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General pathology (pathophysiology) > Special pathology - hepatic disease > Flashcards

Special pathology - hepatic disease Flashcards

1
Q

The liver of domestic animals has how many lobes?
Each liver lobe is composed of ?

A

5-6, species dependently
Each liver lobe is composed of lobules. There are approx. 700,000 lobules in a liver.

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2
Q

the portal triad consists of?

A

hepatic artery
portal vein
bile duct

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3
Q

Hepatic Sinusoid

A

Vascular spaces, termed sinusoids, run between the hepatic plates (cords).

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4
Q

main exocrine function of the liver

A

Production and excretion of bile

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5
Q

Bile is composed of: (5)

A

-water
-cholesterol

-bile acids
-bilirubin

-inorganic ions, other constituents

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6
Q

purposes for bile synthesis: (3)

A

excretory route (for metabolic by-products)
facilitation of digestion
buffers to neutralize acids

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7
Q

Functions of bile acids: (3)

A

-maintenance of cholesterol homeostasis
-stimulation of bile flow
-intestinal absorption of fats and fat-soluble vitamins

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8
Q

Bile acids are synthesized in the liver from cholesterol and are conjugated with

A

glycine or taurine before being excreted into the bile, in order to facilitate their interaction with other components of the bile and
to prevent precipitation into calculi when they are secreted.

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9
Q

The quantities of bile acids required far exceed

A

the liver’s capacity to produce them!

Thus, using the enterohepatic circulation, bile acids are reabsorbed from the ileum,
extracted from the portal blood, and resecreted into bile.

Interruption of this process results in fat malabsorption and a deficiency of fat-soluble vitamins.

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10
Q

Bilirubin is produced from

A

the metabolic degradation of hemoglobin.

The majority of bilirubin is derived from normal extrahepatic breakdown of senescent erythrocytes with a minor contribution from degradation of tissue heme-containing proteins.

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11
Q

Gut bacteria deconjugate bilirubin in the GI tract and degrade it to

A

colorless urobilinogens.

The urobilinogens are excreted in the feces, with minimal reabsorption and excretion into urine too.

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12
Q

Residual urobilinogen is metabolized by bacteria into the brown pigment called

A

stercobilin, imparting the typical color to feces.

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13
Q

Name 4 plasma lipids.

A

cholesterol,
triglycerides,
phospholipids, and
lipoproteins

Hepatocytes can synthesize fatty acids when energy levels are high, and they can oxidize fatty acids as an energy source when necessary.

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14
Q

xenobiotic definition

A

all substances foreign to the body

e.g. drugs, toxins etc.

Cytochrome P450 enzymes of the smooth endoplasmic reticulum (microsomes) of the hepatocytes serve as the major site of metabolism of these substances in preparation for excretion in bile or urine.

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15
Q

what is Cytochrome P450

A

a major group of hepatic enzymes that play a significant role in the detoxification of xenobiotics among other tasks

Cytochrome P450 enzymes of the smooth endoplasmic reticulum (microsomes) of the hepatocytes serve as the major site of metabolism of xenobiotics in preparation
for excretion in bile or urine

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16
Q

endogenous substances (steroids that are lipophilic)
require conversion to ? for elimination from the body

A

require conversion to water-soluble forms for elimination from the body

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17
Q

The liver is responsible for synthesis of approximately ?% of body proteins.

A

The liver is responsible for synthesis of approximately 15% of body proteins.

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18
Q

Synthesis of the majority of plasma proteins occurs mainly within

A

the rough endoplasmic reticulum of hepatocytes.

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19
Q

Proteins produced in the liver include plasma proteins:
(7)

A

albumin
variety of transport proteins
lipoproteins

clotting factors II, V, and VII to XIII
plasminogen

some acute phase proteins (e.g. CRP, SAA)
components of the complement system (C1- C9)

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20
Q

Highly toxic ammonia is generated through catabolism of

A

amino acids.

Metabolic conversion of ammonia into urea, a far less toxic compound, occurs through the urea cycle, which occurs almost exclusively in the liver.

