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Phase 2a > ICS Pharmocology > Flashcards

ICS Pharmocology Flashcards

1
Q

what is teh difference between pharmacodynamics and pharmacokinetics

A
  • Pharmocodynaims - what the drig does to eh bodu
    Pharmacokinetics - what the bod does to the drug
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2
Q

what are teh 4 aspects of pharmaco dynamics

A

Sumation 1+1=2
Synergism 1+1>2 (taking paracetamol and ibroprofen provides more pain relief
Antagonism 1+1=0
Potentiation 1+1+1=1.5

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3
Q

what are the thre routes of administration for drugs

A

systemic - enteral (GI base such as oral or rectal)) and par-enteral (non GI basically by needle, IV,IM,SC,Inhelation)
Local- topical, transpermal. inhelation, intranasal

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4
Q

what is the problem with enteral based drugs

A

they have to cross teh membranes, alot of them wont reahc circulation as they are metabolised by the gut or liver

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5
Q

whihc syetm of drug giving is teh fastest

A

IVm no membranes and no first pass metabolism

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6
Q

what is bioavailabiloty and teh equation for it

A

Bioavailability is the extent to which an administered drug reaches systemic circulation depending on the first pass metabolisation, for IV it is assumed to be 100%
AUC oracl / AUC IV x100

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7
Q

what are teh drug targest

A

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

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8
Q

what does drug distrabution depent on

A

Distribution depends on:
Blood flow to area
Permeability of capillaries
Binding to proteins (albumin = slower)
Lipophilicity
Volume of distribution

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9
Q

how and why does teh liver metabolise drugs

A

lipid soluble dugs cannot pass through teh kidney
phase 1 - make teh drug hydrophillic using chytochrome p450
phase 2 - make drug polar, thsi si he biggets change
some drugs can induce or inhibit teh cytochrome p450 enzymes
after this they are water solube so can pass though teh kidneys

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10
Q

define druggability

A

a biological target that its known to bin with high affinity ti a drug wit a therapputic benefit to teh patient

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11
Q

wha is a receptor

A

A component of a cell that interacts with a specific ligand* and initiates a change of biochemical events leading to the ligands observed effects

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12
Q

what are teh 4 receptors in teh body

A

Ligand-gated ion channels
nicotinic ACh receptor

G protein coupled receptors
beta-adrenoceptors

Kinase-linked receptors
receptors for growth factors

Cytosolic/nuclear receptors
steroid receptors

teh most commen is teh G proetin

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13
Q

what are ligand gated ion channels

A

membrane protines that allow ions to pass though causing a shirt in electriiciy via cations and anions

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14
Q

what are g protien couple receptors

A

largest and most diverse]
targeted by more that 30% of drugs
light energy, peptides, lipids, sugars and protiens interact with them
they are guanine neucleotide binding protines and they hydrolise Guanosine di and triphosphate
they are molectlar switches and catalyse GDP to GTP tjough using ATP
they tehn cause secondary molecules to be released

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15
Q

what are kinase linked receptors

A

nzymes that catalzye teh transfer of phosphate groups between protiens. it is called phosphorilation

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16
Q

wha is a nucler receptor

A

ligand binding receptors taht causes modified gene transcrripton taht feten respond to steriod hormones

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17
Q

define agonist and antagonist

A

agonist- binds to a receptor and activats it
antagonist - binds to a receptor and reduces teh effcte og teh agonist

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18
Q

what is teh two state model of receptor activation

A

describes how drugs activate receptors by inducing or supporting a conformational change in the receptor from “off” to “on”.

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19
Q

what is teh EC50

A

teh concentraion tat gives hakf of teh maximal response

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20
Q

what does a sigmoidal concentraion response curve mean

A

as the done increases teh respose inreases initially but will level off

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21
Q

what is teh Emax

A

teh maximum efficancy

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22
Q

define intrincis activity

A

Intrinsic activity(IA) orefficacyrefers to the ability of a drug-receptor complex to produce a maximum functional response

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23
Q

what is teh difference between potency and efficancy in drugs

A

potency - a lower dose is needed to achieve teh same affcect
efficancy - Refers to the relative ability of a drug-receptor complex to produce a maximum functional response.

