GI including liver Flashcards
What is IBD (inflammatory bowel disease)?
inflammation of bowel caused by genetics/ environment/ poor immune system. (more common in young adults)
- Crohns - patchy transmural inflammation of gut mucosa affecting any part of GIT
*genetics (NOD2) , M=F,
- Ulcerative colitis- continuous inflammation of superficial mucosa layer from rectum
*genetics (HLA2, HLAB27, p-ANCA)
- directly linked to primary sclerosing cholangitis
Presenting symptoms of IBD (with history)
Crohn’s
- mainly non-bloody diarrhoea
- crampy abdominal pain
- WEIGHT LOSS
- extreme fatigue
UC
- more frequent bloody diarrhoea
- autoimmune: uveitis
- Primry sclerosing cholangitis
BOTH non-bowel related (autoimmune): arthritis, erythema nodosum (red bumps), jaundice (raised bilirubin + ALP)
Examination findings of IBD
UC: usually none but if severe fever, tachycardia, tender/distended abdomen, clubbing, oral ulcers, angular stomatitis, anaemia (visible pallor, conjunctival pallor), jaundice (PSC)
Crohn’s: abdominal tenderness, clubbing, angular stomatitis, skin/joint/eye problems
Investigations + findings of IBD
Bedside:
- Stool microscopy and culture: exclude infective colitis/ GASTROENTERITIS
- Fecal calprotectin from stool sample - sign of non-specific bowel inflammation
Bloods
- FBC - low Hb, high platelets (anaemia= chronic disease) high WCC
- LFTs - low albumin
- High ESR (suggests chronic inflammation) – inflammatory marker
- CRP may be high or normal - inflammatory marker
Imaging:
- AXR: could show evidence of toxic megacolon,
- Erect CXR: if there is a risk of perforation
- Colonoscopy/ flexible sigmoidoscopy + biopsy GOLD STANDARD
How to distinguish between crohns and ulcerative colitis (biopsy/ endoscopy)?
Crohns: non-caseating granulomas, fistulas, strictures, cobblestone appearance
UC: pseudopolyps, continuous inflammation from rectum
Management for Crohn’s
Acute Exacerbation
- Fluid resuscitation, may also be on oral iron
- IV/oral corticosteroids
- 5-ASA analogues (e.g. mesalazine and olsalazine)
- Analgesia
- Parenteral nutrition may be necessary
● Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb
Long-Term
- Corticosteroids (prednisolone/ dexamethosone) - induce remission
- Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
- Anti-TNF agents: (e.g. infliximab and adalimumab)
*Can try liquid therapy diet for Crohn’s/ small kids
Lifestyle changes advised for Crohns
- stop smoking (but smoking better in UC)
- low fibre diet
Management for UC
Acute:
- Corticosteroids- hydrocortisone (for SEVERE acute flare ups)
- 5-ASA analogues - decreases the frequency of relapses (useful for MILD to moderate disease)
- Immunosuppresion (azothioprine)- maintain remission if multiple exacerbations
- Biological therapies (anti-TNF therapies)
- Surgery=> more for UC - Proctocolectomy with ileostomy – surgical removal of colon, rectum and anal canal
mechanism + side effects of steroids (prednisolone)
glucocorticoid receptors interact with specific DNA sequences to increase anti-inflammatory gene produces + reduce pro-inflammatory products.
- short term: weight gain, Cushing syndrome, mood swings,
- long term: diabetes, adrenal suppression, osteoporosis, avascular necrosis, thin skin
mehcanism + side effects of immunosupressants (azathioprine)
reduce DNA/RNA production of lymphocytes/ interleukins => suppresses immune system => anti-inflammatory
Side effects:
- nausea, flu-like
- bone marrow suppression
- pancreatitis (raised amylase)
- hepatotoxicity
- increased cancer risk
- increased hypersensitivity => skin rashes
mechanism and side effects of biologics (anti-TNFa)
monoclonal antibodies against TNFa which reduce disease activity by reducing neutrophil accumulation + granuloma formation and cause cytotoxicity to CD4+ T cells.
Side effects:
- redness, itching, bruising, pain, or swelling at the injection site
- headache, fever, rashes
prognosis for IBD
IBD patients should have a colonoscopy every 5 years as they are at increased risk of colorectal cancer
Crohns - chronic relapsing condition
● 2/3 of patients will require surgery at some stage
● 2/3 of these patients require more than 1 operation
Ulcerative colitis - normal life expectancy
complications of IBD
- fistulas (narrow passage connecting organs together)
- malnutrition
- bowel obstruction
- colorectal cancer
- intestinal perforation/ rupture
what is coeliac disease?
autoimmune disease triggered by eating gluten. T cells attack small intestine so can’t absorb nutrients.
How to diagnose coeliac disease from history?
=> diarrhoea + weight loss
- STEATORRHEA (fatty stools)
- fatigue
- bloating/ gas
- abdominal pain
- nausea/ vomiting
Investigations for coeliac disease
bloods:
- FBC (low Hb/ low ferritin/ low b12) ANAEMIA
- anti-transglutaminase antibody test
=> if high level of suspicion/ positive AB test => duodenal biopsy when on gluten (atrophied tissue)
Management for coeliac disease
- lifelong gluten free diet
- can prescribe gluten-free food (biscuits/flour/bread/pasta) - monitor response and repeat tests
complications of coeliac disease (if untreated)
- anaemia
- dermatitis herpetiformis
- osteoporosis/ osteopenia
- infertility
- hyposplenism (give them flu jabs)
- increased cancer risk
prognosis of coeliac disease
if treated => very good
untreated => fatal
Define IBS
- chronic, relapsing disorder of lower GI tract with recurrent episodes of abdominal pain/ discomfort >6 months
+ altered stool passage
+ abdominal bloating
+ passage of mucus
+ symptoms worse on eating
causes of IBS
- environmental
- genetic
Trigger symptoms:
- enteric infection
- GI inflammation (secondary to IBD)
- dietary factors (alcohol, caffeine, spicy/fatty foods)
- Antibiotics
- stress/ anxiety/ depression (affect brain-gut axis)
presenting symptoms of IBS
- >6 months colicky abdominal pain (pain relieved on defecation)
- >6 months bloating
- >6 months change in bowel habit (altered stool consistency, rectal mucus)
- symptoms worsened by eating
- other symptoms: lethargy, nausea, back pain, headache, bladder problems, fecal incontinence
Examination signs of IBS
usually normal
- distended abdomen + mildly tender on palpation in illiac fossa
Investigations + findings for IBS
*usually diagnosed by exclusion + history
- Bloods (FBC=> anaemia, ESR/ CRP => inflammatory markers) TFTs
- Coeliac serology (anti-transglutaminase antibodies - exclude coeliac disease)
- Stool microscopy, sensitivity and culture (exclude infection)
- USS (exclude gallstone disease)
- Sigmoidoscopy
Management of IBS
- Dietary modification (avoid fibre, lactose, fructose, wheat, starch, caffeine, alcohol, fizzy drinks, )
Medical
- antispasmodics (for bloating)
- prokinetics (increases GI motility)
- anti-diarrhoea/ loperamide (for diarrhoea)
- low dose tricyclic anti-depressants
Psychological therapy:
- CBT
- Psychotherapy
complications of IBS
- physical/psychological morbidity
- colonic diverticulitis
define GORD
reflux of stomach contents (acid +/-bile) causing oesophageal inflammation due to failure of anti-reflux barrier
Reflux barrier:
- folds of stomach
- intrabdominal portion of oesophagus
- LOS
- sling fibres of gastric cardia
causes of GORD
- lower oesphageal sphincter hypotension
- hiatus hernias
- oesophageal dysmotility (systemic sclerosis)
- increased gastric acid secretion/ delayed gastric empyting
- drugs- NSAIDs
Lifestyle:
- smoking
- alcohol
- pregnancy
- caffeine
- irregular meals
- obesity
- XS excerise => infcreased intra-abdominal pressure
presenting symptoms of GORD
- heart burn/chest pain
- watery brash (saliva + acid regurgitation)
- bitter taste on tongue
- belching/burping
- odynophagia (pain on swallowing)
- worse on lying down/ bending, after eating + alcohol
Non-oeosophageal
- aspiration => wheeze, cough, laryngitis => Resp team
- hoarseness, sore throat, globus sensation (stuck in throat) => ENT team
RED FLAGS: (malignancy => 2WW)
- Dysphagia
- Anorexia
- Weight loss
- Odynophagia
- Iron deficiency Anaemia
- GI bleeding
examination findings of GORD
- generally normal
- epigastric tenderness
- wheeze on auscultation
Investigations for GORD
*usually clinical diagnosis
- upper GI Endoscopy + biopsy (look at mucosal break - area of erythema separate from normal mucosa + exclude malignancy in >55)
- 24hr pH monitoring + manometry- speed of peristalsis (normal =40)
catheter inserted from nose => oesophagus (reflux episodes over 24hrs, how long pH<4.5)
- +/- barium swallow (confirm hiatus hernia, oeopshageal peristalsis)
Management of GORD
- lifestyle (weight loss, stop smoking, less caffeine/alcohol/ spicy foods / citrus fruit, EAT >3hrs before bed, raise bed head)
- Medication: PPI (lansoprazole), antacids/ alginates (Gaviscon), , H2 blocker (ranitidine) start high dose=> lower single daily dose
- Surgical: antireflux surgery, Nissen’s fundoplication (wrap fundus around lower oesophagus)
- regular Endoscopy - keep checking for barrets oeopshagus
Anti-reflux surgery:
- reduce hiatus hernia
- 2-3 cm of lower oeosphagus
- repair fundus defect
- wrap gastric fundus around lower oesophagus - prevents reflux (usually 360- Nissens fundoplication, 180- partial wrap)
Indications for anti-reflux surgery
- unresponsive to medical management (check compliance + for duration 12-18 months)
- complications (Barrett’s, peptic stricture)
- extra-oeospheageal manifesations (asthma, hoarseness, chest pain)
- younger patients who don’t want to be on lifelong medication
Complications of GORD
- oesophagitis
- barrets oesophagus => oesophageal cancer
- peptic strictures
- oesophageal ulceration
- laryngitis
- anaemia
Complications of surgery:
- dysphagia (odema)-need liquid diet
- gas bloat/ flatulance- new anti-reflux valve can’t burp/belch
- convert from laprascopy to open surgery
- failure to conrol/ reuccurent symptoms
*
define gastritis
inflammation of mucosal lining of stomach
types of gastritis
- erosive + haemorrhagic gastritis - caused by NSAIDs, trauma, burns
- non-erosive/ chronic gastritis- in antrum due to H.pylori
- atrophic gastritis => neuroendocrine tumours/ pernicious anaemia
- reactive gastritis
Describe pathophysiology of atrophic gastritis
autobodies against parietal cells
- less HCL => increased gastrin production => gastric epithelial hyperplasia => increased risk of tumours (neuroendocrine)
- less IF => less B12 absorption => pernicious anaemia
Define peptic ulcer disease
GI ulceration due to increased gastric acid and pepsin. Most commonly gastric/ duodenal (rarer: oesophagus/ Meckel’s diverticulum)
Causes of peptic ulcers
imbalance of acid production
- H-pylori
- NSAIDs
- smoking
- alcohol
- bisphosphonates
- RARE: Zollinger-Ellison syndrome (gastrin-secreting tumour/ hyperplasia of pancreatic islet cells => increased acid production)
presenting symptoms of peptic ulcers
- epigastric pain radiating to back
- relieved by antacids
- (75%) gastric ulcer - worse after eating
- (95%) duodenal ulcer- relieved by eating
- can have haematemesis, melena
examination findings of peptic ulcers
- Usually normal
- some epigastric tenderness
- signs of anaemia (conjuctival pallor, koliconichyia)
Investigations for peptic ulcer disease (in <55 with no red flags)
Bedside
- H-pylori breath test/ stool antigen test
- Stool occult
Bloods
- FBC- Hb, MCV (anaemia)
- amylase (exclude pancreatitis)
- LFTs
- U&Es- check for dehydration
- serum gastrin
- IV Secretin test (for Zollinger-Ellison syndrome)=> secretin causes a rise in gastrin
- clotting screen
Other
- GI Endoscopy + biopsy (DIAGNOSTIC)
Gold standard investigation for peptic ulcer (>55 / red flags)
Upper GI endoscopy
Different ways to measure H.pylori
- urea breath test
- blood antibody test => presence of IgG against H-pylori
- stool antigen test
- Campylobacter-like organism test- biopsy + urea + pH indicator, if H-pylori present converts urea=> ammonia (yellow=> red colour change) urease enzyme
Management of peptic ulcer disease
- IV fluid resus
- monitor vitals
- Endoscopy- if bleeding => laser coagulation/ electrocoagulation
- Surgery - if perforated ulcer
if H.pylori infection=> triple therapy Non H-pylori
=>PPIs/ H2 antagonist
=> stop NSAIDs (if needed use misoprostol)
- Stop NSAIDs
- Eradicate H.pylori (Triple therapy- clarithromycin + amoxicillin + PPI-omperazole)
- Check on gastric ulcer healing with repeat endoscopy 6-8 weeks later
- If reccurent ulcers think other cause
Complications of peptic ulcer disease
- haemorrhage
- perforation
- obstruction/ pyloric stenosis (due to scarring/ penetration)
Define colorectal cancer
cancer in bowel
- most common in sigmoid/ rectum
Presenting symptoms of colorectal cancer
Left sided pain
- fresh red PR bleeding
- constipation + diarrhoea
- abdominal mass
Right sided pain (insidious)
- iron deficiency anaemia
- weight loss
- fever
- diarrhoea
- bowel obstruction (vomiting, nausea, acute abdomen, shock, distension)
Rectal
- tenesmus (FEEL MASS haven’t completely gone to loo)
- PR bleeding
Risk factors for colorectal cancer
- poor diet (fatty, red meat)
- alcoholics
- obesity
- diabetes
- genetic syndromes (FAP, IBD, lynch syndrome, peutz-jegher)
- ethnicity (Ashkenazi Jews)
Investigations for colorectal cancer
Bedside
- PR exam
- Abdo exam
- ECG
- Stool culture
- assess if fit for surgery
Bloods
- FBC- anaemia
- LFTs- metastasis
- U&E- dehydration
- CRP- inflammation
- tumour markers - CEA, AFP
Imaging
- barium enema
- CT abdo
- CT CAP +colonoscopy => staging
- OGD
What would be seen on barium enema of bowel osbtruction/ colorectal cancer?
Apple core strictures
Genetic conditions that cause colorectal cancer
- hyperpigmentation of mucosal membranes => peutz-jegher (autosomal dominant)
- 321 rule - >3 relatives, 2 generations, 1 >50 with CRC => Lynch syndrome (endometrial/gastric/ ovarian cancer risk)
- >100 polyps => familial adenomatous polyposis (inhibits APC tumour suppressor gene)
How to stage colorectal cancer?
Dukes criteria
- A- mucosa + submucosa involvement
- B- muscle layer involvement
- C- lymph node metastasis
- D- distant metastasis
Management of colorectal cancer
- A+B => surgery
- C => surgery + adjuvant chemo
- D => chemo +/- surgery +/- radiotherapy
Types of surgery for colorectal cancer
- right sided=> right hemicolectomy
- left sided => left hemicolectomy
- transverse colon => extension hemicolectomy
- sigmoid => Hartmann’s
- rectal => create anal stump
Management for emergency bowel obstruction + colorectal cancer risk
defunctioning stoma - cut ileum and create stoma to allow large bowel to rest
Define oesophageal carcinoma
malignant tumour of the oesophagus. 2 histological types:
- squamous cell carcinoma (more common in LEDC)
- adenocarcinoma (more common in western world)
Causes of oesophageal carcinoma
SCC
- alcohol
- achalasia
- scleroderma
- tumours
- Plummer-wilson
- nutritional deficiencies
Adenocarcinoma
- GORD
- Barrett’s oeosphagus
Presenting symptoms of oesophageal carcinoma
- can be asymptomatic
- progressive dysphagia (initially worse for solids => liquids)
- hoarseness
- weight loss
- fatigue
- odynophagia (painful on swallowing)
- cough
- regurgitation
Examinations findings of oesophageal carcinoma
- usually no signs
- metastatic disease => supraclavicular lymphadenopathy, hoarseness, hepatomegaly
Investigations for oesophageal cancer
Imaging
- OGD + biopsy
- CXR - exclude perforation
- Barium swallow (can see shouldering)
- Staging: CT CAP, PET, endoscopic ultrasound
Other: bronchoscopy, blood gas, lung function tests
Management of oesophageal carcinoma
- early stage => surgery (oesophagectomy/ oesophagogastrectomy) + adjuvant chemo/radiotherapy
- late/ metastatic => palliative chemo, stent, laser treatment for lesion
Define pancreatic cancer
malignancy of the exocrine/endocrine tissues of the pancreas
*most tumours in head of gland + exocrine tissue
causes of pancreatic cancer
- UNKNOWN
- some hereditary (FAP, HNPCC, MEN, Von-hippel Lindau syndrome)
Risk factors for pancreatic cancer
- older age (>60)
- smoking
- alcohol
- chronic pancreatitis
Presenting symptoms of pancreatic cancer
- non-specific symptoms
- FLAWS - fever, lethargy, anorexia, weight loss, nausea
Examination findings of pancreatic cancer
- jaundice
- Epigastric tenderness/ mass
- palpable gallbladder + painless
- If metastatic => hepatomegaly, splenomegaly, lymphadenopathy
