GI Flashcards
what is malabsorption
failure to fully absorb nutrients due to epithelium destruction or a prblem in the lumen so food is not digested
weight loss despite adequate food intake
3 CFs of malabsorbtion
weight loss
steatorrhoea
anaemia
causes of malabsoption
poor intake defective epithelial tranpsort decreased surface area lymphatic obstruction surgery lack of digestive enzymes poor intraluminal digestion
causes of a decrease in SA causing malbsorption
coeliac = villous atrophy
extensive parasites - giardia
bowel resection
crohns
causes of lymphatic obstruction = malabsorption
TB
lymphomas
causes of surgery causing malabsoption
small intestine resection of bypass
e.g of lack of digestive enzymes causing malabsorption
lactose intolerance
e.g of poor intraluminal digestion causing malabsorption
pancreatic insuffic (pancreatitis, CF) defective bile secretion (gall stones) bacterial overgrowth = brush border damage
what is peritonitis
inflam of the peritoneum assos with the rupture of an internal organ
what is the peritoneum
a serous membrane lining the cavity of the abdomen and covering abdominal organs
what is the peritoneal cavity
a closed sac lined by mesothelial cells that secrete surfactant
causes of peritonitis
perforation of GI tract (trauma, peptic ulcer)
autoimmune - SLE
primary = spontatneous bacterial infections
secondary = localised = acute inflam - acute appendicitis, acute cholecystitis
generalized = irritation due to infection (E. coli)/chem irritants due to intest contents leakage (peptic ulcer)
RF of peritonitis
peritoneal dialysis, ascites
what is spontaneous bacterial peritonitis
neutrophils in ascitic fluid when ascites is secondary to a chronic liver disease assos with E. coli and S. pneumonia
CFs of peritonitis
borderline rigitidiy guarding fever abdo pain exab by movement and coughing (hence lay still) n+v tender hard abdo perforation = sudden onset = shock SEPSIS if low bp
what is characteristic of the abdo pain in peritonitis
exab by movements and coughing, relieved staying still
signs of peritonitis
fever
tender hard abdo
tachycardia
guarding
symptoms of peritonitis
nausea and vomiting
severe abdo pain - exab by movement and coughing (LAY STILL)
Dx of peritonitis
erect CXR = gas under diaphragm
ascitic tap = culture
bloods - rule out pancreatitis
Mx of peritonitis
broad spec antibiotics
percutaneous catheter drainage
what is IBS
group of abdominal symptoms for which no organic cause can be found - diagnosis by exclusion
3 types of IBS
IBS-D
IBS - M
IBS - C
epdiemiology of IBS
female
stress
western world
less than 40
Triggers of IBS
depression, anxiety, psychological stress/trauma
gastrointestinal infection
eating disorder
pelvic surgery
cancer red flag symptoms when patient for IBS
over 50 yo with change in bowels unexplained WL PR bleed rectal/abdo mass anaemia fam histroy of ovarina/bowel cancer increased inflam markers
CFs of IBS main one
abdo pain releived on passing stool
CFS of IBS
abdo pain relieved on passing stool \+2 of; altered stool passage bloating mucus in stool poor sleeping painful periods (dysmenorrhoea) symptoms worse on eating lethargy, back ache, nausea bladder symptoms (urgency, nocturia)
what exabberates IBS
stress
menstruation
gastroenteritis
Dx of IBS
exclude other causes
FBC - anaemia
colonoscopy - crohns UC colorectal cancer
serology - coeliac - tTG and EMA antibodies
ESR and CRP - inflam
stool sample - faecal calprotectin (IBD)
DDx of IBS
lactose intol
caeliac
IBD - crohns UC
colorectal cancer
Mx of IBS
lifestyle modifications
pain/bloat - antispasmodic - buscopan / mebeverine
constip = laxitive - senna
diarrhoea - loperamide (antimobility)
pain - low dose tricyclic antidepressant = amitriptyline
antispasmodic for treating IBS
buscopan, mebeverine
antimotility for IBS Mx
Loperamide (for diarrhoea)
drug for constipation in IBS
laxative = Senna
pain relief in IBS
amitriptyline
life style modifications for IBS
FODMAP diet small regular meals avoid alcohol and caffiene avoid fizzy drinks increase fibre - soluble fibre softens stool insol increases gut motility
what does FODMAP stand for
fermentable, oligosaccharides, disacharides, monosacharides, polyols
what is crohns disease
transmural granulomatous inflammation in any part of the GI tract - chronic XS immune response to an unknwon trigger
where is Crohns most likely to affect in the GI tract
terminal ileum to proximal colon
RFs for crohns
smoking, appendectomy,
fam history
genetic
microscopic features of Crohns
no crypts absesses,
goblet cells present
transmural.
