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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
Q

Type A insulin resistance (female)

A

Velvety hyperpigmentation of the skin, polycystic ovaries, elevated androgen levels, severe insulin resistance

26
Q

Lipoatrophic diabetes

A

Hyperglycemia, subcutaneous fat loss, insulin resistance, hypertriglyceridemia, acanthosis nigricans, hepatic steatosis (fat accumulation)

27
Q

Diabetes in pregnancy - types and consequences (3)

A

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
Q

Honeymoon period - type 1 DM

What happens at end?

A

First 1-2 years, insulin secretion still possible, little insulin treatment necessary

Abrupt transition to overt diabetes (infection, other trigger)

29
Q

Polyuria, polydipsia, polyphagia, weight loss muscle weakness

Severe symptom? Usual cause? Other cause?

Lab finding?

A

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
Q

What causes ketoacidosis in type 1 DM?

A

Increased FFAs –> ketogenesis (liver)

31
Q

Polyphagia, polydipsia, polyuria - explain each

A

Polyphagia - increased fat and muscle breakdown
Polyuria - osmotic diuresis (sugar)
Polydipsia - volume depletion by polyuria

32
Q

Diabetic ketoacidosis - symptoms

Treatment?

A

Abdominal pain, fruity odor, deep labored breathing, CNS depression

Tx = insulin, correct acidosis, treat underlying cause (infection, etc)

33
Q

Why does ketoacidosis happen less frequently in type 2?

A

Portal vein insulin levels keep hepatic fatty acid levels low

34
Q

Common severe symptom in type 2 DM

A

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
Q

Diabetic presents w/ dizziness, confusion, sweating, palpitations, and tachycardia

Treatment?

Is this common?

A

Hypoglycemia (missed meal, physical exertion, insulin OD)

Tx = glucose

MOST COMMON acute complication of DM

36
Q

Chronic DM –> large blood vessels

A

Accelerated atherosclerosis (large/medium arteries) –> MI, stroke, LE ischemia, LE gangrene

37
Q

Chronic DM –> small blood vessels

A

BM thickening –> Retinopathy/cataracts/glaucoma, nephrosclerosis, peripheral/autonomic neuropathy

38
Q

Hyperglycemia in chronic DM causes glycation of proteins. What are the specific products of this? (2)

A

HbA1C, AGEs

39
Q

AGEs (advanced glycation end products) in small vessel growth

A

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
Q

AGEs in vessel destruction and atherosclerosis

A

Crosslink collagens –> decreased elasticity, increased leakiness, increased LDL/cholesterol trapping and deposition

41
Q

AGEs and PKC

A

AGEs –> glycolytic intermediate buildup –> de novo DAG production –> PKC activation –> VEGF/TGF-beta/PAI-1 –> microangiopathy

42
Q

Chronic DM –> oxidative stress

A

Persistent hyperglycemia –> metabolism to fructose –> uses up the NADPH –> reduced glutathione deficiency –> deficient antioxidants –> increased susceptibility to ROS

43
Q

A baby with hyperplastic islets of langerhaans. What to suspect?

A

Mother w/ diabetes

44
Q

Chronic DM – glomerulus

Result of the nodular glomerulosclerosis?

A

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
Q

Chronic DM – renal arteries/arterioles

Chronic DM – renal infections

A

Renal vascular arteriolosclerosis (hyaline thickening - HTN) and atherosclerosis (macrovascular Dz)

Pyelonephritis, NECROTIZING PAPILLITIS (papillary necrosis)

46
Q

Chronic DM – eyes (3)

A

Cataract (opacification of lens)
Glaucoma (increased IOP, optic nerve damage)
Proliferative retinopathy/neovascularization (hypoxia-VEGF)

47
Q

Increased PAI-1

A

Plasminogen activation inhibitor (PAI) –> inhibited fibrinolysis –> increased atherosclerosis

48
Q

First sign of diabetic nephropathy

Patient’s with this should be screened for ____

A

Microalbuniuria (30-300 mg/day)

Macrovascular disease and CV issues

49
Q

Untreated diabetic microalbuniuria –> _______

Accompanied by?

A

Overt macroalbuminuria

HTN

50
Q

Diabetic neuropathies (3)

A
  • Distal extremity polyneuropathy (sensory and motor)
  • Autonomic neuropathy (bowel, bladder, ED)
  • Mononeuropathy (sudden wristdrop/footdrop/CN palsy)
51
Q

Diabetic infections (3)

A
  • TB
  • Pneumonia
  • Pyelonephritis
52
Q

Pancreatic neuroendocrine tumors - likelihood of benign/malignant

A

Insulinomas - benign (90%)

OTHER - malignant (60-90%)

53
Q

Pancreatic neuroendocrine tumors - genetics (5)

A

MEN1
PTEN, TSC2 (tumor suppressor loss)
ATRX, DAXX

54
Q

Most common clinical syndromes w/ PanNETs (3)

A

Hyperinsulinism (most common)
Hypergastrinemia (Z-E syndrome)
MEN

55
Q

Hypoglycemic episodes after fasting/exercise - confusion, stupor
Mass in pancreas

A

Insulinoma

56
Q

Small encapsulated tumor in pancreas, monotonous cells that look like giant islets, preserved architecture, amyloid deposition

A

Insulinoma

57
Q

Hypoglycemia, mass in pancreas, no amyloid, enlarged islets

Causes? (3)

A

Hyperinsulinism –> hyperplasia of islets

Maternal DM, B-W syndrome, Beta-cell K+ channel or sulfonylurea receptor mutation(s)

58
Q

Peptic ulceration, diarrhea, mass in/near pancreas or duodenum

A

Zollinger-Ellison syndrome (Gastrinoma)

59
Q

Mild diabetes mellitus (blood glucose not super high), skin rash, anemia, pancreatic mass

Name of skin rash?

A

Glucagonoma (alpha cell tumor)

Necrolytic migratory erythema

60
Q

Diabetes mellitus, cholelithiasis, steatorrhea, hypochlorhydria, pancreatic mass

A

Somatostatinoma (delta cell tumor)

61
Q

Watery diarrhea, hypokalemia, achlorhydria, pancreatic mass

A

WDHA syndrome - VIPoma

Endocrine 2 (12 decks)

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