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Pathophysiology Exam 3 > Lecture 30 > Flashcards

Lecture 30 Flashcards

1
Q

Islet Cell Tumors

A
  • aka Pancreatic Neuroendocrine Tumors (NETs)
  • Derive from neuroendocrine cells in islets of Langerhans
  • May be benign or malignant
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2
Q

Malignant Pancreatic Neuroendocrine Tumors (NETs)

A
  • Pancreatic Endocrine cancer or islet cell carcinoma
  • Present with multiple metastatic tumor deposits in the liver
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3
Q

Why is the removal of localized tumors usually curative?

A
  • Most islet cell tumors are nonfunctional and often reach a large size before being discovered
  • Most islet cell tumors develop in the tail of the pancreas and do not produce common duct obstruction and jaundice (common in ductal pancreatic adenocarcinomas)
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4
Q

How are metastatic pancreatic neuroendocrine tumors treated?

A

Octreotide (somatostatin analog) may ameliorate hormonal symptoms but does not cure

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5
Q

Insulinomas

A

Most common functioning pancreatic endocrine tumors

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6
Q

How is insulin synthesized?

A
  1. Insulin gene transcripts code for precursor protein (pre-proinsulin)
  2. Removal of its signal peptide in the endoplasmic reticulum of pancreatic beta-cells converts it to proinsulin
  3. Proinsulin is cleaved by two endopeptidases (proprotein convertases 1 and 2) that remove the internal C peptide linking the alpha and beta chains
  4. Equimolar amounts of insulin and C-peptide are stored in secretory granules of beta cells and both are released into portal circulation
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7
Q

What is used as a means of distinguishing T1DM and T2DM?

A

C-peptide levels in peripheral circulation (T1DM has decreased C-peptide levels and T2DM has normal or increased C-peptide levels)

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8
Q

Explain the process of insulin secretion.

A
  • Insulin release is stimulated by plasma glucose concentration
    1. Glucose enters beta cells via facilitated diffusion
    2. Increased intracellular glucose increases the ATP/ADP ratio -> blockage of the ATP-sensitive K+ channel in the PM
    3. Depolarization -> opens voltage dependent calcium channels -> increase the amplitude of free cytosolic Ca2+ levels
    4. Increased intracellular calcium triggers docking and fusion of neurosecretory granules with the plasma membrane -> exocytosis of insulin into extracellular environment
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9
Q

Neonatal Diabetes

A

Mutations of components of the K(ATP) channel

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10
Q

Explain the process of glucose uptake.

A
  1. Insulin binds to its receptor (tyrosine kinase)
  2. Receptor phosphorylates insulin receptor substrates (family of cytoplasmic adaptor proteins that transmit signals from the insulin and IGF-1 receptors)
  3. Includes translocation of Glut-4 transporter to the plasma membrane and influx of glucose
  4. Glycogen synthesis, glycolysis, fatty acid synthesis
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11
Q

Glucose transporter type 4 (GLUT4)

A

Insulin-regulated glucose transporter (facilitated diffusion) found primarily in adipose tissues and striated muscle (skeletal and cardiac)

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12
Q

What are the two types of glucose transporters?

A
  1. Glucose transporter proteins (GLUTs/ Solute Carrier Family SLC2A)
  2. Sodium-dependent glucose transporters (SGLTs)
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13
Q

Glucose transporter proteins

A
  • Transport glucose through facilitated diffusion
  • 14 expressed in the body (other substrates as well: fructose, myoinositol, urate)
  • Some are insulin regulated and some are not
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14
Q

Sodium-dependent glucose transporters

A

Energy-coupled mechanism (active transport)

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15
Q

Fed-state metabolism (Increased glucose metabolism)

A

Increased plasma glucose -> stimulates beta pancreatic cells and inhibits alpha pancreatic cells -> increase insulin -> muscle, adipose, liver -> increase glucose transport, glycolysis, glycogenesis, lipogenesis -> decrease plasma glucose

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16
Q

Fasted-state metabolism (decreased plasma glucose)

A

Decreased plasma glucose -> (1) stimulate alpha cells of pancreas and (2) inhibits beta cells of pancreas

  1. Increases glucagon -> liver -> glycogenolysis, gluconeogenesis, ketones -> Increase plasma glucose -> for use by brain and peripheral tissue
  2. Decreased insulin -> muscle and adipose tissue -> lactate, pyruvate, amino acids, fatty acids -> liver -> (1)
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17
Q

What can tumors with a hormonal syndrome present with?

A
  1. Hyperglycemia (due to glucagon-secreting tumors)
  2. Hypoglycemia (due to insulin-secreting tumors)
  3. Achlorhydria (due to somatostatin-secreting tumors
  4. Peptic ulcers (due to gastrin secreting tumors)
  5. Secretory diarrhea (Pancreatic Diarrhea): due to malignant VIPoma inducing glycogenolysis and hyperglycemia -> stimulate GI fluid secretion
18
Q

Type 1 Diabetes

A
  • Insulin-dependent
  • Lack of insulin because of a destruction of beta cells
  • Require exogenous insulin to maintain life
  • Beta cell damage by the action of cytokines and autoantibodies produced by inflammatory cells
  • Susceptible to ketosis
19
Q

