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ENDOCRINOLOGY

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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

CONTENTS
GENERAL FEATURES OF ENDOCRINOLOGY ................................................................................................................... 7
PHYSIOLOGY OF ENDOCRINOLOGY ............................................................................................................................... 7
FEATURES OF PHYSIOLOGY OF ENDOCRINOLOGY .................................................................................................... 7
SECOND MESSENGERS .............................................................................................................................................. 7
RECEPTORS PHYSIOLOGY .......................................................................................................................................... 8
LOCATION OF RECEPTORS ........................................................................................................................................ 9
GROUP I LIPOPHILIC RECEPTORS ............................................................................................................................ 10
GROUP II HYDROPHILIC HORMONES (BIND TO CELL MEMBRANE) ........................................................................ 10
G PROTEIN COUPLED RECEPTOR............................................................................................................................. 10
NITRIC OXIDE........................................................................................................................................................... 11
PITUITARY GLAND ....................................................................................................................................................... 12
DEVELOPMENT OF PITUITARY GLAND .................................................................................................................... 12
ANATOMY OF PITUITARY GLAND ............................................................................................................................ 12
PHYSIOLOGY OF PITUITARY GLAND ........................................................................................................................ 13
GROWTH HORMONE .............................................................................................................................................. 14
GIGANTISM ............................................................................................................................................................. 14
ACROMEGALY ......................................................................................................................................................... 14
DWARFISM .............................................................................................................................................................. 15
PROLACTIN .............................................................................................................................................................. 15
HYPERPROLACTINEMIA ........................................................................................................................................... 15
PITUITARY TUMOURS.............................................................................................................................................. 16
PITUITARY APOPLEXY .............................................................................................................................................. 16
SHEEHAN SYNDROME ............................................................................................................................................. 17
SYNDROME OF INAPPROPRIATE SECRETION OF ADH ............................................................................................. 17
DIABETES INSIPIDUS ................................................................................................................................................ 18
POLYURIA ................................................................................................................................................................ 18
THYROID GLAND ......................................................................................................................................................... 19
DEVELOPMENT OF THYROID ................................................................................................................................... 19
ANATOMY OF THYROID .......................................................................................................................................... 19
PHYSIOLOGY OF THYROID ....................................................................................................................................... 19
THYROID HORMONES ............................................................................................................................................. 20
HYPERTHYROIDISM ................................................................................................................................................. 20

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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

HYPOTHYROIDISM .................................................................................................................................................. 21
CRETINISM .............................................................................................................................................................. 22
STRUMA OVARY ...................................................................................................................................................... 22
THYROTOXICOSIS .................................................................................................................................................... 22
GRAVES DISEASE .................................................................................................................................................... 23
GOITRE .................................................................................................................................................................... 23
PENDRED SYNDROME ............................................................................................................................................. 24
THYROIDITIS ............................................................................................................................................................ 24
HASHIMOTOS THYROIDITIS .................................................................................................................................... 25
DE QUERVAIN THYROIDITIS .................................................................................................................................... 25
THYROID NODULE ................................................................................................................................................... 25
MALIGNANCY OF THYROID GLAND ......................................................................................................................... 26
FOLLICULAR CARCINOMA ....................................................................................................................................... 27
PAPILLARY CARCINOMA .......................................................................................................................................... 28
MEDULLARY CARCINOMA ....................................................................................................................................... 29
ANAPLASTIC CARCINOMA ....................................................................................................................................... 29
ANTITHYROID DRUGS.............................................................................................................................................. 30
THYROID SURGERY .................................................................................................................................................. 30
THYROID STORM ..................................................................................................................................................... 31
THYROID IMAGING.................................................................................................................................................. 31
THYROGLOSSAL CYST .............................................................................................................................................. 31
CALCIUM METABOLISM .............................................................................................................................................. 32
GENERAL FEATURES OF CALCIUM METABOLISM ................................................................................................... 32
DEVELOPMENT OF PARATHYROID GLAND .............................................................................................................. 32
ANATOMY OF PARATHYROID GLAND ..................................................................................................................... 32
PHYSIOLOGY OF PARATHYROID GLAND .................................................................................................................. 33
CALCIUM ................................................................................................................................................................. 33
PARATHROMONE .................................................................................................................................................... 34
CALCITONIN ............................................................................................................................................................ 34
HYPERPARATHYROIDISM ........................................................................................................................................ 34
OSTEITIS FIBROSIS CYSTICA ..................................................................................................................................... 35
PARATHYROID HYPERPLASIA .................................................................................................................................. 35
PARATHYROID ADENOMA ...................................................................................................................................... 35
PRIMARY HYPERPARATHYROIDISM ........................................................................................................................ 36
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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

SECONDARY HYPERPARATHYROIDISM ................................................................................................................... 36


