PATHO FINAL Flashcards
FUNCTIONS OF THE ENDOCRINE SYSTEM
COMMUNICATION SYSTEM THAT USES CHEMICAL MESSENGERS OR HORMONES THAT HELP US TO TRANSMIT INFO FROM CELL TO CELL OR ORGAN TO ORGAN
HORMONES
CHEMICAL MESSENGERS
WHAT DOES THE ENDOCRINE SYSTEM OVERLAP WITH
NERVOUS SYSTEM AND IMMUNE SYSTEM
*TERMS LIKE NEUROENDOCRINE IMMUNE SYSTEM
WHAT DOES THE ENDOCRINE SYSTEM DO
- GROWTH AND DEVELOPMENT
- SEX DIFFERENTIATION- REPRODUCTION
- METABOLISM-DIGESTION, USE AND STORAGE OF NUTRIENTS, REGULATION OF SOME ELECTROLYTES AND FLUIDS
- ADAPTATION TO AN EVERY CHANGING ENVIRONMENT- HOMEOSTASIS
HOW DO HORMONES FUNCTION AS CHEMICAL MESSENGERS
MOVE THROUGH BLOOD TO DISTANT TARGET SITES OF ACTION.
CAN ACT LOCALLY AS PARACRINE OR AUTOCRINE MESSENGERS
MOST ARE PRESENT IN BODY FLUIDS AT ALL TIMES IN VARYING AMOUNTS
CHARACTERISTICS OF HORMONES
SINGLE HORMONE CAN EXERT VARIOUS EFFECTS IN DIFFERENT ISSUES–> ESTRODIAL—FROM OVARY BUT DOES THINGS IN ALL KINDS OF TISSUES
SINGLE FUNCTION CAN BE REGULATED BY SEVERAL HORMONES-LIPOLISIS- BREAKDOWN OF FAT— TAKES SEVERAL HORMONES
RECEPTORS ON CELL (SURFACE OR INTRACELLULAR) REACT
TO HORMONE TO PRODUCE EFFECT
WHERE ARE HORMONES RELEASED
ENDOCRINE GLANDS
1. PITUITARY GLAND
2. THYROID GLAND
3. ADRENAL GLAND
4. PANCREAS
CLASSES OF HORMONES
AMINES
AMINO ACIDS
PEPTIDES
POLYPEPTIDES
PROTEINS
STEROIDS
FATTY ACIDS
PARACRINE HORMONES
ACT LOCALLY
DO NOT ENTER THE BLOOD STREAM
EX: SEX HORMONES ON THE OVARY
AUTOCRINE
PRODUCES SOME KIND OF BIOLOGIC EFFECT ON THE CELL THAT ACTUALLY PRODUCES IT
*EX: INSULIN EFFECT ON PANCREAS BECAUSE THEY ACT ON THE SAME PANCREATIC CELLS
RELEASING HORMONES FROM THE HYPOTHALAMUS DO WHAT
TELL THE PITUITARY WHAT TO RELEASE INTO THE BLOOD
BESIDES RELEASING HORMONES, WHAT ELSE CAN THE HYPOTHALAMUS RELEASE
PITUITARY INHIBITING HORMONES
HORMONES FROM THE PITUITARY TELL SPECIFIC PERIPHERAL GLANDS TO WHAT
GROW AND PRODUCE THEIR HORMONES
HYPOTHALAMUS-PITUITARY-TARGET CELL SYSTEM
HYPOTHALAMUS –> RELEASING HORMONES OR PITUITARY INHIBITING HORMONES –> TELL PERIPHERAL GLANDS TO PRODUCE HORMONES
ROUTE OF THE HYPOTHALAMUS PITUITARY TARGET CELL SYSTEM
CNS INPUT
HYPOTHALAMUS
RELEASING HORMONE
ANTERIOR PITUITARY
TROPIC HORMONE
TARGET GLAND
HORMONE
TARGET CELL
PHYSIO EFFECT
EXAMPLES OF HORMONES WITH 24 HR FLUCTUATION
THOSE THAT REGULATE OUR SLEEP/WAKE CYCLE
EXAMPLES OF HORMONES WITH A 28 DAY PERIOD
MENTAL CYCLE
HOW IS HORMONE SECRETION MOST OFTEN REGULATED
NEGATIVE FEEDBACK THAT MONITOR SUBSTANCES AND STIMULI IN THE BODY TO PRODUCE A RESPONSE
WHAT IS THE MASTER GLAND AND WHY
PITUITARY GLAND
CONTROL THE FUNCTION OF THE MAJORITY OF OUR TARGET ENDOCRINE GLANDS AND CELLS
WHAT DO TROPIC HORMONES DO
STIMULATE OR INHIBIT THE TARGET GLAND THEY ARE LOOKING AT
