Endocrinology Flashcards

1
Q

Composition of thyroid follicle

A

follicular cells

colloidal substance inside

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2
Q

Composition of colloid substance in thyroid follicle

A

A glycoprotein called thyroglobulin

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3
Q

Function of thyroglobulin

A

Store thyroids hormones extracellular

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4
Q

Thyroid hormones are the reserves of which amino acid

A

Tyrosine

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5
Q

Why are thyroid hormones bones to pretend carriers in circulation

A

Because they are hydrophobic molecules

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6
Q

Function of thyroid hormones

A

Maintain metabolic homeostasis (Intermediary metabolism, body weights, oxygen requirements, body temperature)

Control of growth , reproduction, differentiation

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7
Q

Names of thyroid hormones

A

Thyroxine T4

3,5,3’ triiodothyronine T3

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8
Q

Which thyroid hormones is secreted in larger amounts

A

T4 (80 µg)

T3 is only 5 µg

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9
Q

Which territories has a greater biological activity than the other one

A

T3 about 10 times more activity 24

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10
Q

Major sources of iodine for thyroid hormone

A

IodiZed salt
Iodated bread
dairy products

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11
Q

Daily requirement of iodide in diet for thyroid hormone

A

75 µg a day (10g of iodated salt )

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12
Q

Steps of iodide cycle

A
Uptake 
 oxidation 
Organification 
coupling 
storage
 release
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13
Q

Iodide uptake

A

Transported from interstitial fluid

Concentrated in epithelial cells through Na/I symporter

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14
Q

Iodide uptake regulation

A

Uptake influenced by TSH and inhibited by perchlorate and thiocyanate

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15
Q

Oxidation of iodide

A

Thyroid peroxidase oxidize iodide and form I2

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16
Q

Iodide organification

A

Thyroid peroxidase helps form Mono-iodotyrosine and then di-iodotyrosine

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17
Q

Coupling of iodide

A

Catalyzed by thyroid peroxidase
2 x diiodotyrosine form T4

1 diiodotyrosine and 1 mono iodiotyrosine (T3)

Requires thyroglobulin for ether o bridges

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18
Q

Iodide storage

A

8000 ug of iodide stored in thyroid

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19
Q

Iodide release

A

Colloid droplets containing thyroglobulin with the hormones fuse with lysosomes

Hydrolysis of content with digestion of thyroglobulin and release of iodinated AA

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20
Q

Iodothyronine deiodinases function

A

Activation and inactivation of thyroid hormones

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21
Q

Types of Iodothyronine deiodinases

A

Type 1 deiodinase

Type 2 deiodinase

Type 3 deiodinase

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22
Q

Type 1 deiodinase

A

Converts t4 to T3 in liver kidney thyroid and brain

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23
Q

Type 2 deiodinase

A

Source of intracellular and circulatory T3

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24
Q

Type 3 deiodinase

A

Inactivation of T3 and t4

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25
Q

Wolf chaikoffs effect

A

Adaption to increase in plasma iodine

Inhibitor of NIS to reduce iodine extraction
Inhibits organification process

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26
Q

Which thyroid hormone is more potent

A

T3 (10x more than t4)

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27
Q

Main source of circulating T3

A

Monodeiodination of t4 (80%)

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28
Q

Transport of thyroid hormones

A

Thyroid binding hormones (70%)

Transthyretin (10% of T4)

Albumin (25% of T3 , 15% T4)

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29
Q

Primary carrier of T4 in CSF

A

Transthyretin

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30
Q

Excretion of thyroid hormones

A

Glucuronidqtion

Excreted via bile into feces

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31
Q

2 mechanisms of control of thyroid hormones synthesis

A

Autorégulation with iodine levels

Hypothalamus and anterior pituitary regulation

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32
Q

TSH action

A

Increases iodide transport into follicular cells

Increases production and iodination of thyroglobulin

Increases endocytosis of colloid form lumen into follicular cells

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33
Q

TSH MOA

A

Bind GPCR in thyroid follicle

Activated Gs
Increase of cAMP and PKA activation .

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34
Q

TSH release regulation

A

Inhibited by thyroid hormone with negative feedback at anterior pituitary ( reduce synthesis of TSH, decrease pituitary receptors for TRH, inhibit TRH synthesis)

Thyrotropin releasing hormone (TRH) released from hypothalamus stimulate release of TSH ( GPCR with IP3 and DAG action )

Dopamine, somatostatin, glucocorticoids inhibits TSH release

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35
Q

Impact of diet on thyroid hormone.

A

High carbohydrates diet increases T3 and metabolic rate ( diet induced thermogenesis)

Low carbohydrates diet decrease T3

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36
Q

Carbohydrate metabolism of T3 and T4

A

Low amount enhance glycogenesis with insulin

Large amount promotes glycogenolysis

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37
Q

Lipid metabolism of T3 and T4

A

Increase fat mobilization and oxidation of fatty acids when high amount

Low amount lead to increased serum cholesterol

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38
Q

Effects of TH on cardiovascular

A

Increase heart rate, contractility, cardiac output

Promote vasodilation , increase blood flow

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39
Q

Th effect on CNS

A

Alterations. In mental state
When small -> sluggish state
When high -> anxiety , nervousness

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40
Q

Th effect on reproductive system

A

Low levels can be linked to infertility

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41
Q

Thyroid hormone action

A

GH, prolactin production and secretion

GH action

Glucose intestinal réabsorption

Increase in mitochondrial oxidative phosphorylation

Enzyme synthesis

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42
Q

Hypothyroidism more common in men or women

A

Women

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43
Q

Hypothyroidism impact in infancy

A

Growth and mental retardation ( cretinism )

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44
Q

Hypothyroidism types

A

Primary
Secondary
Severe generalized hormone resistance

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45
Q

Causes of primary hypothyroidism

A

Endemic iodine deficiency

Destruction of thyroid tissue by surgery or during treatment of hyperthyroidism

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46
Q

Characteristics of primary hypothyroidism

A

Low thyroid hormones with high TSH stimulation

Enlarged goiter due to increased activity

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47
Q

Primary hypothyroidism symptoms

A
Cold intolerance 
Lethargy
 constipation 
slow mental function and motor activity 
weight gain 
decreased appetite 
abnormal menses .m
dry thick skin 
hair loss
 horse voice
 stroke volume and heart rate decreased
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48
Q

Hyper thyroidism more common in men or women

A

Woman

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49
Q

Main causes of hyperthyroidism

A

Graves’ disease which is auto immune

Toxic uni nodular of multi nodular goiter’s or inflammation of thyroid gland

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50
Q

Characteristics of Hyper thyroidism

A

Hi thyroid hormones level

low response of TSH to TRH

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51
Q

Hyperthyroidism symptoms

A
Heat intolerance 
nervousness 
irritability 
emotional instability 
pounding heart
 Fatigue
 weight loss 
increased food ingestion 
increased bowel movements 
abnormal menses
. tachycardia 
atrial arrhythmias
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52
Q

What’s unique feature appear in the Hyperthyroidism

A

Infiltrative ophtalmopathy

Which is protuberance of eyes

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53
Q

Composition of endocrine system

A

Endocrine glands

Hormones

Target organ

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54
Q

Endocrine gland

A

Ductless glands which secrete chemical products in interstitial space to reach circulation

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55
Q

Hormones

A

Chemical products released in very small amounts from cell and exert biological action on target cell

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56
Q

Classic Endocrine organs

A
Hypothalamus
 thyroid gland 
adrenal glands 
ovaries
Pituitary gland 
 parathyroid glands 
 testes
 pancreas
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57
Q

Hormones released by the hypothalamus

A

GHRH (gonadotropin releasing hormone)

CRH( corticotropin releasing hormone)

TRH (thyrotropin releasing hormone)

GnRH (gonadotrophin releasing hormone )

Somatostatin
Dopamin
antidiuretic hormone
oxytocin

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58
Q

Hot hormones released by the thyroid gland

A

T3
T4
Calcitonin

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59
Q

Hormone released by adrenal glands

A
Cortisol 
Aldosterone 
adrenal androgens 
Epinephrine 
norepinephrine
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60
Q

