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142 Cards in this Set
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Regulation of gastric secretion |
Secretory healing and defence mech regulated by overlapping neural endocrine paracrine and autocrine control pathways
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Cephalic phase
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Activated by thouht taste and smell of food and swallowing, mostly cholinergic
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Gastric phase
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Chemical effects of food and distension of stomach
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Intestinal phase
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Only a small amount of acid, mediators controversial.
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Gastrin blocking
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Response to food eliminated
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Gastric acid source, effects |
G cells in gastric Antrum |
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Effects of histamine
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Stim parietal cells to secrete acid
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Inhibitors of gastric acid
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Somatostatin from d cells
Cholecystokinin Secretin Neurotensin Glucagon like peptide |
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Intragastric pH
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1.4
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Primary stim for acid secretion
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Histamine 2 receptors
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Pancreatitis
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Associated with enzymatic destruction / autodigestion
Acute leads to chronic causing exocrine and endocrine failure |
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Acute pancreatitis presentation |
Sudden onset severe epigastric son with vomiting mainly on the first 12h |
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Causes of pancreatitis |
Alcohol |
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Why does alcohol cause pancreatitis |
Decreases protein secretion |
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Biochem tests for pancreatitis
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Enzymes released due to acinar cell disruption
Amylase rises within 6-12 hours of the onset, returns to normal within 3-5 days Serum lipase rises within 4-8 hours returns to normal within 8-14 days Liver function tests - raised enzymes or bilirubin indicate gallstones Calcium falls, Ranson's criteria Blood glucose , endo failure and hyperglycaemia Blood gasses, hypoxia and multiple organ failure |
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Macroamylasaemia |
No symptoms but mimics acute pancreatitis Polymerisation or binding to a molecule prevents urinary excretion causes elevated serum and low urinary amylase |
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Malabsorption causes
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Abnormalities of gut wall |
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Malabsorption presentation |
Weight loss tiredness failure to thrive lethargy fatigue |
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Malnutrition investigations |
FBC ESR vit B12 folate iron clotting calcium coeliac screen |
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Breath hydrogen test
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Take sample, give glucose, half hour intervals It also means there is decreased absorption |
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Nutritional assessment
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Measurements of body composition |
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Complications of malnutrition
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Reduced immune function
Poor wound healing Decreased muscle function |
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Malnutrition clinical appearance
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Lax skin and loss of subcutaneous fat, may be masked by oedema
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Albumin measurement
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Used as a poor measurement for nutrition |
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Nutritional support
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Oral, enteral (NG NJ PEG) or paraenteral nutrition support TPN alone or in combo
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TPN complications
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Malposition of central venous catheter and possible pneumothorax |
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Refeeding problems
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Liver decreases glucogenesis thus conserving muscle and protein |
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Oesophageal atresia |
Oesophagus doesn't join up, pause along it |
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Oesophageal varices |
Result from any cause of portal hypertension |
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Treatment of oesophageal varices
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Scleropathy
Ballon tamponade |
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Eosinic oesophagitis more common in
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Children
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Reflux oesophagitis
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Sometimes also duodenal contents
Symptoms dysphagia heartburn acid rash regurgitation haematemesis melaena Inflam cells in epithelium Basal zone hyperplasia Elongation of papillae with capillary congestion |
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Complications of reflux oesophagitis |
Bleeding |
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Barrett's oesophagus
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Where squamous normal epithelium replaced by metaplasic columnar epithelium which is visible macroscopically
