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Preclineazy Sahana Mahesh ANATOMY & PHYSIOLOGY OF THE LOWER GI TRACT KEY LOWER GI ANATOMY HISTOLOGY ABSORPTION & GUT PHYSIOLOGY OVERVIEW CELIACS, IBD, BOWEL OBSTRUCTION APPROACHING ABDOMINAL XRAYS (OSCE STYLE) INSERT SESSION TIMELOWER GI ANATOMY FOREGUT LOWER GI MIDGUT • Jejunum, ileumm • Cecum ANA TOMY • Ascending colon • colonmal 2/3 of transverse HINDGUT • colonl 1/3 of transverse • Descending colon • Rectum • Anal canal THE MIDGUT PERITONEUM & MESENTER Y MESENTERY INTRAperitoneal: suspended by Suspends organs within the abdominal mesentery cavity RETROperitoneal: not suspended by Contains vessels & lymphatics mesentery and lie between parietal peritoneum and abdo wall PERITONEUM Lines abdominal cavity (similar to pleura or serous pericardium) Parieta: lines abdo wall Visceral: covers organs THE GREATER SAC Formed by greater mentum Further divided into 2 compartments by transverse mesocolon Supracolic compartment TRANSVERSE MESOCOLON Infracolic compartment THE GREATER SAC Formed by greater mentum Further divided into 2 compartments by transverse mesocolon Supracolic compartment Left paracolic Right paracolic gutter gutter Infracolic compartment THE GREATER SAC Formed by greater mentum Further divided into 2 compartments by transverse mesocolon Drains fluids such as blood, pus or Supracolic bile away from nearby structures compartment When supine, fluid may accumulate in the subphrenic spaces via the Left gutters Right paracolic paracolic gutter gutter When upright, fluid from the stomach, duodenum or gallbladder Infracolic may run down the gutter to collect in compartment the iliac fossa or pelvis KEY ANATOMICAL FACTS OF THE GUT FOREGUT MIDGUT HINDGUT VERTEBRAL T12-L1 L1 L3 LEVEL ARTERY Celiac trunk Superior Inferior mesenteric artery mesenteric artery VEIN Portal vein Superior Inferior mesenteric vein mesenteric vein Vagusnerve Vagusnerve Pelvic splanchnic INNERVATION nerves T5-T9 thoracic T10-T12 thoracic L1-L2 lumbar splanchnic nerves splanchnic nerves splanchnic nerves MIDGUT ARTERIAL SUPPLY ABDOMINAL DISTAL DUODENUM, HEAD OF AORTA PANCREAS, UNCINATE PROCESS ASCENDING COLON, CAECUM, INFERIOR APPENDIX, ILEUM PANCREATICODUODENAL ARTERY ILEOCOLIC SUPERIOR ARTERY MESENTERIC ARTERY JEJUNAL & ILEAL ARTERIES MIDDLE COLIC RIGHT COLIC ARTERY ARTERY ARTERY JEJUNUM & ILEUM ASCENDING COLON TRANSVERSE COLON HINDGUT ARTERIAL SUPPLY ABDOMINAL DISTAL 1/3 TRANSVERSE COLON AORTA & DESCENDING COLON SUPERIOR MESENTERIC ARTERY RECTUM LEFT COLIC ARTERY SUPERIOR RECTAL INFERIOR ARTERY MESENTERIC ARTERY SIGMOID ARTERIES DESCENDING COLON & SIGMOID COLON‘WATERSHED’ AREAS SPLENIC FLEXURE Areas vulnerable to ischemia in the colon These areas are supplied by the most terminal branches of arteries, making them vulnerable to hypoperfusion RECTOSIGMOID JUNCTIONA 62-year old woman on the ward complains of bloody stools and crampy LLQ abdominal pain. She has just undergone an aortic valve replacement. She has a history of antiphospholipid syndrome. Bloods show raised lactate. Colonoscopy shows ulceration and edema of the descending colon. What abdominal blood vessel is most likely involved? A) Superior mesenteric artery B) Middle colic artery C) Right colic artery D) Left colic artery E) Superior rectal arteryA 62-year old woman on the ward complains of bloody stools and crampy LLQ abdominal pain. She has just undergone an aortic valve replacement. She has a history of antiphospholipid syndrome. Bloods show raised lactate. Colonoscopy shows ulceration and edema of the descending colon. What abdominal blood vessel is most likely involved? A) Superior