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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?

A
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10
Q

⭐️

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?

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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
What are function and non functional ademonas?
26
Symptoms of pituitary ademas depend on what? How is it dx?
27
What are two diseases of Hypersecretion of Growth Hormone ?
Gigantism, Acromegaly
28
Gigantism * When does problem occur? * Typically due to what? What are other causes? * Sometimes accompanied by what?
* 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
29
Giantism: * Caused by over excretion of what? * What are the sxs? * What is going on with the mammosomatotoph cells?
30
Acromegaly * When does this occur? * Typically due to what? * What are some other causes? * Can have what effect?
* 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
31
Acromegaly: * hormonal disorder caused by what? * What is there a lot of? * What type of effect? * What are the sxs?
32
Growth hormone deficiency: * Where is GH secreted from? * What does GH normally do? * What are the sxs in children and adults?
33
Dwarfism * What type of genetic disorder? * What is the mutation?
34
ADH * Where is it made? * When does it get secreted? * What does ADH cause to the blood vessels?
35
How does AHD affect the renal system?
36
What is the difference in urine for DI and DM?
37
38
What happens in DI?
ADH is not working
39
What are the 4 types of DI?
40
Central DI: * Problem is with what? What happens? * Often caused by damage to what?
41
Nephrogenic DI * What are the causes? * What is the defects in?
42
What are the overall effects in DI?
43
SIADH * What is the cause? * What is the pathway down?
44
What are the causes of SIADH?
45
What are the different types of SIADH?
46
What is the pathway of thyroid hormones (hypothalamus, pit, and thyroid gland)
47
What cells secrete calcitonin?
Parafollicular cell
48
What does T3 cause?
49
* What does follicular cells do? * What happens to T4?
50
Hyperthyroidism * What is high? * What can be the cause? * What does it result in?
51
Hyperthyroidism * What are the causes?
* 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
Hyperthyroidism: * What causes large release of pre-formed thyroid hormones * What else can happen?
53
Hyperthyroidism: * What happens with toxic nodular goiter?
54
Hypothyroidism: * Lacks what? Decreased what? * What is primary and secondary?
55
What are two major causes of hypothyroidism?
56
Hypothyroidism: * What surgery can cause this? * What is congenital hypothyroidism?
57
Secondary hypothyrodism * What is the cause? * What does it damage?
58
What happens when there is an increase in plasma calcium?
59
What happens when there is an decrease in plasma calcium?
60
Hyperparathyroidism Primary * What happens? * What levels are messed up?
61
Hyperparathyroidism Primary * What are the causes?
62
Primary hyperparathyrodism: * What happens to the calcium? What does that cause?
63
Secondary hyperparathyrodism: * What is it caused by?
## Footnote Decrease calcitriol: lack of sunlight and poor intake of vit D
64
Hypoparathyroidism: * What is low and high? * What are the sxs? * What is it caused by?
65
66
67
Explain how insulin and glucagon work
68
Explain how normal pancreas, T1D and T2D work?
69
T1D * What is the cause? * How can it be genetic? * What are the sxs?
70
T2D * How does it work? * What are the risk factors?
71
72
Adenral gland * What is produced/secreted? * Highly what? * Secrete on what? * Half life? * Bind to what? * What are the layers?
* 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
Primary adrenal insufficiency: * What is the problem? What can it not produce? * What happens to the gland? * What are the causes?
74
Primary adrenal insufficiency * When do sxs occur? * What are the sxs?
75
What is primary, secondary, tertiary cortiadrenal insufficiency?
76
What is cushing syndrome and disease?
77
Cushing sydrome: * ACTH can mimic what? What does that cause? * Inhibits what? (2) * What are the sxs?
78
What are the causes of cushing syndrome?
79
Pheochromocytoma: * What is the cause? * Where are other sites?
80
What are the causes of pheochromocytoma?
81
Hyperaldosteronism: * What happens to the lab levels?
82
Hyperaldosteronism: * What are the primary causes?
83
Hyperaldosteronism: * What are the secondary causes?

Clinical Medicine 3 (27 decks)

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