Hormones released by the ovaries

A

Estrogen

progesterone

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61
Q

Hormones released by the pituitary gland

A

Growth hormone
Prolactin
ACTH (adrenocorticotropic hormone)

MSH (mélanocyte stimulating hormone)

TSH (thyroid stimulating hormone )

FSH (follicle stimulating hormone)

LH (luteinizing hormone)

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62
Q

Hormone released by the parathyroid glands

A

Parathyroid hormone

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63
Q

Hormones produced by the pancreas

A

Insulin
glucagon
somatostatin

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64
Q

Hormones released by the testes

A

Testosterone

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65
Q

Possible chemical structure of hormones

A

Proteins
Glycoproteins
steroids
amines

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66
Q

Most Abundant form of hormone

A

Protein glycoproteins

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67
Q

Pathway of protein hormone synthesis and release

A

Sensitized as a pre-prohormone
Converted to prohormone
Packaged in the Golgi apparatus to a hormone
Stored in secretory vesicles
Secreted through exocytosis in the interstitium with a calcium intake gradients

68
Q

What are steroid hormone Derived from

A

Cholesterol

69
Q

What are Amine Hormone derived from

A

Tyrosine

70
Q

Two means of transport of hormones

A

As free hormone

bound to carrier proteins

71
Q

What type of hormone can be transported as free hormone

A

Peptides Protein and glycoprotein

72
Q

What type of four months require carrier proteins

A

Steroid hormone

thyroid hormone

73
Q

Main type of hormone carrier proteins

A

Globulins Synthetized by the liver

74
Q

What factor determines half life of Hormones

A

Binding to carrier proteins which regulates excretion from circulation and dynamic equilibrium

75
Q

What organs are responsible for the inactivation of hormones

A

The liver via bile And kidney

76
Q

What is l Hormone receptor desensitization

A

Decreased response to prolong exposure to Hormone

77
Q

What are or some cases of hormone receptor desensitization

A

Down regulation with sequestration and hormone receptor endocytosis

Inactivation through phosphorylation

Truncation of intracellular signaling

78
Q

What are Some factors controlling hormones

A

Central nervous system through Autonomic centers

Hormonal control with some hormones stimulating or inhibiting release of other hormones

Nutrient or ion regulation like glucose with insulin and glucagon

Negative and positive feedback

79
Q

Name of rhythm of most hormones

A

Circadian rhythm

80
Q

What rythm exist within the circadian rhythm and control cortisol levels

A

Ultradian rythm

81
Q

Two types of neurons which mediates endocrine function

A

Magnocellular (posterior pituitary)

Parvocellular (anterior pituitary)

82
Q

What’s structure connect the pituitary gland to the hypothalamus

A

Pituitary stalk

83
Q

Three parts of pituitary glands

A

Anterior / adenohypophysis
Posterior / neurohypophysis
intermediates / pars intermedia

84
Q

Why if there is disconnection of the pituitary stalk to the hypothalamus only prolactin levels increases

A

PIF ( prolactin releasing inhibiting factor) released normally by hypothalamus is not acting on prolactin anymore

85
Q

All hormones of hypothalamic pituitary axis are pulsation except … ?

A

TRH

86
Q

Sheehan syndrome

A

Occur in pregnancy

Enlargement of pituitary glands which becomes vulnerable to infarction

87
Q

Hypothalamic control of GH

A

GHRH

GHIH/ somatostatin

88
Q

What can increase secretion of growth hormones

A
Sleep 
starvation 
stress 
puberty related hormones
 exercise 
hypoglycemia
89
Q

What can decrease secretion of growth hormone

A
Somatostatin 
Somatomedins
 obesity 
hyperglycemia 
pregnancy
90
Q

Direct Actions of growthhormone

A
Decreases Cellular glucose uptake
Increases lipolysis
Increases Protein synthesis in muscle mass 
increases lean body mass
Increase production of IGF
91
Q

Causes of Laron dwarfism due to deficiency in GH

A

Lack of anterior pituitary GH
hypothalamic dysfunction
D’ailier to generate IGF
GH receptor deficiency

