ICS Pharmocology Flashcards
what is teh difference between pharmacodynamics and pharmacokinetics
- Pharmocodynaims - what the drig does to eh bodu
Pharmacokinetics - what the bod does to the drug
what are teh 4 aspects of pharmaco dynamics
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
what are the thre routes of administration for drugs
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
what is the problem with enteral based drugs
they have to cross teh membranes, alot of them wont reahc circulation as they are metabolised by the gut or liver
whihc syetm of drug giving is teh fastest
IVm no membranes and no first pass metabolism
what is bioavailabiloty and teh equation for it
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
what are teh drug targest
Cellular receptors
Enzymes (ACE inhibitors)
Membrane ion channels (Lidocaine)
Membrane transporters (PPIs)
what does drug distrabution depent on
Distribution depends on:
Blood flow to area
Permeability of capillaries
Binding to proteins (albumin = slower)
Lipophilicity
Volume of distribution
how and why does teh liver metabolise drugs
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
define druggability
a biological target that its known to bin with high affinity ti a drug wit a therapputic benefit to teh patient
wha is a receptor
A component of a cell that interacts with a specific ligand* and initiates a change of biochemical events leading to the ligands observed effects
what are teh 4 receptors in teh body
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
what are ligand gated ion channels
membrane protines that allow ions to pass though causing a shirt in electriiciy via cations and anions
what are g protien couple receptors
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
what are kinase linked receptors
nzymes that catalzye teh transfer of phosphate groups between protiens. it is called phosphorilation
wha is a nucler receptor
ligand binding receptors taht causes modified gene transcrripton taht feten respond to steriod hormones
define agonist and antagonist
agonist- binds to a receptor and activats it
antagonist - binds to a receptor and reduces teh effcte og teh agonist
what is teh two state model of receptor activation
describes how drugs activate receptors by inducing or supporting a conformational change in the receptor from “off” to “on”.
what is teh EC50
teh concentraion tat gives hakf of teh maximal response
what does a sigmoidal concentraion response curve mean
as the done increases teh respose inreases initially but will level off
what is teh Emax
teh maximum efficancy
define intrincis activity
Intrinsic activity(IA) orefficacyrefers to the ability of a drug-receptor complex to produce a maximum functional response
what is teh difference between potency and efficancy in drugs
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.
what are teh two mechanisims of antagonists
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
what is teh affinity and efficancy for agonists and antagonists
Agonists
Have affinity and efficacy
Antagonists
Have affinity but zero efficacy
what is inverse agonism
When a drug that binds to the same receptor as anagonistbut induces a pharmacological response opposite to that of theagonist
what is teh diffence between tolerance and desensitization
tolerance - reduction in agonist effect over time
desensitisation - a defence mechanism whihc is vety quick where it is degraded
wht are the factors governing drug action
Receptor-related
affinity
efficacy
Tissue-related
receptor number
signal amplification
how do statins work
they block teh rate limiting step in teh cholesterol pathway to reduce teh levels of LDL
what are inducers ans inhibitors of P450 enzymes in teh liver
inducers, speed up teh metabolism of otehr drugs
inhibirots, decrease teh cytochrome p450 activity reslutingin teh reduced metabolisation of oter drugs
what are teh two different rates of elimination
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
define uniporters, symporters and antiporters
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.
what is an example of a drug that is an agonist
salbutamol inhalor - beta 2 receptor agonist
what is an examle of a drug that is an antagonist
propanalol, beta blocker for hypertension
definine efficany
How well the ligand (drug) activates the receptor – e.g. full or partial agonist?
define potency
Binding affinity of the drug for the receptor
define first pass metabolism
Metabolism of the drug by the gut and liver before it reaches the bloodstream
define bioavailability
Fraction of drug that reaches systemic circulation unaltered
what is teh process of paracetamol metabolism
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
How does a paracetamol overdose work
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 `
what is teh treatment of a paracetamol overdoes
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
what are teh features o teh autonimuc NS
two neuron chain, smooth muscles, cardica muscles and goands, leads to exitation or inhabition
where are teh ganglion located in teh sympathetic and parasympathetic neviur symptims
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
what are teh pre and post ganglionnic neurotransmitter
Sympathetic - nictotinic (acH) preganglionnic and noraadrenaline on alpha and beat postgangionnic
Parasympathetic - ach on nicotinic pre, ach on muscaneric post
how many muscaerinic receptors ar there and where are they found
5
M1: Brain
M2: Heart
M3: All organs with parasympathetic innervation
M4: Mainly CNS
M5: Mainly CNS
what type of receptors are muscaneric
G protiens found on teh outside of cells
who is a sexy they?
