4. Hormone
Secretory product of ductless gland
Released in catalytic amount
Into blood stream Transport to specific target
cells or organs
Elicit physiologic, morphologic, and biochemical
responses
5. The biological function of multicellular living
organisms are well co-ordinated
Nervous system Endocrine system
Internal
environ
ment
External
environm
ent
Co-ordinates the function
through transmission of impulses
via nerve fibers
Chemical
reaction
Transport of
various
substances
Fuction through wide range of
chemical messanger , the
hormones
6.
7. GLANDS SECRETIONS
Pituitary gland
(hypophysis)
Adenohypophysis and neurophypophysis
Adenohypophysis- growth hormone(GH)
or somatotropins, follicle stimulating
hormones(FSH) luteinizing hormone(LH),
prolactin, thyrotropin or thyroid-stimulating
hormones(TSH) and corticotropin or
adrenocorticotropic hormone(ACTH)
Neurohypophysis- stores the antidiuretic
hormone(ADH) or vasopressin and oxytocin
synthesized by hypothalamus
Thyroid gland Thyroxine (T4) and triiodothyronine(T3), the C
cells or parafollicular cells secrete calcitonin
Parathyroid gland parathormone
Adrenal glands
(superarenal
glands)
Outer cortex region- cortisol, aldosterone and
sex steroids. Inner medullary region-
catecholamines(adrenaline and noradrenaline)
8. Pancreatic
islets(islets of
langerhans)
Insulin, glucagon, and somatostatin.
Gonads ovaries secrets- Oestrogen and
progesterone(female sex steroids) and testes
secrets- testosterone(male sex hormone)
Pineal gland Melatonin and other biogenic amines
Placenta Human chorionic gonadotropin(HCG),
Oestrogen, progesterone, somatotropins and
relaxin
Gastrointestinal
mucosa
Gastrin, secretin, cholecystokinin-
pancreozymin(CCK-PZ) etc
kidneys Erythropoietin, prostaglandins and 1,25-
dihydroxycholecalciferol and helps in activation
of angiotensin production
Atrial muscle cells Atrial natriuretic peptides(ANP) and many
peptides
Skin vitamin D now considered as hormone
9.
10. A. Depending upon the chemical structure-
Amines or Amino
acid derivatives
Protiens and
polypeptides
Steroid hormones
1. Catecholamines
(epinephrine and
norepinephrine)
2. Thyroid (T4) and
tiidothyronine
(T3)
1. Posterior
pituitary
hormones
(antidiuretic
hormone and
oxytocin)
2. Insulin
3. Glucagon
4. parathormone
5. other anterior
pituitary
hormones
1. Glucocorticoids
2. mineralocorticoid
3. sex steriods
4. vitamin D
11. B. Depending upon the mehanism of action-
Binds
Group 1 hormones-
Intracellular receptor
Action by forming a
HORMONE- RECEPTOR
COMPLEX
It includes steroids, retinoids,
and thyroid hormones
12.
13.
14. GROUP SECOND MESSENGER HORMONES
GROUP II- A Cyclic AMP(cAMP) 1. Adrenocorticotropic
hormone (ACTH)
2. Antidiuretic hormone (ADH)
3. Angiotensin II
4. Calcitonin
5. Corticotropic hormones
6. Catecholamine
7. Folicullar- stimulating
hormone
8. Glucagon
9. Luteinizing hormone(LH)
10. Paratharmone
11. Somatostatin
12. Thyroid- stimulating
hormone (TSH)
15. Group II- B Cyclic GMP(cGMP) Atrial natriuretic
factor(ANF) and nitric
oxide
Group II- C Calcium/ or
phosphatidyl inositol/
or both
1. Acetylcholine(Ach)
2. Catecholamine
3. Gastrin
4. Oxytocin
5. Thyrotropin-
releasing
hormone(TRH)
6. Gonadotrophin-
releasing
hormone(GnRH)
7. Platelet- derived
growth
factor(PDGF)
16. Group II- D Kinase or
phosphatase cascade
1. Human chorionic
somatotropin(H
CS)
2. Erythropoietin
3. Growth hormone
4. Insulin
5. Insuln like
growth
factor(IGF-I and
IGF-II)
6. Nerve growth
factor(NGF)
7. Prolactin
8. other
17. Hormone transport- After secretion into blood it is circulated
in two forms
Unbound form Bounded form
Catecholamine
Most peptides
Protein hormones
Steroids
Thyroid hormones
Vitamin D
hormone binding to protein is advantageous as:
1. Protects against clearance by kidneys
2. Degradation of liver will slow down
3. provides Reserve of hormone
18. 1. peptide hormone- shorter half life
2. Steroid
3. Thyroid hormone
Half life of 1. insulin is 5 min
2. growth hormone is <30 min
3. thyroxine is 5-7 days
4. triiodothyronine is 1-3 days
5. cortisol is 90-100 min
Longer hormone because they
bind to plasma protein
19.
