1. endocrine chart
The following set of slides covers many of the major hormones of the
body and certain clinical conditions related to each. Please note that this
information is not inclusive but rather focuses on the major aspects of
each hormone and condition. Students should view the slides and fill in
their endocrine charts with information as they proceed. The goal is to
provide students with an overview of certain hormones and conditions.
Students will be able to use their charts on the test on the endocrine
system as a reference.
Viewing the slides in slide show format will make them easiest to follow.
2. controlled by: releasing hormone (GHRH) & inhibiting hormone
(GHIH) from hypothalamus
major targets:
liver, skeletal
muscle, bone
Growth hormone (GH of hGH)
stimulates release of IGF’s
(insulin-like
growth factors)
increases cell/tissue growth
especially in bone & muscle
tissue
indirect
actions
increases lipolysis (fat breakdown) &
increases blood glucose
direct
actions
released from: anterior pituitary
+
GHRH
stimulates
release
GHIH
inhibits
release
3. What happens with deficiency or
excess of GH?? (go to the clinical
conditions pages of your chart)
4. • slowed bone growth
• short stature
• normal body proportions
• cause: hyposecretion during growth
years (before epiphyseal plate closure)
pituitary dwarfism
• hormone involved: hGH
• symptoms:
5. pituitary giantism
• cause: hypersecretion during growth
years (before epiphyseal plate closure)
• hormone: hGH
• symptoms:
• excessive height
• abnormal increase in
length of long bones
• normal body proportions
6. acromegaly
• thickening of bones of
hands, feet, face
• no change in height
• cause: hypersecretion in
adult (usually due
to a pituitary tumor
• hormone: hGH
• symptoms:
changes seen from early
adulthood onward
7. TSH
thyroid
gland
target
hormone: TSH
(thyroid-stimulating
hormone)
TSH also is
controlled
by negative
feedback of
thyroid
hormones
increases secretion
of thyroid hormones
(tri-iodothyronine (T3)
& thyroxine (T4) from
the thyroid gland
action:
T3 & T4
+
released from:
anterior pituitary
(thyrotropin releasing hormone
TRH
Controlled by
from the
hypothalamus
8. Think about what hypo- and
hypersecretion of TSH might lead to.
(coming later)
9. ACTH
adrenal cortex of
the adrenal gland
target =
ACTH also is
controlled by
negative
feedback of
cortisol
hormone: ACTH
(adrenocorticotropic
hormone)
cortisol
action =
increases secretion
of glucocorticoids,
mainly
+
released from:
anterior pituitary
controlled by CRH (corticotropin releasing hormone)
from the
hypothalamus
10. Follice stimulating hormone (FSH)
& Luteinizing hormone (LH)
target = ovaries &
testes
actions = stimulate hormone secretion
(testosterone in male, estrogen & progesterone
in female) and production of eggs & sperm
hormones: FSH & LH
released from:
anterior pituitary
GnRH (gonadotropin releasing
hormone)
controlled by
+
from the
hypothalamus
11. Prolactin
action = milk production
post partum
target = breast
controlled primarily by
from hypothalamus
PIH (prolactin inhibiting
hormone = dopamine)
So if a hormone is controlled by an inhibiting hormone, then
how do you increase the secretion of that hormone???
