pituitary

thyroid

parathyroid

adrenal

pineal 

pancreas

gonads

thymus

other structures no solely endocrine

-secretes at least 9 hormones

growth hormone

thyroid stimulating hormone

follicle-stimulating hormones

oxytocin

antidiuretic hormone

-size of pea

-two lobes-posterior/anterior

-located in the anterior neck on the trachea

-largest purely endocrine gland in the body

-produces the major metabolic hormone thyroid hormone

-thryoid hormone is two different hormones

-T₄ and  T₃

-Hormones increase metabolism, protein synthesis, growth, development in most cells

-located on the posterior portion of the thyroid 

-usually 4 per person, but can vary greatly

-secretes hormone parathyroid hormone

-single most important hormone in controlling calcium levels in blood

-stimulates osteoclasts to reabsorb calsium from the bones into the blood

-pyramid shaped organs located atop each kidney

-each gland is structurally two glands: the adrenal medulla and the adrenal cortex

-each region produces its own hormones

-cortex hormones-

-aldosterone, cortisol, testosterone, estrogen

-medullary hormones

-epinephrin,nonepinephrin

-located behind stomach

-mixed gland composed of endocrine and exocrine gland cells

-produces insulin and glycogen which control blood glucose levels

-produce steroid sex hormones

-women: ovaries

-small oval organs located in the abdominal pelvic cavity

-produce estrogen and progesterone

-men:testes

-located in the scrotum

-produce testosterone

Pineal Gland

-located in the brain

-secretes melatonin

-causes drowsiness

-highest at night 

-located deep to the sternum

-large in infants and decreases in size and function with age

-secretes thymopoietins, thymic factor, and thymosins

-essential for development of T lymphocytes and immune resonse

-stomach-gastrin

-Kidneys- erythropoietin, renin

-heart-atrial natriuretic peptide

-others

hypothalamus

pituitary

pineal

Thyroid

parathyroid

thymus-below thyroid

adrenals

pancreas

testicles

ovaries

-stimulate activity in the organ-systems of the body

-inhibit or stimulate release of other hormones

-nervous

-gastrointestinal

-cardiovascualr

-hepatic

-renal systems

-each hormone has a specific relationship with its target cells

-for a hormone to affect the cell, the cell must have a specific protein receptor

Hormone-AHD

Target-posterior pituitary

Hormone Function- stimulate release of hormones by posterior pituitary

-Growth hormone

-Thyroid-stimulating hormone

-Follicle-stimulating Hormone

-Luteinizing hormone

*secreted by anterior pituitary

-all cells-target

-function- growth and development; protein synthesis; breakdown of fats for energy

*anterior pituitary

Target- Thyroid gland

Function- increase thyroid function, stimulate release of thyroid hormones (T3 and T4)

*anterior pituitary

-Target- ovaries/testes

-Function- increase estrogen release/increase sperm production

*ant pituitary

-ovaries/testes

-stimulate ovulation/increase testosterone release

-antidiuretic hormone

-oxytocin

*posterior pituitary

-Target- Kidneys

-Function- reabsorption of water, increased blood volume, increased blood pressure

*posterior pituitary

-Target- uterus, mammary glands(females)/ Ductus deferens, prostate gland (males)

Function- female- labor contractions, milk secretion

male- contractions of ductus deferens and prostate, ejection of secretions

Thyroxine- T4

Triiodothyronine- T3

Calcitonin- CT

*thyroid

-target- most cells

- increase metabolism, protein synthesis, growth and development

*thyroid

-target- most cells

-function- increase metabolism, protein synthesis, growth and development

*thyroid

-bones, kidneys

-decrease demineralization of bone

Parathyroid hormone- PTH

-bones, kidneys

-Increase calcium in blood by demineralizing bone

Thymosins

lymphocytes

increase effectiveness of immune system

Aldosterone

cortisol

epinephrine

norepinephrine

*adrenal

-Kidneys

-increase reabsorption of water and sodium ions in kidneys

most cells

-anti-inflammatory effects, tissue, cataabolism, response to stress; increases synthesis of glucose and glycogen formation

*adrenal

-Target- most cells

-respond to stress (increase heart rate, increase blood flow to muscle, decrease blood flow to internal organs); increase glycogen breakdown and release of lipids from adipose tissue

sympathetic nervous system

*adrenal

-most cells

-vasoconstriction

insulin

glucagon

*pancreas

-all cells (except those of brain, kidneys, GI, epithelium, and RBCs)

-increase glucose transport out of blood and into cells

*pancrease

Liver, adipose tissues

breakdown of glycogen in liver, release glucose from liver into blood, release of fat stores

-glucose is the body's primary energy source

-endocrine system is responsible for maintaining normal blood glucose levels

-pancreas releases insulin and glucagon

-adrenal glands release epinephrine, norepinephrine, and cortisol

-pituitary releases growth hormone

Regulation of Body Energy Cont.

