FE balance Flashcards

1
Q

Osmolarity changes through the nephron

A
  1. isosmotic fluid leaving the proximal tubule becomes progressively more concentrated at the descending limb. Only water reabsorbed.
  2. removal of solute in the thick ascending limb creates hyposmotic fluid. ions reabsorbed but no water
  3. permeability to water and solutes in the distal tubule and collecting duct is regulated by hormones. Variable reabsorption of water and solutes based on body’s needs
  4. final urine osmolarity depends on reabsorption in the collecting duct
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2
Q

what is vasopressin released by

A

posterior pituitary gland

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3
Q

explain how vasopressin is released into the blood

A
  1. made and packaged in cell body of neuron
  2. vesicles are transported down the cell
  3. vesicles containing AVP are stored in posterior pituitary
  4. AVP is released into blood
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4
Q

what is the stimulus for vasopressin release

A

when we need more water
- high plasma osmolarity
- low blood volume
- low blood pressure

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5
Q

what does vasopressin do

A

controls the addition of water pores (aquaporin-2; AQP2) into the apical membrane of collecting duct cells

results in increased water reabsorption and more concentrated urine. Pulling back water if it is needed
- response may be graded (need a bit of h2o, secrete a little vasopressin, more if needed) and depends on the amount of hormone released

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6
Q

what kind of relationship is the effect of plasma osmolarity on vasopressin secretion

A

linear relationship

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7
Q

what is the the homeostatic response to decreased blood pressure

A

sensor: carotid and aortic baroreceptors
input signal: sensory neuron to hypothalamus
integrating center: hypothalamic neurons that synthesize vasopressin
output signal: vasopressin released from posterior pituitary
target: collecting duct epithelium
tissue response: insertion of water pores in apical membrane
systemic response: increased water reabsorption to conserve water

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8
Q

what is the homeostatic response to decreased atrial stretch due to low blood volume

A

sensor: atrial stretch receptor (if there is less blood it will not need to stretch)
input signal: sensory neuron to hypothalamus
integrating center: hypothalamic neurons that synthesize vasopressin
output signal: vasopressin released from posterior pituitary
target: collecting duct epithelium
tissue response: insertion of water pores in apical membrane
systemic response: increased water reabsorption to conserve water

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9
Q

what is the homeostatic response to osmolarity greater than 280 mOsM

A

sensor: hypothalamic osmoreceptors
input signal: interneurons to the hypothalamus
integrating center: hypothalamic neurons that synthesize vasopressin
output signal: vasopressin released from posterior pituitary
target: collecting duct epithelium
tissue response: insertion of water pores in apical membrane
systemic response: increased water reabsorption to conserve water

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10
Q

what type of hormone is aldosterone

A

steroid hormone

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11
Q

where is aldosterone made and released

A

adrenal cortex

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12
Q

what does aldosterone do

A

acts on principal (P) cells of the distal tubule and collecting duct to increase sodium reabsorption

if we turn this up to increase sodium gradient, water will follow via osmosis

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13
Q

what is the stimulus of aldosterone release

A

angiotensin 2 (low blood pressure and the Renin-Angiotensin system; RAS)

hyperkalemia (High potassium concentration in plasma)

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14
Q

renin-angiotensin-aldosterone system

A

stimuli is low BP or BV
granular cells of the afferent arteriole produce the enzyme renin which is released into circulation to act of angiotensinogen (inactive, produced by liver)

renin converts angiotensinogen to ANG 1 and then ACE (angiotensin-converted enzyme located on all vascular endothelial cells) which is active and acts on adrenal cortex

aldosterone is released from adrenal cortex to increase sodium reabsorption

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15
Q

what are the other targets of ANG 2

A

cardiovascular control center - increase CO, SV, HR
arterioles: powerful vasoconstrictor, increase R and BP
hypothalamus: increases vasopressin release, thirst and salt appetite

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16
Q

what are the buffers in acid base balance

A

bicarbonate in extracellular fluid
proteins, hemoglobin and phophates in cells
phosphates and ammonia in urine

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17
Q

what are the three mechanisms to maintain normal pH

A

buffers, regulation of ventilation and kidneys (in this order)

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18
Q

renal compensation in pH homeostasis

A

H+ secreted and bicarbonate reabsorbed at the proximal tubule

fine regulation of acid-base balance occurs at the collecting duct

interaclated 1 cells (interspersed between P cells) contain high levels of carbonic anhydrase

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19
Q

type A I cells

A

secrete H+ and reabsorb bicarbonate

response to acidosis

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20
Q

type B I cells

A

secrete bicarbonate and reabsorb H+

response to alkalosis

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21
Q

function of calcium in extracellular matrix

A

calcified matrix of bone and teeth

22
Q

function of calcium in extracellular fluid

A

neurotransmitter release at synapse
role in myocardial and smooth muscle contraction
cofactor in coagulation cascade
cement for tight junctions
influences excitability of neurons

23
Q

function of intracellular calcium

A

muscle contraction and signal in second messenger pathways

24
Q

hydroxyapatite

A

calcified extracellular matrix

25
Q

osteoblasts

A

synthesize bone

26
Q

osteoclasts

A

resorb bone (breakdown)

27
Q

parathyroid hormone origin

A

parathyroid glands

28
Q

parathyroid hormone chemical nature

A

84-amino acid peptide

29
Q

parathyroid hormone biosynthesis

A

continuous production, little stored

30
Q

parathyroid hormone transport in circulation

A

dissolved in plasma

31
Q

parathyroid hormone half-life

A

less than 20 mins

32
Q

parathyroid hormone factors affecting release

A

decrease in plasma calcium

33
Q

parathyroid hormone target cells or tissues

A

kidney, bone, intestine

34
Q

parathyroid hormone target receptor

A

membrane receptor acts via cAMP

35
Q

parathyroid hormone whole body tissue reaction

A

increase plasma calcium

36
Q

parathyroid hormone action at cellular level

A

increase vitamin D synthesis; increase renal reabsorption of calcium, increase bone reapsorption

37
Q

homeostatic loop for calcitirol

A

stimulus: endogenous precursors converted to your body via sunlight/ diet
vitamin D
liver
calcitrol

increase plasma calcium shuts of PTH secretion

38
Q

calcitirol chemical nature

A

steroid

39
Q

calcitirol transport in circulation

A

bound to plasma protein

40
Q

calcitirol stimulus for synthesis

A

decrease calcium indirectly via PTH

41
Q

calcitirol tager cells or tissues

A

intestine, bone and kidney

42
Q

calcitirol target receptor

A

nuclear

43
Q

calcitirol whole body reaction

A

increase plasma calcium

44
Q

calcitonin chemical nature

A

32-amino acid peptide

45
Q

calcitonin biosynthesis

A

typical peptide

46
Q

calcitonin transport in circulation

A

dissolved in plasma

47
Q

calcitonin half-life

A

less than 10 mins

48
Q

calcitonin factors affecting release

A

increase plasma calcium concentration

49
Q

calcitonin target cells or tissues

A

bone and kidney

50
Q

calcitonin target receptor

A

G protein-coupled membrane receptor

51
Q

calcitonin whole body or tissue action

A

prevents bone reabsorption, enhances kidney excretion

52
Q

calcitonin action at molecular level

A

signal transduction pathways appear to vary during cell cycle