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Endo/Repro 2 Final > 4. Robbins: Endocrine Pancreas > Flashcards

4. Robbins: Endocrine Pancreas Flashcards

1
Q

Endocrine pancreas is made up of ________.

A

Islet of langerhans, located in the neck and tail of the pancreas.

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2
Q

What cells make up the islet of langerhans?

A

[4 major cell types and 2 minor cell types]

  • 4 major cell types
      1. Alpha cells
      1. Beta cells
      1. Delta cells (ς)
      1. PP cells
  • 2 minor cell types
      1. D1 cells
      1. Enterochromaffin cells
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3
Q

Function of alpha and beta cells

A
  1. Alpha cells: secrete glucagon => ↑ glycogenolysis in liver => [↑ blood sugar/glucose]
  2. Beta cells: secrete insulin => [regulates glucose utilization] & [↓ blood sugar/glucose]
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4
Q

Function of delta and PP cells

A
  • Delta cells: secrete somatostatin => [suppress release of insulin and glucagon_]_
  • PP cells: secrete pancreatic polypeptide => [GI effects: ↑ secretion of GI enzymes & inhibits intestinal motility]
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5
Q

Function of D1 cells and enterochromaffin cells

A
  • D1 cells: secrete VIP (vasoactive intestinal polypeptide) =>
    1. [glycogenolysis and hyperglycemia]
    2. stimulates [GI secretion => diarrhea]
  • Enterochromaffin cells: make serotonin & source of pancreatic tumors that cause from carcinoid syndrome.
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6
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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7
Q

What is the main job of the islet of langerhans?

A

Glucose homeostasis: regulated by

    • release of glucose from liver
    • utilization of glucose by tissue
    • Insulin and glucagon
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8
Q

How is insulin release regulated?

A
  1. GLUT-2 (glucose transporter) to move to takes glucose into B-cells.
  2. Glucose is metabolized => makes ATP
  3. ATP inhibits membrane K+ channel
  4. Membrane is depolarized => Ca2+ influx
  5. Ca2+ influx => insulin release.
  6. Insulin causes GLUT-4 to move into the plasma membrane and promote glucose uptake in target cell.
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9
Q

How is insulin processed?

A

Proinsulin => cleaved in B-cell to [insulin & C-peptide]

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10
Q

How can we measure if insulin was administered by meds or made by the body?

A

Measure C-peptide, a marker of endogenous insulin.

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11
Q

Insulin and glucagon effects during fasting vs feeding stages

A
  • Fasting
    • [​↓ insulin and ↑ glucagon] => hepatic gluconeogenesis and glycogenolysis & ↓ glycogen synthesis => ↑ blood glucose (mainly by liver) prevent hypoglycemia
  • Meal
    • ↑ glucose load causes [↑ insulin and ↓ glucagon] => glucose uptake and utilization to prevent hyperglycemia
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12
Q

What is the major insulin responsive site for postprandial glucose utilization and critical to prevent hyperglycemia?

A

Skeletal muscle

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13
Q

Insulin effects on adipose tissue

A
  1. ↑ glucose uptake
  2. ↑ lipogenesis
  3. ↓ lipolysis
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14
Q

Insulin effects on liver

A
  1. ↑ Glycogen synthesis
  2. ↑ Lipogenesis
  3. ↓ Gluconeogenesis
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15
Q

Insulin effects on striated muscle

A
  1. ↑ glucose uptake
  2. ↑ glycogen synthesis
  3. ↑ protein synthesis
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16
Q

Main job in insulin

A

MOST potent anabolic hormone:

    • Growth- promoting effects
    • Tell body how to utilize glucose
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17
Q

What cell?

A

B-cells (insulin): => dark reaction

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18
Q

What cell?

A

D cells (somatostatin)

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19
Q

What cell?

A

a cells (glucagon)

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20
Q

What cell?

A

EM of B-cell with membrane-bound granules, dense rectangular core and halo.

