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mechanism s of disease > Lecture 12: Accessory Digestive Organs and Nutritional Disorders (Exam 3) > Flashcards

Lecture 12: Accessory Digestive Organs and Nutritional Disorders (Exam 3) Flashcards

1
Q

What diseases were covered in this lecture in the liver, gall bladder, and pancreas?

A

Liver
-Hepatic Circulatory Disorders
-Viral Hepatitis
-Toxic Liver Damage (ethanol)
Eclampsia

Gall Bladder
-Cholestasis
-Cholecystitis

Pancreas
-Neuroendocrine tumors
-Gastrinoma
-Insulinoma
-Somatostinoma
-Diabetes Mellitus (type II)
-Acute v. Chronic Pancreatitis

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2
Q

Give a summary of the liver

A

parenchyma: hepatocytes
-Large cells with lots of organelles
-Divide so the liver can regenerate

Function
-Detoxification
-Bile production
-Blood Proteins
-Glycogen Storage

Receive blood directly from the GI tract
-Perfusion determines susceptibility to toxins

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3
Q

What is the Liver Vasculature?

A

both systemic and functional vasculature

Systemic
-through the Proper Hepatic Artery

Functional
-from the digestive tract
-through the portal vein
Blood enters the parenchyma (sinusoids) and drains into the central vein
-Exits liver through Hepatic Vein

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4
Q

What forms the portal triad?

A

bile duct, portal vein, hepatic artery

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5
Q

What is Liver perfusion?

A

-parenchyma is organized into lobules
-hepatocytes closest to entry receive most nutrients, as well as the heaviest dose of toxins/drugs

Use portal acinus
supplies oxygenated blood to hepatocytes

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6
Q

What is the classic hepatic lobule?

A

(fluid flow) drains blood from the portal vein and the hepatic artery to the hepatic or the central vein

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7
Q

What is the portal lobule?

A

(fluid flow) drains bile from hepatocytes to the bile duct

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8
Q

What is liver disease?

A

the liver responds to injury using well-defined ways

-hepatocyte-based response
-degeneration/intracellular accumulations
-Death-necrosis or apoptosis
-Inflammation
-regeneration
-fibrosis-failure of regeneration

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8
Q

What is liver disease?

A

the liver responds to injury using well-defined ways

-hepatocyte-based response
-degeneration/intracellular accumulations
-Death-necrosis or apoptosis
-Inflammation
-regeneration
-fibrosis-failure of regeneration

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9
Q

What are clinical liver syndromes?

A

Hepatic Failure
- Absence of general functions
-cells do not function properly

Cirrhosis
-Increased resistance to blood flow in the liver

Bilirubin metabolism failure

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10
Q

What is Cirrhosis?

A

-accumulation of bile formation
-nodules of functional tissue are sufficient for maintenance
-greenish color is due to bile accumulation
-alcoholic liver, but the end-stage disease is similar to cirrhosis resulting from other causes

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11
Q

What causes fibrosis in the liver?

A

Quiescent stellate cells in the space of disc

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12
Q

What is the function of stellate cells?

A

Vitamin A storage

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13
Q

When a stellate cell is activated, what can occur?

A

turns into myofibroblast
-proliferation occurs
-contraction
-Chemotaxis
-Fibrogenesis

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14
Q

What are Kupffer cells?

A

located above endothelial cells of hepatocytes

when activated they release cytokines that promote proliferation, contraction, and chemotaxis

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15
Q

What is Bilirubin?

A

-senescent red blood cells are destroyed by phagocytic cells
-in the spleen, liver, and bone marrow
-bilirubin is a yellowish pigment
-seen in fading bruises as RBCs from hemorrhage are removed

Not water soluble (at pH 7.4)
-travels through blood bound to albumin
-conjugated to glucuronic acid for excretion in bile
-eventually fecal matter

Excess bilirubin
-Jaundice- yellowing of the skin
-Icterus- yellowing of sclera

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16
Q

What is Cholestasis?

A

impaired bile formation/flow

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17
Q

What is Hepatitis?

