Gastroenterology Flashcards
where oesophageal star and end
C5
T10
stages of swallowing
4 (0-3)
oral
pharyngeal
upper oesophageal
lower oesophageal
sequence of stages of swallowing of the 2 shincter
CC
OO
CO
how to determine motility of oesophagus
manometery
what is LOS resting pressure / relaxation mediated by
inhibitory noncholinergic nonadrenergic neurons of myenteric plexus (NCNA)
causes of functional disorders of the oesophagus
Abnormal contractions: (Hypermobility
Hypomobility
Disordered coordination)
Failure of protective mechanisms: GORD
achalasia causes
Loss of ganglion cells in aurebach’s myenteric plexus in LOS wall
decreased inhibitory neuron activity
cannot relax properly
secondary achalasia causes
chagus disease (parasite)
protozoa infection
amyloid
What diseases is hypermotility of oesophagus seen in
Chagas disease
Protozoa
Amyloid
Sarcoma
Eosinophilic oesophagitis
what is achalsia
increased resting pressure of LOS
relaxation too late or weak
swallowed food collects in oesophagus cause increased pressure throughout with dilation of oesophagus
achalasia treatment
pneumatic dilation (PD)
to weaken LOS by circumferential stretching to stretch muscles of LOS
what is heller’s myotomy
A continuous myotomy performed for 6cm on the oesophagus and 3 cm onto the stomach
split the muscle
treatment of achalasia
What is dor fundoplication
partial wrapping of the stomach around the esophagus to make a low-pressure valve) performed to prevent reflux from the stomach into the esophagus following the myotomy.
risks of heller’s myotomy and dor fundoplication
oesophageal and gastric perforation
vagus nerve division
splenic injury
what is scleroderma
autoimmune
hypomotility in early stages
atrophy of smooth muscles of oesophagus
reduced resting pressure of LOS
CREST syndrome
what is CREST syndrome
calcinosis,
Raynaud’s
esophageal dysmotility, sclerodactyly,
telangiectasia
what is corkscrew oesophagus
diffuse oesophageal spasm
incoordinate contractions
dysphagia and chest pain
treatment for corkscrew oesophagus
forceful PD of cardia
how to find iatrogenic oesophageal perforation
oesophagogastroduodenoscopy (OGD)
what is Boerhaave;s oesophageal perforation
sudden increase in intra-oesophageal pressure with negatvie intro thoracic pressure
what is foriegn body oesophageal perforation
disk batteries (cause electric burn if in mucosa)
magnets
sharp objects
dishwasher tablet
acid/alkali
what is trauma type oesphageal perforation
neck = penetrating
thorax = blunt force
clinical features of trauma type oesopheal perforation
dysphagia
blood in saliva
haematemesis
surgical empysema
types of oesphageal perforation (4)
iatrogenic
trauma
foreign body
Boerhaave’s
where are the areas of oesophagus prone to perforation
cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphincter constriction
management for oesophageal perforation
IV fluids
borad spectrum AB
bloods (G&S)
definitive management for oesophaeal perforation (2)
conservative management with covered metal stent
operative management (primary repair is optimal, oesophagectomy is definitive)
why LOS usually close
act as barrier to against reflux of harmful gastric juice (pepsin and HCl)
what are the mechanisms of protection after reflux (3)
volume clearance (oesophageal peristalsis reflux)
pH clearnace
epithelium (barrier properties)
mechanism of inhibiting reflux
Ach, alpha adrenergic agonists cause increased pressure in oesophageal sphincter
cause inhibition of reflux
mechanism of promoting reflux
Beta adrenergic agonists, dopamine NO, gastric juice, fat cause decreased pressure in oesophageal sphincter
promote reflux
what happens if fail to protect oesophageal
GORD
stOmach acid leaks up into oesophagus
causes of GORD
reduced sphincter pressure
reduced saliva production cause pH clearance
abnormal peristalsis cause volume clearance
What increases LOS pressure
Acetylcholine
Alpha-adrenergic agonists
Hormones
Protein-rich food
