Endocrinology Flashcards
(271 cards)
1
Q
a.k.a suprarenal gland
A
Adrenal Gland
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’
3
Q
Two kinds of Hormones produced by adrenal glands.
A
Steroid hormones - 90%
Neuropeptides - 10%
4
Q
True or False.
Steroid Hormones (Inner Medulla)
Neuropeptides (Outer cortex)
A
False.
Steroid Hormones (Outer cortex)
Neuropeptides (Inner medulla)
5
Q
Percent composition of adrenal cortex?
A
90%
6
Q
Three Divisions of Cortex
A
Glumerulosa: salt (10%)
Fasiculata: sugar (75%)
Reticularis (15%)
7
Q
Salt hormones are controlled by what division of cortex?
A
Glumerulosa (10%)
8
Q
Fasciculata controls what horomones
A
Sugar hormones: Cortisol
9
Q
True or False. Clinical manifestation of HYPERaldosteronism includes;
Hyperkalemia
Hypotension
Metabolic acidosis
A
False. Hyperaldosteronism
Hypokalemia
Hypertension
Metabolic alkalosis
10
Q
Triad of Pheochromocytoma
A
Sweating (Diaphoresis)
Headache
Palpitation
11
Q
Condition with increased Cortisol level
A
Cushing’s Syndrome
12
Q
Increase of neuropeptides (Epinephrine/Norepinephrine)
A
Pheochromocytoma
13
Q
Congenital Adrenal Hyperplasia
A
Cells proliferate but function of adrenal is loss. Characterized by Hirsutism/Virilization and inability to conceive (.
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)
15
Q
Synthesizes ALDOSTERONE
A
Zona Glumerulosa
16
Q
Function of Aldosterone
A
- Reabsorbed: Na+ Excreted: K+
- Acid base balance
- Regulation of blood pressure
17
Q
True or False.
Aldosterone promotes retaining K+, excreting Na+
A
False.
Retaining sodium, excreting potassium
18
Q
Produces glucocorticoids (ex. cortisol and cortisone) and androgen precursors (Dehydroepiandosterone [DHEA])
A
Zona Fasciculata (70-75%)
19
Q
No. 1 Hormone to assess the adrenal cortex function
A
Cortisol
20
Q
Take part on the production of SEX hormones (testosterone & progesterone) by producing the active DHEA-S.
A
Zona Reticularis
21
Q
It can be converted to testosterone and progesterone.
A
Active DHEA-S
22
Q
True or False:
ACTH - Aldosterone
Angiotensin II - Cortisol
A
False.
ACTH - cortisol
Angiotensin II - Aldosterone
23
Q
It controls/regulates Cortex steroidogenesis.
A
ACTH
Angiotensin II
24
Q
True or False. All adrenal hormones comes from FREE CHOLESTEROL.
A
True.
25
Released during low cortisol levels, stress and Circadian Signals.
Corticotropin Releasing Hormone (CRH)
26
True or False. Conditions which CRH is not released except;
a. High Cortisol
b. Srtess
c. Circadian Signals
d. NOTA
A:
b. Stress
c. Circadian Signals
27
Circadian Rhythm of Cortisol (peak)
4 am - 8 am
28
Rate Limiting Step of Adrenal Gland
Conversion of Cholesterol to Pregnenolone by Cytochrome P450
29
True or False. Angiotensin II is released by HIGH blood pressure and volume
False. Stimulated by LOW blood pressure and volume
30
Triggers to release Aldosterone
Hyperkalemia
| Angiotensin II
31
Converts angiotensin I to an active form of angiotensin, which is Angiotensin II
Angiotensin Converting Enzyme (ACE)
32
Activates ANGIOTENSINOGEN
RENIN
33
True or False. Angiotensin I is more potent and active form that releases ALDOSTERONE
False. Angiotensin II
34
Functions of Angiotensin II
1. Release Aldosterone
2. Vasoconstriction
3. Increase Blood Pressure and Volume
4. Release ADH
Note: 1st two are major function
35
Identify what is responsible for conversion:
1. Angiotensinogen-to-Angiotensin I
2. Angiotensin I- to- Angiotensinogen II
A:
1. Renin
2. ACE
36
Percent composition of cortex that produces cortisol
70%
37
Primary activator in the production of cortisol
Adrenocorticotropic Hormone (ACTH)
38
Functions in Glucose metabolism during hypoglycemia which has 'HYPERGLYCEMIC EFFECT'
Cortisol
39
Which among the ff is the function of Cortisol?
a. Lipogenesis
b. Glycolysis
c. Glycogenolysis
d. NOTA
A: NOTA
Because Cortisol promotes;
Lipolysis
Gluconeogenesis
Glycogenesis
40
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
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.
