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Clinical Medicine 3 > Dr. Houston (Endocrine) > Flashcards

Dr. Houston (Endocrine) Flashcards

1
Q

What are the different chemical messengers? (3)

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2
Q

What happens when a hormone is secreted into the blood?

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3
Q

What are the examples of non classical hormone producing glands?

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4
Q

How does humoral, neural and hormonal stimulation work?

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5
Q

What is the mechanism of water soluble hormone?

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6
Q

What is the mechanism of lipid soluble hormone?

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7
Q

Hormone regulation occurs through feedback control
* What types of feedbacks (2)
* Endocrine cell has ability to do what?
* Enables endocrine cell to do what?

A
  • The mechanism is usually negative feedback, although a few positive feedback are known.
  • Endocrine cell has ability to “sense” biologic consequences of secretion of that hormone.
  • Enables endocrine cell to adjust its rate of hormone secretion to produce the desired level of effect, ensuring homeostasis
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8
Q

How does a negative, positive and short/long feedback mechanisms work?

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9
Q

⭐️

Peptide:
* How is it synthesized?
* How is it stored?
* Solubility?
* Receptors?
* Effects?
* Examples?

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10
Q

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Steroid:
* How is it synthesized?
* How is it stored?
* Solubility?
* Receptors?
* Effects?
* Examples?

A

blue box

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11
Q

⭐️

Amino acid derivative:
* How is it synthesized?
* How is it stored?
* Solubility?
* Receptors?
* Effects?
* Examples?

A

pink box

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12
Q

What is the relationship between hormone secretion, carrier protein bind and hormone degradation?

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13
Q
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14
Q

Where is the hypothalamus?
What are the two types of pituitary glands?

A
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15
Q

Explain the difference in how anterior pit and posterior pit work?

A
  • Anterior pituitary hormones are synthesized and secreted in response to hypothalamic-releasing hormones carried in the hypophyseal portal circulation.
  • Magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus, whose axons terminate in the posterior lobe, synthesize posterior pituitary hormones.
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16
Q

how does the long and short loop feedback mechanism work?

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17
Q

What cells secrete oxytocin and ADH?

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18
Q

What are the hormones released from ant pit?

A

FLAT PG

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19
Q

What are the hormones released from the posterior pit?

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20
Q

Explain the different types of different types of hypersecretion disorders (primary, secondary, 3°)

A

3°: The problem originates in the hypothalamus.
* ↑ CRH, ↑ ACTH, ↑ Cortisol

2°: The problem originates in the anterior pituitary.
* ↓ CRH, ↑ ACTH, ↑ Cortisol

1°: The problem originates in the adrenal cortex.
* ↓ CRH, ↓ ACTH, ↑ Cortisol

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21
Q

What are general causes of hypo and hyper secretion?

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22
Q
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23
Q

What are all the different cells in anterior pituitary?

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24
Q

Pituitary adenomas:
* Cells do what? What does that form?
* Can be classifed by what? (What are the two catogories?)
* What can it cause?

A

Cells: Somatrope, corticotroph, lactotroph, thyrotroph and gonadotroph

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25
Q

What are function and non functional ademonas?

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26
Q

Symptoms of pituitary ademas depend on what? How is it dx?

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27
Q

What are two diseases of Hypersecretion of Growth Hormone ?

A

Gigantism, Acromegaly

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28
Q

Gigantism
* When does problem occur?
* Typically due to what? What are other causes?
* Sometimes accompanied by what?

A
  • Problem occurs before closure of epiphyseal plate
  • Typically due to anterior pituitary adenoma causing hypersecretion of GH.
  • Other causes include hypothalamic tumor, ectopic GH from other tumors, genetic disorders
  • Sometimes accompanied by excess prolactin secretion – break milk, decreased menstruation, male breasts
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29
Q

Giantism:
* Caused by over excretion of what?
* What are the sxs?
* What is going on with the mammosomatotoph cells?

A
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30
Q

Acromegaly
* When does this occur?
* Typically due to what?
* What are some other causes?
* Can have what effect?

A
  • Problem occurs after closure of epiphyseal plate
  • Typically due to anterior pituitary adenoma causing hypersecretion of GH and IGF-1.
  • Other causes include hypothalamic tumor, ectopic GH from other tumors, genetic disorders
  • Can have a diabetogenic effect
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31
Q

Acromegaly:
* hormonal disorder caused by what?
* What is there a lot of?
* What type of effect?
* What are the sxs?

