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Endo-Repro Midterm > Physiology > Flashcards

Physiology Flashcards

1
Q

Define each of the following: endocrine, paracrine, autocrine, juxtacrine, and neurocrine

A
  • endocrine: communication over long distance (through circulation)
  • paracrine: cells communicate over relatively short distances (different cell types)
  • autocrine: cell signals itself/same cell type by releasing ligand that binds to its own surface
  • juxtacrine: cell signal stays attached to secreting cell when it binds to receptor on adjacent cell
  • neurocrine: similar to paracrine but w/ neurons
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2
Q

How are protein and peptide hormones synthesized?

A

DNA -> mRNA -> preprohormone (ribosome) -> pro hormone (ER) -> hormone (golgi)

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3
Q

How are protein and peptide hormones stored and secreted?

A

stored in secretary vesicles until stimulated - increased intracellular Ca -> activation of GPCR -> increased cAMP -> increased PKA

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4
Q

What are amine hormones derivatives of? Give 4 examples.

A
  • derivatives of tyrosine

- Epi, NE, Dopamine, and thyroid hormones

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5
Q

What are steroid hormones derived from? Give 7 examples?

A
  • cholesterol

- cortisol, aldosterone, estradiol, estriol, progesterone, testosterone, and calcitriol

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6
Q

What is positive feedback?

A

hormone action causes more secretion of hormone; uncommon

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7
Q

What is negative feedback?

A

hormone action directly or indirectly inhibits further hormone secretion

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8
Q

What are 3 types of negative feedback?

A
  • long-loop: hormone down line feeds back to beginning
  • short-loop: hormone secreted by gland inhibits further secretion
  • ultrashort loop: gland inhibits its own hormone secretion
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9
Q

How are receptors up-regulated?

A

increase synthesis, decrease degradation, activation

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10
Q

How are receptors down-regulated?

A

decrease synthesis, increase degradation, inhibition

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11
Q

What happens when a hormone receptor is down-regulated?

A

response to hormone declines even though levels remain high

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12
Q

Explain the adenylyl cyclase system

A
  • hormone binds to receptor by Gs or Gi protein
  • activation/inhibition of adenylyl cyclase
  • increase/decrease cAMP
  • second messenger (PKA) amplifies signal for physiological actions
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13
Q

Explain the PCL system

A
  • hormone binds to receptor
  • coupling via Gq to PLC
  • intracellular IP3/Ca increased
  • second messenger (PKC or calmodulin) amplifies signal
  • physiological action
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14
Q

Explain steroid hormones secondary messenger system

A
  • hormone diffuses across cell membrane
  • binds to receptor protein (cytosol or nucleus)
  • hormone-receptor complex becomes transcription factor
  • new mRNA
  • new proteins
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15
Q

ANP vs NO in guanylyl cyclase system

A
  • ANP: GTP -> cGMP -> activates cGMP dependent kinase -> phosphorylates protein responsible for ANPs physiological affects
  • NO: diffuses out of endothelial cells -> binds to and activates cytosolic guanylyl cyclase -> GTP to cGMP -> smooth muscle relaxaion
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16
Q

Explain receptor tyrosine kinases. Give 3 examples

A
  • insulin, IGF-1, prolactin

- intracellular domain has intrinsic tyrosine kinase (phosphorylates itself when activated)

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17
Q

Explain tyrosine kinase associated receptor. Give an example.

A
  • growth hormone
  • intracellular domain non-covalently associated w/ tyrosine kinase (JAK); associated protein (JAK) phosphorylates tyrosine on itself when activated
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18
Q

Where are catecholamines synthesized?

A

in cytosol and secretory granules

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19
Q

Where does cholesterol used to make steroid hormones come from?

A
  • mostly take up as LDL through receptor mediated endocytosis
  • some made de novo from acetyl CoA
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20
Q

What 2 actions do steroid hormones have?

A
  • genomic: modulate gene transcription by interaction w/ intracellular nuclear receptors
  • Nongenomic: specific receptor mediated actions or direct steroid membrane interactions
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21
Q

Why do endocrine organs have such a large blood supply?

A

endocrine glands/organs release hormones into the CV system

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22
Q

Where is the hypothalamus located?

A

below the thalamus, behind the optic chiasma, surrounding the 3rd ventricle

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23
Q

What are the 3 direct targets of the hypothalamus and through what?

A
  • anterior pituitary: through releasing hormones (RH) and inhibiting hormones (IH)
  • kidneys and uterus: through oxytocin and AHD
  • Adrenal medulla: sympathetic innervation
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24
Q

Where is the pituitary gland located? How does it connect to the hypothalamus?

A
  • below the hypothalamus, within hypophyseal fossa of sphenoid bone
  • connected to hypothalamus through infundibulum
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25
Q

What is the embryologic origin of the anterior and posterior pituitary?

A
  • derived from ectoderm
  • Posterior pituitary and infundibular stalk = infudibulum
  • Anterior pituitary = Rathke’s pouch
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26
Q

What are the 3 parts of the anterior pituitary?

A
  • pars tubercles (wraps around stalk)
  • pars intermedia (posterior wall of Rathke’s pouch)
  • pars distalis (majority of gland where hormone production occurs)
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27
Q

What are the 2 parts of the posterior pituitary?

A
  • infundibular stalk (bridge between hypothalamus and posterior pituitary)
  • pars nervosa (actual posterior pituitary)
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28
Q

How does the hypothalamus communicate w/ both anterior and posterior pituitary?

A 
anterior = neurohormones
posterior = axons from hypothalamus
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29
Q

How would the pars distalis and pars nervosa stain on a histological slide?

A

pars distalis = darker staining

pars nervosa = lighter staining (neural tissue)

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30
Q

What do each of the 5 cell types of the anterior pituitary secrete: somatotrophic, thyrotropic, corticotropic, gonadotropic, mammotropic

A
  • somatotropic: growth hormone (GH)
  • thyrotropic: thyroid stimulating hormone (TSH)
  • corticotropic: adrenocorticotropic hormone (ACTH); melanocyte stimulating hormone (MSH)
  • gonadotropic: follicle stimulating hormone (FHS) and luteinizing hormone (LH)
  • mammotropic: prolactin
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31
Q

How do each of the following cells of the anterior pituitary stain on a histologic slide: somatotrophic, thyrotropic, corticotropic, gonadotropic, mammotropic

A
  • Acidphils (red): somatotrophs and mammotrophs

- Basophils (dark staining): corticotrophs, thyrotrophs, and gonadotrophs; B-FLAT (FSH, LH, ACTH, TSH)

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32
Q

What is the function of the posterior pituitary?

A

stores ADH and oxytocin synthesized by the hypothalamus

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33
Q

What is the hypothalamic-hypophyseal portal system?

A

system of blood vessels that connects anterior pituitary and hypothalamus; indirect method of communication

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34
Q

What is the hypothalamic-hypophyseal tract?

