diseases of the mouth, oesophagus, stomach and small bowel Flashcards
what is jaundice
the yellowing of the sclera (white of eyes) and the skin. It is caused by an increase in the blood levels of bilirubin
what is bilirubin
The normal byproduct of breakdown of RBCs and it travels through your liver, gallbladder, and digestive tract before being excreted.
what vessels are in the interlobular portal triad
- Biliary duct
- Branch of hepatic artery
- Branch of hepatic portal vein
what do the left and right hepatic ducts unite to form
common hepatic duct
what is formed when the common hepatic duct joins with the cystic duct
Bile duct
what is formed when the bile duct descends posteriorly to the 1st superior part of the duodenum and then joins with the main pancreatic duct
Ampulla of Vater
where does the Ampulla of Vater drain through and into
it drains through the major duodenal papilla into the second part of the duodenum
what are the sphincters in the area of the bile duct
- Bile duct sphincter - at distil end of bile duct
- Pancreatic duct sphincter - at the distal end of the pancreatic duct
- Sphincter of Oddi - surrounds the end portion of the common bile duct and pancreatic duct
what investigation is used to study the biliary tree and the pancreas
ERCP - endoscopic retrograde cholangiopancreatography
how can jaundice form
Obstruction of the biliary tree by gallstones if carcinoma at the head of the pancreas causing the bile to flow back up to the liver instead of being created into the duodenum. These extra hepatic obstructive causes of jaundice
What are the anatomical relationships of the pancreas to the:
1) stomach
2) duodenum
3) splenic vessels
1) anteriorly lies the stomach
2) the duodenum surrounds the head of the pancreas
3) superoposteriorly
what are functions of the exocrine and endocrine pancreas
- Exocrine - acinar cells - pancreatic digestive enzymes into the main pancreatic duct
- Endocrine - islets of Langerhans - insulin and glucagon into the blood stream
what vessel does blood travel to the pancreas
Mainly branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal and superior mesenteric arteries, respectively.
what is a cause of pancreatitis
blockage if the ampulla by the gallstone
where will pain be felt in regards to the pancreas
Pain in the epigastric region and or umbilical region. It can also radiate through to the patients back
what part of the duodenum is intraperitaneal and which is retroperitoneal
- intraoeriteneal = superior
- retroperitoneal = descending, horizontal and ascending
where does the duodenum start
the pyloric sphincter
what does the duodenum secrete
peptide hormones into the blood
what area of the duodenum does the superior pancreaticoduodenal (gasproduodenal artery) supply
supplies proximal parts 1 and 2 (foregut)
what area of the duodenum does the inferior pancreaticoduodenal ( superior mesenteric artery) supply
supplies distal parts 3 and 4
what are plaice circulares
The lining of the small intestine consists of a series of permanent spiral or circular folds, termed the plicae circulares, which amplify the organ’s surface area, promoting efficient nutrient absorption.
for the jejunum an ileum where does the arterial blood come from and where does the venous drainage from
- arterial blood from superior mesenteric artery via the jejunal and ill arteries
- venous drainage from the jejunal and ill veins to the superior mesenteric vein at hepatic portal vein
what are the main groups of lymph nodes draining abdominal organs
- celiac = foregut organs
- superior mesenteric = midgut organs
- inferior mesenteric = hingut organs
- lumbar = kidneys, posterior abdominal wall, pelvis and lower limbs
aetiology of oral pre-malignancy and cancer
- tobacco
- alcohol
- HPV
- diet and nutrition
- Candida
what is the uk recommended units of alcohol for men in a week
14
why does alcohol cause oral cancer
Ethanol (procarcinogens) is converted to Acetaldehyde (AA carcinogen, mutagen) using Alcohol dehydrogenase which exists in the mouth. Acetaldehyde is the converted to Acetate using aldehyde dehydrogenase
what effects does diet and nutrition have on oral cancer
Low in vitamin A, C, iron increase the risk of oral cancer.
