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Physiology > L11-13: Renal System > Flashcards

L11-13: Renal System Flashcards

1
Q

What are the features of the nephron?

A

~1 million nephrons per kidney
~80% cortical
Juxtamedullary nephrons (concentrated urine)

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2
Q

What is the difference between cortical and juxtamedullary nephrons?

A

Juxtamedullary stretch far in to the medulla and are much longer in comparison to cortical nephrons

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3
Q

What are the main structures in the nephron?

A

Bowman’s capsule
Proximal convoluted tubule (PCT)
Loop of Henle (descending and ascending limb)
Distal convoluted tubule (DCT)
Collecting duct

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4
Q

What is the distribution of blood flow to the kidney?

A

Cortex - 93%
Medulla - 7%

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5
Q

What is the overall approximate blood flow to the kidney at rest?

A

~1.2L/min at rest

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6
Q

What is the anatomical structure of the vascular supply to the nephron?

A

Afferent arterioles feed into the glomeruli then efferent arterioles leave the glomeruli and wrap around the nephron then peritubular capillaries to renal veins to inferior vena cava

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7
Q

Why is it important that there is a close anatomical relationship between tubules and vasa recta?

A

It is important for function

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8
Q

What are the functions of the kidney?

A

Homeostatic regulation of water and ion content of blood
Excretion of metabolic waste products and foreign substances
Production of hormones

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9
Q

What hormones does the kidney produce?

A

Erythropoietin - RBC synthesis
Renin - Na+ balance
Activation of vitamin D - Ca2+ balance, bone prostaglandins and kinins

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10
Q

What is filtered in glomerular filtration?

A

All plasma constituents except proteins >67kDa

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11
Q

How does the glomerular filtration barrier restrict movement?

A

Based on size and charge

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12
Q

What is the filtration fraction and how much is it in glomerular filtration?

A

It is the plasma that filters in the nephron and ~20% at this stage

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13
Q

What is the glomerular filtration rate?

A

~180 liters/day

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14
Q

Where is the filtration barrier in the renal corpuscle positioned?

A

Between the lumen capillary and the lumen of Bowman’s capsule

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15
Q

What is the composition of the filtration path from lumen of capillary to Bowman’s capsule?

A

Fenestration pores
Endothelium
Basement membrane
Podocytes (and foot processed)

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16
Q

Which substances filter in the glomerulus?

A

Water
Na+
K+
Ca2+
Cl-
Glucose
Urea
Creatine
Uric acid

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17
Q

What is not filtered in the glomerulus?

A

RBCs
Serum albumin

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18
Q

What are the different pressures controlling filtration?

A

Hydrostatic pressure of blood (promotes movement into capsule)
Colloid osmotic pressure (caused by proteins movement into capillaries)
Hydrostatic pressure of fluid in BC (opposes movement of fluid in capsule)

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19
Q

What pressure drives the filtration?

A

Capillary hydrostatic pressure

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20
Q

How does an increase in resistance of blood flow impact filtration?

A

Afferent: reduces blood flow into the glomerulus
Efferent: increases blood flow/pressure in glomerulus

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21
Q

How does a decrease in resistance of blood flow impact filtration?

A

Afferent: reduces blood flow to glomerulus
Efferent: increases blood flow out of/ decrease pressure in glomerulus

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22
Q

What happens to GFR and RBF over a range of arterial pressures?

A

They maintain relatively constant

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23
Q

What happens in a myogenic response due to auto regulation?

A

Increase BP
Stretch smooth muscle cells
Vasoconstriction
Decrease renal blood flow, hydrostatic pressure and glomerular filtration rate

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24
Q

What happens in tubuloglomerular feedback due to auto regulation?

A

Fluid flows through tubule which influences arteriole resistance and GFR

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25
Q

How do macula dense cells impact flow?

A

Sense distal tubule flow releasing paracrine that affect afferent arteriole diameter

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26
Q

What is the process of tubuloglomerular feedback?

