[M6] Part 3: Adrenal Gland Flashcards
Multifunctional organ that produces hormones or substances that are essential for life.
ADRENAL GLAND
It is a pyramidal/pyramid-like shaped endocrine gland, located ___ and ___ to the ___
ADRENAL GLAND;
superior (upper) ;
medial (middle) ;
kidneys
Composed of 2 conjoined glands:
ADRENAL GLAND
WHAT ARE THE 2 CONJOINED GLANDS OF ADRENAL GLAND
Adrenal cortex
Adrenal medulla
Outer part of the adrenal gland.
ADRENAL CORTEX
90% of total adrenal gland
ADRENAL CORTEX
ADRENAL CORTEX is ___ of total adrenal gland
90%
ADRENAL CORTEX In cross section: ____
yellowish in color
Major site of steroid hormone production
ADRENAL CORTEX
ADRENAL CORTEX is the Major site of ___
steroid hormone production
ADRENAL CORTEX is Derived from __
mesenchymal cells
Derived from mesenchymal cells
ADRENAL CORTEX
Composed of 3 zones with distinct tissues.
ADRENAL CORTEX
3 ZONES OF ADRENAL CORTEX
G-ZONE
F-ZONE
R-ZONE
Outer part zone of Adrenal cortex
G-ZONE
10% of the total adrenal cortex
G-ZONE
G-ZONE is AKA
zona glomerulosa
G-ZONE
Hormone produced: __
aldosterone
aldosterone is a ___
mineralocorticoid
regulates sodium which is an electrolyte
aldosterone
75% of the total adrenal cortex
F-ZONE
F-ZONE is AKA
zona fasciculata
AKA zona fasciculata
F-ZONE
F-ZONE
Hormone produced: ____
glucocorticoids
F-ZONE produces glucocorticoids hormones such as ___ and ____
cortisol and cortisone
Example of glucocorticoids
cortisol and cortisone
stored form of cortisol
cortisone
F-ZONE Also produces ____
adrenal androgens
Example of adrenal androgens produced by the F-ZONE
dehydroepiandrosterone (DHEA)
DHEA stands for
dehydroepiandrosterone (DHEA)
precursor for other sex androgens/sex hormones (active androgens)
dehydroepiandrosterone (DHEA)
15% of the total adrenal cortex
R-ZONE
R-ZONE is aka
zona reticularis
AKA zona reticularis
R-ZONE
R-ZONE FUNCTION
It sulfates DHEA
R-ZONE sulfates DHEA
by the Addition of ____ to the ____ forming ____ (___)
sulfate ;
DHEA ;
sulfated DHEA ;
DHEAS
Purpose of DHEAS
serves as the major precursor for active androgens and estrogen
serves as the major precursor for active androgens and estrogen
DHEAS
main adrenal androgen
DHEAS
CRH stands for
corticotropin-releasing hormone
Main regulator of Adrenal cortex
(CRH)
the production is in response to three factors
corticotropin-releasing hormone (CRH)
3 factors involved in the production of CRH
Low cortisol level
Stress
Circadian Rhythm
CRH:
Circadian Rhythm
What is the peak conc.
6am-8am
CRH:
Circadian Rhythm
What is the Lowest conc.
10pm-12mn
REGULATION:
- CRH which is produced by the ____, will stimulate the ____ to secrete ____
hypothalamus;
pituitary gland
ACTH.
REGULATION:
- ACTH will stimulate the ____ to produce ___.
adrenal cortex;
Steroid hormones
T/F: all hormones produced by the adrenal cortex is steroid
T
all hormones produced by the adrenal cortex is ___
steroid
In order to produce steroid hormones, kailangan niya ng ____.
precursor
main precursor for steroid hormones
Cholesterol
REGULATION:
- ACTH will stimulate the ___ of ____ inside the ____ of adrenal cortex
transport ;
cholesterol ;
mitochondria
REGULATION:
4. when the cholesterol is inside the mitochondria, it will undergo the process ____
steroidogenesis
process that involves the production of steroid hormone
steroidogenesis
REGULATION:
- First product produced: ____
pregnenolone
serves as a substrate for all adrenal cortex hormones
pregnenolone
REGULATION:
- The production of the adrenal cortex hormone is influenced by the ____
negative feedback system.
