2402 ch 17 endocrine system (part 3) ppt.pdf
TRANSCRIPT
90
Clinical Application: Hyperparathyroidism
! Parathyroid adenoma #1 cause ! Serum calcium imbalance
! Paired, pyramid shaped, on superior surface of kidney
! Retro-peritoneal
! 2 regions: ! Medulla ! Cortex
! 5 layers
Adrenal Glands (Suprarenal)
adrenal gland
92
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
93
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)
94
Explain the RAA Pathway:
95
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
96
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)
97
Describe how glucocorticoids are regulated:
! Negative feedback
! Controlled by CRH (corticotropin releasing HM) & ACTH (adrenocorticotropic HM) from anterior pituitary
98
Good Summary
Figure 17.21 pg
683
2 3
1
3
5
4
High doses of cortisol: Increase retention of Na+, H2O
4 5 6
6
7 8
1 2
Stimulation Inhibition
Cortisol
STIMULUS
CONTROL CENTER
The hypothalamus releases corticotropin- releasing hormone (CRH) into the hypothalamo-hypophyseal portal system.
RECEPTOR
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).
Cortisol levels increase inhibiting release of CRH and ACTH.
NET EFFECT
Increase of all nutrients in the blood.
Cortisol
EFFECTORS: Effectors respond to cortisol in the following ways:
Liver
Stimulation of protein catabolism (occurs in all cells except hepatocytes)
Stimulation of lipolysis Inhibition of lipogenesis
Stimulation of gluconeogenesis (use amino acids and fatty acids)
Adipose connective tissue
All cells
ACTH
CRH
Hypothalamus
Variables that act on the hypothalamus: • Negative feedback by cortisol • Time of day • Stress
Decrease inflammation Suppress the immune system Inhibit connective tissue repair
Cortisol bound by carrier proteins (e.g., CBG)
Amino acids Glucose Amino acids
Glycerol fatty acids
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Fig. 17.22
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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.)
Perc
ent d
evia
tion
from
the
mea
n
0 0 8
Both emotional stress (e.g., anxiety, anger, fear) and physical stress (e.g., fever, trauma, or intense exercise) increase the release of cortisol.
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100
50
–50
–100 24 16
Hours
(a)
(b)
Cortisol level is increased by stress.
Cortisol release fluctuates based on the time of day (circadian rhythm).
24 hours
Sleep
101
Clinical Applications: ! Hyperadrenocorticism or
Cushing’s Disease ! Etiology - Usually excess
ACTH due to pituitary tumor
! Sx
! Hypocorticism or Addison’s Disease ! Etiology – genetic or
autoimmune
! Sx
102
Recall the role of androgens: ! DHEA
! Insignificant in males ! Important in females
! Libido ! Converted to estrogen
! Clinical Application: ! Congenital Adrenal Hyperplasia
http://www.dshs.state.tx.us/newborn/cah2.shtm
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Characterize the role of the adrenal medulla:
! Chromaffin cells secrete epinephrine &
norepinephrine
! Hormones are sympathomimetic (Mimic SNS
effects)
! Enhance fight or flight response
105
Characterize the pancreas:
! Location
! Consists of acinar & islet cells
! Both endocrine & exocrine in function
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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
4
5 2 3 4
1 2 3
Insulin
Pancreas Stimulation Inhibition
NETEFFECT
Decreased blood glucose (fatty acids and amino acids are also decreased in the blood)
CONTROL CENTER
Beta cells within pancreas release insulin.
Beta cells within the pancreas detect an increase in blood glucose levels.
RECEPTOR
Insulin stimulates target cells (effectors).
Insulin Negative feedback Insulin release is inhibited as blood glucose levels decrease to normal.
Insulin
Liver tissue 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
Increased glycogenesis Decreased glycogenolysis and gluconeogenesis
Adipose connective tissue All cells (especially muscle)
1 STIMULUS
Increase in blood glucose
EFFECTORS: Effectors respond to insulin in the following ways:
Glucose Glucose
Amino acids Fatty acids
5 2 3 4
1 2 Glucagon
STIMULUS
Decrease in blood glucose
Pancreas
CONTROLCENTER
Alpha cells within the pancreas release glucagon.
RECEPTOR
Alpha cells within the pancreas detect a decrease in blood glucose levels.
Gucagon stimulates target cells (effectors).
Glucagon
Increased blood glucose and fatty acid levels (note—no change in amino acids or proteins).
NET EFFECT
Negative feedback Glucagon release is inhibited as blood glucose levels increase to normal.
Glucagon
Adipose connective tissue Liver
Increased glycogenolysis and gluconeogenesis Decreased glycogenesis
Increased lipolysis Decreased lipogenesis
3 Glucose
Glycerol fatty acids
4 EFFECTORS: Effectors respond to glucagon in the following ways:
Stimulation Inhibition
1
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Serum glucose levels are regulated by glucagon & insulin secretion:
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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
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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
114
Gonads produce gametes & hormones: Testes
! Testes
! Produce testosterone
! Regulate sperm production
! Maintains male sexual characteristics
! Produce inhibin which inhibits FSH
115
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
116
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
117
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)
118
III. The Stress Response ! What is Stress? ! Eustress vs.
Distress ! Body’s
homeostatic mechanisms attempt to counteract stress
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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
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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
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2. Resistance Reaction
! Initiated by hypothalamic releasing HM ! corticotropin,
growth hormone & thyrotropin releasing hormones
! Results ! Allow body to
continue to fight a stressor
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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
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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
127
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