TERTIARY HYPERPARATHYROIDISM ........................................................................................................................ 36
HYPOPARATHYROIDISM .......................................................................................................................................... 36
PSEUDOHYPOPARATHYROIDISM ............................................................................................................................ 37
PSEUDOPSEUDOHYPOPARATHYROIDISM ............................................................................................................... 37
VITAMIN D............................................................................................................................................................... 37
VITAMIN D INTOXICATION ...................................................................................................................................... 38
FEATURES OF RICKETS............................................................................................................................................. 38
DIAGNOSIS OF RICKETS ........................................................................................................................................... 39
TREATMENT OF RICKETS ......................................................................................................................................... 39
VITAMIN D RESISTANT RICKETS .............................................................................................................................. 39
OSTEOMALACIA ...................................................................................................................................................... 39
FEATURES OF OSTEOPOROSIS................................................................................................................................. 40
CAUSES OF OSTEOPOROSIS .................................................................................................................................... 40
DIAGNOSIS OF OSTEOPOROSIS ............................................................................................................................... 41
TREATMENT OF OSTEOPOROSIS ............................................................................................................................. 41
HYPERCALCEMIA ..................................................................................................................................................... 42
HYPERCALCEMIC CRISIS .......................................................................................................................................... 43
TUMOUR LYSIS SYNDROME .................................................................................................................................... 43
TETANY .................................................................................................................................................................... 43
DRUGS OF CALCIUM METABOLISM ........................................................................................................................ 44
ENDOCRINE PANCREAS ............................................................................................................................................... 44
GENERAL FEATURES OF ENDOCRINE PANCREAS .................................................................................................... 44
PHYSIOLOGY OF ENDOCRINE PANCREAS ................................................................................................................ 44
NESIDIOBLASTOSIS .................................................................................................................................................. 45
HYPERGLYCEMIA AND HYPOGLYCEMIA .................................................................................................................. 45
CAUSES OF DIABETES MELLITUS ............................................................................................................................. 45
GENERAL FEATURES OF DIABETES MELLITUS ......................................................................................................... 46
TYPES OF DIABETES MELLITUS ................................................................................................................................ 46
TYPES OF MODY ...................................................................................................................................................... 47
DIABETES IN PREGNANCY ....................................................................................................................................... 47
COMPLICATIONS OF DIABETES MELLITUS .............................................................................................................. 48
DIABETIC KETOACIDOSIS ......................................................................................................................................... 48
NON KETOTIC HYPEROSMOLAR COMA ................................................................................................................... 48
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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

JOINT MANIFESTATIONS OF DIABETES ................................................................................................................... 48


EYE MANIFESTATIONS OF DIABETES ....................................................................................................................... 49
RENAL MANIFESTATIONS OF DIABETES .................................................................................................................. 50
DIAGNOSIS OF DIABETES MELLITUS ........................................................................................................................ 50
TREATMENT OF DIABETES MELLITUS...................................................................................................................... 51
ALPHA GLUCOSIDASE INHIBITORS .......................................................................................................................... 51
THIAZOLIDONEDIONES ........................................................................................................................................... 52
BIGUANIDES ............................................................................................................................................................ 52
MEGLITINIDE ........................................................................................................................................................... 53
EXENATIDE .............................................................................................................................................................. 53
SULPHONYLUREAS .................................................................................................................................................. 53
FEATURES OF INSULIN ............................................................................................................................................ 54
TYPES OF INSULIN ................................................................................................................................................... 55
ACTION OF INSULIN ................................................................................................................................................ 55
ADRENAL GLAND......................................................................................................................................................... 56
GENERAL FEATURES OF ADRENAL GLAND .............................................................................................................. 56
ANATOMY OF ADRENAL GLAND ............................................................................................................................. 57
PHYSIOLOGY OF ADRENAL GLAND .......................................................................................................................... 57
ADRENAL TUMOUR ................................................................................................................................................. 58
ADRENAL HYPERPLASIA .......................................................................................................................................... 58
ADRENAL CARCINOMA ........................................................................................................................................... 58
FEATURES OF CUSHING SYNDROME ....................................................................................................................... 59
MANAGEMENT OF CUSHING SYNDROME .............................................................................................................. 59
ECTOPIC ACTH PRODUCTION .................................................................................................................................. 60
FEATURES OF CONN SYNDROME ............................................................................................................................ 60
HYPERALDOSTERONISM ......................................................................................................................................... 60
FEATURES OF ADDISONS DISEASE ......................................................................................................................... 60
MANAGEMENT OF ADDISONS DISEASE ................................................................................................................. 61
WATERHOURSE FRIEDRICHSON SYNDROME .......................................................................................................... 61
GENERAL FEATURES OF CONGENITAL ADRENAL HYPERPLASIA .............................................................................. 61
TYPES OF CONGENITAL ADRENAL HYPERPLASIA .................................................................................................... 62
MANAGEMENT OF CONGENITAL ADRENAL HYPERPLASIA ..................................................................................... 62
GENERAL FEATURES OF STEROID DRUGS ............................................................................................................... 63
INDICATIONS OF STEROIDS ..................................................................................................................................... 64
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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

SIDE EFFECTS OF STEROID DRUGS .......................................................................................................................... 64