92
Q

Excess GH before puberty

A

Gigantism

93
Q

Excès Gh After oubeeety

A

Acromegaly

94
Q

Adrenal glands different parts

A

Adrenal cortex outer layer

adrenal medulla inner layer

95
Q

Type of hormones secreted in adrenal cortex

A

Steroid hormones

96
Q

Type of steroid hormones found in the adrenal cortex

A

glucocorticoids
mineralocorticood
androgens

97
Q

What Hormone from the pituitary gland triggers secretion of the steroid hormones in the adrenal cortex

A

ACTH

98
Q

Glucocorticoids function

A

Increase glucose level by gluconeogenesis in liver

Increase protein and fats catabolism

Inhibits ACTH secretion

Sensitize arterioles to action of noradrenaline (blood pressure action )

Allow water excretion

Anti-inflammation effects on the body

99
Q

How do you use glucocorticoids in therapy

A

In auto immune disease like rheumatoid arthritis

in transplantations of organs

Control asthma

100
Q

Example of glucocorticoids

A

cortisol

101
Q

How is cortisol transported into the blood

A

Cortisol binding globulin transcortin

102
Q

Rhythm of secretion of cortisol

A

Diurnal -

Highest in the morning lowest at night

103
Q

What time should you take a sample of cortisol levels

A

Between 8 AM to 9 AM

104
Q

Main mineralocorticoid

A

Aldosterone

105
Q

Function of aldosterone

A

Conserve sodium in the kidney help in secretion of potassium and allow water retention to stabilize blood pressure

Increase sensitivity of the taste buds to sources of sodium

Act on sweat glands to reduce less of sodium in perspiration

106
Q

Secretion of aldosterone stimulated by

A

Sodium level drop in blood
Potassium levels rise in blood
Angiotensin II
AC TH in stress condition and in congenital adrenal hyperplasia

107
Q

Type of androgens

A

Androstenedione (A)
Dehydroepiandrosterone (DHEA)
DHEA sulphate

108
Q

At what stage of life do you have a rise in androgens

A

During puberty

109
Q

Disorders of hyper function of adrenal cortex

A
Cushing’s syndrome ( excess cortisol) 
Conns syndrome ( excess aldosterone)
110
Q

What type of people at risk of Cushing’s syndrome

A

Diabetics

111
Q

Causes of Cushing’s syndrome

A

ACTH dépendant

ACTH indépendant

Iatrogenic

112
Q

ACTH dependent Cushing’s syndrome

A

Pituitary hypersécrétion of ACTH
Mostly due to adenoma (60%)
Ectopic ACTH secretion (bronchial cancer)
ACTH therapy

113
Q

AC TH independent Cushing syndrome

A

Excessive production of adrenal hormones themselves

could be due to adenoma, adrenal carcinoma, or in glucocorticoid therapy

114
Q

Iatrogenic causes

A

Google cortical therapy for some other disorder like rheumatoid arthritis or in organ transplants

115
Q

What is the difference between Cushing syndrome and Cushing’s disease

A

Cashing disease means that the pituitary is involved

Cushing’s syndrome when other cause

116
Q

Pseudo Cushing syndrome

A

Patient appear cushingoid

Occur in severe depression and alcoholism

117
Q

Clinical feature of Cushing syndrome

A
Truncal obesity (moon face, protuberant abdomen )
Thinning of skin
Purple stretch marks on the breasts arms abdomen thighs
 excessive bruising 
Hirsutism 
skin pigmentation (elevated ACTH)
hypertension 
Glucose intolerance 
muscle weakness 
menstrual irregularities
 back pain
Psychiatric disturbances
Euphoria 
depression
118
Q

Cushing syndrome biochemistry

A

Hypokalemia
Kaliuresis
Glucose intolerance
Metabolic alkalosis

119
Q

Investigation of Cushing syndrome

A

Initial screening test for Cushing’s syndrome

24h urinary cortisol excretion

Low dose dexamethasone surpression test.

Diurnal rythm of plasma

Insulin hypoglycemia test

120
Q

24 h urinary cortisol excretion test

A

Urine collected over 24h period
Free cortisol measured.

Cushing syndrome excluded if cortisol < 300nmol/24h

Not specific to tell if pseudo Cushing’s syndrome

121
Q

Disorders of hyper function of adrenal cortex

A
Cushing’s syndrome ( excess cortisol) 
Conns syndrome ( excess aldosterone)
122
Q

What type of people at risk of Cushing’s syndrome

A

Diabetics

123
Q

Causes of Cushing’s syndrome

A

ACTH dépendant

ACTH indépendant

Iatrogenic

124
Q

ACTH dependent Cushing’s syndrome

A

Pituitary hypersécrétion of ACTH
Mostly due to adenoma (60%)
Ectopic ACTH secretion (bronchial cancer)
ACTH therapy

125
Q

AC TH independent Cushing syndrome

A

Excessive production of adrenal hormones themselves

could be due to adenoma, adrenal carcinoma, or in glucocorticoid therapy

126
Q

Iatrogenic causes

A

Google cortical therapy for some other disorder like rheumatoid arthritis or in organ transplants

127
Q

What is the difference between Cushing syndrome and Cushing’s disease

A

Cashing disease means that the pituitary is involved

Cushing’s syndrome when other cause

128
Q

Pseudo Cushing syndrome

A

Patient appear cushingoid

Occur in severe depression and alcoholism

129
Q

Clinical feature of Cushing syndrome

A
Truncal obesity (moon face, protuberant abdomen )
Thinning of skin
Purple stretch marks on the breasts arms abdomen thighs
 excessive bruising 
Hirsutism 
skin pigmentation (elevated ACTH)
hypertension 
Glucose intolerance 
muscle weakness 
menstrual irregularities
 back pain
Psychiatric disturbances
Euphoria 
depression
130
Q

Cushing syndrome biochemistry

A

Hypokalemia
Kaliuresis
Glucose intolerance
Metabolic alkalosis

131
Q

Investigation of Cushing syndrome

A

Initial screening test for Cushing’s syndrome

24h urinary cortisol excretion

Low dose dexamethasone surpression test.

Diurnal rythm of plasma

Insulin hypoglycemia test

132
Q

24 h urinary cortisol excretion test

A

Urine collected over 24h period
Free cortisol measured.

Cushing syndrome excluded if cortisol < 300nmol/24h

Not specific to tell if pseudo Cushing’s syndrome

133
Q

Disorders of hyper function of adrenal cortex

A
Cushing’s syndrome ( excess cortisol) 
Conns syndrome ( excess aldosterone)
134
Q

What type of people at risk of Cushing’s syndrome

A

Diabetics

135
Q

Causes of Cushing’s syndrome

A

ACTH dépendant

ACTH indépendant

Iatrogenic

136
Q

ACTH dependent Cushing’s syndrome

A

Pituitary hypersécrétion of ACTH
Mostly due to adenoma (60%)
Ectopic ACTH secretion (bronchial cancer)
ACTH therapy

137
Q

AC TH independent Cushing syndrome

A

Excessive production of adrenal hormones themselves

could be due to adenoma, adrenal carcinoma, or in glucocorticoid therapy

138
Q

Iatrogenic causes

A

Google cortical therapy for some other disorder like rheumatoid arthritis or in organ transplants

139
Q

What is the difference between Cushing syndrome and Cushing’s disease

A

Cashing disease means that the pituitary is involved

Cushing’s syndrome when other cause

140
Q

Pseudo Cushing syndrome

A

Patient appear cushingoid

Occur in severe depression and alcoholism

141
Q

Clinical feature of Cushing syndrome

A
Truncal obesity (moon face, protuberant abdomen )
Thinning of skin
Purple stretch marks on the breasts arms abdomen thighs
 excessive bruising 
Hirsutism 
skin pigmentation (elevated ACTH)
hypertension 
Glucose intolerance 
muscle weakness 
menstrual irregularities
 back pain
Psychiatric disturbances
Euphoria 
depression
142
Q

Cushing syndrome biochemistry

A

Hypokalemia
Kaliuresis
Glucose intolerance
Metabolic alkalosis

143
Q

Investigation of Cushing syndrome

A

Initial screening test for Cushing’s syndrome

24h urinary cortisol excretion

Low dose dexamethasone surpression test.

