neurology pharmac Flashcards
(122 cards)
1
Q
levodopa is converted to dopamine in brain by
A
dopa decarboxylase enz
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
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
4
Q
dopamine agonists that can be used in PD
A
ergot derivative dopamine agonist– BROMOCRIPTINE
Non ergot dopamine agonist – prami-prexole and ropinirole
5
Q
what enzymes degrade dopamine
A
COMT - catechol-o-methy transferase (inhibited by capones)
MAO-b monoamine oxidase B (inhibited by selegiline)
6
Q
name COMT inhibitors used in parkinsons disease
A
CAPONES–enta and tol –entacapone and tolacapone
7
Q
anticholinergic drug that can help tremors of parkinsons disease
A
benz tropine (similar to atropine) trihexy phenidyl
8
Q
treatment of medically intractable essential tremor
A
high frequency DBS to ventro-intermediate thalamic nucleus
9
Q
serotonergic neurons that are under the action of SSRI are situated in (Remember SsRi—)
A
raphe nucleus of brainstem
SsRi—- serotonin – raphe
10
Q
what does locus coerulus secrete
A
two words– locus coerulus
two word product – nor -epinephrine
two word function –flight - fight
11
Q
Drug used to abort febrile seizure if they are more than 5 min
A
Benzodiazepines
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
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
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
15
Q
what is the dangerous side effect of barbiturates
A
Respiratory depression and coma
16
Q
Flumazenil is used in
A
overdose of Benzodiazepine and non benzodiazepine hypnotics
because it is a competitive antagonist of GABA receptor
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.
18
Q
which CNS drug is contraindicated in porphyria
A
barbiturates
19
Q
acute BZD withdrawl can cause
A
seizures
20
Q
Use of barbiturates have been obsolete except in two uses
A
phenobarbitone in epilepsy
thiopentone in anaesthesia
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.
22
Q
jet lag sydrome drug if taken before the start of flight
A
melatonin
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
24
Q
contraindication of sumatriptan
A
Acute MI since it can cause coronary angiospasm
avoided in pts in CAD or prinzmetal angina
25
peripheral conversion of L Dopa by COMT enzyme give
3-OMD 3 O methyl dopa
| entacapone is COMT inhibitor used to incresase LDOPA delivery to brain
26
drugs which prevent central (in brain) degradation of L dopa
Entacapones and MAO B inhibitors (seligiline and rasagiline)
27
four drugs for alzheimers disease
| remember-- cholinergic activators and glutamate antagonists
3 act via AChE inhibition ---DONE RIVA GALA
Donepezil- rivastigmine -galantamine
1 act via NMDA receptor antagonism to prevent Calcium mediated excitotoxicity --MEMANTINE
28
Mechanism of action of memantine
Acts as NMDA receptor antagonist
| prevents neuronal excitotoxicity mediated by Calcium.
29
unique side effect of amantadine --- PD drug
livedo reticularis -- LINEAR MACULES OF ERYTHEMA AND bluish discolouration.
Due to post capillary constriction
due to local release of norepinephrine.
30
of all parkinson disease drug... only drugs effective in drug induced (phenothiazine induced) parkinsonism
anticholinergics
31
glutamate is main excitatory neurotransmitter in brain. It acts on which receptors in post synaptic membrane
```
NMDA (allows calcium entry )
Ion channel causing sodium influx
AMPA receptor (aminoacid)
```
32
Only drug for ALS
riluzole --- decreases glutamate excitotoxicity
| increases survival
33
Only drug for Chorea and tardive dyskinesia of huntingtons disease
Tetrabenazine--- Vesicular monoamine transporter inhibited..
| Dopamine vesicle is not packed or released.
34
potency of inhalational anesthesia is measured by
MAC -- minimum alveolar concentration.
| required to prevent 50 percent patients from moving during a surgical incision.