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21
Q

What cell?

A

Left: a-cell with dense, round center

Right: delta cells

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22
Q

The most important stimulus for insulin synthesis and release is ______.

A

Glucose

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23
Q

What are incretins?

A

Hormones released from cells in GI after a meal (oral glucose) that help to promote insulin release

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24
Q

What are 2 incretins?

A
  1. Glucagon-like-peptide 1 (GLP-1)
  2. Glucose-dependent insulin-releasing polypeptide (GIP)
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25
Q

MOA of incretins

A
  1. GLP-1 and GIP act on B cells in pancrease => ↑ insulin release
  2. GLP-1 acts on a-cells and suppresses glucagon release => ↓ blood glucose (↓ glucose release from liver )
  3. Inactivated by DPP-4 (dipeptidyl peptidase-4)
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26
Q

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

A
  1. - GLP-1 receptor AGO
  2. - DPP-4 inhibitors (↓ breakdown of incretins)
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27
Q

How is the incretin-effect affect in T2DM?

A

Blunted:

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28
Q

Diabetes Mellitis

  • What is it?
  • Leading cause of what in the US:
  • More common in:
  • Lease common in:
A
  • Problem with NL glucose homeostasis => hyperglycemia
    • 1. Defective insulin secretion
    • 2. Defective insulin effect
  • ESRD, adult-onset blindness, non-traumatic LE amputation due to atherosclerosis
  • MC = american indian/alaska native > Black and hispanic
  • LC: Asian and white
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29
Q

NL blood glucose

A

70- 120 mg/dL

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30
Q

Fasting plasma glucose for DB Diagnosis

A
  1. Fasting plasma glucose > 126 mg/dL
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31
Q

Which value of HbA1C is considered diagnositc for diabetes?

A

> 6.5 %

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32
Q

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

A

≥ 200 mg/dL

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33
Q

What are 4 genetic syndromes associated w/ diabetes?

A
  1. - Down syndrome
  2. - Klinefelter syndrome
  3. - Turner syndrome
  4. - Prader-Willi syndrome
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34
Q

What are T1DM and T2DM?

A

T1DM: AI disease that causes immune-mediated destruction of pancreatic B-cells => absolute deficiency of insulin.

  • T- cells lose self-tolerance against antigens on B- cells

T2DM: Caused by combination of resistance to insulin & inadequate secretory response by B-cells => relative insulin deficiency.

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35
Q

T1DM

  • Onset:
  • AutoAB:
  • Pathology:
A
  • Onset
    • Usually childhood & adolesnce
  • AutoAB
    1. Anti-insulin ab
    2. Anti-GAD ab
    3. anti-ICA512 ab
  • Pathology
    1. Insulitis (inflammtory infiltrate of T-cells and MO)
    2. B-cell depletion
    3. Islet atrophy
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36
Q

T1DM

  • Genetics:
  • Clinical:
    • Weight
    • Insulin levels
    • DKA?
A
  • Genetics
    • MHC class II; HLA-DR3 or DR4 with DQ8.
  • Clinical
    1. NL or WL
    2. Progressive ↓ in insulin
    3. Severe and w/o insulin therapy: DKA
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37
Q

T2DM

  • Onset:
  • AutoAB:
  • Pathology:
A
  • Onset:
    • Adult, but increasing incidence in childhood and adolescence
  • AutoAB:
    • None
  • Pathology:
    1. No insulitis
    2. Amyloid deposits
    3. Mild B-cell deposition
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38
Q

T2DM

  • Genetics:
  • Clinical:
    • Weight
    • Insulin levels
    • DKA?
A

Genetics:

  • Genetics AND environment are important
    • Strong familial predisposition: majority have a 1st degree relative with T2DM
    • Obesity (esp central) = major RF

Clinical:

  • 80% are obese
  • Early = ↑ in blood insulin bc of B-cell compensation; Later = NL/moderate ↓ in insulin bc B-cell exhaustion
  • Severe => hyperglycemic hyperosmotic syndrome (HHS)
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39
Q

Pancreas must be ___ destroyed to give overt T1DM symptoms (Hyperglycemia + ketosis)

A

>90%

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40
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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41
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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42
Q

What causes insulin resistance in T2DM?

