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PA3201 final > Digestive pathology 3 > Flashcards

Digestive pathology 3 Flashcards

1
Q

what is the most common pathological finding of the lver

A

Jaundice

color change due to elevated bilirubin in the body

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2
Q

what is the process of decay of senescent RBCs

A

happens in macrophages

  • Globin chain split off-> heme is present without surrounding globin
  • Heme then separates into iron and unbound unconjugated bilirubin
  • release of unbound unconjugated bilirubin in the blood
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3
Q

What is the liver phase of bilirubin transformation

A
  • unconjugated unbound bilirubin gets into liver
  • liver phase of bilirubin biochem transformation is done via uridine glucosyl treansferase
  • -that enzyme eventually binds unconjugated bilirubin w glucose, creating conjugated bilirubin
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4
Q

Boweel stage of bilirubin transformation

A

In the bowel there is urobilinogen
80% of urobilogen is converted into urobilin (what causes brown stool)
20% returned to circulation
10% released thru kidney

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5
Q

Causes of bilirubin elevation (4)

A
  1. Plasma elevation of unconjugated bilirubin
  2. Plasma elevation of unconjugated/conjugated bilirubin
  3. Unconjugated hyperbilubrubinemia
  4. Congugated hyperbulirubinemia
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6
Q

Why does plasma elevation of unconjugated bilirubin happen

A
  • overprod of bilirubin (due to excessive decay of RBCs)
  • Impaired bilirubin uptake by the liver
  • abnormalities of bilirubin conjugation
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7
Q

Why does plasma elevation of both unconjugated and conjugated bilirubin occur

A
  • hepatocellular disease
  • impaired canalicular excretion of bilirubin
  • biliary obstruction
  • conjugated hyperbilirubinemoa
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8
Q

why does unconjugated hyperbilirubinemia

A

hemolysis
extravasation of blood into tissue
dyserythropoiesis
stress situations

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9
Q

Why does conjugated hyperbiliruvinemia occur

A

(usually occurs with any problem below the liver*)

-Biliary obstruction
-viral hepatitis
-alcoholic hepatitis
-nonalcoholic steatohepatitis
-primary biliary cirrhosis
etc etc

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10
Q

Fraction of conjugated bilirubin below 20%=

A

Unconjugated hyperbilirubinemia

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11
Q

fraction of conjugated bilirubin bw 20-50% (+causes_

A

-mixed Jaundice

causes= hepatitis, tumor of liver

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12
Q

Fraction of conjugated bilirubin greater than 50% (+causes)

A

conjugated hyperbilirubinemia

causes= bile duct obstruction, either intra hepatic, extra hepatic or post hepatic

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13
Q

Clinical manifistations of jaundice

A 
yellow pigmented skin
yellow sclera
malabsorption
light colour chalky stools
dark beer like urine
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14
Q

viral hepatitis + Alcoholic hepatitis ALT and AST ratio

A

Viral hep- ALT more elevated than AST

Alcoholic hep- AST elevated than ALT

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15
Q

What is elevated in cholestasis and cholestatic cirrhosis

A

Elevation of serum alkaline phosphatase

Elevation of gama glutamyl transferase

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16
Q

What markers will you see in a hepatocyte function problem

A

Changes in serum albumin

Changes in prothrombin time

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17
Q

What will you see in tumors of kindney

A

Increase in alpha fetal protein

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18
Q

mc of fatty liver disease

A

alcoholism

metabolic changes and conversion of ethanol into triacyglyerol. Deposition of triacyglyerol through the tissue

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19
Q

What is liver cirrhosis

A

Ongoing liver damage w liver cell necrosis followed by fibrosis and hepatocyte regeneration result in liver function (end stage liver disease)

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20
Q

what are the fibrotic changes in liver cirrhosis stimed by

A
  • chronic inflammation
  • cytokine release-> which signals collagen deposition
  • direct stimuli via hepatitis viruses
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21
Q

Examples of chronic liver disease that leads to cirrhosis

A

Chronic inflammatory pathology (hepatitis)
Chronic hepatic vascular disease
Cholestasis (obstruction of bile flow)

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22
Q

What are the common causes of macronodular cirrhosis

A

Viral hepatitis (B/C)

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23
Q

mc causes of micronodular cirrhosis

A

Chronic alcoholism (nodules less than 3mm in size)

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24
Q

chronic pres of longstanding liver cirrhosis

A
  • Portal hypertension + Caput medusae
  • Markedly decreased detox of liver
  • Excessive estrogen prod of liver
  • Decreased synthesis of hepatic tissue\
  • Decreased gluconeogeneis
25
Q

What is a typical symptom of end stage liver disease

A

Peripheral edema

26
Q

Portal hypertension and what does it lead to

A

Portal hypertension is defined as an increase in pressure in portal vein in the liver

  • ascites
  • splenomegaly
  • portosystemic shunting
  • esophageal varices
27
Q

What is ascites

A

Changes in architecture of liver build up in area of portal vein

  • leads to increase in pressure in peritoneal capillaries and starts seeping thru walls of capillaries
  • liquid leaks thru accumulates in peritoneal cavity
28
Q

What does splenomegaly lead to

A

Causes suppression of hematopoiesis which results in Anemia/ leukopenia/ thrombocytopenia (manifests as patients propensity to bleed)

29
Q

What is portosystemic shunting of blood

A
  • pressure in portal systems build up to a point where we have no ability to expand anymore
  • -as a result there are several sites of portal caval anastomoses
30
Q

