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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

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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
What can be used to observe chronic HepB infection?
can use IHC for HepBsAg accumulation
25
Describe HepC infection?
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
What are consequences for Hepatitis?
Loss of liver function -hypoproteinemia -hyperbilirubinemia -anemia Infection/stress cause. additional damage -Cirrhosis
27
What is Chronic Hepatitis Symptoms
-fatigue, malaise, loss of appetite, mild jaundice -blood tests -serum transaminase is elevated -hyperglobulinemia, hyperbilirubinemia -Minor hepatomegaly, splenomegaly -hepatic tenderness
28
What are the similarities between toxic and viral damage?
-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
Describe toxic liver injury
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
Describe toxic liver injury
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
Describe necrosis in the liver.
necrotic liver -congested -bile accumulation Acetaminophen overdose -confluent necrosis in zone 3 -surrounds central vein
31
What are common liver toxins?
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
Describe mild v. serious ethanol injury
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
What is alcoholic hepatitis?
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
What are Mallory bodies?
-occurs thru alcoholic hepatitis -Intermediate Filament proteins with ubiquitin -Failure of protein degradation
35
What is NAFLD?
non alcoholic fatty liver disease -can lead to NASH ---> cirrhosis
36
Hepatic Vascular disease
- can be caused by cirrhosis eg sickle cell disease in liver
37
What can cause portal hypertension
Prehepatic causes Intrahepatic causes -Cirrhosis from any cause -primary biliary cirrhosis -massive fatty change -diffuse, fibrosing granulomatous -Amyloidosis Posthepatic causes
38
What is preeclampsia/eclampsia?
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
What is Cholestasis?
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
How does Cholestasis look histologically?
1. enlarged hepatocyte 2. dilated canaliculus 3. apoptotic hepatocyte 4. Kupffer cell disgesting pigment
41
T/F: Sepsis is not a cause of cholestasis.
False
42
What are the mechanisms of sepsis caused cholestasis?
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
What are the common leads to canalicular cholestasis?
Bile plugs within centrilobular bile canaliculi -activated Kupffer cells -Mild portal inflammation
44
What is ductular cholestasis?
-Dilated canals of Hering and bile ductules with bile plugs -Edema and presence of neutrophils in the stroma -Hepatocyte cells death is possible
45
What is Cholecystitis?
-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
What is Cholecystitis?
-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
What disease is Rokitansky aschoff sinus associated with?
Chronic cholecystitis
47
What are the neuroendocrine tumors (benign) that we focused on in the lecture?
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
What is glucagonoma?
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
What is an insulinoma?
-clinically, hypoglycemia produces neurological symptoms -precipitated by exercise or fasting
50
What is diabetes Mellitus?
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
What is the difference between type I and Type II diabetes?
T1 - beta cell destruction, usually leading to absolute insulin deficiency T2 (combination of insulin resistance and beta cell dysfunction
52
What do we see pathologically for T1 and T2 diabetes?
T1 insulitis (immune reaction to the beta cells) autoimmune reaction to islet beta cells T2 amyloidosis in islet
52
What do we see pathologically for T1 and T2 diabetes?
T1 insulitis (immune reaction to the beta cells) autoimmune reaction to islet beta cells T2 amyloidosis in islet
53
What do you see pathologically for diabetic glomerulonephropathy?
-Glomerulosclerosis -diffuse mesangial matrix increase PAS stain Thickened glomerular basement membrane
54
What is Acute v Chronic Pancreatitis
-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
What is acute pancreatitis?
reversible parenchyma injury with inflammation Common causes -biliary tract disease -alcoholism -toxins -trauma -vascular disease
56
What does the activation of trypsin do?
-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
What is autodigestion?
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
What is chronic pancreatitis?
-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
What is the pathogenesis of chronic pancreatitis?
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
Describe Pancreatitis clinically
-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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