35
MAC of 0.4 wakes up the patient from anaesthesia
above 1.5 MAC is not / rarely used
| 2 to 3 MAC is lethal
36
when combination of two inhalational anesthetics are used their MAC are
additive
37
name the important inhaled anesthetics.
nitrous oxide
des halo
methoxy iso en fluranes
38
a drug with high blood solubility has slower induction
| or high blood gas coefficient
because inhaled anaesthetic remains soluble in blood and does not enter brain and needs higher concentration.
39
relation between potency and MAC
lower potency -- high drug conc and higher MAC needed
40
N2O is poor blood and lipid soluble
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
41
Halothane is good blood soluble and good lipid solubility
lower MAC needed to reach good blood concentration hence more potent
high lipid solubility -- more redistribution-- slower induction.
42
two important effects with nitrous oxide
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
43
expansion of which inhaled anesthetics occurs in body cavities
pneumothorax is seen with N2O
44
N2O can cause cerebral vasodilation and increase cerebral blood flow. Adverse effect can be
raised ICT. vomiting
45
adr of methoxy flurane and enflurane
methoxyflurane --- nephrotoxic
| enflurane- proconvulsant
46
malignant hyperthermia is caused by
halothane (inhaled anaethetic)
and/ or
succinyl choline.
Concomitant use is more detrimental
47
Genetic abnormality in malignant hyperthermia
AD Mutated RYR1 receptor (ryanodine receptor)
on sarcoplasmic reticulum skeletal muscles
sustained release of Ca ions from SR
sustained muscle contraction
hyperthermia
48
treatment of malignant hyperthermia
External cooling
bicarbonate infusion and 100 percent oxygen
DANTROLENE---RYR receptor antagonist
49
dissociative anaesthesia
ketamine
| emergence reaction is possible causing hallucinations and vivid dreams
50
mechanism of action of ketamine
NMDA receptor antagonist
51
name IV anaesthetics
Thiopental --- now superseded by propofol
midazolam
ketamine
52
what is dissociative anaesthesia
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
site of action for ketamine
higher than others
cortex and subcortical areas-- because of sensory dissociation
others act of RAS
54
fentanly is an IV anaesthetic, opioid analgesic class.
| During recovery it can cause peristent respiratory depression which can be reversed by
IV naloxone--- opioid antagonist
55
mechanism of action of local anaesthetics
block sodium channels in nerve membranes-- no action potential propagation - palsy
56
Local anaesthetics are given mixed with epinephrine because
epinephrine causes vasoconstriction which helps to
1. reduce bleeding
2. Reduce peripheral escape and toxicity
3. Increased effect of anaesthesia
57
order of nerve blockade in local anesthetics
size > myelination
| Small myelinated fibres> small unmyelinated > large myelinated > large unmyelinated fibres
58
Loss of sensation in spinal or local anesthesia
Pain - temperature ---touch and last to go pressure
59
cocaine action as local anesthetic
Cocaine blocks sodium channels--- hence local anaesthetic effects
and for same reason causes QRS and QT prolongation in heart giving rise to arrhythmias
60
methhaemoglobinemia causing anaesthetic drugs
lidocaine and bupivacaine
61
cause of methhaemoglobinemia
inability of enz methhaemoglobin reductase.
| Which converts ferric Fe3+ back to normal Fe-ous Fe2+
62
Mechanism of action of succinyl choline
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
Complications of importance after succinyl choline
malignant hyperthermia
hypercalcemia (just like mechanism of hyperthermia)
hyperkalemia (muscles loose K+)
64
mechanism of action of non depolarising SM relaxants-- crurare drugs
competitive ACh receptor antagonist.
does not allow ACh receptor bound sodium channels to open
End plate potential is not generated.
65
Two phenomenon with non depolarising SM relaxants--- crurares
Fade phenomen-- after partial blockade--- twitching in muscle can be elicited but they progressively fade.
Post tetanic potentiation of second incoming twitch.
66
Reversal of Stage I blockade of succinyl choline
stage I --- is prolonged depolarisation
NO antidote
giving cholineE inhibitors is detrimental because of non availablity of ACh
67
Reversal of stage II blockade of succinylcholine
Stage II is repolrised by still blocked due to desensitised Ach receptors
Reversed by Cholinesterase Inhibitors
68
reversal of blockade of crurare drugs/// non depolarising
similar to stage II of succinyl choline which is also non depolarised
CholineE inhibitor like neostigmine + Atropine/ glycopyrrolate
69
why is neostigmine used with atropine or glycopyrrolate during reversal of blockade
Neostigmine is CholineE inhibitor
can cause muscarinic side effects like bradycardia
hence atropine/glycopyrrolate to avoid it is used
70
site of action of baclofen to relieve spasticity
GABA -B receptors in spinal cord ---acts as agonist-- inhibitory
71
two uses of dantrolene
malignant hyperthermia syndrome from succinyl choline and inhaled anaesthetics
neuroleptic malignant syndrome -- ie toxicity of antipsychotic medications
72
name four spasmolyitcs or antispasmodics
dantrolene baclofen
cyclobenza-prine ---- anticholinergic effects hence antispastic but acts at CNS level
TIZANIDINE--- Centrally acting Alpha2 agonist
73
which antispasmodic acts centrally
Tizanidine--- Alpha 2 agonist
Cyclobenzaprine--- centrally acting has anticholinergic and TCA like effect.
74
name the three opioid receptor
meu-- B endorphin
Delta- enkephalin
Kappa--------dynorphin
75
Mechanism of action of opioids
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
2. open Post synaptic K channels-- hyperpolarisation
76
Neurotransmittor release blocked by opioids are
Ach & NE
Serotonin
It is analgesic --- Substance P
glutamate
77
which drug is used for long term maintenence therapy after opioid withdrawl-- opioid drug addicts
methadone
| Buprenorphine + Naloxone
78
how does morphine cause vomiting
activate or sensitised CTZ
79
Why do morphine cause miosis
| Name the only opioid drug causing mydriasis
```
because they stimulate Edinger westphal nucleus-- 3rd CN parasympathetic - miosis
Only Meperidine (pethidine ) causes mydriasis
```
80
opioid toxicity is treated with
NALOXONE for acute
| NALTREXONE for relapse prevention once detoxification occurs
81
problem / caution of use of mixed opioid agonist- antagonist (pentazocine or butor-phanol)
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
mechanism of action of tramadol
weak opioid agonist
| SNRI-- serotonin and NE reuptake inhibitor
83
side effects of tramadol
Serotonin syndrome
| seizure threshold reduced--can precipitate convulsions
84
which antiglaucoma drugs can cause change in iris colour and increase in eyelash growth
prostanglandins- F2Alpha
Bimatoprost
Latanoprost
they increase uveoscleral outflow
85
Increase in uveoscleral outflow in glaucoma is done by
Prostaglandins F2Alpha
| Bimato-latano prost
86
Increase in trabecular meshwork and canal of Schelmn outflow in glaucoma
Cholinomimetics-- pilocarpine physostigmine
87
which glaucoma drugs are not used in angle closure glaucoma
Alpha agonist 1- epinephrine, 2- apraclonidine brimonidine
| because they cause mydriasis (normal symphathetic action) and worsen angle closure glaucoma.
88
Drugs used in partial / focal aware seizure
all except BZD
| and ethosuximide
89
only use of ethosuximide
Absence seizure.