granulomas w langerhans giant cells
what is a granuloma
Aggregate of epitheliod Histyocytes - noncaesating
macroscopic features of crohns
skip lesions
cobblestone appearance due to deep ulcers and fissures
thickened and narrowed bowel
anywhere from oesophagus to anus
MNEUMONIC for crohns
driving CROHN for CHRISTMAS Cobble stone High temp Reduced lumen (obstruction) Intestinal fistuale (complic) Skip lesions Transmural Malabsorption Abdo pain /anal (peri) lesions Submucosal fibrosis
how to Dx crohns
colonoscopy and biopsy - transmural inflam, goblet cells, granulomas
bloods - anaemia - Fe and folate defic, increase CRP,
barium swallow - strictures and bowel shortening
stool sample - faecal calprotectin, infection
Mx of crohns
smoking cessation induce remission (glucocorticoid) PREDNISOLONE add on - athioprine if severe = infliximab surgery
the corticosteroid with crohns
prednisolone
Ulcerative colitis what is it
autoimmune inflam disease triggered by colonic bacteria causing inflam in the colonic mucosa only
Relapsing and remitting inflammatory disorder of the COLONIC MUCOSA .
what causes Crohns disease pathophysiology
trigger = Th cells relase inflam cytokines = INFLAM - further mediators (free radicals, proteases), unregulated = increase in inflam and tissue destroyed and invade intestineal mucosa - ULCER and GRANULOMA - TRANSMURAL - fistulae/narrowing
complications of crohns
obstruction, enteric fistulae, perforation = major bleed
symptoms of Crohns
abdo pain (RLQ if ileum)
fatigue
weight loss
N and V
signs of crohns
fever pyrexia dehydration aphthous mouth ulceration abdo tenderness/mass (if inflamed loops) arthritis uveitis perianal (skin tags)
causes of UC
CD8+ cell activation destroying cells in the mucosal submucosa colonic layers
assos w p.ANCA
where does UC affect
never spreads proximal to the ileocaecal valve
what is UC called if only affects rectum
proctitis (50%)
what si UC called if affects rectum and extends to sigmoid and desc colon
L sided colitis (30%)
what is UC called if affects whole COLON
extensive colitis (20%)
RFs for UC
stress infection NSAIDS genetic NOT SMOKING NOT APPENDICECTOMY
peak incidence for UC
for crohns
UC - 15-25 then 55-65
Crohns - 20-40
Ethnic group at risk in IBD
Jewish
Macroscopic features of UC
mucasa red and inflamed = friable
continuous
circumferential inflam
severe - ulcers and pseudopolyps
mircoscopic features of UC
superficial mucosal inflam - mucosal layer only
no granulomas
goblet cell depletion
crypt abssesses
what characteristic of UC on a colonoscopy
drainpipe mucosa (lack of haustrations)
stools test in UC - why?
