Buzzin Flashcards
colonizing oral cavity?
- strep mutans
- prevotella intermedia, porphyromonas gingivalis
late: actinomycetem comitans
PAS stain
pseudohyphae, oral candidiasis
Tzanck smear, multinucleated cells
HSV
lesion in mouth thats bleeding
pyogenic granuloma
what is white and won’t scrape off?
hairy leukoplakia - see hyperparakeratosis w/ balloon cells - think EBV
Luekoplakia = premalignant lesion
Tobacco SCC?
p53 and NOTCH
pink squamous cells and mucin making cells neoplasia in mouth?
mucoepidermoid carcinoma
perineural invasion in mouth?
adenoid cystic carcinoma
polyhydramnios
think atresia
double bubble sign?
duodenal atresia - 30% have trisomy 21
also think annular pancreas
air in stomach on CXR?
think fistula
weak posterior/lateral aspect of diaphragm?
diaphragmatic hernia
high AFT levels in amniotic fluid
think omphalocele (OLDMA) or gastroschisis (YMA)
defect in anterior abdominal wall?
gastroschisis
why meckels?
failed involuation of vitelline duct
appendicitis you think….
maybe meckels in young kids!
projectile non bilious vomiting
pyloric stenosis
hirschsprung disease
megacolon! - see bilious vomiting
acquired megacolon?
chagas disease
pyrosis
heartburn
odynophagia
pain w/ swallowing
achalasia
increased tone of LES
secondarily due to chagas disease: trypanasoma cruzi
hiatal hernias
sliding = upper part of stomach –> diaphragm
rolling: upper fundus slids up esophagus
zenker diverticulum
pouches of esophagus due to increased pressure
mallory-wess laceration
retching/violent vomiting = lengwise tears
boerhaave syndrome
perforation of esophagus due to increased pressure
barrets
metaplasia (replacement): squamous cell to intestinal glandular mucosa w/ goblet cells
ADCA risk - length is most imp. risk factor >3cm
+mucicarcmine staine
ADCA
middle third of esophagus
SCC
mets of cancer in upper third esophagus?
cervical LNs
cancer in middle esophagus spread?
SCC - mediastinal, paratracheal,, tracheobronchial nodes
cancer in lower third esophagus?
think ADCA - spread gastric/celiac nodes
curling stress ulcer?
burns/trauma - proximal D
Cushing stress ulcer?
intracranial disease - see gastric, duodenal, esophageal ulcers
where’s h. pylori?
antrum / duodenum
spiral shaped, curved bacilli
chronic inflamm. of fundus?
AI diseae
chronic inflamm. or whole stomach?
drugs/alcohol
antral gastritis w/ high acid production, no hypergastrinemia
H pylori
+ ammonia in breath
due to urease in H. pylori infection
cancer assoc. w/ h pylori?
ADCA, MALT lymphoma
body/fundus gastritis w/ hypergastrinemia?
AI gastritis
AutoAbs to parietal cells and IF - loss of parietal cells
achlorhydria
defective gastric acid secretion
oxyntic
acid producing mucosa - parietal cells
air under diaphragm in CXR?
think PU that punctured through stomach
hematochezia
bright red blood in stools
EGD
upper GI endoscopy
hypertrophic gastropathies?
metetrier disease: xs secretion of TGF alpha: body/fundus ; w/l diarrhea, Peripheral edema
ZE syndrome : gastrin secreting tumor - see chronic diarrhea , multiple peptic ulcers
epithelial dysplasia in gastric tumor?
benign gastric adenoma/ a type of polyp
virchows node/ sister mary joseph node, axillary/irish node?
think gastric adenocarcinoma
two types of gastric adenomas?