A

Obesity and excess adipocytes cause:

  1. ↑ in bad adipokines => promote hyperglucemia and
  2. ↓ in toxic FFA => release cytoines => + inflammasome => secretion of IL-1β => release of pro-inflammatory cytokines =>
  3. Inflammation: damages B cells and end organs => ↓ response to insulin
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43
Q

Insulin resistance in T2DM results in what?

A
  1. Liver = no gluconeogenesis: high fasting blood glucose levels
  2. Skeletal muscle = failure of glucose uptake and glycogen synthesis after a meal => high post-prandial blood glucose levels
  3. Adipose tissue = activation of “hormone-sensitive” lipase is NOT inhibited => excess TAG breakdown and FFA.
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44
Q

What is required for the development of overt T2DM?

A

B-cell dysfunction

45
Q

Causes of B-cell dysfunction that cause exhaustion:

A
  1. ◦ Lipotoxicity to B cells from FFA
  2. ◦ Glucose toxicity
  3. ◦ Decreased incretin/incretin effect
  4. ◦ Amyloid deposition (cause or effect?)
  5. ◦ Genetics!
46
Q

Monogenic forms of DB are due to either a [primary defect in B-cell or defect in insulin receptor signaling].

What are the 2 types?

A
  1. MODY (Maturity-onset DB of the young)
  2. Insulin receptor mutations
47
Q

What is Maturity-Onset DB of the Young (MODY)?

A
  • DB that resembles T2DM clinically, but occurs in youth
    1. ​↑ blood insulin
    2. No autoAB
    3. Non-ketotic
  • Caused by: LOF mutation of Glucokinase** => primary defect in B-cell function that occurs **without loss of B-cells, affecting B-cell mass and/or insulin production.
48
Q

Insulin receptor mutations

Affect what:

Cause:

A
  • Receptor synthesis, insulin binding or RTK activity
  • Severe insulin resistance + hyperinsulinemia + DB (type A)
  • Pts have: acanthosis nigracans polycytic ovaries, high androgen levels and lipoatrophic DB (hyperglycemia + loss of adipose tissue).
49
Q

What is the difference between gestational DB and pre-gestational/overt DB?

A
  • Gestational DB: previously euglycemic develop impaired glucose tolerance and DB for the first time during PG.
    • due to: genetics/env
  • Pregestational DB: W with pre-existing DB become PG.
50
Q

How does pregnancy affect insulin processing?

A

Pregnancy = “diabetogenic” state that favors insulin resistance.

51
Q

Gestational/pre-gestation DB risks to mom and fetus

A
  • Mom
    • C-section
  • Fetus (used to a hyperglycemic environment)
    1. Neonatal hypoglycemia => seizures => brain damage
    2. Macrosomnia = big ass bb
    3. Congenital malformations
    4. Stillbirth
52
Q

How is the diagnosis of T2DM typically made?

A

After routine blood testing in asymptomatic people.

53
Q
  • Insulin => catabolic/anabolic.
  • Insulin deficient => catabolic/anabolic state
A
  • Insulin => anabolic hormone
  • When deficient => catabolic state
54
Q

Classic Triad of T1DM

  • If severe => ____
  • Combination of what sx should suggest T1DM?
A
  1. Polyphagia (increase appetite), but WL/ muscle loss!
  2. Polyuria (water/electrolyte loss)
  3. Polydipsia (intense thirst)

When severe => DKA

WL (bc insulin deficient = catabolic state) & increased appetite.

