Gastroenterology Flashcards
Describe the anatomy of the oesophagus including: vertebral levels, muscular types, and epithelial cell types
Oesophagus starts at C5 (where the trachea begins and ends at T11 the fundus of the stomach
Upper oesophageal sphincter is between pharynx and oesophagus, Lower oesophageal is at T11
Upper 1/3/ cervical oesophagus which ends at the sternal notch has skeletal muscle and sqaumous epithelial
middle 1/3 thoracic oesophagus is from trachea to diaphragm. Has an upper middle and lower part. the upper and middle have a mixture of skeletal and smooth muscle, the lower is only smooth muscle with columnar epithelial
Describe the phases involved in swallowing
Stage 0= oral, chew to make bolus the sphincters are closed
Stage 1= pharangeal phase, UOS opens as a reflex, LOS opens by vasovagal reflex/receptive relaxation
Stage 2= Upper Oesophageal phase, UOS closes, the superior circular muscle contracts and inferior relaxes, sequential contraction of longitudinal muscle to push bolus down
Stage 3- Lower Oeophageal Phase, LOS closes when bolus moves thru
What test determines oepophageal motility
Manometry: measures pressure
the peristaltic waves should be 40mmHg
LOS resting pressure 20 mmHg and then 15mmHg when in receptive relaxation
What neurotransmitter mediates the relaxation of the LOS
inhibitory noncholinergic nonadrenergic neurones of the myenteric plexus
What are the terms that mean (1) difficulty in swallowing and (2) pain on swallowing
(1) Dysphagia : need to know if occurs for solid, liquid, is intermittent or progressive, precise or vague
(2) Odynophagia
Define regurgitation and reflux
Regurg: return of oesophageal contents from above and obstruction
Reflux: passive return of gastroduodenal contents to the mouth
What are the functional disorders of the oesophagus
Absence of a stricture can be caused by two things
1)Abnormal oesophageal contraction
Hypermotility, Hypomotility and Disordered coordination
What is hypermotility in the oesophagus named
Achalasia (LOS doesnt relax)
What causes achalasia (pathophysiology and cause)
Loss of ganglion cells in Aurebach’s myenteric plexus on LOS wall, decreased inhibitory NCNA neurones. This causes increased resting pressure of LOS so receptive relaxation is too late and too weak. The pressure in LOS is much higher than stomach. This causes food to collect in oesophagus causing pressure and dilation of the rest of the oesophagus which stops peristaltic wave propagation
Primary: aetiology unknown
Secondary: due to diseases causing oeophageal motor abnormalities
What diseases can cause secondary achalasia
Chagas disease
Protazoa infection
Amyloid/sarcoma/eosinophilic oesophagitis
Describe how achalasia will present
weight loss, Odynophagia, insidious onset- have symptoms for ages and if not treated oeophagus keeps dilated
leads to pneumonia or esophagitis
What does achalasia put patients at risk of
Oeophageal cancer
How is achalasia treated and what are the risks
Pneumatic Dilation: Balloon inflated the LOS to weaken and stretch circumferentially, decreases pressure so food can pass
Surgery : Heller’s myotomy whch takes away muscle from above and below sphincter and then Dor fundoplication which folds the anterior fundus over. Risk of oesophageal and gastric perforation, cutting vagus nerve, injuring spleen
What is the term for hypomotility
Scleroderma
What is the cause of scleroderma (pathophysiology and causes)
neuronal defects causes atrophy of the oesophagus’ smooth muscle, peristalsis in the distal portion ceases causing hypomotility. Lower resting pressure in LOS, leads to development of gastroesophageal reflux disease,
What syndrome is associated with GORD
CREST syndrome
calcium deposits, spasm of blood vessels in response to cold or stress, acid reflux, sclerodactyl- thickening of skin on hands, dilation of capillaries
How is scleroderma treated
Check its not an organic obstruction
Prokinetiks like cisapride to improve peristalsis force
if peristalsis has failed usually reversible
Give an example of disordered coordination problems of the oesophagus
corkscrew oesophagus
Describe corkscrew oesophagus
Oesophageal spasm, incoordinate contractions so get dysphagia and chest pain. Pressures from 400-500mmHg. Hypertrophy of circular muscle and see the corkscrew on barium test
How is corkscrew oesophagus treated
Pneumatic dilation may result in a response
What is oesophageal perforation, where its most likely to happen and the causes
Hole in the oesophagus
happens at the three areas of anatomical constriction- the cricopharyngeal constriction, aortic and bronchial constriction, diaphragmatic and sphincter constriction.
It can also be due to cancer, foreign bodies, physiological dysfunction
Causes: OGD procedures (endoscope perforates Killians dehisense which is between the pharynx’s inferior constrictor muscles and the cricopharyngeal muscle) ,Boerhaave’s is spontaneous, foreign bodies, trauma,
What is Boerhaave’s and identify the most common findings/sign
Drinking a lot causes repeated vomiting againsta closed glottis creating sudden increased intra-oesophageal pressure with negative intrathoracic pressure. Creates perforation at the left posterolateral aspect of the distal oesophagus which is the weakest point
vomiting and chest pain are the signs
Describe how foreign bodies and trauma to the oesophagus causes oesophageal perforation, name the symptoms
Foreign bodies- disk batteries can erode and make large holes, magnets, sharp objects, acid/alkali things like drain cleaner burns the oesophagus
Trauma - if neck trauma usually penetrative force, if thorax then blunt force
dysphagia, chest pain, and shortness of breath, blood in saliva
How does oesophageal perforation present
Pain, fever, dyspahgia, emphysema
What investigations should be carried out for oesophageal perforation
Chest X ray, CT scan, swallow test, OGD
look for outline of mediasteinum = air in cavity/pneumomediasteinum
look for air or fluid leaking out
How is oesophageal perforations managed
is a surgical emergency so nil by mouth, IV fluids, broad spectrum ABs and antifungals as lots in the oesophagus . take bloods, tertiary referral centre
conservative management= covered metal stent
operative management is default- primary repair or oesophagectomy
How does the stomach protect against reflux and failure of these mechanisms results in what
LOS usually the barrier against reflux (pepsin and HCl)
3 protective mechanisms:
oesophageal peristalsis reflex, clears volume
saliva pH clearance
epitheliums barrier properties
Failure of protective reflux mechanisms
Gastro-oesophageal refluc Disease GORD
What inhibits and promotes reflux
INHIBITS: Acetylcholine, alpha-adrenergic agonists, hormones, protein rich food, histamine, high intra abdominal pressure all increase LOS pressure and inhibit reflux
PROMOTES: VIP, beta-adrenergic agonists, hormones, dopamine, NO, PGI2, PGE2, chocolate, acid gastric juice, fat, smoking all reduce LOS pressure promoting reflux
What causes normal sporadic reflux
pressure on full stomach, swallowing (as the oesophageal pressure and pH rises after swallowing as saliva is neutral) and sphincter opening transiently (creating low LOS pressure momentarily) are normal
Failure of protective mechanisms results in what, explain
GORD
If there is decreased sphincter pressure
If there is more transient sphincter opening theres more air and CO2 entering,
Hiatus hernia: (1) sliding hiatus hernia where stomach moves through diaphragm which moves the gastrooesophageal junction/ LOS, (2)rolling/paraoesophageal hiatus hernia where portion of stomach is herniates thru diaphragm
Abnormal peristalsis causes lower volume clearance
Reduced saliva production during sleep can reduce pH clearance, smoking can also reduce the buffering capacity of saliva and reduce pH clearance
Defective epithelium mucosal due to alcohol
All of these lead to GORD which can reult in reflux oesophagitis where the lining is damaged and lead to carcinoma
How is GORD investigated and treated
Investigations: Oesophagealgastro duodenoscopy (OGD), oesophagel manometry, 24h oesophageal pH recording
Treat: lifestyle changes (weight loss, smoking ess alcohol) and Proton Pump Inhibitors
Dilation of peptic strictures, Laparoscopic Nissen’s fundoplication
What is the function of the stomahc
Break food into smaller particles through acid and pepsin.