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24
Q

what are teh two mechanisims of antagonists

A

competeative - competefir teh binding sight but do not activate it
non competative - bind to allottirtic sight and change teh shape of it so it cannot work

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25
Q

what is teh affinity and efficancy for agonists and antagonists

A

Agonists
Have affinity and efficacy
Antagonists
Have affinity but zero efficacy

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26
Q

what is inverse agonism

A

When a drug that binds to the same receptor as anagonistbut induces a pharmacological response opposite to that of theagonist

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27
Q

what is teh diffence between tolerance and desensitization

A

tolerance - reduction in agonist effect over time
desensitisation - a defence mechanism whihc is vety quick where it is degraded

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28
Q

wht are the factors governing drug action

A

Receptor-related
affinity
efficacy

Tissue-related
receptor number
signal amplification

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29
Q

how do statins work

A

they block teh rate limiting step in teh cholesterol pathway to reduce teh levels of LDL

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30
Q

what are inducers ans inhibitors of P450 enzymes in teh liver

A

inducers, speed up teh metabolism of otehr drugs
inhibirots, decrease teh cytochrome p450 activity reslutingin teh reduced metabolisation of oter drugs

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31
Q

what are teh two different rates of elimination

A

First order: catalysed by enzymes, rate of metabolism directly proportional to drug concentration, this is when there is more drug than enzyme

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

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32
Q

define uniporters, symporters and antiporters

A

Uniporters: use energy from ATP to pull molecules in.
Symporters: use the movement in of one molecule to pull in another molecule against a concentration gradient.
Antiporters: one substance moves against its gradient, using energy from the second substance (mostly Na+, K+ or H+) moving down its gradient.

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33
Q

what is an example of a drug that is an agonist

A

salbutamol inhalor - beta 2 receptor agonist

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34
Q

what is an examle of a drug that is an antagonist

A

propanalol, beta blocker for hypertension

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35
Q

definine efficany

A

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

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36
Q

define potency

A

Binding affinity of the drug for the receptor

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37
Q

define first pass metabolism

A

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

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38
Q

define bioavailability

A

Fraction of drug that reaches systemic circulation unaltered

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39
Q

what is teh process of paracetamol metabolism

A

95% gets conjugated with gluceronide sulfates and is fine and then excreted in teh ureine
5% goes down teh CYP450 route and become toxic NAPQI whihc has to then be conjugated by glutathione to become non toxic again

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40
Q

How does a paracetamol overdose work

A

the regular pathway beomces overloaded and teh P450 system gets used more. this means that all teh glutathione gets used up and the NAPQI builds up and damages the hepatocytes leading to liver necrosis `

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41
Q

what is teh treatment of a paracetamol overdoes

A

Activated charcoal - <1 hour of ingestion of >150mg/kg paracetamol
<8 hours – wait until 4 hours from ingestion then measure plasma level and send for urgent analysis. results suggest acute liver injury > intravenous N-acetylcysteine
Staggered overdose = paracetamol taken over a period of more than 1 hour
- Treatment nomogram in unreliable
- Based on paracetamol levels and further blood tests
Liver transplant
- Low blood pH, high blood lactate, poor blood clotting, hepatic encephalopathy

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42
Q

what are teh features o teh autonimuc NS

A

two neuron chain, smooth muscles, cardica muscles and goands, leads to exitation or inhabition

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43
Q

where are teh ganglion located in teh sympathetic and parasympathetic neviur symptims

A

In the sympathetic system, the ganglion is within a chain adjacent to the spinal cord

In the parasympathetic system, the ganglion is within or very close to the effector organ

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44
Q

what are teh pre and post ganglionnic neurotransmitter

A

Sympathetic - nictotinic (acH) preganglionnic and noraadrenaline on alpha and beat postgangionnic
Parasympathetic - ach on nicotinic pre, ach on muscaneric post

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45
Q

how many muscaerinic receptors ar there and where are they found

A

5
M1: Brain
M2: Heart
M3: All organs with parasympathetic innervation
M4: Mainly CNS
M5: Mainly CNS

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46
Q

what type of receptors are muscaneric

A

G protiens found on teh outside of cells

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47
Q

who is a sexy they?

