Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm Exam 3 > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

what are seizures:

A

sudden, transient episodes of brain dysfunction and altered behavior due to ABNORMALLY EXCESSIVE, SYNCHRONOUS, AND RHYTHMIC FIRING (electrical discharge) of certain populations of hyper-excitable neurons in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are convulsions?

A

Seizure when motor neurons are activated = involuntary contractions of skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of seizures:

A

1) CNS injury - altered excitation thresholds of certain cerebral neurons - head trauma, stroke, tumors
2) Congenital abnormalities in brain -birth trauma
3) Genetic factors - defective genes coding for voltage-gated ion channels or GABA receptors
4) infections, hypoglycemia, hypoxia, toxic and metabolic disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is epilepsy?

A

chronic neurological disorder characterized by recurrent seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

primary epilepsy origin?

A

unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

secondary epilepsy origin?

A

identifiable cause (trauma, tumor, infection, development anomalies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Partial epileptic seizures - types:

A
  • simple partial
  • complex partial
  • partial becoming generalized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Simple partial-

1) type of seizure?
2) spread?
3) consciousness?
4) motor/sensory manifestation?

A

1) Partial epileptic
2) least complicated; *Minimal spread of abnormal neuronal discharge
- USUALLY JUST ONE LIMB IS AFFECTED
3) NO LOSS OF CONSCIOUSNESS - person alert and can remember it
4) Limited motor/sensory manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complex partial-

1) type of seizure?
2) affects how and what parts of brain
3) consciousness?
4) behavior after?

A

1) Partial epileptic
2) **Starts in small brain area (one lobe) and quickly spreads to other areas ex) limbic system which effects alertness and awareness
3) ALTERED CONSCIOUSNESS with potential automatisms (lip smacking, fumbling, swallowing)
4) Strong emotional feelings, gradual recovery of consciousness after 30-120sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Partial becoming generalized seizures:

1) type of seizure:
2) where/how affect brain?

A

1) Partial epileptic

* *2) partial that spreads throughout brain and progresses to a generalized seizure –> TONIC CLONIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Generalized seizures types:

A

1) absence (PETIT MAL)
2) tonic-clonic (Grand mal)
3) tonic
4) atonic
5) clonc and myoclonic
6) infantile spasms
7) status epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Absence (Petit Mal) seizure:

1) type?
2) start and stop?
3) consciousness?
4) who gets?
5) how get?

A

1) generalized seizure - Entire brain - bilateral brain effects
2) Sudden start and stop 10-45 seconds
3) **BRIEF LOSS OF CONSCIOUSNESS - ranges from no motor signs to symmetrical jerking or movement of eyelids, extremities or entire body
4) CHILDREN GET THIS <15yo - May dev into tonic-clonic
5) Inducible by hyperventilation, stress or flashing lights

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tonic clonic seizures:

1) type?
2) what affected?
3) consciousness?
4) phases?

A

1) generalized seizure
2) Tonic spasms and major convulsions of entire body (bilateral)
3) LOSS OF CONSCIOUSNESS - Profound CNS depression after
5) a) Aura=patients sense seizure coming on
b) Tonic=muscle tensing and rigidity of all extremities – then tremors
c) clonic=convulsions due to rapid and repeating muscle contractions and relaxing –> uncontrolled shaking of the body
d) stupor and sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tonic

1) type?
2) consciousness? effects on person/brain?

A

1) generalized seizure

2) Loss of consciousness with severe hypertonic spasms and autonomic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Atonic

1) type?
2) effects on person?
3) who gets often?

A

1) generalized seizure
2) **sudden loss of postural tone **resulting in falls or dropping of head and torso if in sitting postion
3) children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clonic and myoclonic

1) type?
2) consciousness? Effect on person?

A

1) generalized seizure

2) loss of consciousness with rhythmic clonic contractions phase and time matched to EEG pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

infantile spasms

1) type?
2) what happens?

A

1) generalized - epileptic syndrome and not a seizure type

2) recurrent myoclonic jerks of the body with sudden flexion or extension of the body and limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  • *status epilepticus
    1) type?
    2) what happens?
A

1) generalized seizure
* *2) continuous or very rapid recurring seizures - tonic clonic type

**MEDICAL EMERGENCY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

3 stages of mechanism to epileptic seizure

DONT WORRY ABOUT THIS

A

1) initiation
a) abnormal function of Ca ion channels - increased generation of AP
2) Synchronization of surrounding
a) decreased inhibition of GABA - GABA INHIBITS so less inhibition
b) other areas start getting funky
3) propagation –> recruitment of normal neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Goal of antiepileptic meds?

A

restore normal patters of electrical activity - prevent CNS damage by uncontrolled reoccurence

so we inhibit seizures but cant cure seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Antiepileptic meds eliminate seizures in what % of patients?

What % do not respond to these meds?