Investigations for pancreatic cancer
Bloods
- Tumour markers (Ca-19-9, CEA)
- LFTs (obstructive => high GGT, ALP, bilirubin)
Imaging:
- CT scan (within 2 weeks) + Staging CT CAP
- USS abdomen- exclude gallstones/ only if CT not possible
- MRCP - look for blocked bile/pancreatic duct, ERCP - biopsy, tissue diagnosis, stenting
Management of pancreatic cancer
- early (surgery + adjuvant chemo)
- late (palliative chemo +/- surgery +/- raiotherapy)
Label ERCP
A- endoscope
B-duodenum
C- leads
D-common bile duct
E- dilated intrahepatic duct
F- sternotomy clip
G- ampullary stricture
complications of pancreatic cancer
- diabetes
Define gastric cancer
Malignancy of the stomach
- adenocarcinoma (most common)
- leimyosarcoma
- stromal tumours
risk factors for gastric cancer
- genetic (FAP)
- poor diet (processed foods, salt, low vit C)
- smoking
- alcohol
- atrophic gastritis
- pernicious anaemia
- H. pylori infection
- post-gastrectomy
- blood group A
- hypogammaglobulinanaemia
presenting symptoms of gastric cancer
early
- appetite loss
- epigastric discomfort
- indigestion
- nausea
- heart burn
Late
- Haematemesis
- weight loss
- stomach pain
- dysphagia
- jaundice (metastasis)
- ascites (metastasis)
examination findings of gastric cancer
- epigastric mass
- abdominal tenderness
- ascites/ jaundice (metastasis)
- conjunctival pallor (anaemia)
- virchow’s node
- sister mary joesph nodule (metastatic node in umbilicus)
- krukenburg’s tumour (ovarian mass due to metastasis)
investigations for gastric cancer
- bloods - FBC (anaemia), LFTs (metastasis)
- Upper GI endoscopy + biopsy
- CT CAP- for staging
- Endoscopic USS
- Liver ultrasound + bone scan - for tumour staging
- Laprascopy
Management of gastric cancer
- SURGERY (fit/ early) = subtotal/ total gastrectomy
- Endoscopic mucosal resection (early stages)
- Chemo- metastatic
- Radiotherapy
- Monoclonal antibodies (Trastuzumab- blocks HER2 - blocks growth signals to gastric cancer cells)*stage IV
Define biliary colic
gallstone causing obstruction in gallbladder/ common bile duct causing biliary tree contraction to relieve obstruction
*x3 more common in females
types of gallstones
- mixed (cholesterol, calcium bilirubinate, phosphate, protein)
- pure cholesterol stones
- pigment stones- black (calcium bilirubinate), brown (bile duct infestation)
risk factors for gallstones (6Fs)
- fat
- forty
- fertile
- female
- family history
- fair (caucasian)
- diabetes
- drugs: ocreotide/ OCP
- haemolytic disorders (sickle cell, hereditary spherocytosis, thalassemia) => pigment stones
- crohn’s (due to poor enterohepatic recycling of bile salts)
presenting symptoms of biliary colic
- sudden severe constant RUQ pain => radiating to right scapula
- pain usually after fatty meals
- nausea
- vomiting
examination findings of biliary colic
RUQ/ epigastric tenderness
investigations for biliary colic
Bloods
- FBC (raised WCC)
- LFTs
- amylase (exclude pancreatitis)
- blood culture
Bedside
- urinalysis
- ECG
Imaging
- Abdo + biliary tree USS
- Abdo X-ray (only 10% of stones = opaque)
- Extra: MRI, ERCP, MRCP
Management for biliary colic
- conservative => low fat-diet
- remove symptomatic stones in CBD using ERCP then check LFTs are normal => cholecystectomy
complications of gallstones
In gallbladder:
- biliary colic (obstruction of gallbladder/common bile duct)
- acute cholecysitits (inflamed gallbladder)
- gallbladder cancer
- gallbladder empyema (pus)
Outside gallbladder:
- acute cholangitis (infection of bile duct)
- obstructive jaundice
- gallstone ileus
- Mirizzi syndrome= common hepatic duct obstruction due to stone in gallbladder/ cystic duct
- Bouveret syndrome- gastric outlet obstruction
*cholelithiasis (presence of gallstones in gallbladder)
Define cholecystitis
gallbladder inflammation usually due to stone/ sludge formation in the gallbladder neck.
Presenting symptoms of cholecystitis
- unwell, fever
- prolonged RUQ pain => radiating to shoulder (irritates diaphragm C3-5)
- pain worse after eating fatty foods
Examination signs of acute cholecystitis
- tachycardia
- +ve Murphy’s sign
- pyrexia
- RUQ/ epigastric tenderness
- local peritonism (guarding + rebound tenderness)
Investigations for acute cholecystitis
Bedside:
- urinalysis - check for haematuria (renal colic)
Bloods
- FBC- raised WCC (cholecystitis/cholangitis)
- LFTs - exclude cholangitis (high GGT +ALP)
- Blood cultures
- amylase - exclude pancreatitis
Imaging
- US of billiary tree/ abdomen - thickened gallbladder wall, calculi (only 20% of stones are opaque)
- CXR - exclude perforated viscus
- MRCP - only for complicated gallstone disease
Management of acute cholecystitis
Medical:
- NBM
- IV fluids + analgesia
- Antibiotics
- If symptoms persist (abscess/empyema) => drainage
Surgical:
- Laprascopic cholecystectomy
Complications of acute cholecystitis
- empyema
- abscess
- cancer?
cholecystectomy
- infection
- bleeding
- bile leak
- fat intolerance (no gallbladder => no bile)
- post-cholecystectomy syndrome (dyspepsia, nausea, RUQ pain)
Define acute cholangitis
infection of the bile duct
Causes of acute cholangitis
- gallbladder/ bile duct obstruction by stones
- ERCP
- tumours (pancreatic, cholangiosarcoma)
- parasites (ascariasis)
- bile duct stricture/ stenosis
- cholecystectomy => dilate common bile duct
presenting symptoms of acute cholangitis
- Charcot’s triad (fever, RUQ pain=> spread to right shoulder, jaundice)
- Reynold’s pentad (charcot’s + mental confusion + septic shock/hypotension)
- pruritus (itching)
Examination signs of acute cholangitis
- fever
- RUQ pain
- jaundice
- mental confusion
- sepsis
- hypotension
- tachycardia
- mild hepatomegaly
- Murphy’s sign +ve
investigations for acute cholangitis
Bloods
- FBC- high WCC
- high CRP
- LFTs - obstructive picture (raised GGT + ALP)
- U&Es- check for renal dysfunction
- slightly elevated amylase if stone in lower CBD
- blood culture- check for sepsis
Imaging
- US KUB- check for stones
- Abdominal ultrasound - check for gallstones/ biliary tree dilation/obstruction
- CXR- exclude perforation
- contrast CT/MRI - check for cholangitis
- MRCP- check for non-calcified stones
Management of acute cholangitis
Immediate
- ABC
- analgesia, IV fluid, antibiotics
- endoscopic billiary drainage
Surgical
- ERCP (Endoscopic retrograde cholangiopancreatography) + sphincterectomy
- Open bile duct exploration is a last resort due to a high mortality risk
complications of ERCP
- infection
- pancreatitis
- aspiration pneumonia
- duodenal perforation
- haemorrhage
- ascending cholangitis
Complications of acute cholangitis
- liver abscess
- liver failure
- AKI
- septic shock => organ dysfunction
endoscopic drainage can lead to=> Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage
Define Vitamin B12 deficiency
inadequate vitamin B12 to meet demand
Causes of vitamin B12 deficiency
- atrophic gastritis => autoantibodies destory parietal cells =>less IF => less B12 absorption
- gastrectomy
- terminal ileum resection (where B12 absorbed)
- reduced intake (vegans, vegetarians - B12 in red meat)
- malabsorption (crohn’s)
Presenting symptoms of b12 deficiency
- fatigue
- lethargy
- dyspnoea
- headaches
- palpitations
- fainting
- neurological - numbness, parathesia, cognitive/ visual changes
Examination findings of b12 deficiency
- anaemia signs (conjuctival pallor, glossitis, angular stomatits)
- neurological (peripheral neuropathy, degeneration of spinal chord)
- psychiatric (dementia, irirtability, depression)
Investigations for b12 deficiency
- plasma total Homocysteine
- plasma methymalonic acid
- Serum b12 - less relaible
- Bloods- FBC (hypersegmented neutrophils, oval macrocytes
Tests for perniciosu anaemia
- anti-intrinsic factor antibodies
- anti-parietal cell antibodies
- shilling test
Management of B12 deficiency
- neurological symptoms => hydroxocobalamin
- no neurological symptoms + diet related => hydroxocobalamin
- no neurologicl symptoms + non-diet related => cyanocobalamin
advise more B12 in diet (eggs, soya, red meat, dairy)
Define haemorrhoids
Cushions of vascular rich connective tissue located in the anal canal.
