Gastro Flashcards
Differentials liver always say (1)
hepatic dysfunction
AF + acute abdo pain
Acute mesenteric ischaemia
Chronic mesenteric ischaemia symptoms
Severe colicky post prandial abdom pain, weight loss (as eating hurts), upper abdo bruit.
Chronic colonic ischaemia - ischaemic colitis
Inferior mesenteric artery - lower left sided abdo pain plus or minus bloody diarrhoea
Treatment usually conservative, CT may be helpful but lower GI endoscopy gold-standard
PR interval
120-200 ms
QRS interval
<100
Normal axis
-30 to +90
IE hands
splinter haemorrhages, clubbing
Dukes criteria
Hep A symptoms
Abdo pain, fever, N&V
70% symptomatic
Hep A transmission
Faecal oral
Clinical course Hep A
full recovery 2-3 months - no chronic Hep A
Hep A treatment
Supportive care onl
Vaccine - very effective lifelong immunity
Hep A exposure
Can vaccinate after exposure
Hep B curable?
Incurable
Treatment Hep B
Antivirals - entecavir
Hep C treatment
Maviret 8 weeks TD - curable
Liver ask about urine
dark - bilirubin
All histories can ask about
Travel
Hep A lab
HAV IgM antibody
Hep B lab
HBV surface antigen
Hep C lab
HCV antibody
Haemochromatosis check
Ferritin
Ultrasound stone biliary then what?
ERCP, or cholecystectomy
ERCP complications
Pancreatitis
Post-sphincterotomy bleeding
Cholangitis
Failed cannulation
Abdo and throat discomfort
Aspiriation
Infection
Duodenal perforation
Koilonychia
Spooning nails - chronic iron deficiency anaemia
Gastro red flags
Weight loss, dysphagia, bleeding, age >55, odonophagia, family history, lymphadenopathy, persistent vomiting, jaundice, unexplained iron deficiency anaemia
ERCP risk of serious complications
6.9% risk, 0.33% mortality
Odynophagia meaning
Painful swallowing
Gastroscopy complication serious chance
0.13-0.15%
Laxsol =
Docusate + Sennoside B
Docusate mechanism
Stimulant & stool softener
Sennoside B mechanism
Stimulant
Molaxole drug & mechanism
Magrogol - osmolite
Anti diarrhoea
Loperamide
Gastroscopy patient advice
Do not eat or drink for a minimum of 4 hrs before ur appointment
Can do throat anaesthesia spray or sedation - if sedation can’t drive for 24 hrs
Gastroscopy complications
Throat discomfort 1-2 days, abdo discomfort, bleeding if take biopsy, perforation very rare
ERCP overnight
usually discharged arvo, but some stay overnight
ERCP sedation
yes
Colonoscopy preparation
Colonscopy sedation
With or without
Complications and risks colonoscopy
Abdo discomfort, bleeding if polyp removal, perforation, incomplete examination, missed lesions
Hepatic insufficiency increase in estradiol manifestations
Spider angiomas, gynacomastia, palmar erythema, testicular atrophy
Non estradiol related manifestations of hepatic insufficience
Jaundice, nail changes (terry nails (pale beds), muehchke nails (pale lines), clubbing.
Dupeytren’s contractures
Hypertrophic osteoarthropathy
Physical findings of cirrhosis or hepatic insufficiency
Parotid gland enlargement, feto hepaticus (sour breath), ascites, caput medusae, splenomegaly, asterixes
Bruising (abnormal clotting)
Leukonychia (hypoalbuminaemia)
Gall bladder pathology where start?