Endoscopic and histological diagnosis Exclusion of dysplasia and malignancy essential Surveilance for malignancy |
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Malignant risk factors of Barrett's oesophagus |
Male over forty five
Extended segmental disease Long reflux history Early onset of gastroesophafeal reflux Mucosal damage Family history Managed with proton pump inhibitor and surveillance |
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Infectious oesophagitis
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Healthy and immunocompromised
Fungal eg candidiasis mucormycosis aspergillosis Viral HSV and CMV |
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Malignant oesophageal tumours
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Squamous cell carcinoma and adenocarcinoma
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Risk factors for oesophageal squamous cell carcinoma
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Alcohol tobacco Afro Caribbean caustic oesophageal injury achalasia
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Trachoesophageal fistulae
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Connection between oesophagus and trachea
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Adenocarcinoma risk factors
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Barrett's oesophagus tobacco obesity genetic
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Causes of acute gastritis
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NSAIDs alcohol tobacco
Uraemia Chemotherapeutic drugs Stress Ischaemia and shock Gastric irradiation |
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Features of acute gastritis
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Asymptomatic or
Variable epigastric pain Nausea Overt haemorrhage Massive haematemesis |
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Chronic gastritis
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Mucosal inflam leading to atrophy intestinal metaplasia |
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Autoimmune gastritis
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T cell lymphocytes play central role by killing epithelial cells and resulting in gastric atrophy |
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Causes of Chem gastritis
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Long term NSAIDs or alcohol
Reflux of bile and pancreatic juice |
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Peptic ulcer disease |
Most often h pylori induced hyper chlorhydric chronic gastritis
Imbalance of mucosal defences and injurious agents Chronic Epigastric burning aching pain Complications including iron deficiency freak haemorrhage and perforation Treat h pylori and acid suppression |
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Oesophageal web associated with
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Iron deficiency syndrome:
Kolionychia Cheilosis Etc |
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Most common atresia
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With fistula between bottom part of oesophagus and trachea
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Oesophageal motility disorder |
Regurgitation |
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Achalasia
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Cardio spasm, megaoesophagus
Lack of progressive peristalsis and partial / incomplete relaxation of lower oesophageal sphincter Preferentially involved circular layer of muscularis propria which is hypertrophied Progressive dysphagia Nocturnal regurgitation Aspiration of undigested food Caused by T cell mediated destruction or complete absence of myenteric ganglion cells in lower third of oesophagus Treated with oesophagomyotomy or dilatation |
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Causes of achalasia
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Amyloidosis
Chagas' disease Diabetic autoimmune neuropathy Polio Sarcoidosis Surgerical ablation of dorsal motor nuclei Thyroid disease Tumour |
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Complications of achalasia
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Higher risk of oesophageal squamous cell carcinoma
Candida Lower oesophageal diverticula Aspiration Peptic ulceration Stricture Gastroesophageal reflux Barretts oesophagus |
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Hiatus hernia
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Separation of diaphragmatic crura and widening of space between muscular crura and oesophageal wall.
Associated with reflux oesophagitis |
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Complications of hiatus hernia |
Ulceration |
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Congenital diaphragmatic hernia
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Abdominal viscera can enter throat because
Surgical treatment |
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Osmotic diarrhoea
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Excessive osmotic forces by luminal dilutes
Disaccharides deficiency Lactulose therapy Prescribed gut lavage or antacid treatment Bile malabsorption Laxatives |
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Malabsorption
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Improper absorption of gut nutrients producing bulky stools
Steatorrhea / increased osmolarity Usually ablates on fasting |
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Clinical features of malabsorption |
Anaemia |
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Causes of malabsorption |
Defective digestion |
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Coeliac disease
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Immune mediated enteropathies
Triggered by gluten containing cereals Gliadin component largely pathogenic (peptide product of gluten digestion) |
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Coeliac disease presentation
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Anaemia |
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Coeliac diagnosis
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Clinical documentation of malabsorption |
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Intestinal neuro endocrine tumour |
Forty percent in small intestine |
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Carcinoid syndrome |
Ileal tumours causing vasoactive substances released into systemic circulation
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Gastroschitis
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Thickness defect in wall through which evisceration of the intestines has occurred
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Omphalocoele |
Medial abdominal wall defect into which abdominal contents herniate
Defect covered by amnion and peritoneum usually occurs at base of umbilical cord |
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Annular pancreas and duodenal atresia |
Can cause duodenal obstruction and feeding intolerance |
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Meckels diverticulum |
Failed in volition of viteline duct Solitary diverticulum in the distal ileum |
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Hirschsprung disease
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Motor disorder of gut caused by failure of neural crest cells to migrate completely during intestinal development |
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Types of intestinal obstruction |
Herniation |
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Causes of ischaemic bowel disease
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Hypoperfusion - cardiac failure shock dehydration
Acute vascular obstruction |
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Secondary diarrhoea
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Net fluid secretion output greater than half a litre per fat which is isotonic with plasma and peristalsis during fasting
Caused by infections neoplasticism and iatrogenic eg excessive laxative |
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Chrons disease epidemiology
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Most frequently in second decade, second peak in eight
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Ulcerative colitis epidemiology
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Peak in second / third decades, second peak in middle aged men - thought to be because smoking is protective and people stop
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Clinical presentation of UC
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More dramatic diarrhoea onset and more frequently bloody than Chron's
Mucous PR Abdominal pain Systemic features less common than Chron's Extra intestinal manifestations More around rectum |
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Investigation of UC
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Similar as Chron's but colon only because doesn't affect small bowel
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Distribution of UC |
Rectum and continuous involvement of proximal gi |
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Macroscopic features of UC
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Continuous spread from rectum
Worse distally Red granular mucosa Superficial ulceration Pseudopolyps Continuous, no skip lesions and sharp cut off |
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Microscopic features of UC
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Continuous
Acute mucosal inflam Crypt architectural distortion Inflammation limited to mucosa No granulomas |
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Pathogenesis of Chrons
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Genetic
Identified susceptibility genes involved in pathogen recognition at mucosal surfaces eg NOD2 Environmental factors |
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Complications of Chron's / UC
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Toxic megacolon, bowel swells and necrosis, more common in UC. Surgical emergency
Strictures with bowel obstruction - Chron's Fistulae and abscess formation - Chron's Colorectal carcinoma - if disease for more than ten years involving large portion of the colon. But screening program for these people, two year colonoscopy and biopsy of suspicious areas |
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Extraintestinal manifestations of IBD
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Apthous ulcers of the mouth
Primary sclerosing cholangitis - inflammation of the biliary tree Iritis / uveitis Arteritis - speronegative spondyloarthropathies eg ankylosing spondylitis, enteropathic arthropathy Pyoderma gangrenosum Erythema nodosum- hard red lesions, deep inflam of the fat |
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Treatment of IBD - medicine |
Immunosuppression - corticosteroids, oral or topical
Non steroidal immunosuppression eg mesalazine azathioprine methotrexate Immune modulators eg infliximab and adalimumab |
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Surgery for IBD
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Emergency for toxic megacolon or strictures
As an elective procedure eg intractable disease or cancer risk UC may be cured by surgery however Chron's disease can not as it's not a defined part of bowel |
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Prognosis of IBD
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Remission and flares
Rarely fatal although toxic megacolon and bowel perforation from obstruction can be Risk of colorectal carcinoma but not usually an issue because of screening |
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Presentation of Chrons
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Abdominal pain |
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Investigations for Chron's
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Full blood count - anaemia due to iron deficiency and chronic disease |
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Distribution of Chron's
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Patchy. Mouth to anus |
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Macroscopic features of Chron's
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Due to it being a transmural disease
Fat wrapping - fat moves around to protect bowel from inflam response Bowel wall thickening Fistulae Strictures Ulcers - apthous and serpiginous Cobble stoning Skip lesions |
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Microscopic features of Chron's
