Week5.Ch.12.ThePancreas Flashcards

1
Q

Where is the panreas located?

A

The pancreas is located in the retroperitoneal space of the upper abdomen and is closely attached to other retroperitoneal structures, most notably the ganglia and nerves of the celiac plexus.

Because of this close relationship between the pancreas and the retroperitoneal nerves, pain radiating into the back is one of the common features of pancreatic diseases.”

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2
Q

The 3 parts of the pancreas

What tissue?

What cells?

A

The pancreas can be divided into three parts: the head, which lies within the loop of the duodenum; the midportion, which is called the body; and the tail, which extends laterally and left to the hilus of the spleen (see Figure 12-1).

More than 98% of the entire pancreas consists of exocrine tissue-acini, ductules, and ducts.

The endocrine cells are arranged into islets of Langerhans that are scat-tered through the entire organ but are most prominent in the tail”

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3
Q

Explain the drainage of the pancreas

A

The digestive juices produced by the exocrine pancreatic cells drain through the main pancreatic duct into the duo-denum.

The terminal part of the main pancreatic duct is confluent with the common bile duct, forming the ampulla of Vater.

The distal part of the ampulla, encased in the “smooth muscle of the sphincter of Oddi, enters into the lumen of the duodenum, protruding in the form of a small nubbin called the papilla of Vater.

There is often an accessory duct entering the duodenum, which is unrelated to the bile duct.

This close relationship of the head of the pancreas with the duodenum, and the common bile duct, is impor-tant for the understanding of the obstructive symptoms caused by tumors of the head of the pancreas.

Reflux of bile into the pancreatic duct as a result of obstruction of the papilla of Vater may be important in the pathogenesis of pancreatitis. Hormones produced by the endocrine cells are released into the blood circulation; therefore, there is no need for endocrine excretory ducts

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4
Q

Digestive enzymes of the pancreas

A

amylase

lipase

peptidases

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5
Q

Most important consequences of pancreatic diseases

A

Malabsorption and diarrhea

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6
Q

Important to know about pancreatic tumors and anatomy of other organs

A

Because tumors of the head of the pancreas often occlude the common bile duct, obstructive jaundice is a common symptom.

Duodenal obstruction is usually found in more advanced cases

Invasion of the retroperitoneal nerves is a common cause of back pain in patients with pancreatic cancer, but nerve involvement can also occur in those with chronic pancreatitis.”

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7
Q

Things to remember about the pancreas in relation to disease

A
  1. ) The pancreas is part of the digestive tract: improper diet, overeating, alchohol place strain on pancreas and biliary system
  2. )Pancreatic juice contains proenzymes that are activated in the intestine: premature activation can cause tissue destruction
  3. ) Under normal circumstances, pancreatic enzymes can be found in trace amounts in circulating blood
  4. ) Endocine tumors are slow growing and less aggressive than exocine malignant lesions
  5. ) Insulin is the most important hormone secreted by the pancreas
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8
Q

Pancreatitis

A

inflammation of the pancreas, can be acute or chronic

typically sterile chemical inflammation

The inflammation is secondary to tissue destruction caused by digestive enzymes released from damaged exocine pancreatic cells

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9
Q

What is acute pancreatitis?

A

Acute pancreatitis is an acute inflammation of the pancreas and the peripancreatic fat tissue caused by lytic digestive enzymes inappropriately activated after release from damaged pancreatic acinar cells

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10
Q

Most important causes of acute pancreatitis

A

“1) gallstone obstruction of the pancreatic-biliary ductal system, (2) alcohol abuse,

(3) mechanical disruption of the pancreatic acinar cells,
(4) chemical injury of acinar cells by toxins or drugs,
(5) infection and shock, and (
6) netic disorders”

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11
Q

Damage in acute pancreatitis

A

Proteolysis caused by activation of trypsinogen, the inactive form of trypsin, leads to necrosis of tissues.

Elastase acts on the elastic tissue, forming large gaps in the blood vessel wall that result in massive hemorrhage.

The action of lipase on fat cells inside the pancreas and the peripancreatic fat tissues results in fat necrosis.

