Gastro Flashcards
RFs for NAFLD
Obesity
diabetes
dyslipidaemia
rapid weight loss
total parentral nutrition
describe the progression of NAFLD
hepatic fat accumulation without inflammation
–> steatohepatitis,
–> fibrosis,
–>cirrhosis
–> end-stage liver disease.
diagnostic factors of NAFLD
dont drink much ETOH
RFs
deranged LFTs
truncal obesity
hepatosplenomegaly
RUQ pain
medications associated with hepatic steatosis
tamoxifen, corticosteroids, diltiazem, nifedipine, methotrexate, valproate, griseofulvin, intravenous tetracycline, amiodarone, and antiretroviral therapy for HIV.
AST and ALT in NAFLD
both elevated but usually no higher than 300IU/L
AST:ALT ratio usually <1 (which differs from alcoholic LD where ratio is >2)
Investigations for liver conditions
Bloods:
FBC- Hb for anemia
U&Es- Uraemia
LFTs + billirubin
lipids
clotting screen
serum albumin
autoimmune Ab screen
Iron studies
Hep B and C
Imaging:
Liver USS/ fibroscan
Abdo MRI
possible signs in a patient for liver disease
General:
jaundice
abdo distension
unwell looking
bruising/ petechiae
Bronzed appearance- haemochromatosis
Hands/nails:
Leukonychia and mherkles lines- hypoalbuminaemia
Asterixis- uraemia
dupyutrens contracture- chronic liver disease
clubbing- chronic stable liver disease
palmar erythema
Neck:
raised JVP- right sided heart failure secondary to hepatic congestion
face:
Conjunctival pallor- anaemia
Kayserfleisher rings- Wilsons
corneal arcus- hyperlipidaemia
yellowing of sclera- uraemia, billirubinaemia
Xanthelasma- hyperlipidaemia
angular stomatitis- anaemia
chest:
spider naevi
gynaecomastia
abdo:
Ascites
caput madusae
bruising
hepato/splenomegaly
differentials for NAFLD
alcoholic liver disease
autoimmune hepatitis
viral hepatitis
Management of NAFLD
Diet and exercise
consider pioglitazone
vitamin E
liver transplant
complications of cirrhosis
Ascites
Portal hypertension- splenomegaly, hepatopulmonary syndrome
oesophageal varices
uraemic encephalopathy
Hepatocellular carcinoma
hepatorenal syndrome
signs of chronic stable liver disease
Palmar erythema (high oestrogen)
dupyutrens contrcture
clubbing
gynaecomastia (male- failure of liver to break down oestradiol)
spider naevi
signs of portal hypertension
SAVE
Splenomegaly
Ascites
Varices
Encephalopathy
pressure in portal venous system
5-10mmHg
mechanism of hepatic encephalopathy
toxic metabolites such as ammonia/ urea not cleared by the liver
can cross BBB
Mechanism of oesophageal varices
portosystemic shunts are made to minimise portal hypertension at 3 points where the potal system meets the systemic system (oesphagus, anus and round ligament)
causes varices which are very fragile and easly rupture casuing massive upper GI bleeding
mechanism of caput medusae
round ligament (originally umbilicus at birth and closed off) rechannels blood from portal vein to abdominal veins which dilate
mechanism of splenomegaly in chronic liver disease
portal hypertension causes blood to back up into the spleen leading to congestive splenomagaly
–> anaemia, thrombocytopenia and thrombocytopenia as these cells get congested in spleen
mechanism of ascites
- decreased oncotic pressure from hypoalbuminaemia causes water to leak out
- portal hypertension leads to NO release from endothelial cells which causes vasodilation. as a result RAAS is stimulated and more water and Na are retained –> fluid overload
causes of portal hypertension
prehepatic
- obstruction
eg. portal vein thrombosis
intrahepatic
- cirrhosis
- sarcoidosis
