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Pharmacology Final > Final > Flashcards

Final Flashcards

1
Q

Non-specific physical interactions (not absorbed)

A

osmotic diuretics= mannitol
antacids- Mg(oh)2 against hyper acidity
laxatives = MGSO4 osmotic laxative
Chelators= EDTA/ Defeoxamine iron poison/ Lead poison

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2
Q

biochemical interactions without receptor

  1. Inhibition of Enzymes
A

1.1 NON steroidal anti inflammatory drugs
(AChE)
Meloxicam, aspirin, ibuprofen

1.2 ACE inhibitors
angiotensin converting enzyme inhibition, a hypotensive drug
Enalapril

1.3 Acetylcholine inhibitors
acetylcholine enzyme
Neostigmine

1.4 xanthine oxidase inhibitors, same is inhibited
treatment of gout
Allopurinol

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3
Q

biochemical interactions without receptor

  1. Damage to DNA
A

2.1 anticancer drugs cause DNA damage, To treat tumors

Cytabarin

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4
Q

biochemical interactions without receptor

  1. Transporters
A

3.1 Proton pump inhibitors.
inhibit the proton K ATpase pump
to treat hyperacidity

Omeprazole

3.2 Diuretics

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5
Q

biochemical interactions without receptor

4.Ion Channels

A

Local anaesthetics
prevents iron from entering specific channels
Lydicane blocks na+

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6
Q

biochemical interactions with receptors

Ligand gated ion channels

A

1.1 nicotinic acetylcholine receptors
na channels open letting Na enter. Ap is formed. Ca2+ flows out and repolarization occurs

where: in neuromuscular junction, anatomic ganglia and CNS
Neuromuscular junction 2 alpha, beta, o, e
autonomic ganglia 2 alpha and 3 beta
anatgonist is curare

1.2 Gaba A receptor- gated Chloride Ion Channel
stimulationinhibits muscles due to Cl entering the cell causing hyperpolarization
GABA agonists (Narcotics)

Orthosteric: meaning binding happens on GABA alpha site
Allosteric: meaning binding happens on Benzodiazepine site right next to GABA (Diazepam and Alprazolam)

PROPOFOL ACTS AS BOTH, RAPID SEDATION OCCURS WITHIN SECONDS.

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7
Q

biochemical interactions with receptor

G- Protein coupled receptor

A

4 receptors linked to adrenaline
b1- heart induceds tachacardia and has a positive endtropic effect
b2- Bronchodilation, Vasodilation (uterus)
a1- Vasoconstriction
a2- sedative

2.1 G alpha-s Coupled receptor (stimulation)
-receptor type: Beta adrenoreceptor
-Ligand: Adrenaline

Beta1: PKA activates Ca2+, stimulates cardiac contractions, positive inotropic, chronotropic, dromotropic. Less effect on kidney

Beta2: cAMP inhibits MLCK(myosin- like chain Kinase) but promotes MLCP
MLCP stops smooth muscle contraction (relaxation)
Agonists Clenbuterol, Terbutaline

2.2G alpha i ( inhibitory)
Limit prod. of cAMP (inhibits AC)
decrease in chronotrophy and Dromotropic

M2 Cholinergic receptors
ligand:acteylcholine
inhibits AC (adenylate cyclase) which inhibits cAMP
slows heart rate and smooth muscle
stimulation leads to bradycardia
Atropine blocks ligation with Ach

Alpha2
ligand: noradrenaline
sedative, antihypertensive effect.
blocks CA2 from entering vesicles. allows influx of K+ ions
Xylazine (agonist for alpha 2 and a sedative

2.3G alpha q receptors
Ligand as conversion of GDP and GTP
activation of phospholipase C (PLC) and conversion of PIP2 and IP3 and DAG
DAG activates protein kinsae C
alpha 1 receptors: vasoconstriction
h1 receptors : histamine
serotonin receptors

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8
Q

Receptor- ACtivated Tyrosine Kinases

A

contains amino acid Tyrosine
3.1 Insulin receptor substrate
- bind to insulin receptor
-autophosphyrlation
- activation of IP3 K