20. Main mechanism of hormone action are-
I change in the membrane permeablility
II effect on gene expression by binding of
hormones with intracellular receptors
III secondary messenger with activate
intracellular enzymes when hormones combine
with membrane receptors
IV tyrosine kinase activation
22. Sequences of events
1. Transport
2. Internalization
3. Receptor- hormone
complex
4. Conformational
change
5. Activated receptor
hormone complex
6. Binding of the
receptor-hormone
complex to DNA
7. mRNA diffuses in
the cytoplasm
23. SECOND MESSANGER
SYSTEM
1. Adenylyl cyclase –
cAMP system
2. Guanyl cyclase –
cGMP system
3. Membrane
phospholipase –
phospholipid
system
4. Calcium –
calmodulin system
24. By two mechanism
A. Hormone receptors
possessing intrinsic
tyrosine activity:
Insulin and
epidermal growth factor
B. Hormone receptors
that do not possess
intrinsic tyrosine
activity:
Growth hormone
Prolactin- releasing
hormones
Cytokines etc
25. They are measured by hormone assays
bioassay immunoassay
Cytochemical
aasay
Dynamic
tests
By injecting
unknown
sample to
experimental
animals to
assess the
hormone
level. The
effect was
clear dose-
response
relationship
RIA
ELISA
H = antiH + (H+)=
cold
Anti H have affinity
= H
H(plasma) compet
with (H+)= to bind to
antiH
Antiboby hormone complex+
stain= estimated by
spectrophotometer. This is used
for peptide and steriod hormone
More sensitive
Detected in
slices cut from
the enocrine
gland and
cultured
This is useful in
basal level of
hormone
secretion
Suppression type
Used in certain
condition like to
know ACTH
secreting in lung
cancer
Stimulation type
Metyrapone test to
know corticotrophs of
pituitary are normally
functioning
26. Hypothalamic- pituitary gland forms a unique component of
entire endocrine system that regulates.
Growth
Fluid hmeostasis
Functions of thyroid gland
Adrenal glands
Gonads
lactation
27. Development of pituitary gland
ANTERIOR PITUITARY POSTERIOR PITUITARY/
NEUROHYPOPHYSIS
Ectodermal origin
Develops from Rathke’s
pouch
Upward out pouching from
roof of primitive oral cavity
From lowered outpouching of
neuroectodermal tissue from
hypothalamus
28.
29. HORMONES SITE OF ACTONS DISEASES
ANTERIOR
PITUITARY
Growth
hormone(GH)
EXCESS DEFICIENCY
all Somatic cells Gigantism
acromegaly
dwarfism
Adrenocorticotropi
c hormone(ACTH)
Adrenal cortex ACTH dependent –
cushing syndrome
Hypoadrenalin(rar
e)
Thyroid
stimulating
hormone(TSH)
thyroid hyperthyroidism hypothryoidism
prolactin breast hyperprolactinemi
a
---------
gonadotropins gonads hypergonadism hypogonadism
Melanocytic
stimulating
hormone(MSH)
skin hyperpigmentatio
n
------------
POSTERIOR
PITUITARY
Antidiuretic kidneys
------------ Diabetic insipidus
30. Control of anterior
pituitary function
Control of posterior
pituitary function
Growth- hormone releasing
hormone(GHRH)
Corticotropin – releasing hormone(CRH)
Thyrotropin –releasing hormone(TRH)
Gonadotropin- releasing
hormone(GnRH)
Prolactin- releasing hormone(PRH)
Growth- hormone- inhbiting
hormone(GRIH)
Prolactin- inhibiting hormone(PIH)
Oxytocin
Antidiuretic
hormone(ADH)
31. Also called SOMATOTROPIN
it helps in lean body mass and bone mass in adults
Important for postnatal growth and development to adult
size
Synthesized by acidophilic cells called somatotropins of
anterior pituitary
PLASMA LEVELS
Every 1-2 hours there is increase in plasma GH level
Releases in 10-20 pulses per day
VARIATIONS IN PLASMA LEVEL OF GH
birth to early childhood= hormone level increases
children vs adult= children have higher than adult
Puberty= have peak level of GH
Senescences= reduction of GH
32. CIRCULATION
bound to plasma protein
HALF LIFE
20 minutes
METABOLISM
Rapidly metabolized
In liver
Excreted through urine
33.
34. I. Hypresecretion of GH
II. Hyposecretion of GH
HYPERSECRETION OF GH: occurs in tumours of
acidophilic cells(somatotrophs) of the anterior
pituitary.
CAUSES: 1. gigantism
2. Acromegaly
35. In the growing children before closure of
epiphysis of long bone.