55
Q

Severe T1DM and T2DM causes => ________

A
  • Severe T1DM = DKA (occurs less often in T2DM)
  • Severe T2DM = Hyperglycemic hyperosmotic syndrome (HHS)
56
Q

DKA

  • Occurs in T1DM/T2DM?
  • MC occurs due to:
  • Pathology:
A

DKA

  • Severe T1DM, but occasionally occurs in T2DM
  • MC due to factors that increase EPI.
      1. Failure to take insulin
      1. Precursor infections: pneumonia and UTI
  • Pathology
    • [↑ EPI release] => [blocks insulin action => cant process glucose & ↑ glucagon secretion] =>
      • [w/o insulin and glucose for NRG] =>
        • Body breaks down fat via lipase=> FFA are released from adipose tissue => making ketones in liver => ketonemia and ketoneuria (go into urine) => kidneys dump glucose and ketones via osmotic diuresis
        • ↓ peripheral utilization of glucose while glucagon secretion ↑ gluconeogenesis in liver => exacerbating hyperglycemia (250 - 600 mg/dL)
    • => ketoacidotic state (osmotic diuresis and dehydration => shock and ↑ EPI)
57
Q

DKA

  • Names of 2 ketone bodies
  • Diagnose:
  • Clinical manifestations
A
  • Ketone bodies: acetoacetic acid and Beta-hydoxybutyrate
  • Dx: test for ketone bodies
  • Clinical manifestations: fatigue, N/V, abdominal pain, fruity odor, Kassmaul breathing (deep, labored breathing)
58
Q

In patients with DKA, when does metabolic ketoacidosis?

A

When urinary excretion of ketones is compromised by dehydration => metabolic ketoacidosis

59
Q

DKA

  • Triad of symptoms:
  • Resulting in:
  • Presnting signs/sx
A
  • Hyperglycemia, ketonemia, metabolic acidosis
  • Dehydration, polydipsia, polyuria/ketonuria
  • N/V, tachycardia, kassmaul respirations (respiratory alkalosis d/t metabolic acidosis)
60
Q

What causes Kassmaul respirations?

A

Compensatory respiratory alkalosis due to metabolic acidosis seen in DKA

61
Q

How is DKA treated?

A
  1. Insulin
  2. Hydration
  3. Potassium
62
Q

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

A

>90% of Caucasians

63
Q

What is Hyperglycemic Hyperosmotic Syndrome (HHS)?

Most common in whom?

A
  • Acute crisis in T2DM where [chronic hyperglycemic state] causes severe dehydration due a to chronic osmotic diuiresis, MC occuring in older people who do not rehydrate after polyruria.
    • Hyperglycemic state occurs dt:
      • prolonged insulin deficiency,
      • ↑ gluconeogeniesis
      • ↓ glucose uptake]
64
Q

How does HHS differ from DKA?

A
  1. More severe HYPERglycemia (600-1200 mg/dL)
  2. HYPERosmolality (>350 mOsm/L) => obtundation and coma
  3. NO ketones, ketonemia and ketonuria
  4. Severe dehydration and impaired kidney function
65
Q

How do patients with HHS first typically present?

A

Older with AMS, because (-) ketoacidosis and its symptoms delay medical attention until severe dehydration and AMS occur.

66
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
67
Q

Morbitidty associated with chronic DB is due to what?

A
  • Damage to large/medium muscular arteries (diabetic macrovascular disease)
  • Damage to small vessels (diabetic microvascular disease)
68
Q

Chronic DB => diabetic macrovascular disease.

What is the hallmark?

A
  1. *** Accelerated atherosclerosis of aorta and large/medium arteries => MI, stroke, LE gangrene (100x more common in DB than non)
  2. Hyaline arteriolosclerosis => amorphous hyaline thickening of wall of arterioles, narrowing the lumen and causing HTN
69
Q

Chronic DB => diabetic microvascular disease causes what?

A
  • DB retinopathy, nephropathy and neuropathy.
70
Q

MC cause of death in DB?

