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PM Review > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

List 5 Principal Sites involved in signaling of Nausea and Vomiting

A

1) CTZ
2) Cerebral cortex
3) Vestibular apparatus
4) GI tract (mechano and chemoreceptors)
5) Parenchyma
Brainstem (NK receptors)
6) Vomiting center

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2
Q

List neurotransmitters involved in the CTZ

A

Dopamine (D2)
Serotonin (5HT3)

Maybe:
Histamine (H1)
Acetylcholine (Achm)

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3
Q

List neurotransmitters / receptors for nausea in the gut

A

Serotonin (5HT3)
Dopamine (D2)
Muscarinic (Achm)

Opioid

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4
Q

List neurotransmitters / receptors in the vestibular apparatus

A

Histamine (H1)
Acetylcholine (Achm)

Opioid (very high doses)

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5
Q

List neurotransmitters / receptors for nausea in cortex

A

GABA

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6
Q

List 10 non-pharmacological treatments for nausea

A

1) Well ventilated environment with odour control
2) Avoid rapid movements (esp. if provokes nausea)
3) Provide adequate supportive hydration
4) Portion control
5) Avoid sweet preparations
6) Mouthcare
7) Control other contributing symptoms (pain, dyspnea, anxiety etc.)
8) Psychological: relaxation, CBT
9) Acupressure / acupuncture
10) Manage provoking meds with caution

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7
Q

List 6 metabolic causes for nausea

A

Renal failure
Hypercalcemia
HypoNa
Acidosis
Tumoral peptides
Liver failure

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8
Q

List 5 classes of medication for treatment of CINV

A

5HT3 antagonist
D2 antagonist
Prokinetic agents
Corticosteroids
NK-1 antagonists
Benzodiazepines (anticipatory nausea)
Cannabinoid

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9
Q

List 3 prokinetic agents

A

Domperidone
Metoclopramide
Prucalopride

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10
Q

Which neuroleptics used for nausea, also have anti-cholinergic effects?

A

Methotrimeprazine
Prochlorperazine
Olanzapine

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11
Q

List the proposed mechanisms for anti-emetic effect of steroids:

A

1) Reduction in permeability of BBB to chemicals
2) Anti-inflammatory effect +/- reduction in tumor mass
3) Reduce GABA inhibition of anti-emetic neurons
4) Decrease leu-enkephalin in brainstem and gut

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12
Q

Rome criteria for constipation

A

symptoms for 12w/12mo.
<3BM’s/wk
straining
lumpy/dry/hard stools
sensation of block/incomplete emptying
need for manual evacuation

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13
Q

factors causing constipation

A

reduced motility
less moisture
diminished rectal sensation (no sense of distension -> lack of urge)
sphincter dysfunction (rectal)

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14
Q

key neurotransmitters in normal gut function

A

Ach
VIP

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15
Q

key receptors in normal gut function

A

5HT

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16
Q

metabolic problems that cause constipation

A

hypercal
hypokal
uremia
hypothyroid
diabetes

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17
Q

ways in which opioids cause constipation

A

reduced peristalsis
increase fluid absorption
reduced secretions
incr. sphincter tone

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18
Q

opioid receptor types in the gut

A

mu
kappa

stomach and colon

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19
Q

4 practical non-pharm strategies to manage constipation

A
  • movement
  • posture (lean forward)
  • diet
  • abdominal massage
  • attention to privacy
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20
Q

2 opioids classically used for management diarrhea

A

Loperamide (does not cross BBB)
Codeine

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21
Q

How to distinguish secretory from osmotic diarrhea

A

stool anion gap
- >50 - osmotic
- <50 - secretory

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22
Q

4 agents for management of diarrhea, other than opioids.
List the classes

A
  • absorbent (absorp water = bulk)
  • pectin (grated apples), methylcellulose
  • adsorbent (clay surface takes up bacteria and water)
  • kaolin
  • mucosal prostaglandin inhibitor / anti-inflammatory (reduce intestinal secretion, electrolyte excretion)
  • bismuth
  • aspirin
  • somatostatin analogues
  • octreotide
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23
Q

4 key causes (categories) of oropharyngeal dysphagia

A
  • structural
  • neurological
  • myopathic
  • iatrogenic
  • psychogenic (anxiety)
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24
Q

2 key causes (categories) of esophageal dysphagia

A
  • neuromuscular
  • structural
  • vascular (ischemia)
  • iatrogenic
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25
Q

