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Endocrinology Flashcards

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1
Q

a.k.a suprarenal gland

A

Adrenal Gland

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2
Q

True or False. Adrenal Gland is a neuro-endocrine gland located below the kidney.

A

False. Adrenal gland is located ABOVE the Kidney ‘suprarenal’

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3
Q

Two kinds of Hormones produced by adrenal glands.

A

Steroid hormones - 90%

Neuropeptides - 10%

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4
Q

True or False.
Steroid Hormones (Inner Medulla)
Neuropeptides (Outer cortex)

A

False.
Steroid Hormones (Outer cortex)
Neuropeptides (Inner medulla)

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5
Q

Percent composition of adrenal cortex?

A

90%

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6
Q

Three Divisions of Cortex

A

Glumerulosa: salt (10%)
Fasiculata: sugar (75%)
Reticularis (15%)

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7
Q

Salt hormones are controlled by what division of cortex?

A

Glumerulosa (10%)

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8
Q

Fasciculata controls what horomones

A

Sugar hormones: Cortisol

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9
Q

True or False. Clinical manifestation of HYPERaldosteronism includes;
Hyperkalemia
Hypotension
Metabolic acidosis

A

False. Hyperaldosteronism

Hypokalemia
Hypertension
Metabolic alkalosis

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10
Q

Triad of Pheochromocytoma

A

Sweating (Diaphoresis)
Headache
Palpitation

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11
Q

Condition with increased Cortisol level

A

Cushing’s Syndrome

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12
Q

Increase of neuropeptides (Epinephrine/Norepinephrine)

A

Pheochromocytoma

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13
Q

Congenital Adrenal Hyperplasia

A

Cells proliferate but function of adrenal is loss. Characterized by Hirsutism/Virilization and inability to conceive (.

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14
Q

True or False. Congenital Adrenal Hyperplasia is characterized of more FEMALE characteristics than female .

A

False. It is more of Male characteristics (Hirsutism)

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15
Q

Synthesizes ALDOSTERONE

A

Zona Glumerulosa

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16
Q

Function of Aldosterone

A
  1. Reabsorbed: Na+ Excreted: K+
  2. Acid base balance
  3. Regulation of blood pressure
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17
Q

True or False.

Aldosterone promotes retaining K+, excreting Na+

A

False.

Retaining sodium, excreting potassium

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18
Q

Produces glucocorticoids (ex. cortisol and cortisone) and androgen precursors (Dehydroepiandosterone [DHEA])

A

Zona Fasciculata (70-75%)

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19
Q

No. 1 Hormone to assess the adrenal cortex function

A

Cortisol

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20
Q

Take part on the production of SEX hormones (testosterone & progesterone) by producing the active DHEA-S.

A

Zona Reticularis

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21
Q

It can be converted to testosterone and progesterone.

A

Active DHEA-S

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22
Q

True or False:
ACTH - Aldosterone
Angiotensin II - Cortisol

A

False.
ACTH - cortisol
Angiotensin II - Aldosterone

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23
Q

It controls/regulates Cortex steroidogenesis.

A

ACTH

Angiotensin II

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24
Q

True or False. All adrenal hormones comes from FREE CHOLESTEROL.

A

True.

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25
Q

Released during low cortisol levels, stress and Circadian Signals.

A

Corticotropin Releasing Hormone (CRH)

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26
Q

True or False. Conditions which CRH is not released except;

a. High Cortisol
b. Srtess
c. Circadian Signals
d. NOTA

A

A:

b. Stress
c. Circadian Signals

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27
Q

Circadian Rhythm of Cortisol (peak)

A

4 am - 8 am

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28
Q

Rate Limiting Step of Adrenal Gland

A

Conversion of Cholesterol to Pregnenolone by Cytochrome P450

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29
Q

True or False. Angiotensin II is released by HIGH blood pressure and volume

A

False. Stimulated by LOW blood pressure and volume

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30
Q

Triggers to release Aldosterone

A

Hyperkalemia

Angiotensin II

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31
Q

Converts angiotensin I to an active form of angiotensin, which is Angiotensin II

A

Angiotensin Converting Enzyme (ACE)

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32
Q

Activates ANGIOTENSINOGEN

A

RENIN

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33
Q

True or False. Angiotensin I is more potent and active form that releases ALDOSTERONE

A

False. Angiotensin II

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34
Q

Functions of Angiotensin II

A
  1. Release Aldosterone
  2. Vasoconstriction
  3. Increase Blood Pressure and Volume
  4. Release ADH

Note: 1st two are major function

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35
Q

Identify what is responsible for conversion:

  1. Angiotensinogen-to-Angiotensin I
  2. Angiotensin I- to- Angiotensinogen II
A

A:

  1. Renin
  2. ACE
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36
Q

Percent composition of cortex that produces cortisol

A

70%

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37
Q

Primary activator in the production of cortisol

A

Adrenocorticotropic Hormone (ACTH)

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38
Q

Functions in Glucose metabolism during hypoglycemia which has ‘HYPERGLYCEMIC EFFECT’

A

Cortisol

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39
Q

Which among the ff is the function of Cortisol?