Andrew
what do teh M3 receptors do arounf teh body
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
what are pliocarpine eye drops
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
what are two examples fo antimuscaaric drugs
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
what blocks the ACh activity in the somatic nervous system
Nicotinic (N1) receptor blockers inhibit ACh activity in the somatic nervous system
what causes myasthansia graves
blockedge of the transmission of ACH by antibodies cuases skeletal musce weakness
what do the 5 neuroadrenaline receptors do
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
alpha 1 receptors effects and uses
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
alpha 2 effects and uses
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
where are beta 1 receptors found and what does there ahonism cause
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
what are the effects of beta 2 receptirs
bronchi - bronchodilation
bladder - inhibits micturtition
uterus - inhibition of labour
skeletal muscle - increase contraction speed
pancreas - insulin and glucagion secrestion
what are teh 4 factors of pharmokinetics
ADME
Absorption
Distrabution
Metabolism
Excertion
what is teh bioavailabily of oral morphine
50% of it is available
a single doese lasts 3-4 hours
whihc is teh fastest route of administation of opiods
IV, then IM and SC
what is dihydocodine
1.5x more potent than codine
it is already metabolised and so can be used by most people
what type of receptors do opiods work on, and what are they called
G protien coupled receptors, MOP KOP DOP NOP Morphine opiod receptor, delta, kappa, nociceptin)
what are the comparative doses for diamorphine, morphine and pethadine
diamorphine - 5mg
morphine - 10 mg
pethadine - 100mg
what are some side effects of opioids
respiritory depression
sedation
nausea and vomiting
constipation
itching
immune surperssion
endocrine effects
define adverse drug reaction
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.
what are the three catogreis of an adverse drug reaction
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
what is an example of a toxic effect
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
what is an example of a collateral effect
Standard therapeutic doses
Beta blockers causing bronchoconstriction
Broad spectrum antibiotics causing clostridium difficile and pseudomembranous colitis
what is a hypersuspectabiloity reaction
Sub therapeutic doses
Anaphylaxis and penicillin
what are risk factirs for adverse drug reactions
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!
WHAT ARE SOME CAUSES FOR ADR’S
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
what are teh rawlins thompson classifications for adverse drug reactions
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
what is idiosyncracy
Inherent abnormal response to a drug
what is teh process for dealing with an ADR
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
wjat are soe of tegh most common drugs to react to
Antibiotics
Anti-neoplastics
Cardiovascular drugs
Hypoglycaemics
NSAIDS
CNS drugs
what is yellow card reporting
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
what type of receptors are nicotinic, and what type of receptors are muscerinic
- Nivotinic receptors are ligand gated ion channels
- muscarenic receptors are g coupled receptors
what are teh neurotransmitters and receptors of teh parasympatheic NS
Ach - nicotinic 2 receptors
Muscarinic receptors
what are th neurotransmitters and receptros of teh sympathetic NS
ACH binding to nicotinic (N2) receptors
Neuroadrenaline binding to alpha beta receptors
what are Direct-acting Cholinergic agonists and examples
Mimic ACh and bind to ACh receptors
Carbachol (constrict pupil)
Bethanechol (increase smooth muscle tone in GI and GU tract)
Pilocarpine (stimulate saliva secretion)
what are Indirect-acting Cholinergic agonists (reversible) and examples
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)
what are Nicotinic antagonists and examples
Compete with ACh for binding to the nicotinic receptor
Curare, Pancuronium (relax skeletal muscles during surgery)
what are Muscarinic antagonists and examples
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)
what type of receptro is an adrengenic receptor
g protien
bind to guanasine diphosphate, when unactive, t oguanisine triphosphate when active
what do the 2 alpha adrenoceptors do
alpha 1 - vasoconstriction, increased blood pressure,
alpha 2 - increased neuroepinephirein release, inhibition of ACh
what is do the 2 beta adrenoreceptors do
Beta 1 - tachycardia, increased lipolysis, increased renin release, increased contractility