A

neurons that connect the posterior pituitary and hypothalamus; direct method of communication

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35
Q

Explain the function of the 2 plexuses of the hypothalamic-hypophyseal portal system

A
  • primary plexus in the median eminence picks up RH/IH from hypothalamus and takes them to anterior pituitary
  • secondary plexus in the anterior pituitary is where hormones created in anterior pituitary enter the blood
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36
Q

How does the hypothalamic-hypophyseal tract work?

A

Hypothalamic neurons synthesize oxytocin and ADH -> travel to posterior pituitary -> stored in neurosecretory bodies -> released when associated hypothalamic neurons fire to neurosecretory bodies

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37
Q

What is the function of ADH?

A

targets the kidneys to retain Na and water; increase BP

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38
Q

What is the function of oxytocin?

A

targets uterine smooth muscle (contractions) and stimulates lactation; also involved in sexual arousal as well as muscle mass

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39
Q

What causes gigantism? When in life does it occur

A
  • excess production of GH due to a tumor

- occurs in childhood (before growth plates close)

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40
Q

What causes pituitary dwarfism? What do these people look like?

A

hyposecretion of growth hormone; normal body proportion but rarely taller than 4ft

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41
Q

What is the function of the pineal gland and what does it secrete?

A
  • role in growth, development and circadian rhythms

- secretes melatonin and serotonin

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42
Q

Where is the thyroid gland located?

A

below the larynx and anterior to the trachea

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43
Q

What makes up a thyroid follicle?

A

follicular cells surrounding colloid (fluid that contains thyroglobulin -> storage for of T3/T4)

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44
Q

What are parafollicular C cells and what do they secrete?

A

thyroid cells located outside the follicles; secrete calcitonin

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45
Q

What is the function of calcitonin what are its action (3)?

A

lower circulating Ca levels

  • stimulate secretion by kidneys
  • decrease Ca-releasing activity of osteoclasts
  • increase osteogenesis by osteoblasts
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46
Q

What is Grave’s disease? Sx and tx?

A
  • over secretion of T3/T4 due to abnormal antibodies that stimulate TSH receptors
  • Sx: elevated metabolism, rapid HR, weight loss, protruding eyes
    Tx: thyroidectomy or anti-thyroid drugs
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47
Q

What is hypothyroidism? Sx and tx?

A
  • insufficient T3/T4 production
  • Sx: low metabolic rate, weight gain, lethargy
  • Tx: synthetic T3/T4
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48
Q

What causes goiters?

A

thyroid enlargement due to iodine deficiency - follicles make thyroglobulin but cannot make TH

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49
Q

What do parathyroid glands produce and what is its function? What cells produce this hormone?

A

produce parathyroid hormone (PTH) - increases blood Ca levels when low; produced by chief (principle) cells

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50
Q

What actions does PTH have (3)?

A
  • stimulates osteoclasts to resorb bone and release Ca stores
  • increase Ca retention in kidneys
  • kidney create calcitriol (active form of vitamin D) -> increases Ca absorption by intestines
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51
Q

What are the 3 zones of the adrenal cortex and how does each look histologically?

A
  • zona glomerulosa: thin layer on top next to capsule; stains dark pink
  • zona fasciculata: larger middle zone; lighter pink/purple columns
  • zona reticularis: right next to medulla; medium pink
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52
Q

What is produced in the zona glomerulosa? Class of hormone and function?

A
  • aldosterone: influence Na/K levels and secreted in response to low BP
  • mineralocorticoid
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53
Q

What is produced in the zona fasciculata? Class of hormone and function?

A
  • cortisol: mediates glucose metabolism and acts as anti-inflammatory in immune system
  • glucocorticoid
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54
Q

What class of hormones are produced in the zona reticuluaris? Function?

A

androgens - influence secondary sex characteristics

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55
Q

What is the primary cell type of the adrenal medulla? What does it produce?

A

chromaffin cells - secrete Epi and NE

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56
Q

Describe Epi cells and NE cells histologically

A
  • Epi cells: smaller w/ less granules; less electron density (stain gray)
  • NE cells: larger w/ granules; more electron dense (stain black)
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57
Q

What is Addison’s disease? Sx?

A

hyposecretion of both glucocorticoids and mineralocorticoids -> blood glucose and Na levels drop -> severe dehydration and low BP along w/ fatigue and loss of appetite

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58
Q

What is Cushing’s syndrome? Sx?

A

hyper secretion of glucocorticoids due to ACTH-secreting pituitary tumor or adrenal cortex tumor
- Sx: high serum glucose, muscle weakness, lethargy, fat redistribution (buffalo hump and moon face)

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59
Q

What is secreted by each of the following endocrine pancreas cells: alpha, beta, delta, and F-cells?

A
  • alpha: glucagon
  • beta: insulin
  • delta: somatostatin
  • F-cells: pancreatic polypeptide
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60
Q

Describe the insuloacinar portal system

A
  • arterials break into capillary beds and surround pancreatic islets (supplies O2 and nutrients and picks up anything islets want to release into blood stream)
  • go past acinar cells -> helps islets regular acinar cells (local action)
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61
Q

What is the acinar vascular system?

A

vessels that supply only the pancreatic acini and not the islets

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62
Q

What type of sx usually show up w/ pituitary cancers?

A

dizziness and vision problems -> expand up into brain against optic nerves

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63
Q

What neurons in the hypothalamus produce ADH and oxytocin?

A 
ADH = supraoptic nucleus (SON)
Oxytocin = paraventricular nucleus (PVN)
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64
Q

Explain primary, secondary, and tertiary endocrine disorders

A
  • primary: defect in peripheral endocrine gland
  • secondary: defect in pituitary gland
  • tertiary: defect in hypothalamus
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65
Q

What does GH bind directly to?

A

bones and muscle

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66
Q

What are the 3 direct actions of GH?

A

growth, cell reproduction, and metabolism

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67
Q

Name 3 indirect actions of GH

A

signals liver to produce IGF, stimulates hypertrophy and hyperplasia

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68
Q

What 2 hormones does the hypothalamus make that relate to GH? What does each do?

A
  • growth hormone releasing hormone (GHRH) -> stimulates anterior pituitary to secrete GH
  • growth hormone inhibiting hormone (GHIH) = somatostatin (SS) -> inhibits anterior pituitary from secreting GH
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69
Q

What is another name for GH? What cells in the anterior pituitary secrete it?

A

somatotropin -> secreted by somatotrophs

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70
Q

What is produced by the liver in response to GH? What is its 2 functions?

A
  • insulin-like growth factor (IGF-1) = somatomedin C -> inhibits GH from anterior pituitary and stimulates GHIH from hypothalamus
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71
Q

Name 6 things that stimulate GH secretion

A

fasting, hunger, starvation, hypoglycemia, sleep, and Ghrelin

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72
Q

Name 3 things that inhibit GH secretion

A

somatostatin, IGF-1, and inadequate AAs

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73
Q

Describe primary GH insensitivity

A

ghrelin and GHRH activate GH -> GH targets liver but liver is insensitive to it

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74
Q

Describe secondary GH insensitivity

A

GH does not respond to signals from hypothalamus

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75
Q

Describe tertiary GH insensitivity

A

issue w/ GHRH or ghrelin or hypothalamus is insensitive to them

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76
Q

What actions does GH promote in the liver in a fed state?

