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Flashcards in Module 2 Deck (48)
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1
Q

Nervous Systems consist of two main?

A

Central Nervous system and Peripheral Nervous System

2
Q

CNS

A

Central Nervous System - Brain and Spinal corde

3
Q

PNS

A

Peripheral Nervous System - Nerves outside CNS

4
Q

Within the PNS there is Efferent Division and Afferent Division. What is the difference between these nerves?

A

Efferent Division -signals FROM brain/spinal cord

Afferent Division- signals TO brain/spinal cord

5
Q

ANS

A

Autonomic Nervous System: Involuntary- acts largely unconsciously and regulates bodily functions such as the heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal.

6
Q

SNS

A

Somatic nervous system: voluntary portion of the peripheral nervous system -body movements via skeletal muscles. Consists of Efferent and Afferent signals

7
Q

ANS is made up of :
Sympathetic-
Parasympathetic-

A
  • Fight-or flight

- rest and digest

8
Q

How Nerves Transmit Signals

A

When receptors filled, signals transmitted down neuron after which process repeats itself when signal jumps from nerve to nerves. Receptors travel over the synaptic cleft to adjacent nerve endings.

9
Q

Neurotransmitter acetylcholine (ACH)

A

released from nerve ending into synaptic cleft(space between nerves). Function is to carry signals from motor neurons to the body’s skeletal muscles.

10
Q

After ACH travels across synaptic cleft they?

A

bind to receptors on adjacent neuron.

11
Q

After signal transmitted, ACH broken down by?

A

enzyme acetylcholinesterse (ACE) and recycled back into nerve ending for use in next transmission called “re-uptake”

12
Q

Cholinergic Drugs

A

para-sympathomimetic: Stimulate parasympathetic(rest and digest) action at muscarinic, nicotinic receptors. Various drugs that inhibit, enhance, or mimic the action of the neurotransmitter(ACH) of nerve impulses w/in PNS (contracts smooth muscles, dilates blood vessels, increase bodily secretions, and slows heart rate.

13
Q

Acetylcholine

A

neurotransmitter affected. ACH are chemical messages in the brain. Carries signals from motor neurons to the body’s skeletal muscles.

14
Q

Cholinergic agonist drugs

A

mimic action of acetylcholine

15
Q

Anti-cholinesterases

A

inhibit acetylcholine destruction at receptor sites. BLOCK ACH

16
Q

Cholinergic agonist drugs are used for:

A
  • increase bladder tone
  • treat GI distention (bloating and swelling in belly) and atony (loss of strength in a muscle)
  • Reduce eye pressure in glaucoma.
17
Q

Adverse Effects of Cholinergic agonist drugs

A

Cholinergic agonists bind PNS receptors ➡can produce adverse effect in any organ innervated(supplied) by parasympathetic nerves.

  • nausea, vomiting
  • cramps, diarrhea
  • blurred vision
  • decreased heart rate, low blood pressure
  • shortness of breath
  • urinary frequency
  • increased salivation/sweating
18
Q

anti-cholinesterase drugs (ACD) inhibit? Allowing?

A

acetyl-cholinesterase(ACE)

-ACH (acetylcholine) to accumulate in the synaptic cleft, prolonging its effect.

19
Q

2 categories of Anti-cholinesterases drugs:

  • Reversible
  • Irreversible
A
  • Short duration of action; minutes to hours

- long-lasting effects; days to weeks; used as toxic insecticies, pesticides, nerve gas.

20
Q

what are Anti-Cholinesterase drugs used for?

Antidote:

A
  • increase bladder, GI tone
  • Decrease eye pressure in glaucoma
  • Diagnose and promote muscle contraction in myasthenia gravis (weakness and rapid fatigue of muscles under voluntary control)
  • treat dimentia

-cholinergic blocking drugs

21
Q

Adverse Effects from Anti-cholinesterase drugs

A

increased astion of acetylcholine leading to

  • Cardiac arrhythmias
  • nausea, vomiting
  • Diarrhea
  • Shortness of breath, wheezing, tight chest
  • Seizures, headache
  • Anorexia
  • Insomnia
  • Pruritus
  • Urinary frequency, noturia
22
Q

Cholinergic blocking (anti-cholinergic) (cholinergic antagonist) drugs prevent?

A

acetycholine stimulating parasympathetic muscarinic receptors

23
Q

Paradoxical effect

A

can stimulate or depress, depending on doasge (when the opposite happens instead of intended reaction. (pain meds causing pain)

24
Q

Muscarine receptors

A

stimulated by muscarine (an alkaloid derived from mushrooms ) blocked by atropine, belladonna, hyoscyamine sulfate, scopolamine ( all antidotes for cholinergic and nati-cholinesterase drugs)

25
Q

Atropine uses

A

Blocks cholinergic activity on eye➡ mydriasis (dilation of pupil), lasts - 4 hrs.
Anti-spasmodic in GI system
Cardiovascular
-Low dose: decreases cardiac rate (bradycardia)
-High dose: increases cardiac rate (tachycardia)

26
Q

How Atropine works: Acetylcholine (ACH) stimulates ____ and ______ inhibiting ______➡heart rate ____Atropine competes with _____; low dose_____; high dose ______

A

sinoatrial (SA) and atrioventricular (AV) nodes, inhibiting conduction. Heart rate slows. Atropine competes with ACH. Low dose decreases heart rate; high dose increases heart rate.

