Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the 2 routes of administration of a drug?

A

Systemic and local

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 branches of systemic administration of a drug?

A

Enteral (GI tract) and Parenteral (not GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different types of local routes of administration?

A

Topical e.g. topical steroid creams for eczema
Intranasal
Eye drops
Inhalation - can also be systemic depending on drug e.g. salbutamol only affects airways but anaesthetic drug sevoflurane is also given by inhalation but has systemic effects)
Transdermal - can also be systemic depending on drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is systemic administration of a drug?

A

Covers the whole system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is local administration of a drug?

A

Targets a specific area of pathology, without exposing the rest of the system to drugs unnecessarily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the different types of systemic enteral administration?

A

Oral (PO)
Rectal (PR)
Sublingual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the different types of systemic parenteral administration?

A

IV/IM/SC
Inhalation
Transdermal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are pharmacodynamics?

A

Action of the drug on the body (its use!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are pharmacokinetics?

A

Action of the body on the drug (how it’s broken down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do drugs cross membranes?

A

Passive diffusion
Facilitated diffusion
Active transport
Endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

By what route of administration is a drug absorbed the quickest?

A

IV - directly into bloodstream and no membrane crossing or first pass metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are drugs absorbed into the bloodstream?

A

Unless given straight into the bloodstream (IV), drug will need to pass though membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are water soluble drugs absorbed?

A

Water soluble molecules move through membrane by diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are lipid soluble drugs absorbed?

A

Lipid soluble drugs can cross phospholipid membrane directly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are larger drugs absorbed?

A

Larger drugs might need facilitated diffusion from carrier proteins in the membrane, ATP dependent active transport, or are engulfed by the cell through endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is absorption dependent on?

A 
Solubility of drug
Size of molecules
pH
Surface area
Perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens to a drug if it is taken orally?

A

If taken orally, not all of the drug taken gets to the bloodstream – the gut and liver will both start metabolising it first before reaching circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When is bioavailability assumed to be 100%?

A

It is assumed to be 100% if a drug is given IV, but lower if given orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is bioavailability calculated?

A

AUC oral / AUC IV x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is bioavailability?

A

Rate and extent to which an administered drug reaches the systemic circulation

Fraction of drug that reaches systemic circulation unaltered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the drug target types?

A

Cellular receptors
Enzymes (ACE inhibitors)
Membrane ion channels (lidocaine)
Membrane transporters (PPIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does drug distribution depend on?

A 
Blood flow to area
Permeability of capillaries
Binding to proteins (albumin = slower)
Lipophilicity
Volume of distribution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give an example of how blood flow to an area affects distribution.

A

Drug will get to the brain (if can pass through BBB) faster than the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does permeability of capillaries affect drug distribution?

A

Some capillaries have slit junctions that allow drugs through – many in the liver (allows metabolism), none in the brain so harder to get through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does binding to protein affect drug distribution?

A

Drugs may also travel in the blood bound to albumin, which slows the process of distribution as the drug must be FREE FROM ALBUMIN to cross membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does lipophilicity affect drug distribution?

A

Lipophilic drugs can penetrate the cell membrane easily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does volume of distribution affect drug distribution?

A

Higher volume of distribution = drug more in tissues, less in plasma, need to give higher concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where can drug targets be found?

A

Cellular receptors but not all drug targets are receptors on cells (e.g. ramipril, lidocaine, proton pump inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is ramipril?

A

An ACE inhibitor which blocks the angiotensin converting enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is lidocaine?

A

Blocks sodium ion channels and is a local anaesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are proton pump inhibitors?

A

Inhibit membrane transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why is the liver key in the excretion of drugs?

A

Kidney can’t excrete lipid soluble drugs so liver converts lipid soluble drugs into water soluble drugs so they can be excreted by the kidney (2 stages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Summarise the first phase of drug excretion.

A

Make drug hydrophilic (cytochrome p450 catalyses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Summarise the second phase of drug excretion.

A

If still too lipophilic, add something else to make it polar so the drug can’t be absorbed - e.g. acetylation/adding glutathione)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do drugs affect cytochrome P450 enzymes?

A

Drugs can alter the activity of cytochrome P450 enzymes, and therefore alter the rate of metabolism of other drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does alcohol abuse affect drug excretion?

A

Alcohol abuse, both chronic and acute can mess up the P450 system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is a CYP450 inducer?

A

Increases cytochrome P450 activity, and speed up metabolism of other drugs – may result in sub-therapeutic dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a CYP450 inhibitor?

A

Decreases cytochrome P450 activity, reduce metabolism of other drugs – may result in toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Give some examples of CYP450 inducers.

A 
Anti-epileptics: phenytoin, carbamazepine
Rifampicin
St John's Wort
Chronic Alcohol intake
Smokers (CYP1A2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Give some examples of CYP450 inhibitors.

A 
Abx: ciproflaxacin, erythromycin
Isoniazid
Amiodarone
Allopurinol
Anti-fungal: ketoconazole, fluconazole
SSRI: fluoxetine, sertraline
Sodium Valproate
Acute Alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

By what type of kinetics are most drugs eliminated?

A

Most drugs are eliminated through first order kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is first order kinetics?

A

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

The capacity of the elimination system is higher than the concentration of the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is zero order kinetics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When might doses of drugs need to be altered?

A

Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Other than the kidneys, how else can drugs be excreted?

A

Some also excreted by the liver in the bile and then faeces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is signal transduction?

A

Binding of drug to extracellular or intracellular receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does signal transduction occur?