hormone: prolactin
released from:
anterior pituitary
13. Hypothalamus
Hypothalamic-
hypophyseal
nerve tract
Posterior
pituitary
paraventricular
nucleus
actions = 1) contraction of
uterine smooth muscle in
response to pressure on
the cervix during labor
controlled by nerve signals from the uterus & breast via
neuroendocrine reflexes
2) milk ejection
in response to suckling of
an infant in lactating
female
hormone:
oxytocin
targets: uterus & breast
(made in hypothalamus)
released from:
posterior pituitary
14. Hypothalamus
posterior
pituitary
supraoptic
nucleus
• decrease in urine output
• reduction in sweat production
• vasoconstriction (narrowing of
blood vessels)
hormone:
ADH
overall: ADH promotes water conservation;
increases blood volume & raises blood pressure
kidneys sweat
glands
blood
vessels
targets =
controlled by osmoreceptor cells in hypothalamus – these cells respond to
blood osmotic pressure (solute concentration), blood volume and blood
pressure
in response to increased osmotic pressure
of body fluids (ex: during dehydration)
or
decreased blood volume/blood
pressure, will see:
actions =
(made in hypothalamus)
released from:
posterior pituitary
15. diabetes insipidus
• symptoms -
• neurogenic DI -
• nephrogenic DI-
problem is with hypothalamus/pituitary –
see hyposecretion of ADH
receptors for ADH are not responsive
or
kidney (and receptors) are damaged
problem is with the kidney
- involves ADH
• polyuria (excessive urination)
• dehydration
• polydipsia (frequent drinking)
16. SIADH = syndrome of inappropriate ADH secretion
• hypersecretion of ADH
• symptoms:
• fluid retention
• headache
• disorientation
• weight gain
• decreased blood solute concentration
18. thyroxine (T4) & triiodothyronine (T3)
• required for:
• needed for normal development
of skeletal & nervous systems
targets: most body cells
• major metabolic hormone –
as such it increases:
• basal metabolic rate (rate at
which cells produce ATP)
• O2 consumption
• body temperature
Thyroid hormones =
• needed for reproduction
controlled by: TSH from anterior pituitary
TSH
TRH
thyroid
gland
T3 & T4
(numbers 3 & 4 indicate the number of iodine atoms
in the hormone; only use of iodine in the body)
actions:
released
from: thyroid
gland
19. Primary and secondary conditions
In some cases where hormone secretion is controlled by the
anterior pituitary gland, a disorder may result from a problem
with the gland itself or be due to a problem with the controlling
gland, i.e., pituitary gland. If it is the gland itself that is the
problem, then it is a primary condition. On the other hand, if the
controlling gland is the problem then it is a secondary condition.
For example, if there is an issue with thyroid hormone secretion
it might be due to a problem with the thyroid gland itself (primary
condition) or due to a problem with TSH release from the
anterior pituitary (secondary condition).
20. goiter =
• may be associated with
hypo-, hyper- or normal
secretion of thyroid hormone
general term for enlargement of the thyroid gland
• common cause – deficiency of
dietary iodine
Thyroid gland – clinical conditions
can’t make T3 & T4 without iodine
leads to decreased negative
feedback to anterior pituitary
leads to excess secretion of TSH
results in over-stimulation &
enlargement of thyroid gland
21. Congenital hypothyroidism – hormone involved is thyroid
hormone
• dwarfism
• impaired mental
development
cause: severe hyposecretion of thyroid hormone in fetal
life or infancy (due to lack of iodine or to a
poor development of the gland itself)
• thick tongue & neck
symptoms:
22. Myxedema
• edema (swelling) of facial tissues
• goiter if due to lack of iodine
• slow heart rate
• slowed metabolic rate
• mental lethargy
• sensitivity to cold
– hyposecretion of thyroid hormone in adult
causes include:
• thyroid gland defect (primary condition)
• inadequate TSH secretion (secondary condition)
• inadequate dietary iodine
• removal of the thyroid gland
symptoms:
23. • most common cause of hyperthyroidism
• exopthalamous (protruding eyeballs) – distinguishing symptom
Grave’s disease
• cause – excessvie thyroid hormone
secretion caused by antibodies the body
makes that mimic TSH & overstimulate
the thyroid gland (this is an autoimmune
disease)
• may have enlarged thyroid
• symptoms:
• weight loss
• rapid heart rate
• restlessness
• heat intolerance
24. - controlled by blood Ca++ levels – elevated Ca++levels
stimulate secretion
- uncertain physiological role for this hormone
calcitonin - secreted by: thyroid gland
actions: lowers blood calcium by:
• promoting uptake
of Ca++ into bone
matrix by osteoblasts
• inhibiting bone
resorption by
osteoclasts
25. PTH
• bone tissue & kidney
• acts on kidney to retard
Ca++ loss in urine
• stimulates formation of
active Vit. D by the kidney
(Vit D needed for Ca++ absorption
from the intestinal tract)
raises blood Ca++ by targeting:
