Give some of the diseases beta blockers are used to treat

A 
- Angina
• MI prevention
• High blood pressure
• Anxiety
• Arrhythmias
• Heart failure
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39
Q

What are some of the side effects of beta blockers

A
  • Tiredness
  • Cold extremities
  • Bronchoconstriction
  • Bradycardia
  • Hypoglycaemia
  • Cardiac depression
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40
Q

Give an example of a parasympathetic muscarinic antagonist. What would it’s action be

A

Atropine

Used in life-threatening bradycardias and in cardiac arrest (blocks M2 whcih is responsible for slowing heart rate)

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41
Q

Give examples of antibiotics which act on bacteria cell wall

A
  1. Beta lactams (penicillin/cephalosporin)
  2. Vancomycin
  3. Polymyxins
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42
Q

Give examples of antibiotics which act on nucleic acid synthesis

A
  1. Trimethoprim

2. Quinolones

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43
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

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44
Q

Define acute pain.

A

Pain caused by nociceptor activation. It is of short duration,

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45
Q

Define chronic pain.

A

Pain that is on-going or persistent, it lasts for >3-6 months.

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46
Q

Define neuropathic pain.

A

Pain caused by a primary lesion or dysfunction of the nervous system.

47
Q

Define nociceptive pain.

A

Pain caused by actual or potential damage to non neural tissue, it is due to nociceptor activation.

48
Q

Are A delta fibres myelinated or unmyelinated?

A

Myelinated

49
Q

Are C fibres myelinated or unmyelinated?

A

Unmyelinated

50
Q

Describe the type of pain that A delta fibres conveys.

A

Quick, sharp, localised. (A=acute)

51
Q

Describe the type of pain that C fibres conveys.

A

Slow, dull, spread out.

52
Q

What does potency mean?

A

Measure of how well a drug works

53
Q

What is an agonist?

A

A compound that binds to a receptor and activates it

54
Q

What does affinity mean?

A

Describes how well a ligand binds to the receptor

55
Q

What does efficacy mean?

A

Describes how well a ligand ACTIVATES the receptor. (only agonists show efficacy)

56
Q

What are the main actions of NSAIDs and give examples of drugs.

A
  • Analgesic
    • Anti-pyretic (reduces fever)
    • Anti-inflammatory
    e.g. ibuprofen/ASPIRIN
57
Q

How is the mechanism of NSAIDs?

A

They inhibit the enzyme
cyclooxygenase (COX1/2) which are
responsible for prostoglandin synthesis. Prostaglandins are responsible for inflammation and pain. Therefore NSAIDs reduce symptoms of inflammation and pain.

58
Q

What is a disadvantage of long term NSAID use?

A

NSAIDs can cause gastric bleeding. They inhibit COX 1 which is needed for prostaglandin synthesis and prostaglandins are needed for gastric mucus production.

59
Q

Give an example of ACEi and its function

A

Ramipril (anti - hypertensive)

60
Q

What is the mechanism of ACEi?

A
  • Work by inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II
- This means there is less angiotensin II so less bind to
angiotensin receptors (AT1) resulting in reduced vasoconstriction and thus hypertension
  • There is also less aldosterone release further reducing hypertension
61
Q

Give a side effect of ACEi

A

DRY COUGH

  • angioedema
  • AKI/hyperkalaemia
  • hypotension
62
Q

Give an example of a COX inhibitor

A

aspirin/paracetamol/NSAID

63
Q

How does aspirin work?

A

IRREVERSIBLY blocks the active site of the COX enzyme resulting in IRREVERSIBLE INACTIVATION -> Decreased TXA = Decreased Platelet Aggregation = Increased Bleeding Time

64
Q

What kind of drug is clopidogrel/ticagrelor?

A

ADP receptor inhibitor/p2y12 inhibitor

65
Q

How do P2Y12 inhibitors work?

A

Block ADP Receptors = Inhibit Platelet Aggregation

66
Q

What is pain treatment focused on?

A
  1. Reducing excitatory neurotransmitters and nerve excitation.
  2. Enhancing inhibitory neurones.
67
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug.

68
Q

Rawlins-Thompson system: Describe a type A adverse drug reaction.

A
  • Augmented.
  • Very common.
  • Predictable from physiological effects of the drug.
  • Often dose related.
69
Q

Rawlins-Thompson system: Describe a type B adverse drug reaction.

A
  • Bizarre.
  • Unpredictable.
  • Immunological mechanisms and hypersensitivity.
  • Often there is a history of allergy.
70
Q

Rawlins-Thompson system: Describe a type C adverse drug reaction.

A
  • Chronic.

- Occurs after long term therapy.

71
Q

Rawlins-Thompson system: Describe a type D adverse drug reaction.

A
  • Delayed.

- Occurs many years after treatment.

72
Q

Rawlins-Thompson system: Describe a type E adverse drug reaction.

A
  • End of use.

- Withdrawal reaction after long term use; complications of stopping medication.

73
Q

What is the treatment for a type A adverse drug reaction?

A

Reduce the dose.

74
Q

What is the treatment for a type B adverse drug reaction?

A

Withdraw drug immediately!

75
Q

Why are drug interactions such a big problem today?

A
  1. Ageing population.
  2. Polypharmacy.
  3. Increased use of over the counter drugs.
76
Q

Give 5 patient risk factors for drug interactions.

A
  1. Old age.
  2. Polypharmacy.
  3. Renal disease.
  4. Hepatic disease.
  5. Genetics.
77
Q

Give 3 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index.
  2. Steep dose/response curve.
  3. Saturable metabolism.
78
Q

Name 3 types of drug interaction.

