Cell Signaling/Endocrine Flashcards

1
Q

describe the three major types of signaling and give a biological example of each

A

paracine signaling: signaling molecules target adjacent cells
synaptic signaling: signaling molecules (NT) diffuse across synapse to neuron (ACH –> NMJ)
endocrine signaling: signaling molecules travel long distances via bloodstream (hormone)

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2
Q

what determines if a hormone will bind to an intracellular vs cell surface receptor

A
  1. size
  2. solubility
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3
Q

what do kinases and phosphatases do?

A

kinases: enzymes that add a PO4 3-
phosphotases: enzymes that remove PO4 3-

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4
Q

define affinity.

how does KD relate to affinity.

A

the likelihood of something going to bind. 1/KD is the affinity. The lower the KD the higher the affinity.

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5
Q

define specificity.

A

binds only one or a specific family of ligands

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6
Q

define saturability.

A

how many receptors are bound by a ligand

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7
Q

define law of mass action

A

[L] + [R] –> [LR] –> biological response

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8
Q

can ion channels activate intracellular mechanisms?

A

yes

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9
Q

give examples of cell surface receptors

A
  1. ligand gated ion channels (nAChR)
  2. G protein coupled receptors (mAChR, GnRH-R)
  3. serine/threonine receptors (TGFbeta R)
  4. tyrosine kinase receptors (Insulin R)
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10
Q

what type of hormones bind to cell surface receptors

A

protein, peptide and fatty acid derived hormones; large, water soluble
also catecholamines

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11
Q

are cell surface receptors or intracellular receptors faster?

A

cell surface receptors

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12
Q

give examples of intracellular receptors

A
  1. nuclear receptors
  2. mineralocorticoid receptor
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13
Q

what type of hormones bind to intracellular receptors

A

steroids, amino acids, thyroid hormones (small, lipid soluble)

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14
Q

what can cell surface receptors do

A

protein transport, protein synthesis, secretion, ion channels, and gene expression

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15
Q

name two receptors that bind the same ligand

A

nAChR and mAChR

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16
Q

describe adrenergic receptors (alpha 1, alpha 2 and beta) in regard to their G protein and intracellular/biological response

A

alpha 1 - Galpha q/11, increases Ca+2, smooth muscle contraction
alpha 2 - Galpha i, inhibits cAMP, smooth muscle contraction
beta - Galpha s, increases cAMP, heart muscle contraction, smooth muscle relaxation and glycogenolysis

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17
Q

describe muscarinic receptors (1,3, & 5 and 2,4) in regard to their G protein and intracellular response

A

M1,3,5 - Galpha q/11, increase Ca2+ & MAP kinases
M2,4 - Galpha i, inhibits cAMP

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18
Q

what determines if there is a biological response to a hormone

A
  1. specificity
  2. affinity
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19
Q

what are the major classes of hormones

A
  1. protein/peptide hormones
  2. fatty acid hormones
  3. steroid hormones
  4. modified amino acids
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20
Q

how is diabetes an L vs R problem?

A

type 1 diabetes - no beta cells of pancreas so no production of insulin (L problem)
type 2 diabetes - dysfunctional insulin receptors (R problem)

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21
Q

what do intracellular receptors do?

A

regulate gene transcription

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22
Q

what describes a hormones interaction with a nuclear receptor?

A

slow
dimerized HR act as transcription factor

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23
Q

what is the importance of the hypothalamic pituitary vascular system

A

hypothalamus has portal system with anterior pituitary (two capillaries); hypothalamus synthesizes/secretes neurhormones to AP and AP releases trophic hormones into blood stream to target organs

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24
Q

how does the hypothalamus send hormones to the posterior pituitary

A

through neurons, they originate in hypothalamus and axons terminate in posterior pituitary

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25
Q

where are gonadotropes located and what do they secrete

A

anterior pituitary
LH/FSH

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26
Q

where are thyrotropes located and what do they secrete

A

anterior pituitary
TSH

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27
Q

where are somatotropes located and what do they secrete

A

anterior pituitary
Growth Hormone

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28
Q

where are corticotropes located and what do they secrete

A

anterior pituitary
ACTH

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29
Q

where are lactotropes located and what do they secrete

A

anterior pituitary
prolactin (Prl)

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30
Q

what cell types are in the posterior pituitary and what hormones do they release

A

neurons
oxytocin & vasopressin/ADH

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31
Q

Peptide Hormones
solubility:
receptor:
precursor(s):
examples:

A

solubility: soluble
receptor: cell surface receptors
precursor(s): preprohormone (ER) & prohormone (vesicle)
examples: hypothalamic releasing hormones, pituitary hormones, GI/pancreatic hormones, calcitonin, PTH

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32
Q

Fatty Acid Hormones
solubility:
receptor:
precursor(s):
examples:

A

solubility: soluble
receptor: cell surface receptors
precursor(s): *phospholipids + *phospholipase –> *arachidonic acid + *cyclooxygenase (COX) –> eicosanoids
examples: prostaglandins, prostacyclins, leukotrienes, thromboxanes

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33
Q

Steroid Hormones
solubility:
receptor:
precursor(s):
examples:

A

solubility: insoluble
receptor: intracellular receptors
precursor(s): cholesterol & pregnenolone
examples: glucocorticoids, mineralocorticoids, testosterone, estrogen, vitamin D3

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34
Q

Amino Acid Derived Hormones
precursor(s):
examples & their receptors

A

precursor(s): tyrosine
examples:
T3/T4 (intracellular R, insoluble)
catecholamines (E/NE) (cell surface receptor)

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35
Q

Calcitonin
source:
main effect:

A

source: parafollicular cells of thyroid gland (primary) & GI/lung tissues
main effect: decreases calcium in blood via
1. inhibits osteoclasts (suppressing resorption) & increasing Ca deposition in bones
2. inhibits tubular reabsorption of Ca & PO4 3- so increase Ca loss in urine

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36
Q

Parathyroid Hormone
source:
main effect:

A

source: chief cells of parathyroid gland
main effect: increases blood calcium via…
1. tubular reabsorption of Ca in kidney
2. vitamin D production from kidney increases Ca absorption in SI
3. osteoclast resorption

37
Q

describe primary and secondary hyperparathyroidism

A

primary: excess PTH from parathyroid gland = demineralization of bone
secondary: excess Ca loss from renal disease = stimulates PTH

38
Q

what are the calcium pools (calcium storage)

A
  1. intracellular Ca (available for signaling, enzyme activation & muscle contraction)
  2. blood & ECF (unavailable for function bc bound to protein)
  3. bone (majority unavailable)
39
Q

what are the calcium organs

A
  1. kidney
  2. small intestine
  3. bone (major)
40
Q

vitamin D3
source:
main effect:

A

source: stimulated by PTH in the distal tubule of kidney
main effect: increases blood [Ca2+] via…
1. increasing calbindin so SI can increase its absorption
2. initiates transcription for bone to release Ca2+ and PO4 3- via mineralization

41
Q

describe the pathway of inactive and active vitamin D3

A

sunlight –> liver (inactive) –> kidney (active)

42
Q

describe glucose regulation

A

insulin (from beta cells) decrease blood glucose by transporting glucose into fat/muscles and store as glycogen

glucagon (alpha cells) increase blood glucose by increasing glycogenolysis and gluconeogenesis

43
Q

differentiate between adenohypophysis and neurohypophysis

A

adenohypophosis: anterior pituitary origin from oral ectoderm from roof of mouth

neurohypophysis: posterior pituitary origin from neural tissue from floor of diencephalon

44
Q

what is the 2 cell 2 gonadotropin theory in the ovary?

A

LH stimulates theca cells are to synthesize androgens and FSH stimulates granulosa cells to convert androgens to estrogen

45
Q

distinguish different components of male and female reproductive tract

A

testes –> epididymis –> wolffian duct (vas deferens) –> urethra

ovaries –> mullerian duct (uterine tubes) –> uterus –> cervix –> vagina

46
Q

in males what does the external genitalia and prostate gland need?

A

conversion of testosterone —> DHT via 5alpha-reductase

47
Q

in males what does the internal reproductive tract depend on

A

testosterone and AMH

48
Q

where is sperm produced? where do they mature?
where is T produced?

A

produced in seminiferous tubules
mature in epididymis
interstitial space

49
Q

what is required for spermatozoa development

A

counter current heat exchange

50
Q

what transporters transport glucose into muscle and fat cells
what is it dependent on
what organs are they not in

A

GLUT4
insulin-dependent
NOT in brain or liver

51
Q

what species is diabetes mellitus more present in?
pathophysiology?

A

middle/older aged dogs/cats (female dogs more likely than males)
obesity, chronic inflammation, amyloid deposition in islets (cats) and viral infection

52
Q

Oxytocin
effect?
regulation?

A

effect: milk ejection, uterine smooth muscle contraction, maternal behavior
regulation: stimulated by physical & psychological stimuli; inhibited by catecholamines (stress)

53
Q

Vasopressin/Antidiuretic Hormone (ADH)
effect?
regulation?

A

effect: increases water reabsorption by increasing the amount of aquaporin channels in the collecting tubule which increases BP/BV and decreased urine output
regulation: stimulated by increased plasma osmolarity and decreased BP/BV; inhibited by alcohol, increased BP/BV, or decreased plasma osmolarity

54
Q

when is ADH secreted?

A

before thirst

55
Q

contrast central diabetes insipidus vs nephrogenic diabetes insipidus

A

DI: deficiency in ADH
central: no ADH from posterior pituitary
nephrogenic: kidney not responding to ADH due to renal disease or VP receptor/ aquaporin mutation

56
Q

Prolactin
cell that secretes it:
stimulation:
inhibition:
effects:

A

cell that secretes it: lactotropes
stimulation: suckling
inhibition: dopamine
effects: mammary gland growth, stimulates lactogenesis, and stimulates gene transcription that encode milk proteins

57
Q

describe the hypothalamic-pituitary-thyroid axis

A

TRH (hypo)
TSH (AP)
T3/T4 (thyroid gland)

58
Q

T3 primary effects

A

increase BMR, development of fetal/neonatal brain, stimulates growth

59
Q

T3 secondary effects

A

increased heart rate, cardiac output/contractility, vasodilation, CNS/mental state (anxiety/depression), increased GFR, and reproduction/fertility negatively impacted

60
Q

hyperthyroidism
symptoms:
treatment:
more common in:
primary:

A

symptoms: weight loss, angry, anxious, increased appetite
treatment: elimination of thyroid gland, radioactive I131, or inhibit thyroid perioxidase
more common in: cats
primary: benign, hyperplastic thyroid tissue

61
Q

hypothyroidism
symptoms:
treatment:
more common in:
primary, secondary, tertitary:

A

symptoms: obesity, poor coat, lethargy, cold
treatment: supplements of I, T3, or Selenium
more common in: dogs
primary, secondary, tertitary: thyroid disease/iodine deficiency, TSH problem, TRH problem

62
Q

describe the hypothalamic-pituitary-adrenal axis

A

CRH (hypo)
ACTH (AP)
cortisol (adrenal cortex)

63
Q

what is the precursor for ACTH

A

POMC

64
Q

what is the transport protein that binds cortisol to plasma proteins

A

transcortin

65
Q

what zone produces mineralocorticoids

A

zona glomerulosa (outer layer)

66
Q

what zone produces glucocorticoids

A

zona fasiculata (middle layer)

67
Q

what zone produces sex steroids

A

zona reticularis (inner layer)

68
Q

what are the effects of cortisol

A

1.metabolism: increased gluconeogensis, mobilize aa, inhibit glucose uptake, increase fat breakdown
2. antiinflammatory/ immunosuprresive
3. other: fetal development of type 2 alveolar cells, cognitive function, fear, bone formation, wound healing, Ca absorption

69
Q

what are the effects of aldosterone (mineralocorticoid)

A

stimulates transcription of Na/K ATPase Pump = increase Na reabsorption and K secretion in kidney
stimulated by increase in EC [K] and angiotensin II

70
Q

hyperadrenocortisim
cortisol levels:
effect on CRH and ACTH:
primary:
iatrogenic:

A

cortisol levels: high
effect on CRH and ACTH: decreased due to (-) feedback
primary: pituitary dependent (excess ACTH) or adrenal tumors
iatrogenic: excess glucocorticoid therapy

71
Q

hypoadrenocortism
cortisol levels:
effect on CRH and ACTH:
primary:
iatrogenic:

A

cortisol levels: low
effect on CRH and ACTH: increased
primary: injury to adrenal gland tissue, infection or autoimmune
iatrogenic: discontinuation of corticosteroid therapy

72
Q

growth hormone
hypothalamic hormone:
anterior pituitary cell type:
stimulation:
inhibition:
direct growth effects:
indirect growth effects:
metabolic effects:

A

hypothalamic hormone: GHRH
anterior pituitary cell type: somatotropes
stimulation: ghrelin (stomach)
inhibition: somatostatin
direct growth effects: liver, differentiation of chondrocytes
indirect growth effects: bone, muscle, adipose, proliferation of chondrocytes/muscle growth
metabolic effects: protein anabolism, fat catabolism, carb metabolism

73
Q

pituitary dwarfism

A

lack of all pituitary hormones (GH, TSH, ACTH)

74
Q

giantism

A

excess GH from birth before epiphyseal closure (swelling, enlarged peripheral nn, delayed puberty, hypogonadotropic hypogonadism)

75
Q

acromegaly

A

late onset excess GH due to GH secreting pituitary tumor (organ hypertrophy or bony changes, insulin resistance, *male cats)

76
Q

describe the female hypothalamic-pituitary- gonadal axis

A

GnRH (hypo)
LH and FSH (AP gonadotropes)
Estrogen & Inhibin (theca and granulosa cells)

77
Q

what is the dominant follicle first to have/do

A

dominant follicle first to express LH receptor and produce inhibin

78
Q

what causes ovulation

A

dominant follicle produces large amounts of estrogen resulting in an LH surge (+) feedback, this LH surge results in release of the follicle

79
Q

what subunit do gonadotropes and thyrotropes share?

A

they share the alpha glycoprotein subunit (alpha-GSU)

differ in beta subunits

80
Q

what produces the large amount of progesterone during the estrous cycle

A

the corpus lutea (yellow body)

81
Q

describe the follicular phase

A
  1. egg w/ cohort of follicles present and produce FSH to stimulate follicle growth
  2. domintant follicle has LHR and produces inhibin to prevent recruitment of additional follicles
  3. dominant becomes mature and produces E and Inhibin
  4. large amount of E = LH surge
  5. LH results in release of follicle from ovary
82
Q

describe the luteal phase

A
  1. formation of corpus luteum produces P and E, and inhibin
  2. if no pregnancy, PGF2alpha-MRP = death to CL and resets
  3. P and E decrease, LH/FSH increase
83
Q

what day does ovulation begin in animals

A

day zero

84
Q

what hormone does the pre-ovulatory follicle secrete

A

estrogen

85
Q

what are the effects of estrogen

A

follicle growth
secondary sex characteristics
growth/proliferation of epihelial lining of repro tract
feedback to brain
inhibits milk production

86
Q

what are the effects of progesterone

A

prepares endometrium from embryo implantation
breast growth
negative feedback to brain
inhibits milk production
inhibits myometrial contractions

87
Q

most common birth defect of male genitalia

A

cryptochordism

88
Q

effects of testosterone

A

stimulate spermatogenesis
maintain wolffian duct/accessory glands
external genitalia, secondary sex characteristics
stimulate metabolism
affect CNS function/behavior