- controlled by blood Ca++ levels; low Ca++ levels stimulate
release, high levels inhibit
- secreted by parathyroid glands
• promotes bone resorption
by osteoclasts
actions:
26. Hyperparathyroidism
• bones soften and become deformed
• nervous system depression with abnormal reflexes
• muscle weakness
• kidney stones
cause: excess secretion of PTH
symptoms relate to excess removal of Ca++ from bone tissue
27. Hypoparathyroidism
• tingling sensations
• twitching muscles
• convulsions
cause: too little PTH (most often after removal during thyroid
surgery or trauma
symptoms related to hyperexcitable neurons
29. • Cortex
Kidney
• Medulla
Adrenal gland
Zona
glomerulosa
Zona
fasciculata
Zona
reticularis
Medulla
Cortex
Each adrenal gland consists
of an outer cortex and
an inner medulla
each of which produces
different hormones
Each adrenal
cortex itself has
3 layers that
secrete separate
hormones
30. Zona
glomerulosa
Medulla
Cortex
• promotes Na+ retention & K+
excretion by the kidney
• Na+ retention leads to water
retention and this action helps
maintain blood volume and
blood pressure
controlled by: drop in blood
volume & blood pressure or
elevated K+
aldosterone
(a mineralocorticoid –
influences electrolyte & fluid
balance)
target = kidney
actions =
32. Cortisol – secreted by adrenal
cortex
controlled by ACTH (pituitary) &
CRH (hypothalamus)
• stimulates
• gluconeogenesis (new glucose
from non-carbohydrate sources)
• breakdown of fats (lipolysis)
• breakdown of protein
• provides resistance to stress
by mobilizing energy reserves
• high levels of cortisol decrease
inflammation & depress the immune
system
feedback
actions:
targets = many body cells
33. Drugs that resemble cortisol are widely used to reduce
inflammation and depress the immune system.
Hydrocortisone is actually the pharmaceutical preparation of
cortisol itself. You yourself may have used this as a topical
cream to reduce inflammation.
Derivatives such as cortisone and prednisone are commonly
used clinically.
• Since these drugs in some cases may be used in high
doses, they may produce effects in the body that are
comparable to hypersecretion of cortisol by the adrenal
cortex.
• They also have the ability to exert negative feedback on
the pituitary and the hypothalamus and thus may disrupt
the normal control mechanisms for cortisol release.
• Thus, these drugs need to be used very cautiously.
34. Cushing’s
1. excessive secretion from tumor of
adrenal cortex
hormone: excess cortisol or cortisol like substance:
primary
• referred to as
Cushing’s
syndrome
• is a primary
condition
35. Cushing’s (cont.)
2. excessive secretion of ACTH from
tumor of ant. pituitary
secondary
(excess ACTH)
• referred to as
Cushing’s disease
• is a secondary
condition
36. • redistribution of fat to the abdomen
& back (buffalo hump – fat deposit
between scapulae)
In all cases symptoms include:
• facial flushing
• fatigue
3. high doses of corticosteroid drugs
(such as prednisone)
• breakdown of muscle
protein; muscle weakness
• round (moon) face
• elevated blood glucose levels
• poor wound healing
37. hormone: commonly see deficiency of
both cortisol & aldosterone
Addison’s disease
causes: low levels due to
1) a problem with adrenal gland
(often autoimmune) & affects
entire adrenal cortex
3) sudden withdrawal from
glucocorticoid therapy*
*(taking these drugs in high doses long term
will suppress the pituitary, so one needs to
slowly come off of the drugs to allow the
pituitary to recover)
2) a problem with pituitary gland
and ACTH secretion (only affects
cortisol, not aldosterone)
38. symptoms
• electrolyte disturbances
• inability mobilize energy reserves & tolerate stress
• decreased appetite - weight loss
• muscle weakness & fatigue
• hypoglycemia
• bronzed coloration of the skin
40. Adrenal
medulla
epinephrine,
norepinephrine
• controlled by: sympathetic branch
of ANS (important short term
response to stress)
• actions: “fight or flight”
• increased heart rate
• increased blood pressure
• dilated bronchioles
• increased breakdown of
liver glycogen; elevated
blood glucose
• increased BMR
• increased nervousness,
sweating
• secreted by: adrenal medulla
• targets: organs that respond to
sympathetic nervous system stimulation
41. pheochromocytoma
• hormone: epinephrine & norepinephrine
• symptoms - prolonged “fight or flight”
• palpitations
• hyperglycemia
• high blood pressure
• increased BMR
• intense nervousness, sweating
• cause: excessive secretion due to tumor of
adrenal medulla
42. Two hormones from the
pancreas regulate
blood glucose levels:
insulin & glucagon
43. To understand the actions of insulin and glucagon, one
needs first to review the normal metabolic pathway for
glucose inside cells
Remember that glucose is used by cells to make ATP,
primarily by aerobic respiration. In order to be used,
glucose first must enter a cell. Glucose in the blood is
of no use to a cell until it enters.
44. The diagrams on the next two slides show cell
respiration pathways operating inside of cells:
1) when a cell has plenty of glucose
• the glucose is used to make ATP
• glucose not needed immediately for
ATP is converted to glycogen for storage
• when glycogen stores are full the extra
glucose is converted to fat (triglycerides for
storage)
2) when glucose is not readily available inside
a cell
• stored glycogen is broken down to glucose
• stored fats are broken down and used by
cells for ATP synthesis
• if necessary, amino acids from proteins are
used to make ATP
45. fats
(triglycerides)
glycerol
fatty acids
Aerobic respiration glycogen
acetylCoA
Kreb’s cycle ETC
glucose
pyruvic acid
ATP
glucose
plentiful
inside a
cell
1
2
1. glycolysis
(breakdown of glucose
to pyruvic acid to make
ATP)
2. glycogenesis
(production of glycogen
from glucose for storage)
3
3
3. lipogenesis (storage
of excess glucose as fat thru
production of glycerol &
fatty acids)
when a cell has plenty of glucose
• the glucose is used to make ATP
• glucose not needed immediately
for
ATP is converted to glycogen for
storage
• when glycogen stores are full the
extra glucose is converted to fat
(triglycerides for storage)
46. fats
(triglycerides)
glycerol
fatty acids
Aerobic respiration
glycogen
acetylCoA
Kreb’s cycle ETC
glucose
pyruvic acid
ATP
protein
not enough
glucose
inside a cell 6
4
4. glycogenolysis
(breakdown of glycogen to
glucose)
6. gluconeogenesis
(production of glucose from non-
carbohydrate sources)
6
5
5. lipolysis (breakdown
of triglycerides to glycerol &
fatty acids
when glucose is not readily
available inside cells
• stored glycogen is broken down
to glucose
• stored fats are broken down
and used by cells to make ATP
• if necessary, amino acids from
proteins are used to make ATP
47. • increasing glucose uptake into cells
• increasing glycogenesis (formation of glycogen for
glucose storage in liver and skeletal muscle)
• increasing lipogenesis (formation of fats)
actions: works to lower blood sugar levels by:
insulin secretion is controlled by: blood glucose levels;
high levels stimulate release
targets: liver, skeletal muscle, adipose
The job of insulin is to get glucose from the blood into cells
48. • decreasing uptake glucose into cells
• increasing glycogenolysis (breakdown of glycogen)
• increasing gluconeogenesis (formation of new
glucose from non-carbohydrates – fats and
proteins)
actions: works to raise blood sugar levels by:
glucagon secretion controlled by: blood glucose levels;
low levels stimulate release
targets: liver, skeletal muscle (where glycogen stores are)
The job of glucagon is to get glucose out of cells into blood
49. Diabetes mellitus
• condition resulting from an inability to make
insulin or for cells to respond to insulin
• the specifics on diabetes will be covered in the
case study activity in this unit and you can fill in
your chart with information from the case study.