FEATURES:
1. abnormal height
2. huge status
3. becomes giant
4. large hands and feet
5. thick lips
6. Macroglossia
7. thickness of skin
36. Excess secretion of GH in adults
After epiphysis closure of long bone
CLINICAL FEATURES:
* Acromegalic face: • Thick lips
• Macroglossia
• Broad and thick nose
• Promient eye brows
• Thickened skin
• Coarse facial features
* proganthism:
• Protrusion of lower jaw
• Widening of mandible
• Increased space of teeth
37. • Acral part of abnormalities: • large spade like hands
•Thick wide fingers
•Large feet with increase in size of
shoes
• Height normal
• Build stout
• stocky
* kyphosis: due to improper vertebral growth
* Excess growth of internal organs: cardiomegaly,
hepatomegaly, splenomegaly, renomegaly
* Incresed sympathetic activity: causes increased sweating
and hypertension
38.
39.
40. Deficiency of GH in children: leads stunt growth or
dwarfism
Deficiency of GH in adult: results mild anemia
treatment with haematinics like iron
1. reduction in muscle mass
2. hpoglycemia
DWARFISM: short stature may be due to endocrinal or
non endocrinal causes
42. Deficient in early childhood
With the chronological age of 20 years body structure
like that of a normla child of 7-10 years
Features are:
1. Shortness of stature
2. Normal mental activity
3. Plumpness(fatness)
4. Immature faces
5. Delicate extremities
6. Sexual maturity does not occur
With the gonadotropin deficiency
43. Prevents diuresis
Conservation of body water
Causes vasoconstriction so also called as vasopressin or
arginine vasopressin
Synthesis: in the neurons of both paraventricular and
supraoptic nuclei of hypothalamus
Storage: nerve ending of posterior pituitary
Secretion: when impulses from hypothalamus down
axon depolarizes the neurosecretory vesicles
Transport: From capillaries it reaches to target cells and
anterior pituitary by circulating interconnections
Metabolism: kidney and liver
44. kidney
Vasoconstrictor
effect
Anterior
pituitary
• Regulation of water
• decreases excretion
of water
•Action on distal
convoluted tubules
and collecting ducts of
nephron
• ADH in high dose
causes vasocontrition
• Causes increase in
blood pressure
• Main role in blood
pressure hoemostssis in
haemoraahages
• Travel to anterior
pituitary via portal
vein
• combine with
receptor causes
increased ACTH
secretion
45. 1. SYNDROME OF INAPPROPRIATE
HYPERSECRETION OF ADH(SIADH)
2. DIABETES INSIPIDUS
1. SYNDROME OF INAPPROPRIATE
HYPERSECRETION OF ADH(SIADH):
Condition in which ADH secretion increased in the
presence of hypoosmolality
Excessive secretion leads water intoxication i.e
overhydration
It is also called as dilution syndrome
46. Clinical condition of polyuria that occur in deficiency of
ADH
Features:
1. Decreased renal absorption of water
2. Polyurea: passage of large amount of urine
3. Polydipsia: drinking large amount of water
4. Dehydartion: dry tongue
dry mouth
fall in blood pressure
loss in consciousness
47. ACTION : acts mainly on breasts and uterus
ACTION ON BREAST:
contraction of myoepithelial cells and plays a role in milk
ejection
ACTION ON UTERUS:
contracts uterine smooth muscles and plays role in
parturition(labour)
It acts on non pregnant women to facilitate the transport
of sperm in genital tractFactor s which increases
oxytocin:
•On cholinergic stimulation
•Suckling reflex
•Genital tract stimulates during
coitus and labour
Factors which decreases
oxytocin:
•Emotional stress
•Sympathetic stimulation
•Drugs like ethanol and
enkephaline
48. Two principle hormones
1. Thyroxine or T4(3,5,3’,5’-tetraiodothyronine) 90% of
output
2. Triiodothyronine or T3(3,5,3’- triiodothyronine) 10%
output
3. Calcitonin secreted by parafollicular cells which is
concerned with calcium homeostasis
49. They effect the cellular activities of all the tissues
I. On growth and tissue development
II. On metabolic rate in general
III. On metabolism
IV. Respiratory effects
V. Cardiovascular effects
VI. On nervous system
VII. On gastrointestinal tract
VIII.On skeletal muscles
IX. On reproductive system
X. On other endocrinal glands
XI. On kidneys
50. i. In normal body growth and skeletal maturation:
Directly-- Increases protein synthesis and enzymes and
indirectly-- increases production of growth hormone
and somatomedins. Important effects on
Bone development
Teeth development
Normal cycle of growth and maturation
Subcutaneous tissues
ii. Role in tissue differentiation and maturation
iii. role in development of nervous tissues: T3 necessary
for proper axon and dendritic development .
51. Stimulates metabolic activities
Increases basal rate of oxygen consumption
Increases heat production in most of the tissues except
brain, retina, gonads, lungs, and spleen.
52. i. on carbohydrates:
Increases glucose absorption from GIT
Increases glucose metabolism i.e rate of cell uptake of
glucose, Glycolysis, glucogenolysis, insulin secretion.
ii. On fat metabolism:
Mobilization of fat from adipose tissues
Increase level of fatty acids and oxidation of freefatty
acids by cells
Decreases quantity of cholesterol due to increased
excretion in bile.
iii.On protein metabolism:
• Increase in RNA and protein synthesis leading to
+ve nitogen balance
• In high thyroid hormone leads to negative
nitrogen balance
• Thus muscle weakness and creatinine are features
of HYPERTHYROID PATIENTS
iv. Through other hormones: stimualtory effects of
epinephrine, nor epinephrine, cortisol, and
growth hormone on gluconeogenisis, lipolysis,
ketogenesis, and proteolysis of labile protein pool
V. On vitamin metabolism:
• Vitamin are part of enzymes and co enzymes
•Thyroid cause increase vitamin need leading vitamin
deficiency in hyperthyroid
vi. On water and electrolyte balance:
• Regulation of water and electrolyte balance.
53. i. increase in the resting respirarory rate, minute
ventilation and ventilatory responses to hypercapnia
and hypoxia:
Maintains a normal pO2 when O2 utilization increases
and pCO2 when CO2 production is increased
ii. Increase in oxygen- carrying capacity of blood:
Increases in red blood cells
54. i. vasodilatation and increased blood flow to tissues
ii. blood volume: circulation increased because of
Effect of vasodilatation
Activating renin- angiotension- aldosterone and
increases renal tubular sodium reabsorption
iii. Tachycardia: increased heart rate is an physical sign
iv. Force of cardiac contraction: effects via adrenergic
stimulation. Mycardial calcium uptake and adenylyl
cyclase activity are increased enhance contractile
force.
v. cardiac output: increased by increased blood volume,
increased heart rate, increased forceof contraction.
vi. On blood pressure:
• systolic blood pressure is increased due to
increased strength and rate of heart beat
• Diastolic blood pressure is decreased due to
peripheral vasodialataion
• Results into increased pulse pressure but mean
arterial pressure is usually unchanged
55. i. on development of nervous system:
Critical period is upto 1 year
ii. On functioning of nervous tissue in adults:
On central nervous sysetm:
T4 Enhances 1. wakefulness
2. alert
3. Resposivenessto various
stimuli
4. Auditory sense
5. Awareness of hunger
6. Memory
7. Learning capacity
• on peripheral nervous system: increases speed and
amplitude of peripheral nerve reflex
56. Increase in apetite and therefore increase n food intake
Increase inrate of secretion of digestive juices
Increase in motility of GIT: excess of thyroid hormone
causes diarrhoea
Action of thyroid hormone: VIII. ON
SKELETAL MUSCLES:
• slightly increase in hormone makes muscle to react with
vigour
•Excessive quntities of hormone weaken muscles because of
increased protein catabolism
•Lack of hormone causes sluggishness in muscles.
57. In males: lack of hormones causes complete loss of
libido and excess causes impotence
In females: lack of hormones causes menorrhagia and
polymenorrhagia. Irregular periods or even
amenorrhoea
Action of thyroid hormones: X. ON THE
ENDOCRINE GLANDS:
• growth hormone is increased
• Prolactin is decreased
• oestrogen and androgen ratio in males are increased
• occurence of breast engorgement in males in
hyperthyroidism
• Parathyroid hormone and vitamin D are decreased
Action of thyroid hormone: XI. ON
KIDNEY:
kidney size, renal tubular epihelium, renal plasma flow,
glomerular filtration rate. And tubular transport increased
59. Or toxic goiter, or thyrotoxicosis are the other names
AETIOLOGY
autoimmune disease developing thyroid- stimulating
antibodies(TSAb) against TSH receptors also called
LONG ACTING THYRIOD STIMULATOR.
Antibodies
binds to
TSH receptors
Mimic TSH
action on
thyroid growth
and hormone
sythesis
Gland
undergoes
hyperplasia.
60. SYMPTOMS AND SIGNS OF GRAVE’S DISEASE:
1. GENERAL FEATURES:
increase in basal metabolic rate(BMR)
Weight loss
Increased intake of food
Increased heat production causes discomfort
Excessive sweating
Great intake of water in warm environment
2. GOITER: swelling of thyroid gland
Characterized by diffuse goiter
Single or more nodules indicate toxic nodular goiter.
3. CARDIOVASCULAR FEATURES:
Increased pulse rate or sinus tachycardia
Arrhythmia(atrial fibrillation is commonest)
61. 4. NEUROMUSCULAR FEATURES:
Nervousness
Irritability
Restlessness
Psychosis
Tremors of hand
Muscular weakness
Exaggerated tendon reflex
5. GASTROINTESTINAL FEATUES: are diarrhoea or
steatorrhoea
6. DERMATOLOGICA FEATURES: perspiration(increased
sweating or hyperhidrosis), loss of hair and redness of
palm
7. REPRODUCTIVE FEATURES:
• Importence in male
• Oligomenorrhoea or amenorrhoea
• Abortion
• Infertility in females
8. OPHTHALMOLOGICAL SIGNS:
• Lid reaction producing staring look
• Lid lag
• Exopthalmos i.e bulging out of eyeball
62.