↓cortisol = ___CRH
increased
↑CRH
REGULATION:
- However, ____ (inc/dec) cholesterol do not stimulate the ___ (produces aldosterone)
↓cholesterol;
G-ZONE
REGULATION:
- Remember that aldosterone is _____ by ____level bec. aldosterone production is only stimulated by the ____
not influenced ;
cortisol ;
renin-angiotensin aldosterone system (RAAS)
RAAS = activates when there is a ____
↓BV, ↓BP
RAAS = activates when there is a ____
↓BV, ↓BP
↓cortisol = ____ CRH and ACTH
increases
T/F: ↓cortisol = ↑CRH and ACTH but HINDI tataas si aldosterone
T
G-ZONE will only produce aldosterone in response to ____
↓BV, ↓BP
Kidney produces ___
renin
(stimulates the production of aldosterone by the G-ZONE
renin
adrenal cortex hormone synthesis
Steroidogenesis
Before adrenal cortex hormones are produced, kailangan ng ___.
cholesterol
promotes entry of cholesterol to the mitochondria of adrenal cortex
ACTH
STEROIDOGENESIS:
- Cholesterol will be converted to ___ by the enzyme _____
pregnenolone ;
cytochrome p450
Conversion of cholesterol to pregnenolone occurs in ___
mitochondria
STEROIDOGENESIS:
- Once the pregnenolone is produced in the mitochondria, it will be released in the ___/___.
cytosol ;
cytoplasm
this is where the further conversion of pregnenolone to various adrenal cortex hormones.
Cytoplasm
STEROIDOGENESIS:
- In the ____, pregnenolone in the cytosol may migrate to the ____/___
G-ZONE
F-ZONE ;
R-ZONE
STEROIDOGENESIS:
- In the G-ZONE, it will be converted to ____(only produce in response to ___)
aldosterone ;
RAAS
STEROIDOGENESIS:
- Pregnenolone will be converted to ____ in the presence of__________
17α-OH pregnenolone ;
17-OH ase enzymes
17-OH ase enzymes is also known as what in other books
17α-OH ase
STEROIDOGENESIS:
6._____ in the____, will be converted to form ___ and further to ____
17α-OH ase;
F-ZONE;
cortisol;
cortisone
Cortisol is produced in response to ___ and ___
CRH
ACTH
STEROIDOGENESIS:
- The ____ in the ___ may migrate to the ___ to form ___ in the presence of the same enzyme (____).
17-OH pregnenolone;
F-ZONE ;
R-ZONE ;
DHEA ;
17- hydroxylase
Associated with absence or deficiency in the enzyme required for steroidogenesis.
CONGENITAL ADRENAL HYPERPLASIA (CAH)
Inherited family of enzyme disorders
CONGENITAL ADRENAL HYPERPLASIA (CAH)
enzyme required for steroidogenesis.