A

liver produces IGF-1 -> mitogenesis, lipolysis, and differentiation

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77
Q

Explain what happens to GH with normal carb intake but inadequate AA availability

A

GH inhibited -> liver doesn’t produce IGF-1 -> lipogenesis and carb storage

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78
Q

Explain what happens to GH with decreased carbs and normal AA availability

A

GH levels increase -> liver produces IGF-1 -> lipolysis, ketogenic metabolism

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79
Q

How does decreased carbs/normal AAs promote insulin insensitivity?

A

less glucose uptake and increased insulin levels in the blood

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80
Q

What causes acromegaly? Sxs?

A
  • caused by prolonged and excessive secretion of GH in adult life (after closer of growth plates)
  • excessive growth of soft tissue, cartilage, and bones in hands, feet, and face
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81
Q

How would you dx acromegaly?

A

increase serum in GH and IGF-1, failure of oral glucose to suppress serum GH, pituitary enlargement on MRI

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82
Q

What is the HPA axis?

A

hypothalamus-pituitary -adrenal axis

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83
Q

HPA Axis: What is produced by the hypothalamus (PVN)?

A

corticotropin-releasing hormone (CRH)

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84
Q

HPA Axis: What stimulates the release of CRH from the hypothalamus?

A

stress: physical (surgery, infection), emotional (fear), chemical (hypoglycemia)

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85
Q

HPA Axis: What is produced by the anterior pituitary in response to CRH? What cells secrete it?

A

Adrenocorticotropic hormone (ACTH) secreted by the corticotrophs

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86
Q

HPA Axis: What does ACTH stimulate the adrenal glands to secrete?

A

Cortisol

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87
Q

HPA Axis: What inhibiting loops exist in this axis?

A
  • Long loop - cortisol inhibits ACTH and CRH

- Short loop - ACTH inhibits CRH

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88
Q

What is the HPT Axis?

A

hypothalamus-pituitary-thyroid

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89
Q

HPT Axis: What is produced by the hypothalamus (PVN)?

A

Thyroid Releasing Hormone (TRH)

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90
Q

HPT Axis: What is produced by the anterior pituitary in response to TRH? What cells secrete it?

A

Thyroid Stimulating Hormone (TSH) -> thyrotrophs

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91
Q

HPT Axis: What is produced by the thyroid gland in response to TSH?

A

T3 and T4

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92
Q

How is the regulation of prolactin secretion different compared to most other anterior pituitary hormones?

A
  • most hormones stimulated through positive regulation (must be signaled to be made)
  • prolactin controlled through negative regulation (inhibited by hypothalamic dopamine)
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93
Q

What cells synthesize prolactin? What is its main action?

A

synthesized by lactotrophs -> stimulates and maintains lactation

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94
Q

HPT Axis: What factors inhibit TRH secretion?

A

stress (physical, starvation, and infection)

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95
Q

What action does prolactin have on other hormones not in its axis? What is the purpose of this?

A
  • suppresses GnRH (inhibits LH and FSH)

- decreases reproductive function and suppresses sexual drive

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96
Q

What factors stimulate the release of prolactin (4)? What hormone is used?

A
  • pregnancy, breast feeding, sleep, stress

- stimulated by TRH from the hypothalamus

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97
Q

What factors inhibit the release of prolactin (3)?

A

Dopamine + agonists and somatostatin

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98
Q

How does prolactin inhibit itself?

A

stimulates hypothalamic dopamine release -> dopamine inhibits prolactin

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99
Q

What 2 hormones are secreted by gonadotrophs? What is their function?

A
  • Luteinizing hormone (LH) and Follicle Stimulating Hormone (FSH)
  • promotes estrogen and progesterone in females and promotes testosterone in males
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100
Q

What stimulates the secretion of FSH and LH from the anterior pituitary? What hormone can inhibit this process?

A
  • gonadotropin releasing hormone (GnRH) stimulates FSH and LH
  • prolactin inhibits GnRH -> inhibits FSH and LH
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101
Q

What factors can inhibit GnRH besides prolactin?

A

extreme energy deficits and extreme exercise

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102
Q

What is a pituitary adenoma? Name the 3 most common?

A
  • hormone producing tumor in anterior pituitary
  • Prolactinoma (60%)
  • Acromegaly/giantism (20%)
  • Cushing’s disease (10%)
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103
Q

Name 4 common causes of hyperpituitarism?

A

brain damage, pituitary tumors, infections, infarctions

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104
Q

What would hyperpitiuitarism of each of the following hormones be called: ACTH, TSH, GH, PRL, LH and FSH?

A
  • ACHT = Cushing’s disease
  • TSH = TSH secreting adenoma
  • GH = acromegaly/gigantism
  • PRL = prolactinoma
  • LH and FSH = non-functioning adenoma
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105
Q

What would sx be of decreased GH release?

A

short stature in children, no effect in adults

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106
Q

What would sx be of decreased FSH/LH release?

A

infertility/reduced sperm count (males); menstrual irregularity (females)

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107
Q

What sx would be seen with a decrease in each of the following hormones: TSH, ACTH, ADH (posterior pituitary)?

A
  • TSH: hypothyroidism
  • ACTH: loss of pigmentation
  • ADH: diabetes insipidus
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108
Q

What is Sheehan syndrome? What are some of the sx?

A
  • postpartum hypopituitarism due to excessive blood loss during childbirth and damage to the pituitary gland
  • Sx: agalactorrhea, amenorrhea, hypothyroidism
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109
Q

What are the main target tissues of oxytocin? What is its main action in each?

A

breast (milk ejection) and uterus (uterine contraction)

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110
Q

What is pitocin?

A

oxytocin analog given to induce labor

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111
Q

What are the 3 main factors that trigger the release of ADH from the posterior pituitary? How is each measured? Which is most sensitive?

A
  • decreased BP (cardiac and aortic baroreceptors)
  • low blood volume (arterial stretch receptors)
  • increased osmolarity (>280)( hypothalamic osmoreceptors) -> most sensitive
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112
Q

What receptors does ADH affect in the vasculature and kidney?

A

V1 in vasculature

V2 in kidney

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113
Q

What is the overall function of ADH?

A

increases BP and blood volume, decreases osmolarity

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114
Q

What is central neurogenic diabetes insipidus? How does it affect plasma ADH levels?

A
  • failure of hypothalamus to produce ADH or release it from posterior pituitary -> decrease in plasma ADH
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115
Q

What are the causes and sxs of central DI? What is the tx?

