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Physiology and Pharmacology > Renal Anatomy and Disease > Flashcards

Renal Anatomy and Disease Flashcards

1
Q

How much body weight of an average person is water?

A
  • 50-70% (normally 60%)

- in an average person of 70kg is 42L

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2
Q

where is water found in the body?

A
  • in the intracellular compartment or the extracellular compartment
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3
Q

how much water is in the intracellular fluid?

A
  • 62% of the total volume of water in the body

- 25-30L

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4
Q

how much water is found in the extracellular fluid compartments?

A
  • plasma = 7%, 3-4L
  • interstitial fluid = 28%, 11-12L
  • transcellular = 3%, 1.5-2L
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5
Q

what are the cationic concentrations of ICF and ECF?

A

ICF:

  • K+ conc = 148mM
  • Na+ conc = 10mM

ECF:

  • K+ = 5mM
  • Na+ = 140mM
  • this creates conc gradients for K+ to move out of the cell, and Na+ to move into the cell
  • transport pathways are driven by channels and carriers
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6
Q

what are the anionic concentrations of ICF and ECF?

A

ICF:

  • Cl- = 4mM
  • protein = 55mM

ECF:

  • Cl- = 103mM
  • protein = 15mM
  • plasma contains lots of proteins which cannot pass the capillary endothelium as they are too large
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7
Q

what does the total amount of Na+ in the plasma create?

A
  • the effective circulating volume/ECF volume
  • volume of plasma can change which can impact blood pressure
  • changes in plasma are due to renal control as the kidney must handle sodium correctly
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8
Q

what are the typical inputs and outputs of Na+ daily?

A

daily input = 150mM due to diet

  • this input of 150 mM must be excreted to stay in balance
  • we lose 10mM per day in stool and sweat
  • we lose 140mM per day in urine via kidney
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9
Q

what are the typical inputs and outputs of water per day?

A

daily input = 2.6L (1.2L in drink, 1L in food, 0.35L from metabolism)

  • we lose 1.1L per day via respiration, stool and sweat
  • we lose 1.5L per day via urine
  • kidney plays major role in water balance as it is the major route of excretion
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10
Q

what happens if we cannot excrete the sodium and water we have consumed daily?

A
  • sodium becomes accumulated in plasma which changes the ECF volume and therefore changes blood pressure
  • if we cannot excrete water, there is an expansion of the ECF volume and heightened blood pressure
  • excess fluid can accumulate in tissues which can affect lung function
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11
Q

why are kidneys critical?

A
  • they control excretion of sodium and water
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12
Q

what is the general morphology of the kidney?`

A
  • 10cm x 5.5cm
  • located between T12 and L3 vertebrae
  • renal arteries bring blood to kidney, renal veins take blood away
  • renal pelvis leas to ureter which leads to bladder for urine storage
  • 150 grams
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13
Q

what is renal agenesis?

A
  • occurs in 1/2500 foetuses
  • kidneys fail to form
  • incompatible to life
  • high risk of miscarriage if lack of kidney development
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14
Q

what is ectopic kidney?

A
  • occurs in 1/800 post-birth
  • kidneys are not formed in the correct place of the body e.g. in the pelvis
  • causes increased risk of damage and stone formation
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15
Q

what is horseshoe kidney?

A
  • occurs in 1/1000 individuals
  • both kidneys form but are fused across the midline, forming one kidney
  • increased chance of damage and stone formation
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16
Q

what structures can be seen in the longitudinal cross-section of the kidney?

A
  1. capsule: thin fibrous layer around the kidney for structural integrity
  2. cortex: in the light area, below the capsule
  3. medulla: in dark area, beneath the cortex
    - contains medullary rays
    - stripes represent highly capilliarised blood supply
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17
Q

what is the nephron?

A
  • functional unit of the kidney

- 1-1.5 million per kidney

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18
Q

what is the structure of the nephron, and the route of fluid through the nephon?

