gastro Flashcards
LOS anatomical contributions?
left and right crux of diaphragm
phrenosophageal ligament
angle of his - prevents reflux
stages of swallwpoing?
stage 0, oral - chewing and saliva, both sphincter closefd
1 , pharyngeal - UOS open reflexively, LOS opened by vasovagal reflex (receptive relaxation reflex)
2 , UO - UOS closes, contractions of circular and long muscles
3 LO - LOS closes
how can oesophageal motility be measured?
manometry
normal oesophageal pressures?
peristaltic - 40 mmHG
LOS resting - 20 mmHG
LOS receptive relaxation - <5mmHg
what is receptive relaxation mediated by?
inhibitory noncholinergic nonadrenergic neurons of myenteric plexus
what do you call pain on swallowing?
odynophagia
regurg vs reflux?
return of oesophageal contents from above obstruction
passive return of gasproduodenal contents to mouth
what causes oesophageal hypermotilitiy?
achalasia
pathophysiology of achalasia?
loss of ganglion cells in auerbachs myenteric plexus in LOS wall → ↓ activity of inhibitory NCNA neurones (less relaxation , more contraction) → ↑ resting LOS pressure → food collects in oesphagus → ↑ pressure → dilation → peristalsis stops
causes of achalasia?
primary - unknown
secondary - chagas disease, protozoa infection, amyloid, sarcoma, eosinophilic oesophaigtiis
onset of achalasia?
insidious
what does acahalsia largely increase the risk of ?
oesophageal cancer
treatment options for achalasia?
pneumatic dilatation - weakens LOS by stretching or tearing
Hellers myotomy - removal of muscle from stomach and oesophagus
dor Fundoplication - anterior funds folded over oesophagus and sutured to right side of myotomy
peroral endoscopic myotomy
what causes oesophageal hypomotility?
scleroderma
pathophysiology of scleroderma?
neuronal defects → atrophy of oesophageal smooth muscle → distal peristalsis ceases → ↓ LOS resting pressure → GORD develops
causes of scleroderma?
autoimmune
assoicted with CREST syndrome
treatment options for scleroderma?
pro kinetics to improve peristalsis force - cisapride
pathophysiology of corkscrew oesophagus?
incoordinate contractions → dysphasia and chest pain
pressures of 400-500 mmHg
circular muscle hypertrophy
corkscrew appearance on barium swallow
treatment options for corkscrew oesophagus?
forceful pneumatic dilatation of cardia
2 types of vascular anomalies that can. cause dysphagia?
dysphagia lusoria - aberrant right subclavian artery
double aortic arch
3 most likely areas of oesophageal perforations?
cricopharangeal, aortic & bronchial, diaphragmatic constrictions
cause of osphaegal perforations?
iatrogenic boerhaaves foreign body trauma intraoperative malignancy
what procedure is oesophageal perf likely to occur?
OGD especially if diverticula or cancer
how can boerhaaves cause oesophageal perf?
sudden ↑ in intra oesophageal pressure w negative thoracic pressure (vomitting against closed glottis)
symptoms of traumatic oesophageal perf?
dysphagia
blood in salvia
haematemsis
surgical emphysema
how does oesophageal perf usually present?
pain, fever, dysphagia, emphysema
oesophageal perf investigations?
CXR
CT
gastrogaffin swallow
OGD
management of oesophageal perf?
NBM, IV fluids, BS Abs & antifungals ITU/HDU bloods tertiary referal surgery
when is surgery not default management for oesophageal perf?
if theres minimal contamination, its contained or patient is unfit
surgical options for oesophageal perf?
vascularised pedicle flap
dor fundoplication
drains
oesophagectomy
what increases LOS pressure?
acetylcholine , a adrenergic agonists, protein food, high intraabdominal pressure → reflux inhibited
what decreases LOS pressure?
VIP, B adrenergic antagonists, dopamine, NO, chocolate, fat, smoking → promotes reflux
what can causes sporadic reflux?
pressure on full stomach
swallowing
transient sphincter opening
what mechanisms protect the oesophagus following reflux?
volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
epithelium - barrier properties
outline the process of oesophageal protective mechanisms failing (GORD)
↓ sphincter pressure, ↑ transient sphincter opening. ↓ saliva production/buffering capacity, defective mucosa, hiatus hernia
→ → reflux oesphagitis → epithelial metaplasia → carinoma
Ixs for GORD?
OGD
manometry
24 hr oesophageal pH recording
treatment options for GORD?
lifestyle - wt loss, less EtOH, x smoking
PPIs
dilatation peptic strictures
laparoscopic Nissans fundoplication (wrapping funds around oesophagus)
areas of stomach and what they secrete?
cardia & pylorus - mucus
body & fundus - mucus, HCl, pepsinogen
antrum - gastrin
causes of erosive & haemorhagic gastritis?
NSAIDS iscahemia trauma alcohol bruns MOF
what doe erosive & haemorhagic gastritis lead to?
acute ulcer → gastric bleeding/perforation (anywhere in stomach)
cause of nonerosive chronic active gastritis?
