Unit 3 - Formative 5 D2

Front 1

Gross pathology reveals black lumps in the gallbladder.

Back 1

Pigmented cholethiasis (gallstones)

Front 2

What is acalculous cholecysitis?

Back 2

Ischemia due to cysic artery obstruction secondary to inflammation or edema which comrpomies blood flow

Front 3

Acute calculous cholecystitis

Back 3

Chemical irritation and inflammation of the obstructed gallbladder (due to gallstones)

Bile salts are often irritating exposed mucosal walls

Front 4

87yo M critically ill, on long-term TPN w RUQ pain. Abdomen is tender. Murphy’s sign elicited. No similar episodes in past. Ultrasound: No GB wall thickening, pericholecystic fluid present, no gallstones. Diagnosis: ?

Back 4

Acute acalculous cholcystisis

Front 5

Choledocholiathiasis

Back 5

Stones within the bile ducts of the biliary tree

Front 6

Cholangitis

Back 6

Narrowing of bile duct; could be secondary to bacterial infection, inflammation, tumor or gallstone

Front 7

46yo F p/w RUQ pain, jaundice, acholic stools, dark tea-colored urine, no fever. Past history of cholelithiasis. No treatment ever undertaken. Exam: unremarkable. HepB/C neg. Ultrasound: solitary CBD stone, dilated CBD > 1cm. Diagnosis: ?

Back 7

Choledocholiathiasis

Front 8

46yo F p/w fever, RUQ pain, acholic stools, dark tea-colored urine.
If also altered mental status and signs of shock = Raynaud’s pentad

Back 8

Ascending cholangitis

Front 9

72 yo F p/w mild RUQ pain since last several months. She also complains of intermittent episodes of acute colicky pain. She gives past history of gall stones. Her last U/S taken 2 years ago reveal thickend gall bladder, with multiple stones. No pericystic fluid was observed. CBD was not affected. Her present U/S reveals an infiltrative mass occupying most of the gall bladder. Also noticed are gall stones. Cholecystectomy was performed. Gross and histo-pathology are shown. Diagnosis?

Back 9

Carcinoma of the gallbladder

Front 10

Von Hippel Lindau disease

Back 10

vascular neoplasms found in the retina, cerebellum or brain stem in association with congenital cysts in the pancreas, liver and kidney

Front 11

How can you histologically determine a cyst?

Back 11

Cyst lacks a true epithelial lining and is lined by fibrin and granulation tissue

Front 12

A 20-year old woman was first admitted with nausea, weakness, vomiting, dizziness, and visual disturbance. The findings of a fundoscopy were normal, but a CT scan showed a cerebellar tumor in the posterior fossa, which was removed. Histopathologic examination confirmed a cerebellar hemangioblastoma. The patient remained completely asymptomatic until 4 years later, when she presented again with vomiting and dizziness. On admission, an abdominal CT scan showed a 14X10-cm, well circumscribed, thin-walled cyst in the head of the pancreas, and multiple smaller cysts in the tail and body region of the pancreas. She also had bilateral ovarian cysts.

Back 12

Von Hippel Lindau Disease

Front 13

Acute pancreatitis

Back 13

Reversible pancreatic parenchymal injury associated with inflammation

Front 14

What two laboratory findings wil you find in acute pancreatitis?

Back 14

Marked elevation of serum amylase levels during the first 24 hrs followed by rising serum lipase levels in 72-96 hours.

Front 15

Chronic Pancreatitis

Back 15

Inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis, and in the late stages, the destruction of endocrine parenchyma.

Front 16

What is the most common cause of chronic pancreatitis?

Back 16

Long term alcohol abuse

Front 17

What happens to the pancreas of an alcoholic in chronic pancreatitis?

Back 17

Elevated protein concentrations form ductal plugs which calcify; contribute to chronic pancreatitis

Front 18

Mucinous Cystic Neoplasm

Back 18

95% arise in women associated with invasive carcinoma; often at body or tail

Front 19

Histology of Mucinous cystic Neoplasms (Mucinous Cystadenoma)

Back 19

Lined by columnar mucinous epithelium

Front 20

Serous Cystadenoma

Back 20

Benign cystic neoplasms composed of glycogen rich cuboidal cells surroudning small cysts containing clear, thin, straw colored fluid

Front 21

Intraductal Papillary Mucinous Neoplasms

Back 21

arise more frequently in men then women, involve the head of the pancreas instead of the tail

Front 22

Histology of Intraductal Papillary Mucinous Neoplasms

Back 22

Lack the dense ovarian stroma and involve a larger pancreatic duct

Front 23

Solid Pseudopapillary Neoplasm

Back 23

Large, well circumscribed pancreatic masses with solid and cystic components

Front 24

Histology of solid pseudopapillary neoplasm

Back 24

Grows in solid sheets or papillary projectoins

Front 25

Pseudocysts

Back 25

Often manifests as a sac between the stomach and pancreas; usually arise after acute pancreastitis (often chronic alcoholic pancreatitis)

Hapens when body walls of peripancreatic hemorrhagic fat necrosis with fibrous tissue

Front 26

CA 19-9 Use

Back 26

Pancreatic cancer marker

Front 27

What causes cholelithiasis?

Back 27

Supersaturation of bile with cholesterol (cholesterol stones) or bilirubin salts (pigmented stones) promotes stone formation

Front 28

A jaundice patient with a history of gallstones suggests what?

Back 28

common bile duct obstruction (choledocholiathiasis)

Front 29

biliary atresia

Back 29

complete obstruction of bile flow due to destruction or absence of some part of the extrahepatic bile ducts (most common cause of liver failure death in early childhood)

Front 30

annular pancreas

Back 30

pancreatic tissue completely encircles the second portion of the duodenum; can cause duodenal obstruction

Front 31

pancreas divisum

Back 31

failure of fusion of the ventral and dorsal pancreatic primordia; causes secretions to drain only through

Front 32

which enzyme is inappropriately activated in pancreatitis?

Back 32

trypsin, which goes on to activate other enzymes

Front 33

What is the function of the cationic trypsinogen gene PRSS1?

Back 33

PRSS1; codes for a failsafe site on trypin critical for its own activation; if its trypsin will be hyperactive and cause pancreatitis

Front 34

What is the function of serine protease inhibitor, kazal type 1 (SPINK1)?

Back 34

mutation leads to a defective protein that can no longer inactive trypsin, resulting in pancreatitis

Front 35

A pt has a positive urease breath test. Is the organism h. pylori or c. jejuni?

Back 35

H. pylori

Front 36

A pt has a positive H2S production test. Is the organism h. pylori or c. jejuni?

Back 36

C. Jejuni

Front 37

A pt has a positive nitrate reduction test with an organism that grows at 42C (NOT 37C). Is the organism h. pylori or c. jejuni?

Back 37

C. Jejuni

Front 38

Compare the morphology of h. pylori with c. jejuni?

Back 38

h. pylori: spiral w/ 3 unipolar flagella

c. jejuni: comma shaped or "gull winged" with bipolar flagella

Front 39

How is c. jejuni transmitted?

Back 39

Zoonotic: Poultry, dogs, cattle, sheep

Front 40

What is notable about the c. jejuni incubation temperature?

Back 40

Needs 42C, compared to h. pylori which needs 37C

Front 41

Compare the disease course of c. jejuni and c. fetus?

Back 41

c. jejuni: gastroenteritis

c. fetus: systemic intravascular and extraintestinal infections

Front 42

How might you differentiate between c. jejuni and c. fetus?

Back 42

only c. jejuni can grow at 42C, c. fetus needs 37C (similar to h. pylori)

Front 43

What does the S-protein virulence factor for c. fetus do?

Back 43

Helps the organism evade the immune system

Front 44

Tx of choice for campylobacter infections?

Back 44

Erythromycin (broad spectrum); eliminates carriage in 72 hours

Front 45

What is the function of LPS O side chain in h. pylori?

Back 45

Resembles the blood group antigens so it protects the bacteria from immune clearance

Front 46

What si the gold diagnostic standard for h. pylori?

Back 46

Histological examination of gastric biopsy

Front 47

A patient taking antibiotics, pepto bismal, and PPI has stomach ulcers but comes back negative for h. pylori via rapid urease test. What might be happening?

Back 47

The drugs he's taking have decreased the h. pylori load making producing false-negative results.

Front 48

Why does h. pylori being microaerophilic help it grow in the stomach

Back 48

It can grow extremely well in the ciscous mucus layer that coats the gastroepithelium

Front 49

How does the production of urease by h. pylori help it?

Back 49

A byproduct of urease activity, ammonia, neutralizes gastric acids in the local vicinity

Front 50

A mutation in h. pylori hop genes would result in what?

Back 50

An inability of h. pylori to withstand peristalsis or mucosal shedding. (i.e. these genes are adherence genes0

Front 51

What does the VacA virulence factor on h. pylori do to cells?

Back 51

(Vacuolating toxin; causes swelling of cellular compartments)

Front 52

What does the Cag virulence factor on h. pylori do to cells?

Back 52

Cytotoxin associated gene; IL8 induction via Type IV Secretion system for Cag entry attracts inflammatory cells = cell damage

Front 53

Where will h. pylori be dominant in the stomach of an individual with low acid output (for ex. someone on ppi)?

Back 53

Corpus Predominat Gastritis (body)

Front 54

Where is h. pylori normally more pronounced in most patients?

Back 54

Antral predomiantn; higher acid production in body and fundus which is inhibitory to bacterial growth, so it settles in the antrum

Front 55

Which h. pylori gastritis pattern is seen in individuals who develop gastric carcinoma and gastric ulcers?

Back 55

Multifocal atrophic gastritis (corpus, fundus, antrum)

Front 56

What is the triple combo tx for h. pylori infection?

Back 56

PPI, clarithryomycin, beta lactam (amoxicillin) for 7 to 10 days