63. Refers to any abnormal increase in size
IRON DEFIENCY GOITER OF ENDEMIC GOITER:
daily dietary of iodine falls below 10ug(normal
requirement 100-200ug/day)
Decreases the synthesis and secretion of hormone
Leading to increased TSH level and proliferating gland
tissues
Found in regions away from sea coast where water and
soil are low in iodine content
Consumption of iodinsed salt overcomes the problem
of endemic goiter
64. Is a clinical syndrome of low level of circulating
hormone
AETIOLOGY:
1. PRIMARY THYROIDISM: caused by disorders of gland
2. SECONDARY THYROIDISM: caused by anterior
pituitary and hypothalamus
CLINICAL FEATURES:
1. INFANTILE HYPOTHYROIDISM(cretinism)
2. ADULT HYPOTHYROIDISM(myxoedema)
65. Occurs in 1st year of life and is characterized by
mental retardation
Delayed milestones of development
Potbelly
Protruding tongue
Flat nose
Dry skin
Sparse hairs
TREATMENT: should be prompt otherwise mental
deficiency will persist
66.
67. GENERAL FEATUES:
Tiredness
Weight gain without an increase in caloric intake
Decreased heat production
Lower body temperature
Intolerance to cold
Decreased sweating
CARDIOVASCULAR FEATURES:
bradycardia
Hypertension
68. pericardial effusion
Precipitation of angina
NEUROLOGICAL FEATURES:
Movement, speech, thought all slowed
Lethargy
Sleepiness
Delayed relaxation of ankle jerks, aches and pain are
common
Pressure palsy of peripheral nerves(eg. Carpel tunnel
syndrome)
DERMATOLOGICAL FEATURES:
Dry thick skin
Sparse hair
Non pitting oedema due to infiltration by
myxoedematous tissue
REPRODUCTION FEATUES:
•Menorrhagia
•Infertility
•Galactorrhoea
•Impotence
GASTROINTESTINAL FEATURES:
•Constipation
•Adynamic ileus
HAEMATOLOGICAL FEATURES:
•Anemia
69.
70.
71. ACTION OF PTH: primary function is to elevate plasma
calcium conc. And decrease the plasma phosphate conc.
ON THE BONE: stimulates calcium and phosphate
resorption from bone
ON KIDNEY:
i. INCREASE IN CALCIUM REABSORPTION: resorption
of calcium from ascending limb , loop of henle and
distla tubules of kidneys and helps to prevent
hypoclacemia
ii. INHIBITION OF PHOSPHATE REABSORPTION IN
THE PROXIMAL TUBULE: effect produces
phosphaturia and hypophosphataemia.
72. iii. INHIBITION OF REABSORPTION OF Na+ and HCO-
3 IN
THE PROXIMAL TUBULE AND STIMULATION OF Na+-H+
EXCHANGER: causes acidification which prevent the
occurence of metabolic alkalosis .
iv. STIMULATION OF REABSORPTION OF Mg2+ BY THE
RENAL TUBULES:
v. STIMULATION OF SYNTHESIS OF 1,25-
DIHYDROXYCHOLECALCIFEROL action in the kidney
ON INTESTINES: enhances both calcium and phosphate
absorption ------> from intestine indirectly by ---------->
increasing synthesis of ---------> 1,25-
dihydroxycholecalciferol (calcitriol) in the kidney.
75. Acts on three sites: intestine, bone, kidney
Plasma calcium
PTH secretion
calcitriol
Intestinal Ca
absorption
Plasma calcium
Bone Ca
mobilization
Renal Ca
reabsorption
76. SYNTHESIS: in the C- cells or para-follicular cells of
thyroid gland
ACTION:
On bone- to oppose the bone resorption action of PTH
On kidneys- increases loss of calcium and phosphate in
urine. This effect producing hypocalcaemia and
hypophosphataemia.
PHYSIOLOGICAL SIGNIFICANCE :
in children and feotus: skeletal development by
promoting calcium storage in bones.
Protects the bones of mother from excess calcium loss
during pregnancy and lactation
78. low level of plasma calcium due to deficient of PTH
CHARACTERISTIC FEATURES :
HYPOCALCEMIA: serum calcium decreased to 4-8mg/dl
and ionized calcium to 3mg/dl
50% fall in ionized calcium leads to TETANY
HYPERPHOSPHATAEMIA: increase in serum inorganic
phosphate level to 6-16mg/dl
79. CAUSES:
1. HYPOCALCEMIA: cause of increased neuromuscular
irritability leading to tetany.
2. HYPOMAGNESAEMIA: increase in magnesium ion
with neuromuscular irritability.