Urea then enters the systemic circulation (blood urea nitrogen) and is excreted in the urine.

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21
Q

The liver has a significant immune function involved in:
(3)

A

systemic
local
mucosal immunity

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22
Q

Hepatocytes participate in the response to systemic inflammation through the synthess and release of

A

acute phase proteins.

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23
Q

Approximately ?% of the cells in the liver belong to the adaptive immune system or the innate immune system.

A

Approximately 10% of the cells in the liver belong to the adaptive immune system (T and B lymphocytes) or the innate immune system (Kupffer cells, natural killer lymphocytes, and natural killer T lymphocytes).

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24
Q

Compared with other organs, the liver is particularly enriched with cells of the

A

innate immune system, likely a result of the fact it is the site where foreign antigens from the gastrointestinal tract first encounter the innate immune system defenses.

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25
Q

The liver contains the largest pool of (2)

A

mononuclear phagocytes and natural killer cells in the body in most species.

The Kupffer cells provide the first line of defense against infectious agents, endotoxins, and foreign material absorbed from the intestines before they gain access to the systemic circulation.

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26
Q

Disposal of waste molecules such as (2)? and deletion of activated effector T lymphocytes are also important functions of the liver.

A

e.g., products of inflammation such as cytokines and immunoglobulins and deletion of activated effector T lymphocytes are also important functions.

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27
Q

The liver is also involved in transport of secretory

A

immunoglobulin A (IgA), the primary IgG on mucosal surfaces, from plasma cells into the biliary tree an dintestine.

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28
Q

Mechanisms of Liver Injury (6)

A
  • Metabolic bioactivation of chemicals via cytochrome P450 to reactive species
    *Stimulation of autoimmunity
  • Stimulation of apoptosis

*Disruption of calcium homeostasis leading to cell surface blebbing and lysis

*Canalicular injury
*Mitochondrial injury

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29
Q

What is surface blebbing?

A

A bleb is an irregular bulge in the plasma membrane of a cell caused by localized decoupling of the cytoskeleton from the plasma membrane. The bulge eventually blebs off from the parent plasma membrane taking part of the cytoplasm with it.

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30
Q

Acute Hepatitis is

A

Inflammation of the liver parenchyma

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31
Q

Acute Hepatitis is characterized by: (3)

A

-inflammation
-hepatocellular necrosis
-apoptosis

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32
Q

In many forms of acute hepatitis- what cell types accumulate?

A

neutrophils accumulate in response to the usual chemotactic stimuli

Random foci of neutrophilic hepatitis, as a consequence of embolic localization of bacteria, are relatively common in all species.

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33
Q

In neonates—especially calves, lambs, and foals—bacteria, such as Escherichia coli, usually seed the liver via

A

the umbilical veins or less often the portal venous or
hepatic arterial systems.

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34
Q

Acute hepatitis produced by viral infections such as?

A

herpesvirus
- more frequently characterized by a random distribution of necrosis and apoptosis with minimal inflammation or infiltration of lymphocytes.

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35
Q

Chronic Hepatitis is

A

continued hepatic inflammation as a result of persistence of an antigenic stimulus.

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36
Q

Chronic Hepatitis is characterized by: (3)

A

fibrosis;

accumulation of mononuclear inflammatory cells,
including lymphocytes, macrophages, and plasma cells;

frequently- regeneration

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37
Q

Granulomatous hepatitis is

A

refers to the presence of granulomas in the liver.

Liver granulomas are common and are the result of an inflammatory reaction to numerous noxious stimuli.

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38
Q

Chronic suppurative hepatitis is usually manifested as

A

discrete or multiple abscesses.

Focal lesions, such as abscesses or granulomas, often are sufficiently localized so that they do not alter liver function.

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39
Q

Diffuse and severe chronic hepatitis usually leads to loss of

A

hepatic parenchyma, and architectural distortion of the liver as a consequence of fibrosis and nodular parenchymal regeneration.

