GI Flashcards
what is some anti reflux physiological mechanism
Lower oesophageal sphincter formed by the diaphragm
what is oesophagitis
Inflammation of the oesophagus due to reflux
Presentation of GORD
Heartburn, main feature
aggravated by lying down, bending
relieved by antacids
Burning pain
Other Dry cough chronic acid regurgitation water brash and increased production of saliva dysphagia bloating early satiety halitosis enamel erosion
causes and factors associated with GORD,
lifestyle
drugs and diseases
LOS hypotension gastric acid hypersecretion slow gastric emptying loss of oesophageal peristaltic function Hiatus hernia family history pregnancy obesity large meals smoking eating fat chocolate, coffee alcohol drugs like CCB (relax LOS) antimuscarinic H Pylori
diagnosis of GORD
usually a clinical diagnoses and sees its improved by PPI
Investigations for GORD
first line is PPI trial, if symptoms persist past this time then further investigation
Red flags for GORD, things that suggest further investigation is required
Over 55 YO Dysphagia vomiting weight loss GI Bleed hematemesis Persestat symptoms
Further investigations for GORD
Barium swallow- if dysphagia
endoscopy, can show oesophagitis (erosive ulcers) or barrett’s oesophagus
ambulatory PH monitoring
Management in GORD
conservative
50% of management is simple antacids
education: smoke less lose weight, reduce alcohol. raise head when sleeping
eat smaller meals, avoid over eating
education on diet of GORD
avoid certain drugs, CCB Nitrates anticholinergics, these slow oesophageal motility
avoid NSAIDs, Salts, these damage mucosa
Triggers of GORD and foods to avoid
Caffeine, chocolate, spicy food, alcohol, citrus, fizzy drinks
Drug treatment of GORD
can trial antacids
1st line PPI- omeprazole, lansoprazole
can use H2 antagonist if not responding to PPi Ranitidine
surgical management of GORD
endoscopic nissen fundoplication, operation to treat Hiatus hernia
complications of GORD
if prolonged can cause oesophagitis
Barrett’s oesophagus
oesophageal ulcers, perforation hemorrhage or strictures
what is barrett’s oesophagus
pre malignant, epithelium of the oesophagus is usually squamous but after GORD squamous is replaced by columnar epithelium of the stomach since it can tolerate the acid
can become Oesophageal cancer
how is GORD classified
Los angeles GORD classification
categories ulcerations and erosions as mucosal breaks. 1 to 4
diagnoses of barrett’s oesophagus
Endoscopy with biopsy
risk factors for barrett’s oesophagus
Age, white men
prolonged GORD
Smoker
management of barrett’s oesophagus
PPI + surveillance
plus Radiofrequency ablations and endoscopic mucosal resection
Potential esophagectomy
what is chronic idiopathic inflammatory bowel disease
life long long chronic inflammatory disease of bowel split into Ulcerative colitis and crohn’s disease
where does crohn’s affect and where does it most commonly start
anywhere from mouth to anus. most commonly starts at terminal ileum
where does UCs affect
only affects the colon unless ileocecal valve is incompetent or backwash ileitis
epidemiology of crohn’s and UC
Crohn (0.1%) is more common in females. and affects people in 20s onset 15-40 years
UC usual onset is after 35
20-40 years
both get peaks after 60 Years
describe crohn’s lesions
most commonly start in terminal ileum or ascending colon.
