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Internal Medicine > Endocrinology > Flashcards

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
Q

Diabetes insipidus is

A

Complete or partial ADH deficiency

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26
Q

Diabetes insipidus types

A

Central (hypothalamus)
Nephrogenic (kidney)
Transitory (pregnancy)
Primary polydipsia

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27
Q

Diabetes insipidus clinical presentation

A

Polyuria
Polydipsia
Dehydration
Hypoosmotic urine
Plasma hyperosmolality

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28
Q

Central diabetes insipidus causes

A

Tumors
Trauma/surgery
Granulomatosis
Lyphocytic Infundibulo-hypophysitis
Adipsic DI
Cerebral anoxia

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29
Q

Congenital Nephrogenic DI causes

A

mutation of V2 receptor on X chromosome
autosomal recessive mutation of aquaporin 2 water channels

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30
Q

Acquired nephrogenic DI causes

A

Polycystism
Kidney infarction
Sickle cell anemia
Lithium

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31
Q

Transient DI causes

A

Cysteine amino peptidase oxytocinase breaks down oxytosin and ADH

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32
Q

Cystein amino peptidase oxytocinase is produced by

A

Placenta

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33
Q

Primary polydypsia causes

A

Psychiatric patients
Behavioral abnormalities

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34
Q

Diagnosis of DI

A

Disappearance of neurohypophysis signals
Measurement of daily fluid intake and diuresis
Thirst test

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35
Q

Urine osmolality in DI is

A

Less than 200 mosmol/l

Normal is greater than 800 mosmol/l

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36
Q

Plasma osmolality in DI

A

Greater than 285-295 mosmol/l

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37
Q

Differential diagnosis of DI

A

Osmotic diuresis in hyperparathyroidism,
Diabetes melittus
Psychogenic polydipsia
Nephrogenic DI (hereditary)
Polyuretic phase in chronic renal injury

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38
Q

Nephrogenic DI test

A

Desmopressin test

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39
Q

Theraphy for DI

A

Synthetic ADH analog (Minirin)

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40
Q

Anterior pituitary hormones

A

PRL
FSH
LH
TSH
ACTH
MSH (Melanocyte Stimulating Hormone)
STH (somatotropin)

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41
Q

Posterior pituitary hormones

A

ADH
Oxytosin

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42
Q

Pituitary gland diseases

A

Hypo pituitarism
Pituitary Adenomas
Prolactinoma
Acromegaly and gigantism
ACTH adenoma (cushings disease)
TRH adenoma
Gonadotropin adenoma
Non functioning adenoma

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43
Q

Hypopituitarism causes

A

After tumor surgery
Sheehans syndrome

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44
Q

Sheehans syndrome

A

Pituitary necrosis because of extreme blood loss during child birth

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45
Q

Hypopituitarism therapy

A

TSH deficiency - thyroxine
ACTH deficiency - hydrocortisone
STH deficiency - growth hormone

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46
Q

Prolactinoma clinical presentation

A

Female:
Menstrual cycle disorders
Sterility
Galactorrhoea

Male:
Galactorrhoea
Gynacomastia
Low libido
Low spermatogenesis
Low potency

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47
Q

Prolactinoma therapy

A

Dopamine agonists (Bromocriptin, cabergoline)
Surgery

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48
Q

Acromegaly clinical presentation

A

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

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49
Q

Acromegaly and gigantism causes

A

Bitemporal hemianopia

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50
Q

Acromegaly and gigantism therapy

A

1st gen Octreotide - somatostatin analog
2nd gen pasireotide
Dopamine agonist
Radiation

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51
Q

Cushing’s disease clinical presentation

A

Facies lunata
Osteoporosis
Myopathy
Fatigue
Depression
Purple stripes
Skin atrophy, sufusion
Thrombosis
Lower extremities swelling
Secondary hypertension, DM
Decreased libido
Menstrual cycle disorders

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52
Q

Cushings disease diagnosis

A

Increased free cortisol in urine in 24hrs
Lack of cortisol at night (loss of circadian rhythm)
Lack of cortisol suppression after 1mg of dexamethasone