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40
Q

Nonspecific Reactive Hepatitis is (3)

A

a diffuse process

distributed throughout the liver

response to some systemic illness most often within the gastrointestinal tract, or is the residuum of prior liver
inflammation

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41
Q

Nonspecific Reactive Hepatitis Represents a

A

non-specific response to a variety of extrahepatic disease processes,
previous or ongoing febrile illnesses and/or inflammation somewhere in the splanchnic area.

The inflammatory infiltrate is mostly localized in the portal area during this non-specific reaction of the liver.

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42
Q

Cholangitis is

A

Inflammation of the biliary ducts (either intrahepatic or extrahepatic).

There are Several patterns of cholangitis.

The inflammatory cell population and the degree of fibrosis will vary with the type and duration of injury.

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43
Q

Neutrophilic Cholangitis is the

A

most common type of cholangitis.

There are acute and chronic forms.

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44
Q

Neutrophilic Cholangitis is

A

characterized by the presence of neutrophils within the lumen or epithelium of the bile ducts.

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45
Q

Neutrophilic Cholangitis is caused by

A

caused by ascending bacterial infections from the intestine.

Bacterial culture from gallbladder bile is the most rewarding approach and most often reveals
infection with enteric organisms such as Escherichia coli, Enterococcus, Bacteroides, Streptococcus, or Clostridium.

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46
Q

Lymphocytic cholangitis occurs most often in

A

cats.

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47
Q

Destructive Cholangitis is

A

an uncommon syndrome characterized by necrosis of the epithelium of bile ducts.

Inflammation is often present around the areas of biliary destruction and may extend along cholangioles outside of the portal tract.

Certain chemicals, such as trimethoprim-sulfa, have been implicated in this syndrome in dogs.

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48
Q

Cholangiohepatitis is when

A

Inflammation affects both the biliary ducts and hepatic parenchyma.

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49
Q

the principal cellular targets of most liver diseases are (3)

A

The epithelial cells of the liver, hepatocytes and biliary epithelium.

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50
Q

Sublethal injury to hepatocytes is characterized by (3)

A

cell swelling (hydropic degeneration),
steatosis,
or atrophy

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51
Q

lipofuscin is

A

the name given to fine yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion.

this pigment can often be found in affected cells and associated phagocytes after sublethal liver injury.

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52
Q

Random Hepatocellular Degeneration and/or Necrosis can be typical of

A

many infectious agents, including viruses, bacteria, and certain protozoa.

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53
Q

Centrilobular Degeneration and/or Necrosis is

A

particularly common.

this portion of the lobule receives the least oxygenated blood and is therefore susceptible to hypoxia.

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54
Q

Cholestasis is

A

disturbance of flow of all of the constituents of bile

55
Q

hyperbilirubinemia refers specifically to

A

an increased concentration of conjugated or
unconjugated bilirubin in blood

56
Q

Cholestasis can be divided into (3)

A
  1. Intrahepatic cholestasis which can result from hepatocyte disturbances causing issues with metabolization and excretion of bile;

(2) hemolysis, which produces an abundance of bilirubin for excretion and diminishes the supply of oxygen for hepatocyte metabolism (also termed prehepatic hyperbilirubinemia);

(3) inherited abnormalities of bile synthesis that inhibit the excretion of bile.

57
Q

Extrahepatic cholestasis is produced by

A

obstruction of the extrahepatic bile ducts.

It can occur by intraluminal obstruction (by calculi or possibly parasites) or extraluminal constriction by neoplasia or adjacent inflammation, often involving the
pancreas.

58
Q

Cholestasis, if sufficiently severe, can produce

A

a greenish brown discoloration to the liver.

59
Q

Complete biliary obstruction leads to

A

maldigestion of fats due to the reduction in bile acids.

Characteristic clay-colored stool termed acholic feces because of the lack of normal dark pigment, stercobilin, the bilirubin-derived pigment produced by bacterial
metabolism.

