PH 131 - Endocrine System Report

SYSTEMENDOCRINE

HORMONES * HORMONES * HORMONESJANDUSAY * JAVIER * JOVEN * KAMIYA * KALAW

LEONG * LLAMZON * LORENZO * LUKBAN

WHAT TO EXPECT:REPORT OBEJECTIVESSHORT REVIEWDISORDERS and DISEASESREPORT SUMMARY

REPORT OBEJECTIVES

REPORT*OBEJECTIVES

To provide a short review on the Endocrine System

To discuss common & rare Endocrine diseases & disorders

To discuss the effects on normal physiology

To present preventive measures and cures

To provide a short summary on the topics discussed

To familiarize students with Endocrine processes

REVIEW

REVIEWENDOCRINOLOGY

VS.hormones

neurons

REVIEWENDOCRINOLOGY

VS.endocrine

nervous

fastlong-lasting

REVIEWENDOCRINOLOGY

NEGATIVEFEEDBACKMECHANISM

ORGAN HORMONES EFFECT Anterior Pituitary FSH Stimulates activity in ovaries and

testes LH Stimulates activity in ovary

(release of ovum) and production of testosterone

ACTH Stimuates the adrenal cortex Growth Hormone Stimulates bone and muscle

growth TSH Stimulates the thyroid to secrete

thyroxine Prolactin Causes milk secretion

Posterior Pituitary Oxytocin Causes uterus to contracb watert and ducts of mammary glands

Vasopressin Causes kidney to reabsor Thyroid Thyroid Hormone Regulates metabolic rate

Calcitonin Lowers blood calcium levels Parathyroid Parathyroid Hormone Increases blood calcium

concentration Adrenal Cortex Aldosterone Increases Na+ and H2O

reabsorption in kidney Adrenal Medulla Epinephrine Increases blood glucose level

and heart rate Norepinephrine

Pancreas Insulin Decrease blood sugar concentration

Glucagon Increases blood sugar concentration

Ovaries Estrogen Promote female secondary sex characteristics and thickens

endometrial lining Progesterone Maintains endometrial lining

Testes Testosterone Promotes male secondary sex characteristic and spermatogenesis

Horm

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DISEASESAND

DISORDERS

PARATHYROID GLAND

DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND

ADRENAL GLANDPANCREATIC ISLETSEX HORMONES

PITUITARY GLANDDWARFISM &

GIANTISMDIABETES INSIPIDUS

PITUITARY GLANDDWARFISM &

GIANTISMDIABETES INSIPIDUS

Pituitary Gland Disorders

Diabetes Insipidus

Diabetes Insipidus

-(“diabetes”= overflow, “insipidus”= tasteless)

-most common abnormality associated with the dysfunction of the posterior pituitary

-due to defects in antidiuretic hormone receptors or inability to secrete ADH

-can be neurogenic (or central) or nephrogenic

Diabetes InsipidusHow does the normal physiology is disrupted?

Neurogenic DI Nephrogenic DI

A brain tumor, brain surgery or head trauma that damages hypothalamus or posterior pituitary can result to a hypo secretion of ADH.

The kidneys have decreased ability to concentrate urine due to a resistance to ADH action in the kidney.

Diabetes Insipidus

• Symptoms:- excretion of large volumes of urine with resulting dehydration and thirst- bed-wetting

How can normal physiology be regained?

- Hormone replacement, usually for life (for neurogenic DI)

- Subcutaneous injection or nasal application of ADH analogs

- Restriction of salt in the diet and diuretic drugs

Pancreatic Islet DisorderHyperinsulinism

Pancreatic Islet Disorder• Hyperinsulinism- also known as hyperinsulinemia- Usually causes Type 2 diabetes- Occurs when there is reduced sensitivity of

diabetics who undergo insulin therapy- Can also occur when insulin is injected by non-

diabetics. This is usually done by athletes who are trying to enhance their overall anaerobic performances.

Some Causes

-obesity/ overweight-excess glucocorticoids-excess growth hormone-mutations of insulin receptors

3. Hyperinsulinism

How does the normal physiology is disrupted?

