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Endo-Repro Exam 2 > Lecture 5: The Endocrine Pancreas > Flashcards

Lecture 5: The Endocrine Pancreas Flashcards

1
Q

D1 cells of the endocrine pancreas secrete what; what is the effect of this secretory product?

A
  • VIP
  • Induces glycogenolysis and hyperglycemia
  • Stimulates GI secretions –> secretory diarrhea
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2
Q

Which value of HbA1C is considered diagnositc for diabetes?(≥

A

≥6.5%

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3
Q

A fasting plasma glucose of ≥ ______ mg/dL is considered diagnostic for diabetes.

A

A fasting plasma glucose of ≥ 126 mg/dL is considered diagnostic for diabetes.

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4
Q

A random plasma glucose ≥ ______ mg/dL is considered diagnostic for diabetes.

A

A random plasma glucose ≥ 200 mg/dL is considered diagnostic for diabetes.

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5
Q

What are 4 genetic syndromes associated w/ diabetes?

A
  • Down syndrome
  • Klinefelter syndrome
  • Turner syndrome
  • Prader-Willi syndrome
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6
Q

Fasting plasma glucose levels are determined primarily by what?

A

Hepatic glucose output

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7
Q

What is the major insulin-responsive site for postprandial glucose utilization and is critical for preventing hyperglycemia and maintaining glucose homeostasis?

A

Skeletal muscle

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8
Q

What 2 classes of drugs have been created for pt’s with T2DM based on the incretin effect?

A
  • GLP-1 receptor agonists
  • DPP-4 inhibitors (↓ breakdown of incretins)
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9
Q

Which form of diabetes is associated with amyloid deposition in pancreatic islets?

A

Type 2 DM

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10
Q

What are 2 mitogenic functions of insulin?

A
  • Initiation of DNA synthesis in certain cells
  • Stimulation of cell growth and differentiation
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11
Q

Insulin signaling facilitates the trafficking and docking containing which insulin-sensitive glucose transporter to the plasma membrane?

A

GLUT-4

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12
Q

What is the most important susceptibility locus associated with T1DM; what chromosome is it on?

A

HLA gene cluster on chromosome 6p21

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13
Q

Which 2 HLA loci are associated with T1DM?

A
  • HLA-DR3
  • HLA-DR4
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14
Q

Individuals with what concurrent HLA halotypes have the highest inherited risk for T1DM?

A

DR3 or DR4 concurrently w/ a DQ8

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15
Q

The classic manifestations of T1DM (hyperglycemia and ketosis) occur after more than _______% of the beta-cells have been destroyed

A

The classic manifestations of T1DM (hyperglycemia and ketosis) occur after more than 90% of the beta-cells have been destroyed

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16
Q

What is the fundamental immune abnormality underlying the pathogenesis of T1DM?

A

Failure of self-tolerance in T cells specific for islet antigens

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17
Q

What are the 3 circulating islet autoantibodies observed in the majority of pt’s with T1DM as well as asymptomatic family members at risk for progression to overt disease?

A
  • anti-insulin
  • anti-GAD
  • anti-ICA512
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18
Q

Which type of diabetes (T1DM or T2DM) has a stronger genetic component?

A

T2DM —> disease concordance >90% in monozygotic twins

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19
Q

What are the 2 cardinal metabolic defects that characterize T2DM?

A
  • ↓ response of peripheral tissues, especially skeletal m., adipose, and liver to insulin = insulin resistance
  • Inadequate insulin secretion in the face of insulin resistance and hyperglycemia = β-cell dysfunction
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20
Q

Excess FFA’s within macrophages and β cells in the setting ↑ central obesity can activate what; contribute to insulin resistance how?

A

Inflammasome leads to secretion of IL-1β = release of pro-inflammatory cytokines —> insulin resistance

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21
Q

Maturity-onset diabetes of the young (MODY) resembles what type of diabetes?

A

T2DM

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22
Q

How does maturity-onset diabetes of the young (MODY) resemble T2DM?

A
  • ↑ blood insulin
  • NO autoantibodies
  • NON-ketotic
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23
Q

Maturity-onset diabetes of the young (MODY) is most often associated with loss-of-function mutations in which gene?

A

Glucokinase (GCK)

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24
Q

Rare insulin receptor mutations which impair tissue response to insulin can cause what 2 disease states?

A
  • Type A insulin resistance —> acanthosis nigricans
  • Lipoatrophic diabetes —> hyperglycemia + loss of subcutaneous adipose tissue
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25
Q

Women w/ pregestational diabetes (where hyperglycemia was present before conception) have an increased risk for what fetal complications?

