Untitled Flashcards Set
*Up-regulation - ↑ in # of receptors in
deficient hormone
- more sensitive to hormone
3. Mechanisms of interaction of hormone w/target cell
* Peptide & protein hormones, not lipid soluble - so...?
3 Interaction w/plasma membrane receptors
1. First messenger - Hormone
* binds to receptor site on membrane
2. Second messenger produced - Cyclic AMP
*ATP is converted to cyclic AMP by adenylate cyclase
*reaction is stimulated by binding of hormone w/ receptor on membrane (outer)
*note G protein – slowly deactivate
*cAMP ultimately degraded by phosphodiesterase
Note: Ca++ ions may be 2nd messengers
*enters cells when hormone binds
*bind to calmodulin – activates protein kinases...
3. cAMP activates a protein kinase enzyme to phosphorylate a protein
* Response by cell:
*enzyme regulation (↑ or ↓ enzyme production)
*secretion
*protein synthesis
*membrane permeability
*only a little hormone is necessary (chain reaction)
4 Interaction w/ intracellular receptors
1. Receptor sites usually w/in nucleus
2. Binding occurs.
3. Receptor-hormone complex alters DNA expression (turns on or off)
4. mRNA is produced & released to cause protein synthesis
5 Interaction between hormones
1. Permissive effect –prior exposure of another
hormone is required
*↑ in # of receptors?
Ex: estrogen before progesterone in menstrual cycle
2. Synergistic effect – two or more hormones act together
Ex: prolactin (milk production) w/ estrogen
3. Antagonistic effect – opposing actions
Ex: insulin & glucagon from pancreas
6 Site of hormonal action
7 Circulating hormones – affect target areas distant from site of production by glands
* carried by bloodstream
8 Local (Tissue) hormones –affect immediate area of production
*may be produced by all cells
*Eicosanoids - Prostaglandins (PG's)
*lipids
*influences formation of cAMP
*involved in inflammatory response (histamine)
*NO
9 Control of hormonal secretions
* determined by body's needs
10 Negative feedback control systems
*result is opposite the stimulus
* i.e., ↑ hormone will cause a ↓ in production
a. Control by direct stimulation from nervous system
Ex: NE & epinephrine release from adrenal medulla
ADH release from posterior pituitary
b. No nervous stimulation; blood chemical levels stimulate release of hormone
Ex: ↑ glucose blood level; ↑ insulin release
c. Regulating hormones from hypothalamus
1. Releasing hormones - ↑ secretions by gland
2. Inhibiting hormones - ↓ secretions by gland
11 Positive feedback control
*result intensifies stimulus
* Ex: oxytocin (OT) from posterior pituitary...
12 Endocrine glands
13 Pituitary gland – Hypophysis “Master gland”
14 Size 1 – 1.5 cm (.5”) diameter
15 Location
*attached by infundibulum to hypothalamus
16 General structure
*two lobes separated avascular zone → pars intermedia
1. Adenohypophysis
*anterior lobe
*glandular portion
*75% total gland weight
*no direct nerve connection to brain... blood vessels connect
2. Neurohypophysis
*posterior lobe
*stores hormones produced in the hypothalamus
*neural connection to hypothalamus
17 General physiology
1. Adenohypophysis
*receive regulating hormones from hypothalamus
Via Hypophyseal Portal System:
superior hypophyseal arteries
primary plexus (capillaries) regulating hormones
(hypothalamus)
hypophyseal portal veins
secondary plexus (capillaries) hormones
(anterior pituitary)
anterior hypophyseal veins
a. Cell types
*somatotrophs, thyrotrophs, gonadotrophs, lactotrophs, corticotrophs,
b. Hormones
1. Human growth hormone (hGH)
*also known as: somatotropin or somatotropic hormone
* Tropic hormone – stimulates other glands
a. Functions of hGH – stimulate production of insulinlike growth factors (IGF's) by
tissue cells, which...
1.↑ rate of growth & maintain skeletal muscles
2.↑ protein synthesis by ↑ rate of a.a.'s entering cells
3.↓ protein breakdown
4.↑ fat catabolism
5.↓ glucose take up & use by cells
6.↑ blood glucose concentration
*diabetogenic effect - mimics diabetes mellitus
b. Control of hGH release
1. Regulating hormones from hypothalamus
a. GHRH – growth hormone releasing hormone
b. GHIH – growth hormone inhibiting hormone
2. Hypoglycemia – low blood sugar
*promotes GHRH release → stimulate hGH release
3. Hyperglycemia – high blood sugar
*promotes GHIH release
c. Pathology
1. Dwarfism (Pituitary dwarfism)
– hyposecretion of hGH
Treatment? – hGH during childhood while bones can still lengthen
2. Giantism – hypersecretion of hGH during
childhood
*long bones lengthen
Acromegaly – hypersecretion of hGH during
adulthood
*bones of face thicken
2. Thyroid - stimulating hormone (TSH) Thyrotropin
*stimulates thyroid gland (tropic hormone
*release controlled by thyrotropin releasing hormone (TRH) from hypothalamus;
*release of TRH controlled by metabolism, blood chemical levels
(negative feedback)
3. Adrenocorticotropic hormone (ACTH)
*stimulates adrenal cortex
*controlled by corticotropin releasing hormone (CRH)
*release of CRH influenced by stress, low blood glucose, trauma
4. Follicle stimulating hormone (FSH)
*stimulates ovaries to produce eggs & estrogen
*stimulates testes to produce sperm
*release controlled by gonadotropin releasing hormone (GnRH)
5. Luteinizing hormone (LH)
*stimulates ovulation & hormone production in ♀'s
*stimulates testosterone release in ♂'s
*prepares uterus for implantation
*release controlled by GnRH
6. Prolactin (PRL)
*stimulates milk production
*release controlled by PIH (dopamine) & PRH (during pregnancy)
7. Melanocyte stimulating hormone (MSH)
*↑ skin pigmentation; receptors in brain...
*release controlled by...CRH or PIH
2. Neurohypophysis
*posterior lobe of hypophysis
*no glandular material
a. Storage of hormones produced by hypothalamus
*neurosecretory cells – produce hormones
*hormones to posterior pituitary via hypothalamic –hypophyseal tract
*hormones transferred by neurophysins (protein carriers)
- takes approx. 10 hours
*Pituicytes
- cells in posterior pituitary that store hormones
b. Hormones
18 Oxytocin (OT) – Pitocin, commercially
a. Function – stimulates muscle contractions:
*in uterus during labor
*mammary glands during lactation
b. Control - Positive feedback!
*beg. of labor → contractions → afferent impulses to hypothalamus →
↑ contractions
*milk let-down reflex – latent pd. after baby begins suckling (30sec -1min)
2. Antidiuretic hormone (ADH)
a. Function
1. Conservation of body water by reabsorption of water from urine by kidneys
2. Vasopressin – constricts arterioles; ↑ blood pressure
b. Control
1. Osmoreceptors in hypothalamus
– detect changes in osmotic pressure caused by changes in salt & water
conc.
