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Medicine 3 > Renal > Flashcards

Renal Flashcards

1
Q

What are the 2 types of nephron?

A

Cortical and juxtamedullary

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2
Q

What are the two types of capillary beds in the nephron?

A

Glomerular capillaries - high hydrostatic pressure (filtration)
Peritubular capillaries - low pressure (reabsorption)

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3
Q

What are the three main processes of urine modification and composition?

A

Filtration
Reabsorption
Secretion

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4
Q

What is the glomerular filtration rate (GFR)?

A

The volume of fluid entering the Bowman’s capsule per unit time - 180 L/day or ~120 ml/min

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5
Q

How is fluid driven from the capillaries to the Bowman’s capsule?

A

Hydrostatic pressure (20% filtration fraction) due to efferent arteriolar having a smaller diameter than affecting arterioles

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6
Q

Describe the epithelium of the glomerular capillaries

A

Fenestrated and freely permeable to water and many solutes (negatively charged glycoproteins on surface repel ionic proteins). Large molecules cannot pass through

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7
Q

What are the factors that influence ultrafiltration?

A

Change in capillary hydrostatic pressure
Change in colloid osmotic pressure
Change in filtration constant - kidney disease decreasing no. of glomeruli or increasing membrane thickness

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8
Q

What is colloid osmotic pressure?

A

The effect of proteins (albumin) on water in capillaries. If hydrostatic pressure

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9
Q

Why is GFR useful?

A

Tells us how the kidney is functioning to help assess severity of kidney disease and assist drug prescription

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10
Q

Why is insulin clearance useful?

A

Freely filtered and not reabsorbed, secreted or metabolised. Easily measured in urine to give us a good understanding of GFR

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11
Q

How do we use creatinine clearance to measure eGFR?

A

Creatinine blood levels remain constant. We take a urine and serum sample and compare concentrations to give eGFR

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12
Q

What is renal plasma flow (RPF)?

A

The amount of plasma that perfuses the kidneys per unit time

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13
Q

What is a good indicator of RPF?

A

Clearance of para-aminohippuric acid (PAH)

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14
Q

How does a higher filtration fraction affect tubular reabsorption?

A

There is a higher colloid osmotic pressure in the peritubular capillaries and therefore greater forces for tubular reabsorption.

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15
Q

What is autoregulation in the kidney?

A

Ensuring the RBF and GFR remain constant regardless of changes to arterial blood pressure

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16
Q

How is autoregulation in the kidney achieved?

A

Myogenic effects - change in affecerent arteriole contraction in response to pressure and stretch
Tubuloglomerular feedback - NaCl in filtrate detected by co-transporter in juxtaglomerular apparatus and signal for affront arteriole contraction to decrease GFR

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17
Q

What are the factors affecting RBF and GFR?

A

Vasoconstrictors - decrease RBF and GFR (sympathetic nerves, angiotensin 2)
Vasodilators - increase RBF and GFR (prostaglandins, PGE2 and PGI2)

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18
Q

What is the clinical relevance of NSAIDs regarding RBF?

A

NSAIDs block prostaglandin synthesis. If taken when RBF decreased, vasoconstriction may cause acute renal tubular necrosis

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19
Q

What drugs are excreted in bile?

A

Highly-polar compounds with high molecular weight. Major route for drugs metabolites

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20
Q

How are drugs filtered in the kidney?

A

All unbound drug and metabolites freely filtered. Protein bound drugs not filtered but can still be excreted (binding weak and reversible)

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21
Q

What are the contraindications between acid and base drug excretion?

A

Acids and bases are actively secreted so there may be some competition between drugs to be secreted and an increase in drug toxicity.

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22
Q

Why is the acidity or alkalinity or a drug relevant when treating overdoses?

A

Tubule wall is a lipid barrier - ionised compounds cannot pass through

If overdose with acid drug, alkaline diuresis to ionise drug and prevent reabsorption and vica versa

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23
Q

What should be considered when prescribing drugs when patient has renal impairment?

A

Drug elimination. If drug is eliminated in urine then drug elimination may be impaired leading to toxicity

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24
Q

What should be considered when prescribing drugs to a new mother?

