Week 10-12: Gastrointestinal Tract Flashcards
Which Inflammatory Bowel Disease is characterized by bloody stool?
Ulcerative Colitis. In contrast, Crohn’s Disease does not present with bloody stool.
Symptoms of ulcerative colitis, alleviating factors
Crampy lower abdominal pain, relieved by bowel movement; Bloody stool; No mass; Confined to mucosa; Continuous from rectum (colon only); No granulomas;
4 basic GI processes
- Motility - muscular contractions that mix and move forward the contents of the GIT
- Secretion - glands located along the GIT that secrete their contents into the tract, assisting in motility, digestion and absorption
- Digestion - the biochemical breakdown of large particles and molecules into smaller, absorbable particles
- Absorption - small particles are absorbed from the GIT into the blood or lymph
2 broad categories of movement (motility) in GI
1) Mixing movements: Redistribute luminal contents locally, enhancing the exposure to digestive secretions; expose luminal contents to GIT epithelium for absorption.
2) Propulsive movements: Move luminal contents forward. Rate of propulsion varies with specific function of region (e.g., esophagus = rapid; small intestine = slow)
What layers make up the small intestine?
- Muscularis externa is the major smooth muscle layer of the GIT. It has two layers:
- Inner circular layer - responsible for restriction of the lumen
- outer longitudinal layers - responsible for shortening of the GIT
- Myenteric plexus lies underneath, coordinating muscularis externa contractions.
- Inner most layer is the Muscularis Mucosae, which is a thin layer of smooth muscle between the mucosal and submucosal layers.
Explain the role of Ca2+ and Myosin Light Chain Kinase in GI smooth muscle contraction
- increased intracellular Ca2+ leads to binding of Ca2+ and calmodulin.
- the Ca-Calmodulin complex activates Myosin Light Chain Kinase (MLCK)
- MLCK phosphorylates myosin, which can now bind actin and perform shortening of muscle fibres.
- Contraction is terminated when Myosin Light Chain Phosphatase cleaves phosphate from myosin.
How can a smooth muscle cell increase Ca2+ levels for contraction? (2)
1. Calcium-induced calcium release: Depolarisation of membrane brings Ca into cell via voltage gated calcium channels at base of calveoli (indentation at membrane). The influx of Ca induces sarcoplasmic reticulum to release of Ca .
2. Pharmaco-mechanical coupling: IP3 receptor in SR responds to elevated cytosolic levels of IP3 by releasing Ca2+
Describe the role of the Interstitial Cells of Cajal (ICC) as ‘pacemaker’ cells for GI smooth muscle contraction
These are specialized smooth muscle cells of GIT that act as pacemakers for contraction! The undergo spontaneous, transient membrane depolarisations that are propagated to adjacent smooth muscle cells via gap junctions, resulting in SLOW WAVES. Greater # of APs sent along, increases the strength of contraction.
How are the duration and amplitude of slow waves modulated?
By enteric motor neurons in the walls of the GIT.
List the components of ENS
1) Sensory neurons (including mechanoreceptors, chemoreceptors and osmoreceptors)
2) Interneurons (excitatory and inhibitory)
3) Secretomotor cells, which influence… - Smooth muscle - Epithelial cells that secrete or absorb fluid/electrolytes - Enteric endocrine cells
Describe the role of the enteric NS in the regulation of GI motility
The enteric NS can operate entirely in the GI wall without external input (it’s reflexive). Moderate contraction by sending NTs to ICCs and smooth muscle cells in the circular and longitudinal muscle layers, which result in increased intracellular Ca levels and consequent contraction.
Autonomic Nervous System regulation of GI motility
En Passant Innervation: motor axons have multiple varicosities containing NT that can be released into smooth muscle to reach targets The ANS communicates with the ENS
Describe the 3 phases of swallowing
1) ORAL PHASE: pushing food bolus toward the back of oral cavity and up against the palate. Requires tongue.
2) PHARYNGEAL PHASE: Touch and pressure receptors in the pharyngeal nerve (in pharynx) send stimulation to medulla via trigeminal nerve, thus initiating reflexive component of swallowing. Pharyngeal wall contracts, thus pushing food into esophagus. Tongue prevents bolus from travelling backward into mouth. Uvula elevates to seal nasal passages. Vocal cords contract and epiglottis closes over the trachea.
