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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

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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