A

2/3

20% no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Epileptic treatment options:

A

1) meds
2) surgery - temporal lobe related seizures
3) vagus nerve stimulation (VNS) - drug resistant patient with partial seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cyclic Ureides list drugs:

A 
Phenytoin
Forphenytoin
Primidone
phenobarbital
ethosuximide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Tricylcic list drugs:

A

carbamazepine

oxcarbazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

benzodiazepines list drugs:

A

diazepam

lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GABA deriv list drugs?

A

Gabapentin

pregabalin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Other class anticonvulsant drugs list types:

A 
valproic acids
lamotrigine
acetazolamide
tiagabine
topiramate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

anticonvulsants for partial seizures with or without secondarily generated seizures:

A

carbamazepine
phenytoin (PHT)
valproate (VPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

anticonvulsants for tonic clonic (grand mal), tonic, and atonic seizures:

A

carbamazepine
phenytoin
valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

anticonvulsants for absence seizures (petit mal):

A

ethosuximide (ETH)
valproate

AND LAMOTRIGINE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

anticonvulsants for myoclonic seizures:

A

clonazepam

valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

anticonvulsants for status epilepticus:

A 
diazepam
lorazepam
phenytoin
forphenytoin
phenobarbital and primidone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

**Anticonvulsant MOA?

A

INHIBIT FIRING OF CERAIN EXCITABLE CEREBRAL NEURONS

1) Decrease excitatory effects of glutamate and repetitive firing of neurons – block voltage-gated Na channels
2) Increase inhibitory effects of GABA
3) Alter neuronal activation by altering movement of ions (Na,Ca) across neuronal membrane – inhibition of voltage gated Ca channels responsible for T-type Ca currents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Inactivation of Na channel hows? what does this mean?

A

Block INACTIVE STATE=

  • prolong Na channel inactivation
  • neuronal membrane becomes less excitable
  • ***decrease in sustained, high frequency, repetitive discharge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Effects on Ca channels?

Effective against what kind of seizure?

A
  • reduced Ca influx into cells
  • -decreased transmitter released
  • prevent neuronal excitability and spread of activity –> prevention of seizure pattern

-effective against absence seizures (petit mal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

**Two drugs that work on Ca channels?

A

valproate
ethosuximide

USED FOR PETIT MAL (absence seizures)

37
Q

General side effects of anticonvulsants:

A

1) sedation
2) diplopia
3) nystagmus (esp with phenytoin)
4) ataxia (esp with phenytoin)
5) GI upset - nausea, vomit, gastritis
6) avoid abrupt withdraw;
7) decrease efficacy of oral contraceptives
8) teratogenic

38
Q

Which anticonvulsant is safest during pregnancy?

A

phenobarbital

39
Q

Hydantoins which drugs?

A

phenytoin and forphenytoin

40
Q

what the oldest non-sedative antiseizure drug?’

Oldest seizure drug in general?

A

phenytoin

phenobarbital

41
Q

Absorption of hydantoins?

A
  • phenytoin and forphenytoin
  • absorption variable and dependent on formulation
  • poorly soluble
  • highly protein bound
  • *-Forphenytoin is newer and more soluble - IV and IM
42
Q

Phenytoin - pharmacokinetics:

A
  • metabolites are inactive
  • DOSE DEPENDENT (0-order) elimination –> can get a quick buildup of drug with not much change of dose at higher doses (once you saturate the enzymes)
43
Q

Phenytoin MOA:

A

1) blocks and prolongs inactivated voltage gates Na channels = less release of glutamte; blocks high freq firing neurons
2) enhances release of GABA
3) prevents seizure propagation

44
Q

Phenytoin - clinical uses:

A
  • generalized tonic clonic (grand mal)
  • partial seizures
  • status epilepticus
45
Q

Phenytoin side effects:

A
  • sedation -CNS depression
  • ataxia
  • nystagmus
  • diplopia
  • cardiac dysrhythimas
  • hirsutism
  • gingival hyperplasia
  • osteomalacia
  • megaloblastic anemia
  • fetal hydantoin syndrome -teratogenic
46
Q

Drugs that decrease phenytoin metabolism:

A

-competition-
barbiturates -high concentration
warfarin

47
Q

Drugs that increase phenytoin metabolism:

A

-MES induction-
barbiturates-low concentration
carbamazepine

48
Q

Drugs that increase free circulating fraction of phenytoin - displace protein binding:

A

salicylates (aspirin)
valproic acid
kidney failure

49
Q

Carbamazepine- MOA

A

-same as phenytoin-

blocks and prolongs inactivated voltage gates Na channels = less release of glutamate;

50
Q

Carbamazepine- Metabolism:

A

induces its own metabolism by increasing activity of hepatic MES p450s

51
Q

Oxacarbazepine** vs carbamazepine?

A

newer and similar to carbamazepine but shorter half life and active metabolite has longer duration and fewer drug interactions

52
Q

Carbamazepine is the drug of choice for:

A

trigeminal neuralgia - pain disorder

53
Q

Carbamazepine - clinical uses:

A
  • general clonic-tonic seizures (grand mal)

- partial seizures

54
Q

Carbamazepine - side effects:

A
  • CNS depression -osteomalacia, aplastic anemia, megaloblastic anemia
  • SIADH - increased ADH secretion = fluid retention and hyponatremia
  • teratogenic - spina bifida!
55
Q

Carbamazepine - drug interactions:

A

Phenytoin
valproate
phenobarbital

56
Q

Barbiturates - phenobarbital

MOA?