What are some characteristics of asymptomatic invasive oral cancers
- Surface texture: granular (48%) or smooth (33%)
- Elevation: 1mm max in 20% of cases
- No ulceration in 85% and no bleeding in 98%
- Not indurated in 90%
what are high risk sites of oral cancers
90% occurs in the lining of the mouth
10% occurs in salivary glands or bones
what is Erythroplakia
red patch
what is Erythroleukoplakia
red and white patch
what is leukoplakia
white patch
what are warning signs for oral cancer
- Red/ white/ red and white lesion
- Ulcer (exclude trauma, drug, systemic)
- Numb feeling eg lip, face
- Unexplained pain in mouth or neck
- Change in voice
- Dysphagia
what are some orofacial manifestations of cancer
- Drooping eye lid or facial palsy
- Fracture of mandible
- Double vision
- Blocked or bleeding nose
- Facial swelling
what are key questions you should ask for checking for oral cancer
- How long has the pain been present - mouth heals 7-10 days. If there for 3 weeks look at with suspicion
- Is it painful? - pain is usually a late manifestation of oral cancer but would be expected to be a benign ulcer
- Does patient smoke or drink
- What colour is the lesion
what cells line the oesophagus
stratifies squamous epithelium
what is oesophagitis
inflammation that may damage tissues of the oesophagus
what is reflux oesophagitis and what may cause it
inflammation of the oesophagus due to refluxed low pH gastric contents
it may be caused by defective sphincter mechanism +/- Hiatus hernia (where part of the stomach pushes up into. the lower chest through a weakness in the diaphragm)
what is seen under a microscope for reflux oesophagitis
- Basal zone epithelial expansion (basal cell hyperplasia)
- Intraepithelial neutrophils, lymphocytes and eosinophils
what are some complications of reflux oesophagitis
- Ulceration (bleeding)
- Stricture - abnormal narrowing of a bodily passage
- Barretts oesophagus = replacement of stratified squamous epithelium by columnar epithelium
what causes Barretts oesophagus
- Persistent reflux of acid or bile
- May be due to expansion of columnar epithelium from gastric glands or from submucosal glands
- May be due to differentiation from oesophageal stem cells
- Protective response, faster regeneration
what is allergic oesophagitis or ‘eosinophilic oesophagitis’
When eosinophils deposit in the lining of the oesophagus . This can be the result of an allergic reaction to food or the environment
how do you treat eosinophilic oesophagitis
treatment may include steroids/ chromoglycate / montelukast
what are squamous papilloma
small benign (non cancerous) growth that begins in squamous cells - rare tumour in the oesophagus
what are leiomyomas
“fibroids”. Benign smooth muscle tumour that’s a very rare oesophageal tumour
what are lipomas
fatty tumours below skin (not cancer)
what are fibrovascular polyps
intraluminal, submucosal tumour like lesions that usually remain asymptomatic
what are granular cell tumours
mesenchymal soft tissue tumours
what are some common malignant oesophageal tumours
- squamous cell carcinoma
- adenocarcinoma
squamous cell carcinoma aetiology
- Vitamin A, zinc deficiency
- Tannic acid/ strong tea
- Smoking, alcohol
- HPV
- oesophagus
- genetic
explain the pathogenesis of squamous small cell carcinoma
A stepwise progression occurs: Normal –> severe dysplasia –> carcinoma
what does squamous cell carcinoma in the oesophagus cause
obstruction and dysphagia
what is Barretts oesophagus
replacement of stratified squamous epithelium by columnar epithelium with interstitial metaplasia
- Increased risk of developing dysplasia than adenocarcinoma of the oesophagus
what is the pathogenesis of an adenocarcinoma of the oesophagus
genetic factors, reflux disease, others –> chronic reflux, oesophagitis –>Barretts oesophagitis (interstitial metaplasia) –> Low grade dysplasia –> high grade dysplasia –> Adenocarcinoma
what are some mechanisms of metastases for carcinoma of the oesophagus
- Direct invasion
- Lymphatic permeation
- Vascular invasion
