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Endocrine II - Exam 1 > Pancreas Pathology - MT > Flashcards

Pancreas Pathology - MT Flashcards

1
Q

What are the cell types of the Endocrine pancreas?

What do they secrete?

What do the secretions cause to occur?

A
  1. Beta cells, insulin, lowers blood glucose levels
  2. Alpha cells, glucagon, increase blood glucose levels
  3. Delta cells, somatostatin, suppress insulin and glucagon release
  4. PP cells, pancreatic polypeptide, GI stim secretion of gastric/intestinal enzymes and inhibits intestinal motility
  5. DI cells, vasoactive intestinal polypeptide, hyperglycemia and GI fluid secretion and secretory diarrhea
  6. Enterochromaffin cells, serotonin, source of pancreatic tumor with carcinoid syndrome
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2
Q

Recognize Slide and EM histology of granule types of different cells

A

slide 5 of ppt.

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3
Q

In the United States, Diabetes Mellitus is the leading cause of what 3 things?

A

End stage renal disease (nephrosclerosis)

Adult onset blindness

Non-traumatic lower extremity amputations from atherosclerosis of arteries

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4
Q

What is the term for a group of metabolic disorders sharing common feature of hyperglycemia?

A

Diabetes mellitus

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5
Q

What is normal blood glucose range?

A

70-120 mg/dL

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6
Q

How do you arrive at the diagnosis of DM? (types of measurements and their values)

A
  • Fasting plasma glucose >= 126 mg/dL
  • Random plasma glucose >=200 mg/dL
  • 2 hour plasma glucose >=200 mg/dL during oral glucose tolerance test OGTT with loading dose 75 gm
  • HbA1C (glycated Hb) level >=6.5%
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7
Q

What blood glucose levels characterize a prediabetic patient? (Impaired glucose tolerance)

A
  • Fasting plasma glucose b/t 100 and 125 mg/dL (impaired fasting glucose)
  • 2 hour plasm glucose b/t 140 and 199 mg/dL following a 75 gm glucose OGTT
  • HbA1C b/t 5.7% and 6.4%
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8
Q

What causes Type I DM? (pathogenesis)

A

Autoimmune disease processIslet destruction primarily by immune effector cells against endogenous Beta cell antigens

d/t

Failure of self tolerance in T cells specific for islet antigens

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9
Q

Age group affected by Type I DM

A

Can occur at any age (previously thought to affect younger persons under 18)

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10
Q

What causes Type II DM? (pathogenesis)

A
  • combination of:peripheral resistance to insulin
  • inadequate secretory response by pancreatic Beta cells (genetic)
  • Proinflammatory state
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11
Q

predominant type of diabetes in the diabetic population is?

A

DM II, most are overweight

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12
Q

why is prevalence of type 2 DM increasing in adolescents?

A

Obesity

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13
Q

subtypes of type I DM?

A

Immune mediatedIdiopathic

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14
Q

Defining clinical feature of DM type I?Defining Pathology?

A
  • Circulating islet autoantibodies(anti- insulin, anti-GAD, anti ICA512)
  • Diabetic ketoacidosis in absence of insulin therapy
  • Insulitis (Islet inflammatory infiltrate of T cells and Macrophages)
  • Beta cell depletion, islet atrophy
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15
Q

Defining clinical feature and pathology of DM type II?

A

Obese patients,Non ketonic hyperosmolar comas more common

no Insulitis

Amyloid deposition in islet

mild Beta cell depletion

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16
Q

Recognize islet lymphocytic infiltration in Type I DM

A

slide 12

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17
Q

Recognize deposition of amyloid in islet in Type II DM

A

slide 13

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18
Q

What does the honeymoon period in Type I DM refer to?

A

initial 1-2 years following onset of overt Type I DM- exogenous insulin requirements may be minimal b/c of ongoing endogenous insulin secretion

  • After this period, any residual Beta cell reserve is exhausted and inulin requirements increase dramatically
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19
Q

What event can hasten Beta cell destruction, which promotes transition from impaired glucose tolerance to over diabetes? (usually prolonged process)

A
  • Infection (associated w/ increased insulin requirements)
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20
Q

Stages in development of Type I DM are?(precipitating events)

A
  • Genetic predisposition
  • Overt immunologic abnormalities (nml insulin release)
  • Progressive loss insulin release (glucose nml)
  • Overt diabetes
21
Q

What may drive a patient with type 2 DM to get medical attention?

A
  • unexplained fatigue
  • dizziness
  • blurred vision
22
Q

Most of the time, when is the diagnosis of type 2 DM made?

A
  • after routine blood testing in asymptomatic persons

*routine glucose testing recommended for everyone older than 45

23
Q

What is the classic triad of Type I diabetes?