60
Q

Icterus or jaundice is

A

yellowish discoloration of the tissues, particularly those with high elastic tissue content, including the sclera and aorta, due to an increase in bilirubin termed
hyperbilirubinemia.

61
Q

In most species, hyperbilirubinemia can occur once the concentration exceeds

A

0.5 mg/dL, and therefore the patient can be hyperbilirubinemic but not icteric.

62
Q

Maximal accumulation of bilirubin in tissues takes approximately

A

2 days, and this explains why some animals with acute hepatic failure may have only slight icterus.

63
Q

Name the Types of jaundice: (3)
And what are they characterized by

A

Prehepatic – elevated serum levels of unconjugated bilirubiin

Hepatic - elevated unconjugated and conjugated bilirubiin

Post-hepatic - elevated conjugated bilirubiin

64
Q

Prehepatic cause of icterus

A

intravascular hemolysis

common cause in ruminants and likely occurs more often than hepatic damage

65
Q

Horses often manifest icterus with

A

acute hepatic dysfunction or obstruction, but icterus may or may not occur in horses with chronic hepatic disease.

66
Q

Interestingly, “physiologic icterus” is also common in the

A

horse, and horses deprived of feed for several days can become icteric because uptake of bilirubin from the
plasma by hepatocytes is decreased.

67
Q

Icterus in carnivores occurs as a consequence of (3)

A

hemolysis, hepatic dysfunction, or biliary obstruction.

68
Q

hepatic Regeneration is

A

A characteristic feature of the liver to rapidly and efficiently regenerate lost hepatic mass.

In addition to replication of hepatocytes, there is a wave of replication in bile duct epithelium, endothelium, and sinusoidal lining cells that is coordinated with hepatocyte replication.

69
Q

Fibrosis is

A

One of the more common consequences of chronic liver injury.

Pattern of fibrosis is frequently a useful indicator of the type of insult that produces the lesion.

70
Q

The significance of fibrosis depends on

A

its effect on hepatic function and its reversibility.

Despite the considerable regenerative capacity of the liver, hepatic fibrosis, when sufficiently severe, can be lethal.

71
Q

End-Stage Liver or Cirrhosis is

A

diffuse process characterized by fibrosis and the conversion of the normal liver architecture into structurally abnormal lobules.

the final, irreversible result of any one of several different hepatic diseases.

The architecture of the liver is altered by loss of hepatic parenchyma, condensation of reticulin framework, and formation of tracts of fibrous connective tissue.

72
Q

In cirrhosis, the Regeneration of hepatic tissue between fibrous bands leads to

A

the formation of variably sized regenerative nodules.

The entire liver is thus distorted and consists of nodules of regenerating parenchyma separated by fibrous bands, which appear as depressions on the surface.

73
Q

Causes of End-Stage Liver disease (6)

A
  • Chronic toxicity (therapeutic agents or naturally occurring toxins)
  • Chronic cholangitis and/or obstruction
  • Chronic congestion (right side heart failure)
  • Inherited disorders of metal metabolism (copper or iron)
  • Chronic hepatitis
  • Idiopathic
74
Q

Only lesions that affect the majority of the hepatic parenchyma are likely to produce the signs of hepatic failure because focal lesions

A

rarely destroy sufficient parenchyma to deplete the liver’s reserve.

75
Q

Hepatic Encephalopathy

A

Hepatic failure can result in a metabolic disorder of the central nervous system (CNS) termed hepatic encephalopathy.

Neurologic manifestations range from depression and other behavioral changes to mania and convulsions.

Affected animals may walk aimlessly.

The central feature of this disorder is abnormal neurotransmission in the CNS and the neuromuscular system.

76
Q

one of the main factors in the pathogenesis of hepatic encephalopathy is

A

increased concentrations of plasma ammonia derived from amines absorbed from the gastrointestinal tract.

Normally, amines are absorbed from the intestines into the portal blood and metabolized by the liver.

If they bypass the liver and gain access to the systemic circulation, they can exert toxic effects on the brain.