what are some clinical presentations of carcinoma of the oesophagus
- Dysphagia (due to tumour obstruction)
- General symptoms of malignancy (anaemia, weight loss, loss of energy)
what are some histopathology features relating to prognosis of small cell carcinoma
- Tumour diameter
- Depth of invasion
- Pattern of invasion - cohesive vs non-cohesive
- Lymphovascular invasion
- Neutral invasion by tumour
- Involvement of surgical margins
- Metastatic disease
- Extracapsular spread of lymph node metastases
what are some common types of chronic gastritis
- Autoimmune
- Bacterial H.pylori
- Chemical
what is autoimmune chronic gastritis
Autoimmune atrophic gastritis is a chronic inflammatory disease in which the immune system mistakenly destroys a special type of cell (parietal cells) in the stomach. Parietal cells make stomach acid (gastric acid) and a substance our body needs to help absorb vitamin B12 (called intrinsic factor)
what is SACDC (subacute combined degeneration of the cord
when myelin sheath withers away due to lack of vitamin B12
How does H pylori cause gastritis
Both the acid and bacteria irritate the lining and cause an ulcer to form. If left untreated, a H. pylori infection can cause gastritis
how does chemical gastritis occur
- Due to NSAIDs, alcohol, bile reflux
- Direct injury to mucous layer by fat solvents
- Marked epithelial regeneration, hyperplasia, congestion and little inflammation
- May produce erosions or ulcers
what is peptic ulceration
A breach in the gI mucosa as a result of acid and pepsin attack
where can chronic peptic ulcers form
- Duodenum
- Stomach
- Oesophago-gastric junction
- Stomal ulcers
how are chronic peptic ulcers formed
excess acid in the duodenum produces gastric metaplasia and leads to H.Pylori infection, inflammation, epithelial damage and ulceration
microscopically what are some features of peptic ulcers
- Layered appearance
- Floor of necrotic fibrinopurulent debris
- Base of inflamed granulation tissue
- Deepest layer is fibrotic scar tissue
what are some complications of peptic ulcers
- Perforation
- Penetration
- Haemorrhage
- Stenosis
- Intractable pain
what are some benign gastric tumours
- hyperplastic polyps
- cystic funds gland polyps
what are some malignant gastric tumours
- carcinomas
- lymphoma - cancer that begins in infection fighting cells of the immune system (lymphocytes)
- gastrointestinal stromal tumours - abnormal cells in the GI tract
what is the pathogenesis of gastric adenocarcinoma
H.Pylori infection –> chronic gastritis –> intestinal metaplasia/ atrophy –> dysplasia –> carcinoma
what is pernicious anaemia
vitamin B12 deficiency
what is partial gastrectomy
surgical removal of a portion of the stomach
what is HNPCC/ Lynch syndrome
autosomal dominant genetic condition associated with a high risk of colon cancer
what is Menetriers disease
Rare disorder characterised by massive outgrowths of mucous cells in the mucus membrane lining the stomach, resulting in large gastric folds
what are the subtypes of gastric adenocarcinoma
- Intestinal type - exophytic/polypoid mass
- Diffuse type - expands/ infiltrates stomach wall
what is intestinal type of gastric adenocarcinoma
The intestinal-type is the end-result of an inflammatory process that progresses from chronic gastritis to atrophic gastritis and finally to intestinal metaplasia and dysplasia
what is diffuse type of adenocarcinoma
Diffuse gastric cancer is a specific type of stomach cancer, sometimes also called “signet ring cell gastric cancer” or “linitis plastic.” The word “diffuse” is used because this cancer tends to affect much of the stomach, rather than staying in 1 area of the stomac
where can gastric adrenocarcinoma spread to
- Local - directly into other organs
- Lymph nodes - omental
- Haematogenous - to the liver and beyond
- Tanscoelomic - Into peritoneal cavity and ovaries
what is maltoma
MALT lymphoma (MALToma) is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT, and is also called extranodal marginal zone B cell lymphoma.
