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Endocrine Exam > Endocrine Pancreas Pathology > Flashcards

Endocrine Pancreas Pathology Flashcards

1
Q

What is glucose homeostasis regulated by?

A
  • Hepatic release of glucose
  • Tissue utilization of glucose
  • Hormonal control of glucose by insulin and glucagon
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2
Q

What is the regulation of insulin release?

A
  1. GLUT-2 takes glucose into beta cells
  2. Glucose metabolism generates ATP
  3. ATP inhibits the membrane K+ channel
  4. Depolarization results in Ca2+ influx
  5. Ca2+ influx results in insulin release
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3
Q

How is insulin processed?

A
  • Proinsulin is cleaved in the beta cell to form insulin and C-peptide
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4
Q

What is C peptide?

A
  • A marker of endogenous insulin

- Can differentiate from insulin administered as a pharmaceutical agent

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5
Q

What does insulin do in adipose tissue?

A
  • Increase glucose uptake
  • Increase lipogenesis
  • Decrease lipolysis
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6
Q

What does insulin do in striated muscle?

A
  • Increase glucose uptake
  • Increase glycogen synthesis
  • Increase protein synthesis
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7
Q

What does insulin do in the liver?

A
  • Decrease gluconeogenesis
  • Increase glycogen synthesis
  • Increase lipogenesis
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8
Q

What are the incretins?

A
  • Glucagon like peptide (GLP-1)

- Glucose-dependent insulin-releasing polypeptide (GIP)

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9
Q

What is the MOA of incretins?

A
  • Stimulate insulin release and inhibit glucagon release resulting in lower blood glucose
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10
Q

What inactivated incretins?

A
  • Dipeptidyl peptidase-4 (DPP-4)
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11
Q

What causes type 1 diabetes?

A
  • Autoimmune disease due to failure of T-lymphocyte self tolerance
  • T-lymphocytes directed against antigens on the pancreatic beta cells
  • After initial insult, damaged beta cells evoke autoimmune reponse
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12
Q

What is a major link in type 1 diabetes?

A
  • MHC class II genes –> susceptibility loci

- HLA gene cluster on chromosome 6p21, responsible for as many as 50% of T1DM

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13
Q

How do genetics and environment affect type 2 diabetes?

A
  • Majority of patients with T2DM have a first degree relative with T2DM
  • Major risk factor is obesity
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14
Q

What is maturity-onset diabetes of the young (MODY)?

A
  • Resembles T2DM clinically, but happens in youth
  • Blood insulin may be high, normal, or low
  • No autoantibodies
  • Nonketotic
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15
Q

What is the genetic linkage in MODY?

A
  • Most often caused by mutations resulting in loss of function of glucokinase
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16
Q

What are some risks to the fetus in gestational diabetes?

A
  • Neonatal hypoglycemia causing seizures and brain damage
  • Macrosomia
  • Congenital malformations
  • Stillbirth
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17
Q

What is a risk to the mother in gestational diabetes?

A
  • Cesarean section
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18
Q

What is the classic triad fo T1DM?

A
  • Polyphagia
  • Polyuria
  • Polydipsia
  • Severe: diabetic ketoacidosis
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19
Q

How is T2DM usually identified?

A
  • On screening

- Fatigue, vision changes

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20
Q

Who are the autoantibodies checked for diabetes?

A
  • Present in >90% of caucasian children

- Present in <50% of african american and hispanic children

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21
Q

What HLA typing is done for diabetes?

A
  • HLA DR/DQ on chromosome 6
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22
Q

What is the triad of diabetic ketoacidosis?

A
  • Hyperglycemia
  • Ketonemia
  • Metabolic acidosis
23
Q

Who has diabetic ketoacidosis most often?

A
  • More typical of T1DM
24
Q

What are some causes of diabetic ketoacidosis?

A
  • Non-compliance most common underlying etiology

- Precursor infections common (pneumonia or UTI)

25
Q

What is a way to test for diabetic ketoacidosis?

A
  • Test for ketones in the urine
  • Acetoacetic acid
  • Beta-hydroxybutyrate
26
Q

What are some presenting signs of DKA?