A

Via a variety of receptors: ligand-gated ion channels, G protein-coupled receptors etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does signal transduction lead to?

A

Amplification or down-regulation of signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is an agonist?

A

Binds to receptor and activates it by mimicking the endogenous substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What response does an agonist induce?

A

Can be full (causes same response as endogenous substance) or partial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give an example of an agonist.

A

Salbutamol (asthma) is beta 2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is an antagonist?

A

Binds to receptor and prevents its activation - can also bind at another site to the main active site (allosteric site)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What type of reaction takes place when an antagonist binds to a receptor?

A

Can be reversible or irreversible (if a covalent bond forms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Give an example of an antagonist.

A

Propranolol (hypertension) is a beta blocker

Beta blockers like bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do beta blockers do?

A

Block the adrenergic receptors of the sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

When should beta blockers be avoided?

A

Avoid beta blockers in asthmatic patients

Use cardio-selective ones (bisoprolol) if absolutely necessary, rather than propranolol (non-selective)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is efficacy?

A

How well the ligand (drug) activates the receptor – e.g. full or partial agonist?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is potency?

A

Binding affinity of the drug for the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is first pass metabolism?

A

Metabolism of the drug by the gut and liver before it reaches the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does a narrow therapeutic range indicate?

A

Increased risk of toxicity, decreased chance of effective dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Give some examples of drugs with a narrow therapeutic range.

A 
Digoxin
Theophylline
Lithium
Phenytoin
Gentamicin, Vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What happens to paracetamol following a therapeutic dose?

A

Paracetamol is mostly converted to non-toxic metabolites via Phase II metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What happens to paracetamol during phase II metabolism?

A

Here, it conjugates with sulfateand glucuronide, with a small portion being oxidized via thecytochrome P450 enzyme system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What do the cytochromes do to a small fraction of paracetamol during its metabolism?

A

CytochromesP4502E1and3A4convert approximately 5% of paracetamol to a highly reactive intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What happens to NAPQI under normal conditions?

A

NAPQI is detoxified by conjugation with glutathioneto form cysteine and mercapturic acid conjugates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What happens to the phase II metabolic pathways after a paracetamol overdose?

A

The phase II metabolic pathways become saturated, and more paracetamol is shunted to the cytochrome P450 system to produce NAPQI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What happens as a result of increased NAPQI concentration from a paracetamol overdose?

A

Hepatocellular supplies of glutathione become depleted, as the demand for glutathione is higher than its regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What happens once there is not enough glutathione to detoxify NAPQI after a paracetamol overdose?

A

NAPQI therefore remains in its toxic form in the liver and reacts with cellular membranemolecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What can paracetamol overdose result in?

A

Widespread hepatocytedamage and death, leading to acute liver necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the first treatment considered for a paracetamol overdose?

A

Activated charcoal should be considered if patient presents within 1 hour of ingestion of >150mg/kg paracetamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What treatment is given for patients where paracetamol overdose has occurred within the last 8 hours?

A

You should wait until 4 hours from ingestion then measure plasma level and send for urgent analysis.Await result before deciding whether treatment is required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is given if results suggest acute liver injury from paracetamol overdose?

A

Double-check history of paracetamol ingestion, especially the timing, and consider treatment with intravenous N-acetylcysteine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What treatment is given if a patient has taken a staggered overdose of paracetamol?

A

The treatment nomogram in unreliable and instead based on paracetamol levels and further blood tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is classed as a staggered paracetamol overdose?

A

Paracetamol taken over a period of more than 1 hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What might be needed if damage to the liver becomes severe from a paracetamol overdose?

A

Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the need for a liver transplant from a paracetamol overdose?

A

Low blood pH, highblood lactate, poor blood clotting, or significant hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the prognosis of paracetamol overdose with early treatment?

A

Liver failure is rare and death only occurs in about 0.1% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the nervous system divided into?

A

CNS and PNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the CNS?

A

Brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the PNS?

A

All the nerves that connect the centralnervous system to the muscles and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the PNS divided into?

A

Somatic nervous system and autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the somatic nervous system?

A

Controls skeletal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the autonomic nervous system?

A

Further divided into thesympatheticand the parasympathetic and controls internal organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are cholinergic receptors?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the 2 types of cholinergic receptors?

A

Muscarinic and nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What do preganglionic and postganglionic neurons release in the sympathetic nervous system?

A

Different neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What do preganglionic neurons do in the sympathetic nervous system?

A

Release theneurotransmitter ACh, which binds tonicotinic receptors on thecell membrane of postganglionic neuroncell bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What do postganglionic neurons do in the sympathetic nervous system?

A

Most postganglionic neurons release theneurotransmitters adrenaline (epinephrine) andnoradrenaline (norepinephrine) which bind toadrenergic receptors on theplasma membrane of the target organ cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What do preganglionic neurons do in the parasympathetic nervous system?

A

TheACh released bypreganglionic neurons binds tonicotinic receptors on postganglionic neuroncell bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What do postganglionic neurons do in the parasympathetic nervous system?

A

ReleaseACh and it binds to themuscarinic receptors on the target organ cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are cholinergic drugs divided into?

A

Cholinergic agonists and antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are cholinergic agonists?

A

Drugs that mimic or enhance the action of ACh at the neuromuscular junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the effects of cholinergic agonists?

A

Increases GI and GU tone, increases bronchial tone and respiratory secretions. Enhances PSNS activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are cholinergic antagonists?

A

Drugs that inhibit the action of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the effects of cholinergic antagonists?