Diurnal rythm of plasma

Insulin hypoglycemia test

144
Q

24 h urinary cortisol excretion test

A

Urine collected over 24h period
Free cortisol measured.

Cushing syndrome excluded if cortisol < 300nmol/24h

Not specific to tell if pseudo Cushing’s syndrome

145
Q

Low dose dexamethasone suppression test

A

1mg dexamethasone given At night

Blood sample taken next morning

Normal individual have serum cortisol suppressed to less than 50 nmol/l
Failure to suppress suggestive of Cushing syndrome

Not specific

146
Q

Diurnal rythm of plasma

A

Normal patients would have high cortisol in the morning and low Cortisol in the knights

Loss of diurnal variation in patient with Cushing syndrome So cortisol level at night could be raised

Not specific

147
Q

Insulin hypoglycemia test

A

Insulin given IV to lower blood glucose 2.2 mmol/liter

Blood glucose and cortisol measured at 30 45 60 and 90 minutes

Normal patients ( and pseudo Cushing’s) serum cortisol at max at 60 or 90 minutes

patient with Cushing syndrome show little or no response

148
Q

Test used to know the cause of Cushing syndrome

A

Measurement of plasma ACTH

Would be increased or normal in Cushing’s disease

Would be non-detectable in an adrenal tumor

Would be increased or Much increased in Ectopic ACTH secreting tumor

149
Q

What does is use to confirm diagnosis Of Cushing syndrome and it’s cause

A

High dose Dexamethasone suppression test

Cortisol levels decreased to less than 50% in Cushing’s disease

Cortisol level not depressed in adrenal tumor and ectopic ACTH secreting tumor

150
Q

Name of test used to differentiate between Cushing’s disease and ectopic ACTH secretion

A

CRH stimulation test

151
Q

Name of adrenocortical hypofunction disease

A

Addison’s disease

152
Q

Primary Causes of Addison’s disease

A

Destruction of adrenal gland by infection or autoimmune adrenalitis

153
Q

Addison’s disease secondary cause

A

Infiltrative lesion
CAH / Hypoplasia
Inherited mutation in ACTH receptor on adrenal cells

154
Q

Biochemistry of Addison’s disease

A
Hypoglycemia 
Hypomatremia
Hyperkalemia
Raised ureA
Acid base disturbance
155
Q

Clinical features of Addison’s disease

A
Tiredness 
Weakness 
Lethargy
Anorexia
Nausea
Vomiting
Weight loss 
Dizziness 
Pigmentation
Loss of body hair 
Hyperpigmentation when high ACTH (melanocytes stimulating activity)
156
Q

Adrenal crisis

A

Chronic form of adrenal disturbance

Precipitated by stress

157
Q

Clinical symptoms of adrenal crisis

A
High fever 
Dehydration 
Nausea
Vomiting 
Hypotension 
Hypovolaemia 
Hypoglycemic shock 
Hyperkalemia
Hyponatremia 
Hemoconcentration
158
Q

Diagnosis of primary adrenal hypo function

A

Cortisol < 50nmol at 9am

ACTH high because lack of negative feedback

159
Q

Diagnosis of secondary adrenal hypo function

A

Low cortisol and ACTH

160
Q

Conns syndrome

A

Excessive production of aldosterone

161
Q

Conns syndrome causes

A

Adrenal Aldosterone producing adenoma

Diffuse hypertrophy of zona glomerulosa of adrenal cortex

Glucocorticoid remediable aldosteronism

162
Q

Conns syndrome clinical feature

A
Hypokalemia 
Hypertension 
Muscle weakness 
Polydipsia 
Polyuria
163
Q

Biochemistry conns syndrome

A
Hypokalemia 
Kaliuresis
Impaired glucose tolerance 
Metabolic alkalosis
H
164
Q

Diagnosis of conns disease

A

Measure aldosterone , plasma renin activity and do ratio

Very possible if ratio over 2000

165
Q

Confirmatory diagnosis of conns syndrome

A

Saline infusion test (if plasma aldosterone superior to 240 pmol/L)

Posture test