3.2 JAK/ Janus Kinase Inhibitors
- JAK binds to Cytokine receptors
-2STAT bind and are phosphorylated
1 STAT moves into nucleus and begins to stimulate transcription
stimulates production of IL and IgE

JAK INHIBITORS BIND TO THE CYTOKINE RECEPTOR AND STOP SIGNALLING

Oclacitinib for atopic dermatitis. Mainly on JAK-1 inhibits multiple IL’s against inflammation and IL31 (pruritis)

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9
Q

Intracelluar Nuclear Receptors

A

must be lipophilic to cross nuclear membrane (steroids or cortisol)
bound to HEAT SHOCK PROTEIN (HSP90)
Slow process meaning slow acting and long lasting action

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10
Q

drug receptor relations

A

Ligand which binds to recpetor to form a drug- receptor complex
binding is referred to docking the alteration of conformation leads to an effect
strength of binding is known as affinity
Van der Waals forces reversible reactions?

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11
Q

Dissociation constant

A

“K”

equilibrium state between the rate of association and dissociation
Kd= dissociation constant (Kd=kd/ka)
higher Kd means more ligand is released from the receptor
increasing drug meaning increase of receptors occupied.

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12
Q

Efficacy

A

the efficiency of a drug acting
the ability of drug binding to receptors
more recptors more efficient
potency and efficacy are different
E max.
Epinephrine is less efficient than morphine

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13
Q

Potency

A

the impact the drug has on the body
refers to the level of concentration required to reach EC50 on a curve
lower drug concentration needed to reach Ec 50 meaning the drug is more potent. Reaching the same effect with less input.
Fentanyl is more potent than morphine

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14
Q

quantal dose curve

A

describes the effect of a dose, response curve can be on population
we focus on the effect
ED50: effective dose at 50% of population
LD50: lethal dose at 50% of population
TD50; toxic effects seen at 50% of population

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15
Q
A
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16
Q

Therapeutic index

A

is the gap between LD50 and ED50
the higher the gap the more safe the drug is
Remiferentanyl needs *33000 times the initial dose to reach lethal dose

Digoxin only *2
Therapeutic window is the diff between LD50 and TD50 meaning the drug is safe to use within that range

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16
Q

Agonists and Antagonists

A

receptor is either active or inactive. Ligand may acto on either state
Ligands can either be
Full agonist: favours active state, max response with max affinity

Full antagonist: high affinity but will not activate receptor. no response

Partial agonist: sub max response and only partial activation of the receptor. prevents downregulation of receptors.
Heroin downregulates endorphin receptors. Buprenorphine will stimulate the receptors again but even at max dose they wont achieve the same efficacy anymore.

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16
Q

Drug Tolerance

A

2 types of tolerance emerge after prolonged use of drugs.

  1. Pharmacokinetic tolerance: induction of liver enzymes. they get more effective. Phenobarbital to maintain blood plasma.
  2. pharmacodynamic tolerance (desentization)
    opoids and Heroin, inhibits the endorphin receptors.
    Downregulation of receptors occurs

3.sequestration, drug being constantly bound to G protein it will break down. loss of adrenaline recptors.G protein activation prevented by beta Arestin.

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16
Q

Drug Toxicity

A

drug toxicity can be ucaused by genetic predisposition and non selective action, or inappropriate use of drugs
all drugs have an intended (primary) and a secondary (unintended) effects. no drug is entirely specific side effects can be neutral or beneficial. most of the time undesirable.

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16
Q
  1. AGONISTS
A

full agonists
- bind the receptor at an active state

Partial agonists
-will try to bind as many active receptors but fail to reach the same effect.
Heptyl and Octyl derivatives

they both compete with each other and the full agonist has reduced efficiency.

Inverse Agonist
- histamine receptors can existeither active or inactive.
histmaine agonist will stimulate active site
antihistamines work as an inverse agonist and pushes the balance of receptors towards an inactive state.