What are esophageal varices

A

-prob associated w portal hypertension

–submucosal veins of esophagus become dialiated

31
Q

What is hereditary hemochromatosis and what can it lead to

A

mutation in the hemochromatosis gene (HFE) that leads to increased iron absorption from the gut

-Hemochromatosis leads to bronze pigmentation of skin, diabetes mellitus and cardiac arrhythmias

32
Q

What is extrahepatic biliary tract obstruction/cholestatis and what causes it

A

Obstruction of intra and extra hepatic bile ducts causes accumulation of bilirubin in liver

-bile duct/head of pancreas tumor compresses common bile duct, gallbladder stones, tumor of common bile duct

33
Q

What is an intrahepatic biliary tract obstruction/cholestasis and causes

A

blockage of the intra hepatic bile ducts

causes- contraceptive, phenothiazines preg, primary biliary cirrohsis

34
Q

What is a hepatic adenom

A

Often benign
composed of cells that closely resemble normal hepatocytes, but the neoplastic liver tissue is disorganized hepatocyte cords and does not contain normal lobular architecture

35
Q

What is hepatocellular carcinoma and causes

A

Arise in setting of cirrhotic changes

Causes

  • Hepatitis B/C
  • Cirrhosis
  • Alcoholism
  • Ephla toxin
36
Q

What cancers metastisize to the liver and findings associated

A

Any kind can, especially ones from the abdominal cavity

  • Enlarged liver
  • Elevated levels of ALP
  • Elevated bilirubin
  • Some elevation of transaminse levels
37
Q

How is hep A/E, B and C transmited

A

A/E- fecal orally/water

B- Transmitted parentarally, sexually, vertically

C- transmitted parentally, sexuall, IV drugg

38
Q

Hep B serological markers (4)

A

HBsAg- indicates peron is infectipus

anti-HBs- indicates recovery, immunity, vac

Anti- HBc- previous or ongoing inf

IgM anti HBc- recent inf/ accute inf

39
Q

What is cardiac cirrhosis

A

Heart isn’t pumping blood properly which leads to liver congestions and changes to liver parenchyma
(congestive state of liver-> typical findings of cirrhosis)

40
Q

What is extraheypatic biliary atresia

A

Congenital condition where patient born w no biliary ducts outside liver
–Will not survive

41
Q

What is alpha-1-antitrypsin def and what can it cause in future

A
  • Due to def
  • Common manifestation of obstructive pulmonary diesease
  • emphasema later
42
Q

What are the causes of pancreatic pathology (5)

A
  • Low temps and hemorrhagic shock cause hyper percussion of the pancreas
  • alcohol consuption
  • eating rich and fatty foods
  • gallstones
  • viral pathology
43
Q

Effects of alcohol on pancreatic pathology

A
  • alcohol abuse can cause increased permeability of the pancreatic duct to pancreatic digestive enzymes
  • alcohol increases obstruction of pancreatic duct by increasing mucus concentration and therefore behaving like a plug
44
Q

What is acute peritonitis

A

Activation of pancreatic pro enzymes lead to auto digestion of the pancrease
(trypsin is mc pancreatic enzyme which causes activation of pro enzymes)

45
Q

Tests results for acute peritonitis

A

Amylase released into blood

Increase in serum immunoreactive trypsin

46
Q

clinical presentation of acute pancreatitis

A
  • mid epigastric pain w retroperitoneal an dmid thoracic pain
  • nausea and vommiting
  • fever
  • deposition of fluids in third space
47
Q

complications of acute peritonitis

A
  • pancreatic necrosis
  • pancreatic infections
  • pancreatic abscess
  • convulsions
  • ARDS
48
Q

what is chronic pancreatis and causes

A

continuing inflammatory process with exocrine atrophy and fibrosis
– will eventually lead to complete abolishment of endocrie and exocrine function of pancrease

chronic alcohol access is comments cause

49
Q

complicatuons of chronic pancreatis

A
  • intestimal malabsorption and diabetes may occur at advanced stage (since pancreas no longer producing digestive enzymes)
  • Loss of beta cells in Langerhans
  • Lack of pancreatic extract (leads to inability to cleve r factor in b12 leading to def)
50
Q

lab tests for chronic pancreatis

A

amylase/lipase very unreliable

Will see decrease in serum immunoreactive trypsin

51
Q

What is the usually carcinoma of the pancreas and who is it common in/ risk factors

A

usually ductal adenocarcinoma

mc in men (70-80s)
cig smoking
k-RAS gene mutation

52
Q

tumor marker for carcinoma of pancreas

A

CA-19-9

53
Q

mc location of pancreatic adenocarcinoma and s/s`

A

head of pancreas

s/s- Signs of common bile duct obstruction, jaundice, superficial migratory thromo-phlebitis, Retroperitoneal hemmorach causing leakage to skin (bruising)

54
Q

What is acanthosis nigricans and what is it found in

A

found in pancreatic cancer

-severe discolouration of skin (in neck, butt, palms, soes)

55
Q

Common sites of metastisis of pancreatic cancer (2)

A

Left supra clavicular node

pre umbilical metastissi

56
Q

what are the 2 forms of acute cholecystitis (inflammation of gallbaldder)

A

Acalculous- inflammation of gallbladder without presence of gallstones

Cholelithiasis- gallstones present

57
Q

clinical pres of acute cholestitis

A

may present as post prandial biliary colic (right upper quad after eating fatty meals)

  • nausea and vommiting
  • fever
  • US is diagnostic
58
Q

What are majority of gallstones made of

A

cholesterol and some made from bilirubin

59
Q

Risk factros for gallstome

A

w over 40
oral contraceptives
obesity
horomone replacement therapy

PA3201 final (20 decks)

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