gastro

Question 1

3GERD classification (savary miller) & los angeles classification

Answer 1

dx: occur for 2-3 x for 3-6 months. endoscopy if atypical hisotry or for definitive dx.
classification: z line is where the diaphagm crosses the oesopahgus.
solitary erosion,damaging 1 mucosal folds.
multiple erosions- daages more than 1 fold.
3.circumferential erosions.
4. chronic lesions: ulcers/strictures.
5. cylindrical epith-> z line.

los angeles: a-b single or more <5mm on single fold (non spreading).
c- spread to more than 1 fold. not more than 75% circumference.
d- mucosal damage> 75% circumferences.

trx: full dose ppi (4-6 wks) 1 hr [ost eating.if severe then longer 3 months, monitor with endoscopy.
lifestyle.

Question 2

gastritis

Answer 2

mucosa inflammation, acute or chronic (> 6 months).
causes: dietary/ medications. overuse nsaids, aspirin.
excess alcohol, bie reflux, radiation. spice/acidfic food, food poisoning.
bile exposre-> erosion.
chronic: autoimmune/ caffeine/alcohol, benign ulcers, H.pylori-remissions, meds, smoking, reflux.
abdo pain, n+ v, anorexia, headache, reflux, explosive diarrhea.
chronic: heartburn, belching, malabsorption of b12,
complication PUD.
management: NBM (rest), avoid dehydration, switch to telanol, manage food/ meds, antibiotics/antiacdis, b12 injections.

Question 3

acute and chronic gastritis

Answer 3

acute- short term inflammation-> hyperemia, edema, hemorrhage (ulcers, erosions).
etiology: exogenous.
endogenous-> stress, sepsis, shock, ARF, liver failure, azotemia.
indrect radicals . if corrosive ingestion-> heavy hematemesis=> melena, perforation.
contraindicated in corrosive gastritis-> perforation risk.
metoclopramide- N+ V.
analgesics/Abx/corticosteroids.
chronic-> corpus/antrum affected.
class A- stomach body, autoimmune.
b-antrum (H.pylori)
Ab- diffuse (Mix of both sites).
C:special forms (NSAIDS).

syndeys: etiology based, endospci /histology.
nn atrophic: h.pylori
atrophic- diffuse, autoimune
mutlifoical atrophy: type AB.
esophilic: bact,viral and parasitic.
non infectious/ granulatous- sarcoidosis, chrons.
special: type C.
after radiation.

50% asx. dx using egds with biopsy.
2 biospies from anrium and corpus.
trx: ppi+ ABX.
amoxicillin 5 days. rapid urease test.
6-10 days PPI.
metronizaole + clarithromycin.
triple therapy.

Question 4

peptic ulcer

Answer 4

duodenum or gastric (duodenum more common).
bicarbonate mucosa neturalize acid. meds like steroids, nsaids break it Hp.pylori
increase stomach acid (stress,alcohol,smoking, spicy).
epigastric, tenderness,, indigestion, dyspepsia, coffee ground, hematemesis, melena, N+V.
iron deficiency (long/chronic-> cancer too).
eating worsens gastric ulcer, improves ulcer.
food mopes up acid ??
gastric ulcer cancer-> take biopsy.
endoscopy to monitor.

complication-> perforation (peritonitis/acute abdomen-> laparoscopic), scarring/ stricture (pyloric stenosis) distension, reflux, after eating.
zollinger-ellison syndrome-tumour of islet cells increase g-acid secretion.
hyperthyroidism, stress, smoking.
blood group O genetic.
classification: erosive gastritis doesn’t surpass muscularis m.
duodenal ulcer-duodenal bulb.
gastric ulcer-lesser curvature & antrum.
pathology: injury, inhibits pg synthesis (NSAIDS), less protection against acid.
small curvature, otherwise atypical (cancer?).
CF:alarm sx-anaemia, loss weight, anorecia, recent onset, melena, swalloeing issues.

Question 5

dieulafoy lesion

Answer 5

emergency, acute GI bleed, injury to submucosal artery. proximal stomach.
endoscopic hemostasis.
stress ulcer:polytrauma, sepsis, surgery, arf.
curling/; hypovolemic shock-. hypoxia-. low defences.
cushing: brain injury-. vagal stimulation, increase acid-> acetylcholine.
prophylaxis.

nonulcer dyspepsia: bloating, , nausea and belching w/out organic cause.

