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Pharma MT > Pharma Midterm 1 > Flashcards

Pharma Midterm 1 Flashcards

1
Q

Definition of Pharmacodynamics

A

how drug acts on body

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2
Q

Definition of Pharmacokinetics

A

how drug moves in body (Principle of ADME)

(fate of the administered substance)

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3
Q

Meaning of ADME

A

Absorption
Distribution
Metabolism
Excretion

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4
Q

List the non specific physical interaction

A

Osmotic diuretics
Antacids
Laxatives
Chelators

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5
Q

Example of Osmotic diuretics

A

Mannitol (antifreeze or ethanil glycol poisoning)
filtered in bowman’s Capsule, retains water osmotically

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6
Q

Example of Antacids

A

Magnesium Hydroxide
binds to acids to elevate the pH

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7
Q

Example of laxatives

A

Magnesium sulfate
Osmotically retains water in bowels

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8
Q

Example of Chelators

A

EDTA (for Led Poisoning)
Deferoxamine

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9
Q

Example of inhibition of enzymes

A

NSAIDs
ACE inhibitors (Angiotensin)

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10
Q

Example of drug acting on Ion channel

A

Local anaesthetics (Lidocane)

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11
Q

Example of drug acting on Transporters

A

Proton-pump inhibitors (Omeprazole)
Diuretics

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12
Q

Example of Ligand gated ion channel and what inhibits it

A

Acetylcholine channel Receptor are inhibited by nicotinic crurare

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13
Q

How may times G proteins coupled R crosses the membrane?

A

7

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14
Q

Atropine is an antagonist of …

A

Acetylcholine

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15
Q

PKA is activated by which receptor?

A

The Gs coupled receptor

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16
Q

What happens when PKA is activated?

A
  • entry of Ca
  • muscle contraction (positive inotropic effect)
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17
Q

Gq receptors are involved in which muscle contraction? Activated by what?

A

Smooth muscle contraction, vasoconstriction
Noradrenaline

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18
Q

How do Receptor activated tyrosine kinase work?

A

Need phosphorylation to be activated, activate the AKT (Phosphokinase B)

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19
Q

Example of a JAK inhibitor, and which JAK?

A

Oclacitinib, JAK
inhibits IL-4,13 and 31 (most important in allergies)

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20
Q

What is EC50?

A

half maximum effective concentration

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21
Q

How does an intracellular nuclear receptor works?

A
  • Lipophilic receptor drugs attach to NR
  • R in cytoplasm binds to HSP90 (heat shock protein)
  • Ligand + complex can go in nucleus
  • DNA transcription
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22
Q

What is a ligand?

A

Binding + complex with receptor

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23
Q

Define potency

A

power of something to influence

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24
Q

How to calculate the therapeutic index?

A

LD50 / ED50

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25
Q

Example of Pharmacodynamic tolerance

A

Opioids, agonist continuously bin find to R –> down regulation

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26
Q

Example of Pharmacokinetic tolerance

A

Phenobarbital, induction of CYP450 enzymes

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27
Q

Define down regulation

A

Decrease in receptors on cell membrane

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28
Q

Define up regulation

A

Increase in receptors on cell membrane

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29
Q

True or false:
Drugs are entirely specific

A

False, Primary intended effects AND secondary effects

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30
Q

How can drugs be toxic?

A

Genetic predisposition, nonselective action, inappropriate use or administration

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31
Q

Define therapeutic window

A

range of doses that elicits a therapeutic response

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32
Q

A small therapeutic window means …

A

The plasma level of drug must be closely monitored

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33
Q

TD50 stands for

A

toxic response for 50% of population

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34
Q

LD50 stands for

A

lethal response for 50% of population

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35
Q

ED50 stands for

A

therapeutically effective

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36
Q

What are the main types of classification of adverse effects of drugs?

A
  1. “On target”
  2. “Off target”
  3. Production of toxic metabolites
  4. Production of harmful immune response
  5. Idiosyncratic responses
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37
Q

What is “On target” effect?

how can it be adverse?