a. Lipogenesis
b. Glycolysis
c. Glycogenolysis
d. NOTA

A

A: NOTA

Because Cortisol promotes;
Lipolysis
Gluconeogenesis
Glycogenesis

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40
Q

Arrange the ff in the mechanism of Cortisol production:

  1. F-zone release cortisol
  2. CRH activate pituitary to produce ACTH
  3. Hypothalamus-Pituitary-Adrenal Organ Axis is stimulated to produce CRH from hypothalamus.
  4. ACTH act on F-zone
A

Answer:

  1. Hypothalamus-Pituitary-Adrenal Organ Axis is stimulated to produce CRH from hypothalamus.
  2. CRH activate pituitary to produce ACTH
  3. ACTH act on F-zone
  4. F-zone release cortisol.
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41
Q

A condition occurs at birth due to increase number of cells but losing adrenal function due to absent or diminished enzyme activity involved in steroidogenesis

A

CONGENITAL ADRENAL HYPERPLASIA

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42
Q

Most common enzyme abnormality in Congenital Hyperplasia

A

21–Hydroxylase

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43
Q

Hormone used to detect/diagnose Congenital Adrenal Hyperplasia

A

17–hydroxyprogesterone

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44
Q

True or False. Enzyme abnormality of 21-Hydroxylase is INCREASED glucocorticoid and DECREASED adrenal androgen production

A

FALSE. Diminished activity of 21-hydroxylase leads to decrease glucocorticoid and increased adrenal androgen production

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45
Q

Primary Aldosteronism

A

Increased/Excessive production of Aldosterone Secretion that cannot be suppressed by salt or volume replacement (excessive retention of salt).
Inc Aldosterone = Inc Na

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46
Q

Most Common Causes of Primary Aldosteronism

A

Aldosterone Producing Adrenal Adenoma

Unilateral or Bilateral Adrenal Hyperplasia

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47
Q

Screening Considerations of Primary Aldosteronism

A

BP >160/100
Drug Resistant Hypertension
Hypokalemia with hypertension
Presence of Adrenal Mass
Family History of early Hypertension or stroke
First Degree Relatives with Primary Aldosteronism

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48
Q

True or False.

All antihypertensive may not be stopped during test

A

False. All antihypertensive may not be stopped during test, except: Spironolactone (Mineralocorticoid receptor antagonist)

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49
Q

Antihypertensive drug which MUST be stopped during testing because it is a ALDOSTERONE RECEPTOR ANTAGONIST

A

Spirinolactone

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50
Q

Confirmatory test of Primary Aldosteronism

A

Oral Salt Loading/IV Saline Loading

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51
Q

Results from an Initial Diagnosis of Primary Aldosteronism

A

Plasma Aldosterone Concentration (PAC >15ng/dl)

Plasma Renin Activity (PRA >30)

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52
Q

True or False (Morse). Value of Plasma Aldosterone Concentration (should be lesser than 15ng/dl).
Plasma Renin Activity (PRA >30) to Diagnose Aldosteronism.

A

1st statement FALSE

2nd Statement TRUE

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53
Q

Ideal NaCl consumption

A

2 grams

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54
Q

NaCl consumption in Oral salt loading per day, usually 3 days

A

5000 mg (5 grams)

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55
Q

At what volume of Salt should consumed for 3 days?

A

15 g/15000 mg

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56
Q

True or False. In Oral Salt Loading with PA, Potassium is INCREASED to >200 g/meq, while, Urine aldosterone is DECREASED.

A

False. Urine SODIUM must be >200mEq and Urine Aldosterone is INCREASED to >12 micrograms/ 24Hour.

Rationale. Because normally, there should be a negative feedback which Aldosterone is stopped to release with the elevated Na already. But in PA, Aldosterone is consistently released.

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57
Q

IV saline method

A

Infuse 2L of NaCl (Normal saline) for 2 hours.

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58
Q

Test which would indicate if to undergo SURGERY or NOT

A

ADRENAL VENOUS SAMPLING

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59
Q

Aldosterone concentration secretion between 2 adrenal glands.
Ration: >4:1

A

Candidate for SURGERY

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60
Q

Aldosterone concentration secretion between 2 adrenal glands.
Ratio: 3:1 or less

A

NOT FOR SURGERY; Needs medical Management

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61
Q

Main adrenal hyperglycemic hormone

A

Cortisol

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62
Q

Used to measure adrenal insufficiency

A

Cortisol

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63
Q

Inadequate release of hormone in the adrenal cortex

A

Adrenal Insufficiency

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64
Q

Differentiate:
Primary Adrenal Insufficiency
Secondary Adrenal Insufficiency
Tertiary Adrenal Insufficiency

A

Primary: Adrenal Gland is affected. Reduced Reduced Adrenal production with sufficient stimulation
Secondary: Pituitary Gland is Affected. Reduced Adrenal production with insufficient stimulation
Tertiary: Hypothalamus is affected which CRH is not produced

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65
Q

Most Common Cause of Adrenal Insufficiency

A

Autoimmune Destruction

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66
Q

True or False. Suggestive Diagnosis for Adrenal insufficiency.
Cortisol @ 8:00 am: HIGH
ACTH: LOW

A

False.
Cortisol @ 8:00 am: LOW
ACTH: ELEVATED

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67
Q

PRIMARY Adrenal Insufficiency Test

A

ACTH Stimulation Test

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68
Q

SECONDARY Adrenal Insufficiency Test

A

Metyrapone Suppression Test

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69
Q

What is the result of a Normal Patient undergone ACTH stimulation test.

