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(PA school) Human Physiology > Lecture 13: Endocrine control > Flashcards

Lecture 13: Endocrine control Flashcards

1
Q

1) What is the primary type of gland of endocrinology?
2) What type of system are they a part of?
3) What type of signal is involved?

A

1) Ductless endocrine glands throughout the body
2) Functional system that is not anatomically connected
3) Chemical messengers

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2
Q

1) Where do endocrine glands secrete their hormones?
2) What do hormones act on? (distance-wise)
3) What cells do they act on?

A

1) Into blood
2) Distant cells
3) Only act on cells with receptors for the hormone

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3
Q

1) What balance do hormones regulate?
2) What can hormones respond to? Give 3 examples

A

1) Ion/ water balance
2) Adverse conditions
-Infection, trauma, stress

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4
Q

Which of the following do hormones contribute to?:
1) Growth and development
2) Reproduction
3) Digestion and storing nutrients

A

All of the above

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5
Q

What are the major regulatory systems? What type of responses do they consist of?

A

1) Nervous system: rapid precise responses
2) Endocrine system: slower responses

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6
Q

1) What hormones regulate the production or secretion of another hormone?
2) What do these hormones also do? What would happen if they didn’t do this?

A

1) Tropic hormones
2) Maintain structure of their target glands.
-The glands would atrophy.

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7
Q

1) Can a single gland only produce one hormone, or many?
2) Can more than one gland make a type of hormone?
3) Can a single hormone act on different cell types? Why or why not?
4) Is hormone secretion always consistent?

A

1) Many hormones
2) Yes; a single hormone may be produced by multiple glands
3) Yes; for different effects
4) No, hormone secretion can vary considerably
A target cell may respond to multiple hormones
Some hormones are also neurotransmitters

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8
Q

1) Primary function of most hormones is in what?
2) What are hormones’ effects proportional to? Is this the only factor in regulating their effects?

A

1) Regulating homeostasis
2) Plasma concentration; no, many factors influence effects

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9
Q

List 3 (of many) factors that influence a hormones effects

A

1) Availability and sensitivity of target cells
2) Rate of secretion
3) Rate of removal by inactivation and/or excretion (hydrophilic vs lipophilic)

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10
Q

How long do hydrophilic and lipophilic hormones last because of their rates of removal by inactivation and/or excretion?

Which is less vulnerable to excretion via urine?

A

1) Hydrophilic hormones generally last minutes to hours
2) Lipophilic hormones can persist for weeks. Less vulnerable to excretion via urine

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11
Q

Plasma concentration of a hormone is usually regulated by what?

A

Rate of secretion

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12
Q

List and describe 3 mechanisms for controlling secretion

A

1) Negative-feedback control: output counteracts input
2) Neuroendocrine reflexes: sudden increase in hormone secretion
3) Diurnal (circadian) rhythm: repetitive oscillations in hormones

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13
Q

1) “Output counteracts input” describes what type of mechanism to control secretion?
2) A sudden increase in hormone secretion is characteristic of what type of mechanism to control secretion?
3) Repetitive oscillations in hormones describe what?

A

1) Negative-feedback control
2) Neuroendocrine reflexes
3) Diurnal (circadian) rhythm

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14
Q

Endocrine disorders usually result from abnormal ___________ concentrations of hormones caused by _____________ or _____________.

A

plasma; hyper- or hyposecretion

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15
Q

What is a less common cause of endocrine disorders?

A

Target-cell dysfunction

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16
Q

1) Define primary hyposecretion
2) Give 6 potential causes

A

1) Gland abnormality results in decreased hormone secretion
2) Genetic, dietary, chemical/toxic, immunologic, Iatrogenic, idiopathic

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17
Q

Define secondary hyposecretion

A

Gland is normal but there is deficiency of its tropic hormone

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18
Q

1) Define primary hypersecretion
2) Give 3 potential causes. Give an example of one of these causes.

A

1) Gland defect resulting in excessive hormone secretion
2)
-Tumors that ignore regulatory input
-Immunologic (TSH-like antibody stimulating the thyroid gland)
-Drugs

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19
Q

Define secondary hypersecretion

A

Excessive stimulation from outside the gland causes hypersecretion

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20
Q

1) Endocrine dysfunction can occur due to abnormal responsiveness of what to what?
2) What is an inborn cause of endocrine dysfunction?

A

1) Target cells to normal plasma concentrations of a hormone
2) Lack of receptors for a hormone

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21
Q

1) When will target cell responsiveness be pathologic?
2) Can target cell receptors be deliberately altered? Explain and give an example

A

1) When unintentional
2) Yes, as a physiologic control mechanism (ex: down regulation)

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22
Q

1) What is down regulation?
2) What effect does it have?
3) Give an example

A

1) Reduction in number of receptors to a hormone in response to chronically elevated hormone levels
2) Blunts the effect of hypersecretion
3) Insulin receptor down-regulation with chronically elevated insulin

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23
Q

1) True or false: A hormone’s effects can also be influenced by concentrations of other hormones
2) Are target cells only exposed to one type of hormone, or many?

A

1) True
2) Different hormones simultaneously

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24
Q

1) What can hormones alter the receptors for?
2) Give 3 examples of this

A

1) Other hormones
2) Permissiveness, synergism, antagonism

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25
Q

1) Define permissiveness (in the context of hormones altering receptors for other hormones). Give an example.
2) What is the implication of this?

A

1) First hormone enhances target cell responsiveness to second hormone by increasing number of receptors
-Ex: TH and epinephrine
2) One hormone must be present to permit another hormone’s full effect

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26
Q

1) Define synergism (in the context of hormones altering receptors for other hormones). Give an example
2) What does this imply?

A

1) Actions of hormone are complementary, and their combined effect is greater than the sum of their separate effects
-GH hits some Sertoli cells that germinate sperm
2) Each hormone increases the concentration of or affinity to another hormone

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27
Q

Define antagonism (in the context of hormones altering receptors for other hormones)

A

One hormone causes the loss of another hormone’s receptors
-The reason why oxytocin is not released until birth

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28
Q

1) What gland is a small gland below the hypothalamus?
2) What are its parts?