-insulin lowers blood glucose levels by transporting glucose from the blood into the cells for engery

-when glucose levels exceed the body's need for fuel, insulin sweeps the excess glucoe out of blood to be stored as either glycogen in liver and muscles, or fat in adipose tissues

-glucagon, epinephrine, norepinephrine, cortisol, and growth hormone

-work collectively to increase blood glucose levels

-stimulate the release of glucose from glycogen stores

-promote gluconeogenesis

-insulin levels decrease as metabolic demand for glucose increases

-glucose released in response to think increased fuel demand, primarily through function of glucagon

-insulin receptors on muscle cells become more sensitive- increases the muscular uptake of glucose

-normal metabolic processes produce excess energy at rest

-this energy released as heat

-maintains the body's temp within a narrow range

-Body can also regulate heat loss or heat production in response to environmental conditions

-core body temp rises

-physiological heat-dissipating mechanisms begin to function

-radiation of heat from head and neck

-evaporation of sweating

Sensitive to blood temperature

-increases or decreases thyroid-stimulating hormone in pituitary gland

-increased TSH increases production of thyroid hormone, which then increases body temp

-decreased TSH lowers metabolism and body temp

ADH

-forms in hypothalamus

-secreted by pituitary

ADH retains water in body

-increases water reabsorption in the kidneys

-decreases urine volume

-Decreases in blood volume (dehydration) lead to increases in ADH secretion

-Maintaining hydration during activity inhibits the secretion of ADH since, when properly hydrated, there is no need to retain water

Men- stimulate testosterone release, which increases protein sythesis

Women- stimulate estrogen release, which inhibits uptake of glucose

-skin changes

-diaphoresis-hyperhydrosisi excessive sweating

-body or breath odor

-polydipsia-excessive thirst and polyuria-excessive urination

-arthralgia and myalgia

-muscle atrophy and weakness

-amenorrhea and impotence

-confusion or change in mental status

-paraesthesia

-edema and pitting edema

-polyphagia- excessive hunger

-postural hypotention- changes to blood pressure depending on positioning

-lethargy and fatigue

The endocrine glands rarely produce pain

the signs and symptoms of hormonal imbalances are usually more relevant than reports of pain

thyroid can cause pain on palpation

-depending on the condition, observation, palpation, and the assessment of vital signs may be the only physical examination procedures that indicate potential endocrine pathology

- most endocrine diseases require medical laboratory testing to confirm the diagnosis

-normal blood glucose levels

-random: 70-110mg/dL

-fasting:60-80mg/dL

-postprandial:100-140mg/dL

When blood glucose levels become excessively high, glucose spills over into urine

ketones-sign of impending ketoacidosis, a potentially life-threatening condition

Type 1: INSULIN DEPENDENCE- formerly called insulin dpendent diabetes mellitus or juvenile diabetes

-passed from father to daughter and mother to son

Type 2: INSULIN RESISTANCE- formerly known as noninsulin dependent diabetes mellitus or adult onset diabetes

Gestational- can occur during pregnancy

-autoimmune disorder

-pancreas secretes little or no insulin

-without insulin, blood glucose levels become very high

-management requires delicate balance between insulin, diet, and exercise

-abrupt onset

-typically appears before age 25

polydipsia

polyphagia

polyuria

weight loss

may present initially with ketacidosis

-laboratory blood test

-treated with insulin

-produces effects within 5-30 min

-peak effect occurs between 1-4 hours

-duration of 4-8 hours

produces effects within 2-4 hours

peak effect occurs between 8-14 hours

duration up to 24 hours

-require several injections of insulin each day

-injections administered subcutaneously

-it is generally recommended that athletes inject insulin into nonexercising body parts such as abdomen