*Dehydration- ↑ salt; ↓ water (↑ osmotic pressure)
↑ADH; ↓ urine output
* Overhydration - ↓ salt; ↑ water (↓ osmotic pressure)
↓ ADH; ↑ urine output
2. Pain, stress. drugs affects hypothalamus
* ↑ ADH release
c. Pathology
*dysfunction of neurohypophysis
- diabetes insipidis
*hyposecretion of ADH.....note symptoms
*↑ urine ↑ dehydration ↑thirst;
*TRT? ADH
2. Thyroid
a. Structure of glands
19 Lobes
a. Two Lateral lobes on either side of trachea
b. Isthmus – connects 2 lobes
c. Pyramidal lobe – extends upward from isthmus
(may be absent)
20 Cells
a. Follicular cells
*surround thyroid follicles
*produce thyroid hormones
*amines Thyroxine (T4) in ↑ amounts
Triiodothyronine (T3) in ↑ strength
b. Parafollicular cells
*outside follicular cells, away from lumen
* produce calcitonin (CT)
*↑Ca++ uptake in bone tissue (↓ blood Ca++ level)
hypocalcemia used to treat postmenopausal osteoporosis
(Miacalcin)
hypercalcemia release controlled by blood Ca levels
b. Manufacture & release of thyroid hormones
* I- into follicular cells from bloodstream
* I2 united with tyrosine to form thyroid hormone
* Thyroglobulin (TGB) & hormones form thyroid
colloid to store hormone
* Thyroxine-binding globulin (TBG protein) carries
hormones in blood
c. Function of thyroid hormones
1. Regulation of organic metabolism
*calorigenic effect - ↑ body temp. by ↑metabolism
2. Regulate tissue growth; esp. neural tissue
*w/hGH
3. Increase reactivity of nervous system
*↑ cardiovascular function (blood flow; HR)
*↑digestive function
*↑nervousness
d. Control of release of thyroid hormones
*↑ body need for energy (low hormone levels) → TRH → TSH
e. Pathology of thyroid gland
1. Hyposecretion of thyroid hormones
a. During infancy cretinism
*results in dwarfism & mental retardation
*TRT? Thyroid hormones
b. During adulthood myxedema
*slow metabolism; slow HR
*puffy facial features – edema
*TRT? Thyroid hormones
2. Hypersecretion of thyroid hormones
*results in high metabolic rate
*enlarged thyroid (goiter)
*TRT? antithyroid drugs
radioactive iodine
surgery
3. Parathyroid glands (4)
a. Location
*superior & inferior on posterior surface of each lateral lobe of thyroid gland
b. Structure
1. Chief cells (Principal cells)
*actively produce parathyroid hormone (PTH), or parathormone
2. Oxyphil cells
*reserve supply of hormones?
*uncertain function
c. Function of PTH
*↓ blood phosphate (HPO4-2) levels
*also ↑ HPO4-2 in urine
*↑ blood Ca++ and Mg++ levels
Note: antagonistic to calcitonin(w/reference to Ca++)
* ↑ formation of calcitriol in kidneys
* ↑ absorption of Ca++ , Mg++, & HPO4-2 from GI tract into blood
d. Control
*pituitary not involved!
*parafollicular cells affected by blood Ca++ levels
*negative feedback control
low blood Ca++ level → ↑ PTH ↑ blood Ca++
Note pathology -
21 Adrenals -- Suprarenals
a. Location
*superior to each kidney
b. Structure and physiology
1. Adrenal cortex – outer portion of gland
*80-90% of gland
*highly vascularized
a. Zona glomerulosa
* produces mineralocortacoids
*deal w/ homeostasis of mineral concentrations
* Aldosterone - primary hormone of zona glomerulosa
* causes:
*reabsorption of Na+ from urine
*elimination of K+ in urine
Note: Reabsorption of Na+ causes:
*elimination of H+ ions in urine; ↓ blood acidity
*retention of HCO3– ions
*retention of H2O due to ↑ osmotic pressure,
therefore...
*Control of aldosterone release?
Renin-angiotensin pathway
↓ blood pressure → renin released→ angiotensin I produced
aldosterone angiotensin I
↑b.p. ← ↑Na+ ← release ← to II (by ACE)
High K+ concentration → aldosterone released
K+ eliminated
b. Zona fasciculata
*middle section of adrenal cortex
* produces glucocorticoids
1. Three types:
a. Cortisol (Hydrocortisone)
*95% of activity
b. Corticosterone
c. Cortisone
2. Function of glucocorticoids ...energy
a. Combat stress
1. Provides ↑ glucose
*gluconeogenesis – conversion of a substance other than CHO for
energy
(in ↓ blood glucose situations)
*occurs in liver
2. Lipolysis – breakdown of adipose tissue to release fatty acids
3. ↑ protein catabolism to provide amino acids
4. ↑ vasoconstriction by ↑ sensitivity of blood vessels
b. ↓ Immune responses
*anti-inflammatory – balance to inflammation
*note: cortisone shots...
3. Control of release of glucocorticoids
*Negative feedback system involving hypothalamus & pituitary
↓ Hormone level → ↑ CRH → ↑ ACTH → ↑ hormones
Note: Pathology
c. Zona reticularis
* produce gonadocorticoids - androgens
*androgens in ♀’s are converted to estrogen
*androgens in ♂’s are minimal compared to effects of testerone
2. Adrenal medulla
a. Structure
*chromaffin cells –surround blood-filled sinuses
*receives innervation from preganglionic fibers of sympathetic nervous system
*modified sympathetic autonomic ganglion
b. Function
*produce epinephrine (80%) & Norepinephrine
(adrenaline) (noradrenalin)
*hormones are sympathomimetric
*results mimic & intensify sympathetic effects
c. Control
stress → hypothalamus → preganglionic fibers
chromaffin cells → ↑ NE & epinephrine → ↑ fight or flight
4. Pancreas
22 Structure and physiology
1. Heterocrine gland – endocrine & exocrine
2. flattened; 4.5 to 6 “ long
3. posterior & inferior to stomach
4. head, body & tail regions
5. Pancreatic Islets (Islets of Langerhans)
*endocrine portion – 1% of organ
a. Alpha cells – 17% of islets
* secrete glucagon
*↑ blood glucose level thro' glycogenolysis & gluconeogenesis
*control of glucagon secretion?
*alpha cells detect ↓ blood sugar levels
(below normal...90mg/100ml)
*↓ blood glucose → ↑ glucagon
*note sympathetic innervation (exercise)
b. Beta cells – 70% of islet cells
* secrete insulin
*↓ blood glucose level by stimulating entry of glucose into skeletal muscles
via insulin receptors on cells
*control of insulin secretion?
*beta cells detect ↑ blood glucose levels and cause ↑ insulin release
*note parasympathetic innervation (vagus nerve)
Note: hGH & ACTH...?
c. Delta cells – 7 % of islet cells
* secrete GHIH (somatostatin)
*inhibits (controls) secretion of insulin & glucagon
*paracrine activity
d. F cells
*secrete pancreatic polypeptide
*concerned with digestive activity
23 Pathology of pancreas
1. Hyperglycemia - ↑ blood sugar → diabetes mellitus
a. Characteristics
1. Polyuria – excessive urination
2. Polydipsia – excessive thirst
3. Polyphagia – excessive eating
b. Types of diabetes
1. Type I Diabetes – juvenile onset; pre-20 years in age
- insulin - dependent
*insufficient insulin produced
*↓ in # of beta cells ... autoimmune?
Trt? insulin
2. Type II Diabetes – maturity onset; post 40 years in age
- non-insulin dependent
*90% of cases
*lack of insulin receptors on cells
Trt? diet, exercise
5. Pineal gland
*located in roof of third ventricle of brain
*secretion of melatonin
*produced from serotonin
* ↑ production during sleep
*seasonal affective disorder (SAD) due to ↑ production of melatonin during months
with ↓ light
E. Stress Response
*stressor – stimulus that elicits a stress response
*eustress – 'good stress', enables us to deal with extreme physical situations
*distress – 'bad stress', harmful as in illness
1. Fight-or-Flight response – short lived
*↑ hypothalamic stimulation of sympathetic division of ANS
*innervation of adrenal medulla
*↓ parasympathetic stimulation
*↑ glucose & oxygen to tissues...how?
*↑ rennin-angiotensin –aldosterone pathway
*↑ b.p.
2. Resistance reaction
*hormonal primarily; maintains response initiated by fight-or-flight
*hypothalamus releases:
CRH,TRH, & GHRH...result?
*ceases after stressors are removed; parasympathetic ↑
3. Exhaustion
*damage to body tissues may occur if hormone levels remain ↑ for too long a period
*prolonged exposure to stress may ↓ immune response, esp. due to ↑ cortisol levels