3. ALKALOSIS: reduce ionic calcium, produce tetany
CLINICAL FEATURES:
CARPOPEDAL SPASM: occurs flexion at
metacarpophanlangeal joints, extension at
interphalangeal and oppostion of thumb. This posture
is called OBSTETRIC HAND
Pedal spasm is rare, in toes plantarflexed and feet
drawn up
80. TROUSSEAU’S SIGN: occluding the blood supply to limb
about 3min by inflation of a sphygmomanomater cuff
LARYNGEAL STRIDOR(loud sound): spasm of
laryngeal muscles may produce asphyxia.
PARASTHEIAS: tingling senstion in the
peripheral part of limbs, around mouth is
common
CHVOSTEK’S SIGN: twitching of facial muscles
produced by tapping fascial nerve at angle of jaw
MANAGEMENT : intravenous injection of 20ml of 10%
calcium gluconate given to correct hypocalcemia and
relieve tetany.
81. RICKETS
OSTEOMALACIA
OSTEOPOROSIS
RICKETS:
Occuring in children
Due to deficiency of vitamin D in which defective
calcification of bone matrix
MANAGEMENT : supply calcium and vitamin D
82. CRANIOTABES: small rounded areas bones of
skull pressure of finger
WIDENING OF WRIST: widening of lower end of
radius bone
COLLAPSE OF CHEST WALL: flattening side
of thorax with prominent sternum
RICKETY ROSARY: beading of coastochondral
junction of ribs
BOWING OF LEGS OR KNOCK KNEE: occurs
when child starts walking
KYPHOSIS AND PELVIC DEFORMITIES
FRONTAL BOSSING AND POSTERIOR
FLATTENING
83. Defective mineralization of adult bones in epiphyseal
growth plates which are already closed
CLINICAL FEATURES:
SKELETAL
ABNORMALITIES:
1. Skeletal pain, bony
tenderness
2. Muscle weakness and
TETANY
1. with carpopedal
spasm
TREATMENT: similar to rickets
84. Characterized by a
reduction of bone
mass
Per unit volume
With
normal
ratio of
bone
matrix
and
mineralsPATHOGENESIS: mismatch b/w bone resorption
and bone remodelling
CHARACTERISTIC FEATURES :
1. Bone deinsity: reduced ( ground glass appearance seen in
osteomalacia.
2. Incidence of fractures: increased (vertebral,hips and
forearm fracture colles fracture is common
3. Biochemical changes: increased urine excretion of
calcium and hydroxyproline
85. 1. calcium intake from natural sourses
2. moderate excercise
3. oestrogen treatment which arrest rapid
osteoporosis in women after menopause.
86. HORMONES OF ADRENAL CORTEX :
I. Glucocorticoids cortisol
corticosterone
II. Mineralocorticoids: Aldosterone is chief which regulates
sodium balance and extracelullar volume in body
III. Adrenal sex steroids: includes
dehydroepiandrosterone(DHEA) and sulpahte ester
87. HORMONES OF ADRENAL MEDULLA:
Which secretes
catecholamines
Which include
epinephrine,
norepinephrine,
and dopamine
Apart from this it consist
of dynorphins,
neurotensins, encephalin,
somatostatin, and
substance P
88. On
carbohydrates
metabolism
On protein
metabolism
On fat
metabolism
On electrolyte
and water
metabolism
1. Increased
gluconeogenesi
s: increase rate
of glucose
production
2. Decreased
utiliztion of
glucose in
peripheral
tissues.
1. Catabolic effect:
release of
amino acids by
proteolysis in
skeletal muscle
2. antianabolic
effect: inhibit
the syntheisis of
protein.
