GI and Liver Flashcards
What should patients with coeliac receive every 5 years?
PCV vaccine due to hyposplenism
What should patients with spontaneous bacterial peritonitis receive?
Abx prophylaxis
Patients with raised platelets and nausea need what?
Non urgent referral for endoscopy
Management of patient with suspected upper GI bleed?
endoscopy within 24 hours of admission
What is the treatment of wilsons?
Penicillamine
Sudden onset severe abdo pain with vomiting and rapid bloody diarrhoea?
Acute mesenteric ischaemia
Raised transferrin and ferritin with low TIBC suggests what?
Haemochromatosis
Sudden onset abdo pain in someone with peptic ulcer disease?
Perforated peptic ulcer
How are perforated peptic ulcers managed?
- Erect CXR which shows free air under diaphragm
- Refer to general surgery
Tx of C diff?
- Oral vancomycin for 10 days
- If reoccurs: oral fidaxomicin
Anti-mitochondrial antibodies suggest what?
Primary Biliary Cholangitis
First line medication for PBC?
Ursodeoxycholic acid
What is associated with UC?
Primary sclerosing cholangitis
Investigation of choice for suspected pancreatic cancer?
High resolution CT
Management of liver abscess?
Percutaneous drainage with IV Abx - usually amoxicillin, ciprofloxacin and metronidazole
Vomiting followed by severe chest pain and signs of shock?
Oesophageal rupture (Boerhaave syndrome)
What cancer is associated with PSC patients?
Cholangiocarcinoma
What does pernicious anaemia predispose to?
Gastric carcinoma
Management of C diff if symptoms still ongoing after 10 days?
Oral vancomycin and IV Metronidazole
What should be measured to monitor treatment of haemachromatosis?
Transferrin saturation and serum ferritin
Management of haemachromatosis?
- Venesection
- Desferrioxamine
What should be given to patients with suspected variceal bleeding before endoscopy?
Terlipressin
Coeliac disease increased risk of which cancer?
enteropathy associated T cell lymphoma of small intestine
Diarrhoea with greasy stools in swimming pool user?
Giardia lamblia
What is SAAG (serum ascites-albumin gradient) used to measure?
- Portal HTN
- If >11, then portal HTN
How is dyspepsia managed?
- Trial of PPI for 1 month OR test and treatH pylori
- If either is unsuccessful, try the other approach
What are patients with haemochromatosis at risk of?
Hepatocellular carcinoma -> screening with US needed
sweet and fecal breath is indicative of what?
Liver failure
When should PPIs be stopped before upper GI endoscopy?
2 weeks before
Which artery is most likely to be the source of bleeding for someone with peptic ulcer disease?
Gastroduoedenal artery
Tenesmus is generally associated with which IBD?
Ulcerative Colitis
Crohn’s Disease
N – No blood or mucus (PR bleeding is less common)
E – Entire gastrointestinal tract affected (from mouth to anus)
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor
Other
- Terminal ileum
- Ulcer, cobblestone appearance
- Non-caseating granulomas
Ulcerative Colitis
C – Continuous inflammation
L – Limited to the colon and rectum
O – Only superficial mucosa affected
S – Smoking may be protective (ulcerative colitis is less common in smokers)
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis
What is the histology of UC?
- Large bowel
- Mucosal involvement only
- Crypt abscess, reduced goblet cells and no granulomas
- Continuous inflammation
- Pseudo polyps and ulcers may form
What is the histology of Crohns?
- Entire GI tract affected
- Transmural inflammation
- Non-caseating granulomas
- Discontinuous inflammation (skip lesions)
- Cobblestone appearance: fissures and deep ulcers
- Fistula formation
Diarrhoea, fatigue, osteomalacia?
Coeliac disease
What is carcinoid syndrome?
A condition usually when metastases are in the liver and then release serotonin into circulation
How does carcinoid syndrome present?
- Flushing
- Diarrhoea
- Bronchospasm
- Hypotension
- urinary 5-HIAA should be measured with ocreotide to treat
What is a key intervention in patients with asictes?
Restrict dietary sodium
Management of Barret’s?
High dose PPI + endoscopic surveillance
What should be avoided in patients with severe colitis?
Endoscopy -> risk of perforation -> use flexible sigmoidoscopy instead
What are the red flags for GI cancer?
new-onset dyspepsia in a patient aged >55 years
unexplained persistent vomiting
unexplained weight-loss
progressively worsening dysphagia/
odynophagia
epigastric pain
fatigue, erectile dysfunction and arthralgia?
Haemochromatosis
How can haemochromatosis present?
- Bronze skin
- Diabetes
- Liver disease
- Cardiac failure secondary to dilated cardiomyopathy
- Arthritis
signet ring cells are indicative of?
Gastric adenocarcinoma
How does achalasia present?
- Dysphagia of liquids and solids
- Heartburn
- Regurgitation of food
How is achalasia investigated?
- Gold standard: Oesophageal manometry which shows excessive lower oesophageal sphincter tone
- Barium swallow shows bird’s beak appearance
How is achalasia managed?
- Pneumatic balloon dilation
- Surgical intervention: Heller cardiomyotomy
What sign may be seen in pancreatic cancer?
Double duct sign -> dilated common bile duct and dilated pancreatic duct
What does Riglers sign indicate?
- Gas in the peritoneal cavity: sign of perforation
How should gallstones be managed?
If asymptomatic and in the gallbladder, no treatment needed
If in the common bile duct, surgery should be considered
If symptomatic, surgery
What is acute mesenteric ischaemia?
Occlusion of an artery supplying the small bowel, usually superior mesenteric artery
History of AF is common
Sudden-onset, severe pain with normal examination
How does acute mesenteric ischaemic be managed?
- Test serum lactate which will be raised
- Urgent surgery needed: immediate laporotomy
Severe abdo pain, sudden onset and out-of-keeping with exam findings?
Acute mesenteric ischaemia
What is ischaemic colitis?
Occlusion of blood flow to the large bowel resulting in inflammation, ulceration and haemorrhage. Acute but transient.
Where is ischaemic colitis most likely to occur?
Splenic flexure.
(watershed areas such as splenic flexure located at borders of the territory supplied by superior and inferior mesenteric arteries.
How will ischaemic colitis be managed?
Abdo X ray - thumbprinting seen
Supportive treatment, surgery if severe
Indications for surgery in ischaemic colitis?
- generalised peritonitis
- perforation
- ongoing haemorrhage
Ix for ischaemic colitis?
abdo x-ray= ‘thumbprinting’ due to mucosal oedema/haemorrhage
How should a severe flare of UC be treated?
IV corticosteroids
Iron defiency anaemia vs. anaemia of chronic disease
TIBC is high in iron deficiency but low/normal in chronic disease
Think of TIBC as the amount of space in the body to store iron: this will be high in iron deficiency as no iron
What should be given alongside isoniazid to prevent peripheral neuropathy?
Pyridoxine (vitamin B6)
T2DM with abnormal LFTs
NAFLD
What blood test can be done alongside incidental findings of NAFLD?
Enhanced liver fibrosis test
Which drugs are used to maintain remission in Crohns?
Azathioprine or mercaptopurine
Mild vs Moderate vs Severe flares of UC
Mild - <4 stools daily with no systemic disturbance
Moderate - 4-6 stools per day with minimal systemic disturbance
Severe - >6 stools per day with systemic disturbance
What is a severe complication of IBD flare up?
Toxic megacolon -> abdo X-ray needed
Which scores are used in acute GI bleeds?
- Glasgow Blatchford score to identify who can be managed as outpatient
- Rockall score done after endoscopy to identify risk of rebleeding
Alcohol units formula?
volume (ml) * ABV / 1,000
What can be given as prophylaxis for episodes of hepatic encephalopathy?
Lactulose
Metabolic alkalosis + hypokalaemia
Vomiting
Which tool is used to assess for malnutrition in patients?
MUST - malnutrition universal screening tool
What is small bowel bacterial overgrowth syndrome?
- Excessive bacteria in the small bowel
- Diabetes and Scleroderma are associated with this
- Presents like IBS: abdo pain, diarrhoea, bloating
- Hydrogen breath test to diagnose
- Abx usually rifaximin used to treat alongside correcting cause
severe, colicky post-prandial abdominal pain, weight loss, and an abdominal bruit
Intestinal angina/chronic mesenteric ischaemia
‘intestinal angina’, colickly, intermittent abdo pain with non-specific features?
chronic mesenteric ischaemia (rare clinical diagnosis)
What is alcoholic ketoacidosis?
- Euglycaemic ketoacidosis seen in those who drink alcohol excess
- Presents with metabolic acidosis, elevated ketones but NORMAL/LOW glucose levels
- Tx with IV fluids and thiamine
Which test should be used to test for eradication of H pylori?
Urea breath test
What is the most common cause of inherited colorectal cancer?
HNPCC - hereditary nonpolyposis colorectal cancer
What are aminosalicylates associated with?
Agranulocytosis - check FBC
Pain on swallowing (odynophagia) can be a sign of what?
Oesophageal candida
What is used to determine the severity of the C diff infection?
WCC
Bleeding gums and receding
Scurvy
liver and neurological disease
Wilsons disease
Electrolyte imbalances of refeeding syndrome ?
Hypophosphataemia, hypokalaemia and hypomagnesaemia
Abdominal pain, Bloating and Change in bowel habit
IBS
Cholestasis vs liver damage on bloods?
Liver injury - >10 times increase in ALT and <3 times increase in ALP
Cholestasis - <10 times increase in ALT and >3 times increase in ALP
Which drugs can cause cholestasis?
- COCP
- Abx including flucloxacillin, co-amoxiclav
Coeliac disease is associated with deficiency of what?
iron, folate and vitamin B12 deficiency
Which IBD is associated with gallstones?
Crohns
What is used to assess whether glucocorticoid therapy may be beneficial in alcoholic hepatitis?
Maddreys function - serum bilirubin and prothrombin time
Antinuclear antibodies, anti-smooth muscle antibodies and raised IgG levels
Autoimmune hepatitis
dysphagia, glossitis and iron-deficiency anaemia
Plummer-Vinson syndrome
watery green diarrhoea post cholecystectomy
Bile acid malabsorption -> treat with cholestyramine
What is decreased in Wilsons disease?
serum caeruloplasmin
Haemochromatosis is a cause of what?
Hypogonadotropic hypogonadism
Patients with a suspected GI bleed require what?
OGD within 24 hours
What LFTs can indicate pancreatic cancer?
Cholestatic picture
What is an unreliable indicator of iron stored in the body during illness?
Ferritin -> use transferrin saturation instead
What can be used to differentiate between and upper and lower GI bleed?
Urea levels - high in upper GI bleed
Investigations for PSC?
- US scan
- MRCP
What is used for prophylaxis of oesophageal bleeding?
Propranolol
Management of severe alcoholic hepatitis?
Steroids
Which cancers are associated with HNPCC?
- Colorectal
- Endometrial
- Ovarian
- Pancreatic
What is the treatment of hypophosphatemia?
Intravenous infusion of phosphate polyfusor
Most common organism causing SBP?
Gram negs - E coli, Klebsiella
Management of Dysplasia on biopsy in Barrett’s oesophagus
Endoscopic intervention
What should you test to screen for haemochromatosis?
Transferrin saturation
Psychosis is a complication of what?
Wilsons disease
What is the investigation of choice for perianal fistulae in Crohns?
MRI
Bleeding vs perforated peptic ulcer?
Perforated ulcer should present with signs of peritonitis e.g. abdo pain, distension, guarding
Deranged LFTs and AKI in someone with septic shock?
Think ischaemic hepatitis
Patients allergic to aspirin may also react with what?
Sulfasalazine
What is Richter’s hernia?
A rare hernia which causes a firm, erythematous mass -> often presents with symptoms of strangulation (ischaemia/necrosis over the skin)
What should be given for prophylaxis of variceal bleeds?
Propranolol
Management of SBP
Acute: IV Cefotaxime
Abx prophylaxis if they have ascites: Ciprofloxacin until ascites resolves
Back pain worse on lying down, appetite loss and weight loss
Pancreatic cancer
What is the most common type of oesophageal malignancy in patients with GORD?
Adenocarcinoma
What can cause a wheeze in people with GORD?
Inhalation of small amounts of gastric contents
What is the gold standard investigation for GORD?
Oesophageal pH manometry
What surgery can be done for GORD and what does this do?
Nissen fundoplication - fundus wrapped around the abdo oesophagus to improve strength of the gastro-oesophageal junction
What is a complication of Nissen fundoplication?
Dysphagia from compression of the junction
Examination signs of chronic liver disease
- Clubbing
- Palmar erythema
- Dupuytren’s contracture
- Hepatosplenomegaly
- Ascites
What are complications of liver cirrhosis?
- Encephalopathy
- Sepsis
- SBP
- Ascites
- Varices
What dietary advice would you give someone with ascites?
- Fluid restriction
- Low sodium
Why is lactulose given in encephalopathy?
Reduce number of nitrogen producing bacteria in the gut which contribute to hepatic encephalopathy
Why can anti-EMA antibodies be negative in severe malabsorption in coeliac?
Deficiency in proteins such as IgA
Haematemesis + distended abdomen
Variceal bleeding
What is an indicator of pancreatitis severity?
Hypocalcaemia
What is the most common cause of large bowel obstruction?
Tumour then volvulus/diverticular disease
What do Hepatitis B serology markers mean?
HBSAg - acute infection (if > 6 months then chronic infection)
Anti-HBs - immunity
Anti-HBc - previous/current infeection
Causes of different types of jaundice
Pre - Sickle cell, G6PD, Hereditary spherocytosis
Hepatic - Hepatitis, PBC, PSC, EPV, HCC
Post hepatic - biliary atresia, gallstones, pancreatitis
Stages of liver disease
Steatosis -> Fibrosis/Steatohepatitis -> Cirrhosis
When is liver transplant indicated in liver disease?
In chronic liver disease, patients must have stopped alcohol for atleast 6 months
What are complications of GORD?
- Barret’s
- Adenocarcinoma
- Oesophageal stricture
- Chronic cough
What are complications of UC?
- Colon cancer
- Toxic megacolon
- Bowel perforation
Where does volvulus cause large bowel obstruction?
Sigmoid
What is coffee bean sign indication of?
Sigmoid volvulus
What is the management of sigmoid volvulus?
Stable - rigid sigmoidoscopy with flatus tube insertion
Unstable - Urgent laparotomy
Palpable fullness in the gallbladder with painless jaundice?
Think pancreatic cancer
Fever, abdo pain, cirrhosis and portal HTN?
Think SBP
Hypertrophic pulmonary osteoarthropathy is associated with what?
Squamous cell carcinoma of lung
Achalasia increases the risk of what?
Squamous cell carcinoma of the oesophagus
What is the best way to assess someone response to Hep C treatment?
Viral load
Ongoing jaundice + pain post cholecystectomy?
Gallstone in common bile duct
Management of malignant distal obstructive jaundice due to unresectable pancreatic carcinoma
Biliary stenting
Flu like illness with RUQ pain, tender hepatomegaly and deranged LFTs?
Think Hep A
What would biliary colic blood show?
Everything normal
What should you not do in someone with suspected pancreatitis?
Make them nil by mouth - enteral feeding should be offered
What is the treatment for symptomatic perinala fistulae in Crohn’s?
Oral metronidazole
History of vascular disease and lactic
acidosis
Think mesenteric ischaemia
What is the most sensitive/specific test for pancreatitis?
Lipase
What is the marker of choice to assess liver synthetic function?
INR (prothrombin time)
What are some components of Child-Pugh score?
- Bilirubin
- Albumin
- PT
- Encephalopathy
- Ascites
What should be the first investigation in A+E if someone comes in with pain/vomiting?
Erect CXR to look for pneumoperitoneum suggestive of perforation
What are the components of Glasgow score for pancreatitis?
Pa02
Age > 55
Neutrophils
Calcium < 2
Renal function
Enzymes
Albumin
Sugar
Why is US scan helpful in pancreatitis?
Assess for presence of gallstones
What are the 2 signs of pancreatitis?
Grey Turners - Bruising along flanks suggestive of haemorrhagic pancreatitis (sign of retroperitoneal bleeding)
Cullen - Bruising around umbilicus
Pigmented gallstones are associated with what?
Sickle cell anaemia
pseudomembranous colitis is what?
C diff colitis
What is the treatment for cholecystitis?
IV Abx with laparoscopic cholecystectomy within 1 week of diagnosis
What can be used to manage complex anal fistulae?
Draining seton
What is the most common disease pattern in UC and Crohns?
UC - Proctitis
Crohns - Ileitis
What drugs should be stopped in C diff infection?
Opioids
anorectal pain and a tender lump on the anal margin
Thrombosed haemorrhoids
short incubation period and severe vomiting
Staph aureus gastroenteritis
Which Abx can be used for Campylobacter infection if severe/immunocompromised?
Clarithromycin
Charcot’s triad plus hypotension and confusion
Reynolds pentad
What is necessary before a diagnosis of PBC?
Imaging to exclude a extrahepatic biliary obstruction
Management of acute anal fissues?
Bulk forming laxatives
What is Troisier’s sign?
Enlarged hard left supraclavicular lymph node which indicates metastatic abdo malignancy
What are risk factors for gastric cancer?
- H pylori
- Gastric polyps
- Pernicious anaemia
- Gastric ulceration
What does TNM staging assess?
Size of tumour
Presence of lymph nodes
Evidence of metastases
What is the marker for HCC?
AFP
Surgical procedures for pancreatic cancer?
- Pancreaticoduodenectomy
- Whipples
flu-like symptoms, RUQ pain, tender hepatomegaly and deranged LFTs
Hepatitis A
Hepatitis serology
IgM - acute infection
IgG - chronic infection
Severe hepatitis in a pregnant woman
Hep E
Man returns from trip abroad with maculopapular rash and flu-like illness
Think HIV seroconversion
Undercooked pork?
Hepatitis E
Right-sided tenderness on PR exam
Acute appendicitis
What is the surgery for bilateral/recurrent inguinal hernias?
Laparoscopic repair with mesh
Mesalazine can cause what?
Drug induced pancreatitis
lemon tinge to the skin
Pernicious anaemia
pH < 7.3 at 24 hours post paracetamol overdose?
Liver transplant consideration
periodic acid-Schiff- (PAS-) positive macrophages
Whipples disease
dysphagia, iron deficiency anaemia and glossitis
Plummer Vinson syndrome
What is a TIPS procedure?
Artifical channel within the liver used for variceal bleeding refractory ascites
Major complication is hepatic encephalopathy
severe abdominal pain, ascites and tender hepatomegaly
Budd-Chiari syndrome
Which laxative to prescribe when starting patients on opiates?
Senna
Management of diverticulitis flare?
Oral Abx with admission to hospital if symptoms do not improve within 72 hours
Why give albumin for large volume ascites?
reduce paracentesis-induced circulatory dysfunction and mortality
What is usually normal with acute cholecystitis?
LFT tests
classic epigastric pain which is relieved on sitting forwards
Think chronic pancreatitis
What will AST:ALT ratio be in alcoholic hepatitis?
2:1
caput medusae and splenomegaly in a known alcoholic suggest what?
Portal HTN
Antibodies for PBC
Anti-mitochondrial - most common
Anti-smooth muscle
What does a score of 3 or more on Glasgow criteria suggest for pancreatitis?
May need ITU input
slate-grey skin pigmentation
Haemochromatosis
Diarrhoea after rice?
Bacillus cereus
What are the anti emetics of choice in gastroparesis?
- Metoclopramide
- Domperidone
fever, malaise, abdo pain and rose spots on trunk?
Typhoid fever -> treat with fluids and Ciprofloxacin
Raised ALP and bilirubin suggests what?
Cholestatic picture
What marker is raised in cholangiocarcinoma?
CA19-9
MSH2/MLH1 mutation?
HNPCC
What is the AST:ALT ratio in alcoholic liver disease?
2:1 - AST 2 times higher than ALT
Gastroenteritis incubation periods?
1-6 hours: Staph aureus
12-48 hours: Salmonella, E coli
48-72 hours: Shigella, Campylobacter
>7 days: Giardiasis, Amoebiasis
mural thickening of the colon and the presence of pericolic fat stranding in the sigmoid colon
Diverticular disease
What is the weight loss definition for malnutrition?
Loss of >10% in the last 3-6 months
What should the prothrombin time be in order to qualify for liver transplant?
> 100seconds
First line test for coeliac in GP?
Total IgA and IgA tissue transglutaminase
When should a repeat endoscopy be done after the start of PPI therapy for ulcer?
6-8 weeks
Autoimmune hepatitis antibodies?
Type 1 - ANA, anti-smooth muscle
Type 2 - Anti-LKM-1
What can help to confirm SBP from Ascitic fluid?
Raised neutrophils
triad of vomiting, pain and failed attempts to pass an NG tube
Gastric volvulus
Post prandial vomiting and abdo pain in someone with chronic pancreatitis?
Pancreatic pseudocyst
Blockage where does not cause jaundice?
Cystic duct or gallbladder
ALT/AST in the 10,000s?
Think paracetamol overdose
AST vs ALT
AST - alcohol overdose
ALT - drug overdose/viral hepatitis
Suspected cholecystitis in GP?
Refer to hospital for urgent admission
spiral or comma-shaped gram negative
Campylobacter
Ischaemia to the lower GI tract can result mainly into what 3 conditions?
1) acute mesenteric ischaemia
2) chronic mesenteric ischaemia
3) ischaemic colitis
Mesenteric ischaemia vs ischaemic colitis?
Mesenteric: small bowel (typically), due to embolism, sudden onset, severe symptoms, urgent surgery, high mortality.
Ischaemic colitis: large bowel, multifactorial, transient, less severe symptoms, blood diarrhoea, ‘thumbprinting’, conservative Mx
Both: ischaemia to lower GI tract, abdo pain
Predisposing factors to bowel ischaemia?
age, AF, smoking, HTN, DM, cocaine, other causes of emboli eg. endocarditis, malignancy
What is sometimes seen in young pts following cocaine use?
ischaemic colitis
Typical common features of bowel ischaemia?
abdo pain, rectal bleeding, diarrhoea, fever, elevated WBC associated with lactic acidosis
What do blood for bowel ischaemia show?
Elevated WBC associated with lactic acidosis
Ix for bowel ischaemia?
CT
Boerhaaves syndrome?
spontaneous rupture of oesophagus that occurs as a result of repeated episodes of vomiting; rupture usually left side and distal
CP of Boerhaaves syndrome (spontaneous rupture of oesophagus)?
sudden onset severe chest pain that may complicate (lead to or be accompanied by) severe vomiting
severe sepsis secondary to mediastinitis
Diagnosis of Boerhaaves syndrome (spontaneous rupture of oesophagus)?
CT contrast swallow
Mx of Boerhaaves syndrome (spontaneous rupture of oesophagus)?
thoracotomay and lavage is <12hrs onset; >12hrs then insertion of T tube to create a controlled fistula between oesophagus and skin
delays >24hrs associated with high mortality
Appendicitis?
Acute inflam of appendix (small narrow tube connected to the caecum)
Causes of appendicitis?
- luminal obstruction (50%)
- unknown
Causes of luminal obstruction that may cause appendicitis?
- faceolith (hard mass of faecal matter)
- lymphoid hyperplasia during infection
- impacted stool
- foreign body
- appendiceal/caecal tumour
Appendicitis: luminal obstruction leads to…
distension of appendix due to increased mucus production, bacterial overgrowth and suppurative inflam -> impaired lymphatic and venous drainage from appendix -> eventual ischaemia and necrosis, and potential perforation
Peak incidence of appendicitis?
2nd and 3rd decade of life
Appendicitis can be characterised as what?
Uncomplicated (non-perforating) or complicated (perforating)
Cx resulting from delay or misdiagnosis of appendicitis?
perforation: abscess formation, peritonitis, sepsis, intra-abdo adhesions, bowel obstruction
Do all cases of appendicits result in perforation?
natural progression of acute appendicits results in perforation but some may not follow this course and will resolve spontaneously
CP of appendicitis?
- periumbilical or epigastric pain that worsens and migrates to lower quadrant (McBurneys) over 24-48hrs
- pain aggrevated by movement
- low-grade fever (<38), malaise, anorexia (loss of appetite)
- N&V, constipation or diarrhoea
- may present atypically in very young, elderly or pregancy and anatomical position of appendix may vary CPs
Signs on examination for appendicitis?
- tenderness in right lower quadrant, may be worse on coughing or hopping in children
- abdo distension, guarding, rebound tenderness or percussion tenderness, or absent bowel signs (all may suggest peritonitis eg. if perforation has occured)
- palpable abdo mass (appendix mass or abscess)
- Rovsing’s sign
Mx for suspected appendicits?
- emergency admission: specialist assessment
- Imaging: if uncertain but delays surgery; USS (preg, child, breastfeeding), CT or MRI (if USS non-diagnostic)
- Negative imaging= non-operative Mx if uncomplicated: IV fluids and Abx
- GOLD= laparoscopic appendicectomy; can do explorative laparoscopy if progressive/persistent pain to establish/exclude diagnosis
- or may do percutaneous drainage of appendix abscess
Possible post-op Cx from appendicectomy?
small bowel obstruction, superficial wound infection, intra-abdo abscess, stump leakage, stump appendicitis
What is the site of maximal tenderness in appendicitis called?
McBurney’s point= 2/3rds of way along line drawn from umbilicus to anterior superior iliac spine
3 specific signs for acute appendicitis?
- Rovsing’s sign
- Psoas sign
- Obturator sign
Appendicitis: Rovsing’s sign?
palpation of left lower quadrant increased pain felt in right lower quadrant
Appendicitis: Psoas sign?
passive extension of right thigh with pt in left lateral position elicits pain in right lower quadrant
Appendicitis: Obturator sign?
passive internal rotation of flexed right thigh elicits pain in RLQ
How may appendicitis present in infants and young children?
non-specific abdo pain and anorexia, may appear withdrawn
How may elderly pts present with appendicitis?
minimal pain or fever, may present with acute confusion or shock
How may appendicitis present in pregnancy?
Right upper quadrant pain in later stages of pregnancy (appendix displaced by gravid uterus), N&V may be mistaken for pregnancy symptoms
If anatomical position of appendix is different in non-pregnant pt, where may it lie if they present with: right loin pain and tenderness, positive psoas test; muscular rigidity and tenderness to deep palpation absent (due to protection of overlying caecum)?
Retrocaecal/retrocolic appendix
If anatomical position of appendix is different in non-pregnant pt, where may it lie if they present with: vomiting and diarrhoea (due to irritation of distal ileum)?
pre-ileal and post-ileal appendix
If anatomical position of appendix is different in non-pregnant pt, where may it lie if they present with: suprapubic pain and urinary frequency, diarrhoea and tenesmus may be present due to rectal irritation, adbo tenderness lacking, rectal or vaginal tenderness present on right side; microscopic haematuria and lecuocytes +ve on urine dip?
Subcaecal and pelvic appendix
If anatomical position of appendix is different in non-pregnant pt, where may it lie if they present with: pain in left lower quadrant?
Long appendix with tip inflammation
Ix to exclude alternative cause in suspected appendicitis?
- FBC: neutrophil predominant and leucocytosis
- CRP: raised or normal
- Urine dip: exclude UTI
- Pregnancy test
What pts are most likely to be diagnosed with appendicitis clinically?
thin male
Acute cholecystitis?
Inflamm of gallbladder, usually when gallstone completely obstructs gallbladder neck or cystic duct
Acalculous cholecystitis?
gallbladder inflam without gallstones; 5-14%.
Typically in critically ill people due to combination of RFs resulting in bile stasis (due to gallbladder hypo/dysmotility) or bile thickening (dehydration)
Cause of acalculous cholesystitis?
- unknown, but ?functional cystic duct obstruction often present and associated with bile stasis or thickening
- critically ill pts
- or predisposition to bacterial colonisation of static gallbladder bile.
Without treatment, what happens to pt with acute cholecystitis?
May resolve spontaneously within 1-7days; 25-30% will need surgery
Cx of acute cholecystitis?
- gangrenous cholecystitis (necrosis of gallbladder wall)
- perforation of gallbladder
- biliary peritonitis
- pericholecystic abscess
- fistula (between GB and duodenum)
- Jaundice
- Sepsis
Why may pt with acute cholecystitis develop jaundice?
Due to inflam of adjoining biliary ducts- Mirizzi’s syndrome
CP of acute cholecystitis?
- sudden-onset, constant, severe pain in upper right quadrant, lasting several hrs
- tenderness, with or without guarding, in RUQ
- fever, anorexia, N&V, back or shoulder pain, RUQ mass, +ve murphy’s sign
Mx for all pts with suspected acute cholecystitis?
- admit
- Confirm diagnosis= abdo USS and bloods (WCC, CRP, serum amylase)
- Monitoring (BP, pulse, urine ouput)
- Treatment (IV fluids, Abx, analgesia)
- Surgical assessment= cholecystectomy
Type of pain in acute cholecystitis?
- constant, several hrs; can be shorter if gallstone returns to gallbladder lumen or passes into duodenum
- severe, steady
- may radiate to the back
- referred pain from gallbladder felt in right shoulder or interscapular region
When can pt get referred pain in acute cholecystitis?
Right shoulder or interscapular region
What to ask pt with suspected acute cholecystitis?
previous episodes of gallstones or biliary colic (90% have gallstones); (50% who have had one episode of biliary pain will have another within 12m)
RFs for acute cholecystitis?
- recent illness
- trauma
- female
- age
- obesity
- lower fibre diet
Signs of sepsis?
- acute deterioration in pt with strong suspicion of infection
- extreme pain, mottled skin, fever or reduced core temp, rigors or chills and/or SOB
- non-specific= acutely inwell with normal temp
- severe= evidence of multi-organ dysfunction and shock
Murphy’s sign in acute cholecystitis?
inspiration is inhibited by pain on palpation when hand is positioned along costal margin; unreliable in older pts
Mirizzi’s syndrome? (acute cholecystitis)
Gallstone becomes lodged in neck of gallbladder or cystic duct; leads to compression of common hepatic duct causing bile obstruction -> can lead to jaundice.
Differential diagnosis for acute cholecystitis?
- acute cholangitis
- ACS
- acute pancreatitis
- appendicitis
- GI cancer
- GORD
- hepatitis
- peptic ulcer
- right lower lobe pneumonia
- symptomatic gallstones
LFTs in acute cholecystitis?
typically normal; if deranged may indicate Mirizzi syndrome
Ix for acute cholecystitis?
USS first line
Treatment for acute cholecystitis?
IV Abx + early laparoscopic cholecystectomy within 1w of diagnosis
Conditions associated with biliary stasis or thickening?
sepsis, extensive trauma, burns, major surgery, prolonged fasting
Differential diagnosis for appendicitis?
GI:
- gastroenteritis
- intestinal obstruction
- incarerated inguinal hernia
- intussusception
- malrotation of midgut
- Meckel diverticulum
- Biliary colic and acute cholecystitis
- perforated peptic ulcer
- diverticulitis
- pancreatitis
- IBD, IBS, constipation
Urological:
- right ureteric colic
- right pyleonephritis
- UTI
- urinary retention
- testicular torsion
Gynae:
- ectopic
- ruptured ovarian cyst/torsion
- Mittelschmerz
- PID
- Endometriosis, adenomyosis
- fibroids
Other:
- penumonia
- lumbar discitis
- non specific abdo pain
- mesenteric adenitis
- abdo wall abscess/haematoma
- DKA
- shingles
Acute pancreatitis?
Acute inflam process of pancreas with varying involvement of local tissues or more remote organ systems; may not be possible to identify severity based on CP
Classification of severity of acute pancreatitis?
Mild, moderatley severe, severe, recurrent
Mild acute pancreatitis?
absence of local or systemic Cx or organ failure; uneventful recovery and resolves in first week. MOST COMMON
Moderately severe acute pancreatitis?
local Cx and/or transient organ failure that resolves within 48hrs
Severe acute pancreatitis?
persistent single or multiorgan failure for >48hrs
Recurrent acute pancreatitis?
occurs on more than once occasion with full recovery between episodes
Causes/RFs of acute pancreatitis?
- gallstones or alcohol misuse (75%)
- post-endoscopic procedures
- trauma
- surgery
- hyperglyceridaemia
- hypercalcaemia
- drugs
- chronic pancreatitis
- anatomical disorders
- autoimmune conditions
- pancreatic malignancy
- previous episodes
- FHx
Local Cx of acute pancreatitis?
pancreatic necrosis, pseudocyst, abscess, fistulae, thrombosis, haemorrhage
Systemic Cx of acute pancreatitis?
multiorgan failure and sepsis, AKI, acute resp distress syndrome
CP of acute pancreatitis?
- acute sudden onset upper or generalised abdo pain, may be associated with N&/or V, RFs
- signs of shock, fever, sepsis, abdo tenderness and distension
Mx for suspected acute pancreatitis?
- emergency hospital admission for specialist assessment and Mx
Type of pain in acute pancreatitis?
- severe sudden which becomes constant
- localised to epigastric region, right and/or left UQ
- may radiate to BACK or flanks
- generalised with peritonism if peritonitis present
- may be sudden and sharp if caused by gallstones
- if alcohol related= less abrupt onset and poorly localised
degree of pain does not reflect severity
Signs of shock? eg. in acute pancreatitis
tachycardia, tachypnoea and hypotension
What signs are sometimes associated with complicated haemorrhagic pancreatitis (rare)?
- Cullen’s sign
- Grey-Turners sign
- Fox’s sign
Cullen’s, Grey-Turner’s and Fox’s sign (in acute complicated haemorrhagic pancreatitis)?
Ecchymoses (buish discolouration) around umbilicus (CULLEN’S), the flanks (GREY-TURNER’S) or over inguinal ligament (FOX’S)
Differential diagnosis for acute pancreatitis?
- perforated peptic ulcer
- bowel obstruction
- ischaemic bowel
- ruptured AAA
- ruptured ectopic
- MI
- biliary colic, acute cholecystitis, cholangitis
- gastroenteritis
- viral hepatitis
- appendicitis
Specialist assessment and Mx of acute pancreatitis?
Initial:
- resus with IV fluids (crystalloid, aim for urine output >0.5ml/kg/hr
- sup O2
- IV analgesia
- IV Abx if infected pancreatic necrosis
- early nutritional support: enteral nutrition (parenteral feeding if unable to tolerate oral intake)
Surgical:
- endoscopic retrograde cholangiopancreatography (ERCP) to relieve obstruction within 72hrs onset of symptoms= gallstones & cholangitis, jaundice or common bile duct obstruction
- Cholesystectomy= mild acute gallstone pancreatitis arranged during same addmission or deferred until after resolution of severe AP
- Purcutaneous or endoscopic drainage of pancreatic collections and potential Mx of other Cx eg. debridement of necrotic tissue
Initial specialist Ix for acute pancreatitis?
- Bloods= lipase, amylase, liver and renal function, CRP & ESR
- USS (limited but may detect gallstone); CT or/and MRI
- if not improving or underlying cause known= magnetic resonance cholangiopancreatography (MRCP) and/or endoscopic ultrasonography (EUS)
Should you follow up pt with acute pancreatitis?
If have confirmed diagnosis and been discharged from hospital
- advice and support
- Mx RFs
Pathophysiology of pancreatits?
autodigestion of pancreatic tissue by prematurely activated pancreatic enzymes leading to necrosis
What condition may show Cullen’s sign (periumbilical discolouration) and Grey-Turner’s sign (flank discolouration) but is rare?
Acute pancreatitis
Rare features associated with pancreatitis?
ischaemic (Purtscher) retinopathy: may cause temp or permanent blindness
In acute pancreatitis, 75% of pts have raised amylase (>3times upper limit of normal); this does not colerate with disease severity; but what are other causes of raised amylase?
pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, DKA
Is serum lipase useful in acute pancreatitis?
more sensitive and specific than amylase, has long half-life so useful for late presentations >24hrs
When can diagnosis be made for acute pancreatitis?
1) without imaging if characteristic pain + amylase/lipase >3 times normal level BUT early USS imaging important to assess aetiology (eg. gallstones/biliary obstruction) or contrast-CT
Specific scoring systems for acute pancreatitis?
Glasgow score; Ranson score and APACHE II
Common factors that may indicate severe pancreatitis?
- > 55yrs
- hypocalcaemia
- hyperglycaemia
- hypoxia
- neutrophilia
- elevated LDH and AST
Causes of acute pancreatitis (using mnemonic)?
GET SMASHED
G.allstones
E.thanol
T.rauma
S.teroids
M.umps (& coxsackie B)
A.utoimmune eg. polyarteritis nodosa, SLE
S.corpion venom
H.ypertrigluceridaemia, hypercalcaemia, hypothermia
E.RCP
D.rugs
Drugs that may cause acute pancreatitis?
azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valporate
Acute pancreatitis local Cx: peripancreatic fluid collections?
25%
Located in or near pancreas and lack a wall of granulation or fibrous tissue
May resolve or develop into pseudocysts or abcessess
Most resolve so avoid apiration and drainage and may cause infection
Acute pancreatitis local Cx: psudeocysts?
Result from collection of peripancreatic fluid.
Walled by fibrous or granulation tissue and occurs 4w+ after.
Retrogastric.
75% have persistent mild elevation of amylase
Ix= CT, ERCP and MRI or endoscopic USS
Symptomatic- observe for 12w as 50% resolve
Mx= endoscopic or surgical cystogastrostomy or aspiration
Acute pancreatitis local Cx: pancreatic necrosis?
May invl pancreatic parenchyma and surrounding fat.
Cx linked to extent of necrosis.
Early necrosectomy associated with high mortality rate (so avoid unless really indicated).
Sterile necrosis= Mx conservatively
Acute pancreatitis local Cx: pancreatic abscess?
Intraabdo collection of pus associated with pancreas but absent of necrosis.
As result of infected psudeocyst.
Mx: transgastric drainage or endoscopic drainage
Acute pancreatitis local Cx: haemorrhage?
Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de novo or as result of surgical necrosectomy.
Grey-Turner’s sign.
Alcoholic liver disease covers a spectrum of what conditions?
- alcoholic fatty liver disease
- alcoholic hepatitis
- cirrhosis
Ix for alcoholic liver disease?
- gamma-GT elevated
- AST:ALT is normally >2, a ratio of >3 is suggestive of acute alcoholic hepatitis
Mx for alcoholic hepatitis (alcohol liver disease)?
- Glucocorticoids eg. pred used during acute episodes (determined using Maddrey’s discriminant function-DF calculated using prothrombin time and bilrubin conc)
Cirrhosis?
Progressive liver disease due to chronic inflam of liver, usually over 1-20yrs
What happens in liver cirrhosis?
normal liver structure becomes distorted with regenerative nodules surrounded by diffuse fibrosis, affecting synthetic, metabolic and excretory actions
Types of cirrhosis?
Compensated cirrhosis and decompensated cirrhosis
When does a transition from compensated to decompensated cirrhosis occur in some people?
Due to the development of portal HTN and/or hepatocellular dysfunction
Compensated cirrhosis?
inital largely asymptomatic phase when liver still functions effectively
Decompensated cirrhosis?
symptomatic phase with potentially life-threatening Cx eg. jaundice, ascites, hepatic encephalopathy and/or variceal bleeding
RFs for cirrhosis?
- increased alcohol intake
- hep A & C
- autoimmune liver disease
- hameochromatosis or Wilson’s
- Drug-induced liver injruy
- obsesity and/or DMT2 if also NAFLD and increased risk of advanced liver fibrosis
Cx of cirrhosis?
- malnutrition and frailty
- osteoporosis
- infection & sepsis incl. spontaneous bacterial peritonitis
- jaundice
- ascites
- hepatic encephalopathy
- variceal bleeding
- AKI
- hepatorenal syndrome
- heptatocellular carcinoma
CP of cirrhosis?
- pt has RFs
- non-sepcific= malaise, fatigue, anorexia, weight loss, muscle wasting
- Symptoms of chronic liver disease
- Signs of chronic liver disease
- Abnorm LFTs but may be normal
Symptoms of chronic liver disease eg. in cirrhosis?
abnom bruising, bleeding or itch
Signs of chronic liver disease eg. in cirrhosis?
hepatosplenomegaly, spider naevi, clubbing, palmar erythema, proximal nail bed pallor signs of decompensation eg. jaundice peripheral oedema, ascites or hepatic encephalopathy
Signs of decompensation in cirrhosis?
jaundice, peripheral oedema, ascites, hepatic encephalopathy
Ix for cirrhosis?
- LFTs
- FBC
- albumin
- clotting screen and INR
- Hep B and C serology
- autoantibodies and serum Ig
- Fibrosis-4 (FIB-4) score
- Transient elastography to confirm
What may bloods for liver disease/cirrhosis show?
- LFTs and bloods: low platelet, raised AST:ALT, high bilirubin, low albumin or increased prothrombin time or INR
When to refer pt with ?cirrhosis?
- decompensated liver disease= hospital admi or immediate referral to hepatologist or gastroenterologist
- newly diagnosed following imaging= refer hepato or gastro
- alcohol-related liver disease= specialist alcohol services
- end-stage liver disease= palliative MDT if eg. ongoing alcohol use, irrevsersible disease unsuitable for transplant; 2 unplanned liver admissions in last 6m or heaptocellular ca best appropritate for supportive care
Primary care Mx for cirrhosis?
- info
- ensure under specialist follow up for Mx of underlying cause and monitoring for Cx
- lifestyle advice
- assess malnutrition risk, ?dietician
- osteoporosis risk
- vaccines up to date
- review meds in relation to liver function
- Cx
Are liver blood tests for cirrhosis accurate?
Can be normal.
Can be abnormal due to other conditions eg. acute intercurrent illness, bone marrow disease, haemolysis
When to offer referral for transient elastography (or hepato/gastro if not available) if pt is at risk of cirrhosis?
at risk +
- hep C infection
- increased alcohol intake
- or known-related liver disease
?cirrhosis and known hep B infection?
refer gastro
?cirrhosis and known NAFLD and advanced liver fibrosis (based on elevated non-invasive advanced liver fibrosis risk score)?
Referral for transient elastography or acoustic radiation force impulse elastography to diagnose cirrhosis
?cirrhosis and pt obese and/or DMT2?
do not offer tests to diagnose cirrhosis unless they have NAFLD and advanced liver fibrosis
?cirrhosis in pt with additional liver (eg. PBC, PSC, haemochromatosis, Wilson’s)?
liase with pt’s specialist or refer to heapto/gastro
What if ?cirrhosis but cirrhosis is not diagnosed on initial testing?
ensure retesting for cirrhosis every 2yrs for:
- pt with alcohol-related liver disease
- hep C and not shown response to antivirals
- NAFLD and advanced liver fibrosis
Anal fissure?
tear or ulcer in squamous lining of distal anal canal which causes pain on defecation
How are anal fissures classifed?
- acute= <6w
- chronic= 6w+
- primary= no clear underlying cause
- secondary= clear underlying cause
Underlying causes of anal fissure?
- unknown
- constipation, IBD, STI, colorectal ca
Peak incidence of anal fissure?
15-40yrs; primary uncommon in elderly so warrant further Ix
CP of anal fissure?
- anal pain with defacation, - with or without bright red rectal bleeding
- tearing sensation on passing stool
- anal spasm
External examination of the anus may reveal what if a pt has anal fissure?
linear split in anal mucosa
Examination findings of acute anal fissure?
superficial with well-demarcated edges
Exam finding of chronic anal fissure?
wider and deeper with muscle fibres visible in the base; edges often swollen and a skin tag may be visible at the end of the fissure
Exam findings of primary anal fissure?
posterior midline, but 10% occur anteriorly (esp women)
Exam findings of secondary anal fissure?
irregular outline, multiple or occur laterally
What may be needed if it is difficult to examine for anal fissure eg. if pain or anal spasm; or if diagnosis unclear?
Referral for exam under anaesthesia
Mx of anal fissure?
- refer if serious underlying cause suspected
- dietary and lifestyle advice
- simple analgesia and measures to reduce pain: petroleum jelly lubricatn before defecation
- short course topical anaesthetic if extreme pain on defecation
- persisted 1w+ without improvement= rectal GTN ointment 6-8w
- no improvement after topical GTN= botulinum toxin pr ?surgery (sphincterotomy)
- secondary fissure: refer if serious or TUC
Lifestyle advice for pt with anal fissure?
ensure stools soft and easy to pass (high fibre intake, increased fluid intake); good anal hygiene to aid healing; soak in warm shallow bath
When should adults with primary anal fissure be reviewed?
6-8w
advice to reduce risk of recurrence
refer to general or colorectal surgeon if unhealed
When should specialist advice be sought in children with anal fissure?
if not healed after 2w or sooner if signif pain
Differential diagnosis for anal pain with or without bleeding?
- haemorrhoids
- IBD
- sarcoidosis
- infection eg. TB, HIV, syphilis
- maligancy eg. anal carcinoma or lymphoma
- peri-anal abscess
Ascending cholangitis?
Bacterial infection (typically E.coli) of biliary tree
Most common predisposing factor for ascending cholangitis?
gallstones
Charcot’s triad occurs in 20-50% pts with what?
ascending cholangitis
Ascending cholangitis: Charcot’s triad?
RUQ pain
Fever
Jaundice
Ascending cholangitis: Reyonold’s pentad?
RUQ pain
Fever
Jaundice
+
hypotension and confusion
Feature of ascending cholangitis?
- fever, RUQ pain, jaundice, hypotension, confusion
- raised inflam markers
Ix for ascending cholangitis?
USS first like= bile duct dilation and bile duct stones
Mx for ascending cholangitis?
IV Abx + Endoscopic retrograde cholangiopancreatography (ERCP) after 24-48hrs to relieve any obstruction
Ascites?
Abnormal accumulation of fluid in abdomen
Causes of ascites can be grouped into what?
a gradient of <11g/L or a gradient >11g/L
What does SAAG mean?
Serum-Ascites Albumin Gradient= calculation to determine cause of ascites.
SAAG= Serum Albumin - Ascitic Fluid Albumin
SAAG ≥ 11 g/L meaning in ascites?
ascites is due to portal hypertension
SAAG <11g/L meaning in ascites?
ascites due to causes other than portal hypertension
Causes of ascites with SAAG ≥ 11 g/L (indicates portal hypertension)?
- LIVER DISORDERS (most common)= cirrhosis/alcoholic liver disease; acute liver failure; liver mets
- Cardiac= RHF, constrictive pericarditis
- Other= Budd-Chiari syndrome; portal vein thrombosis; veno-occlusive disease; myoxedema
Causes of ascites with SAAG <11g/L?
- Hypoalbuminaiea= nephrotic S; severe malnutrition eg. Kwashiorkor
- Malignancy= peritoneal carinomatosis
- Infections= TB peritonitis
- Other= pancreatitis; bowel obstruction; biliary ascites; post op lymphatic leak; serositis in connective tissue diseases
Mx for ascites?
- reduce dietary sodium and fluid restriction if sodium <125mmol/L
- aldosterone antagonists eg. spironolactone (and often + loop diuretics)
- drainage if tense ascites (therapeutic abdo paracentesis)
- prophylactic oral ciprofloxacin to reduce risk of spontaneous bacterial peritonitis if cirrhosis + ascites with ascitic protein of 15g/L or less, until ascites has resolved
- transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some pts
Large volume paracentesis for the treatment of ascites requires what?
Albumin ‘cover’; this reduces paracentesis induced circulatory dysfunction and mortality
Paracentesis induced circulatory dysfunction eg. in ascites?
can occur due to large vol paracentesis (>5 litres); associated with high rate of ascited recurrence, hepatorenal syndrome, dilutional hyponatraemia and high mortality
Biliary colic?
Colicky RUQ abdo pain caused by gallstones passing through the biliary tree
RFs for biliary colic and gallstone related disease?
Fat
Female
Fertile (pregnancy)
Forty
DM, crohns, rapid weight loss (eg. weight reduction surgery), drugs
Why is obesity a RF for biliary colic?
enhanced cholesterol synthesis and secretion
Why is female a RF for biliary colic?
oestrogen increases activity of HMG-CoA reductase so gallstones 2-3x more common in women
What drugs are RFs for biliary colic?
fibrates, COCP
Pathophysiology of biliary colic?
occur due to increased cholesterol, decreased bile salts and biliary stasis.
pain occurs due to gallbladder contracting against stone lodged in cystic duct
CP of biliary colic?
- colicky (intermittent, crampy) RUQ pain
- worse postpradnially (after eating, espec fatty foods)
- pain may radiate to right shoulder/interscapular region
- N&V
- NO FEVER and LFTS/INFLAM markers NORMAL: in contrast to other gallstone related conditions
Where may biliary colic pain radiate?
R shoulder and interscapular region
Ix for biliary colic (gallstone disease)?
abdo USS and LFTs
if not detected on USS but high suspecion then MRCP or endoscopic USS (EUS)
Mx for biliary colic (gallstone disease)?
referral for elective laparoscopic cholescystectomy
Why may some pts with gallstones experience ongoing jaundice and pain after cholecystectomy?
gallstones may be in the common bile duct (choledocholithiasis)
Cx of gallstones?
- biliary colic
- acute cholecystitis (common)
- ascending cholangitis
- acute pancreatitis
- gallstone ileus
- gallbladder ca
Choledocholithiasis?
Gallstone in common bile duct
Cholelithiasis?
Gallstones
What is a gallstone (cholelithiasis)?
solid deposit that forms within gallbladder
Gallstone disease?
general term that describes presence of 1+ stones in gallbladder or other parts of the biliary tree, and the symptoms and Cx they may cause
When do gallstones occur?
when there is a problem relating to the chemical composition of bile; can result in precipitation of 1 or more of the constituents
Cholesterol gallstone formation is a result of what 3 defects?
cholesterol supersaturation, accelerated cholesterol crystal nucleation and impaired gallbladder motility
What type of diet is associated with gallstones?
high in triglycerides and refined carbs and low in fibre
What medication is associated with gallstones?
somatostatin analogues, glucagon-like peptide-1 analogues and ceftriaxone
Is treatment needed for pts with asymptomatic gallstones found in normal gallbladder and with a normal biliary tree?
No
When should referral be made for bile duct clearance and laparoscopic cholecystectomy in pt with asymptomatic gallstones?
if gallstones found in the common bile duct
When should urgent referral be made for pt with known gallstones?
known gallstones + jaundice or if suspicion of biliary obstruction eg. signif abnormal LFTs
What to do after referring pt with ?gallstones whilst they are waiting for secondary care assessment for possible surgery?
Analgesia:
severe pain= diclofenac or opioid IM
mild to moderate intermittent pain= paracetamol or NSAIDs
Cholestasis?
blockage to flow of bile
Cholecystitis?
inflam of gallbladder
Cholangitis?
inflam of bile ducts
gallbladder empyema?
pus in gallbladder
cholecystectomy vs cholecystostomy?
cholecystectomy= surgical removal of gallbladder
cholecystostomy= inserting drain into gallbladder
Most gallstones are made from what?
cholesterol
Liver and gallbladder anatomy?
right and left hepatic duct leave liver and join together to form common hepatic duct.
cystic duct from gallbladder joins with common hepatic duct halfway along forming the common bile duct.
pancreatic duct from pancreas joins with common hepatic duct further along
when the common bile duct and pancreatic duct join they become the ampulla of Vater which opens into the duodenum.
Sphincter of Oddi is a ring of muscle surrounding ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum.
Where does bilirubin drain and what does raised bilirubin with pale stools and dark urine represent?
Drains from liver, through bile duct and into intestines/ Raised bilirubin (jaundice) with pale stools and dark urine represents obstruction to flow within the biliary system eg. by a gallstone in bile duct or external mass pressing on bile ducts (eg. cholangiocarcinoma or tumour of head of pancreas.
What is ALP and what does it mean if it is raised?
Alkaline phosphatase.
Non-specific marker.
Enzyme originating in liver, biliary system and bone. Abnormal results indicate liver or bone problems.
Raised= pregnancy (produced by placenta); biliary obstruction; liver or bone malignancy; primary biliary cirrhosis; Paget’s disease of bone.
What is ALT and AST?
Alanine aminotransferase and aspartate aminotransferase.
Enzymes produced in the liver.
Markers of hepatocellular injury (damage to liver cells).
ALT and AST slightly high, with a higher rise in ALP?
obstructive picture eg. gallstones
ALT and AST high compared with ALP?
hepatitic picture (hepatocellular injury)
MRCP (magnetic resonance cholangio-pancreatography)?
MRI scan that produces detailed image of biliary system; very sensitive and specific for biliary tree disease eg. malignancy and stones in bile duct.
Eg. used if USS doesn’t show stones in duct but there is bile duct dilation or raised bilirubin suggestive of obstruction
ERCP (endoscopic retrograde cholangio-pancreatography)?
insert endoscope down oesophagus, past stomach, to duodenum and opening of common bile duct (sphinter of Oddi) to access biliary system.
Indication= clear stones in bule ducts
Coeliac disease?
chronic immune mediated systemic disorder in genetically predisposed people, triggered by exposure to dietary gluten.
What is gluten?
major complex protein component of wheat, barley and rye
Non-responsive coeliac disease?
persistent symptoms and enteropathy that do not respond after 6-12m on self-reported gluten-free diet
Refractory coeliac disease?
persistent or recurrent symptoms and villous atrophy on duodenal biopsy, despite strict adherence to gluten-free diet for at least 12m
Cx of undiagnosed, untreated or undertreated coeliac disease?
Reduced QOL; faltering growth in children; nutritonal def incl. anaemia; reduced BMD; hyposplenism; malignancy; refractory coeliac disease
What malignancy are pts with undiagnosed, untreated or undertreated coeliac diease at higher risk for?
Lymphoma and small bowel adenocarcinoma
Conditions associated with coeliac disease?
- DMT1
- autoimmune thyroid disease
- autoimmune liver disease
- selective IgA def
- first degree relative affected
When to suspect coeliac disease?
persistent unexplained GI symptoms; IBS; faltering growth, short stature or delayed puberty in children; prolonged fatigue; persistent or recurrent mouth ulcers; unexplained iron, vit B12 or folate def; suspected dematitis herpetiformis; DMT1; selective IgA def
Consider coeliac disease in pt with what?
- unexplained dep or anxiety
- osteromalacia, penia or porosis, or fragility fractures
- unexplained peripheral nueropathy, ataxia; recurrent miscarriage or subfertility; persitently raised liver transaminases (mild elevation of ALT and AST)
- dental enamel defects
- hyposplenism or asplenia
- Down’s, Turner or William’s syndrome
Ix for coeliac disease?
- height, weight, abdo exam and skin
- Coeliac serology testing
- Gastro referral for endoscopic intestinal biopsy (duodenal biopsy) if serology suggests possible diagnosis
- If serology -ve but high clinical suspicion: consider referral
What should pt do before coeliac serology testing?
ensure eaten gluten-containing foods for min 6w before testing
Mx for coeliac disease?
- education and supporrt
- long-term gluten free diet
What to assess for in pts with coeliac disease?
- persistent or recurrent symptoms despite adherence
- growth and nutritional statis
- osteoporosis risk and ?DEXA scan
- nutrient def incl. annual blood monitoring
- Cx or associated conditions
- referral to dietitian to check dietary adherence and advise on deficiencies
When to refer pt with coeliac disease to appropriate specialist?
if non-responsive or refractory disease or serious Cx
What to give coeliac pts who have hyposplenism?
influenza, meningococcal and pneumococcal immunisation (P booster every 5yrs)
Signs and symptoms of coeliac disease are what?
non-specific and may present with intestinal and extra-intestinal manifestations or be asymptomatic.
CP of coeliac disease?
- Persistent unexplained GI symptoms eg. acid reflux, diarrhoea, steatorrhoea, weight loss, abdo pain, reduced appetite, bloating, constipation
- Prolonged fatigue
- Aphthous ulcers: persistent or recurrent
- Suspected dermatitis herpetiformis
Dermatitis herpetiformis?
immune mediated cutaneous manifestation of coeliac disease.
Symmetrical clusters of itchy blistering skin lesions followed by erosions, excoriations and hyperpigmentation; common on elbows, knees, shoulders, face, sacrum and buttocks.
2 possible extra-intestinal manifestations of coeliac disease?
Aphthous ulcers
Dermatitis herpetiformis
Coeliac serology testing?
1st= total IgA and IgA tissue transglutaminase (tTGA)
2nd line if IgA tTGA unavailable or weakly +ve= anti-EMA antibodies (serum IgA endomysial antibody)
Equivocal coeliac serology result?
- adults= if IgA and tTGA equivocal do anti-EMA antibodies
- children= refer to paeds gastro
Negative coeliac serology test result?
- IgA, tTGA or IgA EMA negative then check for IgA deficiency
- if def present= will cause false-negative IgA
- if IgA tTGA negative and IgA normal then truly negative and coeliac disease unlikely at present; doesn’t rule out it developing in fututre
- strongly suggested but negative= referral
Differential diagnosis for coeliac disease?
- infective gastroenteritis
- non-coeliac gluten sensitivity
- food allergy eg. wheat or cows milk
- AIDS enteropathy
- crohns
- IBS
- diverticular disease
- malignancy
- lactose intolerance
- pancreatic exocrine insufficiency
- peptic ulcer disease
Annual blood monitoring for coeliac disease (consider)?
- coeliac serology (adherence)
- FBC & ferritin
- TFTs
- LFTs
- calcium, vit D, vit B12 and folate
Gluten-free dietary advice?
avoid..
- foods based on wheat, barley and rye eg. cereals, bread, flour, pasta, cakes, biscuits, pasteries
- foods that may contain it as fillers or flavouring eg. sausages, ready meals, soups, sauces
- ?contaminated with gluten during packaging eg. oats, chips- that fried in same as battered fish
- items that contain malt eg. beers
- food labelled: gluten free, very low gluten or crossed grain symbol can be eaten
- avoid risk of cross-contamination at home, travelling, eating out
- alternative sources of starch eg. corn, rice, potatoes
In coeliac disease, repeated exposure to gluten causes what?
villous atrophy which causes malabsorption
Genetic association in coeliac disease?
HLA-DQ2 and DQ8
What does duodenal biopsy +ve for coeliac disease show?
- villous atrophy
- crypt hyperplasia
- increase in intraepithelial lymphocytes
- lamina propria infiltration with lymphocytes
When do children normally present with coeliac disease?
before age of 3 eg. following introduction of cereals into diet.
Failure to thrive, diarrhoea, abdo distension.
Many cases not diagnosed till adulthood.
Does villous atrophy and immunology in coeliac disease reverse on a gluten free diet?
Yes
Diverticula?
sac-like protrusions of mucosa through muscular wall of colon
Diverticula occur where in around 80% of people >85yrs?
sigmoid colon
Diverticulum formation may be associated with what?
low-fibre diet
Majority of people with diverticula have symptoms where?
Left lower abdo.
Minority eg. Asian may be sided sided.
Diverticulosis?
Condition where diverticula are present without symptoms.
What may diverticulosis present with?
Large, painless rectal bleed or found incidentally during Ix for other symptoms.
Diverticular disease?
Condition where diverticula cause symptoms eg. intermittent lower abdo pain, without inflammation and infection.
Diverticulitis?
Condition where diverticula become inflamed and infected.
Diverticulitis CP?
intermittent lower left quadrant abdo pain, fever, malaise, change in bowel habit and occasionally rectal bleeding
Uncomplicated diverticulitis?
Diverticular inflam that does not extend to the peritoneum
Complicated diverticulitis?
diverticulitis associated with Cx such as abscess, peritonitis, fistula, obstruction or perforation
Risk of diverticula increases with…
age
rare <40yrs
Mx for confirmed diverticulosis?
- bulk forming laxatives if constipation
- balanced high fibre diet
- exercise, stop smoking
Mx for diverticular disease?
- urgent admission if signif rectal bleeding
- avoid NSAIDs and opiods eg. codeine
- advice on diet, lifestyle, fluid intake, stop smoking, exercise
- bulk-forming laxatives, simple analgesia or antispasmodic eg. mebeverine
- reassess if persistent or don’t respons
Mx for acute diverticulitis and uncontrollable pain with any features of complicated acute diverticulitis?
Urgent hospital admission: IV Abx, fluid replacement and analgesia.
Urgent surgery if don’t improve or elective if recurrent.
Mx for uncomplicated diverticulitis?
- oral Abx if systemically unwell
- systemically well= no Abx
- analgesia
- re-present if persist or worsen
- referral to secondary care if symptoms persist or deteriorate
- specialist referral to colorectal surgery if frequent or severe recurrent episodes of acute diverticulitis
When to suspect a Cx of diverticulitis?
uncontrolled abdo pain with…
- abdo mass or peri-rectal fullness on PR (intra-abdo abscess)
- abdo rigidity, guarding, rebound tenderness (perforation & perionitis)
- altered mental state, raised resp rate, low SBP, tachy, low temp, no urine output or skin discolouration (sepsis)
- faecaluria, pneumaturia, pyruia or passage of faseces through vagina (colovesical fistula)
- colicky abdo pain, absolute contstipation, vomiting or abdo distension (intestinal obstruction)
Ix for diverticular disease?
- abdo exam; possible pelvic and digital rectal
- referral for imaging or endoscopy to confirm if appropritate
- Consider= FBC; faecal occult blood test; U&E; Kidney function; urinalysis; CRP
Example of an antispasmodic?
mebeverine
Oral Abx for acute uncomplicated diverticulitis if systemically unwell?
co-amoxiclav 500/125mg 3x daily for 5d
or cefalexin 500mg twice daily for 5d
Surgical opitions for acute complicated diverticulitis who don’t respond to medical Mx?
- percut drainage of large abscess
- laparoscopic lavage
- simple colostomy formation
- sigmoid resection with colostomy (Hartmann’s procedure)
- Sigmoid resection with primary anastomosis with or without a diverting stoma
What is a diverticula and where is the usual sight? (histologically)
herniation of colonic mucosa through muscular wall of colon
usual site is between taenia coli where vessels pierce the muscle to supply the mucosa; for this reason, the rectum (lack taenia) is often spared
Specialist Ix for diverticular disease?
- colonoscopy, CT cologram or barium enema= all can identify diverticular disease
- Acutely unwell= plain abdo film and erect CXR to identify perforation; contrast CT abdo and pelvis= to identify acute inflam and presence of local Cx eg. abscess formation
Peptic ulcer disease includes what?
Gastric or duodenal ulcers
Peptic ulcer disease?
breach in the epithelium of gastric or duodenal mucosa, which is confirmed on endoscopy
Most common RFs for development of peptic ulcer disease?
Helicobacter pylori infection and NSAIDs/aspirin
Cx of peptic ulcer disease?
haemorrhage, perforation, gastric outlet obstruction
Ix of peptic ulcer disease?
- H.pylori test
Mx of peptic ulcer disease?
- lifestyle advice, review meds and assess for stress, anx & dep
- H.pylori +ve= full dose PPI 2m + H.pylori eradication therapy
- H.pylori -ve= full dose PPI 4-8w
If proven gastric ulcer then repeat endoscopy and H.pylori test 6-8w later
- +ve= second line H.pylori eradication
- stop NSAIDs or aspirin
- low dose PPI or standard-dose histamine (H2)-receptor antagonist as needed
- can consider long-term acid suppression
Pt on long-term Mx for peptic ulcer disease should be…
- offered annual review
- encouraged to step down or stop treatment if possible
Potential peptic ulcer inducing drugs?
aspirin, NSAIDs, bisphosphonates, corticosteroids, SSRIs, potassium supplements, cocaine
When to consider referral to gastro for peptic ulcer disease?
- refractory or recurrent symptoms despite Mx
- unsuccessful second-line H.pylori erradication regimen
- limited Abx options for H.pylori eradication therapy
- proven gastric ulcer has not healed on repeat endoscopy
- non-peptic cause of ulcer disease suspected
H.pylori test?
carbon-13 ura breath test or stool antigen test
What should pt do before H.pylori test?
do not take PPI 2w before or Abx 4w before
H.pylori eradication therapy?
Triple therapy 7d:
1) PPI: lansoprazole 30mg twice daily
2) Amoxicillin 1g twice daily
3) Clarithromycin 500mg or metronidazole 400mg twice daily
allergic then PPI + clarithro + metron
2nd line therapy= use the Abx that wasn’t used 1st
Peptic ulcer perforation CP?
- sudden epigastric pain, later more generalised
- syncope
Ix for peptic ulcer perforation?
erect CXR if present with acute upper abdo pain= free air under diaphragm
Haemorrhoids? (piles)
abnormally swollen vascular mucosal cushions in anal canal
How are haemorrhoids classified?
internal or external depending on their origin in relation to dentate line
Where is the dentate line?
2cm from anal verge and marks the transition between the upper and lower anal canal
External haemorrhoids?
originate below the dentate line and covered by modified squamous epithelium (anoderm) which is richly innervated with pain fibres
Internal haemorrhoids?
arise above dentate line and covered by columnar epithelium, which have no pain fibres.
What haemorrhoids are itchy and painful?
external
What haemorrhoids are not sensitive to touch, temp or pain (unless become strangulated)?
internal
Internal haemorrhoids are further graded by degree of prolapse, what is 1st-4th degree?
1st degree= projects into lumen of anal canal but do not prolapse
2nd= prolapse on straining but reduce spontaneously when straining stopped
3rd= prolapse on straining and require manual reduction
4th= prolapsed and incarcerated and cannot be reduced
Factors thought to contribute to the development of haemorrhoids?
constipation
straining while trying to pass stool
ageing
heavy lifting
chronic cough
conditions that cause raised intra-abdo pressure eg. preg, childbirth, space-occupying lesions
Cx of haemorrhoids?
ulceration, skin tags, maceration of perianal skin, ishaemia, thrombosis, gangrene
rare= perianal sepsis and anaemia from bleeding
Potential serious underlying pathology of haemorrhoids?
colorectal ca
CP for haemorrhoids?
- bright red painless rectal bleeding seen as streaks on toilet paper, in toilet bowel and/or outside of stool (NOT MIXED)
- anal itching & irritation
- feeling of rectal fullness, discomfort or incomplete evacuation on bowel movement
- soiling
- anal pain (with prolapsed, strangulated interal H or thrombosed external H)
Mx for haemorrhoids?
- ensure stools soft & easy to pass (increase fibre and fluid intake)
- laxatives if constipated
- advice= minimise straining, good anal hygiene
- simple analgesia and/or topical haemorrhoidal preparations
Admission or referral should be arranged for haemorrhoids if….
- diagnosis unclear
- suspect serious pathology
- severe
- does not respond to conservative Mx
- recurrent
Secondary care Mx for haemorrhoids?
- non-surgical= rubber band ligation, injection sclerotherapy, infrared coag/photocoagulation, biploar diathermy or direct-current electrotherapy
- surgical= haemorrhoidectomy, stapled haemorrhoidectomy or haemorrhoidal artery ligation
Ix for haemorroids?
- clinical: exam-> inspect perianal area and perform digital rectal exam if possible without causing pain
- rigid anoscope, proctoscope or rectoscope can be used to diagnose, classify and exclude sinister pathology
What analgesia to avoid in haemorrhoids?
- opioids as cause constipation
- NSAIDs if rectal bleeding
Differential diagnosis of haemorrhoids?
- adenomatous polyps
- anal fissure
- anal or colorectal ca
- rectal prolapse
- STI
- diverticular disease
- anorectal fistula
- IBD
- perianal abscess
- portal hypertension
Haemorrhoidal tissue is part of normal anatomy that contributes to anal continence, where are these mucosal vascular cushions found?
left lateral, right posterior and right anterior portions of anal canal (3, 7 and 11 oclock)
haemorrhoids said to exist when become enlarged, congested and symptomatic
What haemorrhoids are prone to thrombosis?
external
Acutely thrombosed external haemorrhoids?
signif pain and tender lump; purplish, oedematous, tender subcut perianal mass.
if present <72hrs then referal to consider excision; otherwise use stool softeners, ice packs and analgesia; symptoms settle within 10d
Hernia?
protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains it
RFs for abdo wall hernias?
- obesity
- ascites
- ageing
- surgical wounds
Features of abdo wall hernias?
- palpable lump
- cough impulse
- pain
- obstruction (common in femoral hernias)
- strangulation: may compromise bowel blood supply -> infarction
Types of abdo wall hernias? (9)
1) inguinal hernia
2) femoral
3) umbilical
4) paraumbilical
5) epigastric
6) incisional
7) spifelian
8) obturator
9) richter
Types of abdo wall hernias in children? (2)
1) congenital inguinal hernia
2) infantile umbilical hernia
Abdo wall hernia: inguinal?
75% of abdo wall hernias.
95% male. Men have 25% risk of developing.
Above and medial to pubic tubercle; strangulation is rare.
Abdo wall hernia: femoral hernia?
Below and lateral to pubic tubercle.
More common in women, espec multiparous ones.
High risk of obstruction and strangulation/
Surgical repair required.
Abdo wall hernia: umbilical?
Symmetrical bulge under umbilicus.
Abdo wall hernia: paraumbilical?
asymmetrical bulge- half the sac is covered by skin of abdo directly above or below umbilicus
Abdo wall hernia: epigastric?
lump in midline between umbilicus and the xiphisternum.
RFs= extensive physical training, coughing (from lung diseases) or obesity
Abdo wall hernia: incisional?
may occur in up to 10% abdo surgery
Abdo wall hernia: Spigelian?
AKA lateral ventral hernia.
Older pts.
Rare.
Hernia though the spigelian fascia (aponeurotic layer between rectus abdominis muscle medially and semilunar line laterally).
Abdo wall hernia: obturator?
hernia which passes through obturator faroamen.
more common in females.
Typically presents with bowel obstruction.
Abdo wall hernia: Richter hernia?
rare
only antimesenteric border of the bowel herniates through the fascial defect.
Can present with strangulation WITHOUT symptoms of obstruction
Abdo wall hernia: congenital inguinal hernia?
Indirect hernia resulting from a patent processus vaginalis.
1% term babies; more common in premature babies and boys.
60% R sided, 10% bilateral.
SURGICALLY REPAIR soon after diagnosis as at risk of incarceration.
Abdo wall hernia: infantile umbilical hernia?
Symmetrical bulge under umbilicus.
More common in premature and Afro-Caribbean babies.
Vast majority RESOLVE without intervention BEFORE 4-5yrs.
Cx rare.
When do femoral hernias occur?
When section of bowel or any other part of abdo viscera pass into femoral canal.
Why can you get femoral hernias?
It is usually densely packed area of the anterior thigh but it is a potential space that can become occupied by herniated contents via the femoral ring.
Features of femoral hernia?
- lump within groin
- mildly painful
- important to distinguish from inguinal
- typically non-reducible; can be reducible in minority
- cough impulse ABSENT due to small size of femoral ring
Distinguish between femoral and inguinal hernia?
femoral= inferolateral to pubic tubercle
inguinal= supermedial to pubic tubercle
Ix for femoral hernia?
- Diagnosis clinical, can use USS
Important differentials to exclude for femoral hernias?
- lymphadenpathy
- abscess
- femoral artery aneurysm
- hydroccoele or varicocele in men
- lipoma
- inguinal hernia
Cx of femoral hernia?
- incarceration (herniated tissue can’t be reduced)
- STRANGULATION= emergency; tender, non-reducible; systemically unwell; increased risk as time from diagnosis rises and more likely than inguinal
- bowel obstruction= emergency
- bowel ischaemia and rescection -> high morbidity and mortality
Mx for femoral hernia?
- surgical remair NECESSITY due to risk of strangulation= laparoscopically or via laparotomy
- hernia support belts/trusses should NOT be used as risk of strangulation
Features of inguinal hernia?
- groin lump superior and medial to pubic tubercle
- disappears on pressure or when lying down
- discomfort and ache: worse with activity but severe pain uncommon
- strangulation RARE
Indirect vs direct inguinal hernia?
Indirect= hernia through inguinal canal
Direct= through posterior wall of the inguinal canal
Mx for inguinal hernia
treat medically fit pts even if asymptomatic
- mesh repair= open approach if unilateral; laparoscopic if bilateral or recurrent
- hernia truss if not fit for surgery
Following open or laparoscopic mesh repair for inguinal hernia, how long before pt can return to work?
open= 2-3w
L= 1-2w
Cx of inguinal hernia repair?
early= bruising, wound infection
late= chronic pain, recurrence
What does it mean if a hernia is reducible?
herniated tissue can be pushed back into place in abdo through the defect using a hand
What is a hernia that cannot be reduced referred to as?
Incarcerated hernia:
painless but at risk of strangulation
Strangulation of a hernia?
Surgical emergency where blood supply to herniated tissue compromised -> ischaemia or necrosis
What can a strangulated inguinal hernia (1/500) lead to?
permanent loss or perforation of bowel tissue as most inguinal hernias are formed from small bowel
Indications that a hernia is at risk of strangulation?
- episodes of pain in a hernia that was previously asymptomatic
- irreducible hernia
CP of strangulated hernias?
pain; fever; increase in size of hernia or erythema of overlying skin; peritonitic features (guarding, tenderness); bowel obstruction (distension, N&V); bowel ischameia (bloody stools)
Is imaging necessary for strangulated hernia?
NO.
But if obstruction suspected: abdo x-ray or CT. Perforation suspected then erect CXR.
FBC and ABG= leukocytosis and raised lactate
What is it not recommended to do whilst waiting for surgery for strangulated hernia?
DO NOT manually reduce strangulated hernias as can cause more generalised peritonitis/
Mx for strangulated hernia?
immediate surgery= open or laparoscopic with mesh technique (like elective hernia repair) but also remove any dead bowel
Hiatus hernia?
herniation of part of the stomach above the diaphragm
2 types of hiatus hernia?
sliding and rolling
Sliding hiatus hernia?
95%
gastroesophageal junction moves above the diaphragm
Rolling (paraoesophageal) hiatus hernia?
gastroesophageal function remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
RFs for hiatus hernia?
obesity
increased intraabdo pressure eg. ascites, multiparity
Features of hiatus hernia?
heartburn
dysphagia
regurgitation
chest pain
Ix for hiatus hernia?
GOLD= barium swallow most sensitive
but due to the CP
most have endoscopy 1st line and hiatus hernia found incidentally
Mx for hiatus hernia?
- conservative eg. weight loss
- medical: PPI
- surgical: only in symptomatic paraesophageal hernias
Causes of hypospenism?
splenectomy
sickle-cell
coeliac
dermatitis herpetiformis
Grave’s
SLE
amyloid
2 features of hyposplenism?
Howell-Jolly bodies and Siderocytes on blood film
What does the loss of splenic tissue following splenectomy result in?
inability to readily remove immature or abnorm RBCs from circulation; RBC count doesn’t alter signif but cytoplasmic inclusions may be seen eg. Howell-Jolly bodies
What happens in the first few days after splenectomy and also immediately following?
Immediately= a granulocytosis (mainly composed of neutrophils) is seeen and this is replaced by a lymphocytosis and monocytosis over the following weeks.
First few days after= target cells, siderocytes and reticulocytes will appear in circulation
Hyposplenism can result from splenic atrophy due to what?
certain conditions or interventions eg. splenic artery embolisation and splenectomy
Most sensitive diagnostic test for hyposplenism?
Radionucleotide-labelled red cell scan (Howell-Jolly bodies not fully reliable)
Risks associated with hyposplenism?
signif increases risk of post-splenectomy sepsis, espec from encapsulated organsims
due to spleen’s role in detecting and responding to these pathogens
What is crucial for prevention for post-splenectomy sepsis?
Vaccination and Abx prophylaxis.
Asplenic pts should also use medical and mechanical protection when travelling to malaria-endemic areas.
Vaccination schedule used to prevent post-splenectomy sepsis?
- Men C and Hib at 2w post splenectomy (or 2w prior if elective)
- MenACWY one month later
- children <2yrs may need booster
- Pneumococcal vaccine every 5yrs
- Annual influenza
Abx prophylaxis for the prevention of post-splenectomy sepsis?
Penicillin V at least 2yrs and at least until pt is 16yrs. Majority usually for life.
Following splenectomy, pts are at particular risk from what infections?
pneumococcus, Haemophilus, meningococcus and Capnocytophaga canimorsus (dog bites)
Indications for splenectomy?
- trauma: 1/4 iatrogenic
- spontaneous rupture: EBV
- hypersplenism
- malignancy: lymphome or leukaemia
- splenic cysts, hydatid cysts, splenic abscesses
2 causes of hypersplenism?
hereditary spherocytosis or elliptocytosis
Elective splenectomy?
spleen often large
Most laparoscopic
Spleen will be macerated inside a specimen bag to facilitate extraction
Prophylactic aspirin
Cx of splenectomy?
- haemorrhage (from short gastrics or splenic hilar vessels)
- pancreatic fistula (from iatrogenic damage to pancreatic tail)
- thromocytosis (so prophy aspirin)
- Encapsulated bacteria infection eg. strep. pnuemoniae, H. influenzae and Neisseria meningitidis
Post-splenectomy changes?
- platelets will rise first (so ITP given after splenic artery clamped)
- blood film will change over weeks, Howell-Jolly bodies appear
- other blood film changes: target cells and Pappenheimer bodies
- increased risk of post-splenectomy sepsis
Campylobacter?
Commonest bacterial cause of infectious intestinal disease
What is campylobacter infection caused by?
Gram negative baciluus Campylobacter jejuni
How is campylobacter spead and incubation period?
faecal-oral route
1-6 days
Features of campylobacter infection?
- prodrome= headache, malaise
- diarrhoea= often bloody
- abdo pain= may mimic appendicitis
Mx for campylobacter infection?
- self-limiting
- Abx if immunocompromised or severe: high fever, bloody diarrhoea, >8 stools per day, lasted >1w
clarithromycin first line
Cx of campylobacter infection?
- Guillain-Bare
- Reactive arthritis
- Septicaemia, endocarditis, arthritis
What type of bacteria is Clostridioides difficile?
Anaerobic gram positive rod, spore-forming, toxin-producing bacillus
What does c.diff produce?
an exotoxin which causes intestinal damage leading to pseudomembranous colitis
When does C.difficile develop?
when normal gut flora are suppressed by broad-spectrum Abx
What causes C.difficile?
- 2nd & 3rd gen cephalosporins (main)
- clindamycin
- PPI
What is characteristic in c.diff?
raised WCC
Pathophysiology of c.diff?
releases 2 exotoxins (toxin A and B) that act on intestinal epithelial cells and inflam cells resulting in colitis
How is c.diff transmitted?
faecal-oral route by ingestion of spores
Features of c.diff?
- diarrhoea
- abdo pain
- raised WCC
- if severe toxic megacolon may develop
Mild c.diff?
normal WCC
Moderate c.diff?
↑ WCC ( < 15 x 109/L)
Typically 3-5 loose stools per day
Severe c.diff?
↑ WCC ( > 15 x 109/L)
or
an acutely ↑ creatinine (> 50% above baseline)
or
a temperature > 38.5°C
or
evidence of severe colitis(abdominal or radiological signs)
Life-threatening c.diff?
Hypotension
Partial or complete ileus
Toxic megacolon or CT evidence of severe disease
Diagnosis of c.diff?
- Detecting C.diff toxin (CDT) in stool
What only shows c.diff exposure to the bacteria rather than current infection?
C.diff antigen
c.diff toxin= current
Mx of first episode of c.diff infection?
1st: oral vancomycin 125mg 4x day 10days
or
2nd: oral fidaxomicin 200mg 2x day for 10d
or
3rd: oral vancomycin +/- IV metronidazole
Mx of recurrent episodes of c.diff? (20% pts, after 2nd episode its 50%)
- within 12w of symptom resolution= oral fidaxomicin
- after 12w of symptom resolution= oral vancomycin OR fidaxomicin
Mx for life-threatening c.diff infection?
oral vancomycin AND IV metronidazole
also specialist advice as may need surgery
What may be considered for pts who have had 2 or more episodes of c.diff?
faecal microbiota transplant
Prevent spread of c.diff?
- isolation in side room until no diarrhoea (types 5-7 Bristol Stool chart) for at least 48hrs
- PEE if contact with pt with c.diff (gloves and apron)
- hand washing as alcohol gel does not kill c.diff spores
What meds should you review the need to continue if pt has c.diff?
avoid antimotility drugs eg. loperamide and if possible any with anti-peristaltic effect eg. opiods.
review…
- PPI
- laxatives
- meds that cause problems if pt dehydrated eg. NSAIDs, ACEi, ARB, diuretics
Advise to give pt with C.diff?
- diarrhoea should resolve 1-2w
- not usually possible to determine if Abx effective until day 7
- remain infectious while ill and have symptoms
- DO NOT return to school/work until no diarrhoea for >48hrs
refer to hospital if severe
Gastroenteritis?
transient disorder due to enteric infection, usually caused by viruses, characterised by sudden onset diarrhoea with or without vomiting
Food poisoning?
an illness caused by consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses or chemicals
Acute diarrhoea?
3+ episodes of liquid or semi-liquid stool in 24hr period, lasting for <14d where stool takes the shape of the sample pot
Prolonged diarrhoea?
acute-onset diarrhoea that has persisted for >14d
Most infectious diarrhoea is a…. illness
self-limiting
Transmission of infectious diarrhoea?
faecal-oral, foodborne, environmental, airborne
Cx of gastroenteritis?
dehydration, electrolyte disturbance, AKI, sepsis, haemolytic uraemic syndrome, secondary irritable syndrome, IBS
What to ask pt with symptoms of gastroenteritis?
- diarrhoea (blood, mucus, pus); N; V; abdo pain; fever; malaise
- onset, freq, duration
- RFs for developing dehydration eg. co-morbid conditions, fluid & food intake, urine output
- recent food intake
- recent exposure to other cases or outbreaks
- recent foreign travel or hospital admission
- recent drug treatment
Ix for gastroenteritis/diarrhoea?
- clinical
- stool culture and sensitivity if indicated
When would you do a stool culture and sensitivity for pt with gastroenteritis/diarrhoea?
- systemically unwell or possible dysentery (acute painful diarrhoea or blood, mucus or pus in stool)
- prolonged diarrhoea
- recent travel
- contact with affected person or outbreak
Mx for gastroenteritis?
- advise on how to monitor fluid intake & prevent/treat dehydration= oral rehydration salt solution
- Abx, anti-diarrhoeal, anti-emetic and probiotic NOT recommoneded routinely
- hygiene to prevent transmission
- notify public health if notifiable disease
- liase with microbio if specific cause confirmed- need for Abx and/or stool testing for microbio clearance
- emergency admission if needed
Traveller’s diarrhoea?
gastroenteritis when travelling abroad.
3 or more loose to watery stools with or without one or more of: abdo cramps, fever, V or blood in stool
Most common cause of travellers diarrhoea?
Escherichia coli
Most common cause of acute food poisoning?
Staph aureus, Bacillus cereus, or clostridium perfringens
Typical presentation for infection with E.coli?
common among travellers
watery stools
abdo cramps and nausea
Typical presentation for infection with Giardiasis?
prolonged non-bloody diarrhoea
Typical presentation for infection with Cholera?
profuse watery diarrhoea
severe dehydration resulting in weight loss
not common amongst travellers
Typical presentation for infection with Shigella?
bloody diarrhoea
vomiting and abdo pain
Typical presentation for infection with Staph. aureus?
severe vomiting
short incubation period
Typical presentation for infection with Campylobacter?
flu-like prodome followed by crampy abdo pain, fever and diarrhoea which may be bloody.
may mimic appendicitis
Cx= Guillain-Bare
Typical presentation for infection with Bacillus cerus?
2 types of illness seen:
1) vomiting within 6hrs, stereotypically due to rice that has been reheated
2) diarrhoeal illness after 6hrs
Typical presentation for infection with Amoebiasis?
gradual onset bloody diarrhoea, abdo pain and tenderness which may last several weeks
Gastroenteritis is typically caused by infection with what?
E.coli, Giardiasis, Cholera, Shigella, Staph. aureus, Campylobacter, Bacillus cereus, Amoebiasis or Salmonella
Gastroenteritis causes: what has an incubation period of 1-6hrs?
staph aureus and Bacilus cereus (Vomiting subtype, diarrhoeal illness is 6-14hrs)
Gastroenteritis causes: what has an incubation period of 12-48hrs?
Salmonella, E.coli
Gastroenteritis causes: what has an incubation period of 48-72hrs?
Shigella, Campylobacter
Gastroenteritis causes: what has an incubation period of >7d?
Giardiasis, Amoebiasis
Advice to monitor fluid intake and prevent/treat dehydration for pts with gastroenteritis?
- regular fluid intake
- oral rehydration salt solution: small amounts eg. 200-400ml after every loose motion
What to do if pt with gastroenteritis has a specific microbio cause confirmed after stool culture and sensitivity testing in gastroenteritis?
advice from local health protection team regarding need to Abx Mx or stool testing for microbio clearance if any uncertainty
When to urgently admit pt with gastroenteritis to hospital?
systemically unwell and/or features suggesting severe dehydration and/or progression to shcok
intractable vomiting or high-ouput diarrhoea
suspect sepsis
The Salmonella group contains many members, most cause what? What are they?
diarrhoeal disease.
Aerobic gram -ve rods which not normally present as commensals in the gut
What are Typhoid and paratyphoid caused by and CP?
Typhoid= Salmonella typhi
Parathoid= Salmonella paratyphi (types A, B,C)
Termed enteric fevers causing headache, fever, arthralgia
Serotypes of Salmonella that are relatively common causes of bacterial gastroenteritis? Features
Salmonella enteritidis and Salmonella typhimurium.
Source= poultry eg. chicken or eggs
CP: diarrhoea, N&V, abdo cramps, fever, lethargy
When to urgently admit child with gastroenteritis to hospital?
- systemically inwell
- severe dehydration
- progressing to shock
- acute-onset painful blood diarrhoea in previously healthy child
- intractable or biliouis vomiting
- ?sepsis
- clinically deteriorating
- unable to take or no response to ORS
When does diarrhoea and vomiting usually resolve in children with gastroenteritis?
D= lasts 5-7d, stops within 2w
V= lasts 1-2d, stops within 3d
Fluid volume requirement to maintain hydration in children? (eg. in gastroenteritis)
0-10kg= 100mL/kg fluids per day
10-20kg= 1000mL + 50mL/kg for each kg over 10kg per day
> 20kg= 1500mL + 20mL/kg for each kg over 20kg per day
How much to give child eg. with gastroenteritis if using low-osmolarity oral rehydration salt (ORS) solution to rehydrate a child (240-250mOsm/L)?
5yrs or young= 50mL/kg for fluid deficit + maintenance volume of ORS solution over 4hrs. Breastfeeding can continue but no other fluids.
5-11yrs= 200mL ORS after each stool in addition to normal fluid intake
12-16yrs= 200-400mL ORS solution after every loose stool, dose according to fluid loss
after rehydration, for children at increased risk of dehydration= 5mL/kg body weight after each large watery stool
Shigella?
causes diarrhoea (may be bloody), abdo pain
usually self-limiting and doesn’t need Abx
severe/immunocompromised/bloody diarrhoea= ciprofloxacin
What does severity of Shigella depend on?
type
S sonnei (from UK) may be mild but S.flexneri or S.dysenteriae from abroad may cause severe
Crohn’s?
chronic, relapsing-remitting, non-infectious, inflam disease of the GI tract
Where does the inflam in crohn’s affect?
discrete parts of the GIm anywhere from mouth to anus, and affects the full thickness of the intestinal wall
Extra-intestinal manifestations of crohn’s (20% of pts)? May be present before GI symptoms.
- pauci-articular arthritis (<5 joints): asymmetric and self-limiting (w not m)
- erythema nodosum
- apthous mouth ulcers
- episcleritis
- metabolic done disease: osteopenia, porosis and malacia
RFs for Crohn’s?
immune-mediated condition caused by environmental triggering events in genetically susceptible people:
- FHx IBD
- smoking
- previous infectious gastroenteritis
- NSAIDs
Cx of crohn’s?
- psychosocial impact
- abscesses
- strictures
- fistulas
- anaemia
- malnutrition
- faltering growth and delayed puberty
- cancer of small & large bowel
CP of crohn’s?
- persistent diarrhoea 4-6w (incl nocturnal) with possible blood or mucus
- abdo pain
- fatigue, malaise, anorexia, fever
- pallor, clubbing
- apthous mouth ulcers
- abdo tenderness or mass eg. LRQ
- perianal pain, anal or perianal skin tags, fissure, fistula or abscess
- signs of malnutrition and malabsorption (weight loss)
- abnorm. of joints, eyes, liver and skin
Emergency admission for crohn’s?
systemically unwell & blood diarrhoea, fever, tachy or hypotension
Follow up in primary care for Crohn’s?
- lifestyle and support: lifelong condition, stop smoking
- osteoporosis risk
- follow-up with gastro specialist (Mx always initiated by specialist)
- assess for relapse: BMI, CRP
- refer to appropriate specialist if extra-intestinal manifestations
- advice about vaccines: influenzae and pnuemococcal
- referral for pre-conception planning if needed
CP in crohn’s colitis?
faecal urgency, tenesmus (desire to defecate while passing no or little stool), and blood or mucus.
More likely to have extra-intestinal manifestations compared to other areas of GI involement
Ix for crohn’s in primary care?
- FBC: anaemia due to blood loss, increased platelet
- CRP and ESR
- U&Es: ?dehydration & electro distrub
- LFTs: albumin
- Ferritin, B12 folate vit D
- Coeliac serology
- Stool microscopy and culture: ?c.diff
- faecal calprotectin: raised with active inflam
may be normal
Ix for crohn’s?
- bloods and stool sample in primary care then refer to specialist to confirm:
- Colonoscopy and biopsy
- Upper intestinal endoscopy if upper GI tract symptoms
What does colonoscopy and histology of intestinal biopsy show? (6)
- Skip lesions
- deep ulcers
- Cobblestone appearance
- Goblet cells
- Inflammation in all layers from mucosa to serosa
- Granulomas
- Rectal sparing
allows to classify severity
Mx of crohn’s? (specialist)
- induce remission= glucocorticoids
- 2nd= 5-ASA drugs eg. mesalazine
- infliximab useful in refractory disease and fistulating; metronidazole often used for isolated peri-anal disease
- maintaining remission= azathioprine or mercaptopurine
- 2nd= methotrexate
- surgery
Monitoring of crohn’s?
serum ferritin, B12, folate, calcium and vit D
Where does crohn’s commonly affect?
terminal ileum and colon
Why are pts with Crohn’s prone to strictures, fistulas and adhesions?
inflamm occurs in all layers, down to the serosa
When does crohn’s typically present?
late adolescence or early adulthood
What would a small bowel enema (high sens and spec for exam of terminal ileum) show in crohn’s?
- strictures: Kantor’s string sign
- proximal bowel dilation
- Rose thorn ulcers
- Fistulae
1st line drugs to induce and then maintain remission in Crohn’s?
induce= glucocorticoids eg. pred
maintain= azathioprine or mercaptopurine
What must be assessed in pts before starting azathioprine or mercaptopurine to maintain remission in crohn’s?
TPMT activity (thiopurine methyltransferase activity)
Surgery for crohn’s? (80% pts will eventually have)
- stricturing terminal ileal disease= ileocaecal resection
- segmental small bowel resections
- stricturoplasty
- perianal abscess: incision and drainage + Abx
- draining seton for complex perianal fistulae
Perianal fistulae in Crohn’s?
- inflam tract or connection between anal canal & perianal skin
- MRI GOLD for suspected fistulae
-Mx= oral metronidazole; anti-TNF eg. infliximab may also be effective
- complex= draining seton
Common extra-intestinal features of CD and UC related to disease activity?
Arthritis: pauciarticular, asymmetric
Erythema nodosum
Episcleritis
Osteoporosis
Common extra-intestinal features of CD and UC unrelated to disease activity?
Arthritis: polyarticular, symmetric
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis
Crohn’s vs Ulcerative colitis features?
CD= diarrhoea usually NON-BLOODY (except crohns colitis); weight loss prominent; upper GI symptoms: mouth ulcers; perianal disease; abdo mass palpable in right iliac fossa
UC= BLOODY diarrhoea more common; abdo pain in left lower quadrant; tenesmus
Crohn’s vs Ulcerative colitis extra-intestinal features?
CD= gallstones more common (oxalate renal stones) secondary to reduced bile acid reabsorption.
UC= primary sclerosing cholangitis more common
Why are gallstones more common in CD?
oxalate renal stones
impaired bile acid rebsorption increases loss of calcium in bile. Calcium normally binds to oxalate.
Cx of crohn’s vs ulcerative colitis?
CD= obstruction, fistula, colorectal ca
UC= risk of colorectal ca higher
Pathology of crohn’s vs ulcerative colitis?
CD= SKIP LESIONS may be present; can be seen anywhere from mouth to anus.
UC= continuous disease; inflam always starts at rectum and never spreads beyond ileocaecal valve.
Crohn’s vs ulcerative colitis endoscopy (colonoscopy)?
CD= deep ulcers, skin lesions, cobblestone appearance
UC= widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (pseudopolyps)
CD vs UC radiology?
CD= small bowel enema
UC= barium enema
Role of smoking in CD vs UC?
Smoking an increase risk of developing CD and can make it worse.
Smoking protective factor in US: less likely to develop UC and stopping smoking increases risk of UC.
Ulcerative colitis?
Chronic, relapsing-remitting, non-infectious inflam disease of GI tract
UC is characterised as what?
diffuse, continuous, superficial inflam of large bowel, limited to intestinal mucosa, and usually affects the rectum with a variable length of the colon involved proximally
Extra-intestinal manifestations of UC?
uveitis, inflam arthritis, erythema nodosum and pyoderma gangrenosum
IBD?
UC and CD
sometimes can differentiate histologically between 2= IBD type unclassified
Pathophysiology of UC?
exact unknown
immune-mediated condition resulting in impaired epithelial barrier function and chronic inflam caused by envrionmental triggers eg. changes in gut microbiome in genetically susceptible people
Cx of UC?
psychosocial impact, toxic megacolon and bowel obstruction, anaemia, malnutrition, growth failure and colorectal cancer
CP of UC?
bloody diarrhoea >6w, rectal bleeding, faecal urgency and/or incontinence, nocturnal defecation, tenesmus, abdo pain, pre-defecation pain relieved on passage of stool, weight loss, fatigue, malaise, fever.
Pallor, clubbing, abdo distension, tenderness or mass.
Ix for UC?
- FBC, CRP & ESR, U&Es, LFTs, TFTs, ferritin, B12, folate, vit D, coeliac serology
- stool microscopy and culture incl. c.diff toxin and faecal calprotectin
- urgent referral to gastro specialist to confirm diagnosis
Regular review in primary care for UC?
- support and advice
- osteoporosis risk
- follow up with specialist if appropriate
- monitoring
- assess for flare-up
- refer to appropriate specialist if E-I manifestations or to stoma nurse, dietitian or colorectal surgeon
- vaccinations
- advice to be referred to gastro if planning pregnancy to ensure optimal disease control
Specialist Ix for UC?
colonoscopy with biopsy
if severe colitis, AVOID colonoscopy due to risk of perforation= use flexible sigmoidoscopy
barium enema if colonoscopy can’t be performed due to strictures or difficult accessibility
may do upper intestinal biopsy to differentiate from Crohn’s
Macroscopic features of UC on colonoscopy?
- red, raw mucosa, bleeds easily
- no inflammation beyond submucosa
- pseudopolyps (widespread ulceration with preservation of adjacent mucosa which has appearance of polyps)
Histology findings of UC?
- crypt distorsion
- crypt abscesses
- inflam cells infiltrate in lamina propria
- depletion of goblet cells
- infrequent granulomas
Mx for UC?
Mild-moderate= topical (rectal) aminosalicylates (mesalazine and sulfasalazine), if admission not within 4w then add an oral aminosalicylate.
Oral + topical if extensive.
2nd line= corticosteroids
Acute-severe= IV steroids; if no improvement >72hrs then + IV ciclosporin
Maintain remission=
- topical (rectal) (+oral if severe) aminosalicylate daily or intermittent
- if >=2 flares in past year and severe relapse= oral azathioprine or oral mercaptopurine
- biologics eg. infliximab can be used in severe
Severity tool used in UC?
Truelove and Witts’ (adults)
Paediatric Ulcerative Colitis Activity Index (children)
Laxative for constipation in UC?
bulk-forming eg. ispaghula husk or methylcellulose
Avoid what in UC and CD?
NSAIDs- may make symptoms worse
Type of inflammation in UC?
always starts in rectum, never spreads beyond ileocaecal valve and is continuous
Most common site for UC?
rectum
Peak incidence for UC?
15-25yrs and 55-65yrs
Region of abdo pain in CD vs UC?
CD= RIF
UC= LIF
What forms crypt abscesses in UC?
neutrophils migrate through the walls of glands to form them
Barium enema in UC?
- loss of haustrations
- psuedopolyps- superficial ulceration
- long standing disease: colon is narrow and short- drainpipe colon
Risk of what type of cancer is high in UC?
colorectal due to chronic inflam. Worse prognosis due to delayed diagnosis.
lesions may be multifocal
Factors in UC that increase risk of colorectal ca?
- disease duration >10yrs
- pancolitis
- onset <15yrs
- unremitting disease
- poor Mx compliance
What should be decided to be done following risk stratification in IBD pts?
Colonoscopy surveillance for colorectal ca
Colonoscopy surveillance for pts with IBD low risk for ca?
5yr follow up
- extensive colitis with no endoscopic/histo inflam
- OR left sided colitis
- OR crohn’s colitis <50% of colon
Colonoscopy surveillance for pts with IBD intermediate risk for ca?
3yr follow up
- extensive colitis with mild active endo/histo inflam
- OR post-inflam polyps
- OR FHx of colorectal ca in 1st degree relative aged 50yrs+
Colonoscopy surveillance for pts with IBD high risk for ca?
1yr follow up
- extensive colitis with moderate/severe active endo/histo inflam
- OR stricture in past 5yrs
- OR dysplasia in past 5yrs declining surgery
- OR primary sclerosing cholangitis/transplant for primary sclerosing cholangitis
- OR FHx of colorectal ca in 1st degree relative aged 50yrs+
Factors that may trigger flares in UC?
- stress
- meds: Abx, NSAIDs
- stopping smoking
Irritable bowel syndrome? (IBS)
chronic, relapsing and often debilitating disorder of gut-brain interaction
CP of IBS?
abdo pain associated with:
- change in stool form and/or frequency
- may be related to defaecation and bloating
Pathophysiology IBS?
not understood
?multifactorial: bio, psysch and social factors
Prevalence of IBS?
5-20%
When to suspect IBS? (ABC)
> 6m of:
- abdo pain or
- bloating or
- change in bowel habit
- may be relieved by defecation
- altered bowel frequency and stool form (hard, lumpy, loose, watery)
at least 2 of:
- altered stool passage (straining, incomplete evac or urgency)
- abdo bloating, distension, tension or hardness
- made worse by eating
- passage of mucus
Diagnosis of IBS?
diagnosis of exclusion
- clinical
- Ix to rule out other: FBC, ESR & CRP, coeliac serology, faecal calprotectin
Inital Mx for IBS?
- explanation: gut-brain axis
- balanced diet, adjust fibre, adequate fluids
- exercise
- manage associated stress ect.
Medical Mx for IBS if dietary and lifestyle advice doesn’t work?
- Constipation= laxatives but avoid lactulose
- Diarrhoea= loperamide
- Abdo pain/spasm= antispasmodic eg. mebecerine
- Refractory abdo pain= low dose tricyclic or SSRI 2nd line
Referral for IBS?
Gastro:
- uncertain
- atypical, severe, refractory
Mental health:
- >12m and/or psycho cormorbities
Red flag symptoms in IBS?
weight loss, rectal bleeding, positive faecal immunochemical test (FIT), change in bowel habit >60yrs, iron def anaemia, abdo or rectal mass
ROME IV criteria for IBS (for diagnosis in secondary care)?
recurrent abdo pain, >=1 per week in last 3m (onset 6+m prior to diagnosis and associated with 2+:
- related to defaecation
- change in frequency of stool
- change in stool form
Sub-groups of IBS?
based on britsol stool type…
IBS-D (with diarrhoea)
IBS-C (constipation)
IBS-M (both)
IBS-U (unclassified: don’t fall into the other criteria)
Differential diagnosis for IBS?
- malignancy (colorectal, small bowel, ovarian, lymphoma)
- PMS and endo
- anxiety/depression
Constipation:
- functional or drug-induced
- hypothyroidism
Diarrhoea:
- IBD
- Coeliac
- GI indection and secondary lactose intol
- Abx associated
- hyperthroid
- microscopic colititis
- bile acid malabsorption
- laxative misuse
Abdo pain/discomfort:
- diverticular disease
- chronic pancreatitis
- gallstones
- peptic ulcer disease
- GORD
Malnutrition?
state in which a def of nutrients eg. energy, protein, vitamins and minerals causes measurable adverse effects of body composition, function or clinical outcome. Both a cause & consequence of ill health/
Nutrition support be considered in people who are malnourished, how is this defined?
- BMI <18.5kg/m2
- unintentional weight loss >10% within last 3-6m
- BMI <20 and unintentional weight loss >5% within last 3-6m
Nutrition support should be considered in people at risk of malnutrition, defined as what?
- eaten little or nothing for >5d and/or likely to eat little or nothing for the next 5d+
- poor absorptive capacity and/or high nutrient losses and/or increased nutritional needs
Reasons for malnutrition?
- acute illness
- frailty
- ageing
- appetite
- eating & swallowing difficulties
- neuro disease
- chronic conditoons
- psychological
- socioeconomic
Cx of malnutrition?
increased vulnerability to infection and disease, reduced wound healing, pressure ulcers, frailty, falls, reduced function, anxiety, depression, cognitive impairment, social & healthcare costs
When should people be screened for malnutrition?
- initial registration at GP
- routine health checks and immunisations
- med reviews
- contact with community/district nurse
- admission to new care setting eg. care home
- clinical concern
What may cause clinical concern for malnutrition?
- unintentional weight loss
- apathy or fatigue
- poor appetite; early satiety; altered taste; diff swallowing
- altered bowel habit
- recurrent infection or prolonged intercurrent illness
- reduced physical function
- frequent falls
- thin; sarcopenia; loose-fitting clothes, jewllery or dentures
- fraile skin
- poor wound healing
- pressure ulcers
Assessment of pt with or at risk of malnutrition?
- ask: nut intake; unintent weight loss; energy; strength; activity levels; swallowing or appetite issues; mood/cognitive changes; GI sympt; drugs, alcohol, social situation
- exam: BMI; trend in weight loss; signs of malnutrition, acute illness and dehydration; mobility and muscle strength
- consider baseline bloods
Mx of pt with or at risk of malnutrition?
- nutritional care plan, dietary advice and nutrition support
- manage underlying conditions
- set individual goals
- oral nut supplementation if clinically indicated
- refer to dietitian, SALT, occy therapist, physio, mental health or adult social care if indicated
- monitor progress 1-3m
Screening tool for malnutrition?
Malnutrition Universal Screen Tool
Includes: BMI, recent weight change and presence of acute disease
low, medium or high risk
eg. done on admission to hospital or care/nursing homes or if concern eg. thin elderly pt with pressure sores
Dietary advice for malnutrition?
- small frequent meals of nutrient rich foods and drinks
- considered powdered nut supp to be made up with milk
- food first approach: eg. full fat cream added to mash; before prescribing oral nutritional supplements (ONS) eg. Ensure
- if ONS used then take between meals not instead of
Necrotising enterocolitis?
one of leading causes of death in premature infants
tissues in bowel become inflamed and start to die, can lead to perforation, sepsis, death
RFs for necrotising enterocolitis
prematurity
low birth weight
formula feeding
CP of necrotising enterocolitis?
typically 2-3rd week of life
- feeding intolerance
- abdo distension
- bloody stools
can quickly progress to
- abdo discolouration
- perforation
- peritonitis
Diagnosis of necrotising enterocolitis?
Abdo x-ray
Abdo x-ray findings for necrotising enterocolitis?
- dilated bowel loops (asymmetrical)
- bowel wall oedema
- pneumatosis intestinalis (intramural gas)
- portal venous gas
- pneumoperitoneum resulting from perforation
- Rigler sing
- football sign
Rigler sign and football sign on abdo x-ray for necrotising enterocolitis?
Rigler= air both inside and outside bowel
Football= air outlining falciform ligament
Mx for necrotising enterocolitis?
Prophy= antenatal steroids if premature delivery anticipated
Medical (if stage I or II, not III)= withhold oral feeds and replace with parenteral for 10-14d; IV Abx 10-14d; systemic support eg. ventilatory support, fluid resus
Surgical (perforation, obstruction or deterioration)= intestinal resection with stoma formation
Perianal abscess?
collection of pus within subcut tissue of anus that has tracked from the tissue surrounding anal sphincter
more common in men
average age is 40yrs
Most common anorectal abscess (60%)?
Perianal abscess
Features of perianal abscess?
- pain around anus, worse on sitting
- hardened tissue in anal region
- pus-like discharge from anus
- if longstanding= systemic infection
Causes of perianal abscess?
- colonised by gut flora eg. E.coli
- if staph aureus then more likely infection of skin rather than GI tract
Ix for perianal abscess?
- inspection and digital rectal exam
- if uncertain= colonoscopy, bloods (CRP & ESR; cultures)
GOLD= transperineal USS but rarely used unless it has Cx or part of more serious condition eg. IBD
Perianal abscess associated conditions?
- can be caused by IBD espec crohn’s
- DM (due to ability to affect wound healing)
- malignancy
Mx for perianal abscess?
1st= surgical incision and drainage under local; wound then packed or left open and will heal in 3-4w
- Abx if systemic infection
Types of anorectal abscess?
- Perianal= simple abscess of subcut tissue
- Ischiorecal= between obturator internus muscles and external anal sphinter
- Supralevator= when infection tracks superiorly from peri-sphincteric area to above levator ani
- Intersphincteric= rare; between internal and external anal sphincters
- Horseshoe= in potential space between coccyx and anal canal in pelvis; can be result of Cx from another anorectal abscess eg. SL
Secondary peritonitis?
Inflam condition of peritoneum, usually due to spillage of GI or biliary contents into peritoneal cavity.
Secondary peritonitis is frequently precipitated by what?
the perforation of a visceral organ eg. stomach, intestines or gallbladder
Common causes of secondary peritonitis?
- perforated peptic ulcer
- ruptured appendicitis
- diverticulitis
- GI tract perforations that are secondary to trauma or neoplasia
Pathophysiology of secondary peritonitis?
Breach of GI tract integrity -> contam of sterile peritoneal environment -> inflam response= activation of innate immune system, recruitment of neutrophils and release of pro-inflam cytokines.
Severity of secondary peritonitis depends on what?
nature and amount of contaminating material as well as host’s immune response
CP of secondary peritonitis?
- acute severe abdo pain
- localised to site of pathology
- pain may become more diffuse as inflam spreads across peritoneum
- fever, tachy, signs of peritoneal irritation (rebound tenderness and guarding)
Signs of peritoneal irriation eg. in peritonitis?
rebound tenderness and guarding
What may develop in severe cases of secondary peritonitis?
System inflam response syndrome (SIRS) potentially progressing to septic shock
Diagnosis of secondary peritonitis?
- primarily clinical and supported by…
- abdo x-ray= pneumoperitoneum if GI perforation
- USS & CT= more sensitive for intra-abdo abscesses and delineating the extent of inflam
- Bloods= leukocytosis and raised CRP
Mx for secondary peritonitis?
- Urgent surgery + broad spectrum Abx
- Abx should cover common intra-abdo pathogens eg. gram negative bacilli and anerobic bacteria
surgery examples= appendectomy, repair of perforated ulcers, resection of necrotic bowel segments
Spontaneous bacterial peritonitis? (SBP)
form of peritonitis usually seen in pts with ascites secondary to liver cirrhosis
Features of spontaneous bacterial peritonitis?
ascites, abdo pain and fever
Diagnosis of spontaneous bacterial peritonitis?
- paracentesis= neutrophil >250 cells/ul
- most common organism found on ascitic fluid culture= E/coli
Mx of spontaneous bacterial peritonitis?
IV cefotaxime
When should Abx prophylaxis be given to pts with ascites (to prevent spontaneous bacterial peritonitis)?
oral ciproflocacin or norfloxacin
- previous episode of SBP
- fluid protein =<15g/l and either hepatorenal syndrome or Child-Pugh score of 9+
- Pt with cirrhosis and acites with ascitic protein 15g/l or less until ascites has resolved
What is a marker of poor prognosis in SBP (spontaneous bacterial peritonitis)?
alcoholic liver disease
Primary biliary cholangitis?
or primary biliary cirrhosis
Chronic liver disorder typically seen in middle aged females. Interlobular bile ducts become damaged by a chronic inflam process causing progressive cholestasis which may progress to cirrhosis.
Autoimmune.
Itching middle-aged women?
Primary biliary cholangitis
Primary biliary cholangitis associations?
Sjogren’s syndrome (80%)
RA
systemic sclerosis
thyroid
CP of primary biliary cholangitis?
Early: asymptomatic (raised ALP on routine LFTs) or fatigue and pruritus
- cholestatic jaundice
- hyperpigmentation, espec over pressure points
- 10% have RUQ pain
- xanthelasmas, xanthomata
- clubbing hepatosplenomegaly
Late: may progress to liver failure
Diagnosis of primary biliary cholangitis?
- Immunology= anti-mitochondrial antibodies (AMA) M2 subtype (v specific and 98% pts);
smooth muscle antibodies (30%) and
raised serum IgM - Imaging- RUQ USS OR MRCP= BEFORE DIAGNOSIS to exclude extrahepatic biliary obstruction
Mx for primary biliary cholangitis?
1st= ursodexoxycholic acid
- Pruritis= cholestyramine
- Fat-soluble vit supplements
Liver transplant: PBC or also if eg. bilirubin >100; can get recurrence in graft but not common
Role or ursodeoxycholic acid in primary biliary cholangitis?
slow disease progression and improves symptoms
Cx of primary biliary cholangitis?
- cirrhosis -> portal HTN -> ascites, variceal haemorrhage
- osteomalacia and osteoporosis
- signif increased risk of hepatocellular carcinoma
Role of vit B12?
RBC development and maintenance of NS.
Absorption of vit B12?
binds to intrinsic factor and actively absorbed in terminal ileum; small amount passively absorbed without being bound to intrinsic factor
Where is intrinsic factor secreted?
Parietal cells in stomach
Role of intrinsic factors?
binds to vit B12 so B12 can be absorbed in terminal ileum
Causes of vit B12 def?
- pernicious anaemia (most common)
- post gastrectomy
- vegan or poor diet
- disorders/surgery of terminal ileum eg. Crohn’s disease activity or following ileocaecal resection
- metformin (rare)
Features of vit B12 def?
- macrocytic anaemia
- sore tongue and mouth
- neuro symptoms= dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia
- neuropsychiatric symptoms eg. mood disturbances
Mx of vit B12 def?
- if no neuro invl= 1mg IM hydroxocobalamin (B12) 3x each week for 2w, then once every 3m
TREAT B12 def BEFORE FOLIC ACID def
What if pt is folic acid def and B12 def?
Treat B12 def first to avoid precipitating subacute combined degeneration of the cord
Where can abdo pain originate?
- abdo wall
- stomach
- liver
- gallbladder
- spleen
- pancreas
- kidneys
- intestines
- reproductive organs
What does innervation of abdo organs involve?
Somatic and visceral nerve which contribute to nature and perception of pain
Differential diagnosis of abdo pain? (incl medical & unusual)
- peptic ulcer disease
- appendicitis
- acute pancreatitis
- biliary colic
- acute cholecystitis
- AAA
- intestinal obstruction
Medical and unusual causes:
- ACS
- DKA
- pneumonia
- acute intermittent prophyria
- lead posioning
Type of abdo pain in peptic ulcer disease?
Duodenal (more common)= epigastric pain relieved by eating
Gastric= epigastric pain worsened by eating
- Features of upper GI haemorrhage may be seen (haematemesis, melena)
Type of abdo pain in appendicitis?
- initial in periumbilical region then localises to RIF
- Robsing’s sign= more pain in RIF than LIF when palpate LIF
- tachy, low-grade pyrexia, tenderness in RIF
Type of abdo pain in acute pancreatitis?
- severe epigastric pain
- may radiate to back
- usually due to alcohol or gallstones
- vomiting, ileus, low grade fever
- Cullen’s and Grey-Turner’s sign but rare
Ileus?
temp and often reversible cessation of bowel movements and peristalsis, can lead to functional obstruction.
causes= post-op; opiods, antiholinergics, antipsychotics; peritonitis or sepsis; pancreatitis, diverticulitis; trauma; shock; hypokalaemia; hypocalcaemia; hypomagnesia
Type of pain in biliary colic?
- RUQ radiating to right shoulder and interscapular region
- may be following fatty meal
- may persist for hrs
- female, forty, fat, fertile
- obstructive jaundice: pale stools, dark urine
Type of pain in acute cholecystitis?
- continous RUQ pain
- Hx gallstone symptoms
- fever, raised inflam markers and WCC
- Murphy’s sign positive
Type of pain in diverticulitis?
- colicky pain in LLQ
- fever, raised inflam markers and WCC
Type of pain in AAA?
- severe central abdo pain
- radiating to back
- sub-acute (persistent severe abdo pain with developing shock) or catastrophic (sudden collapse)
- ?CVD history
Characterisitc feature of intestinal obstruction?
- Hx of malignancy/previous op
- vomiting
- not opened bowels recently
- tinkling bowel sounds
Tinkling bowel sounds?
Bowel obstruction
Aortic dissection pain vs AAA pain?
AD= severe, sharp, tearing, acute in chest or back
AAA= deep, severe central abdo pain (rupture), radiates to back
Epigastric pain relieved by eating?
duodenal ulcer
Epigastric pain worsened by eating?
gastric ulcer
Constipation?
Defecation that is unsatisfactory due to infrequent stools, difficulty passing stools or sensation of incomplete empyting.
Functional disorder that may develop secondary to another condition.
Rome IV diagnostic criteria for constipation?
spontaneous bowel movements occuring <3x per w
Chronic constipation?
present at least 3m
Faecal loading/impaction?
retention of faeces to the extent that spontaneous evacuation is unlikely
Functional (primary or idiopathic) constipation?
chronic constipation without known cause
Secondary (organic) constipation?
constipation caused by drug or ULC
Population constipation is more common in?
women, elderly, during pregnancy
Assessment of constipation?
- red flags
- normal pattern: freq, consistency
- ?symptoms of impaction and/or incontinence
- associated rectal, abdo, urinary symp
- severity and impact on QOL
- RFs/secondary casues
- self-help or drugs tried
- abdo and rectal exam
Mx of chronic constipation?
- TUC
- advice: fibre, fluids, activity level
- Mx of any faecal loading and/or impaction first
- laxatives step approach
- gradually titrate laxative dose up or down to produce soft formed stools without straining at least 3x week
- if persist then prucalopride
- review
Oral laxatives for constipation?
1st= bulk-forming eg. ispaghula (must have adequate fluids)
2nd= + or switch to osmotic/stool-softening laxative eg. macrogol or 2nd: lactulose
3rd= + stimulant laxative eg. senna (Senokot)
In constipation, what if symptoms are ongoing or refractory to laxatives?
- bloods to exclude ULC
- ?defecatory disorder eg. pelvic floor dyssynergia contributing
When to refer to gastro or colorectal surgeon in constipation?
- suspect serious ULC eg, colorectal ca
- cannot be managed in secondary care
- persist
When to suspect faecal loading or impaction?
- hard lumpy stools which are large and infrequent (eg. every 7-10 days) OR small and relatively frequent (2-3d)
- have to use manual methods to extract faeces
- overflow faecal incontinence or loose stool
When to consider constipation in the elderly?
- confusion, delirium or functional decline
- N or loss of appetite
- overflow diarrhoea
- urinary retention
Mx of faecal loading and/or impaction?
Hard stools= high dose oral macrogol
Soft stools or ongoing hard stools= oral stimulant laxative
If inadequate or too slow then:
- suppository= bisacodyl for soft or glycerol for hard
- mini enema= docusate (softener and weak stimulant)
- still inadequate= sodium phosphate enema
Loin pain typically is in what region?
between lower ribs and buttocks either side of the spine
Where can loin pain originate?
- kidneys
- adrenal glands
- parts of colon
- MSK
- referred from other areas eg. abdo or pelvic organs
What transmit pain signals to the CNS in the renal capsule, ureter and muscles?
renal capsule, ureter and muscles richly supplied with nociceptors that transmit pain signals
Differential diagnosis of loin pain?
- renal colic
- pyelonephritis
- MSK pain (strains or sprains affecting muscles, ligaments or joints)
- radiculopathy (compression/inflam of spinal nerve roots causing referred loin pain)
- ruptured AAA (abdo pain radiating to back can be interpreted as loin pain)
Mx of loin pain?
- identify possible life-threatening conditions eg. ruptured AAA
- abdo, renal and neuro exam
- bloods (FBC, renal function), urinalysis, USS or CT
- pain Mx while Ix is crucial
Differential diagnosis for abdo swelling?
- pregnancy (young female, amenorrhoea)
- intestinal obstruction
- ascites
- urinary retention
- ovarian ca
Characteristic features of ascites?
History of alcohol XS, cardiac failure
Characteristic features of urinary retention?
- Hx of prostate problems
- dullness to percussion around suprapubic area
Characteristic features of ovarian ca?
- older female
- pelvic pain
- urinary symptoms eg. urgency
- raised CA-125
- early satiety, bloating
Dyspepsia?
describes a complex of upper GI symptoms that are typically present for 4+w: upper abdo pain/discomfort, heartburn, acid reflux, nausea and/or vomiting
Gastro-oesophageal reflux disease (GORD)?
chronic condition where there is reflux of gastric contents back into oesophagus, causing heartburn and acid regurg
‘Proven GORD’?
endoscopically-determined reflux disease
‘Proven GORD’ may be due to what?
- oesophagitis= oesophageal inflam and mucosal erosions seen on endoscopy
- endoscopy-negative reflux disease (non-erosive reflux disease)= symptoms of GORD but endoscopy normal
RFs for GORD?
- obesity
- trigger foods eg. spicy
- smoking
- alcohol
- coffee
- stress
- pregnancy
- drugs that decrease lower oesophageal sphincter pressure
What drugs may cause GORD?
those that decrease LOS pressure eg. CCB, anticholinergics, theophylline, benzodiazepines, nitrates,
NSAIDs
10-15% of people with GORD will develop what?
Barrett’s oesophagus; 1-10% of these will develop oesophageal adenocarcinoma over next 10-20yrs
Initial Mx for GORD?
- lifestyle
- Review meds eg. stop NSAIDs
- Antacids eg. Gaviscon but short term only
- full dose PPI 4w to aid healing for proven GORD
- 8w if severe oesophagitis
If H.pylori +ve then eradication regimen
Lifestyle advice for GORD?
sleep with head of bed raised (no additional pillows as may make worse but add wood or bricks under bed head), stop any drugs that make symptoms worse if appropriate, smaller meals, evening meal 3-4hrs before bed
Mx for GORD if refractory or recurrent symptoms?
- alternative diagnosis: cardiac or hepatobiliary disease
- adherence?
- further 4w PPI or double dose
- severe= further w
- or + histamine (H2)-receptor antagonist at bedtime for 2w if confirmed oesophagitis
- or full-dose PPI long-term maintenance if symptoms of severe oesophagitis are controlled
People on long-term Mx for GORD should be what?
- annual review
- encourages to step down or stop if appropriate
When to refer to gastro or GI surgeon for GORD?
- refractory to Mx, persistent or unexplained
- controlled on acid suppression therapy but doesn’t want long-term Mx
- RFs for Barrett’s oesophagus
Specialist Ix for GORD?
- oesophageal manometry if motility disorder suspected eg. achalasia
- ambulatory 24hr oesophageal pH monitoring
- barium swallow to exclude hiatus hernia or motility disorder
Specialist Mx for GORD?
GOLD= laparoscopic fundoplication
Example of PPI for GORD?
lansoprazole 30mg OD (standard/full dose); if double dose then twice d
omeprazole 20mg OD (40mg if severe); if double dose then 40mg OD (or 40mg twice d if severe)
H2-receptor antagonist for GORD?
ranitidine 150mg twice day or 300mg at night
famotidine 20-40mg twice day
Ix for dyspepsia (maybe thinking possible GORD)?
- Test for H.pylori (carbon-13 urea breath test of stool antigen test)
- Trial PPI 4w
- Refer for upper GI endoscopy if recurrent or refractory symptoms despite Mx or second-line H.pylori eradication unsuccessful
- if +ve for H.pylori= first line H.pylori eradication regimen
What once treated for H.pylori?
no need to test for eradication if symptoms have resolved but if repeat testing is needed then carbon-13 urea breath test used
Who needs a 2ww endoscopy for suspected oesophageal or stomach ca?
- All pts with dysphagia
- Upper abdo mass
- > =55yrs with weight loss AND upper abdo pain, reflux or dyspepsia
What pts need non-urgent upper GI endoscopy?
- haematemesis
- > =55yrs with: treat-resistant dyspepsia or raised platelet count (with N&V, reflux, upper abdo pain) or N/V with reflux/dyspepsia/upper abdo pain
Diarrhoea?
Passage of 3+ loose or liquid stools per day (or more frequently than normal)
Acute diarrhoea?
lasts <14d
Persistent diarrhoea?
> 14d
Chronic diarrhoea?
> 4w
Causes of acute vs chronic diarrhoea?
Acute= bacterial or viral infection; meds; anxiety; food allergy; acute appendicitis
Chronic= IBS; diet; IBD; coeliac; bowel ca
Assessment for diarrhoea should include what?
- onset, duration, frequency, severity
- red flags
- underlying cuase
- Cx eg. dehydration
Acute diarrhoea Ix?
Stool sample for M&C if:
- systemically unwell
- blood or pus
- immunocompromised
- recently had Abx, PPI or hospital admission
- foreign travel (also test for ova, cysts and parasites)
- Persistent
- need to exclude infection
Ix for chronic diarrhoea?
Bloods: FBC, U&E, LFTS, Ca, B12, folate, ferritin, TFTs, ESR&CRP, coeliac serology
Onset of diarrhoea within 6hrs of contaminated food suggets what casue?
pre-formed toxin of Bacillus cereus or staph aureus
Red flags for diarrhoea?
- blood, mucus
- recent hospital admission or Abx
- weight loss
- evidence of dehydration
- nocturnal symptoms (organic cause more unlikely)
Signs of mild dehydration?
Lassitude.
Anorexia, nausea.
Light-headedness.
Postural hypotension.
Usually no signs.
Signs of moderate dehydration?
Apathy/tiredness.
Dizziness.
Nausea/headache.
Muscle cramps.
Pinched face.
Dry tongue or sunken eyes.
Reduced skin elasticity.
Postural hypotension.
Tachycardia.
Oliguria.
Signs of severe dehydration?
Profound apathy.
Weakness.
Confusion, leading to coma.
Shock.
Tachycardia.
Marked peripheral vasoconstriction.
Systolic blood pressure less than 90 mmHg.
Oliguria or anuria.
Diagnosis for dehydration?
- clinical
- GOLD= plasma or serum osmolality
Causes of diarrhoea: signs of gastroenteritis?
abdo pain or N&V, diarrhoea
Causes of diarrhoea: signs of diverticulitis?
LIF pain, diarrhoea, fever
Causes of diarrhoea: signs of Abx therapy?
more common with broad spectrum Abx
C.DIFF can be seen
Causes of diarrhoea: signs of constipation causing overflow?
Hx of alternating diarrhoea and constipation may be given; may lead to faecal incontinence in elderly
Causes of diarrhoea: signs of IBS?
common
abdo pain, bloating, change in bowel habit
lethargy, N, backache, bladder symptoms may be present
Causes of diarrhoea: signs of UC?
bloody diarrhoea, crampy abdo pain, weight loss, faecal urgency, tenesmus
Causes of diarrhoea: signs of crohn’s?
crampy abdo pain, diarrhoea, blood less common
mouth ulcers, perianal disease, malabsorption, intestinal obstruction
Causes of diarrhoea: signs of colorectal ca?
depend on site of lesion
diarrhoea, rectal bleeding, anaemia, constitiutional symptoms (eg. weight loss, anorexia)
Causes of diarrhoea: signs of coeliac disease?
children= failure to thrive, diarrhoea, abdo distention
adults= lethargy, anaemia, diarrhoea, weight loss
other autoimmune conditions may coexist
Thyrotoxicosis, laxative abuse, appendicitis and radiation enteritis may be associated with what?
diarrhoea
Diarrhoea: public health indication?
diarrhoea in high risk people (eg. food handlers, healthcare workers, elderly residents in care homes); suspected food posioning (eg. after bbq, restaurant, eggs, chicken, shellfish)
food poisoning is notifiable disease
If diarrhoea is severe, what may bloods show?
- AKI
- hypokalaemia
- hyponatraemia
Achalasia?
failure of oesophageal peristalsis and relaxation of lower oesophageal sphincter (LOS)
What is achalasia due to?
degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated
Achalasia typically presents in who?
middle-aged
both men and women
Dysphagia of BOTH liquids and solids?
Achalasia?
CP of achalasia?
- dysphagia BOTH liquids and solids
- variation in severity of symptoms
- heartburn
- regurg of food- may lead to cough, aspiration pneumonia ect
- malignant change in small no. of pts
Ix for achalasia?
- DIAGNOSTIC (most important)= oesophageal manometry: XS LOS tone which doesn’t relax on swallowing
- Barium swallow: grossly expanded oesophagus, fluid level; bird beak
- CXR= wide mediastinum; fluid level
Bird’s beak appearance on barium swallow?
achalasia
Mx of achalasia?
- 1st line= pneumatic (balloon) dilation
- recurrent/persistent= surgical Heller cardiomyotomy
New-onset dysphagia?
red flag regardless of age or other symptoms; require urgent endoscopy
Causes of dysphagia?
- oesophageal ca
- oesophagitis
- achalasia
- pharyngeal pouch
- systemic sclerosis
- MG
- globus hystericus
Extrinsic causes of dysphagia?
- mediastinal mass
- cervical spondylosis
Oesophageal wall causes of dysphagia?
- achalasia
- diffuse oesophageal spasm
- hypertensive LOS
Intrinsic causes of dysphagia?
- tumours
- strictures
- oesophageal web
- Schatzki rings
Neuro causes of dysphagia?
- CVA
- Parkinson’s
- MS
- MG
- brainstem pathology
Best type of Ix for motility disorders causing dysphagia?
barium swallow
Ix for dysphasia?
- ALL= upper GI endoscopy
- FBC
- Ambulatory oesophageal pH and menometry studies for pts with achalasia or GORD being considered for fundoplication surgery
Heartburn, odynophagia (painful swallowing) but no weight loss and systemically well?
Oesophagitis
What may there be a history of in oesophageal candidiasis causing dysphagia?
HIV or other RFs eg. steroid inhaler use
What may be seen in systemic sclerosis causing dysphagia?
Other features of CREST syndrome may be present, namely Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
Oesophageal dysmotility and LOS pressure decreased
Systemic sclerosis causing dysphasia vs achalasia causing dysphagia?
Achalasia= LOS pressure increased
SS= LOS pressure decreased
In MG you get dysphagia of what?
solids and liquids
Globus hystericus causing dysphagia?
- Hx of anxiety
- intermittent and relieved by swallowing
- painless
What is most common cause of acute upper GI bleed?
oesophageal varices or peptic ulcer disease
Why is urea high in upper GI bleed?
blood is digested into protein (urea is final breakdown product of amino acids in protein)
CP of acute upper GI bleed?
- haematemesis: bright red or coffee ground
- melena: passage of altered blood per rectum, black and tarry
- raised urea (due to the ‘protein meal’ of the blood)
- features associated with particular diagnosis eg.
oesophageal varices= stigmata of chronic liver disease
PUD= abdo pain
Oesophageal causes of acute upper GI bleed?
- varices
- ca
- Mallory Weiss tear
- Oesophagitis
DIfferential diagnosis for acute upper GI bleed can be separated into what groups?
- oesophageal
- gastric
- duodenal
Causes of acute upper GI bleed: CP of oesophageal varices?
- large vol fresh blood
- swallowed blood may cause melena
- associated with haemodynamic compromise
- may stop spontaneously but re-bleeds are common until Mx
Causes of acute upper GI bleed: CP of oesophagitis?
- small vol fresh blood, often streaking vomit
- melena rare
- often ceases spontaneously
- Hx of antecedent GORD symptoms
Causes of acute upper GI bleed: CP of oesophageal ca?
- small vol blood unless a preterminal event with erosion of major vessels
- dysphagia, weight loss
- recurrent until Mx
Causes of acute upper GI bleed: CP of Mallory Weiss tear?
- brisk small to moderate vol of bright red blood following bout of repeated vomiting
- melena rare
- usually ceases spontaneously
Gastric causes of acute upper GI bleed?
- ulcer
- ca
- dieulafoy lesion
- diffuse erosive gastritis
Causes of acute upper GI bleed: CP of gastric ulcer?
- small low-vol bleeds common so present as iron def anaemia
- erosion into signif vessel may produce haemorrhage and haematemesis
Causes of acute upper GI bleed: CP of gastric ca?
- frank haematemesis or altered blood mixed with vomit
- prodromal features of dyspepsia and weight loss
- amount of bleeding variable but erosion of major vessel may produce haemorrhage
Causes of acute upper GI bleed: CP of Dieulafoy lesion?
- arteriovenous malformation
- no prodromal features prior to haematemesis and melena
- can produce considerable haemorrhage
- difficult to detect endoscopically
Causes of acute upper GI bleed: CP of diffuse erosive gastritis?
- haematemesis and epigastric discomfort
- underlying cause eg. NSAIDs
- large vol haemorrhage may occur with haemodynamic compromise
Duodenal causes of acute upper GI bleeding?
- ulcer
- aorto-enteric fistula
Causes of acute upper GI bleed: CP of duodenal ulcer?
- posteriorly sited and may erode gastroduodenal artery
- haematemesis, melena, epigastric discomfort
- occurs several hrs after eating
- periampullary tumours may bleed but are rare
May duodenal ulcers may erode what artery?
gastroduodenal
Causes of acute upper GI bleed: CP of aorto-enteric fistula?
- pts with prev AAA surgery
- rare
- major haemorrhage
- high mortality
Risk assessments for acute upper GI bleed?
- Glasgow-Blatchford score at 1st assessment= ?pts be Mx as outpts or not
- Rockall score= after endoscopy; % risk of rebleeding and mortality; incl- age, features of shock, co-morbidities, aetiology of bleed and endoscopic stigmata of recent haemorrhage
What is the Glasgow-Blatchford score risk assessment?
help determine if pt with upper GI bleed can be Mx as outpatient
- urea, Hb, SBP, gender, HR, melena, syncope, hepatic disease Hx, cardiac failure present
- score of 0= can be Mx as outpatient so can be considered for early discharge
- score >0= high risk GI bleed that is likely to require medical intervention
Resuscitation for acute upper GI bleed?
- ABC, wide-bore IV access x2
- platelet trans if actively bleeding platelet count <50x10*9/l
- fresh frozen plasma to pts with fibrinogen <1g/l or prothrombin time (INR) or APTT >1.5 times normal
- prothrombin complex concentrate to pts taking warfarin and actively bleeding
Mx of acute upper GI bleed?
resuscitation then endoscopy within 24hrs
- no PPI before endoscopy to pts with suspected variceal upper GI bleed
Mx of non-variceal acute upper GI bleed?
- PPI after endoscopy
- further bleeding then repeat endo, interventional radiotherapy and surgery
Mx of variceal acute upper GI bleed?
- terlipressin and prophy Abx at presentation (before endo)
- oesophageal varices= band ligation
- gastric= injections of N-butyl-2-cyanoacrylate
- if not controlled= transjugular intrahepatic portosystemic shunts (TIPS)
Why are pts with liver cirrhosis at risk of oesophageal varices?
Pt with liver cirrhosis at risk of developing portal HTN (increased portal venous system pressure) and one of most signif Cx of this is oesophageal carices.
What is the risk of oesophageal varicies?
Rupture -> severe and life-threatening upper GI bleed
Acute Mx of variceal haemorrhage?
- ABC: resus before endo; blood transfusion may be needed
- Correct clotting: may need FFP, vit K, platelet trans
- Vasoactive agent (terlipressin) and prophylactic IV Abx (quinolones) before endoscopy
- Endoscopy: endoscopic band ligation
- Uncontrolled= Sengstaken-Blakemore tube
- Still fail= TIPSS (connects hepatic vein to portal vein; Cx is exacerbation of hepatic encephalopathy)
What does TIPPS stand for?
Transjugular Intrahepatic Portosystemic Shunt
Prophylaxis of variceal haemorrhage?
- Propanolol
- Endoscopic variceal band ligation: for pts with cirrhosis with medium to large oesophageal varices.
- PPI also given to prevent EVL-induced ulceration
- unsuccessful= TIPSS
Causes of jaundice in pregnancy?
- intrahepatic cholestasis of preg
- acute fatty liver of preg
- HELLP
- Gilbert’s, Dubin-Johnson syndrome may be exacerbated in pregprim
Jaundice?
clinical sign describing yellow pigmentation of skin, sclera and mucous membranes due to raised plasma bilirubin
Jaundice is the result of what?
dysfunction in bilirubin metabolism
How are causes of jaundice characterised?
pre-hepatic
hepatic
post-hepatic
Pre-hepatic causes of jaundice?
haemolytic anaemia, drugs, malaria, Gilbert’s syndrome, Crigler-Najjar syndrome
Intra-hepatic causes of jaundice?
Viral hepatitis, alcohol misuse, autoimmune disorders, drugs, malignancy of biliary system, Dubin-Johnson syndrome and Rotor’s syndrome
Post-heptaic causes of jaundice?
Gallstones, surgical strictures, extra-hepatic malignancy, pancreatitis and parasitic infections
Most important causes of jaundice?
malignancy, alcohol and gallstone disease
Assessment/Ix for pt with jaundice?
- duration of current episode; previous episodes; changes in stool and urine; itching; pain; systemic (fever, arthralgia, myalgia, rash, fatigue, weight loss, N&V); recent travel abroad; Hx of IVDU or blood transfusion; exposure to hepatotoxic drugs; occupation
- exam: signs of chronic liver disease, lymphadenopathy, abdo masses, tenderness or ascites
- Urine sample: bilirubin
- Not acutely unwell= FBC, LFTs, U&E, clotting, hepatitis screen, alpha-1-antitrypsin (metabolic liver disease)
- May need referral or additional screening tests eg. full liver screen and imaging eg. USS or CT
Red flags associated with jaundice?
hepatic encephalopathy (confusion); hepatic dysfunction (bruising); GI blood loss; sepsis; marked abdo pain or tenderness; V; weight loss; paracetamol overdose
When to admit pt for same-day assessment if present with jaundice?
- acutely unwell eg. confusion, fever
- cholangitis suspected
- Bilirubin >100micromol/L
- Renal function abnormal or dehydrated
- Clotting profile abnormal
- Frail/co-morbidities
- Paracetamol overdose
When should pts who do not need admission be referred to secondary care if they present with jaundice?
- 2ww if suspect malignancy
- Bloods show cholestatic or obstructive picture
- bloods show hepatitic picture
- alcohol-related liver disease suspected
- inherited or autoimmune liver disease suspected
What pts with jaundice can be managed in primary care?
if have been diagnosed with hep A or Gilbert’s syndrome
When examining a pt with jaundice, what should you look out for?
- signs of sepsis
- signs of chronic liver disease= palmar erythema, spider naevi, clubbing, leukonychia, Dupuytren’s contractures, gynaecomastia with loss of body hair and testicular atrophy
- signs of liver failure= altered neuromusc function eg. ataxia, nystagmus or asterixis (corarse flapping temor), drowsiness, confusion, bruising, petechiae, purpura
- lymphadenopathy
- masses= hepato or splenomegaly; Courvoiser’s sign (palpable gallbladder)
- Abdo tenderness= Murphy’s sign or widespread
- Visible veins eg. collateral vessels on skin of abdo espec around umbilicus (caput medusae)= chronic liver disease
- ascites
Palmar erythema, spider naeivi, clubbing, Dupuytren;s contractures, gynaecomastia?
Chronic liber disease
Clubbing can be associated with liver…
cirrhosis
Dupuytren’s contracture?
contacture of palmar fascia associated with chronic liver disease due to alcohol misuse, famillial or DM
Ataxia, systagmus, asterixis (coarse flapping tremor), confusion, petechiae or purpura?
Liver failure
Enlargement of supraclavicualar lymph nodes (Troisier’s sign)?
malginancy eg. metastatic pancreatic and gastric ca
LFTs: isolated raised bilirubin?
Often due to Gilbert’s syndrome
- repeat LFT and FBC to ensure no anaemia or haemolysis
LFTs: cholestatic picture?
- Raised ALP
- Causes= primary biliary cholangitis, primary sclerosing cholangitis, biliary obstruction, liver congestion and drug-induced liver injury. Bone disease can also cause raised ALP so repeat and add GGT to confirm liver cause
LFTs: hepatitic picture?
- Raised ALT and AST
- ALP may be raised
- Caused by hepatocellular liver injury secondary to viral hep; NAFLD; alcohol realted liver disease; autoimmune hep or drug induced
LFTs: what can cause ALT to rise to several thousand units per litre (U/L)?
acute viral hepatitis
LFTs: what can produce ALT levels >10,000 U/L?
Acute liver injury from drugs (eg. paracetamol overdose) or ischaemia
LFTs: what can cause AST and ALT to rise to several hundred?
acute alcoholic hepatitis
LFTs: what usually causes ratio of AST:ALT >1 and what causes ALT to rise more than AST?
AST:ALT >1= alcohol-induced hepatocyte damage
ALT rises more than AST= infection
Are AST and ALT raised in obstructive jaundice?
no unless complicated by cholangitis
LFTs: mixed picture?
both cholestasis and hepatocyte damage eg. due to cholangitis associated with stones in common bile duct
LFTs: albumin?
marker of liver synthesising function.
low serum albumin suggests chronic liver disease
What is tested in LFTs?
ALT and AST; ALP; GGT; serum bilirubin; prothrombin time (PT); international normalised ratio (INR); total protein and albumin
Primary sclerosing cholangitis?
biliary disease of unknown aetiology characterised by inflam and fibrosis of intra and extra-hepatic bile ducts
Primary sclerosing cholangitis associations?
- UC: 4% with UC have PSC and 80% with PSC have UC
- Crohn’s
- HIV
Features of primary sclerosing cholangitis?
- cholestasis= jaundice, pruritis; raised bilirubin + ALP
- RUQ pain
- fatigue
Ix for primary sclerosing cholangitis?
- ERCP or MRCP diagnostic= multiple biliary strictures giving beaded appearance
- p-ANCA may be +ve
- liver biopsy (limited)= fibrous obliterative cholangitis described as onion skin
ERCP or MRCP showing multiple biliary strictures giving beaded appearance?
Primary sclerosing cholangitis
Cx of primary sclerosing cholangitis?
- cholangiocarcinoma (10%)
- increased risk colorectal ca
Mx for primary sclerosing cholangitis?
manage Cx and monitor liver damage
eg. ursodeoxycholic acid for pruritis
cure=transplant
Common causes of hepatomegaly?
- cirrhosis if early (later it gets smaller); non-tender firm liver
- malignany: metastatic or primary hepatoma; hard, irregular liver edge
- RHF: firm smooth tender liver edge, may be pulsatile
Other causes of hepatomegaly?
- viral hep
- glandular fever
- malaria
- abscess: pyogenic, amoebic
- hydatid disease
- haem malignancies
- haemochromatosis
- primary biliary cirrhosis
- sarcoidosis, amyloidosis
Causes of hepatosplenomegaly?
- chronic liver disease with portal HTN (unless later cirrhosis)
- infections: glandular fever, malaria, hepatitis
- lymphoproliferative disorders
- myeloproliferative disorders eg. CML
- amyloidosis
Causes of massive splenomegaly?
- myelofibrosis
- chronic myeloid leukaemia
- visceral leishmaniasis (kala-azar)
- malaria
- Gaucher’s syndrome
Other causes of splenomegaly?
massive causes plus…
- portal HTN eg. 2 to cirrhosis
- lymphoprolferative disease eg. CLL, Hodgkin;s
- haemolytic anaemia
- infection: hepatitis, glandular fever
- infective endocarditis
- sickle-cell*, thalassaemia
- rheumatoid arthritis (Felty’s syndrome)
- majority with sickle cell will have atrophied spleen due to repeated infection
Examples of anorectal disorders?
haemorrhoids
anal fissure
proctitis
ano rectal abscess
anal fistula
rectal prolapse
pruritus ani
anal neoplasm
solitary rectal ulcer
Anorectal disorders: summary of haemorrhoids?
Location= 3,7,11 o’clock
Internal or external
Mx= conservative, rubber band ligation, haemorrhoidectomy
Anorectal disorders: summary of anal fissure?
Painful rectal bleeding
Location= midline (posterior 90%) 6 and 12 o’clock; distal to dentate line
Chronic fissure >6/52: triad= ulcer, sentinel pile, enlarged anal papillae
Anorectal disorders: summary of ano rectal abscess?
E.coli, staph aureus
Positions= perianal, ischiorectal, pelvirectal, intersphincteric
Anorectal disorders: causes of proctitis?
Crohn’s; UC; c.diff
Anorectal disorders: summary of anal fistula?
usually due to previous ano-rectal abscess
Intersphincteric, transsphincteric, suprasphincteric and exterasphincteric.
Goodsalls rule determines location.
Anorectal disorders: summary of rectal prolapse?
associated with childbirth and rectal intusscecption.
internal or external
Anorectal disorders: summary of pruritus ani?
very common
children= often related to worms
adults= idiopathic or related to other causes eg. haemorrhoids
Anorectal disorders: summary of anal neoplasm?
Most common= SCC unlike adenocarcinoma in rectum
Anorectal disorders: summary of solitary rectal ulcer?
associated with chronic straining and constipation
histology= mucosal thickening, lamina propria replaced with collagen and smooth muscle (fibromuscular obliteration)
Threadworm (Enterobius vermicularis) or pinworm?
parasitic worm that infects the human gut
Threadworm (Enterobius vermicularis) transmission?
faecal-oral route when threadworm eggs are ingested
can be ingested by hand-to-mouth transfer (after scratching) from the faeces/perianal area of infected person or by handling contaminated surfaces eg. toys, bedding or clothing
Most common parasitic worm infestation in UK?
Threadworm
Who does threadworm (Enterobius vermicularis) most commonly affect?
- <18yrs
- household contacts of infected children
- people living in institutions
Threadworm (Enterobius vermicularis) CP?
- intense perianal itching
- worse at night
- may be asymptomatic
- small white thread-like worms (slowly moving) seen on perianal skin or in stool
- females= can invl genital area so get pruritus vulvae
- nocturnal itching= disturbed sleep and irritabolity
Ix for threadworm (Enterobius vermicularis)?
- clinical
- uncertain= adhesive tape test for eggs (transparent tape applied to perianal area in morning then examined under microscopy)
stool sample not generally recommended
Differential diagnosis for perineal and vulval itch?
- dermatitis
- candidal infection
- pubic lice
- haemorrhoids
- threadworms (rarely confused with other worm infestation because of specific appearance)
Mx for threadworm (Enterobius vermicularis)?
if seen or eggs detected
ALL HOUSEHOLD members too.
- Anthelmintic (mebendazole) single dose + hygiene measures
- <6m old or pregnant= hygiene measures for 6w
Mx for re-infestation of threadworm (Enterobius vermicularis)?
usually due to re-infection.
- consider other causes
- if certain then re-treat pt and household contacts
- reinforce strict hygiene measures
Differential diagnosis for pruritus?
- liver disease
- iron def anaemia
- polycythaemia
- CKD
- lymphoma
- hyper/hypothyroidism
- diabetes
- pregnancy
- ‘senile’ pruritus
- urticaria
- skin disorders: eczema, scabies, psoriasis, pityriasis rosea
Causes of pruritus: summary of liver disease?
- Hx alcohol XS
- Chronic liver disease= spider naevi, bruising, palmar erythema, gynaecomastia
- evidence of decompensation= ascites, jaundice, encephalopathy
Causes of pruritus: summary of iron def anaemia?
- pallor
- Koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis
Causes of pruritus: summary of polycythaemia?
- pruritus particularly after warm bath
- ‘ruddy complexion’
- gout
- PUD
Causes of pruritus: summary of CKD?
- lethargy and pallor
- oedema and weight gain
- HTN
Causes of pruritus: summary of lymphoma?
- pruritus
- night sweats
- lymphadenopathy
- splenomegaly, hepatomegaly
- fatigue
Bright red rectal bleeding?
usually rectal anal canal origin
Dark red rectal bleeding?
usually proximally sited bleeding source
Cause of malaena?
blood that has entered GI tract from gastro-duodenal source due to the effects of the digestive enzymes on the blood itself
Common causes of rectal bleeding?
fissure in ano
haemorrhoids
crohn’s
UC
rectal ca
Type of bleeding in fissure in ano?
bright red rectal bleeding
Type of bleeding in haemorrhoids?
bright red rectal bleeding
Type of bleeding in crohn’s?
Bright red or mixed blood
Type of bleeding in UC?
Bright red bleeding often mixed with stool
Type of bleeding in rectal cancer?
Bright red blood mixed volumes
Main features in history in fissure in ano?
painful bleeding that occurs post defecation in small volumes
usually antecedent features of constipation
Main features in history in haemorrhoids?
post-defecation bleeding noted both on toilet paper and drips into pan
may be alteration of bowel habit and Hx of straining
no blood mixed with stool, no local pain
Main features in history in crohn’s in terms of rectal bleeding?
bleeding (but more common in UC) that is accompanied by other symptoms: altered bowel habit, malaise, Hx of fissures (espec anterior) and abscesses
Main features in history in UC?
Diarrhoea, bleeding, weight loss, nocturnal incontinence, passage of mucous PR
Main features in history in rectal ca?
Alteration of bowel habit; tenesmus may be present; symptoms of met disease
Main features on exam in fissure in ano?
muco-epithelial defect usually in midline posteriorly (anterior fissures more likely due to underlying disease)
Main features on exam in haemorrhoids?
normal colon and rectum
protoscopy may show internal haemorrhoids
internal haemorrhoids usually impalpable
Main features on exam in Crohn’s?
Perineal inspection may show fissure or fistulae. Proctoscopy may demonstrate indurated mucosa and possibly strictures. Skin lesions may be noted at colonoscopy.
Main features on exam in UC?
Proctitis is most marked finding. Perianal disease usually absent. Colonoscopy will show continuous mucosal lesion.
Main features on exam in rectal ca?
Usually obvious mucosal abnormality. Lesion may be fixed or mobile depending upon disease extent. Surrounding mucosa often normal, although polyps may be present.
Ix for pts presenting with rectal bleeding?
ALL pts= digital rectal exam and procto-sigmoidoscopy.
- ?haemorrhoids= young pt with no concerning features then Hx and sigmoidoscopy demonstrating haemorrhoids sufficient. If clear views not obtained then need bowel prep with enema and flexible sigmoidscopy.
- Altered bowel habit= colonoscopy
- XS pain ?fissure= may need exam under local anaesthesia
Ix for staging malignancy of rectum?
Staging= MRI of rectum and CT chest abdo and pelvis.
What Ix should pts with fissure in ano who are being considered for surgical sphincterotomy and females who have obstetric history have?
Ano rectal mamometry testing + endo anal USS
not mandatory as not universally available but if not done then there is absence of info may be continence issues after sphincterotomy
Mx for rectal ca?
anterior resection or abdomino-perineal excision of colon and rectum
total mesorectal excision now standard.
Most resections below peritoneal reflection will require defunctioning ileostomy.
Most pts will need pre-op radiotherapy
Small bowel obstruction?
Passage of food, fluids and gas through small intestines becomes blocked.
Most common cause of small bowel obstruction?
Adhesions (eg. follow prev surgery) then hernias.
Features of small bowel obstruction?
- diffuse central abdo pain
- Bilious vomiting and nausea
- ‘constipation’ with complete obstruction and lack of flatulence
- abdo distension, particularly with lower levels of obstruction
- tinkling bowel sounds (common in early obstruction)
Ix for small bowel obstruction?
- 1st line= abdo x-ray
- GOLD= CT as more sensitive and definitive
What does abdo x-ray show in small bowel obstruction?
- distended small bowel loops with fluid levels
- dilated if small bowel is >3cm diameter
Mx for small bowel obstruction?
- inital= NBM, IV fluids, nasogastric tube with free drainage
- Some pts will settle with conservative Mx but otherwise require surgery
One of the key indications for performing abdo x-ray?
looking for bowel obstruction
Abdo x-ray in small bowel obstruction vs large?
Small:
- max normal diameter= 35mm
- Valvulae conniventes ectend all the way across
Large:
- max normal diameter= 55mm
- Haeustra extend about a third of the way across
Large bowel obstruction?
Passage of food, fluids and gas through large intestines becomes blocked.
Causes of large bowel obstruction?
- Tumour (60%)
- Volvulus
- Diverticular disease
Initial presenting complaint of colonic malignancy in 30% cases?
Large bowel obstruction.
Espec in more distal and rectal tumours as these tend to obstruct earlier due to the smaller lumen diameter.
CP of large bowel obstruction?
- absence of passing flatus or stool
- abdo pain
- abdo distension
- N&V LATE symptoms that may suggest more proximal lesion
- if perforation= peritonism
- symptoms of underlying cause eg. colorectal ca so weight loss ect.
Ix for large bowel obstruction?
1st= abdo x-ray
GOLD= CT (sensitive, specific and can identify aetiology)
Abdo x-ray finding for large bowel obstruction?
Normal diameter limits:
- Caecum= 10-12cm
- Ascending colon= 8cm
- Recto-sigmoid=6.5cm
So any diameter GREATER than this is diagnostic for obstruction
+ presence of free intra-peritoneal gas indicates colonic perforation.
What may presence of free-intra peritoneal gas on abdo x-ray for large bowel obstruction indicate?
colonic perforation
Mx for large bowel obstruction?
urgency depends on whether perforation suspected
- Initial= NBM, IV fluids, nasogastric tube with free drainage
- If cause of obstruction doesn’t require surgery= conservative Mx trialed up to 72hrs, if fail then further Mx (75% will require surgery)
- IV Abx if surgery planned or perforation suspected
- Surgery= emergency if overt peritonitis or evidence of bowel perforation. Irrigation of abdo cavity, resection of perforated segment and ischaemic bowel, and address ULC of obstruction itself
Jaundice is due to hyperbilirubinaemia, occuring at bilirubin levels roughly greater than what?
50umol/L
Where does bilirubin come from?
normal breakdown product from the catabolism of haem and so formed from destruction of RBCs
Normal pathophysiology of bilirubin in the liver?
Bilirubin undergoes conjugation within the liver making it water-soluble -> excreted via bile into GI tract -> majority is egested in the faeces as urobilinogen and stercobilin (metabolic breakdown product of urobilinogen) -> around 10% of urobilinogen is reabsorbed into bloodstream and excreted through the kidneys
jaundice occurs when this pathway is disrupted
Pathophysiology of pre-hepatic jaundice?
XS RBC breakdown -> overwhelms liver’s ability to conjugate bilirubin -> causes unconjugated hyperbilirubinaemia.
Any bilirubin that manages to become conjugated will be excreted normally but it is the UNCONJUGATED BILIRUBIN that remains in the blood that causes the jaundice.
Unconjugated vs conjugated bilirubin?
Unconjugated= form of bilirubin produced when RBCs breakdown. Not been processed by the liver and is not water-soluble so can’t be removed from body easily. Binds to albumin to be transported to the liver.
Conjugated= form that results after liver processess unconjugated bilirubin. Makes it water-soluble (by binding unconjug bilirubin with glucuronic acid) so it can be excreted from body through bile, into GI tract and out in stool.
Pathophysiology of intrahepatic/hepatocellular jaundice?
Dysfunction of hepatic cells -> liver loses ability to conjugate bilirubin.
If it becomes cirrhotic it compressess the intra-hepatic portions of the biliary tree to cause a degree of obstruction.
Leads to both UNCONJUGATED and CONJUGATED bilirubin in the blood- ‘mixed-picture’.
Pathophysiology of post-hepatic jaundice?
Obstruction of biliary drainage. The bilirubin that is not excreted has still been conjugated by the liver so you get CONJUGATED hyperbilirubinaemia.
What type of bilirubin can be excreted in urine?
conjugated as it is water soluble
unconjugated cannot
Why may you get dark urine in jaundice?
Conjugated or mixed hyperbilirubinaemias (as only conjugated bilirubin can be excreted in urine).
In unconjugated hyperbilirubinaemia the urine is normal (unsoluble so can’t be excreted in urine).
Why may you get pale stools in jaundice?
If obstructive picture and there will be reduced levels of stercobilin entering GI tract which normally colours the stool.
LFTs: bilirubin?
quantify degree of any suspected jaundice
LFTs: albumin?
marker of liver synthesising function
LFTs: AST and ALT?
markers of hepatocellular injury
LFTs: alkaline phosphatase (ALP)?
raised in biliary obstruction (as well as bone disease, during pregnancy, and certain malignancies)
LFTs: Gamma-GT (GGT)?
more specific for biliary obstruction than ALP; may be raised in alcohol use
(not routinely performed)
LFTs: AST:ALT ratio >2?
likely alcoholic liver disease
LFTs: AST:ALT around 1?
likely viral hepatitis
Liver screen includes what?
viral serology and non-infective markers.
performed when there is no initial cause for liver dysfunction, tailored to acute or chronic liver failure
Liver screen for acute liver injury?
Viral serology=
- hep A, B, C, E
- CMV and EBV
Non-infective markers=
- paracetamol level
- caeruloplasmin
- antinuclear antibody and IgG subtypes
Liver screen for chronic liver injury?
Viral serology=
- hep B, C
Non-infective markers=
- ceruloplasmin
- ferritin and transferrin saturation
- Tissue Transglutaminase antibody
- Alpha-1 antitrypsin
- Autoantibodies: AMA, ANA, Anti-SMA
Autoantibodies in liver screen eg. for chronic liver injury?
- anti-microchondrial antibody (AMA)
- anti-smooth muscle antibody (Anti-SMA)
- anti-nuclear antibody (ANA)
used to identify autoimmune liver conditions eg. PCS
Cx of liver disease (need to monitor for)?
- Coagulopathy= vit K or fresh frozen plasma (FFP) if needed if evidence of bleeding or rapid coagulopathy. Mx hypoglycaemia orally if possible or 5% dextrose
- Confusion from decompensating chronic liver disease (encephalopathy)= laxatives (lactulose or senna) +/- neomycin or rifaximin to reduce no. of ammonia-producing bacteria in bowel (no. of functional liver cells reduced, some toxins not removed eg. ammonia and can damage nerve cells and astrocytes)
What may low levels of Ceruloplasmin mean?
Wilson’s (copper overload)
Acute liver failure?
Rapid onset hepatocellular dysfunction leading to variety of systemic Cx
Causes of acute liver failure?
- paracetamol overdose
- alcohol
- viral hep (usually A or B)
- acute fatty liver of pregnancy
Features of acute liver failure?
- jaundice
- coagulopathy: raised prothrombin time
- hypoalbuminaemia
- hepatic encephalopathy
- renal failure common (hepatorenal syndrome)
How is liver function best assessed?
Prothrombin time and albumin level.
LFTs not always reflect function of liver accurately.
eg. in cirrhosis the liver’s ability to synthesise proteins is compromised so get low albumin.
Men and women should drink no more than how many units?
14 per week spread evenly over 3d+
1 unit of alcohol is equal to what?
10mL pure ethanol
Examples of 1 unit of alcohol?
- 25ml single measure of spirit (ABV 40%)
- a third of a pint of beer (ABV 5-6%)
- half a 175ml ‘standard’ glass of red wine (ABV 12%)
Calculate no. of units?
(ml x ABV)/1000
Alcoholic ketoacidosis?
Non-diabetic euglycaemic form of ketacidosis occuring in people who regularly drink large amounts of alcohol.
Pathophysiology of alcoholic ketoacidosis?
alcoholics will not eat regularly and may vomit food if they do eat -> episodes of starvation -> malnourished -> after alcohol binge the body starts to break down fat producing ketones -> ketoacidosis
What does alcoholic ketoacidosis typically present with?
- metabolic acidosis
- elevated anion gap
- elevated serum ketone levels
- normal or low glucose conc
Mx for alcoholic ketoacidosis?
IV saline + thiamine (to avoid Wernicke encephalopathy or Korsakoff psychosis)
Angiodysplasia?
Vascular deformity of GI tract which predisposes to bleeding and iron def anaemia
Angiodysplasia is generally seen in who?
elderly
?association with aortic stenosis
Featues of angiodysplasia?
- anaemia
- GI bleeding= upper (melena) or lower (brisk, fresh red PR bleeding)
Diagnosis of angiodysplasia?
- colonoscopy
- mesenteric angiography if acutely bleeding
Mx of angiodysplasia?
- endoscopic cautery or argon plasma coagulation
- antifibrinolytics e.g. Tranexamic acid
- oestrogens may also be used
Leukotrienes (in arachidonic acid metabolism)?
- LTB4: B4 (before) leukocytes comes LTB$
- the rest A, C, D & E constrict the lungs
Endoperoxides (in arachidonic acid metabolism)?
- THROMBOxane think THOMBOSIS= platelet aggregation and vasoconstriction
- prostacyclin is the opposite + decreased uterine tone
- Prostaglandin= increased pain, temp, uterine tone and gastric mucus. Decreased gastric acid. Varying effects on vascular smooth muscle and airways.
Arachindonic acid metabolism?
Phospholipid —(phospholipase A2)—–> Arachidonic acid then either…
—(COX1, COX2)–> endoperoxides
or
–(Lipoxygenase)—> HPETEs
and HPETEs to either—> LB4 or —> Leukotrienes (LA4, LC4, LD4, LE4)
Autoimmine hepatitis?
Unknown aietiology most commonly seen in young females.
Autoimmune hepatitis associations?
autoimmune disorders; hypergammaglobulinaemia; HLA B8, DR3
3 types of autoimmune hepatitis that are characterised depending on what?
the type of circulating antibodies present
Type I autoimmune hepatitis?
- ANA and/or ASMA
- both adults and children
Type II autoimmune hepatitis?
- anti-liver/kidney microsomal type 1 antibodies (LKM1)
- children only
Type III autoimmune hepatitis?
- soluble liver-kidney antigen
- middle-aged adults
Features of autoimmune hepatitis?
- signs of chronic liver disease
- acute hepatitis (25%)= fever, jaundice ect
- amenorrhoea (common)
- ANA/ASMA/LKM1 antibodies, raised IgG levels
- liver biopsy= inflam extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
Mx of autoimmune hepatitis?
- steroids; other immunosupressants eg. azathioprine
- liver transplant
Barrett’s oesophagus?
metaplasia of lower oesophageal mucosa= stratified squamous epithelium replaced by columnar
Risk of what with Barrett’s?
oesophageal adenocarcinoma (50-100fold)
Is there screening for Barrett’s?
no- typically identified who pt has endoscopy for upper GI symptoms eg. dyspepsia
How is Barrett’s subdivided?
short (<3cm) and long (>3cm)
Histological features of Barrett’s?
columnar epithelium may resemble that of the cardiac region of the stomach of small bowel (eg. with goblet cells, brush border)
RFs for Barrett’s?
- GORD (strongest)
- male
- smoking
- central obesity
alcohol isn’t even though it is for GORD and oeso ca
CP of Barrett’s?
asymptomatic but with have coexistent GORD symptoms
Mx of Barrett’s?
- high dose PPI
- if metaplasia (but not dysplasia)= endoscopic surveillance with biopsies every 3-5yrs
- if dysplasia of any grade is identified= endoscopic intervention eg. radiofrequency ablation
Metaplasia vs dysplasia?
M= transformation of one cell type into another type
D= transformation of one cell type to abnormal version of itself
Bile acid malabsorption is a cause of what?
Chronic diarrhoea
Bile acid malabsorption can be what?
primary= XS production of bile acid
or
secondary= underlying GI disorder causing reduced bile acid absorption
What can bile-acid malabsorption lead to?
- chronic diarrhoea
- steatorrhoea
- vit A, D, E, K malabsorption
Secondary causes of bile acid malabsorption?
- pts with ileal disease eg. Crohn’s
- cholecystectomy
- coeliac
- small intestinal bacterial overgrowth
Ix for bile-acid malabsorption?
SeHCAT
(nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT))
- scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
Mx of bile-acid malabsorption?
Cholestyramine (bile acid sequestrant)
Budd-chiari syndrome?
or hepatic vein thrombosis
usually seen in context of underlying haem disease or another precoagulant condition
Causes of Budd-Chiari syndrome (hepatic vein thrombosis)?
- polycythaemia rubra vera
- thrombophilia: activated protein C resistance, antithrombin III def, protein C & S def
- preg
- COCP (20% cases)
Triad of Budd-Chiari syndrome (hepatic vein thrombosis)?
- abdo pain: acute, severe
- ascites= abdo distention
- tender hepatomegaly
Ix for Budd-Chiari syndrome (hepatic vein thrombosis)?
USS with Doppler flow studies
Mx for Budd-Chiari syndrome (hepatic vein thrombosis)?
- anticoagulants mainly
- thrombolysis and stenting
Carcinoid tumours (carcinoid syndrome)?
occurs when mets are present in liver and release serotonin into systemic circulation; may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
Carcinoid tumours (carcinoid syndrome) CP?
- flushing (early)
- diarrhoea
- bronchospasm
- hypotension
- right heart valvular stenosis (left heart in bronchial carcinoid)
- ACTH and GHRH may be secreted so get eg. Cushing’s
- pellagra (rare)= dietary tryptophan is diverted to serotonin by tumour
Ix for Carcinoid tumours (carcinoid syndrome)?
- urinary 5-HIAA
- plasma chromogranin A y
Mx for Carcinoid tumours (carcinoid syndrome)?
- somatostatin analogues eg. octreotide
- diarrhoea= cyproheptadine
Drug-induced liver disease can be divided into what?
- hepatocellular
- cholestatic
- mixed
Drugs that can cause a hepatocellular picture in drug-induced liver disease?
- PARACETAMOL
- sodium valproate, phenytoin
- MAOIs
- halothane
- anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
- statins
- alcohol
- amiodarone
- methyldopa
- nitrofurantoin
Drugs that can cause cholestasis (+/- hepatitis) in drug-induced liver disease?
- COCP
- Abx= co-amoxiclav, fluclox, erythromycin
- anabolic steroids, testosterones
- phenothiazines: chlorpromazine, prochlorperazine
- sulphonylureas
- fibrates
- rare reported causes: nifedipine
Drugs that may cause liver cirrhosis in drug-induced liver disease?
- methotrexate
- methyldopa
- amiodarone
Ferritin?
intracellular protein that binds iron and stores it to be released in controlled fashion at sites where iron is required
What level is classed as increased ferritin?
> 300ug/L in men/postmenopausal women and >200ug/L in premenopausal women
Why may falsely elevated results of ferritin be encountered clinically?
Ferritin is an acute phase protein and may be synthesised in increased quantities in situations where there is inflammation; so take elevated ferritin in context of the clinical picture and blood results.
Causes of increased ferritin?
- Without iron overload (90% pts)= inflammation (due to being an acute phase reactant); alcohol XS; liver disease; CKD; malignancy.
- With iron overload (10%)= primary iron overload (hereditary haemochromatosis) and secondary iron overload (eg. following repeated transfusions)
Best way to test to see whether iron overload is present? (is ferritin actually high or is it just high due to inflam, alcohol ect)
Transferrin saturation=
<45% in females and <50% in males EXCLUDE iron overload
What may cause reduced ferritin levels?
iron def anaemia (iron and ferritin are bound, so the total ferritin levels may be decreased)
What can be useful to determine whether an apparently low Hb and microcytosis is truly caused by an iron def state?
serum ferritin levels
Gilbert’s syndrome?
Autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase.
1-2% of population.
Gilbert’s is due to def of what?
UDP glucuronosyltransferase
Features of Gilbert’s syndrome?
- unconjugated hyperbilirubinaemia (so not in urine)
- jaundice= may only be seen during intercurrent illness, exercise or fasting
Ix and Mx for Gilbert’s syndrome?
Ix= rise in bilirubin following prolonged fasting or IV nicotinic acid
Mx= no treatment needed (benign condition, only mild rise in bilirubin)
Unconjugated hyperbilirubinaemia and jaundice only when pt is ill, exercise or fasting?
Gilbert’s
Is Gilbert’s a serious condition?
No, common and mild.
Benign (harmless)- doesn’t lead to liver damage or serious health problems. Just a condition that affects liver’s ability to process bilirubin.
Hepatic encephalopathy?
May be seen in liver disease. XS absorption of ammonia and glutamine from the bacterial breakdown of proteins in the blood/
What may cause hepatic encephalopathy?
- acute liver failure (most common)
- chronic eg. liver cirrhosis may get mild cognitive impairment- ‘minimal’ HE
- TIPSS may precipitate encephalopathy
Features of hepatic encephalopathy?
- confusion, altered GCS
- asterixus (liver flap), arrhythmic negative myoclonus with a freq of 3-5Hz
- constructional apraxia: inability to draw a 5 pointed star
- triphasic slow waves on EEG
- raised ammonia level (not commonly measured anymore)
Grading of hepatic encephalopathy?
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
Precipitating factors of hepatic encephalopathy?
- infection e.g. spontaneous bacterial peritonitis
- GI bleed
- TIPSS
- constipation
- drugs: sedatives, diuretics
- hypokalaemia
- renal failure
- increased dietary protein (uncommon)
Mx of Hepatic encephalopathy?
TUC
1st= lactulose first line, with + rifaximin for secondary prophylaxis
other= embolisation of portosystemic shunts and liver transplant
Why do lactulose and Abx eg. rifaximin work for hepatic encephalopathy?
L= promotes excretion of ammonia and increases metabolism of ammonia by gut bacteria
Rif= modulate the gut flora resulting in decreased ammonia production
Examples of hepatobiliary conditions?
- viral hepatitis
- congestive hepatomegaly
- biliary colic
- acute cholecystitis
- ascending cholangitis
- gallstone ileus
- cholangiocarcinoma
- acute pancreatitis
- pancreatic ca
- amoebic liver abscess
Key features of viral hepatitis?
- N&V
- anorexia
- myalgia
- lethargy
- RUQ pain
- IVDU or foreign travel
Key features of congestive hepatomegaly?
liver only causes pain if stretched; common way this can occur is as a consequence of congestive HF; cirrhosis may occur in severe disease/
Key features of acute cholecystitis?
- pain similar to biliary colic but more severe and persistent
- pain may radiate to right shoulder or back
- may be pyrexial and Murphy’s sign +ve
Key features of ascending cholangitis?
- infection of bile ducts commonly secondary to gallstones
- triad= fever (rigors), RUQ pain, jaundice
Key features of gallstone ileus?
- small bowel obstruction secondary to impacted gallstone
- may develop if a fistula forms between a gangrenous gallbladder and duodenum
- abdo pain, distention, vomiting
Key features of cholangiocarcinoma?
- persistent biliary colic, anorexia, jaundice, weight loss
- Courvoisier sign (palpable mass in RUQ)
- Sister Mary Joseph Nodes (periumbilical lymphadenopathy)
- Virchow mode (left supraclavicular adenopathy
Key features of pancreatic ca?
- PAINLESS JAUNDICE
- pain can be common presentation
- anorexia, weight loss
Key features of amoebic liver abscess?
- malaise, anorexia, weight loss
- RUQ pain mild
- jaundice uncommon
Hepatorenal syndrome?
Form of impaired kidney function that occurs due to advanced liver disease.
Pathophysiology of hepatorenal syndrome?
Vasoactive mediators cause splanchnic vasodilation -> reduces systemic vascular resistance -> ‘underfilling’ of the kidneys -> this is sensed by juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system -> renal vasocontriction which is not enough to counterbalance the effects of splanchnic vasodilation
2 types of Hepatorenal syndrome?
Type 1 HRS= rapidly progressive; very poor prognosis; doubling of serum creatinine to >221ugmol/L or a halving of the creatinine clearance to less than 20ml/min over period of less than 2w.
Type 2 HRS= slowly progressive; prognosis poor but pts may live for longer
Mx for hepatorenal syndrome?
- GOLD= liver transplant but often too unwell to have surgery
- Vasopressin analogues eg. terlipressin= cause vasocontriction of the splanchnic circulation
- volume expansion with 20% albumin
- TIPSS
4 inherited causes of jaundice and do they cause conjugated or unconjugated hyperbilirubinaemia?
Unconjugated= Gilbert’s and Crigler-Najjar syndrome
Conjugated= Dubin-Johnson syndrome and Rotor syndrome
Key features of Gilbert’s?
autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign
Key features of Crigler-Najjar syndrome type 1?
autosomal recessive
absolute deficiency of UDP-glucuronosyl transferase
do not survive to adulthood
Key features of Crigler-Najjar syndrome type 2?
slightly more common than type 1 and less severe
may improve with phenobarbital
Key features of Dubin-Johnson syndrome?
autosomal recessive.
Relatively common in Iranian Jews
mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
results in a grossly black liver
benign
Key features of Rotor syndrome?
autosomal recessive
defect in the hepatic uptake and storage of bilirubin
benign
Iron studies?
- serum iron
- total iron binding capacity (TIBC)
- transferrin saturation
- ferritin
- Rare= transferrin receptors increased in IDA
Total iron binding capacity (TIBC)?
- transferrin
- raised in iron def anaemia (IDA)
- raised in preg and by oestrogen
Transferrin saturation?
calculated by serum iron/TIBC
Ferritin?
raised in inflam disorders and low in IDA
Results of iron studies in anaemia of chronic disease?
- normo/hypochromic/, normocytic anaemia
- reduced serum and TIBC
- normal or raised ferritin
Ischaemic hepatitis?
diffuse hepatic injury resulting from acute hypoperfusion (sometimes knows as ‘shock liver’). Not inflamm process.
Diagnosis= presence of inciting event eg. cardiac arrest and marked increases in aminotransferase levels (>1000 or 50x the upper limit of normal)
Often occurs in conjunction with AKI (tubular necrosis) or other end-organ dysfunction.
Melanosis coli?
Pigmentation of the bowel wall.
Histology= pigment-laden macrophages.
Associations= laxative abuse espec anthraquinone compounds eg. senna
Metabolic alkalosis?
Caused by loss of H+ ions or gain of bicarbonate. Mainly due to problems of kidney or GI tract.
Causes of metabolic alkalosis?
- Vomiting/aspiration: eg. peptic ulcer leading to pyloric stenos, nasogastric suction; vomiting may also lead to hypokalaemia
- diuretics
- liquorice, carbenoxolone
- hypokalaemia
- primary hyperaldosteronism
- Cushing’s
- Bartter’s syndrome
Mechanism of metabolic alkalosis?
- activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
- aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
- ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
- in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
Molecular biology techniques?
- Southern blotting= detects DNA
- Northern blotting= detects RNA
- Western blotting= detects proteins; uses gel electrophoresis to separate native proteins by 3D structure; eg. confirmatory HIV test
(SNOW DROP= (South, North, West) and (DNA, RNA, Protein)
- ELISA
Enzyme-linked immunosorbent assay (ELISA)?
a type of biochemical assay used to detect antigens and antibodies
a colour changing enzyme is attached to the antibody if looking for an antigen and to an antigen if looking for an antibody
the sample therefore changes colour if the antigen or antibody is detected
an example includes the initial HIV test
3 less common oesophageal disorders?
- Plummer-Vinson syndrome
- Mallory-Weiss syndrome
- Boerhaave syndrome
Key features of Plummer-Vinson syndrome?
Triad= glossitis, iron def anaemia and dysphagia (secondary to oesophageal webs)
Mx= iron supplements and dilation of the webs
Key features of Mallory-Weiss syndrome?
severe vomiting -> painful mucosal lacerations at gastroesophageal junction -> haematemesis.
Common in alcoholics; after many bouts of vomiting.
Boerhaave syndrome?
Severe vomiting -> oesophageal rupture
Peutz-Jeghers syndrome?
autosomal dominant condition characterised by numerous hamartomatous polyps in GI tract.
Prognosis of Peutz-Jegers syndrome?
although polyps themselves don’t have malignant potential, around 50% pts have died from another GI ca by age of 60yrs
Peutz-Heghers syndrome genetics?
autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11
Peutz-Jeghers syndrome features?
hamartomatous polyps in the gastronintestinal tract (mainly small bowel)
- small bowel obstruction is a common presenting complaint, often due to intussusception
- gastrointestinal bleeding
pigmented lesions on lips, oral mucosa, face, palms and soles
Mx of Peutz-Jeghers syndrome?
Conservative unless Cx develop
Pyogenic liver abscess most common organisms found?
staph aureus in children and E.coli in adults
Mx of pyogenic liver abscess?
- Drainage (percutaneous) and Abx:
amoxicillin + ciprofloxacin + metronidazole
or if allergic:
ciprofloxacin + clindamycin
Scoring systems for liver cirrhosis?
- Model for End-Stage Liver Disease (MELD) is newer (particularly pts who are on liver transplant waiting list)
- Child-Pugh classification is older
Child-Push classification for severity of liver cirrhosis?
bilirubin, albumin, PT, encephalopathy ans ascites.
Severity is A (<7), B (7-9) or C (>9)
Model for End-Stage Liver Disease (MELD) scoring system for liver cirrhosis?
bilirubin, creatinine and INR to predict survival.
3 month mortality calculated based on MELD scores.
particularly for pts on liver transplant list
Small bowel bacterial overgrowth syndrome (SBBOS)?
XS amounts of bacteria in small bowel resulting in GI symptoms
RFs for SBBOS?
- DM
- neonates with congenital GI abnormalities
- scleroderma
CP of SBBOS?
overlap with IBS
- chronic diarrhoea
- bloating flatulence
- abdo pain
Diagnosis of SBBOS?
- hydrogen breath test
- small bowel aspiration and culture: less often
- may give Abx as diagnostic trial
Mx for SBBOS?
- TUC
- Abx= rifaximin
Villous adenoma?
colonic polyps with potential for malignant transformation; secrete large amounts of mucous, potentially resulting in electrolyte disturbances
Features of villous adenoma?
- most asymptomatic
- non-spec lower GI symptoms
- secretory diarrhoea
- microcytic anaemia
- hypokalaemia
Whipple’s disease?
rare multi-system disorder caused by Tropheryma whippelii infection.
more common in middle aged men and those who are HLA-B27 +ve
Features of whipple’s disease?
- malabsorption: diarrhoea, weight loss
- large-joint arthralgia
- lymphadenopatjy
- skin: hyperpigmentation and photosensitivity
- pleurisy, pericarditis
- neuro symptoms (rare): opthalmoplegia, dementia, seizures, ataxia, myoclonus
Ix for whipple’s disease?
Jujunal biopsy= deposition of macrophages containing Periodic acid-Schiff (PAS) granules
Mx for whipple’s disease?
guidelines vary
oral co-trimoxazole for 1yr and sometimes preceded by a course of IV penicillin
Wilson’s disease?
autosomal recessive disorder characterised by XS copper deposition in tissues
Metabolic abnormalities from Wilson’s disease?
increased copper absorption from small intestine and decreased hepatic copper excretion
Wilson’s disease is caused by a defect in what gene/chromosome?
Defect in gene ATP7B located on chromosome 13
When does the onset of symptoms in Wilson’s typically occur?
between 10-25yrs
First sign of Wilson’s disease in children vs adults?
children= present with liver disease
adults= neuro disease
Features from Wilson’s result from what?
XS copper deposition in tissues, espec the brain, liver and cornea.
Features of Wilson’s disease?
- Liver= hepatitis and cirrhosis
- Kayser-Fleischer rings
- Neuro= speech, behavioural and psychiatric probems
- renal tubular acidosis (esp. Fanconi syndrome)
- haemolysis
- blue nails
Neurological features of Wilson’s?
- basal ganglia degeneration: in brain; most copper deposited in basal ganglia, particularly in putamen and globus pallidus
- speech, behavioural and psychiatic problems often 1st manifestation
- also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings in Wilson’s?
- green-brown rings in the periphery of the iris
- due to copper accumulation in Descemet membrane
- present in around 50% pts with isolated hepatic Wilson’s and 90% who have neuro invl.
Ix for Wilson’s?
- slit lamp exam for Kayser-Fleischer rings
- reduced serum caeruloplasmin
- reduced total serum copper
- increased 24hr urinary copper excretion
- diagnosis confirmed= genetic analysis of ATP7B gene
Why do you get reduced total serum copper in Wilson’s?
- counter-intuitive but 95% of plasma copper is carried by ceruloplasmin and in Wilson’s ceruloplasmin is reduced
- but free (non-ceruloplasmin-bound) serum copper is increased
- also as copper accumulates in tissues there is less available in bloodstream
Mx of Wilson’s?
Penicillamine (chelates copper) 1st line
(trientine hydrochloride is alternative chelating agent)
Zollinger-Ellison syndrome?
XS levels of gastrin secondary to a gastrin secreting tumour
majority of these tumours found in first part of duodenum; second most common location is the pancreas
In Zollinger-Ellison syndrome, around 30% of gastrinomas occur as part of what?
MEN type I syndrome
Features of Zollinger-Ellison syndrome?
- multiple gastroduodenal ulcers
- diarrhoea
- malabsorption
Diagnosis of Zollinger-Ellison syndrome?
- Fasting gastrin levels (best screen test)
- secretin stimulation test
Mx of Zollinger-Ellison syndrome?
- High dose PPI (manage the extra stomach acid and help stop ulcer developing)
- Curative= surgery
