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princip, pharm, phys, regional > pharm-ponv > Flashcards

pharm-ponv Flashcards

1
Q

who is high risk for ponv?

A
  1. females
  2. Fatties (obese)
  3. full stomach/ fatty foods
  4. history of PONV
  5. motion sickness, migraine
  6. anxiety
  7. use of post op opiates
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2
Q

who is least at risk for PONV

A

smokers

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3
Q

young,girls, non smoker, use of post op opiates has a___% chance of ponv

A

50%

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4
Q

what procedures have higher risk?

A
  1. craniotomy
  2. strabismus repair
  3. ENT/ T&A
  4. orthopedic shoulder repair
  5. certain cosmetic procedures (chest augmentation)
  6. intra-abdominal
  7. Laparoscopic procedures
  8. heria repair (especially under spinal) .
  9. GYN procedures
  10. orchiopexy
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5
Q

what does surgery length do to incidence of PONV

A

longer=more risk

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6
Q

rank the iatrogenic PONV causers (in order of highest incidence to lowest)

  • regional
  • gas/opiates
  • SAB
A
  1. general (gas and opiates)
  2. SAB
  3. regional
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7
Q

what drugs increase chance of PONV

A
  1. opiates (balanced anesthesia)
  2. nitrous
  3. ketamine
  4. anticholinesterases
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8
Q
  1. what conditons increase PONV

2. how does the treatment of this cause PONV

A
  1. pain can cause PONV

2. opiates to treat pain trigger the CRTZ in the brain and cause nausea (very important fact)

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9
Q

what 5 other conditions cause PONV?

A
  1. hypotension (including orthostatic) /dehydraton
  2. hypoxia
  3. hypoglycemia
  4. movement (thru vestibular stimulation)
  5. oral intake too soon after procedure
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10
Q

what are the 3 acts of vomiting?

A

nausea
retching
vomiting

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11
Q

nausea

A

typically associated with decreased gastric motility and increased small intestine tone and reverse peristalsis in small intestine

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12
Q

retching:

A

“dry heaves”, spasmodic respiratory movements conducted with closed glottis causing herination of abdominal esophagus into thoracid cavity due to negative pressure (due to resp effort with glottis closed)

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13
Q

vomiting (phase 1)

A

when gastric and small intestinal contents are expelled
1. deep breath; glottis closes; larynx raises and opens upper esophageal sphincter; soft palate raises to close off posterior nares

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14
Q

vomiting phase 2

A

diaphragm contracts sharply downward; creates neg pressure in thorax which opens esophagus and distal esophageal sphincter

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15
Q

vomiting (phase 3)

A

simultaneous downward movement of diaphragm and contraction of abdomen walls squeezes the stomach elevating intragastric pressure. pylorus is closed and esophagus is open, vomit is expelled.

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16
Q

who is at risk for PONV?

A
  1. children and adolescents
  2. women (d/t gonadotropin and estrogen)
  3. history of PONV
  4. non smokers
  5. anxious persons/ anxiety
  6. obesity (d/t larger gastrc volume, higher chance of reflux, amount of fat soluble drugs accumulated, and gall bladder/gi disease
  7. Oral Intake: excess fatty foods (slows peristalsis), full stomach, currently intoxicated
  8. use of post op opiates
  9. history of motion sickness
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17
Q

can nauser be triggered from multiple things at once?

A

yes

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18
Q

what can stimulation of pharynx cause

A

N/V (ilicits emetic resopnse)

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19
Q

why does car/ motion sickness occur

A

labyrinthine (vestibular) apparats and auricular branch of the tympanum of the ear detects motion stimulus from histhamine or ACH receptors

20
Q
  1. what is the name of the receptors that detect overdistention and altered gastric motility which can lead to N/V?
  2. In what organs of the abdomen are they located?
A
  1. mechanoreceptors

2. bladder, gall bladder, uterus

21
Q
  1. where are chemical stimulus detectors located in the abdomen?
  2. what do they sense?
A
  1. hepatic portal vein detectors

2. cheicals in the venous drainage of gut

22
Q

gastric and duodenal chemoreceptors detect what?

A

irritation from toxins such as serotonin

23
Q

what nerve sends signals regarding nausea to the brain?

A

vagus

24
Q
  1. vagus nerve from gut sends signal to ___,___ & ___ receptors in brain?
  2. what is the name of these areas of the brain?
A
  1. histhamine, cholinergic or enkephalin receptors

2. nucleus tractus solitarius; area postrema and subpostrema

25
Q

what parts of the brain are affected by emotions, sights, smells or thoughts?

A

higher brain centers in the cortex and limbic system

26
Q
  1. where is the chemoreceptor trigger zone (CRTZ , CTZ),

2. what does it do?

A
  1. located in the area postrema on the floor of the fourth ventricle of brain;
  2. identify absorbed toxins, or disturbances (hypotension and metabolic acid-base changes)which is reflected as nausea and vomiting
27
Q

what must coordinate in order for vomiting to occur?