HOW IS THE PITUITARY GLAND DIVIDED
ANTERIOR AND POSTERIOR
WHAT DOES THE ANTERIOR PITUITARY RELEASE
ADH
OXYTOCIN
WHAT DOES THE POSTERIOR PITUITARY GLAND RELEASE
GROWTH HORMONES
TSH
ADRENOCORTICOTROPIC HORMONE
FOLLICLE STIMULATING HORMONE
LUTENIZING HORMONE
PROLACTIN
FEEDBACK REGULATION
SENSORS IN THE BODY DETECT A CHANGE AND ADJUST HORMONE SECRETION TO MAINTAIN BLOOD LEVELS
NEGATIVE FEEDBACK
DECREASE OF HORMONE LEVELS IN THE BLOOD THAT STIMULATES THE ENDOCRINE CELL TO INCREASE HORMONE PRODUCTION
BLOOD LEVEL RISES PRODUCING SOME KIND OF ACTION ON THE TARGET CELL
AFTER ACTION, THE SENSORS WILL START TO DECREASE
EXAMPLE OF NEGATIVE FEEDBACK SYSTEM
THYROID RELEASING HORMONE AND THYROID STIMULATING HORMONE THAT HELP PROMOTE T3 AND T4
INCREASE IN T3 AND T4 CAUSES RELEASE THAT SHUTS DOWN OR SLOWS DOWN THE THYROID
POSITIVE FEEDBACK SYSTEM
RISING LEVEL HORMONE THAT CAUSES ANOTHER HORMONE TO RELEASE THAT STIMULATES THE FIRST
CONTINUED RISE IN THE HORMONE LEVEL AND SOMETHING HAS TO ACT TO SHUT THIS OFF
EXAMPLE OF POSITIVE FEEDBACK
ESTRODIAL DURING MENSTRUAL CYCLE CAUSES INCREASE IN FSH PRODUCTION WHICH INCREASES ESTRODIAL UNTIL WE HAVE THE DEMISE OF THE UTERINE FOLLICLE
THAT DEMISE IS THE STIMULUS THAT SHUTS OFF THE RISE
ALTERED ENDOCRINE FUNCTION
HYPOFUNCTION
HYPERFUNCTION
HORMONE RECEPTOR RESISTANCE
ENDOCRINE HYPOFUNCTION
CONGENITAL DEFECTS
GLAND DESTRUCTION
CONGENITAL DEFECTS
ABSENCE OF OR IMPAIRED FUNCTION
ABSENCE OF ENZYME NEEDED TO MAKE HORMONES
GLAND DESTRUCTION
DECREASED BLOOD FLOW, INFECTION, INFLAMMATION, AUTOIMMUNE RESPONSES, TUMORS
HORMONE RECEPTOR RESISTANCE
ABSENCE OF RECEPTORS
DEFECT IN RECEPTOR BINDING
ENDOCRINE HYPERFUNCTION
EXCESSIVE STIMULATION AND HYPERPLASIA OF THE GLAND
HORMONE PRODUCING TUMOR
ADMIN OF EXOGENOUS HORMONES
HOW ARE ENDOCRINE DISORDERS CLASSIFIED
PRIMARY
SECONDARY
TERTIARY
*DEPENDING ON LOCATION OF DYSFUNCTION IN THE HPT ORGAN SYSTEM
TERTIARY
DYSFUNCTION IN STIMULATION FROM THE HYPOTHALAMUS
SECONDARY
DYSFUNCTION IN STIMULATION FROM THE PITUITARY
PRIMARY
DYSFUNCTION IN THE TARGET ORGAN/GLAND
WHAT HORMONES GENERALLY COME FROM THE HYPOTHALAMUS
RELEASING HORMONES, BUT SOME HAVE INHIBITORY PROPERTIES
WHAT IS THE PRIMARY JOB OF THE HORMONES COMING FROM THE HYPOTHALAMUS
STIMULATE THE PITUITARY TO RELEASE TROPIC HORMONES
GHRH
GROWTH HORMONE RELEASING HORMONE
TRH
THYROTROPIN RELEASING HORMONE
CRH
CORTICOTROPIN RELEASING HORMONE
AIDS IN RELEASE OF HORMONES FROM ADRENAL CORTEX
GRH
GONADOTROPIN RELEASING HORMONE
HYPOTHALAMIC HORMONES
GHRH
TRH
CRH
GRH
SOMATOSTATIN
DOPAMINE
SOMATOSTATIN
INHIBITORY HORMONE
INHIBITS GHRH AND TSH
DELAYS INTESTINAL ABSORPTION OF GLUCOSE
DOPAMINE
INHIBITORY HORMONE
INHIBITS PROLACTIN, FSH, LUTEINIZING HORMONE
