Clinical Application:

Hyperparathyroidism
! Parathyroid adenoma #1 cause
! Serum calcium imbalance

90

Adrenal Glands
(Suprarenal)

adrenal
gland

! Paired, pyramid

shaped, on superior
surface of kidney

! Retro-peritoneal
! 2 regions:
! Medulla
! Cortex
! 5 layers

Anatomy &
Hormones of the
adrenal glands

! 2 structurally &

functionally distinct
areas
! Adrenal cortex
! Mineralocorticoids

affect mineral
homeostasis
! Glucocorticoids affect
glucose homeostasis
! Androgens have
masculinzing effects
! Adrenal medulla
! Modified sympathetic
ganglion of ANS
! Intensifies sympathetic
responses

! Epinephrine &

norepinephrine

92

Describe the function of

aldosterone:
! Aldosterone is the major mineralcorticoid
! Functions:
! Regulate electrolyte concentration in ECF
! increase reabsorption of Na+ w/ Cl-, bicarbonate & H2O
following it
! promotes excretion of K+ & H+

! Secretion regulated by the renin-angiotensin pathway

(RAA)

93

Explain the RAA Pathway:

94

Clinical Application:
Hyperaldosteronism or Conn Syndrome
! Cause of primary aldosteronism = adrenal adenoma in
80% of patients

! Sx = HTN, hypokalemia
! Tx = removal of adenoma
! Corrects HTN & hypokalemia
in most patients
MRI in a patient with Conn
syndrome showing a left adrenal
adenoma.

http://www.ispub.com/journal/the_internet_journal_of_surgery/volume_24_number_1_1/article/conn-s-syndrome

95

Describe the function of

cortisol:
! 95% of glucocorticoids hormonal activity is
due to cortisol

! Functions
! Help regulate metabolism
! Protein catabolism & lipolysis
! Gluconeogenesis
! nutrients available for ATP production

! Resistance to stress
! Anti-inflammatory (Hydrocortisone cream)
! Immunosuppression (Corticosteroids such as
prednisone)

96

Describe how
glucocorticoids
are regulated:
! Negative feedback
! Controlled by CRH

(corticotropin releasing
HM) & ACTH
(adrenocorticotropic
HM) from anterior
pituitary

97

98

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cortisol
STIMULUS
1

Good
Summary
Figure
17.21 pg
683

Stimulation
Inhibition

Variables that act on the hypothalamus:

Negative feedback by cortisol
Time of day
Stress

Hypothalamus
1
2
RECEPTOR
3

8 Cortisol levels
increase inhibiting
release of CRH
and ACTH.

CRH

ACTH

NET EFFECT
7

CONTROL CENTER
3 The hypothalamus
releases corticotropinreleasing hormone
(CRH) into the
hypothalamo-hypophyseal
portal system.

Hypothalamus
responds to various
stimuli.

In response to CRH, the anterior pituitary

releases adrenocorticotropic hormone
(ACTH).

ACTH stimulates the adrenal cortex to

release glucocorticoids (e.g., cortisol)
into the blood.

Cortisol stimulates target cells (effectors).

Increase of all nutrients in

the blood.

Amino acids

Glucose

Cortisol bound by
carrier proteins
(e.g., CBG)

Liver

Cortisol

Amino acids
Glycerol fatty acids

EFFECTORS: Effectors respond

to cortisol in the following ways:

Adipose connective
tissue

All cells

High doses of cortisol:

Increase retention of Na+, H2O
Decrease inflammation
Suppress the immune system
Inhibit connective tissue repair

Stimulation of
gluconeogenesis (use
amino acids and fatty acids)

Stimulation of lipolysis
Inhibition of lipogenesis

Stimulation of protein
catabolism (occurs in all
cells except hepatocytes)

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Percent deviation from the mean

Cortisol release fluctuates based on the time of day (circadian rhythm).

Fig. 17.22

Cortisol levels fluctuate throughout the day.

Notice that in a normal sleep-wake cycle, peak
levels of cortisol correspond to the late stages of
a normal sleep cycle. About half of all cortisol
release occurs when you are asleep, with cortisol
levels peaking right before waking in the
morning. This rhythm of release is regulated by
light and dark cycles detected by the retina as
nerve signals are relayed to the hypothalamus.
(Between individuals, there is significant
variation in normal levels.)

24 hours

150
Sleep
100
50
0
50
100

16

24

Hours
(a)
Cortisol level is increased by stress.
Both emotional stress (e.g., anxiety, anger, fear) and physical stress (e.g.,
fever, trauma, or intense exercise) increase the release of cortisol.

(b)

Clinical Applications:
! Hyperadrenocorticism or
Cushings Disease
! Etiology - Usually excess

ACTH due to pituitary tumor

! Sx

! Hypocorticism or Addisons
Disease
! Etiology genetic or
autoimmune
! Sx

101

Recall the role of androgens:

! DHEA
! Insignificant in males
! Important in females
! Libido
! Converted to estrogen

! Clinical Application:
! Congenital Adrenal Hyperplasia

102

http://www.dshs.state.tx.us/newborn/cah2.shtm

Page 682

Characterize the role of the

adrenal medulla:
! Chromaffin cells secrete epinephrine &
norepinephrine
! Hormones are sympathomimetic (Mimic SNS
effects)

! Enhance fight or flight response

104

Characterize the
pancreas:
! Location

! Consists of acinar &

islet cells

! Both endocrine &

exocrine in function

105

Page 686

Endocrine &
exocrine
functions of
the pancreas:
! Acinar cells = exocrine
(99% of cells)

! Pancreatic islets (islets of

Langerhans) = endocrine
! Alpha (!) cells - glucagon
! Beta (") cells - insulin
! Delta cells somatostatin

(aka GIH, Growth Inhibiting

Hormone)
! F cells - pancreatic
polypeptide

107

Insulin
Pancreas

STIMULUS
1

Stimulation
Inhibition

Increase in blood glucose

RECEPTOR
1

NETEFFECT
5 Decreased blood glucose
(fatty acids and amino
acids are also decreased
in the blood)

CONTROL CENTER

2 Beta cells within the

pancreas detect an
increase in blood
glucose levels.

3 Beta cells within

pancreas release
insulin.

3 Insulin
Negative feedback
Insulin release is inhibited
as blood glucose levels
decrease to normal.

Insulin stimulates target

cells (effectors).

Glucose
Amino acids

Glucose

Fatty acids

Liver tissue

Insulin

EFFECTORS: Effectors respond

to insulin in the following ways:
All cells
(especially muscle)

Adipose connective tissue

Increased glycogenesis
Decreased glycogenolysis
and gluconeogenesis

Most cells

Increased uptake of
glucose by increasing
glucose transport
proteins in the plasma
membrane

Increased uptake
of amino acids, which
stimulates protein
anabolism

Increased lipogenesis
Decreased lipolysis

Glucagon
Pancreas

STIMULUS

Stimulation
Inhibition

1 Decrease in blood glucose

NET EFFECT

RECEPTOR

5 Increased blood glucose

and fatty acid levels
(noteno change in
amino acids or proteins).

2 Alpha cells within the

pancreas detect a
decrease in blood
glucose levels.
3

Glucagon

Negative feedback
Glucagon release is inhibited
as blood glucose levels
increase to normal.

Glucose

Glucagon

CONTROLCENTER
3 Alpha cells within
the pancreas
release glucagon.

4 Gucagon stimulates target

cells (effectors).

Glycerol fatty acids

EFFECTORS: Effectors respond

to glucagon in the following ways:

Liver

Increased glycogenolysis
and gluconeogenesis
Decreased glycogenesis

Adipose connective tissue

Increased lipolysis
Decreased lipogenesis

Serum glucose levels are regulated by

glucagon & insulin secretion:

110

Clinical Application: Diabetes Mellitus

! May be caused by too little insulin, resistance to insulin, or both
! There are three major types of diabetes:
! Type 1 diabetes - usually diagnosed in childhood
! Body makes little or no insulin
! Cause - ?? Genetics, viruses, & autoimmunity

! Type 2 diabetes - more common than type 1

! Usually occurs in adulthood linked to obesity lack of exercise
! Pancreas does not make enough insulin or cells exhibit insulin resistance

! Gestational diabetes - high blood glucose during pregnancy

! Hyperglycemia can cause several problems:

!
!
!
!

Excessive thirst (polydipsia)

Frequent urination (polyuria)
Hunger (polyphagia)
Fatigue

111

Page 688

Gonads produce gametes &

hormones: Ovaries
! Ovaries:
! Produce estrogen
! Produce progesterone
! Estrogen & progesterone along w/ FSH & LH regulate
menstrual cycle, maintain pregnancy, prepare mammary
glands for lactation, maintain female 2o sex characteristics

! Produce inhibin inhibits FSH secretion

! Produce relaxin during pregnancy

113

Gonads produce gametes &

hormones: Testes
! Testes
!
!
!
!

Produce testosterone
Regulate sperm production
Maintains male sexual characteristics
Produce inhibin which inhibits FSH

114

Recall the role of follicle

stimulating hormone (FSH)
! Gonadotropins = FSH & LH
! anterior pituitary release FSH
! initiates formation of follicles
! stimulates estrogen secretion
! stimulates sperm production

115

Role of luteinizing hormone (LH)

! Produced the anterior pituitary
! In females it induces:
! Ovulation
! Formation of corpus luteum
! Secretion of progesterone & estrogen

! In males it:
! stimulates secretion of testosterone

116

Characterize the pineal gland:

! Attached to roof of 3rd ventricle of brain
! Secretes melatonin
! Maintains Circadian rhythms
! More melatonin liberated during darkness than light
! Linked to seasonal affective disorder (SAD)

117

III. The Stress Response

!What is Stress?
! Eustress vs.
Distress
! Bodys
homeostatic
mechanisms
attempt to
counteract
stress
118

Page 685

Describe the stress response:

! Stressful conditions can result in the stress response
or general adaptation syndrome (GAS)

! 3 stages: flight-or-fight, resistance reaction, exhaustion

120

1. Alarm (Fight-or-Flight)
! Initiated by hypothalamic

stimulation of sympathetic
portion of ANS & adrenal
medulla (epinephrine &
norepinephrine)
! Nonessential fxns (SLUDD)

inhibited ! decreased blood flow

to kidneys ! release of renin !
RAA ! aldosterone ! H2O
retention & increased BP
121

122

2. Resistance
Reaction
! Initiated by

hypothalamic
releasing HM
! corticotropin,

growth hormone &

thyrotropin
releasing hormones

! Results
! Allow body to

continue to fight a
stressor
123

124

3. Exhaustion
! Effects of prolonged exposure to cortisol & other
resistance reaction HM:

! Wasting of muscle
! Immunosuppression
! Ulceration of GI tract
! Failure of beta cells
! Insulin resistance

125

Stress can lead to disease:

! Gastritis, Ulcerative colitis,
IBS, Peptic ulcers

! Cardiovascular disease
! Migraines
! Asthma
! Increased incidence of
infectious and autoimmune diseases

! Anxiety / depression
! Post traumatic stress syndrome

126

IV. Aging and the Endocrine System

! Production of hGH decreases
! Production of T3/T4 decreases ! increased TSH
! Thymus atrophies after puberty replaced w/ adipose
! PTH levels increase (decreased Ca+2 intake),
calcitonin levels decrease ! osteoporosis

! Adrenal glands produce less cortisol & aldosterone

! Receptor sensitivity to Glc declines
! insulin secreted more slowly

! Ovaries no longer respond to gonadotropins

127