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Human Disease and Therapeutics > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Neuronal cell body

A

Perikaryon (controls cells)

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2
Q

Excitatory neurotransmitter

A

Glutamate

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3
Q

Inhibitory neurotransmitter

A

GABA (gamma aminobutyric acid)

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4
Q

How does direct action work?

A

Neurotransmitter binds to and opens ion channels

Rapid response by altering membrane potential

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5
Q

How does indirect action work?

A

Binds to G protein and caused and indirect response through secondary messengers
Broader actions with longer lasting effects

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6
Q

What is another name for a ligand gated ion channel?

A

ionotropic

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7
Q

What is a metabotropic receptor?

A

Usually a G protein and have long term effects. There are membrane-delimited (all reaction occur in membrane) and Second messenger ones that require intracellular second messengers

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8
Q

What is an autoreceptor?

A

It is when there is a receptor on the never terminal that binds the neurotransmitter that is released (usually a negative feedback)

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9
Q

What is a heteroreceptor?

A

Receptor on other axon terminals through which neurotransmitters from other neuronal types can influence their function

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10
Q

What make the nerve terminal for acetylcholine unique?

A

There is not acetylcholine transporter (has to return as choline) and uses acetylcholine esterases

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11
Q

What do endorphins bind to?

A

m-opioid receptors that inhibit GABA release causing more excitation

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12
Q

In the autonomic nervous system, how many nerves are used?

A

2, a pre-ganglionic and post-ganglionic

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13
Q

All pre-ganglionic nerves use this neurotransmitter and bind to this type of receptor?

A

ACh and nicotinic

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14
Q

Where do sympathetic nerves originate?

A

Thoracolumbar spine

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15
Q

Where do parasympathetic nerves originate?

A

craniosacral

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16
Q

What is unique about the adrenal medulla?

A

It is directly innervated by the pre-ganglionic nerve and causes release of NE and Epi

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17
Q

Where do parasympathetic pre-ganglionic nerves go?

A

To the ganglia that is closest to the effector organs/tissues

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18
Q

Motor neurons use what neurotransmitter and bind to what type of receptor?

A

ACh and Nicotinic

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19
Q

DA activates what receptors?

A

D1-D5 and alpha and beta adrenergic

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20
Q

What is a seizure?

A

a finite clinical manifestation of abnormal & excessive excitation of a population of cortical neurons

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21
Q

What is epilepsy?

A

syndrome characterized by chronic, recurrent seizures unprovoked by systemic or neurologic insults
3 unprovoked seizures=epilepsy

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22
Q

What is epileptogenesis?

A

sequence of events that converts a normal

neuronal network into a hyperexcitable network

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23
Q

Life time prevalence of seizures?

A

9-10% of the population

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24
Q

Prevalence of epilepsy?

A

1%

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25
Q

What is the biggest inherited cause of epilepsy?

A

Ion channel issues

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26
Q

What is the fastest growing cause of acquired reasons for epilepsy?

A

Trauma

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27
Q

What are common seizure precipitants?

A 
Metabolic and/or Electrolyte Imbalance
Stimulant or other pro-convulsant intoxication
Sedative or ethanol withdrawal
Sleep deprivation
Reduction or inadequate ASD treatment
Hormonal variations
Stress
Fever or systemic infection
Concussion and/or closed head injury
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28
Q

Who is at most risk of getting epilepsy?

A

The young and the old

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29
Q

What is the common cause of epilepsy among all ages?

A

status epilepticus, a seizure lasting longer than 3 minutes

30
Q

Simple partial seizure

A

Localized
Minimal spread
Normal awareness, memory and consciousness
Short duration
Could be different areas of the cortex that are involved

31
Q

Complex partial seizure

A

Localized onset but spreads
awareness, memory, and/or consciousness are lost during seizure
short duration

32
Q

Secondarily generalized seizure

A

begin as partial but end as generalized. tonic (stiffening) and clonic (jerking) phases and postictal phase

33
Q

Another name for tonic-clonic seizure?

A

grand-mal

34
Q

Another name for absence seizure?

A

petit-mal

35
Q

What is characteristic of an absence seizure?

A

spike wave pattern

36
Q

Are grand-mals synchronized or asynchronized?

A

Synchronized

37
Q

Ideal ASD?

A

Effective for the Seizure Type Wide therapeutic index
No organ toxicity
No teratogenicity
No drug-drug interactions Long half-life (t1/2)
No protein binding
Water soluble (easily absorbed) No active metabolites

38
Q

What is the biggest difference between old and new ASDs?

A

newer drugs have fewer drug enzyme interactions

39
Q

What are the three main mechanisms for ASDs?

A

1-increase inhibition
2-reduce excitation
3-modulate inhibition and/or excitation

40
Q

Carbamazepine

A

Used for all types of seizures
May cause steven-johnson’s syndrome
May cause increased absence seizures
Block use-dependent voltage gated ion channels Na+ to stop re-firing of neurons

41
Q

What are the dietary concerns with grapefruit?