A

Andrew

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48
Q

what do teh M3 receptors do arounf teh body

A

Stimulation in the Respiratory System
Produces mucus (airways and nasopharynx)
Induces smooth muscle contraction (bronchoconstriction)

GI tract
Increase saliva production
Increases gut motility
Stimulates biliary secretion

Skin
Only place where Sympathetic system releases ACh
Stimulation of M3 causes sweating

Stimulation of urinary system M3 receptors
Contracts detrusor muscle
Relaxation of internal urethral sphincter

Eye
Causes myosis
Increases drainage of aqueous humour
Secretion of tears

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49
Q

what are pliocarpine eye drops

A

Pilocarpine eye drops are M3 agonists
they increase drainage of aquesou humour whihc reduces occuar pressure and treats glacuocoma.
It can also be used to treat a dry mouth

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50
Q

what are two examples fo antimuscaaric drugs

A

Solifenacin – a treatment for overactive bladder

Blocks M3 receptors in the bladder and inhibits smooth muscle contraction)

Mebeverine – a treatment for irritable bowel syndrome

Blocks M3 receptors in the gut to slow contractility

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51
Q

what blocks the ACh activity in the somatic nervous system

A

Nicotinic (N1) receptor blockers inhibit ACh activity in the somatic nervous system

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52
Q

what causes myasthansia graves

A

blockedge of the transmission of ACH by antibodies cuases skeletal musce weakness

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53
Q

what do the 5 neuroadrenaline receptors do

A

alpha 1 - Contracts smooth muscle (pupil, blood vessels)
Alpha 2 - Mixed effects on smooth muscle
Beta 1 - Chronotropic and inotropic effects on heart
Beta 2 - Relaxes smooth muscle (premature labour, asthma)
Beta 3 - Enhances lipolysis, relaxes bladder detrusor

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54
Q

alpha 1 receptors effects and uses

A

Alpha 1 activation causes vasoconstriction, mainly in the skin and splanchic (abdominal) beds

Noradrenaline is given IV for shock in ITU setting, or to overcome anaesthetic agents alpha blocking effects

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55
Q

alpha 2 effects and uses

A

However, alpha-2 receptors have mixed effects on vascular smooth muscle

They exist in the brain

For example, clonidine is alpha-2 agonist used in ADHD to help concentration

Actually reduces vascular tone and reduces blood pressure

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56
Q

where are beta 1 receptors found and what does there ahonism cause

A

Beta 1 mainly in:
Heart
Kidney
Fat cells

Agonism leads to:
Tachycardia
Increase in stroke volume
Renin release (increase in vascular tone)
Lipolysis and hyperglycaemia

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57
Q

what are the effects of beta 2 receptirs

A

bronchi - bronchodilation
bladder - inhibits micturtition
uterus - inhibition of labour
skeletal muscle - increase contraction speed
pancreas - insulin and glucagion secrestion

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58
Q

what are teh 4 factors of pharmokinetics

A

ADME
Absorption
Distrabution
Metabolism
Excertion

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59
Q

what is teh bioavailabily of oral morphine

A

50% of it is available
a single doese lasts 3-4 hours

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60
Q

whihc is teh fastest route of administation of opiods

A

IV, then IM and SC

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61
Q

what is dihydocodine

A

1.5x more potent than codine
it is already metabolised and so can be used by most people

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62
Q

what type of receptors do opiods work on, and what are they called

A

G protien coupled receptors, MOP KOP DOP NOP Morphine opiod receptor, delta, kappa, nociceptin)

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63
Q

what are the comparative doses for diamorphine, morphine and pethadine

A

diamorphine - 5mg
morphine - 10 mg
pethadine - 100mg

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64
Q

what are some side effects of opioids

A

respiritory depression
sedation
nausea and vomiting
constipation
itching
immune surperssion
endocrine effects

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65
Q

define adverse drug reaction

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug.

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66
Q

what are the three catogreis of an adverse drug reaction

A

toxic effect - they have taken more tan necessary
colleaterall effect - they have taken teh correct dose and reactes
hyper-susceptabiliy effect - tehy have taken less than youd have expected and still reacted

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67
Q

what is an example of a toxic effect

A

Nephrotoxicity or ototoxicity with high doses of aminoglycosides e.g. gentamicin

Can occur if dose is too high or drug excretion is reduced by impaired renal or hepatic function or by interaction with other drugs

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68
Q

what is an example of a collateral effect

A

Standard therapeutic doses
Beta blockers causing bronchoconstriction
Broad spectrum antibiotics causing clostridium difficile and pseudomembranous colitis

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69
Q

what is a hypersuspectabiloity reaction

A

Sub therapeutic doses
Anaphylaxis and penicillin

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70
Q

what are risk factirs for adverse drug reactions

A

PATEINT RISK:
gender (f>m)
age (neonate or geriatric)
polypharmacy
genetics
allergies
hepatic/renal imparement
adhernce problems (the patient doesnt taek it properly)

DRUG RISK:
steep dose response curve
low theraputic index
commonly cuases ADRs

THERE ARE ALSO PRESCRIBER RISKS!