to exclude C difficile
what does bloods show in UC
p-ANCA POSITIVE (neg in crohns)
ESR CRP increased
normochromic/cytic anaemia of chronic disease (iron and b12 defic)
symptoms of UC
diarrhoea as cant absorb water bloody and mucous lower abdo discomfort (LL quadrant) WL Fatigue
signs of UC (intestinal)
pyrexia
dehydration
abdo tenderness/distentsion
tachycardia
extra intestinal signs of UC
clubbing
oral ulcers
erythema nodosum (red lumps under skins)
Complications of UC
toxic megacolon fatty liver changes erythema nodosum on skin increased colon cancer risk arthritis = joints uveitis = eyes
what is toxic megacolon
non obstruction, dilatation of think walled colon = gas filled - emergency
fever hypotension and tachycardia
which is smoking protective for in IBD
UC
Mx of UC
5ASA (aminosalicyclic acid) - induction and maintanence
acute relapses - corticosteroid - prednisolone
suregery (curative)
Mx complications
INFLIXIMAB - biologics - severe
what is the drug used in UC for induction and maintenence
5ASA - aminosalicyclic acid
what used to manage acute relapses of UC and Crohns
corticosteroid - prednisolone
what biologic used for UC and Crohns
infliximab
in UC how to differenciate between proctitis or L sided/extensive
proctitis - freq blood and mucus with urgency and tenesmus
l sided or extensive collitis - bloody diarrhoea. urgency /incontinence at night. 10-0 LIQUID stools/day
which IBD has pseudo polyps
UC
which IBD has granulamtous inflam
Crohns
what is GORDS
prolonged or recurrent reflux of gastric contents into oesophagus
pathophysiology of GORDS
LOS loses tone and increased freq of LOS transient relaxations and so gastric contents reflux into oesophagus - prolonged contact with LO mucosa (has greaer sensitivity to gastric acid and decreased clearance
causes of GORDS
pregnancy (increased abdo pressure) decrease in pressure of LOS - LOS hypotension LOS dysfunction antireflux mechanism impairment - hiatus hernias slow gastric emptying drugs - nitrates, tricyclics, gastric acid hypersecretion alcohol smoking overeating - spicy foods
what is a cause of antireflux mechanism impairment
hiatus hernia
drugs that cause GORDS
nitrates, tricyclics,
CFs of GORDS
food/acid brash =- regurg heart burn - worse lying down, hot drinks, alcohol odynophagia - painful swallowing chronic cough laryngitis
what is characterisitc of heart burn in GORDS
worse on lying down, alcohol and hot drinks
Dx of GORDS
oesophago-gastroduodenoscopy if red flags new onset heart burn and over 45yo
treat based on history
alarm signs in GORDS - get oesophagogastroduodenoscopy
ALARM Help! Anaemia Loss of weight Anorexia Rapid onset of symptoms Melaena
Help! ( haematemesis)
Lifestyle modifications for GORDS
stop smoking
less alcohol
sleep w head raised at night (extra pillow)
Mx of GORDS
lifestyle mod
anatacids - alginate containing - gaviscon/rennie (magnesium trisilicate)
PPIs - omeprazole - blocks gastric acid secretion
H2 recp antagonist - rinetidine - blocks histamine recep - no acid release
complications of GORDS
BARRETTS OESOPHAGUS
peptic stricture
premalig for adenocarcinoma
e.g of a h2 recp anatagonist used in GORDS
rinetidine
e.g of PPI used in gords
omeprazole
e.g of anatacids used in gords and SE
magnesium trisilicate - Mg and Al
SE- Mg = diarr
Al= constip
(gavison, rennies)
how does an antacid work in gords
forms a protective foam layer over the gastric contents
what is a peptic ulcer
a break in superficial epithelial cells pentrating down to the muscualris mucosa of the stomach or duodenum
assos with chronic gastritis
>5mm in diameter
what do fovela cells secrete and where
mucous in cardia
what do parietal cells secrete n where
HCl (H+) in the fundus and body
what do chief cells secrete and where
pepsinogen in the body and fundus
what do g cells secrete and where
gastrin in duodenum and pancreas
what does gastrin do
stimulate parietal cells to secrete HCL
what does brunner glands in duodenum do
secrete mucus rich in bicarb to prevent self digestion from acid
what do prostaglandins do
stim mucous and bicarb
vasodilate BV nearby increasing blood flow promoting epithelial cell growth and inhib acid secretion
what is the cause of peptic ulcer disease
HELIOBACTER PYLORI NSAIDS smoking alcohol mucosal ischaemia
how does H. pylori cause peptic ulcers
colonizes the gastric antrum mucosa and increases gastric acid secretion and decreases duodenal bicarb secretion
produces ammonia so able to survive the acidic conditions
lives in crypts next to acid sensors and alters feedback mechanisms = XS acid produced
causes localised inflam
why do NSAIDs cause peptic ulcers
inhib COX1 which reduces prostaglandin synthesis
why does a decrease in prostaglandin synthesis mean peptic ulcers form
postaglandins inhibit ECL and so decreases histamine production. less HCl from parietal cells.
