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neurology pharmac Flashcards

1
Q

levodopa is converted to dopamine in brain by

A

dopa decarboxylase enz

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2
Q

why is carbidopa combined with levodopa

A

carbidopa inhibts peripheral dopa decarboxylase enz so side effects of peripheray dopamine and epinephrine production are not produced
also carbidopa wont cross the blood brain barrier and hence is safe

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3
Q

which antiviral drug can be used in PD

which increases the synaptic availability of dopamine

A

amantadine is the antiviral drug used in PD because it increases the endogeneous production of dopamine
NMDA antagonism
anticholinergic CNS action

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4
Q

dopamine agonists that can be used in PD

A

ergot derivative dopamine agonist– BROMOCRIPTINE

Non ergot dopamine agonist – prami-prexole and ropinirole

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5
Q

what enzymes degrade dopamine

A

COMT - catechol-o-methy transferase (inhibited by capones)

MAO-b monoamine oxidase B (inhibited by selegiline)

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6
Q

name COMT inhibitors used in parkinsons disease

A

CAPONES–enta and tol –entacapone and tolacapone

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7
Q

anticholinergic drug that can help tremors of parkinsons disease

A 
benz tropine (similar to atropine)
trihexy phenidyl
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8
Q

treatment of medically intractable essential tremor

A

high frequency DBS to ventro-intermediate thalamic nucleus

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9
Q

serotonergic neurons that are under the action of SSRI are situated in (Remember SsRi—)

A

raphe nucleus of brainstem

SsRi—- serotonin – raphe

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10
Q

what does locus coerulus secrete

A

two words– locus coerulus
two word product – nor -epinephrine
two word function –flight - fight

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11
Q

Drug used to abort febrile seizure if they are more than 5 min

A

Benzodiazepines

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12
Q

Why are GABA a receptors inhibitors

A

Gaba is ionotropic affecting chloride ion channel
Chloride is extracellular and eq potential is -75
Hence when gaba induced chloride channels open chloride goes into the cell down the gradient leading to hyperpolarisation
Hence refractory period increases
Hence inhibitory

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13
Q

THREE DRUGS FOR INSOMNIA

A

NON BZD HYPONOTICS– ZOLPIDEM (BZ1 subtype of GABA receptor)
SUVO -REXANT (orexin antagonist)
RAMEL-TEON (melatonin agonist acting on MT1 and 2 in suprachiasmatic nucleus)
BZD – diazepam and alprazolam are also used

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14
Q

Name Benzodiazepines

A

short acting– ATOM- alprazolam, triazolam, oxazepam, midazolam
safe to be used with alcoholics- LOT - lorazepam, oxazepam and temazepam (LORA O TEMA)
rest— diazepam and chlrodizepoxide

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15
Q

what is the dangerous side effect of barbiturates

A

Respiratory depression and coma

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16
Q

Flumazenil is used in

A

overdose of Benzodiazepine and non benzodiazepine hypnotics

because it is a competitive antagonist of GABA receptor

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17
Q

difference of action btn Barbiturates and BZD

A

Barbiturates increase the DURATION of GABA Induced chloride channel opening… GABA being inhibitory it potentiates inhibition– reduced firing of neurons

BZD acts on same GABA A receptor but increases the FREQUENCY OF Cl channel opening
SITE of BZD binding and Barbiturate binding on GABA Is different… Hence together they cause higher CNS depression and coma.

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18
Q

which CNS drug is contraindicated in porphyria

A

barbiturates

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19
Q

acute BZD withdrawl can cause

A

seizures

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20
Q

Use of barbiturates have been obsolete except in two uses

A

phenobarbitone in epilepsy

thiopentone in anaesthesia

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21
Q

barbiturate poisoning is usually suicidal. Treatment is

A

largely and only supportive- no antidote exists.
Gastric lavage, alkalinisation of urine to promote excretion, vasopressors esp dopamine for its renal vasodilating effects, hemodialysis and trying to keep patient alive.