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71
Q

WHAT ARE SOME CAUSES FOR ADR’S

A

Pharmaceutical variation—eosinophilia-myalgia syndrome with L-tryptophan

Receptor abnormality—malignant hyperthermia with general anaesthetics

Abnormal biological system unmasked by drug—primaquine induced haemolysis in patients deficient in glucose 6-phosphate dehydrogenase

Abnormalities in drug metabolism—isoniazid induced peripheral neuropathy in people deficient in the enzyme N-acetyl transferase (that is, those who are slow acetylators)

Immunological—penicillin induced anaphylaxis

Drug-drug interactions—increased incidence of hepatitis when isoniazid is prescribed with rifampicin

Multifactorial—halothane hepatitis

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72
Q

what are teh rawlins thompson classifications for adverse drug reactions

A

Type A (Augmented pharmacological)– predictable, dose dependent, common (morphine and constipation, hypotension and antihypertensive) 80% all ADRs
Type B (Bizarre or idiosyncratic)– not predictable and not dose dependent (anaphylaxis and penicillin)
Type C (Chronic) – osteoporosis and steroids
Type D (Delayed) – malignancies after immunosuppression
Type E (End of treatment) – occur after abrupt drug withdrawal eg opiate withdrawal syndrome
Type F (Failure of therapy) – Failure of OCP in presence of enzyme inducer

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73
Q

what is idiosyncracy

A

Inherent abnormal response to a drug

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74
Q

what is teh process for dealing with an ADR

A

Assess if urgent action is required
Take a history
Review medication history
Review the adverse effect profile of suspected drug
Modify dose, stop or swap
Report

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75
Q

wjat are soe of tegh most common drugs to react to

A

Antibiotics
Anti-neoplastics
Cardiovascular drugs
Hypoglycaemics
NSAIDS
CNS drugs

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76
Q

what is yellow card reporting

A

its a form that is filed in if there is an adverse drig reaction so taht they can be flagged up and prevented in eth furture

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77
Q

what type of receptors are nicotinic, and what type of receptors are muscerinic

A
  • Nivotinic receptors are ligand gated ion channels
    • muscarenic receptors are g coupled receptors
78
Q

what are teh neurotransmitters and receptors of teh parasympatheic NS

A

Ach - nicotinic 2 receptors
Muscarinic receptors

79
Q

what are th neurotransmitters and receptros of teh sympathetic NS

A

ACH binding to nicotinic (N2) receptors
Neuroadrenaline binding to alpha beta receptors

80
Q

what are Direct-acting Cholinergic agonists and examples

A

Mimic ACh and bind to ACh receptors

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

81
Q

what are Indirect-acting Cholinergic agonists (reversible) and examples

A

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

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

82
Q

what are Nicotinic antagonists and examples

A

Compete with ACh for binding to the nicotinic receptor

Curare, Pancuronium (relax skeletal muscles during surgery)

83
Q

what are Muscarinic antagonists and examples

A

Compete with ACh for binding to the muscarinic receptor

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

84
Q

what type of receptro is an adrengenic receptor

A

g protien

bind to guanasine diphosphate, when unactive, t oguanisine triphosphate when active

85
Q

what do the 2 alpha adrenoceptors do

A

alpha 1 - vasoconstriction, increased blood pressure,
alpha 2 - increased neuroepinephirein release, inhibition of ACh

86
Q

what is do the 2 beta adrenoreceptors do

A

Beta 1 - tachycardia, increased lipolysis, increased renin release, increased contractility
beta 2 - vasodilation, decreased peripheral dilation, bronchodilation, increased glucagon