A

1.) Virus that infects hepatocytes
2.) Liver with hepatocytes infected by hepatitis virus
3.) Liver damage secondary to systemic infection

Acute Hepatitis
-massive hepatocyte damage (necrosis)

Chronic Hepatitis
-end-stage of progressive hepatocyte damage
-Liver recovers from the initial injury

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18
Q

What are clinical syndromes for acute and chronic hepatitis?

A

Acute hepatitis
-with submassive hepatic necrosis
a. Asymptomatic
-serological evidence only
-acute with recovery
b. Acute symptomatic hepatitis with recovery
-anicteric or icteric (yellowing)

Chronic hepatitis
-with or without progression or cirrhosis
-similar presentation to toxic liver injury

Acute liver failure
with massive hepatic necrosis

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19
Q

How can you differentiate between acute and chronic hepatitis?

A

Acute
-may have bridging necrosis
-have infiltrates around the portal triad
-apoptosis
-ballooning degeneration
-cholestasis
-damage to hepatocytes
-macrophage aggregation

Chronic
-bridging necrosis
-dense mononuclear infiltrate

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20
Q

What is viral hepatitis?

A

Virus infects hepatocytes
-hepatocytes express viral antigens
-immune system targets hepatocytes

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21
Q

What are the causes of Hepatitis?

A

acute
-primary viral (hepatitis A, B, C, D,E)
-Systemic viral (yellow fever, mononucleosis)

chronic
-most likely with C; minimal with B/D; E only in immunocompromised; never with A
-can be a follow-up to unresolved acute injury, or result from subacute injury

Usually characterized by Cirrhosis
-often linked with hepatocellular carcinoma

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22
Q

Describe HepA infection

A

-passed orally
exposure
2-6 weeks HepA in fecal matter
then decrease
see IgM for initial response but will see IgG (more mature) longer response
-takes time to be recovered

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23
Q

Describe histologically acute HepB

A

-Necrosis of hepatocyte
-macrophage clusters with eosinophilic cytoplasm

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24
Q

What can be used to observe chronic HepB infection?

A

can use IHC for HepBsAg accumulation

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25
Q

Describe HepC infection?

A

Acute
2-26 week incubation time
serum will increase
then Anti-HCV

Chronic
2-26 week incubation time
serum increase (HCV-RNA) never clears
You will see Acidophil body
-apoptotic cell
Mononuclear infiltrate
-surrounding damaged hepatocyte

**reactivation of endogenous HCV strain
**Emergence of new mutant strain

26
Q

What are consequences for Hepatitis?

A

Loss of liver function
-hypoproteinemia
-hyperbilirubinemia
-anemia

Infection/stress cause. additional damage
-Cirrhosis

27
Q

What is Chronic Hepatitis Symptoms

A

-fatigue, malaise, loss of appetite, mild jaundice
-blood tests
-serum transaminase is elevated
-hyperglobulinemia, hyperbilirubinemia
-Minor hepatomegaly, splenomegaly
-hepatic tenderness

28
Q

What are the similarities between toxic and viral damage?

A

-can produce acute and chronic disease
-can result in an immune response
-result in the destruction of hepatocytes (Cirrhosis)

Because the liver is the primary detoxifying organ of the body, toxins must always be eliminated as a potential cause

29
Q

Describe toxic liver injury

A

Zonal necrosis
-Zone 3

Based on perfusion
-portal acinus

Toxins are either:
-predictable and dose-dependent (eg. acetaminophen)
-Idiosyncratic (not dose-dependent).
(eg isoniazid lovastatin)

29
Q

Describe toxic liver injury

A

Zonal necrosis
-Zone 3

Based on perfusion
-portal acinus

Toxins are either:
-predictable and dose-dependent (eg. acetaminophen)
-Idiosyncratic (not dose-dependent).
(eg isoniazid lovastatin)

30
Q

Describe necrosis in the liver.

A

necrotic liver
-congested
-bile accumulation

Acetaminophen overdose
-confluent necrosis
in zone 3
-surrounds central vein

31
Q

What are common liver toxins?

