GI conditions Flashcards
where are the common locations to find squamous cell carcinoma of the mouth? How do they present?
floor of mouth
lateral borders of the tongue
hard, indurated ulcer with raised + rolled edges
what are some precursors to oesophageal adenocarcinoma?
oesophagitis (reversible) -> Barrett’s oesophagus (irreversible?) -> adenocarcinoma
what red flags indicate a 2 week endoscopy referral?
> 55 y/o with new onset pain / reflux with anaemia
weight loss
anaemia - could be indicated by conjunctival pallor
dysphagia + odynophobia
GI bleed - melaena or coffee ground vomiting
worsening GI pain with N+V, low Hb + raised PLT count
what is gastropathy?
epithelial cell damage and regeneration without inflammation
what is gastroparesis? what is it’s treatment?
partial paralysis of the stomach - delayed gastric emptying
treatment = remove cause + correct nutritional deficiencies
–> may requite pro-motility agents / gastric pacemaker
what is functional dyspepsia and what are it’s investigations?
dyspepsia symptoms but no structural abnormality for explanation
investigations = H. pylori excluded via stool antigen test
- young (<50) need no further investigations
- – older or red flag symptoms require endoscopy
does eating worsen or improve pain from duodenal ulcers?
eating improve pain of duodenal
** eating worsens pain when gastric ulcer
what are the investigations for peptic ulcers?
<55 - typical symptoms + positive for H. pylori = start eradication therapy + no further investigations required
older or red flags - endoscopic diagnosis (rapid urease test (CLO) + exclusion of cancer
management of peptic ulcers?
high dose protein pump inhibitors - omeprazole
if H. pylori - eradication therapy
–> amoxicillin (metronidazole if allergic) + clarithromycin
what is the histological change in barretts oesophagus?
metaplasia of the lower oesophagus from squamous to columnar epithelium
what is the management of barretts oesophagus?
PPI - omeprazole
if dysplastic = ablation treatment - photodynamic, laser or cryotherapy
–. destroys epithelium so replaced by normal cells (prevents progression to cancer) - don’t use if no dysplasia
monitored for dysplasia
what is achlasia and what can cause it?
impaired peristalsis (ring of muscles don’t open properly) + failure of LOS to relax
causes-
nerve damage to oesophagus
viral infection
autoimmune condition
what are signs + symptoms of achlasia?
gradually worsening symptoms (few years) until impossible to swallow
dysphagia bringing up undigested food chocking/coughing spontaneous chest pain - due to oesophageal spasm gradual weight loss chest infections
lower oesophageal pressure elevated in >50%
what are the investigations for achlasia?
CXR - dilated oesophagus, fluid level behind heart, absent fundal gas shadow
manometry - small plastic tube, measures pressure at various points
barium swallow - lack of peristalsis, ‘bird’s beak’ due to failure of sphincter relaxation
endoscopy - passes with little resistance
what is the treatment for achlasia?
all palliative
nitrates / pifedipine - relax muscles, side effects = headaches
balloon dilation - often need repeated, may cause rupture
botox injections - needs repeated
Heller’s myotomy = surgery (permanent)
what is Heller’s myotomy? when would it be carried out?
surgery where muscle fibres are cut to make swallowing easier
permanent fix
can cause reflux + heartburn
used for achlasia treatment
how would you discover an oesophageal diverticulum?
barium swallow
what type of bacteria is helicobacter pylori? how does it effect the GI tract?
gram negative aerobic bacteria
forces way into gastric mucosa to avoid acidic environment - breaks created exposes epithelial cells to acid
produces ammonia to neutralise acid - also damages epithelial cells
what investigations are carried out for H. pylori infections?
urea breath test
stool antigen test - no antibiotics or H2 antagonists for 4 weeks
rapid urease test (CLO test) - done during endoscopy, (stomach mucosa biopsy + urea -> if present urease enzymes produce ammonia -> pH test alkaline)
offered to anyone with dyspepsia - 2 weeks PPI free before testing
what is the treatment for H. pylori?