27
Q

Adverse Effects of Atropine use

A

cholinergic blocker adverse effects related to dosage; little difference between therapeutic and toxic dose

  • dry mouth
  • reduced bronchial secretions
  • increased heart rate
  • decreased sweating
28
Q

Adrenergic (sympathomimetic) drugs

A

produce sympathetic effects at alpha, beta, dopamine receptors

29
Q

Neurotransmitters affected by Adrenergic drugs

A

Norepinephrine, epinephrine, dopamine

30
Q

2 types of Adrenergics:
-Catecholamines:
Synthetic Catecholamines have a-

-Non-catecholamines:

A
  • produced by the sympathetic nervous system; not taken orally as destroyed by digestive enzymes; excitatory or inhibitory response (norepinephrine, epinephrine, dopamine)
  • have shorter duration than natural (produced by body) catecholamines

-oral administration; longer duration of action

31
Q

Catecholamines
-Excitatory response:

  • Inhibitory response
    • Potent inotrope
      - Positive chronotropic effect
A

-at alpha receptors (except for intestinal relaxation). Neuron that triggers a positive change in the membrane

  • at beta receptors (except in heart cells)
    - makes heart contractions more forceful
    - causes heart to beat faster
32
Q

Adrenergics

A

working on adrenaline (epinephrine)

33
Q

Adrenergic Action

  • Direct-acting
  • Indirect -acting
  • Dual-acting
A
  • on target organ
  • trigger neurotransmitter release
  • works on target organ AND trigger neurotransmitter release
34
Q

Adrenergics Receptors

  • Alpha receptors
  • Beta receptors
  • Dopamine receptors
A
  • mimic norepinephrine (NOR)
  • mimic norepinephrine (NOR), epinephrine (EPI)
  • mimic dopamine
35
Q

Direct Acting Adrenergics

A

AD drug directly stimulates receptors without interaction with pre-synaptic neuron containing norepinephrine(no NOR is disturbed in presynaps). AD drug only connects to post-synaptic neuron

36
Q

Indirect Acting Adrenergics

A

AD drug stimulates release of norepinephrine (NOR) from pre-synaptic neuron, which then does the binding. AD releases the bodies NOR and this is the binding agent only (NOR

37
Q

Dual Acting Adrenergics

A

Adrenergic drug (AD) stimulates release of norepinephrine (NOR) and binds receptors. Both AD and NOR release and bind to post-synaptic neuron

38
Q

How are Adrenergic drugs used?

A
  • Increase low blood pressure
  • Restore heart rhythm
  • Improve breathing by dilating bronchioles
39
Q

Adverse Effects of Catecholamine

A

restlessness, anxiety, dizziness, headache, palpitations, cardia arrhythmia, hypo-tension, hypertension and hypertensive crisis, stroke, angina, increased blood glucose levels, tissue necrosis (if IV)

40
Q

Non-catecholamine adverse effects

A

headache, restlessness, anxiety or euphoria, irritability, trembling, drowsiness or insomnia, light-headedness, incoherence, seizures, hypertension or hypo-tension, palpitations, bradycardia or tachycardia, irregular heart rhythm, cardiac arrest, cerebral hemorrhage, tingling or coldness in arms or legs, pallor or flushing, angina

41
Q

Adrenergic Blocking Drugs

Classification by site of action:

A

(Sympatholytic) block sympathetic impulses at alpha and beta receptors (NOR and EPI affected)

  • alpha blockers
  • beta blockers
42
Q

Alpha blockers

A
  • occupy receptors on blood vessel
  • blood vessel wall relaxes➡ vessel dilates
  • Dilated vessels= decreased resistance to blood flow
  • decreases blood pressure
43
Q

Alpha Blocker Problem OH

A

Orthostatic hypotension: drop in blood pressure changing position from lying down to standing up; due to redistribution of blood to dialated vessels in legs

44
Q

Alpha blocker drugs are used to:

A
  • decrease hkypertension

- Increase local blood flow

45
Q

Alpha-adrenergic blocker adverse effects caused primarily by?
Symptoms?

A

dilation of blood vessels

  • orthostatic hypotension or severe hypertension
  • bradycardia(slow) or tachycardia(fast)
  • edema
  • difficultly breathing
  • light-headedness
  • flushing
  • arrhythmia, angina(chest pain from lack of blood flow), heart attack
  • spasm of blood vessels in breain
  • shock-like state
46
Q

Beta Blockers

Non-Selective:
2 types

Selective:

A

Occupy beta receptors blocking catecholamines (norepinephrine, epinephrine)

  • Beta1 receptors: in heart; reduce stimulation
  • Beta2 receptors: in bronchi, blood vessels, uterus; cause constriction

beta1 receptors

47
Q

How is a beta blocker used?

A
  • reduce blood pressure
  • reduce heart rate
  • decrease force of heart conractions
  • contrict bronchioles
  • contrict peripheral blood vessels
48
Q

Adverse Effects of Beta-blockers

A

These are drug or dose dependent

  • hypotension
  • bradycardia, peripheral vascular insufficiency, atrioventricular block, heart failure
  • fatigue
  • bronchospasm
  • diarrhea or constipation
  • nausea, vomiting, abdominal discomfort, anorexia, flatulence
  • rash
  • fever with sore throat, spasm or larynx, respiratory distress (allergic response)