87
Q

what are the alpha 1 agonists and antagonists drugs

A

agonists - Decongestants (phenylephrine)

antagonist - Tamsulosin
Doxazosin

88
Q

what are teh alpha 2 agonists and antagonist drugs

A

Agonist - centrally acting vasodilators - clonidine

antagonist - yohimbine

89
Q

what are the beta 1 agonists and antagonist drugs

A

agonists - Inotropes (epinephrine, dopamine, dobutamine)

antagonists - Selective/Non-selective beta-blockers for blood pressure

90
Q

what are beta 2 agonist and antagosit drugs

A

agonist - SABA

Antagonist - non selective beta blockers

91
Q

what is teh most commen drug to treat viruses

A

acyclovir

92
Q

how do beta lactam atibioltics work

A

they inhibit the synthesis of the peptidoglycan layer in the bacterial cell walls

disrupt peptidoglycan production
by binding covalently and irreversibly to the Penicillin Binding Proteins
cell wall is disrupted and lysis occurs
results in a hypo-osmotic or iso-osmotic environment
Active only against rapidly multiplying organisms

93
Q

what are the three cell wall attacking antibiotics

A

beta lactams. vancomycin,

polymyxins (cell membrane)

94
Q

what are the 4 types of beta lactams

A

The 4 types of beta lactams:
penicillins -
ceohalosporins -
carbapenems
monobactams

95
Q

what are 4 penicillin drug names

A

flculoxacillin, amoxicillin, pipericillin, penicillin

96
Q

what are the three key cephalosporins

A

Cefuroxime
Cefotaxime
Ceftriaxone

97
Q

what is a drug example og carbapenems

A

Meropenem

98
Q

hat are two glycopeptides antibiotic drugs

A

Vancomycin
Teicoplanin

99
Q

whihc types of bacteria are more suseptable to beta lactam antibiotics

A

gram-positive usually more susceptible to β-lactams than gram-negative bacteria
`
Differences in the spectrum and activity of β-lactam antibiotics are due to their relative affinity for different PBPs.

100
Q

how do nucleuic acid synthesis antibiotics work ad two examples of it

A

stop the RNA from symthasizing so it cant reproduce

metronidazole
ciprofloxacin

101
Q

what are the 4 classses nd examples of protien synthesis antibiotics

A

Aminoglycosides - Gentamicin
Tetracyclines - Doxycycline
Lincosamides - Clindamycin

Macrolides - Clarithromycin

102
Q

what are two folate synthesis antibiotic drugs

A

Trimethoprim
Co-trimoxazole

103
Q

what is a bacteriacidal antibiotic

A

Kill >99.9% in 18-24 hrs
this is normally antibiotics taht inhibit teh cell walls

104
Q

what is a bacteriacidal antibiotic

A

Kill >99.9% in 18-24 hrs
this is normally antibiotics taht inhibit teh cell walls

105
Q

what are bacteriastatic antibiotics

A

kill >90% in 18-24 hrs

inhibit the growth of bacteria, these are teh antibiotics taht inhibit protien synthesus or DNA replicaiton or metabolism

106
Q

what is the minimum inhibitory concentration

A

the minimum amout of antibiotics yuo can give to stop teh antibiotic form growig and kill it off

107
Q

what 4 things does an antibiotic function rely on

A

release
absorbtion
distrabution
elimination

108
Q

what are teh 4 ways bacteria can avoid antibiotics

A

change antibiotic target (teh receptor it nrmally binds to)
destroy the antibiotic
prevent antibiotic access (change teh channel shape that bacteria uses to get in)
remove teh antibiotic from teh bacteria

109
Q

what are three examples of antibiotic resistance dur to ahcgeing teh antibiotic target

A

Flucloxacillin (or methicillin) is no longer able to bind PBP of Staphylococci – MRSA*

Wall components change in enterococci and reduce vancomycin binding – VRE#

Rifampicin activity reduced by changes to RNA polymerase in MTB – MDR-TB$

110
Q

what is an examples of antibiotic resistance due to destruction of teh antibiotic

A

Beta lactam ring of Penicillins and cephalosproins hydrolysed by bacterial enzyme ‘Beta lactamase’ now unable to bind PBP

111
Q

what are two examples of intrinsic resistance in bacteria

A

Vancomycin cannot penetrate outer membrane of gram negative bacteria

112
Q

what are teh two types of awuired resistance in bacteria

A

spontaneous gene mutation, horizontal gene transfer

113
Q

what are teh three types of horizontal gene transfer in bacteria

A

conjugation - bacteria sex
transduction - insertion of DNA by bacteriophages
Transformation - picking up naked DNA