A

Acetaminophen
-conversion to reactive intermediates
Chlorpromazine (Dopamine antagonist; treats schizophrenia)
-Forms insoluble complexes in bile

-Metabolites
-inhibit membrane enzymes
-impair cytoskeletal functions

Ethanol
-more complicated

32
Q

Describe mild v. serious ethanol injury

A

mild injury
-moderate alcohol intake (6 beers or 8oz. 80 proof liquor
-steatosis (fatty deposits form in liver)
-normally cleared but will accumulate with chronic alcohol intake

Serious injury
-massive intake or chronic effect
-Hepatitis

33
Q

What is alcoholic hepatitis?

A

ethanol has multiple effects on hepatocytes
-affects membrane function (chemical)

-induces/inhibits enzymes that detoxify foreign compounds

-enhances oxygen toxicity

-oxidized to acetaldehyde
-inhibits protein export/metabolism
-alters redox potential

34
Q

What are Mallory bodies?

A

-occurs thru alcoholic hepatitis
-Intermediate Filament proteins with ubiquitin
-Failure of protein degradation

35
Q

What is NAFLD?

A

non alcoholic fatty liver disease
-can lead to NASH —> cirrhosis

36
Q

Hepatic Vascular disease

A
  • can be caused by cirrhosis
    eg sickle cell disease in liver
37
Q

What can cause portal hypertension

A

Prehepatic causes

Intrahepatic causes
-Cirrhosis from any cause
-primary biliary cirrhosis
-massive fatty change
-diffuse, fibrosing granulomatous
-Amyloidosis

Posthepatic causes

38
Q

What is preeclampsia/eclampsia?

A

symptoms: maternal HTN, proteinuria, peripheral edema, coagulation abnormalities (hypercoagulability)

HELLP syndrome
H= Hemolysis
EL= elevated liver enzymes
LP= low platelets

-hemorrhage into the space of disse
-fibrin deposits develop in periportal sinusoids
-develop coagulative necrosis of hepatocytes
-Hematoma may form under Glisson’s capsule

39
Q

What is Cholestasis?

A

systemic retention of bilirubin and other solutes
-excess cholesterol
Xenobiotics
-Other waste products that are not water-soluble

Impaired bile formation and flow
-accumulation of bile in hepatocytes
-Obstruction of bile channels (extra or intrahepatic)
-defects in hepatocyte bile excretion

Symptoms: Jaundice, pruritus, skin xanthomas (cholesterol accumulation), malabsorption (failure to digest/ absorb fat in the intestines)

40
Q

How does Cholestasis look histologically?

A
  1. enlarged hepatocyte
  2. dilated canaliculus
  3. apoptotic hepatocyte
  4. Kupffer cell disgesting pigment
41
Q

T/F: Sepsis is not a cause of cholestasis.

A

False

42
Q

What are the mechanisms of sepsis caused cholestasis?

A

3 different mechanisms
1. Direct effects due to infection within the liver (abscess or cholangitis)
2. Ischemia due to hypotension (esp. if liver is cirrhotic)
3. Circulating microbial products
- most likely to lead to cholestasis, esp. with gram-negative bacteria

43
Q

What are the common leads to canalicular cholestasis?

A

Bile plugs within centrilobular bile canaliculi
-activated Kupffer cells
-Mild portal inflammation

44
Q

What is ductular cholestasis?

A

-Dilated canals of Hering and bile ductules with bile plugs
-Edema and presence of neutrophils in the stroma
-Hepatocyte cells death is possible

45
Q

What is Cholecystitis?

A

-inflammation of the gallbladder
-may be acute or chronic
-maybe both
-almost always associated with gall stones

Acute
-enlarged, tense gall bladder
-Wall is thickened and fluid-filled (edematous)
-Serosa may have hemorrhages beneath
-May be covered with fibrinous exudate
-Finbrinosuppurative is sign of more severe disease

45
Q

What is Cholecystitis?

