Pathology - S2B2 - Pancreas 1

Front 1

What is the anatomical location of the Pancreas?

Back 1

Retroperitoneal

**except the tail

Front 2

80-85% of the glands in the Pancreas are __1__ cells organized into acini that drain into the __2__

Back 2

1. Secretory

2. Duct of Wirsung = Main pancreatic duct

Front 3

The Duct of Wirsung normally drains into the __1__ just proximal to the __2__, but may enter the duodenum directly

Back 3

1. Common Bile Duct

2. Ampulla of Vater

Front 4

What will a gallstone stuck at the Ampulla of Vater normally cause?

Back 4

reflux of bile into the pancreatic duct

Front 5

2 important enzymes that are detectable in the serum after Pancreatic damage

Back 5

1. Lipase

2. Amylase

Front 6

Stimulation of this nerve increases the Pancreatic excretion

Back 6

Vagus nerve

Front 7

What 2 things stimulate the release of Cholecystokinin?

What causes the release of Secretin?

Back 7

Presence of Amino acids and pH < 3 -> Cholecystokinin -> stimulates pancreas to release digestive enyzmes from Acinar cells

Stomach distension -> Secretin -> stimulates pancreas to release Bicarbonate and Water from Ductal cells

Front 8

What do most cancer of the Pancreas arise from?

Back 8

Pancreatic Ducts (Ductal Adenocarcinoma)

Front 9

Pancreatitis: __1__ inflammatory condition of the __2__ pancreas that results from cellular injury to __3__ cells

Back 9

1. Reversible
2. Exocrine
3. acinar

Front 10

Describe how a person would present with Acute/Chronic Pancreatitis

Back 10

Severe, boring Mid-Epigastric and LUQ abdominal pain radiating to the back

Front 11

What are the 2 most common causes of Acute Pancreatitis?

Back 11

1. Alcohol (6 times more common in MEN)

2. Gallstones (3 times more common in women)

Front 12

List 5 complications of Acute Inflammation of the Pancreas

Back 12

1. Shock = pancreatic enzymes eating through the Splenic Artery
2. Peritonitis
3. Hypocalcemia = Ca+ soaps formed during fat necrosis
4. Malabsorption
5. Pseudocyst formation

Front 13

What are the 2 elevated lab findings in Pancreatitis? Which one is elevated first? Which one is more specific for Pancreatitis?

Back 13

Amylase and Lipase

First: Amylase

Specific: Lipase

Front 14

What can Hypocalcemia result in?

What is the cause of Hypocalcemia?

Back 14

Tetani and seizures

Saponification reaction (Ca+ reacting with Fatty acids) in Acute Hemorrhagic Pancreatitis Fat Necrosis

Front 15

What is Chronic Pancreatitis associated with? (3)

Back 15

Alcohol ingestion

Hemochromatosis

Cystic Fibrosis

Front 16

What are 3 complications of Chronic Pancreatitis?

Back 16

1. Pseudocyst formation

2. Malabsorption (Vitamin B12 deficiency)

3. Diabetes

Front 17

Cystic Fibrosis:
-lack of __1__ secretion is linked to impaired secretion of __2__, resulting in unusually viscid secretions
-__3__ of the Pancreas ensues, with resultant __4__ and failure to thrive
-death is almost always due to __5__ complications

Back 17

1. chloride
2. sodium and water
3. Atrophy
4. malabsorption
5. pulmonary

Front 18

Islet cells that secrete Glucagon

Back 18

Alpha cells

Front 19

Islet cells that secrete Insulin

Back 19

Beta cells

Front 20

What groups of people is Type I Diabetes Mellitus most common in?

Races less common in

Back 20

Northern Europeans

Asians, African-Americans, & Native Americans

Front 21

When has Type I DM been noticed to increase in incidence in several studies?

Back 21

Late fall and early winter

Front 22

What HLA do 95% of Type I DM patients express?