Question 6

daintree classification- location

Answer 6

1- antrum
2-gastric body+ duodenal
3- pre-pyyloric
4- cardia.
gastrinoma in syndrome-> measure serum gastrin level at baseline and after stimulation (food).
measure calcium and PTH levels. high.

note other sx like palpable mass, LN, progressive solid -> liquid dysphagia/ odynophagia.
fhx of upper malignancy. jaundice?
biopsy from edge and base of ulcer-> stomach lining distant from ulcer.
dx and subsequent hemostasis trx.
neisser fundoplifcation surgery for perforation.
h2 antagonist like cimetidine.
surgery: bilroth I and II: distal removla of parts of stomach, anastomose body with duodenum
bilroth II: jejunum and the fundus.
roux en Y: jejum atached to fundus and bit of duodenum.
bypass: jejum at cardia level.
surgery results in bile reflux-> type c gastritis-> anastomosis cancer.
vagotomy.

Question 7

complication of ulcers

Answer 7

perforation, melena, hematochezia (undigested blood -> acute/rapid bleeds), haemetesis, penetrate adjacent organs, irregular gastric ulcers-> malignant?

proximal border of duodenal ulcer -. GD artery-> bleeds.
bleed more if anterior wall-> air under diaphragm -> phrenic N-> referred pain to shoulder.
CF: intense/ stabbing pain-> diffuse abdo pain-> distension-> peritonitis.
abdominal x-ray (pneumoperitoneum -> upright), CT w/ h20 soluble contrast.
Trx: emergency surgery, sub-hepatic abscess, pyogenic liver abscess.
perforated duodenal /gastric ulcer, N+V. X-ray diagnosed.
IV ab, percutaneous drainage.

Question 8

pbc

Answer 8

aitoimuen liver disease, t-cells atttack bile duct. 95% women. 35-7-.
impaired bile formation, secretion.
jaundice.
cholestasis (sympatiology) retained toxic metabolites-> damage liver cells-> cirrhosis.
sx: asx in 50%, routinely found on lab tests.
sx: pruritis, fatigue, dry mouth/eyes.
physical: RUQ discmfort, hepaomegaly, hyperpigmentation, jaundice, xanthelasmas -> deposit of fat under skin/ eye.
dx: antimitrocnhdrial antbody (high titer).
lft-GGT and ALP elevated significantly.
confirmed via liver biospy-> dile pathology detected.
trx: decrease liver damage.
urodeoxycholic acid.
cholestryamine (pruritis).
liver transplant.

Question 9

gastric cancer

Answer 9

RF: obesity, age (>70) , h pylori, smoking, acohol, hereditaroy gastric difuse cancer, defet in CDH 1 - e cadherin, diet/ pernicious , chronic gastritis
95% adenocarinoma
5% lymphoma and stroml tumor
most common: pyloric antrum, lesser curvature, cardia, fundus, body
asx - > non specific.
wt loss, indigestion, bloating, N/V, bleeding, fatigue, heartbern,. troiser sign (plapbale lef. supraclavular node-> abdominal malignANCIES.
endoscopy-> gold. CT staging
TNM stage ) epithelium insitu.
4 distat
2-3 local and LN infiltration
survivial: poor prognosis only if caught early
prevention: rich in fruit/ veg, eradicate H. pylor.
endoscopic mucosal resection, neoadjuvant or adjuvant (before surgery), immunotherapy -> nivolumab , trastuzumab.

Question 10

pre-canceorus and gastric cancer.

Answer 10

precancerous condition: changes (dysplasia-> metaplasia-> changes prone to carcinoma).
epithelial-> type G dysplasia.
pathology: low grade dysplasia-> abnormal+ slow growing, low risk- monitor
high grade- endomucosal resection. limited surgical resection
RF: chronic atrophy: long term inflammation, pernicious anaemia.
dx: chromoendoscopy -special staining/ EUS.
CF:pernicious anaemia,. co -presence of thyroid, type 1 DM.
dx: biopsy, serological markers (pepsin, b12, ab against intrinsic factors).
Trx: eliminate pylori,b12 injection.
cancer: include esophagogastric cancer.
epidemic; Korea, japan.
Etiology: exogenous (nitrate/salt food, preserved, dried food).
endogenous- adenomatous polyps, gastrectomy, GERD etc, blood type A, family history hereditary non polyposis Colon C).

pathology: antrum and pyloric . lesser curvature. proximal has poorer prognosis and worser sx.