Ultrasound
THen labs Hep A,B,C
ERCP indications
Suspected or known choledocolithiasis
Jaundic patients with suspected biliary obstruction
Acute cholangitis with obstruction
Post-op biliary leak
Bile duct injury
Carefully selected patients with pancreatics disease
Rate of ERCP cause pancreatitits
3-5%
Hematochezia
Passage of fresh blood in stool
Floating stools due to
Increased gas content of the stool - steatorrhea will manifest as oil droplets
Steatorrhea smell
Will not need to ask
Colonoscopy indications (so many ):)
Acute Lower Gastrointestinal Hemorrhage
Suspected severe IBD to establish diagnosis
Known or suspected colorectal cancer
Unexplained rectal bleeding
Altered bowel habits and rectal bleeding
Altered bowel habit (more frequent and/or looser stool) above age…
Iron deficiency anemia
Imaging shows polyps
Suspected IBD for diagnosis/mapping
Surveillance after diagnosis of adenomatous polyps or colon cancer
IBD surveillance
Family history with FDR <55 or two FDR of any age
FAP, HNPCC, or other familial cancer syndrome
Colonscopy complication rate
0.05-0.28%
Upper Gastrointestinal Endoscopy Indications
Upper gastrointestinal bleeding
Esophageal or gastric foreign body
Caustic ingestion
Dysphagia
Dyspepsia/Reflux with red flag symptoms
Malignancy
Iron deficiency anemia
Persistent vomiting >2 weeks
Pernicious anemia
Coeliac testing
Variceal screening
Ulcer healing confirmation
Non-cardiac chest pain suggestive of oesophageal origin
Liver cirrhosis results from
Chronic inflammation and damage to liver - functional cells are replaced with scar tissue (fibrosis)
Cirrhosis leads to portal HTN
Due to increased resistance of blood flowing through liver
Four most common causes of liver cirrhosis are
Alcohol related liver disease, non-alcoholic fatty liver disease, Hep B, Hep C
Non-invasive liver screen
Ultrasound
Hep B & C serology
Autoantibodies (ANA, SMA, AMA)
Alpha-1-antitrypsin levels
Ferritin & transferrin
Advanced cirrhosis
Thrombocytosis
Low albumin
Increased prothrombin time
Hyponatrenua (fluid retention)
NAFLD diagnose via
Ultrasound - increased echogenicitiy
Cirrhosis ultrasound show
Nodularitiy, enlarged portal vein, splenomegaly, ascites
Hepatocellular carcinoma screened using
Ultrasound
Transient elastography
Fibroscan - used to assess stiffness of the liver using high-frequency sound waves - determine degree of fibrosis to test for liver cirrhosis
liver biopsy to confirm
Cirrhosis
Severity of cirrhosis use
MELD
or
Child-pugh score
Albumin
Bilirubin
Clotting (INR)
Dilation (ascites)
Encephalopathy
Management Cirrhosis
Treat underlying cause (alcohol, diet, antivirals, immunosuppression), monitor for complications, Manage complications, Liver transplant
Portal hypertension
Splenomegaly
Oesophageal varices
Haemorrhoids
Caput medusae
Bleeding Oesophageal Varices
Life threatening emergency - blood transfusion, endoscopy with variceal band ligation.
B-blockers as prophylactic
Spontaneous bacterial peritonitis
Complication of ascitis
Hepatorenal syndrome
impaired kidney function caused by changes in blood flow attributable to portal hypertension
Poor prognosis unless patient has a liver transplant
Hepatic encephalopathy symptoms
Build up of neurotoxic substances- especially ammonia
Presents with reduced consciousness and confusion acutely.
More chronically with changes to personality, memory and food
Hepatic encephalopathy management
Lactulose - poop out the ammonia
ABx - Rifaximin - kills gut bacteria producing ammonia
Alcohol related liver disease progression
Alcoholic fatty liver (steatosis)
->
Alcoholic hepatitis
->
Cirrhosis
Examination findings suggestive of excessive alcohol consumption
Smelling of alcohol
Slurred speech
Bloodshot eyes
Dilated capillaries on the face (telangiectasia)
Tremor
Alcohol related liver disease bloods
- Raised mean cell volume (MCV)
- Raised alanine transaminase (ALT) and aspartate transferase (AST)
- Raised GGT (particularly notable with alcohol-related liver disease)
- Raised alkaline phosphatase (ALP) later in the disease
- Raised bilirubin
- Low albumin
- Increased prothrombin time
Liver imaging options
Ultrasound, fibroscan, CT&MRI, biopsy
CAGE questionnaire to screen for harmful alcohol use
C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?
Alcohol withdrawal
Mild -> delirium tremens
Hallucinations, seizures
Delirium tremens is emergency - Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
Alcohol withdrawal treatment
Benzos
Thiamine (B1) supplements
Wernicke’s symptoms
Confusion, oculomotor disturbance, ataxia
Stages of NAFLD
Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis (NASH)
Fibrosis
Cirrhosis
NAFLD risk factors
Sames as for CVD
Diet, exercise, T2DM, smoking, HTN, hypercholesterolemia, obesity, older
NAFLD blood measure fibrosis
ELF - enhanced liver fibrosis - measure HA, PIIINP< TIMP01 and calculate number indicate whether fibrosis
Which Hep is DNA
B
Faecal oral heps
A & E
Blood heps
B & C
Hep with D
B
Hep LFTs
AST & ALT highhhh
ALP also a bit high & bilirubin
Hep A - treatment
Usually resolves without treatment
Hep B treatment
Most recover within 3 months, 5-15 become chronic
Antivirals slow progression, liver transplant
Hep C treatment
Curable with direct acting antiviral medications
Without treatment 3/4 become chronic
Chronic hep B&C can cause
Liver cirrhosis & hepatocellular carcinoma
Hep E
Rare, mild and cleared within a month
Rarely bad in immunocompromised & pregnant
Autoimmune hepatitis investigations
If Hep immunology -ve
High ALT & AST, raised IgG levels
Autoantibodies
Autoimmune hepatitis management
High dose steroids, immunosuppressants (azathioprine)
Liver transplant may required in end stage liver disease
Haemochromatosis gene
HFE
Autosomal recessive mutation
Haemochromatosis presentation
Chronic tiredness, joint pain, pigmentation (bronze skin), cognitive symptoms, hepatomegaly, diabetes
Haemochromatosis raised ferritin differentials
Infection, NAFLD, hep C, cancer
Can distinguish as transferrin sats are also high
Haemochromatosis treatment
Venesection
Monitoring
Wilsons disease
Accumulation of copper, especially in liver
Wilsons disease presentation
Typically teens or young adults
liver problems, neurological or psychiatric problems
Wilsons disease diagnosis
Serum caeruloplasmin
- low
24 hour urine copper assay - high urinary copper
Alpha-1-antitrypsin deficiency affects
Lungs - COPD & bronchiectasis
Liver - cirrhosis
Primary biliary cholangitis
Autoimmune condition where the immune system attacks small bile ducts in the liver resulting in obstructive jaundice and liver disease - same as primary biliary cirrhosis
Primary biliary cholangitis can lead to
liver fibrosis, cirrhosis and failure
Primary biliary cholangitis presentation
The typical patient is a white woman aged 40-60 years. Often patients are asymptomatic at diagnosis, with the problem picked up on abnormal liver function tests. However, they may present with:
Fatigue
Pruritus (itching)
Gastrointestinal symptoms and abdominal pain
Jaundice
Pale, greasy stools
Dark urine
On examination, there may be:
Xanthoma and xanthelasma (cholesterol deposits)
Excoriations (scratches on the skin due to itching)
Hepatomegaly
Signs of liver cirrhosis and portal hypertension in end-stage disease (e.g., splenomegaly and ascites)
Bloods for primary biliary cholangitis
ALP highhh
Autoantibodies
Treatment primary biliary cholangitis
Ursodeoxycholic acid - non-toxic bile acid protects cholangiocytes from inflammation and damage
Primary sclerosing cholangitis
Intrahepatic AND extrahepatic bile ducts inflamed and damaged - strictures form that obstruct the flow of bile out of the liver.
