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*GIGU I > 17. Endocrine Pancreas Pathology > Flashcards

17. Endocrine Pancreas Pathology Flashcards

1
Q

4 cell types of the islets of langerhans and their phormone products

A

Beta cells — insulin

Alpha cells — glucagon

Delta cells — somatostatin

PP cells — pancreatic polypeptide

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2
Q

Hormone product of D1 cells of the pancreas

A

Vasoactive intestinal polypeptide (VIP)

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3
Q

______ is the transporter responsible for glucose uptake into beta cells. Glucose metabolism generates ATP which inhibits the membrane K+ channel, allowing ____ influx, which results in insulin release

A

GLUT-2; Ca++

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4
Q

During processing, proinsulin is cleaved to form insulin and ____, which a marker of endogenous insulin

A

C peptide

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5
Q

Oral glucose stimulates the release of ______ which stimulate insulin release and inhibit glucagon release resulting in lower blood glucose

A

Incretins

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6
Q

What are examples of incretins?

A

Glucagon-like peptide-1 (GLP-1)

Glucose-dependent insulin-releasing polypeptide (GIP)

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7
Q

Incretins are inactivated by _______

A

Dipeptidyl peptidase-4 (DPP-4)

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8
Q

Difference in age of onset between T1D and T2D

A

T1D: usually childhood and adolescence

T2D: usually adult, increasing incidence in childhood and adolescence

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9
Q

Difference in autoantibodies between T1D and T2D

A

T1D: presence of circulating islet autoantibodies (anti-insulin, anti-GAD, anti-ICA512) [major linkage to MHC class II genes — specifically HLA gene cluster on Chr6p21]

T2D: no islet antibodies [no HLA linkage]

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10
Q

Difference in pathogenesis between T1D and T2D

A

T1D: dysfunction in T cell selection and regulation, leading to breakdown in self-tolerance to islet autoantigens

T2D: insulin resistance in peripheral tissues, failure of compensation by beta cells; multiple obesity-associated factors

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11
Q

What is insulitis, and which type of DM is it associated with?

A

Insulitis = inflammatory infiltrate of T cells and macrophages — associated with T1D

[T2D is NOT associated with insulitis, but may show amyloid deposition in islets]

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12
Q

What disease resembles T2DM clinically, but happens in youth — presenting with increased blood insulin but NO autoantibodies and is nonketotic?

A

Maturity-onset diabetes of the young (MODY)

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13
Q

Maturity-onset diabetes of the young (MODY) is most often caused by mutations resulting in loss of function of _______

A

Glucokinase

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14
Q

Risks to mom vs. risks to fetus with gestational diabetes

A

Mom: cesarean section (usually due to large size of fetus)

Fetus: neonatal hypoglycemia may lead to seizures and subsequent brain damage; macrosomia, congenital malformations, stillbirth

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15
Q

What are the 2 opportunities for gestational diabetes screening?

A

Screen at first prenatal visit for pre-existing DM — measure fasting plasma glucose (FPG), HgbA1c, or random plasma glucose

Screen at 24-28 weeks gestation with oral glucose tolerance test (OGTT) — glucose levels measured while fasting, 1 hour post-oral glucose, and 2 hours post-oral glucose

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16
Q

Classic triad of T1DM

A

Polyphagia
Polyuria
Polydipsia

Severe = diabetic ketoacidosis

[T2DM usually identified on screening — fatigue, vision changes, etc.]

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17
Q

Signs/symptoms of T1DM

A

Increased thirst and frequent urination

Extreme hunger

Weight loss

Fatigue

Irritability or behavior changes

Fruity-smelling breath

18
Q

How is T1DM distinguished from T2DM based on lab results?