3ß-hydroxysteroid isomerase
17α-hydroxylase
11ß-hydroxylase
21ß-hydroxylase
CONGENITAL ADRENAL HYPERPLASIA (CAH)
__ (inc/dec) cortisol and aldosterone production
Decreased
Clinical presentation depends on the enzyme affected
CONGENITAL ADRENAL HYPERPLASIA (CAH)
Types of CONGENITAL ADRENAL HYPERPLASIA (CAH)
3ß-hydroxysteroid isomerase
17α-hydroxylase
11ß-hydroxylase
21ß-hydroxylase
Hypertension: No
Virilization: Slight
3ß-hydroxysteroid isomerase
High Laboratory Value for 3ß-hydroxysteroid isomerase
DHEA
Hypertension: Yes
Virilization: No
17α-hydroxylase
High Laboratory Value for 17α-hydroxylase
Aldosterone
Hypertension: Yes
Virilization: Marked
11ß-hydroxylase
High Laboratory Value for 11ß-hydroxylase
11-deoxycorticosterone
Hypertension: No
Virilization: Marked
21ß-hydroxylase
High Laboratory Value for 21ß-hydroxylase
17-hydroxyprogesterone
development of masculine physical traits among women
Virilization
Example of Virilization
hirsutism
hairy women; usually seen in px with PCOS
hirsutism
Most potent mineralocorticoid
ALDOSTERONE
electron regulating hormones
Mineralocorticoid:
Increase blood pressure through volume expansion by increasing sodium reabsorption
ALDOSTERONE
Stimulates H+and K+ excretion
ALDOSTERONE
ALDOSTERONE Stimulates ____ and ___ excretion
H+
K+
It is unique among the adrenal cortex hormones
ALDOSTERONE
ALDOSTERONE is unique among the adrenal cortex hormones because aldosterone production is not stimulated by ___ and ___
CRH ;
ACTH
ALDOSTERONE is stimulated by the ___
RAAS
RAAS is stimulated by ___ or ___
decreased blood pressure;
blood volume
↓ blood volume/pressure = the ___, specifically the ____ (JG) cells of the ____, will secrete ___
kidneys;
juxtaglomerular ;
nephrons;
renin
Renin will convert ___ to ____
angiotensinogen ;
angiotensin I
Angiotensin I is further converted to angiotensin II by the enzyme____which is produced by the ____
angiotensin converting enzyme (ACE) ;
lungs
Functions of angiotensin II:
1. Stimulate the ____ to produce ___ which will then promote ____ in the________
- It will also stimulate the ___ to produce ____ which will promote ____ in the ____
- It can also ___ (INC/DEC) ___ by causing ____
- It can also __ (INC/DEC) ____ in the ____
- adrenal cortex ;
aldosterone;
sodium reabsorption ;
distal convoluted tubules (DCT) - hypothalamus ;
vasopressin ;
water resorption;
collecting duct - INCREASE;
arterial pressure ;
vasoconstriction - INCREASE;
sodium reabsorption ;
proximal convoluted tube (PCT)
ADLOSTERONE SECRETION
Stimulated by:
Low Blood Pressure
Angiotensin II
ACTH
Elevated serum K+
Progesterone
Dopamine
ALDOSTERONE SECRETION (Stimulated)
Main stimulant
Low Blood Pressure
ALDOSTERONE SECRETION (Stimulated)
Angiotensin II
Low Blood Pressure
ALDOSTERONE SECRETION (Stimulated)
Only stimulates aldosterone production by stimulating the entry of cholesterol in the G-ZONE
ACTH
ALDOSTERONE SECRETION (Stimulated)
It does not directly stimulate the production aldosterone
ACTH
ALDOSTERONE SECRETION
Inhibited by:
Atrial Natriuretic Peptide
Intracellular calcium
Certain drugs:
ALDOSTERONE SECRETION (Inhibited)
What certain drugs inhibit Aldosterone Secretion?
Ketoconazole
ACE inhibitors
NSAIDs
Heparin
Meaning of NSAIDS
Nonsteroidal anti-inflammatory drugs
Example of NSAIDS
Ibuprofen
Also termed as primary aldosteronism in some books
Primary Hyperaldosteronism
Primary Hyperaldosteronism is also termed as ______ in some books
primary aldosteronism
PRIMARY HYPOALDOSTERNISM
a.k.a.
Conn’s disease
PRIMARY HYPOALDOSTERNISM
Caused by:
Aldosterone-secreting adrenal adenoma
Unilateral/Bilateral adrenal hyperplasia
Familial hyperaldosteronism
Adrenocortical carcinomas
Ectopic aldosterone production
PRIMARY HYPOALDOSTERNISM CAUSED BY
Autonomous aldosterone production due to the presence of adenoma and hyperplasia
Aldosterone-secreting adrenal adenoma
Unilateral/Bilateral adrenal hyperplasia
PRIMARY HYPOALDOSTERNISM CAUSED BY
Genetic defect, hereditary
Familial hyperaldosteronism
PRIMARY HYPOALDOSTERNISM CAUSED BY
Associated with carcinoma that produces ACTH
Adrenocortical carcinomas
PRIMARY HYPOALDOSTERNISM CAUSED BY
May nagpo-produce ng aldosterone aside from the adrenal cortex
Ectopic aldosterone production
PRIMARY HYPOALDOSTERNISM
Increased
plasma aldosterone
PRIMARY HYPOALDOSTERNISM
Decreased
plasma renin
Occurs as a result of excess production of renin
Secondary Hyperaldosteronism
SECONDARY HYPERALDOSTERONISM
Increased
aldosterone and renin
Also known as Liddle’s syndrome
PSEUDOHYPERALDOSTERONISM
PSEUDOHYPERALDOSTERONISM
a.k.a
Liddle’s syndrome
PSEUDOHYPERALDOSTERONISM
There are varying levels in ____and ___
renin
aldosterone
PSEUDOHYPERALDOSTERONISM
T/F: Most cases have low aldosterone
T
PSEUDOHYPERALDOSTERONISM
Most cases have low aldosterone except for:
Bartter’s Syndrome
Gitelman’s Syndrome
PSEUDOHYPERALDOSTERONISM
bumetanide-sensitive chloride channel mutation
Bartter’s Syndrome
PSEUDOHYPERALDOSTERONISM
thiazide-sensitive transporter mutation
Gitelman’s Syndrome
PSEUDOHYPERALDOSTERONISM
Both Bartter’s syndrome and Gitelman’s syndrome show an (inc/dec) in aldosterone
Increase
Both Bartter’s Syndrome and Gitelman’s Syndrome are _____ associated
drug associated
Due to destruction of adrenal glands and deficiency of glucocorticoid
ISOLATED HYPOALDOSTERONISM
ISOLATED HYPOALDOSTERONISM
Due to destruction of ____ and deficiency of _____
adrenal glands
glucocorticoid
ISOLATED HYPOALDOSTERONISM
Associated with_____ deficiency
21-hydroxylase
ISOLATED HYPOALDOSTERONISM
When there is a deficiency in 21-hydroxylase, there is an increase in ______
↑ 17-hydroxyprogesterone
HYPERALDOSTERONISM
Diagnostic Tests
Urinary Potassium Excretion
PAC/PRA ratio
Oral Salt Loading:
Saline Infusion Test
Captopril Suppression Test
Urinary Potassium Excretion
Sample
24-hour urine
Urinary Potassium Excretion
________: suggestive of hyperaldosteronism
> 30 mEq/day:
Urinary Potassium Excretion
_____ renal K+ retention
<30 mEq/day:
Urinary Potassium Excretion (<30 mEq/day:)
T/F: You are NOT excreting potassium at this level
F; It does not mean na hindi ka nagtatapon ng potassium
Urinary Potassium Excretion
Two cases why there is a decrease in urininary K+ excretion
If the patient is using diuretics
Gastrointestinal loss
Urinary Potassium Excretion
If the patient is using diuretics, (inc/dec) Na+ _____ (inc/dec) K+ _____
↑ Na+ excretion
↑ K+ reabsorption
Meaning of PAC
plasma aldosterone concentration
Meaning of PRA
plasma renin activity
Most reliable method for screening primary aldosteronism
PAC/PRA ratio
PAC/PRA ratio (Patient considerations)
Patient must remain ______, ___ hours prior to blood collection
During blood collection, the patient should be ______ for __ to ___ minutes
ambulatory. 2
sitting down, 5-15 minutes
PAC/PRA ratio
_____ – suggestive of Primary hyperaldosteronism
> 30
PAC/PRA ratio
_____ – diagnostic of Primary hyperaldosteronism
> 50
Oral Salt Loading
_____ NaCl per day for ____
5000 mg
3 days
Oral Salt Loading
After 3 days, ___ is collected
24-hour urine
Oral Salt Loading
What are measured:
Urine sodium; and
aldosterone
Oral Salt Loading
If urine sodium is ____ and aldosterone is ____, it is suggestive of primary hyperaldosteronism
200 mEq/day
>12 μg/day
primary hyperaldosteronism
Saline Infusion Test
IV infusion of ___ NaCl for ____
2L
2 hours
Saline Infusion Test
What is measured in Saline Infusion Test after IV infusion
aldosterone in the plasma
Saline Infusion Test
Normal
<5 ng/dL PAC
Saline Infusion Test (Normal)
(inc/dec) sodium = (inc/dec) aldosterone
↑ sodium = ↓ aldosterone
Saline Infusion Test
Primary hyperaldosteronism: ____
> 10 ng/dL PAC
aldosterone antagonist
Captopril
Captopril Suppression Test
Normal:
Normal: ↓ aldosterone
Captopril Suppression Test
Primary hyperaldosteronism:
Inc. aldosterone
Captopril Suppression Test
Primary hyperaldosteronism: there will be an increase in aldosterone Specifically, if the PH is _______
aldosterone-producing adenoma (APA)
Stress hormone
CORTISOL
Principal glucocorticoid
CORTISOL
The only adrenal hormone that inhibits ACTH secretion
CORTISOL
CORTISOL
The only adrenal hormone that inhibits ____
ACTH secretion
↑ cortisol = (inc/dec) ACTH
dec
Hyperglycemic hormone
CORTISOL
CORTISOL
increases glucose by stimulating _______and ____
gluconeogenesis
lipolysis
Anti-inflammatory and immunosuppressive actions
CORTISOL
It can inhibit/decrease antibody production
CORTISOL
CORTISOL
Can be used as a therapeutic agent for ______
RA
SLE; and
MS
The body’s natural alarm clock
CORTISOL
Cortisol is stimulated/regulated by _______
ACTH/pituitary gland
ACTH in the circulation is bound to ____ and _______
glycoproteins
transportin
Cortisol can stimulate the body/cells to produce/increase ______
energy metabolism
Cortisol is (inc/dec) during the later stage of ____
Inc
sleep cycle
T/F: Pag tumataas ang cortisol, nagigising ka kasi nag increase din ang energy metabolism of the cells
True
Cortisol increases at _____ (normal sleep cycle)
8am to 10am
CORTISOL LABORATORY ANALYSIS
Cortisol exhibits ___
Diurnal Rhythm
CORTISOL LABORATORY ANALYSIS (DIURNAL RHYTHM)
High levels
8am - 10am
CORTISOL LABORATORY ANALYSIS (DIURNAL RHYTHM)
RV
5 – 25 μg/dL
CORTISOL LABORATORY ANALYSIS (DIURNAL RHYTHM)
Low levels
10pm - 12 mn
CORTISOL LABORATORY ANALYSIS
Specimen
Blood
urine
CORTISOL LABORATORY ANALYSIS (SPECIMEN)
Since the reference value is derived at 8am, collection of _______ must be at 8am
BLOOD
CORTISOL LABORATORY ANALYSIS (SPECIMEN)
Tube used in Blood collection
red top tube
CORTISOL LABORATORY ANALYSIS (SPECIMEN)
What type of urine
24-hr urine
CORTISOL LABORATORY ANALYSIS
Sensitive indicators of adrenal hyperfunction
Urine Free Cortisol:
Urine Free Cortisol: Sensitive indicators of ____
adrenal hyperfunction
CORTISOL LABORATORY ANALYSIS
Urinary Metabolites
17-hydroxycorticosteroids
17-ketogenic steroid
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
Measured using the Porter-Silver method
17-hydroxycorticosteroids
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-hydroxycorticosteroids is measured using ______ method
Porter-Silver method
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-hydroxycorticosteroids: Reagent used
phenylhydrazine in sulfuric acid with alcohol
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-hydroxycorticosteroids
End color
Yellow
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
Measured using Zimmerman reaction
17-ketogenic steroid
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-ketogenic steroid is measured using _______
Zimmerman reaction
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-ketogenic steroid
