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Fall Pharm Block 1 > ANS and Essentials > Flashcards

ANS and Essentials Flashcards

1
Q

What is the preganglionic NT of the ANS?

A

Acetylcholine (Ach)

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2
Q

What are the postganglionic NTs of the ANS?

A

Symathetic: Epi and Norepi
Parasympathetic: Ach

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3
Q

Acetylcholine is deactivating in most parts of the body. The exceptions where Ach is activating are…

A

Gut, kidney, and CNS

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4
Q

A drug that blocks Ach has what affect on CNS?

A

Sedating - Benadryl is an ex.

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5
Q

List the effects of PNS stimulation.

A

Bradycardia, HypoTN, Miosis (constricted pupil), inc blood to skin and viscera, inc peristalsis, inc excretion and salivation

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6
Q

List the effects of SNS stimulation.

A

Tachycardia, HTN, mydriasis (pupil dilation), bronchodilation, inc glucose production in liver, inc blood to skeletal muscles, brain, and heart.

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7
Q

What is the NT of skeletal and smooth muscle?

A

Ach –> paralytics block Ach

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8
Q

List the SNS receptors and their locations and effects.

A 
A1: vasculature
A2: n/a for this class
B1: heart
B2: lungs and vasculature
Alpha constricts and beta dilates
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9
Q

Which receptors do epi and norepi bind to and what is the clinical result?

A

Epi: A1, A2, B1, B2
Norepi: A1, A2, B1
Clinical: Norepi is a more potent vasopressor and provides no bronchodilation

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10
Q

Give an example of a receptor that has different effects in different locations.

A

5-HT

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11
Q

Give an example of a substance that acts differently based on its location and concentration.

A

Interleukins and cytokines

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12
Q

What is the composition of urea and how and where is it made?

A

Urea is made of 2 amines (NH3) and one ketone (C=O). Amino acids are broken down into ammonia which is converted to urea in the liver.

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13
Q

What causes hepatic encephalopathy in hepatitis.

A

Failing liver can’t make ammonia into urea. Ammonia crosses the blood-brain barrier.

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14
Q

Differentiate viruses from bacteria in terms of their replication.

A

Viruses: replicate intracellularly
Bacteria: replicate extracellularly

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15
Q

List the hierarchy of vaccine types from best to worst.

A

Live vaccines > dead vaccines > conjugate vaccines (weak antigen + strong antigen) > toxoids (based on toxin produced by a bacterium)

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16
Q

What is the effect of aldosterone on Na and K?

A

Aldosterone loves Na and hates K –> retain Na and excrete K.

17
Q

What is meant by saying a drug is “dirty” and is that a positive or negative effect?

A

Dirty = drug does more than you want it to. Can be positive or negative –> Lots of side effects but TCAs = antidepressant used to treat insomnia.

18
Q

What is the effect if GABA?

A

GABA is an inhibitory NT –> causes sedation

19
Q

How are dopamine (DA) and Ach levels in the CNS related.

A

Balanced –> if DA increases, Ach decreases and if Ach increases, Da decreases.

20
Q

What diseases result from too much and too little DA?

A

Too much DA = schizophrenia
Too little DA = Parkinson’s
Can have both diseases as they occur in different parts of the brain.

21
Q

What are the precursors to epi and norepi synthesis?

A

phenylalanine and tyrosine

22
Q

What is the precursor for 5-HT (serotonin) synthesis and what is its effect?

A

L-tryptophan –> makes you tired

23
Q

What is the precursor for DA and what is the difference between this precursor and DA?

A

L-dopa –> crosses blood-brain barrier but DA does not.

24
Q

What is the precursor for GABA synthesis?

A

Glutamate

25
Q

Differentiate Addison’s disease from Cushing’s Disease.

A

Addison’s: too little steroid

Cushing’s: too much steroid

26
Q

What are the types of monoamines?

A

DA, norepi, epi, 5-HT, melatonin

27
Q

What enzyme chews up monoamines?

A

Monoamine oxidase (MAO)

28
Q

What enzyme chews up Ach?

A

Acetylcholinesterase

29
Q

What is the specific effect of nerve gasses and insecticides?

A

They are irreversible acetylcholinesterase inhibitors. Drugs we use are reversible inhibitors.

30
Q

In addition to enzyme breakdown, what other way do neurons regulate NT levels?

A

Recycling: reuptake (pulls it in) then pumps it back out

31
Q

What is the precursor to prostaglandins (PGs) and leukotrienes

A

Arachadonic acid

32
Q

What is used to make PGs from their precursor?

A

COX-1 and COX-2

33
Q

How do NSAIDs have their effect?

A

Inhibit COX-1 and COX-2 to dec pain and inflam.

34
Q

How do steroids have their effect?

A

Inhibit formation of arachadonic acid.

35
Q

What is the effect of PGs and angiotensin-2 (AG-2) in the kidneys?

A

PG: dilate afferent arteriole

AG-2: constricts the efferent arteriole

Fall Pharm Block 1 (6 decks)

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