41
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
CONGENITAL ADRENAL HYPERPLASIA
42
Most common enzyme abnormality in Congenital Hyperplasia
21–Hydroxylase
43
Hormone used to detect/diagnose Congenital Adrenal Hyperplasia
17–hydroxyprogesterone
44
True or False. Enzyme abnormality of 21-Hydroxylase is INCREASED glucocorticoid and DECREASED adrenal androgen production
FALSE. Diminished activity of 21-hydroxylase leads to decrease glucocorticoid and increased adrenal androgen production
45
Primary Aldosteronism
Increased/Excessive production of Aldosterone Secretion that cannot be suppressed by salt or volume replacement (excessive retention of salt).
Inc Aldosterone = Inc Na
46
Most Common Causes of Primary Aldosteronism
Aldosterone Producing Adrenal Adenoma
| Unilateral or Bilateral Adrenal Hyperplasia
47
Screening Considerations of Primary Aldosteronism
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
48
True or False.
| All antihypertensive may not be stopped during test
False. All antihypertensive may not be stopped during test, except: Spironolactone (Mineralocorticoid receptor antagonist)
49
Antihypertensive drug which MUST be stopped during testing because it is a ALDOSTERONE RECEPTOR ANTAGONIST
Spirinolactone
50
Confirmatory test of Primary Aldosteronism
Oral Salt Loading/IV Saline Loading
51
Results from an Initial Diagnosis of Primary Aldosteronism
Plasma Aldosterone Concentration (PAC >15ng/dl)
| Plasma Renin Activity (PRA >30)
52
True or False (Morse). Value of Plasma Aldosterone Concentration (should be lesser than 15ng/dl).
Plasma Renin Activity (PRA >30) to Diagnose Aldosteronism.
1st statement FALSE
| 2nd Statement TRUE
53
Ideal NaCl consumption
2 grams
54
NaCl consumption in Oral salt loading per day, usually 3 days
5000 mg (5 grams)
55
At what volume of Salt should consumed for 3 days?
15 g/15000 mg
56
True or False. In Oral Salt Loading with PA, Potassium is INCREASED to >200 g/meq, while, Urine aldosterone is DECREASED.
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.
57
IV saline method
Infuse 2L of NaCl (Normal saline) for 2 hours.
58
Test which would indicate if to undergo SURGERY or NOT
ADRENAL VENOUS SAMPLING
59
Aldosterone concentration secretion between 2 adrenal glands.
Ration: >4:1
Candidate for SURGERY
60
Aldosterone concentration secretion between 2 adrenal glands.
Ratio: 3:1 or less
NOT FOR SURGERY; Needs medical Management
61
Main adrenal hyperglycemic hormone
Cortisol
62
Used to measure adrenal insufficiency
Cortisol
63
Inadequate release of hormone in the adrenal cortex
Adrenal Insufficiency
64
Differentiate:
Primary Adrenal Insufficiency
Secondary Adrenal Insufficiency
Tertiary Adrenal Insufficiency
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
65
Most Common Cause of Adrenal Insufficiency
Autoimmune Destruction
66
True or False. Suggestive Diagnosis for Adrenal insufficiency.
Cortisol @ 8:00 am: HIGH
ACTH: LOW
False.
Cortisol @ 8:00 am: LOW
ACTH: ELEVATED
67
PRIMARY Adrenal Insufficiency Test
ACTH Stimulation Test
68
SECONDARY Adrenal Insufficiency Test
Metyrapone Suppression Test
69
What is the result of a Normal Patient undergone ACTH stimulation test.
A:
| Excessive Production of Cortisol due to overstimulation
70
Expected result with PAI.
A: Low Cortisol level of < 18
71
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.
False. ACTH Stimulation Test
72
What condition is attributed with a Normal ACTH test, but Decreased in Metyrapone Suppression Test?