A
  • Nausea/vomiting
  • Tachycardia
  • Kussmaul respirations
27
Q

What is hyperglycemic hyperosmotic syndrome (HHS)?

A
  • Acute hyperglycemic crisis in T2DM
28
Q

What causes HHS?

A
  • Culmination of prolonged insulin deficiency
  • Increased gluconeogenesis
  • Decreased glucose uptake in peripheral tissues
29
Q

What are the presenting symptoms of HHS?

A
  • Glucose >600 mg/dL
  • Severe dehydration
  • Hyperosmolality –> obtundation, coma
  • Impaired renal function
30
Q

What is hemoglobin A1C?

A
  • Irreversible glycosylation of the hemoglobin tetramer

- Measure of long term diabetic control, since binding takes over 1 month

31
Q

What is a target A1C?

A
  • 6.5-6.7 or lower
32
Q

What does chronic hyperglycemia increase the risk of?

A
  • Stroke
  • MI
  • Lower extremity gangrene
33
Q

What is the most common cause of death in diabetics?

A
  • MI
34
Q

What is the screening done in diabetic nephropathy?

A
  • Use albumin:creatinine ratio in urine
35
Q

What are the three primary pathologic conditions that could occur due to diabetes?

A
  • Glomerular sclerosis
  • Renal vasculature lesions
  • Pyelonephritis
36
Q

What is glomerular sclerosis?

A
  • Thickening of the basement membrane
  • Disruption of the protein cross-linkage that normally makes the membrane an effective filter
  • In consequence, there is a progressive leak of large molecules into the urine
37
Q

What occurs in diabetic retinopathy?

A
  • Neovascularization
  • Hypoxia leads to VEGF overexpression
  • Hemorrhage
  • Blindness
  • Cataracts
  • Glaucoma
38
Q

What is a chronic diabetic complication?

A
  • Neuropathy
  • Distal symmetric polyneuropathy
  • Autonomic neuropathy
  • Diabetic mononeuropathy
39
Q

What are diabetics are an increased risk for?

A
  • Cellulitis
  • Pneumonia
  • Pyelonephritis
40
Q

What are some unifying features of pancreatic neuroendocrine tumors?

A
  • Gross appearance –> solid, tan-yellow
  • Predilection for the pancreatic neck and tail
  • Histology –> well-differentiated neuroendocrine tumors
  • EM – secretory granules
41
Q

What is an insulinoma?

A
  • Small tumors that can produce episodes of symptomatic hypoglycemia
  • Amyloid is a common finding
  • C peptide levels can make diagnosis
42
Q

What is the triad for a gastrinoma?

A
  • Islet cell tumor
  • Gastric acid hypersecretion
  • Peptic ulceration
43
Q

What is a clue to clinical diagnosis for a gastrinoma?

A
  • Ulcers do not respond to conventional therapy
44
Q

What is a gastrinoma also called?

A
  • Zollinger-Ellison syndrome
45
Q

What is seen in somatostatinomas?

A
  • Diabetes
  • Cholelithiasis
  • Steatorrhea
46
Q

What are manifestations of a somatostatinoma? Why?

A
  • Reduced insulin
  • Reduced gallbladder motility
  • Reduced exocrine pancreatic secretions
  • This is all due to somatostatin being a paracrine regulator (usually inhibitory)
47
Q

What is seen in a glucagonoma?

A
  • Mild diabetes

- Necrolytic migratory erythema (groin and LE)

48
Q

What are the 4 D’s of glucagonomas?

A
  • Diabetes
  • Dermatitis
  • Depression
  • DVT’s
49
Q

What is seen in VIPomas?

A
  • Watery diarrhea
  • Hypokalemia
  • Achlorhydria
  • WDHA syndrome
  • Flushing
50
Q

What cell of the pancreas is involved with an insulinoma?

A
  • beta
51
Q

What cell of the pancreas is involved with a gastrinoma?

A
  • G
52
Q

What cell of the pancreas is involved with a somatostatinoma?

A
  • Gamma
53
Q

What cell of the pancreas is involved with a glucagonoma?

A
  • alpha
54
Q

What cell of the pancreas is involved with a VIPoma?

A
  • D1

Endocrine Exam (11 decks)

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