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Endocrinology Flashcards

1
Q

Hormones

A

Chemical messengers

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2
Q

Hormones travel to other organs through

A

Bloodstream

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3
Q

Glands of the Endocrine system

A

Pituitary gland
Thyroid gland
Parathyroid gland
Thymus
Adrenal gland
Pancreas
Ovary and testis

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4
Q

The floor of the third ventricle is formed by

A

Hypothalamus

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5
Q

The hypothalamus ends down with

A

Pituitary stalk

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6
Q

Pituitary stalk follows to the

A

Pituitary gland

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7
Q

Signals from CNS are transmitted to hypothalamus via

A

Neurons and neurotransmitters

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8
Q

The hypothalamus then collects all the signals and information and switches neural to

A

Hormonal signals

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9
Q

What is the main link between nervous and endocrine system

A

Hypothalamus

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10
Q

The central part of hypothalamus is called

A

Median eminence

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11
Q

The pituitary stalk starts from the

A

Median eminence of hypothalamus

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12
Q

Medial Eminence consists of

A

Tubuloinfundibular neurosecretory neurons
and
Capillary network of pituitary portal circulation

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13
Q

What does neurons secrete into bloodstream

A

Neurotransmitters

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14
Q

Neurotransmitters after entering bloodstream becomes

A

Hormones

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15
Q

Hormones from hypothalamus reaches pituitary gland by

A

Pituitary portal circulation

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16
Q

The main unit of neuroendocrinology are

A

Hypothalamus and pituitary gland

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17
Q

The brain sends signals to endocrine glands to

A

Secrete and release hormones

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18
Q

The endocrine glands sends feedback to

A

CNS

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19
Q

What sends inhibition signal to pituitary gland when the hormone reaches a desired amount in blood

A

Hypothalamus

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20
Q

Non endocrine functions of hypothalamus

A

Body temperature
Thirst
Appetite
Mood and consciousness

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21
Q

Hypothalamic hormones

A

Releasing hormones
Inhibiting hormones
Oxytosin and ADH (vasopressin)

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22
Q

Releasing hormones (liberins)

A

Thyroid releasing hormone
Corticosteroids releasing hormone
Gonadotropin releasing hormone
Growth hormone releasing hormone

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23
Q

Inhibiting hormones

A

Somatostatin
Prolactostatin (dopamine)