CF; early satiety. later: hepatomegaly, ascites, palpable tumour in epi region, obstruction. Sister joseph Mary node: indicate metabolise or pelvis spread (painful umbilical nodule)
acanthosis nigricans (specific to adenocarcinoma).
lymph node (lesser+ greater curvature), celiac, paraaortic, mesenteric LN,
cardia carcinoma -> mediastinal LN.#
liver, lung, bones, brain.
peritoneal-> oesophagitis, trans colon, pancreas.
direct-> krukenberg tumour (ovarian
TNM grading
GX- cannot be assessed.
G1,2,3,4- from well differentiated-> poorly differentiated.
dx: biopsy, barium swallow.
labs: anaemia iron deficiency serology (TNF-A).
staging:EUS.
depth tumour and local LN.
abdo-pelvic assessment. throacic CT, diagnostic laparoscopy.
surgery: radical LN removal, resect omentum and radical gastrectomy (roux-en Y bypass).

Question 11

Chrons-IBS

Answer 11

anywhere.
immune related- pathogen in flora (pseudomonas, listeria, mycobacterium).
APC present antigen -. TH1-> cytokines-> inflammatory-> macrophage-> free radical-> platelet activated-> protease.
dysfunction-> tissue destruction.
genetic component, frame shift mutation in NOD2 gene.
gene expression-> dysfunctional protein.
pathogens enter barrier. granulomatous -> transmural ulcers.
cobblestone appearance.
ileum +colon.
CF: pain in right quadrant, watery diarrhoea, malabsorption, weight loss, urgency, anaemia (TI-pernicious)
meds: anti-inflammation, Ab (control gut bacteria), corticosteroids, surgical-> curative for UC.
complication : fistula (enterocutaneous fistula)-perianal, fibrosis/ strictures.
extra-intestinal: arthritis, iritis, erythema nodosoma, etc
obstruction-> constipation/ vomiting,
dx: barium (sticture), colonoscopy.
bloods: crp, leukocyte, high esr, ASCA specific to IBD.
#stool test: c-diff, other causes of gastroenteritis. dettect faecal calprotectin.
trx: lactose free diet. monoclonal Ab (infliximab), azathioprine, sulfasalazines (anti-rhemautic)
surgical not curative: ileorectal, protoccolectmy (endileostomy)
ileocecal resection.

Question 12

jaudnice:

Answer 12

skin eye icterus.
rbc (120 days) macriphages in reticuloendothelial system)-> UC formed (not water solubke)- albumin binds to it-> UGT makes it CB)-> stored in BD-> SI-> urobilinogen-» sterobilin (feces ), yellow urine, blood, liver etc
serum 2.5 mg/dL.
UCB-> extravascular hemolytic anemia .
/(ineffective hemopoesis)- dark urine, pigmented GS, neonatal jaundice (low UGT enzyme)-> kernictuerus.
genetic defect-> gilbert (stress, starvation/ infection -> hemolysis).
CB- dubin nohnson syndrome.obstrucitve jaudnice (GS, pancreatic carcinoma, liver fluke).
pressure-> bakc up bile)-> bile acid, cholesterol, pruritis, xanthomas, , stearrhoea, soluble so dark urine.
viral hepatitis-> heaptocytes-> both rise CB/UCB. bile leak into blood.