Other hydrolytic enzymes, more than 100 of which are present in the pancreatic juice, act on other tissue compo-nents, including carbohydrates, DNA, and RNA”

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12
Q

Acute pancreatitis is pathologically marked by:

A

Acute pancreatitis is pathologically marked by massive edema, hemorrhage, and necrosis of the pancreas (Figure 12-3).

The pancreas appears swollen and is permeated with blood.

Yellow or smudgy brownish-yellow areas of necrosis appear 2 to 3 days after the onset of the attack.

The leakage of digestive enzymes into the abdominal cavity may cause peritoneal irritation, and chemical peritonitis may ensue.

Areas of fat necrosis appear as grayish-yellow discolorations that gradually calcify and become whitish.

By the end of the first week, pseudocysts appear as small cavities filled with liquefied tissue and pancreatic enzymes. These small cavities coalesce into larger pseudocysts, which are typically found in patients who survive the initial attack”

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13
Q

Major complications of acute pancreatitis

A
  1. )Peritonitis complicating acute pancreatitis is typi-cally caused by chemicals and the fluid does not contain bacteria. As already mentioned, it results from the spilling of digestive enzymes from the damaged pancreas.
  2. )Cystic changes resulting from the destruction of the parenchyma of the pancreas are common. When small fluid filled spaces become confluent, larger pseudocysts form. These pseudocysts may replace large portions of the pancreatic parenchyma or may distend the pancreas, compressing and displacing the duodenum or the stomach. The granulation tissue forming the capsule of the pseudocyst will become increasingly fibrotic over time until finally these cystic structures assume the appearance of leather bags filled with murky semifluid material (Figure 12-5).

•Pancreatic abscess develops when the area of pancreatic necrosis becomes infected by the bacteria from the gastrointestinal (GI) tract. In contrast to pseudocysts, which contain liquefied tissue debris and enzymes, the cystic spaces within the liquefied bacte-rial abscess contain pus admixed to bacteria. Like the pseudocyst, pancreatic abscess will be walled off by granulation tissue, which with time becomes more and more fibrotic.

Chronic pancreatitis

Diabetes

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14
Q

Clinical Features of Pancreatitis

A
  • sudden onset
  • abdominal pain, distention, vomiting
  • uncontrolable pain, sweating
  • syncope and shock are in severe disease
  • peritoneal regidity signals peritonitis, which often goes with illieus
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15
Q

Diagnosis of acute pancreatitis

A

leukocytosis

Increased serum lipase and amylase

pancreatic enzymes are also found in urine

biochemical markers 24-72hrs after injury

CT for swelling in pancreas

no effective tx., efforts to minimize damage and prevent shock

-mortality 20%, symptoms of chronic in surviving patients is 20%

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16
Q

What is chronic panreatitis?

A

Characterized by irregular fibrosis replacing normal pancreatic paranchyma

progressive and irreversible, produce exocine and endocrine insufficiency

male to female 3:1

insidious onset, difficult to determine cause, alcohol for 70% of cases. Difficult to determine why some alcoholics develop disease and some do not.

most cases slow and inperceptable

20% have no risk factors

17
Q

Pathology on examination

A

On gross examination, the pancreas does not show typical lobulation but appears smaller, shriveled, and very firm on palpation.

The main pancreatic duct is usually dilated and often contains stones

On cross section, white fibrous tissues may be seen replacing the grayish paren-chyma and extending from the pancreas into the surround-ing fat tissue.

Fibrosis of the pancreas may cause distortion and the common bile duct, duodenum, or pylorus. The common bile duct may become completely obstructed.

18
Q

Chronic pancreatitis can lead to

A
19
Q

Signs of chronic pancreatitis

A
  1. Pain. This is related to the entrapment of nerves in the fibrous tissue, which often extend into the celiac plexus. Fibrosis may cause stenosis of the duodenum, which impedes the passage of food from the stomach into the duodenum, causing pain after eating.
  2. Exocrine pancreatic insufficiency. Destruction of acinar cells reduces the capacity of the pancreas to produce digestive enzymes, which results in malabsorption and steatorrhea. Lack of trypsin and chymotrypsin results in malabsorption of proteins. Lipase deficiency accounts for the fatty stools and inappropriate absorp-tion of fat and fat-soluble vitamins (A, D, K, and E). Most patients lose weight and feel weak. Signs of vitamin deficiency, such as night blindness, secondary to avitaminosis A, or a bleeding tendency, secondary to avitaminosis K, are seen in severe cases.

