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Clinical Chemistry 2 - CEUMLS > Endocrinology Part 3 (Adrenal Gland) > Flashcards

Endocrinology Part 3 (Adrenal Gland) Flashcards

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1
Q

multifunctional organ that produces steroid hormones and neuropeptides essential for life

A

Adrenal gland

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2
Q

pyramid-like shaped gland composed to 2 conjoined gland

A

Adrenal gland

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3
Q

location of adrenal gland

A

superior and medial to the kidneys

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4
Q

outer part of adrenal gland

A

ADRENAL CORTEX

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5
Q

% composition of adrenal cortex with the total adrenal gland

A

90%

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6
Q

% composition of adrenal medulla with the total adrenal gland

A

10%

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7
Q

color of adrenal cortex in cross section

A

Yellowish

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8
Q

color of adrenal medulla in cross section

A

dark mahogany

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9
Q

adrenal cortex is derived from

A

Mesenchymal cells

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10
Q

Major site of STEROID HORMONE production

A

adrenal cortex

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11
Q

3 zones of Adrenal Cortex, each with distinct tissues

A

Zona glomerulosa (G-zone)
Zona fasciculata (F-zone)
Zona reticularis (R-zone)

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12
Q

loc and % of Zona glomerulosa (G-zone) in total adrenal cortex

A

Outer; 10%

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13
Q

loc and % of Zona fasciculata (F-zone) in total adrenal cortex

A

Middle; 75%

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14
Q

loc and % of Zona reticularis (R-zone) in total adrenal cortex

A

Inner; 15%

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15
Q

Hormone produced by G-zone

A

Aldosterone

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16
Q

Hormone produced by F-zone

A

Glucocorticoids (cortisol and cortisone)
Adrenal androgens: dehydroepiandrosterone (DHEA)

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17
Q

Hormone produced by R-zone

A

DHEA-S

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18
Q

a mineralocorticoid (regulates Na2+)

A

Aldosterone

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19
Q

stored form of cortisol

A

cortisone

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20
Q

critical for glucose homeostasis and BP

A

glucocorticoids

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21
Q

precursor for other active androgen or sex hormones, which is sulfated in innermost zona reticularis (R-zone)

A

dehydroepiandrosterone (DHEA)

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22
Q

main adrenal androgen

A

DHEA-S (dehydroepiandrosterone sulfate)

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23
Q

major active precursor for androgens and estrogen

A

DHEA-S (dehydroepiandrosterone sulfate)

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24
Q

inner part of adrenal gland

A

ADRENAL MEDULLA

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25
Q

Adrenal medulla is derived from

A

Neural crest

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26
Q

hormones produced by adrenal medulla

A

amine hormones: CATECHOLAMINES

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27
Q

Composed of Chromaffin Cells

A

adrenal medulla
paraganglia

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28
Q

Function of chromaffin cells

A

secretes catecholamines

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29
Q

enumerate conversion of chole to pregnenolone

A

CRH (hypothalamus)
ACTH (pituitary) - promotes entry of chole into mitochondria
Mitochondria: chole –> pregnenolone by cytochrome P450

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30
Q

Major regulator of adrenal hormone regulation

A

Corticotropin-releasing hormone (CRH)

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31
Q

produced by hypothalamus; stimulate pituitary gland to secrete ACTH

A

Corticotropin-releasing hormone (CRH)

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32
Q

Corticotropin-releasing hormone (CRH) production is in response to:

A
  1. ↓ cortisol level
  2. Stress
  3. Circadian Rhythm
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33
Q

peak in CRH is seen during

A

6-8 AM

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34
Q

lowest CRH level is seen during

A

10-12 MN

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35
Q

Produced by pituitary gland

A

Adrenocorticotropic Hormone (ACTH)

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36
Q

Stimulates the adrenal cortex to produce STEROID HORMONES

A

Adrenocorticotropic Hormone (ACTH)

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37
Q

main precursor of steroid hormones

A

cholesterol

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38
Q

Stimulates transport of free cholesterol inside the mitochondria of adrenal cortex, initiating STEROIDOGENESIS

