Gastroenterology Flashcards
Describe some types of upper GI bleeds and their appearance
Haematemesis - fresh red blood
Biliary vomiting - coffee ground brown colour
Malaena (partially digested blood) - maroon and tar like
List some potential differentials for upper GI bleeding
(Common)
- Peptic ulcer disease
- Oesophageal varices
- Oesophagitis
- Malloy Weiss tear (partial thickness tear)
(Uncommon)
- Cancers of the GI tract
- Boerhaave syndrome (full thickness tear)
- Gastric varices
- Angiodysplasia
- Dieulafoy’s
List 2 assessment scores for Upper GI bleeds, including what it helps to determine
- ROCKALL score
- Simple score based on bedside observations
- However requires an endoscopy (has pre-endoscopy and post-endoscopy score)
- Helps to determine the risk of dying as a result of the upper GI bleed - Glasgow-Blatchford score
- More time-consuming as it requires blood tests and results of these
- Helps to determine the need for hospital admission and need for interventions e.g. endoscopy or blood transfusion
List some investigations that are required for an upper GI bleed
(with an A-E assessment)
Upper endoscopy
- Looks for source of bleeding
- Looks for active bleeding
Venous blood gas
- Quick way of getting Hb
FBC
- Check Hb levels and platelet count (low in chronic liver disease)
U&E
- Raised urea supports upper GI bleeding
Clotting factors
- May need to correct abnormal clotting
LFTs
Also cross matching for significant bleeds (G&S for less significant bleeds)
Outline the steps in management of upper GI bleeds (variceal and nonvariceal bleeding)
Both: check observations to check if haemodynamic instability
Variceal bleeding:
- Gain IV access and IV fluid resuscitation, followed by blood transfusion
- IV Terlipressin (inotrope) and prophylactic IV antibiotics
- OGD is definitive management: oesophageal banding, Linton tube or trans-hepatic portal systemic shunt
- Also consider stopping any offending drugs e.g. anticoagulants and NSAIDs
- If unsuccessful, Sengstaken-Blakemore tube or stenting can control bleeding
Non-variceal bleeding:
- Gain IV access (IV fluids if hemodynamically unstable)
- Definitive treatment depends on the cause: endoscopy (mechanical e.g. clips, thermal coagulation, fibrin or thrombin), embolisation or surgery
- Stop any offending drugs e.g. anticoagulants and NSAIDs
List some of the symptoms and signs of Crohn’s disease
Presentation: Younger age, increased incidence in smokers
Symptoms:
- Frequent loose stools (often without blood)
- Abdominal pain
- Abdominal distension
- Fever
- Unintentional weight loss
- Fatigue
- Mouth ulcers
- Arthritis / joint pains
Signs:
- Fever
- Evidence of perianal disease
- Weight loss
- Pallor / anaemia
List some of the symptoms and signs of ulcerative colitis (UC)
Presentation: Younger age, decreased incidence in smokers
Symptoms:
- Frequent loose stools (often bloody)
- Abdominal pain
- Abdominal distension
- Fever
- Fatigue
- Mouth ulcers
- Arthritis / joint pains
Signs:
- Fever
- Pallor / anaemia
- Abdominal tenderness
List some investigations for Crohn’s disease and ulcerative colitis (and to exclude other diseases)
Bloods - routine bloods to rule out other conditions:
FBC - anaemia or raised platelet count
U&Es - deranged electrolytes or AKI due to dehydration
CRP
Stool test:
- Rule out infective colitis
- Faecal calprotectin - more than 90% specific and sensitive for IBD (raised in active disease but specific to IBD)
Imaging:
Endoscopy = diagnostic OGD or colonoscopy
Abdominal x-ray - used for toxic megacolon or proximal constipation (proximal to area of inflammation)
CT or MRI for complications e.g. fistulas, abscess or strictures
Outline management to induce remission in Crohn’s disease, including if IV Hydrocortisone doesn’t work in 3-5 days
Steroid treatment:
Oral - Prednisolone or Budesonide
IV - Hydrocortisone 100mg QDS (if unwell)
Topical - suppositories or enemas
If IV Hydrocortisone isn’t working after 3-5 days = rescue treatment
- Biologics e.g. Infliximab or Adalimumab
- Surgery (50% of patients requiring rescue treatment will need surgery)
Outline management to induce remission in ulcerative colitis, including if IV Hydrocortisone doesn’t work in 3-5 days
Mild-moderate disease:
-Topical (PR) Mesalazine
- Consider oral corticosteroids e.g. Prednisolone
Severe:
- IV Hydrocortisone (steroids)
May want to use laxatives if there is proximal constipation
If IV Hydrocortisone isn’t working after 3-5 days = rescue treatment
- IV Ciclosporin
- Biologics
- Surgery (50% of patients requiring rescue treatment will need surgery)
Outline the drugs used to maintain remission in Crohn’s and UC, as well as what parameters require regular monitoring
Crohn’s disease:
- Azathioprine
- Mercaptopurine
- Methotrexate
- Biologics e.g. Infliximab or Adalimumab
UC:
- Mesalazine
- Azathioprine (if Mesalazine unsuccessful)
- Biologics (if Mesalazine unsuccessful) e.g. Infliximab or Adalimumab
Regular monitoring of:
- FBCs
- U&Es
- LFTs
Because IBD treatments are immunosuppressive medications
Also regular colonoscopy (starting 10 years after diagnosis) to look for the development of cancers
Outline some ways in which malnutrition may manifest in patients
- Weight loss / loose fitting clothes / muscle wasting
- Poor wound healing
- Prolonged / non-resolving infections
- Apathy (lack of enthusiasm/interest)
- Altered bowel habit
- Reduced appetite
State the method of investigation for malnutrition
MUST screening (Malnutrition Universal Screening Tool)
- 5 step screening tool to identify adults who are: malnourished, at risk of malnutrition or adults who are obese
Outline 5 steps of MUST screening
Step 1:
- Calculate BMI (give score)
Step 2:
- Calculate percentage loss of body weight (give score)
Step 3:
Acute illness or not (give score) - if patient is acutely ill and likely no nutritional
intake for > 5 days
Step 4:
- Add scores for steps 1- 3 to obtain overall risk
Step 5:
- Develop care plan
For the following outcomes from MUST screening, suggest the management options:
1. Low risk
2. Medium risk
3. Severe risk
- Low risk - routine clinical care
- Repeat screening
Hospital – weekly
Care Homes – monthly
Community – annually for special groups e.g. those >75 yrs - Medium risk - observe
- Document dietary intake for
3 days
- If satisfactory, follow low risk rules
- If unsatisfactory, follow local policy and set goals with regular monitoring as above - Severe risk - treat
- Refer to dietitian or implement local policy
- Set goals and regular monitoring as above
Outline how surgery can be used in the management of Crohn’s disease and UC
Crohn’s:
- Surgery can be used when the disease only affects the distal ileum to prevent further flares
- However, Crohn’s commonly affects the entire GI tract
- Surgery can also be used to treat strictures and fistulas
UC:
- Panproctocolectomy (removal of colon and rectum)
- Create a permanent ileostomy or J-pouch (ileo-anal anastomosis
List some parameters that are taken into account in the Glasgow-Blatchford score for Upper GI bleeds
Assess risk of GI bleed and used to determine management pathway
Parameters:
- Raised urea
- Drop in Hb
- Decreased blood pressure
- Increased heart rate
Other factors:
- Malaena
- Syncope
- Liver disease
- Cardiac failure
List some parameters that are taken into account in the ROCKALL score for Upper GI bleeds
Assess risk of mortaility from an upper GI bleed in patients who have had an endoscopy
Parameters:
- Age
- Features of shock e.g. hypotension and tachycardia
- Co-morbidities
- Cause of bleeding e.g. oesophageal varices, Malloy Weiss tear
- Evidence of recent haemorrhage on endoscopy
Why does urea increase in upper GI bleeds?
- Blood in the GI tract gets broken down by digestive enzymes and acid
- Urea is a breakdown product for the blood
- Urea is then absorbed into the intestines
List some things that the liver stores
- Glycogen
- Vitamins
- Iron
- Copper
List some synthetic functions of the liver
- Clotting factor synthesis
- Albumin synthesis
- Bile synthesis
- Glucose synthesis
- Lipid synthesis
List some metabolic (breakdown) functions of the liver
- Bilirubin breakdown
- Ammonia breakdown
- Drug breakdown
- Alcohol breakdown
- Carbohydrate and lipid breakdown
Outline the 3 key characteristic features of acute liver failure (ALF)
Rapid decline in hepatic function with:
1. Jaundice
2. Coagulopathy (INR >1.5)
3. Hepatic encephalopathy
All in patients with no evidence of prior liver disease
If existing disease, called acute-on-chronic liver failure
Outline the symptoms of acute liver failure
- Jaundice
- Itchy skin
- Altered mental status
- Right upper quadrant discomfort
- Nausea
- Features of fluid overload
List some common causes of acute liver failure
- Paracetamol overdose (66% of cases)
- Drug-induced liver injury e.g Aspirin
- Autoimmune hepatitis
- Hepatitis B or A (most common)
- Ischaemic hepatitis
List the classification for acute liver failure (based on time frame ALF developed over)
Hyperacute
- Within 7 days
Acute
- Between 8 and 28 days
Subacute
- Between 29 days and 3 months
List some investigations for suspected acute liver failure
Blood tests:
- Prothrombin time and INR
- Liver function tests (ALT, AST, ALP, bilirubin, albumin)
- Viral serologies
- Autoimmune markers
- Toxicology screening
- Serum amylase and lipase levels (exclude pancreatitis which can occur during ALF)
- Paracetamol levels (low level doesn’t rule out)
Doppler ultrasound - assess for Budd-Chiari syndrome
Chest x-ray - rule out pulmonary cause
Outline the immediate management for acute liver failure
- Admit to ICU if hepatic encephalopathy
- Bed angled to 30 degrees
- Tracheal intubation
- Enteral nutritional support
- Regular CBG monitoring and treat any hypoglycaemia
- Treat any infections aggressively
Outline the presentation of Paracetamol overdose
Same presentation as acute liver failure!
- Recent history of Paracetamol overdose
- Jaundice
- Itchy skin
- Altered mental status
- Right upper quadrant discomfort
- Nausea
- Features of fluid overload
Outline the immediate management of Paracetamol overdose in the following scenarios:
- Ingestion <1 hour ago
- Ingestion <4 hours ago
- Ingestion 4-24 hours
- Ingestion >24 hours and symptomatic
- Staggered overdose
Ingestion <1 hour ago:
- Activated charcoal (with IV anti-emetic)
Ingestion <4 hours ago:
- Wait until 4 hours have passed to take a level
- Treat with N-acetylcysteine based on level
Ingestion within 4-24 hours:
- Start N-acetylcysteine immediately
Ingestion >24 hours and symptomatic
- Start N-acetylcysteine immediately
Staggered overdose:
- Start N-acetylcysteine immediately
State the regional liver service for UHL
Liver unit at Queens Elizabeth Hospital Birmingham
Outline the pathophysiology of chronic liver disease
Chronic liver disease is a gradual deterioration of the function of the liver for > 6 months (includes synthesis of clotting factors, proteins e.g. albumin, detoxification and excretion of bile)
Continuous process of inflammation, destruction, and regeneration of liver parenchyma, which leads to fibrosis and cirrhosis
Outline the common causes of chronic liver disease
Most common general:
- Alcoholic Liver Disease
- NAFLD/NASH
- Chronic Viral Hepatitis
Genetic:
- Alpha-1 antitrypsin deficiency
- Hereditary hemochromatosis
Autoimmune:
- Autoimmune hepatitis (AIH)
- Primary biliary cirrhosis (PBC)
- Primary Sclerosing Cholangitis (PSC)
Others:
- Drugs: Amiodarone, Methotrexate, Phenytoin and Nitrofurantoin
- Budd-Chiari syndrome
- Idiopathic (around 15%)
State the presentation of chronic liver disease
- Ascites
- Oedema
- Jaundice and pruritus
- Easy bruising (prolonged INR/PT and APPT)
- Hepatic encephalopathy
- Asterixis (hepatic flap)
- Varices (oesophageal, rectal or umbilical)
Others (complications of cirrhosis):
- Hepatorenal failure (reduced renal function)
- Increased oestrogen leading to palmar erythema, spider navai and gynecomastia in men
Explain how cirrhosis relates to chronic liver disease
Cirrhosis is a final stage of chronic liver disease
List some of the LFT changes seen in chronic liver disease
- Raised ALT and AST (usually 2-3 Xs normal limit)
- Raised bilirubin (unconjugated> conjugated)
- Raised ammonia
- Decreased albumin
(If chronic liver disease is compensated in early stages, LFTs may be normal)
List some non-specific investigations that can be done to investigate chronic liver disease (other than LFTs)
Ultrasound abdomen:
- Detects size and nodularity (can diagnose cirrhosis)
- Can detect clotting in Budd-Chari and portal vein thrombosis
CT:
- Can show lesion in the liver or obstruction of biliary channels
- Triphasic CT is test of choice in diagnosing hepatocellular carcinoma
Transient elastography (TE)
- Detects early stages of cirrhosis
Doppler scan:
- Can help in diagnosing Budd-Chiari and portal vein thrombosis.
ECG:
- May show delta waves in hepatic encephalopathy
Upper endoscopy:
- Identify and treat oesophageal varices
Liver biopsy:
- Can confirm the diagnosis of chronic liver disease
Outline the management of alcoholic liver disease
- Alcohol abstinence!
- Nutritional support with vitamins, particularly thiamine
- High protein diet
- Referral for liver transplant, but most abstain from alcohol for at least 3 months prior to referral
Outline the management of non-alcoholic fatty liver disease
Has a benign course and does not warrant treatment beyond lifestyle modification
Management of metabolic syndrome components:
- Weight loss
- Increased physical activity
- Reduce cholesterol levels
- Reduce blood pressure
- Optimal control of diabetes and other co-morbidities
If advanced disease, can offer medications as has the potential to progress to cirrhosis in a significant number of patients
- Pioglitazone (decreases steatosis and aminotransferase levels)
- Vitamin E (significantly improves liver function and histological changes)
Outline the management of hepatitis C
Anti-retroviral therapy (expensive!)
Outline the management of hereditary haemachromatosis
Mainstay: venesection
Initial phase:
- Venesection weekly (removal of 500mL of blood) with FBC (checked weekly)
- Continue until serum ferritin is at acceptable level (checked monthly), then go onto maintenance phase
Maintenance phase:
- Typically venesection 3–4 times per year
Also offer blood tests (FBC, LFTs, serum ferritin and transferrin saturation) and genetic testing to immediate family members (genetic condition)
Reduces risk of developing complications related to liver disease or liver cancer
Outline the management of autoimmune liver disease
Requires life-long treatment to prevent cirrhosis and end-stage liver disease
Initial phase:
- Steroid induction therapy with Prednisolone (may add in Azathioprine)
Maintenance phase:
- Maintenance therapy with Azathioprine, introduced 2–4 weeks after initiation of Prednisolone
- Taper down dose as LFTs allow, to reduce steroid-related complication
Aim: Normalization of transaminases and immunoglobulin G
If untreated: can develop cirrhosis and end-stage liver disease
Outline some investigations for abnormal LFTs (non-invasive liver screen)
Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin saturation (hereditary haemochromatosis)
Outline the management of the following complications of chronic liver disease:
- Malnutrition
- Ascites / oedema
- Hepatic encephalopathy
(Exclude complications of portal hypertension)
Malnutrition:
- Regular meals (every 2-3 hrs)
- Low sodium, high protein, high calorie meals
- Avoid alcohol
Ascites / oedema:
- Diuretics (Spironolactone 1st line)
- Dietary salt restriction
- Bed rest
- Ascitic drainage (large volume paracentesis) with albumin infusion
Hepatic encephalopathy:
- Thiamine (B1) replacement
- Lactulose (promotes non-urease-producing bacteria in gut, leading to decreased colonic ammonia production and absorption)
- Rifaximin (decrease the enteric bacterial flora)
Finally, liver transplant
Outline the management of hepatorenal syndrome (complication of portal hypertension)
Hepatorenal syndrome:
- Improve kidney function by increasing renal blood flow
- Albumin (increases circulatory volume)
- Midodrine (peripheral alpha AR agonist, vasoconstriction)
- Octreotide (antagonises vasodilators)
List the management for hepatitis B and C
Hepatitis B:
- Prevention is key = vaccination, however not curable
- Antiviral drugs
1. Nucleoside/nucleotide analogues (NAs) - mainstay
2. Pegylated Interferon Alfa-2a (PEG-IFN)
- Screen for hepatocellular cancer (high risk of development)
- Patient education e.g. not to share items with family/friends like razors
- Family screening and vaccination
Hepatitis C:
- No vaccination, however is curable (90% cure rate)
- Antiviral drugs: Sofosbuvir and Daclatasvir
List some differential diagnoses for malaena
Upper GI bleed
(Common)
- Peptic ulcer disease
- Oesophageal varices
- Upper GI malignancy e.g. ulcerating oesophageal or gastric malignancies
(Less common)
- Gastritis
- Oesophagitis
- Meckel’s diverticulum
- Small bowel tumours
- Vascular malformations
Can be due to a bleed in the small bowel
List some differentials for jaundice (pre-hepatic, hepatic and post-hepatic)
Pre-Hepatic:
- Haemolytic anaemia
- Gilbert’s syndrome
- Criggler-Najjar syndrome
Hepatocellular:
- Alcoholic liver disease
- Hepatitis B or C
- Hereditary haemochromatosis
- Autoimmune hepatitis
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
- Hepatocellular carcinoma
- Iatrogenic, e.g. medication
Post-Hepatic:
- Intra-luminal causes, such as gallstones
- Mural causes, such as cholangiocarcinoma, strictures, or drug-induced cholestasis
- Extra-mural causes, such as pancreatic cancer or abdominal masses (e.g. lymphomas)
List the 4 most common causes of cirrhosis
Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C
List the marker for hepatocellular carcinoma
Alpha-fetoprotein
Outline the general monitoring tests (and their frequency) for chronic liver disease
6 monthly:
- Alpha-fetoprotein testing (for HCC)
- Ultrasound
3 yearly:
- Endoscopy (if no known varices)
Outline the management of oesophageal varices (complication of portal hypertension)
Prophylactic treatment:
- Non-selective beta blockers e.g. Propranolol
- Variceal ligation
- Injection of sclerosant (inflammatory obstruction of vessel)
- Transjugular intrahepatic portosystemic shunt (TIPS)
Active bleeding:
(Supportive)
- IV bolus
- Blood transfusion (FFP) and vitamin K
- Terlipressin (vasopressin)
- Broad-spectrum antibiotics
(Definitive)
OGD with:
- Variceal ligation
- Injection of sclerosant (inflammatory obstruction of vessel)
- Sengstaken-Blakemore tube
List some factors that precipitate hepatic encephalopathy
Electrolyte disturbances
Constipation
Infection
GI bleeding
High protein diet
Medications, particularly sedative medications
Outline the 4 grades of hepatic encephalopathy
Grade 1:
- Psychomotor slowing
- Constructional apraxia (unable to draw a 2D model or assemble an object)
- Poor memory
- Reversed sleep pattern
Grade 2:
- Lethargy
- Disorientation
- Agitation / irritability
- Asterixis
Grade 3:
- Drowsy / reduced conscious level
Grade 4:
- Coma
For the following vitamins, state a food that they can be taken from and what the vitamin is required for:
A
B1
B12
C
D
E
K
A: Root vegetables/liver
- Skin health
B1: Red meat / grains
- Neurone health
B12: Red meat
- Neurones / bone marrow
C: Citrus fruit
- Skin / gums
D: Dairy/fish
- Bones
E: Plant oils
- Antioxidant
K: Leafy vegetables
- Coagulation
List 3 consequences of muscle wasting in the elderly
- More likely to become bed bound
- Respiratory function decreases - increased risk of chest infections
- Reduced skin healing - increased risk of pressure sores
List some risks/complications of parenteral nutrition
Mechanical:
- Thrombosis
- Line damage
- Line blockage
- Pneumothorax (usually occurs on CVC insertion)
- Air embolus (if line left open)
Biochemical
- Electrolyte disturbance
- Hyperglycaemia
- Fluid overload
- Carbohydrate overload
Infectious:
- CVC related bacteraemia or sepsis
State how coeliac disease is diagnosed
- OGD
- Duodenal biopsies is the diagnostic test
Histologically changes:
- Villous atrophy
- Intra-epithelial lymphocytosis
List some complications of chronic coeliac disease
- Anaemia: iron, B12 or folate deficiency
- Hyposplenism
- Osteoporosis
- T-cell lymphoma (small bowel lymphoma)