less prostaglandin therefore = more HCl
why does smoking cause PUD
decrease prostaglanding synth which is a mucosal protective
why does mucosal ischaemia cause PUD
less mucin so less protection = mucosa damaged causing an ulcer
(due to atherosclerosis)
symptoms of PUD
epigastric pain - Gastric ulcers = worse on eating hence weight loss duodenal ulcers = improves on eating N and V bloating haematemesis and melaena dyspepsia (indigestion) heart burn aneamia symptoms - fatigue,m dizziness
complications of Duodenal ulcers
perforation - peritonitis
haemorrhage
gastric outlet obstruction
which type of ulcers is worse on eating
gastic - hence weight loss
duodenal relieved
diagnosis of peptic ulcers
H PYLORI BREATH TEST - urea breath - C13
endoscopy
stool antigen test - H. Pylori
bloods - FBC (anaemia)
explain how to test for H. pylori as cause of Peptic ulcers
H. pylori breath test = positive = urea breath
H. pylori converts urea to ammonia and co2. as it secretes urease
use C 13
stool antigen test also
rapid urease test on a stomach biopsy
specific clinical features of duodenal ulcers
epigastric pain 2-5hrs after eating - radiate to back in panreas affected
more common
specific clin features of gastric ulcers
epigastic pain 1-2 hrs after eating
haematesis or melaena
signs of PUD
melaena
haematesis
epigastic tenderness
Mx of PUD
lifestyle eradicate cause (H. pylori - using triple therapy - (PPI + Amoxicillin + Clarithromycin) PPIs - omeprazole h2 recep antagonists - rantidine STOP NSAIDS
how treat PUD if H pylori the cause
triple therapy =
PPI + amoxicillin + clarithromycin
what PPI use in PUD
omeprazole
what is coeliac disease
gluten sensitive enteropathy
= t cell mediated condition in response to prolamin == malabsoption
what does coeliac disease result in histologically
villous atrophy
crypt hyperplasia
intraepithelial lymphocytosis (increased lymphocytes in lamina propria)
causes of coeliac disease
genetic - HLA DQ2 or DQ8
HLAs assoc with coeliac disease
HLA DQ2 or DQ8
what is it that triggers the immune response in coeliac disease
gliaden = toxic component in gluten resistent to digestion by pepsin and chymotypsin so remains in intestinal lumen
what happens to gliaden in the gut
gliaden peptides pass through epithelium via TFR receptor and get DEAMINATED by TISSUE TRANSGLUTAMINASE (increases immunicity)
they bind to antigen presenting cells and interact w CD4+ cells via HLA class 2 molecules
produces pro inflam cytokines (INF-gamma, TNF)
B cells secrete anti EMAs anti gliadin and anti itTG
activates T nat killer cells causing villous atrophy
gaps in epithelial cells widen = more gliadin IN
what antibodies on serology for coeliac
IgA tTG (tissue transglutaminase) IgA EMA (anti-endomysial antibodies)
what found on bloods of coeliac disease
anaemia (folate and iron defic)
how to Dx coeliac
serology - IgA tTG, anti-endomysial antibodies
intestinal biopsy
HLA typing - HLA DQ2 or DQ8
symptoms of Coeliac
diarrhoea/ constip and steatorrhoea
WL
X to thrive in children
fatigue
signs of coeliac
mouthulcers, angular stomatitis, abdo distenstion
complication of coelica
dermatitis herpeti formis = skin rash due to antibodies Iron deficiency anaemia osteoporosis vit deficiency (vit D, ADEK, iron) MALIGNANCY (small bowel lymphoma..)
what is dermatitis herpeti formis
skin rash die to antibodies found in coeliac disease
how to treat coeliac
strict gluten free diet
monitor complications
i.e DEXA scan for osteoporeosis
vit supplements
what causes acute appendicitis
obstruction by a faecalith
Cfs of appendicitis
central periumbilical pain radiating to R iliac fossa
ANOREXIA
N&V
rebound tenderness and muscle guarding in RIF
diarrhoea
tender mass if appendix abbsess
R shoulder pain if diaphragm irritation
where is the pain in appendicitis
central periumbilical radiating to RIF
R shoulder pain if diaphragm irritation
what is the point of abdo pain called in appendicitis
Mcburneys point (REBOUND = pain)
why do you get abdo pain in appendicitis
increased pressure in appendix due to faecalith plug but mucus production still continues.