A

Whether drug is eliminated in breast milk as may pass to baby

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25
Q

What are the clinical features of acute kidney injury?

A

Oliguria leading to anuria (little urine to no urine)
Electrolyte imbalance (hyperkalaemia and metabolic acidosis)
High blood urea and creatinine (good diagnostic markers)

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26
Q

What are the clinical features of chronic kidney disease?

A

Polyuria
Malaise
Confusion
Electrolyte imbalance

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27
Q

How does the composition of plasma solute compare to that of the ultrafiltrate?

A

Similar concentrations for electrolytes and glucose but much more protein in plasma than ultrafiltrate

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28
Q

What are the normal plasma solute concentrations in mmol/L for Na+, K+, Cl-, HCO3-, H+, glucose and protein?

A 
Na+: 135-145
K+: 3.5-5.0
Cl-: 100-106
HCO3-: 21-28
H+: 37-43
Glucose: 3.9-5.6
Protein: 60-84
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29
Q

What are the normal values for GFR, RPF, PCV (packed cell volume), renal blood flow and cardiac output?

A 
GFR: 120 ml/min
RPF: 600 ml/min
PCV: 40%
Renal blood flow: 1 L/min
Cardiac output: 5 L/min
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30
Q

What mechanism is used to transport solutes for reabsorption from the nephron tubule to the peritubular space?

A

Na+/K+ ATPase pump. Linked to reabsorption of every substance

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31
Q

How do solutes for reabsorption move from peritubular fluid into the peritubular capillaries?

A

Hydrostatic pressure inside capillaries is lower than colloid osmotic pressure

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32
Q

Why is the proximal tubule highly permeable to water?

A

To prevent build up of osmotic gradients so tubular fluid is isosmotic with plasma

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33
Q

How does Na+ move from proximal tubule to epithelial cells?

A

Na+/H+ exchanger
Through tight junctions into lateral space
Symporter mechanisms
Enters alone through membrane channels

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34
Q

What is the process of bicarbonate reabsorption as it cannot pass across apical membrane of epithelial cells?

A

In lumen: H+ combines with HCO3- to form H2CO3. Dissociates to CO2 and water (catalysed by carbonic anhydrase). Diffusion across apical membrane into epithelial cells.
In epithelial cell: CO2 hydrated to form H2CO3 (catalysed by carbonic anhydrase). Dissociation inside epithelial cell to form HCO3- and H+. HCO3- reabsorbed by capillary and H+ used for Na+/H+ exchanger

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35
Q

What drives H2O reabsorption in the proximal tubule?

A

Osmotic gradient by Na+ reabsorption.

Higher oncotic pressure in capillary

36
Q

How does H2O get past lumen epithelium to peritubular capillaries for reabsorption?

A

Through tight junctions between cells and across cells via aquaporin-1 (AQP1) water channels

37
Q

How is Cl- reabsorbed in the proximal tubule?

A

Passively down electrical and concentration gradient and with Cl-/Base antiporters (bases pumped out of epithelial cell to join with H+ that is also pumped out)

38
Q

How is K+ reabsorbed in the proximal tubule?

A

Solvent drag with water and passive diffusion through tight junctions of epithelial cells. Some actively transported back into epithelial cells by Na+/K+ ATPase

39
Q

Why is some urea reabsorbed in the proximal tubule?

A

Reabsorption of Na+ and movement of water concentrates urine in lumen so some moves passively down concentration gradient.

40
Q

Describe solute movement in the descending limb of Henle

A

Limb highly permeable to water (AQP1) but not to NaCl and urea. Passive movement of water out of lumen into highly concentrated medulla

41
Q

Describe solute reabsorption in the thick ascending limb of the loop of Henle

A

Na+/2Cl-/K+ symporter facilitates movement of these solutes into epithelium.
Cl- passively diffuses through channels into medulla
Some K+ leaks back via channels. Lumen become positively charged compared to interstitium driving paracellular diffusion of Na+, Mg2+ and Ca2+
Na+ also enters epithelial cell via Na+/H+ exchanger (leads to HCO3- reabsorption) and then pumped out.