Histamine
High intra-abdominal pressure
INHIBITS REFLUX
what decreases LOS pressure and promotes
acidic food
fats
NO
smoking
What are sliding hiatus hernias
portion of stomach herniated
ligament holding the distal oesophagus down gives way so whole stomach slides up into chest
What is a rolling hiatus hernia
portion of stomach sticks upside
Junction is in place and the stomach herniates alongside the oesophagus
How do you investigate GORD (3)
- OGD - to exclude cancer
or confirm oesophagitis, peptic stricture and barretts - Oesophageal manometry
- 24hr oesophageal pH recording
GORD treatments
lifestyle changes
PPIs
dilation peptic stricutres
laproscopic Nissen’s fundoplication
what is erosive and haemorrhagic gastritis
acute ulcer
gastric bleeding and perforation
what is nonerosive chronic active gastritis and its treatment
helicobacter pylori (H.pylori)
PPi
Triple treatment (amoxicillin, clarithromycin, pantoprazole)
what is atrophic gastritid
fundus
autoantibodies vs part and products of parietal cells
parietal cells atrophy
reduce acid and IF secretion
neural stimulation of gastric secretion
Ach
postganglionic transmitter of vagal parasympathetic fibres
endocrine stimulation of gastric secretion
gastrin
from G cells of antrum
Paracrine stimulation of gastric secretion
Histamine (ECL cells and mast cells of gastric wall)
Endocrine inhibition of gastric secretion
secretin from S.I
paracrine inhibition of gastric secretion
somatostatin (SIH)
paracrine and autocrine inhibition of gastric secretion
PGs
TGF-alpha
adenosine
What are the different types of gastritis
erosive and haemorrhagic
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis
methods of mucosal protection in stomach
Mucus film
HCO3- secretion
Epithelial barrier (tight junctions, strong apical membrane)
Mucosal blood perfusion (good blood supply can get rid of H+ quickly)
what is produced in the cardia and pyloric region
mucus
what is produced in the body and fundus
mucus
HCl
pepsinogen
what is produced in the antrum
gastrin
what are the mechanisms for repairing epithelial defects (epithelial repair and wound healing)
- migration
- gap closed by cell growth (stimulated by EGF, TGF-alpha, IGF-1, GRP, gastrin)
- acute wound healing (BM destroyed and attract leukocytes, macro[hages, phagocytosis of necrotic ells, angiogenesis, regenration fo ECM)
How does migration repair epithelium
Adjacent epithelial cells flatten to close gap
via sideward migration along BM
how are ulcers formed
H. Pylori
Increased gastric juice secretion
Decreased bicarbonate secretion
Decreased cell formation
Decreased blood perfusion
medical treatment for ulcer
PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
clinical outcomes for H.Pylori infection
- asymptomatic or chronic gastritis
- chronic atrophic gastritis, intestinal metaplasia
- gastric or duodenal ulcer
- gastric cancer
surgical treatment for ulcer and medical follow up
Intractability after medical therapy
continuous requirement for steroid therapy / NSAIDS
complications of surgical treatment for ulcer
haemorrhage
obstruction
perforation
When would you opt for elective surgery for ulcers
Rare - most uncomplicated ulcers heal within 12 weeks
if not - change medication, observe additional 12 weeks
Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
where are osmorecceptors found in hypothalamus
organum vasculosum of lamina terminalis (OVLF)
subfornical organ
how angiotensin ll affects ADH secretion
increase
and increase thirst as well
what is ghrelin responsible for
hunger hormone
increase appetite
what is leptin for
inhibit hunger
what is appetite stimulant signal described as
orexigenic
what is appetite suppressive signal described as
anorectic
which part of hypothalamus release orexigenic signal
lateral hypothalamus (feeding centre)
which part of hypothalamus release anorectic signa;
ventromedial hypothalamus (satiety centre)
what happens to lesion in ventromedial hypothalamus (satiety centre)
obesity
what nucleus in hypothalamus release oxytocin and ADH
paraventricular nucleus
what signals does arcuate nucleus in hypothalamus contain
orexigenic and anorectic signals
how is the BBB in arcuate nucleus and why is it in this way
incomplete
to allow access to peripheral hormones
main role of arcuate nucleus in hypothalamus
regulation of food intake
what are the 2 neurone populations in arcuate nucleus
stimulatory (NPY/AGPR neurone)
inhibitory (POMC neurone)
what happens to activation of POMC neurone
inhibit food intake
which receptor is highly expressed in paraventricular nucleus
MCR receptor
how melanocortin system reduce appetite
arcuate nucleus release POMC neurone
POMC cause increase in α– Melanocyte-stimulating hormone (alpha MSH)
alpha MSH increase bind to MC4R in paraventricular nucleus to reduce food intake
how melanocortin system increase appetite
arcuate nucleus release AgRP
cause inhibition in MC4R
increase food intake
what is the in regulating food intake
fat produces circulating hormone
hypothalamus senses the concentration of hormone
then alters neuropeptides to increase/decrease food intake
where does leptin acts on
hypothalamus
role of leptin
regulate appetite (intake) and thermogenesis (expenditure)
where is leptin secreted from (2)
white adipose tissue and gastric mucosa
low level of leptin indicates what
low body fat
high level of leptin indicates what
high body fat
what is leptin resistance
leptin is present but doesn’t signal effectively
where are gut hormones that regulate appetite released
enteroendocrine cells in stomach, pancreas, small bowel
which gut hormones inhibit appetite
peptide YY (PYY)
glucagon like peptide -1 (GLP-1)
which gut hormone increase appetite
ghrelin
how does ghrelin prepare food intake in gut
increase gastric motility and acid secretion
how ghrelin modulates neurone in arcuate nucleus
stimulate NPY/ AgRP neuornes to increase appetite
inhibit POMC neurone
what is ghrelin involved in
increase appetite
regulation of rewards
taste sensation
memory
carcadian rhythm
when is PYY released
in response to feeding
where is PYY released
terminal ileum and colon
effect on PYY on arcuate nucleus
stimulate POMC
inhibit NPY
overall reduce appetite
when is GLP-1 released
response to feeding
effect of GLP-1in appetite
reduces appetite
GLP-1 effects to stomach, liver, pancreas, adipose tissue, heart, brain
stomach: decrease gastric empyting
liver: reduce glucose production
pancreas: increase insulin secretion, reduce glucagon, increase insulin biosynthesis, increase B cell proliferation and reduce apoptosis
adipose tissue: increase glucose uptake and storgae
heart: increase cardiac function and protection
brain: increase neuroprotection and reduce appetite
what organs are associated wit right hypochondriac region (2)
gallbladder
liver
what organs are associated wit left hypochondriac region
pancreas
what organs are associated wit epigastric region
stomach
duodenum
pancreas
what organs are associated wit right and left lumbar region
kidney
what organs are associated wit umbilical region
small bowel
what organs are associated wit right iliac region
appendix
caecum
what organs are associated wit left iliac region
sigmoid colon
what organs are associated wit hypogastric region
bladder
uterus
adnexae
describe the character of pain that produced by kidney stone
colicky
describe the character of pain that produced by liver
constant
describe the character of pain that produced by spleen
constant
radiation of pain that you’d expect produced by gallbladder
upper right quadrant through to back and to right
radiation of pain that you’d expect produced by pancreas head
straight to back and left
radiation of pain that you’d expect produced by pancreas tail
through to back and left
radiation of pain that you’d expect by kidney
in loin and radiates to groin
radiation of pain for small bowel
doesn’t radiate