triple therapy for 7 days
- omeprazole + amoxicillin (metronidazole if allergic) + clarithromycin
how do you test for giardia and amoeba?
stool microscopy
how do you test for salmonella, campylobacter, shigella?
stool culture - salmonella, campylobacter, shigella
blood cultures - salmonella
how do you test for C. Diff?
stool toxin
describe staph aureus in association with gastroenteritis
gram positive coccus
fast incubation - 1hr of eating milk, meat, fish (preformed toxin)
acts on vomiting centre in brain
goes yellow on blood agar - beta haemolysis
list some causes of upper GI haemorrhages
oesophageal varices
mallory-weiss tear - tear of mucous membrane at oesophagogastric junction
peptic ulcers
peptic cancers
what scoring is used in upper GI bleeds?
glasgow-blatchford score - risk of having upper GI bleed
rockall score - post endoscopy for risk of rebleed / overall mortality
how is variceal bleeding treated?
terlipressin - vasoconstrictor (not for ischaemic HD)
+ prophylactic broad spectrum antibiotics at presentation (before endoscopy)
band ligation
injections of sclerosant
TIPS if both fail
why does urea rise in upper GI bleeds?
blood in GI tract gets broken down by the acid and digestive enzymes
–> one of the breakdown products is urea + this urea is then absorbed in the intestines
list the management of upper GI bleeds? (ABATED)
ABCDE resuscitation
Bloods - test for Hb, coagulation, urea, liver disease
Access - 2 large bore canula (for fluids + blood)
Transfuse
Endoscopy - ASAP, within 24hrs is stable
Drugs - stops coagulants + NSAIDs
transfusion treatment is based on the individual presentation, what are the different types of transfusion that would be given for an upper GI bleed?
massive haemorrhage = blood, platelets + clotting factors (fresh frozen plasma)
active bleeding + thrombocytopenia (platelets <50) = platelets
actively bleeding warfarin patients = prothrombin complex concentrate
** transfusing more blood than necessary is harmful **
what is the pathogenesis of appendicitis?
obstruction of the lumen -> lumen fills with mucus -> increased intraluminal pressure -> reduced blood flow to the appendix -> inflammation + ischaemia -> perforation -> peritonitis
what are causes of appendicitis?
obstructed lumen by faecolith (hard stoney mass of faeces)
bacterial
viral
parasites
signs + symptoms of appendicitis?
central pain that migrates to right iliac fossa - worsens when laughs, goes over bumps
anorexia
no bowel movements that day
mild pyrexia + tachycardia
tender, localised pain in RIF
pressing left causes pain on right
pain on flexing hip + internally rotating causes pain
signs of malabsorption?
diarrhoea - fat, globules, offensive
easy bruising
spooning of nails
symptoms of small bowel obstruction?
intermittent pain - colicky (trapped wind, central, cramping
absolute constipation - no farts or stool
vomiting - feeling better after it
burping
abdominal distension
high pitched bowel sounds
list some extra-gastrointestinal manifestations of IBD
eyes - uveitis, conjunctivitis
joints - arthritis, inflammatory back pain
skin - erythema nodosum, pyoderma gangrenosum
liver + biliary tree - sclerosing cholangitis, chronic hepatitis cirrhosis, gallstones
list characteristics of crohn’s disease
No blood or mucus Entire GI Skip lesions Terminal ileum most affected Transmural inflammation Smoking is a risk factor
non-caseating granuloma
cobble stoning
what is the management for inducing and maintaining remission in crohn’s?
inducing -
first line = steroids (oral prednisolone, IV hydrocortisone)
if not enough add immunosuppressant (azathioprine, meracaptopurine)
maintaining -
patient specific, may not require medication
first line = azathioprine or mercaptopurine
list characteristics of ulcerative colitis
Continuous inflammation Limited to colon + rectum Only superficial mucosa affected Smoking is protective Excrete blood and mucus Use aminosalicylates Primary sclerosing cholangitis (PSC)
lack of goblet cells
pseudopolyps
what is PSC?