3) ESOPHAGEAL PHASE: swallowing centre relaxes pharyngeoesophageal sphincter and initiates primary peristaltic waves by interacting with ENS, to propagate the bolus toward the stomach. These are paired with secondary peristaltic waves, which are triggered by stretch and act to dislodge bolus. Gastroesophageal sphincter opens when a peristaltic wave pushes food bolus against it.
What coordinates the motion of swallowing?
The swallowing centre in the medulla oblongata. The initiation of swallowing is voluntary, but once it starts, completion of swallowing in reflexive.
Explain the opening of the gastroesophageal sphincter
The vagus nerve mediates reflexive relaxation of the sphincter when a food bolus is pushed up against it.
Describe primary peristalsis
~5-9 seconds of travel along esophagus
- Inner circular layer of muscularis externa contracts, pinching a ring
- Outer longitudinal muscle layer contracts in front of the inched ring, reducing the length of the tube
- This sequence propagates along the length of the esophagus, pushing luminal contents toward the stomach
What initiates the reflexive phase of swallowing?
Pressure of food against the pharyngeal palate stimulate the trigeminal nerve which signals reflexive swallowing to occur.
What are the 2 major motility paradigms in the small intestine?
- segmentation 2. Migrating Mobility Complex
Explain segmentation
Dominant motility in small intestine right after a meal, responsible for mixing chyme and moving it toward large intestine. Composed of alternating contractions and relaxations of adjacent sections of the intestine.
What initiates segmentation? (3)
distension of the lumen
presence of gastrin
parasympathetic input
What is the migrating mobility complex?
Replaces segmentation following the absorption of a meal. Moves luminal contents along the intestine in periods between meals. Begins at the duodenal-gastric junction and consists of weak peristaltic movements that travel short distances. A second wave begins more distally than the previous to move contents along.
Pathophysiology of achalasia
= functional disorder of the esophagus characterized by increased resting tone and incomplete relaxation of the lower esophageal sphincter, preventing food from entering the stomach.
can be recognized by the ‘bird beak sign’ on radiology.
What is esophagitis (2) and what may cause it (3)?
= inflammation and epithelial damage of esophagus
- May be caused by reflux (GERD), infection of immunocompromised, eosinophilic esophagitis
What is GERD?
= gastric contents leak backward into the esophagus causing irritation/inflammation of esophagus
Barrett’s esophagus: what it is and how it may progress
= distal squamous mucosa of esophagus is replaced by metaplastic columnar epithelium. A response to prolonged injury, columnar epithelium may be more resistance to acid.
Barrett’s esophagus is a complication of GERD that may progress to esophageal adenocarcinoma.
Premalignant dysplasia does not invade lamina propria. Graded based on histologic assessment.
Pathophysiology of diaphragmatic (hiatal) hernias
types (2)
possible presenting Sx (2)
= abnormal protrusion of a segment of the stomach above the diaphragm.
Can be (a) sliding or (b) paraesophageal/nonaxial
Usually asymptomatic, can have reflux or heartburn.
Gastritis: what is it? Acute vs chronic vs chornic active
= inflammation/irritation of the gastric mucosa
ACUTE: sudden onset; often with erosions or ulcer. Often caused by NSAIDs, alcohol, cocaine, stress, trauma.
CHRONIC: Ongoing. Often multifactorial and often combined with acute. Due to infection, autoimmunity, reactive.
CHRONIC ACTIVE: persistent inflammation of the gastric mucosa related to h pylori. Typically affects antrum of stomach and may extend to body. Increased risk of gastric carcinoma and gastric lymphoma.
Peptic ulcer disease: define, possible complications
= acid-induced ulceration of the mucosa and wall of the stomach or duodenum often associated with h. pylori.
Complications: perforation, hemorrahage, obstruction (stenosis), penetration
Carcinoma of the esophagus
didn’t find this in lecture but it is an objective so check CBL research from the week.
Gastric Polyps
= abnormal growth of tissue projecting from a membrane in the stomach
Can be neoplastic (benign or malignant) or non-neoplastic (hyperplastic or fundic gland polyp)
Gastric carcinoma (define, prevalence, appearance)
= malignant neoplasm of gastric epithelium - adenocarcinoma
- Prevalence: more common in certain countries (i.e., Japan and less common in north america)
- Appearance: intestinal-type epithelium with signet ring cells, ulcerating.
Eosinophilic esophagitis
How does it present????
