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Pharmo for medic school > Quick And Dirty Review > Flashcards

Quick And Dirty Review Flashcards

1
Q

Sodium channel blocking drugs (anti epileptics)

A

Carbamazepine
Phenytoin
Valproic acid

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2
Q

Calcium INflux anti seizure

A

Valproic acid

Ethosuximide

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3
Q

Potassium eflux blocker

A

Ezogabine

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4
Q

Glutamate

A

Primary CNS excitatory
Works on AMPA and NMDA
Felbamate
Topirimate

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5
Q

Barbs and gabapentin

A

Barbs potentiates and mimicks gaba
GABApentin promotes release
Tiagabin inhibits reuptake
Vigabatrin inhibits gaba metabolism enzymes

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6
Q

Phenytoin

A

Dilantin, most widely used, good for partial and primary generalized seizures
Selective sodium channel inhibitor
Only hits hyperactive neurons
Above 20mcg/mL nystagmus, cognitive impairement, sedation
Preggo - cleft palate, heart malformations, other serious sides
Hypotension and dysrhythmias
Gingival hyperplasia, rash, ataxia, diplopia,

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7
Q

Phenytoin contras

A

ETOH allergy, TCA coke OD, heart block, sinus brad, adams stokes,
20mg/kg max 10 concentration 10mg/ml

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8
Q

Carbamazepine

A

Tegretol, also selective inhibition of sodium channels, safer/fewer sides than phenytoin, CYP inducer/inhibitor, used for bipolar and neuralgias,

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9
Q

Valproic acid

A

Epival and depakene
Suppression of high frequency Na+
Suppression of Ca2+
Augments GABA

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10
Q

Moderate opioids

A

Codeine and hydro/oxy codone. 30mg = 325 tylenol

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11
Q

Morphine resp depression

A

7 minutes IV, 20 minutes IM, lasts 4-5 hours, N/V worse from first dose
Biliary colic is questionable at best
0.1mg/kg max 2.5 q 15 max 15

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12
Q

PD

A

EPS associated with striatum
Dys and akinesia
Too little dope, too much ACh causes too much GABA
Dope agonists OR Antichols work

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13
Q

Benztropine

A

Antichol for PD, reduce tremor but not bradykinesia, less effective than levadopa but better tolerated

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14
Q

PD other symptoms

A

Depression dementia psychosis autonomic (constipatioon, urinary incontinence, drooling, orthostatic hypotension, and cold intolerance)

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15
Q

3 main sedative/hypnotic drugs

A

Barbs
Benzos
Benzo-like

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16
Q

Barbs

A

Anxiety/insomnia prior to benzos
Powerful resp depression (popular for suicide)
Tolerance, dependence, multiple interactions

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17
Q

Three classes of barbs

A

Ultrashort (thiopental)
Short-intermediate (secobarbital)
Long (phenobarb)

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18
Q

Barbs MOA

A

Enhance inhibitory action of GABA AND mimic GABA

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19
Q

Barbs tox

A

Resp depression
Coma
Pinpoint
TX activated charcoal and maintenance of O2

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20
Q

Common barbs

A 
Phenobarbital (phenobarb)
Amobarbital (amytal)
Pentobarbital (nembutal)
Secobarbital (seconal)
Butabarbital (butisol)
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21
Q

Benzos anxiety

A

Reduce anxiety through limbic system (thalamus, basal ganglia)

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22
Q

Benzos promote sleep through

A

Effects on cortical areas

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23
Q

Benzos muscle relaxation

A

Supraspinal motor areas (cerebellum)

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24
Q

Benzos confusion

A

Confusion and antegrade amnesia (after dosing) from effects on hippocampus and cerebral cortex

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25
Q

Common benzos

A 
Alprazolam (xanax)
Clobazam (onfi)
Clonzaepam (klonopin)
Diazepam (valium)
Estazolam (prosom)
Lorazepam (ativan)
Temazepam (restoril)
Different benzos favor anxiety, insomnia, seizures etc
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26
Q

Flumazenil

A

Anexate, don’t give with TCA OD or pts receiving benzos for status epilep

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27
Q

Benzo like drugs

A

Only for insomnia, not anxiety. Structurally different than benzos but same MOA
Low potential for tolerance, dependence and abuse
Zolpidem (ambien)
Zaleplon (sonata)
Escopiclone (lunesta)

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28
Q

OCD

A

Persistent obsession, compulsion at least 1 hour each day.