Back 22

DR3 or DR4

**compared to only 20% of the population expressing these HLAs

Front 23

__1__ antibodies are detectable in most Type I diabetics, but likely represents a __2__ response to proteins released by destruction of beta cells by __3__

Back 23

1. Beta cells
2. humoral
3. T lymphocytes

Front 24

Seasonal variation of Type I DM in incidence suggests ______ as a possible cause of the abnormal immune response to beta cells

Back 24

Viral infections

Front 25

What are the 2 major risk factors for Type I DM?

Back 25

1. immediate family member with Type 1 DM

2. Caucasians are at a greater risk than other ethnic groups

Front 26

What is the pathology seen in Type I DM?

Back 26

1. Insulitis = inflammation of the islet

2. Beta cell depletion

3. Diffuse fibrosis of the pancreas

Front 27

Most of the pathology seen in Diabetes Type I is due to the __1__, which are thought to be related to the long-term deleterious effects of __2__

Back 27

1. complications

2. Hyperglycemia

Front 28

Normal Pancreas
-ducts are within fibrous septa
-Islets of Langerhans

Back 28

What is this picture showing?

Front 29

Normal Pancreas histology
-Acini of the Exocrine pancreas

Back 29

What is this showing?

Front 30

Isle of Langerhans

Back 30

What is this showing?

Front 31

Acute Edematous Pancreatitis
-edema and inflammatory infiltrate

Back 31

What is this showing?

Front 32

Pancreatic Pseudocyst from Acute Pancreatitis

Splenic Artery bleeding into the pseudocyst

Back 32

What can be seen here?

What could cause it to pulsate?

Front 33

Pancreatic Pseudocyst

Back 33

What is seen here?

Front 34

Hemorrhagic Pancreatitis

Back 34

What can be seen here?

Front 35

Hemorrhagic Pancreatitis

Back 35

What is shown here?

Front 36

Fat Necrosis with formation of calcium-fatty soaps

Back 36

What is this showing?

Front 37

Chronic Pancreatitis with punctate calcifications

Back 37

What is shown here?

Front 38

Chronic Pancreatitis

Back 38

What is shown here?

Front 39

Chronic Pancreatitis

Back 39

What is shown here?

Front 40

Chronic Pancreatitis

Absence of acinar structures & replacement by pink collagen = FIBROSIS

Back 40

What is this showing? How do you know?

Front 41

Cystic Fibrosis, P. aeruginosa, & Bronchiectasis

Back 41

What are the 3 associations here?

Front 42

Cystic Fibrosis in the Pancreas
-ducts are dilated, with fibrosis surrounding them

Back 42

What is this showing?

Front 43

Alpha cells = Glucagon

Beta cells = Insulin

Back 43

What cells are on the left & what do they secrete?

What cells are on the right & what do they secrete?

Front 44

Type I Diabetes Mellitus = Insulitis

Back 44

What is shown here?

Front 45

What are 7 risk factors for Type II Diabetes?

Back 45

1. Obesity
2. Age (generally >30)
3. family history of diabetes
4. lack of regular exercise
5. high BP &/or high conc. of fats in blood
6. history of gestational diabetes or giving birth to a baby weighing > 9 lbs.
7. Blacks, Hispanic, N. Americans, & Asian-Americans

Front 46

Describe the pathogenesis of Type II Diabetes (Non-Insulin Dependent)

Back 46

-Genetically programmed failure of Beta cells to compensate for peripheral insulin resistance
-Multifactorial inheritance
-Altered Beta cell function
-Insulin resistance = may have increased amounts of Insulin, but decreased # receptors (or non-responsive)

Front 47

Describe the pancreatic pathology of Type II Diabetes

Back 47

-No reduction in Beta cells

- May have increased islet fibrosis or Amyloidosis

Front 48

What is the stain for Amyloid?

Back 48

Congo Red stain

Front 49

Type II Diabetes with Amyloid infiltration of the Islet

Back 49

What is shown here?

Front 50

What are the treatments for Type II Diabetes?

Back 50

1. Diet
2. Weight loss and exercise
3. Hypoglycemic drugs
4. Eventually Insulin

Front 51

What is the mode of action for Metformin?