primary sclerosing cholangitis = disease that causes scarring of bile duct - obstruction out of liver to intestines
–> leads to hepatitis, fibrosis + cirrhosis
associated with UC
what is the management for inducing remission of ulcerative colitis?
mild + moderate -
first line = aminosalicylate (mesalazine oral or rectal)
second line = corticosteriods (prednisolone)
severe -
first line = IV corticosteroids (IV hydrocortisone)
second line = IV ciclosporin (immunosuppressant )
what is the management for maintaining remission of ulcerative colitis?
aminosalicylate - mesalazine oral or rectal
azathioprine (immunosuppressant)
list immunosuppressants given for IBD
azathioprine mercaptopurine methotrexate infliximab adalimumab
what surgical interventions can be done in UC?
proctocolectomy = removal of colon + rectum (UC only effects colon + rectum)
patient is either left with an ileostomy or a ileo-anal anastomosis (‘J-pouch’)
–> ileum is folded back on itself + functions like a rectum
what is required for the diagnosis of IBS?
Abdominal pain/discomfort ( ? 3 days a week for 3 months ? )
o Relived on opening bowels OR
o Associated with a change in bowel habit (stool form + frequency)
AND 2 of: o Abnormal stool passage – in complete emptying o Bloating o Worse symptoms after eating o PR mucus
should you recommend a high or low FODMAP diet in IBS?
LOW
avoid - wheat, rye, garlic, onions, milk, yogurt, calorie sweeteners, agave
what genes are associated with coeliac disease?
HLA-DQ2
HLA-DQ8
what antibodies are tested for in coeliac disease?
anti-tissue transglutaminase (anti-TTG)
anti-endomysial (anti-EMA)
what histological features are associated with coeliac disease?
villous atrophy - causes malabsorption
crypt hyertrophy/hyperplasia
symptoms of coeliac disease
dermatitis herpetiformis - itchy skin vesicular rash typically on abdomen
failure to thrive
weight loss
iron deficiency anaemia - due to malabsorption
mouth ulcers
investigations for coeliac disease
must be on gluten diet for 6 weeks prior to testing
raised anti-TTG, anti-EMA
–> total IgA first to exclude IgA deficiency (prevents false negative)
endoscopy + biopsy - villous atrophy + crypt hypertrophy/hyperplasia
biliary colic symptoms
gallstones in cystic duct
sudden onset of constant colicky pain in epigastrium or RUQ
–> may radiate to back
what is murphys sign and what is it a sign of?
murphys sign = inspiratory arrest upon palpation of RUQ
commonly seen in acute cholecystitis (inflammation of gall bladder)
symptoms of acute (ascending) cholangitis
bacterial infection / inflammation of biliary tree
charcot’s triad = RUQ pain, fever, jaundice
septic/unwell -> hypotension, confusion
pathophysio of pre-hepatic (haemolytic) jaundice
excess haemolysis > leads to increase bilirubin (end product of haem breakdown) > accumulation of UNconjugated bilirubin > jaundice
what would the LFTs of pre-hepatic (haemolytic) jaundice look like?
raised total bilirubin normal conjugated bilirubin levels raised unconjugated bilirubin normal urine/stool colour normal ALP, ALT/AST
pathophysio of intra-hepatic (hepatocellular) jaundice
dysfunction of hepatic cells - liver cannot conjugate bilirubin
can lead to cirrhosis -> compresses the intrahepatic portions of biliary tree to cause a degree of obstruction
leads to both unconjugated + conjugated bilirubin in the blood = “mixed picture” LFTs
what would the LFTs of intra-hepatic (hepatocellular) jaundice look like?
raised total bilirubin raised conjugated raised unconjugated dark urine/pale stool raised ALP, ALT/AST - AST/ALT more prominent than ALP (due to liver damage)
what are the true liver function tests - those which reflect synthetic function of the liver?
albumin
prothrombin time
bilirubin
what do raised AST/ALT (transaminases) indicate?
hepatocellular injury
what does a raised ALP (alkaline phosphatase) indicate?
obstruction
what causes post-hepatic jaundice (cholestatic)?