A

A:

Excessive Production of Cortisol due to overstimulation

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70
Q

Expected result with PAI.

A

A: Low Cortisol level of < 18

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71
Q

True or False. Metyrapone Suppression Test is a test done at 8 am (Fasting), given IV with Cosyntropin (250 microgram) and measured after 30 mins, and 60 mins.

A

False. ACTH Stimulation Test

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72
Q

What condition is attributed with a Normal ACTH test, but Decreased in Metyrapone Suppression Test?

A

Secondary Adrenal Insufficiency

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73
Q

True or False. Metyrapone BLOCKS 11 hydroxylase to INCREASE 11-Deoxycortisol with SECONDARY Adrenal insufficiency

A

False.
Normal: Increase 11-Deoxycortisol
SAI: Decrease 11-Deoxycortisol

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74
Q

True or False.
Primary AI: Increase ACTH, decreased cortisol
Secondary AI: Cortisol and ACTH both decreased

A

True.

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75
Q

True or False. Cortisol MUST increase after Insulin consumption.

A

True. Cortisol is a “Hyperglycemic Agent” during hypoglycemia.

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76
Q

also known as the “Cushing’s Syndrome”

A

HYPERCORTISOLISM

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77
Q

Differentiate: Cushing’s Syndrome to Disease

A

Cushing’s disease means there is a tumor in the pituitary gland that produces excessive ACTH (ACTH-producing tumor). While, Cushing’s syndrome are downward metabolic activities or problem or tumor in the adrenal gland which produces cortisol

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78
Q

A tumor in the pituitary gland that produces excessive ACTH.

A

Cushing’s Disease

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79
Q

Complications in downward metabolic activities or problem or tumor in the adrenal gland which produces cortisol.

A

Cushing’s Syndrome

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80
Q

True or False. In Cushing’s diseases ACTH is elevated and Cortisol due to other causes

A

False. Cushing’s disease

presents an ACTH elevation form Pituitary Tumor.

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81
Q

Source of Elevated Cortisol and ACTH from Pituitary Tumors

A

Cushing’s Disease

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82
Q

Test for Cushing’s Syndrome

A

Dexamethasone Suppression Test

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83
Q

True or False.
Secondary Adrenal Insufficiency: Dexamethasone Suppression Test
Cushing’s Syndrome: Metyrapone Suppression Test

A

False.
Secondary Adrenal Insufficiency: Metyrapone Suppression Test
Cushing’s Syndrome: Dexamethasone Suppression Test

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84
Q

Fluid Intake >5L/day and urine volume >3L/day can lead to?

A

FALSE POSITIVE RESULT

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85
Q

What consition can lead to Pseudo-Cushing’s?

A

Depression and Alcoholism

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86
Q

Dexamethasone Suppression Test:

Dose
Time administered
Time of the Day Measured
Result

A

Dose: 1 mg
Time administered: 111:00 om - 12:00 am
Time of the Day Measured: 8:00 am
Result:
Negative: Normal (Suppression: Cortisol <1.8)
Positove: No Suppression (Elevated ACTH = Elevated Cortisol)

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87
Q

True or False. DEXAMETHASONE SUPRESSION TEST can evaluate whether it is Cushing’s SYNDROME or Cushing’s DISEASE

A

False. It cannot assess.

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88
Q

True or False. Late Night salivary Cortisol. Cortisol is greater or equal to the concentration in 8:00 am , present in CUSHING’S SYNDROME.

A

False. Concentration level of Cortisol is present in CUSHING’S DISEASE, due to neglect in diurnal or circadian variation.

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89
Q

True or False. Pseudo-Cushing’s STILL maintains diurnal variability.

A

True. Because there is no tumor, and only due to over reaction of Adrenal glands.

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90
Q

What TEST & what is measured to locate where ELEVATED CORTISOL is originated, whether from ADRENAL or Pituitary after doagnosing Hypercortisolism.

A

Immunoradiometric Assay (IRMA), that measures ACTH

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91
Q

Midnight Salivary Cortisol after Hypercortisolism is established and used IRMA:

Interpret:
>15 micrograms/dL
<5 micrograms/dL

A

> 15 micrograms/dL: Hypercortisolism is ACTH dependent (tumor in the pituitary gland; CUSHING’S DISEASE)
<5 micrograms/dL: ACTH independent (possible affected adrenal gland, CUSHING’S SYNDROME)

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92
Q

Differentiate Pituitary and Ectopic Source of ACTH; or which ELEVATED ACTH is originated whether from Pituitary or other sources.