A

Blocks the ability of acetylcholine to initiate involuntary muscle movements in the lungs, GI tract and GU tract. Balances production of dopamine. Enhances SNS activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the mechanism of direct-acting cholinergic agonists?

A

Mimic ACh and bind to ACh receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Give some examples of direct-acting cholinergic agonists and their therapeutic use.

A

Carbachol (constrict pupil)
Bethanechol (increase smooth muscle tone in GI and GU tract)
Pilocarpine (stimulate saliva secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the mechanism of indirect-acting cholinergic agonists?

A

Inhibit enzyme AChE, increasing the concentration of ACh available at the synapse
(Reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Give some examples of indirect-acting cholinergic agonists and their therapeutic use.

A

Neostigmine, Pyridostigmine (myasthenia gravis, reverse anesthesia)
Donepezil, Rivastigmine, Galantamine (boost cholinergic activity in Alzheimer’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the mechanism of nicotinic antagonists?

A

Compete with ACh for binding to the nicotinic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give some examples of nicotinic antagonists and their therapeutic use.

A

Curare, Pancuronium (relax skeletal muscles during surgery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the mechanism of muscarinic antagonists?

A

Compete with ACh for binding to the muscarinic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Give some examples of muscarinic antagonists and their therapeutic use.

A

Atropine, Scopolamine, Belladonna alkaloids (treat bradycardia, diarrhoea, bladder spasms; dilate bronchi, reduce secretions, dilate pupils; as sedatives, respectively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the catecholamines?

A

Adrenaline and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are adrenergic receptors?

A

Receptors on the surface of cells that get activated when they bind a type of neurotransmitters called acatecholamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are catecholamines involved in?

A

Stimulation of our organs by thesympathetic nervous system (fight or flight)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What type of receptor is an adrenergic receptor?

A

One type ofG-protein coupled receptors or GPCR, because they work directly with intracellular proteins calledguanine nucleotide-binding proteins or G proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What do adrenergic receptors bind to other than catecholamines?

A

They bind to aguanosine diphosphate or GDP molecule when they’re inactive, and to aguanosinetriphosphate or GTP molecule when they’re active.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the different types of adrenergic receptors?

A

⍺₁, ⍺₂, β₁ and β₂

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What do ⍺₁ adrenoreceptors do?

A 
Vasoconstriction
Increased peripheral resistance
Increased blood pressure
Mydriasis
Increased closure of internal sphincter of the bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What do ⍺₂ adrenoreceptors do?

A

Inhibition of noradrenaline release
Inhibition of acetylcholine release
Inhibition of insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What do β₁ adrenoreceptors do?

A

Tachycardia
Increased lipolysis
Increased myocardial contractility
Increased release of renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What do β₂ adrenoreceptors receptors do?

A 
Vasodilation
Decreased peripheral resistance
Bronchodilation
Increased muscle and liver glycogenolysis
Increased release of glucagon
Released uterine smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What do α-agonists do?

A

Bind to α-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction, thus mimicking the effects of sympathetic adrenergic nerve activation to the blood vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Give an example of an alpha-1 agonist.

A

Decongestants (phenylephrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Give an example of an alpha-2 agonist.

A

Centrally-acting vasodilators e.g. clonidine, ⍺-methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Give an example of a beta-1 agonist.

A

Inotropes (epinephrine, dopamine, dobutamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Give an example of a beta-2 agonist.

A

SABA/LABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Give an example of an indirect agonist.

A

Cocaine

Amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Give an example of an alpha-1 antagonist.

A

Tamsulosin

Doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Give an example of an alpha-2 antagonist.

A

Yohimbine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Give an example of a beta-1 antagonist.

A

Selective/Non-selective beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Give an example of a beta-2 antagonist.

A

Non-selective beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What do alpha-blockers (alpha-1 adrenergic receptor antagonists) do?

A

Bind to and inhibit type 1 alpha-adrenergic receptors and thus inhibit smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What do beta lactams contain?

A

Beta-lactam ring in their molecular structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Give some examples of beta lactams.

A

Penicillin derivatives,cephalosporins, monobactams andcarbapenems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

How do beta lactam antiobiotics act?

A

Inhibiting the synthesis of thepeptidoglycanlayer of bacterialcell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the purpose of the peptidoglycan layer in bacteria?

A

Important for cell wall structural integrity, especially ingram-positive organisms, being the outermost and primary component of the wall

130
Q

What is the most widely used group of antibiotics?

A

Beta lactams

131
Q

What does vancomycin do?

A

Inhibits cell wall synthesis bybinding to the D-Ala-D-Alaterminal of the growing peptide chain during cell wall synthesis, resulting ininhibition of the transpeptidase, which prevents further elongation and cross-linking of the peptidoglycan matrix

132
Q

What do polymyxins target?

A

Outer membrane of gram-negative bacteria

133
Q

How do polymyxins work?

A

Because of an electrostatic interaction occurring between the α,γ-diaminobutyric acid (Dab) residue of the positively charged polymyxin on one side and the phosphate groups of the negatively charged lipid A membrane on the other side, divalent cations (Ca2+and Mg2+) are displaced from the negatively charged phosphate groups of membrane lipids. The lipopolysaccharide (LPS) is therefore destabilized, consequently increasing the permeability of the bacterial membrane, leading to leakage of the cytoplasmic content and ultimately causing cell death

134
Q

Explain the endotoxin effect of polymyxins.

