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Physiology Module > Module 4 > Flashcards

Module 4 Flashcards

1
Q 
Reaction Time: Fast
Mediators: Neurons
Type of Message: Electrical impulse
Response Target: External environment
Linking Mechanism: Nerves and synapses
Effectors: Muscles and glands
Function: Nervous coordination
A

NERVOUS CONTROL

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2
Q 
Reaction Time: Slow
Mediators: Hormones
Type of Message: Organic message
Response Target: Internal environment
Linking Mechanism: Blood and circulatory system
Effectors: Organ systems
Function: Chemical coordination
A

HORMONAL CONTROL

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3
Q

released by axon terminals and act locally to control cell functions

A

NEUROTRANSMITTERS

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4
Q
  • local chemical messengers secreted by cells into the extracellular fluid & affect neighboring cells of a different type
  • example: Histamine
A

PARACRINES/JUXTACRINE

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5
Q
  • Affects cells of the same type
  • secreted by cells into the ECF and affects the function of the same cells that produced them by binding to cell surface receptors
A

AUTOCRINES

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6
Q
  • are peptides secreted by cells into the ECF & can function as autocrines, paracrines or endocrine hormones
  • Examples:
    a. interleukins & lymphokines – secreted by helper cells & act on other cells of the immune system
    b. Leptin (adipokines) – secreted by adipocytes
A

CYTOKINES

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7
Q
  • secreted by neurons into the circulating blood and influence the function of cells at another location in the body
  • examples ADH, OTC, and hypophysiotropic hormone
A

NEUROENDOCRINE HORMONES

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8
Q
  • Greek word – HORMAEIN (to arouse or excite)
  • released by endocrine glands into blood stream and influence function of target cells
  • some affect almost all cells and organs (GH, Thyroid hormone, Catecholamines)
  • other affect specific tissues (ACTH, TSH, FSH & LH)
A

Endocrine hormones

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9
Q
  • secreted by ductless glands in the endocrine system
  • play important role in homeostasis
  • essential to the maintenance of the life and well being of an individual and of the species
A

Endocrine hormones

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10
Q
  • Chemical Messengers

- secreted into the blood and acts on another location

A

Hormones

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11
Q

Main site of inactivation of hormone

e.g. Estrogen in males

A

LIVER

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12
Q

Mechanism for removal of hormone

e.g. urine metabolites like VMA), LIVER (bile, feces

A

KIDNEYS

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13
Q

General Characteristics of Hormones

A
  1. Secreted by specific group of cells
  2. Thrown directly into circulation
  3. Exert effects on target tissues which are distant from the source of hormone
  4. Do not create an additional or new function, only modify or alter functions that already exists.
  5. Rate of secretion fluctuates. Increases when there is a need for it; minimal when need not present.
  6. Do not stay in the circulation forever
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14
Q

Hormone Classes

A
  1. PROTEIN HORMONE
  2. BIOGENIC AMINES
  3. STEROID HORMONE
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15
Q
  • More common hormone class; Stored in vesicles
A

PROTEIN HORMONE

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16
Q
  • derivatives of tyrosine
    thyroid hormones (T3 and T4)
    adrenal medullary hormones
  • derivative of histidine:
    histamine (mast cells in connective tissues)
  • derivatives of tryptophan
    melatonin (pineal gland)
    serotonin (blood platelets)
A

BIOGENIC AMINES

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17
Q
  • derivative of Cholesterol

- Synthesized as needed

A

STEROID HORMONE

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18
Q

Produces new proteins from DNA
Lipid-soluble
Reflection Coefficient closer to 0

A

STEROID HORMONES

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19
Q

Modifies existing proteins
Water-soluble
Reflection Coefficient closer to 1

A

PROTEIN HORMONES

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20
Q
  • Transmembrane proteins loop in and out of the cell membrane seven times
  • Make use of G-Proteins
A

G-PROTEIN LINKED HORMONE RECEPTORS

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21
Q
  • Passes through the membranes only once
  • Makes use of intracellular enzymes directly
  • E.g. Leptin and its use of Tyrosine Kinase
A

ENZYME-LINKED HORMONE RECEPTORS

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22
Q
  • Heterotrimeric GTP-binding Proteins
  • Act as TRANSDUCERS
  • Link hormone receptors with 2nd messenger systems (Intracellular Enzymes and Ion Channels)
  • May be Gs Protein (stimulatory) or Gi Proteins (inhibitory)
  • 3 subunits: alpha, beta, gamma
A

G Proteins

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23
Q
  • Most common 2nd Messenger System
  • MECHANISM
    Alpha subunit of G proteins activates Adenylate cyclase and together with ATP —> forms cAMP —> activates protein kinase A
A

cAMP/cGMP System

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24
Q
  • Used by all Hypothalamic Hormones EXCEPT CRH
  • Mediates smooth muscle contraction by hormone/neutrotransmitter (e.g. Motilin in the GI)
  • MECHANISM
    Phospholipase C —> PIP2 —> PIP2 splits into IP3(releases Calcium) and DAG (activates protein kinase C)
A

Phospholipid System (IP3/DAG)

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25
Q
  • Used by Insulin, Growth factors, EPO, Leptin

- Enzyme-linked

A

Tyrosine Kinase

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26
Q
  • Must be transported bound to a protein in the blood

- Active form: FREE, UNBOUND FORM

A

Lipid Soluble Hormones

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27
Q

Hormone Secretion, Transport and Clearance

A
  • Onset of Hormone Effects (Varies from seconds (NE, Epi) to months (T3, GH))
  • Very little amount needed to produce effect
  • Number of Hormone Receptors (never constant)
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28
Q

Mechanism of Hormonal Action

A

On the target cell, the hormone in combination
with the receptor cells act by any of the following
mechanisms:

  1. Alternating the permeability of cell membrane
    - Neurotransmitter substances
  2. Activating the intracellular enzyme - Protein hormones and catecholamines
  3. Activating the gene - Thyroid and steroid hormones
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29
Q

(Regulation of Hormone Secretion)

  • “Products inhibit Precursors”
  • More common
  • E.g. Cortisol inhibiting ACTH Secretion from the Pituitary
A

NEGATIVE FEEDBACK

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30
Q

(Regulation of Hormone Secretion)

  • “Products stimulate Precursors”
  • Rare, exploding
  • E.g. surge of LH before ovulation, Oxytocin during delivery and lactation
A

POSITIVE FEEDBACK

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31
Q

(Regulation of Hormone Receptors)

Decrease in:

  • Receptor Number
  • Receptor Affinity
  • E.g. in the uterus, progesterone down-regulates its own receptor and the receptor for estrogen
A

DOWN-REGULATION OF RECEPTORS

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32
Q

(Regulation of Hormone Receptors)

Increase in:

  • Receptor Number
  • Receptor Affinity
  • E.g. in the ovary, estrogen up-regulates its own receptor and that of LH
A

UP-REGULATION OF RECEPTORS

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33
Q

Hormone Interaction

A
  1. SYNERGISTIC EFFECTS
  2. PERMISSIVE EFFECTS
  3. ANTAGONISTIC EFFECTS
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34
Q