beta 2 - vasodilation, decreased peripheral dilation, bronchodilation, increased glucagon
what are the alpha 1 agonists and antagonists drugs
agonists - Decongestants (phenylephrine)
antagonist - Tamsulosin
Doxazosin
what are teh alpha 2 agonists and antagonist drugs
Agonist - centrally acting vasodilators - clonidine
antagonist - yohimbine
what are the beta 1 agonists and antagonist drugs
agonists - Inotropes (epinephrine, dopamine, dobutamine)
antagonists - Selective/Non-selective beta-blockers for blood pressure
what are beta 2 agonist and antagosit drugs
agonist - SABA
Antagonist - non selective beta blockers
what is teh most commen drug to treat viruses
acyclovir
how do beta lactam atibioltics work
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
what are the three cell wall attacking antibiotics
beta lactams. vancomycin,
polymyxins (cell membrane)
what are the 4 types of beta lactams
The 4 types of beta lactams:
penicillins -
ceohalosporins -
carbapenems
monobactams
what are 4 penicillin drug names
flculoxacillin, amoxicillin, pipericillin, penicillin
what are the three key cephalosporins
Cefuroxime
Cefotaxime
Ceftriaxone
what is a drug example og carbapenems
Meropenem
hat are two glycopeptides antibiotic drugs
Vancomycin
Teicoplanin
whihc types of bacteria are more suseptable to beta lactam antibiotics
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.
how do nucleuic acid synthesis antibiotics work ad two examples of it
stop the RNA from symthasizing so it cant reproduce
metronidazole
ciprofloxacin
what are the 4 classses nd examples of protien synthesis antibiotics
Aminoglycosides - Gentamicin
Tetracyclines - Doxycycline
Lincosamides - Clindamycin
Macrolides - Clarithromycin
what are two folate synthesis antibiotic drugs
Trimethoprim
Co-trimoxazole
what is a bacteriacidal antibiotic
Kill >99.9% in 18-24 hrs
this is normally antibiotics taht inhibit teh cell walls
what is a bacteriacidal antibiotic
Kill >99.9% in 18-24 hrs
this is normally antibiotics taht inhibit teh cell walls
what are bacteriastatic antibiotics
kill >90% in 18-24 hrs
inhibit the growth of bacteria, these are teh antibiotics taht inhibit protien synthesus or DNA replicaiton or metabolism
what is the minimum inhibitory concentration
the minimum amout of antibiotics yuo can give to stop teh antibiotic form growig and kill it off
what 4 things does an antibiotic function rely on
release
absorbtion
distrabution
elimination
what are teh 4 ways bacteria can avoid antibiotics
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
what are three examples of antibiotic resistance dur to ahcgeing teh antibiotic target
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$
what is an examples of antibiotic resistance due to destruction of teh antibiotic
Beta lactam ring of Penicillins and cephalosproins hydrolysed by bacterial enzyme ‘Beta lactamase’ now unable to bind PBP
what are two examples of intrinsic resistance in bacteria
Vancomycin cannot penetrate outer membrane of gram negative bacteria
what are teh two types of awuired resistance in bacteria
spontaneous gene mutation, horizontal gene transfer
what are teh three types of horizontal gene transfer in bacteria
conjugation - bacteria sex
transduction - insertion of DNA by bacteriophages
Transformation - picking up naked DNA
what are teh two examples of gram positive antiobiotic resistance
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
what are teh two classes of NSAIDs
non selective - these are competitive reversible inhibitors of COX 1 and 2 (for example ibruprofen and naproxen)
selective - inhibit COX2 only
how doo NSAIDs work
inhibit teh COX2 enzyme which stops it from producing prostoglandins
how do NSAIDS produce stomach ulcers
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
when would Vancomycin or Teicoplanin antibiotics be used and how
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
what are teh 5 mechanisms antibiotics work by
Inhibitors of cell wall synthesis
Inhibitors of protein synthesis
Inhibitors of nucleic acid synthesis
Anti-metabolites
Inhibitors of membrane function
when would lincosamides (clindamyacin) be used and what type of antibiotic is it
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
what is tetrracyclins (doxycycline) used for
protien synthesis blocker
Activity : Broad spectrum but mainly Gram positive (S. aureus and streps)
Use: cellulitis (if penicillin allergy)
Use: pneumonia
whihc antibiotics can be used to treat both gram pos and neg
Amoxicillin
Amoxicillin-clavulanate
Piperacillin-tazobactam
Meropenem
Cephalexin
Cefuroxime
Ceftriaxone
Cefotaxime
whihc antibiotic is of teh broadest spectrum and is restricted?