affect anywhere in GI tract, lesions tend to skip areas, so lesions are interspersed
the lesion affects transmurally and all the layer of bowel
if it affects the whole GI tract it is known as total collitis
what is it known as when crohn’s affects the entirety of the GI tract
Total colitis
Describe UC lesions
start in rectum, once take cover full rectum (proctitis) it starts to spread up sigmoid and descending colon (Left colitis) and then spreads all the way to the Ileocecal valve (oan colitis)
stops at ileocaecal valve, unless there is backwash ileitis
Inflammation only covers the top layer of bowel (serosa) and is continuous, no interspaced lesion
Describe Crohns macroscopic appearance
small bowel is thickened and has ulcers and fissures that give rise to cobble stone appearance
Describe UC macroscopic appearance
mucosa appears reddened and inflamed
Erythematous appearance
Describe Crohns Biposy result
Transmural inflammation patchy inflammation Granulomatous present in 50% goblet cells present Crypt abscess
Describe UC biopsy result
Affects only serosa continuous inflammation Goblet cell depletion and crypt abscess Granulomas are rare to see
Symptoms of Crohn’s disease
Diarrhoea, abd pain and weight loss
Nausea and vomiting
malaise lethargy and anorexia
aphthous ulceration in mouth
Diarrhoea, very frequent, very malodorous
can be like 5-6 times in an hour so affects Q of L
Symptoms of UC
Diarrhoea with blood and mucous
abd discomfort
malaise lethargy anorexia
can have rectal bleeding
diarrhoea can be episodic or chronic, normal for a while then flares up
Biochemisty, bloods and serology in Crohns disease
Normocytic anemia, can have iron deficency
ESR CRP and WCC elevated
PANCA antibody -ve
ASCA +ve
Biochemistry Bloods and serology in UC
Iron deficeny anemia
ESR and CRP elevated
PANCA antibody present
ASCA -Ve
Investigations in Inflammatory Bowel disease
Bloods, FBC
Stool culture, do this with anyone presenting with diarrhoea - negative
ESR and CRP elevated
Gold standard: colonoscopy Plus Biopsy
can do CT MRI Barium Swallows and all sorts
Crohn’s Management
conservative and non disease modifying treatment
Symptomatic treatment, control diarrhoea (antidiarrhoeal agenst Imodium) control abd pain (analgesics)
stop smoking
Crohn’s management
Disease and pharmacological
Induce remission using prednisolone or (Hydrocortisone if severe)
then afterwards maintain remission using aminosalicylates, 5 ASA
Anti TNF Infliximab can also be used to induce and maintain remission
Crohn’s management
surgery option
resection of extremely inflamed areas
treat complications like strictures of fissures
UC Management
All UC patients are treated with 5-ASA- Sulfasalazine
+ Fluids for dehydration and IV corticosteroids for flare ups
if very severe used Hydrocortisone to induce remission
anti TNF like Infliximab can be used
surgery for resection of terminal ileum or proctocolectomy, or in fissures, strictures, perforations, toxic dilations
what is a 5 ASA and method of action
anti inflammatory only in bowel, because it gets activated when in the lower PH of bowel
UC complications
Colon cancer bowel perforation toxic dilation hemorrhage ankylosing spondylitis (not a complication but can can occur concurrently)
CD Complications
stenosis strictures fistulas abscess forming cancer in ileocaecal malabsorption perforation obstruction
risk factors to inflammatory bowel disease
Family history age groups 20-40 and 60 plus
what is the gene associated with UC
HLA - B27
what is the prevalence of coeliac disease
1%
What is coeliac disease
Inflammation in the small intestine due to autoimmune response triggered by Gliadin in Gluten
Coeliac disease pathophysiology
Gliadin, a protein in Gluten is not broken down in the stomach, it is usually binds to IgG in the Intestines and is destroyed
But in coeliac that IgG Gliadin complex is transported across and is phagocytosis by macrophage and causes inflammation and damage to the small intestine
Presentation of coeliac disease
suspect in weight loss + diarrhoea Abdominal distension - Bloating Anemia - iron deficiency Depression Gas failure to thrive in children dermatitis herpetiformis
what is skin change associated with coeliac disease
dermatitis herpetiformis ( pretty much specific to Coeliac disease)
diseases associated with coeliac disease
Other autoimmune disorders
Type 1 DM
Thyroid disease
IBS
Complications of coeliac disease
Iron deficiency anemia lactose intolerance osteoporosis - since less mineral and ca absorption T cell Lymphoma Increased risk of malignancy
Investigations of Coeliac disease
Needs to be eating gluten for the past 6 weeks