Risk factors for haemorrhoids
- Constipation/ increased straining
- pregnancy
- 45-65 age
- portal hypertension
Classification of haemorrhoids
- Internal- superior haemorrhoidal plexus, above dentate line
- External = below dentate line
*dentate line = line divides the upper 2/3 anal canal from lower 1/3
- Grade 1- no prolapse
- Grade 2- prolapse with defecation but reduces by itself
- Grade 3- prolapse + manually reducible
- Grade 4- proplapse + can’t reduce
*
Presenting symptoms of haemorrhoids
- bright red PR bleeding- on wiping
- Sudden perinatal discomfort
- anal pruitus
- tender anal mass
- Painless (no sensory fibres) unless external => thrombosed
- NO ALARM SYMPTOMS
Examination signs of haemorrhoids
- grade 1/2 can’t be seen on external inspection
- internal haemorrhoids can’t usually be palpated on DRE
Differentials for haemorrhoids
- anal fissure
- anal tags
- polyps
- rectal prolpase
- tumour
Investigations for haemorrhoids
- Abdo exam
- DRE- can see prolapsed haemorrhoids
- Protoscopy- can see internal haemorrhoids
- Rigid/ flexible sigmoidoscopy
Management of haemorrhoids
- 1st degree = conservative
- 2/3rd degree = non-surgical (banding, sclerotherapy)
- 4th degree = surgery
Conservative
- Laxatives
- High fibre diet
- high fluid intake
Banding- applied proximal to haemorrhoids (will fall off after a few days)
Sclerotherapy- fibrosis of dilated veins
Surgery- Morgan- Milligan haemorrhoidectomy
complications of haemorrhoids
- bleeding
- prolapse
- thrombosis
- gangrene
Define ascites
fluid collection in peritoneal cavity
Causes of ascites
- CIRRHOSIS
- portal hypertension (congestive heart failure, pericarditis, fulminant hepatits- XS Paracetamol, Budd-chiari syndrome, alcoholic liver disease)
- hypoalbumin-anaemia (nephrotic syndrome)
- Malignancy , liver metastasis
- infectious peritonitis
presenting symptoms of ascites
- abdominal distension
- risk factors for heart failure (smoking, diabetes, hypertension, high cholesterol, elderly, family Hx)
- history of alcohol consumption (alcoholic liver disease)
- risk factors for hep C (drug user, blood transfusion)
- family Hx (liver disease, autoimmune heaptitis)
- Symptoms of heart failure (SOB +/- odypnoea)
- toxins (paracetamol overdose)
examination findings of ascites
- abdominal distension
- shifting dullness
- abdominal thrills
- signs of liver disease (palmar erythema, leuconycia, jaundice, hepatomegaly)
- raised JVP => congestive HF
- pitting oedema => nephrotic syndrome
Investigations for ascites
Bloods
- FBC (thrombocytopenia => portal hypertension)
- LFT (raised bilirubin)
- U&Es (monitor for hepatorenal syndrome)
- Viral serology (hep A/B/C)
Imaging
- ultrasound
- CT abdo
- MRI abdo
- Abdominal parentesis - check serum albumin levels (cirrhosis)
- Blood culture if non cirrhosis
- Liver biopsy - identify cause
managment of ascites
- diuretics
- abdominal paracentesis- drain fluid
- insertion of a transjugular intrahepatic portosystemic shunt (for portal hypertension)
- Prevent development of spontaneous bacterial peritonitis
Lifestyle
- stop drinking
- reduce fluid intake
- treat cause
Define gastroenteritis (infectious colitis)
acute inflammation of GIT lining
- dysentry = type of gastroenteritis with bloody diarrhoea
Causes of gastroenteritis
caused by toxins, viruses, bacteria, protozoa in contaminated food/ water
Dystentry (bloody gastroenteritis) causes: CHESS
- Campylobacter jejuni
- Haemorrhagic E.coli
- Entomoeba histolytica
- Salmonella
- Shigella
*
Typical causes of gastroenteritis
- elderly with antibiotics overuse = C. Difficile
- young children/ D+V hopsital incident = Norovirus
- Uni student with watery diarrhoea= Campylobacter jejuni
- Travellers diarrhoea = E. coli
- Diarrhoea after meals = S. aureus
Contaminated food
- uncooked meat= stap. aureus, C. perfiringens
- milk + cheese = Listeria, campylobacter
- Eggs + poultry= salmonella
- canned food = botulinum
Presenting symptoms of gastroenteritis
- SUDDEN nausea, vomiting
- DIARRHOEA (watery/ bloody)
- SUDDEN anorexia
- fever + malaise
- SPECIFIC: botulinum (paralysis), mushrooms (renal failure)
Symptoms present:
- toxins (<24hrs)
- virus/bacteria/protozoa (12+hrs)
Ask about
- recent travel history
- antibioitc use
- any close contacts with diarrhoea/vomiting
- recent meals (takeouts/ raw foods/ how food was prepared)
Examination findings of gastroenteritis
- abdominal tenderness
- abdominal distension
- XS nausea/diarrhoea=> dehydration
- hypotension (low bp)
- fever
Investigations for gastroenteritis
Bedside
- stool culture (MC&S)- C.diff => pseudomembranous colitis
Bloods
- FBC
- U&Es- dehydration
- blood culture
Imaging
- AXR/ ultrasound - exlcude perforation (could cause abdo pain)
- Sigmoidoscopy (if IBD suspected)
Management of gastroenteritis
Mild/moderate dehydration
- Bed rest - 48hrs
- Oral rehydration soloution (fluids + electrolytes)
- +/- anti-emetics (ondansetron)
- +/- anti-diarrhoeal (ioperamide) avoid in bloody/infectious diarrhoea as can prolong infection
Severe dehydration
- IV fluids
- +/- anti-emetics
- +/- anti-diarrhoeal
*Only give antibiotics - if SEVERE infection
Specific treatment for C. diff infecitons
- Isolate
- Metronidazole (antibiotic)
- if returns, vancomycin
Complications of gastoenteritis
- dehydration
- electrolyte imbalances
- prerenal failure (dehydration)
- Haemolytic uraemic syndrome (E.coli toxin)
- respiratory muscle weakness (botulinum)
*
Define Haemochromatosis
autosomal recessive genetic disorder that causes increased iron absoprtion in the small intestine
*defect in HFE gene
Presenting symptoms of haemochromatosis
usually asymptomatic and present in later stages:
Early
- weakness
- fatigue
- arthralgia (joint disease)
- erectile dysfunction
Later
- Diabetes
- Hypogonadism => loss of libido, impotence
- bronzed skin
- arrythmias
Examination findings of haemochromatosis
- hepatomegaly (associated cirrhosis)
Investigations for haemochromatosis
Bedside:
- ECG (not diagnostic)
Bloods
- Haematinics: serum ferritin (HIGH), transferrin (LOW), transferrin saturation (HIGH) *not specific
- LFTs/ CRP (exclude other causes for high ferritin)
- fasting blood glucose
- testosterone/ LH/FSH assay (check for hypogonadism)
Imaging
- Liver MRI- check for Fe overload
- Echo (check for cardiomyopathy)
Other:
- Genetic testing (HFE mutation)
- Liver biopsy
Management for haemochromatosis
Stage 0
- 3yr follow up
- lifestyle changes (reduce iron/vit C in diet + supplements, stop alcohol)
- Hep A/B vaccines
Stage 1
- 1yr follow up
- lifestyle changes
- Hep A/B vaccines
Stage 2-4
- Phlebotomy (remove blood to stimulate new RBC production using stored iron) + lifestyle modifications +/- Hep A/B vaccines
- Iron chelation (deferasirox) + lifestyle modification +/- Hep A/B vaccines
*2nd line treatment for patients who can’t give blood- anaemia, severe heart disease, difficult venous access
Why should vit C be avoided in patients with haemochromatosis?
- increases absorption of dietary iron in small bowel
- but can be given in small doses with iron chelation (to increase iron for chelation)
Define peritonitis
inflammation of the peritoneal lining of the abdominal cavity
- Localised (usually resolves with treatment)
- Specialised bacterial peritonitis
- Generalised (worse prognosis)
- Primary- RARE, most common in females- usually resolves with ABs
- Secondary
Causes/ risk factors of peritonitis
Localised
- appendicitis
- cholecysitis
- diverticulitis
- post-surgery
Generalised
- Primary - bacterial cause, ascites, nephrotic syndrome, UTI
- Secondary - bacterial, non-bacterial spillage of bowel contents/blood/bile (e.g. perforated peptic ulcer)
Localised/ secondary generalised common post surgery
Presenting symptoms of peritonitis
- continuous, sharp, stabbing abdominal pain
- pain worsened by movement so patient usually lying still
- vague symptoms if patient has liver disease (confusion from encephalopathy)
Examination findings of peritonitis
Localised
- abdomen tenderness
- rebound tenderness
- guarding
Generalised (worse)
- unwell patient
- signs of sepsis (fever, tachycardia + dehydration)
- patient lying still
- rigid abdomen
- shallow breathing
- generalised abdomen tenderness
- may have reduced bowel sounds (due to paralytic ileus)
Investigations for peritonitis
Bedside:
- pregnancy test
- urine dipstick
Bloods:
- FBC - raised WCC
- U&Es- check for dehydration => AKI (raised urea/creatinine)
- LFTs
- amylase (exclude pancreatitis)
- CRP - bowel inflammation
- blood cultures
- clotting screen
- group & save
- ABG?
