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Endocrine > Adrenals > Flashcards

Adrenals Flashcards

1
Q

What does the adrenal cortex make?

A

Steroidds

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2
Q

What does the adrenal medulla secrete?

A

Catecholamines (NE/E)

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3
Q

Which embryonic tissue are the cortical cells derived from?

A

Mesodermal mesenchyma

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4
Q

Which embryonic tissue are the medullary cells derived from?

A

Neural crest

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5
Q

Where do the following suprarenal branches come from?

Superior suprarenal a.
Middle suprarenal a.
Inferior suprarenal a.

A

Superior suprarenal a. - inferior phrenic a.
Middle suprarenal a. - aorta
Inferior suprarenal a. - renal a.

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6
Q

Once the blood vessels enter the capsule, what does the capsular capillaries, fenestrated cortical sinusoidal capillaries, and medullary arterioles supply?

A

Capsular capillaries- supply capsule
Fenestrated cortical sinusoidal capillaries- supply cortex
Medullary arterioles- traverse the cortex and bring arteriol blood to the medullary capillary sinusoids

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7
Q

What are the 3 layers of the adrenal cortex from superficial –> Deep?

A 
Zona glomerulosa (ZG)
Zona Fasciculata (ZF)
Zona reticulata (ZR)

“Go Find Rex, Make Good Sex”

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8
Q

Where does the R suprarenal v drain?

A

IVC

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9
Q

Where does the L suprarenal v drain?

A

L renal v

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10
Q

What is the hormone released from the ZG?

A

Minerocorticoids

“Go Find Rex, Make Good Sex”

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11
Q

What is the main mineralcorticoid released from the ZG?

A

Aldosterone

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12
Q

What are the H’s released from the ZF?

A

Glucocorticoids (coricosterone and cortisol)

“Go Find Rex, Make Good Sex”

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13
Q

What are the H’s released from the ZR?

A

Gonadocorticoids (DHEA)

“Go Find Rex, Make Good Sex”

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14
Q

What are the H’s released from the adrenal medulla?

A

Catecholamines (NE/E)

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15
Q

Which cells in the adrenal medulla make the catecholamines?

A

Chromaffin cells

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16
Q

What makes the catecholamines different (as far as structure) than the cortical adrenal H’s?

A

They’re peptides rather than steroids.

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17
Q

Which type of SANS fibers inntervate the chromaffin cells (pre- or post-ganglionic)?

A

Preganglionic SANS fibers

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18
Q

Which NT does the preganglionic SANS fibers release to stimulate the chromaffin cells to release the catecholamines?

A

Ach

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19
Q

Which drug depletes catecholamines from the vesicles and inhibits transport?

A

Reserpine

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20
Q

Which H’s from the adrenal cortex induce the conversion of NE –> E in chromaffin cells via enzyme methylation?

A

Glucocorticoids

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21
Q

Which “zona” is the largest in the adrenal cortex?

A

80% is made of the ZF

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22
Q

What triggers the release of cortisol from the ZF?

A

Stress

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23
Q

What are the actions of the glucocorticoids on glucose metabolism?

A

↑ gluconeogenesis, ↑ glycogenolysis

(stressed from seeing a bear –> cortisol released –> glucose put into blood for energy to run away –> can’t run away because those big Mac’s are catching up to you –> trip over a fallen branch –> accept your fate –> turn around –> bear staring at you –> looks you deep in the eyes –> you tightly shut your eyes waiting for the life-ending claw swipe –> hear “are you scared?” –> open 1 eye –> bear pulls its head off and ashton kutcher is inside –> “you’re on punk’d.”)

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24
Q

Why is hydrocortisone used to treat allergies and inflammation? What does hydrocortisone (cortisol) inhibit normally?

A

immune and inflammatory responses

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25
Q

Which hormone stimualtes the release of aldosterone from the ZG?

A

Angiotensin II

“Go Find Rex, Make Good Sex”

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26
Q

Which hormones stimulates the release of cortisol and DHEA from the ZF and ZR?

A

ACTH

“Go Find Rex, Make Good Sex”

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27
Q

Which molecule are all steroid H’s derived from?

A

Cholesterol

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28
Q

Which enzyme converts cholesterol –> pregnenolone?

A

P450scc

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29
Q

Pregnenolone –> ________ –> DHEA

A

17-hydroxypregnenolone

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30
Q

Pregnenolone is also coverted to which molcule to eventually make Aldosterone and Cortisol?