mesenteric artery B) Middle colic artery C) Right colic artery D) Left colic artery E) Superior rectal arteryA B CDUODENUMDUODENUM SHORT & STUBBY VILLI BRUNNERS GLANDS DUODENUM SHORT & STUBBY VILLI ENTEROCYTES 1. BRUNNER’S GLANDS • Secrete alkaline mucus GOBLET CELL 2. SHORT & STUBBY VILLI 3. BRUSH BORDER ENZYMES INTESTINAL • proteases & carbohydrate- GLANDS lysing enzymes BRUNNERS • Why are lipases not present? GLANDS Muscularis mucosaJEJUNUM JEJUNUM TALL & SLENDER PLICAE CIRCULARES VILLI JEJUNUM PLICAE CIRCULARES TALL & SLENDER VILLI 1. PLICAE CIRCULARES • Extensive folding of mucosa 2. TALL & SLENDER VILLI Muscularis mucosa Muscularis externaILEUMILEUM PEYER’S PATCHES ILEUM Villus Muscularis mucosa 1. PEYER’S PATCHES • Diffuse lymphoid tissue Muscularis PEYER’S externa PATCHESJEJUNUM VS ILEUM MACROSCOPIC DIFFERENCES JEJUNUM ILEUM • Wide & thick walled • Narrow & thin walled • Mesentery contains less fat • Mesentery contains more fat • Simple arterial arcades • Complicated arterial arcades • Long vasa recta • Short vasa recta • More folded mucosa & numerous • Less folded mucosa & less villi but villi more lymphatic follicles THE COLON GENERAL FEATURES Diameter 5-7 cm All retroperitoneal except for transverse & sigmoid colonMUSCULARIS EXTERNA THE COLON Mucosa with many goblet 1. THICK MUSCULARIS cells EXTERNA • Represents importance of colon in producing strong peristaltic movements 2. NO VILLI Submucosa MUSCULARIS EXTERNA THE ANAL CANAL Superior rectaluperior rectalDrain to ABOVE PECTINATE LINE Visceral artery veinà IMVà internal iliac Internal haemorrhoids, adenocarcinoma innervation (branch of IMA)plenic vein lymph nodes portal vein • Simple columnar epithelium • Internal anal sphincter is under involuntary control • Internal haemorrhoids are not painful due to visceral innervation BELOW PECTINATE LINE External haemorrhoids, anal fissure, squamous cell carcinoma • Stratified squamous epithelium • External anal sphincter is under voluntary control Inferior rectaInferior rectal artery veinà internal Drain to Somatic (branch of pudendalà superficial • External haemorrhoids are extremely innervation internal internal iliac inguinal lymph painful due to somatic innervation pudendal) common iliac nodes à IVC GUT PHYSIOLOGY MOTILITY ANAL CANAL Enteric nervous system: myenteric plexus, submucosal plexus Internal sphincter External sphincter • Smooth muscle • Skeletal muscle • Autonomic control • Pudendal nerve Autonomic nervous system : • Sympathetic contracts(relaxation) parasympathetic stimulates, • Voluntary control sympathetic decreases > 18 months DEFEACATION: external sphincter relaxes, GUT MOVEMENTS internal sphincter contracts POSTPRANDIAL: villi, pendular and segmentation movements by muscularis and peristaltic waves, receptive relaxation FASTING: migrating motility complex **neurotensin, GLP-1, motilinh as NUTRIENT ABSORPTION SITES STOMACH DUODENUM JEJUNUM ILEUM COLON Absorbed Absorbed Absorbed Cl-, Ca2+ Amino acids, fatty acids,Absorbed Absorbed Fe2+ monoglycerides, Proximal: vit C More electrolytes, Ethanol Glucose, galactose, Fat & water solubleDistal: B12, bile salts water fructose vitamins Secreted Secreted Secreted Pepsin & HCl HCO3-, enzymes Bile, enzymes Saliva & food FLUID BALANCE IN THE GUT Inflow: ~9L/day Bile Gastric secretion Outflow: 6.5L by small intestine, ~1.9L by colon and remainder Pancreatic Small intestine in stools secretion absorption 6.5L Resistance to fluid flow increases away from the mouth and is Colon secretion large intestine determined by tight junctions absorption 1.9L Negative lumen potential promotes anion uptakeA patient has a