A
  • Stillbirth
  • Congenital malformations
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26
Q

Poorly controlled diabetes arising later in pregnancy, regardless of prior history, can lead to what problems for the infant?

A
  • Excessive weight at birth (macrosomia)
  • Problems later in life including obesity and diabetes
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27
Q

How is the diagnosis of T2DM most frequently made?

A

After routine blood testing in asymptomatic pt

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28
Q

Classic triad of T1DM?

A

- Polyuria

  • Polyphagia, BUT losing weight!

- Polydipsia

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29
Q

Autoantibodies associated with T1DM are present more often in which ethnicity, therefore are more reliable indicators of disease?

A

>90% of Caucasians

30
Q

What is the most common precipitating factor of diabtetic ketoacidosis; what are some other factors which may contribute?

A
  • Failure to take insulin (non-compliance) = most common
  • Intercurrent infections –> Pneumonia and UTI’s
  • illness
  • Trauma
  • Certain drugs
31
Q

What is the triad of diabetic ketoacidosis?

A
  • HYPERglycemia
  • Ketonemia
  • Metabolic acidosis
32
Q

The pathogenesis of DKA is associated with the release of what into circulation and how does this contribute?

A
  • Release of epinephrine
  • Which blocks residual insulin action and stimulates the secretion of glucagon
  • ↑ glucagon –> ↑ gluconeogenesis and ↑ blood glucose levels —> exacerbating hyperglycemia —> osmotic diuresis and dehyrdration
33
Q

Insulin deficiency stimulates what enzyme responsible for the production of ketone bodies?

A

Hormone sensitive lipase –> breaks down adipose tissue —> ↑ FFA’s which are esterified to fatty acyl CoA and oxidized by hepatic mitochondria to produce ketone bodies

34
Q

What are the clinical signs/sx’s of pt in DKA?

A
  • Fatigue + N/V + severe abdominal pain
  • Fruity odor
  • Deep, labored respirations (also known as Kussmaul breathing)
35
Q

Which acute hyperglycemia crisis is more common in T2DM and how does it occur?

A
  • Hyperglycemic hyperosmotic syndrome (HHS)
  • Prolonged hyperglycemia –> sustained osmotic diuresis + severe dehydration in a pt who does not drink enough water to compensate for urinary losses
36
Q

How does HHS differ from DKA?

A
  • More severe HYPERglycemia (600-1200 mg/dL)
  • HYPERosmolality (>350 mOsm/L)
  • NO ketones
37
Q

What is the most common acute metabolic complication in both T1DM and T2DM; how does it present clinically?

A
  • HYPOglycemia from either missing a meal, excessive exertion, or too much insulin administration
  • Presents as: dizziness + confusion + sweating + palpitations + tachycardia
38
Q

Which GF released as a result of the AGE-RAGE signaling axis within the vascular compartment is implicated in diabetic retinopathy?

39
Q

The accumulation of what in the lens of pt with chronic hyperglycemia contributes to cataract formation?

40
Q

In tissues that do not require insulin for glucose transport (i.e., nerves, lens, kidneys, and blood vessels), what reaction occurs in the presence of excess intracellular glucose; which cofactor is used for this reaction?

A
  • Glucose metabolized by aldose reductase —> Sorbitol
  • This reaction uses NADPH as cofactor; which compromises GSH regeneration; ↑ susceptibility to oxidative stress
41
Q

What are 5 effects on the vasculature produced by advanced glycation end products (AGEs) formed in the presence of chronic hyperglycemia?

A
  • ↑ release cytokines + GF’s –> TGF-β and VEGF
  • Generation of ROS’s
  • Procoagulant activity
  • Proliferation of smooth m.
  • Cross-linking of matrix proteins –> pro-atherogenic
42
Q

An increase in the number and size of the pancreatic islets is a characteristic morphological feature in which pt’s?

A

NON-diabetic newborns of diabetic mothers

43
Q

What is the morphological hallmark of diabetic macrovascular disease?

A

Accelerate atherosclerosis involving the aorta and large- and medium-sized arteries

44
Q

Which vascular lesion associated with HTN is seen both more prevalent and more severe in diabetics than in non-diabetics?

A

Hyaline atherosclerosis

45
Q

What 3 lesions are encountered in diabetic nephropathy?

A
  1. Glomerular lesions
  2. Renal vascular lesions, mainly arteriolosclerosis
  3. Pyelonephritis, including necrotizing papillitis
46
Q

What are the 3 most important glomerular lesions encountered in diabetic nephropathy?

A
  1. Capillary BM thickening
  2. Diffuse mesangial sclerosis
  3. Nodular glomerulosclerosis
47
Q

The diffuse mesangial slcerosis associated with diabetic nephropathy is caused by an increase in what?