H pylori (antrum)
Tx for H pylori gastritis?
amoxicillin. clarithromycin and pantoprazole for 7-14/7
pathophysiology of atrophic fundal gland gastritis?
autoantibodies against parts and products of parietal cells in fundus → parietal cells atrophy → ↓ acid & IF secretion (( → ↑ gastrin secretion → ECL hyperplasia → carcinoid )) ((→ pernicious anaemia)
what stimulates gastric secretions?
acetylcholine from vagus ps fibres
gastrin from antrum g cells
histamine from ECL and mast cells
what inhibits gastric secretions?
secretin in SI
somatostatin
prostaglandins, TGF-a, adenosine (decreased by NSAIDs)
how does the mucosa protect against acid?
mucus film
HCO3- secretion (requires prostaglandins)
epithelial barrier (tight junctions)
mucosal blood perfusion (will take away any H ions that get through)
mechanisms of repairing epithelial defects?
migration of epithelial cells - close gap
cell growth - stimulated by EGF, TGF-a, IGF1, gastrin
leukocytes and macrophages remove necrotic cells, angiongesis, ECM regeneration, cell division.
what can cause an ulcer formation?
increased HCl secretion h pylori reduced HCO3- secretion ↓ cell formation ↓ blood perfusion
treatment options for ulcers?
PPI/H2 blocker
amoxicillin, clarithromycin, pantoprazole 7-14/7
elective sx
if ulcers don’t heal w medcial tretamet what do you do?
should heal in 12 weeks, if not change medication check serumgastrin (g cell hyperplasia or gastronoma) OGD
when should sx be considered for ulcers?
intractability of medical therapy haemorrhage obstrucion perforation relative eg. need of nsaids or steroids
what is riglers sign?
free intraperitoneal air from perforated viscus
what is indicative of perforated viscus on x ray?
free intraperitoneal and subdiaphrgamatuic air
most common site of ulcers in GIT?
first part of duodenum / pylorus
what criteria is used to assess acute pancreatitis?
modified glasgow criteria
PANCREAS
score ≥3 within 48hrs onset = severe pancreatitis
(or CRP ≥200)
acute pancreatitis management?
fluid resus analgesia pancreatic rest ± nutritional support determine cause severe → HDU
level and structure at subcostal plane?
L3 - IMA
level and structure at supracristal plane?
l4 - bifurcation of aorta
foregut , midgut and hindgut locations?
f - distal oesophagus to 2nd part of duodenum
m - distal 2nd half of duodenum to primal 2/3 transverse colon
h - distal2/3 transverse colon to rectum
differences between visceral and parietal pian?
v - dull, crampy, burning, autonomic, embryological origin
p - sharp, ache, well-localised, somatic
foregut , midgut and hindgut innervation and pain site?
f - t5-t9, epigastrium
m - t10-t11, umbilical
h - l1-l2, suprapubic
constant vs colicky pian?
constant - inflammation, worse with movement, spleen, kidney, liver
tubular obstruction - fluctuates in severity, move to try get comfort, ureter, gallbladder, bowel
colicky pain that becomes constant suggests?
ischemia
what is the most potent stimulus for drinking water?
plasma osmolality increase
where does ADH act?
aquaporin 2 channels in CD
where are osmoreceptors found?
hypothalamus - organum vasculosum of lamina terminals and subfornical organ
how do osmoreceptors lead to ADH release?
concentrated plasma → cells shrink → ↑ proportion of cation channels → membrane depolarises & ↑ firing frequency → ↑ signals to post pitutuirary → ↑ ADH produced → fluid retention and drinking
what are the effects of angiotensin II?
vasoconstriction
↑ sympathetic activity
thirst
stimulate aldosterone release from adrenal cortex zona glomerulosa
water retention via na absorption and k excretion
adh secretion
structure and function of arcuate nucleus?
in hypothalamus
has incomplete BBB allows access to peripheral hormones
stimulatory neurons - NPY & Argp (orexigenic)
inhibitory neurons - POMC (anorexigernic)
regulation food intake by integrating central and peripheral signals
which neuorones does leptin stimulate and inhibit?
stim - POMC
inhibit - NPY & ARGP
what happens when POMC neurons are stimulated?
release a-MSH which stimulates MC4R in the paraventricular nucleus → ↓ food intake
what happens when ARGP neurons are stimulated?
MC4r in paraventrivcular nucleus is inhibited → ↑ food intake
what can cause morbid obesity?
MC4R mutations
POMC deficiency
what is the adipostat mechanism?
adipostat hormone produced from fat → detected b y hypothalamus → alters neuropeptides to increase/decrease food intake
what is leptin?
hormone made by adipocytes and circulates in plasma
acts on hypothalamus to regulate appetite and thermogenesis
eg ↑ leptin → ↓ decreased appetite & ↑ energy expenditure
obesity in relation to leptin?
obese people have ↑ leptin but also have leptin resistance so has no effect
what gut hormones regulate appetite?
ghrelin → stims appetite and gastric emptying
peptide YY → ↓ food intake
when are ghrelin levels highest?
just before meals