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29
Q

3 core symptoms of PTSD

A

Re-experiencing event
Avoiding reminders of the event
Persistent state of hyperarousal

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30
Q

Neuroleptic drugs

A

Reduce and depress nerve functions (slow movement)

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31
Q

Antipsychotic meds

A

Also called neuroleptics because of EPS effects they may produce
Chemically diverse, for schizo, delusional, bipolar, depressive pyschoses
Should not be used for dementia related pychosis (increased mortality)
Created around 1950

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32
Q

Anti depressents

A

Do not alter movement, and so in a different category

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33
Q

Two classes of antipsychos

A

FGAs and SGAs (first and second gen)

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34
Q

FGAs antypsychos

A

Strong blockade of dope receptors, can induce EPS

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35
Q

SGAs anyipsychos

A

Moderate block of dope, stronger block of serotonin

EPS risk lower, but significant risk of effects such as weight gain and the beeties

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36
Q

Specific neuroleptic agents

A

Olanzapine (zyprexa) risperidone (risperdal) quetiapine (seroquel) are 2nd gen, which outsell 1st gen 10-1, haloperidole is 1st gen

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37
Q

FGA MOA

A

Variety or receptors in and outside CNS, to varying degress dope, ACh, histamine, NE
Work by blocking D2 receptors in brain
Primary condition used for is schizo, takes 2-4 weeks, work well
EPS, particularly tardive dyskinesia, is worst side effect generally safe, OD almost unheard of

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38
Q

Tardive dyskinesia

A

Involuntary repetitive movements which may include grimacing, sticking out tongue, smacking of lips, rapid jerking movements, slow writhing movements

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39
Q

EPS acute dystonia

A

Acute dystonia - continuous spasms and contractions of face, neck, tongue, and back upward deviation of the eyes. Hours to days onset, treated with benztropine mesylate, resolve within 5-10mins of treatment

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40
Q

EPS Parkinsonism

A

Muscle rigidity with bradykinesia, shuffling gait, drooling, stooped posture, mask like facies (no expression) 5-30 day onset, treated with benztropine or dimenhydrinate or benadryl

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41
Q

EPS Akathisia

A

Feeling of needing to be in constant motion, rocking while standing or sitting, marching on spot, crossing/uncrossing legs 5-60 day onset
Switch to lower potency antipsycho treat with benzos, beta blockers, antichols

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42
Q

Tardive dyskinesia

A

Irregular, jerky movements primarily in face. Involuntary twisting, squirming movements of tongue, smacking and fly catching movements (takes months to appear, no reliable treatment) prevention is best approach

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43
Q

FGAs muscarinic cholinergic blockade

A

Dry mouth, blurred vision, photophobia, constipation, tachy, dry hot skin, CNS excitation

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44
Q

Other FGA adverse effects

A

Orthostatic hypo (A1 block)
Sedation (H1 block in CNS)
Seizures (reduuce threshold)
Sexy dysfunc (suppress libido, A2 suppression)

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45
Q

Halo

A

Contras parkinsons CNS depression seizure hx 5mg q 15 max 10
Use caution if taking antichol meds, benzos or ETOH
May prolong QT

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46
Q

Benztropine Mesylate

A

Cogentin
ANtichol, antipark for acute dystonic reactions
Increases occular pressure, dose is 1-2mg

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47
Q

SGAs

A

Or atypical antipsychos
Popular in 90s
Metabolic sides (get fatty beeties)
Minor D2 agonisms, strong serotonin 5Ht

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48
Q

Depot forms of neuroleptic agents

A

Haldol, risperidone, sustenna, abilify, zyprexa

49
Q

TCAs

A

Introduced in the 1950s, were first line.
Block neuronal reuptake of NE and sometimes serotonin for depression, bipolar, fibromyalgia, insomnia
8X therapeutic is toxic from antichol properties

50
Q

TCA OD

A

Combo of cholinergic blockade, and direct cardiotox effects

Tachy, AV blocks, Vtach/fib, seizures cardiac arrest

51
Q

Common TCAs

A 
Amitriptyline
Amoxapine
Desipramine (norpramin)
Doxepin
Imipramine (tofranil)
Nortriptyline (pamelor)
Protriptyline (vivactil)
Trimipramine (surmontil)
52
Q

MAOIs

A

More toxic than TCAs, hypertensive crisis from tyramine rich foods (pickled cheese, sausage, soy sauce, beans, snow peas)

53
Q

MAO found in

A

Liver, intestinal walls, terminals of terminals of some neurons
Functions to convert dope, 5HT, NE into inactive

54
Q

MAO OD

A

Tyramine promotes release of NE

HTN, headache, tachycardia, N/V, confusion

55
Q

Common MAOIs

A 
Rasagiline (azilect)
Selegiline (eldepryl, zelapar)
Isocarboxazid (marplan)
Phenelzine (nardil)
Tranylcypromine (parnate)
56
Q

SSRIs

A

1987, N, agitation/insomnia & sexy desfunc
Just as effective but much safer
They selectively block reuptake of serotonin OBVI
Don’t block dope, NE, histamine, cholinergic, A1 receptors