enlarges and presses on visceral nerve fibres
why do u get a fever in appendicitis
appendix obstructed by faecalith
stasis causes bacterial overgrowth (e.coli)
increaseing WBC and pus accumulates causing a fever
patho of ischaemia in appendicitus
faecalith blockage
stasis
bacterial overgrowth- WBC and pus increases pressure further
compromises blood supply and therfeore no oxygen = ischaemia
how can appendicitis lead to peritonitis
iscahemia of appendix wall = weakens = prone to rupture
releasing bacteria into peritoneum
=rebound tenderness and abdo guarding
Dx of appendicitis
clin exam
bloods - increased WBC, increase C reactive protein, ESR
CT and US
Mx of appendicitus
appendectomy
ABX (IV Metronidazole + cefuroxime)
CI of appendicectomy
IBD involving the caecum
what causes gastroenteritis (general)
viral bacterial parasitic fungal antibiotic assos
viral causes of infective diarr
rotavirus (children)
norovirus (winter vomiting, carehomes)
adenovirus
bacterial causes of infective diarr
campylobacter jejuni,
E. coli,
Salmonella (animals),
shigella (blood)
parasitic cause of infective diarr
Giardia lamblia (travel history)
fungal cause of infective diarr
histoplasmosis
antibiotic assoc infective diarr causes
(= C DIFFICILE)
ciprofloxacin
clindamycin
RF for gastroenteritis
forgein travel
poor hygiene
over crowding
new/diff foods
who is at risk for gasteroentertisi
immunosuppresed young old decreased gastric acid secretion travellers
clinical features of infective diarrhoea
blood in stool (=suggests bacterial) vomiting fever fatigue headache muscle pains
Diagnosis of infective diarrhoea
history (eating habits, occupation, travel)
stool culture
C. diff assay
chronic = sigmoidoscopy
Mx of gastroenteritis
rehydration
antibiotics (empirical) for infective
antimobility (loperamide)
life style = wash hands,exclude from work etc
what is C difficile
gram positive spore forming anaerobic bacteria ingested faeco orally
what causes C. diff assos diarhoea
broad spec antibiotics
RFs for C diff assos diarrhoea
age and co morbidities, ABX PPIs long HOSPITAL admission NG tube fed immunocomp
pathology of C. diff assos diarrhoea
colonises stool then to patient (asympt)
when normal colonic microbiota is altered by ABX
environ then favours proliferation
inflamed and ulcerated and a pseudo membrane on endoscopy (inflam exudate)
what see on endoscopy of C diff ass diarrhoea
pseudo membrane
abx assos with C diff diarrhoea
rule of "C" Clindamycin ciprofloxacin cephalosporins ciprofloxacin co-amoxiclav
how to diagnose C diff diarrhoea
stool sample - toxin A or B
clin features of C diff diarrhoea
abdo pain and watery stools
collitis
what conditions make up ischaemia of the colon
acute mesenteric
chronic mesenteria
ischaemic colitis
what is the pathophysic behind acute mesenteric ischaemia
low flow in the superior mesentery artery
causes of acute mesenteric ischaemia
SMA thrombosis or embolism (AF)
mesenteric vein thrombosis
non occlusive diesease ( i.e low flow and poor cardiac output)
CFs of acute mesenteric ischaemia
acute severe abdo out of proportion with signs
rapid hypovolaemia – shock
Dx of acute mesenteric ischaemia
ABG - metabolic acidosis and high lactate (due to intestinal hypoxia - increased lactic acid)
Bloods - Leukocytosis
laparotomy- cut into abdo wall = diagnosis
Mx of acute mesenteric ischaemia
surgery - remove dead bowel
fluid resus
antibiotics - IV gentamicin, IV metronidazole
IV heparin to reduce clotting
Complications of acute mesenteric ischaemia
septic peritonitis
systemic inflamm response syndrome (SIRS)
what is systemic inflam response syndrome
multiple organ dysfunction syndrome mediated by bacteria translocation across dying gut wall
pathophysiology of acute mesenteric ishaemia
sudden interuption of SMA intestinal hypoxia (metabolic acidosis due to increase lactic acid) haemorrhagic infarction and necrosis disrupts mucosal barrier +perforation bacteria and toxins, ROS released sepsis Systemic inflam response sydrome
what is ischaemic colitis
low flow in inferior mesenteric artery resulting in ischaemia of the colon
Cx of ischaemic colitis
