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UWorld - Endocrine > Physiology > Flashcards

Physiology Flashcards

1
Q

What does sunlight exposure do in relation to vitamin D?

A

Converts 7-dehydrocholesterol to cholecalciferol (vitamin D3) in the skin.

(Vitamin D3 then gets converted to its storage form 25-hydroxyvitamin D in the liver and then to its active form 1,25 hydroxyvitamin D in the kidney

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2
Q

What is the function of thyroid peroxidase (TPO)?

A

TPO catalyzes the following

  1. oxidation of iodide to iodine
  2. iodination of thyroglobullin (TG) tyrosine residues
  3. iodotyrosine coupling reaction that forms T3 and T4
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3
Q

Why can exercise cause hypoglycemia in patients with insulin-treated diabetes?

A

Exercise causes increased translocation of GLUT4 receptors to the cell membrane of skeletal muscle.

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4
Q

Which endocrine hormones have a cAMP (g-protein) signalling pathway

A

“FLAT ChAMP”

  • FSH - MSH
  • LH - PTH
  • ACTH
  • TSH
  • CRH
  • hCG
  • ADH (v2 receptor)
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5
Q

Which endocrine hormones have a cGMP signalling pathway?

A

“BAD GraMPa“ –> all cause vasodilation

BNP (natriuretic peptide)

ANP (natriuretic peptide)

EDRF (NO)

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6
Q

Which endocrine hormones have an IP3 signalling pathway?

A

“GOAT HAG”

GnRH Gastrin

Oxytocin

ADH (v1 receptor)

TRH

Histamine

Angiotensin II

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7
Q

Which endocrine hormones have an intracellular receptor signalling pathway?

A

“PET CAT D”

Progesterone

Estrogen

Testosterone

Cortisol

Aldosterone

T3/T4

Vitamin D

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8
Q

Which endocrine hormones have a receptor tyrosine kinase pathway? (MAP Kinase Pathway)

A

think growth factors (GF)

Insulin

IGF-1

FGF

PDGF

EGF

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9
Q

Which endocrine hormones have a non receptor tyrosine kinase pathway? (JAK/STAT Pathway)

A

“PIGGLET”

Prolactin

Immunomodulators (cytokines, IL-2, IL-6)

GH

G-CSF

Erythropoietin

Thrombopoietin

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10
Q

5-alpha reductase deficiency

  1. what is this enzyme used for?
  2. how does it present?
A
  1. Converts testosterone to DHT

2.

Presents in males as an ambiguous external genitalia (individuals often thought to be females) and male internal genitalia.

When testosterone levels increase during puberty, these individuals then develop external male genitalia

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11
Q

What are neurophysins?

A

Carrier proteins for posterior pituitary hormones (oxytocin and ADH)

They carry the hormones from the paraventricular and supraoptical nuclei in the thalamus to the posterior pituitary.

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12
Q

What effects would primary hypothyroidism have on :

  1. TSH
  2. T4
  3. T3
A
  1. Increased TSH (to try and increase TH levels)
  2. Decreased T4
  3. Normal/Decreased T3
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13
Q

Calcium Regulation

  1. What regulates short-term calcium concentrations?
  2. What regulates long-term calcium concentrations?
A
  1. PTH
  2. Calcitriol / 1,25-OH D3 / active Vitamin D
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14
Q

What are the 3 primary effects of PTH?

A
  1. increase osteoclastic bone resorption which releases calcium and phosphate into circulation
  2. increase calcium and decreased phosphate renal reabsorption
  3. increased formation of 1,25-OH D3 (active vit. D) which increases intestinal reabsorption of both calcium and phosphate
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15
Q

Postoperative hypoparathyroidism

  1. when does it usually occur?
  2. what is the result?
A
  1. after a thyroidectomy due to inadvertent damage or removal of the parathyroid gland
  2. decreased PTH
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16
Q

Brown Adipose Tissue

  1. What is its function
  2. Who has the most and why?
A
  1. Heat production
  2. Neonates, since they are more susceptible to hyperthermia
17
Q

Which type of glucose do GLUT transporters prefer to transport, L-Glucose or D-Glucose?

