GI Flashcards
Describe acute pancreatitis
- Etiology
- Symptoms
- Pathophysiology
- Main investigation and treatment
Etiology (two main ones, many others)
Gallstones blocking pancreatic duct or ETOH (increased toxic metabolites). Also, azithioprine can cause this – used in IBD.
Symptoms
Severe pain in epigastrium radiating to the back, fever, nausea and vomiting, Cullen’s and Grey Turner’s Signs, can have severe dehydration
Pathophysiology
Zymogens are activated and digest the pancreas, if there is a blockage, get tissue ischemia from lack of flow –> acinar cell injury –> eventual necrosis of the pancreatic tissue
Treatment
ERCP + antibiotics
Serum lipase will be elevated, maybe amylase too
Eventual cholycystecomy if caused by gallstones
Describe Celiac’s disease
- Etiology
- Symptoms/natural history
- Tests and findings
- Complications
- Treatments
Etiology
Sensitivity to gluten causes disruption of the villous within the duodenum and jejunum. HLADQ2/8 increase suspectibility. T-cell mediated response (autoimmune) to the duo/jej. Higher in caucasians. ~1% of Canadians
Symptoms
Bloating, diarrhea
Tests
anti-transglutamase antibody/anti-endomysial antibody: combined has a high sens/spec but to make a diagnosis, need a scope with multiple tissue biopsies to look for villous atrophy. With overt, partial or total atrophy. With latent, no atrophy or partial with intraepithelial lymphocytes. On PE, dermatatis herpatiformatis
Complications
Malabsorption, most common is Fe deficiency
Non-hodjkins intestinal lymphoma
Treatment
NO GLUTEN!!!
Describe the features of benign vs malignant ulcers
Gross
sharp, punched our borders, if caused by H. pylori, found in duodenum (1st part) VS heaped up margins, malignant-looking tissue
Microscopic
sharp borders, neutrophil and fibrin accumulation at the base of the ulcer VS glands (intestinal) or diffuse (signet cells - will also see markedly thickened stomach wall)
Describe H. pylori’s pathogenesis + histological findings and a chronic disease it causes
- Secreates urease to raise pH
- Sticks to the eptithelium with adhesis
- Toxins - may be related to its malignancy potential
- Flagella - can move around within the mucous
Histo
- Curved bacilli structures
- Intraepithelial neutrophils
- sub-epithelial plasma cells with lymphoid aggregates
Related diseases
- MALT lymphomas
- Chronic gastritis
- gastric and duodenal ulcers
List the causes of esophagitis
- GERD
- Chemical, drugs
- Viral (CMV, herpes), fungal (candida)
- Radiation
- graft vs host disease
- eosinophilic
Describe the pathophysiology of barrett’s esophagus
- Constant irratation/inflammation of the lower esophagus, due to leaky LES (pregnancy, obesity, herniation, smoking and drinking etc)
- Intraepithelial eosphinophilic invasion from GERD, basal zone expansion – > abnormal cell maturation
- Metaplasia of the stratified squamous epithelium to columnar goblet cells that secrete mucous
- Very red + ulcerations
- Considered pre-malignant and requires endoscopal screening (it is reversible)
- Treat the UNDERLYING CAUSE!
Discuss the pathophysiology of IBD and specifically discuss Colitis-associated neoplasms
IBD is composed mainly of two diseases; Crohn’s and Ulcerative colitis. Disrupted balance of Th1 and Th17 cells, microbiota effects as well as epithelial breakdown. Genetics makes up 50% of Crohn’s and about 20% for UC
Crohn’s
skip lesions, most often in the terminal ileum + deep knife like fissures, transmural inflammation and ulceration. Only malignant if present in the small bowel (near rectal area especially)
Colitis
pseudopolyps and ulcers, entire colonic involvement, if becomes dysplastic may do prophylactic colonectomy.
Colon cancer from colitis is called DALM (dysplasta associated lesion or mass)
- 8-10 years of colitis, increased chance with increase severity
- If has PSC, much higher risk
- Requires scope survellience
- difficult because of FLAT malignant tissue
- hyperchromasia, increase nucleation, cribiform appearance
Let’s talk polyps
- 80% of colon cancer starts as a polyps
- Polyps begin with DNA mutation
- Genetic susceptibility is important in screening
-
Convential - low to high grade, starts with APC mutation
-
Tubular
- usually pendunculated, more often low grade but the bigger, the worse
- Tubularvillous
- Villous
-
Tubular
- Sessile serrated
- Refers to appearence on histology
- usually non-cancerous, but has malignant potential
- right colon, and has different stages then convential
- Hyperplastic
- never malignant, the “cute” looking ones
- rectum and colon
Colon cancer
- Etiology
- Histological findings
- Etiology*
- M > F*
50-70
80% from polyps (most common cancer of GI tract)
low fiber, high refined carb, vitamin A, C and E deficiency,
other initiating causes that are rare: CpG methylation, microsattelite instabilty, inflammation from IBD
Histological findings
cause blockages more often if left-sided
varying amounts of glands (amount of differentiation, necrosis within the glands)
sig. desmoplastic response (scarring to malignant cells)
Briefly discuss Acute Cholycystitis
- Severe abdominal pain in the RUQ (can be diffuse)
- radiates to shoulder and back
- Murphy’s sign
- Onset after fatty meal? Questionable
- gallstone blocking the cystic duct
- ultrasound to look for stones —> cholycystecomy
- can have nausea, vomiting and fever
Briefly discuss small bowel infarction
- dull abdominal pain
- diahhrea, vomiting, fever
- elevated WBC, elevated lactate is CLASSIC
- CT or abdo x-ray, or angiogram
Briefly discuss SB obstruction
- colicky pain
- symptoms depend on where/how bad the blockage is
- abdo pain, vomiting, fecal vomiting
- chest x-rays are useful in Dx
Briefly discuss a perforated viscus
- anywhere can perforate, but classically is a peptic ulcer
- can cause pneumoperitoneum
- SURGICAL EMERGENCY
- board rigidity patient, extremely painful everywhere with peritonitis
List the abdominal peritoneal signs
- gaurding
- rebound tenderness
- shake tenderness
- not responsive to analgesics
- absent bowel sounds
Describe the pathophysiology of appendicitis
- obstruction of the lumen
- increased pressure and spasm (visceral pain - usually periumbicular (part of the midgut)
- ischemia
- bacterial invasion and necrosis –> touches the parietal peritoneum –> becomes somatic pain and localizes in the RLQ
- perforates and diffuse peritonitis