114
Q

what are teh two examples of gram positive antiobiotic resistance

A

MRSA
Methicillin resistant Staphylococcus aureus
Bacteriophage mediated acquisition of Staphylococcal cassette chromosome mec (SCCmec)
contains resistance gene mecA
encodes penicillin-binding protein 2a (PBP2a)
confers resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)

VRE
vancomycin-resistant enterococci
Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
Promoted by cephalosporin use

115
Q

what are teh two classes of NSAIDs

A

non selective - these are competitive reversible inhibitors of COX 1 and 2 (for example ibruprofen and naproxen)

selective - inhibit COX2 only

116
Q

how doo NSAIDs work

A

inhibit teh COX2 enzyme which stops it from producing prostoglandins

117
Q

how do NSAIDS produce stomach ulcers

A

they inhibit COX1 and 2 whihc is important fr maintaing teh mucoasal surface n teh stomach, causing breaches and ulcers

selective ones only inhibit COX2 so are less lievly to cuases stomach ulcers

118
Q

when would Vancomycin or Teicoplanin antibiotics be used and how

A

how: IV!

WHY:
- only used on gram positive
- used when there is a patient allergy to penicillin
- used for beta lactam resistant bacteria whihc are gram posiitve such as MRSA

119
Q

what are teh 5 mechanisms antibiotics work by

A

Inhibitors of cell wall synthesis
Inhibitors of protein synthesis
Inhibitors of nucleic acid synthesis
Anti-metabolites
Inhibitors of membrane function

120
Q

when would lincosamides (clindamyacin) be used and what type of antibiotic is it

A

a protien synthesis blocker

for gram pos if there is necrosing fascitiis as it can block teh production fo teh nasty toxins being made

also for cellulitus if tehre is a penicillin allergy

121
Q

what is tetrracyclins (doxycycline) used for

A

protien synthesis blocker

Activity : Broad spectrum but mainly Gram positive (S. aureus and streps)
Use: cellulitis (if penicillin allergy)
Use: pneumonia

122
Q

whihc antibiotics can be used to treat both gram pos and neg

A

Amoxicillin
Amoxicillin-clavulanate
Piperacillin-tazobactam
Meropenem

Cephalexin
Cefuroxime
Ceftriaxone
Cefotaxime

123
Q

whihc antibiotic is of teh broadest spectrum and is restricted?

A

meropenem

124
Q

what are the 2 mechanisms taht asprin does

A

anti inflamitory effect - binding to COX-1/2

Anti platelet - decreased thromboxone A2

125
Q

how do thienopyridine drugs work for antiplatlets

A

metabolised by teh liver ti bind to ADP recetors on platelets and dramatically reduce platelet activation

126
Q

how does dipyriamole work

A

Dipyridamole inhibits phosphodiesterase, which inactivates cyclic AMP . It also stimulates prostacyclin release and inhibits thromboxane A2 formation, like aspirin. This leads to decreased platelet aggregation and vasodilation.

127
Q

what are tw examples of Xa inhibitors for anti coagulation

A

Apixaban, Rivaroxaban

128
Q

how does heparin work and what are its side effects

A

activates antithrombin whihc decreases thrombin and factor A

Bleeding, heparin-induced thrombocytopenia, osteoporosis

129
Q

how does warfrin work and what are its side effects

A

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

it is anti vitamin K which block all vitK dependant factors!

side effects: bleeding, skin/tissue necrosis, teratogenic

130
Q

what does teratogenic mean

A

cna be a drug takne by teh mother whih causes a change in teh structure and function of teh feotus

131
Q

what are throbolytics

A

Activate Plasminogen, which forms the cleaved product Plasmin. Plasmin is a proteolytic enzyme that is capable of breaking cross-links between fibrin molecules, which provide the structural integrity of blood clots

132
Q

what are two examples of thrombolytics

A

Alteplase/Tenecteplase
streptokinase

133
Q

how do loop diuretics work

A

These act at the ascending limb of the loop of Henle 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 s that more water is excterted

134
Q

what are loop diuretcis used for

A

hypertension and oedema often caused by ischaemic heart disease or chronic kidney disease

135
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. Just a reminder that this also means the reabsorption of water is also inhibited, as water follows sodium.