A

GFR increases
Flow through tubule increases
Flow past macula dense increases
Paracine factors released from macula dense
Afferent arteriole constricts
Resistance in afferent arteriole increases
Hydrostatic pressure in glomerulus decreases
GFR decreases

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27
Q

What are GFR and RBF maintained by?

A

Constant auto regulation, neural control and tubuloglomerular feedback

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28
Q

How much of what filters is actually excreted?

A

1% (~1.5L/day)

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29
Q

How much is reabsorbed and where?

A

~99% filtrate reabsorbed
~66% occurs in PCT

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30
Q

How are epithelial cells adapted in the nephron?

A

PCT- highly infolded plasma membrane (full of organelles)
DCT- more columnar
Loop of Henle- Flat and connect less, less organellses
Collecting duct- columnar tight and connect (different variety of cells)

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31
Q

How is the movement of solutes/ fluid facilitated in reabsorption?

A

Leak channels
Paracellular transport
Co- transporter
Antiporter
Membrane pump
Membrane carrier

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32
Q

What is epithelial transcellular transport?

A

Substances cross apical and basolateral membranes of the tubule epithelial cells

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33
Q

What is paracellular transport?

A

Substances pass through the cell-cell junction between adjacent cells

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34
Q

How is the route of reabsorption decided?

A

Depending on electrochemical gradient and permeability of epithelial junctions

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35
Q

How is the PCT adapted for its function?

A

Microvilli on apical surface maximise surface area available for reabsorption
ER, Golgi, lysosomes, vacuoles - all for synthesis of membrane proteins
Interdigitations of basolateral membrane shorten distance to mitochondria (AT)

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36
Q

Which molecules are reabsorbed via paracellular transport?

A

H2O and Cl-

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37
Q

Where does Na+ reabsorption occur?

A

Passively down the apical membrane of the PCT down the electrochemical membrane, ion exchange with other positively charged ions

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38
Q

How is glucose reabsorbed?

A

Co-transport at the apical membrane of the PCT, using carrier at the basolateral membrane

39
Q

How is urate reabsorbed?

A

Organic anion transporters in the PCT, paracellular route, transcellular route, secretion via organic anion transporters

40
Q

What measures are used for reabsorption of glucose?

A

Tm: transort maximum rate
Renal threshold: plasma concentration of substrate at transport maximum
Diabetes mellitus: excessive glucose concentration saturates number of carries and excess glucose appears in urine

41
Q

What is the osmolarity of the tubular fluid and plasma at the PCT?

A

~300mOsm

42
Q

How does osmolarity change through the nephron and what is the effect?

A

Isoosmotic leaving PCT becomes more concentrated in the descending limb
Removal of solute in thick ascending limb creates hypo osmotic fluid
Permeability to water and solutes in DCT and collecting duct is regulated by hormones
Final urine osmolarity depends on reabsorption in collecting duct

43
Q

What happens to the filtration in the Loop of Henle?

A

Descending limb permeable to water , impermeable to solutes
NaCl transport from ascending limb into intersitium
Thick ascending limb of loop impermeable to water

44
Q

How is more concentrated urine formed?

A

Anti-diuretic hormone makes collecting duct permeable to water, so reabsorbed passively driven by osmotic gradient in medullary interstitium
Countercurrent systems maintain osmotic gradient in medullary interstitium

45
Q

What are the properties of countercurrent exchange systems?

A

2 flows in opposite directions
Vessels anatomically very close together
Passive transfer of molecules from one vessel to another

46
Q

What is the countercurrent system between?

A

Vasa recta and collecting duct

47
Q

What is the countercurrent multiplier exchange in the Loop of Henle and vasa recta?

A

Descending limb: H2O reabsorption, increase filtrate osmolarity
Ascending limb: active solute reabsorption, decreased filtrate, osmolarity
Descending vasa recta: H2O reabsorption, solute uptake, increased blood osmolarity
Ascending vasa recta: H2O reabsorption, decreased blood osmolarity

48
Q

Is there a paracellular route in loop of henle reabsorption?