obstruction of biliary drainage –> flow of bile is backed up to liver + overspills it’s constituents into the blood
what would the LFTs of post-hepatic (cholestatic) jaundice look like?
raised total raised conjugated normal unconjugated dark urine/pale stool raised ALP, AST/ALT - (ALP more)
pathophysio of diverticular diasease
thickening of muscle layer due to high intraluminal pressures
–> pouches of mucosa extrude through muscular wall through weakened area near blood vessels to form diverticula
clinical features + complications of diverticular disease
most asymptomatic
intermittent left iliac fossa pain
erratic bowel habit
pericolic abscess perforation (peridiverticulitis) haemorrhage fistula stricture
what causes diverticulitis?
when faees obstruct the neck of the diverticulum -> accumulates bacteria causing inflammation
alters gut motility, increases luminal pressure, disordered colonic microenvironment
clinical features of diverticulitis
LIF pain/tenderness
fever, tachycardia
constipation
left side guarding + rigidity
similar to appendicitis but on left
management of diverticulitis
mild = antibiotics - ciprofloxacin + metronidazole
severe = IV fluids, IV antibiotics + bowel rest
clinical features of ischaemic colitis
sudden onset abdominal pain
passage of bright red blood PR, with or without diarrhoea
distended tender abdomen
AXR - * thumb-printing at splenic flexure *
sigmoidoscopy + biopsy - epithelial cell apoptosis + lamina propria fibrosis
CT to exclude perforation
symptoms + signs of intestinal obstruction
intermittent pain - colicky, central, cramping absolute constipation - no farts/stool burping abdominal distension + tenderness bowel sounds - high pitched fever, tachycardia
**small only - vomiting + feeling better after it
complications of parental nutrition
sepsis
SVC thrombosis
line fracture, leakage, migration
psycho-social
what type of bacteria is yersinia? how is it commonly spread + how do patients present?
gram neg bacillus
raw pork
commonly children -> watery/bloody diarrhoea, abdo pain, fever, lymphadenopathy
adults can present similar to appendicitis
what is hartmanns procedure?
removal of rectosigmoid colon + creation of colostomy - rectal stump sutured closed
usually done in emergency - acute obstruction, tumour, significant diverticular disease
–> colostomy may be permanent or reversed at a later date
risk factors for colorectal cancer
family history of bowel cancer -
familial adenomatous polypois (FAP) - polyps throughout bowel
hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome
biggest risk factor = red + processed meat consumption
IBD
increased age
sedentary lifestyle, obesity (red meat, low fibre), smoking, alcohol
presentation of colorectal cancer
unexplained weight loss
change in bowel habits - looser + more frequent
rectal bleeding
unexplained abdominal pain
iron deficiency anaemia - microcytic anaemia with low ferritin –> fatigue, pale eyelids
abdominal / rectal mass
–> may present with obstruction (tumour blocking bowel) - vomiting, abdo pain, absolute constipation
what method is used for bowel screening in scotland? at what age is this done and how often is it carried out?
faecal immunochemical test (FIT) - human haemoglobin in stool
50-72 y/o in scotland home FIT test every 2 years - if positive = colonoscopy
if risk factors (FAP, HNPCC, IBD) - regular colonoscopy to check
what test can be carried in a GP for those who have suspected colorectal cancer but don’t meet the 2-week referral colonoscopy?
faecal immunochemical test (FIT)
how are colorectal cancers staged?
staging CT - CT thorax, abdomen, pelvis (CT TAP)
MRI for rectal cancers
what are the surgical resection options for colorectal cancer?
right hemicolectomy - caecum, ascending, proximal transverse
left hemicolectomy - distal transverse, descending
sigmoid colectomy
anterior resection - sigmoid + upper rectum
–> increase urgency + frequency of bowel movements, faecal incontinence, difficulty controlling flatulence
abdomino-perineal resection (APR) - rectum + anus
–> permanent colostomy
what is involved in the follow up post colorectal cancer?