71
Q

What is a good measure of glycemic control and why?

A
  • HbA1C levels: glucose becomes irreversibly bound to Hb tetramer, providing a measure of glycemic control over the lifespan of a RBC (120 days) and is affected little by day-day variations.
  • Target A1C levels: below 6.5 - 7
72
Q

How does hyperglycemia damage peripheral tissue?

A

Glucose breaksdown and forms AGEs (advanced glycated end-products) => bind to RAGE receptor on inflammatory cells => AGE-RAGE signaling causes:

  1. ↑ release cytokines + GF’s –> TGF-β ( => deposits excess BM) and VEGF ( => causes diabetic retinopathy)
  2. Generation of ROS’s
  3. Procoagulant activity
  4. Proliferation of vascular smooth m. and synthesis of ECM (=> proatherogenic)
73
Q

Morphological Changes in the Pancreas in T1DM

A
  1. ↓ in the number and size of islets in T1DM
  2. Leukocytic infiltrates in the islet (insulitis) in T1DM
74
Q

How does the size of the islet cell change in T2DM?

A
  1. Subtle reduction
75
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: fetal islets undergo hyperplasia due to maternal hyperglycemia

76
Q

Chronic DB => Diabetic Microangiopathy

A
  1. DB Retinopathy
  2. DB Nephropathy
  3. DB Neuropathy
77
Q

What 3 lesions are encountered in DB Nephropathy?

A
  • 1. Glomerular lesions (MC)
    • Thick BM
    • Disruption of the protein cross-linkages that make the membrane a effective filter => DB capillaries are more leaky than NL to plasma proteins.
  • 2. Renal vascular lesions, mainly arteriolosclerosis
    1. Pyelonephritis, including necrotizing papillitis
78
Q

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

A
  • 1. Thickening of glomerular capillary BM = (in almost cases)
  • 2. Diffuse mesangial sclerosis due to diffuse ↑ in mesangial MATRIX
    • Occurs concurrently with thickening of GBM
  • 3. Nodular glomerulosclerosis (Kimmelstiel-Wilson disease)
79
Q

Matrix depositions in DB nephropathy stain (+) for ____

80
Q

What is nodular glomerulosclerosis that occurs in DB nephropathy?

A

Glomerular lesions become PAS + nodules, often located in periphery of the glomerulus.

81
Q

Grossly, what will the kidney look like in chronic diabetes leading to nephrosclerosis?

A
    • Diffuse granular transformation of the surface
    • Cortex thins
  3. - Contracts (gets smaller)
82
Q

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

A

BOTH afferent and efferent arterioles.

83
Q

Diabetic nephropathy is the leading cause of _____ in the US.

84
Q

How do we screen for diabetic nephropathy?

A

Urine [Albumin: Cr] Ratio (UACR) = gold standard for urine albumin testing.

85
Q

What is Diabetic Retinopathy?

  • Caused by:
  • Results in:
A

DB causes retinopathy neovascularization due hypoxia-induced expression of VEGF =>

  1. Hemorrhage
  2. Blindness
  3. Cataracts (d/t hyperglycemia) and glaucoma (d/t increase intraocular pressure)
86
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

87
Q

Diabetic Nephropathy

  1. ESRD in most common in who:
  2. Earliest manifestation:
A
  1. NA, Hispanics and AA than whites with T2DM.
  2. Microalbuminuria: Low amounts of albumin in the urine (30-300 mg/day)
88
Q

Besides diabetic nephropathy, microalbuminuria is also a marker for what?

What measures should be taken?

A

Comorbid CV disease in T1DM/T2DM.

Screen all patients with microalbuminuria for macrovascular disease and aggressive intervention to reduce RF.

89
Q

Without intervention, which (T1DM/T2DM) is more likely to cause overt nephropathy with with macroalbuminuria ( > 300mg of urinary albumin) in 10-15 years?

A
  • 80% T1DM =
  • 20-40% of T2DM
90
Q

Diabetics have increased susceptibility to what type of infections?