If ascities is present
- ascitic tap (exclude SBP- >250mm^3 neutrophils)
- gram stain + culture
Imaging:
- CXR- exclude perforation
- AXR- exclude bowel obstruction
- USS- exclude stones
Management of peritonitis
Localised
- identify and treat cause (surgery for appendicectomy/ antibiotics for salpingitis)
Generalised
- RESUS: treat sepsis/ shock
- IV fluids
- IV antibiotics (PRIMARY)
- Urinary catheter
- NGT
- central venous line (monitor fluid input)
- Laparotomy (remove infected tissue + drainage)
Specialised bacterial peritonitis (SBP)
- quinolone antibiotics
- cerufoxime + metronidazole
Complications of peritonitis
Early
- sepsis
- resp failure
- multi-organ failure
- paralytic ileus
- abscess
- wound infection
Late
- incisional hernia
- adhesions
define hyposplenism
- dysfunctional spleen or spleen removed during splenectomy
Causes of hyposplenism
- splenectomy (due to spleen trauma, cysts)
- Bone marrow transplant (Graft Vs host disease, splenic irradiation)
- congenital asplenia (missing spleen)
functional hyposplenism
- sickle cell anaemia
- thalassemia major
- Hodgkins Lymphoma
- Coeliac disease
- IBD
Indications for splenectomy
- trauma
- spontaneous rupture
- hypersplenism
- neoplasia (leukaemia/ lymphoma infiltration)
- splenic cysts
- splenic abscess
Investigations for hyposplenism
- Blood film (howel-jolly bodies, Pappenheimer bodies, irregularly contracted cells, target cells)
- Ultrasound/ CT/ MRI imaging
Management for hyposplenism
- vaccines (S. pneumoniae, N. meningitidis, H. influenzae type b and influenza virus)
- antibiotic prophylaxis (1-2yrs after splenectomy)- for patients high risk for penumococcal infections (macrolides)
High risk=
- <16, >50
- don’t respond to pneumococcal vaccine
- immunosuppressed
- haemotological malignancies
Complications of hyposplenism/ splenectomy
- Thrombocytosis (high platelets)
RISK OF INFECTIONS:
- S. pneumoniae (pneumoccocus)
- N. meningitidis
- H. infleunzae type B
- E.coli
- Malaria
define perianal abscess and fistula
perianal abscess= collection of pus
perianal fistulae= abnormal connection between perineal skin and anal canal/rectum
causes of perianal abscess + fistula
- bacterial infection => abscess
- IBD
- Diabetes
- Malignancy
Fistula
- complication of an abscess
- complication of Crohn’s (IBD)- multiple perianal fistuae (pepper pot)
presenting symptoms of perianal abscess / fistula
- throbbing pain in perianal region
- intermittant dishcarge (mucus/ faecal)
- Family Hx of IBD
Examination findings of perianal abscess / fistula
- tender mass (can be fluctuant)= abscess
- small skin lesion near anus (opening of fistula)
- DRE = thickened area (but can’t always be done due to pain/ anal sphincter spasm)
To determine pathway of fistula=> GOODSALL’S rule
- external opening is anterior to transverse line across anus => straight radial tract to anteriorly
- external opening is posterior/ 3cm away => curved tract to midline posteriorly
Investigations for perianal abscess / fistula
Bloods:
- FBC
- CRP
- ESR
- blood culture
Imaging
- MRI
Management of perianal abscess / fistula
SURGICAL TREATMENT
- drainage of abscess
- low Fistula=> laying open (fistulotomy)- minimal damage to anal sphincter =>reduce INCONTINENCE
- High fistula => Seton (non-surgical thread keeping tract open and allows drainage)
- ANTIBIOTICS
external sphincter - voluntary defecation
internal sphincter - involuntary
Complications of perianal abscess / fistula
- RECURRENCE (if not fully excised)
- Incontinence (damage to internal anal sphincter)
- perisiting pain
Define viral gastroenteritis
inflammation of the lining of GIT due to enteropathogenic viruses
viruses damage enterocytes => structural changes to mucosa => malabsorption + loss of brush border enzymes (food intolerance)
*usually spread person-person, food/water borne
causes of viral gastroenteritis
Rotaviruses- airborne
noroviruses- children/elderly high risk (fecal-oral route)
caliciviruses
astroviruses
coronaviruses
enteric adenoviruses
presenting symptoms of gastroenteritis
- mild fever
- nausea + vomiting
- frequent, watery diarrhoea
- abdominal pain
- anorexia (appetite loss)
examination findings of gastroenteritis
- high temp
- dehydrations signs- tachycardia, hypotension, dry mucous membranes
- mild abdominal pain + tenderness
investigations for viral gastroenteritis
bedside:
- urine dip (UTI, infection-glucose)
- pregnancy test
- stool culture - MC&S
bloods
- FBC- Hb (anaemia= chronic cause), raised WCC- infection,
- U&Es- raised urea:creatinine ratio (AKI/ dehydration), Na+/K+ (to give fluids)
stool viral culture (RARE)- identify virus
Imaging:
- AXR- exclude bowel obstruction
risk factors for viral gastroenteritis
- close contact with infected people
- poor hygiene
- contaminated food/water
- extreme ages (younger kids/elderly)
Management for viral gastroenteritis
- oral rehydration or IV fluids crystalloid soloution (for SEVERE DEHYDRATION)
consider if can’t tolerate oral hydration: anti-emetics (neurological side effects)/ anti-diarrhoeal drugs (not for inflammatory causes)
define infectious diarrhoea
diarrhoea caused by infectious agents (bacteria, virus, protozoa)
Define Mallory-weiss tear
tear of mucous membranes in oesophagus near gastro-oesophageal junction => bleeding
*rare
causes of Mallory-weiss
- violent vomiting/ coughing
- alcohol => vomiting
- bulimia
- childbirth
- hiatus hernia - increase abdomen pressure
presenting symptoms of mallory-weiss syndrome
- can be asymptomatic
- abdominal pain
- involuntary retching
- severe vomiting
- melaena (black stools)
- haematemesis (blood in stool)
examination findings of mallory-weiss syndrome
- melaena (PR exam)
- signs of hypovolemia (tachycardia, low bp)
investigations for mallory-weiss syndrome
- Bloods- FBC - check for anaemia
- OGD (oesophago-gastro-duodenoscopy) - look for tear
Management of mallory-weiss syndrome
- usually self-resolving
- if bleeding doesn’t stop => surgery, coagulation therapy, arteriography, injection sclerotherapy
- transfusion if XS blood loss
Complications of mallory-weiss syndrome
- Borrhaeeve’s syndrome - transmural oesophageal perforation
causes of infectious diarrhoea
Viral
- Norovirus- food-borne gastroenteritis
- Rotavirus - most common cause of diarrhoea in children
- Adenovirus
- Astrovirus- common diarrhoea cause in children, elderly, compromised immune system
Bacteria (=> dysenteric disease- BLOODY diarrhoea)
- Salmonella enteritidis- contaminated food/drink
- Esherichia coli- contaminated food/dairy
- Shigella- BLOODY diarrhoea
- Campylobacter- food-borne, BLOODY diarrhoea
- Vibrio infection- raw seafood/sushi
- Staph aureus- EXPLOSIVE diarrhoea (toxins released by bacteria)
- C. difficile - antibiotic overuse
Protozoa (parasite)
- giardia lamblia- contaminated food/person-person EXPLOSIVE diarrhoea
- entamoeba histolytica- faecal-oral transmission, BLOODY diarrhoea
- Cryptosporidium- WATERY stool (GI/resp illness)
What mechanisms cause infectious diarrhoea?
- Increased intestinal secretion of fluid/electrolytes usally due to SECRETORY ENDOTOXINS (E.coli)
- Impaired intestinal absorption of fluids/electrolytes (E.coli, Cryptosporidium, shigella, salmonella, rotavirus)
Presenting symptoms of infectious diarrhoea
DIARRHOEA
- Acute watery diarrhoea (resolves within 10days)
- Bloody diarrhoea (dysentry) - usually invasive enteropathogen
- Perisistent diarrhoea (>14 days) +/- weight loss and signs of nutrient deficiency
- fever
- nausea/vomiting
- abdominal pain
History
- Recent travel history
- Recent oral intake (contaminated food/water)
- anyone else with diarrhoea
What groups are at increased risk of infectious diarrhoea?