CT TAP
serum carcinoembryonic antigen (CEA) - tumour marker blood test
–> predicting relapse
what criteria is used to diagnose IBS?
Rome IV
what are FODMAPs?
a collection of short-chain carbohydrates (sugars) that are not properly absorbed in the gut
A low FODMAP diet is considered a second line dietary intervention for individuals with medically
diagnosed IBS. It should only be trialled under the supervision of a dietitian
list some non-GI symptoms of coeliac disease
recurrent mouth ulcers
prolonged fatigue
anaemia
neurological symptoms
osteomaalacia
what is the pathophysio of achlasia?
Degenerative loss of ganglia from Auerbach’s plexus
pathophysio of cirrhosis
Hepatic stellate cells found in the space of Disse are activated and transformed into myofibroblasts under the influence of cytokines
–> these activated cells synthesise collagen leading to fibrosis
pathophysio of primary biliary cirrhosis
immune system attacks small bile ducts within the liver
first part affected = intralobar ducts (canal of Hering)
causes obstruction of bile (cholestasis)
–> eventually obstruction leads to fibrosis, cirrhosis + liver failure
bile acids, bilirubin + cholesterol overflow into blood as not being excreted
clinical features of primary biliary cirrhosis
fatigue pruritus GI disturbance + abdo pain jaundice pale stools steatorrhoea xanthoma signs of cirrhosis - ascites, splenomegaly, spider naevi
primary biliary cirrhosis investigations
most specific = anti-mitochondrial antibodies
LFTs - ALP raised (obstructive)
blood tests - ESR + IgM raised
liver biopsy = diagnosing + staging disease
primary biliary cirrhosis treatment
ursodeoxycholic acid - reduces intestinal absorption of cholesterol
obeticholic acid ?
colestryamine - binds to bile acids to prevent absorption in the gut –> helps with pruritus
consider immunosuppression
liver transplant @ end stage liver disease
signs of liver cirrhosis
jaundice
hepatomegaly - can shrink in severe
splenomegaly - due to portal hypertension
spider naevi
palmar erythema - due to hyperdynamic circulation
gynaecomastia + testicular atrophy in males - due to endocrine dysfunction
bruising
ascites - cirrhosis causes transudative (low protein)
caput medusae - bulging veins around umbilicus
asterixis - ‘flapping tremor’
what scoring is used in liver cirrhosis?
Child-pugh - indicates severity + prognosis
MELD score - gives percentage estimated 3 month mortality
- helps guide transplant referral
- used every 6 months in patients with compensated cirrhosis
extra-GI manifestations of IBD
eyes - uveitis, conjunctivitis
joints - arthritis, inflammatory back pain
skin - erythema nodosum, pyoderma gangrenosum
mouth ulcers, anaemia
pathophysio of acute pancreatitis
epithelial injury to pancreatic duct - bile reflux, duct obstruction due to stone damage to sphincter of Oddi
–> loss of protective barrier allows autodigestion of pancreatic acini (cells that produce digestive enzymes)
- -> release of lytic pancreatic enzymes:
- proteases - tissue destruction + haemorrhage
- lipases - intra + peripancreatic fat necrosis
most common causes of acute pancreatitsis
alcohol
gallstones
post-ERCP
what is elevated serum amylase a common sign of?
acute/chronic pancreatitis
list characteristics of the 2 main types of inherited colorectal carcinoma
HNPCC - late onset - right sided tumours autosomal dominant inflammatory response (crohns like) defect in DNA mismatch repair mutation in MLH-1, MLH-2, PMS-1 or MSH-6
FAP - early onset - throughout colon autosomal dominant defect in tumour suppression mutation in FAP gene
why can bowel obstructions causes hypovolaemia + shock?