A
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32
Q

Growth hormone deficiency:
* Where is GH secreted from?
* What does GH normally do?
* What are the sxs in children and adults?

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33
Q

Dwarfism
* What type of genetic disorder?
* What is the mutation?

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34
Q

ADH
* Where is it made?
* When does it get secreted?
* What does ADH cause to the blood vessels?

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35
Q

How does AHD affect the renal system?

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36
Q

What is the difference in urine for DI and DM?

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37
Q
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38
Q

What happens in DI?

A

ADH is not working

39
Q

What are the 4 types of DI?

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40
Q

Central DI:
* Problem is with what? What happens?
* Often caused by damage to what?

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41
Q

Nephrogenic DI
* What are the causes?
* What is the defects in?

A
42
Q

What are the overall effects in DI?

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43
Q

SIADH
* What is the cause?
* What is the pathway down?

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44
Q

What are the causes of SIADH?

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45
Q

What are the different types of SIADH?

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46
Q

What is the pathway of thyroid hormones (hypothalamus, pit, and thyroid gland)

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47
Q

What cells secrete calcitonin?

A

Parafollicular cell

48
Q

What does T3 cause?

A
49
Q
  • What does follicular cells do?
  • What happens to T4?
A
50
Q

Hyperthyroidism
* What is high?
* What can be the cause?
* What does it result in?

A
51
Q

Hyperthyroidism
* What are the causes?

A
  • 90% patients serum contains TSH-R antibody called thyroid-stimulating immunoglobulin (TSI) (an IgG antibody) which directed against TSH receptor site
  • TSI formerly called long-acting thyroid stimulator (LATS)
52
Q

Hyperthyroidism:
* What causes large release of pre-formed thyroid hormones
* What else can happen?

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53
Q

Hyperthyroidism:
* What happens with toxic nodular goiter?

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54
Q

Hypothyroidism:
* Lacks what? Decreased what?
* What is primary and secondary?

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55
Q

What are two major causes of hypothyroidism?

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56
Q

Hypothyroidism:
* What surgery can cause this?
* What is congenital hypothyroidism?

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57
Q

Secondary hypothyrodism
* What is the cause?
* What does it damage?

A
58
Q

What happens when there is an increase in plasma calcium?

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59
Q

What happens when there is an decrease in plasma calcium?

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60
Q

Hyperparathyroidism Primary
* What happens?
* What levels are messed up?

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61
Q

Hyperparathyroidism Primary
* What are the causes?

A
62
Q

Primary hyperparathyrodism:
* What happens to the calcium? What does that cause?

A
63
Q

Secondary hyperparathyrodism:
* What is it caused by?

A

Decrease calcitriol: lack of sunlight and poor intake of vit D

64
Q

Hypoparathyroidism:
* What is low and high?
* What are the sxs?
* What is it caused by?

A
65
Q
A
66
Q
A
67
Q

Explain how insulin and glucagon work

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68
Q

Explain how normal pancreas, T1D and T2D work?

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69
Q

T1D
* What is the cause?
* How can it be genetic?
* What are the sxs?

A
70
Q

T2D
* How does it work?
* What are the risk factors?

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71
Q
A
72
Q

Adenral gland
* What is produced/secreted?
* Highly what?
* Secrete on what?
* Half life?
* Bind to what?
* What are the layers?

A
  • Adrenocorticoid production & secretion
  • highly vascularized
  • secrete on demand, do not store
  • long half-lives in the body (hours)
  • Bind to proteins (e.g. albumin) prevents mass excretion in urine
73
Q

Primary adrenal insufficiency:
* What is the problem? What can it not produce?
* What happens to the gland?
* What are the causes?

A
74
Q

Primary adrenal insufficiency
* When do sxs occur?
* What are the sxs?

A
75
Q

What is primary, secondary, tertiary cortiadrenal insufficiency?

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76
Q

What is cushing syndrome and disease?

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77
Q

Cushing sydrome:
* ACTH can mimic what? What does that cause?
* Inhibits what? (2)
* What are the sxs?

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78
Q

What are the causes of cushing syndrome?

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79
Q

Pheochromocytoma:
* What is the cause?
* Where are other sites?

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80
Q

What are the causes of pheochromocytoma?

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81
Q

Hyperaldosteronism:
* What happens to the lab levels?

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82
Q

Hyperaldosteronism:
* What are the primary causes?

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83
Q

Hyperaldosteronism:
* What are the secondary causes?

A

Clinical Medicine 3 (27 decks)

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