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PHYSL 210 > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

Endocrine functions and dysfunctions

A

Function:
– Mood / Behavior
– Reproduction
– Digestion/excretion
– Intermediary metabolism
– Growth
– Puberty

Dysfunction: Result of defect in synthesis, regulation, or hormone action
▪ Growth/retardation
▪ Weight gain/loss
▪ Skin pigmentation/dryness/acne/sweating
▪ Hair growth/loss
▪ Sexual characteristics

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2
Q

Exocrine vs. Endocrine Glands

A

Exo: Empty their secretions into
body cavities or onto body
surfaces by tubular ducts

Endo: Ductless glands that release
their secretions internally
into the bloodstream
– They are highly vascularized because the hormones they make come from dietary precursors and rely on blood for transport

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3
Q

Hormone basics

A

– Chemical messages that regulate homeostasis; set in motion biological reactions
– Have high potency (<10-9
- 10-6 M)
– Act at specific receptors
– Act with a latency (delay) of response
– Have limited storage
– Are secreted irregularly
– Mostly carried in plasma by binding proteins
– Are not an energy source
– Are not incorporated into another molecule

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4
Q

Steroid vs. Protein Hormones

A

Steroid: derived from cholesterol
– cholesterol either comes from dietary sources bound to LDL or synthesized from acetate
– it can be stored as a lipid droplet until needed
Protein: All protein hormones are made from mRNA.
– mRNA -> prehormone -> prohormone -> hormone -> secretory vesicles

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5
Q

Secretory vesicles

A
  • Protect hormones from proteolytic degradation
  • Provide a reservoir in sites of synthesis
  • Provides a transport mechanism
    to the site of release (Plasma membrane)
  • Provides a release mechanism (Exocytosis)
  • Provides for quantal release of consistent hormone amounts

S

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6
Q

Binding proteins

A

Two types of hormones in plasma:
bound and free

  • Only free hormone is active
  • Hormone is inactive when bound to binding protein in plasma

functions:

  • Increases solubility and concentration (Lipid soluble steroid and thyroid hormones)
  • Increases size, protecting hormones from clearance and degradation
  • Inactivates free hormones, providing a buffer against large and sudden changes in hormone concentrations
  • Dynamically regulated with rate of secretion, rate of degradation
    and binding to receptors on target cells
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7
Q

Regulation of Hormone Secretion

A

Dynamically regulated to maintain a steady-state around a set-point
or range, that may vary during the day or with age or physiological
state
– negative and positive feedback

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8
Q

Hormone action and receptors

A

Hormone action is very specific and only binds to certain receptors which then produces a response
– like a lock (receptor) and key (hormone)
cAMP Second Messenger System: proteins must bind to receptors … cannot cross membrane
Signal amplification: binding of 1 hormone = large response (100000)
- Receptors for lipid-soluble hormones are either nuclear or cytoplasmic
- Nuclear: Steroid and thyroid
hormones; genomically mediated
through protein synthesis
-cytoplasmic: Intracellular transport for cytosol-insoluble steroids and reservoir storage and
organelle actions for
thyroid hormones

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9
Q

Receptor regulation

A

Down-regulation (Less receptors)
– Decreased receptor synthesis/increased degradation
– Internalized membrane receptors
– Dislocation of receptor and signal transduction system
- Desensitization (Less affinity)
– Conformational change in Lock structure
Up-regulation (More receptors)
– Increased receptor synthesis/decreased degradation
- Sensitization (More affinity)
– Conformational change in Lock structure

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10
Q

Down Regulation by coated pits

A

Coated pit: Hormone-receptor complexes congregate in certain areas
- Invaginations form -> formation of vesicles in the cell
-> lysozymes cleave the hormone from the receptor
- allows protein hormones to enter the cell

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11
Q

Neurohypophysis

A

hypophysis = pituitary gland
- Anterior lobe is non-nerual tissue and is developed from the Rathke’s pouch or an invagination of the roof of the mouth
- Posterior lobe is neural tissue and is developed from an extension of the hypothalamus.
- intermediate lobe lost at birth
- hypothalamus produces hormones for the posterior pituitary first excreted by the SON (ADH) and paraventricular nuclei (oxytocin)
- infundibulum is the cluster of axons and vessels

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12
Q

Synthesis of Protein Hormones in Nerves

A

For ADH and oxytocin
- development of pre-prohormone -> Pro-pressophysin -> ADH nonapeptide binded to neurophysin -> ADH is released
- neurophysin is an intraneural binding protein not a plasma binding protein; helps to transport the hormone to vesiccles, w/o they could escape because they are very small and be degraded
- Production is in the cell body, packaging is in the Golgi, transport and maturatino along the axon, released or stored in the terminals

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13
Q

ADH

A

Vasoconstriction action:
1. Contraction of blood vessel smooth muscle
2. Increases blood pressure
3. Only occurs at high concentrations
- Hemorrhage
Anti-diuretic action: Refer to renal for mechanism
1. Increases permeability of the renal collecting duct
2. Vasoconstriction reduces glomerular filtration rate
3. Contraction reduces the size of the glomerulosa cells, reducing their
surface area for filtration

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14
Q

Regulation of ADH

A
  1. Plasma volume: baroreceptors sense change in blood pressure caused by changes in volume
  2. Plasma osmolarity: osmoreceptors in hypothalamus, SON and PVN sense changes
  • Examine diagrams on the slides

Other Factors:
ADH secretion increased by: Stress/emotion, Heat, Nicotine, Caffeine
ADH secretion decreased by: Cold, Alcohol

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15
Q

Oxytocin

A
  • posterior pituitary hormone (PVN)
  • Oxytocin actions:
    – Uterine myometrium
    ▪ Parturition
    ▪ Clamping ruptured blood vessels
    ▪ Restoration of uterine size
    ▪ Sperm movement
    ▪ Cervix movement
    – Mammary myometrium
    ▪ Milk let-down
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16
Q

Effects of oxytocin on parturition

A

Positive feedback loop causing uterine contractions during labor
* Initial contractions force fetus downward, stretching cervix and
triggering the neuroendocrine reflex
- Weak uterine contraction = pressure on cervix = oxytocin = strengthens pressure on cervix

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17
Q

Effects of oxytocin on Milk let-down (lactation)

A

Positive feedback loop
– Suckling further increases the release of oxytocin
* Conditioned response
– Visual and auditory stimuli
Other functions: Released during sexual intercourse and stimulates orgasm; also released during social bonding

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18
Q

Regulation of oxytocin

A

Tactile stimuli ↑ secretion
– Genital tract
– Nipples
* Stress ↓ secretion
– Psychogenic/physical

No problems with excess, but impared delivery and lactation without

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19
Q

Anterior pituitary and the hypothalamus

A

blood supply from the hyothamalus controls the secretions of the anterior pituitary
Hypothalamo-hyposphyseal portal vessels: venous or portal blood vessels which run into the anterior pituitary
Nuclei of hypothalamus:
- Magnocellular: larger and longer; synthesize oxytocin and ADH
- Parvocellular: neurons with small cell bodies and axons; produce neural secretions -> blood
- hypothalamus releases both trophic and inhibiting hormones

20
Q

Growth Hormone

A

Acts on most tissues of the body

  • inhibited by SRIF, activated by GHRH
  • Acts through the liver through hormones called somatomedins
  • Somatomedins (IGF-1 and IGF-2) induce growth effects on soft tissue and bone
  • Has some direct effects not mediated by somatomedins
  • ↑ protein synthesis in muscle and liver, ↑ gluconeogenesis (hyperglycemia), and ↑ lipolysis (hyperlipidemia)
  • Somatomedins, growth hormone, and growth hormone inhibiting hormone provide negative feedback
  • Deep sleep, exercise, stress, ↓ blood glucose, ↑ Blood amino acids,
    ↓ blood fatty acids stimulate hypothalamus
21
Q

Changes in Growth Hormone

A

Number and amplitude of growth hormone release episodes increased by dark, sleep, and fasting
- Releasing of GH is episodic

22
Q

Summary of GH

A

synthesized in somatotrophs

Secretion:

  • Episodic
  • More during stress/sleep
  • Less during aging
  • GHRH/SRIF balance

Action:

  • Skeletal/soft tissue growth
  • Hyperglycemia/hyperlipidemia
  • IGF-1 induction (Negative feedback)
23
Q

GH deficiency

A

Isolated GH Deficiency (Type I Dwarfism):
– Defect in GH production
- leads to somatopause in adults: Increased fat/decreased lean mass, metabolic disturbances, impaired immune function (Thymic atrophy)
Laron-type Dwarfism:
– Defect in GH action: GH-receptor dysfunction
– GH levels are not deficient, IGF-1 levels are deficient
* Normal body proportions for age, no intellectual disability, usually mature sexually
Acromegaly: excess growth hormone production in an adult; no growth in height but growth in bones, cartilage, and liver size

24
Q

Prolactin

A

Actions:
– Gonadal modulation: Pro-gonadal when activity is low, anti-gonal when activity is high
‒ Mammary gland development
‒ Lactation
Secretion and associated hormones:
* Prolactin-releasing factors (PRF)
‒ Thyrotropin-releasing hormone (TRH)
‒ Oxytocin
* Gonadal steroids
‒ Estrogen/testosterone increase
‒ Progesterone decrease
* Mammary stimulation
‒ Suckling

25
Q

Prolactin Pathophysiology

A

Excess: Hyperprolactinemia
▪ Gonadal dysfunction, amenorrhea (no menstruation), reduced libido
* Treatment: Dopamine (DA) agonist treatment/tumor removal

Deficiency: Hypoprolactinemia
* Gonadal dysfunction, impaired lactation

26
Q

Adenohypophyseal Pathophysiology

A

Excess: Pituitary diabetes (Hyperglycemia)

Deficiency:
* Hypopituitarism: failure of the pituitary gland to produce one or more of its hormones partially or completely
* Panhypopituitarism: inadequate or absent production of all the anterior pituitary hormones

27
Q

TSH and thyroid hormone (T3 and T4)

A

TSH: Stimulates thyroid gland growth and thyroid hormone synthesis
* Glycoprotein hormone:
- Contains sugar residues-
- 2 subunits: α and β: Biological activity resides in β subunit
- Sugars are essential for biological activity, promote receptor recognition, prevent hormone degradation

Actions of thyroid hormone:
↑ Metabolic rate and heat production;
enhancement of growth and CNS development; enhancement of sympathetic activity
T4 - 4 iodines; precursor to T3 (larrge amount)
T3- more biologically active

28
Q

Thyroid Gland

A

An exocrine gland in early development
- Colloid: site of thyroid hormone synthesis (it is extracellular which is different from other glands)
- Follicular cells: surrounds the cavity with the colloid. When they are active, they increase in size, the colloid decreases in size

29
Q

Thyroid hormone synthesis: Thyroglobulin

A

Glycoprotein synthesized in rough ER of follicular cells and secreted into colloid
* Contains numerous tyrosine residues that provide a template for thyroid hormone synthesis
* NOT a binding protein
Steps:
1. I2 from IF cotransported with sodium ->cell
2. iodine ions diffuse into the lumen
3. thyroglobulin is synthesized in the follicular cell -> colloid. Iodine is oxidized and attached to tyrosine of thyroglobulin (MIT and DIT)
4. MIT or DIT is added to a DIT (coupling)
- 20x more T4 than T3
5. Endocytosis of thyroglobulin with attached T3 and T4
6. Lysozymes release T3 and T4
7. Secretion

30
Q

Thyroid binding proteins

A

Thyroid hormone binding proteins (most bound hormone due to it being hydrophobic)
‒ Only 0.03 % of plasma T4 and 0.5 % plasma T3 free
3 binding proteins:
* TBG → Thyroid-binding globulin (T4 and T3)
‒ Most important
* TBA → Thyroid-binding albumin (T4 and T3)
* TBPA → Thyroid-binding pre-albumin (T4 only)
- Affinity for T4 is much higher than T3
- T3 most often comes from deiodase converting T4 -> T3

31
Q

Thyroid hormone action

A
  1. No specific target sites
  2. Latent, long-lasting responses
  3. Increases oxygen and glucose uptake by most tissues and increases basal metabolic rate (BMR) → CALORIGENESIS
    other actions:
    - Neural activity: ↑ irritability, mentation, beta-receptors; decrease reflex times
    - Cardiovascular action: via beta-receptors (↑ SNS, heart rate, contraction)
    - Intermediary metabolism: Carbohydrate absorption; decrease plasma cholesterol
    - Growth and development: Psychogenic / physical; growth hormone (GH) synergy
32
Q

Thyroid Hormone Receptors

A

‒ Membrane-bound → linked to channels which allow glucose and oxygen to be taken up into the cell
‒ Cytoplasmic → roles in intracellular storage of thyroid hormone or production of ATP in mitochondria
‒ Nuclear → effects on protein synthesis

33
Q

Thyroid Hormone Disorders

A

Excess:
– Hyperthyroidism
– ↑ BMR
Primary thyroid dysfunction:
▪ ↑ T3, T4, toxic goitre/nodules
Secondary (Pituitary, ↑ TSH) or tertiary (↑ TRH) dysfunction:
▪ Goitre
Grave’s Disease:
▪ Long Acting Thyroid Stimulating (LATS) antibodies against the TSH receptor (Goitre)
Deficiency:
– Hypothyroidism
– ↓ BMR
– Endemic goitre
- Iodine deficiency and Primary thyroid dysfunction, ↓ T3 → ↑ TSH → Goitre
– Hashimoto’s Thyroiditis
▪ Antibodies against T3 or T4 or thyroglobulin (Goitre)
– Secondary (Pituitary, ↓ TSH) or tertiary (↓ TRH) dysfunction (Central hypothyroidism, atrophic thyroid)
In utero: cretinism; severely stunted mental and physical development; Irreversible
– In adults: myxedema; accumulation of hyaluronic acid and mucus edema under the
skin

34
Q

Adrenal Cortex

A

Hypothalamus releases CRH/ADH -> anterior pitutary releases ACTH (Stimulates adrenal blood flow, adrenal growth and adrenal
steroidogenesis) -> adrenal cortex produces cortisol, aldosterone and other products
Zones:
Glomerular zone → Aldosterone → No metabolism
- Conn’s syndrome: ↑aldosterone = ↑Na+, ↓K+ = hypertension and kypokalemia, alkalosis
Fascicular zone → Cortisol → Intermediate metabolism
Reticular zone → Androgens → Sex characteristics

35
Q

Cortisol

A

Gradual fall during the day, rise during sleep
Action:
Intermediary metabolism:
‒ Increases blood glucose through anabolic effects on the liver and catabolic effects on other tissues
▪ Stimulates gluconeogenesis in the liver
▪ Stimulation of triglyceride breakdown in adipose tissue
▪ Stimulation of the breakdown of skin, connective tissue and muscle
These actions lead to …
Mobilizes glucose for brain/heart use (Glucose sparing)
‒ ↑ substrate availability (↑ tissue catabolism, ↓ synthesis)
‒ ↑ substrate uptake by the liver
‒ ↑ gluconeogenesic enzymes
‒ ↑ glycogenolysis

the stress hormone: Prevents inflammation, Prevents autoimmunity, mobilizes glucose (Glucocorticoid action)

36
Q

Adrenal insufficiency

A

Addison’s disease: primary
- reduced adrenal secretions = Hypotension, anorexia, weight loss, weakness
Cushing’s disease: secondary; exposed to high levels of cortisol
- due to pituitary (most common), adrenal, or ectopic (tumour that produces ACTH) umour

37
Q

Adrenal Androgens

A

‒ DHEA (Weak androgen, 20 % testosterone potency) synthesized in zona reticularis
‒ Converted to testosterone/estrogens in other tissues
‒ Involved in secondary sexual characteristics (Axillary hair),
libido in females and is a source of estrogen in postmenopausal
women
Adrenogenital syndrome:
‒ Results from excess androgens (therefore less aldosterone and less cortisol) from the adrenal cortex = increased testosterone and masculinity

38
Q

Parathyroid gland

A

Embedded in the thyroid gland (4)
Source of hormone: chief cells in gland
Action:
Plasma calcium (Ca2+) ↑
* Plasma phosphate (PO43-) ↓
* Kidney: ↑ Ca2+ reabsorption↓ PO43-reabsorption, ↑ vitamin D3 activation
* Bone: ↑ bone resorption
* GIT: Indirect effect by ↑ vitamin D3
formation
- high levels of calcium and vitamin D3 (1,25 (OH)2D3) inhibits. Stimulated by low calcium

39
Q

Hyperparathyroidism

A

– Bones, stones and abdominal groans
* ↑ PTH, ↑ Ca2+, ↓ PO43-, ↑ 1,25 (OH)2D3
* Soft tissue calcification (Kidney stones)
* Weak bones, fractures (Bone resorption)
* GIT dysfunction
Causes:
Primary - Normal plasma Ca2+ 9 - 10.5 mg/dL; calcification when Ca2+levels 10 - 12 mg/dL; death at 17 mg/dL
Secondary - ↓ Ca2+, ↑ PTH
– In rickets/osteomalacia (↓ 1,25 (OH)2D3)
▪ Impaired GI uptake of Ca2+
– In renal failure
▪ Impaired renal reabsorption of Ca2+

40
Q

Hypothyroidism and Pseudohypoparathyroidism

A

Primary hypothyroidism:↓ PTH, ↓ Ca2+, ↑ PO4 3-, ↓ 1,25 (OH)2D3
– ↑ neuromuscular activity
▪ ↓ Ca2+, ↓ threshold for excitation, resulting in repetitive responses, reduced accommodation
– Tetany (Ca2+ 6 mg/dL)
– Asphyxia-death (Ca2+ 4 mg/dL)
Trousseau’s Sign: Involuntary contraction of the carpal muscles, due to hypocalcemia and tetany
Chvostek’s Sign: tap nerve on face = snarl

Pseudohypoparathyroidism:
– ↑ PTH, ↓ Ca2+, ↑ PO4 3-, ↓ 1,25 (OH)2D3
– Tissue insensitivity to PTH action

41
Q

Calcitonin

A

Parafollicular cells (C-cells) release calcitonin (Peptide hormone)
Stimulus: ↑ plasma Ca2+

Effects of calcitonin:
Plasma calcium (Ca2+) ↓, Plasma phosphate (PO43-) ↓
* Kidney: ↓ Ca2+ reabsorption, ↓ PO43-reabsorption, ↓ vitamin D3activation
* Bone: ↓ bone resorption
* GIT: ↓ Ca2+ absorption

No excess or deficiency syndromes
Treatment of postmenopausal osteoporosis
– In the absence of estrogen, PTH action on bone is not antagonized
Treatment of Padget’s Disease
– Characterized by excessive osteoclast activity

42
Q

Vitamin D3

A

Cholesterol -> 7-dehydrocholesterol (UV light) ->Vitamin D3
Synthesis of vitamin D3:
- skin accounts for >90% of cholecalciferol (D3),
- <10% from diet in the form of cholecalciferol and ergocalciferol (D2)
- At first very weak activity -> liver forms slightly more active 25-hydroxy vitamin D -> kidney forms very active 1,25-dihydroxy vitamin D and inactive 24,25
Effects of 1,25-dihydroxy vitamin D:
* Plasma calcium (Ca2+) ↑, Plasma phosphate (PO43-) ↑
* Kidney: ↑ Ca2+ reabsorption, ↑ PO43-reabsorption
* Bone: Promote PTH actions
* GIT: ↑ absorption of Ca2+ and PO43-: main site of action -> induces synthesis of vitamin D channels (lumen), binding proteins, ATPase (basolateral)
Stimulus: ↑ PTH, low Ca2+
- it is a steroid hormone
- Protein-bound in plasma (Transcalciferin) and acts through nuclear receptors

43
Q

Vitamin D3 pathophysiology

A

Deficiency:
↓ Vit D, ↓ Ca2+ → poor bone formation
↓ Vit D, ↓ Ca2+, ↑ PTH → ↑ bone resorption
– Rickets in juveniles: Bow-Legged and Knock-Kneed
– Osteomalacia in adults
* Excess:
– VD toxicity -> hypercalcemia (soft tissue calcification)

44
Q

Pancreas

A

Alpha cells → Glucagon 25 %
- stimulate delta and beta
Delta cells → Somatostatin 10 % (paracrine)
- inhibits alpha and beta
Beta cells → Insulin 60 %
- inhibits alpha
SNS: ↑ glucagon, ↓ insulin
PSNS: ↑ insulin, ↑ glucagon

45
Q

Insulin and glucagon

A

Insulin: nutrients -> stored forms = lower
blood glucose
- Primary stimulant of insulin secretion: high plasma glucose
- structure: Proinsulin - Weak insulin-like activity; C-peptide - Weak insulin-like activity

Glucagon: breakdown of stored forms of energy = increase blood glucose
stimulated by nutrients (↓ glucose, ↑ amino acids), GIT hormones (↑ gastrin, CCK, ↓ secretin) and neural stimuli (↑ stress (Sympathetic), ↑ food (Parasympathetic))
actions:
– Glucose:↓ glycogenesis, ↑ gluconeogenesis, ↑ glycogenolysis
– Lipid: ↑ lipolysis, ↓ lipogenesis
– Protein: (Minor) degradation

46
Q

Pancreatic dysfunction

A

Diabetes mellitus: Insulin deficiency/glucagon excess
- Cardinal symptoms of Diabetes Mellitus: Polyuria = ↑ dilute urine, Glucosuria (Glycosuria) = ↑glucose, Polydipsia = excessive thirst, Polyphagia = excessive hunger
Type 1: (Insulin-dependent or juvenile-onset)
– Destruction of the β-cells resulting in decreased insulin release
▪ Autoimmune disease where immune system incorrectly target insulin-producing β-cells
– Treated with insulin injections
– Prevalence: 10 - 20 %
Type 2: (Insulin-independent or adult-onset)
– Associated with insulin resistance
▪ Target cells have decreased response to insulin
▪ May have normal or high plasma insulin levels
▪ Receptor downregulation
– Associated with obesity
– Prevalence: 80 - 90 %
- treated by diet and weight reduction

47
Q

Insulin excess

A

Causes:
▪ Insulin-secreting tumor
▪ Insulin overdose
▪ Reactive hypoglycemia (Hypersensitive beta cells)
– Symptoms:
▪ Hypoglycemia
▪ Sympathetic activation
▪ Insulin shock
– Treatment:
– Glucose for diabetics
– Low carbohydrates for reactive hypoglycemia

PHYSL 210 (16 decks)

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