Reagent::
metadinitrobenzen
CORTISOL LABORATORY ANALYSIS (URINARY METABOLITES)
17-ketogenic steroid
End color
reddish purple
Glucocorticoids are degraded in the ___ and excreted in the ___+ in the form of ___
liver
urine
metabolites
Conditions associated with Cortisol
Hypercortisolism
Hypocortisolism
Example of Hypercortisolism
Cushing’s Syndrome
HYPERCORTISOLISM
Excessive glucocorticoid production due to excessive production of cortisol or ACTH
Cushing’s Syndrome
HYPERCORTISOLISM (CUSHING SYNDROME)
Excessive ____ production due to excessive production of ___ or ___
glucocorticoid
cortisol
ACTH
HYPERCORTISOLISM
↑ ACTH = ___
Cushing’s disease
HYPERCORTISOLISM
↑ cortisol, normal ACTH = ___
Cushing’s syndrome
HYPERCORTISOLISM
Major common cause of Cushing’s Disease
________________
Excess ____ or ___ production
ACTH-secreting pituitary adenoma
ACTH, CRH
HYPERCORTISOLISM
Major common cause of Cushing’s Syndrome
Adrenal tumor
causing autonomous cortisol production
Adrenal tumor
CUSHING’S SYNDROME
Features:
Obesity with thin extremities
CUSHING’S SYNDROME
Other features
Buffalo hump
hirsutism
pendulum abdomen
moon face appearance
easily bruised
CUSHING’S DX
(secondary/primary) hypercortisolism
Secondary
CUSHING’S SYNDROME
(secondary/primary) hypercortisolism
Primary
CUSHING’S DX
Gland affected
Pituitary gland
CUSHING’S SYNDROME
Gland affected
adrenal cortex
CUSHING’S
Which is more serious
CUSHING’S DX
CUSHING’S
Which is less serious
CUSHING’S SYNDROME
CUSHING’S
Which is less common
CUSHING’S DX
CUSHING’S
Which is more common
CUSHING’S SYNDROME
CUSHING’S DX
CAUSE:
Pituitary tumor that secretes ACTH
CUSHING’S DX
INC:
ACTH
CORTISOL
CUSHING’S SYNDROME
Increaaseed
Cortisol
CUSHING’S SYNDROME
Decreased in:
NORMAL ACTH
Develops due to abnormal tumor growth
CUSHING’S DX
Associated with hyperpigmentation
CUSHING’S DX
Develops most often from taking medications that increase cortisol
CUSHING’S SYNDROME
CUSHING’S SYNDROME LABORATORY ANALYSIS
Screening tests
24-hour urine free cortisol
Overnight Dexamethasone Suppression Test
Midnight Salivary Cortisol Test
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Requires accurate collection and urine volume measurement
24-hour urine free cortisol
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Affected by increased fluid intake (_) and urine volume of _
> 5L
3L
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
An increased fluid intake (>5L) and urine volume of >3L can caused false (posi/nega)
false positive
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Cortisol value of ___ above normal is suggestive of ______
24-hour urine free cortisol
3x
cortisol excess
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Administer 1 mg dexamethasone between 11pm and 12am
Overnight Dexamethasone Suppression Test
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Overnight Dexamethasone Suppression Test
Administer ____ between ____ and ____
1 mg dexamethasone
11pm and 12 am
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Overnight Dexamethasone Suppression Test
Blood is then collected at __
___ is measured
8am
cortisol
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Overnight Dexamethasone Suppression Test
Normally, cortisol after dexamethasone administration should be ___
> 1.8 μg/dL
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Also known as late night salivary cortisol test
Midnight Salivary Cortisol Test
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
Midnight Salivary Cortisol Test a.k.a
late night salivary cortisol test