A

1) Pituitary
2) Two distinct lobes; anterior and posterior pituitary

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29
Q

1) What is the anterior pituitary also called? What is it made of?
2) What is the posterior pituitary also called? What is it made of?

A

1) Adenohypophysis; glandular epithelial tissue
2) Neurohypophysis; nervous tissue

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30
Q

1) What do the two lobes of the pituitary have in common?
2) What about the two lobes differs?

A

1) Only their location (and the fact that both are controlled by the hypothalamus by different means)
2) Tissue composition, functions, and control mechanisms

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31
Q

1) How does the anterior pituitary connect to the hypothalamus?
2) What about the posterior pituitary?

A

1) A unique vascular link
2) A neural pathway

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32
Q

1) How are hormones stored in the posterior pituitary? Why?
2) Where are the two hormones that are stored and released here synthesized? What are they?

A

1) As independent vesicles so they can be released individually
2) By the hypothalamus; vasopressin (aka antidiuretic hormone) and oxytocin

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33
Q

1) What does vasopressin/ ADH do? (2 things)
2) What triggers it? (2 things)

A

1) Stimulates water reabsorption in the renal tubule and causes contraction of arteriolar smooth muscle
2) Hypothalamic osmoreceptors and left atrial volume receptors

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34
Q

1) What does oxytocin do? (2 things)
2) What triggers it? (2 things)

A

1) Stimulates uterine smooth muscle contractions (during childbirth) and promotes milk ejection from mammary glands (during breast-feeding)
2) Birth canal and nipple stimulation

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35
Q

Most anterior pituitary hormones are a part of what category?

A

Tropic

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36
Q

List the 6 hormones and one other things synthesized by the anterior pituitary

A

Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Adrenocorticotropic Hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Prolactin (PRL)
Endorphins
Growth hormone (GH)
(FLAT PEG)

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37
Q

1) Which hormone is the only AP hormone that does not stimulate secretion of another hormone?
2) Two most important factors that regulate AP hormone secretion are what?

A

1) Prolactin (PRL)
2) Hypothalamic hormones and feedback by target-gland hormones

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38
Q

1) The secretion of each AP hormone is stimulated or inhibited by what?
2) What are these called?

A

1) One or more of seven hypothalamic hypophysiotropic hormones
2) Inhibiting or releasing hormones (depending on their action)

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39
Q

1) Which hypothalamic hormone stimulates the release of TSH?
2) Which hypothalamic hormone stimulates release of ACTH? What can dysfunction of this cause?
3) What are the two functions of somatostatin? What type of hormone is this?

A

1) Thyrotropin-releasing hormone
2) Corticotropin-releasing hormone
-Dysfunct. can cause immune issues, BP issues, and severe side effects
3) Inhibits release of GH and TSH; hypothalamic

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40
Q

1) What is Gonadotropin-releasing hormone a type of? What does it do?
2) What is GHRH (growth hormone-releasing hormone) a type of and what does it do?

A

1) Hypothalamic hormone; stimulates release of FSH and LH
2) Hypothalamic hormone; stimulates release of GH

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41
Q

1) What does dopamine do? Where does it come from?
2) What is prolactin-releasing hormone and where does it come from?

A

1) Inhibits release of prolactin; hypothalamus
2) Hypothetical hormone; hypothalamus

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42
Q

1) What are the stimulating factors of prolactin?
2) What factor has been hypothesized?

A

1) Very few are known.
2) Existence of prolactin-releasing hormone

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43
Q

What are the 7 hypophysiotropic hormones?

A

1) Thyrotropin-releasing hormone (TRH)
2) Corticotropin-releasing hormone
3) Gonadotropin-releasing hormone (GnRH)
4) Growth hormone-releasing hormone (GHRH)
5) Somatostatin
6) Dopamine
7) Prolactin-releasing hormone (PRLRh)

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44
Q

What is the 3 hormone chain of command involving the hypothalamus and a pituitary?
Describe its 3 steps and give an example for each step

A

Hypothalamic-pituitary axis:
1) Hypothalamic hypophysiotropic hormone regulates:
ex: thyrotropin-releasing hormone (TRH)
2) Anterior pituitary tropic hormone which regulates:
ex: thyroid-stimulating hormone (TSH)
3) Target gland hormone
ex: thyroid hormone (T3, T4)

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45
Q

The unique vascular link between the hypothalamus and the anterior pituitary is called what?

A

Hypothalamic-Hypophyseal Portal System

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46
Q

In the Hypothalamic-Hypophyseal Portal System:
1) What is being combined into what?
2) What do these pass into? What do they do after that?
3) Where do they then drain?

A

1) Hypothalamic capillaries into small portal vessels
2) The anterior pituitary; branch to form AP capillaries
3) Into the systemic venous system

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47
Q

Protein synthesis occurs under the influence of what hormone?

A

Growth hormone

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48
Q

1) True or false: weight gain is the same as growth
2) Give 2 potential causes of weight gain
3) What does growth involve?

A

1) False; weight gain is not the same as growth
2) Retaining water or storing fat
3) True structural growth of tissues

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49
Q

What does growth require? (3 things)

A

Synthesis of proteins, lengthening of bones, increasing the size and number of cells in tissues

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50
Q

List 4 factors that influence growth

A

1) Genetics
2) Diet
3) Health (stress and diseases)
4) Hormones

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51
Q

1) What factor that affects growth significantly alters maximum growth capacity?
2) Why does diet affect growth? What occurs in the case of malnourishment during childhood?
3) Normal levels of what hormones are needed for growth?

A

1) Genetics
2) Protein and amino acids necessary for growth; they do not achieve their full growth potential
3) GH, thyroid hormone, insulin, sex hormones

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52
Q

1) What two health factors can stunt growth?
2) Give 3 examples of the several effects these can have

A

1) Stress (cortisol) and diseases
2) Protein breakdown, long bone inhibition, GH blocking

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53
Q

1) What is the most abundant AP hormone (even in adults)?
2) Does it only have one effect? Explain

A

1) GH
2) No; has other metabolic effects

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54
Q

Give 4 examples of what GH does besides just the general term “growth”

A

1) Stimulates amino acid uptake and protein synthesis
2) Inhibits protein degradation
3) Increases cell division
4) Stimulates bone growth

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55
Q

Does GH directly or indirectly increase protein synthesis? Are the other factors direct or indirect? Explain

A

Directly increases; the other effects are indirect via insulin-like growth factors (IGFs)

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56
Q

What are insulin-like growth factors (IGFs)
structurally and functionally similar to?