A
  • results from damage to pituitary or destruction of hypothalamus
  • Sx include producing a large amount of dilute urine
  • Tx is desmopressin (synthetic analog of ADH)
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116
Q

What is nephrogenic DI? How does it affect plasma ADH levels?

A

kidneys unable to respond to ADH -> increase plasma ADH

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117
Q

What are the causes and sxs of nephrogenic DI?

A
  • drugs such as lithium and tetracyclines, chronic disorders (PKD and sickle cell anemia)
  • sx include producing a large amount of dilute urine
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118
Q

What is SIADH?

A

syndrome of inappropriate ADH secretion -> excessive ADH secretion

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119
Q

What does SIADH cause and what is the tx?

A
  • causes excessive water retention and hypoosomolarity

- Tx include fluid restriction, hypertonic saline, V2 receptor antagonist

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120
Q

How many iodines are connected to T3 and T4? Which is secreted more? Which is more potent?

A 
T4 = 4 iodine, 90% secreted
T3 = 3 iodine, more potent
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121
Q

How is T4 converted to T3 in the periphery and anterior pituitary?

A
  • Type 1 deiodinase in periphery

- Type 2 deiodinase in anterior pituitary

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122
Q

What is the backbone of T3 and T4?

A

tyrosine

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123
Q

What are the 2 intermediates of T3 and T4? How is each made?

A
  • MIT (1 iodine); DIT (2 iodine)
  • DIT + MIT = T3
  • DIT + DIT = T4
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124
Q

What are factors that reduce the conversion of T4 to T3?

A

fasting, medical/surgical stress, catabolic disease

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125
Q

What is organification?

A

process of binding iodine w/ thyroglobulin

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126
Q

What 2 hormones are synthesized in the posterior pituitary?

A

NONE!!! It only stores, does not produce or synthesize!

127
Q

What 2 transporters are on the basolateral membrane of thyroid follicular cells? Functions?

A
  • Na/I symporter: brings Iodine into the cell along w/ Na

- Na/K ATPase: removes Na from cells and brings K in (Na gradient)

128
Q

What 2 transporters are on the follicular lumen side of thyroid follicular cells? Functions?

A
  • Pendrin: Cl/I counter-transporter -> Cl into cell; I into colloid
  • Peroxidase (TPO) - oxidizes iodine in lumen for combo w/ thyroglobulin
129
Q

What does thyroglobulin bind to while in the colloid?

A

T4, T3, and intermediates (MIT and DIT)

130
Q

How does T3 and T4 go from being in the colloid to being released into the blood?

A
  • Tg granules pinocytosed back into cell

- Protease cleaves off T3 and T4 form thyroglobulin and releases them

131
Q

What occurs to MIT and DIT after T3/T4 is released?

A

undergo deiodination into tyrosine and iodine -> recycled in the cell

132
Q

How would perchlorate and thiocyanate inhibit thyroid hormone production?

A

inhibits the Na/I symporter

133
Q

What is PTU and what does it do? What is it used to treat?

A
  • propylthiouracil (PTU) - inhibits peroxidases in thyroid follicles
  • used to treat hyperthyroid/Grave’s disease
134
Q

What is the Wolff-Chaikoff effect?

A

inhibits organifaction

135
Q

How much ingested iodine is usually taken up into the thyroid? What happens to the rest of it?

A

about 25% taken into the thyroid; the rest is excreted by the kidneys

136
Q

In what 2 forms can thyroid hormones circulate in blood?

A

plasma proteins (99%) or free (1%)

137
Q

What are the 3 binding proteins thyroid hormones will bind to?

A
  • Thyroxin-binding protein (TBG)
    Transthyretin (TTR)
    Albumin
138
Q

What synthesizes TBG? Which thyroid hormone does it have a greater affinity for?

A

synthesized by the liver; greater affinity for T4

139
Q

Which thyroid hormone has a longer half life? How long does it take each of them to reach maximum activity?

A
  • T4 - longer half life, reaches max in 10-12 days

- T3 - shorter half life, reaches max in 2-3 days

140
Q

What does a higher level of T3 resin uptake mean?

A

resin picks up whatever T3 is not bound to TBG (higher affinity for T4); higher resin uptake = higher levels of free T3

141
Q

What would you expect resin uptake to look like in hyperthyroidism?

A

increased T4 -> fewer spaces on TBG for T3 -> increased T3 resin uptake

142
Q

What would you expect resin uptake to look like in hypothyroidism?

A

decreased T4 -> more space on TBG for T3 -> decreased T3 resin uptake

143
Q

Explain what changes occur for thyroid hormones in the blood w/ hepatic failure?

A

decreased TBG (synthesized in liver) -> increased T3 resin uptake -> transient increase in free T3/T4 -> inhibition of synthesis (negative feedback)

144
Q

Explain what changes occur for thyroid hormones in the blood w/ pregnancy? What is the overall affect?

A
  • increased TBG -> decreased T3 resin uptake -> transient decreased in free T3/T4 (before 20 weeks) -> increase in synthesis and secretion of T3/T4
  • increase in the total levels of T3 and T4 but levels of free hormones are normal
145
Q

Name 7 functions of thyroid hormone?

A
  • activates nuclear receptors and cAMP second messenger
  • increased metabolic activity
  • conversion of carotene to Vitamin A (hypothyroid = possible blindness)
  • growth
  • maintain cardiac output
  • stimulates GI motility
  • CNS development and excitation
146
Q

How is cholesterol synthesis related to thyroid hormone? What does this mean for hypo- and hyperthyroidism?

A
  • cholesterol and triglycerides in blood inversely related to thyroid hormone
  • hypothyroid = increased cholesterol
  • hyperthyroid = decreased cholesterol
147
Q

Describe the pathophysiology of thyroid hormone on metabolism

A
  • excess: heat intolerance, weight loss, increased BMR

- deficiency: cold tolerance, weight gain, decreased BMR

148
Q

Describe the pathophysiology of thyroid hormone on bone

A
  • excess (adults): osteoporosis
  • excess (children/adolescents): stunted growth
  • deficiency: stunted growth
149
Q

Describe the pathophysiology of thyroid hormone on the CNS

A
  • excess: agitation, anxiety, hyperreflexia

- deficiency: cretinism, slowed movement, impaired memory

150
Q

Describe the pathophysiology of thyroid hormone on the CV system

A
  • excess: tachycardia, increased CO, increased B1 adrenergic receptors (sympathetic)
  • deficiency: bradycardia, decreased CO, heart failure
151
Q

Describe the pathophysiology of thyroid hormone on the GI tract

A
  • excess: diarrhea

- deficiency: constipation

152
Q

What are some of the sx of hyperthyroidism? What is primary and secondary hyperthyroidism called?

A
  • Sx: weight loss, sweating, rapid HR, high BP, heat intolerance
  • Primary: Grave’s disease
  • Secondary: TSH secreting pituitary adenoma
153
Q

What are 4 primary causes of hypothyroidism?