A

drug is binding to intended R
can be adverse if:
* inappropriate concentration
* incorrect tissues

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38
Q

What is “Off target” effect?

A

binds to unintended R

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39
Q

Give examples of production of toxic metabolites?

A
  • lipid peroxidation
  • Reactive oxygen species
  • Depletion of GSH
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40
Q

List the 4 types of harmful immune responses

A
  1. Imediate hypersensitivity
  2. antibody dependent cytotoxic hypersensitivity
  3. immune complex mediated hypersensitivity
  4. delayed type hypersensitivity
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41
Q

Type 1: Imediate hypersensitivity

A

production of IgE

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42
Q

Type 2: antibody dependent cytotoxic hypersensitivity

A

drug binds to the cell, then is recognized by IgG

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43
Q

Type 3: immune complex mediated hypersensitivity

A
  • antibodies form against soluble antigens
  • complexes deposits on tissue
  • can initiate response called “serum sickness”
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44
Q

Type 4: delayed type hypersensitivity

A

1st exposure does not produce response
repeated exposure can trigger a massive immune response

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45
Q

Idiosyncratic responses

A

Rare with no obvious mechanism

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46
Q

Exemples of transcellular transport:

A
  • diffusion
  • filtration
  • active transport
  • pinocytosis, phagocytosis
  • facilitated diffusion
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47
Q

Exemple of intercellular transport:

(btwn endothelial and epithelial cells)

A

filtration

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48
Q

Absorption does not occur when…

A

intraveanous therapy

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49
Q

Absorption determines:

A

the coumpound’s bioavailability

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50
Q

Define the bioavailability

A

fraction of a drug that reaches the bloodstream

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51
Q

What can influence the bioavailability?

A
  • Poor absorption of the GI tract
  • taken with or without food
  • other drugs
  • the hepatic extraction
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52
Q

Give an exemple of the 3 main route of administration:

A

External: skin
Enteral: oral, rectal
Parenteral: IV, IM

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53
Q

What are the absorption sites after oral administration?

A

Stomach (weak acids, lipids), *where drugs are dissolved *
Small intestines (primary site)

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54
Q

Define distribution, and what it depends on

A

reversible transfer of drug from one location to another
-permeability btwn tissues
- blood flow
- ability to bind to plasma proteins

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55
Q

give the classification of distribution to various organs

A

brain, liver, kidney > muscle, skin > fat, bone

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56
Q

Which drugs distribute poorly to CNS

A

Ionized, polar drugs

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57
Q

Whicht types of drugs can cross over the placental barrier?

A

lipid soluble drugs

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58
Q

Define Xenobiotics:

A

coumpounds cannot be used as food and would be harmful if accumulated

( synthetic drugs, natural poisons) has no metabolic function

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58
Q

after metabolism occur what is called the new coumpound ?

A

metabolites

The can be pharmocologically active (prodrugs)

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59
Q

What is the major site of biotransformation?

A

the Liver

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60
Q

What is the Phase 1 of biotransformation in the liver?

A

enzyme is catalysed, frequently a functional group that serves as active centre for sequential conjugation in phase 2

(cytochrome P450)

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60
Q

What is the Phase 2 of biotransformation in the liver?

A

Conjugation reaction

(glucuronyl transferase)

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61
Q

Cytochrome P-450

primary location?
mechanism?
inhibition?

A
  • liver
  • drug is oxidised and oxygen is reduced to water
  • competitive or not, drug - drug interaction
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62
Q

Glucuronyl transferase is not present in which species?

A

Cats

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63
Q

How can a drug be excreted?

A

Kidneys, faeces, sweat, tears, milk and lungs

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64
Q

define the first pass effect

A

drugs taken orally pass across membranes of GI tract into portal vein system and through liver before getting to the general circulation

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65
Q

True or False
Amount of drug in a tissue is generally related to plasma concentration

A

True

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66
Q

Give the 3 types of modelling

A
  • non compartemental
  • compartemental
  • physiologically based
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67
Q

what is the difference between zero order of elimination and first order elimination ?