A

Diffuse ↑ in mesangial MATRIX

48
Q

The glomerular lesions of diabetic nephropathy that take the form of ovoid or spherical, often laminated, nodules of matrix situated in the periphery of the glomerulus are known as what?

A

Intercapillary glomerulosclerosis or Kimmelstiel-Wilson disease

49
Q

Grossly what will the surface of the kidney and cortical tissue show in a patient with long-standing diabetes leading to nephrosclerosis?

A
  • Diffuse granular transformation of the surface
  • Marked thinning of the cortical tissue
  • Overall contraction in size
50
Q

Which arterioles of the kidney (afferent or efferent) are affected by hyaline arteriolosclerosis in long-standing diabetic nephropathy?

A

BOTH the afferent and efferent arterioles

51
Q

Which special pattern of acute pyelonephritis is much more prevalent in diabetics than in nondiabetics?

A

Necrotizing papillitis (or papillary necrosis)

52
Q

What is the gold standard for urine albumin testing?

A

Urine Albumin: Creatinine Ratio (UACR)

53
Q

The most profound histopathologic changes of diabetes are seen in what part of the eye?

A

Retina = Retinal vasculopathy of diabetes

54
Q

What is the fundamental lesions of diabetic retinopathy and how is it induced?

A

Neovascularization due to hypoxia-induced overexpression of VEGF

55
Q

What is the most frequent pattern of involvement seen with diabetic neuropathy?

A

Distal symmetric polyneuropathy of the LE’s that affects BOTH motor and sensory function

56
Q

Diabetics have enhanced susceptibility to what type of infections?

A
  • Skin i.e., cellulitis
  • Tuberculosis
  • Pneumonia
  • Pyelonephritis
57
Q

Intrracellular hyperglycemia stimulates the de novo synthesis of DAG from glycolytic intermediates, which causes excessive activation of what; what are the downstream effects of this?

A
  • Excessive PKC activation
  • Leads to ↑ production of VEGF, TGF-β, and the procoagulant, PAI-1
58
Q

Somatic alterations in which 3 major genes or pathways have been identified as factors associated w/ sporadic pancreatic neuroendocrine tumors?

A
  1. MEN1
  2. LOF mutations, PTEN and TSC2 —> ↑ mTOR signaling pathway
  3. Inactivating mutations of ATRX and DAXX
59
Q

Deposition of amyloid is a characteristic histologic feature of which type of pancreatic neuroendocrine tumor?

A

Insulinoma

60
Q

Levels of what can be useful in making the diagnosis of an insulinoma?

A

Urine C peptide levels

61
Q

Insulinomas are associated with what clinical signs and sx’s; these sx’s are usually precipitated by what?

A
  • HYPOglycemic episodes when blood glucose falls below 50 mg/dL
  • Confusion + stupor + loss of consciousness
  • Episodes precipitated by fasting or exercise
62
Q

Which type of pancreatic neuroendocrine tumor is generally benign and is associated with the lowest rate of metastasis (10%)?

A

Insulinoma

63
Q

How do MEN-1-associated gastrinomas differ morphologically from sporadic gastrinomas?

A
  • MEN-1-associated are often multifocal
  • Sporadic are usually single
64
Q

What is the triad of gastrinomas which constitute Zollinger-Ellison Syndrome?

A
  1. Pancreatic islet cell tumor
  2. HYPERsecretion of gastric acid
  3. Severe peptic ulceration
65
Q

Patients with Zollinger-Ellison syndrome with metastasis where have a shortened life expectancy?

A

Liver; progressive tumor growth causes liver failure within 10 years

66
Q

What are the 4 D’s of Glucagonomas?

A
  1. Diabetes (mild)
  2. Dermatitis (necrolytci migratory erythema)
  3. Depression
  4. DVT’s
67
Q

What is the characteristic rash associated with glucagonomas called and where on the body is this rash seen?

A
  • Necrolytic migratory erythema
  • Groin + lower extremities
68
Q

δ-cell tumors (somatostatinomas) are associated with what 4 clinical manifestations?

A
  • Diabetes
  • Cholelithiasis (gallstones)
  • Steatorrhea
  • HYPOchlorhydria
69
Q

Since somatostatin functions as a paracrine regulator, what 3 things are reduced when somatostatin levels are high?

A
  • Reduced insulin
  • Reduced gallbladder motility
  • Reduced exocrine pancreatic secretions
70
Q

VIPomas are associated with what syndrome and what are the clinical manifestations?

A
  • WDHA syndrome
  • Watery diarrhea
  • HYPOkalemia
  • Achlorhydria
71
Q

20% of patients with VIPomas will also have what presenting sx?

Endo-Repro Exam 2 (11 decks)

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