A

No!

49
Q

How is acid-base balance regulated?

A

Using buffers: cellular proteins, haemoglobin and HPO42-, HCO3-
Respiratory adjustment
Renal adjustment (excreting/ reabsorbing H+, indirectly excreting/ reabsorbing HCO3-)

50
Q

What is acidosis in the kidney?

A

α - Type A intercalated cells in collecting duct excrete H+, reabsorb HCO3-

51
Q

What is alkalosis in the kidney?

A

β - Type B intercalated cells in collecting duct excrete HCO3-, reabsorb H+

52
Q

How is water balance regulated?

A

Diuresis: removal of excess water in urine
Diuretics are drugs that promote urine excretion

53
Q

What does antidiuretic hormone do?

A

It controls the permeability of cells in the collecting duct to H2O

54
Q

How does ADH allow water reabsorption?

A

It binds to receptor on basolateral surface
Stimulates andenylyl cyclase to generate cAMP and activate protein kinase
Increase insertion of aquaporin 2 into apical membrane
Increase water permeability
Increase water reabsorption
Concentrated urine and water conservation

55
Q

Which factors cause water conservation?

A

Osmolarity greater than 280mOsm
Decreased atrial stretch due to low blood volume
Decreased blood pressure

56
Q

How is ADH release controlled?

A

When factors affect water conservation:
Hypothalamic neurons synthesis vasopressin
Vasopressin released from posterior pitutary
Collecting duct epithelium
Insertion of water pores in apical membrane
Increased water absorption to conserve water

57
Q

What are the main controllers of ADH release?

A

Osmoreceptors

58
Q

Where is ADH produced and stored?

A

Produced in cells in supraoptic and paraventricular nuclei of hypothalamus
Stored in vesicles in posterior pituitary gland

59
Q

What changes increase or decrease ADH production?

A

Increase plasma concentration = increase ADH
Decrease plasma concentration = decrease ADH

60
Q

How is AVP made?

A

Arginine vasopressin is made and packaged in the cell body of the neutron
Vesicles are transported down the call
Vesicles containing AVP are stored in posterior pituitary
AVP released into blood

61
Q

What is the feedback loop when there is water deprivation?

A

1- Increased ECF osmolarity
2- Supraoptic & paraventricular nuclei
3- ADH release from posterior pituitary
4- CD made water permeable
5- Water retention by kidney
2- Lateral prepotic area
3- Thirst
4- Drink water

62
Q

What is the feedback loop when there is excessive fluid ingestion?

A

1- Decreased ECF osmolarity
2- Supraoptic & paraventricular nuclei
3- ADH release surpassed
4- CD made water impermeable
5- Water excretion
2- Lateral prep-tic area
3- thirst supressed

63
Q

What are the physiological stimuli for secretion?

A

Heightened emotions, stress
High temperature
Excercise
Pain

64
Q

What factors cause inappropriate secretion?

A

Post-operative
Intracranial disease/injury
Ectopic ADH production
Opiates: Vinblastine Tricyclics
Chlorporpamide, MDMA - ecstasy
Pneumonia
Nicotine

65
Q

Why does nocturnal enuresis (bed-wetting) occur?

A

Delay in development of normal circadian rhythm of ADH

66
Q

How does MDMA impact fluid balance?

A

Stimulated thirst reflex and repetitive behaviour and stimulates ADH secretion so increases fluid in and decreases fluid out
Results in increasing circulating volume and hyponatremia

67
Q

What is the overall effect of ADH?

A

Decreased H2O excretion
Increased blood volume

68
Q

Which diseases is ADH deficiency found in?

A

Diabetes insipidus : polyuria due to deficiency
Central diabetes insipidus: deficiten of ADH secretion
Nephrogenic diabetes insipidus: nephrons don’t respond to ADH

69
Q

Where is most Na+ reabsorbed in the nephron?