- schistosomiosis
post hepatic
- right sided heart failure
- constrictive pericarditis
- Budd-chiari syndrome (hepatic vein obstruction eg. thrombus in PCV or a tumor)
Management of decompensated liver disease
beta blockers may help portal HPTN
Rifaximin- targets GIT bacteria which will reduce ammonia production
lactulose- improvs ammonia clearance
Ascitic tap for WCC and MC&S to rule out SBP- if previously had give prophylactic ciprofloxacin
Ascites- 20% human albumin solution and diuretics (spironolactone/ frusemide) and drain
OGD to look for varices- band ligation if necessary
signs of decompensated liver disease
Ascites
Jaundice
asterixis
encephalopathy
portal hypertension
Main investigations for pt with suspected liver disease
bloods:
FBC- may have anaemia, thrombocytopenia
CRP
U&Es- uraemia
LFTs
Renal function + Cr- hepatorenal syndrome
clotting profile- synthetic marker of liver function
serum albumin
serum hepatitis virology
Immunoglobulins- aSM, amitochondrial, aANCA
caeruloplasmin and Cu- wilsons
Iron studies- haemochromatosis
extra hepatic manifestations of haemochromatosis
arthritis
secondary T2DM and insulin resistance
infertility
secondary causes of diabetes mellitus
cystic fibrosis
pancreatitis
pancreatic cancer
haemochromatosis
phaochromocytoma
cushings
markers of synthetic liver function
albumin
clotting
platelets (liver makes thrombopoetin)
causes of acute liver failure
Hep A&E
paracetamol OD
TB antibiotics
some tropical infections
criteria for hepato-renal syndrome
- Chronic liver disease or acute liver disease with LIVER FAILURE.
- Poor GFR
- Absence of volume depletion
- no nephrotoxic drugs.
6 Absence of shock - No evidence of kidney disease (ie proteinuria or haematuria) / Ultrasound shows no obstruction.
- No improvement in creatinine after withdrawing diruetics or using 1.5 litre of fluid to replete.
types of hepato-renal syndrome
Type 1 is rapidly progessing over 2 weeks. Where as type 2 is more slowly progessing and sometimes a cause can be found such as SBP.
what are the 2 types of autoimmune hepatitis
Type 1: This is the most common type of autoimmune hepatitis. This type patients have ANTI-SMOOTH MUSCLE ANTIBODIES and ANTI-NUCLEAR antibodies.
Type 2: this is rarer, and seen mainly in children, with anti-liver/kidney microsomal type 1 antibodies.
emphysema plus cirrhosis
alpha 1 antitrypsin deficiency
causes of ascites
3C’s and an N
Cirrhosis
Cardiac failure
Cancer
Nephrotic synrome
what is the SAAG and what are different types/ casues
serum ascites albumin gradient
serum albumin- ascites albumin
exudative- SAAG <1.1g/dL
casues (MINP): malignancy, infection (eg.TB), nephrotic syndrome, and pancreatitis
transudative- SAAG >1.1g/dL
Casues: Alcoholic hepatitis, Budd-chiari syndrome, cirrhosis, Kwashiorkor malnutrition
Another way of differentiating between an exudate and a transudate is to assess the ascitic fluid’s lactate dehydrogenase (LDH) level:
LDH <225 U/L = transudate
LDH > 225U/ L = exudate
causes of chronic liver failure
hep B, C and D
alcoholic liver disease
Metabolic associated steatohepatitis/ NAFLD
rare:
Wilsons
Haemochromatosis
Autoimmune hepatitis
alpha1 antitrypsin deficiency
complications of cirrhosis
hepatocellular carcinoma
portal hypertension- rupture of oesophageal varices
ascites and spontaneous bacterial peritonitis
clotting dysfunction and bleeding
uraemic encephalopathy- confusion, reduced GCS, seizure
what is creon
tablet of exogenous pancreatic enzymes