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22
Q

jet lag sydrome drug if taken before the start of flight

A

melatonin

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23
Q

mechanism of action of sumatriptan

A

Serotonin receptor agonist– 5HT1b/1d
inhibtis activation of trigeminal nerve — cluster headache
prevents Vasoactive peptide release—-
induces vasoconstriction — treats headaches

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24
Q

contraindication of sumatriptan

A

Acute MI since it can cause coronary angiospasm

avoided in pts in CAD or prinzmetal angina

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25
Q

peripheral conversion of L Dopa by COMT enzyme give

A

3-OMD 3 O methyl dopa

entacapone is COMT inhibitor used to incresase LDOPA delivery to brain

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26
Q

drugs which prevent central (in brain) degradation of L dopa

A

Entacapones and MAO B inhibitors (seligiline and rasagiline)

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27
Q

four drugs for alzheimers disease

remember– cholinergic activators and glutamate antagonists

A

3 act via AChE inhibition —DONE RIVA GALA
Donepezil- rivastigmine -galantamine
1 act via NMDA receptor antagonism to prevent Calcium mediated excitotoxicity –MEMANTINE

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28
Q

Mechanism of action of memantine

A

Acts as NMDA receptor antagonist

prevents neuronal excitotoxicity mediated by Calcium.

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29
Q

unique side effect of amantadine — PD drug

A

livedo reticularis – LINEAR MACULES OF ERYTHEMA AND bluish discolouration.
Due to post capillary constriction
due to local release of norepinephrine.

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30
Q

of all parkinson disease drug… only drugs effective in drug induced (phenothiazine induced) parkinsonism

A

anticholinergics

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31
Q

glutamate is main excitatory neurotransmitter in brain. It acts on which receptors in post synaptic membrane

A 
NMDA (allows calcium entry )
Ion channel causing sodium influx
AMPA receptor (aminoacid)
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32
Q

Only drug for ALS

A

riluzole — decreases glutamate excitotoxicity

increases survival

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33
Q

Only drug for Chorea and tardive dyskinesia of huntingtons disease

A

Tetrabenazine— Vesicular monoamine transporter inhibited..

Dopamine vesicle is not packed or released.

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34
Q

potency of inhalational anesthesia is measured by

A

MAC – minimum alveolar concentration.

required to prevent 50 percent patients from moving during a surgical incision.

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35
Q

MAC of 0.4 wakes up the patient from anaesthesia

A

above 1.5 MAC is not / rarely used

2 to 3 MAC is lethal

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36
Q

when combination of two inhalational anesthetics are used their MAC are

A

additive

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37
Q

name the important inhaled anesthetics.

A

nitrous oxide
des halo
methoxy iso en fluranes

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38
Q

a drug with high blood solubility has slower induction

or high blood gas coefficient

A

because inhaled anaesthetic remains soluble in blood and does not enter brain and needs higher concentration.

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39
Q

relation between potency and MAC

A

lower potency – high drug conc and higher MAC needed

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40
Q

N2O is poor blood and lipid soluble

A

Poor blood soluble needs more MAC to reach good conc in blood hence less potent.
Poor lipid soluble so poor redistribution (wastage) hence rapid induction

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41
Q

Halothane is good blood soluble and good lipid solubility

A

lower MAC needed to reach good blood concentration hence more potent
high lipid solubility – more redistribution– slower induction.

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42
Q

two important effects with nitrous oxide

A

second gas effect seen with N2O + halothane together – faster induction since halothane will be delivered at higher rate than tidal volume.

diffusion hypoxia– avoided with 100 percent oxygen for few minutes after discontinuation of N2O

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43
Q

expansion of which inhaled anesthetics occurs in body cavities

A

pneumothorax is seen with N2O

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44
Q

N2O can cause cerebral vasodilation and increase cerebral blood flow. Adverse effect can be

A

raised ICT. vomiting

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45
Q

adr of methoxy flurane and enflurane

A

methoxyflurane — nephrotoxic

enflurane- proconvulsant

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46
Q

malignant hyperthermia is caused by

A

halothane (inhaled anaethetic)
and/ or
succinyl choline.
Concomitant use is more detrimental

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47
Q

Genetic abnormality in malignant hyperthermia

A

AD Mutated RYR1 receptor (ryanodine receptor)
on sarcoplasmic reticulum skeletal muscles
sustained release of Ca ions from SR
sustained muscle contraction
hyperthermia

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48
Q

treatment of malignant hyperthermia

A

External cooling
bicarbonate infusion and 100 percent oxygen
DANTROLENE—RYR receptor antagonist