SYNERGISTIC EFFECTS

A

ADDITIVE EFFECTS - same function
- E.g. Epinephrine and NE effects on the heart

COMPLEMENTARY EFFECTS - different function but end product is the same
- E.g. FSH and Testosterone effects on spermatogenesis

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35
Q
  • permit the other hormone to do its function
  • E.g. Cortisol has permissive effects on Epi and NE with regards to blood vessels; T3 has __ on Epi with regards to lipolysis
A

PERMISSIVE EFFECTS

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36
Q
  • inhibit one another

- E.g. Estrogen blocking Prolactin effects on the breasts during pregnancy

A

ANTAGONISTIC EFFECTS

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37
Q
  • Equal to the rate of disappearance of hormone from the plasma/concentration of hormone in each milliliter of plasma
  • Mechanisms: Tissue Destruction, Tissue binding, Bile Excretion, Urine Excretion
A

Metabolic Clearance Rate

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38
Q
  • problem pertaining to the target organ or peripheral gland
A

Primary Endocrine disease

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39
Q
  • problem is in the pituitary gland
A

Secondary Endocrine Disease

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40
Q
  • problem is in the hypothalamus
A

Tertiary Endocrine Disease

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41
Q
  • Causes growth of all or most body tissues
  • Prerequisite: SUFFICIENT INSULIN ACTIVITY and CHO
  • Stimulates increased: MITOSIS, CELL SIZE AND CELL NUMBER
  • Promotes differentiation of specific cell types (e.g., bone growth cells)
  • Single chain; 191 AA residues
  • Pulsatile secretion
A

Growth Hormone (Somatotropin)

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42
Q
  • Relatively low during the day
  • ↑s during first 2 hours of deep sleep
  • Regular nocturnal peak: 1 hour after Stage 3 or 4 deep sleep onset
  • Preceded by nocturnal plasma GHRH peak
A

Growth Hormone (Somatotropin)

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43
Q
  • Biological t½ = 20 mins
  • Serum GH level varies widely
  • GH secretion in women > men
    (highest before ovulation)
  • Rate: highest in late puberty, neonate; lowest in older/obese adults, hypothyroidism, Type 2 DM
A

Growth Hormone (Somatotropin)

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44
Q

Growth Hormone (Somatotropin): AVERAGE PLASMA CONCENTRATION

A
  • 5-20 years old: 6 ng/ml
  • 20-40 years old: 3 ng/ml
  • 40-70 years old: 1.6 ng/mL
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45
Q

Pattern of GH Secretion: Pre-puberty

A
  • Stabilization of 24-hour pulsatile GH secretion rates (200-600 μg/day)
  • Approximate those in post-pubertal young adults
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46
Q

Pattern of GH Secretion: Puberty

A
  • 1.5-3-fold ↑ pulsatile GH secretion
  • With proportionate ↑ in plasma insulin-like growth factor-I (IGF-I)
  • Physiological GH hypersecretion driven by onset of ↑ sex-steroid hormones
  • Correlate with rate of ↑ in height
  • GHRH response: tall adults > ave height
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47
Q

Pattern of GH Secretion: Puberty

A
  • Final height (FH) may partly be determined by inherent GH secretory capacity
  • In normal children with idiopathic short stature - GH treatment significantly ↑ FH in a dose-dependent manner

Mean gain = 1.3 SDS (8 cm) and a broad range of response from no gain to 3 SDS compared to a mean gain of 0.2 SDS in the untreated controls. (Albertsson-Wikland, 2008)

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48
Q

Pattern of GH Secretion: Adulthood

A
  • Starting 18-25 y/o GH secretion ↓s up to pre-pubertal level (
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49
Q

Pattern of GH Secretion: Aging

A
  • ↓ GH secretion
  • Correlated to
  • ↑ total body & visceral fat %; Muscle wasting, ↓ physical fitness, ↓ [testosterone ] or menopause
  • Partly responsible for: ↓ lean body mass; ↓ protein synthesis; ↓ metabolic rate and ↑ adipose tissue
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50
Q

Excessive somatostatin release can lead to

A

↓/deficiency GHRH secretion in aging human

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51
Q
  • is a Protein anabolic hormone, Lipolytic hormone, Diabetogenic hormone, Growth promoter hormone
A

Growth hormone

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52
Q

True or False

Linear bone growth does not happen when the epiphyseal plates close

A

True

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53
Q

Growth Hormone: Effect on Protein Metabolism

A

Anabolic

  • Stimulates AA uptake and CHON deposition
  • ↓ protein breakdown
  • Effect begins in minutes
  • Stimulates collagen synthesis

Produces:

  • (+) Nitrogen balance
  • ↓ BUN and AA (Amino Acids)
  • ↑ excretion of AA 4-hydroxyproline
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54
Q

Growth Hormone: Effect of Carbohydrate Metabolism

A
  • Normal GH level needed to maintain normal pancreatic Islet function which can lead to decreased insulin if no GH
  • decreased CHO use can DIABETOGENIC
  • Mechanism: Impaired insulin function from increased FA blood concentration
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55
Q

Growth Hormone: Effect on Electrolyte Metabolism

A
  • ↑ GI absorption of Ca2+
  • ↓ Na+ and K+ excretion – most probably due to diversion from kidneys to growing tissues
  • (+) Phosphorus balance; ↑ plasma Phosphorus
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56
Q

Growth Hormone: Effect on Fat Metabolism

A
  • Lipolytic
  • ↑ FA mobilization & use for energy
  • ↑ FA to Acetyl CoA conversion
  • ↑ FFA may contribute to GH-induced insulin resistance
  • Effect begins in hours
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57
Q

Summary of GH Actions

A
  1. ↑ protein synthesis rate in most body cells
  2. ↓ Adiposity:
  3. ↑ lipolysis / FA mobilization from adipose tissue
  4. ↑ FA in blood
  5. ↑ FA use as fuel
  6. ↓ glucose uptake
  7. ↑ linear growth
  8. ↑ organ size & function
  9. ↑lean body mass
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58
Q
  • Mediate action of GH on chondrocytes & linear growth, protein metabolism and organ size, and lean body mass
  • Polypeptide growth factors
  • Secreted by liver and other tissues
A

Somatomedins (Insulin-like Growth Factors I & II)

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59
Q

Types of Somatomedins

A
  1. IGF-I (Somatomedin C)

2. IGF-II

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60
Q
  • skeletal and cartilage growth
  • Increases in parallel with GH
  • Both GH- and insulin-dependent
  • Lower in old age: angina pectoris, myocardial infarction, atherosclerosis
  • Earlier death in aging men with low levels
A

IGF-I (Somatomedin C)

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61
Q
  • fetal growth regulator; increased by PRL GH and somatomedins can act both in cooperation and independently to stimulate pathways that lead to growth
A

IGF-II

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62
Q

Stimulate GH Secretion

A
  • decreased glucose
  • decreased FFA
  • increased AA
  • starvation, fasting and protein deficiency
  • Stress
  • Excitement
  • Deep Sleep (stages 3 or 4)
  • Puberty
  • Estrogen, androgen and thyroid hormone
  • GABA
  • Enkephalins
  • Prostaglandin
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63
Q