-some may use an insulin pump

-hypoglycemia

-hyperglycemia

-ketoacidosis

-peripheral and autonomic neuropathy

-retinopathy leading to blindness

-cardiovascular disease

-hypertension

-kidney disorders

-chronic skin ulcers

- poor healing

-blood glucose >200 mg/dL

-gradual onset, abdominal pain, thirst but no hunger, fruity odor on breath, dehydration, lethargy, confusion, loss of consciousness

-blood glucose <70 mg/dL

-sudden onset, headache, hunger but not thirst, blurred vision dizziness, decreased performance, autonomic signs (pallor, diaphoreses, tachycardia, tremors), fatigue, slurred speech, confusion

-much more common than hyperglycemia in type 1 diabetes

-occurs during physical exertion when there is a high level of circulating insulin

-Commonly occurs when an individual injects insulin before exercise and then fails to eat

-athletes must learn to estimate the correct insulin dosage based on the expected intensity and duration of the practice or competition

-use glucometer to monitor BGL 2-4 times a day

-most will start showing signs when levels drop to 50-60 mg/dL

-if an individual recognizes an impending hypoglycemic attack, he should stop activity immediately and consume 30-40g of carbs

-caused by excessively high levels of glucose, which is associated with low levels of insulin

-emotional stress-

-illness or injury

-change in activity level

-addition of a new medication that might stimulate glucose release

-missed insulin dose

-using fat stores for energy and not sugars

-when the body is unable to move glucose from blood to the cells, it turns to fats as an energy source

-ketones are produced as a by product of the breakdown of fats and fuel

-These toxic acids build up in the blood and eventually spill over into the urine

-Ketones are responsible for the fruity odor noticed on the breaths of persons suffering from hyperglycemia and DKA

-glucose reading over 200 mg/dL

-requires urinalysis to screen for ketones

-insulin should be administered immediately

-patient should be transported for medical examination and monitoring

-treatment includes rehydration and restoration of electrolyte balance to correct the acidosis

-normal or high levels of insulin

-Decreased insulin receptor sensitivity

-glucose uptake by the liver and muscles is substantially impaired because the insulin receptors in the liver do not respond to circulating insulin

-BGL remain higher than normal

-positive family history of type 2 and presence of obesity are strong predictors

-Body makes insulin but doesn't use it

-exercise and controlled diet are mainstays in treatment of type 2 

-directly affects blood glucose levels

increases metabolic demand of muscles, which burns more glucose as fuel

increasing the effectiveness of insulin receptors

-low to moderate intensity exercise facilitates muscle glucose uptake in persons with type 2 diabetes

-Since exercise affects glucose levels, athletes with type 1 should discuss adjustment of insulin type, dose, or regimen with their physician

-preparticipation meals and insulin should be adjusted for both expected exercise intensity and blood glucose level at the time of the meal

-BLOOD GLUCOSE LEVES

-immediately before exercise- BLC <100 mg/dL requires a carb snack to raise BGL

-During exercise- = 15 to 30g of carb per half-hour of athletic exercise may be needed to prevent hypoglycemia

-fruit juice

-glucose tablets or gel

-soda

-oranges

-hard candy

-whatever you have

-stop activity at first sign of hypoglycemic attack

-if lose consciousness or seizure, quickly administer glucagon

-be familiar with glucometers and glucagon kits

-most emergency kits include glucagon powder and dissolving liquid to make single dose of 1 mL of glucagon

-injected IM or subcutaneously

-unconscious will regain within 5-20 min after injection

-once conscious eat small snack made up of CHO and proteins

-with type 1 may have a significant hypoglycemic response 6-24hrs after strenuous exercise

-after exercise, the body's muscle and liver glycogen stores must be restored

-existing blood glucose levels are used to synthesize glycogen-- which leads to a further depletion of BGL

-postexercise insulin dose may need to be decreased

-postexercise meal should ensure adequate caloric intake

-failure to inject insulin after exercise may cause hyperglycemia since glucose released during exercise is not countered by insulin secretion

-additional risks (due to polyuria)

-orthostatic hypotension

-dehydration

disorder of pituitary

-uncommon; kidneys are unable to conserve water as they filter blood

-caused by an inadequate secretion of ADH from pituitary

-prevents water from being reabsorbed in the kidneys

-results in large amounts of dilute urine

-polyuria

-polydipsia

-normal blood glucose levels

-hypothalamus or pituitary tumors

-hypothalamus or pituitary infections

-vascular problems that affect the hypothalamus or pituitary

-too much GH causing body tissues to get larger

 -caused by an overproduction of GH

-Continual gowth of bones and soft tissues

-shortened lifespan

-Most common causes of death

-cardiovascular disease secondary to cardiomyopathy, hypertension, and hyperlipidemia

-cancer- secondary to overstimulation and over production of organ cells

Disorder of Pituitary

-tall stature

-thick prominent mandible

-protuding frontal bone

- large thick hands and feet

-barrel chest

-Difficulty Concentrating

-fatigue

-Frequent BMs

-increased appetite, sweating, and weight loss

-heat intolerance

-hair loss

hand tremor, itchy skin, high BP, exophthalmos,palpitations, difficulty sleeping, blood tests reveals TSH is low but TH is high

Nuc-med iodine tx

surgical removal

Thyroid disorder

-autoimmune= most common kind of hyperthyroidism causing the thyroid to produce too much TH

-most common in women over 20

-clinical presentations the same

-may test with a radioactive iodine uptake scan

-treatment is the same as hyperthyroidism

Thyroid does not make enough TH-underactive 

-most comonly caused by thyroiditis

-Hard stools/constipation

-cold sensititivy

-Fatigue/joint and muscle pain/weakness

-thin brittle hair and fingernails

-weight gain

if untreated

-decreased taste and smell

-puffy hands, face, feet

-thick skin

-thinning eyebrows

-levothyroxine is most common supplement

-works best on an empty stomach, 1 hr before food

-requires lifelong Rx therapy

-adrenal disorder

-adrenals do no produce enough hormone (usually cortisol and aldosterone)

-changes in BP, HR, paleness, dark skin, patches, chronic diarrhea, nausea, vomiting, LOA, weakness/fatigue, mouth lesions, salt cravings

hormone therapy

Adrenal disorder

-S/S of being exposed to high levels of cortisol

-S/S- rapid weight gain, fat pad growth along neck and clavicle, round moon face, hypertension, hyperglycemia

treated through steroids of surgery

Metabolic Disorder

-uric acid builds up in the blood causing joint inflammation (typically just one)

-usually so tender it hurts to just have a sheet on it

-Tx: NSAIDs, narcotics, corticosteroids, social habit changes (stay hydrated, dont drink)

metabolic bone disease

lose too much, make too little, both

metabolic bone disease

dysfunctional bone metabolism resulting in large, misshapen bones

-connects the CNS to the rest of the body

-nerve roots

-peripheral nerves

-cerebrum

-diencephalon-hypothalamus, thalamus, pineal body

-Brain stem- medulla oblongata, pons, midbrain

-cerebellum

-motor function

-congnition

-memory

-sensory perception (touch, pressure, pain, temperature)

-special senses (sight, hearing, smell, taste)

-covered by cerebral cortex

-basal ganglia

-corpus collosum

-left receives input from and controls movements of ride side of body

-right does the opposite

-regulates thirst, body temp, water, balance, blood pressure

-regulates homeostasis

-links nervous system to endocrine system

-connects spinal cord to brain

regulates- heart rate, blood pressure, digestion, respiration, coughing, vomiting

coordinates balance

fine motor coordination

posture

bathes spinal cord

supports brain within cranium

3 layers that cover the brain

Pia mater- inner most- lies directly on brain and spinal cord

Arachnoid Mater-middle-subarachnoid space formed between pia mater and arachnoid mater (CSF circulates within this space)

Dura mater- outermost protective covering

-named according to where they exit the spinal column

-each associated with sensory patter (dermatome), motor pattern (myotome), reflex

Peripheral Nerves

fight or flight response

autonomic nervous system

involved in relaxation

autonomic nervous system

syncope or coma

paresthesia

abnormal motor control, coordination, or tone

seizure

headache

changes in vision, hearing, or other senses

changes in mental status

-carry light touch and proprioception impulses from PNS to Brain

-pathways decussate (cross) in midbrain to contralateral cerebrum

-carry pain and temperature impulses from PNS to brain

-pathways decussate in spinal cord

-Family and personal history

-observation/inspection

-special tests

-reflexes,sensation, motor, balance and coordination, cranial nerves

-epilepsy

-muscular dystrophy

-stroke

-certain degenerative CNS disorders

muscle atrophy

tremors

abnormal gait

abnormal gross and fine motor function

-decorticate posturing- injury to cerebral cortex

-Decerebrate posturing- injury to cerebellum

-not breathing, heart rate

arms pronated and wrists flexed

elbows and knees extended

-dilated, fixed pupils

-unequal pupillary response (anisocoria)

-involuntary, rapid eye movements (nystagmus)

-blood or CSF draining from ears

-bruising over mastoid process (battle's sign)

-bruising over the eyelids or periorbital area (racoon sign)

-light touch

-pressure

-pain response

-vibration sense

-temperature

indicates damage to the corticospinal tract

-associated with severe neurological pathology

poke bottom of foot- toes curl in or do nothing- negative

toes splay- positive

-orientation to person, place, and time

-simple serial tests

-seial 7s or serial 3s

-memory of events prior to a head injury (retrograde amnesia)

-memory of events after a head injury (anterograde amnesia)-3 or 5 object recall

-concussion

-epidural or subdural hematoma

-postconcussion syndrome

-spinal cord trauma

-meningitis

-cerebral palsy

-MS

-Epilepsy

-Reflex sympathetic dystrophy

-amyotrophic lateral sclerosis (ALS or Lou Gehrigs disease)

-Infection of the CNS-bacterial, viral

-S/S- stiff neck, terrible headache, violent vomiting

highly contagious

can progress rapidly

can be life threatening

rash

-stiff neck

-terrible headache

-violent vomiting

-high fever

-altered cognition

-syncope

-seizures

-coma

-immediate referral to ER

-antibiotics and corticosteroids

-caused by another virus (mumps, herpes simplex II)

-less contagious than bacterial meningitis

-similar signs and symptoms of bacterial but less severe

-caused by an injury to the brain before, during, or shortly after birth

-results in impairments to posture and motor control

-monoplegic, diplegic, hemiplegic, quadplegic, tetraplegic

-spastic 

-constant spasm

-managed by surgery, PT, OT

Muscle imbalances and excessive tightness

-predisposed to overuse injuries and muscle strains

-anterior knee pain- secondary to flexed knee gait

-low back pain- secondary to hip flexion contracture

-impaired hand-to-eye coordination

-difficulty with controlling racquets, bats, golf clubs

-difficulty with catching and throwing

impaired perception-depth and speed

-degenerative disease that affects the myelin (insulation or coating of nerves) and damages the nerve fibers

-onset usually occurs as young adult

-muscle weakness

-fatigue

-sensory changes

-lack of coordination

-vision problems

medication

excluded from sports participation

-electrical disorder of the brain- 

-Results in seizures

-Does not prevent a person from participating in sports

-Treated with medication-sedatives and tranquilizers

petit mal

grand mal

-protect the athlete from injury

-do not restrain the athlete

-once seizure stops- assess ABCs and other vitals

-assess head, face, mouth, and extremeties for injuries

-calm and reassure the athlete

after seizure, persons will be confused, probably not remember seizure, be fatigued

-first seizure or seizure lasting >5 min warrants medical referral

-occurs following an injury to an extremity

-exact cause unknown

-usuall develops within a few weeks after the original injury

-pain disproportionate to the injury

-extreme skin sensitivity

-inability to or unwillingness to move a joint

-temperature changes in limb

-atrophy

-paleness

-intolerance to cold

Amytrophic Lateral Sclerosis (ALS)

Lou Gehrigs disease

-true etiology is uknown-autoimmune response suspected

-leads to degeneration of nerve fiber and neurons

-progresses from distal to proximal

-most commonly affects middle aged adults

-starts at hands and feet and works towards core

-gradual, progressive weakness (often starts in hands and arms)

-spasticity

-hyperactive reflexes

-tics

-dysarthria

-dysphagia

-supportive to maintain function (mobility, speech, feeding, breathing)

-ALS currently has no cure and half of persons with ALS die within 3 years of onset

-about 10% live 10 years

-respiratory failure usually causes death

immune system attacks nerves eventually causing paralysis

autoimmune