A

Polyuria, polydipsia, polyphagia (urination, thirst, hunger)

*when severe DKA can present

24
Q

DKA arises in insulin deficient or resistant patients b/c?

A

Glucose stores cannot be utilized in muscle, fat, or liver tissue this leads to increased lipolysis and use of FFAs in Ketogenesis in the liver which produces Ketoacidosis presenting as diabetic coma and ketonuria

25
Q

Chronic complications of Diabetes (either type)

A
  • Diabetic Macro and microvascular disease by chronic hyperglycemia
  • Macrovascular disease–> accelerated atherosclerosis–> MI, Stroke (cerebrovascular incidents), Lower extremity ischemia (Gangrene)
  • Microvascular disease–> retinopathy, nephropathy, neuropathy
26
Q

Be familiar with characteristic histology of Type I and Type II DM

A
  • type I has lymphocytic T cell invasion of islets
  • type II has amyloidosis of pancreatic islet
27
Q

Most common cause of death in diabetics is?

A

MI (Macrovascular)

28
Q

What can occur in the kidneys of diabetics?

A

Kimmelstiel Wilson disease (Diabetic nephropathy):

  • glomerular lesions
  • Renal vascular lesions, hyaline arteriolosclerosis
  • Pyelonephritis, necrotizing papillitis
29
Q

What can occur in the eyes of a diabetic patient?

A

hyperglycemia leads to opacification of lens (CATARACTS)

most profound changes are seen in retina

(Diabetic retinopathy)

30
Q

What is the leading cause of End stage renal disease in the United states?

A

Diabetic nephrpathy

31
Q

Sx of Diabetic Neuropathy?

A
  • Burning and tingling pain from distal symmetric polyneuropathy

(affects both sensory an motor function)

  • Sores that develop do not hurt
32
Q

Diabetics are more at risk for what?

A
  • Infections of skin
  • Tuberculosis
  • Pneumonia
  • Pyelonephritis
33
Q

What is a PanNET?

A

Pancreatic neuroendocrine tumor (tumors of pancreatic islet cells, islet cell tumors)

34
Q

critieria for malignancy of PanNETs include?

A
  • metastases
  • vascular invasion
  • local infiltration
35
Q

What is the likelihood of functional insulin secreting PanNET tumors being malignant?

A
  • 90% functional insulin secreting PanNETs are benign

* 60-90% other functioning and non functioning pancreatic endocrine neoplasms are malignant

36
Q

3 most common and distinct clinical syndromes of functional PanNETs

A
  • Hyperinsulinism
  • Hypergastrinemia and zollinger ellison syndrome
  • Multiple endocrine neoplasia (MEN)
37
Q

What is the most common type of Pancreatic endocrine neoplasm?

A

Beta cell tumors (Insulinomas)

38
Q

Clinical signs and sx of Insulinomas

A
  • hypoglycemic episodes where blood glucose can fall below 50 mg/dL of serum
  • confusion, stupor, loss of consciousness

*episodes precipitated by fasting or exercise, relieved by feeding

39
Q

PanNETs well differentiated (recognize picture)

A

slide 36

40
Q

Critical lab finding in the workup of insulinomas are?

A
  • high circulating levels of insulin
  • high insulin to glucose ratio
41
Q

Tx for Insulinoma?

A

surgical resection (usually shows improvement with reversal of hypoglycemia)

42
Q

What is Zolinger Ellison syndrome?

A
  • Gastrinoma (hypersecretion of gastrin usually d/t gastrin producing tumor)
43
Q

Where do gastrinomas usually arise?

A
  • duodenum, peripancreatic soft tissue, pancreas

(gastrinoma triangle)

44
Q

what is the association found in Zollinger Ellison syndrome?

A
  • pancreatic islet cell lesions
  • hypersecretion of gastric acid
  • peptic ulceration severe

* in 93% of patients with gastrinomas

45
Q

Clinical presentation of Gastrinomas

A
  • 50% patients have diarrhea
46
Q

Treatment of Gastrinomas

A
  • H+K+-ATPase inhibitors (PPIs)
  • Total resection of neoplasm when possible
47
Q

prognosis of patients with Gastrinomas

A
  • usually curable with resection
  • if hepatic metastases has occured, shortened life expectancy from progressive liver failure within 10 years
48
Q

Other rare PanNETs

A
  • alpha cell tumor:

incrased serum glucose

  • S cell tumor:

high plasma somatostatin, steatorrhea, DM association

  • VIPoma

watery diarrhea

all patients with severe secretory diarrhea should have a VIP assay performed

  • Pancreatic carcinoid tumor

Serotonin producing

Endocrine II - Exam 1 (6 decks)

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