A

zero : constant amount is eliminated per unit of time
first: constant fraction is eliminated per unit of time

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68
Q

define one compartment model open model:

A

body is 1 continuous fluid with continuous loss due to excretion

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69
Q

what is the two compartemental model

A

the body

has a distribution phase and elimination phase

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70
Q

how many half life is necessary to reach the steady state?

A

5

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71
Q

what is the steady state composed of?

A

average plasma concentration and range of fluctuation

once the steady state acheived, the elimination rate is added

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72
Q

when is the loading dose used?

A

therapeutic concentration in plasma must be reached rapidly

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73
Q

Give 10 factors influencing the drug action

A
  1. receptorial
  2. absorption
  3. distribution
  4. metabolism
  5. gut flora
  6. health status
  7. dosage
  8. feeding
  9. age
  10. gender
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74
Q

exemple of receptorial influence on drug action

A

cat - morphine

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75
Q

exemple of absorption influence on drug action

A

horse - Ampicillin

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76
Q

exemple of distribution influence on drug action

A

dog - Ivermectin

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77
Q

exemple of metabolism influence on drug action

A

Pig - procaine

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78
Q

exemple of gut flora influence on drug action

A

rabbit - Penicillin

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79
Q

exemple of health status influence on drug action

A

Fever- decrease effect on absorption

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80
Q

define tachyphylaxis

A

rapid dvlpmt of drug tolerance

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81
Q

Give an exemple of idiosyncrasy

A

Doberman with Phenylbutazone

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82
Q

What is called a stimulant in neuropharmacology?

A

Psychoactive

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83
Q

What is called an inhibitor in neuropharmacology?

A

Psychotropic

84
Q

list the 3 Autonomic NS medecines

A

Parasympatho-mimetic/lytic
sympatho-mimetic/lytic
ganglionic blockers / stimulant

85
Q

List the somatic NS medecines

A

local anaesthetics
peripheral muscle relaxant

86
Q

In CNS

Exemple of excitatory amino acids

A

Glutamate
Aspartate

87
Q

In CNS

Exemple of inhibitory amino acids

A

Glycine
GABA

88
Q

A choline ester neurotransmitter

A

Ach

89
Q

A monoamines

A

Adrenaline
Dopamine

90
Q

Ach acts on which R and what is its effect?

A

M1, closes K+, Ca2+ and Cl- channels

depo or hyper-polarisation

91
Q

Dopamine

A

precursor of NA, inhibitory effect, act on R D in basal ganglia and limbic system

92
Q

serotonin

A

inhibitory effect

93
Q

GABA

A

Inhibitory, acts on:
- GABAa ligand gated Cl- channel
- GABAb Gi R

94
Q

Glycine

A

inhibits transmission btwn spinal interneurons and motoneurons

95
Q

What are called CNS stimulants?

A

analeptics

96
Q

exemple of analeptic acting on cortex

A

cocaines
ephedrines (appetite suppresant)

97
Q

exemple of analeptic acting on medulla

A

doxapram (resp stimulant)

98
Q

exemple of analeptic acting on spine

A

strychnine (induces reflex excitability of spinal cord)

99
Q

True or false:
Convulsants and respiratory stimulants are used often in clinics

A

False, more as experimental tools

100
Q

what drug can be used in acute resp failure?

A

Doxapram

101
Q

What drug is used as an antidote for poisoning by CNS depressants

A

Picrotoxin

102
Q

Exemple of central analeptics

A

Pentetrazol
Picrotoxin

103
Q

Exemple of peripheral analeptics

A

prectamide
lobelin

104
Q

Exemple of mixed analeptics

A

doxapram

105
Q

Which drugs are methylxanthines?

A

caffein
theophylline
theobromine

106
Q

in high dosage what cardiac effect has methylxanthines?