A

Progesterone

using 3-B-hydroxysteroid dehydrogenase

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31
Q

This is the group of diseases caused by genetically determined deficiency in a variety of enzymes required for cortisol synthesis.

A

Congenital adrenal hyperplasia (CAH)

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32
Q

Which enzyme is needed to covert progestrone to 11-deoxycorticosterone and 11-a-hydroxyprogestrone to 11-deoxycortisol?

A

21-a-hydroxylase

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33
Q

So a deficiency in 21-a-hydroxylase will decrease the synthesis of which H’s?

A

Aldosterone

Cortisol

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34
Q

What happens to DHEA levels in 21-a-hydroxylase?

A

it increases cuz the other’s decrease –> ↑ androgens –> prenatal masculinization in females and postnatal virilization in males

“in 21-a-OH deficiency you look 21 y/o real quick”

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35
Q

Which H accumulates in 11-B-hydroxylase deficiency?

A

11-deoxycorticosterone (mineralcorticoid) and 11-deoxycotisol

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36
Q

So what is the main complaint in 11-B-hydroxylase deficiency?

A

moderate HTN and high virulization

“11 year old MEN with HTN.”

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37
Q

Which H’s accumulate in 17-a-hydroxylase deficiency?

A

aldosterone

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38
Q

So what is the main complaint in 17-a-OH deficiency?

A

Super HTN

“on a scale of 1-10, my BP is at a 17.”

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39
Q

Which AA are catecholamines derived from?

A

Tyr

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40
Q

Which molecule is required fro Phe –> dopa?

A

BH4 (tetrahydrobiopterin)

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41
Q

What is formed when dopa is decarboxylated?

A

Dopamine

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42
Q

Which ion is required fro the hydroxylation of dopamine to form NE?

A

Cu++

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43
Q

What is added to NE to form E using SAM?

A

Methyl group

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44
Q

What are the 2 products when MAO degrades NE?

A

NH4 + an aldehyde

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45
Q

Which enzyme converts NE (using SAM) to an aldehyde by methylating the 3-OH group?

A

COMT

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46
Q

Which 2 factors are required to make SAM?

A

B12 and folate

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47
Q

The products of MAO and COMT eventually parallel to form which final product?

A

VMA

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48
Q

What does an increased VMA in the CSF indicate?

A

Dopamine degradation

like in Parkinsons

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49
Q

What happens to the VMA levels in a pheochromocytoma?

A

they ↑

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50
Q

Where can u measure the levels of VMA?

A

urine

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51
Q

What is the cholesterol mirochondiral transport protein regulated by ACTH?

A

StAR

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52
Q

ACTH also regulates the transport of cholesterol into adrenal cortex cells by regulating what 2 molcules?

A

HDL and LDL

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53
Q

What is the hormone that generated pregnenolone in the mitochondria, that is regulated by ACTH?

A

cholesterol desmolase (CPY11A1)

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54
Q

So pregnenolone is made in the mitochrondria, and where doe sit travel next to continue its reactions?

A

SER

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55
Q

In the ZG, what product returns to the mitochrondria from the SER to make Corticosterone?

A

DOC

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56
Q

In the ZF, what product returns to the mitochrondria from the SER to make Cortisol?

A

11-deoxycortisol

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57
Q

In the ZR, what product returns to the mitochrondria from the final H?

A

trick Q

it never returns to the mitochondria

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58
Q

Which cells does aldosterone work on?

A

Principal cells of the CD

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59
Q

What does aldosterone do to Na and K?

A

reabsorb Na

secrete K

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60
Q

An increase in aldosterone does what do plasma pH?

A

Alkalosis because it ↑ tubular H secretion

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61
Q

What does aldosterone instert into the apical membrane of the principal cells?

A

Na/K ATPases

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62
Q

An increase in which of the following factors stimulates aldosterone secretion?

K in ECF, ATII, Na+ in ECF, ACTH

A

K, ATII and ACTH

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63
Q

What is the syndrome from ↑ aldosterone from a tumor in the ZG?

A

Conn’s syndrome

primary aldosteronism

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64
Q

What happens to the BP, serum K, serum Na, serum pH, and serum renin in Conn’s?

A 
HTN
HypoKalemia
HyperNatremia
Metbolic alkalosis
↓ serum Renin (b/c of ↑ BP)
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65
Q

Which IL do glucocorticoids inhibit as part of its anti-inflammatory effects?

A

IL-2

↓ T-cells

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66
Q

Glucocorticoids induce the synthesis of which factor, which inhibits PLA2 normally, contributing to the anti-inflammatory effects?

A

Lipocortin

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67
Q

What does glucocorticoids do to mast cells which contributing to the anti-inflammatory effects?

A

inhibit release of serotonin and histamine

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68
Q

The inhibition of the production of IL-2 from glucocorticoids helps with what treatment?

A

Prevention of transplant rejection

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69
Q

Which NE receptor do glucocorticoids stimulate to ↑ the vasoconstrictor effect of NE?

A

a1

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70
Q

What is the primary active glucocorticoid in the body?

A

Cortisol

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71
Q

What does cortisol do to proteins?

A

↓ protein synthesis
↑ catabolism of proteins
↑ transport of AA’s to liver (for gluconeogensis)

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72
Q

What does cortisol do to fat?

A

metabolize FA’s –> ↑ FA’s in plasma

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73
Q

What are the 5 things that cortisol does to block the early stages of inflammation?

A
  1. Stabilizes lysosomal membranes
  2. Decreases permeability of the capillaries
  3. Decreases both migration of WBC’s into the inflamed area and phagocytosis of the damaged cells
  4. Suppresses the immune system, causing lymphocyte reproduction to decrease
  5. Reduces fever bc it reduces the release of IL-1 from the WBC’s
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74
Q

So generally what does cortisol do a persons immune system?

A

suppress it

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75
Q

What does cortisol bind to once inside the target cell?

A

Glucocorticoid response elements (GRE)

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76
Q

What do GRE’s do, like any othere steroid H-R complex?

A

increase or decrease txn of genes

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77
Q

What is the cortisol pathway from hypothal –> tissues?

A

hypothal releases CRH –> AHP releases ACTH –> ZF releases cortisol –> liver, fat, muscle, lymphocytes, etc.

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78
Q

What is the condition where the adrenal cortex produces too little adrenocortical hormones?

A

Addisons disease

79
Q

What are the effects of addisons disease?

A

no aldosterone –> hypoNa, hyperK, hypoTN

no cortisol –> low fasting glucose, weakness, low metabolic fxns

80
Q

What is the condition where there is hypersecretion of adrenocortical hormones by the adrenal cortex?

A

Cushings

81
Q

What is the most common cause of cushings syndrome?

A

excess ACTH

82
Q

What are the 4 physical Sx of Cushings?

A

buffalo torso
moon face
acne/hirsuitism
purple striae on belly

83
Q

What is the BP, blood glucose, protein levels in Cushings?

A

HTN
Hyperglycemia
Increased protein catabolism

84
Q

What are the Sx of excess androgens in females?

A

beard, deep voice, baldness, masculine districution of pubic hair, big clitoris, big muscles.

85
Q

What are the Sx of excess androgens in prepubertal males?

A

same as females + rapid development of male sex organs

86
Q

What R is stimulated a ton to cause HTN in Cushings?

A

a1 receptors

87
Q

What bone problem can u get in cushings?

A

Osteoporosis

88
Q

What are teh 4 causes of Cushings?

A
  1. Coricosteroid drugs
  2. Primary adrenal adenoma
  3. ACTH-secreting pituitary adenoma
  4. Paraneoplastic ACTH secretion
89
Q

Is there hypertrophy in one, both, or none of the adrenals in Cushings from Corticosteroid use?

A

none. they both atrophy.

90
Q

Is there hypertrophy in one, both, or none of the adrenals in Cushings from primary adrenal adenoma?

A

Atrophy of the uninvolved kidney

91
Q

Is there hypertrophy in one, both, or none of the adrenals in Cushings from paraneoplastic syndromes?

A

Both

92
Q

Is there hypertrophy in one, both, or none of the adrenals in Cushings from ACTH-sectreting pit adenoma?

A

Both

93
Q

So what drug/test can u do to distinguish between an ACTH-secreting pit adenoma and a paraneoplastic syndrome?

A

High-dose dexamethasone

paraneoplastic DOES NOT respond, pit adenoma has ↓ ACTH

94
Q

What is the syndrome of excess aldosterone?

A

Conn syndrome

95
Q

What is the most common cause of primayr hyperaldosteronism?

A

Adrenal adenoma

96
Q

What are the serum aldosterone and renin in primary hyperaldosteronism?

A

High aldosterone

Low renin

97
Q

Which type of hyperaldosteronism gives you both a high aldosterone AND renin?