POTERIOR PITUITARY HORMONES
ADH
OXYTOCIN
ADH
INCREASE REABSORPTION OF WATER AND SODIUM BY THE KIDNEY THUS INCREASING OUR VASCULAR VOLUME AND OUR OXYTOCIN
OXYTOCIN
STIMULATES UTERINE CONTRACTIONS IN PREGNANT WOMEN
MILK PRODUCTION AFTER CHILDBIRTH
ANTERIOR PITUITARY HORMONES
GH
FSH
LH
TSH
ACTH
GH
GROWTH HORMONE
STIMULATE GROWTH OF BONE AND MUSCLE
PROMOTES PROTEIN SYNTHESIS AND FAT METABOLISM
DECREASES CARB METABOLISM
FSH
FOLLICLE STIMULATING HORMONE
STIMULATES THE GROWTH OF THE OVARIAN FOLLICLE AS WELL AS OVULATION
IN MEN, IT STIMULLATES SPERM PRODUCTION
LH
LUTEINIZING HORMONE
WOMEN-STIMULATE OOCYTE, PRODUCTION OF ESTROGEN, AND PROGESTERONE
MEN- DEVELOPMENT OF TESTI TISSUE, STIMULATE SECRETION OF TESTOSTERONE
TSH
THYROID STIMULATING HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR THYROID HORMONES
ACTH
ADRENOCORTICOTROPHIC HORMONE
STIMULATES THE SYNTHESIS AND SECRETION OF OUR ADRENAL CORTICAL HORMONES
GH SECRETION IS STIMULATED BY
HYPOGLYCEMIA
FASTING
STARVATION
STRESS
GH INHIBITED BY
INCREASED GLUCOSE
FREE FATTY ACID RELEASE
OBESITY
CORTISOL
GH IS ALSO KNOWN AS
SOMADOTROPIN
WHAT DOES GH DO
LATERAL BONE GROWTH
METABOLISM
CARTILAGE GROWTH
WHAT IS THE GROWTH HORMONE RELEASING HORMONE
GHRH
WHAT IS OUR GH INHIBITING HORMONE
SOMATOSTATIN
ACTS OF GROWTH HORMONE
GROWTH PROMOTING ACTIONS
ANTI-INSULINE EFFECTS
*ACTS ON THE LIVER
DOESN’T DIRECTLY CAUSE BONE GROWTH
WHAT DOES THE LIVER PRODUCE FOR BONE GROWTH WHEN STIMULATED BY GH
IGF
IGF
PEPTIDE THAT ACTS ON CARTILATE AND BONE TO PROMOTE THEIR GROWTH
*WILL SEE LINEAR (HEIGHT) GROWTH, INCREASED SIZE AND FUNCTION IN ORGANS, INCREASE IN LEAN MUSCLE MASS
ANTI-INSULIN EFFECTS OF GH
ACTION ON OUR ADIPOSE TISSUE (LYPOLISIS, INCREASE IN FFA TO DECREASE FAT TISSUE), AND CARB METABOLISM (DECREASE USE OF GLUCOSE IN BODY SO INCREASE BLOOD GLUCOSE)
LYPOLISIS
BREAKDOWN OF FATTY TISSUE
WHERE DO THYROID HORMONES ACT TO INCREASE METABOLISM AND PROTEIN SYNTHESIS
NEARLY ALL BODY TISSUES
WHO NEEDS THYROID HORMONES FOR BRAIN DEVELOPMENT
INFANTS
SMALL CHILDREN
WHAT IS IODINE NEEDED FOR
THE PRODUCTION OF THYROID HORMOMNES
WHAT REGULATES THE SECRETION OF THYROID HORMONE
HYPOTHALMIC PITUITARY THEYROID SYSTEM
2 THYROID HORMONES
T4- THYROXINE
T3- TRIIODOTHYRONINE
WHAT IS T3 THE ACTIVE FORM OF
THYROID HORMONE
IN WESTERN CULTURE, WHERE DO WE GET A LOT OF OUR IODINE FROM
IODIZED SALT
TABLE SALT
SEAFOOD
WHY IS T4 CONVERTED TO T3
SO IT CAN PHYSIOLOGICALLY
HOW ARE T3 AND T4 STIMULATED
TSH
THE HYPOTHALAMUS PRODUCES THYROTROPIN RELEASING HORMONE AS A RESULT OF WHAT KIND OF STIMULI
IMPROPER SLEEP
COLD TEMP
STRESS
WHAT DOES TSH ACT ON
DIRECTLY ON THE GLAND ITSELF TO RELEASE T3 AND T4
THIS IS NEGATIVE FEEDBACK
ACTIONS OF THE THYROID HORMONE
INCREASE METABOLISM AND PROTEIN SYNTHESIS
METABOLIC RATE
CARDIOVASCULAR FUNCTION
GI FUNCTION
NEUROMUSCULAR FUNCTION
WHAT DO T3 AND T4 DO FOR THE METABOLIC RATE
INCREASE IT IN ALL BODY TISSUES EXCEPT RETINA, SPLEEN, TESTES, AND LUNG
WHEN METABOLIC RATE INCREASES, WHAT ELSE INCREASES
- USE OF GLUCOSE, FAT, PROTEIN
- CATABOLISM OF CHOLESTEROL IN LIVER
- USE OF VITAMINS
- ABSORBTION OF GLUCOSE FROM GI TRACT
WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO LIPIDS
METABOLIZED FROM ADIPOSE TISSUES
USED AS FUEL
WHEN METABOLIC RATE INCREASES, WHAT HAPPENS TO MUSCLE TISSUES
BROKEN DOWN
USED AS FUEL
WHAT IN THE CARDIOVASCULAR SYSTEM INCREASES WITH A THYROID HORMONE INCREASE
OXYGEN CONSUMPTION
VASODILATION
BLOOD FLOW TO SKIN TO DISSIPATE BODY HEAT GENERATED BY INCREASED METABOLISM
BLOOD VOLUME
CO
VENTILATION
HR
CONTRACTILITY
WHAT INCREASES IN THE GI FUNCTION WITH AN INCREASE OF THYROID HORMONE
MOTILITY
SECRETION PRODUCTION
APPETITE
FOOD INTAKE
WEIGHT LOSS
INCREASE IN THYROID HORMONE CAUSES WHAT NEUROMUSCULAR EFFECTS
- INCREASED MUSCLE REACTION
- NORMAL BRAIN DEVELOPMENT IN THE INFANT
- INTERACTION BETWEEN THYROID AND SYMPATHETIC NERVOUS SYSTEM
WHAT 3 HORMONES DOES THE ADRENAL CORTEX SECRETE
GLUCOCORTICOIDS
MINERALOCORTICOIDS
ADRENAL ANDROGENS
THE HYPOTHALMIC PITUITARY ADRENAL SYSTEM REGULATES WHAT
RELEASE OF GLUCOCORTICOIDS AND ADRENAL ANDROGENS
ADRENAL CORTICAL HORMONES ARE DEACTIVATED BY WHAT
THE LIVER AND EXCRETED IN THE URINE OR BILE
MINERALOCORTICOIDS
FUNCTION IN SODIUM, POTASSIUM, WATER BALANCE
PRIMARY-ALDOSTERONE
GLUCOCORTICOIDS
FUNCTION IN REGULATION OF METABOLISM, CONTROL INFLAMMATORY/IMMUNE RESPONSE, ESSENTIAL FOR STRESS SURVIVAL
PRIMARY-CORTISOL
ADRENAL CORTICAL INSUFFICIENCY
MINERALOCORTICOIDS, GLUCOCORTICOIDS DEFICIENCY
ADRENAL CORTICAL EXCESS
MINERALCORTICOID EXCESS
ANDROGEN EXCESS
GLUCOCORTICOIDS EXCESS
HIRSUTISM
ANDROGEN EXCESS
WITH ADRENAL CORTICALTROPIN RELEASING HORMONES, WHAT ARE EXAMPLES OF STIMULI
STRESS
INFECTION
PAIN
HYPOGLYCEMIA
SLEEP
HEMORRHAGE
TRAUMA
MINERALCORTICOIDS REGULATE WHAT
SODIUM, POTASSIUM, WATER BALANCE
PRIMARY MINERALOCORTICOID
ALDOSTERONE
MINERALCORTICOIDS ARE REGULATED BY
RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
RAAS
ACTION OF MINERALCORTICOIDS
PROMOTE SODIUM, REABSORPTION IN THE DISTAL TUBULES
WATER FOLLOWS SODIUM AND IS EXCRETED IN THE URINE
FUNCTION OF GLUCOCORTICOIDS
STRESS RESPONSE, CONTROL OF INFLAMMATORY/IMMUNE RESPONSE, REGULATE GLUCOSE, PROTEIN FAT METABOLISM
PRIMARY GLUCOCORTICOID
CORTISOL
GLUCOCORTICOIDS ARE REGULATED BY
THE HYPOTHALAMIC PITUITARY ADRENAL SYSTEM
WHAT EFFECT DO ADRENAL ANDROGENS HAVE ON SEXUAL FUNCTION
LITTLE ON NORMAL SEXUAL FUNCTION
PRIMARY ANDROGEN
DEHYDROEPIANDROSTERONE
DHEA
ADRENAL ANDROGENS CONTRIBUTE TO PUBERTY HOW
BODY HAIR GROWTH IN WOMEN
WHATA HAPPENS TO ADRENAL ANDROGENS AS WE AGE
DECLINE IN PRODUCTION
DIABETES INSIPIDUS
ADH DISORDER
DEFICIENCY OR DECREASED RESPONSE TO ADH
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
ADH DISORDERS
EXCESS ADH SECRETION
Where are the releasing hormones released from?
THE HYPOTHALAMUS
Where are the trophic hormones released from?
THE ANTERIOR PITUITARY
What two hormones are released from the posterior pituitary
adh or vasopressin
oxytocin
What is the target organ for TSH?
thyroid
What is released by the target organ in response to TSH
t3 and t4
What is the target organ for ACTH?
adrenal cortex
What is released by the target organ in response to acth
cortisol
androgens
What is the target organ for FSH and LH?
ovarian follicle
What hormones are secreted from the posterior pituitary gland?
oxytocin and adh aka vasopressin
What hormones are secreted from the anterior pituitary gland?
tsh
acth
fsh
lh
Explain the negative feedback mechanism involved in the regulation of thyroid hormones.
The Thyroid Feedback Mechanism. TH regulates TRH gene expression and production through a negative feedback mechanism; TRH expression is high when TH levels are low, and TRH expression is suppressed when TH levels are increased.
What is the physiologic effect of insulin?
carb metabolism
increases rate of transport of glucose across the cell membrane in adipose tissue and muscle
increases rate of glycolysis
stimulates the rate of glycogen synthesis
What is the physiologic effect of glucagon?
Glucagon is secreted into the portal vein and thus has its major physiologic action at the liver to break down glycogen.
What happens to glucose when the liver and skeletal muscle tissue are saturated and can no longer store glycogen?
the “excess” glucose is “converted” to fat tissue through catabolism IN the fat cells, which essentially “grow” with the glucose consumed… and, by the way… this process actually burns off some of the glucose… about 10% of the amount stored is “burned” to store it.
What clinical manifestations would be observed in a child with GH deficiency?
slow height growth each year after a child’s 3rd birthday. A child with GH deficiency may also have a younger-looking face and a chubby body build.
What is the pathophysiology for Diabetes Insipidus (DI)?
when your body doesn’t make enough antidiuretic hormone (ADH) or your kidneys don’t use it properly. Your body needs ADH to retain appropriate amounts of water. Without ADH, your body loses water through urine. Diabetes mellitus is much more common than diabetes insipidus
What is the pathophysiologic difference between type I and type II diabetes mellitus?
In diabetes type 1, the pancreas does not make insulin, because the body’s immune system attacks the islet cells in the pancreas that make insulin. In diabetes type 2, the pancreas makes less insulin than used to, and your body becomes resistant to insulin.
What electrolyte imbalances should the nurse suspect in Addison’s disease?
hyponatremia, hyperkalemia, and hypoglycemia.
What are the clinical manifestations of hypoglycemia?
Fast heartbeat.
Shaking.
Sweating.
Nervousness or anxiety.
Irritability or confusion.
Dizziness.
Hunger.
What clinical manifestations may be seen in a client with Cushing’s Syndrome?
their face get round (“moon face”), they gain weight in unusual ways, bruise easily or feel weak, tired and sad.
What electrolyte is involved in excitatory amino acid injury?
acid glutamate
What is the difference between brain death and a persistent vegetative state?
A persistent vegetative state means the person has lost higher brain functions, but their undamaged brain stem still allows essential functions like heart rate and respiration to continue. A person in a vegetative state is alive and may recover to some degree, given time. Brain death means the person has died.
Describe where production and flow of CSF occurs. What occurs when there is excess of CSF?
Hydrocephalus is a buildup of cerebrospinal fluid (CSF) in the spaces deep inside your brain (ventricles). As a result of the excess fluid, the ventricles widen and put pressure on the brain tissue. In hydrocephalus, the cycle that allows CSF fluid to flow freely is out of balance and fluid builds up in the ventricles.
Order the meningeal layers of the brain starting from the outermost to innermost layer
dura mater
arachnoid
pia mater
Interpret the Glasgow Coma Scale—what does it mean when the client’s GCS is increasing?Decreasing
Based on the level of consciousness, a score is assigned. A higher score indicates a greater level of consciousness. The GCS uses three sites for stimulation. This includes fingertip pressure, trapezius pinch and supraorbital notch.
What cranial nerve is responsible for pupillary changes?
oculomotor nerve
cn iii
what is the formula for cpp
cpp = map - icp
what is normal icp
7-15 mmhg
what is normal cpp
60-80 mmhg
What are the 3 major causes/classifications of increased ICP
brain, cerebrospinal fluid, and blood. Any increase in the volume of its contents will increase the pressure within the cranial vault. An increase in the volume of one component will result in a decrease in volume in one or two of the other components.
Monroe-Kellie Hypothesis
What finally came to be known as the Monro-Kellie doctrine, or hypothesis, is that the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.
What is the difference between a stroke and a TIA?
A TIA is a brief blockage of blood flow to part of the brain, spinal cord or the thin layer of tissue at the back of the eye known as the retina. This blockage may cause temporary stroke-like symptoms. But a TIA doesn’t damage brain cells or cause permanent disability. This is how it differs from a regular stroke.
What vessel is commonly damaged in patients with epidural hematoma?
middle meningeal artery
What acronym do we use to assess for s/s of stroke?
be fast
balance
eyes
face
arm
speech
time
What is the target organ for FSH and LH?
anterior pituitary
A __________ (primary, secondary,tertiary) disorder is associated with damage to the hypothalamus
tertiary
A tumor that causes damage to the thyroid gland is an example of a____________ (primary, secondary, tertiary) disorder.
primary
A tumor that destroys the posterior pituitary gland is an example of a____________(primary, secondary, tertiary) disorder?
secondary
what stimulates the production of gh
ghrh
gh
somadotropin
what inhibits the production of gh
somadastatin
ghih
ghrh and ghih are released from
hypothalamus
growth hormone
igf 1 deficiency
- Idiopathic GH deficiency- Lacks hypothalamic
GHRH - Pituitary tumors, agenesis of the pituitary- Cannot produce GH
- Laron-type dwarfism- Hereditary defect in IGF production
growth hormone
igf1
excess
- Gigantism - childhood* Before puberty and fusion of epiphyseal plates
- Acromegaly – adult* After fusion of epiphyseal plates
gh excess in adults
Overgrowth of the small bones and cartilaginous parts of the skeleton
* Epiphyseal plates closed –don’t grow taller
* Enlargement of the heart and other organs of the body
* Metabolic disturbances resulting in altered fat metabolism and impaired glucose tolerance - can lead to diabetes