A

High Dose Dexamethasone Suppression Test

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93
Q

Difference of High Dose Dexamethasone Suppression Test to Low dose?

A

A: It is administered with 8mg Dexamethasone given at 11PM that INITIALLY suppress the ACTH coming from PITUITARY ALONE.

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94
Q

Interpret the results from High Dose Dexamethasone Suppression Test.

<5 micrograms/dl: _____________
<50% SUPRESSION: ____________
NO SUPPRESSION: ______________

A

<5 micrograms/dl: Normal
<50% SUPRESSION: ACTH from Pituitary
NO SUPPRESSION: Ectopic Source

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95
Q

Gold Standard for determining the source of ACTH production

A

INFERIOR PETROSAL SINUS SAMPLING

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96
Q

True or False. Pituitary ACTH Hypersecretion: if ratio is <2:1 (With CRH) or <3:1 (Without CRH)

A

False. Pituitary ACTH Hypersecretion: if ratio is >2:1 (Without CRH) or >3:1 (with CRH)

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97
Q

Byproduct of Cortisol Synthesis

A

Adrenal ANDROGENS

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98
Q

Composition of Adrenal Medulla

A

10%

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99
Q

Synthesizes Neuro-endocrine peptides that stimulate SYMPATHETIC response promoting flight or fight response.

A

Adrenal Medulla

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100
Q

Three classes of Catecholamines

A

Dopamine
Epinephrine
Norepinephrine

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101
Q

First catecholamine produced

A

DOPAMINE

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102
Q

Last and most ACTIVE catecholamines produced

A

EPINEPHRINE

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3
4
5
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103
Q

Two major enzymes involved in the INACTIVATION of catecholamines.

A 
Catechol-o-methyl transferase (COMT)
Monoamine oxidase (MAO)
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104
Q

Arranged the production of Catecholamine.

  1. DOPA
  2. NOREPINEPHRINE
  3. TYROSINE
  4. EPINEPHRINE
  5. DOPAMINE
A

Tyrosine > Dopa > Dopamine > Norepinephrine > Epinephrine

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105
Q

All reactions take part in the cytoplasm; except

a. Dopamine
b. Epinephrine
c. Norepinephrine

A

A:

c. Norepinephrine. Production is in the Lipid vesicles or outer mitochondrial membranes.

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106
Q

Enzyme that catalyzes the conversion of Norepinephrine (NE) to EPI in the cytosol.

A

Phenylethanolamine N-methyltransferase (PNMT)

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107
Q

Major (80%) catecholamine secretion of Adrenal Medulla.

A

Epinephrine

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108
Q

Ratio of NE:EPI in the circulation

A

9:1

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109
Q

True or False. Inactivation of Catecholamines.
Non-neuronal tissues: Monoamine Oxidase
Neuronal Tissues: Catecholamine-O Methyltransferase (COMT)

A

False.
Non-neuronal tissues: Catecholamine-O Methyltransferase
Neuronal Tissues: Monoamine Oxidase

110
Q

True or False. In circulation EPINEPHRINE is most abundant, present and released by Postganglionic Neurons

A

False. Norepeniphrine is Major Catecholamine product of postganglionic neurons, that is 98% in circulation.

111
Q

Hormones given on patients with Low Blood pressure and Heart Failure

A

Dopamine

Epinepherine

112
Q

Major product in Catecholamine Degradation, that is 30%

A

Vanillylmandelic acid (VMA)

113
Q

Tumors in Adrenal MEDULLA

A

Pheochromocytoma

114
Q

Tumors in SYMPATHETIC GANGLIA

A

Paraganglioma

115
Q

Pheochromocytoma - Paraganglioma (PPGL) are associated with this SYNDROMES.

A

Multiple Endocrine Neoplasia 2
Von Hippen Lindau
Neurofibromatosis type 1

116
Q

Ratio of Multiple Endocrine Neoplasia 2

A

1:2 - 1:5

117
Q

Ratio of Von Hippen Lindau

A

1:10

118
Q

Ratio of Neurofibromatosis type 1 to develop PPGL

A

1:20

119
Q

Main Response of Catecholamines

A

SYMPATHETIC RESPONSE

120
Q

True or False. 90% of cases have singular and benign mass, intra-adrenal and intra-abdominal

A

True.

121
Q

Screening Tests for PPGL

A
  1. Plasma Free Metanephrines (High Risk Patients)
  2. 24-hour Urine fractionated Metanephrines (Low Risk)
  3. Catecholamines
122
Q

True or False. In Plasma Free Methanephrines, patient must be UPRIGHT for 30mins prior to blood sampling

A

False. Because patient must be supine for 30 mins prior to blood sampling. While, UPRIGHT posture leads to increase NE

123
Q

True or False. In detecting/diagnosing PPGL, use the Biproduct or excretion product (VMA).

A

False. Detect the hormone it is producing or near hormone, such as EP, NE, or a Metanephrines.

124
Q

Test done after a repeat 24 hr urine with equivocal result of less than 3 fold elevation of the upper limit.