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16
Q

Antagonists

A

2.1 Non receptor Antagonists
physiological antagonist: histamine inducing anaphylactic shock

chemical anatgonist: counteract agonist. Heparin is an anticoagulant. Protamin is a chemical antagonistas it is strongly positive.

2.2 Receptor Anatagonists

orthosteric binding (same site as agonist)

  • reversible (competitive antagonism) Metatomidine and xylazine are reversed by atapazimol

-irreversible( non competitive active site antagonist)
efficacy is largely decrease and small decrease in potency. Ketamine and NMDA receptors.

-Allosteric binding, binds to a different site.

17
Q

Drug toxicity classification

A

either on target or off target if receptor based
On target: Primary appropriate effect on the appropriate receptor tisse
Off target: leads to side effects and harmful effect undesired

On target adverse effect:
at intended tissue and receptor but: inappropriate concentration with suboptimal pharmakinetics. happens deliberate or accidental, altered pharmacokinetics, liver and kidney disease
changes in pharmacodynamics:
-drug receptor changes, number, state etc.

intended recptor but different tissue.
-antihistamine diphenhydramine HCl on the H1 receptor. Antagonist used to decrease unwanted symptoms of the histamine release in allergic reactions.. crosses BBB?

Off target:
on the unintended receptor.
Thalidomide - enantiomeric pairs, S-enantiomer was a teratogen (birth deformaties) abnormal development of peripheral vessels. R- enantiomer was a sedative
Testing on pregnant animals before human testing

on the unintended receptor and unintended tissue.
use of the beta blockers
B1 receptor antagonists can also acto on beta 2 receptors - increased contractility affecting SM cells

17
Q

Harmful Immune and Idiosyncratic Response and
classification of immune mechanism

A

Drugs are Xenobiotics that the immune system can recognize as foreign material.

immune system has either a hypersensitivity response or autoimmune reaction.

-hypersensitivity type 1-4
type 1 is immediate anaphylactic reactions
type 2 is in response to penicillin or quinidine
type 3 is in response to Cefaclor
type 4 is in response to dermatitis, latex allergy

Idiosyncratic response
-anaphylaxis
-anaphylactoid= pseudo- allergic reaction
Autoimmunity:

17
Q

Formation of toxic metabolites

A

lipid peroxidation

  • lipid peroxidation initiated by ROS, chain reaction, changes membrane permeability. Defense against Vitamin E, Selenium, GSH excretion.

-generation of ROS molecular oxygen is reduced to superoxide anion. Cytotoxic effect is direct, leads to LPO?

-Modification of Sulfhydryl groups, frees sulfhydryl groups maintain cytoplasmic Ca2+ conc. absence leads to lethal hyperglycemia. inactivationof haem enzymes and increased cell permeability.

-Glutathione deficiency, GSH protects cells from oxidative stress. depletion of GSH leads to drug toxicity, decreased cellular protection. ROS convert GSH to GSSG. replenish with NADPH dependant GSSG reductase.

-Paracetamol, never for Cats. it produces covalent protein derivatives which are highly toxic for liver. antidote is N-acetyl cysteine

18
Q

Mechanism and development of drug Toxicity

A

Drug or Metabolites can induce
-receptor specific effects
-protein drug adducts: fibrosis, necrosis, apoptosis and a protective response.
-reaction with small molecules ( leading to cancer or mutation)
-react with DNA (either repairs DNA or leads to Cancer mutation etc.)