Secondary Adrenal Insufficiency
73
True or False. Metyrapone BLOCKS 11 hydroxylase to INCREASE 11-Deoxycortisol with SECONDARY Adrenal insufficiency
False.
Normal: Increase 11-Deoxycortisol
SAI: Decrease 11-Deoxycortisol
74
True or False.
Primary AI: Increase ACTH, decreased cortisol
Secondary AI: Cortisol and ACTH both decreased
True.
75
True or False. Cortisol MUST increase after Insulin consumption.
True. Cortisol is a "Hyperglycemic Agent" during hypoglycemia.
76
also known as the “Cushing’s Syndrome”
HYPERCORTISOLISM
77
Differentiate: Cushing's Syndrome to Disease
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
78
A tumor in the pituitary gland that produces excessive ACTH.
Cushing's Disease
79
Complications in downward metabolic activities or problem or tumor in the adrenal gland which produces cortisol.
Cushing's Syndrome
80
True or False. In Cushing's diseases ACTH is elevated and Cortisol due to other causes
False. Cushing’s disease
| presents an ACTH elevation form Pituitary Tumor.
81
Source of Elevated Cortisol and ACTH from Pituitary Tumors
Cushing's Disease
82
Test for Cushing's Syndrome
Dexamethasone Suppression Test
83
True or False.
Secondary Adrenal Insufficiency: Dexamethasone Suppression Test
Cushing's Syndrome: Metyrapone Suppression Test
False.
Secondary Adrenal Insufficiency: Metyrapone Suppression Test
Cushing's Syndrome: Dexamethasone Suppression Test
84
Fluid Intake >5L/day and urine volume >3L/day can lead to?
FALSE POSITIVE RESULT
85
What consition can lead to Pseudo-Cushing’s?
Depression and Alcoholism
86
Dexamethasone Suppression Test:
Dose
Time administered
Time of the Day Measured
Result
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)
87
True or False. DEXAMETHASONE SUPRESSION TEST can evaluate whether it is Cushing's SYNDROME or Cushing's DISEASE
False. It cannot assess.
88
True or False. Late Night salivary Cortisol. Cortisol is greater or equal to the concentration in 8:00 am , present in CUSHING'S SYNDROME.
False. Concentration level of Cortisol is present in CUSHING'S DISEASE, due to neglect in diurnal or circadian variation.
89
True or False. Pseudo-Cushing’s STILL maintains diurnal variability.
True. Because there is no tumor, and only due to over reaction of Adrenal glands.
90
What TEST & what is measured to locate where ELEVATED CORTISOL is originated, whether from ADRENAL or Pituitary after doagnosing Hypercortisolism.
Immunoradiometric Assay (IRMA), that measures ACTH
91
Midnight Salivary Cortisol after Hypercortisolism is established and used IRMA:
Interpret:
>15 micrograms/dL
<5 micrograms/dL
>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)
92
Differentiate Pituitary and Ectopic Source of ACTH; or which ELEVATED ACTH is originated whether from Pituitary or other sources.
High Dose Dexamethasone Suppression Test
93
Difference of High Dose Dexamethasone Suppression Test to Low dose?
A: It is administered with 8mg Dexamethasone given at 11PM that INITIALLY suppress the ACTH coming from PITUITARY ALONE.
94
Interpret the results from High Dose Dexamethasone Suppression Test.
<5 micrograms/dl: _____________
<50% SUPRESSION: ____________
NO SUPPRESSION: ______________
<5 micrograms/dl: Normal
<50% SUPRESSION: ACTH from Pituitary
NO SUPPRESSION: Ectopic Source
95
Gold Standard for determining the source of ACTH production
INFERIOR PETROSAL SINUS SAMPLING
96
True or False. Pituitary ACTH Hypersecretion: if ratio is <2:1 (With CRH) or <3:1 (Without CRH)
False. Pituitary ACTH Hypersecretion: if ratio is >2:1 (Without CRH) or >3:1 (with CRH)
97
Byproduct of Cortisol Synthesis
Adrenal ANDROGENS
98
Composition of Adrenal Medulla
10%
99
Synthesizes Neuro-endocrine peptides that stimulate SYMPATHETIC response promoting flight or fight response.
Adrenal Medulla
100
Three classes of Catecholamines
Dopamine
Epinephrine
Norepinephrine
101
First catecholamine produced
DOPAMINE
102
Last and most ACTIVE catecholamines produced
EPINEPHRINE
103
Two major enzymes involved in the INACTIVATION of catecholamines.
```
Catechol-o-methyl transferase (COMT)
Monoamine oxidase (MAO)
```
104
Arranged the production of Catecholamine.
1. DOPA
2. NOREPINEPHRINE
3. TYROSINE
4. EPINEPHRINE
5. DOPAMINE
Tyrosine > Dopa > Dopamine > Norepinephrine > Epinephrine
105
All reactions take part in the cytoplasm; except
a. Dopamine
b. Epinephrine
c. Norepinephrine
A:
| c. Norepinephrine. Production is in the Lipid vesicles or outer mitochondrial membranes.
106
Enzyme that catalyzes the conversion of Norepinephrine (NE) to EPI in the cytosol.
Phenylethanolamine N-methyltransferase (PNMT)
107
Major (80%) catecholamine secretion of Adrenal Medulla.
Epinephrine
108
Ratio of NE:EPI in the circulation
9:1
109
True or False. Inactivation of Catecholamines.
Non-neuronal tissues: Monoamine Oxidase
Neuronal Tissues: Catecholamine-O Methyltransferase (COMT)
False.
Non-neuronal tissues: Catecholamine-O Methyltransferase
Neuronal Tissues: Monoamine Oxidase
110
True or False. In circulation EPINEPHRINE is most abundant, present and released by Postganglionic Neurons
False. Norepeniphrine is Major Catecholamine product of postganglionic neurons, that is 98% in circulation.
111
Hormones given on patients with Low Blood pressure and Heart Failure
Dopamine
| Epinepherine
112
Major product in Catecholamine Degradation, that is 30%
Vanillylmandelic acid (VMA)
113
Tumors in Adrenal MEDULLA
Pheochromocytoma
114
Tumors in SYMPATHETIC GANGLIA
Paraganglioma
115
Pheochromocytoma - Paraganglioma (PPGL) are associated with this SYNDROMES.
Multiple Endocrine Neoplasia 2
Von Hippen Lindau
Neurofibromatosis type 1
116
Ratio of Multiple Endocrine Neoplasia 2
1:2 - 1:5
117
Ratio of Von Hippen Lindau
1:10
118
Ratio of Neurofibromatosis type 1 to develop PPGL
1:20
119
Main Response of Catecholamines
SYMPATHETIC RESPONSE
120
True or False. 90% of cases have singular and benign mass, intra-adrenal and intra-abdominal
True.
121
Screening Tests for PPGL
1. Plasma Free Metanephrines (High Risk Patients)
2. 24-hour Urine fractionated Metanephrines (Low Risk)
3. Catecholamines
122
True or False. In Plasma Free Methanephrines, patient must be UPRIGHT for 30mins prior to blood sampling
False. Because patient must be supine for 30 mins prior to blood sampling. While, UPRIGHT posture leads to increase NE
123
True or False. In detecting/diagnosing PPGL, use the Biproduct or excretion product (VMA).
False. Detect the hormone it is producing or near hormone, such as EP, NE, or a Metanephrines.
124
Test done after a repeat 24 hr urine with equivocal result of less than 3 fold elevation of the upper limit.
Clonidine Suppression Test
125
This acts an alpha-2-adrenoceptor agonist and inhibits neuronal NE in patients without PPGL ALONE
Clonidine
126
What dose is given for Clonidine Suppression Test
300mcg/70kg
127
True or False. Plasma Noremetanephrine is measured after 3 hours
True.
128
What will be the possible result?
Patient with PPGL
Patient without PPGL
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
Associated syndrome which has the Highest chance of having PPGFL
Multiple Endocrine Neoplasia 2 (MEN II)
130
Endocrine Gland are __________ gland
Ductless
131
Major Higher Brain Control Center
Hypothalamus
132
Major secretor of Hormones
Pituitary Gland
133
Steroids "one"
Mnemonics: SCATEPAD
```
Cortisol
Aldosterone
Testosterone
Estrogen
Progesterone
Activated Vit. D
```
134
Amines
Epinephrine
Norepinephrine
T3
T4
135
Glycoprotein
Mnemonics: FiSH Erythropoietin , TraSH HCG
FSH
TSH
EPO
HCG
136
Polypeptides
```
ACTH
GH
PTH
Oxytocin
Insulin
Glucagon
```
137
Precursors of Steroid Hormones
Cholesterol
138
Glycoproteins are _____________
Non-protein bound
139
Precursors of Amine Hormones
Tyrosine
140
Hormones synthesized in the Hypothalamus
Oxytocin: Uterine Contraction
| Vasopressin/ADH: Water Reabsorption
141
Love Hormone
Oxytocin
142
Pleasure Hormone
Dopamine
143
Thirst Hormone
AVP/ADH
144
Master Gland
Pituitary Gland
145
Hierarchy of Endocrine System
1.
2.
3.
Hierarchy of Endocrine System
1. Hypothalamus
2. Pituitary Gland
3. End Organs - Thyroid Gland, PTG, Adrenal Gland, Testes, Ovary
146
Pituitary Gland - Other Names
Anterior PG: __________
Posterior PG: _________
Pituitary Gland - Other Names
Anterior PG: Adenohypophysis
Posterior PG: Neurohypophysis
147
Hormones Secreted - Anterior Pituitary Gland
```
TSH
FSH
LH
TSH
ACTH
GH
Prolactin
```
148
Hormones Secreted - Posterior Pituitary Gland
Oxytocin
| Vasopressin
149
Posterior Pituitary Gland only ________ hormone.
STORES
150
Cells in the APG
```
Corticotrophs: ________
Gonadothrophs: _______
Thyrotrophs: ________
Somatotrophs: _______
Lactotrophs: _______
```
Cells in the APG
```
Corticotrophs: ACTH
Gonadothrophs: FSH, LH,
Thyrotrophs: TSH
Somatotrophs: GH
Lactotrophs: Prolactin
```
151
Stress Hormone
Prolactin
152
Other name for Growth Hormone
Somatostropin
153
Major Stimulant for GH secretion
SLEEP
154
Most abundant of all Pituitary Hormones
GH/Somatotropin
155
Tests for GH
GH Deficiency: __________________
Acromegaly/Gigantism: ______________
Tests for GH
GH Deficiency: Insulin Tolerance Test
Acromegaly/Gigantism: Glucose Suppression
156
Tests for GH Deficiency
Confirmatory Test: _____________
2nd Confirmatory Test: ______________
Tests for GH Deficiency
Confirmatory Test: Insulin Tolerance Test
2nd Confirmatory Test: Arginine Stimulation Test
157
FSH acts on _________________
Sertoli Cells
158
LH acts on ____________________
Leydig Cells
159
Functions of LH
1. Ovulation
2. Testosterone production
3. Synthesis of Androgens - Theca Cells
160
Also known as thyrotropin
TSH
161
Activates Cortisol
ACTH
162
Mill Production
Prolactin
163
Major Inhibitor of Prolactin
Dopamine
164
Effect of excess Prolactin
Men: _______
Women: ______
Men: Hypogonadism
Women: Amenorrhea, Galactorrhea
165
Deficiency in ADH
Diabetic Insipidus
166
Types of Diabetic Insipidus
Neurogenic - ________________
Nephrogenic - _______________
Types of Diabetic Insipidus
Neurogenic - Deficiency in ADH; Normal ADH Receptors
Nephrogenic - Sufficient ADH, Defective ADH Receptors
167
Diagnostic Test For Diabetic Insipidus
Overnight Water Deprivation
168
Cells and Hormones Produced by the Thyroid Gland
Follicular Cells: __________
Parafollicular Cells/C Cells: __________
Cells and Hormones Produced by the Thyroid Gland
Follicular Cells: T3 T4
Parafollicular Cells/C Cells: Calcitonin
169
Start of Thyroid Hormone production
11th week of gestation
170
Organized thyroid cells that absorbs iodine
Follicle
171
Most important substrate in Thyroid hormone synthesis
Iodine
172
Active form of Iodine
Oxidized Iodide
173
Synthesized by the follicular cells and the major component of colloid
Thyroglobulin
174
Thyroglobulin is rich in _________
Tyrosine
175
Enzyme that oxidizes trapped iodine and assemble thyroid hormones
Thyroid peroxidase
176
Most Active/Most Hormonal Activity
T3/Triiodothronine/353
177
Two forms of Triiodothyronine
T3 - __________; Active
rT3 - __________; inactive
Two forms of Triiodothyronine
T3 - 3,5,3
rT3 - 3,3,5
178
_____ can be converted back or reverse to T4
rT3
179
Most Abundant fraction of Iodine
T4
180
Prohormone of T3
T4
181
___ is first to increase in Hyperthyroidism
T3
182
Main serum carrier protein of T3 & T4
Thyroxine Binding Globulin (TBG)
183
Enzyme that converts T4 to T3
Iodothyronine 5' deiodinase
184
Enzymes - Thyroid Hormones
____________: Trapped Iodine ----- Oxidized Iodide
____________: t4 --------t3
Enzymes - Thyroid Hormones
Thyroid peroxidase: Trapped Iodine ----- Oxidized Iodide
Iodothyronine 5' - deionidase - : t4 --------t3
185
T3
First increase: ____________
Indicator: ______________
Diagnosis: _____________
T3
First increase: Hyperthyroidism
Indicator: Recovery of Hyperthyroidism
Diagnosis: T3 Thyrotoxicosis
186
T4
Indicator: ________________
Increase: _____________
Distribution: ____________
T4
Indicator: Thyroid Secretory Rate
Increase: NO TSH
Distribution: Most abundant
187
3rd Major Circulating Thyroid hormone
rT3
188
Ratio of T4 to T3
20:1
189
T3 Thyrotoxicosis
Increased:
Normal:
Low:
T3 Thyrotoxicosis
Increased: FT3
Normal: FT4, T4
Low: T4, TSH
190
T4 Thyrotoxicosis
Increased:
Normal:
Low:
T4 Thyrotoxicosis
Increased: T4
Normal: T3
Low: T3, TSH
191
Signs and Symptoms of Hyperthyroidism
```
Tachycardia
Unexplained weight loss
Heat Intolerance
Emotional Lability
Bulging Face
Soft Nails
```
192
Most common cause of Thyrotoxicosis
Graves Disease
193
Commonly Measured or Requested Thyroid Hormones
TSH
| FT4
194
Graves Disease Mechanism - Stimulatory
Presence of Autoimmune antibodies (TRAb) against TSH receptor that STIMULATES the increase production of TSH and Thyroglobulin
195
Riedel's Thyroiditis
Thyroid is WOODY/STONE hard mass
196
Disease: _______________
Shows NO CLINICAL SYMPTOMS
Low TSH
Normal: FT3 FT4
Subclinical Hyperthyroidism
Shows NO CLINICAL SYMPTOMS
Low TSH
Normal: FT3 FT4
197
Diagnostic Test for Graves Disease
TSH Receptor Antibody Test (TRAb)
198
Painful Throiditis
Subacute granulomatous
Subacute non suppurative
De Quervains
199
Reidel's Thyroiditis vs. De Quervain's
Type of Goiter:
Characteristic:
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
Signs and Symptoms of Hypothyrpoidism
```
Bradycardia
Cold Intolerance
Unexplained weight gain
Brittle Nails
Puffy face
```
201
Most Common cause of primary hypothyroidism
Hashimoto's thyroiditis
202
Other names - Hashimoto's Thyroiditis
1. ____________________
2. ____________________
Other names - Hashimoto's Thyroiditis
1. Chronic Lymphocytic Thyroiditis
2. Chronic Autoimmune Thyroiditis
203
Mechanism - Hashimoto's Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis
Mechanism - Hashimoto's Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis
Autoimmune Ab destroys thyroid gland by inhibiting Thyroid peroxidase function - Anti TPO Abs
204
Diagnosis - Hashimoto's Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis
Positive Ab:
Increase:
Decrease:
Diagnosis - Hashimoto's Thyroiditis/Chromic Lymphocytic/Autoimmune Thyroiditis
Positive Ab: Anti-TPO Ab
Increase: TSH
Decrease: T3 T4
205
Peculiar nonpitting swelling of Skin
Myxedema
206
Antibodies in Hashimoto's Thyroiditis
Anti-TPO antibodies
Anti-microsomal
Anti-thyroglobulin antibodies
207
Severe form of Primary Hypothyroidism
Myxedema/Myxedema Coma
208
Most important Thyroid Function test
TSH Test
209
TSH test differentiates ________ and ________ _____thyroidism
TSH test differentiates PRIMARY and SECONDARY HYPOthyroidism
210
3rd major circulating thyroid hormome
rT3
211
Important indicator for Thyroid Cancer and Proof of Thyroid presence
Thyroglobulin Test
212
Indirectly assess T4 in the blood
Free Thyroxine Index (FTI/T7)
213
Measures the available binding sites of TBG and reflects serum level of TBG
T3 uptake
214
TBG is _________ related to T3 uptake
INVERSELY
215
Major site of Steroidogenesis
Adrenal Cortex
216
Stimulates Steriodogenesis
ACTH
217
Cortisol Urinary Metabolites
Method - Cortisol Metabolite Detected - Reagent
Polter-Silber Reaction: ____________ - ___________
Zimmerman: ____________ - ____________
Cortisol Urinary Metabolites
Method - Cortisol Metabolite Detected - Reagent
Polter-Silber Reaction: 17 hydroxycorticosteroid - Phenylhydrazine
Zimmerman: 17 ketogenic acid - Dinitrobenzene
218
Polter-Silber Reaction
End Color:
Detected:
Reagent:
Polter-Silber Reaction
End Color: Yelloe
Detected: 17 HCS
Reagent: Phenylhydrazine
219
Zimmerman Reaction
End Color:
Detected:
Reagent:
Zimmerman Reaction
End Color: Reddish Purple
Detected: 17 ketogenic acid
Reagent: Dinitrobenzene
220
Current Reference Method of 24 hr Urine Free Cortisol
HPLC-MS
221
Screening Tests - Hypercortisolism/Cushing's Syndrome
24 hr UFC
Overnight Dexamethasone Suppression Test
Midnight Salivary Cortisol
222
Confirmatory Tests - Hypercortisolism/Cushing's Syndrome
Low Dose Dexamethasone
Midnight Plasma Cortisol
CRH Stimulation Test
223
Screening Test - Hypocortisolism/Adrenal Insufficiency
ACTH Stimulation Test
224
Confirmatory & Gold Std. - Hypocortisolism/Adrenal Insufficiency
Insulin Tolerance Test
225
Alternative for diagnostic and Confirmatory for Secondary AI
Metyrapone Suppression Test
226
Congenital Adrenal Hyperplasia
Decreased:
Increased:
Congenital Adrenal Hyperplasia
Decreased: Cortisol
Increased: Androgen
227
Congenital Adrenal Hyperplasia
Enzyme deficient: ____________
Diagnostic: __________
Congenital Adrenal Hyperplasia
Enzyme deficient: 21 hydroxylase
Diagnostic: 7 hydroxyprogesterone
228
Screening Tests - Hyperaldosteronism
Plasma Aldosterone Concentration/Plasma Renin Activity Ratio
229
Confirmatory Test - Hyperaldosteronism
Saline Suppression Test
Oral Sodium Loading Test
Fludocortisone suppression test
Captopril Challenge Test
230
Hyperaldosteronism - Plasma Aldosterone Concentration/Plasma Renin Activity Ratio
>30 ratio: _______________
>60 ratio: _______________
Hyperaldosteronism - Plasma Aldosterone Concentration/Plasma Renin Activity Ratio
>30 ratio: Suggestive for Hyperaldosteronism
>60 ratio: Diagnostic for Hyperaldosteronism
231
Occurs due to excessive Renin Production
Secondary Hyperaldosteronism
232
Primary Hyperaldosteronism vs. Secondary Hyperaldosteronism
PAC - aldosterone:
PRC - Renin:
Primary Hyperaldosteronism
PAC - aldosterone: Increase
PRC - Renin: Decrease
Secondary Hyperaldosteronism
PAC - aldosterone: Increase
PRC - Renin: Increase
233
Secondary Hyperaldosteronism
Liddle's Syndrome:
Barterr's Syndrome:
Gitelman's Syndrome:
Secondary Hyperaldosteronism
Liddle's Syndrome: Pseudohyperaldosteronism
Barterr's Syndrome: Bumetanide-sensitive chloride channel mutation