77
Q

toxic products can enter the systemic circulation by two mechanisms:

A

-blood can be shunted to the systemic circulation before it reaches the liver as a result of congenital portosystemic shunts

-or be secondary to portal vein hypertension

78
Q

Glutamine is

A

the most abundant amino acid in the body. The body can make enough glutamine for its regular needs.

79
Q

Shunting of more than ?% of portal blood flow away from the liver is considered abnormal.

A

Shunting of more than 10% to 15% of portal blood flow away from the liver is considered abnormal.

80
Q

Hepatic encephalopathy is common in what species with hepatic failure.

A

Hepatic encephalopathy is common in ruminants and horses with hepatic failure.

and dogs and cats with congenital portosystemic shunts.

and animals with end-stage liver (hepatic fibrosis and nodular regeneration) that leads to shunting of blood within regenerative nodules.

81
Q

Metabolic Disturbances of Hepatic Failure (5)

A

Bleeding Tendencies
Hypoalbuminemia
Vascular and Hemodynamic Alterations of Hepatic Failure
Cutaneous Manifestations of Hepatic Failure
Immunologic Manifestations of Hepatic Failure

82
Q

Bleeding Tendencies due to hepatic failure

A

Impaired synthesis of clotting factors,
reduced clearance of the products of the clotting process, and
metabolic abnormalities affecting platelet function can affect normal clotting, individually or in combiination.

83
Q

Hypoalbuminemia and liver disease

A

Hypoalbuminemia reflects severe and chronic liver disease.

The relatively long half-life of plasma albumin (which ranges from 8 days in the dog to 21 days in cattle), masks the diminished albumin synthesis of the diseased liver for a period of time.

84
Q

plasma albumin half-life

A

ranges from 8 days in the dog to 21 days in cattle

85
Q

Hypoalbuminemia, in combination with portal hypertension, accelerates the

A

forrmation of ascites in affected animals.

86
Q

Vascular and Hemodynamic Alterations of Hepatic Failure involve

A

extensive diffuse fibrosis which increases resistance to portal blood flow through the liver.

This resistance in turn elevates pressure within the portal vein (portal hypertension).

potential for acquired portosystemic vascular anastomoses

increased pressure within the hepatic vasculature causes transudation of fluid (modified transudate) into the peritoneal cavity to produce ascites.

87
Q

acquired portosystemic vascular anastomoses

A

With time, collateral vascular channels open to allow blood in the portal vein to bypass the abnormal liver so
connect the portal vein and its tributaries to the systemic venous circulation.

88
Q

Cutaneous Manifestations of Hepatic Failure are a

A

syndrome of chronic hepatic injury and skin disease

crusting, erosions, and ulceration of the epidermis of the muzzle, mucocutaneous areas of the face, footpads, and pressure points of the skin in some dogs with severe
hepatic disease

The mechanism of cutaneous injury is not understood, but affected animals have characteristic multinodular livers, often with little fibrosis between the nodules.

89
Q

Immunologic Manifestations of Hepatic Failure involve

A

impairment of normal hepatic immune function due to chronic lvier failure

As a consequence, the affected patient frequently develops endotoxemia and an increased risk of systemic infection.

For the most part, this impairment manifests as a reduction of blood filtration by Kupffer cells, which is primarily a result of shunting of portal blood rather than
reduced phagocytic activity.

90
Q

Food containing fat stimulates the secretion of

A

cholecystokinin from the duodenum and jejunum.

91
Q

In response to cholecystokinin, the gallbladder

A

contracts.

92
Q

onstruction by cholelithiasis can lead to

A

hyperbilirubinemia and cholecystitis.

If bile cannot be released from the gallbladder, maldigestion of fats will occur, leading to acholic feces.

93
Q

Larger choleliths can cause

A

pressure necrosis and ulceration of the gallbladder
mucosa or formation of saccular diverticula.

In severe cases, the gallbladder can rupture. Rupture leads to leakage of bile into the peritoneal cavity, which is very irritating and can cause acute peritonitis.