A
  • Bowman’s capsule (BC) surrounds the glomerulus
  • an afferent arteriole brings blood to the glomerular capillary bed:
    1. plasma is filtered and moved out into BC
    2. any fluid that isn’t filtered leaves via efferent arteriole
  • once in BC, filtrate moves down into nephron:
    1. ultrafiltrate moves through the Proximal tubule, through Loop of Henle, then through the Distal tubule into the Collecting Duct
    2. collecting duct drains 6 distal tubules to form urine
    3. urine is formed for storage in the bladder
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19
Q

what are the two types of nephron?

A
  1. Superficial nephron (85%)

2. Juxtamedullary nephron (15%)

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20
Q

what is the superficial nephron?

A
  • nephrons which sit with glomerulus and BC at the periphery of the cortex
  • Loops of Henle enter the outer medulla and drain into the collecting duct
  • make up 85% of total nephrons in kidney
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21
Q

what is the juxtamedullary nephron?

A
  • where the glomerular beds and BCs sit at the fringe of the medulla
  • they have deep Loops of Henle that penetrate the medulla
  • distal tubules drain into the collecting duct
  • these nephrons play biggest role in concentrating urine
  • make up 15% of all nephrons in the kidney
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22
Q

what is renal failure?

A
  • a fall in glomerular filtrate rate (GFR)

- leads to an increase in serum urea and creatinine

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23
Q

what is acute real failure?

A
  • reversible
  • history is short
  • no change to haemoglobin
  • kidney size stays the same
  • there is no peripheral neuropathy
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24
Q

what is chronic renal failure?

A
  • irreversible: dialysis or transplant is needed
  • progressive
  • long history
  • drop in haemoglobin levels
  • kidney size decreases due to damage
  • involves peripheral neuropathy
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25
Q

what is peripheral neuropathy?

A
  • peripheral nerve damage leading to problems with sensation and movement
  • damage to sensory and motor neurons
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26
Q

how does chronic renal failure progress?

A
  • thickening of glomerular membranes
  • damage to glomeruli capillary beds
  • glomerulosclerosis: scarring of glomeruli
  • tubular atrophy: dying off nephrons
  • interstitial inflammation
  • fibrosis
  • reduction in renal size
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27
Q

what is uraemia?

A
  • term to describe the group of severe symptoms of kidney failure
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28
Q

what are the uraemia symptoms of chronic renal failure?

A
  1. failure to excrete salt and water
    - leads to high BP, hyperkalaemia (increased K+) and mild acidosis
  2. poor excretion of urea/creatinine and leakage of protein into urine
    - loss of plasma proteins, anorexia, nausea, vomiting, neuropathy, pericarditis (inflamed pericardium)
  3. failure of erythropoietin production:
    - kidney normally produces this hormone to form haemoglobin
    - loss of hormone causes anaemia and lethargy
  4. failure to excrete phosphate
    - high phosphate levels lower serum Ca2+ conc by precipitation
    - leads to itchy skin and osteoporosis (brittle bones)/osteomalacia (soft bones)
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29
Q

what is precipitation by phosphate?

A
  • metabolic calcification
  • calcium phosphate is deposited in soft tissues
  • causes pruritus (itchy skin) and bone disease
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30
Q

what is the normal GFR?

A

125ml/min

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31
Q

what are the causes of chronic renal failure?

A
  • 30% cases from glomerulonephritis (kidney infection)
  • 25% cases from diabetes mellitus
  • 10% caused by hypertension
  • 5% caused by polycystic kidney disease (inherited)
  • 10% cases unknown
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32
Q

how can chronic renal failure be treated?

A
  1. treating reversible factors by restricting protein, salt and water in diet
  2. taking phosphate binders: take up excess phosphate
  3. taking sodium bicarbonate: combat acidosis
  4. give diuretic drugs: excrete more sodium and water
    - all 4 of these treatments attempt to reduce symptoms and slow progression
    - these do not reverse the illness as it is chronic
  5. dialysis and transplantation is needed at severe level: GFR <5-10ml/min
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33
Q

where does filtration occur?

A
  • in the glomerulus and glomerular capillaries
  • blood plasma enters capillary bed via afferent arteriole
  • any unfiltered plasma leaves via efferent arteriole to peritubular capillaries
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34
Q

where does urine formation occur?

A
  • ultrafiltrate moves down the nephron and is modified by proximal, LoH, distal and collecting
  • at end of collecting duct, urine is formed, stored in the bladder and excreted
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35
Q

what is glomerular filtration?

A

% of plasma that moves from the capillary to the nephron in the BC, to form ultrafiltrate

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36
Q

what is tubular reabsorption?

A
  • ions, solutes and water leave through the tubular lumen of the nephron and enters the peritubular capillaries
  • peritubular capillaries return this fluid to the venous blood supply
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37
Q

what is tubular secretion?

A
  • when substances in the peritubular capillaries are secreted across renal epithelial cells into tubular fluid and lost in urine
38
Q

what is the glomerulus and how is it involved in filtration?

A
  • glomerulus is a capillary bed
  • diameter = 200nm
  • plasma comes in the afferent arteriole to the capillary bed
  • 20% plasma is filtrated into BC (180L/day)
  • 80% goes through efferent arterioles to peritubular capillaries into venous blood
  • forms ultrafiltrate

plasma volume is 3L, so glomerulus filters a volume 60x the plasma volume (180L/day)

39
Q

what does filtration permit and restrict?

A

permits: H20 and small molecules
- ions, solutes, glucose, amino acids

restricts: blood cells and proteins

40
Q

what is contained in the ultrafiltrate?

A
  • protein-free plasma

- 1% albumin is filtered: small molecular weight proteins which are reabsorbed at the proximal tubule

41
Q

what is the transcellular pathway of tubular transport?

A
  • across cell
  • reabsorption: ions, solutes and water which use transport proteins to move across apical and leave via basolateral membranes to enter the peritubular capillary
  • secretion: transport proteins are used to move solutes from peritubular capillary and interstitial fluid from basolateral, to apical, and into the lumen
42
Q

what is the paracellular pathway of tubular transport?

A
  • between cells via tight junctions
  • lets ions, solutes and water move between them
  • reabsorption = from tubular fluid into peritubular capillary
  • secretion = from peritubular capillary into tubular fluid
43
Q

what is the Proximal Tubule?

A
  • bulk reabsorbing epithelium: reabsorption of 70% of the filtrate
  • 70% H2O and Na+ are filtered by glomerulus and reabsorbed by PT
  • 100% glucose and amino acids are reabsorbed
  • 90% bicarbonate is reabsorbed
44
Q

what is transported at the basolateral membrane of the proximal tubule?

A
  1. Sodium-potassium ATPase
    - transports 3Na+ out and 2K+ in using ATP hydrolysis
    - moves ions against electrochemical forces
    - maintains low intracellular Na+ to form conc gradient for Na+ to move across apical side
  2. potassium channel
    - sets up driving force for Na+ uptake at apical membrane
    - sets negative membrane potential as K+ leaves the cell
    - K+ leaves the cell through this channel
45
Q

what is transported at the apical membrane of the proximal tubule?

A
  1. sodium-glucose cotransport protein (SGLT1, SGLT2)
    - uses Na+ gradient from Na-K ATPase to bring glucose into cell
    - glucose moves against conc gradient across apical membrane
    - glucose is then absorbed into peritubular capillary at basolateral side down conc gradient via facilitated diffusion
  2. Sodium-amino acid cotransporters (same as glucose)
  3. NaPiII (sodium-phosphate cotransporter)
    - binds sodium and phosphate
    - uses the electrochemical force of Na+ to bring phosphate into cell
    - phosphate diffuses across basolateral membrane into peritubular capillary
46
Q

what happens to Na+ that enters the proximal tubule from the cotransporters?