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49
Q

dissociative anaesthesia

A

ketamine

emergence reaction is possible causing hallucinations and vivid dreams

50
Q

mechanism of action of ketamine

A

NMDA receptor antagonist

51
Q

name IV anaesthetics

A

Thiopental — now superseded by propofol
midazolam
ketamine

52
Q

what is dissociative anaesthesia

A

profound analgesia+ immobility+ amnesia with light sleep
Pt is unable to process sensory stimuli or react
Pt remains conscious, able to swallow blink eye and has stiffness of muscles

53
Q

site of action for ketamine

A

higher than others
cortex and subcortical areas– because of sensory dissociation
others act of RAS

54
Q

fentanly is an IV anaesthetic, opioid analgesic class.

During recovery it can cause peristent respiratory depression which can be reversed by

A

IV naloxone— opioid antagonist

55
Q

mechanism of action of local anaesthetics

A

block sodium channels in nerve membranes– no action potential propagation - palsy

56
Q

Local anaesthetics are given mixed with epinephrine because

A

epinephrine causes vasoconstriction which helps to

  1. reduce bleeding
  2. Reduce peripheral escape and toxicity
  3. Increased effect of anaesthesia
57
Q

order of nerve blockade in local anesthetics

A

size > myelination

Small myelinated fibres> small unmyelinated > large myelinated > large unmyelinated fibres

58
Q

Loss of sensation in spinal or local anesthesia

A

Pain - temperature —touch and last to go pressure

59
Q

cocaine action as local anesthetic

A

Cocaine blocks sodium channels— hence local anaesthetic effects
and for same reason causes QRS and QT prolongation in heart giving rise to arrhythmias

60
Q

methhaemoglobinemia causing anaesthetic drugs

A

lidocaine and bupivacaine

61
Q

cause of methhaemoglobinemia

A

inability of enz methhaemoglobin reductase.

Which converts ferric Fe3+ back to normal Fe-ous Fe2+

62
Q

Mechanism of action of succinyl choline

A

name is similar and hence action is similar to Ach
Acts on acetyl Choline receptors at NMjn
Sustained depolarisation- does not allow to contract

63
Q

Complications of importance after succinyl choline

A

malignant hyperthermia
hypercalcemia (just like mechanism of hyperthermia)
hyperkalemia (muscles loose K+)

64
Q

mechanism of action of non depolarising SM relaxants– crurare drugs

A

competitive ACh receptor antagonist.
does not allow ACh receptor bound sodium channels to open
End plate potential is not generated.

65
Q

Two phenomenon with non depolarising SM relaxants— crurares

A

Fade phenomen– after partial blockade— twitching in muscle can be elicited but they progressively fade.
Post tetanic potentiation of second incoming twitch.

66
Q

Reversal of Stage I blockade of succinyl choline

A

stage I — is prolonged depolarisation
NO antidote
giving cholineE inhibitors is detrimental because of non availablity of ACh

67
Q

Reversal of stage II blockade of succinylcholine

A

Stage II is repolrised by still blocked due to desensitised Ach receptors
Reversed by Cholinesterase Inhibitors

68
Q

reversal of blockade of crurare drugs/// non depolarising

A

similar to stage II of succinyl choline which is also non depolarised
CholineE inhibitor like neostigmine + Atropine/ glycopyrrolate

69
Q

why is neostigmine used with atropine or glycopyrrolate during reversal of blockade

A

Neostigmine is CholineE inhibitor
can cause muscarinic side effects like bradycardia
hence atropine/glycopyrrolate to avoid it is used

70
Q

site of action of baclofen to relieve spasticity

A

GABA -B receptors in spinal cord —acts as agonist– inhibitory

71
Q

two uses of dantrolene

A

malignant hyperthermia syndrome from succinyl choline and inhaled anaesthetics

neuroleptic malignant syndrome – ie toxicity of antipsychotic medications

72
Q

name four spasmolyitcs or antispasmodics

A

dantrolene baclofen
cyclobenza-prine —- anticholinergic effects hence antispastic but acts at CNS level
TIZANIDINE— Centrally acting Alpha2 agonist

73
Q

which antispasmodic acts centrally

A

Tizanidine— Alpha 2 agonist

Cyclobenzaprine— centrally acting has anticholinergic and TCA like effect.