A

The endotoxin of gram-negative pathogens corresponds to the lipid A portion of the LPS; polymyxins have the ability to bind to and neutralize this LPS molecule released during cell lysis. Finally, another mode of action of the polymyxins is the inhibition of vital respiratory enzymes (inhibition of type II NADH-quinone oxidoreductases [NDH-2]) in the bacterial inner membrane

135
Q

Which antibiotics interfere with folic acid synthesis?

A

Sulfonamides and trimethoprim

136
Q

Which bacteria do quinolones treat?

A

Wide variety of gram-negative and gram-positive bacterial infections

137
Q

Why is quinolone usage threatened?

A

Rising occurrence of resistance, which has been observed in every species that is treated by this drug class

138
Q

How do quinolones work?

A

Quinolone antibiotics inhibit DNA synthesis by targeting two essential type II topoisomerases, DNA gyrase and topoisomerase IV, into toxic enzymes that fragment the bacterial chromosome

139
Q

How does rifampicin work?

A

inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA-dependent RNA polymerase and is used as part of the RIPE regime for the treatment of TB

140
Q

Which antibiotics interfere with nucleic acid synthesis?

A

Sulfonamides
Trimethoprim
Quinolones
Rifampicin

141
Q

Which antibiotics interfere with protein synthesis?

A

Macrolides

Tetracyclines

142
Q

How do macrolides work?

A

Inhibit bacterial protein biosynthesis, and they are thought to do this by preventing peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid (similarly to chloramphenicol) as well as inhibiting bacterial ribosomal translation

143
Q

How do tetracyclines work?

A

Inhibit bacterial protein synthesis by preventing the association of aminoacyl-tRNA with the bacterial ribosome and are used to treat both gram-positive and gram-negative bacterial infections

144
Q

Give some examples of penicillins.

A

Penicillin V/G
Amoxicillin
Ampicillin
Piperacillin/Tazobactam (Tazocin)

145
Q

Give some examples of macrolides.

A

Clarithromycin

Azithromycin

146
Q

Give some examples of tetracyclines.

A

Doxycycline

147
Q

Give some examples of cephalosporins.

A

Cefuroxime

Cephalexin

148
Q

Give some examples of quinolones.

A

Ciprofloxacin

149
Q

What are the 2 different types of NSAIDs?

A

Non-selective NSAIDs

COX2-selective NSAIDs

150
Q

What are non-selective NSAIDs?

A

Competitive reversible inhibitors of COX1 and 2

151
Q

What are COX2-selective NSAIDs?

A

Selectively inhibit COX2 therefore have a different side effect profile

152
Q

Give some examples of non-selective NSAIDs.

A

Diclofenac
Ibuprofen
Naproxen

153
Q

Give some examples of COX2-selective NSAIDs.

A

Celecoxib

Rofecoxib

154
Q

What is the role of the cyclooxygenase (COX) enzyme?

A

Converts arachidonic acid into thromboxanes, prostaglandins, and prostacyclins

155
Q

What is the role of thromboxanes?

A

Platelet adhesion

156
Q

What is the role of prostaglandins?

A

Vasodilation, increase the temperature set-point in the hypothalamus, and play a role in anti-nociception

157
Q

What does aspirin do?

A

Irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2

158
Q

What is the role of COX-1?

A

Gets constitutively expressed in the body, and it plays a role in maintaining gastrointestinal mucosa lining, kidney function, and platelet aggregation

159
Q

What is the role of COX-2?

A

Is not constitutively expressed in the body, and instead it inducibly expresses during an inflammatory response

160
Q

What do NSAIDs inhibit?

A

Most of the NSAIDs are nonselective and inhibit both COX-1 and COX-2

161
Q

When should a COX-2 selective NSAID be used?

A

Because COX-1 is the prime mediator for ensuring gastric mucosal integrity and COX-2 is mainly involved in inflammation, COX-2 selective NSAIDs should provide anti-inflammatory relief without compromising the gastric mucosa

162
Q

What effects does aspirin have in addition to being anti-inflammatory?

A

Anti-platelet effects

163
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX-1/2 = Decreased Thromboxane A2 = Decreased Platelet Aggregation = Increased Bleeding time

164
Q

How does clopidogrel work?

A

The thienopyridine derivatives are metabolised in the liver to active compounds which covalently bind to the adenosine phosphate (ADP) receptor on platelets and dramatically reduce platelet activation

165
Q

How does ticlodipine work?

A

The thienopyridine derivatives are metabolised in the liver to active compounds which covalently bind to the adenosine phosphate (ADP) receptor on platelets and dramatically reduce platelet activation

166
Q

How does dipyridamole work?

A

Inhibits phosphodiesterase, which inactivates cyclic AMP . It also stimulates prostacyclin release and inhibitsthromboxane A2formation, like aspirin. This leads to decreased platelet aggregation and vasodilation

167
Q

Give some examples of anti-platelet drugs.

A

Aspirin
Clopidogrel, ticlodipine (thienopyridine derivatives)
Dipyridamole

168
Q

What is the purpose of anti-coagulants?

A

Act at different points within the coagulation cascade to prolong clotting time.

169
Q

What is the purpose of the coagulation cascade?

A

Stabilise the platelet plug with a fibrin mesh

170
Q

What happens in the coagulation cascade?

A

Two pathways, intrinsic and extrinsic, originate separately but converge at a specific point, leading to fibrin activation

171
Q

Give somme examples of direct inhibitors of factor Xa.

A

Apixaban
Rivaroxaban
Betrixaban
Edoxaban

172
Q

What are the side effects of direct inhibitors of factor Xa?

A

Bleeding (no reversal agent)

173
Q

What does heparin do?

A

Activates antithrombin (decreased thrombin and factor Xa)

174
Q

What is a commonly used LMWH?

A

Dalteparin

175
Q

What does dalteparin do?

A

Activates antithrombin (decreased factor Xa) and have longer half-life

176
Q

How do you monitor use of heparin?

A

Monitor using anti-factor Xa assay

177
Q

What are the side effects of heparins?

A

Bleeding, heparin-induced thrombocytopenia, osteoporosis

178
Q

How does warfarin work?

A

Decreased FII (prothrombin)/VII/IX/X and Protein C/S

179
Q

What are the vitamin K dependent clotting factors?

A

The vitamin K dependent clotting factors can be remembered by 1972 – with the 1 standing for factor X, and then 9, 7 and 2

180
Q

What is prothrombin time?

A

Blood test that measures how long it takes blood to clot

181
Q

What is INR (international normalised ratio)?

A

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

182
Q

What are the side effects of warfarin?

A

Bleeding, Skin/Tissue Necrosis, Teratogenic

183
Q

How are the side effects of warfarin reversed?

184
Q

What does warfarin increase?

A

International Normalised Ratio/ prothrombin time

185
Q

Give some examples of thrombolytics.

A

Alteplase/Tenecteplase (tPA), Streptokinase

186
Q

How do thrombolytics work?

A

Activate Plasminogen, which forms the cleaved product Plasmin. Increased PT

187
Q

What is plasmin?

A

Plasmin is a proteolytic enzyme that is capable of breaking cross-links between fibrin molecules, which provide the structural integrity of blood clots

188
Q

What are the side effects of thrombolytics?

189
Q

What are diuretics used to treat?

A

These are indicated for the treatment of hypertension and oedema often caused by ischaemic heart disease or chronic kidney disease

190
Q

How do loop diuretics work?

A

These act at the ascending limb of the loop of Henlé and reversibly inhibit the Na/K/Cl cotransporter, inhibiting the reabsorption of filtered sodium and chloride ions. This reduces the hypertonicity of the renal medulla, thus inhibiting water reabsorption by the collecting ducts

191
Q

Give some examples of loop diuretics.

A

Bumetanide(Bumex), Ethacrynic acid(Edecrin), Furosemide(Lasix), Torsemide

192
Q

What is the most commonly prescribed loop diuretic?

A

Furosemide

193
Q

What are the side effects of furosemide?

A

Dizziness, electrolyte imbalance, fatigue and headache

194
Q

What are thiazide diuretics prescribed for?

A

Hypertension and heart failure, as well as nephrogenic DI

195
Q

How do thiazide diuretics work?

A

Inhibiting reabsorption of sodium and chloride ions for the distal convoluted tubule by blocking the thiazide-sensitive Na-Cl symporter. This also means the reabsorption of water is also inhibited, as water follows sodium

196
Q

Give some examples of thiazide diuretics.

A

Clorothiazide and bendroflumethiazide

197
Q

What are the common side effects of thiazide diuretics?

A

Alkalosis hypochloraemic;diarrhoea;hyperglycaemia and hyperuricaemia

198
Q

What is spironolactone used to treat?

A

heart failure, hyperaldosteronism, hypertension, and nephrotic syndrome

199
Q

What are the common side effects of spironolactone?

A

Drowsiness,dizziness, nausea,vomiting

200
Q

What are the severe side effects of spironolactone?

A

Hyperkalaemia and anti-androgen effects, e.g. gynaecomastia, loss of libido, erectile dysfunction

201
Q

How does spironolactone work?

A

Within the collecting tubules of the nephron, spironolactone binds competitively to the aldosterone receptor (AR) at the aldosterone-dependent sodium-potassium exchange site. This promotes sodium and water excretion and potassium retention

202
Q

What is affinity?

A

Describes how well a ligand binds to the receptor

203
Q

What is intrinsic activity?

A

Emax of partial agonist ÷ Emax of full agonist

204
Q

What are partial agonists?

A

Partial bind/activation at receptor

205
Q

Give an example of a partial agonist.

A

Buprenorphine for opiod addiction

206
Q

Give an example of an agonist.

A

Alcohol and benzodiazepine at GABA A receptor

207
Q

What does a competitive antagonist do?

A

Instead they reverse the effects of agonists by competing with the agonist to bind (but not activate) receptors thereby preventing agonist from having an effect

208
Q

What happens to the dose curve by adding a competitive antagonist?

A

The dose response curve shifts to the right thereby meaning more agonist is required to illicit the same response

209
Q

What does a non-competitive antagonist do?

A

Binds near the receptor and prevents activation of it but does not bind directly to it so the agonist is still able to bind but just not activate the receptor

210
Q

What happens to the dose curve by adding a non-competitive antagonist?

A

It results in a shift right & down of the dose response curve thereby meaning even more agonist is required to illicit the same response

211
Q

What is the agonist for muscarinic ACh receptors?

212
Q

What is the agonist for nicotinic ACh receptors?

213
Q

What is the antagonist for muscarinic ACh receptors?

214
Q

What is the antagonist for nicotinic ACh receptors?

215
Q

What is the agonist for histamine receptors?

216
Q

What happens when histamine binds to histamine receptors?

A
  • Contraction of the ileum

- Acid secretion from parietal cells

217
Q

What is the antagonist for histamine receptors?

A

Mepyramine

218
Q

What is specificity?

A

No compound is every truly specific. Selectivity is better term to describe activity

219
Q

What happens when mepyramine binds to histamine receptors?

A
  • Reversed contraction of ileum

- No effect on acid secretion

220
Q

Give an example of selective and non-selective agonists.