A
  • agenesis
  • gland destruction: Hashimoto’s
  • inhibit of hormone synthesis and release
  • Transient: post surgical, postpartum
154
Q

What hormone levels would you expect to see in someone with an iodine deficiency?

A
  • decrease in thyroid hormone synthesis
  • increase in TSH levels
  • possible goiter
155
Q

What is the tx for hypothyroidism?

A

replacement doses of T4

156
Q

What is cretinism? What causes it?

A

congenital iodine deficiency/hypothyroidism

Causes: iodine deficiency, maternal intake of anti-thyroid medications, impaired thyroid gland development, genetics

157
Q

Sx of cretinism?

A

feeding problems, respiratory difficulty, protruding tongue, curse facial features, growth/mental retardation, jaundice, dry skin, hypotonia (due to demyelination)

158
Q

What is Hashimoto’s Thyroiditis? What hormone levels would you expect to see?

A
  • thyroid hormone synthesis impaired by thyroglobulin or antibody disruption of TPO (peroxidase)
  • decreased T3/T4 secretion
  • increased TSH levels
  • possible goiter
159
Q

What causes Grave’s disease? Type of endocrine disorder?

A

thyroid stimulating immunoglobulins (TSI) stimulate TSH receptor w/o TSH (primary endocrine disorder)

160
Q

Sx of Grave’s disease?

A

exophthalmos (protrusion of eyeballs) and periorbital edema

161
Q

What hormone levels would you expect to see in someone w/ Grave’s disease? What is the tx?

A
  • decreased TSH levels (loss of feedback)
  • elevated serum free T3/T4
  • circulating TSI (distinguishes Grave’s disease)
  • Tx: PTU (inhibits peroxidase)
162
Q

What can cause goiter?

A
  • Hyperthyroidism: Grave’s disease, TSH producing tumor (secondary)
  • Primary hypothyroidism: iodine deficiency, sporadic hypothyroidism, chronic thyroiditis (Hashimotos)
163
Q

Where would you find GLUT2 and GLUT4 transporters? What does GLUT4 require?

A
  • GLUT2: pancreas (B cells) and liver

- GLUT4: skeletal muscle and adipose tissue (requires insulin)

164
Q

What do pancreatic B cells secrete? Where are they located in islets?

A
  • secrete insulin and peptide C

- located in the center

165
Q

What do pancreatic A cells secrete? Where are they located in islets?

A
  • secrete glucagon

- located peripherally

166
Q

What do pancreatic D cells secrete? What do they use to communicate w/ pancreatic B cells?

A
  • secrete somatostatin

- send dendrite-like processes to B cells

167
Q

What do pancreatic F cells secrete and what does this do?

A
  • secrete pancreatic peptide

- acts like a satiety signal (NPY, PYY)

168
Q

How do cells of islets rapidly communicate w/ each other?

A

through gap junction

169
Q

Describe the blood flow through pancreatic islets and how it aids in communication

A
  • islets receive 10% of pancreatic blood flow
  • blood hits B cells first -> if glucose present, releases insulin -> bathes over other cells -> informs them that insulin has been released
170
Q

Explain the synthesis of insulin?

A

preproinsulin -> proinsulin -> insulin + peptide C

171
Q

What is preproinsulin?

A

signal peptide A and B chains w/ connecting C peptide; no disulfide bonds

172
Q

Describe preproinsulin -> proinsulin?

A

proinsulin still has C peptide attached but no signal peptide

173
Q

How is insulin packaged? What is the final structure of insulin?

A
  • packaged into secretory granules as proinsulin and cleaved into insulin and peptide C
  • insulin = A and B chains connected by disulfide bonds
174
Q

What is C peptide used as a marker of? When does this not work?

A

used as a marker of endogenous insulin secretion, does not work w/ insulin injections (lack peptide C)

175
Q

How does glucose enter pancreatic B cells?

A

GLUT2 through facilitated diffusion

176
Q

What does glucose do once it enters pancreatic B cells?

A

phosphorylated by glucokinase -> G6P -> ATP via glycolysis

177
Q

Explain what ATP synthesized in pancreatic B cells does and what this leads to?

A

closes ATP dependent K channels -> depolarization -> opening of voltage-gated Ca channels -> Ca enters cell

178
Q

What does Ca cause when it enters pancreatic B cells?

A

initiates mobilization of insulin and peptide C vesicles to plasma membrane for exocytosis

179
Q

What are the 2 phases of insulin release? Which one is lost in NIDDM pts?

A

initial burst of insulin and then backs off to become a more gradual release; NIDDM lose that first initial burst

180
Q

To what type of receptor does insulin bind?

A

RTKs

181
Q

What receptor pathway leads to the metabolic effects of insulin?

A

IRS 1-4 -> PKB/AKT -> metabolic effects

182
Q

What receptor pathway leads to the growth effects of insulin?

A

IRS 1-4 -> RAS/GPT -> MAPK -> growth effects

183
Q

What happens to the insulin receptor after insulin binds to it?

A

insulin-receptor complex is internalized by the target cells -> down regulation of receptor by insulin

184
Q

How does insulin affect glucose uptake

A

insulin binds to receptor -> activates downstream pathways -> translocation of GLUT4 to membrane -> glucose enters via facilitated diffusion

185
Q

What can stimulate GLUT4 translocation to plasma membrane independent of insulin?

A

muscle contractions (activates AMPK) -> Exercise good for NIDDM

186
Q

How can exercise cause problems in IDDM?

A

muscle contractions stimulate GLUT4 -> need to time insulin injections around exercise; exercising and the eating and taking insulin will cause BS to drop

187
Q

How does glucagon affect insulin secretion?

A

Though to facilitate insulin secretion - increases slowly between meals and decreases after insulin has been released

188
Q

Name 9 stimulatory factors of insulin secretion

A
  • glucose, FAs, and AAs
  • Cortisol
  • Glucagon
  • GIP/GLP-1 (incretin hormones)
  • K
  • vagal stimulation -> ACh
  • Sulfonylurea drugs
189
Q

Name 6 inhibitory factors of insulin secretion

A
  • decreased blood glucose
  • fasting
  • exercise
  • Somatostatin
  • alpha-adrenergic agonists -> NE
  • Diazoxide (K channel activator)
190
Q

Name the pathway and action of each of the following modulators of insulin secretion: CCK/ACh, GLP-1, Somatostatin

A
  • CCK/ACh - Gq - activate insulin
  • GLP-1 - Gs - activate insulin
  • Somatostatin - Gi - inhibit insulin release
191
Q

Name 4 actions of insulin on skeletal muscle

A
  • increase glucose uptake (GLUT4)
  • increased glycogen synthesis
  • increased protein synthesis
  • increased FA uptake in muscle cells
192
Q

Name 4 actions of insulin on the liver

A
  • promotes glycogen synthesis
  • decreased glujconeogeneis
  • increased lipid storage
  • increased protein synthesis
193
Q

Name 4 actions on insulin on adipose tissue

A
  • increased glucose uptake (GLUT4)
  • increased glycolysis
  • decreased lipolysis
  • promotes FA uptake and storage
194
Q

What affect does insulin have on blood levels of glucose, AAs, FAs, and keto acids?