Type 2 Diabetes

A
  • Non-insulin dependent
  • Insufficient insulin secretion relative to glucose levels
  • No exogenous insulin needed
  • Decrease in tissue response to insulin
  • Insulin resistance of peripheral target tissues: decrease in the number of insulin receptors or deficient postreceptor signaling
20
Q

Cystic Fibrosis cancer risk

A
  • CF patients have a 5-10x higher risk of developing colorectal cancer
  • CF patients that have had a solid organ transplant (ex: lung) have a 20% increased risk of developing colorectal cancer
21
Q

Cystic Fibrosis-related Diabetes

A
  • About 30% of CF patients develop Cystic Fibrosis-related diabetes or CFRD
  • Mucus sticks to pancreas and limits the amount of insulin that is secreted
  • Treated with blood glucose monitoring, insulin injections, and proper diet
22
Q

Diabetic ketoacidosis

A

Serious complication of T1DM but may also occur in T2DM

23
Q

What blocks any residual insulin action in T1DM and stimulates the release of glucagon?

A

Epinephrine

24
Q

What key factors should raise suspicion of diabetes?

A

Combination of polyphagia and weight loss

25
Q

Explain the effects of insulin deficiency.

A
  1. Stimulates lipoprotein lipase
  2. Excessive breakdown of adipose stores and an increase in levels of FFAs -> esterified to fatty acyl CoA in lover
  3. Oxidation of fatty acyl CoA molecules within the hepatic mitochondria produce ketone bodies (acetoacetic acid and beta-hyroxybutyric acid) -> ketonemia and ketonuria
  4. Results in systemic metabolic ketoacidosis
26
Q

How does the unopposed secretion of counter-regulatory hormones play a role in metabolic derangements?

A
  1. Release of epinephrine blocks any residual insulin action and stimulates the release of glucagon
  2. Insulin deficiency and glucagon excess decreases peripheral utilization of glucose while increasing gluconeogenesis (exacerbating hyperglycemia)
  3. Activation of the ketogenic machinery alters the insulin: glucagon ratio (release of ketogenic amino acids by protein catabolism aggravates the ketonix state)
27
Q

What is the result of an absolute insulin deficiency?

A

Leads to a catabolic state -> ketoacidosis and severe volume depletion -> sufficient CNS compromise -> coma or death

28
Q

Atherosclerosis of aorta and larger blood vessels

A
  • Late DM complication
  • Leads to myocardial and brain infarctions and gangrene of lower extremitites
29
Q

Arteriolosclerosis

A

Thickening of the wall of the arterioles and is associated with hypertension

30
Q

Gangrene and DM

A

Feet; caused by blood vessel obstruction as a consequence of vascular arteriosclerosis

31
Q

What causes nonenzymatic glycosylation of proteins?

A

Elevated serum glucose (ex: Hb A1C)

32
Q

Eye complications associated with diabetes

A
  • Total blindness
  • Retinopathy: damage of the retina
  • Cataract: opacity of the lens
  • Glaucoma: impaired drainage of the aqueous humor
33
Q

Kidney diseases associated with diabetes

A
  • Glomerulosclerosis
  • Arteriosclerosis
  • Pyelonephritis
  • Diffuse thickening of the basal lamina of the glomerular capillaries and proliferation of mesangial cells (Kimmelstiel-Wilson lesion)
34
Q

Peripheral neuropathy

A

-Most common form of diabetic neuropathy
- Affects very end of the nerves first (starting with the longest nerves) -> legs and feet often affected first, followed by hands and arms

35
Q

Autonomic neuropathy

A

ANS controls heart, badder, lungs, stomach, intestines, sex organs, and eyes -> diabetes can impact the nerves in any of these areas

36
Q

Radiculoplexus neuropathy

A
  • Diabetic amyotrophy, femoral neuropathy, proximal neuropathy
  • Affects nerves closer to hips or shoulder
  • More common with T2DM or older patients
37
Q

Mononeuropathy

A
  • Focal neuropathy
  • Means damage to just one nerve
  • Sudden onset
  • Ex: carpal tunnel syndrome
38
Q

Gestational Diabetes

A

Any degree of glucose intolerance that develops during pregnancy due to inability to secrete adequate insulin to overcome insulin resistance created by placental hormones

39
Q

Explain what happens with Gestational Diabetes

A
  1. Pregnancy: counter regulatory state
  2. Insulin resistance as well as inability of pancreas to make the additional insulin needed to supply the placenta
  3. Precipitated by the increasing levels of hormone: chorionic somatomammotropin (placental lactogen), progesterone, cortisol, and prolactin (counter-regulatory anti-insulin effects)
40
Q

What can happen with gestational diabetes if untreated?

A
  • Fetal macrosomia: abnormally large body size
  • Neonatal hypoglycemia (due to pancreatic islet hyperplasia and excess insulin secretion)
  • Polycythemia and hyperbilirubinemia in newborn
  • Complications for the mother: increase risk of chronic hypertension and C-section
41
Q

Metabolic Syndrome

A
  • Combination of T2DM, atherosclerosis, and high blood pressure
  • Criteria: central obesity (fasting glucose >110 mg/dL and elevated fasting plasma triglycerides), low plasma HDL levels, blood pressure > 130/85 mmHg
  • Renal disease also associated

Pathophysiology Exam 3 (10 decks)

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