A

inotropic and chronotropic effects on heart
elevation of blood pressure

107
Q

what peripheral effects has methylxanthines?

A

vasodilatation of coronary arteries
increase blood flow to brain, heart, muscle and kidneys
lower blood flow to GI tract

108
Q

Side effect of caffeine?

A

stimulate peptic acid secretion : Peptic Ulcer

109
Q

Clinical use of caffein?

A

acute heart failure
overdosing of anaesthetics
blood circulation disorder

110
Q

What is the WP of caffein?

A

0 days

111
Q

Define a seizure

A

group of symptoms originating from an excitement of neurones

112
Q

why is it important to treat a seizure?

A

the resp. muscle are seizuring and heat can lead in brain oedema

113
Q

Status epilepticus is …

A

Generalized

114
Q

What is the use of long term treatment of epilepsy?

A

a preventing treatment

115
Q

Which guidelines are best to follow in case of an epilepsy treatment?

A

Consensus statement on seizure management in dogs

116
Q

When to start a long term epilepsy treatment?

A
  • seizure > 5min
  • multiple within 3-6 months
  • postictal symptoms occur for > 24 hours
  • Confirmed lesions in the brain
117
Q

For seizures what is the most important inhibitory system?

A

GABAa

118
Q

Which drugs inhibits the calcium influx into the nerf for seizure treatment?

A

Levetiracetam

119
Q

administration of drug for long term seizure treatment

A

orally

120
Q

in which case can we discontinue seizure treatment?

A
  • gradually
  • no seizure for 2 - 3 years
121
Q

Which is the most important drug used in seizure treatment?

A

Phenobarbital

122
Q

What is the effectiveness of phenobarbital on its own?

A

60-90%

123
Q

In which case is phenobarbital not recommended ?

A

Liver failure, intensive metabolism in liver (ROS)

124
Q

What is the auto induction of phenobarbital?

A

induces cytochrom P450 enzyme system

with time will need to elevate the dose

125
Q

How long to reach steady state with phenobarbital?

A

2-3 weeks, take blood sample 1 hour before next administration to check

126
Q

what are the side effects of phenobarbital?

A
  • Sedation
  • elevated liver enzymes
  • hepatotoxicity (not in Fe)
  • pancreatitis
127
Q

how can Potassium bromide be used?

A

alone for mild cases
with phenobarbital

128
Q

what are the pros of potassium bromide?

A
  • not metabolized (so not hepatotoxic)
  • long action (1 daily administration)
129
Q

what can cause potassium bromide in cats?

A

bronchitis and lung oedema

130
Q

what are the side effects of potassium bromide?

A
  • Polyphagia
  • Pruritus
  • Paraparesis
  • Pancreatitis
131
Q

Why would we divide potassium bromide dose in 2

A

to avoid emesis

132
Q

For patients not responding to Phenobarbital or Potassium bromide, what can we combine them with?

A

Levetiracetam

133
Q

is levetiracetam better in a combination or alone?

A

combination

134
Q

what are the pros of Levetiracetam?

A
  • short half life
  • slightly metabolized by liver
  • minimal side effects
135
Q

what are the cons of levetiracetam?

A

has to be given 3 to 4 times a day

136
Q

What is important when giving Imepitoin?

A

Not to miss a dosage as the half life is 2-6 hours (quick plateau)

137
Q

which drug has a minimal changes in patients with impaired liver or kidney?

A

Imepitoin

138
Q

Imepitoin has an effectiveness similar to …

A

Phenobarbital

139
Q

What is the first drug of choice while status epilepticus?

A

Benzodiazepines

139
Q

What is the first drug of choice while status epilepticus?

A

Benzodiazepines

140
Q

Which are the benzodiazepines used for the management of status epilepticus?

A
  • diazepam
  • Midazolam
141
Q

Which drug can be used for the management of status epilepticus and euthanasia?

