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15 Endocrine > 15.9 Endocrine Pancreas > Flashcards

15.9 Endocrine Pancreas Flashcards

1
Q

DKA:

-Tx (3)

A
  1. fluids (because of osmotic diuresis of glucose)
  2. insulin
  3. replace electrolytes (esp K)
    - replace K because giving insulin will reverse the hyperkalemia and put serum K inside cells, leading to hypokalemia. Also, even though DKA pt had hyperkalemia, total K was being lost in the osmotic diuresis.
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1
Q

T2DM

-What is the mechanism by which obesity contributes to this?

A

-Obesity leads to decreased numbers of insulin receptors

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1
Q

Diabetic nephropathy:

-stages of renal damage (3)

A
  1. microalbuminuria–initial preferential involvement of efferent arterioles of glomeruli leads to glomerular hyperfiltration
  2. nephrotic syndrome–hyperfiltration leads to this. characterized by Kimmelstein-Wilson nodules in glomerulus
  3. Chronic renal failure–afferent arterioles damaged later, leading to Diffuse sclerosis of glomerulus
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2
Q

Pt presents with hypoglycemia and you measure high insulin levels.

-Think what? and how to differentiate

A
  1. insulinoma (high C peptide)
  2. exogenous insulin (low C peptide)
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3
Q

Insulin effect on skeletal, adipose tissue

-mech

A
  • increase GLUT4 transporter on surface of cells to allow glucose intake
  • increased glucose uptake leads to increased glycogen synthesis, protein synthesis, and lipogenesis
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4
Q

Diabetes long term complications

-divided into 2 categories of mechanism

A
  1. NEG–non enzymatic glycosylation of vascular basement membranes
    - atherosclerosis, hyaline arteriolosclerosis, HbA1C
  2. Osmotic damage
    - diabetic neuropathy, retinopathy, cataracts
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5
Q

Diabetes: Non-enzymatic glycosylation

-effects (3)

A

NEG of vascular basement membranes:

  1. med/large vessels: atherosclerosis
    - peripheral vascular disease
  2. small vessels: hyaline arteriolosclerosis
    - diabetic nephropathy
  3. glycated hemoglobin: Hb A1C
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5
Q

Pancreatic endocrine tumors:

-assoc with what syndrome

A

MEN 1

PPP:

pituitary, pancreatic, parathyroid

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6
Q

Somatostatinoma

-clinical presentation (2) and why?

A
  1. achlorhydria (inhibition of gastrin)
  2. steatorrhea (inhibition of CCK)
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7
Q

Pancreatic endocrine neoplasms:

-name 4

A
  1. insulinoma
  2. gastrinoma (ZE syndrome)
  3. somatostatinoma
  4. VIPoma
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8
Q

Histology of pancreas islet of Langerhans

-describe

A

beta cells: insulin

alpha cells: glucagon

delta: somatostatin

beta cells in center of islet, alpha surround them, and exocrine acini surround the islet

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9
Q

T2DM

  • what % of diabetics
  • what % of US population
  • arises classically what population
  • genetic predisposition?
A
  • 90% of diabetics
  • 5-10% of US population
  • middle aged, obeses
  • Yes, strong genetic predisposition
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9
Q

T2DM

  • risk for what acute crisis
  • mech
A

Hyperosmolar non-ketotic coma

  • high glucose (>500) leads to life-threatening diuresis with hypotension and coma
  • Ketones are absent because small amount of insulin counteracts glucagon’s effect of lipolysis
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11
Q

Pt presents with T2DM

-would you expect to see high or low insulin levels?

A
  • High, if early in disease
  • Low, if late in disease–beta cell exhaustion causes insulin deficiency. (Give insulin)
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12
Q

T1DM

  • etiology
  • what type of hypersensitivity reaction?
  • assoc with what HLA’s
A
  • autoimmune destruction of beta cells by T lymphocytes
  • type 4 HSR
  • HLA DR3 and DR4
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13
Q

Diabetes: long-term osmotic damage

  • mech
  • effects: (3)
A
  • glucose free enters certain cells, where Aldose reductase converts glucose to sorbitol, resulting in osmotic damage
    1. Schwann cells (myelinate peripheral nerves)–peripheral neuropathy
    2. Pericytes of retinal blood vessels–retinopathy
    3. Lens–cataracts
15
Q

-fasting glucose: normal, prediabetic, diabetic

A

normal 70-99

prediabetic 100-125

diabetic >125

16
Q

DKA:

What type of acidosis?

what happens to serum K and why? (2 mechs)

A
  • anion gap (ketones) met acidosis
  • hyperkalemia because:
    1. K is a buffering mechanism for acidosis–intracellular K leaves cells, allowing H+ to enter cells
    2. Insulin induces K to enter cells (this protects you from hyperkalemia after a meal). T1DM has no insulin.
18
Q

DKA

-in treatment, why give pt K+ even though pt has hyperkalemia?

A
  • Prevent hypokalemia
  • When you give pt insulin, the insulin will push K inside cells, reversing the hyperkalemia to hypokalemia. Also, total K is low since K was excreted in the osmotic diuresis.
19
Q

T1DM

-what may be present in the blood years before clinical disease develops?

A

-Ab against insulin are often present in T1DM, and may be present years before clinical symptoms

20
Q

Diabetes: what glucose levels:

  • random glucose
  • fasting glucose
  • glucose tolerance test
A

random >200

fasting >125

glucose tolerance test: >200, 2 hours after glucose loading

21
Q

VIPoma

-clinical presentation

A

“WDHA”

  1. watery diarrhea
  2. hypokalemia
  3. achlorhydria–VIP inhibits gastric acid secretion

VIP relaxes intestinal smooth m, with NO

Ach and Substance P contract it

22
Q

Names of ketones in DKA

A
  1. beta-hydroxybutyric acid
  2. acetoacetic acid
24
Q

T1DM

  • risk of what deady acute complication?
  • when does it occur
  • mech
A
  • DKA–diabetic ketoacidosis
  • often arises with stress (eg infection)–Epi stimulates glucagon secretion, increasing lipolysis (and gluconeogenesis, glycogenolysis), leading to increased free fatty acids. FFA are converted by liver into ketones to supply energy to brain.
  • Ketones are acidic
25
Q

Insulinoma

  • clinical presentation
  • Tx
  • dx
A
  • presents as episodic hypoglycemia (mental status changes)
  • Tx with glucose
  • Dx with low glucose levels, high insulin, and high C-peptide

15 Endocrine (7 decks)

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