57
Q

SSRIs sides

A

Impotence, delayed/absent orgasm, weight gain, withdrawal syndrome - headache, dizziness, N/V if stopped suddenly

58
Q

Serotonin syndrome

A

Onset 2-72 hours

Agitation, anxiety, hallucinations, sweating, tremors

59
Q

Common SSRIs

A 
Citalopram (celexa)
Escitalopram (lexapro, cipralex)
Paroxetine (paxil, seroxat)
Fluoxetine (prozac)
Fluvoaxmine (luvox)
Sertraline (zoloft, lustral)
60
Q

General anesthetics

A

Drugs that produce unconsciousness and lack of responsiveness to painful stimuli

61
Q

General anesthetics two main groups

A

Inhalation anesthetics

Intravenous anesthetics

62
Q

IV anesthetics

A 
Short acting barbs (thiobarb)
Benzodiazepines
Propofol
Etomidate
Ketamine
63
Q

Benzos

A

Large doses for unconsciousness and amnesia, diazepam, lorazepam, midaz can all be given IV for amnesia

64
Q

Diazepam for induction

A

Unconsciousness within 1 minute

Very little muscle relaxation

65
Q

Midaz for induction

A

Unconsciousness within 80 seconds, dangerous cardioresp effects

66
Q

Propofol anesthetic

A

Unconscious within 60 seconds, lasts 3-5 mins
Sedative-hypnotic
Can cause resp depression, hypotension, risk of bacterial infection

67
Q

Propofol MOA

A

Promotes release of GABA, causing CNS depression, no analgesic actions
Extended sedation infusions up to 4mg/kg/min given
Contras are egg or soy allergy
Dose is 2-2.5mg/kg IV
40mg bolus q10 until desired effects

68
Q

Ketamine

A

Dissociate anesthesia, sedation, immobility, analgesia, amnesia
Can cause delerium, disturbing dreams which decrease with calmed environment and benzos
Schedule 1

69
Q

NMBA block

A

ACH at Nm receptors

70
Q

Order of paralysis

A

Eyes and face, then limbs, abdo, glottis. Last are resp muscles (intercostals and diaphragm)

71
Q

Contras to succ

A

Hypersensitive
HyperK+
Family hx of malignant hyperthermia
Myopathies associated with elevated CK

72
Q

Vec weight based dose

A

0.1mg/kg IV IO maintenance 0.01-0.05mg/kg IV/IO q 20-40

73
Q

5 neurotransmitters

A

NE, ACh, Serotnin, Glutamate, GABA

74
Q

3 things that happen after termination of neurotransmitter

A

Reuptake, enzymatic degrade, diffusion

75
Q

5 effects of muscarinic receptors being activated

A 
Increased gland secretion
Smooth muscle contraction in bronchi and GI
Slowing of HR
Pupil contraction (miosis)
Dilation of vessels
Relaxation of urinary bladder
76
Q

Midaz ceaser dose

A

10 IM 5 IV max 20 total

77
Q

Maintanence ketamine dose

A

0.5mg/kg SIVP q10 prn

78
Q

Acute toxicity triad for barbs

A

Resp depression
Coma
Pinpoint pupils

79
Q

Flumazenil dose

A

0.2mg IV over 15 seconds q1 prn max 3 mg

80
Q

3 uses of benzos

A

Anxiety, insomnia, seizures, combative pts, procedural sedations, ETOH withdrawal, muscle spasms

81
Q

4 mechanisms of adrenergic agonists

A

Direct receptor binding
Promotion of NE release
Inhibit NE reuptake
Inhib NE inactivation

82
Q

A2 activation

A

Reduction of sympathetic outflow to heart/vessels

Relief of severe pain

83
Q

Isoproterenol

A

Activate B1, B2

84
Q

4 ways drugs activate adrenergic receptors

A

Direct binding (most common)
Promotion NE release
Inhibition NE reuptake (TCAs, coke)
Inhibition NE inactivation

85
Q

A1 activation causes 2 main responses

A

Vasoconstriction in blood vessels of skin, viscera, and mucous membranes
Mydriasis of the eye

86
Q

A2 agonists are located

A

presynaptically

87
Q

A2 agonsits therapeutic applications

A

none in PNS

88
Q

A2 in CNS

A

Reduction of sympathetic outflow to heart/blood vessels
Relief of severe pain
Clonidine - reduces sympathetic tone to blood vessels/heart

89
Q

B1 agonists

A 
Heart failure, maintain blood flow to organs in shock (chrono and inotropic effects) 
AV blocks (enhance conduction through AV node)
Asystole - initaite contraction
90
Q

B1 adverse effects

A

Tachycardia, dysrhythmias, angina, increase MVO2

91
Q

B2

A

Lungs and uterUS
Mostly for bronchodilation
Isoproternol hits B1 and B2
Activating B2 has ability to delay preterm labour