A

-inflammation of the gallbladder
-may be acute or chronic
-maybe both
-almost always associated with gall stones

Acute
-enlarged, tense gall bladder
-Wall is thickened and fluid-filled (edematous)
-Serosa may have hemorrhages beneath
-May be covered with fibrinous exudate
-Finbrinosuppurative is sign of more severe disease

46
Q

What disease is Rokitansky aschoff sinus associated with?

A

Chronic cholecystitis

47
Q

What are the neuroendocrine tumors (benign) that we focused on in the lecture?

A

symptoms related to excessive hormone release
Glucagonoma (alpha)
Insulinoma (beta)
Somatostinoma (delta)

diabetes -altered glucose uptake
cholethiasis- impaired bile secretion
steatorrhea- impaired pancreatic excretion

48
Q

What is glucagonoma?

A

Excessive glucose mobilization
-produces hyperglycemia

Patients have a characteristic rash
-Due to malnutrition
-Excessive AA uptake for use as fuel to produce more glucose

49
Q

What is an insulinoma?

A

-clinically, hypoglycemia produces neurological symptoms
-precipitated by exercise or fasting

50
Q

What is diabetes Mellitus?

A

at adipose tissue
increase glucose uptake
increase lipogenesis
decrease lipolysis

at striated muscle
increase glucose uptake
increase synthesis
increase protein synthesis

at liver
decrease gluconeogenesis
increase glycogen synthesis
increase lipogenesis

51
Q

What is the difference between type I and Type II diabetes?

A

T1 - beta cell destruction, usually leading to absolute insulin deficiency

T2 (combination of insulin resistance and beta cell dysfunction

52
Q

What do we see pathologically for T1 and T2 diabetes?

A

T1
insulitis (immune reaction to the beta cells)
autoimmune reaction to islet beta cells

T2
amyloidosis in islet

52
Q

What do we see pathologically for T1 and T2 diabetes?

A

T1
insulitis (immune reaction to the beta cells)
autoimmune reaction to islet beta cells

T2
amyloidosis in islet

53
Q

What do you see pathologically for diabetic glomerulonephropathy?

A

-Glomerulosclerosis
-diffuse mesangial matrix increase PAS stain
Thickened glomerular basement membrane

54
Q

What is Acute v Chronic Pancreatitis

A

-inflammation associated with damage to exocrine tissue
-acute-reversible damage
-Chronic- irreversible damage
-can present as repeated incidents of acute damage that do not fully resolve

55
Q

What is acute pancreatitis?

A

reversible parenchyma injury with inflammation

Common causes
-biliary tract disease
-alcoholism
-toxins
-trauma
-vascular disease

56
Q

What does the activation of trypsin do?

A

-changes associated with acute pancreatitis suggest autodigestion of the pancreas by its own digestive enzymes

-Trypsin is activated in the pancreas, rather than the duodenum
-supported by hereditary pancreatitis
-mutation in the cleavage site (fail-safe; important for deactivation)
-mutation in trypsin inhibitor

57
Q

What is autodigestion?

A

microvascular leakage (edema)
-elastase damages vessel walls

Fat necrosis
-activation of lipases

Parenchymal degradation
-proteases (trypsin, chymotrypsin, etc.)

Thromboses damage weak vessels
-clotting defects

Hemorrhage
-Kallikrein

58
Q

What is chronic pancreatitis?

A

-inflammation with irreversible damage to exocrine parenchyma
-Irreversibly damage-distinction from acute
-Eventually =fibrosis develops, and may even impact endocrine parenchyma

-The most common cause is long-term alcohol abuse
-increased excretion> duct destruction
-directly toxic to acinar. cells

59
Q

What is the pathogenesis of chronic pancreatitis?

A

similar toacute
-duct obstruction
-cell injury

-Oxidative stress has a role in chronic
-Repeated acute episodes
-Perilobular fibrosis
-Duct distortion
-Altered secretion

results in fibrosis and parenchyma loss

60
Q

Describe Pancreatitis clinically

A

-Upper abdominal pain (due to inflammation of the pancreas
-nausea, vomiting, fever, tachycardia, sweating
-icterus/jaundice

Treatments
-IV fluids
-no foods
-medicine for pain

mechanism s of disease (4 decks)

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