Serology testing Look for: anti TTG (transglutaminase) anti EMA (EndoMysial) IgA, and Alpha gliadin
Bloods- HB low Iron Low Ferritin low B12 low
genetic testing HLA testing
Duodenal biopsy is gold standard for investigations
what is the histology of coeliac disease show
this is shown by duodenal biopsy
villous atrophy and crypt hyperplasia
flattened villi and longer crypts
Management of coeliac disease
lifelong gluten free diet
involve a dietician to ensure they still get all essential nutrients from a gluten free diet
can prescribe gluten free flour bread pasta
carry on monitoring EMA testing to see effect
DEXA can to assess if any osteoporosis
what are commonest causes of malabsorption
Coeliac disease
chronic pancreatitis
Crohn’s disease
other causes of malabsorption
Insufficient intake (Malnutrition)
Insufficient absorptive area: due to resection (crohns) coeliac
defective intraluminal digestion: pancreatitis, reduced Bile (due to Biliary obstruction or liver disease or ileal resection) bacterial overgrowth
Defective epithelial transport- genetic mutation
Lymphatic obstruction- lymphoma or TB
Lack of digestive enzymes: Disaccharidase deficiency (lactose intolerance)
Presentation of malabsorption
diarrhoea
weight loss
lethargy
steatorrhea
(anything from crohn’s coeliac or infection, pain,
distention, anemia nausea and vomiting, malaise)
signs of malabsorption
anemia ( iron, B12, Folate)
bleeding disorder easy bruising ( vit K)
oedema (protein)
Osteoporosis (vit D and Ca)
tests for malabsorption
Bloods: FBC Ca B12 Folate INR Coeliac test, anti TTG, EMA AMA PBC, Liver failure investigations (ANA, Anti Trypsin copper and Iron) Stool: check for overgrowth ERCP: biliary stones or pancreatitis)
Common pathogen that lead to malabsorption and how is it treated
Giardia Lamblia (Extensive surface parisitation) diagnosed by biopsy Treat with tetracycline
What is irritanble bowel syndrome
a group of abdominal syndromes where no other cause is found
main causes/RF of IBS
Depression and anxiety psycological stress and trauma GI infection eating disorer physical or sexual abuse Female
IBS prevalence and age of onset
10-20%
usually under 40 Y O
clinical features of IBS
pain or discomfort is alleviated by Defecation
Altered stool form or frequency (constipation and diarrhoea alternating)
Urgency
Incomplete evacuation
Abdominal bloating and distension
mucus PR
Symptoms worsen after food
symptoms exacerbated by stress, menstruation, Gastroenteritis
needs to be chronic (6 Months)
not attributable to other cause (coeliac, infection)
Other symptoms include backache, nausea, Bladder problems
Diagnostic criterias of IBS
6 month history of abdominal pain and discomfort
plus one of the following
symptoms relieved by defecation
alterations in stool form and frequency
Plus 2 of: Urgency frequency Abdominal bloating Mucus PR
further Investigations of IBS
Duodenal biopsy -ve Stool cultures -ve ESR and CRP -ve endoscopy normal colonoscopy normal absence of EMA anti TTG IgA ERCP etc
Management of IBS
Healthy diet
things that make it worst: Fiber, lactose, fructose, wheat, starch, caffeine, alcohol, fizzy drinks.
use of probiotics
potentially refer to psychologist for counseling if think of stress or depression. or to pain clinic, as can coexist
Psychological stress make symptoms worse, abuse
Symptomatic treatment:
Constipation:Bisacodyl
Diarrhoea: Loperamide
what is the differential for haematemesis
Upper GI Bleed. think peptic ulcer is commonest cause
GO Varices
mallory weiss tear
Natural defences of stomach against acid
Alkaline mucus
tight junctions
replacement of damaged cells
Feedback loops
Causes of peptic ulcers
NSAIDs, - inhibit prostaglandins which make mucus
Bile salts due to duodenal gastro reflux, Bile salts strip away mucus layer
H-Pylori
how does H pylori cause Peptic ulcers
secretes Urease, which becomes ammonia then ammonium which causes inflammation and destroys mucosal defence
H pylori is precursor for Gastritis and Peptic ulcers
Risk factors for peptic ulcers
H pylori infection Smoking NSAIDs Duodenal reflux Delayed gastric emptying Stress
Presentation of peptic ulcers
Epigastric pain, relating to meals and hunger
Relived by antacids
can be in L and R UQ
Dyspepsia- Indigestion , feeling bloated
Heartburn and epigastric tenderness
Red Flags that for dyspepsia that make you think to exclude malignancy before thinking peptic ulcers
ALARM Symptoms Anemia - iron deficient Loss of weight Anorexia Recent onset Malena / Haematemesis Swallowing difficult
Differential diagnosis for dyspepsia
oesophagitis/ GORD Duodenal or gastric ulcer Gastric malignancy (ALARM signs) Duodenitis Gastritis non ulcer dyspepsia
duodenal ulcers presentation
Epigastric pain before meals or night
relieved by eating or drinking milk
pain can be localised by finger
Epigastric tenderness
Investigations and management of dyspepsia
if they are Over 55 and show alarm symptoms carry out urgent upper GI endoscopy
Under 55 and no alarm symptoms:
Stop dyspepsia causing drugs,try antacids, and lifestyle changes like with GORD (alcohol, Caffeine, Fizzy drinks, Spicy foods)(sleep upright, don’t overeat)
If symptoms don’t improve carry out H Pylori Test
if -ve use PPI for 4 weeks before doing upper GI endoscope
Investigations for H. Pylori
Non Invasive C 13 Urea Breath test
Treatment for H. Pylori
Triple therapy
1 PPI- Lansoprazole, Omeprazole
2 antibiotics- Amoxicillin and clarithromycin
Complications of peptic ulcers
Hemorrhage and bleed
perforation
malignancy and gastric outlet obstruction (projectile vomiting)
What is H pylori
Gram -ve Curved bacteria present in around 50% f population but asymptomatic
What can H Pylori cause
Gastritis
Peptic ulcers, gastric or duodenal
Gastric cancer
what is zollinger ellison syndrome
Gastrin secreting tumour or hyperplasia in pancreatic islets causing recurrent peptic ulcers
what is gastritis
Inflammation of the gastric mucosa, essentially pre peptic ulcer stage
Describes the redness seen on endoscope
Causes of gastritis
injury to gastric mucosa
commonest cause is H pylori
Irritants, Bile Alcohol, NSAIDs
Autoimmune gastritis - autoimmune disease destroying parietal cells, leads to pernicious anemia
Treatment of gastritis
Treat Underlying disease,
H pylori triple therapy
what are different types of intestinal obstruction
firstly small bowel (60^, commonest) or large bowel
can have Volvulus
Adhesions
Intussusception (Telescoping)
causes of small bowel Obstruction
Adhesions (commonest) often post surgery
Inguinal Hernia
Crohn’s
malignancy
in Children
Appendicitis
volvulus
Intussusception
Pathophysiology of SBO and complications
obstruction causes proximal dilation.
less absorption and increased pressure can cause Perforation
increased secretions and sistension can cause anorexia and vomiting
SBO untreated will cause Ischemia necrosis or peroforation
what is adhesive obstruction
Extra luminal obstruction, usually post surgery, talc from gloves becomes silicon and binds parts of bowel together
what type of obstruction of crohn’s disease
Intramural obstruction
What is a volvulus
Type of SBO extra luminal, occurs when bowel twists around itself in mesentery causing obstruction and can lead to ischemia
what are examples of Intramural obstructions
Crohn’s or Diverticular disease
what is mechanical obstruction
obstructions in SBO
volvulus, Hernia Adhesion
Presentation of small bowel obstruction
Colicky pain, nit localised vomiting is early sign in SBO Constipation is Late sign in SBO distension Projectile or feculent vomiting
shows signs of peritonitis if rupture,
Diagnosis of SBO
CT- Gold standard
`Abd X ray
FBC shows WBC elevated and electrolyte imbalance due to dehydration
Other is laparotomy Laparoscopy
Treatment of SBO
Analgesia + antiemetics Antibiotics, ampicillin + Gentamicin Bowel Decompression: Fluid resuscitation Surgery, Laparotomy to remove obstruction
causes of LBO
commonly malignancy 90%
volvulus
Benign structures ( diverticular disease, ischemia)
Hirschsprung disease
Indication of bowel perforation
Persistent tachycardia
Fever
Abdominal pain and tenderness, rebound tenderness and Guarding
pathophysiology of LBO
Obstruction causes proximal dilation. increased pressure.
This reduced mesenteric blood flow causing ischemia which will lead to dehydration and oedema in bowel.
This can progress to perforation
Presentation of LBO
Colicky pain constipation, early Obstipation no faeces or gas Vomiting, late sudden onset of pain= volvulus weight loss palpable mass in abdomen palpable rectal mass abnormal bowel sounds Blood on DRE rectal bleeding fever tenderness, rebound , guarding
Investigations in LBO
general: FBC:WCC Electrolytes: Imbalance renal function: elevated creatinine serum amylase: can be elevated prothrombin time Increased
Specific Abdominal x ray, Shows dilation CT scan Flexible endoscopy + Biopsy Contrast enema
Treatment of LBO
supportive measures: Antibiotics Gentamicin
IV fluids
potentially transfusion
Surgery emergency Laparotomy
What is Hirschsprung’s disease
Balloon Man disease
congenital disease where no innervation of the colon so dilation and no peristalsis
this causes obstruction
What is diverticulitis
Intramural obstruction in Sigmoid colon (commonly)
Muscular layers has holes every once in awhile.
Increased pressure in lumen (often due to poor fiber diet) causes mucosa to pass though these gaps.
Diverticulitis occurs when fecal matter get stuck in thee gaps and becomes inflamed can become Perforated
Presentation of diverticulitis
Severe pain in Left iliac fossa
Constipation and fever
Abdominal tenderness and potentially a mass
Investigations and management of diverticular disease
Ultrasound or CT of abdomen will show diverticular disease
Fluid and antibiotics amoxicillin or metronidazole
Surgery if perforated
appendicitis pathophysiology and causes
Inflammation of the appendix often due to faecolith, poop stone gets stuck.
this causes localized peritonitis and if left untreated and ruptures will gangrene and rupture causing generalised peritonitis or abscess
Clinical features of Appendicitis
Vague abdominal Pain that will develop into localized severe R Iliac fossa pain
Tenderness, rebound
guarding
Nausea vomiting diarrhoea anorexia
Investigations of Appendicitis
WCC ESR and CRP all elevated
Ultrasound is diagnostic
Can do CT if unclear
Management of appendicitis
Laparoscopic surgery to do appendectomy
IV antibiotics, Cefoxitin
Differential diagnosis of Appendicitis
Gynaecological causes Ectopic or Ovarian Torsion Testicular Torsion Colic, Renal Or biliary Crohn's Intussusception
Causes of localised peritonitis
Any inflammation, Appendicitis, Cholecystitis
causes of Generalised Peritonitis
Infection or perforated
appendix, gallbladder gangrene and perforation and Bowel perforation
Perforated Ulcer
Features of localised peritonitis
Secondary to inflammation
Slower onset and symptoms are that of underlying condition. tenderness, rebound tenderness guarding
Features of generalised Peritonitis
Sudden Onset Acute severe abdominal pain collapse and shock can lead to septicemia rebound tenderness and guarding pain made worse by moving
Investigations for peritonitis
CXR, checks for air under diaphragm Serum Amylase- check acute pancreatitis
Ultrasound CT - Diagnostic
Management of peritonitis
surgically treated
NG tube
Iv Fluid
antibiotics- Metronidazole
What is spontaneous bacterial peritonitis
when there is an infection in ascites: often e coli, kelbestia or enterococci
causes of bowel ischemia
most commonly, Thrombosis or thromboemboli
other occlusive causes is volvulus, tumour, intussusception, herno
and hypovolemic causes like spesis or reduced Co after MI
where is ischemic colitis most likely to occur
Always in large bowel
commonly in Splenic flexure or L colon
Where is mesenteric colitis likely to occur
Small bowel
Mesenteric colitis presentation
Severe abdominal pain, Central and around right iliac fossa
no peritonitis signs but can develop onto hypovolemia, shock, tachycardia hypotension, weak pulse, confusion, reduced urine output
Ischemic colitis presentation
Sudden onset of abdominal pain, round hypochondriac, splenic, o L Iliac fossa, L colon Passage or bright red blood from rectum diarrhea Distended +tender abdomen (peritonitis signs of shock
Investigations of Ischemic colitis
Ultrasound or CT to exclude perforation
AXR
later can do Barium enema
colonoscopy + Biopsy
Investigations of mesenteric colitis
Bloods, Look for loss of plasma = increased HB Increased WCC, metabolic acidosis AXR- rule out other causes Laparotomy- diagnostic CT,MRI angiography also diagnostic
what is gold standard to exclude perforation
CT
Management of ischemic colitis
fluids and antibiotics
metronidazole and gentamicin
ultrasound or CT to Monitor for gangrene
Stricture formation is common so use Barium enema
if IC plus gangrene , perforation, shock, peritonitis= surgery
how to identify stricture formations
Barium enema
Management of Mesenteric colitis
fluid plus antibiotics
gentamicin plus metronidazole
IV heparin
Surgery to remove necrotic bowel
monitor for signs of sepsis