- Intestinal type (non signet ring) - usual type
- assoc. w/ H. pylori
APC/WNT pathway
- occur in gastric antrum/pulorus
- form bulky ulcerative tumors - Diffuse-type (signet ring)
- not assoc. w/ h. pylori
germline loss of fn. in E-cadherin (CDH1 gene)
- infiltrate diffusely in wall of stomach
- linitis plastica
MALToma
marginal zone B cell lymphoma - H. pylori related
arise in site of previous inflammation
CD19/20 +
see lyymphoepithelial lesions
GIST
mesenchymal gastro-intestinal stromal tumor
arise from interstitial cells of cajal
C-KIT/CD117 or PDGFRA mutations
see spindle cell features
C-KIT/CD117 +
mesenchymal GIST
direct vs. indirect hernia?
direct = occur medial to epigastric indirect = lateral to epigastric
target sign on US
think intussuscpetion
red currant jelly stool
intussusception
coffee bean sign?
volvulus
primary vascular related GI bleeding?
Ischemic bowel disease, mural infarction, angiodysplasia, hemorrhoids
cocaine + abdominal pain/bloody diarrhea?
ischemic bowel disease
also think CMV and E. coli
watershed zones?
ischemic bowel disease - think splenic flexure, sigmoid colon, rectum
** most often colon!!!
dysentary
painful bloody diarrhea
secretory diarrhea
persist during fasting - think infectious; viral or enterotoxin
osmotic diarrhea
hypertonic fluid - abates w/ fasting - think lactase defic.
exudative diarrhea
due to mucosal damage –> purulent bloody stoools that persist w/ fasting - think bacterial or IBD
malabsorptive diarrhea
abates w/ fasting : see improper absorption –> bulky stools w/ xs fat
ex. celiac, giardia, CF, chronic pancreatitis
genetics of celiac?
HLA-DQ2/DQ8
diffuse/severe blunting of villi in D/J
malabsorption
dermatitis herpetiformis
subepidermal blistering of skin seen in 10% of celiac pts.
IgA anti-transglutaminase Ab
seen in Celiacs
MTP gene
mutated in abetalipoproteinemia:
oil red-o stain
abetalipoproteinemia:
acanthocytic red cells/ burr cells
abetalipoproteinemia:
guillan barre syndrome
campylobacter enterocoloitis
most common bacterial pathogen in developed countries and travelers diarrhea
see watery/blood diarrhea
bloody diarrhea, fever, ab. pain
shigellosis
rose spots
maculopapular rash on chest and abdomen - typhoid fever - salmonella typhi
may mimic appendicitis
ETEC
watery/secretory noninflamm. diarrhea
EHEC
O157:H7 –> HUS + bloody diarrhea
EIEC
dysentery
EAEC
nonbloody diarrhea, prolonged in AIDS
tropheryma whipplei
Whipple disease - se w/l, diarrhea/steatorrhea, and polyarthritis
see dense accum. of foamy macrophages in SI lamina propria –> accumulate in nodes and joints
** only one affecting lymphatic transport
which kills many children every year?
rotovirus - causes severe wtery diarrhea
AIDS/diarrhea
thik cryptosporidium spp.