Gitelman's Syndrome: Thiazide-sensitive transporter Mutation
234
Liddle's Syndrome
Pseudohyperaldosteronism
235
Barterr's Syndrome
Bumetanide-sensitive chloride channel mutation
236
Gitelman's Syndrome
Thiazide-sensitive transporter Mutation
237
Hypoaldesteronism id caused by deficiency of __________ and _____________ leading to destruction of adrenal glands
Hypoaldesteronism is caused by deficiency of GLUCOCORTICOID and 21 HYDROXYLASE leading to destruction of adrenal glands
238
Principal Adrenal Androgens
DHEA
239
Main precursor of Catecholamines
Phenylalanine
240
Norepinephrine to Epinephrine Ratio
9:1
241
Highest concentration in the Brain/Circulation
Norepinephrine
242
Highest concentration in Adrenal Medulla
Epinephrine
243
Flight or Fight Hormone
Epinephrine
244
Major Metabolite - Norepinephrine
3-methoxy-4-hydroxyphenylglycol (MHPG
245
Major Metabolite - Epinephrine
Vanilyl mandelic acid
246
Major Metabolite - Dopamine
Homovanilic acid
247
Major Metabolite - Serotonin
5-hydroxyindoleacetic acid
248
Pheochromocytoma
Screening Test: ______________
Diagnostic Test: ______________
Pharmacologic Test: _____________
Pheochromocytoma
Screening Test: Plasma Free Metanephrines
Diagnostic Test: 24 hr Urine fractionated metanephrines/normetanephrines
Pharmacologic Test: Clonidine Suppression Test, Glucagon Stimulation Test
249
Most potent male androgen and Principal Androgen hormone in the blood
Testosterone
250
Tests for Male Fertility
Semen Analysis
Testosterone
FSH
LH
251
Major transport protein of Sex hormones
SHBG - sex hormone binding globulin (60%)
252
Most active form of Testosterone
Dihydroxytestosterone
253
Enzyme that converts testosterone to dihyxroxytestoterone (active)
5-alpha-reductase
254
Primary Hypogonadism
a.k.a.
Infertility:
Origin:
Diagnosis:
Primary Hypogonadism
a.k.a. - Hypergonadotropic Hypogonadism
Infertility: Testicular Infertility
Origin: Testicular Origin
Diagnosis: Increased FSH, LH; Decreased Testosterone
255
Secondary Hypogonadism
a.k.a.
Infertility:
Origin:
Diagnosis:
Secondary Hypogonadism
a.k.a. - Hypogonadotropic hypogonadism
Infertility: Pretesticular Infertility
Origin: Pituitary Origin
Diagnosis: Decreased FSH, LH; Decreased/N Testosterone
256
Congenital Testicular Infertility
Klinefelter's Syndrome
Kallman's Syndrome - Cryptorchidism
5 alpha reductase deficiency
Myotonic Dystrophy
257
47XXY
Klinefelter's syndrome
258
Characteristics associated with Klinefelter's Syndrome
Gynecomastia
Small Firm testicles
Azoospermia
259
Testicular Feminization Syndrome
Cryptorchidism
260
Characteristic of Cryptorchidism
Micropenis
| Undescended testicles
261
Most abundant estrogen in post-menopausal women
Estrone (E1)
262
Most potent Estrogn
Estradiol (E2)
263
Most abundant estrogen in pre-menopausal women
Estradiol (E2)
264
Major estrogen secreted in Pregnancy
Estriol (E3)
265
Produced by the corpus luteum that maintains pregnancy
Progesterone
266
Functions of Progesterone
1. Prepares endometrium for embryo implantation
| 2. Maintains Pregnancy
267
Tests for Menstrual Cycle Dysfunction
Estrogen
Progesterone
FSH
LH
268
Tests for Female Infertility
MNEMONICS: THEF LP
DECREASED
```
TSH
HCG
E2
FSH
LH
PRL
```
269
Diagnosis of Down Syndrome - Trisomy 21
Mnemonics - Hi Down
Increased: ________, _______
Decreased: _______, _______
Diagnosis of Down Syndrome - Trisomy 21
Mnemonics - Hi Down
Increased: HCG, Inhibin A
Decreased: Estriol, AFP
270
Gastrin is a diagnostic marker for _________________
Zollinger-Ellison Syndrome
271
Diagnostic marker for Carcinoid tumor
Serotonin