A

D-Glucose

18
Q

what converts the storage form of Vit. D (25-hydroxvitamin D3) in the liver to its active form (1,25-dihydroxyvitamin D3) in the kidney?

A

1-alpha hydroxylase

19
Q

What are the effects of Chronic Kidney Disease (CKD) on Vitamin D?

A

decreased levels of 1,25-dihydroxyvitamin D3

(active form of vitamin D)

20
Q

How does PTH increase bone resorption by osteoclasts?

A
  1. PTH binds receptor on osteoblasts
  2. osteoblasts secrete RANK-L
  3. RANK-L binds the RANK receptors on osteoclasts and their precursors
  4. Activation of NF-KB transcription factor
  5. osteoclasts resorp bone which releases calcium and phosphate into blood
21
Q

GnRH stimulates the release of?

A

FSH and LH

22
Q

What is the function:

  1. LH
  2. FSH
A

1.

LH stimulates the release of testosterone from the leydig cells of the testis

2.

FSH stimulates the release of inhibin B from the sertoli cells of the testis (also required for spermatogenesis)

23
Q

What can taking excess vitamin D supplements result in?

A

Hypercalcemia which results impaired depolarization of neuromuscular membranes

Presents as:

- muscle weakness

- constipation

- confusion

24
Q

Why can patients with granulomatous diseases (TB, Sarcoidosis) have increased levels of 1,25-dihydroxyvitamin D3?

A

The activated macrophages express 1-alpha-hydroxylase so they are able to convert 25-hydroxyvitamin D (storage form in liver) into its active form independent of PTH

25
Q

Why does oral glucose result in a greater insulin release than IV?

A

Since the GI tract releases Incretins (GLP-1 and GIP) in response to oral glucose

26
Q

What is the mechanism of insulin release?

A
  1. Glucose enters pancreatic B cell
  2. Increase in intracellular ATP
  3. K+ channels close
  4. Membrane depolarizes
  5. Opening of voltage-gated Calcium channels
  6. Vesicle release (exocytosis of insulin granules)
27
Q

What are 3 forms of thyroid hormones and how are they produced?

A
  1. T4: produced by the thyroid via TSH stimulation
  2. T3: small amount produced by thyroid, majority is produced via peripheral conversion of T4 –> T3 via 5-deiodinase
  3. rT3: inactive form of T3 produced via peripheral conversion of T4
28
Q

What affects would T3 supplementation have on:

  1. TSH
  2. T4
  3. rT3
A
  1. decreased TSH (via negative feedback)
  2. decreased T4 (due to decreased TSH)
  3. decreased rT3 (due to decreased T4)
29
Q

What is the pathway of insulin synthesis?

A
  1. Preproinsulin (synthesized in RER)
  2. Proinsulin (stored in secretory granules)
  3. Cleavage of proinsulin into Insulin and C-peptide
  4. Vesicles move towards cell membrane and wait for exocytosis
30
Q

What is the pathway of insulin-dependant glucose uptake?

A
  1. insulin binds to an intrinsic tyrosine kinase receptor
  2. receptor gets autophosphorylated
  3. activation of PI3K and MAP-K
    4a. PI3K (in cytoplasm): increased glycogen, protein and lipid synthesis, increased GLUT-4 expression
    4b. MAP-K (in nucleus) -cell growth -DNA sythesis
31
Q

What are the effects of Cortisol in the body?

A

Increased Apetite

Increased BP (upregulates alpha receptors)

Insulin resitance (diabetogenic)

Increased Gluconeogenesis, lipolysis, proteolysis

Decreased Fibroblast Activity (poor wound healing)

Decreased immune Response

Decreased bone formation (decreased osteoblasts)

“Cortisol is A BIG FIB”

UWorld - Endocrine (2 decks)

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