A

Adrenocorticotropic Hormone (ACTH)

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39
Q

1st product produced in steroidogenesis

A

PREGNENOLONE

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40
Q

serves as a substrate for ALL adrenal cortex hormones

A

PREGNENOLONE

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41
Q

FEEDBACK SYSTEM/MECHANISM followed by adrenal cortex hormones production

A

NEGATIVE

↓ cortisol will stimulate ↑ CRH

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42
Q

T/F

decrease in cholesterol will stimulate G-zone (hormone produced: aldosterone)

A

F

↓ chole and cortisol will not increase aldosterone (unstimulated G-zone) since aldosterone is only dependent to RAAS

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43
Q

produced by kidneys in response to ↓ BP, ↓ BV

A

renin

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44
Q

stimulate Aldosterone production by G-zone

A

renin

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45
Q

Adrenal cortex hormone (steroid hormone) synthesis

A

STEROIDOGENESIS

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46
Q

event that takes place in mitochondria during steroidogenesis

A

Cholesterol –> Pregnenolone by cytochrome P450 (CYP450)

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47
Q

what happens next when chole is converted to pregnenolone?

A

Newly synthesized Pregnenolone is then returned to the cytosol
(further conversions of Pregnenolone to various adrenal cortex hormone )

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48
Q

event that takes place in G-zone

A

Pregnenolone –> Aldosterone
*in response to RAAS

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49
Q

event that takes place in F-zone

A

17a-hydroxypregnenolone –> Cortisol –> cortisone
*in response to CRH & ACTH

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50
Q

enzyme that converts Pregnenolone –> 17a-hydroxypregnenolone

A

17-a-hydroxylase

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51
Q

17-a-hydroxypregnenolone in F-zone may migrate to the R-zone to form

A

dehydroepiandrosterone (DHEA) which are sulfated –> DHEAS

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52
Q

major substrate for androgen production such as testosterone and estradiol

A

DHEAS

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53
Q

Associated with absent or deficient enzyme required for steroidogenesis

A

CONGENITAL ADRENAL HYPERPLASIA (CAH)

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54
Q

Inherited family of enzyme disorders

A

CONGENITAL ADRENAL HYPERPLASIA (CAH)

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55
Q

Required steroidogenesis enzymes

A

21ß-hydroxylase
11ß-hydroxylase
3ß-hydroxysteroid isomerase
17α-hydroxylase

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56
Q

cortisol and aldosterone levels in CAH

A

decreased

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57
Q

high lab value caused by deficient 3ß-hydroxysteroid isomerase

A

DHEA

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58
Q

high lab value caused by deficient 17α-hydroxylase

A

Aldosterone

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59
Q

high lab value caused by deficient 11ß-hydroxylase

A

11-deoxycorticosterone

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60
Q

high lab value caused by deficient 21ß-hydroxylase

A

17a-hydroxyprogesterone

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61
Q

effect in hypertension and virilization if 3ß-hydroxysteroid isomerase is deficient

A

HTN: no
Virilization: slight

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62
Q

effect in hypertension and virilization if 17α-hydroxylase is deficient

A

HTN: yes
virilization: no

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63
Q

effect in hypertension and virilization if 11ß-hydroxylase is deficient

A

HTN: yes
virilization: marked

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64
Q

effect in hypertension and virilization if 21ß-hydroxylase is deficient

A

HTN: no
virilization: marked

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65
Q

dev’t of masculine physical traits among women –e.g. Hirsutism (usually with PCOS)

A

Virilization

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66
Q

T/F

Enzyme deficient will increased the substrate in the pathway it convert.

A

T

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67
Q

reason why ALDOSTERONE is increased if 17α-hydroxylase is deficient

A

Pathway continues until aldosterone is produced (In enzyme deficiency, when pathway is blocked, it will continue the other pathway)

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68
Q

most common enzyme deficient that contributes to CAH

A

21 beta-hydroxylase

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69
Q

type of CAH with marked virilization

A

21ß-hydroxylase
11ß-hydroxylase

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70
Q

type of CAH with hypertension

A

17α-hydroxylase
11ß-hydroxylase

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71
Q

Most potent mineralocorticoid (electroregulating hormone)

A

ALDOSTERONE

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72
Q

regulated by aldosterone

A

H+ and K+ excretion
Na2+ reabsorption

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73
Q

effect of aldosterone in BP

A

↑ BP through volume expansion by ↑ sodium reabsorption

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74
Q

secrete renin

A

Juxtaglomerular cells (JG cells) of nephrons (kidneys)

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75
Q

converted by renin

A

Angiotensinogen ———–> Angiotensin I

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76
Q

converted by ACE

A

Angiotensin I ——-> Angiotensin II

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77
Q

angiotensin precursor produced by liver

A

Angiotensinogen

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78
Q

enzyme produced by lungs

A

ACE

79
Q

4 functions of angiotensin II

A
  • stimulate adrenal cortex to produce aldosterone (Aldosterone – Na2+reabsorption in DCT)
  • stimulates hypothalamus to produce ADH (ADH – water reabsorption in collecting duct)
  • ↑ arterial pressure by vasoconstriction
  • ↑ absorption of Na2+ in PCT
80
Q

Aldosterone Secretion is stimulated by

A

 Low BP
 Angiotensin II
 ACTH
 Elevated serum K+
 Progesterone
 Dopamine

81
Q

Aldosterone Secretion is inhibited by

A

 Atrial Natriuretic Peptide
 Intracellular Calcium
 Certain Drugs (ketoconazole, heparin, ACE inhibitors, NSAIDs)

82
Q

acts on ↑ BP by promoting vasodilation and Na2+ excretion

A

Atrial Natriuretic Peptide

83
Q

T/F

ACTH only stimulate aldosterone by stimulation of cholesterol entry to G-zone; does NOT DIRECTLY stimulate aldosterone production (RAAS is still the main stimulant)

A

T

84
Q

aka Primary Hyperaldosteronism

A

Primary Aldosteronism
Conn’s disease

85
Q

increased and decreased values in primary hyperaldosteronism

A

↑: plasma aldosterone
↓: plasma renin

86
Q

causes of Primary Aldosteronism

A
  1. Aldosterone-secreting adrenal adenoma
  2. Unilateral/Bilateral adrenal hyperplasia
  3. Familial hyperaldosteronism
  4. Adrenocortical carcinomas
  5. Ectopic aldosterone production
87
Q

Autonomous aldosterone production

A
  1. Aldosterone-secreting adrenal adenoma
  2. Unilateral/Bilateral adrenal hyperplasia
88
Q

genetics/hereditary primary Hyperaldosteronism

A

Familial hyperaldosteronism

89
Q

Primary hyperaldosteronism caused by cancer that produces ACTH

A

Adrenocortical carcinomas

90
Q

aldosterone production aside from adrenal cortex

A

Ectopic aldosterone production

91
Q

condition with excess renin production

A

Secondary Hyperaldosteronism

92
Q

aldosterone & renin lvl in secondary hyperaldosteronism

A

INCREASED

93
Q

3 Pseudohyperaldosteronism

A

Liddle’s syndrome - ↓ aldosterone
Bartter’s Syndrome - ↑ aldosterone
Gitelman’s Syndrome - ↑ aldosterone

94
Q

Variation in renin & aldosterone conc. but in most cases aldosterone is ↓

A

Pseudohyperaldosteronism

95
Q

aka Bartter’s Syndrome

A

bumetanide-sensitive chloride channel mutation

96
Q

aka Gitelman’s Syndrome

A

thiazide-sensitive transporter mutation

97
Q

Due to adrenal gland destruction and glucocorticoid deficiency

A

Isolated Hypoaldosteronism

98
Q

Associated with 21-hydroxylase deficiency

A

Isolated Hypoaldosteronism

99
Q

associated with ↑ 17a-hydroxyprogesterone

A

Isolated Hypoaldosteronism

(increased in 17a-hydroxyprogesterone is due to 21-hydroxylase deficiency)

100
Q

Diagnostic Tests for Aldosterone

A

Captopril Suppression Test
Urinary Potassium Excretion
Plasma Aldosterone Concentration (PAC)/Plasma Renin Activity (PRA) ratio
Oral Salt Loading
Saline Infusion Test

101
Q

Aldosterone antagonists

A

Captopril

102
Q

normal effect of captopril in aldosterone?
what is the abnormal effect?