Ulcerative colitis associated with
Primary sclerosing cholangitis
Primary sclerosing cholangitis presentation
Often patients are asymptomatic at diagnosis, with the problem picked up on abnormal liver function tests. However, they may present with:
Abdominal pain in the right upper quadrant
Pruritus (itching)
Fatigue
Jaundice
Hepatomegaly
Splenomegaly
Primary sclerosis cholangitis investigations
LFTs - ALP raised
Autoantibodies NOT helpful
MRCP - shows bile duct strictures
Management primary sclerosing cholangitis
ERCP - treat dominant strictures - otherwise no treatments
Liver transplant
Primary liver cancer is usually
Hepatocellular carcinoma - risk if have cirrhosis (from any cause)
Presentation liver cancer
Usually non-specific
Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Upper abdominal mass on palpation
Hepatocellular carcinoma tumour marker
Alpha-fetoprotein
management hepatocellular carcinoma
Surgery if early, radiofrequency ablation, radiation, targeted drugs.
Cholangiocarcinomas
Types of cancer originate in bild ducts - associated with primary sclerosing cholangitis
Cholangiocarcinoma presentation
Obstructive jaundice - pale stools, dark urine, generalised itching
Tumour marker cholangiocarcinoma
CA19-9
GORD long term
Oesophagus - squamomus epithelium replaced with columnar (metaplasia)
Premalignant condition
Treat with monitoring endoscopically, PPI, radiofrequency ablation
GORD exacerbated by
Greasy & spicy food, coffee, alcohol, NSAIDs, stress, smoking, obesity, hiatus hernia
Dyspepsia means
Indigestion - non specific
Covers the symptoms of GORD
Gord red flag
Suspicious of cancer - DYSPHAGIA - urgent endoscopy
Weight loss, >55 yrs
Hiatus hernia
Herniation of stomach up through diaphragm
Management GORD
Lifestyle, stop NSAIDS, omeprazole, surgery
Anyone with dyspepsia can offer
H. Pylori test
Need two weeks without using a PPI before testing for H. Pylori for accurate result.
Stool antigen test
Urea breath test
H pylori antibody test (blood)
Rapid urease test (during endoscopy)
H pylori eradication involves
PPI + two antibiotics - amoxicillin + Clarithromycin for 7 days
Peptic ulcer risk factor
H Pylori
NSAIDs
+ stress, alcohol, caffeine, smoking, spicy foods
Peptic ulcer bleeding risk increased if
NSAIDs, aspirin, anticoags, Steroids, ssri
Peptic ulcer diagnosed
Endoscopy, during which do rapid urease test (CLO Test)
Management peptic ulcers
Stop NSAIDs, treat H pylori infection, PPI
Peptic ulcer complication
Bleeding, perforation, strictures
Upper GI bleed causes
Peptic ulcer, oesophageal varices, stomach cancers
Crohn’s - symptoms compared with UC
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 (don’t set the nest on fire)
Ulcerative colitis features as opposed to crohns
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
IBD diagnosis
Faecal calprotectin is around 90% sensitive and specific for inflammatory bowel disease in adults. It is used as an initial test before moving on to endoscopy. Colonoscopy + intestinal biopsies
UC management
Mild to moderate - aminosalicylate first line
Severe - steroids
Surgery
Crohn’s management
Steroids first line
Enteral nutrition as alternative (treats nutritional deficiencies, improve gut microbiome, removing inflammatory foods)
Methotrexate, azathioprine
Surgical resection
IBS
At least 6 months of abdo pain or discomfort with at least one of
- pain relieved by opening bowels
- change in frequencies
- change in consistency
IBS management
Low fodmap diet, probiotic supplements
Loperamide for diarrhoea
Laxatives - husk - for constipation
Coeliac disease linked with
T1DM, thyroid disease
Coeliac antibodies
Anti-tissue transglutaminase antibodies (anti-TTG)
Coealiac disease presentation
Often asymptomatic
Failure to thrive in young children
Diarrhoea
Bloating
Fatigue
Weight loss
Mouth ulcers
Diagnosis
antibodies
Endoscopy & jejunal biopsy - villous atrophy, crypt hyperplasia
