Gastroenterology Flashcards
Symptoms/presentation of Dyspepsia?
Oesophageal:
- Odynophagia
- Dysphagia
- Heartburn
Gastric
- Epigastric pain
- nausea and vomiting
- Bloating
General:
- Weight loss
- Appetite increase/decrease
Causes of Dyspepsia?
Oesophageal causes:
- GORD
- Barret’s oesophagus
Gastro-duodenal
- PUD- gastric and duodenal
- Gastric cancer
- Functional dyspepsia
Other causes:
- Biliary diseases (gall stones)
- Jaundice
- Pancreatic diseases
Management of Dyspepsia
- Investigate possible causes for dyspepsia (H pylori, gastric or Oesophageal cancer, Drugs, stress/trauma)
- Refer for OGD- if meets the criteria
- Life-style management: Weight loss (if high BMI), Elevate the head while sleeping, Stop smoking, Reduce alcohol consumption
- Medicinal management: Depends on the cause, Anyone with uninvestigated dyspepsia must be treated with PPI.
WHat is gold standard for dyspepsia
OGD
gold standard for investigating dyspepsia.
What is the criteria to be eligible for OGD?
>55 years
Dyspepsia
Alarm symptoms:
- Weight loss- unintentional
- Persistent GI bleed
- Difficulty swallowing/ inability to swallow
- Persistent vomiting
- Fe deficiency anaemia
- Epigastric mass
- Haematemesis
Pathology of GORD
Three main mechanisms: Poor oesophageal motility decreases clearance of acidic material. A dysfunctional LES allows reflux of large amounts of gastric juice. Delayed gastric emptying can increase the volume and pressure in the reservoir until the valve mechanism is defeated, leading to GORD.
The opening of the LOS results in a backflow/ aspiration of gastric content and acid into the oesophagus causing irritation and inflammation of the lining of the oesophagus. Persistent acid reflux damages the oesophageal mucosa causing complications
Complications of GORD
Oesophagitis, Oesophageal stenosis, Barrett’s oesophagus
Hiatus hernia (but note HH does not always cause GORD)
oesophageal adenocarcinoma
ulceration: rarely→haematemesis, melaena,↓F
Symptoms/Presentations of GORD
- Heartburn: related to meals. Worse lying down / stooping, Relieved by antacids
- Waterbrash
- Regurgitation
- May present with odynophagia
- Nocturnal asthma
- Chronic cough
- Laryngitis, sinusitis
Investigations of GORD
- Isolated symptoms don’t need Ix
- Bloods:FBC
- CXR:hiatus hernia may be seen
- OGD if: >55yrs, Symptoms >4wks, Dysphagia, Persistent symptoms despite Rx, Wt. loss, OGD allows grading by Los Angeles Classification
- Ba swallow:hiatus hernia, dysmotility
- 24h pH testing ± manometry
- pH <4 for >4hr
Management of GORD?
Lifestyle modifications:
- Weight loss
- Stop smoking
- Reduce alcohol
- Elevate head while sleeping
- Small regular meals ≥ 3h before bed
- Stop drugs: NSAIDs, steroids, CCBs, nitrate
Medications
- OTC antacids: Gaviscon, Mg trisilicate
- 1:Full-dose PPI for 1-2mo -Lansoprazole 30mg OD
- 2:No response→double dose PPI BD
- 3:No response: add an H2RA -Ranitidine 300mg nocte
- Control: low-dose acid suppression PR
Surgery
- Nissen Funoplication : usually laparoscopic approach, mobilise gastric funds and wrap around lower oesophagus. Repai diaphram and close any diaphragmatic hiatus
- Complications: gast- bloat: inability to belch/vomit. Dysphagia if wrap too tight
Differential Dx for GORD
- Oesophagitis: Infection: CMV, candida, IBD, Caustic substances / burns
- PUD
- Oesophageal Ca
What is peptic ulceration?
Ulcer in stomach or duodenum - most benign but gastric ulcers can be malignant
- It is a defect of the gastric/ duodenal mucosa which extends to the muscularis mucosa
- Gastric ulcer: defect of the gastric mucosa that is >0.5cm and extends to the muscularis mucosa
- Duodenal ulcer: defect of the duodenal mucosa extending to the muscularis mucosa
Causes of PUD?
H pylori infection
H pylori
NSAIDs and aspirin
Stress- also called curling ulcers
Neuroendocrine tumors- Zollinger Ellison tumour
How does H pylori and NSAIDS/aspirin cause PUD?
H pylori infection
H pylori🡪 produces Urease🡪 breakdown urea into NH3🡪 creates an alkaline environment that favors bacterial colonization🡪 release of bacterial cytotoxins 🡪 cause damage to the mucosa lining of the stomach
NSAIDs and aspirin
Inhibition of COX 1 and COX2🡪 decreased prostaglandins🡪 decreased mucosal blood flow, inhibition of mucosal epithelium proliferation, decreased HCO3-🡪 Damage to the mucosa–> ulcer
Presentation of Barret’s metaplasia?