no fluid is absorbed in colon due to obstruction –> fluid loss into GI tract + reduced fluid in intravascular space = hypovolaemia
== ‘third-spacing’
causes of bowel obstruction
adhesions - small bowel
hernias - small bowel
malignancy - large bowel
volvulus - large bowel
diverticular disease
strictures
intussusception - bowel slides into adjacent part (young kids 6months - 2yrs)
signs of peritonitis
guarding - tensing abdo muscles when palpated
rigidity - involuntary persistent tightness
rebound tenderness - rapidly releasing pressure on abdomen creates worse pain than pressure itself
coughing test
percussion tenderness
signs + symptoms of haemorrhoids
constipation + straining
sore/itchy anus
feeling a lump around or inside anus
painless, bright red bleeding –> after opening bowels, NOT mixed with the stool
what are the 3 main complications of hernias?
incarceration - when irreducible, can lead to obstruction + strangulation
obstruction - when causes blockage in passage of faeces, absolute constipation
strangulation - irreducible AND base of hernia becomes tight cutting off blood supply (ischaemic/gangrenous tissue) = surgical emergency
how can you distinguish between direct + indirect inguinal hernias?
when pressure applied
indirect - hernia reduced to deep inguinal ring (mid way from ASIS to pubic tubercle) + remains reduced
direct = irreducible
what is the difference between direct + indirect inguinal herniation?
indirect = herniates through inguinal canal
- reducible
- lateral to epigastric artery
- lies within spermatic cord (layers of abdo wall)
direct = herniates through hesselbach’s triangle
- irreducible
- medial to inferior epigastric artery
- lies parallel to spermatic cord
what do LFTs look like in hepatitis?
high AST/ALT
less of a rise in ALP
which strains of hepatitis are self-limiting (no increased risk of hepatocellular carcinoma)?
A + E
how is hep A spread?
faecal oral - poor hand hygiene, in foreign markets touching lots of food
how do you diagnose hep A?
presence of hep A IgM
IgG will be detectable for life
treatment for hep A?
supportive, avoid alcohol
how is hep B spread?
3 B’s
Blood
Babies - pregnant mother to child (vertical transmission)
Body fluid - sex hehe
incubation = 1-6months
endemic - recent travel?
HBsAg –> negative
HBcAb –> positive
HBsAb –> positive
what do these hep B serology results indicate?
resolved HBV infection
HBcAb IgG
HBsAg –> negative
HBcAb –> negative
HBsAb –> positive
what do these hep B serology results indicate?
vaccinated
HBsAg –> positive
HBcAb –> positive
HBsAb –> negative
what do these hep B serology results indicate?
active infection
if HBcAb IgM present - acute
what does the presence of HBeAg in serology results imply?
implies high infectivity
e antigen = marker of viral replication
management of HBV
antivirals:
first line = interferon alfa
tenofovir - reduces viral replication
notify public health
how is hep C spread? symptoms?
blood + bodily fluids
most asymptomatic - release when they get chronic symptoms
when does a hep C infection become chronic?
presence of HCV RNA > 6months
hep C = commonest hep to develop hepatocellular carcinoma (via cirrhosis)
diagnosis of hep C
HCV-PCR test - if positive -> HCV RNA
chronic if HVC > 6 months
–> liver biopsy to assess damage
treatment of hep C
curable
protease inhibitors for 8-12 weeks
daclatasvir + sofosbuvir
sofosbuvir + simeprevir
–> always 2+ drugs (reduces resistance)
no vaccine available
which viral hepatitis exacerbates HBV
hep D
–> requires hep B to function
diagnosis = HDV RNA PCR on blood
characteristics of hep E
similar to hep A
self-limiting mostly
faecal-oral spread
zoonotic spread - pigs
diagnosis = blood for HEV IgM
causes and risk factors of haemolytic uraemic syndrome
causes - E coli 0157, shigella –> shiga/shiga-like toxin (verotoxin)
risk factors = NSAIDS, anti-motility agents (loperamide), antibiotics
HUS signs + symptoms
petechiae (red spots on skin) oliguria (low urine volume) fever bloody diarrhoea high WBC, low platelets
(acute renal failure, thrombocytopenia, haemolytic anaemia)
PSC symptoms
jaundice * CHRONIC * RUQ pain pruritus fatigue hepatomegaly
PSC investigations
gold = MRCP - bile duct lesions/strictures
LFT - cholestatic picture (raised ALPs)
PSC treatment
ursodeoxycholic acid - slows disease progression
colestyramine - helps pruritus, binds to bile acids preventing absorption
ERCP - stent strictures
liver transplant = curative
sudden onset colicky pain in RUQ, radiates to back, worst postprandially (after meals)
biliary colic - gallstones
investigations for cholecystitis
USS - gallstones + thickening of gall bladder wall
2nd line (if diagnosis unclear) = cholescintigraphy (HIDA scan)
management of ascending cholangitis
fluids + IV antibiotics (broad spectrum)
ERCP - drain bile ducts, ?stent idk
what is a TIPS procedure?