malabsorption disease. She developsparasthesiasand muscle cramps. ECG shows a prolonged QT interval. Which of the following structures is likely to be damaged? A) Kidneys B) Duodenum C) Jejunum D) Terminal ileum E) PancreasA patient has a malabsorption disease. She developsparasthesiasand muscle cramps. ECG shows a prolonged QT interval. Which of the following structures is likely to be damaged? A) Kidneys B) Duodenum C) Jejunum D) Terminal ileum E) Pancreas KEY P A THOLOGIES LOWER GI TRACT OBSTRUCTIONLIAC DISBOWEL DISEADISEASEUC DIFF INFECTION BOWEL OBSTRUCTION PATHOPHYSIOLOGY • Bowel obstruction leads to stasis of luminal contents and gas proximally: 1. Gaseous abdo distension 2. Vomiting 3. Bowel ischaemia due to compression of vessels Complications of these? COMMON CAUSES SBO LBO • Bowel adhesions Malignant • Incarcerated tumours hernia • Diverticulitis • Meckel • Volvulus diverticulum BOWEL OBSTRUCTION PATHOPHYSIOLOGY CLINICAL FEATURES • Bowel obstruction leads to stasis of • Colicky abdo pain luminal contents and gas proximally: • Nausea & vomiting 1. Gaseous abdo distension • Earlier onset & more vomit in SBO 2. Vomiting • Constipation/obstipation • Late onset in proximal SBO 3. Bowel ischaemia due to • Abdo distension compression of vessels • More severe in LBO Complications of these? COMMON CAUSES MANAGEMENT • Abdominal xray: distended bowel loops SBO LBO • Bowel adhesions • Malignant tumours (369 rule) • Incarcerated • Small bowel > 3cm • Diverticulitis • Large bowel > 6cm hernia • Volvulus • Caecum > 9cm • Meckel • CT is more definitive diverticulum • IV fluids, NG tube drainage, surgeryA 78-year old man presents to A&E with colicky abdominal pain that started 12 hours ago. He reports not having opened his bowels in 5 days, which is abnormal for him. He has started feeling nauseated and has just had a bout offecal vomiting. Examination shows diffuse abdominal tenderness and auscultation reveals high -pitched ‘tinkling’ bowel sounds. What is the most likely underlying cause of this man’s presentation? A) IBD B) Fecal impaction C) Adhesions D) Colorectal carcinoma E) Meckel diverticulumA 78-year old man presents to A&E with colicky abdominal pain that started 12 hours ago. He reports not having opened his bowels in 5 days, which is abnormal for him. He has started feeling nauseated and has just had a bout offecal vomiting. Examination shows diffuse abdominal tenderness and auscultation reveals high -pitched ‘tinkling’ bowel sounds. What is the most likely underlying cause of this man’s presentation? A) IBD B) Fecal impaction C) Adhesions D) Colorectal carcinoma E) Meckel diverticulum CELIAC DISEASE Autoimmune disorder characterised by intestinal hypersensitivity to gluten KEY FACTS PATHOPHYSIOLOGY Consuming gluten • HLA-DQ2 & HLA-DQ8 association • Immune response to gliadin • Symptoms: tTg is released diarrhoea/steatorrhea, It modifies gliadin from flatulence/bloating, abdo pain, gluten N&V, loss of appetite • Dermatitis, peripheral neuropathy Dermatitis herpetiformis Pathogenic T cells react to Blistering rash over extensor surfaces DIAGNOSTICS modified gliadin • RaisedtTg IgA on bloods (make sure to check for IgA Chronic intestinal deficiency first) inflammation • Endoscopy is confirmatory Impaired absorption of 1. lymphocytic infiltration nutrients especially in 2. Crypt hyperplasia distal duodenum & 3. Villous atrophy proximal jejunum IBD: ULCERATIVE COLITIS PATHOPHYSIOLOGY FEATURES OF UC 1. Dysregulation of immune system “ULCCCERS” (inflammation, recruitment of CD4 Th2 cells, NK cells) Ulcers Autoantibodies pANCA aginst enterocytes 2. Dysregulated intestinal Large intestine epithelium/mucosa (ulceration, erosions, Continuous necrosis) 3. Begins in rectum and spreads Colon cancer proximally (not past large bowel) Crypt abscesses Extends proximally ETIOLOGY Red diarrhoea HLA-B27, Ashkenazi Jew association Sclerosing NSAIDs may exacerbate cholangitis Smoking, appendectomy protective IBD: ULCERATIVE COLITIS MACROSCOPIC FINDINGS e.g. BIOCHEMICAL FINDINGS colonoscopy 1. Elevated CRP, ESR Erythematous mucosa 2. Raised faecal calprotectin Deep ulceration 3. Detection of p-ANCA antibodies Pseudopolyps (benign) MICROSCOPIC FINDINGS e.g. IMAGING histology Abdominal XRAY may show loss of Crypt abscesses haustra if severe (leadpipe appearance) No granulomas TYPICAL CLINICAL FEATURES Bloody diarrhoea Mucus in stool Urgency & tenesmus Abdominal pain IBD: CROHN’S DISEASE PATHOPHYSIOLOGY 1. Dysregulation of immune system (inflammation, recruitment of CD4 Th17 cells, NK cells) 2. Obstruction, fibrotic scarring, stricture and strangulation of bowel 3. Abscess and fistula formation ETIOLOGY HLA-B27, Ashkenazi Jew association SKIP LESIONS Younger patients (15-35) Smoking may predispose/exacerbate TRANSMURAL INFLAMMATION Usually terminal ileum affected, rectum spared MOUTH to ANUS involvement But mostly commonly affects terminal ileum and colon IBD: ULCERATIVE COLITIS MACROSCOPIC FINDINGS e.g. BIOCHEMICAL FINDINGS colonoscopy or endoscopy 1. Elevated CRP, ESR 2. Raised faecal calprotectin Cobblestone mucosa Skip lesions MICROSCOPIC FINDINGS e.g. TYPICAL CLINICAL FEATURES histology Watery diarrhoea Non-caseating granulomas Abdominal pain Transmural inflammation Weight loss Lymphoid hyperplasia Malabsorption symptoms due to…. IBD: ULCERATIVE COLITIS MACROSCOPIC FINDINGS e.g. BIOCHEMICAL FINDINGS colonoscopy or endoscopy 1. Elevated CRP, ESR 2. Raised faecal calprotectin Cobblestone mucosa Skip lesions MICROSCOPIC FINDINGS e.g. TYPICAL CLINICAL FEATURES histology Watery diarrhoea Non-caseating granulomas Abdominal pain Transmural inflammation Weight loss Lymphoid hyperplasia Malabsorption symptoms due to… B12 & bile salt malabsorption (most commonly). IBD: EXTRAINTESTINAL MANIFESTATIONS RELATED TO DISEASE ACTIVITY EPISCLERITIS (CROHN’S) APTHOUS ULCERS (CROHN’S) ERYTHEMA NODOSUM OLIGOARTICULAR ARTHRITIS OSTEOPOROSIS GALLSTONES (ONLY CROHN’S) RENAL STONES (ONLY CROHN’S) IBD: EXTRAINTESTINAL MANIFESTATIONS RELATED TO DISEASE ACTIVITY UNRELATED TO DISEASE ACTIVITY EPISCLERITIS (CROHN’S) UVEITIS APTHOUS ULCERS (CROHN’S) PYODERMA GANGRENOSUM ERYTHEMA NODOSUM AXIAL ARTHRITIS POLYARTICULAR ARTHRITIS DIGITAL CLUBBING OLIGOARTICULAR ARTHRITIS OSTEOPOROSIS PRIMARY SCLEROING CHOLANGITIS (UC) GALLSTONES (ONLY CROHN’S) AUTOIMMUNE HEPATITISU( ) RENAL STONES (ONLY CROHN’S)IBD: EXTRAINTESTINAL MANIFESTATIONS ERYTHEMA NODOSUM Most often in Crohn’s PYODERMA GANGRENOSUM IBD: MANAGEMENT ULCERATIVE COLITIS CROHN’S DISEASE INDUCE REMISSION INDUCE REMISSIONdepends on severity & locationAMINOSALICYLATES, CAN ADD ON AMINOSALICYLATES +/- STEROIDS AZOTHIOPRINE Surgery can be curative e.g. protectomy Surgery can help but not curative e.g. hemicolectomy COLOSTOMY ILEOSTOMY UROSTOMY LEFT ILIAC FOSSA RIGHT ILIAC FOSSA RIGHT ILIAC FOSSA SOLID FAECES LIQUID FAECES URINE FLUSH WITH SKIN SPOUTED SPOUTEDA patient with confirmed Crohn’s disease developsparasthesiasin her feet. She says she has had multiple falls in the past few weeks. On examination, there is complete loss of proprioception and vibration. What is the cause of her symptoms? A) Thiamine deficiency B) Hypocalcemia C) B12 deficiency D) Bile salts deficiency E) Guillain-Barre syndromeA patient with confirmed Crohn’s disease