94
Q

Infectious agents or injurious substances can enter the gallbladder via

A

reflux of intestinal bacteria into the cystic duct, particularly if there is dysfunction of or injury to the sphincter regulating bile flow into the intestine.

95
Q

Hematogenous entry of Infectious agents or injurious substances can enter the gallbladder via the

A

hepatic circulation, through the venous circulation or through the bile into the intestine, where they can then be absorbed and distributed via the systemic circulation.

96
Q

gallbladder rupture can lead to

A

acute peritonitis due to leakage of irritating bile salts into the abdominal cavity.

97
Q

Passive hepatic Congestion (Acute and Chronic) can be a consqeunce of

A

cardiac dysfunction

Right-sided heart failure produces elevated pressure within the caudal vena cava that later involves the hepatic vein and its tributaries.

98
Q

Chronic hepatic passive congestion is particularly common in

A

aged dogs and occurs secondary to right atrioventricular valve insufficiency resulting from valvular endocardiosis (myxomatous degeneration).

99
Q

Acute passive hepatic congestion can occur as a consequence of

A

acute right-sided heart failure, which has a wide variety of causes.

100
Q

Congenital Portosystemic Shunts are

A

abnormal vascular channels that allow blood within the portal venous system to bypass the liver and to drain into the systemic circulation.

101
Q

A congenital shunt can be either

A

intrahepatic or extrahepatic in location but is usually limited to a single relatively large-caliber vessel.

102
Q

Shunts occur most commonly in

A

the dog and cat.

Affected animals are typically stunted and frequently develop signs of hepatic encephalopathy.

The liver is small and may have a characteristic histologic appearance of small or absent portal veins within the portal tracts, reduplication of arterioles, and lobular
atrophy.

103
Q

Portal Vein Thrombosis refers to

A

partial or total obstruction of blood flow into the liver caused by thrombosis within the extrahepatic portal venous system.

104
Q

Portal vein thrombosis is uncommon in all species, but it is reported most commonly in

A

dogs.

105
Q

Portal Vein Thrombosis can occur with diseases associated with hypercoagulability including

A

liver disease,
hyperadrenocorticism,
protein-losing nephropathy,
protein-losing enteropathy,
neoplasia, and
various immune-mediated and infectious diseases.

It can also be induced by damage to the portal vein or by local inflammatory disorders, including pancreatitis.

106
Q

Portal Hypertension is

A

Increased pressure within the portal vein which can arise from disturbances of venous blood flow.

107
Q

Hepatocellular Steatosis (Lipidosis) is

A

the presence of excessive lipid within the liver

the Rate of triglyceride accumulation within hepatocytes exceeds either their rate of metabolic degradation or their release as lipoproteins.

Hepatocellular steatosis is not a specific disease entity but can occur as a sequel to a variety of perturbations of normal lipid metabolism.

With progressive accumulation of lipid, the liver enlarges and becomes yellow.

108
Q

6 main causes for hepatic steatosis

A

1) Excessive entry of fatty acids into the liver (excessive intake or increased mobilization of FFAs)

2) excessive dietary intake of carbs

3) abnormal hepatocyte function with accumulation of triglycerides

4) increased esterification of fatty caids to triglycerides

5) decreased apoprotein synthesis

6) impraied secretion of lipoprotein from liver because of toxins/drugs

109
Q

Bovine fatty liver syndrome, also known as fatty liver disease, is mechanistically similar to

A

ketosis and is especially common in ruminants with high energy demands.

110
Q

Feline fatty liver syndrome is a distinct syndrome of

A

idiopathic hepatocellular steatosis recognized in cats.

111
Q

The accumulation of lipids in the liver in the diabetic animal is the result of

A

increased fat mobilization and decreased use of lipids by injured hepatocytes.