A
  1. Synergy; interaction of 2 compounds leads to a greater combined effect.
  2. Antagonism; one drug blocks another.
  3. Other.
79
Q

How might drug interactions affect drug metabolism?

A

If a drug inhibits or induces CYP450 it might affect the metabolism of another drug.

80
Q

How does grapefruit juice affect CYP450? And what drugs might this impact on?

A

Grapefruit juice is a CYP450 inhibitor, it affects CYP3A4 specifically and increases the bioavailability of some drugs e.g. Ca2+ channel blockers and immunosuppressants.

81
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide.

82
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation.
83
Q

Describe the dose-response curve for morphine.

A

As dose increases response increases. This association is initially rapidly and then the graph plateaus. It is not sigmoidal!

84
Q

Name a protein that can inhibit apoptosis.

A

BCL-2; it inhibits pro-apoptotic proteins e.g. caspase and therefore inhibits apoptosis.

85
Q

What disease might develop in someone with a non-functional BCL-2 protein?

A

Cancer.

86
Q

Where are mast cells found?

A

They are only found in tissues, not in the blood!

87
Q

Name a local anaesthetic.

A

Lidocaine.

88
Q

How do local anaesthetics work?

A

They inhibit pain by stopping impulse conduction in sensory nerves.

89
Q

What drug inhibits ACh release at the NMJ?

A

Botulinum toxin.

It is used to treat urinary incontinence and also cosmetically as a muscle relaxant.

90
Q

Describe the action of botulinum toxin at the NMJ,

A

Botulinum toxin inhibits Ach release at the NMJ. Protease degrade vesicle proteins.

91
Q

How do diuretics work?

A

They inhibit ‘symporters’ in the loop of henle.

- This leads to increased H2O excretion and decreased salt reabsorption and so BP decreases.

92
Q

Give an example of loop of henle diuretics.

A
  • Furosemide, act on the ascending loop.

- Thiazides, act on the distal tubule.

93
Q

How can drugs be developed?

A
  1. Serendipity, by chance. e.g. penicillin.

2. Rational drug design. e.g. propranolol.

94
Q

Describe how rational drug design works.

A

Rational drug design is focused on developing an antagonist from an agonist. It looks at solubility, electrostatic charge and bulk.

95
Q

How does heparin work?

A

Activates Antithrombin (decreased thrombin and factor Xa)

96
Q

What are the SE of heparin?

A

Bleeding, thrombocytopenia (heparin-induced thrombocytopenia), osteoporosis

97
Q

How does warfarin work?

A

Anti-Vitamin K = Decreased FII (prothrombin)/VII/IX/X and Protein C/S

98
Q

What are SE of warfarin?

A

Bleeding, Skin/Tissue Necrosis, Teratogenic

99
Q

How does RAAS respond to LOW BP?

A
  1. Baroreceptors in afferent vascular walls detect low pressure
  2. Decreased Na+ transport to macula densa cells
  3. Increased sympathetic stimulation (beta 1)
  4. JG cells release RENIN
100
Q

What are the effects of angiostensin II? (6)

A
  1. Systemic arteriole vasoconstriction
  2. Kidney efferent>afferent constriction = Increase
  3. Glomerular Pressure = Maintain GFR despite lowered overall kidney blood flow
  4. Kidney proximal tubule/thick ascending limb Na+/H+ exchanger stimulation = Increased Na+/HCO3/H20 reabsorption
  5. Adrenal cortex = Aldosterone release
  6. Posterior Pituitary = ADH release
101
Q

What are the functions of ACE?

A

Catalyses conversion of angiotensin I to angiotensin II

Degraded by bradykinin

102
Q

How do loop diuretics e.g. FUROSEMIDE work?

A

Inhibit Na/K/Cl cotransporter of thick ascending limb

103
Q

When are loop diuretics used?

A

Oedematous States (HF, Cirrhosis, Nephrotic Syndrome, Pulmonary Oedema), HTN, Hypercalcaemia

104
Q

What are SE of loop diuretics?

A

ototoxicity, hypokalaemia, dehydration, AKI, gout

105
Q

How do thiazide diuretics work?

A

Inhibit Na/Cl cotransporter of distal tubule

106
Q

What is a spironolactone?

A

Competitive aldosterone receptor antagonists in collecting tubules (K+ SPARING)

107
Q

Give some of SE for corticosteroids

A
  • weight gain
  • buffalo hump/ moon face
  • depression/anxiety
  • thin skin
  • hypertension
108
Q

How does methotrexate work?

A

prevents folate synthesis = prevents DNA synthesis

109
Q

Describe monitoring for pts on methotrexate

A

baseline, every 2-3 months

CXR, FBC, LFT, U&E (not cxr every 2 months)

110
Q

What are the consequences of prescribing a drug with a narrow therapeutic ratio? (example?)

A

Increased risk of toxicity, decreased chance of effective dose e.g. digoxin, vancomycin)

111
Q

What is the procedure for poisoning <1hr of ingestion?

A

PO activated charcoal

112
Q

What is the pathology of paracetamol overdose?

A
  1. Phase 2 conjugation pathway saturated
  2. Alternative pathway used = NAPQI = glutathione depletion
  3. Glutathione depletion = liver/renal necrosis
113
Q

How do you treat paracetamol overdose?

A

IV N-acetylcysteine

MY PHASE 2A MEDICINE (14 decks)

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