A

Enhances phasic GABA_A receptor responses = increases opening time of CL channel

57
Q

Phenobarbital - clinical uses?

A

Status epilepticus

58
Q

Primidone- importance to seizures?

A

drug is metabolized to phenobarbital by liver = same effects

59
Q

Ethosuximide - treats what condition?

A

petit mal - absence seizures

60
Q

**ethosuximide - MOA?

A

blocks presynaptic T-type Ca channels –> blocks high frequency firing of neurons

61
Q

**Drug of choice for absence seizures?

A

ethosuxamide and Valproic acid

62
Q

Valproic acid - MOA?

what is diffference?

A
  • same as other petit mal - absence seizure drug ethosuxamide

blocks presynaptic T-type Ca channels –> blocks high frequency firing of neurons

-this one is less sedating

63
Q

***Valproic acid - side effects?

A
  • Potential for hepatotoxic syndrome

- teratogenic risk - spina bifida

64
Q

*Benzodiazepines- diazepam

MOA?

A

-potentiates GABA_A responses by increasing the frequency of channel opening (Cl ion channels are opened for longer = hyperpolarization and stuff so cant fire)

65
Q

*Diazempam - clinical uses?

A

status epilepticus - tonic clonic

66
Q

*Lorazepan -
drug class?
used for?

A
  • benzodiazepine -

- used for status epilepticus - longer durition of action than diazepam

67
Q

*Diazepam - side effects:

A
  • sedative effects

- tolerance

68
Q

What is the prefered intial agent for status epilepticus?

A

diazepam

69
Q

gabapentin - MOA?

-what is it?

A
  • block presynaptic volt gated Ca channels = decreases excitatory transmission
  • amino acid –> analog of GABA
70
Q

Gabapentin - clinical uses?

-uses with use?

A
  • generalized tonic clonic seizures (Grand mal)
  • neuropathic pain - posthepetic neuralgia and fibromyalgia

short T1/2 = 6hrs

71
Q

Adverse effects of gabapentin:

A

somnolence
dizziness,
ataxia
GI issues

72
Q

Pregabalin - what is it?

A

similar to gabapentin - GABA analong

73
Q

Lamotrigine - MOA?

-similar to what agent?

A
  • blocks presynaptic volt gated Na and Ca channels

- similar to Carbamazepine

74
Q

Lamotrigine - Clinical uses:

A

partial seizures
generalized seizures
tonic clonic gran mal
absence seizures petit mal

75
Q

**Lamotrigine - Adverse effects:

A

Stevens Johnson syndrome - allergic reaction that looks like it sucks

76
Q

Lamotrigine - interactions:

A

Volproate (get rash)

carbamazepine

77
Q

*Felbamate

MOA?

A

block Na channels and glutamate receptors

78
Q

*Felbamate

clinical uses?

A

adjunct for seizure states

79
Q

*Felbamate adverse effects:

A

aplastic anemia

hepatic failure

80
Q

*Topiramate
adverse effects:
interactions?

A
  • sedation, confusion, paresthesias, anorexia

- acidosis with zonisamide

81
Q

Zonisamide - adverse: DONT NEED TO KNOW FOR DURIC EXAM

A

urinary stones
mental clouding
tremors

82
Q
  • *Tiagabine
  • MOA?
  • clinical uses?
  • adverse?
A
  • inh of GABA uptake
  • partial seizures
  • sedation, dizzy, headache, tremor
83
Q

Vigabatrin DONT NEED TO KNOW FOR DURIC EXAM

-ae?

A

visual defects

may cause absence seizures or psychotic reactions

84
Q

Centrally acting muscle relaxants

-used for?

A

1) spasticity - an exaggerated muscle stretch reflex syndrome - after injury to CNS (brain/spine)
2) Spasm - increase inmuscle tension seen after musculoskeletal injuries and inflammation (injury is local)

85
Q

goal of centrally acting muscle relaxants?

A

normalize muscle excitability without causing a profound decrease in muscle fnction

86
Q

Drugs used as muscle relaxants:

A
  • Benzodiazepine -Diazepam

- Baclophen -

87
Q

Benzodiazepine - Diazepam - MOA as centrally acting muscle relaxant

A

**-more GABA_A (Cl ion cahnnels) inh of alpha motor neurons

***-treatment of spams with excess exertion, MS, cerebral palsy, injury

88
Q

**Baclofen - MOA as centrally acting muscle relaxant

A

**-works at GABA_B receptor agonist: (G-protein effect on K channels) - more K conductance = hyperpolarization = reduction in Ca influx = less excitatory transmitter release downstream inh effect on muscles

  • **-reduces spasticity with MS spinal and brain injury
  • LESS SEDATION THAN DIAZEPAM

Pharm Exam 3 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions