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Group 5 Report on Pathophysiology
Citation preview
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
on
e S
um
mary
EN
DO
CR
INO
LOG
Y
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
DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND
ADRENAL GLANDPANCREATIC ISLETSEX HORMONES
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
HYPERTHYROIDISMT3
OVERACTIVETISSUE IN THETHYROID GLAND
PRODUCINGTOO MUCH
WHATAND
T4TRIIODOTHYRONINE& THYROXINE
CAUSESGRAVE’S DISEASE
TOXIC THYROID ADENOMATHYROIDITISNORMAL?WHATWHATWHAT
SYMPTOMS?HIGH EXCITABILITY; METABOLISM
MILD TO EXTREME WEIGHT LOSSMUSCLE WEAKNESS; TREMORS
exophthalmosDEVELOPMENT OFPROTRUSION OF EYEBALLS
EDEMATOUSTISSUES
& DEGENERATIVEMUSCLES
TREATMENT!SURGICAL REMOVAL OF GLANDLESSEN IODINE INTAKE
HYPOTHYROIDISMTOO LITTLET3T4A
ND
CAUSESAUTOIMMUNI
TY
AUTOIMMUNITYAGAINST THE
THYROID=
DETERIORATION
ASSOCIATED WITH
THYROID GOITER
THYROID GOITER
GOITERENDEMIC COLLOID &IDIOPATHIC NONTOXIC
IODINE DEFICIENT
NOT IODINE DEFICIENT
SYMPTOMS?FATIGUE; SLEEPINESS; SLUGGISH
WEIGHT GAIN; CONSTIPATIONFAILURE OF TROPHIC FUNCTIONSANDmyxedema
TREATMENT!MORE IODINE
ORAL MEDICATON
PARATHYROID GLAND
DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND
ADRENAL GLANDPANCREATIC ISLETSEX HORMONES
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
PARATHYROID GLANDHYPERPARATHYROIDI
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
PARATHYROID GLANDHYPERPARATHYROIDI
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
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ADRENAL GLANDPARATHYROID GLAND
DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND
PANCREATIC ISLETSEX HORMONES
ADRENAL GLANDCUSHING’S SYNDROME
ADDISON’S DISEASE
CUSHING’S DISEASE
CU
SH
ING
’SS
YN
DR
OM
E
CU
SH
ING
’S
• 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)
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
ADRENAL GLANDPARATHYROID GLAND
DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND
PANCREATIC ISLETSEX HORMONES
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
ADRENAL GLANDPARATHYROID GLAND
DISEASES&DISORDERSTHYROID GLANDPITUITARY GLAND
PANCREATIC ISLETSEX HORMONES
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
’SD
ISE
AS
E
• 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
ISE
AS
E
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)
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studies!
She had puffiness around her nose and eyes. Her menses gegan at age 16 and were irregular with scant flow. She had no
interest in the opposite sex. There was an absence of
pubic hair. She was constipated, gained weight easily, had dry skin and hair, had anemia, and she tired
easily.
What can she be suffering from?
What can she be suffering from?
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
• 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