- age: infants, young children, elderly
- immunocompromised (HIV/AIDS/ chemotherapy)
- exposure to enteropathogens (recent travel/ contaminated food/water)
- antibiotic use + elderly/cancer patients
Examination findings of infectious diarrhoea
- check for signs of dehydration (raised HR, low bp, high RR, reduced skin turgor, dry mucous membranes)
- +/- painful swollen joints (reiter’s syndrome)
- guillan-barre syndrome- autoimmune nerve damage (C. jejuni infection)
Investigations for infectious diarrhoea
Bedside
- Urine dip
- Stool MC&S (FIRST LINE)
Bloods
- FBC - check for anaemia, high WCC (infection)
- CRP/ESR- inflammation marker
Imaging
- Abdo ultrasound (for unwell patients => check bowel obstruction/ severity of infectious colitis)
- Endoscopy + biopsy (for perisitant diarrhoea - shows atrophy of cells/ protozoal cysts or exclude IBD/infectious colitis
Other
- Biopsy- mucosal oedema (sign of infection)
- PCR test on stool - check for viral infections
Management of infectious diarrhoea
- Oral rehydration therapy
- Supportive treatment = IV fluids (in severe dehydration for fluid + electrolyte replacement
- anti-diarrhoeal medications
- antimotility = Ioperamide
- antisecretory agents
- Treat cause => antibiotics (cholera/dysentry, not always needed)/ anti-virals
- analgesia/ anti-pyretics (for fever/pain)
*
define malabsorption
- difficulty digesting nutrients
- difficulty absorbing nutrients
Causes of malabsorption
Difficulty digesting
- lactose intolerance (missing lactase enzyme)
- Whipple disease (bacterial infection effects digestion + absorption)
Difficulty absorbing nutrients
- Crohn’s- damage to intestine
- cystic fibrosis (affects pancreas => reduced enzyme secretion- less proteins/fats/vit A,D,E,K absorbed)
- Chronic pancreatitis
- Zollinger-Ellison - pancreatic insufficiency
- Coeliac disease (autoantibodies attack villi of small bowel)
- Pernicious anaemia (attacks parietal cells => less IF=> less B12 absorption)
- parasites (giardia lamblia)
*
Presenting symptoms of malabsorption
- avoiding specific foods
- bloating/gas
- chronic diarrhoea
- steatorrhoea (Coeliac)
- growth failure
- weight loss
- +/- oligoamenorrhoea (stop menstruating)
- +/- bleeding (low Vit K)
- +/- oedema (protein/calorie malnutrition)
Ask about
- Family Hx (coeliac, Crohn’s, CF, lactose intolerance)
Investigations for malabsorption
Bedside
- Stool MC&S
Bloods
- FBC- anaemia (low Hb)
- ESR/CRP
- Vitamin B12
- Iron studies (ferritin)
- Clotting screen (Vit K deficiency)
- serum albumin
- Calcium
- LFTs
- coeliac screen (autoantibodies)
Imaging
- abdominal US (check gallbladder/liver/pancreas)
Breath hydrogen test - check for intestinal bacterial overgrowth
Management of malabsorption
- Nutritional support
Depends on cause
- Coeliac - gluten-free diet
- Pancreatic insufficiency => oral replacement of enzymes
- crohn’s => steroids
- blockage of bile => SURGERY
- pernicious anaemia => B12/ folate injections
Complications of malabsorption
- coeliac => infertility, small bowel adenoma
- anaemia
- stunted growth
- rickets/osteomalacia/osteoporosis (low Ca2+)
define malnutrition
state resulting from lack of uptake/intake of nutrition leading to changed body composition + body cell mass leading to low physical/mental function and clinical outcome from disease
- undernutrition- not getting enough nutrients
- overnutrition- getting too many nutrients
causes of malnutrition
- disease related anorexia- reduced appetite (feeling sick/diarrhoea)=> cancer, liver disease, COPD
- malabsorption - Crohn’s/ UC
- mental health problems- depression, schizophrenia=> low desire to eat
- eating disorders - anorexia, bulliemia
- dementia- can forget to eat
- increased energy requirement => healing after surgery/burns, tremors
- medicine side effects reducing appetite
- elderly -poor dentition/ disabilities
- swallowing difficulty (dysphagia)
symptoms of malnutrition
- unintentional weight loss (5-10%)
- low BM1 (<18.5)
- lack of intrest in eating/drinking
- feeling tired
- feeling weakness
- getting ill more often/ longer recovery time
- stunted growth in children
What’s is used in hospital to diagnose malnutirition?
MUST (malnutrition universal screening tool)
- based on BMI/ unplanned weight loss
- assessed within 6hrs
- if diagnosed => refer to dietician
Investigations for malnutrition
Bedside
- BMI
- stool culture (check for parasites => malnutrition)
- mid upper arm diameter
Bloods
- FBC- check for anaemia/ infection
- blood glucose
- U&Es- dehydration
- B12/folate levels
- iron studies - ferritin
- TFTs
- Ca2+/ zinc/ vitamin levels
- cholesterol (low)
- albumin - BUT is reduced by inflammation
management for malnutrition
- Lifestyle => balanced diet, increase snacking,
- Nutritional supplements (oral nutrition)
- Enteral feeding (NGT, NJT, NDT)
- Parental feeding (IV -nutrients into venous blood) - only if dysfunctional GIT (Crohn’s, short bowel syndrome, ischaemic bowel disease, cancer)
Problems with enteral feeding (NGT)
- refeeding syndrome (too many nutritents too quickly)
- metabolic- deranged electrolyte, hyperglycaemia
- mechanical - tube displacement, tube blockage
- aspiration
- nausea/vomiting/diarrhoea
- tube infection
problems with parenteral nutrition
- mechanical - arrhythmias, thrombosis
- catheter related infections
- metabolic- deranged electrolytes
What is refeeding syndrome and it’s pathogenesis?
- when starved individual is fed nutrients too quickly
When starved
- less insulin release
- gluconeogenesis/ glycogenolysis
when fed
- increased insulin => glycogenensis
- Na+/water retention => oedema
- hypokalemia/ low Mg2+/ phosphate
- used up thiamine (co-enzyme in carb metabolism) => WERNIKE’S ENCEPHALOPATHY
Consequences:
- wernicke’s encephalopathy
- respiratory depression
- arrythmias/ tachycardia/ HF => cardiac arrest/ DEATH
How is refeeding syndrome managed?
- micronutrients
- monitor electrolytes
- thiamine supplements
- monitor fluid output (Na+/K+)
define Hepatitis A & E viruses
hepatitis caused by hepatits A virus (HAV) or Hepatitis E virus (HEV)
- HAV = picornavirus
- HEV= calicivirus
- small non-enveloping single stranded RNA virus
- (common in developing countries- poorer sanitation)
- 3-6 week recovery
Describe how HAV/HEV are transmitted?
via faecal-oral route
- replicate in hepatocytes and are secreted into bile
- Immune response causes liver inflammation/ hepatocyte necrosis
- Infected cells killed by CD8+ / NK cells
*Incubation of virus = 3-6 weeks
Presenting symptoms of HAV/HEV
Early
- fever, malaise
- anorexia
- nausea/ vomiting
Late- signs of hepatitis
- dark urine
- pale stools
- jaundice
- itching
*Incubation of virus = 3-6 weeks
Examination findings of HAV/HEV
- pyrexia
- tender hepatomegaly
- jaundice
- palpable spleen
- absence of chronic liver disease signs
Investigations for HAV/HEV
Bedside - urinalysis
- +ve biliubin
- raised urobilinogen
Bloods
- LFTs - raised ALT, AST, ALP
- high ESR
- low albumin
Viral serology
- anti-HAV IgM- acute illness phase (disappears >5 months)
- anti-HAV IgG- recovery phase/ lifelong
- anti-HEV IgM (1-4 weeks after)
- anti-HEV IgG
Management of HAV/HEV
- Bed rest + Treat symptoms
- anti-pyretics
- anti-emetic
- cholecystyramine (for severe pruitus)
Prevention (NOTIFIABLE DISEASE)
- clean water/sanitation/ good hygiene
- passive immunisation (IM antibody) for short term protection
- active immunisation with attenuated HAV virus when travelling to endemic countries
*IMMUNISATION only for HAV virus
Complications of HAV/HEV
- fulminant hepatic failure (>80% mortality)
- post-hepatic syndrome
- cholestatic hepatitis => prolonged jaundice/itching
define Hepatitis B and D viruses
Hepatitis B
- Hepatitis caused by infection of HBV (Hep B virus)
- acute or chronic (viraemia + hepatic inflammation >6months)
- Double stranded DNA virus
Hepatitis D
- Hepatitis caused by infection of HDV (Hep D virus) is a defective virus
- can only co-infect with Hep B/ with a carrier of HBV
- single stranded RNA virus
Transmission of HBV
- Sexual contact
- bloodborne
- vertical transmission (mother => baby)
Risk factors for HDV
- IV drug user
- sexual contact with HBV carriers
- unscreened blood/blood products in haemodialysis
- infants of HBeAg/HBsAg positive mothers
What viral proteins are produced by HBV?