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Acute mucosal inflammation
Crypt architectural distortion Extension of inflam beyond the mucosa inducing fissuring ulcers Fibrosis neuronal and muscular hypertrophy Granulomas |
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Ideas for pathogensesis of appendicitis
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Luminal obstruction causes accumulation of mucus
Causes ischaemia of wall and obstruction to blood flow Followed by bacterial infection that spreads from damage mucosa into the wall |
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Treatment of diverticular disease
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Supportive therapy if uncomplicated
Antibiotics with anaerobic and aerobic cover Nil by mouth to reduce risk of perforation Surgery for complications of repeated episodes of diverticulitis |
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Intestinal obstruction - presenting features
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Constipation with or without overflow diarrhoea
Abdominal swelling Abdominal pain Vomiting and fecal vomiting Dehydration Respiratory compromise due to pressure on diaphragm |
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Examination findings on obstruction of bowel
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Abdominal distension
Absent or tinkling bowel sounds Abdominal tenderness Dehydration |
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Causes of abdominal obstruction
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Obstruction like gall stones faecal impaction and foreign bodies
Obstruction within the wall like tumours inflam structures volvulus endometriosis and intussusception External obstruction eg adhesions (most common in small bowel) hernias and external tumours |
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Investigation of obstruction abdominal
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Bloods
Abdominal x days CT/USS |
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Management of bowel obstruction
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Nil by mouth
IV fluids Nasogastric tube Most will resolve due to supportive therapy esp those with adhesions underlying cause is usually survey ante Otherwise treatment of cause. Usually surgery |
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Complications of obstructive bowel
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Bowel perforation with subsequent peritonitis
Bowel ischaemia Sepsis Pneumonia due to respiratory compromise or aspiration of vomit Prognosis is dependant on overlying cause |
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Pseudobstruction of the bowel
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All signs and symptoms but no mechanical blockage |
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Causes of peritonitis |
Perforation pf an abdominal viscus |
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Presentation of peritonitis
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Abdominal pain although bursting may cause transient relief |
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Clinical features of appendicitis
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Abdominal pain starting in umbilical region then moving to the right iliac fossa (McBurneys point) |
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Investigations of peritonitis |
Elevated white cell count CRP and electrolyte abnormalities |
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Peritonitis macroscopic features
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Dull grey shiny peritoneum
Thin development of frank pus Location depends on source |
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Management of peritonitis
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Supportive eg oxygen and fluids
Antibiotic broad spectrum Surgery to explore and repair and wash out |
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Peritonitis complications
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Electrolyte abnormalities due to sequestration of fluid in peritoneum
Sepsis Abscess formation Adhesion with subsequent bowel obstruction risk |
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Polyps
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Mushroom like growths
Most common in colon and recum May be benign or pre malignant May be associated with polyposis syndromes eg FAP, will have colonectomy in young adults to prevent cancer |
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Hyper plastic polyps
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Small and benign
Increase with age |
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Inflammatory pseudopolyps
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Bulging inflamed mucosa as a result of adjacent inflam process
May be very large but benign |
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Adenomatous polyps
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Common
Not malignant but have some abnormalities seen in cancer Are precursor lesions will become cancer if left long enough Show nuclear and architectural abnormalities that are also seen in colorectal carcinomas Not invasive |
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Management of adenomatous polyps
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Surveillance endoscopy
Try to remove all May require surgery if large Seeing increased number as a result of the bowel cancer screening |
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Investigations of acute appendicitis
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Not really because we get them to surgery asap
Fbc Elevated CRP Pregnancy test USS/CT scan not required unless presentation atypical |
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Colorectal carcinoma risk factors and protective
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More common in men
Age Physical inactivity IBD Obesity Smoking Red meat Low fibre Alcohol Protective High vegetable consumption HRT and OCP High folate and NSAID use |
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Presentation of colorectal carcinoma
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Change in bowel habit