136
Q

what are some examples of thiazide diuretics

A

clorothiazide and Bendroflumethiazide

137
Q

what are some side effects fo thiazide diuretics

A

alkalosis hypochloraemic; diarrhoea; hyperglycaemia and hyperuricaemia to name a few.

138
Q

how do potassium sparing diuretics work

A

it binds competitivly to the aldosterone receptors at the aldosterne dependant sodium potassium exchange site

thsi promotes na and water excretion and potassium retention

139
Q

what is an example of a potassium saving diuretic and some side effects

A

sprionolactone

hyperkalemia, antiandrogen effects, loss of libido, erectike disfunction

140
Q

what are 4 drug targets

A

receptors, enzymes, transporters, ion channels

141
Q

defie affinity and efficancy

A

affinity - binding to teh receptor
efficity - how well teh drug activated teh receptor

for exampe an anatagonist woud have good affinity and bad efficancy

142
Q

definr potency

A

the strength of a drug, how well it works

if a drug has teh same effect at a lower concentration, it is more potent

143
Q

what are teh 4 areas of pharmocokinetics

A

ADME

administration
distrabution
metabolism
excretion

144
Q

DEFINE POTENCY AND EFFICANCY

A

Potency denotes the amount of drug needed to produce a given effect. Efficacy: Refers to the relative ability of a drug-receptor complex to produce a maximum functional response

145
Q

what are the neurotransmitters and receptors used for the sympathetic pathway

A

Sympathetic- between teh pre ganglionic and the post, the post gangioonic receptors is epinephreine

146
Q

what are the neurotransmitters and receptors used for the parasympathetic

A

parasympathetic - Ach is the neurotransmitter for both nerves, teh first receptor is nicotinic and teh second is muscarinic

147
Q

what are the neurotransmitters and receptors used for the somatic

A

somatic - just ach and is only one nerve, the receptor is nicotinic

148
Q

what are three drugs whihc work on Ach receptros

A
  • botulinum toxin - BOTOX - causes ach release inhibition which causes paralysis
    • Curare causes muscle paralysis by acting as a competitive acetylcholine (ACh) antagonist
      Ach -ase inhibitors - causes a decreased degridation of Ach which leads to increased concentration
149
Q

what is a cholinergic crisis and teh symptoms of it

A
  • Cholinergic crisis - over stimulation and prduction of ACH
    • Remember by SLUDGE
    • Salivation
    • Lacrimation
    • Urination
    • Defication
    • Gi distress
      Emesis (vomiting)

ACH inhibitors will cuase side effects oposite to sluge

150
Q

where are teh three muscerinic receptors foud

A

M1 - brain
M2 - heart
M4- lungs

151
Q

what is teh athwya for teh formation of adrenaline

A

tyrosine
L dopa
dopamine
neuroadrenaline
adrenaline

152
Q

whree are teh alpha 1 and 2 receptors found

A

blood vessles and sphincters cusing vasoconstriction and bladder contraction and pupil dilation

alpha agonists will cuase bladder release for example teh drug -Tamsulosin- can be used to treat men with prostate problems

153
Q

what are teh two beta receptos and where are they fous

A

1- in teh heart and is ionotrophic (increased force of contraction)

2 - lungs - causes bronchodilation you can use it to treat asthma

154
Q

agonist and antagonist for dopamine uses

A

agonist - for prolacteremia, acromegally and parkinsons

antagonist - for antisickness (metroclopramide) and psychic disorders

155
Q

agnoist drug uses for GABA

A

agonist - benzodiazipenes - larazapan and diazapan are used for anxiety, sleep disorders and epilepsy

156
Q

histamine antagonist drug types

A

H1 - allergys (loratadine)
H2 - for GORD as it decreases stomach acid secretion (ranitidine)

157
Q

whihc is teh main excitatory and mian inhibitory neurotransmitter

A

excitatory - glutamate
inhibitory - GABA

158
Q

what are teh antibiotics for community aquired pneuminia

A

amoxicillin for typical (s.pneumonia,)

clarthromycin for atypical (legonella, c.pneumonia, m.pneumoia)

159
Q

treatment for TB and a side effect for each

A

remeber RIPE

you take teh fist 2 for 6 months and then the second 2 for teh two months after that.

