k18 - fisiologi adrenal
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fisiologiTRANSCRIPT
© 2012 Pearson Education, Inc.
Fisiologi Sistem EndokrinC h a p t e r
18
Kelenjar Adrenal
Tujuan Pembelajaran1. Menjelaskan fisiologi hormon korteks adrenal2. Menjelaskan fisiologi hormon medula adrenal
Figure 18-14a The Adrenal Gland
Right superioradrenal arteries
Celiac trunk
Right adrenalgland
Right middleadrenal artery
Right inferioradrenal artery
Right renal artery
Right renal vein
A superficial view of the leftkidney and adrenal gland
Right and left inferiorphrenic arteries
Left adrenal gland
Left middleadrenal arteryLeft inferioradrenal arteries
Left adrenal vein
Left renal artery
Left renal vein
Superior mesentericartery
Abdominal aorta
Inferior vena cava
Figure 18-14c The Adrenal Gland
Adrenalcortex
Capsule
Adrenalmedulla
Zonareticularis
Zonafasciculata
Zonaglomerulosa
Adrenal gland
The major regions of an adrenal gland
LM 140
Cholesterol
Pregnenolone Dihydroepi- andr♂sterone
Progesterone 17-Hydroxyprogesterone Androstenedione
TestosteroneCortisolCorticosterone
Aldosterone(Mineralocorticoid)
(Glucorticoids)
Testes
Estradiol
Ovaries
(Androgens)
Figure 18-3 G Proteins and Hormone Activity
Hormone
Proteinreceptor
G proteinactivated
Hormone
Proteinreceptor
G proteinactivated
Effects on cAMP LevelsMany G proteins, once activated, exert their effects by changing the concentrationof cyclic-AMP, which acts as the second messenger within the cell.
Increasedproduction
of cAMPadenylatecyclaseActs as
secondmessenger
kinase
Activatesenzymes
Opens ionchannels
If levels of cAMP increase,enzymes may be activatedor ion channels may beopened, accelerating themetabolic activity of the cell.
Examples:• Epinephrine and norepinephrine (β receptors)• Calcitonin• Parathyroid hormone• ADh, ACTH, FSH, LH, TSH• Glucagon
Examples:• Epinephrine and norepineph- rine (α2 receptors)
In some instances, G proteinactivation results in decreasedlevels of cAMP in thecytoplasm. This decrease hasan inhibitory effect on the cell.
Enhancedbreakdown
of cAMPPDE
Reducedenzymeactivity
Hormone
Proteinreceptor
G protein(inactive)
G proteinactivated
Figure 18-4a Effects of Intracellular Hormone Binding
Receptor
Diffusion throughmembrane lipids
CYTOPLASM
Target cell response
Alteration of cellularstructure or activity
Translation andprotein synthesis
Binding of hormoneto cytoplasmic ornuclear receptors
Transcription andmRNA production
Gene activation
Binding ofhormone–receptorcomplex to DNA
Nuclearpore
Nuclearenvelope
Receptor
If we are talking about hormones, we always have to think abaout :
1. The name2. The glands/ the cells3. The target cells4. Function in the target cells5. The stimulaters6. The inhibitors7. Feed back mechanism
Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Mineralocorticoid
• Aldosteron• Source: Zona Glomerulosa (outermost region)• Target Sel:
• Tubulus distal• Taste bud
Mineralocorticoid
• Efect:• Stimulates conservation of sodium ions and elimination of potassium
ions• Increases sensitivity of salt receptors in taste buds
• Stimulator:• Drop in blood Na+, blood volume, or blood pressure via RAA• Rise in blood K+ concentration
Mineralocorticoid
• Inhibitor:• Rise in blood Na+, blood volume, or blood pressure• Drop in blood K+ concentration• ANP & BNP
• Feed back mechanism
Glucocorticoid
• For example, cortisol (hydrocortisone)• Liver converts cortisol to cortisone• Source: Zona Fasciculata • Target sel:?
Glucocorticoid
• Efect:1. Metabolic efect:
overall effect: increase plasma glucose levels,
often at the expense of proteins and fatsa. Carbohydrate
• gluconeogenesis• decrease glucose utilization(anti- insulin effect)
b. Protein• proteins are mobilized • lean body mass decreases
Glucocorticoid
• Efect:1. Metabolic efect:
c. Fat• causes lipolysis (enhances catecholamines)• expectations: person will be thin, but if excessive cortisol see unusual fat
distribution (i.e. “buffalo hump”)
d. Increases Hunger
Glucocorticoid
• Efect:2. Other Effects:
a. Fetal Development• Cortisol aids in maturation of the lungs, especially with the production of
surfactant
b. Adultsi. Anti-inflammatory
• during tissue damage, phospholipase A2 activity increases releasing arachadonic acid to aid in synthesis of prostaglandins & leukotrienes
• glucocorticoids enhance production of macrocortin which inhibits phospholipase A2 and thus the inflammatory response
Glucocorticoid• Efect:2. Other Effects:
b. Adultsii. Immune Response
• glucocorticoids suppress the immune system by decreasing the number of T lymphocytes
• used frequently after organ transportsiii. Vasoconstriction
• Glucocorticoids necessary for vasocontriction effects of the catecholaminesiv. Stimulates Erythropoietinv. Increases Bone Reabsorbtionvi. Decreases REM Sleep
Glucocorticoid• Stimulator:1. CRH
2. ACTH3. Hypoglicemia4. Stress
* Stress and hypoglycemia can also trigger the release of CRH
Glucocorticoid
• Inhibitor:-• Feed back mechanism
Androgen
• DHEA• Source: Zona Reticularis• Target sel: ?• Efect:• sexual characteristics• Anabolic
Androgen
• Stimulator• ACTH
• Inhibitor• Feed back mechanism
18-6 Adrenal Glands
• The Adrenal Medulla
• Contains two types of secretory cells
• One produces epinephrine (adrenaline)
• 75% to 80% of medullary secretions
• The other produces norepinephrine (noradrenaline)
• 20% to 25% of medullary secretions
18-6 Adrenal Glands
• Epinephrine and Norepinephrine• Activation of the adrenal medullae has the following
effects:• In skeletal muscles, epinephrine and norepinephrine
trigger mobilization of glycogen reserves• And accelerate the breakdown of glucose to provide ATP
• This combination increases both muscular strength and endurance
• In adipose tissue, stored fats are broken down into fatty acids • Which are released into the bloodstream for other
tissues to use for ATP production
18-6 Adrenal Glands
• Epinephrine and Norepinephrine• Activation of the adrenal medullae has the following
effects:
• In the liver, glycogen molecules are broken down
• The resulting glucose molecules are released into the bloodstream
• Primarily for use by neural tissue, which cannot shift to fatty acid metabolism
• In the heart, the stimulation of beta 1 receptors triggers an increase in the rate and force of cardiac muscle contraction
Table 18-5 The Adrenal Hormones
Table 18-9 Clinical Implications of Endocrine Malfunctions
The Hormonal Responses to Stress
• General Adaptation Syndrome (GAS) • Also called stress response• How body responds to stress-causing factors
• Is divided into three phases
1. Alarm phase
2. Resistance phase
3. Exhaustion phase
Figure 18-20 The General Adaptation Syndrome
Alarm Phase (“Fight or Flight”)
BrainGeneralsympatheticactivation
Sympatheticstimulation
Adrenal medulla
Epinephrine,norepinephrine
Immediate Short-TermResponses to Crises
• Increased mental alertness• Increased energy use by all cells• Mobilization of glycogen and lipid reserves• Changes in circulation• Reduction in digestive activity and urine production• Increased sweat gland secretion• Increased heart rate and respiratory rate
Figure 18-20 The General Adaptation Syndrome
Resistance Phase
Renin-angiotensinsystem
Sympatheticstimulation
Growth hormone
PancreasGlucagon
ACTH Adrenal cortex
Glucocorticoids
Mineralocorticoids(with ADH)
Kidney
Long-Term MetabolicAdjustments
• Mobilization of remaining energy reserves: Lipids are released by adipose tissue; amino acids are released by skeletal muscle• Conservation of glucose: Peripheral tissues (except neural) break down lipids to obtain energy• Elevation of blood glucose concentrations: Liver synthesizes glucose from other carbohydrates, amino acids, and lipids• Conservation of salts and water, loss of K+ and H+
Figure 18-20 The General Adaptation Syndrome
Exhaustion Phase
Collapse of Vital Systems
• Exhaustion of lipid reserves• Cumulative structural or functional damage to vital organs• Inability to produce glucocorticoids• Failure of electrolyte balance