Bleeding PR Abdominal pain / distension Anaemia more right side Systemic features - weight loss and malaise Bowel obstruction / perforation usually left sided tumours |
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Colorectal carcinoma investigations
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Microcytic anaemia |
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Treatment of acute appendicitis
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Laproscopic appendicectomy |
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Diverticular disease
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Diverticulosis is outpouchings of bowel mucosa through muscle layer |
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Pathogensesis of diverticulosis
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Low fibre diet
Increased intravenously pressure required for low fibre stools Causes outpouchings where blood vessels penetrate muscularis propria Most common on left side of colon Becomes inflamed when diverticulum obstructed |
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Diverticulitis presentation
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Left iliac fossa pain
Fever Constipation diarrhoea vomiting nausea Can have rectal bleeding |
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Investigations for diverticulitis
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Bloods elevated white cell count and crp
CT scan Colonoscopy and barium enema contraindicated as risk of perforation |
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Complications of diverticulitis
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Diverticular abscess |
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Pyloric stenosis of the newborn |
More common in males, becomes metabolically alkalotic through projectile vomiting Can palpate stomach - distended and peristalsis visible Treated with surgery |
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C. difficile infection |
Gut flora disrupted by antibiotics |
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C. difficile presentation |
Recent antibiotics |
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Treatment of C. difficile
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Oral vancomycin or IV metromidazole
Stop other antibiotics If relapse repeat Fecal transplant |
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Shigella
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Classic cause of bacillary dysentery |
Caus
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Salmonella typhi and paratyphi |
Cause enteric fever |
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Salmonella path
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Invades small and large mucosa
Multiplication in mesenteric LNs can lead to reticulocyte infection and bacteraemia Abdo cramps and diarrhoea Excrete for over 8 weeks in faeces |
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Campylobacter
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Most common cause of diarrhoea
Contact with uncooked meat Commonest cause of bloody diarrhoea Young adults Diagnosis wih selective culture Fluids and antibiotic management, erythromycin but antibiotics not usually used |
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Cryptosporidium
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Infection follows oocyst ingestion
Drinking water and swimming pools Young children Chronic diarrhoea in hiv and aids Diagnosis through stool microscopy |
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Amoebic dysentery |
Abdo pain and bloody diarrhoea
Colitis |
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Commonest cause of diarrhoea worldwide
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Rotavirus.
Vaccination campaign in progress |
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Complications of gastroenteritis |
Electrolyte disturbances
Lactose intolerance Malnutrition Post infective malabsorption syndrome Reactive arthirits Others |
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How do viruses cause diarrhoea
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Damage intestinal villi so unable to absorb macromolecules
These exert osmotic pressure drawing water out |
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Staph aureus toxin |
Heat stable, found in food, diarrhoea and vomiting 1-6h after ingestion and settles in 8-12h
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Bacillus cereus
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Aerobic sport forming rod that loves moist slow cooking food
Quick acting emetic toxin 1-6h Or a diarrhoea one in vivo Diarrhoea and abdo cramps after 8-16h |
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Cholera pathology
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Quite susceptible to gastric acid so need to ingest a lot
Produces enterotoxin coded for by bacteriophage Binds to epithelial cells, causes a cyc activation, secretory diarrhoea of isotonic fluid. Causes severe dehydration as exceeds capacity of colon to reabsorb Incubation 12h to 5d Rice water stools as much to 30l per day Circulatory collapse |
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Management of cholera
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ORT prompt
IV if cannot tolerate or losses too great Adjunctive antibiotics Eg aIthromycin erythromycin doxycycline Oral vaccine not that great but useful if at risk Hygiene essential |
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Enterotoxigenic E. coli |
Two toxins
Travellers diarrhoea Supportive management |
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Enterohaemorrhagic E. coli
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Most dangerous |
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Scleropathy |
Injection of medicines into blood vessels to make it shrink eg in oesophageal varices |
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Causes of intussception |
Mostly seen in infants and children Enlarged mesenteric lymph nodes and Peyer's patches in bowel wall (adenovirus infection?), can act as apex as intusseptum propelled by peristalsis Meckel's diverticulum Intraluminal mass (adults) |
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