1. Lipolytic effect:
stimulate
hydrolysis of
stored
triglycerides at
maximal rate its
presence is
necessary for
growth
hormone
2. lipogenic effect:
in excess fat
accumulation in
abdomen and
trunk(trunked
obesity)
becomes thin,
1. retention of
sodium and
water
2. Promotion of
diuresis: b
inactivation of
ADH by liver
89. 1. Effect on
muscle
2. Effect on bone 3. Effect on
connective tissue
4. Effect on
vascular system
• cotractility and
work
performance
maintained
• decrease in
muscle mass and
strength: by
excess cortisol
results decrease
muscle protein
synthesis and
increase muscle
catabolism
• increased bone
resorption
• inhibition of
bone formation
• thinning of
skin
• thinning of
walls of
capillaries
• sustaining
myocardial
performnace
• maintaining
normal blood
volume
90. 5. Effects on
kidnys:
6. Effects on
central nervous
system
7. Effects on
gastrointestinal
tract
8. Effects on
blood cells and
lymphatic organs
• increase in GFR
by glomerular
plasma flow
• rapid excretion
of water load
• increase in
calcium and
phosphate
excretion
• modulate
excitability
behaviour and
mood
• increase gastric
secretion and
lead to peptic
ulcer
• excess leads to:
•Eosinopenia and
basopenia
• lymphopenia
• neutrophilia
• polycythaemia
• thrombocytosis
91. Anti –inflammatory
effect
Anti-immunity effect Anti-allergic effect
• inhibits activity of
phospholipase A2
• stabilize lysosomal
membrane
• inhibits migration of
circulating leucocytes
to site of inflammation
• inhibits leukotriene
• decreases collagen
formation
• inhibits both cellular
and humoral immunity
by decreasing the
proliferation of L cells
and B cells
• reduces the no. Of
basophils and protects
against release of
secretory products of
granulocytes, mast
cells. macrophages
92. Adrenal cortex: GLUCOCORTICOIDS: ACTION:
IV. ROLE IN FETAL LIFE
Maturation of central nervous system, retina, skin, and
lungs
Adrenal cortex: GLUCOCORITICOIDS:
ACTION: V. ROLE IN STRESS:
Various stress eg: trauma, cold, illness, starvation, are
associate with activation of hypothalamic- hypophyseal
adrenal axis . Increase secretion of hormone helps to
adaptation to various stress
93. It includes: 1. aldosterone: is chief
2. deoxycortisterone(DOC)
3. 18-hydroxy-deoxycorticosterone(18-OH-
DOC) in small amount
94. A. PRIMARY ACTIONS
On renal tubules:
1. Sodium reabsorption
from tubular fluid into
tubular cells
2. Potassium excretion
3. Hydrogen excretion
On sweat glands, salivary
glands and colon:
Glands secretion --------
contain sodium chloride --
------ ducts absorb sodium
chloride while passing -----
---- potassium exreted
Colon: sodium reabsorption
from colon and potassium
excretion in faeces
96. 1. CUSHING SYNDROME:
Causes:
Seen tumours of pituitary cells
In adrenal adenoma and adrenal carcinoma
Excessive glucocorticoids administration
97. Characteristics features:
Muscle weakness
and backpain due
to protien
catabolism
Sodium and
water retention
causes oedema,
hypertension
Hyperglycemia
may lead to
glycosuria and
adrenal diabetes
Susceptibility to
osteoporosis
and bone
fracture
Hirsutism and
menstrual
irregularitiesd
ue to more
adrenal
androgens
Susceptibilty
to infections
Psychological,
emotional. And
personality
changes
truncal or centripetal obesity like 1.
buffalo hump( collection of fat at
upper back)
2. Moon face( on face)
3, purple striae or cutaneous
abdominal striae or livid stretch
marks(skin and subcutaneous tissue
becomes thin due to protein
catabolism & excess stretching
causes rupture of subdermal tissue
causing purple striae
Blackening of skin
Suceptibility to
peptic ulceration
98. 2. HYPERALDOSTERONISM:
Characteristic features:
Sodium and water
retention
Hypokalemia occurs
due to increased
potassium excretion
producing muscle
weakness
Metabolic alkolosis
occurs due to secretion
of more amount of
hydrogen into renal
tubules
99. 3. ADRENOGENITAL SYNDROME:
Characteristic features:
In pre-pubertal
males: excessive
androgen
produce
precocious
pseudopuberty
In males: oestrogen
producing cells may
produce female like
secondary sexual
characters such as
enlargement of
breasts, atrophy of
tests. Loss of libido,
and feminine body
In females:
development of male
secondary sexual
characteristics such
as beard, muscular
body. Breaking of
voice, male type hair
growth, enlargement
of clitoris and
amorrhoea
101. Glucocorticoids insufficient
produces:
1. Weight loss, malaise
2. Anorexia, nausea
3. Vomiting, weakness and
diarrhoea
4. It is essential for adoptation
of stress
5. Addison’ s disease if
exposed to any type of stress
may lead to fatal
Characteristic features: Mineralocorticoids deficiency:
produces hyponatraemia,
hyperkalaemia, acidosis, and
decreased ECF volumewith
hypotension
Loss of androgen causes sparse of
hair in femlaes
Increased ACTH secretion causes
diffuse pigmentation of skin and
mucus membrane
102. I. METABOLIC EFFECTS:
General metabolic
effects
On carbohydrate
metabolism
On fat metabolism
•Increased haet
production
•Increased oxygen
consumption and
carbondioxide output
•Raised basal metabolic
rate(BMR)
•Glycogenolysis
stimulated in liver
•Glycogenesis reduced
in liver
•Gluconeogenesis is
increased
•Insulin secretion
inhibited
•Glucagon secretion
stimulated
•ACTH secretion
stimulated
•Increase lipolysis by
stimulating hormone
sensitive lipase in
adipose tissue
103. II. PHYSIOLOGICAL ACTION :
On CNS
Lead to arousal and alerting responses producing
anxiety, apprehension and coarse tremors of
extremities
On GIT
Causes relaxation of smooth muscle of wall of the
gut, decreasing tone and motility which produces
constipation
On urinary
baldder
Produces retention of urine by relaxing detrusor
muscles
On Skin
On pilomotor muscle producing piloerection of
hair
On skeletal
muscle
During excercise hormone increases blood supply
104. On eyes
Causes dilatation of pupil by contracting dilator
pupil lae
On
respiration
Relaxes smooth muscle of bronchioles producing
bronchodilatation which increases rate and force
of respiration
On blood
•Reduces blood coagulation time
•Increases RBC count
•Increases plasma protein concentration
•Neutrophilia occurs due to sequestrated
neutrophil into blood
105. Phaeochromocytoma is a rare beningn tumour arising
from epinephrine and nor epinephrine secreting
chromaffin cells of adrenal medulla
CLINICAL FEATURES:
episodic and norepisodic hypertension with postural
drop
attacks of tachycardia, palpitaion, sweating, pallor,
headache, and chest discomfort
abdominal pain, vomiting, constipation, and glucose
intolerance
weight loss and weakness
106. HORMONES:
Beta cells secretes insulin
alpha cells secrets glucagon
delta cells are intermixed. These are
sourses of somatostatin
ACTION OF INSULIN:
I. Metabolic effects
II.Effects on ion transport
III.Role in cell growth and
development
107. I. Metabolic effects
On carbohydrate
metablism
On lipid metabolism On protien metabolism
• Insulin increases
uptake of glucose in
skeletal, cardiac,
smooth muscle,
adipose tissue,
leucocytes, mammary
glands
• others are not insulin
dependent
• gluconeogenesis
•Glycogenolysis
•glycolysis
• Favouring lipogenesis
• decreasing lipolysis
• reducing ketogenesis
• Stimulates protein
• syntheisis Inhibites
protein degredation
108. II. on ion transport:
increases potassium, magnesium uptake into skeletal
muscle cells from ECF
on electrolyte balance is to increase reabsorption of
potassium and sodium by tubules of kidney
109. III. In cell growth and development:
Anabolic action
Important as growth hormone for promotion of
normal growth
Direct
stimulatory
effect on
macromolecules
Macromolecules in tissues such as cartilage,
bone
Stimulation of
other growth
hormone
Includes insulin like growth factor 1 and 2,
epidermal growth factors, nerve growth
hormone, relaxin
110. On carbohydrate
metabolism
Acts on liver ------- increases blood sugar level ---
----- by increasing glycogenolysis and
gluconeogenesis n liver
On lipid
metabolism
Activates lipase in adipose tissue ----- releases
FFA and glycerol into circulation ------ in liver
FFA oxidised ----- produces energy and ketone
On protein
metabolism
Increases amino acid uptake of liver -----
promotes gluconeogensis thus lower the plasma
amino acids
Calorigenic
effect
Action require th epresence of glucocorticoids
and T4
Other action
•Inhibitions of renal tubular sodium
reabsorption reslting in natriuresis
•Increase force of contraction of heart
•Stimulates secretion of growth hormone,
insulin, and prancreatic somatostatin
111. Diabetic mellitus hypoglycemia
Primary diabetic
mellitus:
•Insulin –
dependent diabetic
mellitus(IDDM /
type I)
•Non insulin
dependent diabetes
mellitus(NIDDM/
type II)
Secondary
diabetic mellitus:
•Associated with
certain pathologic
condition such as
pancreatic, cystic
fibrosis,
acromegaly,
cushing syndrome
Hypoglycemia
in non diabetic
Hypoglycemia
in diabetic
(more
common)
112.
113.
114. Cardinal
symptoms
Include poluuria, poludipsia, polyphagia, weight
loss,
Biochemical
signs
Include hyperglycemia, glycosuria, ketosis,
ketouria, and ketoacidosis
complication
s
• predisposition to infections due to impaired
phagocytic function
•Include ketotic coma and non ketotic
hyperosmolar coma
•Chronic complications include atherosclerosis
and microangiopathy (vascular lesion in which
capillary basement membrane becomes thicker) ---
--- causes diabetic retinopathy, diabetic
nephropathy, diabetic neuropathy
115. CNS symptoms also called
neuroglycopenic symptoms
•It is depressed when blood
glucose level falls below 50-
70mg%
•Which results into hallucination,
extreme nervousness, tremors,
confusion, difficulty in conc.,
incoordination, convulsion and
drowsiness
•If blood glucose level falls again
lower then coma will occur
•Treatment – glucose intraveously
CVS smptoms:
•Palpitaion,
tachycarida,
cardiac
arrhythmias
GIT
symptoms:
includes
nausea and
vomting
Skin
symptoms:
are sweating
and
hypothermia
116. I. textook of human physiology for dental students,
author Indhu Khurana, 2nd edition
II. textbook of human physiology for BDS author- AK
jain ,4th edition
III. textbook of physiology, koeppen stanton, 6th edition