•Endocrine insufficiency. Destruction of the islets of Lang-erhans occurs at a slower rate than does the loss of exocrine pancreatic cells. Nevertheless, in later stages of the disease more than 70% of patients have signs of diabetes mellitus”

20
Q

Adenocarcinoma of the pancreas

-risk factors

A

4th major cause of death in males, 5th in females

Risk factors not clearly defined: smoking

chronic pancreatitis can increase risk

disease of old age

21
Q

Location of pancreatic cancers

A

-tumors of the pancreatic head tend to obstruct the bile duct and cause jaundice

22
Q

Metastases in pancreatic cancer

A

At time of dx

40% lymph

40% distant organs

20% limited to pancreas

23
Q

Symtpoms of pancreatic cancer

A

Non specific: weight loss, n&v, loss of appetite

Depend on location of the tumor: upper abdominal pain suggests pancreas

tumors of pancreatic head obstruct the pancreatic head obstruct the comon bile duct and cause jaundice. The gallbladder may be dilated and palpated on physical exam (Couvoisiers sign).

Tumors of body and tail do not cause jaundice, but invade celiac plexus and cause pain

Splenomegaly may occur as a result of obstruction of splenic vien

Migratory thrombophlebitis (Trousseaus sign)

Liver metastases cause enlargement of liver

Metasteses of duodenum cause obstruction

Peritoneal seeding causes ascites and protruding abd.

24
Q

Tumors of the endocrine pancreas

A

Called islet cell tumors

rare, usually low grade malignant or benign

usually hormonally active - used to determine diagnosis of which cells are involved (any 4 cell types in the inslet of L.)

most common insulinomas, followed by gastrinomas

glucagonomas, somatostatinomas, and vasoactive polypeptide secreting tumors are less common

25
Q

Cells in the pancreas

A

Alpha: glucagon (20%)

Beta: Insulin (70%)

Delta: somatostatin and polypeptide (10%)

26
Q

Definition of DM

A

Heterogenous group of systemic disorders characterized by hyperglycemia, complex disturbances of carbohydrate, lipid, and protein metabolism, and a variety of organic changes related to blood vessel pathology

Consequence of relative or absolute insulin deficiency, or abnormal response of target cells to insulin

27
Q

Most important causes of metabolic disturbances in DM

A
  1. )An absolute deficiency of insulin (e.g., lack of beta cells secondary to islet cell destruction)
  2. ) A relative deficiency of insulin (e.g., when the demand for insulin exceeds the supply)
  3. ) Interference with insulin binding to target tissues (e.g., tissue resistance to insulin as a result of faulty insulin receptors or antibodies to insulin or insulin receptors”
28
Q

Insulin

A

Produced in the beta cells in the islet of L.

Inulin is secreted during hyperglycemia by promoting its release in the liver cells for glycolysis and glycogenesis of serum glucose

insul also stimulates influx of glucose in striated muscle for energy

stimulates the synthesis of proteins from amino acids

stimulates fat formation from triglycerides in fat cells (lipogensis)

all these are mediated by the activated of cellular insulin receptors

29
Q

Insulin effects can be partically counteracted by

A

glucagon

pituitaru growth hormone

steriod hormones

epi

30
Q

Excess glucose results in

A

spills over into urine- glycosuria

leads to osmotic diuresis and polyuria

31
Q

Lacticacidosis

A

Utilization of glucose in stiated muscle is impaired

Use of anearobic glycolysis instead of oxidative aerobic glycolysis is used for energy production

Results in excessive lactic acid

32
Q

Ketoacidosis

A

Inadequate utilization of fats and reduced lipogenesis result in accumilation of free fatty acids which are oxidized into ketones

Ketogenesis is another cause of acidosis

33
Q

Hyperglycemia and other tissues

A
34
Q
A