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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
List non-pharm interventions to address oropharyngeal dysphagia
- 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
26
Best short term intervention for malignant esophageal obstruction
stenting (better short term outcomes) RT (better long term outcomes)
27
5 complications of NG tubes
- aspiration - pain - nasopharyngeal ulceration - sinusitis - bleeding
28
5 complications of PEG tubes
bleeding pain infection leakage displacement mucosal overgrowth / ulceration
29
list 4 treatments for esophageal spasm
- CCB's (diltiazem) - smooth muscle relaxants (anticholinergic -TCA's in Uptodate)) - Botox - PDE-5 inhibitors
30
distinguish heartburn from dyspepsia
heartburn - retrosternal burn dyspepsia - epigastric pain / burning, early satiety, post-prandial fullness
31
How is dyspepsia classified
functional vs secondary
32
secondary causes of dyspepsia
GERD PUD esophagitis mass r/o gastroparesis
33
Which nerves are involved in hiccup pathophysiology (afferent and efferent)? Which neurotransmitters are involved?
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
3 non-pharm techniques for hiccup mgmt
- vagal stimulation - lift uvula, pull tongue - glottic stimulation - nebulized saline, cotton swab touch to palate - sympathetic - fright - increase pCO2 - breathe into bag
35
4 pharmacological agents for hiccups
anti-D - metoclop, chlorpromazine anti-convulsant - gabapentin smooth m. relaxant - baclofen BZP - midazolam anaesthetic - nebulized lidocaine
36
List key receptor triggers for nausea in: - GI tract - Cortex - CTZ - Vestibular apparatus
- GI tract - 5HT3 - Cortex - GABA, 5HT2 - CTZ - 5HT3, D2, NK1 - Vestibular apparatus - H1, M
37
Key receptors in the VC
H1 M 5HT2 NK1
38
Key receptors controlling gastric emptying
D2 5HT4 MLN (motilin)
39
3 receptors controlling gastric secretion
SST (somatostatin) M H2
40
3 ways in which opioids cause nausea
direct effect on CTZ slowing of gut - mechanoreceptor trigger - VC/NTS vestibular sensitization
41
3 psychological interventions for nausea
- breathing / relaxation therapy - hypnosis - behavioural therapy with systemic desensitization (anticipatory nausea)
42
3 non-pharmacological options for nausea
ginger acupuncture/pressure (P6 meridian) smaller meals calorie dense (high protein, low fat) bicarbonate (renal failure)
43
mechanism of methotrimeprazine
anti D2 anti 5HT2 anti M anti H1 anti adrenergic
44
mechanism of haldol
heavy anti D2 some 5HT3
45
mechanism of olanzapine
heavy anti D (D1-4) anti M some 5HT2/3
46
Prochlorperazine
anti D2 anti H1 some anti M some 5HT2
47
mechanism of metoclopramide
anti -D2 anti - 5HT4 some anti 5HT3
48
mechanism of domperidone
anti-D2 (peripheral)
49
mechanism of ondansetron and granisetron
heavy anti-5HT3
50
mechanism of scopolamine
heavy anti-M
51
mechanism of cyclizine
anti-H1 some anti-M
52
mechanism of aprepitant
anti-NK1
53
which anti-depressant has anti-5HT3 property?
mirtazapine
54
basic pathophysiology of anorexia - cachexia
negative protein and energy balance driven by: - reduced intake - abnormal metabolism
55
define cachexia
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
3 stages of cachexia:
pre-cachexia cachexia refractory cachexia
57
what are the key aspects of the cachexia assessment
- stores - extent of depletion (BMI, wt loss history) - muscle mass and strength - intake - impact - function/psychosocial effect - catabolic drivers
58
what is reversibility of anorexia cachexia dependent on?
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
how should treatment for anorexia cachexia be stratified by prognosis?
>2-3 mo. survival - consider nutritional interventions less than that - supportive care and symptom management
60
Outline an approach to management of potentially reversible cancer anorexia cachexia:
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
What medications are supported by evidence for cancer - associated cachexia
medroxyprogesterone acetate corticosteroids
62
define anorexia
loss of appetite or reduced caloric intake
63
3 ways muscle loss occurs in cancer
- chemo - cytotoxic to muscle - inflammation - stimulates atrophy genes and proteolysis - inflammation - inhibit anabolic effect of growth hormone, and insulin like growth factor
64
2 ways fat loss occurs in cancer
- reduced intake / nutrition - tumor releasing lipolytic factors
65
missed cause of fatigue, anorexia / cachexia in males with cancer
hypogonadism
66
anorexia - cachexia most common in which 3 cancers?
- pancreas - lung - upper GI
67
anorexia cachexia less common in which 2 cancers?
- breast - hematological
68
what are key psychological concerns in patients with cachexia?
pressure to eat foreshadowing of death body image loss of control compromised function / role
69
Assessment tool for anorexia cachexia
PG-SGA patient generated subjective global assessment
70
What blood test correlates with cachexia severity and prognosis
CRP
71
Tests for muscle mass / strength
- grip test - 6 min walk test imaging - dual energy XR or CT
72
How to steroids vary in their risk of myopathy? What is the main role in anorexia cachexia?
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
What is the role of megesterol acetate
Short term intervention - almost all fat gain, may have catabolic effect on muscle
74
Distinguish neurogenic bowel in UMN vs. LMN lesions - pathophysiology - approach to management of constipation
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
What are some non-traumatic etiologies of neurogenic bowel?
stroke MS cancer
76
How do you distinguish between UMN and LMN cause of neurogenic bowel?
DRE - tight (UMN), loose no volitional contraction (LMN)
77
General principles in management of neurogenic bowel
- 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
2 meds to treat hepatic encephalopathy (other than lactulose)
PEG - acute Rifaximin LOLA L-ornithine L-aspartate

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