Gambar Sistem Endokrin

 

Endocrine Systems

Body systems maintain homeostasis

Homeostasis

Homeostasis is essential for  survival of cells Female

Cells Cells make up body systems Opening image Slide 1

 

Thyroid gland

Figure

Right lobe

Trachea

Isthmus

Left lobe

19.1 Page 702 Slide 2

 

Colloid

Blood Thyroid follicular follicular cell

*Endoplasmic reticulum/Golgi complex

Lysosome

Figure

TGBI == Iodine T hyroglobulin Thyroglobulin MIT = Monoiodotyrosine

DIT Di-iodotyrosine e T3== Di-iodotyrosin Tri-iodothyronine T4 = Tetraiodothyronine Tetraiodothyronine (thyroxine)

19.2 Page 703 Slide 3

 

Stress

Cold in infants

Hypothalamus

Thyrotropinreleasing hormone (TRH)

Anterior pituitary

Thyroid-stimulating hormone (TSH)

Thyroid gland Thyroid hormone (T3 and T4) Figure

Metabolic rateof and heat production; enhancement growth and CNS development; enhancement of  sympathetic activity

19.3 Page 705 Slide 4

 

Anterior pituitary

Thyroid-stimulating immunoglobulin immunoglobuli n (TSI)

No TSH

(No stimulation)

Thyroid gland

Thyroid hormone Figure

19.4 Page 706 Slide 5

 

Adrenal cortex

Adrenal medulla

(S ee ee next slide)

Adrenal gland

Figure

19.7a Page 708 Slide 6

 

Connective tissue capsule Zona glomerulosa

Zona fasciculata Cortex

Zona reticularis

Medulla

Figure

19.7b Page 708 Slide 7

 

Diurnal rhythm

Stress

Hypothalamus Corticotropin-releasing hormone (CRH)

Anterior pituitary Adrenocorticotropic hormone (ACTH) Adrenal cortex

Cortisol

Metabolic fuels and building blocks available to help resist stress

Blood glucose (by stimulating gluconeogenesis and inhibiting glucose uptake) Blood amino acids (by stimulating protein degradation) Blood fatty acids (by stimulating lipolysis)

Figure

19.8 Page 710 Slide 8

 

Hypothalamus

GnRH

CRH

Anterior pituitary

FSH,

LH

ACTH

Adrenal cortex

Gonads

Enzyme absent No sex hormone production (androgens or estrogens)

No gamete production

Androgen

No cortisol

Virilization = Normal pathway that does not occur  FSH = Follicle-stimulating hormone ACTH = Adrenocorticotropic hormone LH = Luteinizing hormone GnRH = Gonadotropin-releasing hormone CRH = Corticotropin-releasing Corticotropin-releasing hormone

Figure

19.11 Page 714 Slide 9

 

Stressor 

Specific response characteristic of type of stressor  Body Nonspecific generalized response regardless of type of stressor = Stress response

Figure

19.12 Page 716 Slide 10

 

Stressor  Hypothalamus

CRH

nervous Sympathetic system

Posterior  pituitary

Anterior  pituitary ACTH

Vasopressin Adrenal medulla

Adrenal cortex

Epinephrine

Cortisol

Glucagon-secreting cells Glucagon-secreting Insulin-secreting cells Endocrine Arteriolar  smooth muscle pancreas Vasoconstriction

Glucagon

Insulin Blood flow through kidneys

Renin

Angiotensin

Aldosterone

Figure

19.13 Page 718 Slide 11

 

Food

intake

Dietary protein

Dietary carbohydrate

Dietary triglyceride fat

D I G E S T I O N

Absorbable units

Amino acids

Glucose

Fatty

acids

Monoglycerides

A B S O R P T I O N

Metabolic in body pool Body proteins (structural or  secretory products)

Storage, structural, and functional macromolecules macromolecu les in cells

Glycogen storage in liver and muscle

Triglycerides in adipose tissue stores (fat)

Amino acids

Urea Urinary excretion (elimination from body)

Oxidation to CO2 + H2O + ATP (energy)

Glucose

Fatty

acids

Expired (elimination from body)

Use as metabolic fuel in cells Figure

19.14 Page 720 Slide 12

 

Factors

that increase blood glucose

Factors

that decrease blood glucose

Transport of glucose into cells:  ±±For utilization for energy production  ±±For storage as glycogen through glycogenesis as triglycerides

Glucose absorption from digestive tract Blood glucose Hepatic glucose production:  ±±Through glycogenolysi glycogenolysis s of stored glycogen  ±±Through gluconeogenesis

Urinary excretion of glucose (occurs only abnormally, when blood glucose level becomes so high it exceeds the reabsorptive capacity capacity of kidney tubules during urine formation)

Figure

= Factors subject to hormonal control to maintain blood glucose level

19.15 Page 724 Slide 13

 

Blood glucose concentration Gastrointestinal hormones

Blood amino acid concentration

Major control Food

intake

Parasympathetic stimulation

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 Slide 14

 

Insulin deficiency

Hepatic glucose output

Glucose uptake by cells

Hyperglycemia

Intracellular  glucose deficiency

Triglyceride synthesis

Polyphagia

Alternative energy source

Polyuria Dehydration

Amino acid uptake by cells

Protein degradation

Blood fatty acids

Glucosuria Osmotic diuresis

Lipolysis

Muscle wasting Blood amino acids

Weight loss

Gluconeogenesis

Polydipsia

Ketosis

Cellular  shrinking Blood volume

Peripheral circulatory failure

Nervous system malfunction

Low cerebral blood flow

Metabolic acidosis

Increased ventilation

Aggravation of  hyperglycemia

Diabetic coma Figure

Renal failure

Death

19.17 Page 727 Slide 15

 

Blood glucose

a cell

Blood glucose

b

cell

Insulin

Glucagon

Blood glucose to normal

a cell

b

Glucagon

cell

Insulin

Blood glucose to normal

Figure

19.18 Page 731 Slide 16

 

High-protein meal (little carbohydrate) carbohydrate)

Blood amino acid concentration

b

cells

a cells

Insulin

Promotes cellular  uptake and assimilation of amino acids

Glucagon

Glucose uptake by cells

Hepatic glucose output

Hepatic glucose output

(Effects counteract each other) Hypoglycemia Hyperglycemia

Blood glucose remains normal

Figure

19.19 Page 732 Slide 17

 

Central canal Osteocyte

Lamella Canaliculi

Osteon

Blood vessel from marrow Central canal Figure

Vessel in in central canal

19.20 Page 738 Slide 18

 

Osteocyte

Osteoblast

Osteocytic± osteoblastic bone membrane Osteoblast

Mineralized bone

Outer  surface

Blood vessel

Central canal Bone fluid

Canaliculi

Lamellae Figure

19.21a Page 739 Slide 19

 

In canaliculi

Mineralized bone: stable pool of Ca2+

In central canal

Plasma

Bone fluid: labile pool of Ca2+

Fast

exchange

Slow exchange (Bone dissolution)

= Membrane-bound Ca2+ pump

Figure

19.21b Page 739 Slide 20

 

Plasma Ca2+

Plasma Ca2+

Parathyroid glands

Thyroid C cells

PTH

Calcitonin

Plasma Ca2+

Plasma Ca2+

Figure

19.22 Page 740 Slide 21

 

Precursor in skin (7-dehydrocholesterol)

Dietary vitamin D Sunlight

Vitamin D3 Hydroxyl group (OH) Liver enzymes

25-OH D3 PT H

Hydroxyl group

+

Plasma Ca2+

Kidney enzymes Plasma PO4

3-

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

Promotes intestinal absorption of Ca2+ and PO4 3-

19.23 Page 741 Slide 22

 

Relieves

Plasma Ca2+

Parathyroid glands

PTH

Kidneys

Renal tubular  Ca2+ reabsorption

Bone

Activation of vitamin D

Mobilization of  Ca2+ from bone

Intestine Urinary excretion of Ca2+

Absorption of  Ca2+ in intestine Figure

19.24 Page 742

Plasma Ca2+

Slide 23

 

Relieves

Plasma PO43-

(Because of inverse relationship between plasma PO43- and Ca2+ concentrations caused by solubility characteristics of calcium phosphate salt) Plasma Ca2+

Kidneys

Parathyroid glands

Activated vitamin D

PTH

PO43- reabsorption by kidneys

Ca2+ reabsorption by kidneys

Urinary excretion of Ca2+

Ca2+ absorption in intestine

(Counteract each other) Urinary excretion of PO43-

No change in plasma Ca 2+

PO43- absorption in intestine Figure

Plasma PO43-

19.25 Page 743 Slide 24