Question 13

additional jaudncie notes

Answer 13

normal< 1.23 mg/dl.
abnormal>2.5-2 mg/dl.
jaudnice>4-5 mg/dl.
prehepatic: hemolyiss, congenital (gilberti)
intrahepatic: accompanied with deranged ALP, AST,ALT (<1000 uL) suggest infx, hepatits, drug intoxication.
post hepatic: cholestatic jaundice.
-biliary cirrhosis )parasitic)
carcinoma, choledolithasisi, bile strictures, pregnancy.
CF: pale stool, malapsorption in water soluble vitamins.

pseudoauncie: excess carotene vegetables.no slceral icterus, sphenolskin exposure to

Question 14

UC

Answer 14

only rectum and large intestine.
affects mucosa-> submucosa.
th1 attack the tissues (flares-> remission (healing)). cross reactivity of P-ANCA with the gut flora-> immune mediated (autoimmune).
bloody, mucosal diarrhea, wt loss, painless, anemia microcytic and iron deficiency, erythema nodosa, tenesum (infammation) , urgency, left quadrant pain. systemic sx
colonoscopy and imaging-enema barium
complications: toxic megacolon.
extra intestial : pyoderma gangrenosm, conjuctivits, episcleritis, clubbing etc.
trx: anti ifnlammatory sulfsalazone, immunosuppresant, biolgics (infliximab), coelctomy (curative).
it works its way around, circumferential and continous.
sulfide- active inflammation.
genetic predisposition- fhx (female- teen-30th).
can be proctitis, left sided colitis or pancolitis.
criteria of true love and witts used for admission and iv therapy.
mild: < 4 stools/24rs. no systemic manifestation.
moderate: 4-6.
severe: >6 stools/day, systemic -tachy, esr> 30.
labs: low albumin.
serum gamma -gltamyl trasnferase-> damage liver + alcohol intake.
stool: calprotectin, lactoferrin. mucosal infammation. rule out other bacterias.

Question 15

acute pancreatitis:

Answer 15

glasgon imrie score (pancrease)
pa02< 8kpa
age>55
neu>15 x 109
calcium,< 2mmol
enzymes: LDH/AST
albumin<32 g/L
sugar> 10mmol.
trx: treat underlying cause.
IV fluid, Ab (supportive).
monitor input/output (catheter).
BUN-> indicate how much needed
anaglesic-opiates
NGT (keep NBM), tolerate nutrient.
surgery-necrosis, pseudocyst, abscess, ostruction, vascular complication, uncertainty
endocrine-insulni, glucagon, somatostatin-GIH.
exocrine- bicarbonate, digestive (trypsinogen, elastase, lipase, amylase).
early activation-necrosis, fat necrosis, damage (cellular or majority),inflammation, edema, ischemia.
IGETSMASHED
I-idiopathic, G-GSB, E-ethanol, T-trauma.S-steroid, M-microbio-mumps, hepatits.TB), a-Autoimmune, S-scorpia sting, H-hypercalemia, hyper triglycerides, E-ERCP,emboli, D-drugs - direutics gliptine,opiates
SX: band like pain, N+ V, fever, appetite, GBS, epigastric radiate to back, rebound , guarding, cullen/turner haemorrhage.
secondary: hypovolemic.
dx: abdo pain, elevated ERCP, CT/US (after 48hrs).
hypocalcaemia- fat necrosis-> fatty-> ind ca2+.
complication: pseudocyst-juice collections), chronic, necrosis, infection, abscess, peripancreatic fluid collection.
chornic: diabetic, reduced functio/firbotic. alchol cause.
similar sx.
chronic pain, lack of enzyes-> strictures- obstruct bile/ juice,pseudocyst and abscess.
mNgement: cesstion, analgesia, replacemnt of enzyme in creon tabelt.
mLbaopriton-> stearrhea, deficiency in fat soluble vitamins, ercp, surgery needed.

Question 16

panreatic cancer

Answer 16

poor prognosis, common in head of pancrease. obstructive painless jaundice.
courviosier sign (seen in cholanigocaricnoma).
sx: N+V, wt loss (tumor related anorexia), worsening of DM2 or new onset DM., vague (CBH, N+V), non specific sx, migratory thrombo
trosseua sign of malignancy-> migratory throbocyotplebitis ( reoccurs at different sites).
dx: imaging, ercp (biopsy, peructaneous), TAP (metastiasis), Ca19-9 (cholanigocarcinoma.
mRCP (assess biliary).

trx: stent, palliative, radicl chemo/ radiotherapy, PPPD (modified whipples),total pancreatectmy, distal.
hepatobilary MDT -> approach. 25 % survival- 5 years.

Question 17

precancerous and carcinoma of colon

Answer 17

adenocarinoma of rectum/colon.
hereditary, sporadic or familail. older age (>50 yrs). mostly L -sided (5-6 cm).
split rectum into upper and lower part.
RF / etiolgy: familial adenomatous polyposis (excess polyps), hrediratynon polyposis colorectal cancer.
hereditary , fHX, adenomas, IBS< smoking, processed meat, nsaids, low fiber diet.
pentz jeghens sund-> autosomal. hamartous, hyperpigmentation of buccal mucosa, bleeding polyps-> obstruct.
apc gene (t -suppressor-> daage-> malignant polpys0> sessile/ pedunculated.

cf: R sided-> melena, diarrhea,
L-sided: CBH, melena, abdo pain colicy -> pbstructive.
recum -> hematochezia, decrease caliber stool, tenesmus, pain etc.
sx based on location and staging.
advanced: obstruction, palpable.
metastic-> liver (ascites, distension), lungs-> dysnpnoea, cough, PE, hemoptysis), LN involvement.
DX: colonoscopy + bisopy.
double contrast enema -> aple core filling.
FBC, ocult blood , sigmoidsoocpy, CT/MRI.
CEA tumors -> CA19.9.
TNM + duke :
A-limited to mucosa ,B muscle wall,C LN involvement,Distant
trx: radio/chemo.
neo/adjuvant.
colecromy, regional LN dissection.
regimens: folinic acid, floroquiracil etc.

Answer 18

mutated apc doesnt stop sporaidc growth.
adenomatos and serrated (normal, serrated are more mutated dna repair gene , saw sooth appearnace).
ascending: pain, weight. late diagnosis, anemia,melena
descending: lumen narrowing, early detected.

Question 19

cirrhosis

Answer 19

regeneratie nodules- colinoes of cells, fibrotic and collagen.
end stage disease.
stellate cells in perisinusoidal space. damaged hepatocyte-> activate stellate (store vit A)-> TGF-B-> produce collagen-> compress central V and sinuosids (key for wound healing but constant-> fibrotic)
portal triad-portal V, A and bile duct.
fluid into peritoneal cavity-> ascites.
congestive splenomegaly-> backs up fluid ito spleen.
portosystemic shunt-> renal vasoconstrictive-> low fltrate-> hepatorenal failure.
blood diversion -> liver function-> low detoxification-> heaptic encephalopathy (build up ammonia)-. asterixis/coma.
estrogen in blood.
UC blood-> jaundice-> albumin.
low clotting factor -> coagulation issues.
ealry -> comepnsatory.
asx or non specific (wt loss wekanes, fatigue.
deocmpensated- pruritis, ascites, easy bruising.

dx: bisopy.
lab : bilirubin, AST> ALT, GGTP, thrombocytopenia.
trx: transpalnt, prevent further damange, antiviral if hepatitis C,

Question 20

viral hepatitis

Answer 20

virus DNA inside hepatocyte, MHC 1 expressed, cd8 complex - cytotoxic killing-> inflammation -> damage.
pathology: council man body.
sx: fveer, malase, nausea, hepatomegaly, pain.
ALT>AST (last to return to noral).
atypical lymphocytosis (large)- stimualted via antigen.
jaudnice -UCB-CB, CB leakage and hepatocyte cannot convert.
dark urine, urobilinogen increase (intestinal micorbes, cannot go back to liver-> urine )
acute, after 6 months-> chronic and post necrotic (portal tract).
5 types:
HVA: feco oral, travellers. acute. serology: IgM activate, igG -> recovery vaccine.
HEV: similar, contamnated water, sea food.
same. no vaccination. if pregnant-> fulminant hep.
HCV: childbrith, sex,, iv drug user.
test: enyme immunosay- not protecctive igG.
recombinant immunoblot is more specific.
HCV RNA test- pcr standard (1-2 wk -> rna).
decreasing-> recovery, if levels same -> chronic.
HBV: same as HCV. acute and chronic.
linked to cancer.
dpeneds on age: if younger than 6 -> chronic.
markers: surrface Ag .
core antigen: HbcAg.
E antigen -> active infection secreted via host cell.
acute: DNA virus. igM detected-. attack core.
igG attack super villian (surface Ag). Important.
chronic-> looks healthy. contagious and infective.
post necrotic cirrhosis and hepatocellular carcinoma.
HDV is super infection (more severe) or co infection (igG isnt protective antibody in this stage and only igM is ).

Question 21

autoimmune hepatitis

Answer 21

idiopathic, combo of environmental and genetic. F>M.
HLA on chromosome 6. (regulate immune).
exposed to alloantigen.
other assisociation-> hashimotosi.
asymtpomatic to cirrhosis + fulminant hepatitis and symtomatic.
ALT more associated with Liver.
type 1: ANA (80%). ASMAS (own SM)
serum albumin low..
pT prolonged.
type II: less common. antibodies against kidney/ liver microsome, cytosol liver.
younger girls.
trx: suppress immune.
azathioprine (inhibit synthesis of b and t- cells).
corticosteroids, transplant,

Question 22

alcoho induced liver disease

Answer 22

detoxified in liver.
ADH works to , cyto p450, catalase peroxisome ethanol-> acetyladehyde.
fat production excess-> fatty liver, (heavy, greasy, tender, yellow deposit).
steatosis.
trx: stop alcohol.
ROS-> damage cells.
acetylaldehyde->
mallory body in alcohol hepatocytes.
CF: pain, liver function reduced, N+V, liver mass increase.
dx: hepatomegaly, increase GGTP, AST>ALT, hyperlipiddemia. sparkling lvier on USS>
trx: antioxidant, transmetil-> overcome intra hepatic cholestasis (prevent jaundice and bile spilling).
hepatitis: splenomegaly. hyaline, mallory body seen, PMN infiltration, fibrosis.
immune complex form.
weakness, anorexia, pain, increase temp, hematemesis, melena, ascites.
labs: anaemia, LFT
trx: correct diet, corticosteroids (suppress inflammation), anabolic steroids, hepatoprotectives (legalon, carsils), transmetil.

Question 23

hepatic encephalopathy

Answer 23

reversible syndrome involving neurophysiatric abnormalities with underlying disease.
decompensated!- alcoholic related, non alcohol fatty liver, hepatitis (B/c), wilsons.
epidemiology- almost 50% occurence, results n hospitalisation
idipopathic cause
portosysemic shunting- no clearing of toxins, bypass normal liver (increase w/ severity).
overall decrease liver function-> neurotoxins-> brain dysfunction (ammonia), GABA, manganese, short chain fatty Acids).
NH3-> urea cycle fails. cross BBB-> alter cellular pathway.
affect ketoglutarate-> glutamate-> glutamine (decrease att / consumption)-> oedema-> oxidative stress.
hypoxia, meds, constipation, excess proteins, hypokalemia, hypovolemia, RF, surgery/procedure (TIPS), bleeds GI (ammonia in gut), bacterial peritonitis.
clinical: mild (perosnality changes-apathy), sleep wake cycle revers,e shrot term memory affected, impaired cognition, slurred/slow speech.
stage II-> asterixis, lethargy, drowsy, reduced attention, abnormal clock drawing test- indicative.
stage III: ataxia, positive Babinski, hyperactive reflexes.
stage 4: coma, only respond mild to painful stimulus.
Dx: late/end stage liver disease. exclude other disease. arterial ammonia.
EEG
trx underlying cause, ab, K+ supplements, reduce toxins.
lactulose-> titrate to 2-3 stools a day (reduce absorption-> increase osmotic laxative effect)
rifaimin 400 mg, zinc (defiinecy), neomycin in refractory.
swallow evaluation.
west haven cirtiera: severity of HE.
type A - acute
type 2: bypass liver.
type C: cirrhosis.
grade 1-4 (coma).