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53
Q

Cushings disease treatment

A

Surgery

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54
Q

Diabetes mellitus is acute or chronic

A

Chronic

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55
Q

Diabetes mellitus is characterised by

A

Persistent hyperglycemia

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56
Q

Persistent hyperglycemia in DM is due to

A

Impaired insulin secretion
Resistance to insulin

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57
Q

Types of DM

A

Type 1
Type 2
Gestational DM
Secondary DM

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58
Q

Etiology of DM type 2

A

Genetic and environment

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59
Q

Hyperglycemia causes

A

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)

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60
Q

Incretin

A

Gastric Inhibitory Polypeptide (GIP)
Glucagon Like Peptide 1 (GLP1)

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61
Q

Insulin resistance in liver leads to

A

Increased fasting plasma glucose

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62
Q

Insulin resistance in muscles leads to

A

High postprandial glucose

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63
Q

Increased insulin production by Beta cells leads to

A

Progressive beta cells failure

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64
Q

Insulin resistance in adipose tissue leads to

A

Increased free fatty acids in plasma due to increased lipolysis
Decreased lipogenesis
Decreased glucose uptake

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65
Q

INCRETIN abbreviation

A

Intestine Secretion Insulin

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66
Q

Alpha cells in DM type 2

A

It produces more glucagon and increases post prandial glucose level in blood

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67
Q

Glucose reabsorption takes place in which part of kidney tubules

A

PCT

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68
Q

The transporters that take part in glucose absorption in kidneys are

A

SGLT-2 (90%)
SGLT-1 (10%) (straight descending part of PCT)

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69
Q

Brain insulin resistance

A

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

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70
Q

Diabetes Mellitus clinical features

A

Polyuria
Polydipsia
Polyphagia

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71
Q

Diabetes mellitus signs

A

Kussmaul’s breathing because of metabolic ketoacidosis
Dehydration
Weigt loss
Altered level of consciousness
Acute coronary disease
Stroke
Kidney disease
Vision loss
Diabetic foot

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72
Q

Diabetes Mellitus diagnosis
Free Plasma Glucose while fasting is

A

Greater than 7 mmol/l is diabetic

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73
Q

Fasting is

A

No calorie intake for 8 hours or more

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74
Q

Glycated hemoglobin HbA1C for adults is

A

Greater than 6.5% is diabetic

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75
Q

2hPG in a 75g OGTT is

A

Greater than 11.1 mmol/l is diabetic

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76
Q

2hPG is

A

2 hour post prandial or 2hr plasma glucose

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77
Q

Random PG is

A

Greater than 11.1 mmol/l is diabetic

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78
Q

75g OGTT for GDM is diabetic when it exceeds

A

Fasting : 5.1 mmol/l (92 mg/dl)
1 h : 10 mmol/l (180 mg/dl)
2h : 8.5 mmol/l (153 mg/dl)

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79
Q

Microvascular chronic complications of DM

A

Retinopathy, cataract, glaucoma
Nephropathy
Neuropathy

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80
Q

Macrovascular chronic complications of diabetes

A

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

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81
Q

Drugs used to treat diabetes

A

Metformin
Sulfonylureas
Thiazolidinediones
Insulin

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82
Q

Incretin based drugs

A

Dipeptidyl Peptidase-4 (DPP-4) inhibitors
Glucagon like peptide-1 (GLP-1) Analogues

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83
Q

Co transporter inhibitors

A

Sodium Glucose Cotransporter-2 (SGLT-2) inhibitors

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84
Q

More diabetes drugs

A

Alpha glucosidase inhibitors
Metiglinide analogues
Pramlintide

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85
Q

Diabetics have increased risk of

A

Cardiovascular
Peripheral vascular
Cerebro vascular diseases

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86
Q

DM type 1 is

A

Absolute insulin deficiency because of Beta cell damge in pancreas

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87
Q

Which diabetes is autoimmune

A

Type 1 DM

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88
Q

Osmotic diuresis means

A

Glucose attracts water so more glucose in kidney tubules leads to Polyuria

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89
Q

Blurring of vision in diabetes is caused by

A

Accumulation of glucose in eye vessels and leads to inflammation because of hyperosmotic condition

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90
Q

Amino acids are converted to what in diabetes during chronic weight loss

A

Glucose and ketone bodies

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91
Q

Hyperglycemia leads to a condition that affects peripheral nerves called

A

Paraesthesia

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92
Q

Insulin drugs

A

Insulin lyspro
Insulin aspart
Insulin glulisin
Insulin glargin
Insulin detemir

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93
Q

Questions that are asked during examination

A

Current symptoms
Life history
Family history
Pharmacotherapy history

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94
Q

Examination

A

Examination by systems

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95
Q

After examination things to be done are

A

Give conclusion diagnosis
Laboratory diagnosis
Instrumental tests

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96
Q

Types of symptoms

A

General symptoms
Specific symptoms

97
Q

Cerbral complication of DKA is

A

Cerebral edema

98
Q

Sudden drop in serum osmolality leads to

A

Edema and other complications like dehydration because of Polyuria

99
Q

Diabetic Keto Acidosis and Hyperosmolar Hyperglycemic State can lead to decreased

A

Serum Potassium

100
Q

Adrenal cotex layers

A

Zona glomerulosa (outer)
Zona fasciculata (middle)
Zona reticularis (inner)

101
Q

Zona glomerulosa secretes

A

Minerelocorticoids

102
Q

Zona fasciculata secrets

A

Glucocorticoids

103
Q

Zona reticularis secretes

A

Adrenal Androgens

104
Q

Minerelocorticoids example

A

Aldosterone

105
Q

Glucocorticoids example

A

Cortisol

106
Q

Adrenal androgens example

A

Androstenedione
DHEA
DHEAS

107
Q

Which layer of adrenal cortex is predominantly under the control of ACTH

A

Zona fasciculata
Zona reticularis

108
Q

Which layer of adrenal cortex is predominantly under the control of Renin Angiotensin Aldosterone System

A

Zona glomerulosa

109
Q

Adrenal cortex hormones are circulated in blood stream bound to?

A

Plasma protiens (globulins)

110
Q

Adrenal cortex hormones are broken down in

A

Liver and excreted via kidneys

111
Q

Cushing syndrome is chronic hypersecretion of

A

Glucocorticoid (cortisol)
And also maybe androgens

112
Q

Etoiology of cushing’s disease is

A

ACTH dependent:
Ectopic ACTH
Pituitary adenoma

113
Q

Etiology of cushing syndrome

A

ACTH independent:
Adrenal adenoma
Adrenal carcinoma
Nodular hyperplasia

114
Q

ACTH is elevated in

A

Ectopic ACTH secretion
And little elevation in pituitary tumor of adenohypophysis

115
Q

ACTH is suppressed in

A

Adrenal carcinoma or adenoma
Or maybe in nodular hyperplasia

116
Q

Cushings disease clinical picture

A

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
Q

Hypertension in cushing disease is by

A

Increased vascular tone by cortisol
And also by renal sodium absorption

118
Q

Osteoporosis in cushing disease is caused by

A

Increased calcium elimination by kidney due to cortisol elevation and compensatory increased activity of parathyroid gland

119
Q

Diagnosis of cushings disease are

A

Urine 24 hr
Elevated steroid metabolites in urine
Elevated plasma cortisol
MRI
CT
UZ

120
Q

Differential diagnosis of cushings

A

Dexamethasone 1mg suppression test

121
Q

Hyperaldosteronism types

A

Primary and
Secondary

122
Q

Primary hyperaldosteronism is

A

Increased aldosterone without RAAS increase

123
Q

Secondary aldosteronism is

A

Increase in aldosterone with RAAS increase

124
Q

Primary hyperaldosteronism

A

Conns syndrome
Adrenal tumor
Glucocorticoid suppressed hyperaldosteronism

125
Q

Pathogenesis of hyperaldosteronism

A

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
Q

Nephrogenic diabetes in hyperaldosteronism is caused by

A

Hypokalemia

127
Q

Laboratory diagnosis of primary hyperaldosteronism

A

Decreased serum potassium
Increased K in urine
Renin decreased in plasma even after volume depletion

128
Q

Treatment of primary aldosterone

A

Spironolactone

129
Q

Secondary hyperaldosteronism is caused by

A

Renal artery stenosis
Liver cirrhosis
Congestive Heart Failure
Nephrotic syndrome
Renin secreting tumor

130
Q

What is primary adrenal cortical insufficiency

A

Addison’s disease

131
Q

Addison’s disease etiology

A

Autoimmune adrenalitis
Cortical atrophy
Amyloidosis
Hemochromatosis
Infection (TB, fungal infection, AIDS)

132
Q

When do we find clinical manifestation in addison’s disease

A

After 90% cortical damage

133
Q

Clinical signs of addison’s disease

A

Anorexia
Weakness
Hyperpigmentation except palms and soles
Hypotension
Vomiting pain diarrhoea (GIT symptoms)
May cause hypoglycemia
Menstrual disorders

134
Q

Addison’s laboratory diagnosis

A

Hyponatremia
Hyperkalemia
Normocytic anemia
Esnophilia
Low plasma and urine cortisol
Low DHEA
Low aldosterone
ACTH elevated

135
Q

Diseases of hyperpigmentation

A

Hemochromatosis
Wilson’s hepatolenticular degeneration
Multiple polyposis
Progressive cachexia (anorexia nervosa, malignancy)

136
Q

Addison’s disease treatment

A

Substitution therapy
Hydrocortisone
Fludrocortisone

137
Q

Secondary adrenocortical insufficiency etiology

A

ACTH deficiency
Chronic use of corticosteroids
After pituitary surgery in cushings disease

138
Q

Clinical signs of secondary adrenocortical insufficiency

A

No hyperpigmentation
Absence of signs of Minerelocorticoid deficiency

139
Q

Secondary adrenocortical insufficiency laboratory diagnosis

A

Low ACTH along with low cortisol

140
Q

Acute adrenocortical insufficiency etiology

A

Insufficient substitution
Haemorrhage in adrenal cortex due to anticoagulant therapy or infection or coagulation disorder
Discontinuation of glucocorticoid therapy

141
Q

Acute adrenocortical insufficiency signs

A

Shock
Hypotension
High fever
Acute abdomen
Coma
Cyanosis
Petechial haemorrhage
Haemorrhage

142
Q

Acute adrenal insufficiency laboratory diagnosis

A

Hyponatremia
Hyperkalemia
Hypoglycemia
Azotemia
Esnophilia
Dexamethasone does not help in hormonal findings
Low cortisol

143
Q

Acute adrenocortical insufficiency treatment

A

Volume compensation by IV fluid
Hormone replacement

144
Q

Adrenal medulla origin

A

The sympathetic nervous and adrenal medulla have same ectodermal origin

145
Q

The hormones secreted by adrenal medulla are

A

Epinephrine and
Nor epinephrine

146
Q

Epinephrine and nor epinephrine are

A

Catecholamines (Amines)

147
Q

Adrenaline is secreted in

A

Adrenal medulla

148
Q

Nor adrenaline is secreted in

A

Post ganglionic sympathetic nerve endings and to a lesser extent in adrenal medulla

149
Q

Epinephrine and nor epinephrine are broken down in ________and entered via _____________

A

Liver and excreted by kidneys

150
Q

Pheochromocytoma

A

It is a catecholamine secreting tumor of adrenal medulla

151
Q

Methylation of nor adrenaline to adrenaline is by

A

Phenylethanolamine N methyl transferase (PNMT)

152
Q

Methylation of nor adrenaline to adrenaline is dependent on

A

Cortisol

153
Q

More nor adrenaline is secreted by

A

Large tumours

154
Q

Smaller tumours have corticomedullary blood supply so they secrete more

A

Cortisol and large PNMT activation

155
Q

Extradrenal tumours secrete only

A

Nor epinephrine

156
Q

Pheochromocytoma clinical signs

A

Hypertension
Paroxysms like
Palness redness
Palpitaion
Sweating
Headache

157
Q

Diagnosis of pheochromocytoma

A

Catecholamines and metabolites in the urine
Plasma catecholamines
Functional tests
CT
MRI

158
Q

Level of glucagon in pheochromocytoma is

A

Increased

159
Q

Adrenogenital syndrome

A

Increased secretion of DHEA and androstenedione in adrenal cortex that are extraadrenally converted to testosterone

160
Q

Congenital adrenal hyperplasia

A

Hereditary deficiency of an enzyme (21 hydroxylase) necessary for synthesis adrenocorticorticosteroids especially cortisol

161
Q

The main regulatory factor for synthesis of ACTH and CRH is

A

Cortisol

162
Q

When there is increased secretion of cortisol there is also increased secretion of

A

Adrenal androgens

163
Q

21 hydroxylase deficiency is

A

Complete
Incomplete

164
Q

Complete deficiency of 21 hydroxylase is

A

Cortisol and aldosterone deficiency

165
Q

Incomplete 21 hydroxylase deficiency is

A

Only cortisol deficiency

166
Q

CAH complications during puberty in children

A

Isosexual precocious puberty in boys and
Heterosexual precocious puberty in girls

167
Q

Signs of CAH in girl during birth is

A

Female pseudohermaphroditism
Fused labia
Persistent urogenital sinus
Developed clitoris

168
Q

In adulthood in CAH signs are

A

Hirsutism
Menstrual disorder
Virilization

169
Q

CAH diagnosis

A

Elevated DHEA, DHEAS and androstenedione in serum
Low cortisol
High ACTH

170
Q

CAH therapy is

A

Corticosteroids to suppress ACTH

171
Q

Virilization

A

Increased muscle mass
Clitomegaly
Deep voice
Breast atrophy
and Hirsutism

172
Q

Hirsutism vs hypertrichosis

A

Hirsutism is androgen dependent hair growth in male pattern

Hypertrichosis is androgen independent hair growth

173
Q

Effects of triiodothyronine (T3)

A

Increased tissue thermogenesis
Decreased systemic vascular resistance
Increased cardiac inotropy and chronotropy

174
Q

Parathyroid gland location and number

A

Behind thyroid gland and there are 4 of them

175
Q

Parathyroid gland action on bone

A

Bone resorption increases serum calcium and decrease phosphorus because of excretion of phosphorus in urine

176
Q

Parathormone action on kidneys

A

Increased reabsorption of calcium in kidney tubules and
Increases production of vitamin D

177
Q

Parathormone action on intestine

A

Increased calcium absorption

178
Q

Primary parathyroidism etiology

A

Hyperplasia
Carcinoma
Solitary adenoma

179
Q

Secondary parathyroidism etiology

A

Hypocalcemia
Is under feedback mechanism

180
Q

Tertiary parathyroidism etiology

A

Chronic secondary parathyroidism leads to autonomy of parathyroid gland and leads to tertiary parathyroidism

PTH is not under negative feedback

181
Q

Laboratory diagnosis of hyperparathyroidism

A

Increase serum calcium
Decreased serum phosphate
Increased PTH
Increased alkaline phosphate
Increased phosphoresis 24hrs
Increased calcimuresis 24hrs

182
Q

Parathyroidism differential diagnosis

A

Sarcoidosis
Hypercalcaemia associated with malignancy
Thiazide diuretics

183
Q

Hyperparathyroidism treatment

A

Surgery

184
Q

Treatment for hypercalcaemia

A

Rehydration
Dialysis
Diuretics
IV bisphosphonates to inhibit osteoclastic bone resorption
IV bisphosphonates (Zoledronic acid)

185
Q

Secondary hyperparathyroidism etiology

A

Terminal chronic renal failure (hyperphosphataemia)
Malabsorption syndrome (hypophosphataemia)

186
Q

Hypoparathyroidism etiology

A

Destruction of parathyroid gland
Developmental disorder
Inactive PTH
Resistance to PTH
Functional disorder in PTH secretion (hypomagnesaemia)

187
Q

Element required for the production of PTH is

A

Magnesium

188
Q

Symptoms and signs of hpoparathyroidism

A

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
Q

Chovstek’s sign

A

Hemifacial contraction (angle of the mouth)

190
Q

Trousseau’s signs

A

Carpal spasm

191
Q

Erb’s sign

A

Muscles hyper excitability

192
Q

Hypoparathyroidism treatment

A

IV calcium
Calcitriol
Ergocalciferol

193
Q

Cause of cataracts in hypoparathyroidism

A

Low calcium in aqueous humour and high sodium in it which leads to damage of lens