19
Q

Extracorporeal INteractions

A

Physical incompatibility
- when two drugs are mixed in syringe or infusion
- change in consistency, shape, viscosity, etc. of the original dose form.
- Mixing/ Dilution of infusions and injections, Ivermectin and Isopropyl

  • change in pH (tetracyclines, alkaline solutions)
    -mixing of lipophilic and hydrophilic ointments (suppository bases)
    -ionisation (pentobarbital and xylazine, opoids or ketamine)
  • eutetics ( methol+camphor+ aspirin vs. Antypyrin+ Sulphur)
  • Adsorption (glass over plastic, sticking to surface)

Chemical incompatibility
multiple types of reactions: oxidation, reduction, hydroxylation, double replacement. insoluble complex formation(ca2+ and oxytetracyvline)

Physicochemical incompatibility
-oxytetracycline+ ca gluconate = dark green colour and forms precipitate
-ivermectin + physiological saline =cloudy perticipate
-pentobarbital+ xylazine = solid perticipate
-Menthol+ Camphor: Eutectic formation

19
Q

Drug Interactions and types

A

can be interactions between drugs and feed, toxins and endogen metabolites

types:
Extracorporeal - reactions occurring outside the body. can be physical, chemical or physicochemical incompatibilities.

Intracorporeal- reaction occur within the body. can be positive drugs that amplify each other.
Additive/ potentiation: CNS inhibitors
Synergism: Antibacterial agent

or negative: Therapeutic incompatibility
Pharmacodynamic interactions
Pharmacokinetic interaction
-can occur at any point in the ADME process

20
Q

Intracorporeal interactions

A

Receptorial
1. Competitive (Direct) two drugs acting on the same receptor site. physical blocking of a receptor
Agonist vs Antagonist ( fentanyl vs Naloxon)
Agonist vs Partial Agonist (Fentayl vs Butorphanol)
Medeto/Dexmedetomidine vs. Atipamezole
Pilocarpine vs Atropine

  1. Non-Competetive (non-direct). Allosteric: Same organ/tissue and same receptor. same organ different receptor:
    -aminoglycoside+non depolarising muscle relaxant
    -H1 antihistamines+ hypnosedatives
    -combination of antihypertensive or antirhythmics
    physiological
    -acts on different tissue
    -adrenergic vs cholinergic drugs
    -adrogens vs oestrogens

Non-receptorial
- chelating agents EDTA
-Absorbents: activated carbon
-Acid neutralisers (Al (OH)3 )

21
Q

Pharmacokinetics Interactions

A

Absorption
-physiochemical reactions

Distribution

Metabolism
-biotransformation (aiming to form water soluble molecules)
-Phase 1 - main enzyme CYP450
-Phase 2 - conjugationn and formation of less reactive metabolites.

22
Q

CYP450 enzyme

A

NADH/NADPH
NADPH cytochrome P450 reductase
O2 (mostly oxidative reaction)
CYP1
CYP2
CYP3

23
Q

CYP mediated interactions

A

Decreased efficacy
increase duration of action

Chicken and turkeys: Ionophore coccidiostats (monensin, narasin, salinomycin) + Tiamulin/ Valnemulin is highly TOXIC

Increased level = cimetidine+Lidocaine
Monepantel induces CYP1A, 2B, 2C, 2E, 3A`

24
Q

Elimination

A

urine ph influences the rate of excretion of drugs
Procaine, Antihistamines, Caffeine, Pethidine,
penicillins remain longer in the urinary tract. therefore good for UTI

25
Q

Species, Subspecies and Bloodlines

A

Receptorial
-xylazine (bo. are particulary sensitive)
-morphine( fe. sensitive)

absorption
-ampicillin (&cefaclor) absorption 60% ca. 30%bo.
-Atropine in horses, cattles and humans are very sensitive.

Distribution
-ivermectin: collies, shelties, bobtails, crosses BBB leading to paralysis
Barbiturates: Greyhounds are particularly sensitive (low body fat)

Metabolism
-Salycilates, Phenols: cats are sensitive
Sulphonamides: Dogs sensitive
Procaine: Pigs
Atropine: White rabbits and goats high levels of atropine esterase

Gut Flora
-Penicillin: Rabbit and hamsters are sensitive due

26
Q

Health status, Condition

A

Fever: reduce stomach emptying negative absorption effect
Diarrhea: increased gut motility (flushed out quickly)
Illnss: makes animals unwilling to eat
organ phosphates: liver renal failure
Fat levels:increased fat decreases sensitivity needing a higher dose

27
Q

Dosage

A

dose determines level of effect like xylazine and atropine

28
Q

Route of application

A

MgSO4 acts as a laxative orally but as an muscle relaxant I.V.
Insulin : only I.V.

