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PSL300 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Adrenal medulla

A

Modified sympathetic ganglia, secreted catecholamines

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2
Q

Adrenal cortex

A

Steroid factory, it secretes steroid hormones

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3
Q

Main catecholamine

A

epinephrine, it is secreted in enough quantity to exert effects

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4
Q

chromaffin cell

A

post ganglionic sympathetic neuron

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5
Q

Catecholamines

A

Epinephrine, norepinhrine, dopamine

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6
Q

Stimulus for release of epinephrine

A

Activation of the sympathetic nervous system - fight or flight response

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7
Q

role of epinehrine in skin, intestine, kidney

A

intestine: muscle relaxation, arteriole contriction
skin and kidney: arteriole contriction

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7
Q

role of epinehrine in liver and fat

A

liver: glucose release (via glycogenolysis)
fat: fatty acid release

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8
Q

role of epinehrine in muscle, brain and resp

A

muscle: arteriole contraction (alpha receptors), arteriole relxation (beta receptors)
brain: increased alertness
resp: bronchodilator

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9
Q

Reactions of anaphylactic shock

A

bronochospasm (contriction of airways), decrease in blood pressure

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10
Q

How does epipen counteract symptoms of anaphylactic shock?

A

bronchodilation, vasoconstriction in skin, kidney, intestine and vasodilation in skeletal and cardian muscles.

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11
Q

Parts of adrenal cortex

A

Zona glomelurosa, zona facilutata, zona reticularis

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12
Q

what does zona glomerulosa secrete

A

aldosterone

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13
Q

what does zona fasciculata secrete

A

glucocorticoids - cortisol

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14
Q

Weak androgens

A

Less than 20% activity of testosterone but they are converted to more potent androgens and estrogens in peripheral tissue

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14
Q

what does zona reticularis secrete

A

sex steroids

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15
Q

What increases androgen production?

A

ACTH

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16
Q

physiological role of androgens in children

A

Male prenantal development, also contribute to andrenarche - pubic hair, body odor, oily skin, acne - for both males and females

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17
Q

physiological role of androgens in adult men

A

no physiological role - testes provide androgens for males

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18
Q

physiological role of androgens in women

A

although ovaries provide estrogen, androgens maintain pubic and axillary hair, source of estrogen after menopause

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19
Q

Aldosterone

A

its actd on the distal tubule of increase Na+ absorbtion and K+ secretion

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20
Q

Cortisol

A

Main glucocoricoid, secreted by zona fasiculata

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21
Q

role of cortisol

A

mediation long term stress

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22
Q

what is the control pathway of secretion of cortisol

A

hypothalamic-adrenal-pituatary pathway

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23
Q

diurnal rhythm

A

continious secretion of costisol

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24
Q

short term stress

A

nerve impulse –> spinal cord –> preganglionic sympathetic fibres –> adrenal medulla (secretes amino acid based hormones) –> catecholamines

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25
Q

short term stress response

A
  1. heart rate and blood pressure increases
  2. bronchioles dilate
  3. liver converts glycogen to glucose and releases glocse to blood
  4. blood flow chnages, reducing digestive system activity
  5. metabolic rate increases
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26
Q

prolonged stress

A

hypothalamus –> CRH released –> corticoptropic cells of anterior pituatary –> ACTH –> targets blood –> adrenal cortex –> steroid horones secreted

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27
Q

long term stress response

A
  1. kidneys retain sodium and water
  2. blood volume and blood pressure rise
  3. proteins and fats converted to glucose or broken down for energy
  4. blood glucose increases
  5. Immune system supressed
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28
Q

What is cortisol protective against?

A

Hypoglycemia through the permissive effect

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29
Q

Metabolic effect of cortisol

A

they primarily catabolic
1. promotes glucogenesis
2. brakdown of skeletal muscle proteins
3. enhances lipolysis
4. supresses the immune system

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30
Q

How is cortisol used as a drug to supress the immune system?

A
  1. inhibit inflammatory responses
    specififc uses: poison ivy, allergies, asthma
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30
Q

cortisol regulation

A

it is regulated through the negative feedback loop.
cortisol supresses both CRH and ACTH production, inturn stopping its own production.

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31
Q

what can long term use of cortisol drugs do

A

inhibition of ACTH secretion and atrophy cortisol secretig cells

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32
Q

addisons disease (adrenal insifficiency)

A

hyposecretion of adrenal steroid hormones.
it causes destruction of the adrenal by autoimmunity, sometimes infection

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33
Q

symptoms of addisons disease

A

hypotension (low aldosterone –> low Na + reabsorbtion –> increased water loss –> low blood volume) , hypoglycemia. (low cortisol –> low blood glucose levels)

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34
Q

Cushings syndrome - excess cortisol

A

caused by tumours, cortisol therapy

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35
Q

symptoms of cushings syndrome

A

hyperglycemia, muscle protein breakdown, lipolysis but build up of fat on trunk and facem increased apetite, mood elevation but then followed by depression and problems with learning

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35
Q

What does excessive water loss do?

A

It can cause disease (hypotension/shock)
there is less extracellular fluid –> decreased blood pressure

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36
Q

How is water distributed in the body?

A

2/3 in intracellular fluid
1/3 in extracellular fluid - 75% interstitial and 25% plasma

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37
Q

Symptoms of excessive water loss

A

confused, chess pain, low blood pressure, no urine

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38
Q

What does too much water in the body do?

A

back up in legs, abdomen and lungs
it can cause difficulties walking and breathing

39
Q

How is urine formed in the nephron?

A

Filtration, reabsoprtion and secretion

40
Q

What is the nephron/kidney responsible for

A
  1. excreting waste
  2. regulating blood volume
  3. controlling electrolytes
  4. blood pH
  5. Vitamin D (via PTH)
41
Q

Mechanism in nephron

A
  1. After fluid (isoosmotic) leaves the proximal tubule, it goes into the descending limb of the loop of henle. here the fluid gets more conc s only water is reabsorbed.
  2. in the ascending limb ions are reabsorbed (hypoosmotic)
  3. in the distal tubule, hormones manage the reabsorption of water and ions.
  4. lastly, urine osmolarity will depend on reabsorption in the collecting duct; most reabsorption happens here.
42
Q

Osmolarity

A

Concentration of a solution expressed as total number of solute particles per litre

43
Q

Function of Vasopressin

A

Increases water reabsorption in the kidneys - conserves body water, water balance and fluid homeostasis, increases blood volume and blood pressure

also regulates the permeability of cells in the kidney - increased permeability - high reabsorption and low urine output

44
Q

Function of Aldosterone

A

increase Na+ reabsorbtion and K+ secretion
it acts on the distal tubule and collecting duct

45
Q

Function of Atrial Netriuetic peptide and BNP

A

decrease Na+ and water reabsorption ( lowers blood pressure). Increase K+ reabsorption.

it suppresses renin, aldosterone and vasopressin

46
Q

where is vasopressin synthesized and secreted from

A

Syntheisized in the hypothalamus and secreted from the posterior pituitary

47
Q

Other name for vsaopressin

A

Antidiuretic hormone ADH

48
Q

Bond in vsaopressin

A

disulfide bond between cys-cys

48
Q

Stimuli for vasopressin release and how it is detected

A

Low blood pressure - detected by reduced stretch of atrial walls and aortic and carotid arteries
high plasma osmolarity - detected by osmoreceptors in hypothalamus - MODT IMP STIMULUS

49
Q

Regulation of vasopressin release

A
  1. low blood pressure and high osmolarity are detected
  2. PASSES TO HYPOTHALAMIC neurosecretory cells
  3. passed neurosecretory terminals in pituitary
  4. ADH released
  5. increased H2O permeability and water reabsorption takes place in collecting duct
50
Q

What does increase in vasopressin cause?

A

thirst

51
Q

process of water pore binding and reabsorption of water

A
  1. vasopressin binds to receptor
  2. cAMP released - signal cascade caused
  3. aquaporin 2 water pores form on membrane of collecting duct lumen
  4. water is reabsorbed into blood
  5. osmolarity of blood reduces
51
Q

Where does vasopressin insert water pores?

A

Vasopressin inserts water pores into distal convulated tubule or in collecting duct cell membranes

52
Q

where is aldosterone sythesized?

A

adrenal cortex

53
Q

How is aldosterone synthesis controlled?

A

it is controlled by negative feedback: simple (K+, osmolarity) and complex (renin-angiotensin II)

53
Q

what are stimulators for aldosterone synthesis?

A

High K+ in plasma - most important stimulus
Angiotensin II (via blood pressure) - low bp
through RAAS - renin angiotensinogen pathway

53
Q

regulation of aldosterone synthesis and action

A
  1. high K+ in plasma and low blood pressure (activates RAAS pathway) are the stimuli
  2. Causes adrenal cortex to synthesize aldosterone
  3. aldosterone goes to P cells of collecting duct
  4. this causes increased Na+ reabsorption and K+ secretion
54
Q

what is the inhibitor for aldosterone synthesis?

A

high osmolarity in extracellular fluid

54
Q

What does aldosterone act on?

A

distal tubule and collecting duct

55
Q

What does aldosterone prevent degradation of?

A

Apical Na+ channel

56
Q

MAIN aldosterone action

A
  1. aldosterone combines with a cytoplasmic receptor
  2. Hormone-receptor complex initiates transcription in the nucleus.
  3. Translation and protein synthesis make new channels and pumps.
  4. aldosterone-induced proteins module existing channels and pumps
  5. result is increased Na+ reabsorption and K+ secretion
57
Q

Renal juxtaglomerular cells

A

they secrete the enzyme renin when blood pressure falls

57
Q

What does aldosterone increase expression of

A

Na+ and K+ channels and Na+/k+ ATPase

58
Q

Renin-angiotensin pathway

A
  1. the drop in blood pressure is sensed by the kidney
  2. renin is released
  3. renin cleaves angiotensinogen (produced by liver) to produce angiotensin I
  4. ACE produced by the lungs will cleave angiotensin I to produce angiotensin II
  5. angiotensin II is active and it
58
Q

what does angiotensin do

A
  1. increases vsaopressin
  2. stimulates thirst
  3. potent vasoconstricutor
  4. increases proximal tube Na+ retention
59
Q

BNP

A

in ventricles (myocardial cells) and neurons

60
Q

Atrial Natriuretic peptide

A

in atria (myocardial cells) and neurons

61
Q

CNP

A

in the brain, pituitary, vessels, and kidneys

62
Q

ANP release

A
  1. increased blood volume causes increased atrial stretch
  2. myocardial cells stretch and release ANP
63
Q

ANP effect on hypothalamus

A

less vasopressin
therefore, high NaCl and water excretion. decreased blood volume and decreased BP.

64
Q

ANP effect on kidney

A

tubule: less Na+ reabsorption
afferent arteriole: greater glomerular filtration rate and decreased renin ( low blood pressure) - also decreased aldosterone

65
Q

ANP effect of adrenal cortex

A

less aldo sterone - greater nacl and water excretion, decreased blood volume, decreased blood pressure

66
Q

ANP effect on medulla oblongata

A

decreased sympathetic output - decreased blood pressure.

67
Q

Why is calcium critical for normal physiology ?

A
  1. intracellular signalling
  2. hormone secretion
  3. blood clotting
  4. neural excitability
  5. muscle contraction
  6. building and maintaining bone
68
Q

descibe calcium in bone

A

calcium in bone is mainly in crystals - hydroxyapatite
A small fraction is ionized and readily exchangeable with ECF and plasma.

68
Q

locations of calcium

A
  1. extracellular matrix
  2. extracellular fluid
  3. intracellular Ca2+
69
Q

Where does calcium have the ability to move?

A

between bone and ECF (both ways), kidney and ecf (both ways), cell and ecf (both ways), small intestine to ecf

70
Q

3 cells in bones

A

osteoblasts, osteoclasts and osteocytes

71
Q

osteoblasts

A

bone forming cells

72
Q

osteoclasts

A

break down bone
1. they are attached to bone matrix
2. they secrete HCl and proteases - low pH
3. acid and proteases break down the matrix
4. Ca2+ released becomes part of ionised Ca2+ pools - enters bloodstream

73
Q

osteocytes

A

maintain bone, they are retired osteoblasts that are surrounded by bone matrix

74
Q

making bone

A

creating calcium phosphate complexes ( calcium crystallization)

75
Q

bone dynamics

A
  1. osteoclast precursors –> osteoclast - they create pits - ACTIVATION
  2. osteoblast precursors fill in the pit, forming osteoid - REVERSAL and BONE FORMATION
76
Q

Osteoclast formation

A

RANKL on osteoclasts interact with RANK on osteoclast precursors.
differentiation nd fusion takes place forming osteoclast.

77
Q

RANK

A

receptor activator of nuclear factor kappa B

78
Q

RANKL

A

RANKL

79
Q

Osteoproteregin (OPG)

A

Secreted by osteoblasts, it blocks RANK and RANKL interaction - preventing formation of osteoclasts

80
Q

Action of Denosumab

A
  1. it specifically binds to RANKL
  2. mimics the effect of OPG
  3. mops up RANKL not letting it bind to osteoclasts
81
Q

3 hormones that control plasma Ca2+ levels and what do they act on

A

parathyroid hormone, calcitriol, and calcitonin
act on: bone kidneys digestive tract

82
Q

Where is parathyroid hormone released from

A

parathyroid glands - 4 tiny glands

83
Q

function of parathyroid hormone

A

increases plasma Ca2+ conc by effluc of Ca2+ from bone and decreased loss of Ca2+ in urine.
stimulus: low plasms conc

84
Q

What happens when Ca2+ is bound to Gq receptor

A

PTH secretion is inhibited
PTH synthesis is reduced

85
Q

PTH effects on bone

A
  1. PTH acts on osteoblasts by increasing cAMP to increase RANKL and decrease OPG expression
  2. More osteoclasts form leading bone resorption
86
Q

Organs critical in the development of cacitriol

A

Skin, Liver, Kidney

87
Q

What does calcitriol target to increase serum calcium?

A

intestine, bone, kidney

88
Q

Formation of calcitriol

A
  1. precursor of vit D3 (7-dehyrocholestrol) in skin needs UV light to transform to cholecalciferol (vit D3)
  2. In liver cholecalciferol transforms to 25-hydroxycholecalciferol.
  3. PTH acts on it and in kidney it becomes calcitriol (vitamin D3 hormone).
89
Q

How does cacitriol act?

A
  1. it increases Ca2+ uptake from small intestine
  2. renal Ca2+ reabsorption and mobilization from bone.
89
Q

Calcitriol and vitamin D nuclear receptor binding

A
  1. Calcitriol and vitamin D nuclear receptor bind
  2. in nucleus. the complex and retinoic acid receptor become a heterodmer.
  3. they then bind to the vitamin D response element on DNA
  4. transcription stimulated, mRNA formed.
90
Q

how is blood phosphate controlled?

A

PTH: increases phosphate release from bone and decreases phosphate reabsorption form kidney
calcitriol: increases phosphate absorption by intestine and reabsopriton by kidney.

PSL300 (19 decks)

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