A

normal: ↓ aldosterone

primary hyperaldosteronism (Aldosterone-producing adenoma [APA]): ↑ aldosterone (AUTONOMOUS PROD)

103
Q

sample used in urinary potassium excretion and oral salt loading

A

24 hr urine

104
Q

principle of Urinary Potassium Excretion

A

aldosterone promotes K+ excretion in urine

105
Q

value suggestive of hyperaldosteronism in Urinary Potassium Excretion

A

> 30 mEq/day

*↑ Aldosterone = ↑ K+ excretion

106
Q

value suggestive of renal potassium retention in Urinary Potassium Excretion

A

<30 mEq/day

107
Q

2 cause of ↓ urinary K+ excretion:

A
  1. Diuretic use – ↑ Na2+ excretion, ↑ K+ reabsorption
  2. GI loss
108
Q

Most reliable method for screening primary aldosteronism

A

Plasma Aldosterone Concentration (PAC)/Plasma Renin Activity (PRA) ratio

109
Q

Special Patient Consideration in PAC/PRA ratio

A

 Ambulatory/walking: 2 hr prior blood collection
 Seated for 5-15 mins: during blood collection

110
Q

value suggestive of primary hyperaldosteronism in PAC/PRA ratio

A

> 30

111
Q

value diagnostic of primary hyperaldosteronism in PAC/PRA ratio

A

> 50

112
Q

administered in oral salt loading for diagnosing primary aldosteronism; what is the duration?; what is collected after?

A

5,000 mg/day for 3 days

24 hr urine is collected after 3 days

113
Q

what is measured in oral salt loading

A

urine sodium
urine aldosterone

114
Q

values suggestive of primary aldosteronism in oral salt loading

A

urine sodium: >200 mEq
urine aldosterone: >12 μg/day

115
Q

administered in saline infusion test and its duration? what is measured?

A

IV infusion of 2L NaCl for 2 hr
plasma aldosterone

116
Q

effect of saline infusion in aldosterone

A

↓ aldosterone (since there is already ↑ Na2+)

117
Q

normal PAC for saline infusion test

A

<5 ng/dL

118
Q

PAC for saline infusion test suggestive of primary hyperaldosteronism

A

> 10 ng/dL

119
Q

what is required to consider if it is primary adrenal insufficiency

A

90% of adrenal gland must be destroyed

120
Q

Used for Androgen excess diagnosis

A

Plasma DHEA
Plasma DHEAS

121
Q

aka CORTISOL

A

stress hormone

122
Q

Principal glucocorticoid

A

CORTISOL

123
Q

Only adrenal hormone that inhibits ACTH secretion

A

CORTISOL

124
Q

Hormone regulated by ACTH

A

Cortisol

125
Q

ACTH in circulation is bound to

A

Glycoproteins
Transcortin

126
Q

effect of cortisol in glucose

A

INCREASE GLU
Hyperglycemic (stimulates gluconeogenesis & lipolysis)

127
Q

Has an anti-inflammatory and immunosuppressive actions by inhibiting Ab production

A

cortisol

128
Q

used as therapeutic agent for RA, SLE, MS

A

cortisol

129
Q

Body’s natural alarm clock

A

cortisol

130
Q

reason why there is increased cortisol at the end of sleep

A

↑ energy metabolism by the cells

131
Q

hormone that exhibits diurnal rhythm

A

cortisol

132
Q

↑ cortisol levels are seen during

A

8-10am

133
Q

↓ cortisol levels are seen during

A

10pm-12mn

134
Q

ref value of cortisol

A

5-25 ug/dL

135
Q

specimen for cortisol

A

Blood - 8am collection (red top tube)
24 hr Urine

136
Q

Sensitive indicators of adrenal hyperfunction

A

Urine Free Cortisol

137
Q

All glucocorticoids degraded in the liver and excreted in urine in these forms (urinary metabolites):