A

Clonidine Suppression Test

125
Q

This acts an alpha-2-adrenoceptor agonist and inhibits neuronal NE in patients without PPGL ALONE

A

Clonidine

126
Q

What dose is given for Clonidine Suppression Test

A

300mcg/70kg

127
Q

True or False. Plasma Noremetanephrine is measured after 3 hours

A

True.

128
Q

What will be the possible result?

Patient with PPGL
Patient without PPGL

A

Patient with PPGL: Partially/No suppression (< 40%) of Noremetanephrine and Elevated Baseline Noremetanephrine.

Patient without PPGL: Total Suppression (> 40%) of due to inhibition of neuronal NE

129
Q

Associated syndrome which has the Highest chance of having PPGFL

A

Multiple Endocrine Neoplasia 2 (MEN II)

130
Q

Endocrine Gland are __________ gland

A

Ductless

131
Q

Major Higher Brain Control Center

A

Hypothalamus

132
Q

Major secretor of Hormones

A

Pituitary Gland

133
Q

Steroids “one”

Mnemonics: SCATEPAD

A 
Cortisol
Aldosterone
Testosterone
Estrogen
Progesterone
Activated Vit. D
134
Q

Amines

A

Epinephrine
Norepinephrine
T3
T4

135
Q

Glycoprotein

Mnemonics: FiSH Erythropoietin , TraSH HCG

A

FSH
TSH
EPO
HCG

136
Q

Polypeptides

A 
ACTH
GH
PTH
Oxytocin
Insulin
Glucagon
137
Q

Precursors of Steroid Hormones

A

Cholesterol

138
Q

Glycoproteins are _____________

A

Non-protein bound

139
Q

Precursors of Amine Hormones

A

Tyrosine

140
Q

Hormones synthesized in the Hypothalamus

A

Oxytocin: Uterine Contraction

Vasopressin/ADH: Water Reabsorption

141
Q

Love Hormone

A

Oxytocin

142
Q

Pleasure Hormone

A

Dopamine

143
Q

Thirst Hormone

A

AVP/ADH

144
Q

Master Gland

A

Pituitary Gland

145
Q

Hierarchy of Endocrine System

  2. 3.
A

Hierarchy of Endocrine System

  1. Hypothalamus
  2. Pituitary Gland
  3. End Organs - Thyroid Gland, PTG, Adrenal Gland, Testes, Ovary
146
Q

Pituitary Gland - Other Names

Anterior PG: __________
Posterior PG: _________

A

Pituitary Gland - Other Names

Anterior PG: Adenohypophysis
Posterior PG: Neurohypophysis

147
Q

Hormones Secreted - Anterior Pituitary Gland

A 
TSH
FSH
LH
TSH
ACTH
GH
Prolactin
148
Q

Hormones Secreted - Posterior Pituitary Gland

A

Oxytocin

Vasopressin

149
Q

Posterior Pituitary Gland only ________ hormone.

A

STORES

150
Q

Cells in the APG

Corticotrophs: \_\_\_\_\_\_\_\_
Gonadothrophs: \_\_\_\_\_\_\_
Thyrotrophs: \_\_\_\_\_\_\_\_
Somatotrophs: \_\_\_\_\_\_\_
Lactotrophs: \_\_\_\_\_\_\_
A

Cells in the APG

Corticotrophs: ACTH
Gonadothrophs: FSH, LH,
Thyrotrophs: TSH
Somatotrophs: GH
Lactotrophs: Prolactin
151
Q

Stress Hormone

A

Prolactin

152
Q

Other name for Growth Hormone

A

Somatostropin

153
Q

Major Stimulant for GH secretion

A

SLEEP

154
Q

Most abundant of all Pituitary Hormones

A

GH/Somatotropin

155
Q

Tests for GH

GH Deficiency: __________________
Acromegaly/Gigantism: ______________

A

Tests for GH

GH Deficiency: Insulin Tolerance Test
Acromegaly/Gigantism: Glucose Suppression

156
Q

Tests for GH Deficiency

Confirmatory Test: _____________
2nd Confirmatory Test: ______________

A

Tests for GH Deficiency

Confirmatory Test: Insulin Tolerance Test
2nd Confirmatory Test: Arginine Stimulation Test

157
Q

FSH acts on _________________

A

Sertoli Cells

158
Q

LH acts on ____________________

A

Leydig Cells

159
Q

Functions of LH

A
  1. Ovulation
  2. Testosterone production
  3. Synthesis of Androgens - Theca Cells
160
Q

Also known as thyrotropin

A

TSH

161
Q

Activates Cortisol

A

ACTH

162
Q

Mill Production

A

Prolactin

163
Q

Major Inhibitor of Prolactin

A

Dopamine

164
Q

Effect of excess Prolactin

Men: _______
Women: ______

A

Men: Hypogonadism
Women: Amenorrhea, Galactorrhea

165
Q

Deficiency in ADH

A

Diabetic Insipidus

166
Q

Types of Diabetic Insipidus

Neurogenic - ________________
Nephrogenic - _______________

A

Types of Diabetic Insipidus

Neurogenic - Deficiency in ADH; Normal ADH Receptors
Nephrogenic - Sufficient ADH, Defective ADH Receptors