A

They causes an increase in carbamazepine levels because they block the enzyme that metabolizes it

42
Q

Ethosuximide

A

only drug that focuses on absence seizures

reduces t-type Ca 2+ channel currents

43
Q

Phenobarbitol

A 
All types of seizures
cheap
long term cognitive, memory, and behavior effects
Big time INDUCER
may cause absence seizures
44
Q

Phenytoin

A

all types
gingival hyperplasia
zero order kinetics at high doses
Block use-dependent voltage gated ion channels Na+ to stop re-firing of neurons

45
Q

Topiramate

A

all types
Weight loss
inc. metabolism of estrogen
word-finding difficulty

46
Q

Valproic acid

A 
all types
weight gain
reye-like syndrome, hepatic failure
don't give if pt has liver issues
neural tube defects (spina bifida)
47
Q

What are the two types of parasympathetic receptors?

A

Nicotinic and muscarinic

48
Q

Muscarinic agonists, functions, antagonists?

A

Agonists-ACh, bethanechol, pilocarpine
Function-rest and digest
Antagonists-atropine, scopolamine

49
Q

What are the 2 nicotinic receptors?

A

Muscle and Neuronal

50
Q

Nicotinic (muscle) agonist, function, and antagonist?

A

Agonist-ACh
Function-neuromuscular junction
Antagonist-succinylcholine

51
Q

Nicotinic (neuronal) agonist, function, and antagonist?

A

Agonist-ACh
Function-autonomic ganglia, adrenal medulla, CNS
Antagonist-mecamylamine

52
Q

What are the two classes of neuromuscular blockers?

A

Depolarizing-succinylcholine, depolarized neuron making it so it cannot react to further signals
Non-depolarizing-competes with ACh

53
Q

3 cholinesterase inhibitors

A

physostigmine-short duration, used for glaucoma antidote for atropine
Donepezil-used for Alzheimer’s
Sarin-nerve gas

54
Q

What does botulinum toxin do?

A

Prevent release of ACh

55
Q

What cholinergic drugs are used in dentistry?

A

Cevimeline-xerostomia in Sjogren’s

Pilocarpine-xerostomia in radiotherapy

56
Q

Alpha 1 receptors

A 
Agonist-Epi>NE, phenylephrine
Tissues and actions
-radial muscle of iris/dilates pupil
-GU and GI sphincters/contract
-Vasculature/Contracts
Antagonist-prazosin
57
Q

Alpha 2 receptors

A 
Agonist-Epi>NE, clonidine, guanfacine
Tissues and actions
-Vasculature/Contracts
-NE terminals/decrease NE release
-Brainstem/decrease NE release
58
Q

If a drug ends in -olol what is it?

A

Beta blocker

59
Q

Beta 1 receptors?

A

Agonist-Epi=NE, isoproterenol
Tissue and action
-Heart/everything increases
Antagonists-propranolol

60
Q

Beta 2 receptors?

A

Agonists-Epi»»NE, isproterenol, albuterol, and terbutaline
Tissue and actions
-Ciliary muscle of eye/ relaxation for far vision
-vasculature/relaxation/dilation of skeletal muscle vasculature
-lung smooth muscle/relaxation
-bladder and uterine wall/relaxation
Antagonists-propranolol

61
Q

What happen in the liver under adrenergic stimulation of Beta 2 and Alpha receptors?

A

Gluconeogenesis and glycogenolysis

62
Q

D1 receptors?

A

Agonist-DA and fenoldapam
Tissue and action
-Kidney/increase blood flow, increase GFR, and sodium excretion
-vasculature and heart/vasodilation

63
Q

D2 receptors?

A

Agonist-DA
Tissues and actions
-DA nerve terminals/negative feeback
-chemoreceptor trigger zone/nausea and vomiting

64
Q

Barorecetors do what?

A

Maintain BP

65
Q

Depending on the speed that Epi is given and the dose what happens?

A

Slow dose not much, increase HR and decrease TPR

High dose-more alphas get involved so increased HR and increased TPR

66
Q

What does Epi do to the eye?

A

dilates pupil (mydriasis)

67
Q

How can pilocarpine be used to treat glaucoma?

A

acts on muscarinic receptors on iris sphincter muscle causing them to contract, also causes ciliary muscles to contract opening the trabecular meshwork through increased tension. This facilitates fluid flow decreasing the pressure.

68
Q

What are the mixed adrenergic drugs?

A

ephedrine, ephedra, and pseudoephedrine

uses as decongestants and dietary supplements

69
Q

How do indirect adrenergic drugs (Amphetamines, cocaine, methylphenidate, SSRIs, TCA,s) work?

A

Block re-uptake of DA

70
Q

What can food with tyramine do if taking an MAO inhibitor?

A

if taking an MAO inhibitor it gets into the blood stream and gets into nerve terminals and displaces NE

71
Q

Non-selective alpha antagonists?

A

phenoxybenzamine, phentolamine

Orthostatic hypotension

72
Q

What is tamsulosin?

A

Flomax, benign prostatic hypertrophy

alpha 1 antagonist

Human Disease and Therapeutics (4 decks)

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