A

decreases blood levels of all of them

195
Q

What causes IDDM?

A

destruction of B cells -> can’t produce insulin

196
Q

How does IDDM lead to DKA?

A

increased blood levels of ketoacids and decreased utilization of them -> acidosis

197
Q

What is the normal effect of insulin on K?

A

helps Na/K ATPase maintain activity -> brings K into cells and decreases blood levels

198
Q

What affect can IDDM have on K levels?

A

intracellular hypokalemia and extracellular hyperkalemia (K shifts out of cells)

199
Q

How does diabetes causes osmotic diuresis/glucosuria?

A

increased blood sugar exceeds reabsorption capacity of kidneys -> water/electrolyte reabsorption decreases - increased urination and increased glucose in urine

200
Q

What is the current tx for IDDM?

A

insulin replacement

201
Q

Explain the process of insulin resistance in a NIDDM pt

A

takes more insulin to maintain normal blood sugar levels -> eat a meal and exaggerated sugar response -> pancreas creates exaggerated amount of insulin -> liver, skeletal muscle and adipose tissue don’t respond to insulin -> liver continues to release glucose b/c its not receiving any

202
Q

What will appear on blood work of a pt w/ NIDDM?

A

increased blood glucose levels and increased insulin levels

203
Q

What can be an early sign of NIDDM?

A

Non-Alcoholic fatty liver disease

204
Q

What are treatments for NIDDM?

A
  • calorie restriction
  • weight reduction
  • exercise
  • sulfonylurea drugs
  • incretin analog of GLP-1
  • insulin sensitizers (Metformin)
  • Bariatric surgery
205
Q

What is the incretin effect?

A

GI tract hormones that are needed to facilitate release of insulin -> lost in NIDDM

206
Q

What is the main stimulator of glucagon? What else can stimulate it?

A
  • decreased blood glucose (main)
  • CCK
  • Fasting
  • B-adrenergic agonists
  • ACh
207
Q

What 2 main things inhibit glucagon secretion?

A

Insulin and somatostatin

208
Q

What are 3 main actions of glucagon?

A
  • increase blood glucose (through liver)
  • stimulate lipolysis (adipose and skeletal)
  • ketoacids produced from FAs
209
Q

What effect does extracellular Ca have?

A

effects cell excitability (especially nerve fibers)

210
Q

Where is 99% of Ca stored? What is the biologically active form of Ca?

A

99% stored in bones and teeth; free, ionized form is active

211
Q

What effect does hypocalcemia have on APs? What are some sx of hypocalcemia?

A
  • reduces activation threshold for Na channels -> spontaneous APs
  • Sx: hyperreflexia, spontaneous twitching, muscle cramps, numbness/tingling
212
Q

What effect does hypercalcemia have on APs? What are some sx of hypercalcemia?

A
  • decreases membrane excitability

- Sx: constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy

213
Q

How do acidemia and alkalemia affect free ionized Ca levels?

A
  • academia: increased free ionized Ca (less space on albumin due to high H)
  • alkalemia: decreased free ionized Ca (more space on albumin due to lack of H)
214
Q

What is PTH’s overall effect on Ca levels? How does it do this?

A
  • overall: increases plasma Ca
  • bone: increases bone resorption (indirectly through osteoclasts)
  • kidneys: increases Ca reabsorption and urinary cAMP
  • intestines: increases Ca absorption (indirectly by activating vitamin D)
215
Q

What is PTH’s overall effect on Pi levels? How does it do this?

A
  • overall: decreases serum Pi
  • intestine: increases Pi absorption (indirectly by activating vitamin D)
  • kidney: decreases Pi reabsorption (inhibits Na/P symporter in
216
Q

What is Vitamin D (Calcitriol) overall effect on Ca levels? How does it do this?

A
  • overall: increases serum Ca
  • bone: promotes osteoclast formation and bone resorption
  • kidney: increases Ca reabsorption
  • intestines: increases Ca absorption
217
Q

What is Vitamin D (Calcitriol) overall effect on Pi levels? How does it do this?

A
  • overall: increases serum Pi
  • intestine: increases Pi absorption
  • kidney: increases Pi reabsorption
218
Q

What is Calcitonin’s overall effect on Ca and Pi levels? How does it do this?

A
  • overall: decreases serum Ca and Pi
  • bone: inhibits osteoclastic-mediated bone resorption
  • kidney: promotes Pi and Ca excretion
219
Q

Where is the majority of Pi stored?

A

bone (85%)

220
Q

What cells synthesize and secrete PTH? What is the stimulus for secretion?

A
  • synthesized by chief (principle) cells in parathyroid gland
  • stimulated by decrease in plasma Ca levels
221
Q

Via what receptor does PTH work?

A

GPCR (Gs) - stimulates cAMP

222
Q

What is the CaSR and where is it located?

A

calcium sensor receptor located in the kidney and parathyroid gland to sense Ca levels

223
Q

What inhibits PTH secretion?

A

high Ca levels

224
Q

What inhibits the PTH gene specifically?

A

Vitamin D - PTH needed to activate vitamin D in the kidney (negative feedback)

225
Q

What does vitamin D promote in the kidney and parathyroid gland?

A

CaSR

226
Q

What does chronic hypercalcemia do to PTH levels?

A

decreases synthesis and storage of PTH and increased breakdown

227
Q

What does chronic hypocalcemia do to PTH levels? What effect does this have on the parathyroid gland?

A

increases synthesis and storage of PTH -> hyperplasia of parathyroid gland (secondary hyperparathyroidism) due to low Ca

228
Q

What does severe hypomagnesemia do to PTH?

A

inhibits PTH synthesis

229
Q

What type of hormones are PTH and Vitamin D?

A

PTH: peptide

Vitamin D: steroid

230
Q

What form of vitamin D comes from UV light and diet? Is it active?

A
  • cholecalciferol (Vitamin D3)

- no, inactive prohormone

231
Q

What is the main circulating form of Vitamin D? Where does it come from?

A

25-OH-cholecalciferol made in the liver via 25-hydroxlase

232
Q

What is the active form of Vitamin D and what makes it? Where is it made?

A

1,25-(OH)2-cholecalciferol made in the kidney via 1a-hydroxylase

233
Q

What stimulates and inhibits 1a-hydroxylase expression

A
  • Stimulated by PTH

- Inhibited by high levels of Ca and Vitamin D (negative feedback)

234
Q

What is PTH’s short term and long term effects on bone?

