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Anatomy 403 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

General functions of endocrine system

A
  • regulate cellular metabolism (TH)
  • maintain water, electrolyte, and nutrient balance (insulin, aldosterone, ADH)
  • promote growth and development (GH,TH)
  • control reproduction (estrogen, testerone)
  • help the body cope with stress (cortisol)
  • regulate digestion and adsorption of food (GI hormones)
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2
Q

hormone imbalance

A
  • hypo/hyper
  • weight gain/loss
  • increase/decrease BP
  • infertility, etc.
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3
Q

endocrine glands

A

secrete substances into the bloodstream

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4
Q

hormones

A

chemical messengers of the endocrine system

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5
Q

paracrine agent

A

in the same tissue

ex: histamine, nitric oxide (NO), cytokines

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6
Q

nervous system

A
  • fast/wired
  • APs (electrical) and NTs at synapses (chemical)
  • short duration
  • local effects
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7
Q

endocrine system

A
  • slow/wireless
  • hormones into blood (chemical)
  • long duration
  • widespread effects
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8
Q

Peptides/Proteins

A
  • amino acids
  • range in size from 3 amino acids to full proteins
  • more of these than the other two
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9
Q

Amines

A
  • derivatives of tyrosine
  • TH
  • Epi
  • NE
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10
Q

steroids

A

made from cholesterol

  • 85% from liver
  • 15% from diet
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11
Q

peptide hormones

A
  • composed of amino acids
  • most hormones are proteins/peptides
    ex: GH, insulin, ADH, LH, FSH
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12
Q

peptide hormone synthesis

A

peptide hormones are processed and packaged into secretary vesicles for exocytosis

  • transcription –> DNA –> mRNA
  • translation
  • synthesis –> rough ER
  • packaging –> Golgi
  • storage –> vesicle
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13
Q

cells that secrete lots of peptides have:

A
  • increased rough ER
  • increased Golgi
  • increased secretory vesicles
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14
Q

properties of peptides hormones

A
  • hydrophilic
  • vesicle storage
  • soluble in blood
  • extracellular receptors (use 2nd messengers)
  • fast effect (modify existing proteins)
  • short 1/2 life (rapidly degraded)
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15
Q

vesicle storage

A

release is controled

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16
Q

soluble in blood

A

no transport needed

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17
Q

rapidly degraded

A

because unbound in blood

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18
Q

signaling transduction pathway

A
  1. hormone-receptor binding activates a G protein
  2. G protein activates adenylate cyclase
  3. adenylate cyclase produces cAMP
  4. cAMP activates protein kinases
    - -> 2 nd messenger
  5. protein kinases phosphorylate enzymes. This activates some enzymes and deactivates others
  6. activated enzymes catalyze metabolic reactions with a wide range of possible effects on the cell
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19
Q

steroid synthesis occurs in

A

mitochondria and smooth ER

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20
Q

steroid synthesis depends on

A
  • cell type
  • enzymes expressed
    ex: ovaries express aromatase
    testes do NOT
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21
Q

cells that synthesize steroid hormone have:

A
  • increase mitochondria
  • increase smooth ER
  • increase specific enzyme
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22
Q

properties of steroid hormones

A
  • hydrophobic
  • membrane permeant
  • need binding/transport proteins
  • intracellular receptors
  • slow effect (synthesize proteins)
  • long 1/2 life
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23
Q

binding proteins of steroid hormones

A
  • transport hydrophobic / lipophilic substances
  • hormones inactive when bound
  • creates storage pool
  • reduce metabolic clearance rate
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24
Q

cellular response to steroid hormone

A
  1. dissociates from transport protein
  2. diffuses into target cell
  3. binds to receptor complex
  4. complex binds to DNA (hormone response elements)
    - -> alter gene expression
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25
Q

what two categories why tyrosine break into?