A

Pentobarbital

142
Q

pros of pain

A

risk prevention

143
Q

cons of pain

A
  • catabolic state (cortisol)
  • loss of appetite
  • resp depression
  • delayed wound healing
144
Q

define sensitization

A

sense pain worse after 2 or multiple times experiencing pain

145
Q

3 levels of pain sensitization

A
  • peripheral sensitization
  • central sensitization
  • cortical reoganization
146
Q

difference between opioids and opiates

A

opioids : natural and synthetics
opiates: natural (morphin)

147
Q

True or false :
Analgesics act on nociception and nerve fibres

A

False, not on nerve fibres if need of amputation need to use a nerve block

148
Q

Pharmacological effects of analgesics

A

Sedation, euphoria (not cats and horses), cough relief and antidiarrheal

149
Q

What are the receptors targeted by opioids?
Which are pre-post synaptic?

A

Kappa, delta (presynaptic only)
Mu (pre and post-synaptic)

150
Q

Which opioid receptor has the strongest effects?

A

Mu

151
Q

Which opioid receptor agonist used are extremely safe?

A

Kappa agonist

152
Q

Exemple of full agonist of opioid R

A

Morphine
fentanyl

153
Q

Exemple of full antagonist of opioid R

A

Naloxone

vanish side effect AND effect

154
Q

Exemple of partial agonist of opioid R

A

buprenophine

155
Q

Exemple of agonist-antagonist of opioid R

A

butorphanol

antagonist: Mu R
agonist: Kappa R

156
Q

Which drugs would be used against significant pain?

A

Morphine
Fentanyl

157
Q

How can fentanyl be administered?

A

Topically

158
Q

how long does it take to morphine to have its’ max effect?

A

15-45 min

159
Q

Side effects of opioids

A
  • Resp drepression
  • Emesis
  • Bradycardia
  • Obstipation
  • hyperthermia
  • histamine release
160
Q

which opioid drug causes the most severe respiratory depression and bradycardia?

A

Fentanyl

161
Q

Which opioid weak full agonist is unpredictable in dogs?

A

Tramadol

162
Q

Which analgesic has a ceiling effect?

A

Buprenorphine

163
Q

What is buprenorphine used for?

A
  • soft tissue surgery
  • pancreatitis
164
Q

Which analgeasic is very safe?

A

Butorphanol

165
Q

Exemples of other analgesics?

A
  • ketamine
  • NGF (antagonist NMDA R)
  • Amantadine (antagonist NMDA R)
  • Gabapentin
166
Q

Define sedatives or tranquilizers

A

Induce calming by reducing irritability or excitement

167
Q

define hypnotics

A

induce sleep and treatment of insomnia

168
Q

define psychotherapeutic drugs

A

influence behaviour, mood and emotional reactions

169
Q

What are the major tranquilisers (neuroleptics)

A

Phenothiazine derivates
Butyrophenones

170
Q

What are the major hypnosedatives?

A

Alpha agonist
Anxiolytics

171
Q

Mecanism of action of phenothiazine tranquillisers

A

antagonist to :
- Dopamine R
- adrenoreceptor
- muscarinic R
- H1 R
- 5-HT-R

172
Q

pharmacological effect of phenothiazine

A

-sedation
- inhibition of body temparature regulation
- potentiation
- antihistamine effect

173
Q

Administration of phenothiazine tranquilisers

A

buccal, rectal

174
Q

Side effect of Phenothiazine tranquiliser

A
  • hypotension
  • irritation, allergy
  • epilepsy
  • bulldogs, boxers may be oversensitive
175
Q

Examples of phenothiazine tranquilisers

A

Chlorpromazine
Propiopromazine
Acepromazine
Promethazine

176
Q

Butirophenone tranquilisers mechanism of action

A

dopamine inhibition
NA inhibition
anticholinergic effects in CNS

177
Q

side effect of butirophenone tranquilisers

A

transient salivation or panting
hypotension

178
Q

Exemple of butyrophenones

A

Azaperone

179
Q

Examples of alpha 2 agonists

A
  • xylazine
  • detomidine
  • medetomidine
  • dexmedetomidine
  • romofidine
180
Q

Pharmacological effects of alph agonist?

A

-analgesia
sedato hypnotic
vasoconstriction
GI smooth muscle relaxation

181
Q

side effects of Xylazine

A
  • emesis
  • sweating in horses
  • tympani in ruminants
182
Q

Which specie is detomidine used for

A

used for Equine

183
Q

how can detomidine be used

A

alone or with ketamine, thiopentone and opioids

184
Q

medetomidine and dexmedetomidine are develloped for?

A

cats and dogs

185
Q

what is romifidine frequently used with?

A

buthorphanol

186
Q

What type of drug is Atipamezole and Yohimbine

A

Alpha 2 adenoreceptor, blocking and antagonist

187
Q

How can diazepam be used?

A

Prevention and control of epilepsy
sedation

188
Q

contraindications of diazepa

A
  • liver diseases (cats and foals)
  • paradoxical reaction ( cat, greyhound)
189
Q

pharmacological effect of barbiturates

A

CNS, circulation, respiration - inhibitio

190
Q

Example of a long lasting barbiturate and middle long lasting

A

long lasting: Phenobarbital
middle long lasting: amobarbital, butobarbital

191
Q

how do local anaesthtics work?

A

blocks conduction in nerve fibres

192
Q

what are the 2 chemical types of local anaesthetics

A
  • esters (Procain)
  • amides (lidocain)
193
Q

Mechanism of action of local anaesthetics?

A

blocking NA+ channels

194
Q

LA block conduction in which order

A

non-myelinated axons
small myelinated axons
large myelinated axons

195
Q

give the order of the disappearance of nervous functions

A
  • pain
  • warmth
  • touch
  • deep pressure
  • motor function
196
Q

What influences the activity of LA

A
  • do not work on inflammed tissue
  • application with vasoconstrictor medecines increase the duration of activity and decrease the toxicity
197
Q

Give the stages of anaesthesia

A

Stage 1 -disordered consciousness
stage 2 - excitement
stage 3 - surgical anesthesia
stage 4 overdose

198
Q

Examples of injectable anaesthtics

A
  • barbiturates
  • propofol
  • imidazole anaesthetics
  • NMDA R antagonist (ketamin)
199
Q

Examples of inhalation anaesthetics

A
  • Isoflurane
  • sevoflurane
  • dinitrogen monoxide
  • desflurane
200
Q

Barbiturates are only applicable

A

IV

201
Q

Short, ultra short acting barbiturates

A

Pentobarbital
Methohexital
Thiopental

202
Q

which breed are barbiturates not used

A

Grey hounds (oversensitive)

203
Q

Which anaesthetic is safe to use in liver failure patient?

A

Propofol

204
Q

Opiods have to be combined with which anaesthetics?

A

Propofol
Imidazole anaesthetics
Steroid anaesthetics

205
Q

How should imidazole anaesthetics be administered and why?

A

IV, causes severe tissue irritation

206
Q

With which drugs can Ketamine be used

A
  • Xylazine
  • Medetomidine
  • Detomidine
  • Diazepam
  • Acepromazin
  • Butorfanol
207
Q

What do we need for a balanced anaesthesia

A

combination of :

  • antimuscarinic
  • sedatives
  • opioids
  • anaeasthetics and muscle relaxants
208
Q

combinations for light plane anaesthesia

A

xylazine- ketamine
Dex/Me/Detomidine - ketamine
xylazine - zoletil
medetomidine - zoletil
xylazine - butorphanol
medetomidine - butorphanol
thiopental - guaiphenesin
azaperone - metomidate (swine)

209
Q

combinations used for neuroleptanalgesia

A

Etorphine - acepromazine
butorphanol - acepromazine
fentanyl - fluanisone
fentanyl - droperidol

Pharma MT (3 decks)

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