causes of pancreatitis
Idiopathic
Gall stones
ERCP
Trauma
Steroids
Malignancy, mumps
Autoimmune
Scorpion venom
Hhypercalcamia, hypertriglyceride
Ethanol
Drugs (sulfonamides, azathioprine, NSAIDs, diuretics)
Management of GORD
supportive
- smaller meals
- dont eat 2hrs before bed
- avoid citrusy foods
medical
- gavisocn
- PPIs
surgical
- fundoplication
what is the montreal classification of crohns
A- age of onset
L- disease location
B- disease behaviour
A1: ≤16 years
A2: 17-40 years
A3: > 40 years
L1: terminal ileum
L2 : colon
L3: ileocolon
L4: upper gastrointestinal
B1: Inflammatory
B2: stricturing
B3: penetrating
what is the montreal classification of UC
extent
E1: ulcerative proctitis; involvement limited to rectum (rectosigmoid junction)
E2: left sided ulcerative colitis: involvement limited to portion of colorectum distal to splenic flexure
E3: extensive ulcerative colitis: involvement extends proximal to splenic flexure
severity
S0: ulcerative colitis in clinical remission; no symptoms of UC
S1: mild UC ≤ 4 bloody stools daily, lack of fever, pulse <90 bpm, haemoglobin >105g/L, ESR < 30mm/hr
S2: moderate ulcerative colitis: > 4-5 stools daily but with minimal signs of systemic toxicity
S3: severe ulcerative colitis: ≥ 6 bloody stools daily, pulse > 90 bpm, temperatures > 37.5°C, haemoglobin < 105 g/L, ESR > 30 mm/hr
eosinophilia plus iron deficiency anaemia
think parasitic infection such as giardia or strongoloides
what would you give if someone with Cdiff diarrhoea was not responding to vancomycin?
oral fidaxomicin
if fulament colitis suspected then refer to surgery
drugs that cause liver cirrhosis
Amiodarone
methotrexate
methyldopa
Drugs that cause cholestasis
clauvulanic acid
penicillins
oestrogens
erythromycin
chlorpromazine
Infective causes of bloody diarrhoea
E.coli
Salmonella
shigella
campylobacter
causes of dysphagia
obstructive:
- oesophageal/ gastric carcinoma
- oesophageal web
- oesophageal strictures
- external compression: goitre, thymoma, lung cancer
motility issue:
- achalasia
- stroke
- MG
- systemic sclerosis
- MND
- parkinsons
scoring systems used in upper GI bleed
Glasgow-Blachford score- calculated before a procedure to determine whether a patient will need to be admitted for medical intervention
AIMS65 -
used to calculate the risk of in-hospital mortality in patients with an upper GI bleed
Rockall score-
used after GI endoscopy to determine the percentage risk of rebleeding and mortality in patients with upper GI bleeding
differentials for dysphagia
Painful to swallow:
- tonsilitis
- oesphagitis
Mechanical/ obstruction
- oesophageal cancer
- oesphageal web
- oesophageal stricture
- external compression (thymoma, goitre, lung Ca)
- pharyngeal puch
Motility disorder
- achalasia
- stroke
- bulbar/pseudobulbar palsy
Ix for non neuro casues of dysphagia
REFERRAL UNDER 2WW to exclue oesphageal Ca
OGD
Barium swallow
manometry
Differentials for dyspepsia
GORD
Gastric/ duodenal ulcer
- NSAIDs, steroids, H.pylori
Upper GI Ca
Achalasia
oesophagitis (think HIV with candida)
Functional
redflag features with new dyspepsia
ALARM
Anaemia
Loss of weight
Anorexia +/- abdo pain
Recent symptoms
Meleana/ haematemesis
features of a pancreatic pseudocyst
Pseudocysts can be asymptomatic or present with signs of biliary obstruction (abdominal pain, jaundice) or gastric outlet obstruction (post-prandial vomiting) due to mass effect of an enlarging pseudocyst on adjacent structures. There is also the risk of secondary infection