Neurotransmitters that stimulate GH secretion

A

Dopamine
Acetylcholine
Serotonin
Norepinephrine

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64
Q

Inhibit GH secretion

A
  • Somatostatin
  • Increased glucose and FFA
  • Somatomedins (IGF)
  • GH
  • Beta adrenergic agonist
  • Cortisol
  • Senescence
  • Obesity
  • Pregnancy
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65
Q
  • Excessive activation of somatotropes or (+) acidophilic pituitary tumors
  • Excessive GH before puberty/ fusion of epiphyses with shaft
  • Rapid growth of all body tissues
  • Hyperglycemia due to Eventual degeneration of overactive pancreas and can lead to DM
  • Panhypopituitarism in most, if untreated: Death by early adulthood
A

Gigantism

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66
Q

other cells in the pituitary are unfunctional

A

Panhypopituitarism

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67
Q

Management for Gigantism

A
  • microsurgical tumor removal

- Pituitary gland irradiation

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68
Q
  • Excessive GH after puberty / epiphyseal fusion with shaft
  • Thicker and enlarged bones
    Hands, feet
    Membranous bones (cranium, nose, forehead, supraorbital ridge, mandible, vertebrae)
  • Continued growth of soft tissues (tongue, liver, kidneys)
  • Prognathism, huge brows, huge tongue, large hands with spade fingers
  • Deep guttural voice
  • Oily skin
A

Acromegaly

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69
Q
  • a type of GH excess
  • Joint deformities or frank arthritis
  • Secondary DM
  • Sleep apnea
  • Kyphosis

↑ coronary risk:

  • Poor glucose tolerance
  • Hypertension
  • Lipid problems
  • Life shorter by average 10 years (vs. normal person)
A

Acromegaly

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70
Q

Management for Acromegaly

A

Normalized by treatment of adenoma (surgery, octreotide, radiation)

Ocreotide - somatotropin analog

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71
Q

If adult onset – typically with other Anterior Pituitary hormone deficiencies

If childhood onset – dwarfism

A

Growth Hormone Deficiency

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72
Q
  • ↓ secretion of all AP hormones

- May be congenital, slowly or suddenly develop

A

Panhypopituitarism

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73
Q

Causes of Panhypotituitarism

A
  • Pituitary tumor
  • Suprasellar cysts
  • Enlarged Rathke’s pouch remnants
  • Pituitary infarction and necrosis from post-partum hemorrhage (Sheehan syndrome)
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74
Q

Causes:

Panhypopituitarism during childhood

  • Hypothalamic dysfunction, GHRH deficiency
  • Pituitary destruction, GH deficiency

Isolated GH deficiency

  • Biologically incompetent GH
  • GH receptor deficiency
A

(Pituitary) Dwarfism

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75
Q

Causes

  • Unresponsive GH receptor (Laron dwarf/ GH insensitivity)
  • Hereditary inability to form somatomedin C (IGF-I) (African pygmy; Levi-Lorain dwarf)
A

(Pituitary) Dwarfism

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76
Q

(Pituitary) Dwarfism: Manifestations:

A
  • Proportional body parts
  • Short stature
  • Delayed skeletal maturation
  • Greatly ↓ development rate
  • Does not go through puberty
  • Insufficient gonadotropic hormones for sexual maturation
  • If only GH deficient (1/3) → mature sexually & reproduce
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77
Q

Panhypopituitarism in Adult: Causes

A
  • Pituitary destruction
  • Tumors: Pituitary adenoma, craniopharyngioma, chromophobe tumors
  • Surgery, radiation, trauma
  • Sheehan’s syndrome
  • Empty sella syndrome
  • Stroke
  • Infectious meningitis (e.g., TB meningitis)
  • Vascular problems (e.g., cavernous sinus thrombosis, sarcoidosis)
  • Post-surgical cure of acromegaly
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78
Q

Panhypopituitarism in Adult: Manifestation

A
  • Hypothyroidism (e.g., lethargy)
  • Depressed glucocorticoid production by adrenals (e.g., weight gain)
  • Suppressed gonadotropic hormone secretion (e.g., lost sexual function)
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79
Q

Panhypopituitarism in Adult: Treatment

A

Most signs & symptoms treatable by adrenocortical and thyroid hormones

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80
Q

Medical Uses of Human Growth Hormone

A
  1. Dwarfism and replacement therapy in growth-deficient children - Human GH synthesized by E. coli
    - if purely GH deficiency → completely treatable if given early
  2. Turner’s syndrome -2nd X chromosome in females either absent or deformed → growth & development problems
  3. Renal insufficiency (kidney failure)
  4. HIV - to treat muscle wasting
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81
Q

Medical Uses of Human Growth Hormone 2

A
  1. Anti-aging:
    - Increased protein deposition, esp. in muscles
    - ↓ fat deposits
    - Feeling of invigoration of energy
    - GH + exercise: ↑ type II muscle fibers in elderly
  2. Physical performance enhancer in sports
    - Used for perceived anabolic effects on muscle growth and recovery (e.g., in weight lifting, body building, football, etc.)
    - Combined with anabolic steroids, erythropoietin
    - Studies: no ↑ muscle size or strength after hGH injection
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82
Q 
-10-20%
Hormone product: Adrenocorticotropic Hormone (ACTH)
Stain Affinity: Basophilic
Hypothalamic Hormone Control: CRH
Target: Adrenal, Adipose
Peripheral Hormone Involved: Cortisol
A

Corticotrope

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83
Q
  • 30-50%
    Hormone product: Growth Hormone (GH) to Somatotropin
    Stain Affinity: Acidophilic
    Hypothalamic Hormone Control: GHRH, GHIH (somatostatin)
    Target: All Tissues (major in LIVER)
    Peripheral Hormone Involved: Insuline-like growth factor-I (IGF-I)
A

Somatotrope

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84
Q 
- 10-15%
Hormone product: Follicle Stimulating Hormone (FSH); Luteinizing Hormone (LH)
Stain Affinity: Basophilic
Hypothalamic Hormone Control: GnRH
Target: GONADS
Peripheral Hormone Involved:
Estrogen
Progesterone
Testosterone
Inhibit
A

Gonadotrope

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85
Q 
10-30%
Hormone product: Prolactin (PRL)
Stain Affinity: Acidophilic
Hypothalamic Hormone Control: PIH
Target: Breast, Gonads
Peripheral Hormone Involved: None
A

Lactotrope (Mammotrope)

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86
Q

3-5%
Hormone product: Thyroid Stimulating Hormone (TSH)
Stain Affinity: Basophilic
Hypothalamic Hormone Control: TRH
Target: Thyroid Gland
Peripheral Hormone Involved: Triode-thyronine

A

Thyrotrope

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87
Q

▪ Also called the Neurohypophysis

▪ Composed mainly of glial-like cells called pituicytes

A

POSTERIOR PITUITARY GLAND

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88
Q

▪ do not secrete hormones
▪ act to support large numbers of terminal nerve fibers and terminal nerve endings from nerve tracts that originate in the supraoptic and paraventricular nuclei of the hypothalamus

A

Pituicytes

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89
Q

▪ Anti-diuretic hormone (ADH) or vasopressin and Oxytocin
▪ Synthesized in the cell bodies of the supraoptic and paraventricular nuclei
▪ Transported with “carrier” proteins called NEUROPHYSINS down to the nerve endings in the neurohypophysis (requires several days)

A

Neurohypophysial Hormones

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90
Q

▪ ADH is formed primarily in the supraoptic nuclei
▪ Oxytocin is formed primarily in the paraventricular nuclei
▪Each of these nuclei can synthesize about one sixth as much of the second hormone as of its primary hormone

A

Neurohypophysial Hormones

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91
Q

▪ Both are polypeptides, each containing nine amino acids
▪ Vasopressin: Cys-Tyr-Phe-Gln-Asn-Cys-Pro-ArgGlyNH2
▪ Oxytocin: Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-GlyNH2
▪ The similarity of the molecules explains their partial functional similarities

A

ADH and Oxytocin

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92
Q

▪ Injection (as small as 2 nanograms) can cause decreased excretion of water by the kidneys
▪ Without this hormone, the collecting tubules and ducts become almost impermeable to water and allows extreme loss of water into the urine
▪ causes insertion of aquaporins which causes absorption of water from the collecting tubules and ducts by osmosis

A

Anti-diuretic Hormone (ADH)

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93
Q

Vasoconstrictor Effect of ADH

A

▪ Low concentrations of ADH cause water reabsorption
▪ Higher concentrations of ADH have a potent effect of constricting the arterioles throughout the body
▪ Stimulus: decreased blood volume
▪ Decreased stretch signal from atrial stretch receptors, baroreceptors of the carotid, aortic, and pulmonary regions

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94
Q

Regulation of ADH

A

▪ Secretion of ADH primarily regulated by osmotic & volume stimuli
▪ Most important physiologic stimulus for ADH secretion: ↑ plasma osmolarity
▪ Hypovolemia or volume contraction also potent stimulus
▪ H2O is conserved in the body while Na & other solute continue to be excreted in the urine → causes dilution of the solutes in the ECF → correcting the initial excessively concentrated ECF

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95
Q
  • State of excess free water excretion

Manifested by :

  • Excretion of excessive amounts of dilute urine
  • Excessive thirst
  • Reduction of fluid intake will not affect the concentration of the urine
A

Diabetes Insipidus (DI)

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96
Q

▪ Total or partial loss of the ability to synthesize or release AVP
▪ Causes: brain tumor; head trauma and brain surgery that damages the posterior pituitary or hypothalamus
▪ Loss of free water leads to an ↑ in plasma osmolality

A

Central Diabetes Insipidus

97
Q

▪ Hyperosmolality cannot increase AVP sufficiently but usually results in a large increase in thirst

▪ In many patients with this disease, the patient has:

a. high water intake and output
b. normal plasma osmolality

▪ It is only when water intake is restricted that the severe hyperosmolality becomes apparent

A

Central Diabetes Insipidus

98
Q

▪ Levels of ADH is normal or elevated but the renal tubules cannot respond appropriately to ADH

A

Nephrogenic Diabetes Insipidus

99
Q

Nephrogenic Diabetes Insipidus: Causes

A
  • Failure of the countercurrent mechanism to form a hyperosmotic medullary interstitial
  • ADH receptors in distal tubules and collecting ducts maybe non-functional or kidneys damaged
  • Drugs : lithium (drug for bipolar disorder) and tetracyclines
100
Q

Treatment of Diabetes Insipidus

A
  1. Central DI: Synthetic analog of ADH like desmopressin (subcutaneous or nasal spray)
  2. Nephrogenic DI:
    - Correct the underlying renal disorder for hypernatremia: low Na diet
    - Diuretic that enhances sodium excretion: Thiazides
101
Q

▪ Overproduction of ADH not accounted for by hyperosmolality or non-osmotic stimuli to ADH
▪ Excessive secretion of ADH → reduces urine output
→ retention of water and increase in volume of ECF
→ secondary increase in urine output
→ urine formed is concentrated
→ Na+ and other ions excreted in urine
→ low Na+ in ECF

A

Syndrome of Inappropriate Anti-diuretic Hormone (SIADH)

102
Q

Low Sodium in the blood can lead to

A

Brain swelling, seizures, coma and eventually Death

103
Q

Treatment of SIADH

A

▪ Aimed towards correcting hyponatremia and its symptoms

  • Loop diuretic (furosemide): promotes free water excretion
  • Isotonic and sometimes, hypertonic saline
  • Fluid intake restriction to 0.5 to 1.0 L/day
  • Aquaretics/vaptans: agents that competitively block ADH action and increase water excretion
  • Demelocycline (an older tetracycline)
104
Q

▪ Powerfully stimulates contraction of the pregnant uterus
▪ Facilitates bonding or attachment between mother and infant
▪ Causes milk to be expressed from the alveoli into the ducts of the breast
▪ Psychogenic factors and sympathetic activation can inhibit OTC secretion and depress milk ejection

105
Q

▪ This hormone is at least partially responsible for causing birth of the baby:

  • In a hypophysectomized animal, the duration of labor is prolonged
  • Amount of oxytocin in the plasma increases during labor, especially during the last stage
  • Stimulation of the cervix in a pregnant animal elicits nervous signals that pass to the hypothalamus and cause increased secretion of oxytocin
106
Q

▪ Brand names: Syntocinon®, Pitocin ®
▪ Used therapeutically to decrease immediate postpartum bleeding
▪ Used to induce labor
▪ OTC assists in ovulation & in the termination of the corpus luteum

A

OXYTOCIN as a Drug

107
Q

More Reasons to Breastfeed

A

▪ Oxytocin is not only extensively interconnected to the cortisol, noradrenaline and several neurotransmitter systems to produce long-term effects
▪ It is also highly correlated to resilience to stress, growth, healing and well-being.

108
Q
  • Central 20% of the adrenal gland
  • Neuroectodermal in origin
  • Functionally related to ANS
  • Secretes catecholamines in response to sympathetic stimulation
  • An enlarged specialized sympathetic ganglion
A

Adrenal medulla

109
Q
  • Discharge catecholamines into the bloodstream
  • Composed of chromaffin cells
  • Catecholamines are secreted into the blood to act as hormones
  • Source of ALL circulating epinephrine and ~30% of circulating norepinephrine
A

Adrenal medulla

110
Q
  • Innervated by cholinergic preganglionic sympathetic neurons
  • Contains granules
A

chromaffin cells

111
Q

Adrenal medulla: Vascularity

A
  • Blood is carried from cortex to medulla
    Few medullary arterioles (oxygen- and nutrient-rich blood)
    Numerous cortical sinusoids (rich with cortical hormones)
  • Medullary arterioles and cortical sinusoids&raquo_space; medullary plexus of vessels&raquo_space; single suprarenal vein
112
Q

(Adrenal Medulla: Vascularity)

Consequence of high concentration of cortisol from cortex bathe chromaffin cells

A
  • Cortisol inhibits neuronal differentiation of the medullary cells
  • Cortisol induces expression of PNMT (converts NE to epinephrine)
113
Q
  • Outer 80% of the adrenal gland
  • Mesodermal in origin
  • Secretes CORTICOSTEROIDS which are all synthesized from cholesterol
A

Adrenal cortex

114
Q
  • Thin layer underneath the capsule
  • Secretes ALDOSTERONE because it contains aldosterone synthase
  • Controlled mainly by ECF concentrations of angiotensin II and potassium (Both stimulate aldosterone secretion)
A

Zona glomerulosa

115
Q
  • Middle and widest layer
  • Straight cords of large cells with “foamy” cytoplasm
    filled with lipid droplets
  • Secretes CORTISOL AND CORTICOSTERONE, and small amounts of androgen and estrogen
  • Controlled by hypothalamo-pituitary-adrenal axis ACTH
A

Zona fasciculata

116
Q
  • Deep layer
  • Secretes ADRENAL ANDROGENS DEHYDROEPIANDROSTERONE (DHEA) AND ANDROSTENEDIONE, and small amounts of estrogen and glucocorticoids
  • Controlled by ACTH and cortical androgen-stimulating hormone*
A

Zona reticularis

117
Q

MNEMONICS for the ADRENAL MEDULA LAYERS

A

“It gets sweeter as you go deeper”
Glomerulosa - Salt (Mineralocorticoid)
Fasciculate - Sugar (glucocorticoid)
Reticular - Sex (androgens)

118
Q

Principal corticosteroids

A
  1. Aldosterone (principal mineralocorticoid)
  2. Cortisol (principal glucocorticoid)
  3. Adrenal cortex also produce small amounts of sex hormones (androgenic hormones)
119
Q

Affects the electrolyes (“minerals”) of the ECF sodium and potassium

A

Aldosterone (principal mineralocorticoid)

120
Q
  • Exhibits important effects that increase blood glucose concentration
  • Protein and fat metabolism
A

Cortisol (principal glucocorticoid)

121
Q
  • All are chemical modifications of cholesterol
    4 rings with 21 carbons
  • Progesterone, glucocorticoids, and mineralocorticoids are 21-carbon steroids
  • Androstanes are 19-carbon steroids
  • Estranes (produced primarily in the ovaries) are 18-carbon steroid
A

Adrenocortical hormones

122
Q

Mnemonic

A

21 - pregnanes
19 - androstanes
18 - estranes

123
Q

Synthesis of adrenocortical hormones

A
  • Each layer is specialized to synthesize particular hormones
  • Depending on the presence or absence of enzymes
    (17,20- lyase in zona fasciculata: androgenic steroid
    Aldosterone synthase in zona glomerulosa: aldosterone)
124
Q

The rate-limiting reaction in steroidogenesis is the __ because cholesterol is stored in the cytoplasm and CYP11A1 (cholesterol desmolase) is located in the inner mitochondrial membrane

A

transfer of cholesterol from the outer to the inner mitochondrial membrane

125
Q
  • Principal mineralocorticoid
  • Synthesized only by the zona glomerulosa
    Due to presence of aldosterone synthase
    Cannot synthesize glucocorticoids
  • Regulated primarily by RAAS (Minimally influenced by ACTH)
A

Aldosterone

126
Q

Aldosterone: Transport and metabolism

A
  • Only ~60% bind to plasma proteins, 40% in free form
  • half-life: ~20 mins
  • Almost all inactivated by the liver in one pass(Conjugated especially to glucuronic acid and to a lesser extent sulfates)
  • Excretion
    Bile then feces: ~25%
    Urine: remaining
127
Q

Aldosterone: Physiologic actions

A

Three actions on the late distal tubule and collecting ducts of the kidney:

  1. Increases Na+ reabsorption (principal cells)
  2. Increases K+ secretion (principal cells)
  3. Increases H+ secretion (α-intercalated cells)
128
Q

Aldosterone: Physiologic actions 2

A

Excess increases ECF Volume and arterial pressure but has only small effect on plasma sodium concentration.
»Simultaneous osmotic absorption of almost equivalent amounts of water
»Stimulate thirst and increased water intake

129
Q
  • Excess causes hypokalemia and muscle weakness
  • Too little causes hyperkalemia and cardiac toxicity
    Stimulates transport of potassium into ICF
    Alters the electrical excitability of the nerve and muscle fiber membranes
    Weakness of heart contraction, development of arrhythmia, heart failure
A

Physiologic Action of Aldosterone

130
Q

Physiologic Action of Aldosterone in Colon, salivary glands and sweat glands

A
  • Promotes Na+ and water absorption
  • Effect on salivary glands: for conservation of salt when excessive quantities of saliva are lost
  • Effect on sweat glands: for conservation of salt in hot environments
131
Q
  • has a proinflammatory, profibrotic effect on the cardiovascular system, causes LVH and remodeling
  • Binds to mineralocorticoid receptor (MR), an intracellular receptor
  • Similar to cortisol (alters gene expression)
A

Aldosterone

132
Q

Cellular Mechanism of Aldosterone

A
  • Aldosterone diffuses readily to the interior of the tubular epithelial cells (Lipid soluble)
  • Combines with receptor protein
133
Q

Has a stereomolecular configuration that allows only aldosterone or very similar compounds to combine with it

A

receptor protein

134
Q

Cellular Mechanism of Aldosterone 2

A
  • Aldosterone-receptor complex diffuses into the nucleus
  • mRNA, in conjunction with the ribosomes, causes protein formation.
    (1) one or more enzymes and (2) membrane transport proteins required for sodium, potassium, and hydrogen transport through the cell membrane
135
Q

Aldosterone: Regulation of secretion

A
  • Almost entirely independent of regulation of cortisol and androgens by zona fasciculata and reticularis
136
Q

Major stimuli for aldosterone production

A
  1. Increased angiotensin II

2. Increased serum [K+]

137
Q

What is the effect of increased sodium ion concentration in aldosterone secretion?

A

very slightly decreases aldosterone secretion

138
Q
  • is necessary for aldosterone secretion but has little effect in controlling the rate of secretion in most physiological conditions
139
Q

Major actions of angiotensin II on the adrenal cortex

A
  1. Specifically increase output of aldosterone
  2. increased growth (hypertrophy) and vascularity of the zona glomerulosa; no effect on other two zones
  3. increased StAR and aldosterone synthase enzyme activity
140
Q
  • Principal naturally occring glucocorticoid in humans
  • Synthesized in zona fasciculata/ reticularis
  • ≥ 95% of glucocorticoid activity of the adrenocortical secretions (Small but significant: corticosterone)
141
Q

Cortisol is bound predominantly (>90%) when in circulation. Where?

A
  1. cortisol-binding globulin (i.e. transcortin)

2. Albumin (5-7%)

142
Q

Circulating half-life of cortisol?

A

60-90 minutes; Because of the high degree of binding in circulation

143
Q
  • predominant site of steroid inactivation

- inactivates cortisol and conjugates them so that they can be excreted more readily by the kidney

144
Q

Mechanism of action

A

Acts through glucocorticoid receptor (GR)

145
Q

How does Cortisol increase gene transcription?

A
  1. Rapid translocation of the cortisol-GR complex into the nucleus
  2. Cortisol-GR complex interacts with glucocorticoid response elements (GREs) in the DNA
  3. Recruitment of coactivator proteins
  4. Assembly of general transcription factors
146
Q

How does Cortisol decrees gene transcription?

A
  1. Rapid translocation of the cortisol-GR complex into the nucleus
  2. Interaction with negative glucocorticoid response elements (GREs)
  3. Recruitment of corepressor proteins; OR interference with ability of transcription factors to activate gene expression
147
Q

Metabolic Action of Cortisol

A
  • Catabolic and diabetogenic
  • ↑ blood glucose
  • Increase lipolysis
148
Q

How does Cortisol increase blood glucose?

A
  1. Stimulates gluconeogenesis in liver
    - Enhance gene expression of hepatic gluconeogenic enzymes
  2. Inhibit protein synthesis, ↑ proteolysis in muscle
    - Provide rich source of carbon for hepatic gluconeogenesis
149
Q

How does Cortisol promotes glucose sparing?

A
  1. Decreases glucose utilization by tissues
  2. Decreases insulin sensitivity of adipose tissue
  3. ↓ Glut4-mediated glucose uptake
    - Potentiates effects of catecholamines on lipolysis
150
Q

How does Cortisol Act on Cardiovascular?

A
  1. Permissive actions on catecholamines - Good cardiac output and blood pressure
  2. Stimulates EPO synthesis
151
Q

ANTI-INFLAMMATORY and IMMUNOSUPPRESSIVE ACTIONS of Cortisol

A
  • ↓ production of proinflammatory cytokines
  • ↑ production of anti-inflammatory cytokines
  • Stabilizes lysozomal membranes ↓ release of proteolytic enzymes that augment local swelling
  • Inhibit leucocyte migration to site of injury
152
Q

ANTI-INFLAMMATORY and IMMUNOSUPPRESSIVE ACTIONS of Cortisol

A
  • Inhibit phagocytic activity of neutrophils
  • At high levels:
    ↓ circulating T-lymphocytes (esp. helper T cells)
    ↓ ability of T-lymphocytes to migrate to site of antigenic stimulation
  • Promote atrophy of thymus and other lymphoid tissue
  • Inhibit cell-mediated immunity
153
Q
  • has an almost global effect in reducing all aspects of inflammatory process
  • does not impair antibody production by B-lymphocytes
154
Q

ACTIONS ON REPRODUCTIVE SYSTEM of Cortisol

A
  • depress reproductive behavior and function

↓ the function of the reproductive axis at the hypothalamic, pituitary and gonadal levels

155
Q

ACTIONS ON BONE METABOLISM of CORTISOL

A
  • ↑ bone resorption

- Inhibit osteoblast bone-forming functions

156
Q

How does Cortisol increase bone resorption?

A
  • ↓intestinal Ca+2 absorption
  • ↓ renal Ca+2 reabsorption
  • As a result: Lower serum Ca+2 ↑ PTH secretion
157
Q

ACTIONS ON THE KIDNEYS of CORTISOL

A
  • Inhibit secretion and action of ADH (thus ADH antagonist)

- ↑ GFR by increasing cardiac output and acting directly on the kidney (Vasodilation of the afferent arteriole)

158
Q

CORTISOL: EFFECTS ON THE CNS

A

Glucocorticoid receptor in the limbic system

  1. Decreases REM sleep
  2. Increases slow-wave sleep
  3. Increases awake time
159
Q

CORTISOL: ACTIONS ON FETAL DEVELOPMENT

A
  • Required for normal development of CNS, retina, skin, GI tract and lungs
  • In the lungs, induces differentiation and maturation of type II alveolar cells
160
Q

How does Cortisol affect the Connective tissue?

A

Inhibit fibroblast proliferation and collagen formation

161
Q

Action of Cortisol in Gastrointestinal tract?

A
  1. Trophic effect on GI mucosa
  2. Stimulates appetite
  3. Stimulates gastric acid and pepsin secretion
162
Q

Cortisol: Regulation of secretion

A
  1. Regulated by hypothalamus-pituitary-adrenal axis
    Hypothalamus: corticotropin-releasing hormone/factor (CRH)
    Pituitary gland: adrenocorticotropic hormone
  2. Almost entirely controlled by ACTH from anterior pituitary
  3. Norigenic and systemic stress
  4. strong diurnal rhythmic regulation from suprachiasmatic nucleus
  5. CRH chronically increases proopiomelanocortin (POMC) gene expression
163
Q
  • surges early predawn and morning hours then decline continually throughout the day and night
164
Q

is the precursor of ACTH and other peptides such as melanocyte-stimulating hormone (MSH)

A

proopiomelanocortin (POMC)

165
Q

Immediate of Acute effects when ACTH binds to melanocortin 2 receptor (MC2R) of the zona fasciculata

A
  1. Cholesterol is rapidly mobilized from lipid droplets
    - activation of cholesterol ester hydrolase
  2. Cholesterol is rapidly transported to mitochondrial membrane - Rapidly increases StAR protein gene expression and activates StAR protein
  3. Ultimately increase pregnenolone
166
Q

Chronic effects when ACTH binds to melanocortin 2 receptor (MC2R) of the zona fasciculata

A
  1. ↑ gene transcription of steroidogenic enzymes and their coenzymes
  2. ↑ expression of LDL and HDL receptors
167
Q

Long term effects when ACTH binds to melanocortin 2 receptor (MC2R) of the zona fasciculata

A

Trophic actions on zona fasciculata and reticular

  • ↑ size and functional complexity of organelles
  • ↑ size and number of cells
168
Q
  • Produces dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione
  • Only small amounts of potent androgens are normally produced by adrenal cortex
  • In females, adrenal androgens are major androgens
    For pubic and axillary hair
    For libido
A

Adrenal androgens

169
Q
  • main product adrenal androgen
  • Become detectable at ~6 years old: adrenarche
  • Continually increase, peak during mid-twenties and progressively decline with age (DHEA exhibit same pattern)
  • Most abundant circulating hormone in young adults
170
Q

Formation of DHEA and DHEAS

A
  1. Zona reticularis expresses cofactors or conditions that enhance the 17,20-lyase function of CYP17, generating DHEA from 17-hydroxypregnenolone
  2. expresses DHEA sulfotransferase (SULT2A1 gene), which converts DHEA into DHEAS
  3. 3β-HSD is expressed at much lower levels
    - androstenedione is a minor product compared to DHEAS and DHEA
171
Q

Metabolism and fate of DHEAS and DHEA

A
  1. DHEAS can be converted back to DHEA by peripheral sulfatases
  2. DHEA and androstenedione can be converted to active androgens (testosterone and dihydrotestosterone) peripherally in both sexes
  3. DHEA binds to albumin and other globulins in blood with low affinity so efficiently excreted by the kidney
    half-life: 15-30 mins
  4. DHEAS binds to albumin with high affinity
    half-life: 7-10 hours
172
Q

Contribution of adrenal androgens to active androgens

A

Men: negligible
Women: for the growth of axillary and pubic hair and for libido

173
Q

Regulation of secretion of DHEAS and DHEA

A
  1. ACTH: primary regulator
    zona reticularis shows the same atrophic changes as the zona fasciculata in conditions with little or no ACTH
  2. DHEA and androstenedione display same diurnal pattern as cortisol
174
Q

Other unknown factors regulate zona reticular function (DHEAS and DHEA)

A
  1. Adrenarche occurs in the face of constant ACTH and cortisol levels
  2. Rise and decline of DHEAS is not associated with a similar pattern of ACTH and cortisol production
175
Q

The adrenal cortex secretes an entirely different group of hormones, called __

A

corticosteroids

176
Q

21-B-Hydroxylase

A 
Aldosterone: Decreased
Cortisol: Decreased
Androgens: Increased
ACTH: Increased
Blood Pressure: Decreased
Accumulating substrate: 17-hydroxyprogesterone
177
Q

11-B-Hydroxylase

A 
Aldosterone: Decreased
Cortisol: Decreased
Androgens: Increased
ACTH: Increased
Blood Pressure: Increased
Accumulating substrate: 11-deoxycorticosterone
178
Q

17-alpha-Hydroxylase

A 
Aldosterone: Increased
Cortisol: Decreased
Androgens: Decreased
ACTH: Increased
Blood Pressure: Increased
Accumulating substrate: Pregnenolone
179
Q
  • One of the largest endocrine glands
  • Located below the larynx on each side of the trachea
    - Weighs 15 to 20g in adults
A

Thyroid Gland

180
Q

(Thyroid Gland)

secrete hormones, cuboidal (inactive) to columnar (active)

A

Follicular Cells

181
Q

(Thyroid Gland)

- Scattered among follicular cells and in spaces between the spherical follicles which secrete calcitonin

A

Parafollicular Cells

182
Q

(PARATHYROID GLAND)

– Produce PTH
– Small, polygonal, darkly staining, abundant cells
– Contain lakes of glycogen giving them a water clear appearance

A

Chief Cells

183
Q

(PARATHYROID GLAND)

– Function unknown
– Large, light staining, fewer in numbers
– Only present at age 6 onwards

A

Oxyntic cells

184
Q

Percentage synthesized: 93%
Half-life: More (6 days)
Affinity for binding plasma protein: More
Binding to nuclear receptor: Less (10% of the receptors)
Onset of Action: 4x slower (2 days)

185
Q

Percentage synthesized: 7%
Half-life: Less (1 day)
Affinity for binding plasma protein: Less
Binding to nuclear receptor: More (90% of the receptors)
Onset of Action: 4x faster (12 hours)

186
Q

Steps in Synthesis of Thyroid Hormones

A
  1. Iodide trapping
  2. Formation and secretion of thyroglobulin
  3. Oxidation of iodine
  4. Organification of thyroglobulin
  5. Storage and secretion
187
Q
  • Basal membrane of the thyroid actively pumps iodide to the cell interior (Na-I symporter)
  • Concentrates the iodide to about 30 - 250 times its concentration in the blood
  • Stimulated by TSH
A

Iodide Trapping

188
Q
  • Thyroid cell endoplasmic reticulum and Golgi apparatus synthesize the glycoprotein thyroglobulin and secrete to the follicle colloid
A

Formation of Thyroglobulin

189
Q
  • Conversion of iodide to nascent iodine I0 or I3
  • Promoted by PEROXIDASE and its accompanying hydrogen peroxide
  • Peroxidase is located in the apical membrane of the cell or attached to it, so the iodine will be readily available
  • When peroxidase is blocked or hereditarily absent, the rate of synthesis of thyroid hormone falls to zero
A

Oxidation of Iodine

190
Q
  • Binding of iodine to thyroglobulin
  • Oxidized iodine is associated with IODINASE, which speeds up the binding
  • Iodine binds with about 1/6 of the tyrosine molecules in thyroglobulin
A

“Organification” of Thyroglobulin

191
Q
  • successive stages of iodination of tyrosine
  • COUPLING of iodotyrosine molecules
  • may occur in a matter of minutes or even days
A

Final Formation of Thyroxine (T4) and Triiodothyronine (T3)

192
Q

Release of Hormones from Thyroid Gland

A
  • Apical surface of the cell sends out pseudopods to form pinocytic vesicles that engulf some colloid
  • Lysozymes fuse with the vesicles which have proteases that digest thyroglobulin
  • T4 and T3 will be in free form then diffuse to basal membrane into surrounding capillaries
  • T4 and T3 now enter circulation
193
Q

Fate of Thyroglobulin

A
  • About ¾ of iodinated tyrosine will not become T3 or T4 and remain only as mono- or diiodotyrosine that are cleaved from thyroglobulin as well
  • Iodine is cleaved from these through the DEIODINASE ENZYME, which makes all the iodine available again for hormone synthesis
  • Congenital absence of deiodinase enzyme causes iodine deficiency due to failure of recycling
194
Q

Daily Secretion of T4 and T3

A
  • 93% of hormone released from thyroid is T4, only 7% is T3
  • During ensuing days, T4 is slowly deiodinated to T3 which is more readily available in the tissues
  • Delivery is about 35 micrograms of T3 per day
195
Q

Transport of T4 and T3 to Tissues

A
  1. Upon entering the blood, 99% of T4 and T3 bind to transport proteins secreted by the liver:
    – Main: Thyroxine-binding globulin
    – Less: Thyroxine-binding prealbumin and albumin
    – Half of T4 is released to tissues in 6 days
  2. Half of T3 is released to tissues in 1 day (due to lower affinity to binding proteins)
  3. Upon entering tissues, T4 and T3 bind with intracellular proteins (T4 > T3 binding)
  4. Hormones are stored and used slowly in the next few days or weeks
196
Q

• Unique: can produce and store hormones for up to 3 months
↓TBG: liver & kidney disease
↑TBG: estrogen or pregnancy

A

Thyroid Hormone

197
Q

FORMS OF THYROID HORMONE IN PLASMA

A

– Thyroxine Binding Globulin :70%
– Transthyretin or Thyroxine Binding Prealbumin : 20%
– Thyroxine Binding Albumin: 10%
– Free Thyroxine : 0.03%

198
Q

Latency of Thyroid Hormones

A
  • After injection of thyroxine to the blood, the basal metabolic rate only increases after 2 to 3 days
  • Once activity begins, it lasts for 10-12 days then decreases with a half-life of 15 days
  • Triiodothyronine has a latency of 6-12 hours
  • Maximal cellular activity happens in 2-3 days
  • Latency is due to binding to protein and their slow release and from how these are used in the cell
199
Q
  • Thyroid hormone receptors are located in the DNA
  • Forms a heterodimer with retinoid X receptor (RXR) on DNA
  • On binding with thyroid hormones, they initiate transcription and eventual translation into intracellular proteins
  • Whole process takes about minutes to hours (explains latency)
A

Thyroid Hormones Activate Nuclear Receptors

200
Q

Actions of Thyroid Hormones

A
  • Increases O2 consumption and Basal Metabolic Rate (BMR)&raquo_space; Increases mitochondria and Na-K-ATPase pump activity
  • Stimulates carbohydrate, fat and protein metabolism
  • Increases requirements for vitamins
  • Increases blood flow, Cardiac Output, Heart Rate, Heart Strength
201
Q

How does Thyroid Hormone stimulate carbohydrate, fat and protein metabolism?

A
  • Increases glucose uptake, gluconeogenesis, glycogenolysis
    Decreases cholesterol, phospholipids and triglycerides but increases fatty acids
  • Increases cholesterol secretion to bile and number of liver LDL receptors
  • Increase protein synthesis
  • Needed for Growth
202
Q

Actions of Thyroid Hormones

A
  • Increases respiration
  • Increases gastrointestinal motility
  • Increases cerebration
  • Increases muscle vigor (reason for Fine Muscle Tremors)
  • Increases risk for somnolence
  • Loss may cause loss of libido, impotence, menstrual changes
203
Q
  • Hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as contrast medium
  • Typically occurs with comparatively small increases in iodine intake, in people who have thyroid abnormalities that cause the gland to function without the control of the pituitary
A

Jod-Basedow Effect

204
Q
  • Reduction in thyroid hormone levels caused by ingestion of a large amount of iodine
  • Autoregulatory phenomenon that inhibits organification in the thyroid gland (inhibition of peroxidase), the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream
  • Lasts several days (around 10 days), after which it is followed by an “escape phenomenon“
A

Wolff-Chaikoff Effect

205
Q

– Resumption of normal organification of iodine and normal thyroid peroxidase function
– Due to decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell

A

Escape phenomenon

206
Q
  • Increased metabolic rate
  • Excitability, restlessness
  • Exophthalmos (sometimes but not always)
  • Increased appetite but with weight loss, protein wasting and muscle weakness (thyrotoxic myopathy)
  • Pre-tibial Myxedema (20% of patients)
  • Tachycardia, increased Cardiac output
  • Fine Tremors
  • Diarrhea
A

Hyperthyroidism

207
Q
  • Decreased metabolic rate
  • Slow thought process, poor memory
  • Elevated plasma cholesterol and other lipids (atherosclerosis)
  • Fatigue, increased somnolence, weight gain
  • Whole body myxedema
  • Prolonged relaxation phase of Deep Tendon Reflexes (DTRs)
  • Hoarse voice
  • Constipation
A

Hypothyroidism

208
Q 
– Autoimmune disease, anti-TSH receptor antibodies
– Classic Triad:
• Exophthalmos
• Goiter
• Pre-Tibial Myxedema
A

Graves Disease

209
Q

– Plummer’s Disease

– Most common cause of hyperthyroidism in those >50 y.o.

A

Toxic Multinodular Goiter

210
Q

– Results from congenital lack of thyroid gland, genetic defect of the thyroid gland or lack of iodine in the diet
– Skeletal growth

211
Q

Most Common cause of Primary Hypothyroidism

A

Iodine deficiency

212
Q

– Auto-immune disease presenting with increased
lymphocytes and macrophages destroying the
thyroid
– Anti-Thyroglobulin, Anti-Microsomal antibodies

A

Hashimoto’s Thyroiditis

213
Q 
(Bone)
– Ground Substances
• ECF + Chondroitin Sulfate + Hyaluronic Acid
• Gelatinous medium
– Collagen Fibers
• 95% of Organic Matrix
• for TENSILE STRENGTH
A

ORGANIC MATRIX

214
Q

(Bone)
– Ca10(PO4)6(OH)2
– for COMPRESSIONAL STRENGTH

A

BONE SALTS

215
Q

Continuous in response to bone stress

A

Bone Remodeling

216
Q

Osteoblast - Secrete Collagen & Ground Substance where calcium precipitates

A

BONE DEPOSITION

217
Q

Osteoclasts - Secrete Lysosomal enzymes, Citric Acid and

Lactic Acid

A

BONE ABSORPTION

218
Q

– 99% as hydroxyapatite in Bone
– 0.1% in the interstitium

–

A

BODY CALCIUM

219
Q

Calcium Metabolism

A

Positive calcium balance
– Calcium Intake > Calcium Excretion

Negative calcium balance
– Calcium Intake

220
Q

Effect of PTH

A

Intestine: Indirectly INCREASES CALCIUM and PHOSPHATE absorption by inc. vitamin D metabolite

Kidney: DECREASE CALCIUM excretion and INCREASED PHOSPHATE excretion

Bone: CALCIUM and PHOSPHATE RESORPTION INCREASED by continuous high concentrations. Low intermittent doses increase bone formation

221
Q

Net Effect of PTH on Serum Levels

A

Serum Calcium increased, Serum phosphate decreased

222
Q

Effect of Active Vitamin D metabolite

A

Intestine: INCREASED CALCIUM AND PHOSPHATE absorption

Kidney: Increased resorption of Phosphate. Loss of CALCIUM in the urine

Bone: Direct effect - INCREASED CALCIUM and PHOSPHATE resorption
Indirect effect - promoting MINERALIZATION by INCREASING THE AVAILABILITY OF CALCIUM AND PHOSPHATE

223
Q

Net Effect of Active Vitamin D metabolite on Serum Levels

A

BOTH INCREASED in serum CALCIUM and PHOSPHATE

224
Q

Vitamin D Synthesis

A

Vitamin D comes from Cholesterol

  1. Starts at the Skin: Calciol (Cholecalciferol)
  2. 1st activation: Liver Calcidiol (25 hydroxyCholecalciferol)
  3. 2nd activation: Kidney Calcitriol (1,25 dihydroxyCholecalciferol)
225
Q

Secreted by the Parafollicular cells of the Thyroid

Decreases plasma calcium concentration
– Decreases number and activity of osteoclast
– Effects in Children > Adults

A

Calcitonin

226
Q

Effects on Parathyroid Hormone Secretion:

A

– Magnesium effect on PTH is similar to calcium
o Hypomagnesemia stimulates PTH secretion
– Increased phosphate forms calcium phosphate which reduces stimulation of Ca-sensitive receptors which trigger an increase in PTH

227
Q
  • Hypercalcemia
  • Hypophosphatemia
  • Osteitis Fibrosa Cystica – Due to great osteoclastic activity
  • Increases Alkaline Phosphatase – Secreted by osteoblast in an attempt to neutralize osteoclast activity
A

HYPERPARATHYROIDISM

228
Q

Primary Hyperparathyroidism Effect on Serum and Urine

A

SERUM
Calcium: Increased
Phosphorus: Decreased
Alkaline Phosphatase: Increased or None

URINE
Calcium: Increased
Phosphorus: Increased

229
Q

Secondary Hyperparathyroidism Effect on Serum and Urine

A

SERUM
Calcium: None or Decreased
Phosphorus: Increased
Alkaline Phosphatase: Increased or None

URINE
Calcium: Decreased
Phosphorus: Decreased

230
Q

Hypocalcemia: interferes with normal muscle contraction and nerve conduction
– Paresthesias
– Tetany and Seizures
– Possible laryngeal spasm
– Fatigue, headaches, bone pain and insomnia, crampy abdominal pain
– Chvostek’s sign

A

HYPOPARATHYROIDISM

231
Q

– secretes pancreatic juice to duodenum

232
Q
  • secretes insulin and glucagon directly into the blood.
A

Islets of Langerhans

233
Q

▪ 60% of islet cells
▪ Lies in the middle of each islet
▪ Secretes insulin and amylin

A

Beta cells

234
Q

▪ 25% of islet cells

▪ Secretes glucagon

A

Alpha cells

235
Q

▪ Around 10% of total

▪ Secretes Somatostatin

A

Delta cells

236
Q

▪ Minority in islet cells

▪ Secrets pancreatic polypeptide – uncertain function

237
Q

▪ Small protein with MW 5,808
▪ Composed of two amino acid chains linked with 2 disulfide bridges
▪ Starts as insulin preprophormone from RER of beta cells resulting to proinsulin

238
Q

are cleaved in golgi apparatus insulin and peptide fragments (proinsulin has no intrinsic activity)

A

Proinsulin

Physiology Module (8 decks)

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