A
  • Short term: bone formation (direct effect on osteoblasts)

- Long term: increases bone resorption (indirect effect on osteoclasts)

235
Q

Explain what each of the following factors are in bone: M-CSF, RANK, RANKL, OPG

A
  • M-CSF (macrophage colony stimulating factor): induce stem cells to osteoclasts
  • RANK: cell surface receptor on osteoclasts/precursors
  • RANKL: cell surface protein produced by osteoblasts (mediator of osteoclast formation) -> binds to RANK
  • OPG (osteoprotegerin): protein produced by osteoblasts; decoy for RANKL -> inhibits RANKL/RANK interaction
236
Q

What is the action of PTH and Vitamin D on RANKL and OPG?

A
  • PTH: increases RANKL, decreases OPG

- Vitamin D: increases RANKL

237
Q

What is the action of PTH in the PCT of kidneys?

A

inhibits Na/P symporter -> Pi excreted in urine

238
Q

In which part of the nephron does PTH increase Ca reabsorption?

A

DCT

239
Q

What specific action does active vitamin D have on intestinal cells? How does this increase Ca absorption?

A
  • increases protein synthesis of calbindin -> Ca binding protein that shuttles Ca from intestinal lumen through cell
  • some Ca can diffuse paracellularly but to increase absorption, calbindin is required b/c high intracellular Ca concentrations can cause apoptosis
240
Q

What transporters are used to move Ca in and out of intestinal cells?

A
  • into cell: TRPV6 Ca channel (diffuses down its gradient)

- out of cell: Ca ATPase

241
Q

What causes primary hyperparathyroidism? What effect does it have on PTH, Ca, Pi, and active vitamin D levels?

A
  • due to parathyroid adenoma
  • increased PTH secretion
  • increased plasma Ca (hypercalcemia)
  • decreased Pi (hypophosphatemia)
  • increased activation of vitamin D
242
Q

What are 2 causes of secondary hyperparathyroidism?

A
  • increased PTH levels secondary to low Ca
  • Renal failure
  • Vitamin D deficiency
243
Q

How will renal failure effect PTH, Ca, Pi, and vitamin D levels?

A
  • decreased vitamin D (due to kidney damage)
  • increase PTH (due to low vitamin D and Ca)
  • decrease Ca (due to decreased vitamin D)
  • increase Pi (due to decreased GFR)
244
Q

How will Vitamin D deficiency effect PTH, Ca, Pi, and vitamin D levels?

A
  • decreased vitamin D (obviously)
  • increased PTH (due to low vitamin D and Ca)
  • decrease Ca (due to decreased vitamin D)
  • decreased Pi (due to increased PTH)
245
Q

How will hypoparathyroidism effect PTH, Ca, Pi, and vitamin D levels?

A
  • decreased secretion of PTH
  • decreased vitamin D
  • decreased Ca
  • increased Pi
246
Q

What are the sxs and tx of hypoparathyroidism?

A

Sx mostly associated w/ hypocalcemia: muscle cramps, numbness/tingling, seizures
Tx: oral Ca supplement and active form of vitamin D

247
Q

What is albright heredity osteodystrophy?

A
  • pseudohypoparathyroidism type 1A

- Gs for PTH in bone and kidney defective (does not form cAMP)

248
Q

How will albright hereditary osteodystrophy effect PTH, Ca, Pi, and vitamin D levels?

A
  • increased PTH (can’t perform actions)
  • decrease Ca
  • increase Pi
  • decrease vitamin D
249
Q

What is the phenotype of albright heredity osteodystrophy?

A

short stature, short neck, obesity, subcutaneous calcifications

250
Q

What is PTH-related peptide (PTHrP)?

A

peptide produced by malignant tumors - binds and activates PTH receptors w/o requiring PTH

251
Q

How will humoral hypercalcemia of malignancy effect PTH, Ca, Pi, and vitamin D levels? What else will be increased?

A
  • PTHrP increased
  • decreased PTH
  • increased Ca
  • decreased Pi
  • decreased vitamin D (normal for cancer)
252
Q

What is familial hypocalciuric hypercalcemia?

A

mutation that inactivates CaSR in parathyroid glands and Ca receptors in ascending limb of kidney - decreased sensitivity to Ca levels (requires higher levels of Ca to stimulate receptor)

253
Q

How will familial hypocalciuric hypercalcemia effect PTH, Ca, Pi, and vitamin D levels?

A
  • normal/high levels of PTH
  • increased Ca
  • normal Pi and vitamin D
254
Q

What causes rickets?

A

insufficient amount of Ca and Pi available to mineralize growing bone in children

255
Q

Pseudovitamin D-deficient rickets type I vs type II

A
  • Type I: decreased 1a-hydroxylase

- Type II: decreased vitamin D receptor - vitamin D resistance

256
Q

How does estradiol affect Ca levels through the bone, kidney, and intestines?

A
  • kidney: increases Ca reabsorption
  • intestines: increases Ca absorption
  • bone: promotes survival of osteoblasts and apoptosis of osteoclasts (bone formation)
257
Q

Which population is most at risk for osteoporosis and why?

A

postmenopausal women due to decreased strong (decreased bone formation)

258
Q

Which catecholamine does the adrenal medulla produce more of?

A

Epi - 80%

259
Q

What hormones are decreased and increased w/ 21-hydroxylase deficiency?

A
  • sex hormones increased

- decreased cortisol and mineralcorticoids

260
Q

What are some sx of 21-hydroxylase deficiency?

A

hypotension (decreased aldosterone), Na and volume loss, hyperkalemia, elevated renin

261
Q

How would males and females present w/ 21-hydroxylase deficiency?

A

Females: sexual ambiguity
Males: normal phenotype w/ precocious pseudo-puberty

262
Q

What group of hormones increases w/ 11B-hydroxylase deficiency? What does this cause in females?

A

increased androgens; causes virilization of female fetuses

263
Q

What specific hormone is increased in 11B-hydroxylase deficiency and what does it do?

A

11-deoxycorticosterone (can stimulate MR -> HTN)

264
Q

What are some sx of 11B-hydroxylase deficiency?

A

HTN, hypokalemia, suppressed renin secretion

265
Q

What hormone groups are decreased and increased in 17a-hydroxylase deficiency? What are some sx?

A
  • decreased androgens and cortisol
  • increased mineralocorticoids
  • Sx: HTN, hypokalemia, hypogonadism
266
Q

What effect does cortisol have on each of the following: liver, muscle, fat, skin, immune system, endocrine, and GI?

A
  • liver: increased gluconeogenesis
  • muscle: protein breakdown
  • fat: lipolysis in extremities, central fat deposition
  • Skin: collagen breakdown and fragile blood vessels
  • Immune: decreased inflammation -> increased infections
  • Endocrine: insulin resistance
  • GI: decreased Ca absorption (risk of osteoporosis)
267
Q

What do glucocorticoids inhibit as part of negative feedback?

A

CRH and ACTH

268
Q

What is ACTH derived from?

A

POMC

269
Q

How is ACTH connected w/ MSH? What can occur if you have excess ACTH?

