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Endocrine & Reproduction II Exam #2 > Endocrine Pancreas Pathology > Flashcards

Endocrine Pancreas Pathology Flashcards

1
Q

Where do the majority of the islets of Langerhans exist within the endocrine pancreas?

A

In the neck and tail

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2
Q

What is secreted by the following cells of the endocrine pancreas?

Alpha cell
Beta cell
Delta cell
D1 cell
PP cell
A 
Alpha cell - glucagon
Beta cell - insulin
Delta cell - somatostatin
D1 cell - VIP
PP cell - pancreatic polypeptide
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3
Q

What is the step-by-step mechanism of insulin release? (5)

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

What is the marker of endogenous insulin levels? How is it produced?

A

C-peptide (helps differentiate what is produced vs. what is ingested). It is produced when proinsulin is cleaved to insulin and C-peptide.

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5
Q

Effects of insulin on adipose (3)

A

Increased glucose uptake
Increased lipogenesis
Decreased lipolysis

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6
Q

Effects of insulin on striated muscles (3)

A

Increased glucose uptake
Increased glycogen synthesis
Increased protein synthesis

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7
Q

Effects of insulin on the liver (3)

A

Decreased gluconeogenesis
Increased glycogen synthesis
Increased lipogenesis

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8
Q

What does oral glucose intake stimulate the release of?

What do they do?

What inactivates them?

A

Incretins (GLP-1, GIP, etc.).

Incretins stimulate insulin release and inhibit glucagon release resulting in lower blood glucose.

DPP-4 inactives incretins.

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9
Q

What is the onset like in T1DM vs. T2DM?

A

T1DM: childhood and adolescence typically
T2DM: usually adult

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10
Q

Which antibodies are circulating in T1DM?

A

Islet antibodies (anti-insulin, anti-GAD, anti-ICA512)

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11
Q

What is the pathogenesis of T1DM vs. T2DM?

A

T1DM: dysfunction in T-cell selection and regulation leading to breakdown in self-tolerance to islet auto-antigens.

T2DM: insulin resistance in peripheral tissues, failure of compensation by beta cells.

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12
Q

What pathological features are seen in the endocrine pancreas in T1DM vs. T2DM?

A

T1DM: insulitis (inflammatory infiltrate w/ T-cells and Mo); beta cell depletion; islet atrophy.

T2DM: no insulitis; amyloid deposition in islets; mild beta cell depletion.

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13
Q

Which genes are associated with the susceptibility loci in T1DM?

Which chromosome?

A

MHC class II genes

Chr. 6p21 (approx. 50% of T1DM)

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14
Q

At what point destruction of islet cells does T1DM ensue?

A

> 90% of islet cells destroyed

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15
Q

What 2 features must be present to cause T2DM?

A

Insulin resistance + beta cell dysfunction

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16
Q

What is Maturity-onset diabetes of the young (MODY)?
What are 3 features?

What is the genetic linkage?

A

It resembles T2DM, but in youth.

  • increased blood insulin
  • NO auto-Abs
  • non-ketotic

Mutations causing a loss of function of glucokinase.

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17
Q

Classic triad of T1DM includes what?

A

Polyphagia, Polyuria, Polydipsia

18
Q

How is T2DM usually identified?

A

On screening; may have vision changes, fatigue.

19
Q

Why is T1DM more difficult to diagnose in AA and Hispanic children?

What HLA typing can be helpful?

A

Because auto-antibodies exist in <50% of AA and Hispanic children (90% in Caucasian).

HLA DR/DQ on chr. 6

20
Q

What type of DM does diabetic ketoacidosis usually occur in?

What is the most common cause?

What is common as a precursor to its onset?

What is the triad?

A

T1DM

Non-compliance is most common etiology

Precursor infections: pneumonia, UTIs

Hyperglycemia, ketonemia, metabolic acidosis

21
Q

What are 5 steps to developing diabetic ketoacidosis?

A
  1. Body cannot use glucose, so it accumulates in blood (epinephrine released).
  2. Glucagon is released, promoting GNG.
  3. Insulin deficiency promotes FFA release, generating ketones.
  4. Shock, dehydration (more epinephrine).
  5. Kidneys dump glucose and ketones, causing an osmotic diuresis.
22
Q

Which 2 ketones accumulate in diabetic ketoacidosis?

How is ketoacidosis diagnosed?