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24
Q

Diabetes insipidus causes decreased reabsorption of water in

A

Distal kidney tubules

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25
Diabetes insipidus is
Complete or partial ADH deficiency
26
Diabetes insipidus types
Central (hypothalamus) Nephrogenic (kidney) Transitory (pregnancy) Primary polydipsia
27
Diabetes insipidus clinical presentation
Polyuria Polydipsia Dehydration Hypoosmotic urine Plasma hyperosmolality
28
Central diabetes insipidus causes
Tumors Trauma/surgery Granulomatosis Lyphocytic Infundibulo-hypophysitis Adipsic DI Cerebral anoxia
29
Congenital Nephrogenic DI causes
mutation of V2 receptor on X chromosome autosomal recessive mutation of aquaporin 2 water channels
30
Acquired nephrogenic DI causes
Polycystism Kidney infarction Sickle cell anemia Lithium
31
Transient DI causes
Cysteine amino peptidase oxytocinase breaks down oxytosin and ADH
32
Cystein amino peptidase oxytocinase is produced by
Placenta
33
Primary polydypsia causes
Psychiatric patients Behavioral abnormalities
34
Diagnosis of DI
Disappearance of neurohypophysis signals Measurement of daily fluid intake and diuresis Thirst test
35
Urine osmolality in DI is
Less than 200 mosmol/l Normal is greater than 800 mosmol/l
36
Plasma osmolality in DI
Greater than 285-295 mosmol/l
37
Differential diagnosis of DI
Osmotic diuresis in hyperparathyroidism, Diabetes melittus Psychogenic polydipsia Nephrogenic DI (hereditary) Polyuretic phase in chronic renal injury
38
Nephrogenic DI test
Desmopressin test
39
Theraphy for DI
Synthetic ADH analog (Minirin)
40
Anterior pituitary hormones
PRL FSH LH TSH ACTH MSH (Melanocyte Stimulating Hormone) STH (somatotropin)
41
Posterior pituitary hormones
ADH Oxytosin
42
Pituitary gland diseases
Hypo pituitarism Pituitary Adenomas Prolactinoma Acromegaly and gigantism ACTH adenoma (cushings disease) TRH adenoma Gonadotropin adenoma Non functioning adenoma
43
Hypopituitarism causes
After tumor surgery Sheehans syndrome
44
Sheehans syndrome
Pituitary necrosis because of extreme blood loss during child birth
45
Hypopituitarism therapy
TSH deficiency - thyroxine ACTH deficiency - hydrocortisone STH deficiency - growth hormone
46
Prolactinoma clinical presentation
Female: Menstrual cycle disorders Sterility Galactorrhoea Male: Galactorrhoea Gynacomastia Low libido Low spermatogenesis Low potency
47
Prolactinoma therapy
Dopamine agonists (Bromocriptin, cabergoline) Surgery
48
Acromegaly clinical presentation
Prominent supra orbital arches Folds on forehead Large nose Large ears Thick lips Macroglossia Increased spacing between teeth Large hands and feet Oily skin Hirsutism in women Enlarged thyroid gland (multinodular goiter) Increased sweating Arthralgia Myopathy Carpal tunnel syndrome Headache Neuropathy PTG DM Hypertension Cardiomyopathy Rhythm disorder Sleep apnea Lumbago
49
Acromegaly and gigantism causes
Bitemporal hemianopia
50
Acromegaly and gigantism therapy
1st gen Octreotide - somatostatin analog 2nd gen pasireotide Dopamine agonist Radiation
51
Cushing’s disease clinical presentation
Facies lunata Osteoporosis Myopathy Fatigue Depression Purple stripes Skin atrophy, sufusion Thrombosis Lower extremities swelling Secondary hypertension, DM Decreased libido Menstrual cycle disorders
52
Cushings disease diagnosis
Increased free cortisol in urine in 24hrs Lack of cortisol at night (loss of circadian rhythm) Lack of cortisol suppression after 1mg of dexamethasone
53
Cushings disease treatment
Surgery
54
Diabetes mellitus is acute or chronic
Chronic
55
Diabetes mellitus is characterised by
Persistent hyperglycemia
56
Persistent hyperglycemia in DM is due to
Impaired insulin secretion Resistance to insulin
57
Types of DM
Type 1 Type 2 Gestational DM Secondary DM
58
Etiology of DM type 2
Genetic and environment
59
Hyperglycemia causes
Decreased incretin level Increased glucose reabsorption by kidneys Lipolysis Decreased glucose uptake by muscles Neurotransmitter dysfunction Increased glucagon secretion by alpha cells of islets Decreased insulin secretion Increased Hepatic Glucose Production(HGP)
60
Incretin
Gastric Inhibitory Polypeptide (GIP) Glucagon Like Peptide 1 (GLP1)
61
Insulin resistance in liver leads to
Increased fasting plasma glucose
62
Insulin resistance in muscles leads to
High postprandial glucose
63
Increased insulin production by Beta cells leads to