low flow in IMA underlying atherosclerosis and vessel obstruction
Rf of ischaemic colitis
cotraceptive pill
thrombophillia
vasculitis
nicorandil drug
Cfs of ischaemic colitis
BLOODY diarrhoea
LLQ pain
complications of ischaemic colitis
perforation
sepsis
peritonitis
Dx of ischaemic colitis
colonoscopy (when recovered to exlcu strictures)
urgent CT to excl perforation
barium enema - thumb printing of submucosal swelling at splenic flexure
Mx of ischaemic colitis
conservative
if gangrenous - resus and bowel resection (peritonitis and hypovolaeimic shock)
what is gastritis
inflamm assos with mucosal injury
what protective mechanism to gastric cells have in the stomach
secrete mucin to protect from low pH in stomach
Cx of gastritis main one
Heliobacter pylori infection
causes of gastritis (detailed)
H. pylori
autoimmune gastritis (vs parietal cells and IF = pernicious aneamia)
duodenogastric reflux - bile salts enter and damage mucin production)
granulomas (crohns, sarcoidosis)
viruses - herpes simplex
mucosal ischaemia ( low blood supply less mucins = more acid)
chemical - NSAIDs aspirin alcohol ( inhib prostaglandins which stim mucous production)
causes of gastritis menumonic form
DRAG HIV Drugs (NSAIDs, aspirin, alcohol) Reflux (duodenogastric) Autoimmune Granuloma (crohns)
H pylor
Ischaemia of mucosa
Virus (herpes simplex)
Cfs of gastritis
N+V
abdo bloat
haematemesis
Prevention of gastritis
PPIs alongside NSAIDs ( to prevent bleeding from actue stress ulcers and gastritis
Tx of gastritis
etradicate h pylori if positive - triple therapy (PPI and 2 of metronidazole, bismuth, amoxicillin, tetracycline)
decrease stress
remove Cx agents
PPI or H2 receptor antagonists
complications of H pylor gastitis infection
GASTRIC CANCER
peptic ulcers
inflam and metaplasia
Dx of gastritis
endoscopy
biopsy
DDx of gastritis
GORDs
peptic ulcer disease
gastric carcinoma
how to confirm cause of gastritis is H. pylor
urea breath test
foeacal antigen test
how does H pylori cause gastritis
colonises mucous layer in gastric antrum
adhers to epithelial cells in gastric pits under MUCOUS LAYER SO PROTECTED
damages by enzyme release -
urease converts urea to ammonium = toxic to gastric mucosa so less mucous produced
chem mediators produced = induce inflam = ulcers and more acid
why can H pylori survive in stomach
adherres to epithelium UNDER mucus layer so is protected
what is a hernia
protrusion of organ or tissue out of the body cavity it normally lies
Causes of hernias
muscle weakness (age trauma) body strain - pregnancy contsipation heavy lifting, chronic cough
what is an inguinal herna
protusion through the inguinal canal
2 types of inguinal hernia and the difference
indirect and direct
direct = MEDIAL to inferior epigastric vessels
indirect = LATERAL to inferior epigastric vessels and protrudes through the INTERNAL INGUINAL RING (follows spermatic cords path)
which hernia can go to the scrotum
indirect inguinal hernia
which hernia lies LATERAL to inferior epigastric vessels
indirect
which hernia lies medical to inferior epigastric vessels
direct
CFs of an inguinal hernia
visible lump
pain/ache on exertion
Mx of inguinal hernia
surgery
Rfs of inguinal hernais
male smoker,
history of hernias (weak abdo wall)
2 types of hernias
hiatus and inguinal
what is a hiatus hernia
part of the stomach herniates through the oesohphageal hiatus of the diaphragm
2 types of hiatus hernai
rolling and sliding
what is a sliding hiatus hernia
gastro oesophageal junction slides up into the chest
get gastric acid reflux as LOS less competent
what is a rolling hernia
gastro oesopheal junction remains in the abdo but bulge of stomach herniates into chest alongside oesophagus = still intact hence no gross acid reflux
which hernia causes acid reflux and why
sliding hiatus hernia - gastro - oesp junction slides up into chest so LOS less competent
rolling, it remains in the abdo below diaphragm
in which hiatus hernia does the gastro oespho junction remain below the diaphragm
rolling
CFs of hiatus hernias
rolling - none as no reflux, pain if severe due to strangulation
sliding - acid reflux
