Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > PNS Meds > Flashcards

PNS Meds Flashcards

1
Q

Recall how peripheral nervous system is classified

A

somatic nervous system: you control the movement

autonomic nervous system: involuntary, SNS and PSNS

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

Examples of processes controlled by ANS

A

blood pressure
heart rate & breathing
body temperature
balance of water and electrolytes
body fluids production (saliva, sweat, tears)
digestion
urination
defecation
sexual response

You do not need to control these process!

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

Tell which neurotransmitter binds to cholinergic receptors

A

Acetylcholine

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

Recall what neurotransmitters trigger an adrenergic receptor

A

Norepinephrine
Epinephrine
Dopamine

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

List the 3 subtypes of cholinergic receptor subtypes

A

Nicotinic N
Nicotinic M
Muscarinic

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

Describe what happens when a nicotinic N receptor is stimulated

A

Nicotinic N is found in the adrenal medulla
–> release epinephrine

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

Describe what happens when a nicotinic M receptor is stimulated

A

Nicotinic M is found in neuromuscular junction –> contraction of skeletal muscle

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

Recall the effects of muscarinic receptor actions throughout the body

A

Eyes: accommodation (ciliary muscle contraction) and pupil constriction

Heart: decreased rate
Lungs: bronchial constriction
GI tract: increased secretions and intestinal motility
Urinary bladder: increased pressure

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

List the 3 adrenergic receptor subtypes

A

Alpha 1, Beta 1, and Beta 2

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

Recall what happens when alpha 1 receptors are stimulated

A

Eye: pupil dilation
Arteries and veins: constriction
Male sex organs: constriction & ejaculation
Bladder: contraction of bladder and sphincter

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

Identify where beta 1 receptors are located

A

Heart: increased rate and FOC
Kideys: renin increase

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

Recall what happens when beta 2 receptors are stimulated

A

Arterioles: dilation (deliver more blood to heart, muscle, etc.)
Bronchi: dilation
Uterus: relaxation (slow down labor!)
Skeletal: increased contraction
Liver: glycogenolysis

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

Recall what neurotransmitter stimulates muscarinic receptors

A

Acetylcholine

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

Compare cholinergic and anticholinergic effects

A

Enhance the effects of Ach, increasing the actions of PSNS

Competitively block the effects of Ach, increasing SNS activity

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

Recite what occurs when the muscarinic receptors are activated by the cholinergic drug bethanechol

A

Bethanechol activates muscarinic receptors in the bladder!

increase bladder pressure, relaxation of smooth muscles and sphincter

Allows urine to leave the bladder –> commonly used in post-partum patients and patients with neurogenic atony of bladder

In short: relief of urinary retention

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

What groups of patients should be cautious with bethanechol

A

Bethanechol could enhances muscarinic receptors in other parts of the body

–> caution for patients with asthma, cardiac problems, peptic ulcers, or intestinal obstruction

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

Anticholinergic drugs are also known as…

A

parasympatholytic drugs

antimuscarinic drugs

muscarinic blockers

**anticholinergics block the actions of Ach at muscarinic receptors

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

Discuss the effects of atropine on the body

A

Atropine is an antagonist to muscarinic receptors

Recall that muscarinic receptors are located in eyes, heart, GI tract, lungs, urinary bladder.

Thus, its parasympatholytic effects include pupil dilation (mydriasis), increased HR, decreased saliva flow, open airways, decreased urinary activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

List 4 therapeutic indications for atropine

A
  1. bradycardia
  2. eye disorders
  3. preanesthetic
  4. muscarinic poisoning
20
Q

Describe the mechanism of action of the neuromuscular blockers (NMBs)

A

Neuromuscular blockers (NMBs) prevent Ach from activating nicotinic M receptors at the skeletal neuromuscular junction

–> cause skeletal muscle paralysis!
The patient no longer has control of skeletal muscles, which include the diaphragm.

21
Q

Recognize the rationale of using general anesthetics and/or analgesics with NMBs

A

Since NMBs do not affect CNS, the patient is fully awake and aware of pain.

–> general anesthetics and/or analgesics must also be given to the patient

22
Q

Describe the four important parts of neuromuscular junction

A
  1. Axon
  2. Motor-end-plate
  3. Muscle fiber (tubular cell called a myocyte)
  4. Myofibril

If we take a closer look…
- presynaptic terminal
- synaptic vesicles (store NTMs)
- sarcolemma
- nicotinic M receptors
- mitochondrion (cell’s powerhouse, producing ATP)

23
Q

Describe the rationale of using sedation with neuromuscular blockers (NMBs)

A

Sedation is ALWAYS used with NMBs to decrease the anxiety that would come from a person being totally paralyzed while still awake.