what is GIST ( gastrointestinal stromal tumour)
Very rare gastric tumour which are stromal in nature, producing spindle cell masses driven by mutations in the KIT oncogene
what is dyspepsia
Epigastric pain or burning (epigastric pain syndrome), postprandial fullness (postprandrial distress syndrome). Early satiety (postprandial distress syndrome)
what are the foregut structures
- oesophagus
- stomach
- duodenum
- pancreas
- gallbladder
what are organic causes of dyspepsia
- peptic ulcer disease
- drugs (esp NSAIDs, COX2 inhibitors)
- gastric cancer
what is functional dypepsia
Functional dyspepsia is a term for recurring signs and symptoms of indigestion that have no obvious cause.
what are causes of peptic ulcer disease
- H pylori
- NSAIDs
- gastric dysmotility
what is H.pylori
Gram -ve microaerophilic flagellated bacillus. Acquired in infancy but consequences not until later in life
what are the consequences for H.pylori
- no pathology
- peptic ulcer disease
- gastric cancer (almost all non cardia gastric adenocarcinoma)
what is the homeostasis mechanism of gastric acid secretion
- G cells in the distal part of the stomach are stimulated by acid.
- G cells stimulate the production of Gastrin that then enters the blood stream and stimulates the parietal cells to produce acid
how do we diagnose a H.pylori infection
- gastric biopsy can gain tissue to be used to get info on a urease test (if helicofactor is present), histology, culture/sensitivity
- urease breath test
- FAT (faecal antigen test)
- Serology (IgA anitbodies) - not accurate with increasing patient age
what is urease
Urease, an enzyme that catalyzes the hydrolysis of urea
how do you treat peptic ulcer disease
- all people should get :
> antisecretory therapy ie proton pump inhibitors
> tested for presence of H.pylori - H.pylori +ve the eradicate and confirm
- H.pylori -ve then antisecretory therapy
- withdraw NSAIDs
- lifestyle (difficult)
- non-HP/ non-NSAID ulcers - nutrition and optimise comorbidites
- no firm dietary recommendations
what is eradication therapy for H.pylori
- “tripple therapy” for 1 week =
PPI+ amoxycillin 1g bd + clarithromycin 250mg bd
PPI + metronidazole 400mg bd + clarithromycin 250mg bd
- 2 week regimens
> higher eradication rates
> poorer compliance - dual therapy = PPI + 1 antibiotic not recommended
- quadrouple therapy + culture directed therapy
what are complications of peptic ulcer disease
- anaemia
- bleeding
- perforation
- gastric outlet/ duodenal obstruction - fibrotic scar
what are causes of GORD
- incompetent closing of lower oesophageal sphincter
- poor oesophageal clearance
- barrier function/ visceral sensitivity
what are symptoms of GORD
- heartburn
- acid reflux
- waterbrash
- dysphagia
- odynophagia
- weight loss
- chest pain
- hoarseness
- coughing
what are some investigations for GORD
- endoscopy
- Ba swallow
- oesophageal manometry and pH studies
what are alarm symptoms
- dysphagia
- weight loss
- anaemia
- vomiting
- F/H UGI cancer
- Barretts
- Pernicious anaemia
- PUD surgery > 20 years
what are complications of GORD
- oesophagitis
- schatzki’s ring
- adenocarcinoma of the oesophagus
what is the pathogenesis of adenocarcinoma
normal –> ongoing erosive damage for years –> oesophagitis (reversible) –> more errosive damage for years –> Barretts oesophagus (irreversible) –> adenocarcinoma (too late)
what is the management of GORD
- symptom relief
- healing oesophagitis
- prevent complications
- lifestyle modifications (stop smoking, loose weight is obese, prop up the bead head, avoid provoking factors)
what are the dug managment of GORD
- Antacids - symptomatic relief, no benefit in healing or preventing complications
- proton pump inhibitors - block the acid pumping mechanism and prevent ongoing acid production in the stomach eg Ranitidine, Omeprazole
they help heal all grades of oesophagitis
what are some features of Barretts oesophagus
- 10% of GORD patients
- Intestinal metaplasia
- Irreversible
- increased risk of adenocarcinoma
- PPI +/- surveillance
what is low grade dysplasia management
- surveillance more frequently every 3 month s
- optimise their PPI dose 40mg twice daily
what is high grade or persistent low grade dysplasia management
- remove with endoscopic mucosal resection
what is Hiatus hernia
- sliding hiatus hernia
- paraesophageal hiatus hernia
what is gastroparesis
condition where there is poor emptying of the stomach without a physical blockage in the pyloris
what are symptoms of gastroparesis
- feeling of fullness
- nausea
- vomiting
- weight loss