NEUROBLASTOMA .................................................................................................................................................. 64
CAUSES OF PHEOCHROMOCYTOMA ....................................................................................................................... 65
FEATURES OF PHEOCHROMOCYTOMA ................................................................................................................... 65
EXTRA ADRENAL PHEOCHROMOCYTOMA .............................................................................................................. 66
DIAGNOSIS OF PHEOCHROMOCYTOMA ................................................................................................................. 66
TREATMENT OF PHEOCHROMOCYTOMA ............................................................................................................... 67
PINEAL GLAND ............................................................................................................................................................ 67
MULTIPLE ENDOCRINE NEOPLASIA ............................................................................................................................. 68
GENERAL FEATURES OF MULTIPLE ENDOCRINE NEOPLASIA .................................................................................. 68
MEN I ...................................................................................................................................................................... 68
MEN IIA ................................................................................................................................................................... 68
MEN IIB ................................................................................................................................................................... 68
POLYGLANDULAR SYNDROME ................................................................................................................................ 69
CARCINOID .................................................................................................................................................................. 69
FEATURES OF CARCINOID ....................................................................................................................................... 69
MANAGEMENT OF CARCINOID ............................................................................................................................... 70
OBESITY ....................................................................................................................................................................... 70
WEIGHT GAIN AND WEIGHT LOSS .............................................................................................................................. 72

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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

KEY TO THIS DOCUMENT


Text in normal font Must read point.
Asked in any previous medical entrance
examinations
Text in bold font Point from Harrisons
text book of internal medicine 18th
edition
Text in italic font Can be read if
you are thorough with above two.

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GENERAL FEATURES OF ENDOCRINOLOGY

ENDOCRINOLOGY

GENERAL FEATURES OF ENDOCRINOLOGY


System favors oscillatory responses
Paracrine regulation
C21
C19
Somatostatin secreted by
Melatonin is secreted by
Endocrine manifestations produced by
Investigation of choice for Primary and Metastatic
Neuroendocrine Tumour (except Insulinoma)
Best imaging modality for neuroendocrinal tumours
Lifelong treatment is necessary in

Positive feedback system


Somatostatin release inhibits Insulin release
Cortisol, Progesterone
Androgen
D cell
Pineal gland
Ketoconazole
Somatostatin Receptor Scintigraphy
Radionucleide scan
Myxedema, Addisons disease, Juvenile diabetes

PHYSIOLOGY OF ENDOCRINOLOGY
FEATURES OF PHYSIOLOGY OF ENDOCRINOLOGY
Hormone synthesized as peptide precursor
NOT a peptide hormone
Which hormone has NO Intracellular Storage
Vasodilator
Hormone NOT acts by increasing protein synthesis

Insulin, PTH, rennin, angiotensin II


Progesterone
Calcitriol
ANP
Vasopressin

SECOND MESSENGERS
Bio organic computer
Transmission of regulatory signals through ECF
NOT an example for transmission of
regulatory signals
Various cells respond differentially to second
messenger because they have
Used for cell signaling
Second messengers are
Secondary messengers
Acts as second messenger
Intraneuronal second messenger
Hormone using phospholipase C as messenger
NOT a second messenger
Production of cAMP from ATP requires
Membrane bound enzyme catalyzing formation of cyclic
AMP from ATP
Membrane bound enzyme that catalyses formation of
cAMP from ATP

Protein kinase and phosphatase


Synaptic signals through neurotransmitters, endocrine
signals through hormones, G protein coupled receptors
Direct contact through gap junctions
Different enzyme composition
NO
Substance that increase or decrease function
cAMP, IP3, DAG, cGMP
Ca++
Calmodulin
Angiotensin II
Guanylate cyclase
Adenyl cyclase
Adenylate cyclase
Adenylate cyclase

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PHYSIOLOGY OF ENDOCRINOLOGY

ENDOCRINOLOGY
cAMP acts through
All known effects of cyclic AMP in eukaryotic cells result
from
Secondary derivative of biologically important
nucleotides
cAMP mediates
cAMP mediates
Decrease in cAMP is caused by
Adenyl cyclase is inhibited by
Cyclic AMP is inactivated by
NOT using cAMP as second messenger
NOT mediated by cAMP
NOT using cAMP as second messenger
cGMP as second messenger for
cGMP act on
Secretion of atrial natriuretic peptide
increases when there is
Cyclic GMP is a second messenger of
Second messenger is produced from
A phosphorylated derivative is acted upon by
Phospholipase C as a part of second messenger system
Substances act to increase release of Ca++ from
endoplasmic reticulum
Calcium release from endoplasmic reticulum is
triggered by
Inositol triphosphate and diacyl glycerol
are derived from

Activation of protein kinase


Activation of protein kinase
Cyclic AMP
Glucagon, LH, FSH
Corticotrophin, Dopamine, Glucagon
Alpha 2 receptor
Somatostatin
Phosphodiesterase
Vasopressin
Estrogen
Vasopressin, Growth hormone
ANP, NO
Atrial natriuretic peptide
Increased in central venous pressure
Insulin
Phosphatidyl Inositol
Phosphatidylinositol
Inositol triphosphate
Inositol triphosphate
Phosphatidyl inositol 4,5 bisphosphate
(PIP2)

RECEPTORS PHYSIOLOGY
Membrane receptor
Intracellular receptor
Intracellular receptor
Steroid receptor superfamily belongs to
Steroid receptor superfamily present in
Lipophilic acting on nuclear receptor
Cytoplasmic receptor
NOT highly specific binding with single
type of nuclear receptor
Acts through tyrosine kinase receptor
Receptors which are transcription factors
Steroids bind to
Binds to steroid receptors
Belongs to steroid receptor super family
Does NOT bind to steroid receptors
Steroid hormone do NOT have attachment site for
Receptors on cell membrane that activates ion channel
after binding with agonists

For specific action, Molecular transport


Mainly on nuclear surface, Steroids act on them
Vitamin D3, Cortisone, Thyroxine, Androgen
Zinc finger motif
Vitamin D3, Thyroxine
Thyroxine
Cortisol
Glucocorticoid
Insulin
Estrogen, glucocorticoids, Vitamin D
Cytosolic receptors and heat shock proteins
Steroids, Transcriptional factors, Steroid response
element
Vitamin D3 receptor, thyroid receptor, retinoid receptor
Transcriptional mediators
Transcription repressors
Nicotinic cholinergic, GABA A receptors

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PHYSIOLOGY OF ENDOCRINOLOGY

ENDOCRINOLOGY
Does NOT act by intracellular receptor
Does NOT have intracellular receptor
NOT have cell surface receptor
Which DOES NOT have Cell membrane receptor
True about receptor action
Operating time of following receptor is in milliseconds
C terminal end of androgen receptor is concerned with
Receptor mediated action NOT seen in
Receptor blocking agent has
Adrenaline, noradrenaline and dopamine acts through
Dopamine, norepinephrine, serotonin all have the
following type of receptors
GABA B is associated with
GH, prolactin and erythropoietin are
associated with
EDF, PGDF and insulin receptors are
associated
Aldosterone receptor NOT present in
Mineralocorticoid receptor NOT found in

Insulin
Adrenaline
Thyroxine
Steroids
Binding sites are non specific and one drug can displace
other
Ligand gated ion channels
Ligand binding
General anesthetics
Increased Affinity for receptor and Intrinsic activity
Seven pass receptor
7 pass receptor
G protein coupled receptor
JAK STAT receptor
Tyrosine kinase receptor
Liver
Liver

LOCATION OF RECEPTORS
Muscarinic receptors

Nicotinic receptors
Alpha adrenergic receptors

Beta adrenergic receptors

Vasopressin receptors
Histamine receptors

Serotonin receptors

M1 gastric glands, M2 AV node, M3


smooth muscle, ocular system, endocrine
glands
Nm neuromuscular junction, Nn
ganglia, adrenal medulla
Alpha 1 vascular smooth muscle,
prostatic urethra, dilator papillae. Alpha
2 blood vessels, brain
Beta 1 heart, JG cells. Beta 2 bronchus,
GIT, bladder, uterus, liver, skeletal muscle
spindle, blood vessles. Beta 3 adipose
tissue, coronary vessels
V1 vascular smooth muscle, platelets. V2
collecting duct. V3 pituitary
H1 smooth muscles and endothelial cells,
H2 parietal cells, H3 CNS, H4 Mast
cells, eosinophils, T cells, dendritic cells
5HT1B/1D constriction of cranial
vessels, 5HT3 vomiting, 5HT4 - peristalsis

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PHYSIOLOGY OF ENDOCRINOLOGY

ENDOCRINOLOGY

GROUP I LIPOPHILIC RECEPTORS


CYTOPLASMIC RECEPTORS
Glucorticoids & Mineralocorticoids
Androgen,Estrogen
Retinoic acid
Vitamin D3 (1,25(OH) 2 D2

NUCLEAR RECEPTORS
Thyroid Hormones

GROUP II HYDROPHILIC HORMONES (BIND TO CELL MEMBRANE)


C-AMP
CRH
FSH
TSH

C-GMP
ANF
NO

LH
Adrenaline
D1 to D5

MSH
ACTH
Alpha 2 adrenergic
Beta adrenergic
Parathromone
V2
Glucagon
HCG
Angiotensin
II(Epithelium)
Somatostatin
Calcitonin
Lipotropin
5HT1
H2
M2

Ca/IP3/DAG
Oxytocin
M1,M3
V1(Vascular smooth
muscle)
GnRH
GHRH
Angiotensin
II(Vascular
&Smooth muscle)
PDGF
Substance P
Gastrin
CCK
TRH
Alpha 1 adrenergic
5HT2
H1

Kinase/Phosphatase
Growth Hormone
Prolactin
Insulin
EGF
FGF
IGF I & II

NGF
PDGF
Erythropietin
M-CSF

G PROTEIN COUPLED RECEPTOR


Small G proteins
G protein

Rab, ras, rho/rac


G channels, Phosphorylase formation, Made up of 3
units, Related to ras oncogene

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PHYSIOLOGY OF ENDOCRINOLOGY

ENDOCRINOLOGY
G protein activation leads to
Metabotropic receptor
G protein coupled receptor is
G protein coupled receptor
In G protein coupled receptor, amino
terminal end faces
In G protein couples receptor, carboxy
terminal end faces
Carboxy terminal end is associated with
Normally GDP is associated with
G protein receptor complex

G protein acts as inhibitory and excitatory because of


difference in
Action of alpha subunit of G protein
If there is Gs alpha sub unit gain of function mutation
Gs
Gi
Gq

Gh

Generation of second messenger


Single sub unit structure, interact with G
protein, effects are for long period
Metabotropic receptor
G proteins act as inhibitory and excitatory because of
difference in alpha subunit
Extracellular side
Cytoplasmic side
Alpha, beta and gamma
Alpha
Interacts with transmembrane domain, GTP to GDP,
Adenyl cylase activation leads to increased CAMP,
Helical structure, Binds to ligand at cell surface
Alpha subunit
Breakdown of GTP to GDP
Increased cAMP
Stimulates adenyl cyclase, increases
protein kinase A. eg beta1 and beta2
Inhibits adenyl cyclase. Example alpha 2
Activates phospholipase C which in turn
increases protein kinase C. example alpha
1
Activates phosphodiesterase. Example
rods and cones

NITRIC OXIDE
Nitric oxide
Nitric oxide
Nitric oxide
Nitric oxide

Molecules from which nitric oxide can be


released in vivo
Endothelial relaxing factor is
EDRF is
Nitric oxide is produced in
Nitric oxide synthase requires
Calcium independent/ inducible nitric oxide synthase
Inducible form of nitric acid synthase is

Free radical, Vasodilator, Oxidizing agent, Catalyst


Vasodilator, Derived from arginine
cGMP, regulate vascular tone, penile erection, low
concentration in cigarette smokers
Formed from L-arginine by NO synthetase, causes
vasodilatation of all vessels, used in portal
hypertension, interacts with Hb, used in erectile
dysfunction, used in pulmonary hypertension, caused
systemic hypotension, Least systemic effect, Better
ventilation perfusion match
Arginine, amyl nitrite, isosorbide dinitrite
Nitric oxide
Nitric oxide
Endothelium
NADPH, FAD, FMN, Heme iron
NOS 2
Macrophage

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PITUITARY GLAND

ENDOCRINOLOGY
present mainly in
Mechanism of action of nitric oxide
Causes release of NO from endothelial cell
Nitric Oxide does NOT act via
Primary action of nitric oxide in gastrointestinal tract
Inhaled gas used to prevent pulmonary artery pressure
in adults and infants
Nitric oxide produces its antiaggregatory action by
increasing levels of
Inhaled gas used to decrease pulmonary artery pressure
in infants and adults
Increasing nitric oxide
Release of NO is associated with

cGMP
ADP, acetylcholine
Membrane bound receptor
Smooth muscle relaxation
Nitric oxide
cGMP
Nitric oxide
Glycerine trinitrate, sodium nitroprusside, hydralazine
Hydralazine, Nitroprusside, Nitroglycerine

PITUITARY GLAND
DEVELOPMENT OF PITUITARY GLAND
Pituitary gland arises from
Adenohypophysis arise from
Anterior Pituitary develops from
Posterior pituitary develops from
Diverticulum from floor of diencephalon
form
Oncocytes are associated with
Oncocytes are NOT seen in

Ectoderm
Roof of Stomodeum
Craniopharyngeal tube, Rathkes Pouch
rd
Floor of 3 ventricle in the region of Infundibulum
Posterior pituitary
Kidney, Salivary glands, endocrine glands
Pineal gland

ANATOMY OF PITUITARY GLAND


Weight of pituitary gland
Pituitary gland
Type of cells in neurohypophysis
Most abundant cells in pituitary
Most earliest cells in pituitary
Most resistant cells in pituitary
Least found cells in Pituitary
Pituitary related to each side by
Pituitary inferiorly related by
Pituitary separated from optic chiasma by
Arterial supply of Pituitary
Endocrine gland having portal circulation
Venous drainage from neurohypophysis is routed
through

600 mg
Situated deep in sella, Sphenoidal air cells lie inferior to
it, Supplied by a branch of internal carotid artery
Pituicytes
Somatotroph
Corticotrophs
Thyrotrophs
Thyrotrophs
Cavernous sinus
Sphenoid air cells
Diaphragmatic sella
Superior & Inferior Hypophyseal artery branch of
Internal Carotid artery
Hypophysis cerebri
Portal vessels to adenohypophysis, Inferior hypophyseal
veins to dural venous sinuses, Capillaries to median
eminence and hypothalamus

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PITUITARY GLAND

ENDOCRINOLOGY
NOT a route of Venous drainage from neurohypophysis
Pituitary bright spot is due to
Herring body
Best view to visualize pituitary fossa on X-ray skull
Best view for detecting sella turcica on X ray
J shaped sella is seen in

Superior hypophyseal veins to ventricular tachycytes


High phospholipid content of posterior pituitary
Posterior pituitary
Lateral skull view
Lateral view
Mucopolysacchroidoses, Achondroplasia, Optic chiasma
glioma, Neurofibromatosis I, Hydrocephalus

PHYSIOLOGY OF PITUITARY GLAND


Pituitary has no control over
Sequence of acquired pituitary hormone loss
FSH & LH are produced by
Acidophilic Cells
Basophilic cells of pituitary secrete
Alpha and beta subunits seen in
ACTH level highest during
Prolactin produced by
Lactation is mediated by
Oxytocin differs from vasopressin at
Vasopressin receptors
Vasopressin acts on
Vasopressin acts by
Vasopressin acts via
Vasopressin is under control of
ADH

Increases ADH secretion


Vasopressin is inhibited by
Administration of exogenous vasopressin does NOT
increase urine osmolality
NOT true about ADH
NOT a function of vasopressin
Deficiency of vasopressin results in
Conivaptan
Selective V1 blocker
Selective V2 blocker
Myoepithelial cells are found in
Factor essential for myoepithelial cell contraction
Ejection of milk from breast
Hormone responsible for stimulating milk let down
reflex
Neurophysin is found in
Initial Investigation for Hyperpituitarism
Septooptic dysplasia is associated with
Obese female, hypertension, chronic headache, normal
pituitary function

Adrenal medulla
GH FSH/LH TSH - ACTH
Anterior Pituitary
Growth hormone, Prolactin
TSH, ACTH, LH
LH, HCG
Early morning
Anterior Pituitary
Prolactin
Position 3 and 8
V1 vascular smooth muscle, V2 collecting duct, V3
anterior pituitary
Intramedullary collecting duct
Water transport across collecting duct
IP3 - DAG
Caudal ventrolateral medulla
Postoperative increase in secretion, Neurosecretion,
Increased secretion when plasma osmolality is high, Act
on distal tubule and increase permeability
Fluoxetine
Alcohol
Renal hyposensitivity to ADH
Increased secretion when plasma osmolality is low
Increasing thirst
Inability of kidney to concentrate urine
Non selective V1 and V2 blocker
Relcavaptan, nelivaptan
Lixivaptan, mozavaptan, tolvaptan
Salivary gland, mammary gland, parotid
Oxytocin
Oxytocin
Oxytocin
Oxytocin
Serum IGF-1
HESX1 gene
Empty sella syndrome

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PITUITARY GLAND

ENDOCRINOLOGY
MC endocrinal abnormality associated
with empty sella
Transection of pituitary stalk
NOT occur after transection of pituitary stalk

No abnormality
Diabetes insipidus, hyperprolactinemia, hypothyroidism
Diabetes mellitus

GROWTH HORMONE
Somatomedin mediates
Most physiological effects of growth hormone mediated
by
NOT a neurotransmitter
Anabolic action of protein is mediated by
Potent stimulator of growth hormone
Growth hormone secretion inhibited by
9 year old boy, growth retardation propensity to
hypoglycemia. Short stature, micropenis, increased fat
and high pitched voice. Bone age 5 years.
Growth hormone deficiency is associated with
Deficiency of growth hormone
Insulin provocative test is useful in differentiation of
short stature as a result of
TRH stimulation test is useful in diagnosis of disorders
of
Tests for growth hormone
Laron syndrome
Growth hormone releasing factor
(GRFoma)

Deposition of chondroitin sulphate


Somatomedin
Somatomedin
Growth hormone
Arginine
Hyperglycemia
Growth hormone deficiency

Obesity, micropenis, doll like facies


Proportionate dwarfism, Symptomatic hypoglycemia,
Delayed tooth eruption, Sexual infantilism
Hypopituitarism
Growth hormone
L-arginine test, L-dopa test
Growth hormone insensitivity, growth failure
Lung

GIGANTISM
Gigantism occur in
NOT a feature of gigantism

Enuch
Mental retardation

ACROMEGALY
MC cause of Acromegaly
Acromegaly is due to excess of
Depressed nasal bridge NOT seen in
Hypoglycemia is NOT a feature of
Paradoxical response to GH release to TRH is seen in
Heel pad thickness is increased in
MC cause of increased heel pad thickness
Acromegaly is associated with
Confirmatory investigation for acromegaly
TRH stimulating test useful in diagnosing

GH Producing pituitary adenoma


Growth hormone
Acromegaly
Acromegaly
Acromegaly
Acromegaly
Heel injury
Increased GH, somatomedin C
Glucose induced GH suppression
Acromegaly, Hyperthyroidism

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PITUITARY GLAND

ENDOCRINOLOGY
Serum IGF-1 test for
Drug of choice in acromegaly
Drug used for Acromegaly
True about Octreotide
Long acting octreotide
Side effect of octreotide
NOT true about octreotide
Octreotide NOT used in
Octreotide NOT used in
NOT true about octreotide

Acromegaly
Octreotide
Pegvisomant (GRH receptor Antagonist)
Used in secretory diarrhea
Sandostatin
Delays gall bladder emptying
An absorbent
Glioma
Glucoganoma
Effective orally

DWARFISM
Etiology of Nutritional dwarfism
Disproportionate Dwarfism

Chronic malnutrition
Hypothyroidism

PROLACTIN
Prolactin is secreted by
Only hormone for which no stimulator has been
isolated
Normal prolactin level
Normal prolactin level in a woman of reproductive age
Milk production

Increased prolactin associated with


Prolactin
TRH stimulates release of
Hyperprolactinemia is associated with
Prolactin secretion is increased by
Prolactin secretion NOT increased by
Hormone secretion inhibited by Dopamine
Prolactin secretion of decreased by
Secretion of prolactin affected by
Prolactin antagonist
Prolactin secretion inhibited by
Secretion of prolactin affected by
Prolactin deficiency is tested by

Anterior Pituitary
Prolactin
10 25 microgram/L
25 ng/ml
Secretion by contraction of lactiferous sinus,
Neuroendocrine part of posterior pituitary is involved,
Oxytocin involved, Affected by emotion
Increased estradiol
Decreases gonadotrophin action
TSH, GH, Prolactin
Amenorrhoea, Galactorrhea, Infertility
Chlorpromazine
Dopamine
Prolactin
L- DOPA, Bromocriptine
Dopamine
Dopamine
Bromocriptine
Dopamine
TSH test

HYPERPROLACTINEMIA
Causes of Hyperprolactinoma
Hyperprolactinemia caused by
Investigation of choice for hyperprolactinemia
Gynaecomastia is NOT seen in
NOT true about hyperprolactinemia

Chronic renal failure, Thyrotoxicosis, Metoclopramide


Methyldopa, phenothiazines, metoclopramide
Prolactin estimation
Hypoprolactinemia
Elevated prolactin levels are always

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PITUITARY GLAND

ENDOCRINOLOGY
associated with adenoma

PITUITARY TUMOURS
Pituitary tumour
MC type of Pituitary adenoma
MC Pituitary tumour
30 year old woman, secondary amenorrhoea for 3 years
along with galactorrhoea
NOT true about prolactinoma in pregnancy
Middle age female increasing visual loss, breast
engorgement, irregular menses. investigation of choice
26 year female, prolactin 65 ng/L second month
Treatment of Choice for Prolactinoma
MC cause of Panhypopituitarism
Galactorrhoea
Amenorrhoea, Galactorrhoea, Bitemporal hemianopia
Amenorrhoea, galactorrhoea, increased prolactin. CT
scan reveal
Loss of erection, low testosterone, high prolactin
Tumour less than 1 cm
Percentage of conversion of microadenoma to
macroadenoma
Visual defect caused by tumor of Pituitary gland
pressing Optic chiasma
Lactational amenorrhoea is due to
Weak Giants
Expansion & Ballooning of sella
Enamel like superstructure is seen in
Somatotrophic adenoma
NOT a feature of pituitary eosinophilic
adenoma
Gold standard investigation for pituitary
adenoma
Earliest method of diagnosing pituitary tumors
Best way to distinguish between pituitary tumor from
ectopic ACTH producing tumor
Most preferred approach for pituitary surgery at
present time

10% of brain tumours, erodes sella and extends into


surrounding area, differentiated by RETICULIN stain
Prolactinoma
Prolactinoma
Prolactinoma
Macroadenoma>1% associated with bad prognosis
Serum prolactin
Routine obstetric care
Bromocriptine (oral dopamine agonist)
Pituitary adenoma
Inappropriate secretion of milk containing fluid from
breast
Prolactin secreting Pituitary macroadenoma
Pituitary adenoma
Pituitary adenoma
Microadenoma
5%
Bitemporal hemianopia
Prolactin induced inhibition of GnRH
Pituitary adenoma
Pituitary Adenoma
Craniopharyngioma
Eosinophilic staining
Adrenal hypercortisolism
Contrast enhanced MRI
CT scan
Petrosal sinus sampling
Trans sphenoidal

PITUITARY APOPLEXY
Hypocalcemia seen in
Associated with pituitary apoplexy
NOT a cause of pituitary apoplexy

Hypopituitarism
Diabetes mellitus, sickle cell anemia, hypertension
Hyperthyroidism

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PITUITARY GLAND

ENDOCRINOLOGY

SHEEHAN SYNDROME
Postpartum pituitary necrosis
Empty sella, amenorrhea, failure of lactation
NOT a cause of primary amenorrhoea
Most effective drug in Sheehans syndrome
Drug essential in Sheehan syndrome
Loss of libido in postpartum necrosis best treated with

Sheehans syndrome
Sheehan syndrome
Sheehan syndrome
Corticosteroids
Cortisone
Low dose testosterone

SYNDROME OF INAPPROPRIATE SECRETION OF ADH


Free water clearance regulated by
Circulatory form of ADH
Form of ADH circulating in plasma
ADH acts on
For concentration of urine by ADH, absorption of water
occurs from
When NaCl injected into internal carotid artery, it
causes release of ADH by stimulating
Greatest stimulator of ADH secretion
ADH is stimulated by
Concentration of urine due to
SIADH is due to
MC cause of SIADH
Malignant tumour producing ACTH, ADH
SIADH secretion is seen in
SIADH caused by
SIADH
SIADH
SIADH
Syndrome of inappropriate ADH is characterized by
Inappropriate ADH secretion
Findings in SIADH
Hyponatremia with Isovolemia
SIADH associated with
Finding in SIADH
Edema
NOT seen in SIADH
SIADH NOT associated with
Treatment of SIADH
Drug of choice for SIADH
Vasopressin antagonist act on
Treatment of SIADH
NOT used in SIADH
Drug NOT used in SIADH

ADH
Free form
Free form
Medullary Collecting duct
Collecting duct
Supraoptic nucleus
Hyperosmolality
Angiotensin II, Standing, Hyperosmolarity
Angiotensin II, Aldosterone, ADH, ANP
Excess ADH
Ectopic ADH by Small Cell Cancer
Oat cell cancer
Lung abscess, vinca alkaloids, bronchial adenoma
Vincristine, vinblastine, cyclophosphamide
Hyponatremia, Low Plasma osmality, High urine
Osmolality, Hyponatremia
Increased urine Na+, Increased urine osmolality
Na+ < 135, Uric acid < 4 mg/dl, K+ normal
Hyponatremia and urine sodium excretion > 20 mEq/L
Water intoxication, expanded fluid volume,
hypomagnesemia, concentrated urine
Increased urine Na+, Increased urine osmolality
SIADH
Hypogammaglobulinemia
Normal Blood Pressure
Does NOT occur in SIADH (excess Vasopressin)
Low BP due to volume depletion
Interstitial nephritis
Fludrocortisones, demeclocycline, hypertonic saline
Demeclocycline
Medullary collecting duct
V2/V1a antagonist (Conivaptan)
Desmopression
Desmopressin

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PITUITARY GLAND

ENDOCRINOLOGY

DIABETES INSIPIDUS
Normal serum osmolality
Normal urine osmolality
MC cause of diabetes insipidus in pregnancy
Causes of diabetes insipidus
Nephrogenic diabetes is caused by
NOT a cause of diabetic insipidus
Inheritance of Diabetes insipidus
Central diabetes insipidus
Nephrogenic diabetes
A child is crying excessively even after being given feed.
He is passing large quantities of urine and reportedly
getting dehydrated. Urine examination shows no
proteinuria and a specific gravity of 1004. most likely
diagnosis
Diabetes insipidus is associated with
Diabetes insipidus associated with
Diabetes insipidus
Hypertonic contraction of fluid volume is caused by
Recessive Nephrogenic diabetes
X linked nephrogenic diabetes
Urinary Osmolality in Diabetes Insipidus
Hyponatremia NOT seen in
Diagnosis of diabetes insipidus require
Hickey hare test
Drug of choice for lithium induced diabetes mellitus
Treatment of lithium induced diabetes insipidus
Main stay of treatment for nephrogenic diabetes
insipidus
Drug of choice for central /neuogenic diabetes insipidus
Chlorpropamide is used in
NOT used for diabetes insipidus
Drug NOT used in diabetes insipidus

285 - 295 mosm/L


350 - 1000 mosm/L
Severe pre eclampsia
Head injury, Histiocytosis, Viral encephalitis
Hypokalemia, sarcoidosis, hypercalcemia
Multiple sclerosis
X linked recessive
Low urine osmolality, Normal to high serum osmolality
Renal tubule unresponsive to ADH
Diabetes insipidus

Increased serum osmolality, Decreased urine osmolality


Hypernatremia
Water deprivation test is required
Diabetes insipidus
Aquaporin 2
V2 receptor
30 mmol/L
Diabetes insipidus
Water deprivation test
Diabetes insipidus
Amiloride
Thiazide diuretics, K+ sparing diuretics
Thiazide or amiloride diuretics, Salt restriction
Desmopressin
Central diabetes insipidus
Furosemide
Furosemide

POLYURIA
Polyuria is caused by
9 year old female polyuria, polydipsia, metabolic
acidosis, on slit lamp examination crystal deposits are
seen in cornea
Cerebral salt wasting syndrome
Head injury, raised ICT, put on ventilator and started on
IV fluids and diuretics. 24 hours later urine output 3.5
litres. sodium 156 mEq/L, osmolarity 316 mOsm/kg
Decreased serum and urine osmolality along with
reduced serum sodium
Investigations done in women with polyuria > 6L/day

Hypercalcemia, primary hyperaldosteronism,


nephrogenic diabetes insipidus
Cystinosis

Polyuria, hypotension, dystautonomia


High output due to diuretics

Psychogenic polydipsia
Water deprivation test, Plasma and urine osmolality

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