A
  1. - Skin i.e., cellulitis
  2. - Tuberculosis
  3. - Pneumonia
  4. - Pyelonephritis
91
Q

Tumors that occur in the pancreatic islet cells are called what?

A

Pancreatic Neuroendocrine Tumors (PanNETS)

92
Q

PanNETs all look the same.

What are the unifying features (gross, histology, on EM)?

A
  • Most commonly occur in neck and tail and pancreas
  • Gross: Solid; tan- yellow
  • Histo: Well-differentiated small, round blue cell tumors (NE tumors)
  • EM: have secretory granules.
93
Q

Mutations in sporadic pancreatic neuroendocrine tumors:

A
  1. MEN1
  2. LOF mutations in PTEN and TSC2 —> ↑ mTOR signaling pathway
  3. Inactivating mutations of ATRX (alpha-thallasemia/mental-retardation syndrome, X- linked) and DAXX (death-domain associated protein)
94
Q

4 Functional Pancreative Endocrine Neoplasms: which is the MC?

A
  1. Insulinoma ***
  2. Gastrinoma
  3. Somatstatinoma
  4. Glucagonoma
  5. VIPoma
95
Q

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

A

Insulinoma

96
Q

Insulinoma

  1. What are they?
  2. Symptoms
  3. Common histological finding:
  4. Diagnosis is made measuring _______.
A
  • Solitary, small encapsulated tumors (< 2cm) of B-cells that secrete insulin and cause episodes of symptomatic hypoglycemia (< 50 mg/dL)
    • ​=> [Confusion, LOC, stupor] that occurs after fasting/exercise (relieved after giving glucose)
  • Amyloid
  • C-peptide levels
97
Q

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

A

Insulinoma

98
Q

Triad of Gastrinoma

A
  1. Islet cell tumor
  2. Gastric acid hypersecretion
  3. Peptic ulceration*

*GA hypersecretion and peptic ulcers => Zolinger-Ellison Syndrome

99
Q

How are the ulcers produced by Gastrinomas different from those found in general population?

A
  1. Unresponsive to regular therapy.
  2. Occur in the jejunum (in addition to dudodenum and stomach)
    • (peptic ulcers in jejunum = assume ZE syndrome)
100
Q

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

A
    • MEN-1-associated are often multifocal
    • Sporadic are usually single
101
Q

Metastasis in Gastrinomas

A

More than 1/2 of gastrinomas are locally invasive or have already metastasized when diagnosed

102
Q

If peptic ulcers are found in jejunum => assume _______

A

ZE Syndrome

103
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

104
Q

What are the 4 D’s of Glucagonomas?

A
  1. Diabetes (mild)
  2. Dermatitis (necrolytic migratory erythema = pathognomic rash) in groin and LE
  3. Depression
  4. DVT’s
105
Q

What is necrolytic migratory erythema?

A

Pathogneumonic rash caused by glucagonma, causing [erythema, superificial areas of epidermal necrosis => shed, form bullae and crust].

106
Q

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

A
  • Symptoms often subtle = hard to diagnose
  • Clinical manifestations:
    • 1. Diabetes
    • 2. Cholelithiasis (gallstones)
    • 3. Steatorrhea
    • 4. HYPOchlorhydria
107
Q

Somatostatinoma

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

A
  1. ↓ insulin
  2. ↓ gallbladder motility
  3. ↓ exocrine pancreatic secretions
108
Q

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

A
  • Increase VIP (vasoactive intestinal peptide) secretion by D1 cells => intestinal fluid secretion =>
  • WDHA syndrome
      • Watery diarrhea
    • - HYPOkalemia
    • - Achlorhydria
109
Q

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

  • What else gives you this symptoms?
  • Metastatic rate?
A

- Flushing

- Carcinoma tumors

- 80% metastatic rate

Endo/Repro 2 Final (11 decks)

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