Appears red as compared to the adjacent pink squamous cell mucosa of the oesophagus
The transition zone (Z line) is shifted upwards
The physiological transformation zone separating the squamous cells from the columnar cells
Pre-malignant change- requires close monitoring
Increased risk of Oesophageal adenocarcinoma
Treatment for Barret’s Oesophagus?
PPI
Biopsies to rule out dysplasia and cancer
Low grade dysplasia= need radio-ablation or endoscopy every 6-12 months taking biopsies every 1cm
Oesophageal adenocarcinoma Pathology?
- It is associated with Barret’s oesophagus
- Intestinal metaplasia- Tumour produces mucins
- Tumour mutations in TP53
- It occurs in the distal colon
- Hence lymph node spread- gastric and coeliac nodes
- Usually presents after lymph node metastasis and hence poor prognosis as compared to squamous cell carcinoma
Investigations for Oesophageal adenocarcinoma
Endoscopy
Biopsy
Oesophageal squamous cell carcinoma
- Oesophageal squamous-cell carcinomas may occur as ______ ________tumors associated with _____ and ______ cancer, due to field cancerization
- Primary oesophageal cancer however is more commonly an _________
- Anal cancers are normally ________ _______ ________
- Oesophageal squamous-cell carcinomas may occur as second primary tumors associated with head and neck cancer, due to field cancerization
- Primary oesophageal cancer however is more commonly an adenocarcinoma
- Anal cancers are normally squamous cell carcinomas
Adenocarcinoma
- Stomach is lined by ______ ________ normally
- Risk factors for cancer = ________, diet, __ ______ ______
- Two types of gastric adenocarcinoma: _______ vs _______
- Intestinal type forms glands (polypoid)
- Stomach is lined by glandular epithelium normally
- Risk factors for cancer = smoking, diet, H pylori infection
- Two types of gastric adenocarcinoma: Intestinal vs Diffuse type
- Intestinal type forms glands (polypoid)
Epidemiology of squamous cell carcionoma
Male > female (4:1)
More seen in the African American population
Epidemiology of Oesophageal Adenocarcinoma?
Male > female (7:1)
More seen in the Caucasian population
What is Crohn’s disease?
Inflammation that can involve one small area of the gut, or multiple areas with normal bowel in between: SKIP LESIONS
AKA Cobblestone appearance
Commonly affects the terminal ileum and ascending colon- resulting in RLQ pain
Transmural Inflammation: Damage extends beyond the submucosal layer and through the depth of the entire intestinal wall (unlike UC)
micro organisms related to Crohns
Mycobacterium paratuberculosis as well Pseudomonas and Listeria species
Complications of Crohns
fistulae, abscess, bowel obstruction, perforation, toxic megacolon, kidney stones, Bowel cancer (adenocarcinoma), gallstones
Patho fo UC
AUTOIMMUNE Th2 mediated rxn, where cytotoxic T cells target abnormal gut bacteria or p-ANCA antibodies, thus eroding the lining of the intestines, and ulceration
The circumferential inflammation can destroy the haustras of the colon leading to a smooth section of colon which is called the “lead pipe” sign.
Prevalent in non-smokers/ex-smokers*
Classifications of UC
- Proctitis: Just the rectum
- Proctosigmoiditis: Involves the rectum and sigmoid colon
- Left sided Colitis: Involves the descending colon up to the splenic flexure
- Extensive Colitis: Extending to the hepatic flexure
- Pancolitis/Universal colitis: The entire colon is affected, associated with Backwash Ileatis (inflammation of the terminal ileum)
Difference between Crohns and UC
What is Diverticulitis?
Inflammation of abnormal pouches called diverticula (can develop on the walls of the large intestine, or any other hollow structure). Usually 0.5c,-1cm large
True Diverticula: involve all layers of the intestine
Pseudo diverticula: Muscle layers are not included MOST COMMON
When abdominal outpouching occurs without inflammation, it is called ________
diverticulosis
Risk factors for Diverticulitis?
Obesity, lack of exercise, low fibre diet, Smoking, Connective tissue disorders (genetic), Family history, NSAIDs, Common in the western world, Elderly, Females
Symptoms of Diverticulitis?
Symptoms: MOST CASES ARE ASYMPTOMATIC
- Lower abdominal pain (sudden onset)- mostly affects the Sigmoid colon- LLQ pain and tenderness
- Erratic bowel habits
- Symptoms of infection (fever, tachycardia), Nausea, Diarrhea, Constipation, Fever, blood/mucus in the stool
Investigations and Treatment for Diverticulitis?
Raised CRP and ESR, USS, CT, Barium enema, Sigmoidoscopy
Treatment
If less severe: analgesia, Fibre, Antibiotics, Fluid resus
Surgical resection if acutely unwell
What is Coeliac’s disease?
An AUTOIMMUNE DISORDER where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel. It usually develops in early childhood but can start at any age.
1 in 100 people have it. Family History increases risk to 1 in 10.
Pathophysiology of Coeliac’s Disease
Gluten is a large molecule, that is broken down to smaller ones in the gut, and it is the breakdown products that are toxic (gliadins). The main toxic peptide is α-Gliadin.
Autoantibodies are created in response to exposure to gluten, which target the epithelial cells of the intestines, leading to inflammation in the small bowel (particularly jejunum)
It causes atrophy of the intestinal villi, and crypt hypertrophy, so the surface of the bowel becomes flattened, and the surface area for absorption becomes greatly reduced (malabsorption)
Important antibodies to know for coeliac disease?
- Anti-TTG (anti-tissue transglutaminase)- attacks TTG, which is responsible for gluten breakdown
- Anti-EMA (Anti-endomysial)
- DGP (deaminated gliadin peptide)
Clinical features of Coeliac Disease
Often asymptomatic (can be mistaken for IBS), Steatorrhea, failure to lose/gain weight, abdo pain, cramps, bloating, distension, diarrhoea, fatigue, mouth ulcers, anaemia, dermatitis herpetiformis, osteomalacia, Vit D and calcium deficiency, neurological (ataxia, epilepsy)
Coeliac disease diagnosis?
Check for total IgA levels whilst on gluten diet
- Raised Anti-TTG antibodies serology (FIRST LINE)
- Raised anti-endomysial antibodies
- deaminated gliadin peptide (DGP) – in cases of patients who have a IgA deficiency
Duodenal Biopsy to confirm
Genetic testing for HLADQ2 and HLADQ8
What is IBS?
- Irritable bowel syndrome (IBS) is a group of symptoms—including abdominal pain and changes in the pattern of bowel movements without any evidence of underlying damage (like inflammation, ulcers etc).
- It has been classified into four main types depending on whether diarrhoea is common, constipation is common, both are common, or neither occurs very often
IBD vs IBS?
IBD has structural damage to the bowel (ie inflammation, ulceration) in ADDITION to IBS symptoms
Diagnosis of IBS
What is the criteria used called
Other pathology should be excluded:
- Normal FBC, ESR and CRP blood tests
- Faecal calprotectin negative to exclude inflammatory bowel disease
- Negative coeliac disease serology (anti-TTG antibodies)
- Cancer is not suspected or excluded if suspected
Symptoms should suggest IBS:
Abdominal pain / discomfort pain for ≥12wks which has 2 of:
- Relieved by defecation
- Change in stool frequency (D or C)
- Change in stool form: pellets, mucu
AND 2 of:
- Abnormal stool passage: incomplete/urgency
- Bloating/Distention
- Worse symptoms after eating
- PR mucus
ROME CRITERIA
Risk factors for IBS
Female, stress, gastroenteritis (nota/rotavirus)
Treatment for IBS?
- A low FODMAPS diet:
F- fermentable
O- oligosaccharides 🡪 sucrose (Wheat, rye, legumes and various fruits and vegetables, such as garlic and onions.)
D- disaccharides 🡪 lactose (Milk, yogurt and soft cheese)
M- monosaccharides 🡪 fructose (Various fruit including figs and mangoes, and sweeteners such as honey
Andmitriptyline
P- polyols 🡪 sugar free sweeteners ( Certain fruits and vegetables including blackberries and lychee, as well as some low-calorie sweeteners like those in sugar-free gum.)
- Avoid caffeine and alcohol
- Probiotics, regular small meals, reduced processed food, physical activity, for constipation: soluble fibres, laxatives, stool softeners, for pain: anti-diarrhoeals (ie loperamide), antimuscarinics, antispasmodics (mebeverine)
- Manage stress, anxiety and depression- CBT
- Amitriptyline
Genetic connections with coeliac disease
Genetic connections:
HLA-DQ2 gene (90%)
HLA-DQ8 gene
What are Gallstones?
Incidence?
RF?
Symptoms
Formation of hard stones in the gallbladder
Incidence increases with age. More common in women.
F – Fat
F – Fair
F – Female
F – Forty
Most are asymptomatic and are discovered when they cause biliary colic etc
What are the types of gallstones?
- Cholesterol gallstones are the most common stones -supersaturation of bile with cholesterol –Gallbladder stasis -cannot been seen on X-RAY . However if they have enough CaCO3
- Bilirubin gallstones are the 2nd most common stones: AKA pigmented
- can be seen on X-RAY as the bilirubin binds to calcium
–associated with : hemolytic disease, E.coli
What if the stones are brown in colour?
- sign of infection (caused by bacteria Ecoli)
- causes calcium + UBC
- browness is due to hydrolysed phospholipid too in it.
What is biliary colic? and where would you find pain?
Biliary colic, also known as symptomatic cholelithiasis, a gallbladder attack or gallstone attack, is when a colic (sudden pain) occurs due to a gallstone temporarily blocking the cystic duct.
- Intermittent RUQ pain that comes in waves
- Pain MAY radiate to R shoulder tip
- Typically starts in the evening and lasts till the morning
- Recurring condition, usually managed with diet adjustment
What is Cholecystitis? and where would you find pain?
- Inflammation of the cystic duct due to gallstone obstruction
- Prolonged colicky pain which MAY radiate to the shoulder tip
- Inflammation->Fever + leucocytosis
- Murphy’s Sign. There will be RUQ pain that is usually worse on inspiration.
What is Choledocholithiasis? where would you get pain?
- Common bile duct obstruction
- No inflammation -> no fever or leucocytosis
- Obstructive jaundice
- Dilated hepatic ducts
- RUQ pain> 6h
What is Cholangitis? where would you get pain?
Infection of the gallbladder and CBD
Charcot triad-> fever, jaundice and RUQ pain
Reynolds triangle -> hypotension (shock) +altered mental status + Charcoat triangle. This occurs when the infection becomes more advanced
RUQ pain
Murphy sign
Complications of gallstones?
- Cholecystitis , Acute cholangitis + Mirizzi syndrome
- Empyema +perforation
- Jaundice -> obstructive jaundice
- Acute pancreatitis -> epigastric pain, radiates to the back , curling makes it better
- Cancer of the gallbladder
- Gallstone ileus
A bowel obstruction requires immediate medical treatment. If it’s not treated, there’s a risk that the bowel could split open (rupture).
What is PRIMARY SCLEROSING CHOLANGITIS
Primary (not caused by something else)
Sclerosing (hardening/fibrosis of tissue)
Cholangitis (inflammation of bile ducts)
Disorder caused due to the chronic inflammation of the intra hepatic and extra hepatic bile ducts leading to fibrosis
More commonly occurs in males (around 30-50 years)
Causes of PRIMARY SCLEROSING CHOLANGITIS
The exact cause is unknown but it has a strong association with autoimmune disesases, especially inflammatory bowel disease (most commonly UC).
In most patients, there is presence of antibodies such as pANCA and ANA antibodies but these are not specific for the disease.
It is linked to HLA DR3 and HLA B8
Associated diseases for PRIMARY SCLEROSING CHOLANGITIS
UC
Crohn’s (much rarer)
AIH
HIV
Sclerosing Cholangitis vs Biliary Cirrhosis
WHat is PRIMARY BILIARY CHOLANGITIS?
Disorder caused due to the chronic inflammation of the intra hepatic bile ducts leading to fibrosis
More commonly occurs in females (around 30-65 years)
Presentation of PRIMARY BILIARY CHOLANGITIS
Think of PPBBCCS
- Often asympto and Dx incidentally (↑ALP)
- Jaundice occurs late
- Pruritus and fatigue
- Pigmentation of face
- Bones: osteoporosis, osteomalacia (↓vit D)
- Big organs: HSM
- Cirrhosis and coagulopathy (↓vit K)
- Cholesterol↑: xanthelasma, xanthomata
- Steatorrhoe
What is appendicitis?
causes?
Inflammation of the appendix
Can occur at any age but most commonly in the elderly or in the 2nd decade of life.
It is due to the obstruction of the appendix lumen by hyperplasia of the lymphoid tissue, feces, worms, foreign body etc.
Patho of appendicitis?
Once the lumen is obstructed, it can lead to bacterial overgrowth, ischemia, inflammation etc.
If untreated, it can lead to necrosis, peritonitis, gangrene, perforation etc
Pain in Appendicitis?
Visceral pain
n the early stages, the pain will be poorly localized to the periumbilical or epigastric region. This is because the organ is poorly innervated by the lesser splanchnic nerves which localise the pain to the centre of the abdomen.
Pain in Appendicitis?
Somatic pain
In the later stages, as the inflammation becomes worse, it spreads to the parietal peritoneum in that area, so the pain can be localized. This is because the peritoneum is supplied by the same nerve as the respective dermatome.
So, initial pain will be in the periumbilical region and then will localize to the RIF as the inflammation becomes worse
How is the pain in appendicitis described?
It is described as constant and sharp
What is Mcburney’s point?
2/3’s of the way along an imaginary line from the umbilicus to the anterior superior iliac spine on the right hand side
What is Rovsing’s Sign?
pain felt in the LRQ when the LLQ is palpated
Psoas sign –
increased pain during passive extension of the right hip
Obturator sign
pain felt on passive internal rotation of the flexed hip
what does Washboard ridgidity
This shows that there is peritonitis. the pain is exacerbated by the slightest movement (e.g. rolling, coughing, even breathing) as this moves the peritoneum.
Characteristics fo autoimmune hepatitis?
- Increased IgG levels
- Antibodies against:
Liver specific proteins
Non-live specific proteins
Mononuclear infiltrate within the liver:
Monocytes, macrophages, lymphocytes, plasma cells, macrophages and mast cells
Key definitions relating to gallbladder and gallstones?
- Cholestasis
- Cholelithiasis:
- Choledocholithiasis:
- Biliary colic:
- Cholecystitis:
- Cholangitis:
- Gallbladder empyema:
- Cholecystectomy:
- Cholecystostomy:
- Cholestasis: blockage to the flow of bile
- Cholelithiasis: gallstone(s) are present
- Choledocholithiasis: gallstone(s) in the bile duct
- Biliary colic: intermittent right upper quadrant pain caused by gallstones irritating bile ducts
- Cholecystitis: inflammation of the gallbladder
- Cholangitis: inflammation of the bile ducts
- Gallbladder empyema: pus in the gallbladder
- Cholecystectomy: surgical removal of the gallbladder
- Cholecystostomy: inserting a drain into the gallbladder
atients with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction.
TRUE OR FALSE
TURE
Ix for gallstones
LFTs- raised bilirubin, ALP
USS- first line
In a raised ALT and AST with higher rise in ALP , this suggest?
cholestasis an”obstructive picture”
If ALT and AST are high compared with the ALP level, this is more indicative of…
a problem inside the liver with hepatocellular injury “a hepatitic picture”
A raised ALP is consistent with ______ ___________ in presence of right upper quadrant pain and/or jaundice.
A raised ALP is consistent with biliary obstruction in presence of right upper quadrant pain and/or jaundice.
What is (MRCP)
A magnetic resonance cholangio-pancreatography (MRCP) is an MRI scan with a specific protocol that produces a detailed image of the biliary system. It is very sensitive and specific for biliary tree disease, such as stones in the bile duct and malignancy.
MRCP is used in a number of scenarios for gaining a detailed picture of the biliary system, such as identifying biliary strictures or congenital abnormalities.
With gallstone disease, MRCP is typically used to investigate further if the ultrasound scan does not show stones in the duct, but there is bile duct dilatation or raised bilirubin suggestive of obstruction.
What is ERCP
Complications
An endoscopic retrograde cholangio-pancreatography (ERCP) involves inserting an endoscope down the oesophagus, past the stomach, to the duodenum and the opening of the common bile duct (the sphincter of Oddi). This gives the operator access to the biliary system.
The main indication for ERCP is to clear stones in the bile ducts.
Key complications of ERCP are:
- Excessive bleeding
- Cholangitis (infection in the bile ducts)
- Pancreatitis
Complications of cholecystectomy include:
- Bleeding, infection, pain and scars
- Damage to the bile duct including leakage and strictures
- Stones left in the bile duct
- Damage to the bowel, blood vessels or other organs
- Anaesthetic risks
- Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
- Post-cholecystectomy syndrome
What is Post-cholecystectomy syndrome
Post-cholecystectomy syndrome involves a group of non-specific symptoms that can occur after a cholecystectomy. They may be attributed to changes in the bile flow after removal of the gallbladder. Symptoms often improve with time. Symptoms include:
- Diarrhoea
- Indigestion
- Epigastric or right upper quadrant pain and discomfort
- Nausea
- Intolerance of fatty foods
- Flatulence
What is Wilson Disease?
How is it inherited?
What gene and what chromosome?
Wilson disease is the excessive accumulation of copper in the body and tissues. It is caused by a mutation in the “Wilson disease protein” on chromosome 13. The Wilson disease protein also has the catchy name “ATP7B copper-binding protein” and is responsible for various functions, including the removal of excess copper in the liver. Genetic inheritance is autosomal recessive.
Clinical Features of Wilson disease?
think of CLANKAH
Cornea
- Kayser-Fleischer rings (70%, may need slit-lamp)
Liver Disease
- Children usually present c̄acute hepatitis.
- Fulminant necrosis may occur
- →cirrhosis
Arthritis
- Chondrocalcinosis
- Osteoporosis
Neurology
- Parkinsonism:bradykinesia,tremor, chorea, tics
- Spasticity, dysarthria, dysphagia
- Ataxia
- Depression, dementia, psychosis
Kidney
- Fanconi’s syn. (T2 RTA)→osteomalacia
Abortions
Haemolytic anaemia
- Coombs’ negative
Copper deposition in the liver leads to ____ _____ and eventually liver cirrhosis. Copper deposition in the ______ _____ ______ can lead to neurological and psychiatric problems.
Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis. Copper deposition in the central nervous system can lead to neurological and psychiatric problems.
Ix of Wilson Disease?
- Bloods:↓Cu,↓caeruloplasmin
NB. Caeruloplasmin is an acute-phase protein and maybe high during infection. It may also be low protein-deficient states: nephroticsyndrome, malabsorption
- ↑24h urinary Cu
- Liver biopsy:↑hepatic Cu
- MRI:basal-ganglia degeneration
Management for wilsons disease
Treatment is with copper chelation using:
- Penicillamine (lifelong)
- Trientene
eating typically worsens the pain of ______ ulcers and improves the pain of _________ ulcers.
eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
Management for peptic ulcer?
Peptic ulcers are diagnosed by endoscopy. During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.
Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers
First, Second and Third line Medication for IBS
First Line Medication:
- Loperamide for diarrhoea
- Laxatives for constipation. Avoid lactulose as it can cause bloating. Linaclotide is a specialist laxative for patients with IBS not responding to first-line laxatives
- Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)
Second Line Medication:
- Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)
Third Line Medication:
- SSRIs antidepressants
What is hiatus hernia
A hiatus hernia is when part of your stomach moves up into your chest. It’s very common if you’re over 50. It does not normally need treatment if it’s not causing you problems
Explain the classification of Hiatus Hernia?
Sliding (80%)
- Gastro-oesophageal junction slides up into chest
- Often assoc. c̄GORD
Rolling (15%)
- Gastro-oesophageal junction remains in abdomen but abulge of stomach rolls into chest alongside theoesophagus
- LOS remains intact so GORD uncommon
- Can→strangulation
Mixed (5%)
Ix for Hiatus Hernia
- CXR:gas bubble and fluid level in chest
- Ba swallow: diagnostic
- OGD: visualises the mucosa but can’t exclude hernia
- 24h pH + manometry:exclude dysmotility or achalsia
Tx for Hiatus Hernia
- Lose wt.
- Rx reflux
- Surgery if intractable symptoms despite medical Rx.-Should repair rolling hernia (even if asympto) as it may strangulate
What is hereditary haemochromatosis
How is it inherited
What gene on what chromonsome:
Hereditary hemochromatosis (he-moe-kroe-muh-TOE-sis) causes your body to absorb too much iron from the food you eat. Excess iron is stored in your organs, especially your liver, heart and pancreas. Too much iron can lead to life-threatening conditions, such as liver disease, heart problems and diabetes
AR
HFE gene (High FE) on Chr6 (C282Y
Patho haemochromatosis
- Inherited, multisystem disorder resulting from abnormaliron metabolism.
- ↑intestinal Fe absorption (↑enterocyte DMT +↓hepatocyte hepcidin)→deposition in multiple organ
Clinical features of Haemochromotosis
Myocardial
- Dilated cardiomyopathy
- Arrhythmias
Endocrine
- Pancreas: DM
- Pituitary: hypogonadism→amenorrhoea, infertility
- Parathyroid: hypocalcaemia, osteoporosis
Arthritis
- 2ndand 3rdMCP joints, knees and shoulders
Liver
- Chronic liver disease→cirrhosis→HCC
- Hepatomegaly
Skin
- Slate grey discolouration
Ix of Haemochromatosis
- Bloods:↑LFT,↑ferritin,↑Fe,↓TIBC, glucose, genotype
- X-ray:chondrocalcinosis
- ECG, ECHO
- Liver biopsy:Pearl’s stain to quantify Fe and severity
- MRI:can estimate iron loading
Treatment for haemochromotosis
Iron removal
- Venesection: aim for Hct <0.5
- Desferrioxamine is 2ndline
General
- Monitor DM
- Low Fe diet
Screening
- Se ferritin and genotype
- Screen 1stdegree relatives
Transplant in cirrhosis
Patho of Wilson’s Disease
- Mutation of Cu transporting ATPase
- Impaired hepatocyte incorporation of Cu intocaeruloplasmin and excretion into bile.
- Cu accumulation in liver and, later, other organ
Symptoms and signs of PSC
Symptoms
- Jaundice
- Pruritus and fatigue
- Abdo pain
Signs
- Jaundice: dark urine, pale stools
- HSM
Complications of PSC
Bacterial cholangitis
↑Cholangiocarcinoma
↑CRC
Ix for PSC
- LFTs:↑ALP initially, then↑BR
- Abs:pANCA (80%), ANA and SMA may be +ve
- ERCP/MRCP:“beaded” appearance of ducts
- Biopsy:fibrous, obliterative cholangitis
Associated diseased with primary bilary cirrhosis ?
rimary biliary cholangitis is associated with metabolic or immune system disorders, including thyroid problems, limited scleroderma (CREST syndrome), rheumatoid arthritis, and dry eyes and mouth (Sjogren’s syndrome)
What are the types of Liver function tests?
ALT- Markers of hepatocellular damage, localised to liver
AST- Markers of hepatocellular damage, synthesised by liver, heart, skeletal muscle and brain
Billirubin- Assessing degree of jaundice
gGT- Cholestasis
ALP- Cholestasis – sources are bone and liver
Albumin- Synthetic function
Prothrombin time - Synthetic function
Liver function tests- imaging
- USS- Ultrasound is usually first line. Identifies any obstructive pathology present or gross liver pathology
- Fibroscan
- MRI
- MRCP- Used to visualise the biliary tree. Usually performed if obstructive jaundice is suspected or US is inconclusive
- X rays – hepatic angiogram
- CT
- Biopsy- Performed when the diagnosis has not been made despite the above investigations
What is Jaundice?
yellow appearance of the skin, sclerae and mucous membranes resulting from an increased bilirubin concentrations in body fluids
What are the types of jaundice?
- Pre-hepatic
- Hepatic/ intrahepatic/ hepatocellular
- Post-hepatic
Pre-hepatic jaundice and also be called?
haemolytic jaundice
What is pre hepatic jaundice?
Excessive red cell breakdown which overwhelms the liver’s ability to conjugate bilirubin 🡪 unconjugated hyperbilirubinemia
Any bilirubin that manages to become conjugated is excreted normally
Unconjugated bilirubin in the blood causes jaundice
ALT, AST, ALP will be normal
Examples of conditons that can see pre hepatic jaundice?
- Examples
- Haemolytic anaemia
- Malaria
- Sickle cell thalassemia
- SLE
What is hepatic jaundice?
- Due to dysfunction of the hepatic cells
- Liver loses the ability to conjugate bilirubin
- Liver may become cirrhotic 🡪 compromises the intra-hepatic portions of the biliary tree to cause some obstruction
- Both unconjugated and conjugated bilirubin are found in blood
- High ALT, AST and ALP (higher ALT&AST)
Examples of conditions where you can hepatic jaundice?
- Alcoholic liver disease
- Viral hepatitis
- Primary biliary cirrhosis
- Hepatocellular carcinoma
What is Post-hepatic jaundice
- AKA obstructive jaundice
- Due to obstruction of biliary drainage
- Bilirubin that has been conjugated by the liver is not excreted
- Excess conjugated bilirubin = conjugated hyperbilirubinemia
- High ALP, AST and ALT (higher ALP)
What is Acute liver failure?
Onset of hepatic decompensation within 6 months, results in loss of function in 80-90%
Causes of Acute Liver failure?
- Drugs
50% of cases in the UK due to paracetamol overdose
others inc NSAIDs and ecstasy
- Infection
Viral hepatitis, CMV, HSV, EBV
- Acute fatty liver in pregnancy
Unmetabolized fetal fatty acids enter maternal circulation and accumulate in mothers liver
- Wilsons disease
AR, copper accumulates in the liver
- Budd-Chiari
Occlusion of hepatic vein
Abdo pain + ascites + liver enlargement
Clinical features of Acute liver failure?
- Jaundice
- Bruising (coagulation disturbance)
- Ascites
- Tachycardia and hypotension
- Due to reduced systemic vascular resistance
- Signs of encephalopathy
- Sweet smell on breath
Complications of acute liver failure
- Hepatic encephalopathy = altered level of consciousness
- Impaired protein synthesis = measured by serum albumin + prothrombin time in blood
What is Chronic liver failure
Progressive destruction/regeneration of liver parenchyma leading to fibrosis and cirrhosis (> 6 months
Causes of chronic liver failure
- Metabolic
Hereditary haemochromatosis -Accumulation of iron, reacts with H2O2 to form free radicals
NAFLD
Wilsons disease
- Toxic and drugs
Alcohol
Drug induced is rare 🡪 methotrexate, amiodarone
- Infections – hep b & c
- Autoimmune
Primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis
Clinical features of Chronic liver failure?
- Nail clubbing
- Palmar erythema
- Spider nevi
- Gynaecomastia
- Feminising hair distribution
- Small irregular shrunken liver
- Anaemia
- Caput medusae
Complications of chronic liver failure?
- Portal hypertension
- Synthetic dysfunction
- Hepatopulmonary syndrome
- Hepatorenal syndrome
- Encephalopathy
- Hepatocellular carcinoma
What is portal hypertension?
- Increased blood pressure in the hepatic portal system (portal venous system) usually due to hepatic cirrhosis
- Obstruction may prevent the blood flow from the portal vein into the IVC
- Causes the blood to accumulate in the hepatic portal system 🡪 increasing the pressure 🡪 PORTAL HYPERTENSION
- Portosystemic Shunts- anastomoses between portal and systemic systems, due to portal HTN the blood backs up and varices form- these can rupture
- Features (ABCDE)- ascites, bleeding, caput medusae, diminished liver function and enlarged spleen
What is hepatic encephalopathy?
Reduced blood to liver 🡪 reduced liver function
Increased ammonia crosses BBB
Can be gradual or sudden
In advanced stages 🡪 coma
Clinical features of heaptic encephalopathy
Asterixis, lethargy, movement problems, changes in mood or changes in personality, altered consciousness, seizures
What is treatment for hepatic encephalopathy?
Treatment = Oral lactulose
What is Hepatopulmonary syndrome
Syndrome of shortness of breath and hypoxemia caused by vasodilation in lungs of patients with liver disease
Causes of hepatopulmonary syndrome?
Due to formation of microscopic intrapulmonary arteriovenous dilations
Thought to be due to increased liver production or decreased liver clearance of vasodilators, e.g. NO
Dilation of blood vessels 🡪 over-perfusion relative to ventilation 🡪 V/Q mismatch
Increased gradient between the partial pressure of O2 in alveoli and adjacent arteries
What is Hepatorenal syndrome?
Life-threatening medical condition that consists of rapid deterioration of kidney function in individuals with cirrhosis or fulminant liver failure
Occurs due to portal hypertension
What is HEpatocellular carcinoma
Malignant tumour of the liver which occurs primarily in patients with pre-existing liver cirrhosis or chronic hepatitis
Most common type of primary liver cancer
Malignant tumour of the liver which occurs primarily in patients with pre-existing liver cirrhosis or chronic hepatitis
Most common type of primary liver cancer
What is the adenoma- carcinoma sequence?
A stepwise pattern; of mutational activation of oncogenes ( ie Kras) and inactivation of tumour suppressor genes (eg p53) that results in cancer
Environmental factors that leads to GI cancer development
- Smoking
- Alcohol
- Diet; processed meat ( especially red meat), increased obesity risk, green vegetables and diet high in fibre protective against colorectal cancer
- Chronic inflammation ie patients with ulcerative colitis have increased risk of developing colorectal cancer
- Upper GI cancer; H pylori infection?
Hallmarks of cancer
Hallmarks of cancer
Environmental factors that leads to GI cancer development
- Smoking
- Alcohol
- Diet; processed meat ( especially red meat), increased obesity risk, green vegetables and diet high in fibre protective against colorectal cancer
- Chronic inflammation ie patients with ulcerative colitis have increased risk of developing colorectal cancer
- Upper GI cancer; H pylori infection?
what is Colorectal cancer development in relation to TSG and Oncogenes
- Inactiviation of APC
- Activation of Kras
- Inactivation of p53
what is Colorectal carcinogenisis in IBD development in relation to TSG and Oncogenes?
Same genes different order
- P53
- Kras
- APC
what is Colorectal carcinogenisis in IBD development in relation to TSG and Oncogenes?
Same genes different order
- P53
- Kras
- APC
what is Colorectal cancer development in relation to TSG and Oncogenes
- Inactiviation of APC
- Activation of Kras
- Inactivation of p53
APC KRA and P53
which of these are tumour supressor genes?
APC and P53
APC KRas and P53
Which of these are oncgenes?
KRas
APC KRas and P53
Which of these are oncgenes?
KRas
APC KRA and P53
which of these are tumour supressor genes?
APC and P53
Difference between HNPCC and FAP
Difference between HNPCC and FAP
Pathology of Colorectal Cancer
Most common : adenocarcinoma ( a malignant tumour formed from glandular structures of the epithelial tissue)
Less common; mucinous adenocarcinoma, signet ring cell carcinoma, small cell carcinoma
Glandular dysplasia is the premalignant lesion, when it forms a poly it is commonly referred to as an adenoma
Adenomas classified as tubular, tubulovillous and villous (the is the worst one)
Adenomas are also graded in terms of dysplasia (low or high)
Staging using TNM for Corectal Cancers
Tumour staging
Staging using TNM for Corectal Cancers
Lymph nodes staging
Staging using TNM for Corectal Cancers
Metastasis staging
Staging using TNM for Corectal Cancers
Metastasis staging
Pathology of gastric cancers?
Pathology of gastric cancers?
Staging using TNM for Corectal Cancers
Lymph nodes staging
Staging using TNM for Corectal Cancers
Tumour staging
Pathology of Colorectal Cancer
Most common : adenocarcinoma ( a malignant tumour formed from glandular structures of the epithelial tissue)
Less common; mucinous adenocarcinoma, signet ring cell carcinoma, small cell carcinoma
Glandular dysplasia is the premalignant lesion, when it forms a poly it is commonly referred to as an adenoma
Adenomas classified as tubular, tubulovillous and villous (the is the worst one)
Adenomas are also graded in terms of dysplasia (low or high)
What are the causes of acute pancreatitis?
Gallstones - Obstruct sphincter of Oddi causing reflux . Bile salts irritates pancreatic duct
Ethanol - Increases acinar cell secretion, decreases ductal cell secretion → thickened pancreatic juice . ROS damages the cells
Trauma - Usually ruptured duct in the body of the pancreas from direct trauma (vertebral column)
Drugs - sodium valporate, furosemide, thiazides, Azathioprine
What are the causes of acute pancreatitis?
Gallstones - Obstruct sphincter of Oddi causing reflux . Bile salts irritates pancreatic duct
Ethanol - Increases acinar cell secretion, decreases ductal cell secretion → thickened pancreatic juice . ROS damages the cells
Trauma - Usually ruptured duct in the body of the pancreas from direct trauma (vertebral column)
Drugs - sodium valporate, furosemide, thiazides, Azathioprine
Name some drug induced Jaundice
Name some drug induced Jaundice
Viral Hepatitis
There are types A-E
explain how they are spread and their cause
Viral Hepatitis
There are types A-E
explain how they are spread and their cause
