Gastrointestinal Flashcards
List 5 Principal Sites involved in signaling of Nausea and Vomiting
1) CTZ
2) Cerebral cortex
3) Vestibular apparatus
4) GI tract (mechano and chemoreceptors)
5) Parenchyma
Brainstem (NK receptors)
6) Vomiting center
List neurotransmitters involved in the CTZ
Dopamine (D2)
Serotonin (5HT3)
Maybe:
Histamine (H1)
Acetylcholine (Achm)
List neurotransmitters / receptors for nausea in the gut
Serotonin (5HT3)
Dopamine (D2)
Muscarinic (Achm)
Opioid
List neurotransmitters / receptors in the vestibular apparatus
Histamine (H1)
Acetylcholine (Achm)
Opioid (very high doses)
List neurotransmitters / receptors for nausea in cortex
GABA
List 10 non-pharmacological treatments for nausea
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
List 6 metabolic causes for nausea
Renal failure
Hypercalcemia
HypoNa
Acidosis
Tumoral peptides
Liver failure
List 5 classes of medication for treatment of CINV
5HT3 antagonist
D2 antagonist
Prokinetic agents
Corticosteroids
NK-1 antagonists
Benzodiazepines (anticipatory nausea)
Cannabinoid
List 3 prokinetic agents
Domperidone
Metoclopramide
Prucalopride
Which neuroleptics used for nausea, also have anti-cholinergic effects?
Methotrimeprazine
Prochlorperazine
Olanzapine
List the proposed mechanisms for anti-emetic effect of steroids:
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
Rome criteria for constipation
symptoms for 12w/12mo.
<3BM’s/wk
straining
lumpy/dry/hard stools
sensation of block/incomplete emptying
need for manual evacuation
factors causing constipation
reduced motility
less moisture
diminished rectal sensation (no sense of distension -> lack of urge)
sphincter dysfunction (rectal)
key neurotransmitters in normal gut function
Ach
VIP
key receptors in normal gut function
5HT
metabolic problems that cause constipation
hypercal
hypokal
uremia
hypothyroid
diabetes
ways in which opioids cause constipation
reduced peristalsis
increase fluid absorption
reduced secretions
incr. sphincter tone
opioid receptor types in the gut
mu
kappa
stomach and colon
4 practical non-pharm strategies to manage constipation
- movement
- posture (lean forward)
- diet
- abdominal massage
- attention to privacy
2 opioids classically used for management diarrhea
Loperamide (does not cross BBB)
Codeine
How to distinguish secretory from osmotic diarrhea
stool anion gap
- >50 - osmotic
- <50 - secretory
4 agents for management of diarrhea, other than opioids.
List the classes
- 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
4 key causes (categories) of oropharyngeal dysphagia
- structural
- neurological
- myopathic
- iatrogenic
- psychogenic (anxiety)
2 key causes (categories) of esophageal dysphagia
- neuromuscular
- structural
- vascular (ischemia)
- iatrogenic
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
Best short term intervention for malignant esophageal obstruction
stenting (better short term outcomes)
RT (better long term outcomes)
5 complications of NG tubes
- aspiration
- pain
- nasopharyngeal ulceration
- sinusitis
- bleeding
5 complications of PEG tubes
bleeding
pain
infection
leakage
displacement
mucosal overgrowth / ulceration
list 4 treatments for esophageal spasm
- CCB’s (diltiazem)
- smooth muscle relaxants (anticholinergic -TCA’s in Uptodate))
- Botox
- PDE-5 inhibitors
distinguish heartburn from dyspepsia
heartburn - retrosternal burn
dyspepsia - epigastric pain / burning, early satiety, post-prandial fullness
How is dyspepsia classified
functional
vs
secondary
secondary causes of dyspepsia
GERD
PUD
esophagitis
mass
r/o gastroparesis
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
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
4 pharmacological agents for hiccups
anti-D - metoclop, chlorpromazine
anti-convulsant - gabapentin
smooth m. relaxant - baclofen
BZP - midazolam
anaesthetic - nebulized lidocaine
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
Key receptors in the VC
H1
M
5HT2
NK1
Key receptors controlling gastric emptying
D2
5HT4
MLN (motilin)
3 receptors controlling gastric secretion
SST (somatostatin)
M
H2
3 ways in which opioids cause nausea
direct effect on CTZ
slowing of gut - mechanoreceptor trigger - VC/NTS
vestibular sensitization
3 psychological interventions for nausea
- breathing / relaxation therapy
- hypnosis
- behavioural therapy with systemic desensitization (anticipatory nausea)
3 non-pharmacological options for nausea
ginger
acupuncture/pressure (P6 meridian)
smaller meals
calorie dense (high protein, low fat)
bicarbonate (renal failure)
mechanism of methotrimeprazine
anti D2
anti 5HT2
anti M
anti H1
anti adrenergic
mechanism of haldol
heavy anti D2
some 5HT3
mechanism of olanzapine
heavy anti D (D1-4)
anti M
some 5HT2/3
Prochlorperazine
anti D2
anti H1
some anti M
some 5HT2
mechanism of metoclopramide
anti -D2
anti - 5HT4
some anti 5HT3
mechanism of domperidone
anti-D2 (peripheral)
mechanism of ondansetron and granisetron
heavy anti-5HT3
mechanism of scopolamine
heavy anti-M
mechanism of cyclizine
anti-H1
some anti-M
mechanism of aprepitant
anti-NK1
which anti-depressant has anti-5HT3 property?
mirtazapine
basic pathophysiology of anorexia - cachexia
negative protein and energy balance driven by:
- reduced intake
- abnormal metabolism
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)
3 stages of cachexia:
pre-cachexia
cachexia
refractory cachexia
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
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)
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
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)
What medications are supported by evidence for cancer - associated cachexia
medroxyprogesterone acetate
corticosteroids
define anorexia
loss of appetite or reduced caloric intake
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
2 ways fat loss occurs in cancer
- reduced intake / nutrition
- tumor releasing lipolytic factors
missed cause of fatigue, anorexia / cachexia in males with cancer
hypogonadism
anorexia - cachexia most common in which 3 cancers?
- pancreas
- lung
- upper GI
anorexia cachexia less common in which 2 cancers?
- breast
- hematological
what are key psychological concerns in patients with cachexia?
pressure to eat
foreshadowing of death
body image
loss of control
compromised function / role
Assessment tool for anorexia cachexia
PG-SGA
patient generated subjective global assessment
What blood test correlates with cachexia severity and prognosis
CRP
Tests for muscle mass / strength
- grip test
- 6 min walk test
imaging
- dual energy XR or CT
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
What is the role of megesterol acetate
Short term intervention - almost all fat gain, may have catabolic effect on muscle
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
What are some non-traumatic etiologies of neurogenic bowel?
stroke
MS
cancer
How do you distinguish between UMN and LMN cause of neurogenic bowel?
DRE - tight (UMN), loose no volitional contraction (LMN)
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
2 meds to treat hepatic encephalopathy (other than lactulose)
PEG - acute
Rifaximin
LOLA L-ornithine L-aspartate
