Basis Of Pharmacology Flashcards

1
Q

2 general divisions of nervous system

A

CNS

PNS

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2
Q

Divisions of PNS

A

Autonomic
Somatic
Enteric

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3
Q

Divsions of CNS

A

Brain

Spinal cord

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4
Q

Functions of frontal lobe

A
Personality 
Concentration 
Memory 
Judgement 
Abstract thoughts 
Motor function 
Motor control of speech
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5
Q

What results can happen if frontal lobe damaged

A
No expression of language 
Motor weakness
Personality changes
Behavorial changes 
Cant plan sequence of complex movements
Cant focus
Cant do tasks
Cant problem solve
Mood changes
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6
Q

Functions of parietal lobe

A

Coordination of sensory informatioon
Analysis and interpretation of sensory information
Centre for memory
Spatial awareness

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7
Q

Results of damage to parietal lobe

A
Anomia 
Agraphia 
Cant read or draw objects 
Cant differentiate left or right
Mathematics difficulties
Loss of spatial awareness 
Eye and hand coordination loss
Visual field deficitis
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8
Q

Occipital lobes functions

A

Visual interpretations

Perception of retina signal s

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9
Q

Results of damage to occipitla lobe

A
Visual agnosia 
Visual field deficits
Cnt locate objects in visual fields 
Visual hallucinations 
Word blindness
Reading, writing, recognizing objects difficulties
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10
Q

Functions of temporal lobes

A

Auditory receptive areas

Interpretation of visual, auditoru , and somatic integration

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11
Q

Temporal lobe damage can lead to

A
Auditory hallucinations 
Prosopagnosia
Wernickes aphasia 
Short term memory loss
Personality changes 
Can identify and verbalize seen objects
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12
Q

Thalamus functions

A

Alertness

Sensations

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13
Q

Hypothalamus functions

A
Hormones regulation 
Fluid balance 
Sleep wake cycle 
Blood pressure regulation 
Emotional responses 
Temperature rgulation 
ANS regulation
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14
Q

Damage to hypothalamus leads to

A

Diabetes insipidus

Temperature control loss

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15
Q

Pons functions

A

Heart
Respiration
Blood pressure

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16
Q

Damage to pons lead to

A
Facial sensation loss
Corneal reflex loss
Facial muscle droopimng
Cant gaze outwards
Corneal reflex loss
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17
Q

Midbrain functions

A

Auditory reflex

Visual reflexes

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18
Q

Midbrain damages lead top

A

Ptosis
Diplopia
Dilated pupils
Cant gaze up down or inward

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19
Q

Medulla oblongata functions

A

Connects brain and spinal cors with sensory and motor fibers

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20
Q

Medulla oblongata damage lead to

A
Cant swallow
Loss of gag and cough reflex
Vomiting 
Tongue protrusion 
Respiratory pattern changes
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21
Q

Cerebellum functions

A

Coordination of movements
Controls balance, posture, muscle tone, awareness
Cognitive functions like attenttion, language, emotion

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22
Q

Cerebellum damage lead to

A
Disturbed gait and walking 
Impaired balance 
Incoordination 
Cant reach out and grab objevts\
Dizziness 
Vertigo
Slurred speech 
Cant make rapid movements
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23
Q

2 major cells classes

A

Neurons

Neuroglial cells

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24
Q

Neuroglial cells

A

Astrocytes
Oligodendrocytes
Ependymal cells
Microglia

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25
Q

Neurons functions

A

Excitation

Nerve impulse conductions

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26
Q

Amount of neurons in the brian

A

About 100 billion neurons

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27
Q

Astrocytes function

A
BBB integrity 
Take up, store, release some neurotransmitter 
Remove and disperse excessive ion 
Neuronal guidance 
Presenting antigen to immune system
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28
Q

Most common clinical disorder with astrocytes

A

Astrocytomas - tumors

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29
Q

Oligodendrocytes functions

A

Myelination of CNS neurons

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30
Q

Clinical disorders of oligodendrocytes

A

Multiple sclerosis

Oligodendroglioma

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31
Q

Schwann cells functions

A

myelination of peripheral nerves

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32
Q

Schwann cells disorders

A

Benign tumor - schwannomas ( loss of tumor supressor gene neurofibromin)
Leucodystrophies

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33
Q

Microglia functions

A

Macrophages of brain

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34
Q

Neuroglia that cause inflammation seen in parkinsons disease

A

Microglia

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35
Q

Ependymal cells functions

A

Movement of CSF

Line central canal in spinal cord

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36
Q

enzyme responsible for transferring acetyl-coa to choline

A

Choline acetyltransferase

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37
Q

Origin of choline

A

Blood and synthetized in the liver by methylation of ethanolamine by decarboxylation of serine

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38
Q

Enzyme that terminates cholinergic signal

A

Acetylcholine esterase

39
Q

2 receptor types for cholinergic signaling

A

Muscarinic

Nicotinic

40
Q

Type of muscarinc receptors

A
M1
M2
M3
M4
M5
41
Q

M1 rceptors found in

A

CNS specially Cortex and hippocampus

42
Q

Decrease in function or density of M1 receptor linked to

A

Dementia

43
Q

M2 receptors specialized for which type of cell

A

Cardiac cells

44
Q

Action of M2 receptors

A

Inhibitory response Gi protein

Activates K channels

45
Q

M3 receptors found in

A

Exocrine glands

Smooth muscles in GIT and organs

46
Q

M4 receptor action

A

Inhibition , activate K+ channels

47
Q

M5 receptors function

A

Excitatory

48
Q

Nicotinic receptors function

A

Ionotropic receptors

Open cation channel

49
Q

2 types of nicotinic receptors

A

Muscular

Neuronal

50
Q

3 ways neurotransmitters are cleared at synapse

A

1- reuptake
2- breadown and eventual reuptake of part of products
3- destruction by glial cells