A
  • catecholamines

- thyroid hormones

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26
Q

properties of catecholamines

A
  • hydrophilic
  • vesicle storage
  • soluble in blood
  • extracellular receptors
  • fast effect
  • short 1/2 life
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27
Q

properties of thyroid hormones

A
  • hydrophobic
  • membrane permeant
  • needed binding proteins
  • intracellular receptors
  • slow effect
  • long 1/2 life
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28
Q

catecholamines hormones

A
  • DA
  • NE
  • Epi
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29
Q

Thyroid hormone hormones

A
  • T4

- T3

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30
Q

hormone receptors

A
  • determine which tissues response to an endocrine “broadcast”
  • only cells with a receptor for a hormone will respond to that hormone
  • even if cells possess the same receptor, cellular response can differ
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31
Q

endocrine glands

A
  • glands NOT anatomically connected
  • form a system in a functional sense
  • some glands have multiple (non-endocrine) functions
  • some glands secrete multiple hormones
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32
Q

infundibulum

A

connects hypothalamus and pituitary

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33
Q

hypothalamus

A

master gland

- responds to many stimuli and instructs pituitary what to do to maintain homeostasis

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34
Q

inputs to hypothalamus

A
  • hormone
  • general sense (pain, touch, temp, suckling)
  • higher centers (emotion)
  • special senses
  • blood conditions (glucose, osm, temp)
  • –> lacks blood brain barrier
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35
Q

pituitary gland

A
  • 2 lobes
  • different origins and different mechanisms of action
  • size of garbanzo bean
  • lies in pocket of sphenoid bone just below hypothalamus
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36
Q

anterior pituitary (adenohypopohysis)

A

glandular pituitary

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37
Q

anterior pituitary develops from

A

epithelial tissue in mouth

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38
Q

posterior pituitary (neurohypophysis)

A

neural pituitary

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39
Q

posterior pituitary develops from

A

nervous tissue in brain

- neural extension of hypothalamus

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40
Q

posterior pituitary

A
  • hormones are made in cell bodies of hypothalamus and stored in axons in posterior pituitary
  • action potential from hypothalamus = hormone release from axon terminal in bloodstream
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41
Q

peptide hormones in posterior pituitary

A
  • ADH

- oxytocin

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42
Q

ADH

A
  • AKA: vasopressin
  • released in response to: increase osmolarity
  • stimulates water retention by kidneys and vasoconstriction (Increased BP)
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43
Q

ADH result

A
  • increase blood volume
  • decrease urine production
    = decrease blood osmolarity
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44
Q

oxytocin (OT) causes

A
  • contraction of uterine smooth muscle during birth

- milk secretion from breast tissue upon suckling

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45
Q

anterior pituitary

A
  • no neural connection

- system of blood vessels

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46
Q

advantages of portal system in anterior pituitary

A
  • local route for blood flow (very little in general regulation)
  • hypothalamus hormones doesn’t get dilutes so doesn’t need as much
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47
Q

anterior pituitary hormones

A
  • releasing hormones (RH)

- inhibiting hormones

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48
Q

releasing hormones

A
  • ON

- stimulate anterior pituitary to secrete hormones

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49
Q

examples of releasing hormones

A
  • TRH
  • GnRH
  • CRH
  • GHRH
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50
Q

inhibiting hormones

A
  • OFF

- prevent anterior pituitary from secreting hormones

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51
Q

examples of inhibiting hormones

A
  • somatostatin (SS)
  • -> AKA: growth hormone inhibiting hormone
  • prolactin inhibiting hormone (PIH)
  • -> actually dopamine (DA)
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52
Q

prolactin (PRL)

A

milk production

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53
Q

advantages of three hormone feedback system

A
  1. amplification
    - only need small amount of starting hormone
  2. multiple feedback pathways
    - limits extremes in hormone secretion
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54
Q

hypersecretion

A

increased amounts of hormones

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55
Q

hyposecretion

A

decreased amounts of hormones

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56
Q

primary

A

primary with final gland in axis

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57
Q

secondary

A

problem with tropic hormone (pituitary)

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58
Q

receptor

A

either receptor doesn’t respond (desensitized), or nonexistent or permanently turned on

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59
Q

signal transduction

A

problem with protein in pathway

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60
Q

hypertrophy

A

gland overstimulated and grows

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61
Q

atrophy

A

gland shrinks

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62
Q

thyroid gland

A

largest pure endocrine gland

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63
Q

follicular cells

A

follicule

- site of TH synthesis

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64
Q

C cells

A

secrete calaitonin

Ca+2 regulation

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65
Q

T4 (thyroxine)

A
  • 90% of secretion
  • -> higher affinity for transport protein
  • “storage pool” in blood
  • converted to T3 in target cells
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66
Q

T3 (triiodothyronine)

A
  • most active form
    • 4x more potent
  • R inside target cells have higher affinity for T3
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67
Q

synthesis of TH

A
  1. iodide is cotransported with Na+
  2. diffusion
  3. iodide is oxidized and attached to rings of tyrosines in thyroglobulin
  4. the iodinated ring of one MIT or DIT is added to a DIT at another spot
  5. endocytosis of thyroglobulin containing T3 and T4 molecules
  6. lysosomal enzymes release T3 and T4 and TG
  7. T3 and T4 secretion
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68
Q

exception for thyroid hormone

A
  • conjugation of TG allows storage inside colloid until needed
  • can be stored
  • TSH regulates release
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69
Q

mechanism of TH action

A
  • affects virtually every cell
  • can affect transcription of > 100 proteins
  • once bound, can control function for many days
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70
Q

major functions of thyroid hormone

A
  • increases basal metabolic rate
  • permissive to actions of Epi, NE
  • essential for CNS development (fetus) and activity (adults)
  • permissive for overall growth and development
  • increases epidermal growth / turnover (skin/hair)
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71
Q

TH increases basal metabolic rate

A
  • increase heat production
  • rate at which cells burn fuel to maintain basic life functions
  • increases number of mitochondria
  • increases Na+/K+ ATPase activity
  • increase glucose concentration
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72
Q

TH permissive actions of Epi, NE

A
  • increases SNS activity

- increases beta-adrenergic receptor expression –> cells are more responsive to Epi and NE

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73
Q

TH essential for CNS development and activity

A
  • neural growth
  • synapse formation
  • number of glia
  • myelination
74
Q

TH permissive for overall growth and development

A

needed for normal production of GH

75
Q

cretinism

A

absence of TH in development

  • poorly developed CNS
  • severe mental retardation
  • decreased growth
  • caused by dietary lack of iodine
76
Q

hypothyroidism caused by

A
  • iodine deficiency
  • radiation
  • autoimmune destruction (very common in females)
77
Q

hypothyroidism results in

A
  • low metabolism
  • fatigue
  • weight gain
  • decreased HR (decreased beta-AR, decreased Epi/NE effect)
  • cold intolerance
78
Q

myxedema

A

dry skin, mucus and protein build up under the skin

79
Q

goiter

A
  • decreased TH leads to increased TSH
  • TSH increases size and number of follicular cells
  • if goiter due to iodine deficiency highly treatable
80
Q

goiter pathway

A
  1. No Iodine = No TH
  2. no feedback
  3. increase TSH secretion
  4. TSH increases size and number of follicular cells
81
Q

hyperthyroidism caused by

A
  • tumor

- auto-antibodies that stimulate TSH-R

82
Q

hyperthyroidism results in

A
  • nervousness
  • anxiety
  • weight loss
  • heat intolerance
  • hyperglycemia
  • high resting HR
83
Q

exophthalmos

A

eye bulge out

  • antibodies attack eye muscles
  • may also be goiter
  • can be treated by removing thyroid / beta-blocker
84
Q

how many layers does the medulla of the adrenal glands have?

A

1 layer

85
Q

what type of tissue it the medulla of the adrenal glands?

A

nervous tissue

86
Q

what is the medulla of the adrenal glands controlled by?

A

sympathetic nervous system

87
Q

what does the medulla secrete?

A

epinephrine and norepinephrine

88
Q

how many layers does the cortex of the adrenal glands contain?

A

3 layers

89
Q

what is the inner most layer of the adrenal glands of the cortex?

A

zona reticularis

90
Q

what is the middle layer of the adrenal glands of the cortex?

A

zona faciculata

91
Q

what is the outer most layer of the adrenal glands of the cortex?

A

zona glomerulosa

92
Q

what does the zona reticularis secrete?

A

estrogen and testosterone

93
Q

what does the zona faciculata secrete?

A

cortisol

94
Q

what does the zona glomerulosa secrete?

A

aldosterone

95
Q

what type of tissue is the cortex of the adrenal glands?

A

glandular tissue

96
Q

aldosterone

A
  • 90%
  • mineralocorticoids
  • increase Na+ reabsorption in kidneys
  • increase H2O retention (H2O follows Na+)
  • increase blood volume = increase BP
97
Q

adrenal medulla

A
  • catecholamines
  • modified sympathetic ganglion that does not give rise to postganglionic fibers = hormones are secreted (neuroendocrine reflex)
98
Q

functions of adrenal catecholamines

A
  • dilates respiratory airways
  • increases HR and BP
  • dilates blood vessels to heart and skeletal muscle –> vasodilation
  • mobilizes glucose, fatty acids –> hormone effect only
  • increases alertness –> hormone effect only
  • dilates pupils
  • reduces digestive activity
  • inhibits bladder emptying
  • Epi reinforces SNS effects NE during “fight or “flight” stress response”
99
Q

androgens

A
  • similar to testosterone but 20% as potent –> plays role in females, fetus and puberty
  • also, source of estrogen in men and post menopausal females
100
Q

stress

A

anything that disrupts homeostasis

101
Q

stress examples

A
  • phycological stress
  • daily exercise
  • trauma
  • surgery
  • infection
  • starvation
  • sleep deprivation
102
Q

functions of cortisol (basal levels)

A
  • fetal/neonatal development of brain, intestines, lungs, glands
  • liver glucose production between meals
  • anti-inflammatory / anti-immune (prevent hyper-response)
103
Q

cortisol liver glucose production between meals

A
  • break down of fats and proteins for energy

- mobilizes glucose (gluconeogensis, decrease glucose use)

104
Q

cortisol anti-inflammatory / anti-immune

A

without this function autoimmune disorders develop

105
Q

functions of cortisol in stress

A
  • metabolic effects (glucose sparing)
  • support SNS responses
  • stimulates erythropoietin (EPO) (replace RBC’s)
  • bone resorption
  • anti-inflammatory / immunosuppression
  • psychological / analgesic
  • inhibition of non-essential functions
106
Q

cortisol in stress metabolic effects

A

mobilizes glucose, fatty acids, and amino acids

107
Q

cortisol in stress supports SNS response

A
  • vasoconstriction
  • increased HR and RR
  • bronchodilation
108
Q

cortisol in stress stimulates EPO

A
  • in case of bleeding
109
Q

cortisol in stress bone resorption

A
  • Ca+2 mobilization

- to repair broken bones and blood clotting pathway

110
Q

cortisol in stress anti-inflammatory / immunosuppression

A
  • decrease antibodies

- decrease leukotrienes and prostaglandins

111
Q

drugs used as cortisol mimics

A
  • cortisone
  • prednisone
  • dexamethasone
112
Q

cortisone

A

synthetic cortisol

- equipotent

113
Q

prednisone

A

4x as potent as cortisol

114
Q

dexamethasone

A

30x as potent as cortisol

- used for RA

115
Q

cortisol in stress psychological / analgesic

A
  • elevates mood (short term)

- endorphins co-released with ACTH inhibit pain

116
Q

cortisol in stress inhibition of non-essential functions

A
  • reproduction/growth
  • LH/FSH decrease
  • sex hormones decrease
117
Q

effects of chronic stress

A
  • weight loss (muscle)
  • impaired growth
    • —> these two have increased protein catabolism
  • high BP (SNS effect)
  • polycythemia (increased RBC)
  • decrease bond density
  • decrease immune response
  • decrease fertility
118
Q

adrenal insufficiency

A

Addison’s disease

119
Q

Addison’s disease caused by

A
  • tuberculosis
  • tumors
  • autoimmune destructions
120
Q

tuberculosis

A

destroys adrenal cells

121
Q

Addison’s disease results in

A
  • low BP (decreased SNS, decreased aldosterone)
  • low blood glucose
  • anxiety, fatigue
  • weight loss
  • muscle weakness / pain
  • hyperpigmentation of skin
122
Q

cortisol hypersecretion

A

Cushing’s syndrome

123
Q

Cushing’s syndrome caused by

A

tumors (adrenal/pituitary)

124
Q

Cushing’s syndrome results in

A
  • osteoporosis
  • thin skin
  • muscle weakness
  • immunosuppression
  • high blood glucose (mimics diabetes)
  • high BP (increased SNS)
  • redistribution of fat
125
Q

brain

A
  • done by about 5 years (size)

- development into 20’s

126
Q

total body height

A
  • 2 periods of rapid growth
  • -> first 2 years
  • -> puberty
127
Q

what is growth influenced by?

A
  • genetics

- environment

128
Q

requirements for normal growth

A
  • adequate nutrition (especially protein)
  • freedom from chronic illness/disease
  • freedom from chronic stress
  • normal host of hormones
129
Q

normal host of hormones promoting growth

A
  • growth hormone (GH)
  • insulin - like growth factors (liver)
    • –> these two work together for growth
  • insulin
  • thyroid hormone
  • testosterone
  • estrogens
  • other peptide growth factors
130
Q

what gland secretes growth hormone?

A

anterior pituitary

131
Q

insulin (in fetus)

A

protein synthesis

132
Q

thyroid hormone

A

permissive: allows GH to have growth effects but does not medicate those effect on growth

133
Q

testosterone

A

stimulates GH and IGF secretion at puberty, stimulates protein synthesis, closure of epiphyseal plates

134
Q

estrogens

A

stimulates GH and IGF secretion at puberty, closure of epiphyseal plates

135
Q

other peptide growth factors

A

> 60

- stimulate differentiation and cell division

136
Q

increased IGF does what?

A
  • increased cell division
  • increased protein synthesis
  • increased bone growth
  • increased blood glucose
137
Q

functions of growth hormone

A
  • postnatal growth (espically bones)
    • –> increased osteoblasts
  • protein synthesis (muscle)
  • secretion of IGF-1
  • fetal development
  • cell division
  • mobilize glucose and fatty acids
138
Q

end result of growth hormone

A
  • protein synthesis
  • catabolize fat for energy
  • prevent glucose storage
139
Q

what does insulin promote?

A

growth during fetal / childhood development

140
Q

with age:

A
  • decreased GH
  • decreased muscle formation
  • increased fat formation
141
Q

dwarfism

A
  • GH / IGF-1 / GF deficiency or receptor insensitivity
  • decreased done growth
  • decreased muscle development
142
Q

hypersecretion of GH

A

caused by slow growing pituitary tumor

143
Q

gigantism

A

excess GH before epiphyseal plates close

- will be excessively tall

144
Q

acromegaly

A

excess GH after epiphyseal plates close

145
Q

acromegaly results in

A
  • bone thickening –> hands, feet, head
  • enlarged organs (heart)
  • hyperglycemia (mimic diabetes)
146
Q

absorptive state

A

after meal:

  • anabolic processes exceed catabolism
  • increased insulin
  • most glucose used for fuel
  • glucose stored by glycogenesis
  • gluconeogensis is suppressed
147
Q

post absorptive state

A

between meals:

  • catabolic processes increase
  • glucagon
  • glucose is released by glycogenolysis
  • gluconeogensis stimulated
  • fatty acids oxidized for fuel
148
Q

beta cells

A
  • contain 1% of insulin
  • secreted during and immediately following a meal (during absorptive state)
  • increased absorption of glucose in most cells
149
Q

alpha cells

A
  • contain 1% of glucagon

- secreted between meals (during post absorptive state)

150
Q

effects of insulin

A
  1. facilitates the entry of glucose into muscle, adipose and most other tissues
  2. stimulates liver to store glucose as glycogen
151
Q

effects of glucagon

A
  1. causes liver to convert stored glycogen into glucose and release into bloodstream
  2. stimulates gluconeogenesis
152
Q

diabetes mellitus - type 1

A

type 1 / insulin-dependent / juvenile onset

- 5%

153
Q

diabetes type 1 caused by

A

destruction of beta cells (autoimmune) –> no insulin secretion

154
Q

diabetes type 1 results in

A

hyperglycemia “starvation in the midst of plenty”

155
Q

diabetes type 1 effects

A
  1. extreme hyperglycemia
  2. increased fat catabolism
  3. atherosclerosis
  4. increased urine volume = osmotic diuresis
156
Q

extreme hyperglycemia

A

nerve damage and blindness

157
Q

increased fat catabolism

A

ketoacidosis (coma)

158
Q

atherosclerosis

A
  • hypertension
  • kidney damage / vessel damage
  • amputations
159
Q

diabetes mellitus - type 2

A

type 2 / non - insulin dependent / adult - onset

- 95%

160
Q

diabetes type 2 caused by

A
  • desensitized insulin receptors on target cells

- often associated with obesity and inactivity

161
Q

diabetes type 2 effects

A
  • hyperglycemia
  • other symptoms like type 1, but usually milder
  • insulin secretion normal to elevated
162
Q

diabetes type 2 treated with

A

diet and exercise

163
Q

too high Ca+2 homeostasis

A

cardiac arrhythmia / decrease neuromuscular excitability

164
Q

too low Ca+2 homeostasis

A

increased excitability of neurons and muscles

- tremors in muscles

165
Q

where is majority of Ca+2 stored?

A

in the bones

166
Q

what is the parathyroid hormone?

A

peptide

167
Q

what does the parathyroid hormone do?

A

secreted when Ca+2 levels fall

168
Q

hyperparathyroid

A
  • weaker bones / bone pain
  • constipation
  • gall / kidney stones
  • muscle weakness / fatigue
169
Q

calcitonin

A

secreted when increased Ca+2

170
Q

where is calcitonin found?

A

from parafollicular cells (c-cells) in thyroid gland

171
Q

calcitonin effects

A
  • increased Ca+2 storage in bone
  • decreased blood Ca+2
  • increased osteoblast
  • decreased osteoclast
172
Q

parathyroid hormone pathway

A
  • decrease plasma calcium
  • increase parathyroid hormone secretion
    1. increase bone resorption
    • -> increase osteoclasts
    • -> decrease osteoblasts
      1. increase calcium reabsorption in the kidneys and decrease urinary excretion of calcium
      2. increase calcium absorption into blood & increase active vitamin D
173
Q

25-OH D

A

calcidol

174
Q

calcitrol

A

active form of vitamin D

175
Q

parathyroid hormone within vitamin D pathway

A

increases active vitamin D

176
Q

calcitonin role in children

A

bones in kids are highly active and release increase Ca+2 (about 5g/day)

177
Q

calcitonin role in adults

A
  • doesn’t have much of an effect on adult
  • kidney correct increased Ca+2 in adults
  • adults need PTH but don’t need calcitonin
  • only about 0.3 g/day
178
Q

androgen/estrogen/progesterone

A

growth/reproduction

179
Q

GI tract

A

sections/motility

180
Q

lepin (adipose)

A

appetite

181
Q

ANP (heart)

A

blood pressure

182
Q

EPO (kidney)

A

RBC production

Anatomy 403 (13 decks)

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