A

afferent stimuli detect the need to vomit and coordinate the response in the vomiting center in the lateral reticular formation of the brainstem close to foruth ventricle.

28
Q

what are the receptors that have a role in receiving emetic impulses?

A

histhamine, serotonin, opiod, muscarenic, and dopaminergic

29
Q

how do antihisthamines block nausea?

A

antagonizes H1 & H2

30
Q

what does H2 stimulation cause?

A

increased gastric hydrogen ion concentration

31
Q

where are H2 receptors found besides the stomach/

A

in the CNS with some in the heart

32
Q

how does a H2 blocker work?

A

blocking histhamine stimulation of H2 receptors prevents increases in cAMP (cAMP activates the proton pump of gastric parietsl cells which secrete H+ ion)

33
Q

H2 blockers are used to manage ____ reactions?

A

allergic

34
Q

what is one concern regarding H2 blockers and the lungs?

A

H2 blockers leave H1 stimuation unopposed (H1 stimulation potentially causes bronchospasm). (although side effects are uncommon).

35
Q

other side effects of H2 blockers are…

A

diarrhea, confusion, and drug interactions (mostly with cimetidine (tagament)

36
Q

what is the method of elimination for H2 blockers ?

A

renal and hepatic

37
Q

H1 blockers
name some of the many uses:
give an example:

A

1 anti nausea/ anti motion sickness

  1. serotonin blocking action
  2. anticholinergic activity
  3. antiparkinson effect
  4. local sedation
  5. benadryl 25-100 mg
38
Q

antihisthamines (H1 & H2 blockers) can cause what changes in drug absorption?

A

alter absorption of other PO meds by increasing pH

39
Q

rantidine

  1. what class of histhamine blocker?
  2. uses?
  3. what doesnt it affect?
  4. less ___ side effects than cimetidine:
  5. less hepatic _____ ______ than cimetidine;
A
  1. H2 blocker
  2. gerd, duodenal and stress ulcers, prevention of aspiration
  3. does NOT affect gastric volume, gastric emptying, or pancreatic secretions
  4. CNS
  5. hepatic enzyme induction
40
Q

Rantidine brand name?

  1. onset:
  2. peak:
  3. durtion:
  4. dose:
A

zantac

  1. onset: 15 minutes IV, 30 min PO
  2. Peak: 1-2 hours IV, 2-3 hrs PO
  3. duration: 6-8 hours IV, 8-12 PO
  4. dose: 50 mg IV; 150 mg bid PO
41
Q

cimetidine:
onset:
duration:
dose:

A

tagament
60 min
6 hrs
300 mg IV

42
Q 
famotidine
s/e:
onset:
peak:
duration:
dose:
A 
pepcid
same as zantac, safe profile
30 min IV, 60 min PO
10-12 hrs po and IV
20 mg iv and po
43
Q

nizatidine
dose:
dose for active ulcer:

A

Axid
150 mg for gerd
300 mg for active ulcer

44
Q 
phenothiazines 
1.class:
2.method of action:
3.side effects:
4.what action causes side effects:
common phenothiazines:
A
  1. antipsychotics
  2. dopamine receptors in CRTZ
  3. dopaminergic side effects: tardive dyskinesia, parkinson effects
  4. compazine, phenergan
45
Q

promethiazines: prochlorperazine
1. moa
2. may cause hypotension-how?
3. extrapyramidal side effects treated with ?
4. elimination?
5. onset?
6. peak?
7. duration?
8. dose? daily max?

A

compazine

  1. direct effect on CRTZ
  2. by alpha blockade
  3. benadryl
  4. hepatic
  5. less than 5 min
  6. 15-30 min
  7. 2-4 hours
  8. 2.5-10 mg (max less than 40 mg/day)
46
Q

Phenthiazines: promethiazine

  1. class
  2. side effects
  3. why not good for not a good H1 blocker
  4. action:
  5. onset:
  6. duration
  7. dose
A

phenergan

  1. phenothiazine derivitive
  2. no antipsychotic effects at theraputic doses, but EPSs are possible
  3. H1 antihisthamine effects not enough to be theraputic
  4. sedative, antiemetic and anticholinergic effects
  5. 2-5 minutes
  6. <2 hours
  7. 12.5-50 mg iv
47
Q

metoclopramide

  1. origin:
  2. what is its action on peristalsis and lower esophageal sphincter?
  3. what is its action on GI muscle?
  4. affects on dopamine?…where?
  5. what is the action on the vomiting reflex and peristalsis?
  6. dose:
  7. side effects:
A

reglan

  1. derived from procainamide
  2. speeds gastric emptying by stimulating upper gi tract gastric motility and increases lower esophageal sphincter tone
  3. sensitizes GI smooth muscle to effects of ACH
  4. antagonism of central & peripheral dopamine effects in CRTZ
  5. reverses gastric immobility and cephalad peristalsis during vomiting reflex
  6. 10 mg
  7. mask like face, EPSs, depression, agitation, jitters, confusion, irregular heart beat, exacerbates porphyria

princip, pharm, phys, regional (18 decks)

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