List some extra-intestinal manifestations of ulcerative colitis
Correlates with disease activity:
- Erythema nodosum (red swellings on skin)
- Mouth ulcers (aphthous ulcers)
- Episcleritis (reddening of eye tissue)
- Joint pain (acute arthropathy)
Generally correlates with disease activity:
- Pyoderma gangrenosum (painful skin ulcers)
- Anterior uveitis (eye inflammation)
Doesn’t correlate with disease activity:
- Sacroiliitis (painful sacroiliac joint)
- Ankylosing spondylitis (inflammation and fusion of spine)
- Primary sclerosing cholangitis (narrowing of bile ducts)
Outline the scale used for alcohol withdrawal for patients admitted to hospital and rough management plan
Glasgow modified alcohol withdrawal scale - gives a score based on A HOST (Agitation, Hallucinations, Orientation, Sweating, Tremor)
- Assesses withdrawal risk
- Suggests the dose of Benzodiazepine required as well as the frequency of monitoring (how often the score should be recalculated)
Management:
- Oral benzodiazepine (Diazepam or Lorazepam) given, with symptom triggered dosing of medication
- IV Diazepam given if severe delirium tremens
Wernicke-Korsakoff Syndrome - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Caused by a thiamine (vitamin B1 deficiency)
- Alcohol reduces the absorption of thiamine, reduces stores in the liver and reduces enzyme activity that converts thiamine into an active state
- Generally caused by alcoholic disease but can also be caused by malnutrition
- Wernicke syndrome occurs first in an acute phase and if left untreated, will progress to chronic irreversible Korsakoff syndrome
Presentation:
Wernicke syndrome (triad)
1. Confusion / mental state changes
2. Ataxia
3. Eye movement dysfunction
Korsakoff syndrome:
- Memory impairment, specifically short-term memory loss (sometimes also have long-term memory loss)
Management:
- Thiamine replacement therapy (either prophylactically or as treatment)
- Alcohol abstinence
- Improved nutrition
If caught early, Wernicke’s syndrome can be reserved fully
List the 4 stages of hepatic encephalopathy (liver failure)
Stage 1
- Altered mood and behaviour
- Sleep disturbance
- Dyspraxia
Stage 2
- Drowsiness
- Confusion
- Slurring of speech
- Personality change
Stage 3
- Incoherency
- Restlessness
- Asterixis
Stage 4
- Coma
Outline 3 microscopic features of Crohn’s disease
- Villous atrophy
- Crypt hyperplasia
- Lymphocyte infiltration
Outline the King’s College referral criteria for liver transplant in the following scenarios
- Paracetamol induced acute liver failure
- Non-Paracetamol induced acute liver failure
Paracetamol induced acute liver failure
- Acidosis (< 7.3)
- Or 3 all of the following: raised INR (> 6.5), raised serum creatinine AND bad encephalopathy grade 3 or 4
Non-Paracetamol induced acute liver failure
INR > 6.5 (prolonged prothrombin time)
Any three of:
- Age <10 or >40
- Drug-induced liver failure
- 1 week from 1st presentation of jaundice to encephalopathy
- Raised bilirubin (≥300µmol/L)
- Prolonged prothrombin time >50s
Outline the criteria for safe discharge after a Paracetamol overdose
- Patient is asymptomatic
- LFTs normal (ALT specifically)
- INR normal
- Paracetamol concentration below treatment line on nonogram
- Provided with safety netting advice / psychiatry review if intentional overdose
List some factors predisposing someone to refeeding syndrome
- Low BMI (< 16)
- Low levels of PoMP already, prior to refeeding (phosphate, magnesium or potassium)
- Little or no nutritional intake for 10 days propr
- Unintentional weight loss already (15% over 3-6 months)
Gastro-Oesophageal Reflux Disease (GORD) - state the following:
- Pathophysiology
- Investigations
- Management
Pathophysiology:
- Reflux of gastric content through the lower oesophageal sphincter, into the oesophagus
Investigations:
- Epigastric (or retrosternal) pain
- Acid regurgitation
- Bloating
- Nocturnal cough
- Hoarse voice
Red flag: dysphagia (2 week wait for direct-access endoscopy)
Management:
- Lifestyle changes
- Antacids (e.g. Gaviscon) short term only
- 4 week trial of PPI
- Histamine H2-receptor antagonists (e.g. Famotidine)
- Alter worsening medications (e.g. NSAIDs, bisphosphonates)
- Consider H pylori testing
- Last line: laparoscopic fundoplication surgery
List some things that worsen symptoms of Gastro-Oesophageal Reflux Disease (GORD)
- Alcohol
- Hot drinks / food
- Spicy food
- Stress
- Obesity
- Smoking
- NSAIDs
Outline h pylori testing and eradication therapy
Testing:
- Either carbon‑13 urea breath test or stool antigen test
Eradication - 7 day course of triple therapy BD with:
- Clarithromycin
- Amoxicillin
- (M)etronidazole
- Lansoprazole
If unsuccessful, try anotehr 7 days and use Metronidazole instead of Amoxicillin
Routine re-testing is not necessary after treatment
State 4 types of tests that can be used to diagnose H pylori
All tests require 2 weeks without using a PPI prior to testing
- Stool antigen test
- Carbon-13 urea breath test
- H. pylori antibody test (blood)
- Rapid urease test performed during endoscopy (CLO test)
Outline changes in cell type in Barrett’s oesophagus
Squamous epithelium -> columnar epithelium (metaplasia)
State management options for a patient with confirmed Barrett’s oesophagus
- PPI
- Endoscopic monitoring for progression to adenocarcinoma
- Endoscopic ablation (e.g. radiofrequency ablation) for low-high dysplastic changes to mimimise cancer risk
Irritable bowel syndrome (IBS) - state the following:
- Pathophysiology
- Investigations
- Management strategies
Pathophysiology:
- Disturbance of the gut-brain interaction (functional disorder), F>M (particularly younger women)
Investigations:
- Stool culture, faecal calprotectin
- Bloods: FBC, WCC, CRP, ESR, anti-TTG antibody and IgA tests, Ca-125 for ovarian cancer
Criteria for diagnosis:
- At least 6 months of the following symptoms (‘IBS’ mnemonic):
a. Intestinal pain relieved by opening bowels
b. Bowel habit abnormalities (increased or decreased frequency)
c. Stool abnormalities (watery, mucus)
- At least 2 of the following:
a. Straining and urgency
b. Bloating
c. Mucus
d. Symptoms worse after eating
Management strategies:
Lifestyle advice
* Good fluid intake
* Regular small meals
* Low FODMAP diet
* Reduce stress where possible
* Regular exercise
Medications (varies based on symptoms)
* Consider 12-week trial of probiotics (discontinue if ineffective)
* Loperamide / bulk-forming laxatives for bowel habits
* Antispasmodics for cramps e.g. Mebeverine, hyoscine butylbromide or peppermint oil
* Linaclotide is a specialist drug for constipation if others are unsuccessful
Alternative treatment options:
* CBT
* Antidepressants (SSRI and tricyclics)
* Specialist referral
List some conditions to exclude in the diagnosis of IBS (irritable bowel syndrome)
- IBD (chrohn’s and UC)
- Coeliac
- Thyroid disturbance
- Bowel cancer (+ pancreatic cancer, ovarian cancer)
- Diverticulitis
- Gastroenteritis
- Bowel obstruction
List the 4 main types of laxatives and give some examples of each
- Bulk-forming e.g. Isphagula Husk, Methylcellulose
- Osmotic e.g. Movicol or Lactulose
- Stimulant e.g. Senna or Bisacodyl, Sodium picosulphate
- Stool softener e.g. Docusate sodium
State some key conditions to rule out for a patient presenting with constipation
- Bowel obstruction
- Bowel cancer (ovarian cancer or other cancers causing local compression)
- Hypothyroidism
- Hypercalcaemia
- IBS
- Neurological conditions e.g. MS, Parkinson’s disease