42
Q

Describe solute reabsorption in the thin ascending limb of the loop of Henle

A

Passive reabsorption but impermeable to water

43
Q

What is the role of the ascending limb of the loop of Henle in concentrating urine?

A

Reduces osmolality of tubular fluid (becomes hypoosmotic). Makes medullary interstitium hyperosmotic which leads to osmosis of water out of descending limb

44
Q

How is solute reabsorption continued in the early distal convoluted tubule?

A

Na+/Cl- symporter transports Na+ and Cl- across apical membrane.
Cl- diffuses our through channels
Na+ pumped out (drives further transport)
H+ secreted by Na+/H+ exchange to help bicarbonate reabsorption
K+ reabsorbed

45
Q

Why is there a net gain of blood HCO3- at the end of filtration?

A

High concentration of carbonic anhydrase in cytoplasm of intercalated cell to produce HCO3- (absorbed) and H+ to be secreted. Important in acid-base balance.

46
Q

What are the two types of cell in the late distal tubule/collecting duct?

A

Principal cells: reabsorb Na2+ and water. Secrete K+

Intercalated cells: secrete H+. Reabsorb HCO3- and K+

47
Q

What are the effects of aldosterone in the late distal tubule/collecting duct?

A

Increase Na+ reabsorption in principal cells: increased no. of active apical Na+ channels and basolateral Na+ pump
Increase K+ secretion in principal cells: increase no. of active apical K+ channels and basolateral Na+ pump which draws in K+
Increases H+ secretion in intercalated cells: stimulates H+ ATPase pump.

48
Q

How is aldosterone secretion affected by hyperkalaemia and hypokalaemia?

A

Hyperkalaemia increases aldosterone secretion and hypokalaemia decreases aldosterone secretion

49
Q

What is the consequence of hypoaldosteronism?

A

Hyperkalaemia

50
Q

What is the consequence of hyperaldosteronism?

A

Hypokalaemia and metabolic alkalosis

51
Q

What is the effect ADH on late distal tubule/collecting duct?

A

ADH increases water permeability of late distal tubule/collecting duct via aquaporin 2 (AQP2) in the apical membrane so water reabsorption is increased.

52
Q

What is the effect of ADH on the inner medullary collecting duct?

A

Increases permeability to urea through ADH-dependent facilitated diffusion transporter on the apical membrane. This is important to maintain osmotic gradient between interstitium and collecting duct as water is reabsorbed into the interstitium when ADH is present, disrupting the osmotic gradient.

53
Q

What happens to urea if it is reabsorbed from the inner medullary collecting duct?

A

Recycled back into descending and ascending loops of Henle

54
Q

What is diabetes insipidus?

A

Central diabetes insipidus: Inadequate secretion of ADH
Nephrohenic diabetes insipidus: tubule insensitivity to ADH

Tubule impermeable to water = polyuria & polydipsia (thirst)

55
Q

What is the difference between osmolality and osmolarity?

A 
Osmolality = no. of solute particles in 1 kg water
Osmolarity = no. of solute particles in 1 L water
56
Q

What is the vasa recta?

A

Blood vessel that runs parallel to the loop of Henle

57
Q

What is the function of the vasa recta?

A

Supply nutrients and oxygen to nephron

Remove excess water and solutes that would dissipate gradient

58
Q

Describe the movement of water and solutes into and out of the vasa recta

A

In the descending vasa recta, H2O moves out and solutes move in
In the ascending vasa recta, H2O moves in and solutes move out

59
Q

What are the effects of a high ECF osmolality (excess water intake)?

A

Water moves into cells - swell

60
Q

What are the effects of a low ECF osmolality (water loss/salt intake)?

A

Water moves out of cells - shrink

61
Q

What stimulates thirst and ADH (increased water intake/retention)?

A

Increasing osmolality detected by osmoreceptors and decrease in blood volume/pressure

62
Q

What are the clinical manifestations of excess sodium?

A 
Renal failure
Weight gain
Oedema formation
Hypertension
Nocturia
63
Q

What are the clinical manifestations of sodium deficit?

