Brainscape's Knowledge GenomeTM

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


See full index

MQW U3 > Pharm > Flashcards

Pharm Flashcards

1
Q

What DA pathway controls movement?

A

Nigrastriatal

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

What DA pathway controls reward and perception?

A

Mesolimbic

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

What DA pathway controls executive function?

A

Mesocortical

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

What DA pathway controls pituitary prolaction function?

A

Tuberoinfundibular

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

2 Post-synaptic enzymes that terminate DA action:

A

MAO A or B

COMT

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

Hyperfunctioning Migrostriatal pathway causes:

Hypofunctioning causes:

A

Hyper: dyskinetic movemnt
Hypo: dyskinetic movement, parkinsonism

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

Hyperfunctioning Mesolimbic pathway causes:

Hypofunctioning causes:

A

Hyper: Addiction, hallucinations
Hypo: amotivation, apathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hyperfunctioning Mesocortical pathway causes:

Hypofunctioning causes:

A

Hyper: hypervigilance
Hypo: inattention

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

Hyperfunctioning Tuberoinfundibular pathway causes:

Hypofunctioning causes:

A

Hyper: hypoprolactinemia
Hypo: hyperprolactinemia

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

What drugs to enhance DA synthesis?

A

Levodopa: DA precursor
Carbidopa: combined therapy to prevent peripheral DA activity –> lower side effects

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

Results of low and high DA activity:

A

Low: distractable
High: hypervigilant

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

ADHD: ___ DA activity at ___

A

low, anterior cingulate

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

Parkinson: ___ DA activity at ___

A

low, striatum

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

Why is MTHFR enzyme important?

Genetics?

A

Creates L-methylfolate, which is the form that can cross BBB

TT alleles bad –> less DA made

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

Bupropion:
Treats?
Class?
Affects what pathway?

A

Antidepressant
NDRI
Mesocortical

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

Amphetamines mechanism:

A
  • Block DAT

- Increase VMAT2 –>more DA release

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

Methylphenidate mechanism:

A

-Block DAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 wakefulness promoting stimulant drugs:
Treats?
Side effects?

A
  • Modafinil, Armodafinil
  • Narcolepsy
  • Off label: ADHD
  • P450-3A4 inducer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Selegiline:
low dose is used for for?
high dose is used for?

A

Low dose: MAO-B selective –> Parkinson

High dose: MAO A and B –> Depression

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

Rasagiline mechanism:

treats?

A
  • MAO-B inhibitor

- Parkinson’s

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

MAOIs for Depression:

A
  1. Isocarboxazid
  2. Phenelzine
  3. Tranylcypromine
  4. Selegiline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Serotonin Syndrome

A
  • MAOI decrease Serotonin breakdown
  • Adding Serotonin drug –> toxic levels in CNS
  • Tremor, muscle spasm, vital changes, hyperthermia, delirium, coma, death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

COMTi drugs:
treats?
effect on neurotransmitters?

A
  • Entacapone, Tolcapone
  • Parkinson’s
  • elevate DA and NE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

D2 receptor agonists:

treats?

A
  • Bromocriptine, pramipexole, ropinerole, Apomorphine injection
  • Parkinson’s or Restless leg Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

D3 receptor agonists:

treats?

A
  • Aripiprazole
  • Antipsychotic for Schizo
  • Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Amantadine mechanism:

treats?

A
  • Release DA, block DAT, stimulate D2

- Parkinson’s, Influenza

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

Reserpine treats:

A

HTN, Schizo psychosis, causes Depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tetrabenazine treats:

A

Huntington’s Chorea by lowering DA availability

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

D2 receptor antagonist affects which pathways?
treats?
classification?

A

ALL; they are non-selective

Schizophrenia

FGAs (high, low potency), SGAs

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

What causes EPS?

Symptoms?