Transjugular Intra-hepatic portosystemic Shunt (TIPS)
creation of connection between hepatic vein + portal vein + insertion of stent
–> allows blood to flow from portal to hepatic veins - relieves pressure in portal system + varices
pathophysio of ascites
Increased pressure in portal system causes fluid to leak out of capillaries in liver + bowel into peritoneal cavity – low albumin = low plasma volume
–> reduces blood pressure in kidneys
Kidneys release renin in response – leads to increased aldosterone secretion (via RAAS) + reabsorption of fluid + sodium retention in kidneys
management of ascites
low sodium diet
anti-aldosterone diuretics = spironolactone
paracentesis
prophylactic antibiotics against SBP if <15g/L protein
monitor U&Es
complications of cirrhosis
ascites + spontaneous bacterial peritonitis (SBP)
varices
hepatorenal syndrome
hepatic encephalopathy - excess ammonia - confusion, flappy hands
hepatocellular carcinoma
hepatic encephalopathy treatment
laxatives - lactuloses - promotes excretion of ammonia
antibiotics - rifaximin - reduces bacteria producing ammonia
nutritional support
haemochromatosis
def = genetic iron overload disorder – deposition of iron in tissues
- autosomal recessive
- mutations in human haemochromatosis protein (HFE) gene on chromosome 6
diagnosis = serum ferritin, genetic testing
complications = cirrhosis, cardiomyopathy, pancreatic failure, no erections ://
treatment = venesection (weekly protocol of removing blood to decrease total iron)
Wilson’s disease
Def = excessive accumulation of copper in the body + tissues
- Wilson’s disease protein on chromosome 13 –
ATP7B copper-binding protein
- autosomal recessive
clinical features
- neurological - - dysarthria (speech difficulties),
dystonia (abnormal muscle tone), Parkinson’s
–> psychiatric – depression, full psychosis
- hepatic – chronic hepatitis > cirrhosis
- kayser-fleischer rings in cornea – deposition if
copper
treatment = copper chelation drugs – penicillamine, trientene
what is Budd-Chiari?
thrombosis in hepatic vein - causes acute hepatitis
jaundice, tender hepatomegaly, ascites (chronic)
diagnosis = US treatment = anticoag, stent, treat hepatitis
autoimmune hepatitis
type 1 - adults + kids (ANA/ASMA antibodies)
type 2 - kids only (LKM1 antibodies)
Ix = presence of antibodies, liver biopsy (interface hepatitis with piecemeal necrosis)
Tx = steroids induce remission, azathioprine (immunosuppressants)
palliative treatment of hepatocellular carcinoma
sorafenib = kinase inhibitors - inhibit proliferation of cancer
–>can extend life by months
scoring of pancreatitis
Glasgow score = used to assess severity -> 3+ = severe
One point for each (PANCREAS mnemonic)
- P – paO2 < 60
- A – Age > 55
- N – neutrophils – WBC > 15
- C – calcium < 2
- R – uRea > 16
- E – enzymes – LDH > 600 or AST/ALT >200
- A – Albumin < 32
- S – Sugar – glucose >10
management of pancreatic cancer
operable -
total pancreatectomy
distal pancreatectomy
pylorus-preserving pancreaticoduodenectomy (PPPD) = modified Whipple
radical pancreaticoduodenectomy = Whipple
in operable (palliative) - stents / bypassing biliary obstruction palliative chemo/radio