Progressive beta cells failure
64
Insulin resistance in adipose tissue leads to
Increased free fatty acids in plasma due to increased lipolysis Decreased lipogenesis Decreased glucose uptake
65
INCRETIN abbreviation
Intestine Secretion Insulin
66
Alpha cells in DM type 2
It produces more glucagon and increases post prandial glucose level in blood
67
Glucose reabsorption takes place in which part of kidney tubules
PCT
68
The transporters that take part in glucose absorption in kidneys are
SGLT-2 (90%) SGLT-1 (10%) (straight descending part of PCT)
69
Brain insulin resistance
After eating and increased glucose there is inhibitory response from hypothalamus but in DM type 2 there is no inhibition because the hypothalamus is resistant to insulin
70
Diabetes Mellitus clinical features
Polyuria Polydipsia Polyphagia
71
Diabetes mellitus signs
Kussmaul’s breathing because of metabolic ketoacidosis Dehydration Weigt loss Altered level of consciousness Acute coronary disease Stroke Kidney disease Vision loss Diabetic foot
72
Diabetes Mellitus diagnosis Free Plasma Glucose while fasting is
Greater than 7 mmol/l is diabetic
73
Fasting is
No calorie intake for 8 hours or more
74
Glycated hemoglobin HbA1C for adults is
Greater than 6.5% is diabetic
75
2hPG in a 75g OGTT is
Greater than 11.1 mmol/l is diabetic
76
2hPG is
2 hour post prandial or 2hr plasma glucose
77
Random PG is
Greater than 11.1 mmol/l is diabetic
78
75g OGTT for GDM is diabetic when it exceeds
Fasting : 5.1 mmol/l (92 mg/dl) 1 h : 10 mmol/l (180 mg/dl) 2h : 8.5 mmol/l (153 mg/dl)
79
Microvascular chronic complications of DM
Retinopathy, cataract, glaucoma Nephropathy Neuropathy
80
Macrovascular chronic complications of diabetes
Transient ischemic stroke Coronary artery disease High blood pressure Peripheral vascular disease due to narrowing of blood vessels in leg and leads to decreased blood flow
81
Drugs used to treat diabetes
Metformin Sulfonylureas Thiazolidinediones Insulin
82
Incretin based drugs
Dipeptidyl Peptidase-4 (DPP-4) inhibitors Glucagon like peptide-1 (GLP-1) Analogues
83
Co transporter inhibitors
Sodium Glucose Cotransporter-2 (SGLT-2) inhibitors
84
More diabetes drugs
Alpha glucosidase inhibitors Metiglinide analogues Pramlintide
85
Diabetics have increased risk of
Cardiovascular Peripheral vascular Cerebro vascular diseases
86
DM type 1 is
Absolute insulin deficiency because of Beta cell damge in pancreas
87
Which diabetes is autoimmune
Type 1 DM
88
Osmotic diuresis means
Glucose attracts water so more glucose in kidney tubules leads to Polyuria
89
Blurring of vision in diabetes is caused by
Accumulation of glucose in eye vessels and leads to inflammation because of hyperosmotic condition
90
Amino acids are converted to what in diabetes during chronic weight loss
Glucose and ketone bodies
91
Hyperglycemia leads to a condition that affects peripheral nerves called
Paraesthesia
92
Insulin drugs
Insulin lyspro Insulin aspart Insulin glulisin Insulin glargin Insulin detemir
93
Questions that are asked during examination
Current symptoms Life history Family history Pharmacotherapy history
94
Examination
Examination by systems
95
After examination things to be done are
Give conclusion diagnosis Laboratory diagnosis Instrumental tests
96
Types of symptoms
General symptoms Specific symptoms
97
Cerbral complication of DKA is
Cerebral edema
98
Sudden drop in serum osmolality leads to
Edema and other complications like dehydration because of Polyuria
99
Diabetic Keto Acidosis and Hyperosmolar Hyperglycemic State can lead to decreased
Serum Potassium
100
Adrenal cotex layers
Zona glomerulosa (outer) Zona fasciculata (middle) Zona reticularis (inner)
101
Zona glomerulosa secretes
Minerelocorticoids
102
Zona fasciculata secrets
Glucocorticoids
103
Zona reticularis secretes
Adrenal Androgens
104
Minerelocorticoids example
Aldosterone
105
Glucocorticoids example
Cortisol
106
Adrenal androgens example
Androstenedione DHEA DHEAS
107
Which layer of adrenal cortex is predominantly under the control of ACTH
Zona fasciculata Zona reticularis
108
Which layer of adrenal cortex is predominantly under the control of Renin Angiotensin Aldosterone System
Zona glomerulosa
109
Adrenal cortex hormones are circulated in blood stream bound to?
Plasma protiens (globulins)
110
Adrenal cortex hormones are broken down in
Liver and excreted via kidneys
111
Cushing syndrome is chronic hypersecretion of
Glucocorticoid (cortisol) And also maybe androgens
112
Etoiology of cushing’s disease is
ACTH dependent: Ectopic ACTH Pituitary adenoma
113
Etiology of cushing syndrome
ACTH independent: Adrenal adenoma Adrenal carcinoma Nodular hyperplasia
114
ACTH is elevated in
Ectopic ACTH secretion And little elevation in pituitary tumor of adenohypophysis
115
ACTH is suppressed in
Adrenal carcinoma or adenoma Or maybe in nodular hyperplasia
116
Cushings disease clinical picture
Obesity (central type) Facies lunata Acne Hirsutism Thin skin Dark pigmentation in cushing disease (ACTH dependant) Muscle weakness Emotional Mental disorders Decreased libido Hypertension Osteoporosis
117
Hypertension in cushing disease is by
Increased vascular tone by cortisol And also by renal sodium absorption
118
Osteoporosis in cushing disease is caused by
Increased calcium elimination by kidney due to cortisol elevation and compensatory increased activity of parathyroid gland
119
Diagnosis of cushings disease are
Urine 24 hr Elevated steroid metabolites in urine Elevated plasma cortisol MRI CT UZ
120
Differential diagnosis of cushings
Dexamethasone 1mg suppression test
121
Hyperaldosteronism types
Primary and Secondary
122
Primary hyperaldosteronism is
Increased aldosterone without RAAS increase
123
Secondary aldosteronism is
Increase in aldosterone with RAAS increase
124
Primary hyperaldosteronism
Conns syndrome Adrenal tumor Glucocorticoid suppressed hyperaldosteronism
125
Pathogenesis of hyperaldosteronism
Na retention K loss Increased extracellular fluid Suppression of renin release K release from cells H+ entry into cells Renal H+ loss Hypokalemic alkalosis
126
Nephrogenic diabetes in hyperaldosteronism is caused by
Hypokalemia
127
Laboratory diagnosis of primary hyperaldosteronism
Decreased serum potassium Increased K in urine Renin decreased in plasma even after volume depletion
128
Treatment of primary aldosterone
Spironolactone
129
Secondary hyperaldosteronism is caused by
Renal artery stenosis Liver cirrhosis Congestive Heart Failure Nephrotic syndrome Renin secreting tumor
130
What is primary adrenal cortical insufficiency
Addison’s disease
131
Addison’s disease etiology
Autoimmune adrenalitis Cortical atrophy Amyloidosis Hemochromatosis Infection (TB, fungal infection, AIDS)
132
When do we find clinical manifestation in addison’s disease
After 90% cortical damage
133
Clinical signs of addison’s disease
Anorexia Weakness Hyperpigmentation except palms and soles Hypotension Vomiting pain diarrhoea (GIT symptoms) May cause hypoglycemia Menstrual disorders
134
Addison’s laboratory diagnosis
Hyponatremia Hyperkalemia Normocytic anemia Esnophilia Low plasma and urine cortisol Low DHEA Low aldosterone ACTH elevated
135
Diseases of hyperpigmentation
Hemochromatosis Wilson’s hepatolenticular degeneration Multiple polyposis Progressive cachexia (anorexia nervosa, malignancy)
136
Addison’s disease treatment
Substitution therapy Hydrocortisone Fludrocortisone
137
Secondary adrenocortical insufficiency etiology
ACTH deficiency Chronic use of corticosteroids After pituitary surgery in cushings disease
138
Clinical signs of secondary adrenocortical insufficiency
No hyperpigmentation Absence of signs of Minerelocorticoid deficiency
139
Secondary adrenocortical insufficiency laboratory diagnosis
Low ACTH along with low cortisol
140
Acute adrenocortical insufficiency etiology
Insufficient substitution Haemorrhage in adrenal cortex due to anticoagulant therapy or infection or coagulation disorder Discontinuation of glucocorticoid therapy
141
Acute adrenocortical insufficiency signs
Shock Hypotension High fever Acute abdomen Coma Cyanosis Petechial haemorrhage Haemorrhage
142
Acute adrenal insufficiency laboratory diagnosis
Hyponatremia Hyperkalemia Hypoglycemia Azotemia Esnophilia Dexamethasone does not help in hormonal findings Low cortisol
143
Acute adrenocortical insufficiency treatment
Volume compensation by IV fluid Hormone replacement
144
Adrenal medulla origin
The sympathetic nervous and adrenal medulla have same ectodermal origin
145
The hormones secreted by adrenal medulla are
Epinephrine and Nor epinephrine
146
Epinephrine and nor epinephrine are
Catecholamines (Amines)
147
Adrenaline is secreted in
Adrenal medulla
148
Nor adrenaline is secreted in
Post ganglionic sympathetic nerve endings and to a lesser extent in adrenal medulla
149
Epinephrine and nor epinephrine are broken down in ________and entered via _____________
Liver and excreted by kidneys
150
Pheochromocytoma
It is a catecholamine secreting tumor of adrenal medulla
151
Methylation of nor adrenaline to adrenaline is by
Phenylethanolamine N methyl transferase (PNMT)
152
Methylation of nor adrenaline to adrenaline is dependent on
Cortisol
153
More nor adrenaline is secreted by
Large tumours
154
Smaller tumours have corticomedullary blood supply so they secrete more
Cortisol and large PNMT activation
155
Extradrenal tumours secrete only
Nor epinephrine
156
Pheochromocytoma clinical signs
Hypertension Paroxysms like Palness redness Palpitaion Sweating Headache
157
Diagnosis of pheochromocytoma
Catecholamines and metabolites in the urine Plasma catecholamines Functional tests CT MRI
158
Level of glucagon in pheochromocytoma is
Increased
159
Adrenogenital syndrome
Increased secretion of DHEA and androstenedione in adrenal cortex that are extraadrenally converted to testosterone
160
Congenital adrenal hyperplasia
Hereditary deficiency of an enzyme (21 hydroxylase) necessary for synthesis adrenocorticorticosteroids especially cortisol
161
The main regulatory factor for synthesis of ACTH and CRH is
Cortisol
162
When there is increased secretion of cortisol there is also increased secretion of
Adrenal androgens
163
21 hydroxylase deficiency is
Complete Incomplete
164
Complete deficiency of 21 hydroxylase is
Cortisol and aldosterone deficiency
165
Incomplete 21 hydroxylase deficiency is
Only cortisol deficiency
166
CAH complications during puberty in children
Isosexual precocious puberty in boys and Heterosexual precocious puberty in girls
167
Signs of CAH in girl during birth is
Female pseudohermaphroditism Fused labia Persistent urogenital sinus Developed clitoris
168
In adulthood in CAH signs are
Hirsutism Menstrual disorder Virilization
169
CAH diagnosis
Elevated DHEA, DHEAS and androstenedione in serum Low cortisol High ACTH
170
CAH therapy is
Corticosteroids to suppress ACTH
171
Virilization
Increased muscle mass Clitomegaly Deep voice Breast atrophy and Hirsutism
172
Hirsutism vs hypertrichosis
Hirsutism is androgen dependent hair growth in male pattern Hypertrichosis is androgen independent hair growth
173
Effects of triiodothyronine (T3)
Increased tissue thermogenesis Decreased systemic vascular resistance Increased cardiac inotropy and chronotropy
174
Parathyroid gland location and number
Behind thyroid gland and there are 4 of them
175
Parathyroid gland action on bone
Bone resorption increases serum calcium and decrease phosphorus because of excretion of phosphorus in urine
176
Parathormone action on kidneys
Increased reabsorption of calcium in kidney tubules and Increases production of vitamin D
177
Parathormone action on intestine
Increased calcium absorption
178
Primary parathyroidism etiology
Hyperplasia Carcinoma Solitary adenoma
179
Secondary parathyroidism etiology
Hypocalcemia Is under feedback mechanism
180
Tertiary parathyroidism etiology
Chronic secondary parathyroidism leads to autonomy of parathyroid gland and leads to tertiary parathyroidism PTH is not under negative feedback
181
Laboratory diagnosis of hyperparathyroidism
Increase serum calcium Decreased serum phosphate Increased PTH Increased alkaline phosphate Increased phosphoresis 24hrs Increased calcimuresis 24hrs
182
Parathyroidism differential diagnosis
Sarcoidosis Hypercalcaemia associated with malignancy Thiazide diuretics
183
Hyperparathyroidism treatment
Surgery
184
Treatment for hypercalcaemia
Rehydration Dialysis Diuretics IV bisphosphonates to inhibit osteoclastic bone resorption IV bisphosphonates (Zoledronic acid)
185
Secondary hyperparathyroidism etiology
Terminal chronic renal failure (hyperphosphataemia) Malabsorption syndrome (hypophosphataemia)
186
Hypoparathyroidism etiology
Destruction of parathyroid gland Developmental disorder Inactive PTH Resistance to PTH Functional disorder in PTH secretion (hypomagnesaemia)
187
Element required for the production of PTH is
Magnesium
188
Symptoms and signs of hpoparathyroidism
Cramps Spasms Stridor Chvostek’s sign Trousseau’s sign Erb’s sign Prolonged QT interval Intracranial calcification (basal ganglia calcification) Cataracts (because of calcification of eye) Mental retardation
189
Chovstek’s sign
Hemifacial contraction (angle of the mouth)
190
Trousseau’s signs
Carpal spasm
191
Erb’s sign
Muscles hyper excitability
192
Hypoparathyroidism treatment
IV calcium Calcitriol Ergocalciferol
193
Cause of cataracts in hypoparathyroidism
Low calcium in aqueous humour and high sodium in it which leads to damage of lens
194
Cause of calcification (intracranial) in hypoparathyroidism
Calcium phosphate product accumulation due to low calcium and high phosphate
195
What are lydig cells
Interstitial cells
196
Lydig cells are stimulated by which hormone
LH
197
Lydig cells secrete
Androstenedione Testosterone
198
What makes up 90% of testis volume
Seminiferous tubules
199
Seminiferous tubules are stimulated by
FSH
200
Sperms are produced and transported via
Seminiferous tubules
201
Spermatozoa are feed by which cells
Sertoli cells
202
Where are sertoli cells located
Walls of seminiferous tubules
203
Inhibin is produced by which cells
Sertoli cells
204
Negative feedback of LH is by
Testosterone
205
Negative feedback of FSH is by
Inhibin
206
In peripheral tissue testosterone is converted to
Dihydrotestosterone (DHT) , more active form
207
In adipose tissue testosterone is converted to
Estradiol
208
Male hypogonadism
Androgen deficiency and affects other organs
209
Hypogonadism can include dysfunction
Endocrine function of testis (androgen production) Exocrine function of testis (sperm production) Or Both
210
Primary hypogonadism
Testis insufficiency
211
Secondary hypogonadism
Hypothalamus and pituitary insufficiency
212
Target organ androgen insensitivity/ resistance
Androgen receptor defect 5 alpha reductase deficiency
213
Congenital Primary hypogonadism etiology
Klinefelter’s syndrome Cryptochidism Noonan’s syndrome Lyedig cell aplasia Bilateral anorchia Myotonic dystrophy Androgen biosynthesis defect
214
Acquired primary hypogonadism etiology
Trauma Inflammation After chemotherapy/ radiation Chronic diseases Narcotics, alcohol Aging
215
Klinefelter’s syndrome
XXY (one extra X chromosome) Causes primary hypogonadism
216
Klinefelter’s syndrome diagnosis
Decreased testosterone Increased LH/ FSH Azoospermia Karyotype of 47, XXY
217
Klinefelter’s syndrome treatment
Testosterone replacement
218
Secondary hypogonadism etiology
Panhypopituitarism Isolated LH deficiency Isolated FSH deficiency LH and FSH deficiency With normal sense of smell With hyposmia or anosmia (Kallmann’s syndrome) Prader willi syndrome Cerebellar ataxia Biologically inactive LH Hyperprolactinemia
219
Kallmann’s syndrome
Genetic disorder Insufficient GnRH from hypothalamus LH and FSH are not produced Greater in males Anosmia
220
Kallmann’s syndrome diagnosis
Decreased testosterone Decreased LH Decreased FSH Olfactory bulb is missing on MRI
221
Kallmann’s syndrome treatment
Testosterone replacement Gonadotropin replacement
222
Ovarian hormones
Estrogen Progesterone Testosterone Anti-mullerian hormone (AMH) Inhibin A and B
223
Main hormone in premenopausal women is
Estradiol
224
Estrogen hormone that increases in pregnancy is
Estriol
225
The main hormone after menopause is
Estrone
226
In women testosterone produced by ovary is converted to
Estradiol
227
Anti mullerian hormone (AMH) function is
Development of ovarian follicles
228
Inhibin A and B function
Regulates FSH release
229
The mean age of menstrual cycle is called
Menarche
230
Two phases of menstrual cycle are
Follicular phase Luteal phase
231
Three phases of endometrium during menstrual cycle
Proliferative Secretory Degenerative
232
Luteolysis occurs if
Pregnancy does not occur
233
Amenorrhea
No menarche by age 16 No menses for more than 3 cycles
234
Physiological amenorrhea
Before puberty During pregnancy During lactation After menopause
235
Pathological amenorrhea
Primary: by age 16 Secondary: no menses for 3 cycles
236
Hypothalamic amenorrhea
GnRH deficiency A.Kallmann’s syndrome (genetic) B.Endocrine causes: Functional hypothalamic amenorrhea Amenorrhea in female athletes Amenorrhea in anorexia nervosa and bulimia C.Anatomical abnormal CNS tumors Sarcoidosis
237
Kallmann’s syndrome
GnRH deficiency Primary amenorrhea Hyposmia
238
Pituitary amenorrhea Genetic causes
Autosomal recessive mutation that causes Decreased FSH LH PRL TSH GH rGnRH FSH mutation that leads to Decreased FSH and E2 Increased LH
239
Pituitary amenorrhea Endocrine and anatomic causes
Hyperprolactinemia Anatomic are Pituitary neoplasm Pituitary destruction

Internal Medicine (5 decks)

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