A

17-hydroxycorticosteroids
17-ketogenic steroid

138
Q

Method for 17-hydroxycorticosteroids determination

A

Porter Silber Method

139
Q

Reagent for 17-hydroxycorticosteroids determination

A

Phenylhydrazine in sulfuric acid (H2SO4) + alcohol

(Porter Silber Method)

140
Q

Endcolor for 17-hydroxycorticosteroids determination

A

Yellow

(Porter Silber Method)

141
Q

Method for 17-ketogenic steroid determination

A

Zimmerman reaction

142
Q

Reagent for 17-ketogenic steroid determination

A

Meta-dinitrobenzene

(Zimmerman reaction)

143
Q

Endcolor for 17-ketogenic steroid determination

A

reddish-purple

(Zimmerman reaction)

144
Q

aka HYPERCORTISOLISM

A

Cushing’s Syndrome

145
Q

Excessive glucocorticoid production

A

Cushing’s Syndrome

146
Q

Major common cause of Hypercortisolism

A

1) ACTH-secreting pituitary adenoma – CD
2) Autonomous Cortisol production (adrenal tumor) – CS
3) Excess ACTH or CRH production - CD

147
Q

Features of Cushing’s Syndrome

A

Obesity with thin extremities
Buffalo hump
Hirsutism
Pendulum abdomen
Moonfaced

148
Q

condition with ↑ cortisol, ↓/N ACTH

A

Cushing’s Syndrome / Primary hypercortisolism

149
Q

condition with ↑ ACTH, ↑ cortisol

A

Cushing’s Disease / Secondary hypercortisolism

150
Q

Cause of Cushing’s Disease / Secondary hypercortisolism

A

pituitary tumor (autonomously secretes ACTH)

151
Q

Less serious, More common hypercortisolism

A

Cushing’s Syndrome

152
Q

More serious, Less common hypercortisolism

A

Cushing’s Disease

153
Q

Develops due to tumor growth, associated with hyperpigmentation

A

Cushing’s Disease

154
Q

Develops most often from taking medications that increases cortisol

A

Cushing’s Syndrome

155
Q

Screening Tests for HYPERCORTISOLISM

A

24-hour urine free cortisol
Overnight Dexamethasone Suppression Test
Midnight Salivary Cortisol Test / Late Night Salivary Cortisol Test

156
Q

Confirmatory Tests for HYPERCORTISOLISM

A

Low-dose Dexamethasone Suppression Test
Midnight Plasma Cortisol
Corticotropin-Releasing Hormone Stimulation test

157
Q

screening test that requires accurate collection and urine volume measurement

A

24-hour urine free cortisol

158
Q

In 24-hour urine free cortisol, if cortisol is 3x above normal it indicates?

A

suggestive of cortisol excess

159
Q

sources of false positive in 24-hour urine free cortisol

A

Increased fluid intake: >5L/day
Urine volume: >3L

160
Q

administered in Overnight Dexamethasone Suppression Test and time of administration? type of specimen and time of collection?

A

1mg dexamethasone
11-12pm
blood at 8 am

161
Q

Results of Overnight Dexamethasone Suppression Test

A

Normal = <1.8 ug/dL
Cortisol excess = >1.8 ug/dL

162
Q

requirement for Midnight Salivary Cortisol Test / Late Night Salivary Cortisol Test

A

avoid smoking prior to collection

163
Q

administered in Low-dose Dexamethasone Suppression Test and time of administration? type of specimen and time of collection?

