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Endocrine 2 > Robbins - Endocrine Pancreas > Flashcards

Robbins - Endocrine Pancreas Flashcards

1
Q

Pancreatic polypeptide - function

A

Stimulates gastric and intestinal enzyme secretion, inhibits intestinal motility (constipation)

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2
Q

VIP - function

A

Induces glycogenolysis (hyperglycemia), stimulates gastrointestinal fluid secretion (secretory diarrhea)

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3
Q

Enterochromaffin cells - function

Tumor of these cells?

A

Secrete serotonin

Carcinoid syndrome

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4
Q

Diabetes mellitus –> secondary damage to _______

A

Kidneys, eyes, nerves, blood vessels

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5
Q

Diagnosing DM (4)

A
  • Fasting glucose > 126
  • Random glucose > 200
  • 2-hour glucose (OGTT) > 200
  • HbA1c > 6.5%
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6
Q

Why must serum glucose tests be repeated (except the random glucose)?

A

Acute stressors can cause transient hyperglycemia (infection, burn, trauma)

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7
Q

Diagnosing prediabetes (impaired glucose tolerance) (3)

How often does this become overt diabetes in 5 years?

A
  • Fasting glucose 100-126
  • 2-hour glucose (OGTT) 140-199
  • HbA1c 5.7-6.4

25% of the time

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8
Q

Anti-GAD, Anti-ICA512 autoantibodies

A

Type 1 DM

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9
Q

Insulin levels: type 1 vs type 2

A

Type 1: progressive decline

Type 2: elevated (early), then normal or decreased (late)

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10
Q

Most common symptom w/o treatment: type 1 vs. type 2

A

Type 1: ketoacidosis

Type 2: nonketotic hyperosmolar coma (HHS)

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11
Q

Genetics - type 1 vs. type 2

A

Type 1: HLA-DR3/4, HLA-DQ8 (bad), CTLA4, PTPN22, AIRE

Type 2: TCF7L2, PPARG, FTO (diabetogenic, obesity-related)

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12
Q

Membrane-bound granule w/ dense, rectangular core and distinct clear halo around the granule

A

Beta-cell (insulin)

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13
Q

How are DM type 1 and Hashimoto’s thyroiditis similar?

A

Both require T-cell self-tolerance breakdown, causing autoantibody formation

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14
Q

Insulitis

Seen in what?

A

Inflammatory infiltrate of T-cells and macrophages, causing beta-cell depletion and islet atrophy

Type 1 DM

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15
Q

Type 2 DM - what is seen in islets?

A

Amyloid deposition, mild beta-cell depletion

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16
Q

C-peptide

A

Peptide byproduct of insulin proteolytic activation in the Golgi complex of beta-cells

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17
Q

Can measure C-peptide levels in someone _______

A

Receiving exogenous insulin, to determine function of beta-cells

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18
Q

What all is required for the onset of autoantibody formation in type 1 DM?

A

Genetic susceptibility + environmental stimulus (virus, other)

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19
Q

Autoantibody targets in type 1 DM

A

Insulin, GAD enzyme, ICA512 (islet cell autoantigen)

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20
Q

How does obesity lead to insulin resistance?

A

Free fatty acids, adipokines, inflammation –> decreased insulin release and increased resistance of target tissues

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21
Q

Insulin resistance in:

  • Liver
  • Skeletal muscles
  • Fat
A

Liver = increased gluconeogenesis
Skeletal muscles = decreased glucose uptake
Fat = increased LPL activity –> excess circulating FFAs

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22
Q

Types of monogenic diabetes

A
  • Beta-cell function mutation

- Insulin receptor mutation

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23
Q

Most common form of beta-cell function mutation (monogenic diabetes)

A

MODY (maturity-onset diabetes of the young)

- GLUCOKINASE mutation

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24
Q

Type A insulin resistance

Cause?

A

Severe insulin resistance, hyperinsulinemia, diabetes

Mutation of insulin receptor/signaling (monogenic DM)