CUSHING’S SYNDROME LABORATORY ANALYSIS (Screening Tests)
The patient should avoid smoking prior to collection
Midnight Salivary Cortisol Test
CUSHING’S SYNDROME LABORATORY ANALYSIS
CONFIRMATORY TESTS
Low-dose Dexamethasone Suppression Test
Midnight Plasma Cortisol
Corticotropin-releasing Hormone Stimulation test
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
0.5 mg of dexamethasone is administered every 6 hours for 2 days
Low-dose Dexamethasone Suppression Test
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Low-dose Dexamethasone Suppression Test
___ of dexamethasone is administered every ___for ___
0.5 mg
6 hours
2 days
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Low-dose Dexamethasone Suppression Test
0.5 mg of dexamethasone is administered ___(total for 2 days)
8 times
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Low-dose Dexamethasone Suppression Test
For every administration, blood is collected after ____
__ times din ang collection of blood
15 minutes
8
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Low-dose Dexamethasone Suppression Test
Normally, there should be (inc/dec) cortisol
Decreased
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Low-dose Dexamethasone Suppression Test
Patients with ________ show an (inc/dec) cortisol
hypercortisolism
inc
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Special Requirement:
The patient should be admitted to the hospital before ___ because the patient should be ____ during blood collection
Midnight Plasma Cortisol
10pm
asleep
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
It will identify if the in cholesterol is ACTH dependent or ACTH-independent
Corticotropin-releasing Hormone Stimulation test
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Corticotropin-releasing Hormone Stimulation test
It will identify if the increase in cholesterol is ________ or _________
ACTH dependent
ACTH-independent
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Corticotropin-releasing Hormone Stimulation test
___ and ___ are measured after the administration of __
Cortisol
ACTH
CRH
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Corticotropin-releasing Hormone Stimulation test
ACTH-dependent: (dec/inc) ACTH, cortisol
inc
CUSHING’S SYNDROME LABORATORY ANALYSIS (CONFIRMATORY TESTS)
Corticotropin-releasing Hormone Stimulation test
ACTH-independent: (inc/dec) ACTH, (inc/dec) cortisol
↓ ACTH, ↑ cortisol
What condition is associated with Hypocortisolism?
Addison’s Disease
Primary adrenal insufficiency
Addison’s Disease
Hypocortisolism will only occur if_____ of the adrenal gland is destroyed
90%
Addison’s Disease
What is associated with Addison’s Disease
Hypocortisolism; and
hypoaldosteronism
HYPORCORTISOLISM - ADDISON’S DX
Primary Adrenal Problem
o Autoimmune adrenalitis
o Fungal disease
o HIV Infection
o Tuberculosis
o Bilateral Adrenal Hemorrhage
o Adrenoleukodystrophy
o Infiltrative processes
o Metastasis
antibody against adrenal gland
Autoimmune adrenalitis
HYPORCORTISOLISM - ADDISON’S DX
OTHER CAUSES
o Secondary to ACTH deficiency
o Glucocorticoid therapy
o Tumors
o Developmental abnormalities
o Malignancies
HYPORCORTISOLISM - ADDISON’S DX
Secondary adrenal insufficiency
Secondary to ACTH deficiency
HYPORCORTISOLISM - ADDISON’S DX
Most common cause
Glucocorticoid therapy
HYPORCORTISOLISM - ADDISON’S DX
Causes hypocortisolism
Glucocorticoid therapy
HYPORCORTISOLISM - ADDISON’S DX
HYPOCORTISOLISM (↑ cortisol = (inc/dec) CRH = (inc/dec) ACTH = (inc/dec) cortisol)
↑ cortisol = ↓ CRH = ↓ ACTH = ↓ cortisol