A

Acetoacetic acid + Beta-hydroxybutyrate

Test for ketones in urine

23
Q

DKA uniting pathophysiology (3)

Resulting in (3)

Presenting sings/symptoms (3)

A

Pathophysiology: hyperglycemia, ketonemia, acidosis

Resulting in: dehydration, polydipsia, polyuria/ketonuria

Presenting signs/symptoms: N/V, tachycardia, Kussmaul respirations

24
Q

What are Kussmaul respirations?

A

Compensatory alkalosis for metabolic acidosis (a decrease in PCO2 decreases the [H+]; pH increases)

25
Q

How is DKA treated? (3)

A

Insulin, hydration and K+

26
Q

Hyperglycemic hyperosmotic syndrome (HHS) is an…

What is it a culmination of?

Presenting signs/symptoms?

What is a unique feature?

A

Acute hyperglycemic crisis in T2DM

Culmination of prolonged insulin deficiency: increased GNG, decreased glucose uptake in peripheral tissues.

Glc > 600 mg/dl
Severe dehydration
Hyperosmolality (>350 mOsm) - obtundation, coma
Impaired renal function

There are NO ketones

27
Q

Extreme hyperglycemia: DKA or HHS?

A

HHS (extreme); DKA has hyperglycemia, but not extreme

28
Q

What is hemoglobin A1C?

What does it measure?

What is the target range?

A

Irreversible glycosylation of the Hgb tetramer = Hgb A1C

Measure of long-term diabetic control (binding takes place over 1 mo.)

Target A1C is 6.5-7 or less

29
Q

Increased risk of which diseases/processes in patients with chronic hyperglycemia? (3)

A

Stroke
MI (2x - most common COD)
LE gangrene (100x)

30
Q

Advanced glycated end products can have which effects on vasculature? (5)

A 
Cytokines and GFs (TGF-b and VEGF)
ROS
Procoagulant activity
SM proliferation
Cross-linking matrix proteins (proatherogenic)
31
Q

What are 3 primary pathologic lesions in diabetic nephropathy?

A

Glomerular sclerosis - thickening of BM, disruption of protein cross-linkage which causes leakage of protein into the urine.

Renal vascular lesions - arteriosclerosis

Pyelonephritis

32
Q

How is diabetic nephropathy screened?

It is the leading cause of…

A

Albumin:creatinine ratio

ESRD in the US

33
Q

What is Kimmelstein-Wilson disease?

A

A renal disease associated with longstanding DM. It leads to destruction of small vessels in the kidney and nodular mesangial matrix accumulation in the glomeruli (PAS +).

34
Q

Diabetic retinopathy causes ________, which leads to… (3)

What other ocular complications occur in DM? (2)

A

Neovascularization

  • hypoxia leads to VEGF overexpression
  • hemorrhage
  • blindness

Cataracts and Glaucoma

35
Q

What are the unifying features of pancreatic neuroendocrine tumors? (4)

A

Gross appearance - solid, yellow/tan

Predilection for pancreatic neck and tail

Histology: “well-differentiated neuroendocrine tumors”

EM: secretory granules

36
Q

Pancreatic neuroendocrine tumors: which is least likely to metastasize?

A

Insulinoma: 10% risk of Mets.

All others are 60-80% risk of Mets.

37
Q

Amyloid is most common histological finding in which NE pancreatic tumor?

A

Insulinoma

38
Q

What is the triad in a Gastrinoma?

A

Islet cell tumor
Gastric acid hypersecretion
Peptic ulceration

39
Q

What is a clue to clinical diagnosis of a Gastrinoma?

A

Peptic ulcers that do not respond to conventional therapy

40
Q

What are the major manifestations of a Somatostatinoma? (3)

Why?

A

Reduced insulin
Reduced Gb motility
Reduced exocrine pancreatic secretions

Somatostatin functions as a paracrine regulator, so its manifestations are typically inhibitory.

41
Q

What is pathognomonic of a Glucagonoma?

What are the symptoms? (4)

It may cause…

A

Necrolytic migratory erythema - erythema, epidermal necrosis progressing to epidermal shedding, bullae formation and crusted erosions.

4 D’s - diabetes, dermatitis, depression and DVTs.

It may cause a mild DM.

42
Q

What is WDHA?

Which NE tumor does it occur in?

A

Watery diarrhea, hypokalemia, achlorydia

Occurs in patients with a VIPoma

Endocrine & Reproduction II Exam #2 (10 decks)

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