24
Q

List 3 common indications when paralysis with NMBs is used

A
  1. surgery
  2. endotracheal intubation
  3. mechanical ventilation
25
Q

Explain the healing benefits of paralysis with intubation

A
  • NMBs eliminate the gag reflex when being intubated
  • Patients feel uncomfortable being intubated (it makes them feel air hungry)
  • When patients are critically ill, they will not waste energy they need to heal on “fighting” the mechanical ventilator
26
Q

Specify the route of administration of neuromuscular blockers (NMBs)

A

Must be given IV

NMBs cannot cross blood brain barrier –: no impact on CNS (paralysis, not sedation)

It cannot cross placenta either, minimal effects on a fetus

27
Q

Identify the pharmacologic effects of NMBs in the skeletal muscles and the central nervous system (CNS)

A
  • leads to severe muscle relaxation (aka flaccid paralysis)
  • no impact on CNS
28
Q

List 2 life-threatening adverse effects of NMBs

A
  1. respiratory arrest
  2. cardiovascular effects (hypotension)
29
Q

Recite the 2 types of NMBs

A
  1. competitive NMBs (aka non-depolarizing NMBs)
  2. depolarizing NMBs
30
Q

What are the characteristics of competitive NMBs?

A

The onset of paralysis is quick, but it takes 20-45 min to reach the peak and then decline gradually. It takes 1 hour for the complete recovery.

Competitive NMBs are used for longer procedures.

31
Q

What are the characteristics of depolarizing NMBs?

A

The onset of paralysis is quick, and its effect is ultrashort-acting. It reaches the peak after 1 min and fades after 4-10 minutes.

32
Q

5 examples of competitive NMBs

A

Atracurium
Cisatracurium
Pancuronium
Rocuronium
Vecuronium

they end in “-ium”

33
Q

Which competitive NMBs are good choice for patients with renal/hepatic dysfunction?

What is the risk factor?

A

Atracurium and Cisatracurium

They have the risk of hypotension due to histamine release (histamine cause peripheral vasodilation)

Atracurium: cholinesterase in plasma break it down
CIsatracurium: spontaneous degradation

34
Q

Which competitive NMBs have no risk of hypotension?

A

Pancuronium: excreted through urine, may produce tachycardia

Rocuronium: eliminated by hepatic metabolism

Vecuronium: excreted in the bile

35
Q

Example of depolarizing NMB

A

Succinylcholine

36
Q

Describe the mechanism of action of succinylcholine

A

Succinylcholine binds to Ach receptors and cause a prolonged (delayed) depolarization of motor-end-plate

–> results in flaccid paralysis of skeletal muscle

37
Q

Specify the indication for succinylcholine

A

used for muscle relaxation during intubation

38
Q

What would happen when pt has low pseudocholinesterase activity and receives succs?

A

No rapid succinylcholine degradation
–> paralysis may last for hours!

***Pseudocholinesterase is a plasma enzyme produced in the liver that is responsible for the metabolism of the common anesthesia drugs, succinylcholine, and mivacurium, as well as ester local anesthetics

39
Q

Describe postoperative myalgia due to succinylcholine

A

Pt may develop muscle pain in neck, shoulders, and back within 12-24 hours after surgery, due to muscle contractions

(the exact cause is unknown)

40
Q

What electrolyte imbalance may happen with succinylcholine?

A

Hyperkalemia

Succs promote the release of K from tissues.

41
Q

Identify patients in whom significant hyperkalemia is most likely to occur with succinylcholine

A

Hyperkalemia is rare, but could be life-threatening.

Most likely to occur in patients with major burns, multiple trauma, denervation of skeletal muscle, or upper motor neuron injury.

42
Q

Recite the life-threatening adverse effect of succinylcholine

A

malignant hyperthermia (severe reaction to certain drugs used for anesthesia)

43
Q

List 6 clinical features of malignant hyperthermia

A
  • muscle rigidity
  • elevated temperature
  • cardiac dysrhythmias
  • unstable blood pressure
  • electrolyte imbalance
  • metabolic acidosis
44
Q

Describe the treatment of malignant hyperthermia

A
  • immediately discontinue succinylcholine
  • lower body temp (ice packs & cold saline infusion)
  • administer IV dantrolene
45
Q

Describe the mechanism of dantrolene

A

Dantrolene is a direct-acting skeletal muscle relaxant. It reduces the metabolic activity of skeletal muscle –> reduction of high fever and muscle rigidity

46
Q

Compare pros & cons of dantrolene

A
  • treats malignant hyperthermia & NMS and effect is reported withing minutes of administration
  • has a risk of hepatotoxicity
47
Q

List 2 drug classes that interact with succinylcholine

A

cholinesterase inhibitors (result in more intense effects)

some antibiotics (aminoglycosides, tetracyclines, etc. can intensify the succs effect)

Pharmacology (20 decks)

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