meropenem
what are the 2 mechanisms taht asprin does
anti inflamitory effect - binding to COX-1/2
Anti platelet - decreased thromboxone A2
how do thienopyridine drugs work for antiplatlets
metabolised by teh liver ti bind to ADP recetors on platelets and dramatically reduce platelet activation
how does dipyriamole work
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.
what are tw examples of Xa inhibitors for anti coagulation
Apixaban, Rivaroxaban
how does heparin work and what are its side effects
activates antithrombin whihc decreases thrombin and factor A
Bleeding, heparin-induced thrombocytopenia, osteoporosis
how does warfrin work and what are its side effects
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
what does teratogenic mean
cna be a drug takne by teh mother whih causes a change in teh structure and function of teh feotus
what are throbolytics
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
what are two examples of thrombolytics
Alteplase/Tenecteplase
streptokinase
how do loop diuretics work
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
what are loop diuretcis used for
hypertension and oedema often caused by ischaemic heart disease or chronic kidney disease
how do thiazide diuretics work
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.
what are some examples of thiazide diuretics
clorothiazide and Bendroflumethiazide
what are some side effects fo thiazide diuretics
alkalosis hypochloraemic; diarrhoea; hyperglycaemia and hyperuricaemia to name a few.
how do potassium sparing diuretics work
it binds competitivly to the aldosterone receptors at the aldosterne dependant sodium potassium exchange site
thsi promotes na and water excretion and potassium retention
what is an example of a potassium saving diuretic and some side effects
sprionolactone
hyperkalemia, antiandrogen effects, loss of libido, erectike disfunction
what are 4 drug targets
receptors, enzymes, transporters, ion channels
defie affinity and efficancy
affinity - binding to teh receptor
efficity - how well teh drug activated teh receptor
for exampe an anatagonist woud have good affinity and bad efficancy
definr potency
the strength of a drug, how well it works
if a drug has teh same effect at a lower concentration, it is more potent
what are teh 4 areas of pharmocokinetics
ADME
administration
distrabution
metabolism
excretion
DEFINE POTENCY AND EFFICANCY
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
what are the neurotransmitters and receptors used for the sympathetic pathway
Sympathetic- between teh pre ganglionic and the post, the post gangioonic receptors is epinephreine
what are the neurotransmitters and receptors used for the parasympathetic
parasympathetic - Ach is the neurotransmitter for both nerves, teh first receptor is nicotinic and teh second is muscarinic
what are the neurotransmitters and receptors used for the somatic
somatic - just ach and is only one nerve, the receptor is nicotinic
what are three drugs whihc work on Ach receptros
- 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
- Curare causes muscle paralysis by acting as a competitive acetylcholine (ACh) antagonist
what is a cholinergic crisis and teh symptoms of it
- 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
where are teh three muscerinic receptors foud
M1 - brain
M2 - heart
M4- lungs
what is teh athwya for teh formation of adrenaline
tyrosine
L dopa
dopamine
neuroadrenaline
adrenaline
whree are teh alpha 1 and 2 receptors found
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
what are teh two beta receptos and where are they fous
1- in teh heart and is ionotrophic (increased force of contraction)
2 - lungs - causes bronchodilation you can use it to treat asthma
agonist and antagonist for dopamine uses
agonist - for prolacteremia, acromegally and parkinsons
antagonist - for antisickness (metroclopramide) and psychic disorders
agnoist drug uses for GABA
agonist - benzodiazipenes - larazapan and diazapan are used for anxiety, sleep disorders and epilepsy
histamine antagonist drug types
H1 - allergys (loratadine)
H2 - for GORD as it decreases stomach acid secretion (ranitidine)
whihc is teh main excitatory and mian inhibitory neurotransmitter
excitatory - glutamate
inhibitory - GABA
what are teh antibiotics for community aquired pneuminia
amoxicillin for typical (s.pneumonia,)
clarthromycin for atypical (legonella, c.pneumonia, m.pneumoia)
treatment for TB and a side effect for each
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
what drig is given for cellulitus and whihc bacteria causes it
group B strep or S aureus
flucoxacillin
what antibiotic fr a UTI
nitro furantoin
or trimethroprim however can affect folic acid levels so should be avoided for teh first 12 weeks
what is teh antibiotic for gonorrhoea
doxycyclin
what is teh treatment for chlamydia
azithromycin or doxycyclin
treatment for H.pylori
CAP!
clarythromycin, amoxicillin and PPI (omeprazole)
what is teh treatment for gastroenteritis
caused by campylobacter - clathythromycin
shigella or salmonella - ciprofloxacin
what is teh treatment for meningitus
ceftriaxone, amoxicaillin if listeria is suspected
giver steriods simulationsly
what are teh 4 pain types
nociceptive, cancer, neuropathic, chrhronic non cancer
what is the defornition of acute pain
pain that lasts less tahn a week and is nociceptive
how should adverse drug reactions be reported
via teh yellow card scheme!!!! to teh MHRA
what is teh rawlins and thompson adverse drug reactions 5 types
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?
define protine binding and what does tghis mean
protien binding - it binds to alot of protines in teh blood, if this is hight it wont reach as many receptos as quickly
what are pateint factors that can interact with drugs
age, polypharmy, genetics, hepatic or renal disease
how can apsorbtion effect drugs
acidity of stomach
motility of the stomahc
solubility in teh blood stream
what are some CTP450 inhibitors and inducers, and what effect does this have on drugs
inhibitors - erethromycin, grapefruit juice, cause increased theraputic effect
inducers - alcohol, st johns wort, thsi cuases decareased theraptic effect of teh drug
what is a factor that can change the excretion of drugs
drugs which are acidic will be excreted faster if urine is weakly basic and the same vise vera
what are the two naturally occuring opiods
morphine and codine
what is teh equivelent dose of morphine, diamorphine and pethadine
10mg morphine
5mg diamorphine (heroin)
100mg pethadine
define tolerence and efine dependance
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
what is teh treatment for an opioid overdose
NALOXONE!!!
what is teh main antiplatelet and what would this be given for
asprin, arterial throbi
what is teh mechanism of asprin
a cox 1 inhibitor, decreases levels of thromboxone A2 which normally activates platelts
what is a drg other than asprin that is an antiplatelet and what is its mechanism
clopidogrel - P2Y12 inhibition
what are teh 4 anti coagulents
when high, ducks thoughup
heparin
warfrin
DOACs (direct oral anticoagulation)
thrombolytics
what is teh mechanism of heparin
activates antithrombin 3 and inhibits clotting factor x
what is teh mechanism of warfrin
antivitamin k
what is teh mechanisms of thrombolytics and a drug name
activates plamin to degrade fibrin
an example is aleplase whihc is given IV
what is teh antidote to someone bleeding who is on warfrin
vitamin k!
what are two examples of DOACs
apixiban and rivoroxiban
what is a side effect of PPIs
increased risk of fractures
what is a risk of loops and thiazide diuretics
hypokalemia and dehydration
what are some side effcets of steroids
cateracts
ulcers (decrased immune response)
striae
hypertension
increased infection riskj
pancreatitus
osteoporesis