A

Vomiting, diarrhoea
Weight loss
Syncope
Orthostatic hypotension

64
Q

What are the actions of aldosterone?

A

Promote sodium reabsorption in the late distal tubule/collecting duct. Stimulates:
Na+ reabsorption
K+ secretion
H+ secretion

65
Q

What is the site of renin release?

A

Granular cells of juxtaglomerular apparatus

66
Q

What factors stimulate renin release?

A

Low Na+ delivery to distal tubule (macula densa)
Low ECF volume and BP (catecholamines)
Low renal perfusion pressure (renal baroreceptor)

67
Q

What are the actions of renin-angiotensin aldosterone system (RAA)?

A

Low Na+, ECF vol, BP
Renin release
Converts angiotensinogen to angiotensin I (liver)
ACE converts angiotensin I to angiotensin II
Aldosterone release

68
Q

What are the effects of angiotensin II?

A

Increased aldosterone secretion -> Increased proximal Na+ reabsorption
Increased thirst
Increased ADH secretion
Sympathoexcitation -> vasoconstriction

69
Q

How is the renin-angiotensin-aldosterone system regulated?

A

Angiotensin II inhibits renin secretion both directly and by increasing ADH secretion

70
Q

What stimulates aldosterone release?

A

Angiotensin II
K+
ACTH

71
Q

How does aldosterone affect K+ secretion?

A

Increased activity of Na+/K+ ATPase
Increased K+ permeability of luminal membrane (K+ leaks back into lumen)
Increased Na+ reabsorption (lumen more electronegative)

72
Q

What is the renal response to low BP?

A 
Baroreceptors detect low BP
RAA system activation
Increased Na+ reabsorption and thirst
Volume and BP restored
(Converse for increase in BP)
73
Q

What is the renal response to low solute concentration?

A

Detected by osmoreceptors
Decreased ADH release
Decreased water reabsorption (increased excretion)
Increase in osmolality

74
Q

What is the equilibrium equation responsible for the acid-base balance?

A

H2O + CO2 H2CO3 H+ + HCO3-

75
Q

How do kidneys respond to alkalaemia?

A

Inhibit H+ secretion (decrease HCO3- reabsorption)
Excrete HCO3- in urine
(converse applies for acidaemia)

76
Q

Why does the kidney secrete ammonium?

A

Response to acidosis. Kidney responds to acidosis by secreting H+ bound to NH3 (=NH4+) in proximal tubule. NH4+ reabsorbed in ascending limb of loop of Henle into interstitium. NH3 from interstitium diffuses into collecting duct to bind to H+ for excretion.

77
Q

What is the purpose of diuretics?

A

Increase Na+ excretion (natriuresis) followed by water. Decrease ECF volume (oedema, BP)

78
Q

How do osmotic diuretics work and give an example?

A

Mannitol. Increase osmolality of tubular fluid in PCT and loop of Henle. Reduce passive reabsorption of H2O. Used in cerebral oedema (increased osmolality removes fluid from brain)

79
Q

How do loop diuretics work and give an example?

A

Furosemide. Block Na+/Cl-/K+ symporter of thick ascending limb (block at Cl- site)

80
Q

What are the effects of loop diuretics?

A

Prevents creation of hypertonic interstitium
Increase Na+ delivery to DCT (promotes K+ loss)
Decrease Na+ delivery to macula densa (promotes renin release)
Loss of Ca2+ and Mg2+ (loss of transepithelial potential)

81
Q

How do thiazides work and give an example?

A

Chlortalidone. Inhibit Na+/Cl+ symporter in DCT

82
Q

Why do thiazides not work in renally impaired patients?

A

Secreted by weak acid transported in DCT

83
Q

What diuretics cause hypokalaemia and alkalosis and how?

A

Loop and thiazides. Increase Na+ delivery to DCT which stimulates aldosterone Na+ pump in exchange for K+ and H+

84
Q

How do potassium sparing diuretics work?

A

Aldosterone receptor antagonists e.g. spironolactone prevent insertion of Na+ pumps and channels

Na+ channel blockers e.e amiloride

85
Q

Why is K+ important in the body?

A

Excitability of nerve and muscle

Medicine 3 (8 decks)

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