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9.1 Endocrine Flashcards

1
Q

Where is GH secreted from?

A

Ant pit

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2
Q

Where is Thyroid hormone secreted from?

A

Thyroid

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3
Q

Where are glucocorticoids (cortisol) secreted from?

A

Zona fasiculata of adrenal cortex

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4
Q

Where is progesterone secreted from?

A

Ovaries

and placenta

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5
Q

Where is prolactin secreted from?

A

Anterior pit

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6
Q

Where is Oxytocin secreted from?

A

Paraventricular nucleus of hypothalamus, and stored in post pit.

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7
Q

where is ANP secreted from?

A

Heart
ANP = atrial natriuretic peptide
aka ANH atrial natriuretic hormone

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8
Q

Where does glucagon come from?

A

Alpha cells of the pancreas

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9
Q

Where is testosterone secreted from?

A

Leydig cells of testes
In females- ovaries
Also from Zona Reticularis of adrenal cortex

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10
Q

Where is FSH secreted from?

A

Ant pit

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11
Q

Where is vasopressin secreted from?

A

Vasopressin = ADH

Supra Optic Nuclei of hypothal, and stored in the post pit

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12
Q

Where is calcitonin secreted from?

A

Parafollicular C cells of thyroid

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13
Q

Where is TSH secreted from?

A

Ant pit

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14
Q

Where are Epi and NE secreted from?

A

Chromaffin cells of the adrenal medulla

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15
Q

Where is insulin secreted from?

A

Beta cells of the pancreas

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16
Q

Where is estadiol secreted from?
Estriol?
Estrone?

A

Estradiol- ovaries
Estriol- placenta
Estrone- fat cells

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17
Q

Where is estrogen secreted from in males?

A

Testes

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18
Q

Where is PTH secreted from?

A

Parathyroid glands

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19
Q

Where is somatostatin secreted from?

A

Delta cells in pancreas

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20
Q

Where is LH secreted from

A

Ant pit

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21
Q

Where are mineralocorticoids secreted from?

A

Zona glomerulosa of the adrenal cortex

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22
Q

Where is ACTH secreted from?

A

Ant pit

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23
Q

Hormones of post pit

A

Oxytocin and Vasopressin (ADH)

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24
Q

Hormones of ant pit

A

FLAT PiG

FSH
LH
ACTH
TSH

Prolactin
Growth hormone

also endorphins (but they’re NTs, not hormones)

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25
Q

What hormone increases blood glucose level and decreases protein synthesis?

A

Glucocorticoids (eg cortisol)

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26
Q

What hormone stimulates metabolic activity?

A

Thyroid hormone

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27
Q

What hormone stimulates bone and muscle growth?

A

GH, but GH has to stimulate IGF-1, which is what actually causes the effects.

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28
Q

What hormone stim’s the adrenal cortex to synth and secrete cortisol?

A

ACTH

AdrenoCorticoTropic Hormone

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29
Q

What hormone prepares the endometrium for implantation and is responsible for maintenance of pregnancy?

A

Progesterone

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30
Q

Signaling: Which hormones use cAMP?

A 
Most of the ant pit hormones.
FLAT CHAMP:
FSH
LH
ACTH
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH

plus Calcitonin and Glucagon!

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31
Q

Signaling: what hormones use cGMP?

A

Think vasodilators.
ANP
NO (EDRF)

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32
Q

Signaling: what hormones use IP3?

A 
Releasing hormones (except CRH, which uses cAMP)
GGOAT:
GnRH
GHRH
Oxytocin
ADH (V1 receptor)
TRH
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33
Q

Signaling: what hormones use a steroid receptor?

A 
The steroid hormones:
PETT VAG:
Progesterone
Estrogen
Testosterone
T3 and T4 (thyroxine)

Vitamin D
Aldosterone
Glucocorticoid (cortisol)

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34
Q

Signaling: what hormones use Tyrosine Kinase?