A
  • they are moved out by the Na-K ATPase on the basolateral membrane to maintain low intracellular sodium

reabsorption of sodium drives water reabsorption

47
Q

what happens to the phenotype of mice when NaPiII is knocked out?

A

mice cannot make the NaPiII protein:

  • less phosphate reabsorption
  • decreased plasma-phosphate levels due to phosphate being lost in the urine

there is more phosphate in the tubular fluid:

  • causes increased calcification due to precipitation, leading to the formation of intraluminal stones (nephrolithiasis)
  • deposits renal parenchyma (nephrocalcinosis)
  • causes renal damage
48
Q

how does bicarbonate reabsorption occur at the proximal tubule?

A

NHE3 (sodium-hydrogen exchanger) on apical membrane:

  • as Na+ enters cell, H+ leaves
  • H+ that leaves binds to bicarbonate to form carbonic acid
  • carbonic anhydrase causes carbonic acid to dissociate to CO2 and H2O at apical membrane
  • CO2 diffuses into the cell down conc gradient
  • H2O moves into cell via aquaporins
  • inside the cell, carbonic anhydrase in the ICF forms recombines CO2 and H2O to form carbonic acid
  • carbonic acid forms bicarbonate

bicarbonate and sodium are reabsorbed at the basolateral membrane by a cotransporter

  • one bicarbonate and 3Na+ enter the peritubular capillary
  • bicarbonate maintains pH in the plasma
49
Q

what happens to the phenotype of mice when NHE3 is knocked out?

A

mice cannot reabsorb bicarbonate due to lack of H+ secretion:

  • causes acidosis, so plasma is reduced by 0.1pH, which impacts electrolytes
  • impacts systole in cardiac cycle due to lack of Na+ reabsorption
  • mice lose more fluid
50
Q

why does losing NHE3 cause major issues?

A
  • inhibition of H+ secretion
  • inhibition of sodium and bicarbonate reabsorption
  • fall in fluid reabsorption
  • drop in plasma bicarbonate, leading to acidosis
  • fall in BP due to decrease in ECF volume as lack of water reabsorption
51
Q

what is the transport maximum?

A
  • rate of transport has a maximum limit as there are a limited number of protein carriers in the cell membrane

example: increase in plasma glucose causes increase in rate of filtration
- at a certain point, whatever is being filtered is reabsorbed, so nothing appears in the urine
- transport max of glucose = 375mg/min

52
Q

why can some glucose appear in the urine? what is it an indication of?

A
  • when reabsorption becomes constant
  • the renal threshold is extrapolated due to plasma glucose level being above glucose in the urine
  • this threshold can indicate diabetes mellitus
53
Q

how does secretion occur in the proximal tubule?

A

2 systems:

  • organic cations
  • organic anions
  • rapid removal of compounds via excretion
  • removal of plasma protein-bound substances of peritubular capillaries to tubular fluid
  • removal of foreign compounds e.g. penicillin (not always helpful)
54
Q

why is a high dose of penicillin needed when treating an antibiotic infection?

A
  • the proximal tubule filters it into the urine very quickly
55
Q

what is the role of the Loop of Henle?

A
  • concentrates the urine
  • reabsorption of Na+, Cl- and H2O
  • reabsorption of Ca2+ and Mg2+
  • site of action of loop diuretics
56
Q

what are diuretics?

A
  • class of drug which increases urine flow rate to lose excess fluid
57
Q

what are the 3 structures of the loop of Henle?

A
  1. thin descending limb
    - water permeable
    - impermeable to Na+ and Cl-
  2. Thin ascending limb
    - permeable to Na+ and Cl-
    - impermeable to water
  3. thick ascending limb
    - permeable to Na+ and Cl-
    - impermeable to water
58
Q

what is transported at the basolateral membrane of the Thick Ascending Limb of the Loop of Henle?