Consequences of these disruptions

1. Insulin stimulates too much uptake of glucose by cells. Thus, there is decreased blood glucose level, or hypoglycemia.

1. Epinephrine, glucagon and human growth hormone are secreted.

2. Anxiety, sweating, tremor, increased heart rate, hunger and weakness occur.

Severe hypoglycemia 3. Mental disorientations, convulsions, unconsciousness and insulin shock.

3. Hyperinsulinism

How can normal physiology be regained?

- immediate intravenous administration of large quantities of glucose

- administration of glucagon (or, less effectively of epinephrine) can cause glycogenolysis in the liver and thereby increase blood glucose level extremely rapidly

**Permanent damage to the neuronal cells of the nerous system usually occurs when treatment is not given immediately.

PARATHYROID GLAND



THYROID GLANDGOITER

HYPERTHYROIDISMHYPOTHYROIDISM

GOITERWHY, YES. THIS IS A….

GOITER?ENLARGEMENTWHAT IS A GOITER?

OF THETHYROID.

GOITERNORMAL

PHYSIOLOGYThyroid Hormones (T3 & T4)

- produced by cells in thyroid gland- regulated by thyroid stimulating hormone (TSH)- produced through the attachment of iodine atoms to ring structures of T3 and T4

SYMPTOMSAHEM! AHEM!

Breathing and swallowing difficultiesCoughing and hoarseness

GOITERCAUSES

Endemic Goiter due to iodine deficiency Iodine deficient therefore Thyroid Hormone is not produced

Pituitary gland produces more Thyroid Stimulating Hormone

Thyroid enlarges Hashimoto’s Thyroiditis (destroys thyroid gland)

Damage on thyroid gland therefore insufficient thyroid hormone is produced

Pituitary gland secretes more Thyroid Stimulating Hormone

Throid enlarges Graves’ Disease Immune system produces Thyroid

Stimulating Immunoglobin Thyroid enlarges, producing my

Thyroid Hormone Causes hyperthyroidism

TREATMENT

Surgery- thyroidectomy Lugol’s IodineRadiocative Iodine

POSSIBLE COMPLICATIONSHYPERTHYROIDISMHYPOTHYROIDISM

PARATHYROID GLAND



PARATHYROID GLANDHYPERPARATHYROIDI

SM

HYPOPARATHYROIDISM

PARATHYROID GLAND* control calcium within the blood.

* control how much calcium is in the bones, and therefore, how strong and dense the bones are!

* As the blood filters through the parathyroid glands, they detect the amount of calcium present in the blood

making more or less parathyroid hormone (PTH). Calcium level in the blood is too low: the parathyroid cells make more parathyroid hormone.

FUNCTION &NORMAL PHYSIOLOGY


SM

HYPOPARATHYROIDISM

…occurs when your parathyroid glands make too much PT and cause you to have too much calcium in the bloodstream.

CAUSES OF TOO MUCH PTH:Growth on the parathyroid glands!

Enlargement of 2 or more of the parathyroid glands! OR medical conditions (like, lessay, kidney failure and rickets...)

HYPERPARATHYROIDISM

Normally, the amount of calcium going into your bones matches the amount of calcium passing out of your bones.

This means that the amount of calcium in your bones should stay about the same all the time. If you have

hyperparathyroidism, more calcium is coming out of your bones than is going back in. When this happens, your bones might hurt, ache or become weak. Weak bones break more easily and heal slower than normal bones.

PHYSIOLOGY&IMPLICATIONS

HYPERPARATHYROIDISM

Feeling weak or tired most of the timeGeneral aches and pains

Frequent heartburn Nausea & Vomiting; Loss of appetite

An increase in bone fractures or breaksConfusion and memory loss

Kidney stones; Excessive urinationHigh blood pressure

THE SYMPTOMS

HYPERPARATHYROIDISMSURGERY

DRINK PLENTY OF WATERLIMIT INTAKE OF CALCIUM AND

VITAMIN DDO NOT SMOKEEXERCISE DAILY

TREATMENT

HYPERPARATHYROIDISM


SM

HYPOPARATHYROIDISM

HYPOPARATHYROIDISM

Hypoparathyroidism is a rare condition in which your body secretes abnormally low levels of parathyroid hormone

(parathormone). This hormone plays a key role in regulating and maintaining a balance of your body's levels

of two minerals — calcium and phosphorus.The low production of parathyroid hormone in

hypoparathyroidism leads to abnormally low ionized calcium levels in your blood and bones

and to an increased amount of phosphorus.