194
Q

Cause of calcification (intracranial) in hypoparathyroidism

A

Calcium phosphate product accumulation due to low calcium and high phosphate

195
Q

What are lydig cells

A

Interstitial cells

196
Q

Lydig cells are stimulated by which hormone

A

LH

197
Q

Lydig cells secrete

A

Androstenedione
Testosterone

198
Q

What makes up 90% of testis volume

A

Seminiferous tubules

199
Q

Seminiferous tubules are stimulated by

A

FSH

200
Q

Sperms are produced and transported via

A

Seminiferous tubules

201
Q

Spermatozoa are feed by which cells

A

Sertoli cells

202
Q

Where are sertoli cells located

A

Walls of seminiferous tubules

203
Q

Inhibin is produced by which cells

A

Sertoli cells

204
Q

Negative feedback of LH is by

A

Testosterone

205
Q

Negative feedback of FSH is by

A

Inhibin

206
Q

In peripheral tissue testosterone is converted to

A

Dihydrotestosterone (DHT) , more active form

207
Q

In adipose tissue testosterone is converted to

A

Estradiol

208
Q

Male hypogonadism

A

Androgen deficiency and affects other organs

209
Q

Hypogonadism can include dysfunction

A

Endocrine function of testis (androgen production)
Exocrine function of testis (sperm production)
Or Both

210
Q

Primary hypogonadism

A

Testis insufficiency

211
Q

Secondary hypogonadism

A

Hypothalamus and pituitary insufficiency

212
Q

Target organ androgen insensitivity/ resistance

A

Androgen receptor defect
5 alpha reductase deficiency

213
Q

Congenital Primary hypogonadism etiology

A

Klinefelter’s syndrome
Cryptochidism
Noonan’s syndrome
Lyedig cell aplasia
Bilateral anorchia
Myotonic dystrophy
Androgen biosynthesis defect

214
Q

Acquired primary hypogonadism etiology

A

Trauma
Inflammation
After chemotherapy/ radiation
Chronic diseases
Narcotics, alcohol
Aging

215
Q

Klinefelter’s syndrome

A

XXY (one extra X chromosome)
Causes primary hypogonadism

216
Q

Klinefelter’s syndrome diagnosis

A

Decreased testosterone
Increased LH/ FSH
Azoospermia
Karyotype of 47, XXY

217
Q

Klinefelter’s syndrome treatment

A

Testosterone replacement

218
Q

Secondary hypogonadism etiology

A

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
Q

Kallmann’s syndrome

A

Genetic disorder
Insufficient GnRH from hypothalamus
LH and FSH are not produced
Greater in males
Anosmia

220
Q

Kallmann’s syndrome diagnosis

A

Decreased testosterone
Decreased LH
Decreased FSH
Olfactory bulb is missing on MRI

221
Q

Kallmann’s syndrome treatment

A

Testosterone replacement
Gonadotropin replacement

222
Q

Ovarian hormones

A

Estrogen
Progesterone
Testosterone
Anti-mullerian hormone (AMH)
Inhibin A and B

223
Q

Main hormone in premenopausal women is

A

Estradiol

224
Q

Estrogen hormone that increases in pregnancy is

A

Estriol

225
Q

The main hormone after menopause is

A

Estrone

226
Q

In women testosterone produced by ovary is converted to

A

Estradiol

227
Q

Anti mullerian hormone (AMH) function is

A

Development of ovarian follicles

228
Q

Inhibin A and B function

A

Regulates FSH release

229
Q

The mean age of menstrual cycle is called

A

Menarche

230
Q

Two phases of menstrual cycle are

A

Follicular phase
Luteal phase

231
Q

Three phases of endometrium during menstrual cycle

A

Proliferative
Secretory
Degenerative

232
Q

Luteolysis occurs if

A

Pregnancy does not occur

233
Q

Amenorrhea

A

No menarche by age 16
No menses for more than 3 cycles

234
Q

Physiological amenorrhea

A

Before puberty
During pregnancy
During lactation
After menopause

235
Q

Pathological amenorrhea

A

Primary: by age 16
Secondary: no menses for 3 cycles

236
Q

Hypothalamic amenorrhea

A

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
Q

Kallmann’s syndrome

A

GnRH deficiency
Primary amenorrhea
Hyposmia

238
Q

Pituitary amenorrhea
Genetic causes

A

Autosomal recessive mutation that causes
Decreased
FSH
LH
PRL
TSH
GH

rGnRH
FSH mutation that leads to
Decreased FSH and E2
Increased LH

239
Q

Pituitary amenorrhea
Endocrine and anatomic causes

A

Hyperprolactinemia

Anatomic are
Pituitary neoplasm
Pituitary destruction

Internal Medicine (5 decks)

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