A
  1. Sodium-potassium ATPase
    - sets up driving force for influx of sodium across the apical membrane
    - maintains low intracellular sodium
  2. Barttin-CLCK chloride channel
    - Barttin is a protein beta-subunit which transports CLCK to basolateral membrane of TAL
    - CLCK is a channel which allows chloride to diffuse into the peritubular capillary via facilitated diffusion
  • allows for absorption of NaCl
  • Ca2+ and Mg2+ are absorbed by paracellular transport as they follow NaCl
59
Q

what is transported at the apical membrane of the thick ascending limb of the Loop of Henle?

A
  1. NKCC2: Na-K-Cl cotransporter
    - uses Na+ electrochemical force to bring 2Cl- and K+ into cell
    - Na+ is reabsorbed into peritubular capillary via Na-K ATPase on basolateral membrane
    - Cl- is reabsorbed by CLCK on basolateral membrane
    - drives transport of water
  2. ROMK: potassium channel
    - K+ is recycled at the apical membrane into tubular fluid
    - this sets up the negative membrane potential across apical membrane for TAL to function
    - if there is not enough K+ in tubular fluid, NKCC2 cannot work
60
Q

what is Bartter’s syndrome?

A
  • mutation of the thick ascending limb
  • recessive genetic mutation: inherited

symptoms:

  • saltwasting and polyuria due to lack of NaCl and H2O reabsorption
  • decrease in ECF volume -> hypotension
  • hypokalaemia: low K+ plasma
  • metabolic alkalosis
  • hypercalciuria: increased Ca2+ in urine due to less reabsorption of Ca2+ and Mg2+ due to less NaCl reabsorption
  • nephrocalcinosis
61
Q

what causes Bartter’s syndome?

A

Loss of function mutations:
1. Mutation in NKCC2 causes inability to reabsorb NaCl

  1. CLCK mutation leads to accumulation of Cl- in the cell
    - high intracellular Cl- conc stops NKCC2 from working
    - this stops reabsorption of NaCl
  2. ROMK mutation means K+ cannot be recycled across apical membrane, so there is less K+ in tubular fluid
    - this stops NKCC2 function so less NaCl reabsorption
62
Q

what happens to the phenotype of mice when ROMK is knocked out?

A

these mice cannot make the ROMK channel:

  1. salt wasting: fractional excretion of Na+ and Cl- is high as K+ is no longer recycled on apical
    - causes loss of NaCl in urine
  2. polyuria: urine flow is higher
    - knockout mice lose more water due to less NaCl reabsorption
  3. mice have acidosis rather than alkalosis which humans have
    - there is no difference in wildtype and knockout mice in plasma K+
    - doesn’t fully reflect human patients with lack of ROMK
63
Q

what are 2 examples of loop diuretics and what do they do?

A
  • both inhibit NKCC2 to inhibit NaCl reabsorption and water reabsorption
  • cause an increase in urine flow rate
  • lower ECF volume to treat high blood pressure
  • have Bartter’s-like symptoms so must be dosed correctly to avoid hypotension
64
Q

what is the role of the early distal tubule?

A
  1. reabsorption of NaCl
  2. reabsorption of Mg2+

sensitive to thiazide diuretics

65
Q

what is transported at the basolateral membrane of the early distal tubule?

A
  1. sodium-potassium ATPase
    - uses ATP to maintain low intracellular Na+ conc by exchanging 3Na+ out of cell for 2K+ into cell
  2. K+ channel
  3. CLCK
66
Q

what is transported at the apical membrane of the early distal tubule?

A
  1. NCC: sodium-chloride cotransporter
    - Na+ across apical membrane is driven by the electrochemical gradient
    - binds Na+ and Cl- and undergoes conformational change to bring them into the cell

Na+ is reabsorbed by Na-K ATPase
Cl- is reabsorbed by CLCK

  1. Magnesium channels
    - located on apical membrane, but there are no magnesium transporters on the basolateral membrane
    - it is unknown how magnesium is reabsorbed
67
Q

what is Gitelman’s syndrome?

A
  • recessive genetic mutation in NCC (inherited)
  • salt wasting and polyuria
  • hypotension
  • hypokalaemia
  • metabolic alkalosis
  • hypocalciuria (different to Bartter’s) - decrease in Ca2+ in urine
68
Q

what causes Gitelman’s syndrome?