167
Q

Diagnostic Test For Diabetic Insipidus

A

Overnight Water Deprivation

168
Q

Cells and Hormones Produced by the Thyroid Gland

Follicular Cells: __________
Parafollicular Cells/C Cells: __________

A

Cells and Hormones Produced by the Thyroid Gland

Follicular Cells: T3 T4
Parafollicular Cells/C Cells: Calcitonin

169
Q

Start of Thyroid Hormone production

A

11th week of gestation

170
Q

Organized thyroid cells that absorbs iodine

A

Follicle

171
Q

Most important substrate in Thyroid hormone synthesis

A

Iodine

172
Q

Active form of Iodine

A

Oxidized Iodide

173
Q

Synthesized by the follicular cells and the major component of colloid

A

Thyroglobulin

174
Q

Thyroglobulin is rich in _________

A

Tyrosine

175
Q

Enzyme that oxidizes trapped iodine and assemble thyroid hormones

A

Thyroid peroxidase

176
Q

Most Active/Most Hormonal Activity

A

T3/Triiodothronine/353

177
Q

Two forms of Triiodothyronine

T3 - __________; Active
rT3 - __________; inactive

A

Two forms of Triiodothyronine

T3 - 3,5,3
rT3 - 3,3,5

178
Q

_____ can be converted back or reverse to T4

A

rT3

179
Q

Most Abundant fraction of Iodine

A

T4

180
Q

Prohormone of T3

A

T4

181
Q

___ is first to increase in Hyperthyroidism

A

T3

182
Q

Main serum carrier protein of T3 & T4

A

Thyroxine Binding Globulin (TBG)

183
Q

Enzyme that converts T4 to T3

A

Iodothyronine 5’ deiodinase

184
Q

Enzymes - Thyroid Hormones

____________: Trapped Iodine —– Oxidized Iodide
____________: t4 ——–t3

A

Enzymes - Thyroid Hormones

Thyroid peroxidase: Trapped Iodine —– Oxidized Iodide
Iodothyronine 5’ - deionidase - : t4 ——–t3

185
Q

T3

First increase: ____________
Indicator: ______________
Diagnosis: _____________

A

T3

First increase: Hyperthyroidism
Indicator: Recovery of Hyperthyroidism
Diagnosis: T3 Thyrotoxicosis

186
Q

T4

Indicator: ________________
Increase: _____________
Distribution: ____________

A

T4

Indicator: Thyroid Secretory Rate
Increase: NO TSH
Distribution: Most abundant

187
Q

3rd Major Circulating Thyroid hormone

A

rT3

188
Q

Ratio of T4 to T3

A

20:1

189
Q

T3 Thyrotoxicosis

Increased:
Normal:
Low:

A

T3 Thyrotoxicosis

Increased: FT3
Normal: FT4, T4
Low: T4, TSH

190
Q

T4 Thyrotoxicosis

Increased:
Normal:
Low:

A

T4 Thyrotoxicosis

Increased: T4
Normal: T3
Low: T3, TSH

191
Q

Signs and Symptoms of Hyperthyroidism

A 
Tachycardia
Unexplained weight loss
Heat Intolerance
Emotional Lability
Bulging Face
Soft Nails
192
Q

Most common cause of Thyrotoxicosis

A

Graves Disease

193
Q

Commonly Measured or Requested Thyroid Hormones

A

TSH

FT4

194
Q

Graves Disease Mechanism - Stimulatory

A

Presence of Autoimmune antibodies (TRAb) against TSH receptor that STIMULATES the increase production of TSH and Thyroglobulin

195
Q

Riedel’s Thyroiditis

A

Thyroid is WOODY/STONE hard mass

196
Q

Disease: _______________

Shows NO CLINICAL SYMPTOMS
Low TSH
Normal: FT3 FT4

A

Subclinical Hyperthyroidism

Shows NO CLINICAL SYMPTOMS
Low TSH
Normal: FT3 FT4

197
Q

Diagnostic Test for Graves Disease

A

TSH Receptor Antibody Test (TRAb)

198
Q

Painful Throiditis

A

Subacute granulomatous
Subacute non suppurative
De Quervains

199
Q

Reidel’s Thyroiditis vs. De Quervain’s

Type of Goiter:
Characteristic:

A

Reidel’s Thyroiditis

Type of Goiter: Painless Goiter
Characteristic: Woody/Stone Hard thyroid

De Quervain’s
Type of Goiter: Painful Goiter
Characteristic: Neck pain, Increased ESR & TG

200
Q

Signs and Symptoms of Hypothyrpoidism

A 
Bradycardia
Cold Intolerance
Unexplained weight gain
 Brittle Nails
Puffy face
201
Q

Most Common cause of primary hypothyroidism

A

Hashimoto’s thyroiditis

202
Q

Other names - Hashimoto’s Thyroiditis

  1. ____________________
  2. ____________________
A

Other names - Hashimoto’s Thyroiditis

  1. Chronic Lymphocytic Thyroiditis
  2. Chronic Autoimmune Thyroiditis
203
Q

Mechanism - Hashimoto’s Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis

A

Mechanism - Hashimoto’s Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis

Autoimmune Ab destroys thyroid gland by inhibiting Thyroid peroxidase function - Anti TPO Abs