A

In the PCT

70
Q

Where is no Na+ reabsorbed in the nephron?

A

In the thin loop of henle

71
Q

Which hormone axis is activated to increase the reabsorption of Na+?

A

Renin-angiotensin-aldosterone

72
Q

What happens in the renal corpuscle when renin is released?

A

Decrease NaCl at macula densa
Stretch receptors in afferent arteriole sense decrease BP
Increase in renal sympathetic nerve stimulation due to central decrease BP

73
Q

What happens in the renin-angiotensin-aldosterone axis?

A

Angiotensin in plasma
Renin stimulates angiotensin I production in plasma
ACE (angiotensin converting enzyme) added
Forms angiotensin II in plasma
Stimulating aldosterone in adrenal cortex
So increased Na+ reabsorption (DCT & CD)
So increase in extracellular fluid

74
Q

How does the renin-angiotensin-aldosterone axis act?

A

As a negative feedback loop

75
Q

What is the cellular action of aldosterone?

A

Aldosterone binds to receptor in cytoplasm
Initiating transcription
Increase in ENaC channels in apical surface increases Na+-K+ pumps
Na+ reabsorption Cl- follows and K+ secretion

76
Q

What is aldosterone?

A

A steroid hormone synthesised in adrenal cortex, stimulation by angiotensin II

77
Q

What is the overall effect of aldosterone?

A

Decrease in NaCl and H2O excretion
Increase in blood volume

78
Q

Where does angiotensin II act?

A

Arterioles, cardiovascular control centre, hypothalamus and adrenal cortex

79
Q

How does angiotensin II act?

A

Acts on the brain to create sensation of thirst
Powerful vasoconstrictor
Stimulates release of aldosterone

80
Q

What is angiotensin II effect on baroreceptor reflex?

A

Inhibits baroreceptor reflex and increases release of norepinephrine from sympathetic postganglionic fibres

81
Q

What is the overall effect of angiotensin II?

A

Decreases NaCl and H2O excretion
Therefore increasing blood volume and BP

82
Q

When does atrial natriuretic peptide get released?

A

When blood volume increases causing atrial stretch

83
Q

What is the effect of atrial natriuretic peptide?

A

Causes decrease in ADH in hypothalamus
Inhibits aldosterone in adrenal cortex
Increase GFR decrease in NaCl & H2O reabsorption and renin in kidney
All causing an increase in NaCl sonf H2O excretion

84
Q

What is atrial natriuretic peptide produced?

A

By the atria in response to stretch

85
Q

What does atrial natriuretic peptide inhibit?

A

Thirst and ADH, aldosterone and renin release

86
Q

What is the overall effect of atrial natriuretic peptide?

A

Increases NaCl and H2O excretion therefore decreasing blood volume and BP

87
Q

What is nephrolithiasis?

A

Formation of renal calculi (kidney stones) crystalline structures composed mostly of calcium oxalate salts

88
Q

How do renal calculi form?

A

Due to higher than normal ion and solute concentration in filtrate

89
Q

Where do renal calculi form?

A

In nephron loop, DCT and/or collecting system
Adhere to epithelium

90
Q

What are the two rings of sphincter muscles in the renal system?

A

Internal - smooth muscle, normal tone keeps it contracted
External - skeletal muscle controlled by somatic motor neurones, tonic stimulation from CNS maintains contraction

91
Q

What is urine?

A

Where fluid leaves the collecting duct and flows through the ureter to the bladder

92
Q

What is the bladder?

A

Hollow organ expands to hold ~500ml
Smooth muscle wall
Nech of bladder continuous with urethra

93
Q

What is the mechanism of micturition?

A

Stretch receptors fire
Parasympathetic neurones fire, motor neurones stop firing
Smooth muscle contracts, internal sphincter passively pulled open and external sphincter relaxes

Physiology (6 decks)

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