Back 51

makes muscle cells and fat cells utilize glucose in the peripheral tissue

Front 52

What is the mode of action for Sulfonylureas and Thiazolidinediones?

Back 52

Stimulate pancreas to make more insulin

Front 53

-

Back 53

-

Front 54

Describe the pathogenesis leading to the complications seen in Diabetes

Back 54

Nonenzymatic protein glycosylation through the polyol pathway

Front 55

Explain the accelerated atherosclerosis as a complication of diabetes

Back 55

-

Front 56

Nodular Glomerulosclerosis = Kimmelstiel-Wilson disease
-pink nodules

ACE inhibitors

Back 56

What is shown here?

What can prevent this complication?

Front 57

Papillary Necrosis = diabetes affects small vessels and end arteries

Papilla can slough off and occlude to ureter = hydroureter and kidney swelling

Back 57

What is shown here? What is there risk of?

Front 58

Describe the characteristics of Background Retinopathy

Back 58

1. Hemorrhages
2. Microaneurysms
3. "cotton-wool" exudates
4. DOES NOT NORMALLY IMPAIR VISION!!

Front 59

What is the pathogenic cause of Diabetic Retinopathy?

Back 59

Osmotic damage

Front 60

Background Retinopathy
-follow the vessels out
-vessels are thicker than normal and hemorrhaging can be seen
-Starburst cotton-wool spots are seen at 3 o'clock

Back 60

What is shown here?

Front 61

What is Proliferative Retinopathy?

Back 61

Neo-vascular proliferation in the retina, which OBSCURES vision

Front 62

What are common complications of Proliferative Retinopathy?

Back 62

Retinal detachment and blindness

Front 63

Proliferative Retinopathy

Back 63

What is shown here?

Front 64

Proliferative Retinopathy with Microaneurysms (due to Osmotic damage from increased Sorbitol)

Back 64

What is seen here?

Front 65

What is another name for Gallstones?

Back 65

Cholelithiasis

Front 66

What are the 10 F's that are associated risk factors for Cholesterol or Mixed Gallstones?

Back 66

1. Fat = obese
2. Forty and above
3. Fertile = multiparous
4. Flatulent = intestinal disease or malabsorption
5. Female

with Fatty, Foul, Fetid, Floating Feces

Front 67

What drugs can cause an increased risk for Cholesterol or Mixed Gallstones (Cholelithiasis)?

Back 67

Cholesterol-lowering drugs
- Clofibrate
- Cholestryramine

Front 68

When would a man be at an increased risk for developing Cholesterol Gallstones?

Back 68

if he was on hormone therapy to treat Prostatic Carcinoma

Front 69

What ethnicities are at increased risk for Cholesterol/Mixed Gallstones?

Back 69

Pima & Navajo Indians

Scandinavian countries & Latin America

Front 70

List 4 examples of GI tract disorders that could lead to Cholesterol/Mixed Gallstones

Back 70

1. Malabsorptive disorder
2. Ileal resection for obesity
3. Cystic Fibrosis with Pancreatic insufficiency
4. Chronic Diarrheal states

Front 71

What are the risk factors associated with Pigmented Gallstones?

Back 71

1. Hemolytic anemias
2. Alcoholic Cirrhosis
3. Infected bile (E. coli)
4. Parasitic infections

Front 72

Examples of Hemolytic Anemias or Hemoglobinopathies that can cause Pigmented stones

Back 72

1. Malaria
2. Sickle Cell anemia
3. Polycythemia vera

Front 73

What Parasitic infections can cause Pigmented (bilirubinate) stones?

Back 73

Ascaris or Clonorchis sinensis

Front 74

What is the most common type of Gallstone?

Back 74

Mixed stone = composed primarily of cholesterol but also contain variable amounts of bilirubin and calcium salts

Front 75

What clinical manifestation is characteristic of Cholelithiasis?

Back 75

fatty food intolerance

Front 76

What is the most common stone associated with Cholecystitis?

