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Robbins Pathology- Endocrine (Chapter 24) > Chapter 24- Endocrine Pancreas > Flashcards

Chapter 24- Endocrine Pancreas Flashcards

1
Q

What is the process of insulin release

A

1) GLUT2 take glucose into the cells
2) Glucose generates ATP
3) ATP inhibits the membrane potassium channels
4) Depolarization results in calcium influx
5) Calcium influx causes insulin release

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2
Q

What are the locations that Islets of Langerhans are located

A

Neck and tail of pancreas

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3
Q

What is the effect of insulin on the adipose tissue

A

Increased glucose uptake

Increased Lipogenesis

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4
Q

What is the effect of insulin on striated muscle

A

Increased glucose uptake
Increased glycogen synthesis
Increases protein synthesis

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5
Q

What is the effect of insulin on the liver

A

Increased glycogen synthesis
Increased lipgenesis
Decreased gluconeogensis

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6
Q

What is the serum marker that is indicative for endogenous insulin

A

C peptide, as it is only created which insulin is cleaved into its activated form.

*Can be used to differentiate synthetic and endogenous insulin

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7
Q

What causes the release of incretins

A

Oral glucose

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8
Q

What are the incretins

A
  • Glucagon like peptide-1 (GLP-1)

- Glucose dependant insulin releasing polypeptide (GIP)

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9
Q

What is the mechanism of action for incretins

A

Stimulate insulin release and inhibit glucagon release, resulting in a lower blood sugar level

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10
Q

What is the role of dipeptidyl peptdidase 4 (DDP-4) on incretin levels

A

Inactivate incretins, so the blood glucose level will rise

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11
Q

What is the significance of DDP on potential diabetes treatment

A

By blocking DDP4, there will be less incretin breakdown. As a result, there will be more blood glucose uptake and a reduction in the serum blood levels

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12
Q

What is the major gene linking to T1D

A

MHC class 2 on chromosome 6p21

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13
Q

How much of the pancreas must be destroyed to see T1D symptoms

A

> 90%

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14
Q

What are the major risk factors for T2D

A
  • First degree relatives, so there is a familial aspect

- Obesity

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15
Q

What is are the characteristics of maturity onset diabetes of the young (MODY)

A

T2D like, but in the young:

  • Increased blood insulin
  • No Autoantibodies
  • NOnketotic
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16
Q

What is the genetic link to MODY

A

Mutations resulting in the loss of function in glucokinase

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17
Q

When is the time to scan for gestation DM

A
  • At the time of initial visit

- Second visit, at 24 to 28 weeks gestation.

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18
Q

What is the triad for diabetes

A
  • Polyphagia (eating more)
  • Polyuria (peeing more)
  • Polydipsia (drinking more)
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19
Q

How is T2D usually identified on screening in children

A
  • Fatigue or vision changes
  • Increased thirst and urination
  • Extreme hunger
  • Weight loss
  • Irritability of behavior changes
  • Fruity smelling breath
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20
Q

What is the HLA typing for T1 or T2D

A

HLA DQ/DR on chromosome 6

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21
Q

What is a large deciding factor on T1 or T2DM

A

Presence of autobodies

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22
Q

How does the level of antibodies in T1D different between races

A
  • Present in >90% of Caucasian children

- Present in < 50% of African American and Hispanic children

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23
Q

Diabetic ketoacidosios is more commonly seen in which form of diabetes

A

Type 1

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24
Q

What is the triad of diabetic ketoacidosis

A
  • Hyperglycemia
  • Ketonemia
  • Metabolic acidosis
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25
Q

What are the common causes of diabetic ketoacidosis

A
  • Noncompliance*** most common

- Precursor infections such as pneumonia and UTI

26
Q

How to test for ketones

A

IN the urine

27
Q

What are the usual clinical presenting signs from DKA

A
  • Nausea/Vomiting
  • Tachycardia
  • Kussmaul respiration’s
28
Q

What is Hyperglycemic hyperosmotic syndrome (HHS)

A

Acute hyperglycemic crisis in T2DM

29
Q

What are the presenting features for HHS that differentiation for DKA

A
  • Hyperglycemia (>600)
  • Severe dehydration
  • Hyperosmolaloty (can cause coma)
  • Impaired renal function
  • NO KETONESSS****
30
Q

What is the most common cause of death in diabetics

A

Myocardial infarction

31
Q

What are diabetics at a higher risk for

A
  • Stroke
  • MI (2x)
  • Lower extremity gangrene (100x)
32
Q

What are the major complications of diabetes in the eye

A

Retinopathy, cataracts, glaucoma

33
Q

What are the major complications of diabetes in the kidney

A

Nephropathy

34
Q

What are the major complications of diabetes with neuropathy

A

Pain, numbness, feet wounds and gangrene

35
Q

What are the major complications of diabetes in the brain

A

TIA, cognitive impairment

36
Q

What are the effects of advanced glycated end products

A
  • Cytokines (TGF-Beta, VEGF)
  • Reactive oxygen species
  • Procoagulation
  • Proliferation of smooth muscle
  • cross linking of matrix proteins (proatherogenic)
37
Q

What is the leading cause of end stage renal disease in the US

A

-Diabetic nephropathy

38
Q

What are the three leasions seen during diabetic nephropathy

A
  • Glomerular sclerosis
  • Renal vascular lesions
  • Pyelonephritis
39
Q

What is the happening during the glomerular sclerosis as a result of diabetic nephropathy

A

-Thickening of the basement membrane and disruption of the cross linkages that make the membrane a filter

40
Q

What are the pathological changes seen in diabetic nephropathy

A
  • Early basement membrane thickening

- Kimmelstiel-Wilson disease (Nodular mesangial matrix accumulation in glomerulus)

41
Q

What is the gold standard for testing for diabetic nephropathy

A

Urine albumin testing (UACR), as the first sign on diabetes is protein in the urine due to loss of filter function

42
Q

What are the physical changes seen during diabetic retinopathy

A
  • “Cotton wool” spots
  • Hemorrhages and aneurysms

**Due to the neovascularization

43
Q

What is the process that diabetes causes retinopathy

A

Neovascularization due to hypoxia leading to increased VEGF and blood vessels

44
Q

What are some of the eye conditions that are seen as a result of diabetes

A
  • Cataracts

- Glaucoma

45
Q

Which infections are diabetics at a higher risk for

A
  • Cellulitis
  • Pneumonia
  • Pyelonephritis
46
Q

Which portion of the pancreas are at a higher risk for pancreatic neuroendocrine tumors

A

Neck and tail

47
Q

What are the histological findings for a pancreatic neuroendocrine tumor

A

-Well differentiated with secretory granules

48
Q

What type of cell tumor and rate of metastasis in an insulinoma

A

Beta cell with 10% metastasis

49
Q

What type of cell tumor and rate of metastasis in an gastrinoma

A

G cells with 60% metastasis

50
Q

What type of cell tumor and rate of metastasis in an somatostatinoma

A

Delta cell with 80% metastatic rate

51
Q

What type of cell tumor and rate of metastasis in a glucagonoma

A

Alpha cell with 60% rate of metastasis

52
Q

What type of cell tumor and rate of metastasis in an VIPoma

A

D1 cell with 80% rate of metastasis

53
Q

What is the common histological finding in insulinoma

A

Amyloid

54
Q

What are the characteristics of the a insulinoma

A
  • Small tumors causing hypoglycemia

- C peptides levels are used to make the diagnosis

55
Q

What are the symptoms, aka the triad of gastrinoma

A

Aka Zollinger ellison syndrome:

  • Islet cell tumor
  • Gastric acid hypersecretion
  • Peptic ulceration
56
Q

How are gastrinomas usually found

A

Ulcers that do no respond to the normal therapy

57
Q

What is the triad of a somatostatinoma

A
  • Diabetes
  • Cholithiasis
  • Steatorrhea
58
Q

What is the cause of the triad that is normally seen in a somatostatinoma

A
  • Reduced insulin (diabetes)
  • Reduced gallbladder motility (gallstone)
  • Reduced exocrine pancreatic secretions (steatorrhea)
59
Q

What are the clinical presentations of a glucagonoma

A

4 D’s

  • Diabetes
  • Dermatitis (necrolytic migratory erythema in groin or LE)
  • Depression
  • DVTs
60
Q

What are the clinical presentations of a VIPoma

A

WDHA syndome:

  • Watery diarrhea
  • Hypokalemia
  • Achlorhydria

*Can also result in flushing in 20%

Robbins Pathology- Endocrine (Chapter 24) (5 decks)

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