A

Secondary hyperaldosteronism (RAAS activation)

98
Q

Why does 21-a-hydroxylase deficiency lead to b/l adrenalo hyperplasia?

A

no synthesis of aldosterone or cortisol –> no neg feedback to ACTH –> hyperplasia of adrenals

99
Q

Which CAH is the most common, 21-b, 17-a, or 11-B hydroxylase deficiency?

A

21-B-hydroxylase deficiency (90%)

100
Q

What is the classic syndrome assocaited with acute adrenal insufficiency?

A

Waterhouse-Friderichsen syndrome

101
Q

What happens to kids in WF syndrome?

A

N. meningitis infection –> DIC –> hemorrhagic necrosis of adrenal glands.

102
Q

In WF syndrome, the lack of cortisol can lead to what problem?

A

Death

103
Q

What do the adrenals classicaly look like in WF syndrome?

A

Sack of blood

104
Q

What is the most common cause of Addisons in the West?

A

Autoimmune destruction

105
Q

What is the most common cause of Addisons in developing world?

A

TB

106
Q

What is the most common cause of Addisons in metastatic carcinomas?

A

Lung CA

107
Q

What skin changes occur in Addisons?

A

↑ ACTH –> hyperpigmentation

108
Q

Which 2 markers are elevated in the screening of a pheocromocytoma?

A

urine metaneprines and VMA

109
Q

What is the drug you HAVE to give pre-op before surgical removal of a pheo?

A

Phenoxybenzamine

110
Q

What are the 4 components to the “rule of 10’s” in pheochromocytomas?

A

10% b/l
10% familial
10% malignant
10% located outside the adrenal medulla

111
Q

What is the most common location for a pheo outside the adrenal medulla?

A

Bladder wall

112
Q

What 3 things are associated with pheochromocytomas?

A

MEN 2A/2B
vHL disease
NFM1

113
Q

Which form of cancer shows up as a yellow well circumscribed nodular lesion, adenocortical adenomas or carcinomas?

A

Adenomas

prolif of the glands –> more yellow and shit

114
Q

What do adrenocortical carcinomas show on cur surface?

A

variegated, poorly demarcated lesions contains areas of necrosis, hemorrhage and cystic change

gross-looking.

115
Q

What gene is mutated in MEN 2A/B, which is assocaited with a pheo?

A

RET

116
Q

Which form of MEN is characterized by abnormalities involving the parathyroid, pancreas, and pituitary glands; thus the mnemonic device, the 3Ps?

A

MEN-1

117
Q

What is the fxn of MEN1, which is lost in the MEN-1 disease?

A

it’s a tumor suppressor gene

118
Q

What are the 3 components of the MEN-2?

A

MEN-2A
MEN-2B
Familial medullary thyroid cancer

119
Q

What are the 3 components of the MEN-2A (sipple) syndrome?

A

Pheochromocytoma
Medullary carcinoma
Parathyroid hyperplasia

120
Q

In addition to the pheo and medullary thyroid carcinoma, what other 2 things are a part of MEN-2B?

A 
Marfanoid habitus (like marfans)
Mucocutaneous ganglioneuromas
121
Q

What is a variant of MEN-2A, in which there is a strong predisposition to medullary thyroid cancer but not the other clinical manifestations of MEN-2A or MEN-2B?

A

Familal thyroid CA

122
Q

Since MEN-2A/B can cause life-threatening thyroid carcinoma, what is the screening method?

A

Screen at-risk family members (cuz of the RET mutation)

123
Q

Which drug inhibits the following rxns?

Pregnenolone –> progesterone
17-hydroxypregnenolone –> 17-hydroxyprogesterone
Dehydroepiandrosterone –> androstendione

A

Trilostane

124
Q

Which drug inhibits the following rxns?

11-deoxycorticosterone –> corticosterone
11-deoxycortisol –> cortisol

A

Metyrapone

125
Q

So what enzyme does trilostane inhibit?

A

3B-hydroxysteroid dehydrogenase

Stan goes to 3B’s

126
Q

And what enzyme does metyrapone inhibit?

A

11B-hydroxylase

Tyra has 11 foreheads

127
Q

Which glucocorticoid R is expressed in the organs of excretion (kidney, colon, salivary glands, sweat glands) and hippocampus?

A

Type I

128
Q

Where is the type II glucocorticoid receptor located?

A

Many tissues

129
Q

After long use of glucocorticoids, why must u taper the pt off of them?

A

Allow the hypothalamic-pituitary-adrenal (HPA) axis to regain full activity

(remember it’s supressed in steroid therapy)

130
Q

How much more does prednisone have the anti-inflammatory potency of cortisol?

A

4-5x

131
Q

How much more does methylprednisone have the anti-inflammatory potency of cortisol?

A

5-6x

132
Q

How much more does dexamethasone have the anti-inflammatory potency of cortisol?

A

18x

133
Q

What is the DOC for primayr adrenal insufficiency?

A

Oral hydrocortisone

134
Q

What is the therapeutic goal of hydrocortisone?

A

to administer the smallest possible effective dose of glucocorticoid so as to minimize the adverse effects of chronic glucocorticoid excess

135
Q

What are the 3 components of the early inflammatory response, and are blocked by cortisol?

A

Thromboxanes
Prostaglandins
Leukotrienes

136
Q

What is the biggest limitation to glucocorticoid therapy?

A

Doesnt correct the underlying disease, just limits the effects of inflammation

137
Q

What are the 2 major adverse rxns to long-term glucocorticoid treament?

A

Susceptibility to infection

DM

138
Q

What does glucocorticoids do to the gut, which can lead to osteoporosis?

A

inhibits vit D absorption of Ca++ –> hyperPTH –> ↑ osteoclast activity –> osteoporosis

139
Q

Inhaled, cutaneous, and depot preparations (intramuscular) of glucocorticoids avoids what?

A

High systemic levels

140
Q

Inhaled glucocorticoids are the treatment of choice for what condition?

A

Chronic asthma

141
Q

What is the treament of acute adrenal insufficiency?

A

large dose of IV glucocorticoid

142
Q

What is the enzyme that must be present in order to convert an inactive form of glucocorticoid to an active one?

A

11B-HSDI enzyme

143
Q

What separates the fetus from the mother, making it safe to use prednisone?

A

The placenta

144
Q

Normally, the maternal liver acitvates the prednisone to prednisolone, but what does the placenta have to convert the prednisolone back to the inactive prednisone?

A

placental 11B-HSD II

145
Q

Why cant the fetus activate prednisone?

A

the liver doesnt fxn during fetal life

146
Q

Generally, the agents that inhibit hormone synthesis at the early steps have what effects? later steps?

A

Early- broad effects

Later- more selective

147
Q

Minerealcorticoids regulate Na reabsorption in what 4 organs/glands?

A

Sweat glands
Salivary glands
Colon
Kidney

148
Q

Why can’t u give aldosterone itself as a therapeutic agent?

A

The liver converts > 75% of aldosterone to an inactive metabolite

149
Q

What is the other drug used, which has a minimal first-pass hepatic metabolism and a high mineralcorticoid to glucocorticoid potency ratio?

A

Fludrocortisone

“flew right past the liver”

150
Q

What 2 things must u measure in fludrocortisone treatment?

A

serum K

BP

151
Q

Which drug is a competitive agonist to the mineralcorticoid receptor, but can cause gynecomastia?

A

Spironolactone

152
Q

What is the mineralocorticoid receptor antagonist that binds selectively to the mineralocorticoid receptor, thus limiting the adverse effects?

A

Eplerenone

153
Q

What is the main ion problem in aldosterone R antagonists?

A

hypoKalemia

154
Q

What is the msot common cause of primary adrenal failure?

A

autoimmune adrenalitis (Addisons)

155
Q

This is the condition where pts with unrecognized adrenal failure who develop an intercurrent illness such as pneumonia, and experience dehydration and hypotension out of proportion to the severity of the illness.

A

Adrenal crisis

156
Q

Which form of adrenal failure (1o or 2o) requires glucocorticoid AND mineralocorticoid replacement?

A

Primary

(if the adrenals are screwed (primary), yer Cortisol and Aldosterone and DHEA are screwed. If the problem is the ant pit (secondary), aldosterone can still be triggered for release by the RAAS system, so u dont need to replace it).

157
Q

What are the 2 drugs for glucocorticoid replacement?

A

Hydrocortisone or prednisone

158
Q

What is the drug used for mineralcoricoid replacement?

A

Fludrocortisone

159
Q

What is the best screening test for Cushing syndrome?

A

24-hr urinary free cortisol excretion

160
Q

What are the 3 main causes of primary aldosteronism?

A

Aldosteronoma, idiopathic b/l hyperplasia, adrenocortical carcinoma

161
Q

Which cells are increased in a pheo?

A

Chromaffin cells

162
Q

What are the Sx of a pheo?

A

Episodic Headache, Palpitations, Sweating, and HTN

163
Q

What scan is used to localize a pheo?

A

T2 MRI with I-MIBG

164
Q

What are the things called when there are small adrenal masses that are incidenal and found either in CTs for other reasons or autopsies?

A

Adrenal incidentaloma

165
Q

What are the clinical features of hypogonadism in adult males?

A

Decreased libido and potency, decreased ejaculate volume, infertility, decreased stamina, decreased sexual hair growth, and gynecomastia

166
Q

What are the clinical features of hypogonadism in male adolescence?

A

Delayed puberty and growth, with an absence of a pubertal growth spurt, eunuchoid habitus (ratio of arm span to height is >1), high pitched voice, poor muscle development, and a female pattern of fat distribution

167
Q

What syndrome can cause a small firm teses in a hypogonadal male?

A

Klinefelter’s Syndrome

168
Q

What serum H levels are low in male hypogonadism?

A

Testosteronee

169
Q

What is the chromosomal abnormality in Klinefelters?

A

47 XXY

170
Q

What is the syndrome characterized by hypogonatrotrophic hypogonadism and anosmia?

A

Kallman’s syndrome

171
Q

What are the 2 main causes of gynecomastia?

A

Excess estrogen

Absolute increase in estradiol production

172
Q

An increase in B-hCG for a gynocomastia male implies what etiology?

A

HCG-secreting tumor

http://thechart.blogs.cnn.com/2012/11/08/home-pregnancy-tests-may-detect-mens-cancer/

173
Q

What 2 things define primary amenorrhea?

A

when menarch has not occured by 16 y/o with normal secondary sex characteristics or by age 14 in the absence of secondary sex characteristics

174
Q

What defines secondary amenorrhea?

A

when a woman with a previous menstal fxn doesnt menstruate for 3 cycles or 6 months

175
Q

What are the 3 main causes of primary amenorrhea?

A

Adal dysgenesis (45%), constitutional delay of puberty (20%), and mullerian agenesis (15%)

176
Q

What are the 4 main causes of secondary amenorrhea?

A

Hypothalamic Dysfxn (40%), polycystic ovarian syndrome (30%), pituitary dz (20%), and ovarian failure (10%)

177
Q

A woman with vaginal dryness, hot flashes, and loss of secondary sex characteristics may have low levels of what H?

A

Estrogen

178
Q

In secondary amenorrhea, what test must u do to exclude pregnancy?

A

hCG level

179
Q

What are the 2 tests in seocndary amenorrhea to evaluate thyroid dysfxn?

A

Prolactin and TSH levels

180
Q

In the measurement of Estradiol, LH, and FSH for seocndary amenorrhea, what might an increase in FSH with low estradiol indicate?

A

Primary ovarian failure

181
Q

What are the levels of FSH and LH in hypothalamic pituitary disorder?

A

both are inappropriately low

182
Q

What cancer can estrogen therapy put u at risk for?

A

Endometrial CA

183
Q

What is the chromosomal abnormality in Turner syndrome?

A

45 XO

184
Q

What are the clinical manifestations fo Turners?

A

Webbed neck, low set ears, micrognathia, shield like chest, short metacarpals and metatarsals, increased carrying angle at the elbows, renal developmental abnormalities, and cardiovascular anomalies (coarctation and aortic stenosis).

185
Q

This is the syndrome in females under 25, and it is a distorted perception of weight and body image that leads to poor nutrition.

A

Anorexia nervosa

186
Q

What are the clinical manifestations of anorexia nervosa?

A

amenorrhea, bradycardia, hypotension, constipation, growth of lanugo hair, and in severe cases, dependent edema

187
Q

This is the Excessive androgen induced hair growth in the androgen sensitive areas of the female body.

A

Hirsutism

188
Q

This is the masculinization of secondary sex characteristics and the sex organs and is the result of pronounced androgen stimulation.

A

Virilization

189
Q

What 3 diseases can cause Hirsutism?

A

PCOS
CAH
ACTH-dependent Cushings

190
Q

What is the most common cause of hyperangrogenism in females?

A

PCOS

191
Q

What are the 2 metabolic disorders assocaited with PCOS?

A

Glucose intolerance and DMII

192
Q

What is the inheritance of CAH?

A

AR

193
Q

What are the 2 therapies used in the management of idiopathic Hirsutism and polycystic ovarian syndrome?

A

Metformin and insulin sensitizing agents

Endocrine (4 decks)

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