51
Q

2 types of postsynaptic receptors

A

Receptor directly linked to ion channel

Receptor linked to GPCR which lead to activation and modulation of iom channel

52
Q

Acetylcholine released by

A

Neurons in voluntary muscles for contraction

Neurons that control Heartbeats

53
Q

Where do you find muscular nicotinic receptors

A

In the neuromuscular junction

54
Q

Where do you find the meuronal nicotinic receptors

A

In the post synaptic terminal in autonomic ganglia

55
Q

Type of neuron involved in short term memory consolidation

A

Cholinergic neuron

56
Q

type of neuron that is found in tegmétum of brainstem which lowers portion of the central nervous system affecting arousal sleep cycle and initiation of REM sleep phase

A

Cholinergic neurons

57
Q

Disease caused by blocking of nicotinic acetylcholine receptors by antibodies

A

Myasthenia gravis

58
Q

Symptoms of myasthenia gravis

A
Fatigue 
muscle weakness 
Eyelid and mouth drooping 
difficulty swallowing 
double vision 
unsteady walk
59
Q

What type of neuron is dying in alzheimer patient

A

Ach releasing neuron

60
Q

Main drugs action in treating Alzheimer’s disease

A

Drugs that inhibits acetylcholinesterase and increases acetylcholine in the brain

61
Q

Example of drugs that’s inhibit acetylcholinesterase

A

Donepezil

Rivastigmine

62
Q

What are some examples of drugs that’s our acetylcholinesterase inhibitors and are very toxic

A

Organophosphates (Chlorpyrifos parathion diazinon)

63
Q

Example of organophosphate used as nerve gases

A

Sarin
Tabun
VX

64
Q

What is the main accidentally neurotransmitter in the central nervous system

A

Glutamate

65
Q

What is the main function of ultimate in the central nervous system

A

Synaptic plasticity with the removal of old unused synapse and potentiation and formation of new synapse

66
Q

What prevents the glutamate from traversing from blood to the brain

A

Blood brain barrier

67
Q

Precursor molecule of glutamate

A

Glutamine

68
Q

Where is glutamate formed

A

In the astrocytes and then transported into

69
Q

Explain the glutamate cycle neuron astrocytes

A

Glutamate Is released in the synaptic cleft
small part of glutamate taken up by presynaptic neuron
most of the glutamate enter astrocytes by EAAT1 and EAAT2 transporters
Glutamate transforms into glutamine by glutamine synthetase inside astrocytes which requires ATP and ammonia
Glutamine exported interneuron which complete cycle

70
Q

Regarding glutamate synthesis What happens when there’s too much ammonia

A

LIVER ENCEPHALOPATHY

Ammonia crosses BBB and transfrom glutamate to glutamine so decreased ATP and glutamate and GABA dysregulation

71
Q

What are the types of glutamate receptors

A

AMPA receptors
NDMA Receptors
Kainate receptors
Metabotropic receptors

72
Q

Ampa receptor action

A

Ligand gated ion channel that allow influx of calcium and sodium
Efflux of potassium

73
Q

NMDA receptor action

A

Ionotropic receptor

74
Q

major inhibitory neurotransmitter

A

GABA

75
Q

GABA synthesis

A

Glutamate to GABA By glutamate decarboxylase

76
Q

Types of GABA Receptors

A

GABA a
GABA b
GABA c

77
Q

GABA A RECEPTOR ACTION

A

Chloride influx

78
Q

GABA B receptor action

A

Gi protein Inhibit adenylate cyclase
Increase potassium permeability
Less calcium activity

79
Q

Gaba c receptors action

A

Ionotropic receptor

Connected to chloride channel

80
Q

Types of catecholamines

A

Noradrenaline
Adrenaline
Dopamine

81
Q

Catechomines are derived from this AA

A

Tyrosine

82
Q

Catecholamines formation pathway

A

Tyrosine Ring hydroxylation -> dopa
Dopa decarboxylation -> dopamine
Dopamine hydroxylation -> norepinephrione
NE methylation -> epinephrine

83
Q

What competitive inhibitor act on dopa decarboxylase

A

Alpha methyldopa

84
Q

What is the link netween parkinsons disease and catecholamine

A

Insufficient formation of dopaine in the brain

85
Q

What is L dopa a good a good treatment for parkinsons disease

A

Because can cross BBB

86
Q

2 enzymes involved in inactivation of catecholamines

A

COMT

MOA

87
Q

MAO inhibitors are used in the treatment of

A

Depression

88
Q

Subtypes of adrenergic receptors

A

A1
A2
B1
B2

89
Q

A1 receptor action

A

Postsynaptic neuron

Excitatory action of NE

90
Q

A2 receptor action

A

Presynaptic neuron

Inhibitory effect of NE

91
Q

B1 receptor action

A

Neuronal receptor with excitatory effects

92
Q

B2 receptor action

A

Integration of nervous and immune system

93
Q

Alpha 2 agonist used as veretinary anelgesic

A

Medetomidine