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NPB 101 > ENDOCRINE SYSTEM > Flashcards

ENDOCRINE SYSTEM Flashcards

1
Q

hydrophilic vs lipophilic hormone mode of action at target cell

A

receptors are expressed on target tissues ➞ when bound: initiates biochemical chain of events (cascade) that alters cell fx

hydrophilic work at target cell membrane via secondary active transport w/ G-coupled protein receptors

  • ex: under acute stress need fuel (glucose) EP works at membrane receptor & causes stored glucose to be broken down & released immediately

lipophilic act via intracellular receptors to induce transcription & translation

  • diffuse into cell faster but synthesizing then acting takes longer
  • ex: cortisol increases transcription of genes that make glucose in AM ➞ necessary for big gaps btwn meals but gradual process
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2
Q

hydrophilic hormone pathways

A

second messenger pathway cAMP: cyclic adenosine monophosphate
1. extracellular 1st messenger (hormone) binds to G-protein-coupled receptor in target cell membrane
2. G-protein-coupled recpeptor activates G-protein
3. subunit ⍺ moves along inner cell membrane & activates adenyl cyclase
4. adenyl cyclase **converts ATP to cAMP **
5. cAMP activates protein kinase A
6. protein kinase A activates protein via phosphorylation
7. activated protein carries out response

second messenger pathway IP3/DAG/Ca²⁺
1. extracellular first messenger (hormone) binds to G-protein-coupled protein receptor in target cell membrane
2. G-protein-coupled receptor activates G-protein
3. subunit ⍺ moves along inner cell membrane & activates phospholipase C
4. phospholipase C converts PIP2 to IP3 & DAG
5. IP3 mobilizes intracellular Ca2+ from ER ➞ activates calmodulin ➞ activates CaM kinase ➞ activates inactivated protein that carries out response
AND
5. DAG activates protein kinase C ➞ phosphorylates activates inactivated protein that carries out response
* Ca2+ increase can bring about smooth muscle contraction (intestines, blood vessels) or secretion of other hormones via CaM kinase
* ex: vasoconstriction or GI
* protein kinase C has many specific protein targets to regulate by phosphorylation
* capable of amplification

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3
Q

lipophilic hormone pathway

A

uses intracellular (cytoplasmic or nuclear) receptors to regulate gene transcription
* effects are generally slower onset & longer lasting
* capable of amplification
1. free lipophilic hormone diffuses through plasma membrane
2. hormone binds to receptor & activates ➞ turns into transcription factor: protein that recognizes specific genes & regulates their activity
3. hormone receptor complex binds with DNA’s hormone response element
4. binding activates gene
5. activated gene transcribes mRNA
6. new mRNA leaves nucleus
7. ribosomes read mRNA to synthesize new proteins
8. new protein is released from ribosomes & folds
9. new protein brings about response

ex: estrogen binds to ER & ↑ transcription of genes inducing growth of uterus & mammary glands
ex: glucocorticoids bind to GR to ↑ transcription of genes involved in gluconeogenesis (in liver)

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4
Q

endocrine regulation systems

A
  1. negative feedback control driven by
    a. direct sensing: ex: BG major driver of insulin/glucagon secretion
    b. HPT axis: hormone in control system provides feedback — ex: hypothalamus-pituitary-gonad axis
  2. neuroendocrine reflexes result in sudden rapid increase in hormone secretion — ex: secretion of EP from adrenal gland in response to increased SNS output
  3. circadian rhythms: rate of secretion fluctuates characterized by repetitive oscillations Q24, responsive to day/night — ex: cortisol releases BG ➞ glucocorticoid: glucose-regulating steroid of adrenal gland
  4. receptor #, availability, or responseiveness: ↑ # of receptors ↑ sensitivity or hormone but too much hormone for too long > overstimulation ➞ desensitize # of receptors − ex: anabolic steroids
  5. other hormonespermissiveness: one hormone must be present for another to work
    synergism: combiined action of seceral hormones is greater than sum of separate effects
    antagonism: 1 hormone causes loss of another’s receptors
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5
Q

effective plasma concentration regulated by:

A
  1. rate of secretion
  2. conversion or activation: must be activated to bind to receptor
  3. transport: lipophilic hormones must circulate through brief associations with proteins ➞ hormone synthesis set to account for [blood] + [needed for receptors]
  4. inactivation & excretion: always metabiolic processes that change hormones & inactivate them ➞ then excreted out by urine
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6
Q

endocrine disorders caused by:

A

too little hormone activity
1. hyposecretion − ex: type I diabetes
2. ↑ removal from blood ex: normal BG but β cells signal release of insulin
3. abnormal tissue responsiveness to hormone: non-functional downstream receptors, lack of target-cell receptors, or lack of enzymes essential for response

too much hormone activity
1. hypersecretion potentially from tumor secreting too much in uncontrolled way
2. ↓ plasma protein binding to hormone: too much free, biologically active hormone
3. ↓ removal of hormone from blood

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7
Q

regulation of hormone secretion

A
  1. hypothalamic-pituitary (thyroid/adrenal/gonad)-axis: changes sensed are relayed to hypothalamus where info is integrated ➞ acts on other glands to regulate secretion
  2. changes sensed directly by hormone-secreting cells which are then corrected
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8
Q

absorptive state vs post-absorptive state

A

absorptive state: fed state – body stores fuel
* anabolic
post-absorptive state: fasted state > body is not consuming/digesting energy it needs > uses energy stored from absortive state
* catabolic

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9
Q

glycogenesis

A

glucose ➞ glycogen results in ↓ BG

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10
Q

glycogenolysis

A

glycogen ➞ glucose results in ↑ BG

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11
Q

gluconeogenesis

A

glycerol +/− AA ➞ glucose results in ↑BG

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12
Q

protein synthesis

A

AA ➞ proteins results in
↓ blood AA

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13
Q

protein degradation

A

protein ➞ AA resilts in
↑ blood AA

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14
Q

fat synthesis
(lipogenesis or triglyceride synthesis)

A

fatty acids + glycerol ➞ triglycerides results in
↓ blood fatty acids

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15
Q

fat breakdown
(lipolysis or triglyceride degradation)

A

triglycerides ➞ fatty acids & glycerol
↑ blood fatty acids

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16
Q

consequences of hypoglycemia vs hyperglycemia

A

hypoglycemia:

  • neurological problems
  • coma
  • death
  • more acutely dangerous
  • 4 major homones ↑BG
    1. glucagon
    2. GH
    3. cortisol
    4. epinephrine

hyperglycemia:

  • glucotoxicity leading to retinopathies, peripheral nerve damage, poor kidney fx, & atherosclerosis ➞ deposition of fatty plaques on inner arterial walls
  • osmotic diueresis (polyuria) dehydration: too much glucose leaving in urine ➞ water will follow
  • long-term toxicity
  • only 1 hormone ↓BG: insulin
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17
Q

insulin synthesis

A

synthesized & secreted from β cells in islets of Langerhans: clusters of endocrine cells of in the pancreas

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18
Q

insulin function

A
  • insulin = major absoroptive-state hormone
  • travels through blood to facilitate glucose uptake & storage in target cells
  • glucose = major regulator of insulin
  • β cells monitor [ATP], not [glucose]
    * no receptor for glucose
    * [ATP] = stimulus
  • major job of insulin: enhance glucose uptake via transporter protein GLUT4 in cells
    * GLUT4 = insulin-dependent
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19
Q

insulin major job

A

enhance glucose uptake via transporter protein GLUT4 cells

  • glucose = water soluble ➞ needs passage into cell
  • GLUT-4 = proteins that fuse inner cell membrane w/ outer cell membrane ➞ poke hole that is selective for glucose
  • insulin receptors in membrane initiate cascade of events that leads to moving GLUT4 proteins
  • glucose flows w/ concentration gradient
  • without insulin receptor stimulation, cell pulls GLUT4 transporters back
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20
Q

insulin-mediated glucose uptake & storage

A

insulin-dependent:
* GLUT4 transport in muscles & stored as glycogen
* GLUT4 transport in adipose tissue (fat) stored as triglycerides via de novo lipogenesis

insulin-independent:
* glucose can diffuse in/out of liver cells always w/ concentration gradient via GLUT2
* brain is always using glucose
* does not store glucose
* GLUT2 protein transport in brain always open

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21
Q

INSULIN ABSORPTIVE STATE OVERALL EFFECTS

A

carbohydrate metabolism:
1. enhances glucose uptake via GLUT4
2. ↑ liver & skeletal muscle glycogenesis
3. inhibits liver & muscle glucogenesis
4. inhibits liver gluconeogenesis
↑ insulin ➞ ↓ [BG]

fat metabolism
1. Enhances glucose uptake in adipocytes for triglyceride synthesis
2. Increases adipocyte triglyceride synthesis
3. Inhibits adipocyte lipolysis
↑ insulin ➞ ↓ [fatty acids] in blood

protein metabolism
1. enhances AA uptake into muscle & liver
2. ↑ protein synthesis
3. decr proteolysis
↑ insulin ➞ ↓ [AA] in blood

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22
Q

in the absorptive state

A

insulin-mediated glucose uptake & storage
* anabolic

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23
Q

in the post-absorptive state

A
  • catabolic
  • ⍺ cells in islets of langerhans in pancreas synthesize & secrete glucagon
  • glucagon = major post-absorptive state hormone
    • maintains fasting BG
    • no major effect on lipolysis, doesn’t do anything with protein
    • no effect on brain or skeletal muscle in regards to fuel metabolism
  • [glucose] = major regulator of glucagon secretion
    • ↓ circulating [fatty acids] & ↑ [AA] also stimulate glucagon secretion
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24
Q

GLUCAGON POST-ABSORPTIVE STATE OVERALL EFFECTS:

A

carbohydrate metabolism:
1. inhibits liver glycogenesis
2. ↑ liver glycogenolysis
3. ↑ liver gluconeogenesis
↑ glucagon ➞ ↑ [BG]

fat metabolism:
1. ↓ triglyceride synthesis
2. ↑ lipolysis
↑ glucagon ➞ ↑ [fatty acids] in blood

protein metabolism: minimal effect

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25
Q

diabetes mellitus

A
  • insulin defficiency ➞ BG is dangerously high
  • “starvation in the face of plenty”➞ without insulin as a stimulus that BG levels are high body feels like it is in starvation mode/fasting state when it is not
  • most common of all endocrine disorders
  • elevated BG = indicator
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26
Q

characteristics of type 1 diabetes

A

level of insulin secretion: little -none

age of onset: childhood ➞ “juvenile diabetes”

percentage of diabetics: 10-20%

basic defect: autoimmune destruction of β cells ➞ pancreas cannot sufficiently produce insulin

tx:
* insulin injections (caution: driving BG too low)
* dietary management
* exercise

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27
Q

characteristics of type II diabetes

A

level of insulin secretion: may be normal or exceed normal

age of onset: adulthood

percentage of diabetics: 80-90%

basic defect: reduced sensitivity of insulins target cells
* insulin resistance: intracellular signaling pathways that transmit insulin don’t work
* takes more insulin to have same effect on glucose

tx:
* dietary control & weight loss
* exercise
* oral hypoglycemic drugs

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28
Q

diabetes without insulin

A
  • cannot move glucose out of blood into fat
  • not able to move into resting skeletal muscle
  • liver cannot store as glycogen, even though glucose uptake is unaffected
  • liver senses no glucose ➞ pathway reverses
  • causes hyperglycemia & cannot store glucose
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29
Q

diabetes effect on insulin

A

carbohydrate metaboilsm: without insulin:

  1. cannot increase cell-glucose uptake
  2. cannot ↑ liver & skeletal muscle glycogenesis
  3. cannot inhibit liver & skeletal muscle glycogenesis
  4. cannot inhibit liver gluconeogenesis
    ↑BG
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30
Q

diabetes effect on glucagon post-absorptive state hormone

A
  1. inhibits liver glycogenesis = stops liver from storing glucose
  2. ↑ liver glycogenolysis = liver breaks glycogen to glucose
  3. ↑ liver gluconeogenesis = liver creates new glucose
  4. ↑ glucagon ➞ ↑ [BG]
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31
Q

pituitary gland in general

A
  • all pituitary hormones are peptides ➞ easily stored
  • sits right below hypothalamus
  • split into anterior & posterior
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32
Q

posterior pituitary

A

neural portion ➞ hormones are released in response to neural input from hypothalamus
* direct relationship with hypothalamus

posterior pituitary hormones:

  1. vasopresin: fluid balance & BP regulation
    • causes vasoconstriction
    • antidiuretic: causes water to move out of kidney tubules back into blood ➞ concentrating urine/↓ amount of urine
    • smooth muscle
  2. oxytocin: uterine contractions & milk ejection during breastfeeding
    • influences pair-bonding & parent-offspring bonding
    • reprod ➞ not homeostasis
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33
Q

anterior pituitary

A

glandular portion ➞ produces hormones in response to hypothalamic releasing & inhibiting

  • indirect relationship w/ hypothalamus
  • median eminence: cluster of capillaries at base of hypothalamus
  • hypothalamic hormones are released in median eminence & travel down hypothalamic hypophyseal portal system ➞ where 1 capillary bed joins another capillary bed
  • hypothalamic hormones secreted in tiny tiny amounts ➞ once hit anterior pituitary diluted in blood & indetectable in systemic bloodstream
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34
Q

hypothalamic control of anterior pituitary

A

tropic hormones: regulate hormone secretion by another endocrine gland ➞ stimulate & maintain endocrine target tissues

hormones of the anterior pituitary:
* TSH: thyroid stimulating hormone
* ACTH: adrenocorticotropic hormone
* GH: growth hormone
* LH: luteinizing hormone
* FSH: follicle-stimulating hormone
* prolactin

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35
Q

GHRH: growth hormone-releasing hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
peripheral hormone(s)

A

GHRH: growth hormone-releasing hormone
↓
GH: growth hormone
↓
liver
↓
insulin-like growth factor 1

  • somatostatin inhibits GHRH
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36
Q

hypothalamic releasing/inhibiting hormone
⇣
GH
⇣
endocrine organ
⇣
peripheral hormone(s)

A

GHRH: growth hormone-releasing hormone
↓
GH: growth hormone
↓
liver
↓
insulin-like growth factor 1

  • somatostatin inhibits GHRH
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37
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
liver
⇣
peripheral hormone(s)

A

GHRH: growth hormone-releasing hormone
↓
GH: growth hormone
↓
liver
↓
insulin-like growth factor 1

  • somatostatin inhibits GHRH
38
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
insulin-like growth factor 1

A

GHRH: growth hormone-releasing hormone
↓
GH: growth hormone
↓
liver
↓
insulin-like growth factor 1

  • somatostatin inhibits GHRH
39
Q

CRH: corticotropin-releasing hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
peripheral hormone(s)

A

CRH: corticotropin-releasing hormone
⇣
ACTH: adrenocorticotropin hormone
⇣
adrenal glands
⇣
glucocorticoids

40
Q

hypothalamic releasing/inhibiting hormone
⇣
ACTH
⇣
endocrine organ
⇣
peripheral hormone(s)

A

CRH: corticotropin-releasing hormone
⇣
ACTH: adrenocorticotropin hormone
⇣
adrenal glands
⇣
glucocorticoids

41
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
adrenal glands
⇣
peripheral hormone(s)

A

CRH: corticotropin-releasing hormone
⇣
ACTH: adrenocorticotropin hormone
⇣
adrenal glands
⇣
glucocorticoids

42
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
glucocorticoids

A

CRH: corticotropin-releasing hormone
⇣
ACTH: adrenocorticotropin hormone
⇣
adrenal glands
⇣
glucocorticoids

43
Q

hypothalamic-pituitary-endocrin-axis pathway

A

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
peripheral hormone(s)

44
Q

(TRH) thyrotropin-releasing hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
peripheral hormone(s)

A

(TRH) thyrotropin-releasing hormone
⇣
TSH: thyroid-stimulating hormone
⇣
thyroid gland
⇣
thyroxine (T4) & triiodothyronine (T3)

45
Q

hypothalamic releasing/inhibiting hormone
⇣
TSH
⇣
endocrine organ
⇣
peripheral hormone(s)

A

(TRH) thyrotropin-releasing hormone
⇣
TSH: thyroid-stimulating hormone
⇣
thyroid gland
⇣
thyroxine (T4) & triiodothyronine (T3)

46
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
thyroid
⇣
peripheral hormone(s)

A

(TRH) thyrotropin-releasing hormone
⇣
TSH: thyroid-stimulating hormone
⇣
thyroid gland
⇣
thyroxine (T4) & triiodothyronine (T3)

47
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
T3 & T4

A

(TRH) thyrotropin-releasing hormone
⇣
TSH: thyroid-stimulating hormone
⇣
thyroid gland
⇣
thyroxine (T4) & triiodothyronine (T3)

48
Q

gonadotropin releasing hormone (GnRH)
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
peripheral hormone(s)

A

gonadotropin releasing hormone (GnRH)
⇣
LH: luteinizing hormone & FSH: follicle stimulating hormone
⇣
gonads
⇣
sex hormones

49
Q

hypothalamic releasing/inhibiting hormone
⇣
LH & FSH
⇣
endocrine organ
⇣
peripheral hormone(s)

A

gonadotropin releasing hormone (GnRH)
⇣
LH: luteinizing hormone & FSH: follicle stimulating hormone
⇣
gonads
⇣
sex hormones

50
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
gonads
⇣
peripheral hormone(s)

A

gonadotropin releasing hormone (GnRH)
⇣
LH: luteinizing hormone & FSH: follicle stimulating hormone
⇣
gonads
⇣
sex hormones

51
Q

hypothalamic releasing/inhibiting hormone
⇣
anterior pituitary hormone
⇣
endocrine organ
⇣
sex hormones

A

gonadotropin releasing hormone (GnRH)
⇣
LH: luteinizing hormone & FSH: follicle stimulating hormone
⇣
gonads
⇣
sex hormones

52
Q

hypothalamic-pituitary-endocrine-axis control

A
  1. activity of a specific axis is maintained within an optimal range around individual-specific set points
    • peripheral hormones regulate multiple systems w/out competing — feedback
  2. hypothalamus can integrate a lot of info to determine set point of axis b/c hypothalamic hypophysiotropic neurons receive inputs from all levels of brain
  3. abnormalities in peripheral hormone levels
53
Q

problem: destruction of the endocrine gland (hyposecretion)

effects on endocrine hormone:

effects on APH:

explanation:

A

effects on endocrine hormone: ↓

effects on APH: ↑

explanation:
* no gland to secrete endocrine hormone
* APG senses no hormone ➞ directs secretion
* lost ⊝ feedback ➞ APG responds

54
Q

problem: destruction of APG (hyposecretion)

effects on endocrine hormone:

effects on APH:

explanation:

A

effects on endocrine hormone: ↓

effects on APH: ↓

explanation:
* no APG = no secreting APH
* no APH = no endocrine hormone
* driver is gone

55
Q

problem: endocrine tumor (hypersecretion)

effects on endocrine hormone:

effects on APH:

explanation:

A

effects on endocrine hormone: ↑

effects on APH: ↓

explanation:
* APG senses high levels of endocrine hormone ➞ halts APH production
* excess endocrine hormone drives pituitary secretion down

56
Q

problem: APG tumor (hypersecretion)

effects on endocrine hormone:

effects on APH:

explanation:

A

effects on endocrine hormone: ↑

effects on APH: ↑

explanation:
* APH stimulates secretion of endocrine hormone
* excess APH secretion stimulates endocrine gland to produce even more endocrine hormones

57
Q

GH

A

growth hormone

  • secreted by anterior pituitary upon stimuation by GHRH from hypothalamus
    • GHRH is inhibited by somatostatin
  • secreted most ~3h after sleep ➞ diurnal
  • stimulates liver to secrete insulin-like growth fator I (IGF-1)
    • IGF-1 stimulates chondrocyte growth & osteoblast differentiation
    • promotes long-bone growth until puberty
    • estradiol accelerates bone building osteoblasts that catch up & seal growth plate
    • estrogen needed for bone density
  • thyroid hormone is permissive for effects of GH
  • growth-promoting actions:
    • ↑ cell division
    • ↑ protein synthesis (↓blood AA)
    • ↑ bone growth
  • metabolic effects:
    • ↓ glucose uptake by resting muscles (↑BG) which stimulates gluconeogenesis (^ BG)
    • ↑ glucose output by liver (glycolysis) ➞ (↑BG)
    • ↑ lipolysis (↑blood fatty acids)
58
Q

pathophysiology of GH excess & insufficiency

A
  1. no GH or GH receptor defect ➞ dwarfism
  2. pituitary tumor ➞ hypersecretion of GH
    * if before puberty: excess growth in long bone
    * if after puberty: no effect on length (plate already sealed) but bone can growth thicker/wider/denser = acromegaly
59
Q

thyroid gland

A
  • gland on neck over trachea
  • follicular cells: thyroid secreting cells that form spheres around **colloid lumen **
  • colloid =** thyroglobulin**: large glycoprotein made of tyrosines where thyroid hormone synthesis occurs
  • TSH acts on follicular cells
  • burst of TH at birth/early development
60
Q

TH synthesis under TSH

A
  • made in colloid
  • iodide must go through K+/- symporter
  • iodide coupled with tyrosine
  • synthesized through phagocytosis: TSH signals follicular cells to eat colloid
61
Q

TSH stimulates:

A
  • follicular cells to pump iodine& make thyroglobulin & colloid
  • enzymes to couple tyrosines with iodide
  • keeps gland healthy ➞ enough #s of follicles to synthesize TH
62
Q

major effects of TH

A
  1. metabolism
      - how efficiently cells convert fuel to energy
  - determinant for BMR
  - ↑ rate of O2 consumption
  -  thermogenic
  2. ↑HR, strength of contractions ➞ permissive for SNS (mainly heart)
  3. growth ➞ permissive for GH
  4. development of CNS & senses ➞ brain maturation depends on:
    - **cerebellum development**: ability to learn, execute smooth motor skills, speak, write
- **myelination of cortex & peripheral nerves**: of AP
- **oligodendrocytes & schwann cell maturation**: self-supportive cell fx
- **special senses**: vision, hearing
63
Q

thyroid disease

A
  • # 2 disease affecing america
  • 1/10 prevalence
  • serious consequences: preg women with undiagnosed hypothyroidism risk miscarriage & fetal development problems
64
Q

hypothyroidism

A
  • too little TH produced
  • ↓BMR
  • ↓HR
  • cold easily
  • ↑ weight: fuel stored not burned
  • easily fatigued
  • finished alertness
  • poor memory
  • goiter if b/c of hormone receptor problen/if hormone gland is overstimulalted
  • reversible w/ TH replacement therapy or iodine in diet
65
Q

causes of hypothyroidism

A
  1. primary failure of thyroid gland
  2. autoimmune disease (Hashimoto’s thyroiditis)
  3. secondary to TRH and/or TSH difficiency
  4. not enough iodine
66
Q

hyperthyroidism

A
  • ↑BMR
  • ↑HR
  • excessive respiration/easily overheated
  • ↓ weight, fuel burned not stored
67
Q

hyperthyroidism causes

A

grave’s disease:

  • autoimmune
  • produces antibodies that trick thyroid into thinking its TSH ➞ mimics TSH ovestimulating thyroid
  • TSH ↓ from thyroid gland b/c ⊝ feedback
  • exopthalmos: bulging eyes
  • ↓ weight, heat intolderance, insomnia, ↑HR
68
Q

goiter

A

enlarged thyroid gland

  • follicular cells are constantly added to make up for loss of TH
  • thyroid gland is overstimulated
  • can be hypo or hyper
69
Q

effects of hypothyroidism from a hypothalamic/pituitary tumor on

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↓[T3/T4] (thyroid hormone)

↓[TSH]

goiter present: no

70
Q

effects of hypothyroidism on the thyroid gland (Hashimoto’s) on

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↓[T3/T4] (thyroid hormone)

↑[TSH]

goiter present:
* inflammation early on
* loss of gland entirely later

71
Q

effects of hypothyroidism from iodine insufficiency on

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↓[T3/T4] (thyroid hormone)

↑[TSH]

goiter present: yes

72
Q

effects of hyperthyroidism on the thyroid gland (grave’s disease) on

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↑[T3/T4] (thyroid hormone)

↓[TSH]

goiter present: yes

73
Q

effects of hyperthyroidism from a thyroid gland tumor on:

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↑[T3/T4] (thyroid hormone)

↓[TSH]

goiter present: no, localized tumor nodule

74
Q

effects of hyperthyroidism b/c of hypothalamic/pituitary excess on

[T3/T4] (thyroid hormone)

[TSH]

goiter present

A

↑[T3/T4] (thyroid hormone)

↑[TSH]

goiter present: yes

75
Q

adrenal gland

A
  • stress ➞ preparation
    • real or percieved threat to homeostasis
    • physical or psychological
    • ex: temp or exams
  • important for integrated stress response
  • near kidney
  • cortex = outer layers (not including connective tissue)
  • medulla = inner
  • secretes both lipophilic & hydrophilic (only lipophilic controlled by HPA)
76
Q

HPA-controlled AG hormones

A

glucocorticoids from middle 2 layers of cortex

  • CRH ➞ ACTH
  • ACTH = peptide ➞ makes 2º messenger coupled receptor signaling cascade to initiate steroid synthesis
    1. ACTH activates G-protein coupled receptor in membrane of cortex (middle 2 layers)
    2. receptor activates adenyl cyclase ➞ ↑ in cAMP activates protein kinase A
    3. phosphorylation of protein kinase A activates steroidogenic enzymes
77
Q

ACTH

A

adrenocorticotropic hormone

  • released by anterior pituitary when stimulated by glucocorticotropic releasing hormones (CRH)
  • stimulates adrenal glands to produce glucocorticoids
    • major: cortisol
    • minor: aldosterone
78
Q

cortisol

A
  • metabolic effects:
    • ↑BG (gluconeogenesis)
    • ↑blood fatty acids (lipolysis in specific areas)
    • ↑blood [AA] (proteolysis for fuel of gluconeogenesis)
    • permissive for effects of SNS: EP & NE
  • behavioral effects:
    • initial: euphoria & alerntess
    • chronic: excessive exposure associated with emotional lability, insomnia, & depression
    • CRH & ACTH have direct effects on learning & memory
  • at ↑[cortisol] natural & sympathetic glucocorticoids (cortisol, cortisone, prednisone, dexmethasone) = immunosuppressive & antiinflammatory
  • chronic cortisol ↑ BG ➞ adrenal diabetes ➞ hypoglycemia & suppressed immune sys & breaks down muscle & bone
79
Q

metabolic fuel: carbohydrate

circulating form:

storage form:

major storage site:

role:

A

circulating form: glucose

storage form: glycogen

major storage site: liver, muscle

role: first energy source, essential for brain

80
Q

metabolic fuel: fat

circulating form:

storage form:

major storage site:

role:

A

circulating form: free fatty acids

storage form: triglycerides

major storage site: adipose tissue

role: primary energy resevoir; energy source during fast

81
Q

metabolic fuel: protein

circulating form:

storage form:

major storage site:

role:

A

circulating form: AA

storage form: body protein

major storage site: muscle

role: source of glucose for brain during a fast; last reservoir to meet other energy needs

82
Q
  1. abnormalities in peripheral hormone levels caused by:
A

a. peripheral endocrine gland ➞ primary enocrine disorder
b. pituitary gland ➞ secondary enocrine disorder
c. hypothalamus ➞ tertiary enocrine disorder
* most difficult to identify b/c so few hypothalamic peptides in miniscule amounts

83
Q

the body’s response to stressors

A

largely the same

84
Q

type I diabetes

A
  • no/almost no insulin secretion
  • autoimmune destruction of β cells
  • tx: insulin injections = only
    • dietary management & exercise can help
85
Q

type II diabetes

A
  • insulin secretion may be normal or too high
  • reduced sensitivity of insulin target cells
    • isulin resistance: signalling pathways dont work ➞ takes more glucose to have same effect
  • tx:
    • dietary control & weight loss
    • exercise
    • oral hypoglycemic drugs
86
Q

diabetes mellitus

A
  • ↑ BG levels
  • high fat diets ↓ insulin sensitivity ➞ accumulation of fat interferes w/ downstream signaling pathways of insulin receptors
  • untreated: ↑ fatty acids in blood from ↑ lypolysis & ↓ triglyceride synthesis
  • without insulin:
    • cannot move glucose out of blood into fat (no triglyceride sythesis)
    • cannot move glucose into resting skeletal muscle
    • liver cannot store as glycogen even though uptake is unaffected
  • causes hyperglycemia & cannot store glucose
87
Q

insulin absorptive state overall effects

A

carbohydrate metabolism
* enhances glucose uptake via GLUT4
* ↑ liver & skeletal muscle glycogenesis
* inhibits liver & muscle glycogenesiis
* inhibits liver glyconeogenesis

fat metabolism
* enhances glucose uptake in adipocytes for triglyceride synthesis
* inhibits adipose lipolysis

protein metabolism
* enhances AA uptake in muscle & liver
* ↑ protein synthesis
* inhibits proteolysis

88
Q

NE vs EP

A

NS= focused FOF response: ↑ alertness, arousal, & attention, constricts vessels, maintains BP during stress, ↑ systolic BP

EP = general FOF response: ↑ HR, dilates muscles increases blood flow to muscles, ↑ breathing, ↑ BG, ↑ strength & physical performance

89
Q

glucagon effects

A

carbohydrate metabolism
* inhibits liver glyconeogenesis
* ↑ liver glycolysis
* ↑ gluconeogenesis

fat metabolism
* ↓ triglyceride synthesis
* ↑ lipolysis

no effects on protein metabolism

90
Q

insulin dependent vs insulin independent

A

insulin dependent via GLUT4 transport:
* resting muscle cells stored as glycogen
* adipocytes stored as triglycerides

insulin dependent via GLUT2 transport:
* brain but cannot be stored
* liver (but insulin facilitates glycogen storage, glycogenesis

91
Q

4 hormones that ↑ BG

A
  1. glucagon
  2. EP
  3. cortisol
  4. IGF-1

NPB 101 (13 decks)

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