A

FIG PIP:
FGF
IGF-1
GH

PDGF
Insulin
Prolactin

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35
Q

How do steroid hormones (PETT VAG) effect a response?

A

Hormones pass thru lipid cell mbr and bind to a receptor in the cytoplasm or in the nucleus.
The receptor transforms to expose a DNA-binding domain, and an enhancer element binds to the DNA.
This causes transcription of mRNA, which makes proteins, which produce the response.

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36
Q

What is SHBG? How does it affect males vs females?

A

SHBG = sex hormone binding globulin. (It binds testosterone)
Only free hormone is functional, so any hormone bound by SHBG is inactive.
In men, increased SHBG means decreased free testosterone, which leads to gynecomastia
In women, decreased SHBG leads to increased free testosterone, causing hirsutism.

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37
Q

How do steroid hormones travel through the bloodstream?

A

Steroid hormones are lipophilic and insoluble in plasma, so they have to circulate bound to specific binding globulins, which increase their solubility and allow them to be delivered to the target organ.

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38
Q

Post pit embryo and hormones

A

Post pit = neurohypophysis
Comes from neuroectoderm
Vasopressin (ADH) and Oxytocin are made in the hypothalamus and stored there.

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39
Q

Ant pit embryo and hormones

A 
Ant pit = adenohypophysis
Comes from surface ectoderm- specfically, oral ectoderm (Rathke's pouch)
FLAT PiG and MSH:
FSH, LH, ACTH, TSH
Prolactin, GH
MSH (melanotropin)

Many of the ant pit hormones generate cAMP for signalling.

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40
Q

What are the hormonal subunits?

A

alpha subunit- common to TSH, LH, FSH and hCG.

Beta-subunit- unique to each hormone. Determines hormone specificity.

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41
Q

POMC

A

Pro-opio-melano-cortin.
Larger precursor to ACTH, which also contains sequences for other hormonal peptides, like MSH.
So, whenever ACTH is overproduced, MSH will also be overproduced- bc what is really in excess is the POMC.
This is why Addison’s (incrsd ACTH) has hyperpigmentation- it’s from the increased MSH.

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42
Q

What are the acidophilic and basophilic hormones of the ant pit?

A

B-FLAT:
Basophilic = FSH, LH, ACTH, TSH
Acidophilic = Prolactin, GH

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43
Q

How is prolactin regulated? and how does it regulate?

A

Prolactin secretion from the ant pit is inhibited by dopamine (the dopamine comes from the arcuate nucleus of the hypothalamus).
Prolactin inhibits its own secretion by increasing dopamine synthesis and secretion.

Prolactin secretion is increased by TRH.

In addition to regulating itself, Prolactin inhibits GnRH (which inhibits FSH, LH and therefore est, prg, test)

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44
Q

Prolactin function

A

Milk production in breast
Inhibits GnRH synthesis and release, therefore:
Inhibits ovulation (F)
Inhibits spermatogenesis (M)

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45
Q

Drug Rx for prolactinoma

Drug Rx to stimulate prolactin secretion

A

Dopamine agonists (bromocriptine) inhibit prolactin secretion (bc dopamine inhibs its release).

Dopamine antagonists (haloperidol, antipsychotics) stimulate secretion (since blocking dopamine means there will not be inhibition)

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46
Q

What hormone does TRH regulate?

A

Promotes rls of TSH and(!) prolactin

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47
Q

What hormone does Dopamine regulate?

A

It inhibits the release of prolactin

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48
Q

What hormone does CRH regulate?

A

CRH causes release of ACTH (which causes rls of cortisol)

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49
Q

What hormone does GHRH regulate?

A

GHRH causes release of GH, which causes rls of IGF-1

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50
Q

What hormone does Somatostatin regulate?

A

Somatostatin is a “anti-digestion” hormone.

SS decreases secretion of GH and TSH too.

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51
Q

What hormone does GnRH regulate?

A

GnRH causes rls of FSH and LH, which go on to stimulate estrogen, progesterone, and testosterone.

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52
Q

What hormone does Prolactin regulate?

A

Prolactin inhibits GnRH

Note: this is why hyperprolactinemia causes hypo-gonadism.

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53
Q

Pituitary adenoma

A

Usu a prolactinoma.
Findings: amenorrhea, galactorrhea, low libido, infertility (Hyperprolactinoma = hypogonadism bc Prolactin inhibits GnRH)
Can impinge on optic chiasm and cause bitemporal hemianopia.
Rx: bromocriptine or carbergoline (dopamine agonists- dopamin inhib’s prolactin rls)

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54
Q

Sheehan’s syndrome

A

Post-partum hypopituitarism.
During pregnancy, the ant pit enlarges (increased lactotrophs), but the blood supply stays the same.
So, if there is severe bleeding during delivery (hemorrhage), there will be hypotension and therefore hypoperfusion of the pituitary, increasing the risk of pit infarction.
Classic sign is no lactation after delivery, but since all ant pit hormones are affected, can cause fatigue, anorexia, amenorrhea, loss of pubic/axillary hair.
Can cause decreased ACTH, TSH, gonadotropins, GH, and of course, Prolactin.

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55
Q

Hyperprolactinemia (sx, causes)

A

Main sx is hypogonadism (bc prolactin inhib’s GnRH) so in females, infertility, oligo/amenorrhea, and rarely galactorrhea (no sx in post-menopausal females bc they are already hypogonadal)
In males, hypogonadism (low testosterone) causes decrsd libido, impotence, infertility, gynecomastia, rarely galactorrhea

Causes: 
Pregnancy, nipple stimulation
Stress (physical, psychological)
Prolactinoma
Dopamine antagonists (haloperidol, antipsychotics, metoclopramide, methyldopa)
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56
Q

Acromegaly

A

Excess GH in adults
Impaired glucose tolerance (insulin resistance)
Lg tongue w deep furrows, deep voice, lg hands/feet, coarse facial feat

Rx: Pit adenoma resection, followed by octreotide administration (octreotide = somatostatin)

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57
Q

What is the effect on glucose in acromegaly? Why?

A

There is impaired glucose tolerance (insulin resistance).

Acromegaly is excess GH, and GH is a counter-regulatory hormone (like glucagon), so it causes resistance to insulin.

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58
Q

How is a Dx of acromegaly made?

A

Increased serum IGF-1 (bc of incrsd GH)
or
Failure to suppress serum GH following an oral glucose tolerance test.

IGF-1 is measured instead of GH bc GH is secreted in a pulsatile fashion (and at night)

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59
Q

When is increased GH normal?

A

stress
exercise
hypoglycemia

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60
Q

Gigantism

A

Increased GH in children- which causes increased linear bone growth.

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61
Q

Where is somatostatin made?

A

throughout the GI tract, esp by D cells in gut mucosa, and pancreatic islet cells.
Also md in nervous system.

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62
Q

What does somatostatin do?

A

It’s anti-gut (shuts down digestion) and anti- anterior pituitary

In the CNS, PNS, peripheral organs: SS decreased endocrine and exocrine secretion; reduces splanchnic blood flow, reduces GI motility and GB contraction, and inhibs secretion of most GI hormones.

63
Q

Somatostatin analog

A

Octreotide

also somatostatin LAR and lanreotide-P

64
Q

Use for octreotide (SS analog)

A

Pit excess: acromegaly, thyrotropinoma, ACTH-secreting tumors

GI endocrine excess:
Zollinger-Ellison syndrome (incrsd gastrin)
Carcinoid syndrome (incrsd serotonin)
VIPoma (increased VIP hormone)
Glucagonoma, Insulinoma

Can use if you need to reduce splanchnic circulation- portal HTN d/t bleeding esophageal varices; bleeding peptic ulcers.

Also certain diarrheal dz

65
Q

What embryological feature is a pituitary adenoma assoc with?

A 
Rathke's pouch.
The adenohypophysis (ant pit) originates from Rathke's pouch of the oral ectoderm (surface ectoderm).
66
Q

50yo F w double vision, amenorrhea, headaches

A

Prolactinoma (compressing the optic chiasm and causing visual disturbances- most likely biemporal hemianopia)

67
Q

Dx: on MRI, there is replacement of tsu in the sella turcica w CSF

A

Empty sella syndrome
Usu subclinical- be there is enough pit tsu lining the sella turcica that it’s okay.
Can possibly have a deficiency of a pit hormone, but usu just fine.

68
Q

What hormones share a common alpha subunit?

A

TSH
FSH
LH
b-hCG

69
Q

Where is PTH produced?

A

Chief cells of Parathyroid

70
Q

What is the function of PTH?

A

It increases serum Ca2+:

  • increases bone resorption of Ca2+
  • increases kidney resorption of Ca2+ in the DCT

It gets rid of phosphate:
-increases bone resorption of phosphate
then,
-decreases kidney resorption of phosphate
(so takes it from bone and dumps it in urine)

It increases Vit D production, bc it stimulates 1-a-hydroxylase in the kidney, which converts 25-OH to the active form (1,25)

71
Q

Does PTH stimulate osteoblasts or clasts?

A

Both.

Osteoblasts directly, and osteoclasts indirectly.

72
Q

How is PTH regulated?

A

Decreased free serum Ca2+ means increased PTH

Decreased free serum Mg2+ means decreased PTH
Decreased Mg2+ is caused by diarrhea, aminoglycosides, diuretics, alch abuse

73
Q

How do hypo and hyper Ca2+ relate to PTH?

A

Hypocalcemia causes increased PTH, and increased PTH causes hypercalcemia.

74
Q

Where does Vit D come from?

A

Vit D2- plants

Vit D3- sun

75
Q

What happens to Vit D2 and D3 when the are absorbed/ingested

A

Both are converted to 25-OH Vit in the liver. Then, they go to the kidney, where I-alpha-hydroxylase (which is stimulated by PTH) converts them to 1,25 (OH)2 Vit D, which is the active form.

76
Q

What is the active form of Vit D?

A

1, 25 (OH)2 aka calcitrol

77
Q

What is the function of activated Vit D

A

To put Ca2+ and phosphate in your blood:

  • increases absorption of dietary Ca2+ and dietary phosphate from the gut
  • increases resorption of Ca2+ and phosphate from the kidney.
78
Q

How does PTH affect Vit D production?

A

It enhances it, bc PTH stim’s 1-alpha-hydroxylase, which converts inactive to active Vit D

79
Q

How does Ca2+ affect Vit D production?

A

Decreased Ca2+ causes increased Vit D production (so that Vit D can abs more Ca2+ from the gut)

80
Q

How does phosphate affect Vit D production?

A

Decreased phosphate causes increased Vit D production (so that it can abs more phosphate from the gut)

81
Q

How does Vit D affect Vit D production

A

Negative feedback- it inhibits its own production

82
Q

How are Vit D and PTH similar/different in action?

A

Vit increases Ca2+ and phosphate in the blood

PTH increases only Ca2+ in the blood. It pulls phosphate out of bones (like Vit D), but it spills it out in urine (unlike Vit D, which keeps it in blood)

Also, increased PTH means more Vit D is activated. (1-a-hydroxylase)

83
Q

Vit D deficiency results in which disease?

A

Adults- osteomalacia

Kids- rickets

84
Q

T/F 24, 25 (OH)2 Vit D is an active form

A

False. It’s inactive

The active form is 1, 25

85
Q

What happens to Vitamin D levels in sarcoidosis? Why?

A

Sarcoidosis features granulomas, which are made of lots of macrophages. Macrophgs can generate Vit D, so there’s an increase in Vit D levels. (Notably, this leads to hypercalcemia, since more Vit D means more Ca2+ absorbed from the gut)

86
Q

Calcitonin source

A

Parafollicular C cells of the thyroid

87
Q

What is a neoplasm of the parafollicular C cells of the thyroid called?

A

Medullary thyroid carcinoma

88
Q

What does calcitonin do?

A

It decreases bone resorption of Ca2+.
It opposes the actions of PTH (but, it does NOT really affect Ca2+ homeostasis)
Calcitonin tones your bones! (keeps Ca2+ inside them)
It can be helpful in building bone and in osteoporosis

89
Q

How is calcitonin regulated?

A

By serum Ca2+ levels

If there is increased Ca2+ in the serum, calcitonin will be secreted by the thyroid.

90
Q

Cause of primary, secondary, tertiary hyperparathyroidism

A

Primary: increased PTH, usu d/t adenoma
Secondary: decreased Ca2+, causing increased PTH
Tertiary: Chronic renal dz, causing refractory (hard to treat) increase in PTH

91
Q

Primary hyperparathyroidism

A

Increased PTH
Usu d/t adenoma.
Stones, bones, groans
Causes hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, increased ALP (d/t bone turnover), and increased cAMP in urine.
Often asympt or px’s w weakness and constipation (groans)

92
Q

Osteitis fibrosa cystica

A

aka von Recklinghausen’s syndrome
Cystic bone spaces filled w brown fibrous tsu (brown tumors of bone), causing bone pain. Result of primary hyperparathyroidism.

93
Q

Secondary hyperparathyroidism.

A

Decreased Ca2+, leading to increased PTH.
Hyperplasia d/t decreased Ca2+ gut abs and increased phosphorus, most often in chronic renal dz.
Decreased Vit D bc of kidney dysfn causes decreased Ca2+ gut abs.
See hypocalcemia, but hyperphosphatemia
Increased ALP (bony turnover) and increased PTH.

94
Q

Why is there hypocalcemia and hyperphosphatemia in secondary hyperPTH?

A

Secondary Hyperparathyroidism is due to decreased Ca2+ abs from the gut, esp w renal dz
Even tho PTH is increased, the amt of Ca2+ absorbed from the gut can’t be high- since the kidneys are damaged, Vit D isn’t converted to the active form and can’t absorb Ca2+, even if PTH is there to convert it.

PTH increases phosphate resorption from bone and usually excretes it in urine- but since the kidneys are dmgd, they can’t excrete- so they phosphates build up in the blood.

95
Q

What is renal osteodystrophy?

A

Bone lesions d/t secondary hyperparathyroidism, d/t renal dz

96
Q

Cause/findings of hypoparathyroidism

A

Cause: accidental surgical incision (thyroid surgery), autoimmune destruction, DiGeorge syndrome
Findings: hypocalcemia, tetany

97
Q

What signs are used to identify hypoparathyroidism?

A

Chovstek’s sign- tap facial nerve in cheek and get contraction of facial muscles (indicated hypocalcium)
Trousseau’s sign: occlude brachial artery w BP cuff, see carpal spasm.

98
Q

Pseudohypoparathyroidism

A

Clinically looks like hypoPTH, but in fact PTH is high.
aka Type I, Albright’s hereditary osteodystrophy.
Autosomal-dom
Kidney unresponsiveness to PTH.
Causes hypocalcemia, shortened 4th/5th digits, and short stature
PTH is high, it’s just that kidney can’t see it.

Since PTH is so high, can cause osteitis fibrosa cystica (brown tumors of bone) seen in hyperparathyroidism.

99
Q

What are the typical causes of pancreatitis?

A
  1. Alcohol use
  2. Gall stones
    (these 2 are by far the most common)
  3. Hypertriglyceridemia (treat w fibrates)
  4. Hypercalcemia (from Hyperparathyroidism)
100
Q

What are the typical causes of depression?

A
  1. Mjr depressive disorder/psychological causes

Endocrine causes:

  1. Hypothyroidism
  2. Hyperparathyroidism
101
Q

What is usually the cause of hypercalcemia?

A

90% of cases are d/t primary hyperparathyroidism (mostly adenoma, but some hyperplasia) or d/t malignancy

10% is d/t
excess vit D ingestion
excess antacid/milk ingestion (milk-alkali)
granulomatous dz (excess vit D)
increased bone turnover
thiazide diuretics (decreased renal excretion)

102
Q

When hypercalcemia is caused by malignancy, what specific cancers cause it?

A

Sq cell cancer (esp lung) via PTHrp
Renal cell carcinoma
Breast cancer mets
Multiple myeloma

103
Q

Causes of hypocalcemia

A

Hypoparathyroidism
Poor Ca2+ intake
Acute pancreatitis

104
Q

How do bisphosphonates work?

A

They inhibit osteoclast activity.

They reduce the formation and the resorption of hydroxyapatite (the calcium form in bone)

105
Q

2 most common causes of primary hyperparathyroidism

A
  1. solitary parathyroid adenoma

2. parathyroid hyperplasia

106
Q

What agents can be used to treat osteoporosis?

A 
Bisphosphonates
Ca2+
Vit D
Pulsatile PTH
Calcitonin
Estrogen
Testosterone
Tamoxifen, Raloxifene
107
Q

Signs/Sx of Hypothyroidism

A 
Hypo = slow
Cold intolerance (decreased heat production)
Weight gain (but decreased appetite)
Hypoactivity, lethargy, fatigue, weakness
Constipation
Decreased reflexes
Myxedema (facial/periorbital)
Dry, cool skin, coarse, brittle hair
108
Q

Lab findings in Hypothyroidism

A

Increased TSH (sensitive test for primary hypothyroidism)
Decreased total T4
Decreased free T4
Decreased T3 uptake

109
Q

Signs/Sx of hyperthyroidism

A 
Hyper = fast
Heat intolerance (increased heat production)
Weight loss, but increased appetite
Hyperactivity
Diarrhea
Increased reflexes
Chest pain, palpitations, arrhythmias
Warm, moist skin; fine hair
110
Q

Lab findings in hyperthyroidism

A

Decreased TSH (if primary)
Increased total T4
Increased free T4
Increased T3 uptake

111
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

112
Q

What are the dz’s causing hypothyroidism?

A

Hashimoto’s thyroiditis
Cretinism
Subacute thyroiditis (deQuervain’s)
Riedel’s thyroiditis

113
Q

What are the dz’s causing hyperthyroidism?

A

Graves dz
Toxic multinodular goiter
Jod-Basedow phenomenon

114
Q

What is Hashimoto’s thyroiditis

A

Hypothyroidism (most common cause).
Auto-imm disorder: anti-microsomal Ab and anti-thyroglobulin Ab
Assoc w HLA-DR5
Hurthle cells on histo.

Slow course
Moderately enlarged, NON-tender thyroid.
Lymphcyte infiltrate w germinal centers.

Risk factor for developing thyroid lymphoma.

Can have thyrotoxicosis during follicular rupture- so may be hyPERthyroid early in course.

115
Q

T/F an enlarged thyroid means hypothyroidism.

A

False

It can mean hypothyroidism- but it can also mean hyperthyroidism, or a euthyroidism (goiter)

116
Q

Hypothyroidism w lymphocytic infiltrate

A

Hashimoto’s thyroiditis

117
Q

Hypothyroidism w macrophage and eosinophil infiltrate

A

Riedel’s thyroiditis

will also see fibrosis on histology

118
Q

Cretinism

A

Hypothyroidism.
(severe congenital fetal hypothyroidism)

Endemic cretinism: occurs when endemic goiter is present d/t lack of iodine in diet.

Sporadic cretinism: caused by defect in T4 formation or developmental failure in thyroid formation.

Pot-bellied, pale, puffy-faced child w protruding tongue and umbilicus. Small stature, MR (since thyroid hormone is needed for CNS maturation)

119
Q

Subacute thyroiditis (deQuervain’s)

A 
Hypothyroidism
Self-limited, usu following a flu-like illness.
Elevated ESR and jaw pain, early inflam
V Tender (!!) thyroid gland.
Histology shows granulomatous inflam.

Can be hyperthyroid early in course.

Lymphocytic subacute thyroiditis is painless.

120
Q

Subacute thyroiditis causes elevated ESR and jaw pain. What non-thyroid-related pathology also causes these sx?

A

Temporal arteritis.

Subacute thyroiditis (deQuervain’s) will have a very tender thyroid.

121
Q

Where are thyroid hormones formed?

A

T4 is from the follicles of the thyroid gland.

T3 is formed in the blood- there is peripheral conversion of T4 to T3.

122
Q

T/F the only purpose for iodine in the body is to make T3 and T4

A

True.
Iodine has no other use.
T3 and T4 contain iodine and control the body’s metabolic rate.

123
Q

What is the function of thyroid hormones?

A
  1. Bone growth (synergism w GH)
  2. CNS maturation
  3. Increased B1 receptors in the heart (so increased CO, HR, SV, contractility)
  4. Increased BMR via increased Na+/K+ ATPase activity: increases O2 consumption, Respi rate, body temp
  5. Increased glycogenolysis, gluconeogenesis, lipolysis (so breaking down glycogen in liver, making glucose, breaking down fat)
124
Q

Thyroid storm involves what receptor?

A

B1 receptor stimulation.

Rx: B-blockers like propranolol

125
Q

How is thyroid hormone regulated?

A

TRH from the hypothalamus stimulates the ant pit to rls TSH, which stimulates the follicular cells of the thyroid to make T4. T4 is converted to T3 peripherally.

There is negative feedback on the ant pit by the free T3 (it decreases the ant pit’s sensitivity to TRH)

TSI (thyroid stimulating immunoglobulin) is like TSH- it stimulates follicular cells.

126
Q

T3 functions

A 
4 B's:
Brain maturation
Bone growth
Beta-adrenergic effects
BMR (increased)
127
Q

What is TBG? When is it increased or decreased?

A

Thyroxine-binding globulin
It binds most of the T3/T4 in blood.
Only free hormone is active.

In hepatic failure, TBG is decreased.
In pregnancy or OCP use, TBG is increased (bc estrogen increases TBG)

128
Q

Which thyroid hormone has greater affinity for receptors?

A

T3 binds with greater affinity than T4.

129
Q

What is peroxidase?

A

Enz responsible for oxidation and organification of iodide.

Also responsible for coupling MIT and DIT.

130
Q

Where is thyroid hormone produced?

A

In the thyroid follicular cell (border of follicle) and in the lumen of the thyroid follicle (inside of follicle, aka colloid)

131
Q

How is iodide brought into the lumen of the follicle?

A

Iodide is actively absorbed from the blood by iodide trapping: Na+ and iodide are co-transported into the follicular cell thru the basolateral (blood) side of the follicular cell, and then passes out the other side of the cell into the lumen of the follicle, where it is oxidized and concentrated.
Then, it’s ready to be bound to tyrosine residues on the TG (thyroglobulin)

132
Q

How does TG (thyroglobulin) get to the lumen of the thyroid follicle?

A

TG is synth’d by the RER in the follicular cell. Then, it’s secreted (secretory pathway) by exocytosis

133
Q

How is thyroid hormone made?

A

TG from the follicular cell is secreted into the lumen of the follicle; meanwhile, iodide is also brought in and is concentrated.
Iodine is bound to tyrosine residues on the TG by the enz thyroperoxidase. This forms MIT and DIT.
DIT + DIT = T4
MIT + DIT = T3
(but it’s still all attached together at this point)
The complex is endocytosed back into the follicular cell. Then, proteases in the cell break down the complex to liberate the T3 and T4, and they go out of the follicular cell and into the blood.

134
Q

Where do anti-thyroid drugs propylthiouracil and methimazole act?

A

They inhibit MIT and DIT formation (from TG and Iodine)

135
Q

What is Graves’ dz?

A

Hyperthyroidism (most common cause)
Auto-imm, w TSI and TSH receptor Ab (that stimulate the receptor)
It’s a Type II HPS (anti-self Ab)

Px: opthalmopathy (proptosis, EOM swelling); pretibial myxedema, diffuse goiter
Often px’s during stress (eg childbirth)

Histo: decreased colloid inside the follicle

136
Q

Thyroid storm (thyrotoxicosis)

A

Stress-induced catacholamine surge, which causes arrhythmia and death.

Seen as serious complication of Graves’, other hyperthyroid disorders.
Also in Jod-Basedow

Rx: propranolol (B-blocker)

137
Q

Toxic multinodular goiter

A

Hyperthyroidism.
Focal patches of hyper-fn’g follicular cells working independently of TSH d/t a mutation in the TSH receptor.
Causes increased rls of T3 and T4
Nodules are NOT malignant.

138
Q

Jod-Basedow phenomenon

A

Hyperthyroidism
Thyrotoxicosis if a pt w an iodine deficiency goiter is made iodine replete (given lots of iodine)
Seen when pt given radiocontrast dye w iodine in it becomes hyperthyroidic.

139
Q

What are the anti-thyroid drugs and what are they used for?

A

Propylthiouracil
Methimazole

Used for hyperthyroidism
If prego: use propythiouracil

140
Q

Mechanism and toxicity of propylthiouracil and methimazole (anti-thyroid)

A

Inhibit organification of iodide and coupling of thyroid hormone synthesis- they inhibit the iodination of tyrosyl groups, so iodine is not attached to thyroid hormone.

Toxicity: skin rash, agranulocytosis (rare), aplastic anemia
(zidovudine HIV drug also has agran and aplastic anemia as a side effect)

141
Q

Medical professional w pride in recent weight loss + hyperthyroidism

A

Thyroid Hormone abuse (TH increases BMR)

142
Q

Hyperthyroidism w single thyroid nodule? w multiple thyroid nodules?

A

Single: Toxic thyroid adenoma

Multiple: Toxic multinodular goiter

143
Q

Hyperthyroidism w Hx of thyroidectomy or thyroid radio-ablation

A

Taking too much exogenous thyroid hormone

144
Q

Papillary carcinoma

A 
most common kind of thyroid cancer 
excellent pgx
ground glass/orphan annie nuclei
psamomma bodies
nuclear grooves
increased risk if had childhood irradiation
145
Q

Follicular carcinoma

A 
Cancer of thyroid follicle
Good pgx
Uniform follicle
40% a/w Ras mutation
More common in iodine deficient areas
146
Q

Medullary carcinoma

A

Thyroid carcinoma in the parafollicular C cells
produces calictonin
sheets of cells in amyloid stroma
A.w MEN 2A and 2B

147
Q

Undifferentiated/anaplastic thyroid cancer

A

Mainly in older pts

V poor pgx

148
Q

Lymphoma (thyroid cancer)

A

Assoc w Hashimoto’s thyroiditis (hypothyroid)

149
Q

TSH and thyroid hormone levels in Graves’

A

Graves = Ab to the TSH receptor that stimulate the receptor. If receptor is stimulated by the Ab, it will signal to make Thyroid hormone- so T3 and T4 will be high. This will feedback and cause decreased TSH. But, the TSH receptor will still be stimulated bc of the Ab.

150
Q

What kind of thyroid cancers activate receptor tyrosine kinases?

A

Papillary carcinoma and medullary carcinoma

151
Q

What kind of cancer might a pt get if he has Hashimoto’s thyroditis?

A

Lymphoma

152
Q

Thyroid cancer a/w rearrangements in RET oncogene or NTRK1?

A

Papillary carcinoma

153
Q

The most common mutation in the BRAF gene (a serine/threonine kinase) can produce which kind of thyroid cancer?

A

Papillary carcinoma

154
Q

First and second most common thyroid cancers

A

Most common: Papillary carcinoma (70-75%)

2nd: Follicular carcinoma (10%)

* DIT each session (34 decks)

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