- HBcAg- core antigen
- HBsAg- surface antigen
- HBeAg- e antigen
*HDV has HBsAg antigen
Presenting symptoms of HBV/HDV
Early
- fever, malaise
- anorexia
- nausea, vomiting
- diarrhoea
- RUQ pain
- serum sickness type illness (fever, arthralgia, polyarthritis, urticaria, maculopapular rashes)
Later
- jaundice
- pale stools
Examination findings of HBV/HDV
Acute
- jaundice
- pyrexia
- tender hepatomegaly
- splenomegaly
- cervical lymphadenopathy
- sometimes urticaria/ maculopapular rash
Chronic
- usually no findings
- some signs of chronic liver disease
Investigations for HBV/HDV
Bloods
- LFTs- high ALT,AST, ALP, bilirubin
- clotting screen (high PT- in severe disease)
Viral serology (GOLD-STANDARD)
- Acute HBV => +ve HBsAg, IgM anti-HBcAg +/- HBeAg
- Chronic HBV => +ve HBsAg, IgG anti-HBcAg +/- HBeAg
- HDV infection => IgM/IgG against HDV
*HBV vaccinated => +ve anti-HBsAg antibody
Other
Liver biopsy (if ascites present/ clotting affected)
Management for HBV
Acute HBV
- bed rest + symptom treatment (anti-pyretics, anti-emetics, cholestyramine- for pruitus)
- NOTIFIABLE DISEASE
Chronic HBV
- anti-viral treatment (if +ve HbeAg, detectable HBV by PCR, decompensated cirrhosis)
- interferon alpha (augments anti-viral mechanism)
- nuceloside analogues
- On medication for life
Prevention of HBV
- Safe sex
- blood screening
- sterilise instruments
- passive immunisation=> Hep B antobodies for infants with +ve HBeAg mothers
- active immunisation => recombinant HBsAg vaccine for at risk pp/ have +ve HBV mothers
Complications of HBV
- Fulminant hepatic failure
- Chronic HBV (10%)
- Cirrhosis
- Hepatic cellular carcinoma
- HDV => acute liver failure/ rapid disease progression
Define Hepatitis C virus
hepatitis caused by infection with Hepatitis C virus (HCV) often chronic
- single stranded RNA virus
- Has multiple genotypes
- Can take up to 12 months to recover
How is HCV transmitted?
PARENTERAL
- Sexual
- vertical
What patients are at risk of HCV?
- IV drug user
- haemodilaysis
- recipients of unscreened blood products
- tattoing
- non-sterile acupuncture
- health care workers
Presenting symptoms of HCV
- 90% ASYMPTOMATIC
- 10% jaundice + mild-flu
Examination findings of HCV
- NO SIGNS usually
- some signs of chronic liver disease
- can have extrahepatic (rashes/ renal dysfunction)
Investigations for HCV
Bloods
- LFTs- acute (high ALT,AST,ALP,bilirubin), chronic (x8 higher AST+ALT)
- Reverse transcriptase PCR => detects + genotypes HCV
- Viral serology
- IgM anti-HCV antibodies (acute)
- IgG anti-HCV antibodies (chronic)
Other
Liver biopsy (check degree of liver inflammation)
features:
- chronic hepatitis
- lymphoid follicles in portal tracts
- fatty change
- cirrhosis
Management of HCV
Acute => symptomatic (anti-pyretics, anti-emetics, cholecystyramine) + BED REST
Chronic
- pegylated interferon alpha
- nucleoside analogue (ribavirin)
- Monitor HCV viral load for treatment efficacy
Prevention of HCV
- safe sex
- needle exchange schemes for drug users
- instrument sterilisation
Which viral hepatitis doesn’t have a vaccine?
Hepatitis C
Complications of HCV
- fulminant hepatic failure
- chronic HCV (80%) => CIRRHOSIS (20%)
- hepatocellular carcinoma
Define autoimmune hepatitis
chronic hepatitis with autoimmune features with circulating autoantibodies and hyperglobulinanaemia
Pathogenesis of autoimmune hepatitis
environmental agent (virus/drugs) triggers hepatocyte expression of HLA antigens which are attacked by T cells
Inflammatory changes (similar to chronic viral hepatitis)= lymphoid infiltration to portal tracts and hepatocyte necrosis
Types of autoimmune hepatitis
- Type 1 classic
- ANA, Anti-smooth muscle antibodies (ASMA), Anti-actin antibodies, Anti-soluble liver antigen
Type 2
- Antibodies to liver/kidney microsomes (ALKM-1)
- antibodies to liver cytosol antigen (ACL-1)
Presenting symptoms of autoimmune hepatitis
- can be asymptomatic and discovered through abnormal LFT finding
- Check FHx for autoimmune diseases
- rule out alcoholic/ viral hepatitis
Insidious symptoms:
- Malaise
- fatigue
- anorexia
- weight loss
- nausea
- jaundice
- amennorrhoea
- epistaxis
Acute hepatitis (25%)
- fever
- anorexia
- nausea/vomiting/ diarrhoea
- RUQ pain
- serum sickness (arthralgia, polyarthritis, maculopapular rash)
Examination signs of autoimmune hepatitis
- chronic liver disease signs (spider naevi)
Late signs:
- ascites
- oedema
- hepatic encephalopathy
Cushingoid features (round face, acne, hirsutism)
Investigations for autoimmune hepatitis
Bloods
- LFTs- high ALT/AST, ALP, GGT, bilirubin, LOW albumin
- FBC- low Hb, WCC, platelets (hyposplenism from portal hypertension)
- Clotting- high PT (severe disease)
- Hypergammaglobulinanaemia - ANA, ASMA, Anti-LKM antibodies
Liver biopsy- check for hepatitis/ cirrhosis
To exclde other causes:
- Viral serology - rule out viral hepatitis
- urinary copper (Wilson’s)
- ferritin/transferrrin saturation (haemochromatosis)
- a-1 antitrypsin
- anti-microbial antibodies (PBC)
- ERCP - rule out PSC
Management of autoimmune hepatitis
Immunosuppressants
- steroids (prednisilone)
- maintenance phase (azothioprine/ 6-mercaptopurine (steroid-sparing agents)
- Test for TPMT1 activing before starting azothioprine
Monitor
- Ultrasound/ alpha-fetoprotein every 6-12 months to detect hepatocellular carcinoma in cirrhosis patients
- Hep A/B vaccines
- Liver transplant - if patient intolerant to immunosuppression
Complications of autoimmune hepatitis
- Fulminant hepatic failure
- cirrhosis
- complicatios of portal hypertension => ascites, varices
- Hepatocellular carcinoma (HCC)
- Corticosteroid side effects => thin skin, Cushings, impaired wound healing
Prognosis of autoimmune hepatits
- 5yr survival with treatment = 85%
- 5yr surival without = 50%
- 5yr survival with transplant= >80%
Define alcoholic hepatitis
liver inflammation due to chronic alcohol use (>15yrs)
Presenting symptoms of alcoholic hepatitis
mild
- Epigastric/ RUQ pain
- low grade fever
- nausea
Severe
- jaundice
- abdominal discomfort/ swelling
- swollen ankles
- GI bleeding
Examination findings of alcoholic hepatitis
mild
- hands (palmar erythema, dupyutrens contracture)
- face (facial telangiectasia- red lines)
- chest (spider naevi, gynaecomastia)
- hepatomegaly
- easy bruising
severe
- jaundice
- tachycardia
- fever
- hepatomegaly
- ascites
- encephalopathy (liver flap, drowsy, disorientation - XS ammonia crosses blood-brain barrier)
- bruising
Investigations for alcoholic hepatitis
Bloods
- FBC (low Hb + platelets, high MCV + WCC)
- LFTs (high AST:ALT, high GGT +ALP, high bilirubin, low albumin)
- U&Es- low urea + K+
- clotting - low PT
Imaging
- USS - check for malignancy/ stones
- CT/MRI liver
Other
- GI endoscopy
- liver biopsy- exclude other types of hepatitis
- EEG - encephalopathy
Management of alcoholic hepatitis
acute:
- thiamine + vitamins (NG tube)
- correct K+/ Mg/ glucose
- oral lactulase for encephalopthy (reduce ammonia)
- monitor urine output + diuretics (for ascites)
- steroids - FOR INFLAMMATION reduce mortality
*Hepatorenal syndrome => n-acetylcysteine/ glypressin
Complications of alcoholic hepatitis
- cirrhosis
- acute liver decompensation
- hepatorenal syndrome= cirrhosis + ascites + renal failure
Pathophysiology of hepatorenal syndrome
- splanchnic vessels to intestines VASODILATE (NO, prostaglandins released by liver damage)
- reduced blood volume detected by JGA => activates RAAS
- VASOCONSTRICTION of renal vessels
- KIDNEY failure
define Liver cirrhosis
scarring of the liver due to previous liver damage (hepatitis, alcohol)
Architectural changes to hepatocytes = more fibrosis, nodular regeneration
Causes of liver cirrhosis
- chronic alcohol misuse
- hepatitis (viral/ autoimmune)
- Drugs (methotrexate, hepatotoxic drugs)
- Inherited (a1-antitrypsin deficiency, haematochromatosis, CF, Wilson’s)