= a type of esophagitis characterized by numerous eosinophils within the squamous mucosa and associated with dysphagia
may present as difficulty swallowing, food impaction, heartburn
Looks like rings in the trachea on endoscopy. Biopsy needed to confirm eosinophils. Must exclude GERD.
causes of GERD (5)
- low resting tone in lower esophageal sphincter
- delayed esophageal clearance
- delayed gastric emptying
- increased abdominal pressure
- increased acid production
Symptoms of GERD
Variable - heartburn, water brash, belching, retrosternal pain
How is GERD diagnosed? (2)
when is endoscopy warranted?
Clinically - history and relief with medication (PPI)
Endoscopy warranted if…
- heartburn presents with alarm symptoms (bleeding, weight loss)
- Persistent reflux or previous severe erosive esophagitis
- History of esophageal stricture with persistent dysphagia
What are some complications that may occur with GERD?
- stricture (scarring)
- ulceration
- bleeding
- barrett’s esophagus
- adenocarcinoma
What may be seen on biopsy of GERD?
- increased inflammatory cells in the epithelial layer (eosinophils, neutrophils, excess T lymphocytes)
- basal cell hyperplasia
- elongation of lamina propria
Treatment for GERD
- PPI to decrease acid production
- Antacids
- Diet modifications
- Weight loss
Endoscopic and histologic features of Barrett’s esophagus
Endoscopy:
- red vevety GI type mucosa between pale squamous mucosa. Tongues extend upward from gastroesophageal junction or may be a broad band moving the who junction up.
Histology:
- squamous epithelium replaced by columnar epithelium or intestinal type and may see other types of glandular epithelium.
Treatment for Barrett’s Esophagus
- anti-reflux therapy
- endoscopy every 1-2 years to assess for dysplasia, carcinoma
Tests for h pylori
Serology
urea breath test
stool antigen test
biopsy
Composition of gastric juice (3)
- Water
- Organic compounds (Intrinsic Factor, Pepsinogen, Lipase, Mucus)
- Ions (Na+, K+, H+, Cl-, HCO3-)
Progression of Type 2 Diabetes (stages; 3)
Insulin blood levels and appropriate treatment at each stage
Early
- Abnormal oral glucose tolerance test (OGTT) but normal fasting glucose
- Treat with diet and exercise
Overt, but mild T2D
- Moderate fasting hyperglycemia develops (~7 mM)
- Treat with diet and exercise and add oral hypoglycemic agents (sulfonylureas), insulin-sensitizing drugs (metformin), DPP-4 inhibitors, and/or GLP-1 analogues.
Advanced:
- Severe fasting hyperglycemia (>9 mM)
- Insulin dependence often required
Possible causes of insulin resistance?
- Involves genetic and/or acquired defects in insulin action. Can arise as part of other syndromes (i.e., PCOS) or rare gene mutations.
- Associated with obesity (especially central obesity)/BMI
- Associated with inflammation in adopose tissue (macorphages produce TNFalpha)
Characteristics of insulin secretion in type 2 diabetes
- Impaired glucose-induced insulin secretion from B cells
- Impaired proinsulin processing –> manifests as hyperproinsulinemia
- B cells become unable to compensate for increasing insulin resistance and produce decreasing amounts of insulin
Causes of decline in unsulin secretion in type 2 diabetes (3)
- Glucose and lipid toxicity to beta cells
- Increased # islet macrophages that make pro-inflammatory cytokines
- Toxic amyloid deposits build up in pancreas
Monogenic forms of diabetes (2)
Mature onset diabetes of the young (MODY)
Neonatal diabetes mellitus
MODY
Mature Onset Diabetes of the Young
~2-5% of all type 2 diabetes. All associated with renes that regulate B cell mass or function
Neonatal Diabetes Mellitus
Rare: born with type 2 diabetes; a single gene type
Formerly diagnosed as type 1 diabetes, which influences the efficacy of treatment. Now treated with sulfonylureas
Gestational Diabetes Mellitus (progress, risk to infant)
Appears during pregnancy and disappears following birth. Pregnant women become insulin resistant and insulin secretion increases.
>50% of GDM women later develop T2D.
Carries risk for the infant (increased size, dificult birth)
Reducing progression of type 2 diabetes
lifestyle modifications are very effective for slowing progression of diabetes. Metformin is also effective but not actually as much as lifestyle changes!
what do parietal cells produce and where are they located?