74
Q

name the three opioid receptor

A

meu– B endorphin
Delta- enkephalin
Kappa——–dynorphin

75
Q

Mechanism of action of opioids

A

block synaptic transmission for pain
1. Close presynaptic Calcium channels– fusion of vesicle and release cannot happen– Ach and NE release from presynapntic memb blocked

  1. open Post synaptic K channels– hyperpolarisation
76
Q

Neurotransmittor release blocked by opioids are

A

Ach & NE
Serotonin
It is analgesic — Substance P
glutamate

77
Q

which drug is used for long term maintenence therapy after opioid withdrawl– opioid drug addicts

A

methadone

Buprenorphine + Naloxone

78
Q

how does morphine cause vomiting

A

activate or sensitised CTZ

79
Q

Why do morphine cause miosis

Name the only opioid drug causing mydriasis

A 
because they stimulate Edinger westphal nucleus-- 3rd CN parasympathetic - miosis
Only Meperidine (pethidine ) causes mydriasis
80
Q

opioid toxicity is treated with

A

NALOXONE for acute

NALTREXONE for relapse prevention once detoxification occurs

81
Q

problem / caution of use of mixed opioid agonist- antagonist (pentazocine or butor-phanol)

A

they are partial kappa agonist with partial agonism or antagonism at Meu receptors
hence when used on drug addicts who take full agonists usually — like morphine heroine codeine meperidine
would cause competition for opioid receptors
and withdrawl symptoms arise which are difficult to treat because even naloxone cannot treat it (since it is pure antagonist)

82
Q

mechanism of action of tramadol

A

weak opioid agonist

SNRI– serotonin and NE reuptake inhibitor

83
Q

side effects of tramadol

A

Serotonin syndrome

seizure threshold reduced–can precipitate convulsions

84
Q

which antiglaucoma drugs can cause change in iris colour and increase in eyelash growth

A

prostanglandins- F2Alpha
Bimatoprost
Latanoprost
they increase uveoscleral outflow

85
Q

Increase in uveoscleral outflow in glaucoma is done by

A

Prostaglandins F2Alpha

Bimato-latano prost

86
Q

Increase in trabecular meshwork and canal of Schelmn outflow in glaucoma

A

Cholinomimetics– pilocarpine physostigmine

87
Q

which glaucoma drugs are not used in angle closure glaucoma

A

Alpha agonist 1- epinephrine, 2- apraclonidine brimonidine

because they cause mydriasis (normal symphathetic action) and worsen angle closure glaucoma.

88
Q

Drugs used in partial / focal aware seizure

A

all except BZD

and ethosuximide

89
Q

only use of ethosuximide

A

Absence seizure.

90
Q

mechanism of action of ethosuximide

A

blocks thalamic calcium channels—- prevents release of neurotransmitter

91
Q

drugs used in absence seizures

A

ethosuximide
lamotrigine
valproic acid

92
Q

mechanism of action of valproic acid

A

causes sustained inactivation of sodium channels

inhibits GABA transaminase – hence increases GABA concentration– inhibitory no seizures

93
Q

mechanism of action of lamotrigine

A

Blocks sodium channels — inhibits glutamate release

94
Q

unique adverse reactions of lamotrigine

A 
Steven johnson syndrome 
Hemophagocytic lymphangiohistiocytosis (BLACK BOX WARNING)
95
Q

mechanism of action of vigabatrin and its black box warning

A

vi- gaba trin
Increases GABA by irreversibly inhibiting GABA transaminase
ADR- Permanent vision loss

96
Q

reuptake of GABA by GAT transporter in presynaptic membrane

and clearence of GABA by glial cells is inhibited by

A

tiagabine

97
Q

degradation of GABA by transaminase is inhibited by

A

Valproate

vigabatrin

98
Q

drugs for eclampsia seizures

A

Magsulf

benzodiazepines

99
Q

Drug for trigeminal neuralgia

A

carbamazepine

100
Q

drug for peripheral neuropathy and post herpetic neuralgia

A

Gabapentin

101
Q

Succinyl choline can lead to prolonged paralysis in patients with

A

Genetic polymorphisms
Involving BCHE butrylcholine esterase
Which is also known as pseudocholine esterase
Pt having this gene mutations have increased succinly choline at NMJ
Prolonged paralysis

