30: Clinical Endocrinology Flashcards

1
Q

What is the honeymoon period in T1DM?

A

The period of time following diagnosis where the pancreas can produce a significant amount of insulin to reduce insulin needs (~10% remaining)

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2
Q

What are the counter regulatory hormones to insulin?

A
  • Glucagon
  • Catecholamines
  • Cortisol
  • Growth hormone
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3
Q

What are the actions of insulin?

A

ANABOLIC

Stimulates: glucose uptake, glycolysis glycogen synthesis, protein synthesis, uptake of ions

Inhibits: gluconeogenesis, glucogenolysis, lipolysis, ketogenesis, proteolysis

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4
Q

Why are fluctuations in blood sugar throughout the day important?

A

Creates gradients that allow glucose to enter the cell (aid uptake)

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5
Q

What is the mechanism of action of insulin

A
  • Bind to insulin receptor on cell
  • Stimulates translocation of GLUT4 to cell surface
  • Allows glucose to be taken up by the cell via passive diffusion
  • Stimulate glycogen syntehsis, fatty acid synthesis
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6
Q

Where does energy at birth come from?

A

20% from metabolising ketones

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7
Q

What is the mechanism of ketone production?

A
  1. White fat - activation of hormone sensitive lipase causes lipolysis of triglycerides (inhibited by INSULIN)
  2. Liver - NEFA taken up by hepatocytes, undergoes oxidation to Acetyl CoA
  3. Mitochonrdia - Acetyl CoA broken down into ketones
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8
Q

What are the 3 important ketones?

A
  • Acetoacetate
  • Beta hydroxybutyrate
  • Acetone
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9
Q

Ketones require ____ + ___

A

Lack of insulin + excess glucagon

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10
Q

How does DKA affect the ion gap?

A
  • Increases

- Dissociation of acids means H+ free to bind to bicarbonate (CO2 and H2O)

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11
Q

Why might a patient being treated for DKA have hyperchloremia?

A
  • Fluid replacement with 0.9% NaCl

- Salt loading and normalising of Na (salt lost in urine) but no net loss of Cl - causes hyperchloremia

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12
Q

Why does urine testing with a ketone strip tend to underestimate the extent of acidosis in DKA?

A
  • Reaction occurs in the presence of acetoacetate

- In DKA AcAc pushed to BOHB (less to react and cause colour change)

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13
Q

Why are bedside tools poor for measuring severe acidosis?

A

Too saturated

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14
Q

Where is the majority of intracellular K stored?

A

Muscle

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15
Q

K is regulated with a feed___ mechanism

A

Forward - does not rely on serum levels to trigger reaction

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16
Q

How do:

  • Insulin
  • cAMP and glucagon
  • Aldosterone

Affect serum K

A
  • Insulin stimulates Na/K/ATPase and inc. K uptake
  • cAMP and glucagon stimulated by protein rich meal, shift transtubular K gradient and inc. GFR
  • Aldosterone promotes K uptake by cells and renal excretion
17
Q

Acidosis increases/decreases K loss from cells

A

Increases

18
Q

What effect can beta blockers have on K levels?

A
  • Prevent muscle reuptake

- Inc s[K]

19
Q

What are the 3 determining factors of K secretion?

A
  1. Activity of Na/K/ATPase
  2. Permeability of luminal membrane
  3. Electrochemical gradient from lumen -> blood
20
Q

Why do a lot of diuretics decrease serum K?

A

Inc. distal tubular flow results in decreased serum K