List non-pharm interventions to address oropharyngeal dysphagia

A
  • diet modifications (thicker, easy to chew etc)
  • oral care (address xerostomia)
  • exercises
  • techniques (triple swallow, positioning/turning
  • hygiene post meal
  • parenteral/enteral feeding
  • electric stimulation
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26
Q

Best short term intervention for malignant esophageal obstruction

A

stenting (better short term outcomes)

RT (better long term outcomes)

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27
Q

5 complications of NG tubes

A
  • aspiration
  • pain
  • nasopharyngeal ulceration
  • sinusitis
  • bleeding
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28
Q

5 complications of PEG tubes

A

bleeding
pain
infection
leakage
displacement
mucosal overgrowth / ulceration

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29
Q

list 4 treatments for esophageal spasm

A
  • CCB’s (diltiazem)
  • smooth muscle relaxants (anticholinergic -TCA’s in Uptodate))
  • Botox
  • PDE-5 inhibitors
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30
Q

distinguish heartburn from dyspepsia

A

heartburn - retrosternal burn

dyspepsia - epigastric pain / burning, early satiety, post-prandial fullness

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31
Q

How is dyspepsia classified

A

functional
vs
secondary

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32
Q

secondary causes of dyspepsia

A

GERD
PUD
esophagitis
mass

r/o gastroparesis

33
Q

Which nerves are involved in hiccup pathophysiology (afferent and efferent)?

Which neurotransmitters are involved?

A

Afferent - vagus nerve - irritation anywhere along its path
Efferent - phrenic nerve - diaphragmatic contraction, recurrent laryngeal nerve - closure of glottis

Central - poorly localized

Neurotransmitters - GABA, dopamine

34
Q

3 non-pharm techniques for hiccup mgmt

A
  • vagal stimulation - lift uvula, pull tongue
  • glottic stimulation - nebulized saline, cotton swab touch to palate
  • sympathetic - fright
  • increase pCO2 - breathe into bag
35
Q

4 pharmacological agents for hiccups

A

anti-D - metoclop, chlorpromazine
anti-convulsant - gabapentin
smooth m. relaxant - baclofen
BZP - midazolam
anaesthetic - nebulized lidocaine

36
Q

List key receptor triggers for nausea in:
- GI tract
- Cortex
- CTZ
- Vestibular apparatus

A
  • GI tract - 5HT3
  • Cortex - GABA, 5HT2
  • CTZ - 5HT3, D2, NK1
  • Vestibular apparatus - H1, M
37
Q

Key receptors in the VC

A

H1
M
5HT2
NK1

38
Q

Key receptors controlling gastric emptying

A

D2
5HT4
MLN (motilin)

39
Q

3 receptors controlling gastric secretion

A

SST (somatostatin)
M
H2

40
Q

3 ways in which opioids cause nausea

A

direct effect on CTZ
slowing of gut - mechanoreceptor trigger - VC/NTS
vestibular sensitization

41
Q

3 psychological interventions for nausea

A
  • breathing / relaxation therapy
  • hypnosis
  • behavioural therapy with systemic desensitization (anticipatory nausea)
42
Q

3 non-pharmacological options for nausea

A

ginger
acupuncture/pressure (P6 meridian)
smaller meals
calorie dense (high protein, low fat)
bicarbonate (renal failure)

43
Q

mechanism of methotrimeprazine

A

anti D2
anti 5HT2
anti M
anti H1
anti adrenergic

44
Q

mechanism of haldol

A

heavy anti D2
some 5HT3

45
Q

mechanism of olanzapine

A

heavy anti D (D1-4)
anti M
some 5HT2/3

46
Q

Prochlorperazine

A

anti D2
anti H1
some anti M
some 5HT2

47
Q

mechanism of metoclopramide

A

anti -D2
anti - 5HT4
some anti 5HT3

48
Q

mechanism of domperidone

A

anti-D2 (peripheral)

49
Q

mechanism of ondansetron and granisetron

A

heavy anti-5HT3

50
Q

mechanism of scopolamine

A

heavy anti-M

51
Q

mechanism of cyclizine

A

anti-H1
some anti-M

52
Q

mechanism of aprepitant

A

anti-NK1

53
Q

which anti-depressant has anti-5HT3 property?

A

mirtazapine

54
Q

basic pathophysiology of anorexia - cachexia

A

negative protein and energy balance driven by:
- reduced intake
- abnormal metabolism

55
Q

define cachexia

A

complex metabolic syndrome associated with an underlying illness, characterized by loss of muscle with or without the loss of fat.

prominent clinical feature is weight loss in adults (classically defined as >10% of body mass)

56
Q

3 stages of cachexia:

A

pre-cachexia
cachexia
refractory cachexia

57
Q

what are the key aspects of the cachexia assessment

A
  • stores - extent of depletion (BMI, wt loss history)
  • muscle mass and strength
  • intake
  • impact - function/psychosocial effect
  • catabolic drivers
58
Q

what is reversibility of anorexia cachexia dependent on?

A

catabolic drivers
- stage of disease, tumor type and prognosis, treatments available
- systemic inflammation (CRP>10 signals those who may benefit from early nutritional intervention)

59
Q

how should treatment for anorexia cachexia be stratified by prognosis?

A

> 2-3 mo. survival - consider nutritional interventions

less than that - supportive care and symptom management

60
Q

Outline an approach to management of potentially reversible cancer anorexia cachexia:

A

identify and treat secondary factors
- GI, oral, psychological, metabolic/endocrine
optimize nutrition (caloric deficit is common)
exercise (preserve muscle mass / function)
anti-inflammatory (omega 3 fatty acids)

61
Q

What medications are supported by evidence for cancer - associated cachexia

A

medroxyprogesterone acetate

corticosteroids

62
Q

define anorexia

A

loss of appetite or reduced caloric intake

63
Q

3 ways muscle loss occurs in cancer

A
  • chemo - cytotoxic to muscle
  • inflammation - stimulates atrophy genes and proteolysis
  • inflammation - inhibit anabolic effect of growth hormone, and insulin like growth factor
64
Q

2 ways fat loss occurs in cancer

A
  • reduced intake / nutrition
  • tumor releasing lipolytic factors
65
Q

missed cause of fatigue, anorexia / cachexia in males with cancer

A

hypogonadism

66
Q

anorexia - cachexia most common in which 3 cancers?

A
  • pancreas
  • lung
  • upper GI
67
Q

anorexia cachexia less common in which 2 cancers?

A
  • breast
  • hematological
68
Q

what are key psychological concerns in patients with cachexia?

A

pressure to eat
foreshadowing of death
body image
loss of control
compromised function / role

69
Q

Assessment tool for anorexia cachexia

A

PG-SGA
patient generated subjective global assessment

70
Q

What blood test correlates with cachexia severity and prognosis

A

CRP

71
Q

Tests for muscle mass / strength

A
  • grip test
  • 6 min walk test

imaging
- dual energy XR or CT

72
Q

How to steroids vary in their risk of myopathy?
What is the main role in anorexia cachexia?

A

Fluorinated steroids (dex) have a higher risk of muscle catabolism (pred. preferred)

Role:
- short term appetite boost if longer prognosis
- EOL sx. support refractory cachexia with short prognosis

73
Q

What is the role of megesterol acetate

A

Short term intervention - almost all fat gain, may have catabolic effect on muscle

74
Q

Distinguish neurogenic bowel in UMN vs. LMN lesions
- pathophysiology
- approach to management of constipation

A

UMN - hyper-reflexic bowel, incr. tone intestinal wall and anal sphincter
(peristalsis intact ->fecal retention/impaction from tight sphincter)
- suppository or disimpaction needed

LMN - areflexic bowel, flaccid sphincter
(slow peristalsis -> constipation with incontinence)
- use bulk agent like fiber to prevent accidents

75
Q

What are some non-traumatic etiologies of neurogenic bowel?

A

stroke
MS
cancer

76
Q

How do you distinguish between UMN and LMN cause of neurogenic bowel?

A

DRE - tight (UMN), loose no volitional contraction (LMN)

77
Q

General principles in management of neurogenic bowel

A
  • routine is critical (time on toilet 30min post meal)
  • toilet routine:
  • abdominal clockwise massage x 5 min, followed by digital stimulation x 20-30s, manual disimpaction +/- supp
  • consider senna QHS
  • next steps: enema, mg citrate, lactulose
78
Q

2 meds to treat hepatic encephalopathy (other than lactulose)

A

PEG - acute
Rifaximin
LOLA L-ornithine L-aspartate

PM Review (19 decks)

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