A

0.5mg dexamethasone every 6 hr for 2 days
Blood collection every 15 mins after

164
Q

Results of Low-dose Dexamethasone Suppression Test

A

Normal = ↓ cortisol
Hypercortisolism = ↑ cortisol

165
Q

Special Requirement in Midnight Plasma Cortisol

A

Px admitted to the hospital before 10pm
Blood collection while asleep

166
Q

Identifies if increased cortisol is ACTH-dependent or independent

A

Corticotropin-Releasing Hormone Stimulation test

167
Q

Measure Cortisol & ACTH after CRH administration

A

Corticotropin-Releasing Hormone Stimulation test

168
Q

Differentiate ACTH-dependent to ACTH-independent

A

ACTH-dependent ↑ cortisol ↑ ACTH
ACTH-independent ↑ cortisol ↓ ACTH

169
Q

aka Addison’s Disease

A

Primary adrenal insufficiency (hypocortisolism)

170
Q

Primary Adrenal Problems

A

o Autoimmune adrenalitis – Ab against adrenal gland
o Fungal disease
o HIV Infection
o Tuberculosis
o Bilateral Adrenal Hemorrhage
o Adrenoleukodystrophy
o Infiltrative processes
o Metastasis

171
Q

Other causes of Addison’s dse

A

o Secondary to ACTH deficiency – secondary adrenal insufficiency
o Glucocorticoid therapy
o Tumors
o Developmental abnormalities
o Malignancies

172
Q

Secondary to ACTH deficiency

A

secondary adrenal insufficiency

173
Q

most common cause of Addison’s dse

A

Glucocorticoid therapy

cause hypocortisolism due to neg. feedback loop
↑ cortisol = ↓ CRH = ↓ ACTH = ↓ cortisol

174
Q

Screening test for HYPOCORTISOLISM

A

ACTH Stimulation Test
Metyrapone Suppression Test (MTS)

175
Q

Confirmatory test for HYPOCORTISOLISM

A

Insulin Tolerance Test

176
Q

requirement in ACTH Stimulation Test

A

Px in fasting state

177
Q

Procedure for ACTH Stimulation Test

A
  • Obtain baseline in fasting state: measure ACTH & Cortisol
  • Administer 200ug cosyntropin (synthetic ACTH)
  • Collect blood after 30-60 mins
  • Measure ACTH & Cortisol
178
Q

what is administered in ACTH Stimulation Test

A

200ug cosyntropin (synthetic ACTH)

179
Q

Result of ACTH Stimulation test

A

o Primary Hypocortisolism: low cortisol
o Secondary Hypocortisolism: low cortisol
*perform MTS to differentiate

180
Q

used for confirmation of secondary hypocortisolism

A

Metyrapone Suppression Test (MTS)

181
Q

Blocks certain enzymes in steroidogenesis

A

Metyrapone Suppression Test (MTS)

182
Q

administered in Metyrapone Suppression Test (MTS)? time of administration? specimen type and time of collection?

A

30mg Metyropone = midnight
collect blood = 8 am

183
Q

Result of Metyrapone Suppression Test (MTS)

A

↑ 11-deoxycorticosterone (blocks 11ß-hydroxylase, increasing its substrate): >7ug/dL
↓ Aldosterone = <5ug/dL

184
Q

after MTS, Secondary hypocortisolism is indicated by?

A

decreased ACTH

185
Q

NORMAL effect of Insulin Tolerance Test in cortisol and ACTH

A

↑ cortisol, ↑ ACTH

due to insulin administration causing hypoglycemia

186
Q

ABNORMAL effect of Insulin Tolerance Test in cortisol and ACTH

A

Hypocortisolism – ↓ cortisol & ACTH, regardless of glucose concentration

187
Q

Insulin Tolerance Test is not performed among px with

A

CV disease
Seizure disorder

188
Q

Produced as by-products of cortisol synthesis regulated by ACTH

A

ANDROGENS

189
Q

Precursors for the production of more potent androgens and estrogens in tissues

A

ANDROGENS

190
Q

Stimulants of Androgen

A

ACTH
Prolactin
Pro-opiomelanocortin
T cells

191
Q

DHEAS will serve as precursors to more active androgens such as:

A

Testosterone
5-dihydrotestosterone
Androstenedione

192
Q

DHEAS can also serve as precursors to estrogens such as:

A

Estradiol
Estrone

193
Q

Excess of this hormone results to virilization

A

Androgen

194
Q

Normal Values of Androgen

A

Plasma DHEAS: 4mg/day
Plasma DHEA: 7-15mg/dL

*If values are greater than the normal values = Androgen excess

Clinical Chemistry 2 - CEUMLS (9 decks)

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