29
Q

Feeding

A

decreases BV
phytoestrogens increase activity of metabolising enzymes

30
Q

Gender and sex

A

testosterone increases metabolic activity which decreases drug utilisation
LD50 values can be higher in males.
Pregnant females cannot give anti-progesterone drug. (induce uterine contractions)

31
Q

Age

A

Young

Old:
change in gastric secretion, pH, blood flow motility. body compositions, protein binding changes
metabolism decreases and clearance becomes more reliant on environmental factors. excretion suffers decreased renal clearance and increased half life .

32
Q

Tolerance

A

subjects reaction to drug decreases
resistance can build up (opioids)
Tachyphylaxis: rapid development of drug tolerance
Drug immunity Body becomes insensitive drug

33
Q

Drug dependance Abuse

A

consider in the case of prescribing controlled drugs
Habituation and addiction

34
Q

Idiosyncrasey

A

Hypersensitivity
genetic issues causing enzymatic anomaly
Dobermann and Phenylbutazone

35
Q

Allergy/ Anaphylaxis

A

uncommon and unwanted
type 1-4
anaphylaxis: systemic, immediate hypersensitivity due to IgE mediated release of mediators from mast cells and basophils
Anaphylactoid: Pseudo-allergic reaction. No IgE mediation and unknown causation mechanism.
Autoimmunity: Immune cells begin to attack the body own cell

36
Q

direct parasympathomimetics

A

acetylcholine
carbachol
bethanechol
methacholine
pilocarpine

37
Q

indirect parasympathomimetics

A

physostigmine
neostigmine
pyridostigmine
edrophonium
Organophophates

38
Q

parasympathomimetics pharmadynamics

A

eye- constriction m. sphincter pupillae
cardivascular- bradycardia, negative chronotropic effect
gi tract- smooth muscle contraction
vomiting, diarrhoea
respiratory tract- bronchoconstriction
urinary tract- bladder contraction

nicotinic receptor, muscarinic receptor ACh- receptor

39
Q

parasympatholytics

A

atropine
glycopyrrolate
homatropine
Tropicamide
Ipratropium
Benethimid
Butyl-scopolamide

40
Q

Sympathomimetics

A

non specific
-adrenaline
-noradrenaline
-dopamine
-ephedrine

specific
-alpha1 agonist, pheynyephrine, xylometazoline, oxymetazoline, naphazoline, tetryzoline, Phenylpropanolamine
-beta 1 agonist, dobutamine, isoproterenol
-beta 2 agonist, isoproterenol, clenbuterol, salbutamole, terbutaline, salmeterolem, isoxsuperine

41
Q

sympatholytic drugs

A

non specific alpha antagonist, Phenoxybenzamine, Tolazoline
alpha 1 antagonist, prazosine, doxasozine
alpha 2 antagonist, yohimbine and atripamezole
beta 1 antagonist, Metoprolol, Atenolol
beta 1 and beta 2 anatagonist
non specifi antagonist- propranolol

42
Q

tranquilisers

a- adrenoreceptor
dopamingeric receptor
histamine receptor
5ht receptor- serotonin
Muscarinic receptor

A

Phenothiazines
-propromazine
-acepromazine
-chlorpromazine
-Prometazine
-
Butyrophenones
-azaperone
-Droperidol, Fluanisone, Haloperidol

43
Q

sedato hypnotics

reduced motor activity and vasoconstriction, hypotension,

optical, ear canal surgery and dentistry

A

alpha 2 agonist
-xylazine
-medetomidine
dexmedetomidine
-romifine
-detomedine

benzodiazepines
-diazepam
-alprazolam (xanax)
-midazolam
-zolazepam

barbiturates
-phenobarbital
-amobarbital
-butobarbital

other compounds:
alcohols, aldehydes, Br-, Mg2+

44
Q

Opiods

A

Pharmacology Final (3 decks)

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