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25
Type A insulin resistance (female)
Velvety hyperpigmentation of the skin, polycystic ovaries, elevated androgen levels, severe insulin resistance
26
Lipoatrophic diabetes
Hyperglycemia, subcutaneous fat loss, insulin resistance, hypertriglyceridemia, acanthosis nigricans, hepatic steatosis (fat accumulation)
27
Diabetes in pregnancy - types and consequences (3)
Pregestational - pre-existing DM --> risk of stillbirth and congenital malformations Gestational - diabetogenic development in pregnancy --> resolves after delivery --> OVERT DIABETES 10-20 yrs later Poor DM control LATE in pregnancy --> large size at birth, increased risk of obesity and diabetes later in life
28
Honeymoon period - type 1 DM What happens at end?
First 1-2 years, insulin secretion still possible, little insulin treatment necessary Abrupt transition to overt diabetes (infection, other trigger)
29
Polyuria, polydipsia, polyphagia, weight loss muscle weakness Severe symptom? Usual cause? Other cause? Lab finding?
Type 1 DM Ketoacidosis - usually failure to take insulin - OR increased epinephrine (infection, illness, other) --> blocks insulin, stimulates glucagon Labs = acetoacetic acid, beta-hydroxybutyric acid
30
What causes ketoacidosis in type 1 DM?
Increased FFAs --> ketogenesis (liver)
31
Polyphagia, polydipsia, polyuria - explain each
Polyphagia - increased fat and muscle breakdown Polyuria - osmotic diuresis (sugar) Polydipsia - volume depletion by polyuria
32
Diabetic ketoacidosis - symptoms Treatment?
Abdominal pain, fruity odor, deep labored breathing, CNS depression Tx = insulin, correct acidosis, treat underlying cause (infection, etc)
33
Why does ketoacidosis happen less frequently in type 2?
Portal vein insulin levels keep hepatic fatty acid levels low
34
Common severe symptom in type 2 DM
Hyperosmolar hyperosmotic syndrome (HHS) - severe dehydration in patients who can't drink enough water to compensate for the polyuria (older, disabled) --> Impaired mental status, severe dehydration
35
Diabetic presents w/ dizziness, confusion, sweating, palpitations, and tachycardia Treatment? Is this common?
Hypoglycemia (missed meal, physical exertion, insulin OD) Tx = glucose MOST COMMON acute complication of DM
36
Chronic DM --> large blood vessels
Accelerated atherosclerosis (large/medium arteries) --> MI, stroke, LE ischemia, LE gangrene
37
Chronic DM --> small blood vessels
BM thickening --> Retinopathy/cataracts/glaucoma, nephrosclerosis, peripheral/autonomic neuropathy
38
Hyperglycemia in chronic DM causes glycation of proteins. What are the specific products of this? (2)
HbA1C, AGEs
39
AGEs (advanced glycation end products) in small vessel growth
Bind RAGE (receptor) on inflammatory cells and vessels --> cytokines, growth factors (TGF-beta), ROS generation, procoagulant activity, enhanced SM and matrix proliferation Causes basement membrane deposition and matrix proliferation (small vessels)
40
AGEs in vessel destruction and atherosclerosis
Crosslink collagens --> decreased elasticity, increased leakiness, increased LDL/cholesterol trapping and deposition
41
AGEs and PKC
AGEs --> glycolytic intermediate buildup --> de novo DAG production --> PKC activation --> VEGF/TGF-beta/PAI-1 --> microangiopathy
42
Chronic DM --> oxidative stress
Persistent hyperglycemia --> metabolism to fructose --> uses up the NADPH --> reduced glutathione deficiency --> deficient antioxidants --> increased susceptibility to ROS
43
A baby with hyperplastic islets of langerhaans. What to suspect?
Mother w/ diabetes
44
Chronic DM -- glomerulus Result of the nodular glomerulosclerosis?
Glomerular/tubular BM thickening + PAS-POSITIVE mesangial increase/sclerosis + PAS-POSITIVE peripheral nodular glomerulosclerosis (KIMMELSTIEL-WILSON nodules) K-W nodules expand --> OBLITERATE THE TUFT
45
Chronic DM -- renal arteries/arterioles Chronic DM -- renal infections
Renal vascular arteriolosclerosis (hyaline thickening - HTN) and atherosclerosis (macrovascular Dz) Pyelonephritis, NECROTIZING PAPILLITIS (papillary necrosis)
46
Chronic DM -- eyes (3)
Cataract (opacification of lens) Glaucoma (increased IOP, optic nerve damage) Proliferative retinopathy/neovascularization (hypoxia-VEGF)
47
Increased PAI-1
Plasminogen activation inhibitor (PAI) --> inhibited fibrinolysis --> increased atherosclerosis
48
First sign of diabetic nephropathy Patient's with this should be screened for ____
Microalbuniuria (30-300 mg/day) Macrovascular disease and CV issues
49
Untreated diabetic microalbuniuria --> _______ Accompanied by?
Overt macroalbuminuria HTN
50
Diabetic neuropathies (3)
- Distal extremity polyneuropathy (sensory and motor) - Autonomic neuropathy (bowel, bladder, ED) - Mononeuropathy (sudden wristdrop/footdrop/CN palsy)
51
Diabetic infections (3)
- TB - Pneumonia - Pyelonephritis
52
Pancreatic neuroendocrine tumors - likelihood of benign/malignant
Insulinomas - benign (90%) | OTHER - malignant (60-90%)
53
Pancreatic neuroendocrine tumors - genetics (5)
MEN1 PTEN, TSC2 (tumor suppressor loss) ATRX, DAXX
54
Most common clinical syndromes w/ PanNETs (3)
Hyperinsulinism (most common) Hypergastrinemia (Z-E syndrome) MEN
55
Hypoglycemic episodes after fasting/exercise - confusion, stupor Mass in pancreas
Insulinoma
56
Small encapsulated tumor in pancreas, monotonous cells that look like giant islets, preserved architecture, amyloid deposition
Insulinoma
57
Hypoglycemia, mass in pancreas, no amyloid, enlarged islets Causes? (3)
Hyperinsulinism --> hyperplasia of islets Maternal DM, B-W syndrome, Beta-cell K+ channel or sulfonylurea receptor mutation(s)
58
Peptic ulceration, diarrhea, mass in/near pancreas or duodenum
Zollinger-Ellison syndrome (Gastrinoma)
59
Mild diabetes mellitus (blood glucose not super high), skin rash, anemia, pancreatic mass Name of skin rash?
Glucagonoma (alpha cell tumor) Necrolytic migratory erythema
60
Diabetes mellitus, cholelithiasis, steatorrhea, hypochlorhydria, pancreatic mass
Somatostatinoma (delta cell tumor)
61
Watery diarrhea, hypokalemia, achlorhydria, pancreatic mass
WDHA syndrome - VIPoma

Endocrine 2 (12 decks)

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