Question 24

metabolic liver disease- hemoatochromosis

Answer 24

primary- high iron. defect on HFE gene (AR), decrease r
secondary: thalassemia TBF.
gene mutation regulates protein increasing iron absorption form gut.
m>F (menstrual loss). normal iron content 3-4 g.
treatment- constant phlebotomy, deforaxamine etc.
complication: ROS, direct collagen formation.
triad: micronodular cirrhosis, DM (fibrosis of kidney), bronzing in skin (melena), arrhythmia, CHF, arthritis, joint pain, infertility (hypogonadism - 2nd to pit dysfunction)
labs: ferritin, high iron, decreased TIBC.
serum Fe> 36 micro mol/L.
serum transferin >90%.
unsaturated fe2+ binding capacity. deferoxamine (iron chelating agent).
trx
wilson: increased cu2+. AR
ceruloplasmin protein binds in liver- plasma-> albumin-> tissue.
also excreted in bile.
defect in ceruloplasmin, accumulation, decrease biliary excretion.
CF: keyser fleisher (split lamp) ring in cornea, cirrhosis, haemolysis, psychosis.irreersible effect on kidney.
abdo pain, jaundice, ascites, parkinsonism (dystonia, personality changes, dysarthia (inability to produce speech).

labs: low ceruloplasmin, high hepatic Cu2+. coombs-ve for hemolytic anemia in ALF.
trx: depenicillamine.

Question 25

liver cancer
and metastasis.

Answer 25

benign- haemangioma, focal hyperplasia, hepatocellular adenoma (oral contraceptive, steroids), -estrogen linked (high in young women).
asx. if large-> fullness, nausea, upper abdo pain.
dx: US. contrast CT, MRI. biopsy.
trx: surgical -> exceeding 5cm/conservative treatment sufficient.
discontinue contractive. treat complications. resect if malignant transformation, remove adenomas.
simple cysts.-incidental, congenital.
asx.
dx: sonographic. laparoscopic resection if sx.
malignant: HCC or from cholangiocarcinoma.
hepatocellular.
solitary tumour-cirrhotic, chronic hepatitis (type C+B). non alcoholic fatty liver disease
increase in alpha fetoprotein.
pathology: distinct 3 types
hanging- stalk vascular.
pushing-fibrous capsule.
infiltrative-.> invades vascular structure.
CF: RUQ, palpable mass, ascites, wt loss, obstrucitve jaudnice, hemobilia.
dx: afp> 500 microg/ml( specific).
US, CT , MRI imaging. biopsy to confirm.
paraneoplastic syndrome (sx related to only tumor)- EPO production, hypoglycemia, hypercalcemia->pTH deranged.
TNM-not accurate.
liver Italian programme-child Pugh score (PT time, albumin, encephalopathy, jaundice, bilirubin, ascites ) , level AFP, liver morphology, PV thrombosis.
trx: curative, hepatectomy, transplant.
palliative, embolization, percut ablation. vaccination against HBV.

Question 26

cholecystolithiasis, cholecystitis.

Answer 26

cholangitis -> choledolithaissis or acute pancreatitis if bile outflow obstrucited.
acute cystitis- cholelithiasis.
biliary colic-. RUQ, after fatty meal. continous and afebrile, n+V. or asx.
ivnestigaition: LFT, wbc, crp, alp.US used
treatment -lapaorsopci cholecystectomy
5x f: fertile (estrogen icnreases cholesterol), fat, forty, fair, female.
chlolesterol, pigment and mixed stones.
rf: high choolesterol & low bile salt

analgesia and avoid hihg fat diet.extracorepal shock wave lithotripsy.
acute cholecystitis- galstone, bile stasis-> inflamaotyr enymes->distension, protaglandin released-> ischeia, necrosis and perfroation.
pain radiate to R scapula. murphey sign.febrile. no jaundice.

acute cholangitis: tumors, GBS, surgery.
bile slude- infection-> ascendng infection
charcout triad: fever, RJQ, jaudnice.
altered MS (hypotension) , sepsis.
raised biliaey pressure-> bactereceia.
pruritis, tea colored urine,stearrhoea/pale.
raised alctate and alp raised.
ercp, following mcrp.
iltuion of CBD.
iv flids, ab. sphicncterectomy and and stent.
percutanoeus choangiopancretography is 2nd line if patient is too unwell.
cholecytokinin-contraciton of GB- colic pain. radiate to pain.
pigment stone- black/brown.
cholesterol- pale yelllow.
mirizi syndrome-> CBD obstruction.
brown spec ab- cpehalosporin, cefuroxime, gentamicin. NBM.
+ve ortner sign (tp edge of right costal arch
chronic: recurrent attack with temp occlusion of cystic duct.
vague sx. porcelain calficiation of GB. pericholecystic fluid, diluted.