A

Isoprenaline is a NON-SELECTIVE B-adrenoceptor agonist so it activated both B1 (heart) & B2 (lungs) receptors
- Whereas salbutamol is a SELECTIVE B2-adrenoceptor agonist, but at very high concentrations it loses its specificity so will activate both B1 and B2

221
Q

How do you calculate clearance?

A

Rate of appearance in urine ➗ Plasma concentration

222
Q

What is renal blood flow?

A

18% of cardiac output = 1L/min

223
Q

What is renal plasma flow?

A

60% of blood flow = 600mls/min

224
Q

What is glomerular filtration?

A

12% of renal blood flow = 130mls/min

225
Q

What are first order reactions?

A

Rate is directly proportional to the concentration of drug (rate ∝ [drug])

226
Q

What are second order reactions?

A

Rate is directly proportional to the square of the concentration of the drug (rate ∝ [drug]2)

227
Q

What are third order reactions?

A

Rate is directly proportional to the cube of the concentration of the drug (rate ∝ [drug]3)

228
Q

What are zero order reactions?

A

Rate is unrelated to the concentration of the drug (rate ∝ [drug]0)

229
Q

What are the 3 compartments of the body according to pharmacokinetic theory?

A

Plasma (5 litres), Interstitial (15 litres) & Intracellular (45 litres)

230
Q

What affects aspirin uptake?

A

Gastric pH

231
Q

What does a raised gastric pH do to aspirin uptake?

A

A raised pH results in the reduced uptake of aspirin from the stomach and thus a reduction in bioavailability

232
Q

Which compartment are proteins/large molecules active in?

A

Proteins/large molecules are only active in the plasma compartment (5L)

233
Q

Which compartment are water soluble molecules active in?

A

Water soluble molecules are active in plasma and interstitial compartment
(5L + 15L)

234
Q

Which compartment are lipid soluble molecules active in?

A

Lipid soluble molecules are only active in the intracellular fluid (45L)

235
Q

How do you calculate volume of distribution?

A

Volume of distribution = Total amount of drug in body ➗ Concentration of drug in plasma

236
Q

What is volume of distribution?

A

It is the volume (litres) that the drug would occupy if it was distributed through all the compartments as if they were all plasma

237
Q

What is elimination?

A

The elimination of a drug is from the plasma compartment

238
Q

What is clearance?

A

The removal of drug from the plasma by either liver or kidney is CLEARANCE

  • The volume of plasma that can be completely cleared of drug per unit time (mls minute-1 (ml/min))
  • The rate at which plasma drug is eliminated per unit plasma concentration (mls minute-1 (ml/min))
239
Q

What is hepatic blood flow?

A

Hepatic blood flow is 24% of cardiac output (3/4 from portal vein and 1/4 from hepatic artery)

240
Q

What is hepatic extraction ratio (HER)?

A

The proportion of drug removed by one passage through the liver

241
Q

When does liver failure affect drug metabolism?

A

There is minimal effect on drug metabolism until at least 70% of functioning liver is lost

242
Q

Which drugs have active metabolites?

A
  • Prednisone
  • Isosorbide dinitrate - Codeine
  • Diamorphine
  • L-dopa
  • Cortisone
  • Morphine
243
Q

What are the adverse effects of muscarinic agonists?

A
  • Diarrhoea
  • Urination
  • Miosis (excessive pupil constriction)
  • Bradycardia
  • Emesis (vomiting)
  • Lacrimation (tears)
  • Salivation/sweating
  • Remember by DUMBELS!
244
Q

What does the parasympathetic nervous system do?

A
  • Acetyl choline
  • Rest & digest
  • Constricts pupils
  • Stimulates tears
  • Stimulates salivation
  • Lowers heart rate
  • Reduces respiration
  • Constricts blood vessels
  • Stimulates digestion
  • Contracts bladder
245
Q

What does the sympathetic nervous system do?

A 
Noradrenaline
• Fight or flight
• Dilates pupil
• Inhibits tears
• Inhibits salivation
• Activates sweat glands 
• Increases heart rate
• Increases respiration 
• Inhibits digestion
• Release of adrenaline 
• Relaxes bladder
• Ejaculation in males
246
Q

How is adrenaline synthesised?

A

TYROSINE > DOPA > dopamine > noradrenaline > adrenaline

247
Q

What are the effects of alpha-1 adrenoreceptors?

A
  • Vasoconstriction
  • Pupil dilation
  • Bladder contraction
248
Q

What are the effects of alpha-2 adrenoreceptors?

A

Presynaptic inhibition of noradrenaline (negative feedback) i.e. when blood sugar is low then alpha-2 in pancreas will be stimulated to reduce noradrenaline release thereby reducing insulin levels being released from the pancreas

249
Q

What are the effects of beta-1 adrenoreceptors?

A
  • Increased force of heart contraction (positive inotropic
    effect)
  • Increased heart rate
  • Increased electrical conduction in heart
  • Increased renin release from kidney
  • Increased blood pressure
250
Q

What are the effects of beta-2 adrenoreceptors?

A
  • Bronchodilation
  • Vasodilation
  • Reduced GI motility
251
Q

What are the effects of beta-3 adrenoreceptors?

A
  • Increased lipolysis

- Relaxation of bladder

252
Q

What do adrenergic agonists target?

A
  • Blood vessels (Alpha-1)
  • Heart (Beta-1)
  • Bronchial smooth muscle (Beta-2)
253
Q

What are the effects of adrenergic agonists?