92
Q

Adrenergic antagonists LPT

A

Direct blockade of adrenergic receptors, nearly all cause reversibly (competitive) blockade

93
Q

A1 and A2 antags

A

Phentolamine for prevention of necrosis following extravasation of IV A1 blockers and reversal of soft tissue anesthesia

94
Q

Beta 1 blockers

A

Metoprolol, labetalol, bisoprolol, atenolol, esmolol
Reduced heart rate, force of contraction, and impulse conduction through AV
A fib by lowering sinus nodal discharge rate
Conduction of atrial impulses through AV node is slowed

95
Q

Beta blockers others

A

Angina, HTN, MI, CHF, pheochromocytoma

96
Q

Excitation contraction coupling

A

Process by which an action potential in a motor neuron leads to contraction of a muscle

97
Q

6 steps of a muscle contraction

A

Action potential releases ACh into junction
ACh binds to nic M on motor end plate
Binding causes depol
Depol creates muscle action potential
Muscle action potential causes calcium release from SR
Calcium allows actin/myosin to interact and contract muscle

98
Q

Non depol NMBA

A

Competitive, bind to Nic m and block ACh.

Eyes/face then limbs abdo glottic and last intercostals and diaphragm

99
Q

NMBA sides

A

Hypotension from nic m block and histamine release
No crossing of BBB
Rule 1, don’t be a dick

100
Q

Depol NMBA

A

Only succ
Binds to nic M and causes depol, fasciculations occur, prevents repol for 4-6 mins at EMS dose
Peak paralysis 1 min, max 10
Malignant hypertherm (1 in 25,000) causes Muscle rigidity and temp up to 43 from increased Ca2+ release from SR

101
Q

Succ degraded by

A

Pseudocholinesterase

102
Q

Hyperk succs

A

Rare for enough k+ from succ to causes severe hyperk, more likely to occur in major burns, significant trauma, rhabdo

103
Q

Succ slide

A

Anectine
Contras hyperk, family hx of malig hypertherm, pseudocholinerserate defic, myopathies with elevated CK
Adult 1.5mg/kg max 150
peds 1.5-2.0 mg/kg

104
Q

Addtional consids succ

A

Don’t be a dick, give sedsation first
Don’t give for difficult airways
Takes 60-90 seconds
Acute airway burns will not cause hyper k

105
Q

Roc slide (lol get it?)

A

Zemuron
only contra is hypersens
1mg/kg repeat 0.5mg/kg IV/IO prn
Ped samesies

106
Q

Roc additional consids

A

Don’t be a dick, give sedation first
Micins (antibis) Dipine (ccb) can potentiate effects of roc
Increases in BP, hrt rate, or bronchospasm possible
No histamine release
Peaks 1-3 mins, lasts 20-40

107
Q

Vecuronium

A

Norcuron, NMBA, only contra is hypersens
0.1mg/kg maintain at 0.01-0.05mg/kg q 20-40
Peds same

108
Q

Vecuronium addtional consids

A

Don’t be a dick
micins and ccbs potentiate effect
Nohistamine release

109
Q

Pancuronium

A

Pavulon, NMBA, only contra is hypersens

0.1mg/kg maintain at 0.01mg/kg q 20-40 peds samesies

110
Q

Panc additional consids

A

Was prototype NMBA
Don’t be a dick
No histamine release
30-45% hepatic metab

111
Q

2 basic steps in process by which neurons influence bevhaior of post synaptic cells

A

Axonal conduction, AP travels down neuron

Synaptic transmission - info carried across gap b/w neuron and postsynaptic cell

112
Q

Axonal conduction synaptic transmyssion

A

Most drugs act on altering synaptic transmission, only a few alter axonal conduction.
Synaptic trans can produce more selective effects
Local anesthetics alter axon conduction (not selective as all axons are alike)

113
Q

5 steps in receptor activiting

A

Transmitter synthesis, storage, release
Receptor binding
Termination of transmission

114
Q

Peripheral nervous system includes

A

Autonomic which has parasympa and sympa

Somatic motor system voluntary nervous system

115
Q

Three principal functions of ANS

A

Regulat heart, secretory glands, smooth muscle

116
Q

Parasympa 7 functions

A

Slow hrt rate, increase GI secretions, empty bladder, empty bowel, focus eye for near vision, constrict pupil, contract smooth muscle

117
Q

Sympa 3 main functions

A

Regulate cardiovasc (bloodflow to brain, dedistribute blood, compensate for blood loss)
Reg of body temp (blood flow to skin, secretion of swetat, piloerection)
Fight or flight (increase hrt and BP, shunt blood from skin/viscera, dilate bronchi, dilate pupils, mobilize stored energy)

118
Q

Two main site for parasympa drug actions

A

Between pre and post ganglionic neurons

Junctions between effector organs and postganglionic neurons

Pharmo for medic school (26 decks)

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