- Primary billiary cholangitis = autoimmune => bile ducts destroy liver
- Vascular - Budd-chiari syndrome (occlusion of hepatic veins)
- Non-alcoholic steatohepatitis
Presenting symptoms of liver cirrhosis
- early non-specific (anorexia, weight loss, fatigue, nausea, weakness)
- reduced function (bruising, ascites, leg swelling - slowed blood flow through liver so increased pressure in hepatic portal vein)
- reduced detoxification (jaundice, galactorrhea, amenorrhoea)
- portal hypertension (ascites)
examination findings of liver cirrhosis (A=>N)
- Ascites
- Bruises
- Clubbing + Caput medusa
- Duputrens contracture
- palmar Erythema
- Fat spleen
- Gynaecomastia
- Hepatomegaly, hair loss
- Itching (bile deposits on skin)
- Jaundice
- Leukonycia (hypoalbuminanaemia)
- Mini testes
- Spider Nevi
- Other (steroids, pregancy)
- Parotid enlargement
- Terrys nails (distal white, proximal is red)
- Xanthelesma
hands (palmar erythema, clubbing, leuconykia, terry’s nails)
face (xanthelesma, jaundice, hair loss)
chest (gynaecomastia, spider nevi)
abdomen (ascites, hepatomegaly, splenomegaly, caput medusa, bruising)
Investigations for liver cirrhosis
Bloods
- FBC - low Hb, platelets
- LFTs- raised ALP/ GGT/ AST/ALT/bilirubin, low albumin
- serum alpha-fetoprotein (marker of liver cancer raised in chronic liver disease)
- Prolonged PT (clotting)
Identify cause:
- viral serology (Hep B/C)
- Iron studies (Haematochromatosis)
- a-1 antitrypsin levels
- caeruloplasmin (Wilson’s)
- Anti-mitochondrial antibody (PBC)
- ANA, AMSA (autoimmune hepatitis)
Ascitic Tap
- MC&S- check for infection
- biochemistry (low glucose, protein, amylase, albumin)
- >250mm/L neutrophils = bacterial peritonitis
Liver biopsy
- histology (nodular appearance, fibrosis)
- grading (inflammation)
- staging (arhcitectural distortion)
Imaging
- US - biliary obstruction, ascites
- CT/MRI - hepatocellular carcinoma
Endosocpy (look at varices)
Management of liver cirrhosis
- Treat CAUSE
- Avoid alcohol, NSAIDs, opiates, sedatives, hepatotoxic drugs
- Enteral feeding, NGT
- Treat complications:
Ascites
- diuretics
- Na+ restrict => Fluid restrict if Na+ too high
- monitor weight
Encephalopathy
- lactulose (reduces gut absorption of ammonia)
- phosphate enemas
Spontaneous bacterial peritonitis
- Antibiotics (metronidazole, cefuroxime)
- Prophylaxis for reccurent infection- Ciprofloxacin
Surgery
- TIPS (transjugular intrahepatic portosystemic shunt => reduces portal hypertension)
- Liver transplant (CURATIVE)
Complications of liver cirrhosis
- Pulmonary hypertension + Ascites
- Variceal Bleeding/ haemorrhage
- Encephalopathy (ammonia not broken down by liver => passes thorugh BBB => brain)
- Spontaneous bacterial peritonitis
- Hepatocellular carcinoma
- Renal failure (hepatorenal syndrome)
- Pulmonary hypertension (hepatopumonary syndrome)
How is the prognosis of liver cirrhosis graded?
Child-pugh score
Based on albumin, PT, bilirubin, ascites, encephalopathy
Define liver failure
liver dysfunction of healthy liver (acute liver failure) or acute deterioration of chronic liver disease (acute-on-chronic liver failure) leading to
- jaundice (elevated unconjugated bilirubin)
- encephalopathy (reduced ammonia breakdown => BBB to brain)
- coagulapathy (reduced clotting factors/platlets)
How to classify liver failure?
by onset from jaundice to development of encephalopathy
- hyperacute = <7 days
- acute= 1-4 weeks
- subacute = 5+ weeks
Causes of liver failure
- paracetomol overdose
- Viral Hepatitias (A=>E)
- malignancy
- Other: autoimmune hepatitis, Budd-chiari, Wilson’s, Haematochromatosis, poisonous mushrooms, pregnancy
Presenting symptoms of liver failure
- asymptomatic
- non-specific (nausea, jaundice, fever)
Examination findings of liver failure
- ascites
- bruising/ bleeding
- splenomegaly
- pyrexia (infection)
- asterix
- encephalopathy (ataxia, confusion, opthalmoplegia)
- smell of pear drops
- Kaiser-flaeisher rings (Wilson’s)
Investigations for liver failure
Bloods
- FBC- Hb (anaemia), WCC (infection)
- glucose
- LFTs (raised bilirubin/ CCT/ALP/AST/ALT, low albumin)
- U&Es- hepatorenal failure
- ESR/CRP
- Coagulation screen
- ABG
- group and save
Identify cause
- viral serology- hepatitis
- iron studies/Ferritin- Haemotochromatosis
- caeruloplasmin -Wilson’s
- paracetomol levels
- autoantibodies (ANA, AMSA)
Ascitic tap
- Spontaneous bacterial peritonitis (neutrophil >250mmol/L)
- MC&S
- biochemisty (glucose, amylase, albumin)
Imaging
- Liver US/ CT
- Doppler ultrasound - Budd-chiari
EEG- monitor encephalopathy
haemolytic jaundice LFT results
unconjugated bilirubin = increased
conjugated bilirubin = normal
urine urobilinogen = increased
ALT/AST = normal
ALP = normal
hepatic jaundice LFT results
unconjugated bilirubin = increased
conjugated bilirubin = increased
urine urobilinogen = increased
ALT/AST = increased
ALP = normal/mild increase
cholestatic jaundice LFT results
unconjugated bilirubin = normal
conjugated bilirubin = increased
urine urobilinogen = decreased
ALT/AST = normal/mild increase
ALP = increased
Management of liver failure
- RESUS (ABC)- oxygen, fluids, cannula, transfusion?
- Treat cause
- N-acetylsteine for paracetomol overdose
- anti-virals for viral Hepatitis
Treat/ prevent complications
- monitor vitals (vitals, PT, creatinine, pH, urine output)
- encephalopathy (lactulose, phosphate enemas)
- coagulopathy (IV vitamin K, FFP, platelet infusion)
- antibiotic and antifungal prophylaxis
- renal failure (haemodialysis, nutition)
- protect gastric mucosa (PPIs)
- cerebral oedema (mannitol)
- hypoglycaemia treatment
Surgery- Liver transplant
Why do patients with liver failure get cerebral oedema?
- liver doesn’t clear nitrogenous compunds, so astrocytes in clear it which reqiures convert glutamate => glutamine
- Glutamine changes osmotic balance in cells and causes fluid shift to brain cells
- Cerebral oedema (rasied ICP)
What drugs to avoid in liver failure?
- sedatives
- NSAIDs
- opiates
- other drugs metabolised in liver
what is gastrointestinal perforation?
perforation of wall of GIT with spillage of bowel contents into blood
common causes for gastrointestinal perforation
large bowel: diverticultis, colorectal cancer, appendicitis
gastroduodenal: perforated ulcer
small bowel (RARE):trauma, infection, crohn’s
oseophagus: borrhaeve’s perforation
what drugs can increase risk of gastrointestinal perforation?
NSAIDs
steroids
bisphosphonates
presenting symptoms of GI perforation
very UNWELL
shock signs
pyrexia
pallor
dehydration
examination findings of GI perforation
loss of liver dullness (overlying gas)
peritonitis signs:
- guarding
- rigidity
- rebound tenderness
- absent bowel sounds
investigations + findings for GI perforation
- Bloods- FBCs, U&Es (high urea after GI bleed), LFTs
- CXR - air under diaphragm
- AXR- abdominal gas shadowing
- Gatrograffin swallow- if oesophageal perforation
management plan for GI perforation (large bowel/ gastroduodenal/ oesophageal)
immediate:
- IV fluids + electrolytes
- antibiotics (cefuroxime, metronidazole)
surgical:
- for large bowel=> peritoneal lavage + resect perforated section (Hartmann’s procedure)
- for gastroduodenal =>laparotomy, peritoneal lavage and closed with omental patch
- for oesophageal => pleural lavage, repair oesophagus
what is Hartmann’s procedure?
removing the affected section of the bowel and creating an alternative path for faeces to be passed
why are gastric ulcers biopsied?
check for malignancy
prognosis for GI perforation
- large bowel
- gastroduodenal
- high risk of faecal peritonitis if untreated => SEPSIS (death)
- perforated gastric carcinomas have poor prognosis
complications of GI perforation
- peritonitis (large/small bowel)
- shock, sepsis, mediastinitis (oesophagus)
common side effects of metronidazole (antibiotic)
- nausea
- diarrhoea
- metallic taste in mouth
