-secreted by cells called endocrine cells

-secreted into blood and carried to targets

-very low concentrations

-act by binding receptors

-extension of neural tissue

-secretes neurohormones

-Vasopressin (ADH)- "water homeostasis"

-produces zero hormone

secretes 6 hormones

-thyroid stimulating hormone (TSH)

-Adrenocorticotripon (ACTH)

-Growth Hormone (GH)

-Follicle stimulating hormone (FSH)

-Leutinizing Hormone (LH)

-Prolactin

secretes: thyrotropin relasing hormone (TRH), Corticotropin releasing hormone (CRH), Growth hormone releasing hormone (GHRH), Growth hormone inibiting hormone (GHIH), Gonadotropic releasing hormone (GRH), Prolacting releasing hormone, Prolactin inhibiting hormone (dopamine)

primary effect is on the Na/K pumps

increase metabolic rate

calorigenic-producing heat

thyroid deficiency in infancy

reversible upon restoration of normal thyroid hormone levels

heat intolerant, metabollic rate is really cranked up

increased protein catabolism

irritablitly, insomnia, excitable reflexes

increased T3 or T4, decreased TSH

Graves' Disease

reduced secretion of thyroid hormones

decreased protein synthesis

cold intolerant-low metabolism

slowed heart rate

myxedema-fluid is held onto and makes thick skin

enlarged thryoid gland

may be present with hypo, hyper, or euthyroid (normal) states

chromafin cells secrete epinephrine

sympathetic nervous system

zona glomerulosa

zona fasiculata

zona reticularis

-different zone contain different complements of enzymes involved in hormone production

called adrenocorticoids

mineralocorticoids

Glucocorticoids

aldosterone is main example

secreted by zona glomerulosa

regulate Na absorption and K secretion at kidney

Glucocorticoids

secreted by zona fasiculata and reticularis

regulates body's response to stress

affect protein, carb, lipid metabolism

affects blood glucose levels

inhibits inflammation and the immune response

hypercortisol

either ACTH increase, Cortisol increase, or an iatrogenic--medically induced--excess of cortisol

hyperglycemia

protein depletion leading to muscle wasting, fragility of tissue

moon facies, buffalo hump

hypertension

hyposecretion of cortisol and aldosterone

hypoglycemia, poor stress tolerance

excess Na excretion and K retention

secreted by anterior pituitary

increase cell size (hypertrophy)

increase cell number (hyperplasia)

produced in the liver and are released into bloodtream for transport to target tissues

-hormone in response to GH

Hydroxyapaptite

the end of long bones

located between the epiphysis and shaft in growng bowns

Also known as the growth plate

lay down cartelidge

responsible for increase in bone length

defincient growth hormone secretion

irreversible, stunting of growth, poor muscle development, and higher than normal body fat

sits on spinal coloumn

endocrine and exocrine gland

b cells and a cells

b- insulin

a- glucagon

nutrients enter the bloodstream from the GI tract, glucose is in abundant suppl.

excess nutrients stored as glycogen, triglycerides, or protein

Post absorptive state

nutrients are not being absorbed by the GI tract and energy must be supplied by the body's endogenous stores

keep plasma glucose at appropriate levels to supply brain

secreted by b cells

anabolic hormone- promotes synthesis of energy storage molecules

increase in plasma glucose levels directly stimulate b cells to secrete insulin

synthesis of fatty acids and triglycerides

synthesis of glycogen in liver

protein synthesis

Using GLUT-4

feeding and absorption of nutrients

respond to stimulation from the parasympathetic nervous system--rest and digest

GIP (glucose dependent insulinotropic peptide)- secreted by intestinal tract in resonse to presence of food

sympathetic stimulation inhibits insulin secretion

facilitates movement of glucose into most cells

stimulates formation of glycogen (glycogenesis) in liver and skeletal muscle

increases transport of amino acids into cells

enhances protein synthesis

promotes movment of fatty acids into tissue

increases glucose transporters on adipose tissue-GLUT-4

increases metabolic pathways forming triglycerides

secreted by alpha cels

catabolic hormone-break things down

promotes glycogenolysis and gluconeogenesis

promotes ketone formation-fatty acids

promotes breakdown of proteinds-amino acids

no synthesis

breakdown of glycogen

formation of glucose by gluconeogenesis

promotes breakdown of protein in liver

promotes gluconeogenesis

effects of glucagon on lipids

promotes breakdown of triglycerides freeing up glycerol and fatty acids

glycerol for gluconeogenesis

fatty acids transported to liver and converted to ketones

fasting glucose concentration is too high

indicative of diabetes mellitus-disease involving defects of insulin production of target tissues

-nutrient intake is intermittent yet our body needs nutrients readily availabe 24hrs/day--efficient storage process

-the brain depends primarily on glucose, the level must be maintained

the muscle cell

may extend the length of the entire muscle

hocky stick like

2 binding sites, actin and myosin ATPase

head portion is called the cross bridge

G-actin denotes the individual globular component of actin

two strands of F-actin twisted together

threadlike molecule that lies in the 'groove' of the actin spiral

at rest blocks binding site on actin for myosin

3 binding sites

-tropomyosin

-actin binding site

-Ca++

myosin binds to ATP=> becomes ADP + Pi--activation of myosin head

-when myosin attaches to actin it is called the power stroke

-ATP must bind the myosin ATPase to detach myosin

-binds to Ca binding site on troponin

-troponin 'dragging' tropomysoin away from actin

-myosin binds to actin

-the Ca was released from SER and must be pumped back in via ATP pumps during relaxation

-one of the first steps of a muscle contraction

-ALWAYS excitatory and will be an action potential

what the action potential is conducted along

adjacent to SER of myofibril where Ca++ is located

cross bridge cycling and ends at point of peak tension

-Ca++ release exceeds reuptake

longest of 3 phases

Ca++ reuptake exceeds release

progressively more frequent stimulation, relaxation period becomes even shorter

-individual periods of very brief relation can be distinguished

maximal tension is reached

individual tensions cannot be identified

most the muscle fiber can develope

length tension curve relates to the sliding filament mechanism of tension development

OPTIMAL LENGTH

x=5 fibers

y=7 fibers

x+y= 12 fibers

contractile element- consists of the sarcomeres

-what actually produces the tension

series elastic element 

the tendons

dones not actively generate force rather it passively transmits the force generated by the contractile elements to the skeletal components to which it is attached

muscle shortening does not occur

load is greater than tension which muscle can generate

tension is generated which is at least equal to the force opposing it

-sarcomeres shorten and the series elastic elements lengthen

replinsh ATP

creatine phosphate +ADP↔ATP+ creatine

provides for about 10 seconds

with or without oxygen

means of rapidly producing large amounts of ATP

last for about a minute

in the presence of oxygen, glycogen and fatty acids can be processed completely through oxidative pathways

contracting muscles for an extended ammount of time.

fast fibers- contain myosin ATPase with fast activity

Slow fibers- contain myosin ATPase with slow activity

fatigue easily-relatively few mitochondria

relatively larger

fewer capillaries

Rich in mitochondria-high resistance to fatigue

relatively smaller

good capillary supply

contain myglobin

oxygen binding protein acts as oxygen reserve

imparts red color to tissue

slow myosin ATPase

typically smaller fibers

intermediate size fibers

fast myosin ATPase high oxidative capacity

Fast glycolitic fibers

larger fibers

fast myosin ATPase

High glycolytic capacity

sheets

in the walls of internal organs and blood vessels

very efficient with energy

uninucleated, not striped

no t tubles or sarcomeres

-still utalizes Ca++ but does not have an SER like skeletal muscle

-cells act as a 'single unit'

-due to extensive linking with gap junction

-contain pacemaker cells which can initiate depolarization of the entire muscle

-stretching may induce contraction

-resting level of contraction 'tone'

act as individual units

no gap junctions

no pacemaker cells

stretching does not cause contraction

do not maintain a level of resting tone

initiates the cross bridge formation

myosing light chan phosphatase is required to inactivate myosin

smooth muscle therefore contractios are slower than skeletal muscle

-no problem with fatigue

when a contraction is caused without a change in membrane potential

smoot muscle does not need an action potential

striated

made up of two kinds of cells: contractile and autorhythmic

make up 99 percent of the heart

utilize actin and myosing to create tension

1 percent of cardiac cells

do not create tension "conductive cells"

junctions that contain both desmosomes and gap junctions

depolarization travels via gap junctions

votage dependent Ca++ channels than open Ca channels on the SER

called Ca mediated Ca release

-90 resting potential, lower than cell

plateau phase to ensure heart does not go to tetany

sodium channels open quickly

do not create tension

pacemaker potential

funny sodium channels

do not have voltage gated sodium channels-Ca++

works together with contractile cells

located in right atrium

determines heart rate in normal situations

built in pause button

near tricuspid valve

conducts slowly

release of nor-epinephrine to b₁ receptors on SA node

speeds the heart rate up

enjances opening of funny channels and Ca++ channels

travel via vegus nerve

ACH binds to muscarinic receports on SA node

slows down the heart rate by inhibiting funny channels

enhances K channels