102
Q

Pts with genetic polymorphisms with BHCE GENE have prolonged paralysis from which anaesthetic agents

A

Succinyl choline
Mivacurium
Cocaine effects are prolonged

103
Q

Succinyl choline is ineffective in producing paralysis in standard doses in which patients

A

Myasthenia gravis
Avoided
Because of less number of acetylcholine receptors in these patients
No effect of succinyl cholin

104
Q

Cytch P450 inducers

A

Cbz barbiturates phenytoin
Rifampin greisofulvin
St johns wort - HERBAL TO TREAT DEPRESSION
Modafinil– STIMULANT TO TREAT NARCOLEPSY
Cyclophosphamide

105
Q

Cyto 450 inhibitors

A

Grapefruit juice
Azole antifungal
Isoniazid

Protease inhibitors - ritonavir
Cimetidine
Fluroquinolones clarithromycin
Amiodarone

106
Q

How can levetriacetam modulate Glutamate and GABA release

A

Because they bind to synaptic vesicle protein -2A

And modulAtes release of neurotransmittor

107
Q

Which neurotransmitter release is modulAted by levetriacetam

A

Glutamate and GABA

108
Q

Name the three drugs which inhibit cortical sodium channel currents
And hence prevent seizures

A

Pcv drugs

Phenytoin
Carbamazapinr
Valproate

Of these valproate also has action to increase GABA level and hence is considered broad spectrum

109
Q

Motor end plate acetylcholine gated ion channel is

A

Ionotropic
Two ach needed to bind at two binding sites
To open the ion channel
Opens sodium in calcium in and potassium out channel

110
Q

Name choline esterase inhibitors which can have cns effects

A

Only tertiary amine which are lipophilic will cross bbb to have CNS effects
4 drugs
Done riva galantamine/— alz dz drugs
Physostigmine— used to revert both central and peripheral effects of atropine toxicity

111
Q

Dopamine receptors in mesolimbic pathway are blocked by which drugs

A

Haloperidol and resiperidone like antipsychotic medications

Used to treat schizophrenia and bipolar mood disorders

112
Q

Morphine is metabolised by liver into

A

Active metabolites by glucoronidation

Morphine 3 glucoronide
Morphine 6 glucoronide

Which Are then renally excreted
Morphine 6 glucoronide is infact more active than morphine itself

113
Q

Morphine is avoided in renal dysfunction because

A

Morphine metabolites are glucoronide conjugate products from liver
They are active metabolites
after glucoronidation they are renally excreted
In renal failure they accumulate leading to opioid toxixity

114
Q

In renal dysfunction for pain

Instead of morphine which opioids are to be used

A

Fentanyl

Hydromorphone

115
Q

What drug is pergolide

Where is it used

A

Pergolide is D2 agonist
Used in parkinsons disease
Only modest improvement as monotherapy
But still can be used in early case to delay starting levodopa

116
Q

Which parkinsons disease drug is used to delay disease progression

A

Selegiline
MAO b inhibitor
It is also used when mptp is the causative agent
Because mptp is converted to toxic pd causing product mpp+
This can be prevented by selegiline

117
Q

Use of methylphenidate

A

ADHD- it is in an indirectly acting

sympathomimetic

118
Q

Which drug is used to treat ADHD

A

Methylphenidate- indirect sympathomimetic acts as a stimulant

Alpha 2 agonists— guanfacine and clonidine
Atomoxetine

119
Q

Fluorinated inhaled anaesthetics result in hypotension during anaesthesia because

A

They cause myocardial depression
Reduce cardiac output causes hypotension
Ventricular and atrial pressures increase

120
Q

Halothane and sevoflurane are preferred inhaled anaesthetics in asthma patients because——

A

Routine inhaled anaesthetics cause decrease in lung mucociliary clearence

And halothane and sevoflurane have bronchodilation effects hence preferred in ashtmatics

121
Q 
Essential tremor is most common movement disorder
Familial
Autosomal dominant
Improves with alcohol intake
Treatment is
A

Non selective beta blocker
Propranolol
By its cns effects

122
Q

Uses of propranolol

Non selective b blocker

A

First line in essential tremor
In bleeding varices to reduce portal venous pressure
In migraine prophylaxis

Flash Facts (23 decks)

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