A
  • ACTH cleaved into MSH in non-pituitary tissues

- excess = hyperpigmentation

270
Q

At what time of the day is there a major increase in cortisol? How is this used clinically?

A

early in the morning; dexamethosome suppression test is given overnight to get results in the morning

271
Q

What is a normal response for low dose dexamethosome suppression test? What is abnormal and what does it indicate?

A
  • normal: suppression of ACTH and cortisol secretion

- no suppression = cushing

272
Q

What is a normal response to the cosyntropin stimulation tests (CST)? How would adrenal insufficiency (primary and secondary) respond?

A
  • normal: cortisol increases
  • primary adrenal insufficiency: cortisol remains the same or rises small amount
  • secondary adrenal insufficiency: cortisol greatly increases
273
Q

What is Cushing syndrome? What happens to cortisol and ACTH levels?

A
  • hypersecretion of cortisol (elevated cortisol levels)

- ACTH depends on etiology: adrenal tumor = low ACTH; non-pituitary neoplasms can secrete high ACTH

274
Q

How will Cushing syndrome respond to a high dose dexamethosome test?

A
  • Adrenal tumor: ACTH decreases but cortisol remains high

- Ectopic ACTH secreting tumor: ACTH and cortisol remain high

275
Q

What is Cushing disease and what causes it? What happens to cortisol and ACHT levels?

A
  • hypersecretion of ACTH due to a pituitary tumor

- high ACTH and cortisol

276
Q

How will Cushing disease respond to high dose dexamethosome test?

A

suppresses ACTH and decreases cortisol down to normal-high levels

277
Q

Name 6 signs/sxs of Cushing’s

A
  • moon face
  • hirsutism
  • bruising (breakdown of collagen)
  • ABD adiposity
  • stretch marks
  • Buffall hump (excess fat deposit on back of neck)
278
Q

What is Addison disease and what causes it?

A

primary adrenal insufficiency (hyposecretion of all adrenal steroids) usually due to autoimmune restriction of adrenal gland

279
Q

What will ACTH and cortisol levels be in Addison’s disease?

A

high ACTH and low cortisol

280
Q

How will Addison’s disease respond to the Cosyntropin test?

A

no change in cortisol levels (adrenals can’t respond to ACTH)

281
Q

What are the signs and sxs of Addison’s disease?

A
  • hyperpigmentation (MSH from high ACTH)
  • weight loss and muscle weakness
  • hypoglycemia
  • hypotension
  • hyponatremia and hyperkalemia (due to loss of aldosterone)
282
Q

What causes secondary adrenal insufficiency? What will ACTH and cortisol levels be?

A
  • caused by exogenous glucocorticoid administration (pituitary problem)
  • low ACTH and cortisol
283
Q

How will secondary adrenal insufficiency respond to the cosyntropin test?

A

increase in cortisol (adrenals are functional)

284
Q

What is the overall function of aldosterone?

A

increases Na reabsorption, increases K excretion, and increases H excretion

285
Q

What is the function of 11B-HSD2? Why is it important?

A
  • metabolizes cortisol to cortisone in kidney

- protects MR from cortisol binding and keeps it available for aldosterone

286
Q

What is Conn syndrome?

A

primary hyperaldosteronism - hyper secretion of aldosterone due to adrenal neoplasm

287
Q

What effect does excess aldosterone (Conn syndrome) have?

A

Increased aldosterone -> increased Na and H20 reabsorption -> increased blood volume/BP -> hypokalemia

288
Q

What is primary hypoaldosteronism?

A

hyposecretion of aldosterone due to destruction of the renal cortex or defects in aldosterone synthesis

289
Q

What is secondary hypoaldosteronism?

A

hyposecretion of renin from juxtaglomerular cells of kidney - inadequate stimulation of aldosterone

290
Q

What effect does ACTH deficiency have on aldosterone?

A

very little/no effect due to RAAS still being functional

291
Q

What is the rate limiting step in catecholamine production?

A

tyrosine -> DOPA via tyrosine hydroxylase

292
Q

Where is dopamine stored after production and what happens to it?

A

stored in chromaffin granules and converted to NE

293
Q

What stimulates tyrosine to DOPA and dopamine to NE?

A

sympathetic stimulation

294
Q

What stimulates NE to Epi and where does it occur?

A

cortisol stimulation - occurs in the cytoplasm of chromaffin cells

295
Q

What are 2 enzymes that metabolize catecholamines?

A
  • monoamine oxidase (MAO)

- COMT

296
Q

What is used to determine the amount of catecholamine production?

A

Vanillylmandelic acid (VMA)

297
Q

What is a pheochromocytoma?

A

tumor of chromaffin tissue -> produces excess catecholamines

298
Q

What are the sxs of a pheochromocytoma?

A

HTN, orthostatic hypotension, headaches, sweating, palpitations, CP, flushing, anxiety

299
Q

Describe the RAAS system?

A

decreased renal perfusion -> renin secreted -> Ang II -> ADH (water reabsorption) and Aldosterone (salt reabsorption) -> increased blood volume

300
Q

What is MEN?

A

AD group of diseases w/ tumors in at least 2 endocrine glands

301
Q

What group of cells are affected in MEN?

A

amine precursor uptake and decarboxylation cells (APUD) - neuroendocrine cells that secrete amines

302
Q

What is mutated in MEN Type 1?

A

MEN1 gene -> menin (tumor suppressor)

303
Q

What are the 3 locations of tumors in MEN1?

A

parathyroid, endocrine pancreas, pituitary

304
Q

Which organ is most frequently involved in MEN1? What is the first clinical manifestation from this organ?

A

parathyroid glands -> hyperparathyroidism

305
Q

What is the 2nd most common manifestation of MEN1 and what disease is it associated with?

A

pancreas (pancreatic islets) -> involves gastronomas (ZE syndrome)

306
Q

What do most pituitary tumors in MEN1 secrete? How does this manifest in men and women?

A
  • secrete prolactin -> prolactinemia
  • women: galactorrhea and amenorrhea
  • men: impotence
307
Q

What is mutated in MEN Type 2?

A

RET protooncogene (codes for RTK important for cell growth and development)

308
Q

What is the most common manifestation in MEN2?

A

medullary thyroid carcinoma (MTC) - malignant transformation of parafollicular C cells

309
Q

What 3 manifestations appear in MEN2A?

A

medullary thyroid carcinoma, pheochromocytoma (adrenal), and parathyroid

310
Q

What is different about pheochormocytomas in MEN2A than sporadic pheohromocytomas?

A

secrete greater amounts of Epi

311
Q

What are the 3 most common manifestations in MEN2B?

A

mucosal neuromas, medullary thyroid carcinoma (MTC), and pheochromocytoma

312
Q

What manifestation is not usually seen in MEN2B?

A

hyperparathyroidism

313
Q

What is cutaneous lichen amyloidosis?

A

itchy skin condition present in MEN2A

Endo-Repro Midterm (3 decks)

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