Back 76

Mixed stone

Front 77

What is the most common cause of both Acute and Chronic Cholecystitis?

Back 77

Gallstones
-80% of acute
-90% of chronic

Front 78

How do you diagnose Cholecystitis?

Back 78

Murphy's sign = inspiratory arrest in response to palpation of the RUQ during deep inspiration

Front 79

Acute Cholecystitis
-fibrinous exudates
-red, congested = inflammation

Back 79

What is shown here?

Front 80

Cholecystitis with stones (cholelithiasis)

Back 80

What is seen here?

Front 81

Cholecystitis with cholelithiasis

Back 81

What is seen here?

Front 82

Porecelain Gallbladder
-due to Dystrophic Calcification of the gallbladder
-late complication of Chronic Cholecystitis

Back 82

What is seen here?

Front 83

Porcelain Gallbladder
-consequence of transmural chronic inflammation
-extensive fibrosis during the repair phase with scarring and DYSTROPHIC CALCIFICATION

Back 83

What is seen here?

Explain the pathogenesis

Front 84

What 2 things are present in 75-90% of cases of Carcinoma of the gallbladder?

Back 84

Chronic Cholecystitis

Cholelithiasis

Front 85

What is a high-risk condition for Gallbladder Adenocarcinoma?

Back 85

Porcelain gallbladder

Front 86

Gallbladder Adenocarcinoma:
1. Gender preference
2. Age preference
3. Ethnic distribution
4. 5 year survival

Back 86

1. Female:Male = 2:1
2. Average age = 65
3. Pima and Navajo indians
4. 1% five-year survival

Front 87

Gallbladder Adenocarcinoma
-opened up, thicker than normal
-fibrotic area

Back 87

What is seen here?

Front 88

Gallbladder Adenocarcinoma
-Left: GB is thickened
-Right: glandular structures indicating Adenocarcinoma

Back 88

What is shown here?

Front 89

What is the difference b/w Acute Interstitial Pancreatitis & Acute Hemorrhagic Pancreatitis?

Back 89

Interstitial = mild inflammation characterized by widening edema and widening of interstitial spaces that contain scattered inflammatory cells

Hemorrhagic = Pancreatic Acinar cell injury results in activation of pancreatic enzymes and enzymatic destruction of pancreatic parenchyma

Front 90

What are the most common drugs associated with causing Acute Pancreatitis?

Back 90

1. Azathiopurine
2. Mercaptopurine
3. Corticosteroids
4. high dose Estrogen

Front 91

Pseudocyst:
-massive necrosis leads to __1__ necrosis of the pancreatic tissue, which becomes enclosed by __2__.

Back 91

1. liquefactive

2. Granulation tissue

Front 92

What are 5 systemic complications of Acute Hemorrhagic Pancreatitis?

Back 92

1. Shock = due to increased vascular permeability caused by pancreatic enzymes

2. DIC = pancreatic enzymes in circulation leads to formation of platelet and fibrin thrombi in small vessels

3. ARDS = due to enzymatic injury of the alveolar-capillary units in the lung -> hyaline membranes

4. Renal failure = due to shock

5. Subcutaneous Fat Necrosis = due to lipase enzymes from pancreas

Front 93

Explain Fat Necrosis and the Saponification reaction

Back 93

Acute Hemorrhagic Pancreatitis causes release of Lipases which digest Fat, releasing Fatty acids which form Calcium soaps

Front 94

Define Chronic Pancreatitis

Back 94

Chronic inflammation with FIBROSIS leading to a progressive loss of pancreatic function
-reduction in size
-often shows calcifications

Front 95

What do pigmented stones result from?

Back 95

precipitation of excess insoluble unconjugated Bilirubin

Hemoglobin -> Heme -> Biliverdin -> Bilirubin

Front 96

What is the most common primary tumor of the Gallbladder?

Back 96

Adenocarcinoma of the Gallbladder

Front 97

Type of Diabetes that may cause Ketoacidosis?

Back 97

Type 1 Insulin Dependent Diabetes