HORMONES
HORMONE RECEPTORS:
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TSH
Protein Hormones
Catecholamines
Thyroid Hormones
Steroid Hormones
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Cytoplasmic receptors
MODE OF ACTION OF STEROID HORMONES:
Hormone + Receptor
TR complex
DNA
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HR complex
PremRNA
mRNA
Ribosomes
Protein
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Response
MODE OF ACTION OF PROTEIN HORMONES & CATECHOLAMINES
ECE
Cytoplasm
CAMP
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ATP
Protein Kinase A
Response.
Adrenal Gland
Thyroid gland
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TH, ADH
Mineralocorticoids
Glucagon, Catecholamines
Hypophysis/Pituitary Gland
Adenohypophysis
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Ant. Pituitary
Master Gland
Ectodermal
Develops from Rathke's pouch
Neuromypophysis
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Post Pituitary.
Neuroectodermal in origin
Developed from ventricle
Pars distalis
Pars intermedia
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Pars tuberalis
Pars nervosa.
Hormones of Ant. Pituitary
Somatotrophs/Somanotropes
Lactotrophs/Lactotropes
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Corticotrophs - ACTH & B-lipotropin
Thyrotrophs - TSH
Gonadotrophs - FSH, LH
Classical Tropic Hormones - ACTH, TSH, FSH, LH
Ant. Pituitary
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Chromophobes - taken no stain; secrete no hormone
Chromophils - take stain; secrete hormone
Regulation of Ant. Pituitary Secretion
Hypothalamus controls ant. pituitary by secreting releasing & inhibiting hormones which are called neurohormones. These hormones are transported to ant. pituitary through hypothalamic portal vessels.
Hormones of Hypothalamus: (all are peptide hormones except Dopamine)
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- Growth Hormone Releasing Hormone (GHRH)
- Corticotropic Releasing Hormones (CRH)
- Thyrotropin Releasing Hormone (TRH)
- Gonadotrophin Releasing Hormone (GnRH)
- Growth Hormone Inhibiting Hormone (Somatostatin)
- Prolactin Inhibiting Hormone (Dopamine)
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Regulation of GH Secretion
Hypoglycemia, fasting, starvation
Exercise, stress, trauma.
Hypothalamus
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GHIH/Somatostatin
GHRH
GHRP
Anterior Pituitary
GH
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Liver
Other tissues.
Somatomedin
Action of GH:-
GH acts on bones, growth & protein metabolism through somatomedin secreted by liver.
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Somatomedin: substance through which GH acts.
Types
IGF-I/Somatomedin C
IGF-II
Related to insulin except there is C-chain extension of A-chain & domain
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Acts on bones & protein metabolism
Insulin Like IGF
Role in fetus growth
Duration of Action:
GH
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IGF-I/Somatomedin C
Loose binding with plasma protein. Released from plasma protein rapidly
Binds with plasma protein strongly
Released slowly from plasma protein
Action lasts for short duration
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Action continuesly for long duration
Mode of Action of Somatomedin C/IGF-I
Via 2nd messenger cAMP
GH Receptor/GHS [Growth Hormone Secretagogue]
GH + GHS (transmembrane receptor) - cytokine family
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Mainly liver cells
HR complex
Intracellular Enzyme Pathways
Somatomedin secretion.
Hormones of Post. Pituitary
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- ADH/Vasopressin
- Oxytocin.
Neurohypophysis doesn't secrete any hormones
ADH & Oxytocin - synthesized in hypothalamus.
Hypothalamo-hypophyseal tract (axonic flow)
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Post pituitary.
Stored at Nerve endings.
When myelinated from Hypothalamus reach post pituitary, hormones are released from Nerve endings.
Neurohormones
Neurophysin winding protein which transport ADH & Oxytocin from Hypo post pituitary via hypothalamo-hypophyseal tract.
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Neurophysin I/Oxytocin Neurophysin
Winding protein for oxytocin.
Neurophysin II/ADH Neurophysin.
Winding protein for ADH/Vasopressin.
Secreted by supraoptic nuclei of hypothalamus (mainly)
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Paraventricular nucleus (in small qty)
Actions:
ADH
+Vasopressin V2 Receptor
ADH-Receptor complex
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Gs
GTP
AC
ATP
cAMP
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PKA
AQ-2
Increase reabsorption of plasma volume
ADH + V1R, Vasoconstriction
Peripheral Resistance
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Vasoconstriction
Plasma osmolality
ADH/Vasopressin
Aquaporin-3, 7- always open
Aquaporin-2
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Glomerulus
PCT
Loop of Henle
DCT
Renal Tubules
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Principal Cell
Normally bound to water keeps it off
Bound to ATP turns it on
Diabetes insipidus
(Polyuria, polydipsia)
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Oxytocin
Endometrium
Myometrium
Perimetrium
Hyposecretion
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Uterine Inertia
Postpartum Haemorrhage.
Less common in ant. Pituitary.
Hypersecretion
Pitocin (synthetic oxytocin)
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Given during labor
Stretching of cervix of Uterus.
Ca storage
Ca++
DAG
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PL-C
Increase intracellular [Ca++]
Increase contraction
Milk Let
Ejection of Milk
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Love & Trust
THPT Axis
Paraventricular nucleus
Oxytocin
TRH
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Ant. Pituitary
Portal system
Hypothalamus
Thyroid Hormone
Follicular Cells
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Simple cuboidal epithelial cell
Tyrosine
Steps of Thyroid hormone synthesis
TRH stimulate thyrotrophs from hypothalamus (Peptide hormone)
Ant. Pituitary release TSH.
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TSH + Follicular cells to synthesize Thyroglobulin
Iodide trapping
Oxidation of Iodide TPO
Organification of Tyrosine + Thyroglobulin
Coupling of DIT & MIT
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Storage-known
Endocytosis of Thyroglobulin with T3 & T4
Lysosomal Enzymes cleave T3 & T4 out of Thyroglobulin
Exocytosis of T3 & T4 into blood plasma.
Release of Thyroid
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Follicular cells send extensions- Pseudopods around thyroglobulin mediated by PSEUDOPODS
Thyroglobulin comes into pinocytic vesicle
Mode of Action of Thyroid Hormone
T3, T4
Glucose
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Glycogen
Liver
Blood
Glycogenolysis
Hyperglycemia
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Gluconeogenesis
Increase LDL uptake
LDL had cholesterol
T3, T4
TBG
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Thyroid Hormone through lipid bilayer
Cellular ATP
Increase O2 usage
TBMR
Increase Heat production
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Increase no of mitochondria
Hypertrophy
Heart:
Non contractile
Myocardium
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B-Adrenergic Receptor
Norepinephrine
Increase contractility
Increase CO
Increase HR/BP
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5' Deiodinase
Retinoic Acid
Transcription Factor
Hormone response Element
Protein into membrane
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Skin.
Stratum corneum
S. Lucidum
S. Granulosum
S. Spinosum
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S. Basale
Blood vessels
Sweat glands
Sweat
Smooth muscle
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GIT
Glands
Increase metabolism
Increase secretion
Transport of Thyroid Hormones
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By 3 types of proteins:
- Thyroxine-Binding Globulin (TBG)
- Thyroxine binding Prealbumin (TRPA)
- Albumin
Glycoprotein
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Of Transthyretin (TTR)
Great affinity for Thyroxine
Transports most of hormone
Transports 1/3 of T4
Transports 1/3 of TH.
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Regulation of secretion of TH. (Negative feedback control)
- Decrease TBMR
- Leptin from adipose tissue
- Alpha-melanocyte stimulating hormone from pituitary
- Increase I2 intake.
- Stress.
- Somatostatin-PIH
- Dopamine
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Hypothalamus
TRH
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Ant. Pituitary
TSH
Secretion receptor
Thyroid gland
(T3, T4)
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Mode of Action:
In larger cells (cells of liver, muscle & kidney), most of T4 is deiodinated to form T3
True intracellular hormone is T3, rather than T4
Bound with plasma protein
Found freely in plasma.
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Increase binding affinity for thyroid hormone receptor.
TH acts by activating the genes & using the genetic transcription.
Sequence of Events:
T3- enter the nucleus
Binds with Thyroid Hormone Receptor (TR)
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Contained to DNA strand
Always bound to another receptor (RXR Retinoic acid
THR complex formed
RNA polymerase & phosphoprotein kinase
Initiates transcription
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Large no. of mRNA is formed.
Synthesis of Nuclear Proteins.
Functions of Thyroid Hormones
- Increase BMR
- Stimulate growth in children.
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Increase O2 consumption of tissues.
TBMR
Increase heat production.
Calorigenic Action
Protein Metabolism: Increase synthesis of protein
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Decrease catabolism of protein
Using the translation of RNA
Using the transcription of DNA TORNA
Using the Activity & No. of mitochondria: Increase ATP Product
Using the Activity of cellular enzymes like
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Alpha-glyceral po4 dehydrogenase & oxidative enzymes
Carbohydrate Metabolism:
Accelerate Gluconeogenesis
Increase Glycogenolysis.
Increase Glucose absorption from GIT tract.
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Fat Metabolism:
Thyroxine decreases fat storage by mobilizing it from adipose tissues. Mobilized fat is converted into free FA & transported by blood
The free FA in blood.
CVS: Increase HR - acts directly on heart
Increase force of contraction.
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Increase blood vessels
Increase metabolic rate
Increase qty of metabolites production
Vasodilation
Increase Arterial BP: - Increase rate & force of contraction
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Increase CO
Increase BP
Mean Press - unaltered
Systolic BP-Increase
Diastolic BP-Decrease
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Pulse A. Pressure
CNS:- Thyroxine-essential for development & maintainance of normal functioning of CNS.
CNS development: Thyroxine-important for brain development during fetal life & in few yrs of post natal life.
On normal function of CNS:-
Thyroxine-stimulating factor for CNS, especially brain
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Increase blood flow to brain
Normal functioning of brain needs the mu of T4.
Hypersecretion of T4- excess stimulation of CNS.
Excess worries.
Hypothyroidism
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Myxedema-adults
Cretinism-children.
Myxedema: general edematous appearance
Causes:
- disease of thyroid gland.
- genetic disorder
- I2 deficiency.
- deficiency of TSH/RH
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Common Cause: Hashimoto's Thyroiditis - late middle aged
Autoimmune antibodies lead to destruction of gland.
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Symptoms: edematous appearance throughout the body
- swelling of face
- Bagginess under eyes.
- Non pitting type of edema i.e when pressed, it does not make pits.
Accumulation of [hyaluronic Acid
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Chondroitin SO4
Atherosclerosis: hardening of wall of arteries
Accumulation of fats deposited & Increase plasma level of cholesterol.
Produces Arteriosclerosis
Thickening & stiffening of arterial wall
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Anemia (RBCs)
Decrease body wet.
Constipation.
Menorrhagia & polymenorrhea.
Cretinism
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Hypothyroidism in children, stunted growth
Causes:-
- Congenital absence of thyroid gland.
- genetic disorder
- lack of I2 in diet
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Symptoms:
New born baby appears normal as the lining of birth (T3, T4 might have was supplied from mothers
Few weeks after birth, baby starts developing signs
Sluggish movement
Croaking sound while crying.
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Unless treated immediately, the baby will be mentally retarded permanently
Skeletal growth more affected then soft tissue
Stunted growth + bloated body.
Tongue- so big that hangs with dripping of saliva
Loud croak + swallowing
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Breathing
Cretin
Mental retardation.
Body is disproportionate
Reproductive function affected.
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Pituitary Dwarf
CNS- normal.
Body parts- proportionate
May be normal
Goiter - enlargement of thyroid gland.
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Toxic Goiter
Goiter in hyperthyroidism
Enlargement of thyroid gland with Increase in TH (due to thyroid tumor)
Non Toxic Goiter
Enlargement of thyroid gland without Increase in hormone secretion.
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(Hypothyroid goiter).
Based on causes
Endemic Colloid Goiter
I2 deficiency goiter.
Non toxic goiter due to I2 deficiency
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Intake < 50mg/day
Lack of I2 no hormone formation.
By feedback mechanism
Hypothalamus
TRH Increase
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Ant. Pituitary
TSH Increase
Thyroid cells to secrete Thyroglobulin into Thyroid follicles.
As there is no hormone to be cleaved, Thyroglobulin remains as it is & is accumulated in follicles of gland Increase in size of gland.
Idiopathic Non Toxic Goiter
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(unknown cause).
Enlargement without I2 deficiency
Cause: may be due to
- thyroiditis
- deficiency of enzymes.
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Ex- Peroxidase, TPO iodinase,
5-deiodinase.
Required for TH synthesis
Some food stuffs contains goitrogens, TH inhibitors
Ex- turnip, cabbage, soyabea
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Becomes active during I2 intake.
Hyperthyroidism.
Grave's Disease: autoimmune disease.
Most common cause of hyperthyroidism
Normally, TSH combine with surface receptors of thyroid cells
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Synthesis & secretion of th
B lymphocytes (plasma cells) produces autoimmune Abs
Thyroid stimulating Abs (TSAbs)
Lar wer TSH
Binds with membrane receptor of TSH
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cAMP system of thyroid follicular cells
Hypersecretion of th.
TS Abs- lasts for long time upto 12ms.
TSH- lasts for an hr
[TSA]=0 Increase in plasma.
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Adrenal Gland
Life saving gland/
Essential endocrine gland.
Adrenal Cortex
Outer portion
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80% of gland.
Adrenal Medulla
Central portion
20%
Zona Glomerulosa
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Zona Fasciculata
Zona Reticularis.
All adrenocortical hormones are steroids in nature.
Name corticosteroids
Cytoplasmic receptor
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Mineralocorticoids
Glucocorticoids
Sex hormones
Zona Glomerulosa
Synthesis
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Paraventricular Nuclei
Corticotropin Releasing Hormone
ACTH
Lungs
ACE
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Angiotensin II
Angiotensin I
Zona Glomerulosa
Zona Fasciculate
Zona Reticularis
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Adrenal medulla
Renin
JG cells
Decrease BP
ANP
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Atrial Natriuretic Peptide
Increase TBP
Functions of Mineralocorticoid:
Transport
Transcortin
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Corticosteroid - Albumin Binding Globulin
94% Transport.
Aldosterone & circulates on its own.
It has to wind to transport protein as it is an steroid
Synthesis of Aldosterone
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Mechanism of Action:
Aldosterone Increase Increase activity of (ENals)
Insertion of these channels inca om from cytoplasm
Gene for (sgk) serdem & glucocorticoid regulated kinase.
Increase activity of ENac activity
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Activates genes for other proteins.
Synthesis of Aldosterone
Cholesterol
Cholesterol desmolase
Pregnenolone
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3-B hydroxysteroid dehydrogenase
Progesterone
21-B-hydroxylase
11 deoxy corn costerone
11-B hydroxylate
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Glucocorticoid
Mineralocorticoids/ Corticosterone
18-A-hydroxylase &
Aldosterone
18-R-dihydroxy dehydrogenase
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Conn's Syndrome
Increase hyperaldosteronit
Prolonged excess secretion of aldosterone from adrenal cortex due a de non to tamom of 2. glomerula
Features:
- Increase to Not absorption & its exchange with H+ & K+ in DCT
- Hyponatremia Increase Net Increase TECly & Increase B.P
- Mexuesion in urine Hypokalemia.
- musculer weakness.
- Metabolic alkalosis free Ca++ Tetany.
- Hypokalemic neuropathy (renal tubules demy) polyuria, polydipsia, Decrease conc. ability of Kidney.
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Aldosterone escape.
5- desence of intravascular vol.
Functions of Mineralocorticoids.
Aldosterone
Colife saving hormone.
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(Na) death within 2 days 2 weeks.
Na
acts on OCT & collecting auch (Peeler)
Increase Na EnaL, Increase No absorption
ECF
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Hypernatriuria
Na absorbed from renal tubules
simultaneously no vallo absorbed.
TECF volume
Increase Na absorption Increase (Na+)
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n2o absorbed simultaneously
BP-
TECF YOU & Twood you
TRA
Aldosterone
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Escape
K+:-
Increase K+ excretion through renal neuveres
Hypokalemia.
n+:-
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Increase Na reabsorption from renal tubules
(Note annet pes)
tuinler unerion of(n+]
+(n+) in ECF
Aldosterone maintain Acid we baan.
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Adosterom
Increase Hyposecretion
Acidosis.
Alkalosis
Conn's Syndrome
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Aldosterone Escape - 2° effect of excess Mineralocorti
Escape of kidney from salt-retaining effects of excess administration/secretion of Aldosterone.
Increase Aldosterone level
ENGU.
Increase duorption of Na & Ho from renel tubules
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TECF volume
Increase arterial B.P.
Pelcretion of AND BNP & CNP
(C-type namuretic peptide) from cardiac muscle.
Exuena of Na+
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Excursion of Not Increase wo through urine
Decrease ECF volume
LIVER
Angiotensinogen
Increase [K+]-Hyperkalemia.
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Decrease [Na+)-Hyponatremia
Decrease ECFAMA
Decrease BP
Renin
TGAK
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Angiotensin-I
Angiotensin
ACE lungs.
Angiotensin II
Adrenal Cortex
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2 Glomerulosa
Increase small art
Increase discharge of
Decrease [K+]
Increase [Ng+]
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TECE YOU
Excretion of K+
Retention of Nat
Retention of no
Increase
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Kidneys
Increase
Aldosterone
Zona Fasciculata
Stimule
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Hypoglycemia
Long term,
Chronic
Stress
eg: Trauma
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Starvation
Cornires.
Paraventricular Nucleos
Corticotropin elleaning nomine
Corticotroper (ACTH)
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Cortisol
Glycogenoty is (Indirectly)
Gluconeogenisic
Glycogeners (Direct (w)
Protein caracolin
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depresses immune systu
Adipose Tissue
Adipocytes
Tram transtornh
corncom usia
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Just lunding Glolentin
Liver
Glyure
Glucose
Glycogen
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GLYLOGENER
MUA CREA
Prettin
catalection
AA
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Ra
Smooth Muicer Ce
Increase rensinuity et
Alpha Adrenergic retentor for NORER
Vasoconstriction
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TR-
This download link is referred from the post: MBBS Lecture Notes for all subjects (updated for 2021 syllabus) - All universities
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