Releases food in a controlled and steady rate
Kills parasites and bacteria
Describe what substances/molecules are found in different regions f the stomach
In the cardia and pyloric regions (top and bottom valve parts) its only mucus
Body and fundus have parietal and chief cells to make acid : mucus, HCl, pepsinogen
Antrum: gastrin
What types of gastritis are there
1) Erosive and haemorrhagic gastritis: causes and acute ulcer so bleeding and perforation. Causes of this can be NSAIDs, alcohol, multi-organ failure, burns, trauma and ischamia
2) Nonerosive, chronic active gastritis: helicobacter pylori acts on antrum to increase gastrin so acid secretio is increased resulting in a gastral and duodenal ulcer
3)Atrophicgastritis: Autoantibodies act on the parietal cells in the fundus, kparietal cells atrophy so less pepsinogen, intrinsic factors and acid secretion. (More acid secretion need means G-cell and Enterocromaffin like-cells hyperplasia which can lead to epithelial metaplasia and carcinoma. Less intrinsic factors means vitamin B12 cannot be absorbed so get pernicious anaemia)
All three can lead to :
Reactive gastritis which results in epithelial metaplasia and carcinoma
Describe the regulation of gastric secretion: both the stimulation and inhibition
Stimulation:
ACh acts on M1 receptors of vagal parasymapthetic fibres: stimulates acid secretion, G cells secrete gastrin and enterochromaffin cells which release histamine
Gastrin from the antrums G cells (makes partietal cells make H+/K+ pump work and chief cells to make pepsinogen to pepsin
Histamine (enterochromaffin like cells and mast cells) binds to H2 receptors, parietal cells will make HCl
Inhibition:
Secretin : inhibits antral G cells so no gastrin (less activation of parietal and chief cells)
Somatostatin: inhibits histamine release, and the H+/K+ATPase that parietal cells need
Prostaglandins PGs (E2 and I2), TGF-alpha and adenosine
How is the stomach protected from ulcer formation
1) Mucus film protects from pepsin and H+
2) HCO3 secretion from surface epithelium maintains a pH gradient, and if bicarbonate meets a proton will make water and Co2 (prostaglandins stimulate HCO3/ NSAIDs like ibuprofen inhibits this effect- so take NSAIDs with acid suppressant)
3)Epithelial barrier: EGF from salivary glands stops H+
4) Mucosal blood perfusion: Blood flow contributes to protection by supplying the mucosa with oxygen and HCO3-, and by removing H+ and toxic agents diffusing from the lumen into the mucosa.
If there is damage to the epithelium how does the body repair itself, explain the two phases
Migration: adjacent epithelial cells flatten and slide across the basement membrane to close the gap
Cell Growth to close the gap stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin
Describe acute wound healing
Acute Wound Healing: basement membrane destroyed in wounds so attract leukocytes and macrophages to phagocytose the necrotic cells, promote angiogenesis and regenerate ECM after repairing basement membrane. Epithelial cells then close by restitiution/migration and cell division
What causes ulcer formation
Helicobacter pylori disturbs the barrier function
NSAIDs (ibuprofen and aspirin) or smoking reduces prostoglandin synthesis so less inhibiton of HCl or pepsin so get too much gastric acid which is chemical aggression
Lower HCO3- secretion
Decreased cell fromation
Decreased blood perfusion to take protons away due and mucosal protection decreases
How are ulcers of the stomach treated
Medical: Proton pump ingibitor or H2 blocker, if CLO test shows its due to H.pylori then triple AB’s (amoxiccilin, clarithromycin, pantoprazole) for 1-2 weeks
Surgical:
if ulcer doesnt heal in 12 weeks then observe for another 12. Check serum gastrin and then do OGD and biopsy the four quadrants of the ulcer if it is refractory (non healing)
After surgery then may need continuous NSAIDs, complications of surgery are haemorrhage, obstruction and perforation.
If gastrin levels are high after 24 weeks what two diagnoses are possible
g cell hyperplasia or gastrinoma Zollinger-Ellison Syndrome (tumour secreting gastrin which causes lots of ulcers)
What three factors control thirst
Osmolality (conc)
Blood volume reduced
Blood pressure reduced
What hormone regulates osmolality, how does it work and where
ADH/Vasopressin
is stored in the posterior pituitary and when released binds to the V2 receptor on the kidneys collecting duct to insert aquaporin 2 channels. When ADH is high in the plasma it means anti diuresis is achieved and small amounts of urine passed. Also binds to the V1 receptor to cause constriction
In which regions of the hypothalamus are osmoreceptors located
Organus vasculosum of the lamina terminalis / circumventricular organs
Subfornical Organ
Describe the process of ADH release
Osmoreceptors in the organus vasculosum of the lamina terminalis and the subfornical organ. When plasma is more concentrated/ high osmolality, water moves out the osmoreceptors and they shrink. Shrinking means the membrane: cation channels increases so more activation and the membrane depolarises. A positive charge therefore moves across the osmoreceptor and fires and action potential which triggers supraoptic magnocellular nuceli which stimulates ADH producing cells in the posterior pititary to increase ADH. ADH is released, fluid retention occurs through ADH binding to V2 receptors and inserting aquaporin 2 channels, and thirst is triggered
How is relief of thirst sensation caused
Receptors in the mouth, pharynx and oesophagus decrease thirst sensation even before sufficient water has been absorbed- this is short lived but to ensure not too much is drunk
Completely relieved when plasma osmolality is decreased or blood volume/ arterial pressure decreased
Describe how the body responds to changes in blood pressure/volume
When blood pressure/volume drops then juxtaglomerular cells of the renal afferent arteriole release renin. Renin breaks down angiotensinogen that the liver produces into angiotensin I. Angiotensin I is then broken down to angiotensin II by ACE. Angiotensin II then increases sympathetic activtiy and causes vasoconstriction, causes ADH secretion, stimulates thirst and stimulates the zona glomerulosa of the adrenal cortex to release aldosterone which will then absorb Na+ and Cl- and excrete K+
How is body weight homeostasis achieved
Reduction of adipose tissue increases food intake and reduces energy expenditure and reduces sympathetic nervous system activity
Increase does the opposite
What are the terms meaning appetite stimulant and appetite suppressant respectively
Stim- Orexigenic
Supp- Anorectic
What nucleus in the brain regulates food intake
Arcuate nucleus
How is appetite regulated
(1) Leptin (2) Ghrelin, PYY and gut hormones (3) neural input all give infromation to the hypothalamus. The arcuate nucleus of the hypothalamus has an incomplete BBB so allows access to these peripheral hormones, when ghrelin is produced due to an empty stomach it stimulayes synthesises info producing either appetite stimulant/orexigenic neuropeptides such as NPY and AGRP. When PYY and other gut hormones like GLP-1 and CCK are relasease from a full stomach the arcuate nucleus produces suppressive/anorectic neuropeptides such as POMC (in PYY’s case it will also inhibit NPY) . It sends this info to the paraventricular nucleus that has neurones that terminate in the posterior pituitary.
Leptin is in proportion to adipose tissue in the body, If it is high it signals to stop eating and burn fat
Describe the difference between the two orexigenic neuropeptides
AGRP inhibits POMC to encourage eating (inhibits the inhibitor double negative)
NPY directly stimulates
How does the neuropeptide that stimulates a decrease in food intake work. What is this system called
Melanocortin system
POMC triggers neuropeptides such as alpha-MSH which act on the paraventricular nucleuses MC4R receptor to decrease food intake. However AGRP which inhibits POMC has to be inhibited for POMC to be activated
What mutations of the CNS could possibly affect appetite
POMC deficiency and MC4-R deficiency
Signals from amygdala: emotion, memory, reward
Other parts of the hypothalamus
Problems with the vagus nerve to the brain stem
What is the hormone produced by fat and what does it do, give an example of one
Adipostat, hypothalamus senses the concentration and alters the neuropeptides adjustingly
Leptin is an example, is made in white adipose tissue and enterocytes, circulates in plasma and acts on hypothalamus to regulate appetite and energy expenditure. Leptin is in direct proportion to amount of body fat. If it is high it decreases food intake and increases thermogenesis/energy expenditure
What mechanisms can affect leptins effect on fat regulation
Congenital leptin deficiency : absent leptin
Decreased leptin expression/secretion from adipose tissue : cant regulate
Leptin resistance
What gastrointestinal hormones control appetite and food intake, where are they produced and how do they work
Enteroendocrine cells in the stomach pancreas and small bowel secrete gastrointestinal hormones
ghrelin stimulates appetite when stomach is empty. Increases gastric motility and acid secretion. Directly modulates arcuate nucleus to stimulate ARGP and NPY peptides whilst inhibiting POMC neurones. Regulates reward, taste sensation, memory and circadian rhythm. LEvels spike before a meal
Peptide tyrosine tyrosine (PYY) inhibits food intake when stomach distended. Reelased in the terminal ileum and colon once feeded, Inhibits NPY release, stimulates POMC neurones to reduce appetite
What are some concequences of obesity
Sleep apnoea
Depression
Bowel cancer
Osteoarthritis
Gout
Stroke
MI
HYpertension
Diabetes
What is Rigler’s sign
Double wall sign, sign of pneumoperitoneum (free intraperitoneal air)
What are the signs of duodenal perforation
Riglers sign, subdiaphragmatic air , pain, vomiting, pyrexia
How are duodenal perforations managed
I.V fluids and AB’s
Surgery: laproscopic omental pathc
What are the clinical signs of pancreatitis
Amyalse levels high, pyrexial, epigastic pain, vomiting, fatty foods aggravate
How is pancreatitis investigated and managed
Fluids and painkillers, avoid fatty foods
US to see gallstones, if gallstones present then MRCP ( if gallstones may see dilated cyctic duct and a stricture below due to the stone)
Describe the embryology of the digestive tube and how this affects blood supply
Distal oesophagus to proximal part of of 2/3 of duodenum is foregut. The blood supply to this region is the coeliac trunk
Distal half of 2/3 of duodenum to proximal 2/3 of transverse colon is midgut. Blood from Superior mesenteric artery
Dital 1/3 of transverse colon to rectum is hindgut. Blood from inferior mesenteric artery
Which organs and issues are associated with colicky pain, and which constant
Colicky :
Ureter stones
Kidney stones
Cholelithiasis (stone in gallbladder)
Choledocholithiasis (in common bile duct)
Colon
Constant: kidney, spleen, liver problems
Describe radiation of pain of the upper six quadrants and what organ theyre associated with
Right hypochondriac : gallbladder radiates through the back and to the right
Epigastric : stomach, duodenum, pancreas: straight through to back
Left hypochondriac: pancreas: through back to righ
Right Lumbar and Left Lumbar: kidneys radiate from loin to groin
Umbilicus doesnt usually radiate
How would appendicitis present
Central epigastric pain then shifts to right iliac region.
Gradual onset
Constant pain
No radiation of pain
nausea, anorexia, fever
worse on movement
dull ache
How would bowel obstruction present
Central/epigastric pain
gradual
colicky
vomiting if bowels not open
Farting relieves pain
Moderate pain
How would uriteric colic present
Loin pain that radiates to groin
sudden onset
Colicky
vomiting
severe pain
How would cholelithiasis or choledocholithiasis present
Right upper quadrant that radiates to right shoulder
sudden onset
colicky
nausea and indigestion
after eating and fatty foods make worse
Since the GI tract has such a high antigen load what immunological state is it in
Restrained activation state as has to tolerate the resident microbiota, dietary ntigens but also respond to pathogens
What four major phyla of bacteria live in the gut microbiota
Bacteroidetes
Firmicutes
Actinobacteria
Proteobacteria
descirbe what symbionts, commensals and pathobionts are
Symbionts - bacteria that live in bowel and dont harm
Commensals- get an advantage from the host such as nutrients in bowel
Pathobionts- no advantage or harm but if become too much can lead to harm
What is the term that describes an altered microbiota composition
Dysbiosis
What are some causes of dysbiosis
Infection/Inflammation
Dietary changes
Xenobiotics
Hygiene
Genetics
Bacteria then produce bacterial metabolites and toxins which can affect different systems in the body
What is the difference between microbiota and microbiome
Microbiota is a specific region of the microbiome
Describe the mucosal defence in detail
Physical Barriers
Epithelial barrier: has a mucus layer made by goblet cells, monolayer of epithelium with tight junctiosn and Paneth Cells in the small intestine which secrete antimicrobial peptides called defensins and lysozyme
Peristalsis moves bacteria along
Enzymes and the acidic pH kill
Commensal bacteria: compete for guts nutrients and binding sites, make antimicrobial signals and act on the hosts immune system to prevent invasion
After invasion Immunological Barrier
MALT
GALT
What is MALT and GALT
MALT (Mucosa Associated Lymphoid Tissue): in submucosa under epithelium, lymphoid masses that contain lymphoid follicles which are surrounded by HEV postcapillary venules which are high endothelial venules that allow access from gut to the lymphocyte circulation. Examples are tonsils and adenoids
GALT (Gut Associated Lymphoid Tissue)- responsible for innate and adaptive immune responses, has B and T cells, dendritic cells, epithelial and intra-epithelial lymphocytes.
Non organised:
- intra-epithelial lymphocytes (between eneterocytes)
- Lamina propria lymphocytes
Organised:
-Peyer’s patch (small int)
- Caecal patch (large int)
- Isolated lymphoid follicles
- Mesenteric lymph nodes
What is the difference between the small and large intesitines non organised GALT
Small intestine: Stem cells in the crypt make enterocytes that divide up to microvilli. Paneth cells are in the crypt, Lots of intra-epithelial lymphocytes, Macrophages, T cells,
LArge intestine: Goblet cells increase, lymphoytes decrease
Describe Peyer’s Patches in detail including location, structure and how they sample antigen
Along the submucosa of the small intestine, especially the ileum. Development requires exposure to bacterial microbiota so get more with age.
Peyers patches are lymphoid follicles covered with follicle associated epithelium (no goblet cells or other things or microvilli, thinner so is exposed to the microbiota) The FAE also contains M cells which uptake the antigen through IgA receptors (IgA-bacteria complexes move in) . Contains naive T cells, B cells and dendritic cells. Dendritic cells use trans-epithelial antigen sampling reach out and grab antigen
Once antigen is inside the Peyer’s patch
what happens
Dendritic cells take antigen on MHCII to T cells which will become Treg cells and influence the naive B-ceels which express IgM to switch class to IgA, B cells then become IgA secreting plasma cells. These cells populate the lamina propria. The dendritic cells need to activate more lymphocytes so will move to the mesenteric lymph node so lymphocyte proliferation occurs, it will move into venous circulation through thoracic ducts and either move to MALTS, skin, tonsils or to the lamina propria to produce more antibodies and secrete them into the lumen
The dimeric IgA formed moves throught th epithelial cells in a vesicle and is released into the lumen as secretory IgA (sIgA) which binds to the antigen in the lumen stopping invasion.
How do naive T cells find their way to Peyers patch
Gut honing cascade directs T cells to Peyers pathes. Will move through high endothelial venules to where they need to be in the lamina propria, roll across the HEV,
the HEV’s MAdCAM-1 Adhesion molecule will activate the T cells by binding to T cells alpha4beta7 integrin will, arrest them and roll them into lamina propria.
Why is enterocyte turnover time important
Short turn over time because they are the first line defense against GI pathogens and substances in the diet can damage them. The effects of this are short lived as the enterocytes are replaced.
What can affect enterocyte turnover rate
Radiation causing impaire production
Describe how cholera infects
Transmitted thru faecal-oral route in contaminated food and water
Vibrio cholerae serogroups O1 and O139 cause cholera-acute bacterial disease. They move into the small intestine, make contact with the enterocytes and release cholera enterotoxin. Cholera enterotoxin is endocytosed into the lamina propria where it increases adenylate cyclase activity, increases cAMP and activates the cystic fibrosis transmembrane conductance regulator to move Na+, K+, Cl-, HCO3- and water into the gut lumen
What are the symptoms of cholera infection and how is it treated
Severe dehydration, Watery diarrhoea, vomiting, nausea and abdominal pain.
Take bacterial stool culture or a rapid dipstick test
Rehydrate via oral route treats it
What vaccine is used to prevent cholerae infection
Dukoral an oral vaccine
Describe the viral causes of gastroenteritis and how to treat them
Rotavirus: RNA virus which replicates in enterocytes, causes diarrhoea. Treat by oral rehydratopn, take the live attenuated oral vaccine Rotarix
Norovirus: RNA virus that takes 24-48 hours, faecal-oral transmission, will shed virus for 2 weeks, causes oubreaks in closed communities, get acute gastroenteritis and recover in 1-3 days. Sample PCR to diagnose.
both present with Vomiting, abdominal cramps, darrhoea for 1-3 days . Do PCR testing on stool sample. Both just rehydrate maybe give antiemetics/antidiarrhoea drugs
Describe the 5 bacterial causes of gastroenteritis
Campylobacter (jejuni/coli)- from undercooked meat, untreated water and unpasteurised milk, has low infective dose so highly virilant. Dont usually treat maybe azithromycin. Self limited watery maybe bloody diarrhoea, fever, abdoinal pain. Take stool and bloof culture
E.coli: gram negative, harmless (1) enterotoxigenic E.coli causes watery diarhoea and is a cholera like toxin, often treavel (2) Enteroinvasive E.coli causes bloody diarrhoea, a shigella like illness due to inflammation (3) Enterohaemorrhagic/Shiga toxin-producing E.coli is the O157 serogroup causes loss of kidney function and hameolytic uraemic sydrome, bloody diarrhoea, not much fever. Take a stool or blood culture
Clostriduym difficile: Exists naturally inside, if enter a dysbiotic state that favours the pathogen then get sick. Risk factors are age, hospital stay length, being in a nursing home, within 2 months of antibiotic use sucha as penicillin, cephlasporins, clindamycin or fluroquinolones). Signs : diarrhoea watery/bloody, pain, tender abdomen. Pseudomembrane formation, toxic megacolon or fulminant colitis. Stool sample and sigmoidoscopy. Should isolate the patient give Metronidazole and Vancomycin or Faecal Microbiota Transplantation.
Cholera also
What two terms describe excessive thirst and drinking and (2) inappropriate or lack of thirst
Polydipsia
Adipsia
Define anorexia and obesity
Anorexia : lack or loss of appetite for food
Obesity: abnormal or excessive fat accumulation that poses a risk to health
Three causes of primary polydipsia
Mental illness
Brain injury
Organic brain damage
What is secondary polydipsia, list 5 causes
Medical issues that disrupt osmoregulation or alter ADH
Diabetes insipidus (impaired ADH production) and diabetes mellitus, kidney failure, sickle cell, addisons (hypoadrenocorticism), conns syndrome (primary aldosteronism)
diuretics, laxative, antidepressant
dehydration due to fever, vomiting, diarrhoea, underhydration
Describe how the body would respond to lower Blood pressure
Describe the two ways in which ADH secretion can be stimulated
LOW BLOOD PRESSURE
renal afferent arterioles juxtaglomerular cells detect low blood pressure and secrete renin, renin cleaves the livers angioteninogen into angiotensin II, whih the lungs ACE converts to Angiotensinogen II. Angiotensinogen II causes vasoconstriction and increases sympathetic activity to lower GFR, causes thirst, acts on zona glomerulosa to secrete aldosterone which pulls in sodium and water at the distal convuluted tubule and proximal collecting duct (aldosterone only released when drop in blood pressure). But also causes ADH secretion which acts on the V2 receptors in the proximal collecting duct to insert aquaporin 2 channels.
DETECTS HIGH OSMOLALITY
Osmoreceptors in the organus vasculosum of the lamina terminalis and the subfornical organ. When plasma is more concentrated/ high osmolality, water moves out the osmoreceptors and they shrink. Shrinking means the membrane: cation channels increases so more activation and the membrane depolarises. A positive charge therefore moves across the osmoreceptor and fires and action potential which triggers supraoptic magnocellular nuceli which stimulates ADH producing cells in the posterior pititary to increase ADH. ADH is released, fluid retention occurs through ADH binding to V2 receptors and inserting aquaporin 2 channels, and thirst is triggered
What problem impairs aldosterone regulation
Conn’s syndrome: secretes too much aldosterone from a tumour
What is the key difference in the presentation of diabetes mellitus and diabetes insipidus
Diabetes mellitus: will pee a lot to get rid of glucose
Diabetes insipidus: cannot concentrate pee due to an ADH insufficiency so wont pee much
How is obesity treated
if BMI 40 or BMI 35 + comorbidity then gastric bypass or sleeve gastrectomy
After bariatric surgery GLP1, GLP2, which stimulate insulin release and inhibity glucagon release as well as PYY which controls satiety and anorexogenic are elevates so will eat less. Ghrelin also decreases so there is less NPY appetite (NPY is an orexigenic hormone which causes appetite)
Describe how C.difficile infections will present
high creatinine (affects kidney function), high WBC
rigler’s sign (air in the bowel) indicated pneumoperitoneum from small bowel obstruction that perforates
fever, diarrhoea, tummy pain and distention
positive stool test for c.diff
How are c.diff infections managed
Move patient to side room as infectious, discontinue any antibiotics which may have caused the dysbiosis. Give fluids, nutrition to manage diarrhoea
What are the treatments for different classes of severity for c.diff infecctions
not severe: antibiotic therapy: oral vancomycin or metronidazole or fidaxomicin, Faecal microbiota transplantation
Severe if WCC over 15 and creatinine over 150
Fulminant colitis : leads to hypotension/shock, ileus (lose bowel function), toxic megacolon
for these the same antibiotics, lose monitoring and early surgical consultation
What are the indications for surgery in c.diff patients
Colonic perforation
Necrosis/full-thickness ischameia
Intra-abdominal hypertension/abdominal compartment syndrom
Signs of peritonitis or worsening abdo exam ]End-organ failure
Pseudomembranous colitis: is severe colonic disease get yellow-white plaques forming pseudomembranes on the mucosa which is confirmed by endoscopy and biopsy
How would ulcerative colitis present
Diarrhoea with rectal bleeding
urgency and mucus secretion
high platelet count, WBC , CRP
sigmoidoscopy/ total colonoscopy shows chronic inflam with no granulomas, continuous left sided inflammatory changes (U.C starts from rectum upwards)
How is ulcerative colitis managed
5-ASA (aminosalicylic acid), then prednisolone then immune suppressors- axathioprine and methotreaxate. biologics, diet, FMT, AB’s
What are the different severities of ulceritive colitis
based on clinical disease activity index, Montreal classification, trulov &Witt scores
Mild: 4 bowl movements a day, not system toxicity, normal ESR/CRP, mild symptoms
give 5-ASA
Moderate: more than 4 BM, some anameia, mild symptoms and systemic toxicity, nutiriotn maintained, no weight loss
prednisolone (corticosteroids) and immune suppressors
Severe: more than 6 BMa, severe anaemia and toxicity, inc ESR/CRP, weight loss
biologics- infliximab, continue immune suppressors and steroids, consult about surgery
What are the risk factors of ulcerative colitis
Autoimmunity, CHF, hepatotoxicity, bone marroe suppression, demyelinating disease
Define malnutrition
State in which deficiency, excess or inbalance or energy, protein or other nutrients results in a meaurable adverse affect on body composition, function and clinical outcome
Whoo are at risk of malnutrition
PPL at risk are over 65, have alcohol or drug dependency, Gi dysfunction, crhonic disease
What are some causes of malnutrition in a hospital setting
1) Maldigestion, malabsorption : Function, length or loss of Gi tract/ bowel
drug-nutrient interactions
2) Reduced Intake : Taste changes, food options, nil by mouth, fatigue, inactivity
3) Altered metabolism: resting energy expenditure changes (hypometabometabolism after injury then longer hypermetabolic pahse with inc catabolism/ high O2 consumption, see body wasting.)
What is the impact of malnutrition in clinical settings
physical function decline and poorer clinical outcomes such as death after operation, complications, hospital length stay. less wound healing and response to treatment
How is malnutrition diagnosed
MUST screening tool
Dieticial assesses nature and acause by looking at diet, clinical, body composition etc
Who should be given nutrition support
Malnourished : BMI less than 18/ unintentional weight loss more than 10% in 3-6months/ BMI under 20 + 5% weight loss in 3-6m
At risk of malnutrition: eaten little for more than 5 days or have poor absorptive capacity/ high nutrient losses/ increased nutritional needs due to catabolism etc
How is malnutrition treated
1st = oral route : oral nutritional support : includes fortification of meals and snacks, changing meal patterns, practical support, diet counselling, nutritional supplements
2nd if GI tract is functioning and accessible then Enteral feeding. Naso-gastric tube if cant access stomach then nasoduodenal or nasojejunal. If for more than three months gastrostomy or jejunostomy
3rd paraenteral tube feeding if tube feeding not possible, return to enteral or oral feeding as soon as possiblr
What are the complications of enteral feeding
misplacement can go into lung, blockage, buried bumper
metabolic complications maybe hyperclycaemia or deranged electrolytes
may have aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea
If a nasogastric tube is misplaced what do you do
aspirate the pHshould be 5.5. and below, if above then chest x-ray
Define paraenteral nutrition
delivery of nutrients, electrolytes, and fluid directly into the venous blood
where is the access point for paraenteral nutrition
central venous catheter at superior vena cava and right atrium
What are the complications of parenteral nutrition
catheter related infection from hand hygiene
pneumothorax, haemothorax, cardiac arrhythmia
hyperglycaemia, deranged electrolytes, abnormal liver enzymes, oedema
Can albumin be used to mark malnutrition, explain
No, albumin made in liver and is a negative acute phase protein.
The acute phase response is when theres inflammatory stimulus, monocytes and macrophages are activated and release cytokines, especially IL-6. Cytokines act on liver to synthesise c reactive protein, amyloid a, haptoglobin etc but down regulate albumin and transferrin. see high CRP but low albumin.
Albumin is thus a poor predictor of malnutrition in acute phase
As reintroduce oral, enteral or paraenteral feeding to a malnourished or starved individual, what do you put the patient at risk for, explain it
Refeeding Syndrome : are starved so have used glycogen stores, protein catabolismhas occured, protein and vitamin depletoion , K+ and Na+ may still be normal. then switch to refeeding which causes insulin secretion, protein and glycogen is made, glucose is taking up leads to rapid fall of extracellular levels of K+, Mg, PO43-, thiamine. get salt and water retention
causes: arryhtmia, high HR, CHF, cardiac arrest
respiratory depression
coma, seizures. encephalopathy, wernicke’s encephalopy
Who are at risk of refeeding syndrome
risk : no food/little intake for 5 or more days
high risk (one or more of):
- BMi under 16
- 15% unintentional weight loss in 3-6m
- little/no food for more than 10 days
- low K+, Mg2+, PO4
high risk (two or more of):
- BMI under 18.5
- 10% unintentional weight loss in 3-6m
- little/no nutrition for more than 5 days
-PMx of alcohol abuse or on insulin, chemotherapy, antacids, diuretic etc any drugs
Extremely high risk:
BMI under 14
little to no intake over 15days
How is refeeding syndrome avoided
start by upping by 10-20 kcal/kg, carbs should be 40-50% of energy,micronutrients given from onset
keep correcting electrolytes daily
give thiamine from onset of feeding usually 30 mins before
monitor fluid shifts
What is the difference between clear and free fluids
A clear liquid diet, where you only drink things like water, tea, and broth, usually in prep for surgery.
A full/free liquid diet is similar, but it includes all fluids and foods that are normally liquid as well as foods that turn to liquid when at room temperature, foods that are easy to pour or can be sucked through a straw. It gives you more nutrition, protein and calories than a clear liquid diet.
Describe types of colorectal cancer and what cell type of cancer it is
usually patients over 50
Adenocarcinoma (glandular epithelium affected)
Sporadic
Familial: if family history
Hereditary Syndrome: Family history, get at young age with specific gene defects
How does colorectal cancer develop
get APC mutation and COX-2 overexpression so develop a polyp which then becomes a small adenocarcinoma then with k-ras mutations it gets bigger and p53 mutation it grows and eventually loss of 18q results in colon carcinoma .
What are the risk factors of colorectal cancer
past history of colorectal cancer, adenoma, UC or radiotherapy
1st degree relative under 55yrs got
relatives with genetic predispositions
smoking, obesity, socioeconomic status
How will colorectal cancer present
66% in descending colon and rectum
33% in sigmoid colon and rectum
If caecal and right sided cancer
iron deficiency anaemia: bleed slowly, not enough to notice
Diarrhoea
distal ileum obstruction
palpable mass
Left sided and sigmoid cancer:
PR bleeding, mucus, thin stool (tumour obstructs stool so becomes thin)
Rectal carcioma:
PR bleeding, mucus, tenesmus (feel like need to go), anal, perineal and sacral pain
Late signs:
bowel obstruction
local invasion: bladder symptoms and female UTIS
metastises: liver, lung, regional lymph node, peritomeum
If late stage colorectal cancer begins to effect the peritoneum what is seen
Sister Mary Joseph nodule (tumour seen thru bellybutton)
When examining a patient with colorectal cancer what signs are you looking for to determine whether its primary or metastasised
Primar:
abdominal mass, on digital rectal exam is smaller than 12cm and reached with the finger, use a rigid simoidoscopy, checkfor abdominal tenderness and distention
Mets:
hepatomegaly
monophonic wheeze
bone pain
What investigations are used to diagnose colorectal cancer
Faecal occult blood test:
- Guaiac test (hemoccult) have to avoid red meat, melons, horse-radish, vitamin C and NSAIDs for 3 days
- FIT (Faecal Immunochemical Test) detects faecal occult blood
Blood Tests:
- FBC as may be anaemia or low ferritin
- Tumour markers: CEA useful for meauring but not diagnostic
DIAGNOSIS ::::: Colonoscopy: to visualise lesions under 5mm, can remove small polyps, sedation
CT Colonoscopy/Colonography: visualise lesions over 5mm,no sedation, if lesions then need colonoscopy to diagnose
MRI pelvis: rectal cancer to check mesorectal lymph involvement and help to decide whether chemotherapy before or after surgery
CT chest/abdo/pelvis: to stage cancer
How is colorectal cancer managed
Surgery
stent, radiotherapy, chemotherapy
If obstructing colon carcinoma then :
- for right + transverse colon:
resection and primary anastomosis
- for left sided obstruction:
Hartmanns procedure (colostomy that will be reversed)
primary anastomosis with intraoperative bowel lavage and defunctioning ileostomy
palliative stent
List the different types of resection of the colon
Right hemicolectomy 9right colon removed then ileocolic anastomosis)
Extended right Hemicolectomy ( right and part of transverse colon removed then ileocolic anastomosis)
Left Hemicolectomy with colorectal anastomosis
Sigmoidectomy
What are the most common types of liver cancers, describe them
Hepatocellular cancers- primary cause, usually have cirrhosis, can be caused by aflatoxin 9toxins made by mould). 4-6 months survive without medication, systemic chemo is ineffective, so surgical excision is most effective, can use: liver transplant, transarterial chemoembolisation or radio frequency ablasion. less than 30% survive 5 yrs and only 5-15% can get the surgeyr
Cholangiocarcinoma : common hepatic duct due to primary scleorising cholangitis and ulcerative colitis , liver fluke (parasite in raw fish), choledochal cyst (cyst in bile duct). less than 6 months, systemic chemo is ineffective, surgical excision best choice. % year survival is 20-40%, 20-30 can get the surgeyr
Gallbladder cancer: gallstones can cause, porcelain GB too, or chronic typhoid infection. 5-8 month without med. systemic chemo ineffective so must do surgical excision. 5 year survival 64% if stage II, 44 if III, 8 if IV, less than 15% can get surgery
Colorectal cancer or any secondary liver metastases, less than a year survival without treatment, could use radiofrequency ablasion but surgical excision is optimal. 5 year survival of 25-50%, 25% can get the surgery
Describe pancreatic cancer, the most common form of it, groups of people that are more likely to get it and risk factors
common and lethal (incidence and mortality equivalent) as most present late and only 15-20% have a resectable disease
pancreatic ductal adenocarcinoma most common
more common in western/industrialised countries, most between 60-80 yrs, men more common.
risk factors: chronic pancreatitis, T2D, occupation (insecticides, aluminium), cigarrette smoking, family history 1-3 1st degree relatives increase chance by 2,6,30. espcially SPRIK1, PRSS1, CFTR genes
Describe the pathogenesis of pancreatic cancer
pancreatic intraepithelial neoplasias evolve through non-invasuve neoplastic precursor lesions, they are less than 5mm diameter and cant be seen in imaging but aquire genetic alterations along the way that lead to cancer.
PANIN-1A from ERBB2 and KRAS mutations
PANIN-2 from CDKN2A
PANIN-3 from TP53 BRCA2
How does pancreatic cancer present
HEAD OF PANCREAS
- Jaundice (common bile duct compressed), no pain and Courvoisiers sign of a papable gallbladder
- weight loss: anorexia, alabsorption, diabetes
-pain: epigastrum, radiates to back
-acute pancreatitis
- vomiting if duodenum is obstructed
-gastrointestinal bleeding if duodenal invasion or varices due to portal vein or splenic vein occlusion
BODY AND TAIL OF PANCREAS
- asymptomatic
- weight loss
- vomiting at late stage if affects duodenaljejunum flecture
no jaundice as onlyoccurs in head of pancreas when tumour obstructs the CBD
What investigations are used for pancreatic cancer
Tumour marker CA19-9 : is falsely elevated in pancreatitis, hepatic dysfunction and obstructive jaundice. Over 200u/ml is 90% specificity
Ultrasonography : identify pancreatic tumours, dilated bile ducts, liver mets
Dual-phase CT: looks for organ and vascular invasion and mets can predict resectibility
MRI detect resection similar to CT
MRCP: ductal imaging
ERCP: confirms double duct sign (CBD and pancreatic duct dilated) , aspirates biliary system, can put stent to relieve jaundice
EUS: sensitive for small tumours
Laprascopy and laparoscopic US: mets
PET: occult metastases
How are pancreatic cancers treated
Whippies operation (takes pancreas head)
if tail then take tail and spleen away
What are neuroendocrine tumours
from gastroenteropancreatic tract, can be anywhere, arise from secretory cells of neuroendocrine system
sporadic in 75%, genetic in 25%
MEN1 (multiple endocrine neoplasia type !) causes parathyroid tumours, pancreatic and pituitary
How do neuroendocrine tumours present
asymptomatic
secretion of their hormones and metabolites can be found , but liver usually takes care of
Carcinoid syndrome: vasodilation (red face), bronchoconstriction, increased intestinal motility, endocrdial fibrosis (left sided regurg)
insulinoma, glucagonoma, gastinoma (zollingere-ellison), VIPoma, Somatostatinoma
How are neuroendocrine tumours diagnosed
investigate and use histology to dianose
Biochemical Assessment: Chromoganin A secreted, insulin, gastrin, somatostatin, PPY can be raised so measure in fasted satat. SCreen calcium, PTH, prolactin, GH. 24hr urinary 5-HIAA which is a metabolite of 5-HT
Imaging:
Ct +/- MRI
bowel imaging: endoscopy, barium follow through, capsule endoscopy
Endoscopic US
SOmatostatin receptr scintigraphy 68Ga-DOTATATE PET/CT which is somatostatin labelled with gallium will light up
How are neuroendocrine tumours graded
Grade:
G1: less than 2/10 High power field and less than 2% Ki-67 indec
G2, 2-29/10 HPF, 3-20% Ki67 indext
G3, over
What are the treatments of neuroendocrine tumours
Curative resection
cytoreductive resection if small
Liver transplant
RFA
Chemoembolisation or embolisation
SIRT
somatostatin receptor radioneucleotide therapy
What are some causes of dysphagia
Upper: pharyngeal cancer, pharyngeal puch, parkinsons, stroke, MND: pain to swallow
Lower: oesophageal or gastric cancer, stricture, lung cancer, achalasia : food would feel stuck
A mechanical or neurological cause of difficulty swallowing would be indicated by what
both solids and liquids being hard to swallow
How can angina be related to pain after meals
Because blood moves to bowels to aid digestion so woudl limit blood supply but would happen a while after. and on exertion too
How are upper GI malignancies staged
CT chest abdo pelivis
T1- at linign, T2- beyong lining but in organ, T3- out of serosa, T4 in adjacent organ
before T3 can do surgery, once moved outside organ then biologics to shrink tumour then operate and chemo
N1 1-2 lymph nodes close to tumour, n3 7 or more
M1 is distant metastases
How are apprpriate surgery patient selected
ECOG score
Grade 0- all fine
Grade 1- can move, light house work etc
Grade 2- moving more than 50% of waking hours, doesnt work
Grade 3- limited self care, 50% in chair
Grade 4 - disabled no self care
Grade 5 dead
What is ramipril
ACEi
What types of anaemia would cause
1) microcytic
2) normocytic
3) macrocytic
1) iron deficiency, anaemia of chronic disease, thalassaemia (disorder of Hb) , sideroblastica anaemia (cant use iron stores0
2) ABCDE- aplastic anaemia, bleeding, chronic disease, desrtuction - Haemolysis, Endocrine disorders (hypothyroidism or hypoadrenalism)
3) FAT RBC = foetus (preganant), Alcohol, Thyrodi disorder, Reticulocytosis, B12/folate deficiency, cirrhosis
What is iron deficiency caused by
blood loss: increased demand like growing or pregnant or decreased absorption
GI: aspirin/NSAID, colonic adenocarcinoma, gastric carcinoma,
non GI: menstruation, blood donation, haematuria, epistaxis
symptoms that suggest colorectal cancer
blood or mucus in stool
faecal incontinence
Tenesmus
change in bowel habit
How does bowel ischaemia present, what are two common types and their causes
sudden crampy abdominal pain, severity depends on how much affected, bloody loose currant jelly stood, fever and septic shock signs
Acute mesenteric ischaemia: small bowel ischamia, occulusive due to thromboemboli, sudden onset with abdominal pain rly bad, ex-smoker, high serum lactate
Ischaemic colitis: large bowel ischaemis, due to low blood flow states or atherosclerosis, mild and gradual, moderate pain and tenderness
What are the risk factors for bowel ischaemia
over 65
cardiac arrythmias AF mostly
atherosclerosis
sickle cell disease
hypercoagulation
vasculitis
hypotension from shock
If bowel ischaemia is suspected what investigations should be carried out
Bloods: FBC (high neutrophils), VBG (lactic acidosis rise due to ischameia so will cause what looks like metabolic acidosis)
Imaging- CT Angiogram to show disrupted flow, vascular stenosis, pneumatosis intestinalis, ischaemic colitis’ thumbprint sign
Endoscopy: show oedema, cyanosis or mucosal ulceration caused by ischamic colitis
For ischaemic colitis how should the patient be managed
IV as hypotensive
bowel rest
broad spectrum ABs
NG tube
anticoagulation
keep doing abdominal exams and imaging
For bowel ischaemia what signs indicate that a surgery is needed adn what two surgical approaches can be taken
If small bowel ischaemia/acute mesenteric ischameia, if have signs of sepsis or periotinitis, haemodynamic instability, massive bleeding, fulminant colitis with toxic megacolon
then do exploratory laparotomy to resection the necrotic bowel or surgical embolectomy/mesenteric arterial bypass
endovascular revascularisation: if have no sign of ischaemia then baloon angioplasty/thrombectomy
embolectomy of SMA in embolic AMI (emoblisms usually from left auricle in AF, endocarditis vegetations, mural infarct
endovascular management of SMA thrombus in thrombotic AMI ( due to atherosclerosis
arterial bypass of SMA (from hypotension or hypoperfusion usually due to trauma causing vasospasm in shock so dont perfuse, those with vasopressor requirements or undergoing dialysis so large amounts of fluids removed
How does acute appendicitis present
periumbilical pain that moves to RLQ. anorexia, anusea, vomiting, fever, bowel changes
McBurney’s point: tender RLQ
Blumberg sign: rebound tenderness in RIF
Rovsing sign: palpate LLq and get pain in RLW
Psoas sign: flex right hip against resistance and get RLQ pain
Obturator sign: internal rotation of hip with hip and knee flexion causes RLQ pain
what investigations are needed for a patient that presents with acute appendicitis
Bloods: FBC (high neutrophils), high CRP, haematuria in urinalysis, electrolyte imbalances if keep vomiting
Imaging: CT always, USS instead if a child or pregnant, MRI if pregnant and didnt find on USS
Diagnostic Laparoscopy: if imaging inconsistent and still in pain
what is the score used to check whether appendicitis is likely
Alvarado score
RLQ pain = 2
WCC high = 2
fever =1
rebound tenderness= 1
pain migration = 1
anorexia = 1
nausea or vomiting = 1
neutrophilia left shift = 1
if 4 or less its unlikely, if 7 or more liekly. if inbetween possible
What is the management of acute appendicitis
IV, analgesia, IV or PO AB’s
if abscess, phlegmon or sealed perforation then resuscitate, IV AB and percutaneous drainage
Ct guided drainage
Surgical management
Interval appendicectomy: as despite conservative management usually happens again
Laproscopic better than open as less pain, lower infection chance, less hospital stay,
What are the two things that can cause a bowel obstruction
paralytic ileus: bowel doesnt function like after surgery
Mechanical: blocking
How can mechanical bowel obstruction be classfied
site of pain, high is mall bowel, low is larger
if its simple then bowel is occluded but no blood problem, if strangulating then blood supply of involved segment of intestine is cut off and can cause ischaemia
causes in lumen: faecal impaction, gallstone ileus
in wall: chrons disease, tumours, diverticulitis of colon
outside wall: strangulated hernia, volvulus, adhesions (from surgery scars) or bands
What are the most common causes of small bowel obstruction
Adhesions from surgery
neoplaia
incarcerated hernia
chrons disease
What are the most common causes of large bowel obstruction
colorectal carcinoma
volvulus
diverticulitis
faecal impaction
hirchsprungs disease
what are the signs of small bowel obstruction and large bowel obstruction
SBO:
colickly, central abdominal pain
early onset or vomiting, vomits large amount, bilious/green vomit
complete constipation is. late sign
dont really get distended abdomen , usually have previous abdominal operation
LBO:
abdominal pain is colicky or constant
late onset of vomiting or no vomiting, initially green vomit then faecal vomiting
complete constipation is a early sign
distended abdomen is early and signficant sign
IN BOTH:
dehydration, high pitched tinkling bowel sounds or absent bowel sounds, diffuse tenderness
How is bowel obstruction diagnosed
Presence of symptoms
Examination: search for hernias and abdominal scars
need to know whether simple or strangulating
What symptoms suggest a patient has a strangulating bowel obstruction
character of pain changes from colicky to continuous
tachycardia
fever
peritonism
bowel sounds absent or reduced
leaukocytosis
increased c reactive protein
What are the common hernial sites and what are the three types of hernias
Epigastric, umbilical, incisional, inguinal and femoral
Neck of sac
Strangulated hernia
Richter’s hernia (only part of the border protrudes thru not the other side
What investigations are needed for bowel obstructions
Bloods:
WCC and CRP usually normal if raised then strangulation
U&E
VBG if vomiting: low Cl-, K+ with metabolic alkalosis
VBG if strangulation: metabolic acidosis from lactate
Imaging:
- erect CXR/AXR:
SBO will see dilated small bowel loops less than 3cm central and proximal to obstruction.
LBO: dilated large bowel over 6cm, caecum will be 9cm, more peripheral
- Ct abdo/pelvis
transition point (site of obstruction and dilation of loops, detect tumpurs and unusual hernias
On a X-ray describe the differences between a SBO and LBO
SBO: ladder pattern of centrally placed dialted loops, striations pass completely across the width
LBO: distended peripherally, haustrations of taenia coli so lines arent all the way through the width of the bowel
How is bowel obstruction managed
if no sign of ischaemia:
NBM, IV fluids, analgesia, , antiemetics, correct electrolytes.
NG tube, urinary catether and gradually inc food
Faecal impaction : stol evacuation
Sigmoid volvulus: rigid sigmoidoscopic decompression
SBO: oral gastrogaffin which can resolve adhesional SBO
What are the indicators that a bowel obstruction requires surgery and what surgical procedures are available
Haemodynamic instability or signs of sepsis
Complete obstruction with signs of ischaemia
closed loop obstruction
persistant bowel obstruction for more than 2 days eve with management
Operations:
Exploratory Laparotomy/Laparoscopy
Restoration of intestinal transit
bowel resection with primary anastomosis or temporary stoma formation
How does GI perforation present
sudden severe abdominal pain with distension, abdominal guarding, regidity, rebound tenderness. Pain on movement, anuse, vomiting, complete constipation, fever, high HR, high breathing, hypotension, low or absent bowel sounds
if its perforated :
-peptic ulcer: sudden epigastric pain, referred shoulder, NSAIDs, steroids taken
- perforated diverticulum: LLQ pain, constipation
-appendix: migratory pain, anorexia, RLQ pain
- malignancy:weight loss, anorexia, PR bleeding
What investigations should be requested if a GI perforation is thought to be the problem
BLoods:
FBC (neutrphils high), urea, creatinine high
VBG: lactic acidosis
Imaging
erect CXR: subdiaphragmatic fee air called pneumoperitoneum
CT abdo/pelvis: pneumoperitoneum, free GI content, mesenteric fat stranding,
How are GI perforations managed
NBM, NG instead
IV
broad spec AB
IV PPI
paraenteral analgesics and antiemetics
urinary catheter
if localised peritonitis with no signs of sepsis then IR guided drainage of intra-abdominal collection, frequent abdominal examinations with imaging
What is the surgical management of GI perforations
if generalised peritonitis with signs of sepsis
exploratory lapraotomy/ laparascopy
close perforation with or without omental patch
resect perforated segrment with stoma or primary anastamosis
tale intra abdominal fluid for microscopy culture and sesitivity, peritoneal lavage
if malignant then intraoperative biopsy
if appendix perforated then lap or open appendicectomy
What biliary and pancreatic causes can lead to acute abdominal pain
Biliary Colic:
RUQ pain radiates to shoulder, nausea. will find stones on USS. analgesics, antiemetics, cholecystectomy
Acute cholecystitis (inflam of GB and cystic duct):
severe RUG pain, fever, high WCC/CRP, see thickened gallbladder wall on USS, murphys sign, murphys sign. give IV fluids. ABs, analgesics, blood cultures, cholecystectomy. NO JAUNDICE
Acute cholangitis: (common bile duct)
jaundice, RUQ pain and fever which is Charcot’s triad. elevated LFTs, WCC/CRP, blood BC&S is positive. USS shows biliary dilation. IV AB, fluids, analgesia, ERCP to clear bile duct or add stent
Acute pancreatitis:
severe epigastric pain radiates to back, nausea, vomiting, history of gallstones or alcohol. High amylase/lipase, high WCC, low Ca2+. fluid rescuscitation, O2, analgesia, aniemetics, admission score
Distended abdomen with coffee bean sign on xray is a typical sign of what
volvulus of sigmoid colon (loop of intestine twists around itself
What management is effective when treating sigmoid volvulus
sigmoidocope with soft ribber rectal tube passed along the sigmoidoscope which untwists the volvulus, releases lots of flatulus and faeces
if a sigmoid volvulus is left untreated the patient is at risk of what
the loop of bowel may have its blood supply eventually cut off and necrosis
How to manage a patient with sigmoid volvulus when sigmoidoscope and rectal tube failed
Exploratory laparotomy and sigmoid colectomy with end colestomy (hartmann’s procedure)
In acute mesenteric ischamia, which vein could be affected and what patients does this occur in
Superiro mesenteric vein thrombosis
patients with:
portal hypertension
portal pyaemia
sickle cell disease
What is portal pyaemia
air within the SMV and portal venous system in the liver.
form of septic thrombophlebitis of portal venous system, you ger bugs and puss inside the portal vein from bowel dying and bacteria/pathogen translocating up too the portal system
is a complication of intraabdominal sepsis : diverticulitis and appendicitis
on scan will see black spots on liver and at SMV