rifampicin - red pee/tears
isoniazid - peripheral neuropathy
pyrazinamide - hepatitis
ethambutol - optic neuropathy

160
Q

what drig is given for cellulitus and whihc bacteria causes it

A

group B strep or S aureus

flucoxacillin

161
Q

what antibiotic fr a UTI

A

nitro furantoin

or trimethroprim however can affect folic acid levels so should be avoided for teh first 12 weeks

162
Q

what is teh antibiotic for gonorrhoea

A

doxycyclin

163
Q

what is teh treatment for chlamydia

A

azithromycin or doxycyclin

164
Q

treatment for H.pylori

A

CAP!

clarythromycin, amoxicillin and PPI (omeprazole)

165
Q

what is teh treatment for gastroenteritis

A

caused by campylobacter - clathythromycin
shigella or salmonella - ciprofloxacin

166
Q

what is teh treatment for meningitus

A

ceftriaxone, amoxicaillin if listeria is suspected

giver steriods simulationsly

167
Q

what are teh 4 pain types

A

nociceptive, cancer, neuropathic, chrhronic non cancer

168
Q

what is the defornition of acute pain

A

pain that lasts less tahn a week and is nociceptive

169
Q

how should adverse drug reactions be reported

A

via teh yellow card scheme!!!! to teh MHRA

170
Q

what is teh rawlins and thompson adverse drug reactions 5 types

A

ABCDE

augmented - is it a commen side effcect for example dry coungh on ace inhibitors
bizare - allergic reaction
chronic - cushings from steriods
delayed - has there been a drug used in teh past?
end of use - withdrawl?

171
Q

define protine binding and what does tghis mean

A

protien binding - it binds to alot of protines in teh blood, if this is hight it wont reach as many receptos as quickly

172
Q

what are pateint factors that can interact with drugs

A

age, polypharmy, genetics, hepatic or renal disease

173
Q

how can apsorbtion effect drugs

A

acidity of stomach
motility of the stomahc
solubility in teh blood stream

174
Q

what are some CTP450 inhibitors and inducers, and what effect does this have on drugs

A

inhibitors - erethromycin, grapefruit juice, cause increased theraputic effect
inducers - alcohol, st johns wort, thsi cuases decareased theraptic effect of teh drug

175
Q

what is a factor that can change the excretion of drugs

A

drugs which are acidic will be excreted faster if urine is weakly basic and the same vise vera

176
Q

what are the two naturally occuring opiods

A

morphine and codine

177
Q

what is teh equivelent dose of morphine, diamorphine and pethadine

A

10mg morphine
5mg diamorphine (heroin)
100mg pethadine

178
Q

define tolerence and efine dependance

A

tolerance - overstimulation of receptor menas that there is a desensatisation and more needs to be given in order to reach teh same effect

dependence - teh psychological state of craving euphoria

179
Q

what is teh treatment for an opioid overdose

A

NALOXONE!!!

180
Q

what is teh main antiplatelet and what would this be given for

A

asprin, arterial throbi

181
Q

what is teh mechanism of asprin

A

a cox 1 inhibitor, decreases levels of thromboxone A2 which normally activates platelts

182
Q

what is a drg other than asprin that is an antiplatelet and what is its mechanism

A

clopidogrel - P2Y12 inhibition

183
Q

what are teh 4 anti coagulents

A

when high, ducks thoughup

heparin
warfrin
DOACs (direct oral anticoagulation)
thrombolytics

184
Q

what is teh mechanism of heparin

A

activates antithrombin 3 and inhibits clotting factor x

185
Q

what is teh mechanism of warfrin

A

antivitamin k

186
Q

what is teh mechanisms of thrombolytics and a drug name

A

activates plamin to degrade fibrin

an example is aleplase whihc is given IV

187
Q

what is teh antidote to someone bleeding who is on warfrin

A

vitamin k!

188
Q

what are two examples of DOACs

A

apixiban and rivoroxiban

189
Q

what is a side effect of PPIs

A

increased risk of fractures

190
Q

what is a risk of loops and thiazide diuretics

A

hypokalemia and dehydration

191
Q

what are some side effcets of steroids

A

cateracts
ulcers (decrased immune response)
striae
hypertension
increased infection riskj
pancreatitus
osteoporesis

Phase 2a (18 decks)

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