A
  • Vasoconstriction (Alpha-1)
  • Positive inotropic effect (Beta-1)
  • Bronchodilation (Beta-2)
254
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

255
Q

What is the positive role of pain?

A
  • Warning of tissue damage
  • Immobilisation for healing
  • Protection of the species: establishment of memory
256
Q

What are the physiological effects of pain?

A
  • Increased heart rate
  • Increased blood pressure
  • Increased respiratory rate
257
Q

What is chronic pain?

A

Ongoing persistent pain greater than 3-6 months

258
Q

Summarise adverse drug reactions (ADRS)

A
  • A - Augmented
  • B - Bizarre
  • C - Chronic
  • D - Delayed
  • E - End of use
259
Q

How do you identify the type of ADR?

A
  • Is there a history of allergy? - Type B (Bizarre)
  • Is it predictable from the mechanism of action? Does it seem
    dose-related? - Type A (Augmented)
  • Has the patient been using the medication for a long time? - Type C (Chronic)
  • Is the patient withdrawing from a medicine? - Type E (End of Use)
  • Has the patient uses a drug in the past that could be causing a problem now? - Type D (Delayed)
260
Q

What is mast cell degranulation?

A

Cross linking of IgE receptors releasing:

  • Histamine
  • Thromboxanes, prostaglandins
  • Tumour Necrosis Factor (TNF)
261
Q

What are the main clinical features of anaphylaxis?

A

• Exposure to drug, immediate rapid onset
• Rash withe characteristic blotches
• Swelling of lips, face, oedema, central
cyanosis (go blue/purple)
• Wheeze
• Hypotension (Anaphylactic shock)
• Cardiac arrest

262
Q

What is the alternative presentation of anaphylaxis?

A
  • Cardiorespiratory arrest

* NO SKIN CHANGES!

263
Q

What markers should be identified if an ADR is suspected?

A

• Type A : Serum concentration - plasma monitoring
• Type B:
- Tryptase - released from only mast cells - BEST TEST TO CONFIRM ALLERGY BASED ADR
- Urine Methylhistamine - breakdown product of histamine

264
Q

What are the drug risk factors for drug interactions?

A
  • NARROW therapeutic index
  • Steep dose/response curve
  • Saturable metabolism - e.g. paracetamol and alcohol are metabolised at a SET RATE
265
Q

Give some examples of drugs that are weak acids.

A 
• Aspirin - try to alkalinise urine to help increase excretion
with aspirin overdose
• Ibuprofen
• Paracetamol
• Warfarin
266
Q

Give some examples of drugs that are weak bases.

A
  • Amphetamine
  • Atropine
  • Propranolol
  • Salbutamol
267
Q

How long are fluids discontinued for after surgery?

A

Nil by mouth policy for fluids is 2 hours - due to fear of aspiration under anaesthesia

268
Q

What antagonist is given to reverse overdose?

269
Q

How much of an oral drug is the equivalent to it parentally?

A

10mg orally is equivalent to 5mg parenterally (sub-cutaneous, intramuscular & IV)

270
Q

What do you administer to a patient with opioid induced respiratory depression?

A

Administer naloxone - IV is fastest route - 400 micrograms per ml

271
Q

What is gate control theory?

A
  • There is a balance of activity between large (A beta fibres) and
    small (A delta fibres & C fibres) fibres
  • Interneurons of the substansia gelatinosa regulate the input in
    Lamina V (dorsal horn of spinal cord)
  • If A beta fibres are NOT stimulated by nociceptive stimulus then the pain signal goes through to the brain and is perceived
  • If A beta fibres ARE stimulated then the pain signal is halted and does not reach the brain and is thus not perceived
  • This means that low intensity stimulation of the skin or peripheral nerves or vibration in order to stimulate the A beta fibres will generate analgesia
272
Q

What are the applications of gate control theory?

A
  • Rubbing site of injury
  • Application of heat
  • TENS - trans cutaneous nerve stimulation of A beta fibres
  • Spinal cord stimulaiton
273
Q

What is adrenaline used for?

A
  • Anaphylaxis - reduced blood pressure & increased bronchoconstriction
  • Cardiac arrest
  • Acute hypotension
274
Q

What type of drug is adrenaline?

A

Non-selective since it works at any alpha or beta adrenoceptor

275
Q

Give some examples of selective adrenergic alpha-1 agonists.

A

Phenylephrine & Oxymetazoline

276
Q

What do phenylephrine and oxymetazoline do?

A

• Results in vasoconstriction
• Useful as a nasal decongestant since vasoconstriction results in
less fluid leakage from vessels

277
Q

Give some examples of selective adrenergic alpha-2 agonists.

278
Q

What does clonidine do?

A

It inhibits noradrenaline release therefore is useful as an anti-hypertensive

279
Q

What does dobutamine do?

A

Have a positive inotropic effect in the heart thus increase force of heart contraction

280
Q

Give some examples of selective adrenergic beta-1 agonists.

A

Dobutamine

281
Q

Give some examples of selective adrenergic beta-2 agonists.

A

Salbutamol

282
Q

What does salbutamol do?

A

Results in bronchodilation

283
Q

Give some examples of selective adrenergic beta-3 agonists.

A

Mirabegron

284
Q

What does mirabegron do?

A

Results in the relaxation of the bladder

285
Q

What does tamulosin do?

A

Relaxes bladder neck, thus aids in urination, useful in men with enlarged prostates who find it difficult to urinate

286
Q

What does doxazosin do?

A

Is a vasodilator, thus reduces blood pressure i.e. is an anti-hypertensive

287
Q

Give some examples of adrenergic alpha-2 antagonists.