They are located in oxyntic glands of stomach body and they produce HCl and Intrinsic factor
What do chief cells produce?
pepsinogen (turned to pepsin by HCl) and lipase
What do ECL cells produce?
histamine
what do D cells produce?
somatostatin
what do G cells produce?
Gastrin
how is gastrin released and what does it do in the stomach?
Gastrin is released into the blood stream (endocrine) from G cells in the pyloric glands of the stomach. It acts on parietal cells to increase HCl secretion and on Chief Cells to increase pepsinogen secretion. It also increases contractions of the stomach.
Mechanism of acid production by parietal (oxyntic) cells
- Stimulation of the stomach stimulates the tubulovesicles to fuse with the canaliculi of parietal cells to form long microvilli
- H+/K+ ATPase proton pump in tubulovesicle membranes is now on microvilli surface and facilitates production of HCl
- The cell received CO2 from blood, which is is taken with water by Carbonic Anhydrase to make HCO3- + H+.
- H+ from this reaction is exported out of the cell into the stomach by the H+/K+ ATPase
- Cl moves from the blood, through the cell, and to the stomach down its concentration gradient, where it combines with H+ int he stomach to make HCl
Define the term ‘zymogen’ and describe the specific conversion of pepsinogen to pepsin.
Pepsinogen is produced by chief cells in the stomach. Pensinogen is cleaved by acid (HCl) to its active form (i.e., pepsinogen is a zymogen), pepsin. Pepsin can also activate more pepsinogen directly - this is called autocatalysis
What are the components of the gastric mucosal barrier?
Mucus (sticky secretions containing mucin and glycoproteins) and bicarbonate
Explain the significance of the gastric mucoasal barrier in mucosal protection
Protects the luminal epithelium from acid and pepsin-based hydrolysis as well as microorganisms.
Where is mucus produced in the stomach lining?
Mucus neck cells of gastric glands secrete clear mucus in response to several stimuli (e.g., mechanical/vagal stimulation, ACh, PGs, bacterial toxins)
Surface epithelial cells continuously secrete viscous mucus with high [HCO3-] via exocytosis. Mucus is held in place by the surfacephosopholipids on the luminal membrane f the cells to lubricate and protect against damage.
Role of prostaglandins (PGs) in the stomach (5)
Involved in the protection of the stomach.
- inhibit acid secretion
- prevent exfoliation of epithelial cells
- increase mucosal blood flow
- stimulate mucus and bicarbonate secretion
- enhance synthesis of surface-active phsopholipids that line the gastric mucosa and hold mucus in place.
Gastrin
(where it comes from, what stimulates it, what it binds to, what it does)
Comes from G cells in the pyloric glands in the antrum of the stomach;
Secreted in response to the peptide NT GRP (gastrin releasing peptide) from enteric neurons and in response to digested protein in the gastric lumen;
Binds to CCK receptors on the basal surface of parietal cells and chief cells to activate them, thus upregulating their products.
Describe the roles played by gastrin, histamine, and ACh in the regulation of gastric secretion
HCl is produced by parietal cells, which have receptors for gastrin (CCK receptor), histamine (H2 receptor), and ACh (M3 receptor).
Gastrin is released by G cells in the pyloric glands of the stomach in response to presence of digested protein or in reposnse to GRP released by enteric neurons. Histamine is released by ECL cells in response to gastrin and in response to ACh stimulation from neurons. ACh action on the parietal cells is the product of direct stimulation from neurons.
Explain how ACh, gastrin, and histamine stimulate the parietal cell in a coordinated fashion
There is thought to be continuous background release of histamine in gastric interstitial fluid to maintain basal acid secretion. Gastrin and ACh can act both via stimulation of histamine and synergistically with histamine direclty on the parietal cell.
What are the three phases gastric secretion
cephalic (psychic), gastric, and intestinal
Describe the stimuli and neural pathways involved in the cephalic phase of acid secretion (3)
Explain inhibition of this pathway (1)
The cephalic phase is responsibel for preparing the stimach for an incoming meal. COnscious thought, smell, and taste stimulate the hypothalamus, which activates parasympathetic outflow from the vagus nerve. This stimulated chief cells and G cells to release acid and pepsin in the stimach before food even arrives in there.
Inhibition: Stomach filling and feelings of satiety result in sympathetic discharge.
Describe the stimuli and neural pathways involved in the gastric phase of acid secretion (non-neuronal and neuronal aspects)
Explain inhibition of this pathway.
Rate of secretion is maximal during the gastric phase. There are two components:
Non-neuronal: Food entering the stomach increases pH, stimulating gastrin release and stimulating parietal cells directly.
Neuronal: Food entering the stomach causes distension, which activates a vago-vagal reflex via mechanoreceptors in the gastric wall. This results in stimulation of acid and pepsinogen release and indirect stimulation of gastrin release.
Inhibition: pH drop in the antrum stimulated D cells in pyloric glands to release somatostatin, which acts locally to inhibit G cell production of gastrin.
Describe the stimuli and neural pathways involved in the intestinal phase of acid secretion
Explain inhibition of this pathway
Nutrients (peptones) in the duodenum stimulate G cells to secrete more gastrin, which then acts on parietal cells and chief cells in gastric glands.
Inhibition: Passage of chyme into duodenum and its breakdown inthe jejunum stimulates the enterogastric reflex arc, leading to production of enterogastrones. Enterogastrones feedback to inhibit G cell, parietal cell, and chief cell activity as well as smooth uscle contraction in the stomach.
Somatastatin. When it is released and what it does
Somatostatin is released from D cells in the pyloric glands in response to pH drop in the antrum. It acts to inhibit the gastric phase of acid secretion by locally inhibiting G cell production of meal-stimulated gastrin.
Enterogastrones
- what are they
- when are they produced
- what do they do
Entrogastrones include secretin (stimulated my acid), SSK (stimulated by AAs and fat), GIP and GLP-1 peptides (stimulated by fat and glucose). They are all hormones produced as a response to chyme passage to duodenum ad jejunum. They act to inhibit the intestinal phase of acid secretion by feeding back to inhibit G cell, parietal cell, and chief cell activity as well as smooth muscle contraction in the stomach.
Why are NSAIDs hard on the stomach?
They inhibit the production of PGs. PGs’ role int hes tomach is to inhibit acid secretion, increase mucosal flow/production, enhance synthesis of surphase phospholipids, and prevent exfoliation of epithelial cells. Inhibiting PGs inhibits this important protective mechanism for the gastric mucosa.
How does h pylori cause harm in the stomach?
What characteristics of h pylori help it survive and do harm in the stomach?
- Mechanism of damage: Inject viruluence factors into epithelial cells, causing them to release nutrients and urea to nourish the bacteria. This damage the epithelial cells and their tight junctions, resulting in inflammation. Cytokines related to inflammation stimulate G cells (++gastrin) and inhibit D cells (–somatostatin), increasing acididty and furthering injury.
- Adapted to survive in the stomach: Flagellated and motile with chemotaxis toward high pH areas of stomach (mucus). Adhesive to epithelial cells. Produces a potent urease, which converts NH3 and CO2 to protect itself from gastric acid and promote further gastrin secretion.
General treatment for h pylori infection in stomach
Standard triple therapyy combined PPI and 2 antibiotics (clarithromycin and amoxicillin or metronidazole)
Peppermint - effect on GI?
worsens heart burn
caffeine - effect on GI disease
worsens heartburn
How does heartburn present?
symptoms
aggravating factors and alleviating factors
post-prandial, retrosternal pain of varying duration and severity. May experience water brash, sour taste, odynophagia (pain with swallowing)
aggravating - supin position, caffeine and peppermint (foods that relax upper esophageal sphincter), fat and protein (foods that delay emptying)
alleviating - antacids
Things that may cause heartburn (5)
peppermint, caffeine, opioids, smoking, alcohol
Define GERD
gastroesophageal reflux disease. Retrograde movement of gastric contents into the esophagus with symptoms AND/OR complications.
reflux esophagitis
Acid damage to esophagus. A common complication of GERD. Caused by increased abdominal pressure, increased volume in stomach, or decreased esophageal clearance.
Treatment for reflux esophagitis (lifestyle, medications, surgery)
- Correct underlying cause
- Lifestyle changes (remove exacerbating factors such as smoking, alcohol, weight)
- Medications: antacids, H2 antagonist (OTC), PPI (slower onset but more effective). Usually stopped after symptoms resolve and relief maintained with lifestyle modification.
- Surgery: Fundoplication - wrapping stop of stomach around the esophagus (rarely performed)
Possible complications of esophagitis (3)
Pain/bleeding
Stricture
Barrett’s esophagus (progresses to adenocarcinoma)
Possible causes of esophagitis and their different manifestations (4)
- Infection (HSV, CMV, candida): typically in immunosuppressed and v painful (odynophagia)
- Inflammatory (eosinophilic): rings form in trachea, exudate produced; can be treated with elimination diet
- Trauma (pill): causes painful swallowing, common in elderly (impaired esophageal clearance)
- Reflux
Dyspepsia - formal definition
“stomach ache”
Rome III definition = one or more of…
- post-prandial fullness
- epigastric pain or burning
- early satiety
Sometimes associated with nausea, bloating, anorexia
Causes of dyspepsia
- Usually no obvious cause: ulcer-like symptoms or dysmotility-like symptoms
Gastritis vs gastropathy
Gastritis = inflammation of gastric mucosa associated with injury (h pyloria, autoimmune, alcohol)
Gastropathy = epithelial cell damage and regeneration without inflammation (NSAIDs, bile reflux, congestion)
causes of acute vs chronic gastritis
Acute (alcohol, early h pylori)
Chronic (autoimmune, late h ylori)
Different physical patterns of gastritis
Antral-based gastritis - infection increases gastrin secretion, which increases parietal cell acid production, causing duodenal damage. May eventually cause metaplasia in stomach or duodenum or produce ulcers in stomach or duodenum.
Corpus-predominant atrophic gastritis or pangastritis - caused by genetically lower acid output, predisposing the body for h pylori infection. Increased risk for ulcers, metaplasia, and gastric CA.
Purpose of a urea breath test
test for h pylori by investigating the presence of urease enzyme which braeks down uria into ammonia and carbon diaoxis. Pt swallows radiolabelled urea and radiolabelled CO2 is measured in breath. Diagnostic for dyspepsia.
Peptic ulcer disease = ?
damage to the mucosal lining of the intestinal surface where acid is implicated in pathogenesis.
May vary from normal mucosal to erosive (damage restricted to superficial mucosa) to ulcerative (damage extends to muscularis mucosa).
Management of peptic ulcer disease
- correct underlying cause
- Lifestyle changes
- Medication: PPI
- Endoscopic: injection around ulcers to stop blood leak coagulation of vessels if ulcer is shallow, place clips to hold ulcer shut, embolizaation (obstruct problem blood vessel), omental patch, other surgical approaches.
Dysphagia
= dysfunctional swallowing. May be progressive (i.e., cancer) or longstanding (physical difference)
How to approach a diagnosis for dyphagia
Where is the issue? transfer (oropharyngeal vs esophageal)
What is the issue? SCC > adenomacarcinoma > pepstic stricture
Pro and con of an abdominal XR for diagnosis of GI diseases
Easy to get, cheap
Won’t show mild inflammatory bowel disease
Pros and cons of doing a barium swallow
Easy and cheap
Low sensitivity and specificity
Good for testing dysphagia
Pros and cons of doing a CT abdomen
3D information, very sensitive and specific.
Expensive
Exposure to ionizing radiation
Best test for severe abdominal pain
CT enterography: what is it and pros/cons
Same as a CT abdomen, but with negative PO contrast and another IV contrast.
Good for showing strictures, intraluminal fillinf defects. Better than plain CT if you are suspecting Crohn’s disease
Physical and histological characteristics of Crohn Disease
- Any part of GIT (‘gum to bum’)
- Patchy distribution
- Transmural inflammation with associated serositis
- Granulomas
- Cobblestone appearance of mucosal surface due to linear ulceration
- Thickened walls, narrowed lumen
- Abscess
- Radiology: string sign
What is pictured here? What may it suggest
Granuloma of the colon, may be Crohn Disease
What diagnosis is supported by this radiograph?
Crohn Disease
Physical and histological characteristics of ulcerative colitis
- Colon only (starts in rectum)
- Continuous involvement
- Inflammation limited to mucosa
- No granulomas
- Affects mucosal layer only
- Absence of goblet cells
- Crypt distortions and abscesses
Describe the two kinds of polyps that can occur in the colon or rectum
Polyps are abnormal tissue growth projecting from a mucous membrane.
Sessile polyp has a broad base
Pedunculated polyp has a stalk
Polyps can be neoplastic (premalignant, malignant) or non-neoplastic
a) acute appendicitis
b) Ulcerative colitis
c) Behcet’s disease
d) gastroenteritis
e) Crohn disease
crohn