112
Q

Hepatic Amyloidosis is

A

a familial/hereditary disease

may be asymptomatic for long intervals, clinical signs may include fever, lymphadenopathy, vomiting, inappetence, weight loss, PU/PD, jaundice, and
hepatomegaly

is a progressive systemic disorder- prognosis is poor

113
Q

Excessive hepatic accumulation of glycogen occurs with metabolic

A

perturbations involving glucose regulation

(including diabetes mellitus and the glycogen storage diseases)

114
Q

dietary lipids digested by

A

pancreatic lipase and phospholipase

115
Q

proteins digested by

A

pancreatic trypsin and chymotrypsin

116
Q

carbohydrates digested by

A

salivary and pancreaatic amylase

117
Q

how do pancreatic secretion maintain pH?

A

they contain electrolytes that buffer

118
Q

α-Amylase breaks what down

A

Breaks down polysaccharides (starch) into the disaccharides (maltose)

119
Q

lipase breaks what down

A

triglycerides into fatty acids and glycerol

120
Q

Trypsin Excreted as what and activated by?

A

Excreted as trypsinogen and activated by enteropeptidase in the intestines.

– Completes the breakdown of the proteins from meat into amino acids.

121
Q

Chymotrypsin A, B, C are activated by

A

enterokinase

– Break down peptide bonds with phenylalanine, tyrosine and tryptophan

122
Q

Pancreatic injury results in the release of

A

pancreatic enzymes into the surrounding parenchyma
leading to further enzyme activation and autodigestion of the pancreatic tissue

123
Q

when trypsin is released into parenchymal tissue during pancreatitis, it an activate the

A

kinin system, complement, and clotting cascades - leading to overwhelming inflammation and necrosis when released into parenchymal tissue during pancreatitis.

124
Q

why can pancreatitis lead to systemic inflammatory response syndrome (SIRS)

A

Trypsin- can activate the kinin system, complement, and clotting cascades - leading to overwhelming inflammation and necrosis.

activated enzymes + vasoactive peptides + inflammatory mediators + embolic debris can also be released into the systemic circulation leading to inflammation and necrosis in other tissues such as the liver and lung and
to systemic inflammatory response syndrome (SIRS).

125
Q

Exocrinepancreatic insufficiency is

A

Deficiency or the absence of pancreatic enzymes, as a result of impaired production, secretion or activity.

*Impaired fat digestion and assimilation (only 20 – 30% of food fat is assimilated)

*Impaired protein digestion (only 40-60% assimilated)

126
Q

Obstruction of the flow of pancreatic juice into the duodenum can be caused by (4)

A

*Pancreatic duct obstruction by stones, tumours, scarring of tissue

*Inflammation of the duodenal bulb mucosa that blocks the sphincter

*Pancreatitis

*Disorders of the neurohumoral regulation of pancreatic juice secretion

127
Q

name 6 hepatic dysfunction markers

A

so markers that may decrease with loss of hepatic function

albumin
bilirubin
cholesterol
coagulation factors
glucose
urea nitrogen

128
Q

name 2 canalicular epithelial enzymes

A

alkaline phosphatase (ALP/AFOS/ALKP)
gammaglutamyltransferase (GGT)

concurrent increase of these increase specificity for liver disease

129
Q

name 2 hepatocellular cytosolic enzymes

A

alanine aminotransferase (ALT)
aspartate aminotransferase (AST)

130
Q

increased ALT can indicate

A

increased hepatocyte necrosis

because is a hepatocellular cytosolic enzyme

131
Q

increased AST can indicate

A

increased hepatocyte necrosis because is a hepatocellular cytosolic enzyme

however, note AST has a muscular isoenzyme so is less specific for hepatic injury

132
Q

hepatic lipidosis typically causes a minimal increase of what hepatic biomarker

A

GGT

gammaglutamyltransferase

133
Q

what is ALP?
increased when?

A

alkaline phosphatase

a hepatocyte canicular epithelial enzyme

increased with cholestatic diseases, biliary obstruction, cholangiohepatitis

134
Q

what is GGT?
increased when?

A

gammaglutamyltransferase,
a hepatocyte canicular epithelial enzyme

increased with cholestatic diseases, biliary obstruction, cholangiohepatitis

General pathology (pathophysiology) (16 decks)

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