204
Q

Diagnosis - Hashimoto’s Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis

Positive Ab:
Increase:
Decrease:

A

Diagnosis - Hashimoto’s Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis

Positive Ab: Anti-TPO Ab
Increase: TSH
Decrease: T3 T4

205
Q

Peculiar nonpitting swelling of Skin

A

Myxedema

206
Q

Antibodies in Hashimoto’s Thyroiditis

A

Anti-TPO antibodies
Anti-microsomal
Anti-thyroglobulin antibodies

207
Q

Severe form of Primary Hypothyroidism

A

Myxedema/Myxedema Coma

208
Q

Most important Thyroid Function test

A

TSH Test

209
Q

TSH test differentiates ________ and ________ _____thyroidism

A

TSH test differentiates PRIMARY and SECONDARY HYPOthyroidism

210
Q

3rd major circulating thyroid hormome

A

rT3

211
Q

Important indicator for Thyroid Cancer and Proof of Thyroid presence

A

Thyroglobulin Test

212
Q

Indirectly assess T4 in the blood

A

Free Thyroxine Index (FTI/T7)

213
Q

Measures the available binding sites of TBG and reflects serum level of TBG

A

T3 uptake

214
Q

TBG is _________ related to T3 uptake

A

INVERSELY

215
Q

Major site of Steroidogenesis

A

Adrenal Cortex

216
Q

Stimulates Steriodogenesis

A

ACTH

217
Q

Cortisol Urinary Metabolites
Method - Cortisol Metabolite Detected - Reagent

Polter-Silber Reaction: ____________ - ___________
Zimmerman: ____________ - ____________

A

Cortisol Urinary Metabolites
Method - Cortisol Metabolite Detected - Reagent

Polter-Silber Reaction: 17 hydroxycorticosteroid - Phenylhydrazine
Zimmerman: 17 ketogenic acid - Dinitrobenzene

218
Q

Polter-Silber Reaction

End Color:
Detected:
Reagent:

A

Polter-Silber Reaction

End Color: Yelloe
Detected: 17 HCS
Reagent: Phenylhydrazine

219
Q

Zimmerman Reaction

End Color:
Detected:
Reagent:

A

Zimmerman Reaction

End Color: Reddish Purple
Detected: 17 ketogenic acid
Reagent: Dinitrobenzene

220
Q

Current Reference Method of 24 hr Urine Free Cortisol

A

HPLC-MS

221
Q

Screening Tests - Hypercortisolism/Cushing’s Syndrome

A

24 hr UFC
Overnight Dexamethasone Suppression Test
Midnight Salivary Cortisol

222
Q

Confirmatory Tests - Hypercortisolism/Cushing’s Syndrome

A

Low Dose Dexamethasone
Midnight Plasma Cortisol
CRH Stimulation Test

223
Q

Screening Test - Hypocortisolism/Adrenal Insufficiency

A

ACTH Stimulation Test

224
Q

Confirmatory & Gold Std. - Hypocortisolism/Adrenal Insufficiency

A

Insulin Tolerance Test

225
Q

Alternative for diagnostic and Confirmatory for Secondary AI

A

Metyrapone Suppression Test

226
Q

Congenital Adrenal Hyperplasia

Decreased:
Increased:

A

Congenital Adrenal Hyperplasia

Decreased: Cortisol
Increased: Androgen

227
Q

Congenital Adrenal Hyperplasia

Enzyme deficient: ____________
Diagnostic: __________

A

Congenital Adrenal Hyperplasia

Enzyme deficient: 21 hydroxylase
Diagnostic: 7 hydroxyprogesterone

228
Q

Screening Tests - Hyperaldosteronism

A

Plasma Aldosterone Concentration/Plasma Renin Activity Ratio

229
Q

Confirmatory Test - Hyperaldosteronism

A

Saline Suppression Test
Oral Sodium Loading Test
Fludocortisone suppression test
Captopril Challenge Test

230
Q

Hyperaldosteronism - Plasma Aldosterone Concentration/Plasma Renin Activity Ratio

> 30 ratio: _______________
60 ratio: _______________

A

Hyperaldosteronism - Plasma Aldosterone Concentration/Plasma Renin Activity Ratio

> 30 ratio: Suggestive for Hyperaldosteronism
60 ratio: Diagnostic for Hyperaldosteronism

231
Q

Occurs due to excessive Renin Production

A

Secondary Hyperaldosteronism

232
Q

Primary Hyperaldosteronism vs. Secondary Hyperaldosteronism

PAC - aldosterone:
PRC - Renin:

A

Primary Hyperaldosteronism

PAC - aldosterone: Increase
PRC - Renin: Decrease

Secondary Hyperaldosteronism
PAC - aldosterone: Increase
PRC - Renin: Increase

233
Q

Secondary Hyperaldosteronism

Liddle’s Syndrome:
Barterr’s Syndrome:
Gitelman’s Syndrome:

A

Secondary Hyperaldosteronism

Liddle’s Syndrome: Pseudohyperaldosteronism
Barterr’s Syndrome: Bumetanide-sensitive chloride channel mutation
Gitelman’s Syndrome: Thiazide-sensitive transporter Mutation

234
Q

Liddle’s Syndrome

A

Pseudohyperaldosteronism

235
Q

Barterr’s Syndrome

A

Bumetanide-sensitive chloride channel mutation

236
Q

Gitelman’s Syndrome

A

Thiazide-sensitive transporter Mutation

237
Q

Hypoaldesteronism id caused by deficiency of __________ and _____________ leading to destruction of adrenal glands

A

Hypoaldesteronism is caused by deficiency of GLUCOCORTICOID and 21 HYDROXYLASE leading to destruction of adrenal glands

238
Q

Principal Adrenal Androgens

A

DHEA

239
Q

Main precursor of Catecholamines

A

Phenylalanine

240
Q

Norepinephrine to Epinephrine Ratio

A

9:1

241
Q

Highest concentration in the Brain/Circulation

A

Norepinephrine

242
Q

Highest concentration in Adrenal Medulla

A

Epinephrine

243
Q

Flight or Fight Hormone

A

Epinephrine

244
Q

Major Metabolite - Norepinephrine

A

3-methoxy-4-hydroxyphenylglycol (MHPG

245
Q

Major Metabolite - Epinephrine

A

Vanilyl mandelic acid

246
Q

Major Metabolite - Dopamine

A

Homovanilic acid

247
Q

Major Metabolite - Serotonin

A

5-hydroxyindoleacetic acid

248
Q

Pheochromocytoma

Screening Test: ______________
Diagnostic Test: ______________
Pharmacologic Test: _____________

A

Pheochromocytoma

Screening Test: Plasma Free Metanephrines
Diagnostic Test: 24 hr Urine fractionated metanephrines/normetanephrines
Pharmacologic Test: Clonidine Suppression Test, Glucagon Stimulation Test

249
Q

Most potent male androgen and Principal Androgen hormone in the blood

A

Testosterone

250
Q

Tests for Male Fertility

A

Semen Analysis
Testosterone
FSH
LH

251
Q

Major transport protein of Sex hormones

A

SHBG - sex hormone binding globulin (60%)

252
Q

Most active form of Testosterone

A

Dihydroxytestosterone

253
Q

Enzyme that converts testosterone to dihyxroxytestoterone (active)

A

5-alpha-reductase

254
Q

Primary Hypogonadism

a.k.a.
Infertility:
Origin:
Diagnosis:

A

Primary Hypogonadism

a.k.a. - Hypergonadotropic Hypogonadism
Infertility: Testicular Infertility
Origin: Testicular Origin
Diagnosis: Increased FSH, LH; Decreased Testosterone

255
Q

Secondary Hypogonadism

a.k.a.
Infertility:
Origin:
Diagnosis:

A

Secondary Hypogonadism

a.k.a. - Hypogonadotropic hypogonadism
Infertility: Pretesticular Infertility
Origin: Pituitary Origin
Diagnosis: Decreased FSH, LH; Decreased/N Testosterone

256
Q

Congenital Testicular Infertility

A

Klinefelter’s Syndrome
Kallman’s Syndrome - Cryptorchidism
5 alpha reductase deficiency
Myotonic Dystrophy

257
Q

47XXY

A

Klinefelter’s syndrome

258
Q

Characteristics associated with Klinefelter’s Syndrome

A

Gynecomastia
Small Firm testicles
Azoospermia

259
Q

Testicular Feminization Syndrome

A

Cryptorchidism

260
Q

Characteristic of Cryptorchidism

A

Micropenis

Undescended testicles

261
Q

Most abundant estrogen in post-menopausal women

A

Estrone (E1)

262
Q

Most potent Estrogn

A

Estradiol (E2)

263
Q

Most abundant estrogen in pre-menopausal women

A

Estradiol (E2)

264
Q

Major estrogen secreted in Pregnancy

A

Estriol (E3)

265
Q

Produced by the corpus luteum that maintains pregnancy

A

Progesterone

266
Q

Functions of Progesterone

A
  1. Prepares endometrium for embryo implantation

2. Maintains Pregnancy

267
Q

Tests for Menstrual Cycle Dysfunction

A

Estrogen
Progesterone
FSH
LH

268
Q

Tests for Female Infertility

MNEMONICS: THEF LP

A

DECREASED

TSH
HCG
E2
FSH
LH
PRL
269
Q

Diagnosis of Down Syndrome - Trisomy 21
Mnemonics - Hi Down

Increased: ________, _______
Decreased: _______, _______

A

Diagnosis of Down Syndrome - Trisomy 21
Mnemonics - Hi Down

Increased: HCG, Inhibin A
Decreased: Estriol, AFP

270
Q

Gastrin is a diagnostic marker for _________________

A

Zollinger-Ellison Syndrome

271
Q

Diagnostic marker for Carcinoid tumor

A

Serotonin

Clinical Chemistry (20 decks)

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