288
Q

What does yohimbine do?

A

Blocks alpha-2 receptor meaning noradrenaline inhibition DOES NOT OCCUR leading to an increase in noradrenaline and other catecholamines such as dopamine

289
Q

What do adrenergic beta-1 antagonists do?

A
  • Results in a reduction in cardiac output as well as a reduction in renin thus a reduction in blood pressure
  • Useful in treating hypertension, angina and arrhythmia
290
Q

What is propanolol?

A

Non-selective i.e. works on all beta receptors

291
Q

Give some examples of beta-1 selective antagonists.

A

Atenolol, Metoprolol, Bisoprolol, Betaxolol

292
Q

What is carvedilol?

A

A non-selective beta & alpha-1 antagonist which not only affects the heart but causes vasodilation too

293
Q

Give some examples of ACE inhibitors.

A

Captopril and enalapril

294
Q

What are ACE inhibitors?

A

Anti-hypertensives

295
Q

How do ACE inhibitors do?

A

Work by inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II meaning there is less angiotensin II so less bind to angiotensin receptors (AT1) resulting in reduced vasoconstriction and thus hypertension as well as less aldosterone release further reducing hypertension

296
Q

What type of drug is enalapril?

A

Pro-drug - this means its ester needs to be enzymatically cleaved by esterase for the drug to be activated

297
Q

How do captopril and enalapril work?

A

Both captopril and enalapril work by binding to ACE active site thereby meaning it is unable to convert angiotensin I to angiotensin II

298
Q

What does captopril mimic?

A

mimic dipeptide; His & Leu

299
Q

What does enalapril mimic?

A

mimics tripeptides; Phe, His & Leu

300
Q

Give some examples of proton pump inhibitors (PPIs).

A

Omeprazole, lansoprazole, pantoprazole & rabeprazole

301
Q

How are PPIs activated?

A

Activated in acidic (i.e. stomach) environments

302
Q

What do PPIs do?

A

They act to inhibit acid secretion

303
Q

What does prostaglandin E2 (PGE2) do?

A

When prostaglandin E2 (PGE2) released from chromaffin cells, binds to EP3 receptors on parietal cells, this causes a reduction in the concentration of H+ and thus acidity of the stomach by reducing the activity of the H+/K+ ATPase pump - PGE2 INHIBITS PARIETAL CELLS

304
Q

What does histamine do to parietal cells?

A

When histamine released from histaminocytes, binds to H2 receptors on parietal cells, this causes the H+/K+ ATPase pump to increase activity resulting in a higher concentration of H+ being pumped into the gastric lumen thereby increasing acidity - HISTAMINE ACTIVATES PARIETAL CELLS

305
Q

Describe how PPIs work.

A

PPIs act to IRREVERSIBLY INACTIVATE the proton pump (H+/K+ ATPase) resulting in a marked reduction in acidity of the stomach, thereby helping with reflux etc.

306
Q

Give some examples of anaesthetics.

A

Lidocaine and procaine

307
Q

How do local anaesthetics work?

A

These local anaesthetics work by interrupting axonal neurotransmission in the sensory nerves. They do this by blocking voltage dependent sodium channels thereby preventing the neurones from depolarising meaning threshold isn’t met and thus no action potential is developed to be propagated

308
Q

Why do anaesthetics result in pain relief?

A

Pain isn’t transmitted to the brain to be perceived

309
Q

Why can local anaesthetics sometimes act on muscles?

A

Local anaesthetics can diffuse through mucus membranes EASILY thus sometimes can act on muscles too

310
Q

What do opioids use in order to work?

A

Opioid drugs simply use the existing pain modulation system - natural endorphins (endogenous morphine) and enkephalins

311
Q

How do opioids work?

A

G protein coupled receptors act via second messengers

They inhibit the release of pain transmitters at spinal cord and midbrain and modulate pain perception in higher centres - euphoria - to change the emotional perception of pain

312
Q

What do opioids block?

A

Descending pain transmission

313
Q

What are the opioid receptors?

A

Morphine (MOP)
Delta (DOP)
Kappa (KOP)
Nociceptin opioid-like (NOP)

314
Q

What do kappa agonists cause?

A

Mental depression instead of euphoria

315
Q

What type of receptors do all the opioids used at present affect?

A

Morphine - MOP

316
Q

Where are opioid receptors found?

A

Midbrain
• Spine
• GI tract - can get constipated with opioid use
• Breathing centre - it communicates using opioid receptors, opioid use can cause respiratory depression

317
Q

What are the relative potencies of morphine, diamorphine and pethidine?

A
  • Diamorphine - 5mg (twice as potent as morphine)
  • Morphine - 10mg
  • Pethidine - 100mg (10 times weaker than morphine)
318
Q

Give some examples of opioids.

A 
Morphine
Diamorphine
Pethidine
Methadone
Oxycodone
Codeine
Fentanyl
Hydrocodone
319
Q

What are the naturally occurring opioids?

A
  • Morphine

* Codeine (weak)

320
Q

What are the synthetic opioids?

A
  • Pethidine
  • Fentanyl (very potent)
  • Alfentanil (very potent)
  • Remifentanil (very potent)
321
Q

Which opioid is a synthetic partial agonist?

A

Buprenorphine - if overdose there is no respiratory depression

322
Q

What are the side effects of opioids?

A
  • Respiratory depression
  • Sedation
  • Nausea & Vomiting
  • Constipation
  • Itching
  • Immune suppression
  • Endocrine effects

Phase 2a (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions