Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

USMLE Step I Pathology > Exocrine Pancreas and Liver Pathology (Pathoma) > Flashcards

Exocrine Pancreas and Liver Pathology (Pathoma) Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Annular Pancreas

A

Devolopmental malformation of pancreas forming ring around the duodenum.

Risk of duodenal obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute Pancreatitis

A

Liquefactive necrosis and fat necrosis and hemorrhage of pancreas

Due to autodigestion of pancreatic parenchyma by pancreatic enzymes

Premature activation of TRYPSIN leads to activation of other enzymes.

MCC: Alcohol (contraction of sphincter of oddi –> decrease pancreatic drainage) or Gallstones

Other causes: Trauma (kid wearing seatbelt), hypercalcemia (autoactivation) and hyeprlipidemia, drugs, scorpion stings, mumps, rupture of posterior duodenal ulcer

Clinical Features: Epigastric pain that radiates to back. N/V. Periumbilical and flank hemorrhage.

Elevation of serum lipase (best test) and amylase. Hypocalcemia

Complications: Shock, pancreatic pseudocyst (can rupture), pancreatic abscess (E. coli infection of abscess), DIC and ARDS (pancreatic enzymes active on clotting factors and endothelium when in blood).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Chronic Pancreatitis

A

Fibrosis of pancreatic parenchyma secondary to recurrent acute pancreatitis

MC due to alcohol and cystic fibrosis (thick secretions –> blockage). Many are idiopathic.

Clinical features: Epigastric abdominal pain radiating to back, pancreatic insufficiency (steatorrhea w/ ADEK def.), dystrophic calcification of pancreas, secondary DM, increased risk for carcinoma

Amylase and Lipase are not good markers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pancreatic Carcinoma

A

Adenocarcinoma arising from pancreatic ducts

MC in elderly (70 = avg. age)

Major risk factors = smoking and chronic pancreatitis

Clinical features: Epigastric pain and weight loss. Usually late. Obstructive jaundice w/ pale stools and palpable gallbladder (head of pancreas). Secondary DM (body or tail)

*Think if thin elderly w/ new DM

Can cause pancreatitis, migratory thrombophlebitis (Trousseu’s sign in 10%)

Serum marker CA 19-9 used to track progress of tumor

Rx: Whipple procedure (En bloc removal of head neck of pancreas, duodenum, and gallbladder)

Terrible outcomes (less than 10% one year survival)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Biliary Atresia

A

Failure to form or early destruction of extrahepatic biliary tree

Leads to biliary obstruction within first 3 months

Presents w/ jaundice (CB) and progresses to cirrhosis (back pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Colelithiasis

A

Gall stones

Due to precipitation of cholesterol or bilirubin in bile due to supersaturation, decreased phospholipids (i.e. cholestyramine), or stasis (increase bacteria –> increased UCB –> stone

Cholesterol is MC stone in West –> radiolucent. Yellow in color

Risk factors: Female (estrogen), Fat (cholesterol), Forty, and Fertile (estrogen), Cofibrate, Native American, Crohn’s disease (decreased bile salts/acids from ileum), Cirrhosis (decreased bile salt production)

Bilirubin stone (usually radiopaque) and looks black in color.

Risk factor: Extravascular hemolysis, biliary tract infection (E. coli, Ascaris lumbricoides, and Clonorchis sinesis) –> increased UCB Bilirubin

Gallstones are usually asymptomatic.

Complications:
Biliary colic -
Acute and chronic cholecystitis
Ascending cholangitis
Gallstone ileus
Gallbladder cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cholesterol Stones

A

MC stone in West. Radiolucent and yellow in color

Risk factors: Female (estrogen), Fat (cholesterol), Forty, and Fertile (estrogen), Cofibrate, Native American, Crohn’s disease (decreased bile salts/acids from ileum), Cirrhosis (decreased bile salt production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bilirubin Stones

A

Usually radiopaque and black in color.

Risk factor: Extravascular hemolysis, biliary tract infection (E. coli, Ascaris lumbricoides, and Clonorchis sinesis) –> increased UCB Bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bilary Colic

A

Waxing and waning RUQ pain.

Due to gallbladder contracting against stone in cystic duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acute Cholecystitis

A

Acute inflammation of gallbladder wall

Impacted stone in cystic duct results in dilitation w/ pressure ischemia, bacterial overgrowth, and inflammation

Presents w/ RUQ *radiating to RIGHT SCAPULA. Fever and elevated WBC, N/V, Increased alk phosp, risk of rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chronic Cholecystitis

A

Chronic inflammation of gallbladder due to chemical irritation from longstanding cholelithiasis

*Hallmark is formation of Rokitansky-Aschoff sinus (mucosa diving into smooth muscle)

Presents w/ vague RUQ pain, especially after eating.

Porcelain gallbladder is a late complication (dystrophic calcification)

Rx: Cholecystectomy, especially if porcelain gallbladder is present (increased cancer risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ascending Cholangitis

A

Bacterial infection of bile ducts

Usually due to ascending infection w/ enteric gram negative bacteria (e. coli)

Presents as sepsis, jaundice, and abdominal pain

Increased incidence with choledocholitiiasis

Remember stasis –> infection behind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gallstone Ileus

A

Gallstone enters and obstructs the small bowel after fistula formation

Obstructs I/C valve. Air in biliary tree!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Gallbladder Adenocarcinoma

A

Arises from glandular epithelium that lines the gallbladder wall.

Gallstones = major risk factor; esp. porcelain gallbladder

Clasically presents as cholecystitis in elderly woman (not normal age of onset for cholecystitis)

Poor prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Jaundice

A

Yellow discoloration of skin; earlies sign is scleral icterus

Due to increased serum bilirubin (>2.5mg/dl

Arises w/ disturbances in bili metabolism.

Causes: Extravascular hemolysis or ineffective erythropoesis, phsyiologic jaundice of the newborn, gilbert syndrome, Crigler-Najjar syndrome, Dubin-Johnson syndrome, Biliary obstruction, viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Extravascular hemolysis

A

Etiology: High levels of UCB overwhelm liver

Labs: High UCB

Clinical Features: Dark urine (increased urobilinogen –> UCB is not water soluble)

Increased risk for pigmented bili stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Physiologic jaundice of the newborn

A

Newborn liver has transiently low UGT activity

Labs: High UCB

Clinical features: UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neuro deficits and death.

Rx: phototherapy (makes UCB water soluble –> gets rid of riboflavin (b2)!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Gilbert syndrome

A

Mildly low UGT activity; automal recessive

Labs: High UCB

Clinical Features: Jaundice during stress (infection). Otherwise not clincally significant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Criggler-Najjar syndrome

A

Absence of UGT

Labs: High UCB

Kernicterus; usually fatal

20
Q

Dubin-Johnson syndrome

A

Deficiency of bilirubin canalicular transport protein; autosomal recessive

Labs: Increased CB

**Liver is dark; otherwise not clincally significant. Rotor syndrome is similar to DJS but lacks liver discoloration

21
Q

Biliary Tract Obstruction

A

Associated w/ gallstones, pancreatic adenocarcinoma, cholangiocarcinoma, parasites, and liver fluke (Clonorchis sinensis)

Labs: Increased CB, Decreased urine urobilinopgen, and increased Alk Phosph

Clinical Features: Dark urine (due to bilirubinuria) and pale stools. Pruritis due to increased plasma bile acids. Hypercholestemia w/ xanthomas. Steatorrhea w/ malabsorbtion of ADEK

22
Q

Viral Hepatitis

A

Inflammation of parenchyma disrupts hepatocytes and small bile ductules

Labs: Increased CB and UCB

Clinical Features: Dark urine due to urine CB; urine urobilinogen is normal or decreased.

Due to Hep ABCDE virus, EBV, and CMV

Hep BCD can progress from acute hepatitis to chronic hepatitis

23
Q

Acute Hepatitis

A

Jaundice (mixed CB and UCB) with dark urine (CB), fever, malaise, and nausea

Elevated liver enzymes (ALT >AST) –> Remember two L’s rule –> alcohol is opposite

Sx last less than 6 months

24
Q

Chronic Hepatitis

A

Sx and serology for more than 6 months

Risk for advance to cirrhosis

25
Q

Hepatitis A Virus

A

Fecal Oral transmission

MC in travelers

Acute hepatitis only

Anti-virus IgM marks active infection. Anti-virus IgG is protective, and its presence indicates prior infection or immunizaiton

26
Q

Hepatitis E

A

Fecal Oral transmission

MC from contaminated water or undercooked seafood

Acute hepatitis only

Anti-virus IgM marks active infection. Anti-virus IgG is protective, and its presence indicates prior infection

Infection in pregnant women is associated w/ fulminant hepatitis (liver failure w/ massive liver necrosis)

27
Q

Hepatits B

A

Parenteral transmission (i.e. childbirth, sex, iv drugs, needlestick)

Results in acute hepatitis; chronic disease in 20%

HBsAG is is first serologic marker to rise and key marker of infection –> if present more than 6 months defines chronic state

HBcAB IgM = key marker of acute battle

HBsAB IgG is indicator of won battle

HBeAG and HBV DNA indicates infectivity (mail a letter to a friend)

Acute (HBsAG, HAeAG, HBcAB IgM);

Window (HBcAB IgM);

Resolved (HBcAB IgG, HBsAB IgG);

Chronic (HBsAG for greather than 6 months, +/-HBeAG, HBcAB IgG);

Immunization (HBsAB IgG)

28
Q

Hepatitis C

A

Parenteral transmission (ie. IV drugs, intercourse, needle stick) risk from transfusion is almost none due to screening of blood supply.

Results in acute hepatitis; chronic disease in most states.

HCV-RNA test confirms infection; decreased RNA levels indicate recovery; persistence indicates chronic disease

29
Q

Hepatitis D

A

Dependent on HBV for infection; superinfection upon coexisting HBV is more sever than coinfection.

30
Q

Cirrhosis

A

End-stage liver damage

Disruption of normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes (think alcoholic who quits and relapses)

Mediated by stellate cell that secretes TGF-B. Lie beneath endothelial cells that line sinusoids.

Portal HTN

Decreased detoxification

Decreased protein synthesis (hypoalbuminemia and coagulopathy –> follow PT)

31
Q

Portal HTN

A

Ascitis

Congestive splenomegaly/hypersplenism (consumption of RBCs and platelets)

Portosystemic shunts (varices, caput medusa, internal hemorrhoids)

Hepatorenal syndrome (rapid renal failure secondary to cirrhosis)

32
Q

Decreased detoxification

A

Mental status changes, asterixis, and coma (due to increased ammonia –> reversible!)

Gynecomastia, spider angiomata, and palmar erythema (decreased estrogen breakdown)

Jaundice

33
Q

Alcohol-Related Liver Disease

A

Damage to hepatic parenchyma due to consumption of alcohol

MCC of liver disease in West

Three patterns of injury:

  1. ) Fatty Liver
  2. ) Alcoholic Hepatitis
  3. ) Cirrhosis
34
Q

Fatty Liver

A

Accumulation of fat in the hepatocytes resulting in heavy, greasy liver.

Resolves w/ abstinence

35
Q

Alcoholic Hepatitis

A

Chemical injury to hepatocytes; generally seen w/ binge drinking

Acetaldehyde mediates damage

Mallory body = damaged intermediated filaments in hepatocytes.

Presents w/ painful hepatomegaly and elevated liver enzymes (AST > ALT) –> Remember 2 L rule. AST is in mitochondria

May result in death

36
Q

Nonalcoholic Fatty Liver Disease

A

Fatty change, hepatitis, and/or cirrhosis

Develops w/o exposure to alcohol

Associated w/ obesity

Dx of exclusion; ALT > AST (AST is mitochondial enzyme)

37
Q

Hemochromatosis

A

Excess body iron leading to deposition in tissues and organ damage

Damage is mediated by generation of free radicals (Fenton-RXN)

HLA- A3

Primary hemochromatosis is due to mutations in HFE, most commonly C282Y

Loss of regulation of enterocyte iron absorbtion

May be secondary to transfusions (i.e. Sickle Cell)

Cirrhosis, secondary DM, bronze skin, cardiac arrhythmia (also restricitve cardiomyopathy) and gonadal dysfunction

Labs: Increased Ferritin, decreased TIBC, increased serum Fe, Increased percent sat

Presents in late adulthood

Brown pigment in hepatocytes –> prussian blue stain (vs. lipofuschin)

Rx: Phlebotomy

Increased risk for hepatocellular carcinoma

38
Q

Wilson Disease

A

Autosomal recessive defect (ATP7B gene) in ATP-mediated hepatocyte copper transport

Results in lack of copper transport into ible and lack of copper incorporation into ceroplasmin

Copper builds up in hepatocytes, leaks into serum, and deposits in tissues

Copper mediated production of hyrdroxyl free radicals leads to tissue damage

Sx: Cirrhosis, Neurologic manifestations (parkinson’s like, chorea like), Kayer’Fleisher rings in cornea, Increased risk for hepatocellular carcinoma

Presents in childhood

Rx: D-penicillamine

Labs increased urinary copper, decreased serum ceroloplasmin, copper in hepatocytes

39
Q

Primary Biliary Cirrhosis

A

AI granulomatous destruction of intrahepatic bile duct.

Classically arises in women (avg. age 40)

Associated w/ other AI diseases

Antimitochondrial antibody!

Cirrhsosis is a late complication

40
Q

Primary Sclerosing Cholangitis

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts

Periductal fibrosis w/ onion skin appearance

Uninvolved regions are dilated resulting in beaded appearance on imaging

Associated w/ ulcerative colitis and p-ANCA

Present w/ obstructive jaundice

Cirrhosis is a late complication

Increased risk for cholangiocarcinoma

41
Q

Reye Syndrome

A

Fulminant liver failure and encephalopathy w/ viral illness (esp chickenpox) who take aspirin

Related to mitochondrial damage of hepatocytes

Present w/ hypoglycemia, elevated liver enzymes, and N/V

May progress to coma and death.

Kawasakis is exception!

42
Q

Hepatic Adenoma

A

Benign tumor of hepatocytes

Associated w/ OCPs –> regresses upon sessation, recurs w/ pregnancy

Risk of rupture and intraperitoneal hemorrhage, esp. during pregnancy.

43
Q

Hepatocellular Carcinoma

A

Risk Factors: Chronic hepatitis, Cirrhosis, Aflotoxins derived from Aspergillis (high incidence in countries that store grain for long periods of time –> p53 mutation.

Increased risk for Budd-Chiari

Poor prognosis –> found late due to cirrhosis hiding it

Alpha-fetoprotein = serum tumor marker

44
Q

Budd-Chiari

A

Liver infarction secondary to hepatic vein obstruction

Presents w/ painful hepatomegaly and ascites

45
Q

Metastasis to Liver

A

MC liver cancer

MC sources: Colon (MCC), pancreas, lung, and breast

Multiple nodules in liver

Clinically may be detected as hepatomegaly w/ nodular free edge of liver

USMLE Step I Pathology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions