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Anatomy and Phyisology > week 2 quiz review > Flashcards

week 2 quiz review Flashcards

1
Q

review of negative feedback loop

A

stimulus will produce a change in normal homeostasis; this is detected by sensors and this input travels along the afferent pathway to the control centre; control centre creates an output which is sent along the efferent pathway to an effector; the response of the effector decreases the original stimulus, thus maintaining homeostasis

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2
Q

stimulus

A

a change great enough to disrupt normal homeostasis conditions

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3
Q

receptors

A

contain sensors that detect the stimulus and create generators or receptors potentials; this information is sent along the afferent pathway to the control centre

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4
Q

bladder at rest

A

motor neurons are firing, detrusor muscle is relaxed, and internal and external sphincters are contracted

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5
Q

what parts of the bladder are controlled by the parasympathetic system?

A

the detrusor and the internal sphincters

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6
Q

what parts of the bladder are controlled by the somatic system?

A

the external sphincter

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7
Q

where is the micturition centre located?

A

the sacral spinal cord

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8
Q

what is the smooth muscle of the bladder

A

detrusor muscle and internal urethral sphincter

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9
Q

what does the contraction of the detrusor muscle do?

A

makes the bladder small, thus increasing pressure inside the bladder

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10
Q

what are the motor neurons synapsing with during bladder at rest?

A

the sphincter muscles, causing these structures to stay contracted

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11
Q

bladder when full

A

sensory receptors detect stretch and send this sensory input to sacral spinal cord; this causes two motor pathways to be stimulated by the parasympathetic system, the first is for the detrusor muscle to contract and the second is the relaxation of the internal sphincter; also during this time the firing of motor neurons ceases

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12
Q

what is the stimulus for ADH secretion?

A

high blood osmolarity and when water reabsorption is low

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13
Q

where and what are the receptors for ADH feedback loop?

A

the osmoreceptors in the hypothalamus

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14
Q

what releases ADH?

A

posterior pituitary gland which is controlled by the hypothalamus

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15
Q

where does ADH act?

A

in the late DCT and collecting ducts

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16
Q

what does ADH bind to?

A

V2 receptors on the basolateral membrane of collecting duct cells

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17
Q

what cells does ADH act on?

A

principal cells

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18
Q

result of ADH feedback loop

A

decreased plasma osmolarity and increased facultative water reabsorption

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19
Q

what produces renin?

A

the juxtaglomerular apparatus

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20
Q

what detects low blood pressure

A

JGA and baroreceptors in the carotid sinus

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21
Q

what is renin?

A

an enzyme that causes the conversion of angiotensinogen to angiotensin I

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22
Q

where is aldosterone released from?

A

the adrenal cortex

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23
Q

ANG II effects

A

increased sympathetic activity, vasoconstriction, increased Na and H20 reabsorption, ADH secretion via posterior pituitary gland, and aldosterone secretion

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24
Q

why is ANG II associated with sympathetic system?

A

because this systems helps to increase blood pressure by increasing heart rate and blood pressure by vasoconstriction; sympathetic system also causes the release of norepinephrine when ANG II binds to AT1 receptors, causing vasoconstriction

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25
Q

when happens when blood pressure conditions are normal?

A

blood vessels are dilated and intrinsic controls override extrinsic controls

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26
Q

what does ANG II bind to?

A

AT1 receptors

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27
Q

how does ANG II cause increased tubular reabsorption of Na and Cl?

A

through increasing Na, Cl, and K channels in the CT; also causes increased activity of the Na/H antiporter, as well as the Na/Cl symporter

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28
Q

what does aldosterone do in simple terms?

A

causes increased activity of the principal cells of the collecting ducts; increases Na, Cl, and K channels here

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29
Q

what does aldosterone bind to?

A

mineralocorticoid receptors within the cell cytoplasm

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30
Q

afferent vs efferent arteriole during normal conditions

A

afferent is typically larger in diameter than the efferent

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31
Q

afferent and efferent arterioles if BP needs to increase

A

afferent will constrict, allows decreased GFR

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32
Q

afferent and efferent arterioles if BP needs to decrease

A

efferent will constrict, allows increased GFR

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33
Q

what kind of hormone is aldosterone?

A

a steroid hormone

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34
Q

where does aldosterone act?

A

mainly in the CT (principal cells)

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35
Q

what is the primary purpose of aldosterone?

A

to increase the activity of the Na/K pump; but also increases sodium, potassium, and chloride channels

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36
Q

ANP

A

released when blood pressure is high from the atria of the heart; functions to inhibit renin and therefore decreased sodium reabsorption

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37
Q

what is a diuretic?

A

a type of drug that causes the kidneys to make more urine, decreasing blood volume and pressure as a result

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38
Q

transport proteins involved in aldosterone mechanism?

A

Na/K pump, Na channels, K channels, Cl channels, and aquaporins

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39
Q

where do osmotic diuretics work?

A

in the PCT

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40
Q

how do osmotic diuretics work?

A

by blocking the sodium-glucose symporter on the apical surface through using mannitol (similar structure to glucose)

41
Q

what water reabsorption are osmotic diuretics associated with?

A

obligatory

42
Q

where do thiazide-type drugs work?

A

in the DCT

43
Q

how do thiazide-type drugs work?

A

through blocking the Na and Cl symporter on the apical side in the DCT

44
Q

what water reabsorption are thiazide-type diuretics associated with?

A

facultative

45
Q

where do loop diuretics work?

A

in the ascending limb

46
Q

how do loop diuretics work?

A

block the Na-K-2Cl symporter on the apical side

47
Q

what water reabsorption are loop diuretics associated with?

A

facultative

48
Q

where do potassium-sparing diuretics work?

A

in the CT

49
Q

how do potassium-sparing diuretics work?

A

they limit the activity of K channels, also causing the Na/K pump to cease; cause the tubule cells to retain more potassium and secrete more sodium

50
Q

what water reabsorption are potassium-sparing diuretics associated with?

A

facultative

51
Q

3 major fluid compartments

A

intracellular fluid, interstitial fluid, and intravascular fluid

52
Q

order of fluid compartments holding the most fluid to the least

A

intracellular fluid > interstitial fluid > intravascular fluid

53
Q

solute concentrations higher in the interstitial fluid and blood plasma

A

Na, Cl, and Ca

54
Q

solute concentrations higher in the cell

A

K, HCO3, Mg, HPO4, and SO4

55
Q

what is released by the kidneys when there are high calcium levels?

A

calcitonin; causes more bones to be built

56
Q

what is released by the kidneys when there are low calcium levels?

A

calcitriol; causes more absorption of calcium from foods in the GI tract

57
Q

negative feedback loop associated with PTH

A

PTH released from parathyroid gland when calcium levels are low; this causes osteoclasts to degrade bone matrix and also for kidneys to release calcitriol

58
Q

where is calcitonin released from?

A

parafollicular cells

59
Q

water input breakdown

A

60% beverages, 10% metabolism, 30% foods

60
Q

water output breakdown

A

60% urine, 28% insensible losses, 8% sweat, and 4% feeces

61
Q

thirst mechanism

A

increased plasma osmolarity (and dry mouth) will activate osmoreceptors in the hypothalamus which will activate the hypothalamic thirst centre; ingestion of water will cause mouth and throat to moisten and for intestines to stretch, allowing for water to be reabsorbed from the GI tract, decreasing plasma osmolarity

62
Q

excess hydration

A

causes ECF osmotic pressure to drop (lower concentration of solutes), causing water to move into the cells and swelling them

63
Q

dehydration

A

cells will shrink and ECF osmolarity increases, causing water to move into ECF from cells

64
Q

acids

A

have higher concentrations of H+ and tend to donate H+

65
Q

bases

A

have higher concentrations of OH- and tend to donate OH-

66
Q

example of a strong acid

A

HCl

67
Q

example of a strong base

A

KOH

68
Q

pH scale

A

1-14; it is a log scale so moves up a factor rather than in a linear fashion

69
Q

buffer systems

A

these convert strong acids and bases into weak ones

70
Q

what is a buffer?

A

a solution that can resist pH change upon the addition of acid or base components; usually consist of weak acids or bases with a salt

71
Q

is HCO3- weak or strong?

A

it is a weak base

72
Q

is H2CO3 weak or strong?

A

it is a weak acid

73
Q

do strong acids and bases dissociate easily or not?

A

easily

74
Q

example of buffer system with Na and why does this work?

A

HCl + NaHCO3 > H2CO3 + NaCl; this works because bicarbonate is a weak base that reacts with a strong acid to produce a weak acid and a salt, thus increasing the pH

75
Q

how do salts form?

A

when an acid reacts with a base in a neutralisation reaction; ex. HCl + KOH > H20 + KCl

76
Q

low pH 2 pathways

A

either involves Na/H antiporter and HCO3 carrier in the PCT or H pump and HCO3/ Cl antiporter in the CT (intercalated cells) on apical surface; brings H+ into urine and HCO3 into bloodstream

77
Q

high pH pathway

A

involves CT and intercalated cells and proton pump is located on the basolateral side and send protons into the bloodstream; at the same time HCO3/ Cl antiporter moves HC3O into the urine and Cl into the cell

78
Q

what is HCO3 usually cotransported with?

A

Cl

79
Q

negative feedback loop for low blood pH

A

chemoreceptors in the medulla and heart send signals to the inspiration centre in the medulla; causes the diaphragm to contract and thus more CO2 to be exhaled

80
Q

why does exhaling CO2 increase blood pH?

A

the less CO2 in the blood, the less H2CO3 will form, and thus less H+ in the blood

81
Q

does HCO3 move in or out of blood when low pH?

A

into the blood

82
Q

carbonic anhydrase

A

enzymes that allow for the bicarbonate shift reaction to occur

83
Q

what is a strong acid?

A

one that 100% dissociates

84
Q

how would a strong acid be neutralised?

A

by combining with a weak base; this will cause it to form a weak acid, along with a salt

85
Q

what is the result of a strong acid being neutralised?

A

the pH will increase

86
Q

example of a strong acid being neutralised

A

HCl + NaHCO3 > NaCl + H2CO3

87
Q

how would a strong base be neutralized?

A

by combining with a weak acid; this will cause it for form a weak base, along with a salt

88
Q

what is the result of a strong base being neutralised?

A

the pH will decrease

89
Q

example of a strong base being neutralized

A

NaOH + H2CO3 > NaHCO3 + H20

90
Q

receptors for low blood pH feedback loop

A

central chemoreceptors in the medulla oblongata and peripheral chemoreceptors in the carotid and aortic bodies

91
Q

control centre for low blood pH feedback loop

A

inspiration centre in the medulla oblongata

92
Q

the more CO2, the more acidic or basic?

A

acidic

93
Q

chloride shift

A

HCO3 and Cl usually move through this in opposite directions; assists with blood pH changes

94
Q

how does a proton pump work?

A

takes ATP, breaks it down to ADP + inorganic phosphate; this energy moves the proton from the inside to the outside of the cell

95
Q

why do we use the HCO3/Cl shift?

A

because the negative charge being taken out needs to be replaced; negative charges inside the cell are important for neuron functioning

96
Q

how is H+ buffered in the urine

A

they either combine with NH3 to form NH4+ or combine with HPO4– to form H2PO4-

97
Q

what does increased blood osmolarity do in regards to the thirst mechanism and how are these signals transferred to the CNS

A

creates dry mouth and decreased saliva activity; these signals are transferred to the CNS by sensory receptors in the mouth/pharynx

98
Q

how is the RAAS system related to thirst mechanism

A

decreased blood volume and pressure activate ANG II; in which this activates the thirst mechanism to cause us to drink more water

Anatomy and Phyisology (94 decks)

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