A
  • High Potency FGA

- Akathisia, Dystonia, Parkinsonism, Neuroleptic Malignant Syndrome

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

Symptoms of Neuroleptic Malignant Syndrome:

A
  1. Hyperthermia
  2. Muscle rigidity
  3. Vital sign instability
  4. Rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Tardive Dyskinesia

A
  • Chronic D2 receptor antagonism
  • Permanent movement disorder side effect
  • Choreic or Athetotic movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

High vs Low Potency FGA drugs:

  • Haloperidol
  • Thioridazine
  • Thiothixine
  • Fluphenazine
  • Chlorpromazine
A

High:
Haloperidol
Fluphenazine
Thiothixine

Low:
Chlorpromazine
Thioridazine

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

Blocking ___ receptor lowers EPS risk

A

Serotonin 2a (5HT2a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Side effects of ‘Dones’ vs ‘Pines’

A

Dones: more EPS

Pines: more sedating, more metabolic syndrome

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

Clozapine risks and benefits

A
  • Risk of agranulocytosis
  • Most metabolic risk of any agent
  • No neuromuscular effect –> no EPS/TD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Blocking what receptor stops psychosis?

A

D2

38
Q

Mechanism of action for Beta blockers in Glaucoma?

A

Reduce aqueous production

39
Q

Suffix for carbonic anhydrase inhibitors:

A

-zolamide

40
Q

Mechanism of action for Carbonic Anhydrase Inhibitors in Glaucoma?

A

Reduce production of aqueous

41
Q

Mechanism of action for Prostaglandin Analog in Glaucoma?

A

Increase uveoscleral outflow w/o effect on aqueous flow or trabecular outflow facility

42
Q

Cocaine mechanism for diagnosing Horner’s Syndrome

A
  • Cocaine = reuptake inhibitor –> NE flood –> pupillary dilation
  • Horner’s Syndrome = dysfunctional PANS –> no pupillary dilation
43
Q

What drug is used to differentiate preganglionic from postganglionic lesions in Horner’s Syndrome?

A

Hydroxyamphetamine: Releases NE

44
Q

Hydroxyamphetamine mechanism for differentiating lesion location in Horner’s Syndrome

A
  • Topical application
  • No pupillary dilation = 3rd order neuron problem = Postganglionic = benign process
  • Dilation = Preganglionic lesion –> requires investigation
45
Q

How do you differentiate Adie’s syndrome from an intracranial aneurysm?

A
  • Low dose muscarinic agonist (Methacholine or Pilocarpine)
  • Chronic denervated nerve in Adie’s syndrom will be hypersensitive –> pupillary constriction
  • Acute trauma neurved from aneurysm will not respond
46
Q

What is light-near dissociation?

A

No pupil response to light, but does have accomodation

47
Q

Most common cause and population affected by Parinaud’s Syndrome

A
  • Midbrain tumor (pineal)

- Young children

48
Q

Common presentation and population affected by Adie’s Syndrome

A
  • Loss of patellar reflex

- Young females

49
Q

What characterizes Argyll-Robertson Syndrome:

A
  • Miotic irregular pupils

- Does not respond to cycloplegics

50
Q

Triptan’s mechanism of action:

A

5HT1 B-D agonist –> vasoconstriction of intracranial EXTRACEREBRAL blood vessels (trigeminovascular system) –> block sterile inflammation reaction

51
Q

In what patient population are triptans contraindicated?

A

Patients w/ vascular disease, uncontrolled HTN, and comlicated migraine syndromes

52
Q

Migraine vs Tension vs Cluster Headache characteristics:

A

Migraine: unilateral, throbbing, moderate-severe, aggravated by activity, relieved by rest

Tension: dull, achy, non-pulsatile, pressure-like, bilateral, mild-medium

Cluster: severe, unilateral, in temporal, orbital or supraorbital areas

53
Q

Most commonly used Beta blocker for Migraine?

A

Propranolol

54
Q

Most commonly used Ca++ Channel Blocker for Migraine?

A

Verapamil

-useful for aura

55
Q

For what patient population is Migraine prevantative therapy recommended?

A
  • 3+ severe headaches/month or
  • 2+ mild-moderate headaches/week or
  • inability to use effective symptomatic therapy
56
Q

2 Anti-epileptics used for migraine prevention

A

Valproic Acid, Topiramate

57
Q

Cluster Headache characteristics:

A
  • Clockwork daily and annual rhythm (same time)
  • Men:women 4:1
  • Some patients have heavy facial features
58
Q

Long-term Cluster Headache prevention drugs:

A
  • Verapamil (Ca++ channel blocker)
  • Topiramate (antiepileptic)
  • Valproic Acid (antiepileptic)
  • Lithium (mood stabilizer)
59
Q

Biogenic Amine Hypothesis of Depression:

A

Depression = too little CNS NE and/or 5HT

60
Q

Scoring of Hamilton Depression Rating Scale (HDRS):

A

Mild= 8-13
Moderate= 14-18
Severe= 19-22
Very Severe= >23

61
Q

What do MAO-A and -B mainly oxidize?

