gambar sistem endokrin

8/3/2019 Gambar Sistem Endokrin

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Slide 1

Opening

image

Homeostasis

Cells

Body systems

maintain

homeostasis

Cells make up

body systems

Endocrine Systems

Homeostasis is

essential for

survival of cells

Female


2/24

Slide 2

Figure 19.1

Page 702

Thyroid

gland

Right lobe Trachea Isthmus Left lobe


3/24

Slide 3

Blood

Thyroid follicular cell

*Endoplasmic

reticulum/Golgicomplex

Colloid

TGB = Thyroglobulin

I = IodineMIT = Monoiodotyrosine

DIT = Di-iodotyrosine

T3 = Tri-iodothyronineT4 = Tetraiodothyronine (thyroxine)

Lysosome

Figure 19.2

Page 703


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Slide 4

Figure 19.3

Page 705

Stress Cold ininfants

Hypothalamus

Thyrotropin-releasinghormone (TRH)

Anterior pituitary

Thyroid-stimulating

hormone (TSH)

Thyroid gland

Thyroid hormone

(T3 and T4)

Metabolic rate and heat production;

enhancement of growth and CNSdevelopment; enhancement ofsympathetic activity


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Slide 5

Thyroid-stimulating

immunoglobulin (TSI)

Anterior pituitary

No TSH

(No stimulation)

Thyroid gland

Thyroid hormone

Figure 19.4

Page 706


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Slide 6

Adrenal

cortex

Adrenal

medulla

Adrenal gland

(See next slide)

Figure 19.7a

Page 708


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Slide 7

Figure 19.7b

Page 708

Connective tissue

capsule

Zona

glomerulosa

Zona

fasciculata

Zona

reticularis

Cortex

Medulla


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Slide 8

StressDiurnalrhythm

Hypothalamus

Corticotropin-releasing

hormone (CRH)

Anterior pituitary

Adrenocorticotropichormone (ACTH)

Adrenal cortex

Cortisol

Blood glucose

(by stimulating gluconeogenesis

and inhibiting glucose uptake)

Blood amino acids

(by stimulating protein degradation)

Blood fatty acids(by stimulating lipolysis)

Metabolic fuels

and building blocks

available to help

resist stress

Figure 19.8

Page 710


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Slide 9

Figure 19.11

Page 714

Hypothalamus

GnRH CRH

Anterior pituitary

FSH, LH ACTH

Gonads Adrenal cortex

No sex hormone production

(androgens or estrogens)No gamete

productionAndrogen

Nocortisol

Enzyme

absent

Virilization= Normal pathway that does not occur

ACTH = Adrenocorticotropic hormone

GnRH = Gonadotropin-releasing hormone

FSH = Follicle-stimulating hormone

LH = Luteinizing hormone

CRH = Corticotropin-releasing hormone


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Slide 10

Stressor

Body

Specific response characteristic

of type of stressor

Nonspecific generalized response

regardless of type of stressor =

Stress response

Figure 19.12

Page 716


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Slide 11

Figure 19.13

Page 718

Stressor

Hypothalamus

Sympathetic

nervoussystem

CRH

Anteriorpituitary

ACTH

Adrenal cortex

Cortisol

Posterior

pituitary

Vasopressin

Adrenal medulla

Epinephrine

Glucagon-secreting cellsInsulin-secreting cells

Endocrinepancreas

Glucagon Insulin

Arteriolar

smooth muscle

Vasoconstriction

Blood flow

through kidneys

Renin Angiotensin Aldosterone


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Slide 12

Food intake

Absorbable units

Dietary proteinDietarycarbohydrate

Dietary triglyceridefat

D I G E S T I O N

Aminoacids Glucose

Fattyacids Monoglycerides

A B S O R P T I O N

Metabolic pool

in bodyBody proteins(structural orsecretoryproducts)

Aminoacids

Urea Urinary excretion

(elimination from body)

Storage, structural, and

functional

macromolecules in cells

Glycogen storagein liver and

muscle

Triglyceridesin adipose tissuestores (fat)

Glucose

Fatty

acids

Oxidation to

CO2 + H2O + ATP (energy)

Expired(elimination from body)

Use as metabolic fuel

in cells

Figure 19.14

Page 720


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Slide 13

Figure 19.15

Page 724

Factors that increase blood glucose Factors that decrease blood glucose

Glucose absorption from

digestive tract

Hepatic glucose production:

Through glycogenolysis

of stored glycogen

Through gluconeogenesis

Blood

glucose

Transport of glucose into cells:For utilization for energy production

For storage

as glycogen through glycogenesis

as triglycerides

Urinary excretion of glucose (occurs

only abnormally, when blood glucose

level becomes so high it exceeds the

reabsorptive capacity of kidney tubules

during urine formation)

= Factors subject to hormonal control to maintain blood glucose level


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Slide 14

Gastrointestinal

hormones

Blood glucose

concentrationBlood amino acid

concentration

Major control

Food

intake

Parasympatheticstimulation

Islet b cells Sympathetic stimulation(and epinephrine)

Insulin secretion

Blood glucose

Blood fatty acids

Blood amino acids

Protein synthesis

Fuel storage

Figure 19.16

Page 726


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Slide 15

Figure 19.17

Page 727

Insulin deficiency

Hepaticglucoseoutput

Glucoseuptakeby cells

Triglyceride

synthesisLipolysis

Amino aciduptake by cells

Proteindegradation

Hyperglycemia Intracellularglucosedeficiency

Bloodfattyacids

Muscle

wasting

Glucosuria

PolyphagiaAlternative

energy source

Bloodamino

acids

Weight

loss

Osmotic diuresis

Polyuria

Dehydration Polydipsia Ketosis

Gluconeogenesis

Cellularshrinking

Blood volume

Peripheralcirculatoryfailure

Renal failure Death

Low cerebral

blood flow

Nervous system

malfunction

Metabolicacidosis

Diabeticcoma

Increasedventilation

Aggravation of

hyperglycemia


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Slide 16

Blood glucose

a cell b cell

Glucagon Insulin

Blood glucose

to normal

Blood glucose

a cell b cell

Glucagon Insulin

Blood glucose

to normal

Figure 19.18

Page 731


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Slide 17

Figure 19.19

Page 732

Promotes cellularuptake andassimilationof amino acids

High-protein meal

(little carbohydrate)

Blood amino acid

concentration

b cells a cells

Insulin Glucagon

Glucose uptakeby cells

Hepatic

glucose output

Hepatic

glucose output

Hypoglycemia Hyperglycemia

(Effects counteract each other)

Blood glucose

remains normal


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Slide 18

Osteocyte

Osteon

Blood vessel

from marrow

Central

canal

Vessel in central canal

Canaliculi

Lamella

Central

canal

Figure 19.20

Page 738


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Slide 19

Figure 19.21a

Page 739

Osteoblast

Outer

surface

Osteocyte

Canaliculi

Osteocyticosteoblastic bone

membrane

Mineralized

bone

Bone fluid

Osteoblast

Blood vessel

Central canal

Lamellae


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Slide 20

In canaliculi In central canal

Mineralized bone:

stable pool of Ca2+Bone fluid:

labile pool

of Ca2+

Plasma

Fast exchange

Slow exchange

(Bonedissolution)

= Membrane-bound

Ca2+ pumpFigure 19.21b

Page 739


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Slide 21

Figure 19.22

Page 740

Plasma Ca2+ Plasma Ca2+

Parathyroid glands Thyroid C cells

PTH Calcitonin

Plasma Ca2+Plasma Ca2+


22/24

Slide 22

Precursor in skin

(7-dehydrocholesterol)Dietary vitamin D

Vitamin D3

Hydroxyl group (OH)

Liver enzymes

25-OH D3

Hydroxyl group PTH Plasma Ca2+

Kidney enzymes

Plasma PO43-

1, 25-(OH)2 D3(active vitamin D)

Promotes intestinal

absorptionof Ca2+ and PO4

+

3-

Sunlight

Figure 19.23

Page 741


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Slide 23

Figure 19.24

Page 742

Relieves Plasma Ca2+

Parathyroid glands

PTH

BoneKidneys

Renal tubular

Ca2+ reabsorption

Activation

of vitamin D

Mobilization of

Ca2+ from bone

Intestine

Urinary excretion

of Ca2+Absorption of

Ca2+ in intestine

Plasma Ca2+


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Slide 24

Relieves Plasma PO43-

(Because of inverse relationship

between plasma PO43- and Ca2+

concentrations caused by solubility

characteristics of calcium phosphate

salt)

Plasma Ca2+

Parathyroid glands

PTH

Kidneys

Activated vitamin D

PO43- reabsorption

by kidneys

Ca2+ reabsorption

by kidneys

Urinary excretion

of Ca2+

Urinary excretion

of PO43-

Ca2+ absorption

in intestine

No change in plasma Ca2+PO4

3- absorption

in intestine

Plasma PO43-

(Counteract each other)

Figure 19.25

Page 743

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