90
mechanism of action of ethosuximide
blocks thalamic calcium channels---- prevents release of neurotransmitter
91
drugs used in absence seizures
ethosuximide
lamotrigine
valproic acid
92
mechanism of action of valproic acid
causes sustained inactivation of sodium channels
| inhibits GABA transaminase -- hence increases GABA concentration-- inhibitory no seizures
93
mechanism of action of lamotrigine
Blocks sodium channels --- inhibits glutamate release
94
unique adverse reactions of lamotrigine
```
Steven johnson syndrome
Hemophagocytic lymphangiohistiocytosis (BLACK BOX WARNING)
```
95
mechanism of action of vigabatrin and its black box warning
vi- gaba trin
Increases GABA by irreversibly inhibiting GABA transaminase
ADR- Permanent vision loss
96
reuptake of GABA by GAT transporter in presynaptic membrane
| and clearence of GABA by glial cells is inhibited by
tiagabine
97
degradation of GABA by transaminase is inhibited by
Valproate
| vigabatrin
98
drugs for eclampsia seizures
Magsulf
| benzodiazepines
99
Drug for trigeminal neuralgia
carbamazepine
100
drug for peripheral neuropathy and post herpetic neuralgia
Gabapentin
101
Succinyl choline can lead to prolonged paralysis in patients with
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
Pts with genetic polymorphisms with BHCE GENE have prolonged paralysis from which anaesthetic agents
Succinyl choline
Mivacurium
Cocaine effects are prolonged
103
Succinyl choline is ineffective in producing paralysis in standard doses in which patients
Myasthenia gravis
Avoided
Because of less number of acetylcholine receptors in these patients
No effect of succinyl cholin
104
Cytch P450 inducers
Cbz barbiturates phenytoin
Rifampin greisofulvin
St johns wort - HERBAL TO TREAT DEPRESSION
Modafinil-- STIMULANT TO TREAT NARCOLEPSY
Cyclophosphamide
105
Cyto 450 inhibitors
Grapefruit juice
Azole antifungal
Isoniazid
Protease inhibitors - ritonavir
Cimetidine
Fluroquinolones clarithromycin
Amiodarone
106
How can levetriacetam modulate Glutamate and GABA release
Because they bind to synaptic vesicle protein -2A
| And modulAtes release of neurotransmittor
107
Which neurotransmitter release is modulAted by levetriacetam
Glutamate and GABA
108
Name the three drugs which inhibit cortical sodium channel currents
And hence prevent seizures
Pcv drugs
Phenytoin
Carbamazapinr
Valproate
Of these valproate also has action to increase GABA level and hence is considered broad spectrum
109
Motor end plate acetylcholine gated ion channel is
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
Name choline esterase inhibitors which can have cns effects
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
Dopamine receptors in mesolimbic pathway are blocked by which drugs
Haloperidol and resiperidone like antipsychotic medications
| Used to treat schizophrenia and bipolar mood disorders
112
Morphine is metabolised by liver into
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
Morphine is avoided in renal dysfunction because
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
In renal dysfunction for pain
| Instead of morphine which opioids are to be used
Fentanyl
| Hydromorphone
115
What drug is pergolide
| Where is it used
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
Which parkinsons disease drug is used to delay disease progression
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
Use of methylphenidate
ADHD- it is in an indirectly acting
| sympathomimetic
118
Which drug is used to treat ADHD
Methylphenidate- indirect sympathomimetic acts as a stimulant
Alpha 2 agonists— guanfacine and clonidine
Atomoxetine
119
Fluorinated inhaled anaesthetics result in hypotension during anaesthesia because
They cause myocardial depression
Reduce cardiac output causes hypotension
Ventricular and atrial pressures increase
120
Halothane and sevoflurane are preferred inhaled anaesthetics in asthma patients because——
Routine inhaled anaesthetics cause decrease in lung mucociliary clearence
And halothane and sevoflurane have bronchodilation effects hence preferred in ashtmatics
121
```
Essential tremor is most common movement disorder
Familial
Autosomal dominant
Improves with alcohol intake
Treatment is
```
Non selective beta blocker
Propranolol
By its cns effects
122
Uses of propranolol
| Non selective b blocker
First line in essential tremor
In bleeding varices to reduce portal venous pressure
In migraine prophylaxis