A

Insulin

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57
Q

What are the two types of insulin-like growth factors (IGFs)? What does each do?

A

1) IGF-I: mediates most of GH’s growth-promoting actions
2) IGF-II: primarily important in fetal development. Role in adults unclear.

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58
Q

1) IGF-I variation stimulates what two things?
2) Give an example of effects of genetic variation in IGF-1 regulation. What is unique about this example?

A

1) hypertrophy and hyperplasia
2) Differentiates the Great Dane (has more IGF1) from the Chihuahua; no other species produces adults with such a wide size range

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59
Q

1) What releases IGF-1? What produces it?
2) Why?
3) Does only GH control its production?

A

1) Released by liver, produced by other tissues which do not actually release it into the blood.
2) Reason unclear, perhaps paracrine function
3) No, a number of other factors

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60
Q

List and describe 3 examples of factors other than GH effecting IGF-1 production

A

1) Nutrition: inadequate food reduces IGF-I despite fasting increasing GH
2) Age: dramatic increase in IGF-I during puberty
3) Tissue-specific: Local factors can increase production. E.g. gonadotropins stimulate IGF-I release into testes or ovaries

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61
Q

What is bone? What does it consist of?

A

1) A living connective tissue
2) Cells that are triggered by osteoblasts to produce extracellular matrix known as osteoid

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62
Q

1) What is osteoid?
2) What hardens it? Where?

A

1) Extracellular matrix made of collagen fibers in semisolid gel with a rubbery consistency.
2) Calcium phosphate crystal deposition within the osteoid

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63
Q

What activity does IGF-1 stimulate in relation to bone growth? What does it do in adolescents?

A

Osteoblastic activity; promotes lengthening

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64
Q

1) What hormones regulate GH?
2) Is there a pattern to GH secretion? Explain.

A

1) Two antagonistic hypophysiotropic hormones: growth hormone-releasing hormone (GHRH) and somatostatin
2) Diurnal; increases up to five times daytime value one hour after onset of deep sleep.

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65
Q

When are there bursts of GH release?

A

In response to exercise, stress, low blood glucose

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66
Q

What are 3 reasons for GH deficiency?

A

1) Dwarfism
2) Laron dwarfism
3) Pygmyism

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67
Q

1) What causes dwarfism?
2) What are the effects of dwarfism?

A

1) GH hyposecretion in children.
2) Short stature, poorly developed muscles (reduced protein synthesis), excess subcutaneous fat (less fat mobilization)

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68
Q

1) What causes Laron dwarfism?
2) What causes pigmyism?

A

1) Unresponsive GH receptors
2) Lacking IGF-I; GH and cell responsiveness normal

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69
Q

1) Does GH deficiency after adolescence produce symptoms?
2) If not, explain why. If so, give examples.

A

1) Produces few symptoms
2) Exs: Reduced muscle mass, decreased bone density, heart disease

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70
Q

1) Hypersecretion of GH is usually caused by what?
2) What do the effects of hypersecretion depend on?

A

1) AP tumor
2) Age during hypersecretion

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71
Q

What effects does hypersecretion of GH have during childhood and after adolescence? What is each called?

A

1) Childhood: Gigantism; rapid growth without distortion of body proportions, soft tissues grow correspondingly.
2) After adolescence: Acromegaly; bones become thick, soft tissues proliferate. Disproportionate growth.
-Bone thickening obvious in the jaws and cheekbones. Hands and feet enlarge.

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72
Q

What do thyroid hormone, insulin, and sex steroids all effect?

A

Growth

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73
Q

When do progesterone and estrogen peak in women?

A

Ovulation

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74
Q

What element of diet can cause primary hyposecretion?

A

Not enough salt

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75
Q

What two hormones need to be working to breastfeed?

A

Oxytocin (eject) and PRL (produce)

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76
Q

Why might a man be producing milk?

A

Prolactinoma in pituitary

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77
Q

1) What does TRH stimulate?
2) What does that then stimulate?
3) What does that then stimulate?

A

1) TRH stimulates TSH
2) TSH stimulates T4
3) T4 stimulates TRH and TSH

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78
Q

Ghrelin can induce ____________ production

A

somatostatin

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79
Q

1) What are the (adult) target organs of growth hormone?
2) What does one of these then stimulate?

A

1) Muscle growth and liver
2) Liver produces IGF1

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80
Q

1) What hormone is permissive to growth hormone? Explain to what extent.
2) What does insulin promote? What does it resemble?

A

1) Thyroid hormone; GH effects are only fully realized when thyroid hormone levels are adequate.
2) Protein synthesis; resembles IGF-I, might interact with its receptors

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81
Q

What two sex steroids contribute to GH? When do they contribute to this?

A

Androgens and estrogen; contribute to puberty growth spurt and stop further growth by closing the epiphyseal plates

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82
Q

What 3 things does GH bind with? What does each do?

A

1) Adipose tissue: Enhances breakdown of triglycerides, making fatty acids available for energy, preserving glucose for the brain (can only use glucose but can’t store glycogen)
2) Skeletal muscles: Decreases glucose uptake by muscles (again, preserves glucose)
3) Liver tissue: Increase glucose output by liver (makes more glucose available)

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83
Q

Why are males taller? (3 reasons)

A

1) Males start puberty 2 years (avg) after females, and benefit from 2 more years of prepubertal growth.
2) Experience a greater steroid hormone growth spurt before their androgens close their growth plates.
3) Androgens also lead to higher GH peaks

84
Q

1) What structure is the “master biological clock”? What does this mean?
2) What is it made of and where is it?

A

1) Suprachiasmatic nucleus (SCN); it’s the pacemaker for circadian rhythms
2) Two clusters of nerve cell bodies in the hypothalamus above the optic chiasm

85
Q

Circadian rhythm affects a lot more than just hormone secretion rates; give examples

A

Gene expression, temperature regulation, metabolism, feeding patterns, behavior, even possible medication effects

86
Q

1) The SCN cycle is about _____ hours, but is able to synchronize with ___________________________.
2) What would happen without this continual adjustment?

A

1) 25; light-dark cues of the environment
2) Circadian rhythms would become progressively out of sync with the light-dark cycle

87
Q

What cycle is the SCN cycle in sync with? How?

A

Light-dark cycle by melatonin secreted by pineal gland

88
Q

Describe how special photoreceptors in the retina transmit to the SCN

A

Photoreceptors contain a protein called melanopsin, and these melanopsin-containing cells inform the SCN of illumination

89
Q

The lack of what input would cause the SCN to increase melatonin production tenfold?

A

Special photoreceptors in the retina transmit to the SCN

90
Q

True or false: Shift work (working outside of the 8a-5p schedule) has a detrimental effect on health

A

True

91
Q

1) What can exacerbate the negative effects of shift work?
2) What are some of these negative effects?

A

1) Especially if those shifts are frequently altered between night and day shifts
2) Fatigue, insomnia, depression, heart disease, diabetes, cancer

92
Q

Give examples of how impaired judgement of fatigued workers is a societal threat

A

1979 Three Mile Island nuclear reactor accident in the Pennsylvania
1986 nuclear accident of Chernobyl in Ukraine
1989 Exxon Valdez oil spill in Alaska
-All may have been due to impaired judgement of workers operating at a time unsuitable for clear thinking

93
Q

What can mitigate some of the negative effects of shift work?

A

Keep shifts stable for 3 weeks to give time to adjust, utilize bright lights and melatonin supplementation strategically to reset circadian rhythm

94
Q

1) Define stress
2) Stress responses are coordinated by what organ via what nervous system?

A

1) A generalized, nonspecific response of the body to any factor that overwhelms, or threatens to overwhelm, homeostasis
2) The hypothalamus via the sympathetic nervous system

95
Q

List 5 types of stressors and give examples of each

A

1) Physical: trauma, surgery, heat, cold
2) Chemical: reduced O2, altered pH
3) Physiologic: heavy exercise, pain
4) Infectious: bacteria, viruses, parasites
5) Psychosocial: anxiety, fear, sorrow, personal conflicts, change in lifestyle

96
Q

Different stressors produce different responses; give an example

A

Cold leads to shivering and vasoconstriction, heat leads to vasodilation

97
Q

1) What gland consists of two lobes of endocrine tissue joined by a narrow middle portion called the isthmus?
2) What is this gland’s shape and location?

A

1) Thyroid gland
2) Bow-tie shape and location

98
Q

1) What are follicles?
2) What are follicular cells?

A

1) Rings of follicular cells enclosing a lumen filled with colloid
2) Secretory cells of the thyroid

99
Q

1) What is an extracellular storage site for thyroid hormone?
2) What is thyroglobulin?
3) What are C cells?

A

1) Colloid
2) Glycoprotein, main constituent of colloid
3) Secretory cell in interstitial spaces between follicles

100
Q

Follicular cells secrete two iodine-containing hormones; what are they?

A

T3: tri-iodothyronine
T4: tetraiodothyronine

101
Q

T3 and T4 are collectively called ___________ hormone, which is an important regulator of ______________

A

Thyroid hormone; BMR

102
Q

What hormone do C cells secrete? What does this hormone do?

A

Calcitonin; plays a role in calcium metabolism

103
Q

What two things are used to synthesize thyroid hormone?

Which is synthesized by the body and which must be obtained from the diet? Which serves no other functions in the body?

A

Tyrosine (AA) and iodine
1) Tyrosine made by body
2) Iodine must be ingested and reduced to iodide. Serves no other functions in the body.

104
Q

1) Thyroid captures iodide from the blood and does what?
2) What one iodide to tyrosine forming monoiodotyrosine (MIT)? What else does it attach and what does this form?

A

1) Transfers it to the follicular cell
2) Thyroperoxidase (TPO); also attaches two iodide to another tyrosine forming di-iodotyrosine (DIT)

105
Q

1) Thyroglobulin joins MIT to DIT to yield what?
2) What else? Why?

A

1) T3 (tri-iodothyronine)
2) DIT to DIT to yield T4 (tetraiodothyronine)

106
Q

Are T3 and 4 instantly used?

A

Stored until secreted

107
Q

What do follicular cells release? Is this substance hydrophilic or phobic?

A

T3 and T4, which are very lipophilic and pass freely across the membrane into the blood

108
Q

1) 90% of thyroid hormone secreted is in ____ form
2) Most secreted T4 is converted to T3 by what 2 things?

A

1) T4
2) Liver and kidneys

109
Q

1) T3 is _____x more potent than T4 (Receptor affinity ______x higher for T3)
2) Which is the active form of thyroid hormone, T3 or T4?

A

1) 10x; 10x
2) T3

110
Q

What are the 5 effects of thyroid hormones?

A

1) Metabolism and heat production
2) Sympathomimetic effect
3) Cardiovascular
4) Nervous system
5) Growth

111
Q

1) What function of thyroid hormone increases BMR, especially rate of O2 consumption?
2) What is this also an important component in?

A

1) Metabolism and heat production
2) Heat production.

112
Q

1) What effect of TH increases responsiveness to catecholamines (epinephrine and norepinephrine)?
2) What kind of relationship is this with target-cell receptors?

A

1) Sympathomimetic effect
2) Permissive relationship

113
Q

1) What cardiovascular effect does TH have?
2) What nervous system effect does TH have?
3) How does TH affect growth?

A

1) Increases heart rate and contractile strength directly and indirectly (E/NE)
2) Crucial for CNS development in children and for normal CNS activity in adults
3) Stimulates GH and increases IGF-I production

114
Q

1) What regulates TH?
2) What is one characteristic of TH that most other hormones don’t have?

A

1) Hypothalamic-pituitary-thyroid axis
2) Thyroid hormone is relatively stable (doesn’t undergo wide variations in secretion)

115
Q

The only known factor that increases thyrotropin-releasing hormone (THRH) secretion is what?

A

Cold exposure in infants (temperature)

116
Q

What 3 things can inhibit TSH and thyroid hormone (TH) secretion?

A

Stress, starvation, and infection

117
Q

List the 3 potential causes of hypothyroidism

A

1) Failure of thyroid gland
2) Deficiency of TRH, TSH, or both
3) Deficient dietary iodine

118
Q

List 4 symptoms of hypothyroidism

A

From decrease metabolic activity:
2) Weight gain (lower BMR)
3) Cold intolerance (lack of calorigenic effect)
4) Hyporeflexia, slow speech, poor memory (nervous system)

119
Q

List 2 causes of hyperthyroidism

A

Grave’s disease (most common): autoimmune disease.
Thyroid tumor

120
Q

How does Grave’s disease (an autoimmune disorder) cause hyperthyroidism?

A

1) Body produces thyroid-stimulating immunoglobulin (TSI, an antibody) that attaches to TSH receptors on thyroid cells.
2) Bypasses negative feedback.

121
Q

List 6 symptoms of hyperthyroidism

A

1) Heat intolerance, sweating (increased BMR)
2) Weight loss
3) Weakness (depletion of protein stores from elevated BMR)
4) Palpitations (cardiovascular)
5) Anxiety, irritability (nervous system)
6) Exophthalmos (Grave’s only) d/t inflammation behind the eye

122
Q

What is a symptom unique to Grave’s disease?

A

Exophthalmos

123
Q

1) Define goiter
2) What does it cause?
3) What can it accompany? Is it always present in these conditions?

A

1) An enlarged thyroid gland
2) Excessive TSH or TSI
3) Hypo- or hyperthyroidism; not necessarily present in either condition

124
Q

List the two types of hypothyroidism and how each affects T3/T4 levels and TRH and TSH levels (and whether or not a goiter is present)

A

1) Primary failure of thyroid: low T3 and T4, high TSH, yes goiter
2) Secondary to hypothalamic or AP failure: low T3 and T4, low TRH and/ or TSH, no goiter

125
Q

For the 3 types/ causes of hyperthyroidism, list how each affects T3/T4 levels and TRH and TSH levels (and whether or not a goiter is present)

A

1) Abnormal presence of TSI (graves disease): high T3 and T4, low TSH, yes goiter
2) Secondary to excess hypothalamic/ anterior pituitary secretion: high T3 and T4, high TRH and/ or TSH, yes goiter
3) Hypersecreting thyroid tumor: high T3 and T4, low TSH, no goiter

126
Q

1) What are the parathyroid glands?
2) What do they secrete?

A

1) Four tiny glands on the posterior thyroid in each corner
2) Parathyroid hormone (PTH)

127
Q

1) What does parathyroid hormone do?
2) What would happen after a few days without it?

A

1) Increases plasma calcium
2) The individual will die of hypocalcemic respiratory spasm

128
Q

Calcium homeostasis involves exchanges between what 4 locations?

A

ECF, bone, kidneys, and small intestine

129
Q

99% of calcium is in ______________ form in the skeleton and teeth

A

crystalline

130
Q

List the 3 places besides bones where calcium is stored and which is biologically active (and the %s within in each)

A

1) 0.9% within soft tissues
2) 0.05% in ECF bound to plasma proteins
3) 0.05% free in the ECF: biologically active; carefully regulated

131
Q

Even small changes in calcium can have profound effects because it’s involved in what 5 functions?

A

1) Neuromuscular excitability
2) Smooth and cardiac muscle excitation-contraction coupling
3) Throughout the body, calcium triggers the release of secretory products by exocytosis
4) Forms the cement that holds tight junctions between cells
5) Cofactor in several steps of the clotting cascade

132
Q

1) What kind of change in free calcium alters neuromuscular excitability?
2) What does decreased calcium do to neuromuscular excitability?
3) What about increased calcium?

A

1) Even a small change
2) Increases sodium permeability and excitability
3) Depresses neuromuscular excitability

133
Q

1) Throughout the body, calcium triggers the release of secretory products by what process? What does this form?
2) What is calcium a cofactor in?
3) Calcium is involved in excitation-contraction coupling for what kind(s) of muscle?

A

1) Exocytosis; the cement that holds tight junctions between cells
2) Several steps of the clotting cascade
3) Smooth and cardiac

134
Q

1) How does PTH use bone as a “calcium bank”?
2) Are the bone-borrowing effects of PTH significant? Why or why not?

A

1) It withdraws calcium-phosphate crystals as needed to raise plasma concentration
2) Bone-borrowing effects of PTH are negligible, bc even a small amount of bone contains massive amounts of calcium

135
Q

1) Excess _______ over years can lead to osteoporosis
2) What substance being increased stimulates redeposition in the bone?

A

1) PTH
2) Calcium

136
Q

1) What does phosphate bind with? What does this do?
2) Kidney responds to increased PTH by doing what 2 things?

A

1) Phosphate will bind to calcium, decreasing plasma concentration
2) Increasing calcium reabsorption and phosphate excretion

137
Q

Describe how plasma calcium is raised (4 steps)

A

1) Calcium is low so PTH is increased
2) Calcium-phosphate is liberated and dissolved
3) Phosphate is eliminated and calcium is kept
4) Plasma calcium rises

138
Q

Besides regulating calcium, what 2 things does PTH enhance or promote?

A

1) Enhances kidney activation of Vit D
2) Promotes absorption of calcium and phosphate in the small intestine activating Vit D (indirectly)

139
Q

1) What substance raises plasma calcium? (reiterating)
2) What stimulates and inhibits this substance?
3) What hormone decreases calcium mobilization from the bone? What produces this hormone?

A

1) PTH
2) Stimulated by decreased calcium, inhibited by increased calcium
3) Calcitonin, hormone produced by the thyroid C cells,

140
Q

1) What 2 things does calcitonin inhibit the reabsorption of in the kidneys?
2) What is a rare property of calcitonin?

A

1) Calcium and phosphate
2) Hypocalcemic effect; it protects against hypercalcemia (which is rare)

141
Q

1) What is vitamin D also called?
2) What is vitamin D?
3) What does vitamin D do?

A

1) Cholecalciferol
2) A hormone produced by the skin from cholesterol (in response to sunlight exposure)
3) Increases calcium reabsorption in the intestine

142
Q

1) Vitamin D is biologically inactive and requires a two-step activation sequence; what is this sequence?
2) What is its active form?

A

1) First in the liver, then the kidneys (vit PTH).
2) Calcitriol

143
Q

What can cause hyperparathyroidism?

A

Hypersecreting tumor

144
Q

List 4 symptoms of hyperparathyroidism and describe each.

A

1) Related to hypercalcemia and hypophosphatemia (mild to severe)
2) Decreased neuromuscular excitability: decreased alertness, poor memory, depression, weakness, cardiac disturbances, mood disorder
3) Thinning of bones: causes fractures.
4) Kidney stones: bc of calcium filtration

145
Q

Where are the adrenal glands?

A

Embedded above each kidney in a capsule of fat

146
Q

List and describe the 2 parts of adrenal glands

A

1) Adrenal cortex: outer layer; secretes steroid hormones
2) Adrenal medulla: inner layer; secretes catecholamines (E/NE)

147
Q

1) What does the adrenal cortex produce?
2) What are these? Are they hydrophilic or lipophilic?

A

1) Adrenocortical hormones
2) Steroid hormones derived from cholesterol (and thus all lipophilic)

148
Q

1) How are adrenocortical hormones categorized?
2) List these 3 categories

A

1) Based on primary action
2) Mineralocorticoids, glucocorticoids, and sex hormones

149
Q

1) What makes up most mineralocorticoids? What does it influence?
2) What makes up most glucocorticoids? What do they do?
3) What are sex hormones of the adrenal cortex similar to? Which of these produced by the AC is the most important?

A

1) Aldosterone; influences mineral (Na+/K+) balance.
2) Mainly cortisol; glucose metabolism and adaptation to stress.
3) Those produced by the gonads; most important is the androgen dehydroepiandrosterone.

150
Q

1) What is the main mineralocorticoid?
2) What does it act on? Why?

A

1) Aldosterone
2) Acts on distal and collecting tubules of kidney to promote Na+ reabsorption and K+ elimination

151
Q

Aldosterone acts on distal and collecting tubules of kidney to promote Na+ reabsorption and K+ elimination. What are the two effects of this?

A

1) Induces osmotic retention of H2O, expanding ECF volume
2) Important in regulating blood pressure

152
Q

1) What would happen without aldosterone? Is this unique?
2) True or false: aldosterone regulation is dependent on anterior pituitary control.
3) The answer to #2 is because ACTH promotes __________, not ___________

A

1) A person would quickly die from too much plasma volume loss; few other hormones lead to death quickly.
2) False; aldosterone is regulated independent of anterior
3) cortisol, not aldosterone

153
Q

Aldosterone is stimulated by what 2 things?

A

1) Renin-angiotensin-aldosterone system
2) Stimulation of adrenal cortex by rising plasma K+

154
Q

1) List 2 causes of aldosterone hypersecretion
2) List the symptoms and what it’s related to

A

1) Adrenal tumor or inappropriate RAAS activity (multiple causes, e.g. renal artery atherosclerosis)
2) Related to hypernatremia and hypokalemia
-High blood pressure, thirst, nausea
-Cramps, constipation, cardiac rhythm disturbance

155
Q

1) Cortisol plays an important role in what? What else is it involved in?
2) What types of actions for other hormones does it have?
3) How does it effect stress?

A

1) Glucose metabolism; also involved in protein and fat metabolism.
2) Significant permissive actions
3) Has stress-resisting effects

156
Q

What is the general metabolic effect of cortisol?

A

Increases blood glucose for the brain at the expense of protein and fat

157
Q

How does cortisol increase blood glucose for the brain at the expense of protein and fat?

A

1) Stimulates hepatic gluconeogenesis, converting amino acids into carbohydrate, when liver’s glycogen is depleted
2) Inhibits glucose uptake except in the brain
3) Stimulates protein degradation, especially in muscle.
-Amino acids made available for gluconeogenesis
4) Facilitates lipolysis in adipose tissue. Fatty acids are made available for body tissues to use instead of glucose

158
Q

1) Give an example of a permissive action of cortisol
2) What is the evolutionary theory behind the effects of cortisol on stress?

A

1) Must be present for catecholamines to induce vasoconstriction
2) Threatened human would need to forego eating; in addition to reserving glucose for the brain, free AA’s would be available to repair tissue injury

159
Q

1) What part(s) of the inflammatory response does cortisol interfere with because of its immunosuppression effects?
2) Describe the negative feedback (of cortisol’s effects on immune response)

A

1) Almost every step of the inflammatory response
2) Lymphocytes can secrete ACTH, leading to cortisol secretion (negative feedback)

160
Q

1) What regulates cortisol?
2) What two structures does cortisol suppress? What feedback is this?

A

1) Hypothalamic-pituitary-adrenal cortex axis
2) Anterior pituitary and hypothalamus; negative feedback

161
Q

Describe the hypothalamic-pituitary-adrenal cortex axis regulation of cortisol (4 steps)

A

1) Hypothalamus: Secretes corticotropin-releasing hormone (CRH)
2) Anterior pituitary: Secretes adrenocorticotropic hormone (ACTH) which acts on
3) Adrenal cortex: Secretes cortisol
4) Cortisol suppress the AP and hypothalamus (negative feedback)

162
Q

What are 3 causes of cortisol hypersecretion (Cushing’s syndrome)?

A

1) Adrenal cortex overstimulation (excess CRH, ACTH, or both)
2) Adrenal tumors
3) ACTH secreting tumors in non-pituitary locations, commonly the lung

163
Q

List 3 symptoms of cortisol hypersecretion (Cushing’s syndrome)

A

1) Excessive gluconeogenesis
2) Hyperglycemia “adrenal diabetes”
3) Atypical fat storage locations (reasons unclear)
-In face, shoulders, abdomen causing a “buffalo hump” or “moon face”

164
Q

1) Does the adrenal cortex produce androgens and estrogens in men, women, or both?
2) Does it produce a lot of androgens & estrogens?

A

1) Both sexes
2) Small amount in comparison to gonads (testes and ovaries)

165
Q

1) How strong is dehydroepiandrosterone (DHEA)? Who is it significant in?
2) What is it involved in? Give 3 examples

A

1) 100x weaker than testosterone. Not significant in males due to testicular testosterone but DHEA makes a significant difference in females
2) Androgen processes: pubic and axillary hair growth, pubertal growth, female sex drive

166
Q

1) The only adrenal sex hormone that is abundant enough to matter is what?
2) What controls this?

A

1) Dehydroepiandrosterone (DHEA)
2) ACTH, not the pituitary gonadotropic hormones

167
Q

slide 76
1) Which is more common, adrenal androgen or adrenal estrogen hypersecretion?
2) What usually causes adrenal androgen hypersecretion?
3) What is adrenal androgen hypersecretion also called and why?

A

1) Androgen hypersecretion is more common; adrenal estrogen hypersecretion is extremely rare.
2) Inherited enzyme deficiency
3) “Androgenital syndrome” due to profound effects on sex characteristics

168
Q

Describe “androgenital syndrome” symptoms in both adult and newborn women

A

1) Adults: Male pattern of body hair (hirsutism). Deep voice. Muscular limbs. Smaller breasts. Amenorrhea.
2) Newborns: Clitoral enlargement and penile appearance; can make it difficult to determine sex.

169
Q

Describe “androgenital syndrome” symptoms in both adult and newborn men

A

1) Adults: No apparent effect. Barely noticeable next to testosterone. DHEA too weak.
2) Prepubertal males: Prematurely develop male sex characteristics: deep voice, beard, sex drive

170
Q

1) If one adrenal gland is removed or nonfunctional, the other compensates through what 2 things?
2) What must occur for adrenocortical insufficiency to occur?
3) What are the two types of adrenocortical insufficiency?

A

1) Hypertrophy and hyperplasia
2) Both glands must be affected
3) Primary adrenocortical insufficiency (Addison’s disease) and secondary adrenocortical insufficiency

171
Q

1) What is primary adrenocortical insufficiency (Addison’s disease) caused by?
2) What is deficient?

A

1) Autoimmune destruction of the cortex from attacking antibodies
2) Both aldosterone and cortisol

172
Q

1) What is secondary adrenocortical insufficiency and what is it caused by?
2) What is deficient?

A

1) Insufficient ACTH due to hypothalamic or pituitary etiology.
2) Only cortisol (aldosterone is independent of pituitary)

173
Q

1) What is the most threatening component of Addison’s that is fatal if severe enough?
2) Describe the usual onset of this component
3) What occurs because of this? What 2 things can this do to the body?

A

1) Aldosterone deficiency
2) So slow that aldosterone is subnormal
3) K+ retention and Na+ depletion (hyperkalemia and hyponatremia); cardiac rhythm disturbance and hypotension

174
Q

List and describe potential effects of cortisol deficiency

A

1) Poor response to stress
2) Hypoglycemia: reduced gluconeogenesis
3) Skin pigmentation: high ACTH which can bind to receptors of melanocyte-stimulating hormone

175
Q

1) What is a modified part of the sympathetic nervous system?
2) What cells does this structure consist of? What are these called?
3) Describe how these cells exert their effects

A

1) Adrenal medulla
2) Modified postganglionic sympathetic neurons called chromaffin cells
3) Don’t have fibers that end on effector organs, they release chemicals directly into blood when stimulated

176
Q

1) Which secretion is more abundant, epinephrine or norepinephrine? Give the percentages each makes up.
2) What produces these hormones and what stores them?
3) How are they secreted?

A

1) Epinephrine secretion (80%) is much more abundant than norepinephrine (20%)
2) Produced within adrenal medulla, stored in chromaffin granules
3) By exocytosis

177
Q

1) All of the _______________ in the body is from the adrenal medulla
2) Most of the ______________ in the body comes from sympathetic postganglionic fibers

A

1) Epinephrine
2) Norepinephrine

178
Q

True or false: Epinephrine and norepinephrine have affinities for different receptor types. Explain.

A

True; such as α1, α2, β1, β2

179
Q

1) Epinephrine secretion always accompanies what?
2) What stimulates its secretion from the adrenal medulla?

A

1) A generalized sympathetic response
2) Sympathetic nervous system

180
Q

What are the 2 general types of epinephrine effects?

A

Organs and metabolic

181
Q

List the 5 ways epinephrine affects organs

A

1) Supports peak exertion in stressful situations
2) Increases cardiac output (rate and strength)
3) Generalized vasoconstriction, increasing blood pressure
4) Vasodilation of coronary and skeletal muscle vessels
5) Bronchodilation

182
Q

What are the 2 metabolic effects of epinephrine?

A

1) Mobilizes carbohydrates and fats to make available to muscles
2) Stimulates hepatic gluconeogenesis and glycogenolysis (glycogen to glucose)

183
Q

1) What does epinephrine do for the heart and respiratory activity?
2) What does epinephrine promote? (3 things)

A

1) Stimulates activity, and provides the energy to sustain that activity.
2) Mental alertness, sweating (heat dissipation), pupillary dilation

184
Q

1) What structure is composed of both exocrine and endocrine tissues?
2) What is its exocrine function?
3) Where are its endocrine cells? How much of the pancreas do they make up?

A

1) Pancreas
2) Alkaline digestive secretion
3) Scattered throughout the pancreas in tiny “island” clusters called islets of Langerhans; 1-2% of total pancreas mass

185
Q

What 5 types of endocrine cells are scattered throughout the pancreas in tiny “island” clusters called islets of Langerhans?
List what each type does and what percent each makes up

A

1) Beta cells (60%) secrete insulin
2) Alpha cells (25%): produce glucagon
3) Delta cells (10%): somatostatin synthesis
4) Gamma cells (4%): pancreatic polypeptide hormone, poorly understood
5) Epsilon cells (1%): release ghrelin
BADGE

186
Q

1) What hormone inhibits the digestive system through various means?
2) How does it do this? (2 ways)
3) Increases in what 2 things can cause this hormone to be released? What type of feedback is this?

A

1) Somatostatin
2) Decreases nutrient digestion and absorption and uses paracrine action
3) Blood glucose and amino acids; negative feedback

187
Q

Paracrine action of somatostatin decreases pancreatic secretion of what 3 things?

A

Insulin, glucagon, and somatostatin itself

188
Q

1) What does insulin lower and promote the storage of? (3 things)
2) What does it promote conversion to? (3)

A

1) Blood glucose, fatty acids, and amino acids
2) Glycogen, triglycerides, and protein

189
Q

What are the 4 effects of insulin that lower blood glucose and promote storage?
[hint: facilitates 1 process, stimulates 1, and inhibits 2]

A

1) Facilitates glucose uptake into most cells
2) Stimulates glycogenesis (conversion of glucose to glycogen) in skeletal muscle and liver
3) Inhibits glycogenolysis (breakdown of glycogen into glucose)
4) Inhibits gluconeogenesis (conversion of amino acids into glucose)

190
Q

What effect does insulin have on fat? What are the 4 ways it does this?

A

Lowers blood fatty acids and promotes triglyceride storage
1) Enhances fatty acid uptake into adipose tissue
2) Increases transport of glucose into adipose tissue
3) Promotes triglyceride synthesis
4) Inhibits lipolysis

191
Q

How does insulin affect protein? What are the 3 ways it does this?

A

Lowers blood amino acid levels and enhances protein synthesis
1) Promotes amino acid uptake
2) Increases amino acid incorporation into protein
3) Inhibits protein degradation

192
Q

1) Primary control of insulin secretion is a negative feedback loop between what 2 things?
2) How does glucose affect this?
3) What is the answer to #2 one of the few examples of?

A

1) Beta cells and blood glucose levels
2) Initiates a chain of events that alters beta cell membrane potential
3) Non-muscle non-nervous tissue undergoing changes in membrane potential

193
Q

Elevated amino acid levels stimulate ________ secretion

A

insulin

194
Q

1) What innervates islets of Langerhans?
2) What does this innervation do?

A

1) Richly innervated by parasympathetic and sympathetic fibers
2)
P: increases secretion
S: decreases secretion

195
Q

1) What are released in response to food increased insulin secretion? What kind of mechanism is this?
2) Give 2 specific examples of what’s released and what they’re called

A

1) GI hormones; feed forward mechanism
2) Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1); called incretins

196
Q

1) What is the most common endocrine disorder?
2) What are its two variants? Define each.

A

Diabetes mellitus:
1) Type 1: lack of insulin
2) Type 2: increased insulin, reduced sensitivity; effectively a lack of response to insulin

197
Q

1) What is is the hallmark of diabetes mellitus (both kinds)?
2) What do both types of diabetes mellitus lead to?
3) What does this mean for the cells?
4) What does this cellular effect lead to?

A

1) Hyperglycemia
2) Decreased glucose uptake
3) The cells are glucose-starved, despite abundance in the blood
4) Glucose-starved cells lead to appetite stimulation

198
Q

1) In diabetes the body can be unable to use glucose, so the body switches to what for energy?
2) What organ converts this substance into a usable energy source? What is this usable energy source called and what is one of their properties?
3) What can the use of this extra energy source eventually lead to? In what type of diabetes is this more common in?

A

1) Fatty acids
2) Liver; into ketone bodies; acidic.
3) Metabolic acidosis; esp. in T1DM bc T2DM usually has enough insulin action to suppress this

199
Q

1) What can the use of fatty acids for energy in diabetes lead to? In what type of diabetes is this more common in?
2) What else does diabetes lead to the breakdown off for energy?

A

1) Can lead to coma or death, esp in T1DM
2) Proteins to free amino acids

200
Q

1) What causes T1DM? What cell types are involved?
2) Why does this happen?

A

1) Autoimmune process involving beta cell destruction by T lymphocytes
2) Reason unclear, possibly genetic/epigenetic

201
Q

1) What mediates T2DM? Define this concept.
2) What do many T2DM patients have? What is this?

A

1) Insulin resistance: down-regulation of insulin receptors in the presence of chronically elevated insulin
2) Metabolic syndrome: cluster of features that predispose to heart disease

202
Q

1) Give examples of metabolic syndrome symptoms
2) How many does a pt have to have to be diagnosed?

A

1) Abdominal obesity, high triglycerides, low HDL, high blood glucose, high blood pressure
2) 3 out of 5

203
Q

1) In general, what does glucagon do?
2) What does glucagon do regarding glucose production and blood glucose?
3) How specifically does it have this effect on glucose? (3 processes)

A

1) Opposes the actions of insulin
2) Increases hepatic glucose production, increasing blood glucose
3) Decreasing glycogenesis, promoting glycogenolysis, stimulating gluconeogenesis

204
Q

1) What does glucagon promote and inhibit regarding fats? What effect does this have?
2) What does glucagon promote and inhibit regarding protein?

A

1) Promotes lipolysis, inhibits triglyceride synthesis
-Increases blood fatty acids
3) Inhibits protein synthesis, promotes protein degradation

205
Q

Give 2 examples of incretins

A

1) Glucose-dependent insulinotropic peptide (GIP)
2) Glucagon-like peptide 1 (GLP-1)

206
Q

List 3 ways glucagon opposes the actions of insulin

A

1) Increases hepatic glucose production, increasing blood glucose
2) Promotes lipolysis, inhibits triglyceride synthesis
3) Inhibits protein synthesis, promotes protein degradation

207
Q

1) When does glucagon secretion increase? What is this in response to?
2) What is the “hormone of fasting” and what does it promote?
3) What is the “hormone of feasting” and what does it promote?
4) What do these fasting and feasting hormones do?

A

1) In postabsorptive state; hypoglycemia
2) Glucagon, promotes retrieval
3) Insulin, promotes storage
4) Work together to regulate nutrients

(PA school) Human Physiology (35 decks)

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