also MAI - can detect w/ acid fast stain
amebiasis
dysentery and liver abscess - caued by entamoeba histolytica seen in india, mexico, colombia –> go to liver, brain and lungs
giardia
deacreased expression of brush border enzymes –> steatorrhea
pANCA
some UC
ASCA
some CD
starts on cessation of smoking
UC
UC
colon and rectum –> retrograde, no skips
mucosa/submucosa - superficial broad based ulcers
can cause megacolon and pseudopolyps
NO granulomas/strictures
bloody mucoid diarrhea
risk of ADCA
CD
regional enteritis unaffected, skip areas transmural linear mucosal ulcers - deep ulcers granulomas!!! fissureing/fistula creeping fat relatively mild diarrhea, ab. pain, RLQ (ileocecal) *** erythema nodosum ADCA fat + vit malabsorption
sessile
flat
pedunculated
polyps w/ stalk
hyperplastic polyps
sessile - no malignant potential - most common
inflammatory polyps
seen in chronic IBD - see rectal bleeding ad mucus discharge - not malignant
hamartomatous polyps
pedunculated - think PJ syndrome of juvenile polyposis
mutated STK11
Peutz-Jeghers syndrome -
see hamartomatous polyps, mucocutaneous hyperpigmentation
increased risk of cancer
SMAD4, BMPR1a mutations
think juvenil polyposis
age <5
see hamartomatous polyps - congenital malformations - digital clubbing - cancer by age 50
adenomas
neoplastic polyps that are not yet malignant - size >4cm has increased malignancy
APC gene mutation
Familial adenomatous polyposis - see numerous adenomas >100 to make ddx
colon cancer by age 30 if not treated
autosomal dominant
MLH1, MSH2 , microsatellite instability due to repair gene defect
think hereditary non-polyposis colorectal cancer HNPCC
see sessile serrated adenomas
autosomal dominant
right sided ADcarcinoma - mucinous subtypes + endometrial cancer
mucinous ADCA
predominantly on right side - has to do with DNA mismatch repair genes or hypermethlaition: MSH2, MLH1, BRAF — think HNPCC or sporadic colon cancer
left sided ADCA?
think typical tubular/villous ADCA with APC/WNT pathway defect
change in bowel habits, rectal bleding, melena, LLQ pain : presents w/ obstruction and is caught more quickly
right sided ADCA?
presents w/ fatigue, w/l, anemia : they don’t often present w/ obstruction
mucinous ADCA
due to MSH2, MLH1, BRAF mutations and DNA mismatch repair problems
where does colon ADCA met to?
regional LNs, lungs, bones, liver *** most common
well differentiated neuroendocrine tumor?
carcinoid tumor ** midgut most aggressive
carcinoid syndrome = serotonin release - episodic skin flushing, diarrhea, bramping, asthma
zones of rectum?
upper zone = columnar epi. (see ADCAs)
middle zone = transitional zone = cloacogenic carcinoma (behaves like SCC but doesn’t make keratin)
lower zone = squamous epi. - see condyloma papilliform - HPV 16/18, mutated E6/E7
anal fistulas assoc. w/?
CD
lymph drainage above dentate line?
perirectal and paravertral nodes
lymph drainage below dentate line?
superficial inguinal /femoral nodes
toxin of H. pylori?
Vacuolating cytotoxin (VacA) causes cell
injury characterized by vacuolization. Another H. pylori gene from a pathogenicity island encodes cytotoxin-associated
antigen (CagA) and is present in many patients with chronic gastritis and peptic ulcers and increases their risk for gastric
cancer.
leather bottle stomach
diffuse gastric ADCA - signet rings are seen
cobblestone appearance of gastric mucosa
leather bottle stomach - diffuse gastric ADCA - signet rings are seen
Sclerosing cholangitis associated w/ what?
UC sometimes CD
Diarrhea with mucus and blood in the stools
Shigella dysenteriae and Entamoeba histolytica.
with E. histolytica can see liver abscess
ompeprazole + Upper GI endoscopy reveals 3 circumscribed, round, smooth lesions in
the gastric body from 1 to 2 cm in diameter. Biopsies are taken and microscopically show the lesions to consist of irregular
glands that are cystically dilated and lined by flattened parietal and chief cells. No inflammation, H. pylori, metaplasia, or
dysplasia is present.
fundic gland polyps
typhoid fever
Salmonella typhi
abdominal pain and diarrhea during week 1 of their illness. By week 2, these patients had splenomegaly
and elevations in serum AST and ALT levels. By week 3, they were septic and had leukopenia. At autopsy, the patients
who died were found to have ulceration of Peyer’s patches.
centrilobular
zone 3 - acetiminophen toxicity
periportal
zone 1
microvesicular steatosis?
pregnancy, Reye syndrome, tetracycline/salicylate toxicity, alcohol
macrovesicular
obesity, diabetes, hep C, EToH
skin/body changes of chronic liver failure?
jaundice, palmer erythema, spider angiomata, terry nails, finger clubbing, “fector hepatis”” - sweet/musty breath, edema/ascities, hypogonadism/gynecomastia
asterixis
hepatic enceophalopathy - “flapping” tremor of hands - jerky irregular flexion patterns - due to ammonia accumulation and liver failure
macronodular cirrhosis
think viral
micronodular cirrhosis
think ethanol
causes of liver cirrhosis?
hep C * most common
alcohol * also really common
hep B* sometimes
mediators causing myofibroblast transformation?
PDGF (migration of stellate cells) and TNF activates stellate cells
TGF beta –> stimulates fibrinogenesis in myofibroblasts
stellate cells secrete VEGF/ANG1 –> vascular remodeling
portal HTN?
due to liver cirrhosis - b/c of fibrosis and sinusoidal remodeling of myofibroblasts –> intrahepatic vascular reistance
pre-hepatic: portal occlusion
Intra-hepatic: due to liver cirrhosis: alcohol + hep
post hepatic: RSHF, hepatic v. outflow obstruction
see varices, ascites, congestive splenomegaly, heptic encephalopathy
high protein ascities?
TB, carcinoma = exudate
low protein ascites?
transudate = albumin loss
eruptive xanthomas, pruritis, jaundice
think cholestasis - inability to excrete bile - backs up showing jaundice
no bile salts to break down fats –> cholesterol retention and xanthomas
bile salts deposit in skin –> pruritis
UDP
uridine diphosphatase = conjugates/ makes direct bilirubin
choluria
dark colored urine - due to bilirubin excretion
rotor/DJ syndrome
mpaired biliary excretion of bilirubin glucuronides is due to a mutation in the canalicular multidrug resistance protein 2 (MRP2)
see elevated conjugated bili/jaundice w/out AST/ALT elevation
DJ has black liver
high unconjugated bili levels?
think Gilbert/Crigler Najar - due to UDP problems
AST/ALT
meausres hepatocyte membrane disruption
ALT found in liver
most common cause of just ALT/AST elevation = NASH
higher AST/ALT ratio is likely ETOH
see very high levels w/ viral infection
ALK Phos and GGT
induced enzymes - think biliary things
seen w/ cholestasis and EtOH
isolated elevated GGT = EtOH
isolated ALK Phos: must rule out bone and placenta
high IgA
alcoholic liver disease
diffuse hypergammaglobulinemia?
cirrhosis, AI hep
IgM high
primary biliary cirrhosis
IgG high
AI hep
Hep A
F-O contamination
1 mos. incubation
third world epidemic - shellfish in US
ACUTE ONLY - does not cause chronic disease
see spike in fecal HAV
see anti-HAV Ab in those having had vacc.
see IgM- anti-HAV after 1 month in those that have been infected
Hep B
ACUTE and CHRONIC (only minority go to chronic)
- horizontal transmission: sex most common
- vertical: seen in Asia!
- 5% progresses to chronic hepatitis, 1% of total gets cirrhosis, .5% of total gets hepatocellular carcinoma
3 mos incubation
histo: “gorund glass appearance” of HBsAg
portal inflatmmion, apopostis w/ acidophil bodies
Dane particles
incomplete dsDNA - think HBV
indicative of active infection of HBV?
HBsAg
Acutely infected w/ HBV?
see HBsAg, IgG Anti-HBc, IgM Anti-HBc**
chronically infected w/ HBV?
see HBsAg, IgG Anti-HBc - don’t see Anti-HBc IgM!!!
what shows if pt. has ever been infected w/ HBV?
IgG Anti-HBc
what shows if pt. has only had HBV vaccination and never been infected?
IgG Anti-HBs - shows immunity to HBV
only thing present during window period indicating acute infection?
IgM - anti-HBc
won’t see anything during 3 mos. incubation gap
chronicity of Hbv?
persistence of HBsAg for more than 6 mos, along with HBeAg and HBV-DNA ::: see it waver
what denotes high infectivity of HBV?
presence of HBeAg and high levels of HBV DNA
what is best indcator of chronicity of HBV?
age - younger age at time of infection = larger chance of increased chronicity
1 cause of cirrhosis in US?
Hep C
Hep C
ACUTE and CHRONIC!!!! - most
parenteral transmission
2 mos incubation
no vaccine - genome is unstable
see HCV RNA - in case of infection - stays w/ chronicity
see anti-HCV in case of resolution
- most common cause of Hep C = Stable chronic hepatitis (not cirrhosis)
- only 15% of total go to cirrhosis
Histo: portal inflammation, bridging fibrosis, lobular inflammation
Hep D
Acute infection
3 mos incubation
parenteral
Absolutely dependent on HBV infection –> superinfection or co-infection
Hep E
“hepatitis A of india”
1 mos incubation
F-O route
same serology as hep A:
Fecal HEV seen during infection
Anti-HEV Ab indicates vaccine / clearance
IgM- anti-HEV - indicates infection - DDx
clonorchis sinensis
think cholangiocarcinomas - these are helminths
AMA
primary biliary cirrhosis (PBC) (a scarring of liver tissue, confined primarily to the bile duct drainage system of the liver).
ASMA
think AI hepatitis
histology same as viral hep - see cluster of periportal plasma cells
Female = Type 1
Children = Type 2
sometimes also 80% have associated high titers of various autoantibodies, including (Type 1) ANA, ASMA, but negative for AMA (Type 2) ALKM1, ACL-1*
Increased frequency HLA-B8 or HLA-DRw3
60% have other forms of autoimmune disease
vinyl chloride
angiosarcoma
zone 1 hepatoxocitiy
think FE overload, Allyl alcohol
Zone 3 hepatoxicity
think CCl4 (carbon tetrachloride), acetaminophen, ethanol
aceta: give n-acetyl cystein as antidote - toxicity due to NAPQ1 –> depletion of GSH
MTX
used to tx. psoriasis/ RA
see periportal fibrosis and cirrhosis
Isoniazid
anti-TB metabolite –> causes liver damage with increased ALT
alcoholic liver disease
all changes begin in zone 3 –> portal tracts
- Fatty liver: micro/macrovesicular
- alcoholic hepatitis: ballooning and mallory bodies - see neutrophils surrounding necrotic hepatocytes
- see fever, jaundice, RUQ pain, high AST:ALT, high alk phos and GGT - cirrhosis
non-alcoholic fatty liver
metabolic syndrome; hyperlipidemia with high TG’s, insulin resistance, high BP
see aST cirrhosis (non alcoholic steatohepatitis)
C2Y82Y, H63D, TF2R
mutations in these genes –> genetic adult hereditary hemochromatosis (autosomal recessive) –> causes gene defect in HFE
hepatocytes unable to recognize iron thus don’t make hepcidin = iron overload! –> ** cirrhosis, bronze skin, ARTHRALGIA
** prussian blue stain **
mutations in juvenile hemochromatosis?
HAMP, HJV
anemia of CD?
chronic inflammm – IL6 –> activates production of hepcidin
Wilson Disease
high copper levels! ATP7B deficiency (controls copper excretion in bile duct)
levels accumulate in liver (cirrhosis/hepatitis), brain (parkinsonian/CNS disorders), eyes (Kayser-Fleischer rings)
on labs see increased urine copper
ATP7B deficiency
Wilson Disease- high copper levels!
ATP7A deficiency
Menkes disease = copper deficiency = “kinky hair disease” –> severe neuro disease
alpha1AT
Autosomal recessive
Pizz gene mutation –> A1AT is a protease normally inhibits neutrophil elastase (this protein is made in liver –> accumulates in liver and causes disease )
seen in neonatal hepatitis and cirrhosis in 40’s assoc. w/ smoking
causes of neonatal cholestasis?
extrahepatic biliary atresia
idiopathic neonatal hep
A1AT
PBC
primary biliary cirrhosis = cholestatis liver disease of destruction of small/medium bile ducts in liver
AMA+ : directed against PCD-E2 in herings canal
seen in middle aged women: pruritis and jaundice
** destruction of midde bile ducts –> periportal hepatocellular damage
PSC
primary sclerosing cholangitis = cholestasis w/ obliterative fibrosis of intra and extrahepatic bile ducts
seen in IBD!!! UC - 90%
male disease - see acute ascending cholangitis
pANCA and ANA elevated!!!
“beading” on ERCP and onion skin fibrosis
beading
PSC
ciliopathies
mutation in polycystin Pc1/Pc2 –> bile duct cystic changes/ fibrosis
Von Meyenberg complex and caroli disease (autosomal recessive) think about ADPKD and manifestations in brain and kidneys
nutmeg liver
acute liver congestion at zone 3
budd-chiari syndrome
obstruction of more than 2 hepatic vv or IVC
sen in polycythemia or clotting disorders
see RUQ pain, ascites, hepatomegaly
zone 3 congestion
HELLPP
hemolysis, elevated liver enzymes, low platelets - seen in pregnancy
which virus has increased risk during pregnancy?
HEV
nodular hyperplasia of liver
most common benign hepatic mask that isn’t vascular - see central scar of stellate cells
assoc. w/ osler-weber-rendu disease
Cavernous hemangioma of liver
commonest hepatic tumor/mass
bleed when disrupted and are benign neoplasms
Hepatic adenoma
rounded smooth borders, no central scar
seen in women on OC’s: prone to rupture
hepatocellular carcinoma
think HBV, HCV, alcohol
elevated AFP!!!
see liver failure, cachexia, varices, hemorrhage
what could get mistaken as focal nodular hyperplasia?
fibrolamellar variant of hepatocellular carcinoma - seen in young females and males, not assoc. w/ HBV, HCV, or cirrhosis
see single large mass w/ malignant hepatocyes
Klatskin tumor
arises from perihilar region of bile duct eptihelium
cholelithiasis
gallstones
5 F’s
cholesterol stones - female, fat, flatulent, fertile, forty
stone formation?
- Increased production/saturation → supersaturatiohn
- Crystallization (nidus)
- Flow (volume, turbulence) – hypomotility leads to sludge
- Accretion (matrix/sludge) – sludge gives nidus something to crystalize on → accretion of cholesterol forming stones
strawberry gallbladder?
Cholesterolosis of the Gallbladder: cholesterol in mucosa
- supersaturated bile and ↑mucosal uptake…can present clinically like acute/chronic cholecystitis
- usually with stones (mechanism unknown if stone absent)
- often called “strawberry gallbladder”
o can cause gallbladder biliary pain
o accumution of cholesterol in mucosa gives it the white/yellow dot background in the pattern of red
black pigement stones
unconj bilirubin - due to chronic hemolysis, SS, thalassemia , CD
brown pigment stones
bili + cholelsterol
e. coli infection, liver flukes (C. sinensis )
cholelithiasis
stones in gallbladder
cholecystitis
inflamm. of gallbladder
choleocholithiasis
stones in bile duct
acalculous cholecystitis
seen in ill - HIV pts - no stones
+ revound, murphys sign
acute cholecystitis
see necrosis, hemorrhage, inflammation/edema
hydrops of gallbladder
- obstruction of cystic duct without inflammation
- results in mucin filled gallbladder
HIDA scan
radioactive dye (given IV) is excreted by the liver (GB not seen in acute cholecystitis …even up to 3 hrs…stone blocks duct) a. pt injected w/ die into vein – fills gallbladder and later will be seen in small bowel – if there is obstruction then die won’t go into gall bladder and will continue into small bowel ---- + study means there is a stone
ECRP
used to evaluate the biliary tree
a. tube is inserted down esophagus, into small bowel – at tip of scope there is alight to visualize the ampulla – can pass a needle into the ampulla and send it up into the biliary tree → inject die into biliary tree and examine for causes of obstruction
b. can also go in a grab stones and pull them out of the ampulla of vater
c. can also use ECRP to place a stent
acute/ascending cholangitis
• Cholangitis = bacterial infection superimposed on an obstruction of the biliary tree most often due to gallstone → ascending cholangitis
- There is secondary bacterial infection…organism is typically from duodenum
- E. coli, Klebsiella, enterobacter ….
• Infection moves up the biliary tree into the liver bile duct system…sometimes resulting in multiple small liver abscesses
• Typically causes: 1)Fever, 2)Jaundice, 3)Abdominal pain (Charcot’s Triad)
- with Hypotension, Mental status changes (Reynold’s Pentad)….increased mortality – watch out!
• Histology: shows inflamm. process due to stone, will see bile ducts are expanded and filled with pus → spills out into liver parenchyma and forms microabscesses and enzymes skyrock → super elevated ALT/AST
rokitanski -aschoff sinuses
Chronic Cholecystitis:
• >90% associated with gallstones (same epidemiology)
• Pathophysiology: repeated bouts of acute inflammation, chemical or bacterial
• Pathology: stiff, thickened wall with variable inflammation and Rokitanski-Aschoff sinuses
• R-A sinus (seen on right) = areas where gallbladder has constricted and surface mucosa is pulled down into wall
• Clinical: highly variable symptoms of pain and “dyspepsia”
• Pathologic findings and clinical symptoms do not correlate well
• Porcelain gallbladder: chronic cholecystitis with calcified wall, higher risk of adenocarcinoma → mandatory surgery
• see fibrotic thickened gray-white wall due to fibrosis and inflammation with many gallstones present in the lumen
• see calcified wall prominently on the CXR/ CT scan
• Have high risk for developing ADCA, MUST COME OUT!
cacinoma of gallbladder
• 2 Xs more common in women, peaks in 7th decade
• Native Americans and Hispanics
• Usually assoc. with gallstones
• Rarely diagnosed preop. or when resectable
– no symptoms until advanced disease
– rare ddx in time
• Vast majority are Adenocarcinoma
• Terrible prognosis; <10% 5 year survival!
• ERBB2 (Her-2/neu) overexpressed (2/3)
• can results in direct liver invasion!
klatskin tumor
cholangiocarcinoma located at jn. or right and left hepatic ducts
PRSS1 mutations:
code for a variant of trypsin that is resistant to inhibitor deactivation
pancreas divisum
ducts do not fuse
- - predisposes to chronic pancreatitis
o see that tail and body (dorsal portion) drains through minor sphincter through the “minor duct of santorini”
o Duct of Wirsung does not develop and very little drains out of papilla of vater (when use ERCP and inject into duct of wirsung – see no flux into the pancreas, only up into the biliary tree)
annular pancreas
- normal pancreas encircles 2nd part of duodenum
- presents with obstruction and other developmental defects
- presents with “double bubble sign” : stomach and proximal duodenum fill w/ air
- see bilious green tinged vomit – due to bile still entering into the small bowel (obstruction is usually below the ampula)
o – may or may not be complete obstruction, and less commonly may present later in adulthood
defects leading to increased pancreatitis?
- PRSS1: mutated trypsinogen resistant to antitrypsin
- SPINK1: SPINK 1 protein is a trypsin inhibitor
- CFRT: some cystic fibrosis variants get pancreatitis
two main causes of acute pancreatitis?
alcohol: seen in males, 40
biliary stones: seen in women, 70
- Alcohol → damage of ductule that’s producing HCO3-
- Drugs → damage of acinus: CCK → zymogens, lipase, amylase
elevated serum amylase and lipase***
DDx of Acute Pancreatitis: clinical DDX!
- epigastric pain radiating to the back
- fever, nausea, vomiting
- elevated serum amylase and lipase***
Morphology:
- Early stages: see diffuse swelling from edema with redness from vasodilation, but no necrosis
- Mid stages: see areas of hemorrhage and peripancreatic fat along with fat necrosis= “saponification”
- Later stages: see complete fat necrosis = complete saponification
most common cause of chronic pancreatitis?
alcohol
see excruciating pain, diabetes, ascities, fat malab, pseudocyts formation and duct obstruction
TRUE CYST
- Have an epithelial lining.
- As all epithelia secrete fluid, the cyst will continue to grow in size, and impinge on adjacent anatomical stuctures (a type of neoplasm)
- Treatment must include excision of epithelium, or they will recur
- Squamous cysts fill with keratin (because keratin is greasy, they were named as though the contents were fatty (i.e. sebaceous cyst of skin and cholesteatoma are misnomers)
o epidermal inclusion cyst of skin, keratocyst of jaw, cholesteatoma of external ear canal/mastoid bone - Serous cysts secrete a watery clear fluid, mucinous cysts mucin
PSEUDOCYST
- Have no epithelial lining Will not grow in size unless connected to a duct
- Treatment is by drainage
- examples include pancreatic pseudocyst, adrenal pseudocyst and old abscess
- represents 75% of all pancreatic cysts – usually occur after a bout of acute pancreatitis
- histology: there is smooth borders no lining of the epithelium – instead is lined by fibrin and granulation tissue
serous cystadenoma
cyst mass w/out atypica- seen in elderly females, straw colored serous yellow fluid in it
neg. mucin stain
mucinous cystic neoplasms
slow growing, painless mass in adult females
makes mucinous fluid
see smooth borders w/ cysts lined by columnar mucinous epithleium
Intraductal papillary mucinous neoplasms
• Typically arise in the main duct of the head of pancreas of males
• May be benign, borderline or malignant
• presents w/ obstruction, that is not a stone
• histology:
– see papillary neoplasm that distends the pancreatic duct
– neoplasms behave like a stone and continue to grow and expand – must be removed in order to keep them from progressing to chronic pancreatitis
– considered “intraductal neoplasm”
pancreatic carcinoma
• 4th leading cause of Cancer Death in US
– Median survival 9 months; 5% 5 year survival
– only 20% completely resectable → s shelf: rectal pouch mass – metastasis
• Diagnosis
– Imaging: CT scan commonest, endoscopic US best (can do biopsy at the same time with US)
– Tissue ddx: FNA cytology or needle core biopsy
– Laboratory: CA 19-9 only for monitoring (classically elevated in pancreatic cancer – a marker to follow tx)
• CANCER IS A TISSUE DIAGNOSIS
• Pathology
– Typically metastasize regional lymph nodesà then liverà then lungs
– Direct local invasion (along nerves, duodenum, stomach, colon, vessels)
– Peritoneal spread with ascites
• Staging for possible surgery
migratory thrombophelbtisi
pancreatic cancer
palpable gallbladder
think pancreatic cancer
STK11 mutation
peutz-jeghers syndrome = inherited risk of pancreatic carcinoma
common somatic alterations in pancreatic ADCA?
- KRAS – growth factor signal transducer
- p16/CDKNA: (cell cycle regulator: tumor suppressor)
Necrosis with portal bridging in liver
chronic hepatitis. Mild steatosis is seen in HCV infection. The incidence of
chronic hepatitis is highest with HCV infection.
AST
level that is higher than the ALT level
characteristic, however, of liver cell injury associated with chronic alcoholism
Piecemeal hepatocellular necrosis
think HCV
ceruloplasmin
Ceruloplasmin is an α2-globulin that
carries copper in plasma. Because copper cannot be secreted into plasma, ceruloplasmin levels are low. in Wilson’s disease
K-RAS
K-RAS mutations are found in more than 90% of pancreatic adenocarcinomas