PHYSIOLOGY&IMPLICATIONS

HYPOPARATHYROIDISM

Tingling or burning (paresthesias) Muscle aches or cramps; Twitching or spasms

Fatigue or weaknessPainful menstruation

Patchy hair loss, such as thinning of your eyebrowsDry, coarse skin; Brittle nails

Headaches; Depression, mood swingsMemory problems

THE SYMPTOMS

HYPOPARATHYROIDISMRESTORE THE CALCIUM

AND MINERAL BALANCE IN THE BODY.Treatment involves calcium carbonate and vitamin D supplements, which usually must be taken for life. Blood levels are measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is recommended.

TREATMENT

HYPOPARATHYROIDISM

ADRENAL GLANDPARATHYROID GLAND


PANCREATIC ISLETSEX HORMONES

ADRENAL GLANDCUSHING’S SYNDROME

ADDISON’S DISEASE

CUSHING’S DISEASE

CU

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• Occurs when your body is exposed to high levels of the hormone cortisol

• Characterized by high plasma levels of ACTH and cortisol

• Another name hypercortisolism

• Can occur from multiple causes including:

1. Adenomas of the anterior pituitary that secrete large amounts of ACTH

2. Abnormal function of the hypothalamus that causes high levels of corticotrophin-releasing hormone (CRH) “ectopic secretion” of ACTH by a tumor elsewhere in the body

3. Adenomas of the adrenal cortex

High blood pressure.High blood sugar.

Suppressed immunity (and more infections).Insulin resistance

Suppressed sex hormones and reduced libido.Suppressed thyroid hormones.

- A round, red, full face, often called a "moon" face. - Muscle weakness and thin limbs.

- Growth of fine hair on the face, upper back, or arms. - A lump of fat (buffalo hump) on the back of the neck.

- Stretch marks over abdomen.

SYMPTOMSCUSHING’S

CUSHING’S

DISEASE

Cushing's syndrome is treated by restoring a normal balance of hormones.

This may involve surgery, radiation treatments or drugs. Tumors on the

adrenal glands are removed by surgery. If there is a tumor on just one adrenal

gland, the other gland usually shrinks and ceases normal productivity.

CUSHING’S

TREATMENT

ADDISON’S

DISEASE

AD

DIS

ON

’S

A disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands.

It may be due to :(1)a disorder of the

adrenal glands themselves (primary adrenal insufficiency) or

(2) inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency)

Addison's disease results from damage to the adrenal cortex.

This damage may be caused by the following:The immune system mistakenly attacking the gland (autoimmune disease)Infections such as tuberculosis, HIV, or fungal infectionsHemorrhage, blood lossTumorsUse of blood-thinning drugs (anticoagulants)

http://www.ncbi.nlm.nih.gov/pubmedhealth/n/pmh_adam/A000077/

ADDISON’S• Changes in blood

pressure or heart rate• Chronic diarrhea• Darkening of the

skin ; Paleness• Extreme Weakness• Unintentional weight

loss• Mouth lesions on the

inside of a cheek• Nausea and vomiting• Salt craving• Slow, sluggish

movementSYMPTOMS

Taking hormones to replace the insufficient amounts being made

by your adrenal glands (glucocorticoids

(cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone))

ADDISON’S

TREATMENT




PANCREATIC ISLETDIABETES MELLITUS

PANCREAS

• retroperitoneal• Exocrine gland• Endocrine gland

-98% of the secreting cells in the pancreas make digestive enzymes

-2% of the cells make hormones that are secreted into the portal vein

Pancreatic Hormones

GLUCAGON INSULIN SOMATOSTATIN

Cell origin alpha beta delta

Target liver liver, adipose tissue, muscle, and satiety

center of hypothalamus

alpha and beta cells

Action release of glucose to the blood from

liver cells

transport of glucose into body cells

inhibition of glucagon and

insulin secretion

Normal Physiology

• Circulating glucose is derived from three sources:1. intestinal absorption during the fed state2. glycogenolysis -breakdown of glycogen3. gluconeogenesis -formation of glucose primarily from lactate and amino acids during the fasting state

• insulin is the key regulatory hormone of glucose disappearance (hypoglycemic hormone), and glucagon is a major regulator of glucose appearance (extremely potent hyperglycemic agent)

Disruptions on Physiology

Insulin and glucagon

• antagonistic interaction• humoral stimuli • potent regulators of glucose metabolism• bi-hormonal definition of diabetes:

diabetic state = insulin deficiency + glucagon excess

Diabetes [Mellitus] Pathophysiology

• glucose concentrations rise due to lack of insulin-stimulated glucose disappearance

• poorly regulated hepatic glucose production

• increased or abnormal gastric emptying following a meal

Type 1 IDDM:autoimmune-mediated

destruction of pancreatic β-cells

• peripheral insulin resistance (insulin insensitivity)

• impaired regulation of hepatic glucose production

• declining beta (ß) cell function, eventually leading to possible ß-cell failure

Type 2 NIDDM: insulin resistance coupled

with progressive β-cell failure and decreased availability of insulin

(most common)

NOTE:

TYPE1 – noticeable early symptoms

TYPE2 – may occur without or gradual development of symptoms

Diabetes Complications (VASCULAR)

Lipidemia, high bloodcholesterol

levels

stroke

heart attacks

renal shutdow

n

Atheros-clerosis

gangrene

blindness

Diabetes Complications (NEURAL)

loss of sensation

impaired bladder function

impotence

loss of sensation

impaired bladder function

impotence

Treatment and Prevention




SEX HORMONESPOLYCYSTIC OVARIES

KLINEFELTER’S DISEASE

PCOS

polycystic ovary syndrome

PCOS

polycystic ovary syndrome

• one of the most common female endocrine disorders

• a health problem caused by hormonal system imbalance: increase in ovarian production and insulin resistance

What causes PCOS?• Resistance to the hormone insulin

diabetes• Too much production of LH compared

to FSH follicles on the ovaries produce more of the male hormone testosterone than the female hormone estrogen adrenal glands start to produce increased amounts of testosterone

• Too much testosterone prevents ovulation

• Estrogen is still produced deficiency in progesterone

Symptoms• irregular or non-existent periods• very light or very heavy bleeding

during your period• mild to moderate abdominal

discomfort• excessive hair growth on your face,

chest and lower abdomen• acne• Infertile• overweight

Management• Lifestyle modification: health

control; exercise• Birth control pills• Diabetes medications• Fertility medications• Surgery - laparascopic

ovarian drilling

KLIN

EFE

LTER

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ISE

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• a condition in which human males have an extra X chromosome instead of the normal XY

• also known as XXY Syndrome or 47, XXY• low testosterone level What causes XXY Syndrome?• X and Y chromosome fail to pair and fail to

exchange genetic material production of an additional X chromosome

KLIN

EFE

LTER

’SD

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Symptoms• Small, firm testes• Osteoporosis (in young or middle-age men)• Motor delay or dysfunction• Speech and language difficulties• Attention deficits• Learning disabilities• Dyslexia or reading dysfunction• Psychosocial or behavioural problems

Management and TreatmentEducational guidanceTherapeutic Options

Medical Options e.g. Testosterone

Replacement Therapy (TRT)

References:

• Elaine N. Marieb, Katja Hoehn. Human Anatomy & Physiology 7th edition• Aronoff, S. et al. Glucose Metabolism and Regulation: Beyond Insulin and

Glucagon. Retrieved from http://spectrum.diabetesjournals.org/content/17/3/183.full

• http://www.hormone.org/Diabetes/diabetes.cfm• Photos from Google images

http://spectrum.diabetesjournals.org/content/17/3/183.full



http://www.hormone.org/Diabetes/diabetes.cfm



• References:Guyton, A. & Hall, J. Textbook of Medical Physiology. 11th EditionTortora, G. & Derrickson, B. Principles of Anatomy and Physiology. 11th Edition

http://emedicine.medscape.com/article/117648-overview