A
  • A = NE, 5HT, Tyramine

- B = DA, phenyethylamine

62
Q

What is the most used TCA for TTH prevention?

A

Amitriptyline

63
Q

What is a common side effect of TCAs?

A

Cardiac arrhythmias

64
Q

What 2 SSRIs have P450 Inhibition

A

Fluoxetine, Paroxetine

65
Q

What is Ketamine’s mechanism of action?

A

Glutamate NMDA receptor antagonist

66
Q

What drug can quitting smokers use to maintain nicotine abstinence?

A

Bupropion - Atypical antidepressant

67
Q

What is the important side effect of Buproprion?

A

Lowers seizure threshold

68
Q

What can happen if you give a Bipolar person tricyclics?

A

Precipitate mania

69
Q

What are the 3 structural parts of local anesthetics?

A
  1. Aromatic ring
  2. Intermediate Linkage
  3. Terminal Amine
70
Q

If there is a big difference between pKa of local anesthetic and physiologic pH, what form will be more common? (uncharged/charged)

A

Charged

71
Q

The (charged/uncharged) form of a local anesthetic can penetrate membranes

A

Uncharged

72
Q

Which structural part of a local anesthetic determines lipid solubility and potency?

A

Aromatic Ring

73
Q

Metabolism of Ester vs Amide Local Anesthetics:

A

Esters: metabolized by plasma enzymes

Amides: Metabolized by hepatic P450 enzymes

74
Q

How and where do local anesthetics bind intracellularly?

A
  • Reversibly

- Intracellular portion of Na channel

75
Q

High risk for CNS toxicity from which 2 Local Anesthetics?

A

Bupivacaine, Ropivacaine

76
Q

Which requires higher dose of Local Anesthetics: CNS or Cardio toxicity

A

Cardiotoxicity

77
Q

What is Transient Neurological Syndrome and which local anesthetics can cause it?

A
  • Severe transient pain from local anesthetic use in spinal anesthesia
  • Lidocaine, Procain, Mepivacaine
78
Q

Which group (ester or amide) of local anesthetics have high allergic reaction rates?

A

Esters – PABA metabolites = known allergen

79
Q

Which nerve fibers are first to be blocked by local anesthetics?

A
  • B and A delta

- Generally: smaller, myelinated nerves blocked first

80
Q

What are toxic side effects of Na+ channel blockers?

What is a side effect?

A

Toxicity = Dizzy, drunk, double vision

Side effect = 15% have rash, rare Steven Johnson syndrome

81
Q

What is a contraindication for Valproate? Why?

A

Pregnancy – 4-8% Teratogenic

82
Q

What drugs can be given for status epilepticus?

A

IV: Phenytoin, Lorazepam, Diazepam, Valproate

83
Q

Absence seizure.

What drug? Mechanism?

A

Ethosuxamide

- T-type thalamus Ca++ channel blocker

84
Q

Mechanisms for Anti-epileptics:

A
  1. Voltage-gated Na+ channel blockers
  2. Voltage-gated Ca++ channel blockers
  3. Glutamate receptor blockers
  4. GABA system agonists
85
Q

Difference between Felbamate and Topiramate

A 
Felbamate = NMDA blocker
Topiramate = AMPA and Kainate receptor blocker
86
Q

Difference between toxicity and side effect

A

Toxicity: Unwanted effect of drug

Side effect: unexpected effect, not related to mechanism of action

87
Q

Which anti-epileptic exhibits no metabolism?

A

Gabapentin

88
Q

What drug has synergistic action/competes with valproic acid

A

Lamotrigine

89
Q

Antiepileptic drug with “word finding” problem toxicity

A

Topiramate

90
Q

What is the Meyer-Overton Rule?

A

Potency of anesthetic gases directly related to their solubility in olive oil

91
Q

What is the gold standard drug for maintenance of general anesthesia?

A

Isoflurane

MQW U3 (11 decks)

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