The renal system 3 Flashcards

1
Q

Fluid homeostasis

A

25% of all arterial blood go through the kidney for cleaning

BP is regulated engough for blood to be cleaned = influences Glomerual Filtration Pressure

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2
Q

Intrinsinc controls

A
  • maintains a nearly constant glomerular filtration

- maintains a nearly constant glomerular filtration rate when mean arterial BP is in the range of 80-180 mmHg

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3
Q

types of renal autoregulation (2)

A

Myogenic Mechanism
Tubuloglomerular feedback mechanism
- kidneys compensate for change in MAP between 80-180 mmHg through pressure autoregulation

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4
Q

Myogenic mechanism

A

Aim: to maintain normal glomerular filtration rate: 120mL/min

  • if high BP -> afferent arterioles constrict -> restricts blood flow into glomerulus -> less GFR
  • if low BP -> dilation of afferent arterioles -> raises glomerular hydrostatic pressure
  • protect glomerulus from high pressure that could damage the filter
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5
Q

Tubuloglomerular feedback

A
  • if high BP - higher blood flow into glomerulus - faster filtrate flow in nephron
  • there will not be enough time to reabosrb all ions
  • many ions still in filtrate
  • macula densa cells in DCT sense high sodium coming past
  • have to send signal to slow down flow
  • DCT loops arounf and sits in front of afferent arteriole
  • DCT comes into contact with the afferent and efferent arteriole
  • several cells involved: juxtaglomerular complex
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6
Q

Juxtaglomerular complex

A
  • macula densa cells: part of the DCT of the same nephron
  • juxtaglomerular = granular cells: specialised muscle cells of the afferent arteriole produce renin to regulate flow
  • Extraglomerular mesangial cells: keep filter clean
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7
Q

Intrinsic control: tubuloglomerular feedback

Macula densa
Granular cells

A
  • flow-dependent mechanism directed by the macula densa
  • if glomerular filtration rate high: filtrate flow rate increases in tubule - filtrate flow rate increases in the tubule
  • Filtrate NaCl concentration will be high because of insufficient time for reabsorption
  • macula densa cells of the juxtaglomerular apparatus respond to high NaCl
  • Granular cells releasing renin = vasoconstricting arteriole -> intense constriction of afferent arteriole -> reduction in blood flow into glomerulus
    = more time to reabsorb ions again
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8
Q

Extrinsic control -> regulation of glomerular filtration rate

A
  • when mean arterial blood pressure extrememely low <80mmHg -> essential blood reaches vital organs -> less through kidneys
  • norepinephrine is released by the adrenal medulla
  • > both cause vascular smooth muscles constrict
  • > constriction of afferent arterioles, inhibiting filtration
  • > release of renin
  • > constriction of afferent arteriole
  • > decrease extracellular fluid vol
  • > mean arterial pressure decreases
  • > sympathetic tone increases -> arteriole constriction
  • > renin decreases
  • > GFR and renal blood flow decreases
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9
Q

Renal effects of angiotensin

A
  • Angiotensin II is a powerful vasoconstrictor
  • works most effectively on the Efferent arteriole
  • increased resistance downstream
  • -> maintains GFR without decreasing RBF
  • > the smaller the efferent arteiole, the more filtrate produced
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10
Q

Antidiuretic hormone

A
  • secreted from the posterior pituitary in reponse to angiotensin II
  • increases water reabsoprtion in the DCT
  • assisting in maintaining mean arterial pressure/ plasma volume through water reabsorption
    More water = more pressure
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11
Q

Aldosterone

A
  • angiotensin II stimulates release of aldosteron from adrenal cortex
  • aldoesteron increases reabsoprtion fo Na in DCT
  • maintains mean arterial pressure indirectly through subsequent water reabsorption
  • released from the adrenal glands
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12
Q

angiotensin converting inhibitiors

A
  • to treat high bloof pressure - used in heart failure where fluid builds up and hydrostatic pressure is too high
  • prevent conversion of angiotensin 1 to 2
  • inhibitors cause:
    vasodilation
  • diuresis (excessive urine production) and decreasemen mean arterial pessure
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13
Q

Fine tuning of osmolarity

A
  • regulation of water and urea

- regulation of salts: Na, K, Ca, H

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14
Q

Regulation of urine osmolarity

A
  • collecting ducts of all nephrons use osmotic gradient to adjust urine osmolarity
  • normal osmolarity of plasma = 300mOsm
  • kidneys can eliminate excess water -> dilute urine up to 1400 mOsm
  • kidneys conserve water -> concentrate urine up to 1400mOsm
  • Kidneys regulate urine volume and osmolarity by varying water and Na reabsorption in distal nephron
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15
Q

Water regulation: ADH

A
  • pituitary releases ADH = vasopressin in response to Angiotenis II
  • ADH increases water permeability in DCT and CD
  • ADH promotes water reabsorption and conrecntration in urine
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16
Q

When is ADH secreted from posterior pituitary?

A

When signals from:
1. osmoreceptors: detect change in ECF osmolarity, located in the hypothalamus and digestive trace
Increased ECF osmoalrity stiu,ulates ADH secretion
2. Baroreceptors
Detects changes in blood volume and pressure. Decreased BP and plasma volume stimulates ADH

17
Q

What cells does ADH act on

A

Type A intercalated cells: mediate acid secretion and bicarbonate reabsorption
Type N intercataled cells: mediate bicarbonate secretion and acid reabsorption
Principal cells reabsorb Na + and water and secrete K

18
Q

Control of water reabsorption process

A
  • pituitary released ADH travels via blood to epithelial cells of DCT
  • > increases number of prinicpal cells their apical plasma membrane of princial cells
  • > aquaoporin’s allow diffusion of water across the plasma membrane
  • > collecting duct becomes permeable to water
  • > ADH promotes water reabsorption and concentration of urine
  • ADH creates aquaporins (doors) for reabsorption
19
Q

Factors influencing ADH secretion

A
Stimulation:
- ADH promotes water reabsorption 
- increased ECF osmolarity
- decresed blood volume
- decreased mean arterial pressure
- stress, nausea, vomiting, nicotine
Inhibition:
- no ADH = water loss
- decreased ECF osmolarity
- hypervolemia
- increased MAP
- alcohol
- diuretics
- obligatory water loss
20
Q

Obligatory water loss

A

minimum vol. of urine that must be excreted to eliminate solutes remaining in tubular fluid = approx. 440mL/day in adults under normal condition

21
Q

PCT reabsorption of sodium

A
  • Apical membrane: sodium symporters/antiporters
  • Basolateral membrane: sodium potassium exchange pump
  • sodium is out of the cell, so that there is vacancy for more sodium to go through
22
Q

DCT reabsorption of sodium

A
  1. aldosterone
  2. atrial natriuretic peptide
    - apical membrnane: co-transport with other solutes - like sodium and cholride going in
    - sodium ion channel - facilitated diffusion
    - sodium reabsorption coupled to K secretion at distal nephron
23
Q

Aldosterone

A
  • released at adrenal cortex when stimulates by presence of angiotensis II through RAAS
  • synthesis of new Na and K channels on apical membrane
  • reabsorption of Sodium
    With high aldosterone, little Na leaves the body -> water follows -> increases BP
24
Q

Atrical natriuretic peptide

A
  • released by cardiac atrial cells it blood vol or pressure elevated
  • ANO increases excretion of sodium by ciliating afferent and constricting efferent arterioles, increaing GFR = increased filtered load of Na+
  • high AN, sodium leaves, K maintanins -> water in filtrate -> decrease BP
25
Q

Renal handling of K

A

-Ratio of extracellular: intracellular K+ is critical to function of excitable cells
-K+ is freely filtered at glomerulus
-Unregulated reabsorption from PCT (60%) and ascending LOH (30%)
-Regulated secretion in late distal tubule and collecting duct (diet dependent)
-Hyperkalaemia: Plasma potassium > normal.
Hypokalaemia: Plasma potassium < normal.
-Aldosterone increases:
Na+/K+ pumps on basolateral membrane
K+ channels on apical membrane
•Facilitates movement of K+ from peritubular fluid to renal tubule

26
Q

Reabsorption of K+ at proximal tubules

A
  • K+ moves from peritubular fluid into cell via Na+/K+ pump
  • K+ moves from tubular fluid across apical membrane
  • K+ also moves between cells to peritubular fluid
  • Moves down gradient via channels in basolateral membrane to peritubular fluid
27
Q

Secretion at distal nephron

A
  • Secretion occurs at Principal cells of distal nephron
  • K+ moves from peritubular fluid into cell via Na+/K+ pump on basolateral membrane
  • Ion channels in apical membrane allow K+ to be secreted into renal tubule
  • Potassium diffuses down concentration gradient from epithelial cells to tubular fluid
28
Q

Calcium regulation

A

-Reabsorption: 70% PCT, 20% ascending LOH, remainder in DT
-Critical to function of all cells, particularly important in heart, muscle and bones
-Plasma concentration regulated through kidneys, digestive tract, bone and skin
-Calcium added to plasma from bone and by absorption from digestive tract
-Calcium removed from plasma by bone and kidneys
Hypercalcaemia: High plasma Ca2+
Hypocalcaemia: Very low plasma Ca2+
-Has to be deposited into the bone as a long time reservoir

29
Q

Low calcium: 2 hormones increase calcium in blood

A

-Secretions triggered by hypocalcaemia
-Parathyroid Hormone (PTH): released from parathyroid glands:
Stimulates Ca2+ reabsorption in ascending LOH and distal tubules
Stimulating resorption of bone (take Ca2+ from bone - move it into blood)
Stimulates activation of calcitriol in kidneys (Ca2+ absorption at gut and reabsorption at kidney)
-1,25-(OH2)D3 or Calcitriol: Steroid hormone synthesized from Vitamin D3
-Synthesized from Vitamin D3 in several steps, last step occurs in the kidney
-Increases plasma calcium by stimulating Ca2+ absorption from digestive tract and reabsorption in distal nephron of kidneys

30
Q

High calcium: calcitonin decreases Ca in blood

A
  • Calcitonin: Hormone secreted from thyroid gland
  • Secretion triggered by hypercalcaemia
  • Increases Ca2+ uptake by bone -> stores Ca2+ in bone = calcification
  • Decreases renal Ca2+ reabsorption
  • Net effect: Decrease plasma Ca2+ levels
31
Q

Renal calculi: kidney stones

A

Crystallised Ca, Mg or uric acid salts in renal pelvis -> stones block ureter, causing pressure and pain

32
Q

Chronic renal disease

A

Glomerular filtration rate <60 ml/min

33
Q

Anuria

A

Abnormally low urinary outpir (<50ml/day)

34
Q

UTI

A
  • dysuria (painful urination),
  • 40% of women
    Short urethra of femals can allow fecal bacteria to easily enter urethra
35
Q

Renal failure

A
  • defined as glomerular filtration rate <15mL/min

- need hemodialysis or transplant