- upper abdominal pain
what are causes of gastroparesis
- idiopathic
- diabetes mellitus
- cannabis
- medication eg opiates, anticholinergenics
- systemic diseases eg systemic sclerosis
what is the management of gastroparesis
- removal of precipitating factors eg drugs
- liquid/sloppy diet
- eat little and often
- promotility agents
- gastric pacemaker
what is achalasia
Motility disorder of the lower oesophageal sphincter failing to relax. it is almost in spasm all of the time. Reduced peristalsis in the body of the oesophagus. Due to obstruction at the LOS –> the oesophagus becomes dilated
what is the management of achalasia
- balloon dilation
- surgical - cardiomyopathy
what are the 2 types of oesophageal cancer
- squamous cell carcinoma
- adenocarcinoma
what is progressive dysphagia
difficulty swallowing initially for red meat etc and eventially not being able to swallow saliva
what are the steps of fat digestion and absorption
- lipolysis
- micellar solubilisation with bile acid
- absorption
- digestion
what is malabsorption
Malabsorption is a disorder that occurs when people are unable to absorb nutrients from their diets, such as carbohydrates, fats, minerals, proteins, or vitamins
what is coeliac disease
Caused by an abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorbtive capacity
what is lactose malabsorption
deficiency of lactase giving a history of diarrhoea, abdominal discomfort, and flatulance following the indigestion of dairy products
what is tropical sprue
colonisation of the small intestine by a infectious agent or alterations in the intestinal bacterial folora
what is whipples disease
Whipple disease is a rare bacterial infection that most often affects your joints and digestive system. Whipple disease interferes with normal digestion by impairing the breakdown of foods, and hampering your body’s ability to absorb nutrients, such as fats and carbohydrates
what is Crohns disease
patients with extensive ill involvement, extensive intestinal resections, enterocoelic fistulas, and strictures leading to small intestinal bacterial overgrowth may develop significant and occasionally devastating malabsorption
what is small bowel bacterial overgrowth
small intestinal bacterial overgrowth (SIBO) occurs when there is an abnormal increase in the overall bacterial population in the small intestine — particularly types of bacteria not commonly found in that part of the digestive tract. This condition is sometimes called blind loop syndrome.
what history should you look at of a patient for malabsorption
- GI symptoms
- Past medical history
- Travel history
- Social history
- Drug history
- Dietary history
what are GI stool symptoms
- Diarrhoea ( duration, fat gobbles, floating, hard to flush away)
what are baseline investigations of the malabsorption
- FBC
- coagulation
- LFT’s
- albumin
- calcium/magnesium
- stool culture
what are the basic steps of management of malabsorption
- treat the underlying causes
- replace the deficiency
- support nutritionally
what supplies blood to the small bowel
Superior mesenteric artery
what can cause ischaemia of the small bowel
- mesenteric arterial occlusion ie mesenteric artery atherosclerosis or thromboembolism from heart
- non occlusive perfusion insufficiency ie shock, strangulation obstructing venous return, drugs, hyper viscosity
what is the most metabolically active part of the bowel wall
the mucosa is the most metabolically active part of the bowel wall and therefore the most sensitive to the effects of hypoxia
what are the degrees of infarction in acute ischeamia of the gut
- mucosal infarct = early ischaemia affecting mucosa
- mural infarct = mucosa and submucosa
- transmural infarct = late ischeamia involving all the layers of the gut
what are some complications of ischaemia of the small bowel
fibrosis, stricture, chronic ischaemia, gangrene, perforation, sepsis and death
what is Meckels diverticulum
Result of incomplete regression of Vitelli-intestinal duct. Its a tubular structure, 2 inches longs, 2 foot above IC valve in 2% of people. It may contain heterotrophic gastric mucosa. It may cause bleeding, perforation or diverticulitis which mimic appendicitis
Are primary or secondary tumours more common in the small bowel
secondary tumours are much more common
what primary tumours are in the small bowel
- lymphomas
- neuroendocrine (carcinoid) tumours
- carcinomas
what are lymphomas
malignant tumours of the lymphoid cells
what are neuroendocrine tumours of the small bowel
Small, yellow, slow growing tumours that are locally invasive.
what is a carcinoid tumour
Carcinoid tumors are a type of slow-growing cancer that can arise in several places throughout your body. Carcinoid tumors, which are one subset of tumors called neuroendocrine tumors, usually begin in the digestive tract (stomach, appendix, small intestine, colon, rectum) or in the lungs
what diseases are primary carcinomas associated with
Crohns disease and Coelaic disease
what is appendicitis
Appendicitis is inflammation of the appendix, a small pouch connected to your large intestine. Causes vomiting, abdominal pain, RIF tenderness and increased white cell count
what are causes of acute appendicitis
- unknown
- faecoliths (dehydration)
- lymphoid hyperplasia
- parasites
- tumours (rare)
what I the pathology of acute appendicitis
- acute inflammation (neutrophils)
- mucosal ulceration
- serial congestion, exudate
- pus in lumen
- Acute inflammation must involve the muscle coat
what may be seen for acute appendicitis
- yellow surface exudate is seen
- wall thickened ready to perforate, containing pus
- mucosal ulceration and mural inflammation
- pus in the lumen
- neutrophils invade the appendix wall
what can be complications of appendicitis
- peritonitis
- rupture
- abscess
- fistula
- sepsis and liver abscess
what is the aetiology of coeliac disease
- Gliadin a component of gluten is the suspected toxic agent
- But tissue injury may be a bystander effect of abnormal immune reaction to Gliadin
- Mediated by T cell lymphocytes which exist within the small intestinal epithelium ‘intraepithelial lymphocytes’
what happens in coeliac disease when there is an increasing loss of enterocytes due to IEL mediated damage
this leads to loss of villous structure, loss of surface area, a reduction In absorption and a flat duodenal mucosa
what is the clinical appearance of coeliac disease
- mucosa may be endoscopically normal or appear attenuated/flat
- lesion worse in proximal bowel so duodenal biopsy is very sensitive
what is the serology of coeliac disease
- antibodies are seen (anti-TTG, anti-endomesial, anti-gliadin)
what are the metabolic effects of coeliac disease
- malabsorption of sugars, fats, amino acids, water and electrolytes
- malabsorption of fats leads to steatorrhea
- reduced intestinal hormone production leads to a reduced pancreatic secretion and bile flow (CCK) leading to gallstones
what are effects of malabsorption
- loss of weight
- anaemia (Fe, Vit B12, folate)
- abdominal bloating
- failure to thrive
- vitamin deficiencies
what are other complications of coeliac disease
- T cell lymphomas of GI tract
- increased risk of small bowel carcinoma
- gall stones
- ulcerative-jejenoilleitis
what vessel supplies blood to the appendix
appendicular artery
what is the aetiology of appendicitis
- no unifying hyposthesis
- obstruction of the lumen with faecolith
- bacterial
- viral (clustering of cases)
- parasites
what is the pathology of appendicitis
- huge variation in macroscopic disease
- lumen may or may not be occluded
- mucosal inflammation
- lymphoid hyperplasia
- obstruction
- build up of mucus and exudate
- venous obstruction
- ischaemia… bacterial invasion through wall
- perforation
what are classic clinical symptoms of appendicitis
- central pain that migrates to the RIF
- anorexia
- nausea
- one or two vomits
- may not have moved bowels
- pelvic: vaguer pain localisation: rectal tenderness
- elderly
what are signs of appendicitis
- mild pyrexia (never high temp initially)
- mild tachycardia
- localised pain in RIF (right iliac fossa)
- guarding
- rebound
what are specific signs of appendicitis
- Rosvings = pressing on the left causes pain on the right
- Psoas = patient keeps the right hip flexed as this lifts an inflammed appendix off the psoas
- Obturator = appendix is touching obturator internus, flexing the hip and internally rotating will cause pain
- pointing = where did it start and where is it now?
what investigations to carry out for appendicitis
- clinical diagnoses
- USS useful in women with kids
- AXR to exclude other causes
- bloods (important CRP, WCC)
- Urinalysis
what is management of appendicitis
- Analgesia
- Antipyretics
- Theatre
- Antibiotics
- Appendicectomy = laparascopic (best) , convert to open sometimes (not first line)
- laparotomy sometimes
how to treat an appendix mass
- antibiotics first line
- can operate or not
- theatre if fails or complicated (tachycardia, worsening pain, increase in size, vomiting or copious NG aspirates (ileus))
how to treat an appendix absess
- not an appendix mass
- usually delayed
- usually has liquidised
- radiologically drains
what can go wrong with a small bowel
- obstruction
what happens with small bowel obstruction
- colicky central pain
- absolute constipation
- vomiting
- burping
- abdominal distension
what is the definition of malnutrition
is a major clinical and public health issue within the United Kingdom with the wider determinants of health including poverty, social isolation and deprivation all exacerbating its incidence (Elia,2003)
what are the effects of starvation
- Metabolic rate decreases.
- Weight will decrease, slow loss almost all from fat stores.
- Decrease in nitrogen losses
- Early small increases in catecholamines, cortisol, GH, then slow fall. Insulin decreased.
- Water is initially lossed then late retention
what are the effects of injury
- Increased metabolic rate …
what is enteral tube feeding
- delivery of a nutritionally complete feed via a tube into the stomach, duodenum or jejunum
what are indications for ETF
- Inadequate or unsafe oral intake, and a functional, accessible GI tract
- ‘If the gut works, use it’ - unconscious patients, neuromusculat swallowing disorder, upper GI obstruction, GI dysfunction
contradictions for ETF
- Lower GI obstruction
- Prolonged intestinal ileus
- Severe diarrhoea and vomiting
- High entercutaneous fistula
- Intestinal ischaemia
what is refeeding syndrome
Refeeding syndrome is a serious and potentially fatal complication of nutritional rehabilitation in patients with severe anorexia nervosa. It occurs in significantly malnourished patients when a diet of increasing calories is initiated orally, by nasogastric (NG) tube and/or delivered intravenously.
what are metabolic features of refeeding syndrome
Hypokalaemia Hypophosphataemia Hypomagnesaemia Altered glucose metabolism Fluid overload
what are physiological features of refeeding syndrome
Arrhythmias Altered level of consciousness Seizure Respiratory failure Cardiovascular collapse Death
how do you screen for malnutrition risk
‘MUST’
what are the main sections for resuscitation of a patients who has GI bleeding
- Airway
- Breathing
- Circulation
- Airway protection
- Oxygen
- IV access
- Fluids
what bore access is needed for a patient with GI bleeding
large bore IV access is mandatory
what are the signs of the ‘100 rule’: poor prognosis group
systolic BP < 100mmHg pulse > 100/min Hb < 100 g/l age > 60 comorbid disease postural drop in blood pressure
what are the main takeaways for an endoscopy for a GI bleed
- Identify cause
- Therapeutic manoeuvres
- Assess risk of rebleeding
what is stigmata of recent haemorrhage
- active bleeding/oozing
- overlying clot
- ‘visible vessel’
what are treatments for bleeding peptic ulcers
- endoscopic treatment (high risk ulcers)
- acid suppression (?infusions)
- interventional radiology
- surgery
- H.pylori eradication - secondary prevention
what are some endoscopic treatment of peptic ulcers
- injection
- heater probe coagulation
- combinations
- clips
- haemospray