A

Autoantibodies — present in T1DM only

HLA typing — HLADR/DQ on Chr6

[note that autoantibodies are more reliably detected in caucasian children with T1DM than AA and hispanic children]

19
Q

Clinical triad of DKA

A

Hyperglycemia (usually of T1DM)

Ketonemia

Metabolic acidosis

[presenting signs/symptoms include dehydration, polydipsia, polyuria/ketonuria, N/V, tachycardia, and Kussmaul respirations]

20
Q

Pathogenesis of DKA

A

Body can’t use flucose, so it accumulates in the blood

Glucagon is released, promoting gluconeogenesis

Kidenys dump glucose and ketones, osmotic diuresis occurs

Shock, dehydration, more epinephrine

Insulin deficiency promotes FFA release generating ketones

21
Q

DKA treatment

A

Insulin
Hydration
Potassium

[hypokalemia will rapidly occur when you give insulin, so you must also give K+]

22
Q

What is hyperglycemic hyperosmotic syndrome (HHS)?

A

Acute hyperglycemic crisis in T2DM

Culmination of prolonged insulin deficiency —> increased gluconeogenesis and decreased glucose uptake in peripheral tissues

23
Q

Presenting signs/symptoms of hyperglycemic hyperosmotic syndrome (HHS) — note which sign makes it different from DKA!

A

Glucose >600 mg/dL

Severe dehydration

Hyperosmolality (>350 mOsm/L) leading to obtundation, coma

Impaired renal function

[NO KETONES! — distinguishes it from DKA]

24
Q

What lab provides a measure of long-term diabetic control?

A

Hemoglobin A1c

25
Q

Major complications of diabetes

A

Eye: retinopathy, cataracts, glaucoma

Kidney: nephropathy

PNS: peripheral neuropathy

Brain: increased risk of stroke and cerebrovascular disease

Heart: coronary heart disease, 2x risk of MI (note it may present differently in diabetics)

Extremities: peripheral vascular disease + neuropathy —> gangrene

26
Q

Most common cause of death in diabetics

A

Myocardial infarction

27
Q

Leading cause of end-stage renal disease in the US

A

Diabetic nephropathy

28
Q

How is diabetic nephropathy tested for, and what are the 3 primary pathologic lesions

A

Albumin:Cr ratio in urine (gold standard)

3 primary pathologic lesions:
Glomerular sclerosis
Renal vascular lesions
Pyelonephritis

29
Q

What is Kimmelstiel-Wilson disease?

A

Nodular glomerulosclerosis associated with diabetic nephropathy

30
Q

Clinical features of diabetic retinopathy

A

Hemorrhages

Abnormal growth of blood vessels

Cotton wool spots

Hard exudates

31
Q

Pathogenesis of diabetic retinopathy

A

Neovascularization —> hypoxia leads to VEGF overexpression, hemorrhage, blindness

32
Q

Unifying features of pancreatic neuroendocrine tumors

A

Gross appearance — solid, tan-yellow

Predilection for the pancreatic neck and tail

Histology — well-differentiated

EM — secretory granules

33
Q

Amyloid is a common histologic finding among just one type of pancreatic neuroendocrine tumors — which one?

A

Insulinoma

34
Q

Insulinomas are small tumors that can produce episodes of symptomatic hypoglycemia (<50mg/dL). What lab finding is used to dx insulinoma?

A

Elevated C peptide levels

35
Q

Triad associated with gastrinoma (Zollinger Ellison syndrome)

A

Islet cell tumor

Gastric acid hypersecretion

Peptic ulceration

[diagnostic clue is when ulcers do not respond to conventional therapy]

36
Q

Triad associated with somatostatinoma

A

Diabetes

Cholelithiasis

Steatorrhea

[somatostatin functions as a paracrine regulator, so manifestations are typically inhibitory — reduced insulin, reduced gallbladder motility, reduced exocrine pancreatic secretions]

37
Q

What pancreatic neuroendocrine tumor presents with mild diabetes and a characteristic rash affecting the groin and lower extremities known as necrolytic migratory erythema?

A

Glucagonoma

38
Q

4 D’s of glucagonomas

A

Diabetes
Dermatitis
Depression
DVTs

39
Q

What pancreatic neuroendocrine tumor might be mistaken for a carcinoid tumor, due to the tendency to induce flushing and diarrhea?

A

VIPoma

40
Q

WDHA syndrome associated with VIPomas (triad)

A

Watery diarrhea

Hypokalemia

Achlorhydria

*GIGU I (67 decks)

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