developsparasthesiasin her feet. She says she has had multiple falls in the past few weeks. On examination, there is complete loss of proprioception and vibration. What is the cause of her symptoms? A) Thiamine deficiency B) Hypocalcemia C) B12 deficiency D) Bile salts deficiency E) Guillain-Barre syndrome CLOSTRIDIOIDES DIFFICILE INFECTION C. DIFF CLINICAL FEATURES • Gram positive rod • Spore-forming C.Diff causes Difficult Diarrhoea • Transmission • Watery diarrhoea (> 3 stools a day with • Community acquired: faeco-oral odor) • Cramping abdo pain, nausea, anorexia • Hospital acquired: contaminated • Fever and dehydration surfaces & medical equipment RISK FACTORS SEVERITY MILD: normal WCC 1. Recentabx (clindamycin, cephalosporins, quinolones) MODERATE: raised WCC, 3-5 stools/day 2. Advanced age SEVERE: raised WCC or raised creatinine 3. PPI use or temp > 38.5 or evidence of severe 4. Severe illness/immunosuppression colitis 5. Recent hospitalization/nursing home LIFE-THREATENING: hypotension, partial 6. IBD or complete ileus, toxic megacolon CLOSTRIDIOIDES DIFFICILE INFECTION MICROSCOPIC FINDINGS • Pseudomembranous colitis • Elevated yellow-white plaques that form pseudomembranes MANAGEMENT Review current Abx therapy & stop FIRST EPISODE • Oral vancomycin 10 days • Second line: fidaxomicin DIAGNOSIS RECURRENT Detection of C.diff toxin in the stool • Oral fidaxomicin C.Diff antigen positivity only shows LIFE-THREATENING exposure to bacteria, rather than current • Oral vancomycin AND IV infection metronidazoleBOWEL IMAGING AbdominalYs and CTS ABDOMINAL XRA Ys Indications for use Gases, masses, • Evidence of bowel obstruction • Evidence of inflammation i.e. bones and stones colitis (?toxic megacolon) • Evidence of bowel perforation SMALL BOWEL LARGE BOWEL Minimal intraluminal gas Around periphery Centrally located Mixture of gas and faeces Small diameter ~3cm Larger diameter 3-5cm Valvulaeconniventes (stack of coins,Haustra (stretch only part-way across go all the way round) the diameter)John Smith 09/07/1992 87269062 ABDO XRA Y: GASES PNEUMOPERITONEUM SMALL BOWEL OBSTRUCTION • Rigler sign • Mutliple gas filled, dilated (>3cm) • Dome sign loop sf bowel • Note valvulae conniventes ABDO XRA Y: MASSES • Look for any organ enlargement (shadows of liver, spleen, bladder) • Look at mucosal lining Ruptured AAA ABDO XRA Y: BONES • Abnormalities of visible bones such as the ribs, spine, sacrum and pelvis • E.g. fractures, scoliosis, degenerative disease, tumours • May be incidental or provide information on the cause of abdo pain Lumbar scoliosis ABDO XRA Y: STONES Look for renal, ureteric and bladder stones/calcification • Trace course of ureter from renal pelvis, along tips of lumbar spine to the ischial spine and medially to the bladder • 80-90% of renal stones are radio-opaque, but will require ______ to confirm their position in the ureter • May be incidental or provide information on the cause of abdo pain Right renal stone ABDO XRA Y: IDENTIFYING PATTERNS LARGE BOWEL OBSTRUCTION THUMBPRINTING PATTERN TOXIC MEGACOLON • Mutliple gas filled, dilated (>5•m) Sign of colitis • Life threatening, acute dilation of loops of bowel in the periphery colon associated with systemic • Haustra toxicity • Super dilated, loss of haustrationABDO XRA Y: IDENTIFYING PATTERNS PNEUMOPERITONEUM • Gas under the diaphragm BARIUM STUDIES CROHN’S DISEASE APPLE CORE STRICTURE • Cobblestone, thumbprinting • usually due to cancer growths pattern • Normal mucosal folds lost PLEASE FILL OUT THE FEEDBACK FORM PLEASE TUNE IN TO OUR REMAINING SESSIONS THIS WEEK! @OSCEazyOfficial @osceazyofficial OSCEazy Osceazy@gmail.com