A

Loss of function mutation:

  • NCC can no longer transport Na+ and Cl- into distal tubule, so there is more NaCl in the urine
  • less NaCl reabsorption means less water reabsorption, causing polyuria

still unknown as to why hypocalciuria is caused

69
Q

how can functions of transporters in mice be observed?

A

xenopus oocyte studies:

  • inject RNA of a protein of interest
  • protein of interest is made and used at the membrane
  • functional analysis of NCC: radioactive Na+ is tracked to see how much radioactivity is in the ICF and thus how much Na+ transport into the distal tubule
70
Q

what are thiazide diuretics?

A

Chlorothiazide:

  • inhibit NCC to reduce NaCl reabsorption
  • reduces water reabsorption to increase urine flow and remove excess ECF volume
  • treats high BP as cardiac output falls due to the lowered ECF volume
  • Gitelman’s-like side effects
71
Q

what is the benefit of carrying one mutation for ROMK, NCC or NKCC2?

A

protects against hypertension

72
Q

what are the roles of the late distal tubule, collecting tubules and cortical collecting duct?

A
  • concentrates urine
  • reabsorption of Na+ and water
  • secretion of K+ and H+ into urine

connecting tubules link late DT to CCD

73
Q

what are the two cell types of the late distal tubule and the cortical collecting duct?

A

Principal:

  • Na+ and water reabsorption
  • K+ and H+ secretion

Intercalated:

  • alpha-intercalated cell
  • beta-intercalated cell
  • H+ secretion and reabsorption
  • bicarbonate secretion and reabsorption
74
Q

what is transported at the basolateral membrane of the principal cell of the late DT and CCD?

A
  1. sodium-potassium ATPase
    - sets up electrochemical driving force of Na+ by keeping intracellular Na+ concentration low
  2. Aquaporins 3 and 4
    - water is reabsorbed to peritubular capillary
    - always open and active
  3. Kir2.3: K+ channel
    - allows K+ reabsorption into the peritubular capillary
75
Q

what is transported at the apical membrane of the principal cell of the late DT and CCD?

A
  1. ENaC: Na+ selective channel
    - allows Na+ to diffuse into cell down the electrochemical gradient
    - Na+ is then lost on the basolateral membrane by ATPase, so net reabsorption
    - water is also reabsorbed by AQP3 and AQP4
    - regulation of ENaC determines the final Na+ conc in urine
  2. aquaporin 2
    - water moves down osmotic gradient across the apical membrane
  3. ROMK:
    - drives potassium secretion across the apical membrane into the tubular fluid and so into urine
76
Q

what is the relationship between Na+ and H+ in the principal cells of the late DT and CCD?

A
  • the more Na+ that is reabsorbed, the more H+ that is secreted into the urine
  • can cause metabolic alkalosis in Bartter’s and Gitelman’s
77
Q

what is the relationship between Na+ and K+ in the principal cells of the late DT and CCD?

A
  • there is an enhanced driving force for Na+ at the principal cell, so more reabsorption by ENaC
  • this causes more secretion of K+
  • in Bartter’s and Gitelman’s syndromes, this process is amplified
  • this causes a major fall in plasma K+ levels due to loss of urine
78
Q

what are the 3 principal cell diseases?

A
  1. Diabetes insipidus: AQP2
    - problem with AQP2 mechanism, so there is a struggle to reabsorb water
    - major loss of fluid in the urine
  2. Liddle’s syndrome: ENaC
    - functional mutation in ENaC subunit
    - causes absorption of too much water which increases ECF volume
    - causes hypertension
  3. pseudohypoaldosteronism
79
Q

what is amiloride?

A

diuretic used to treat high BP:

  • an antagonist of ENaC: blocks Na+ reabsorption across the apical membrane
  • this causes a loss in the osmotic gradient so less water reabsorption
  • more Na+ and water is lost in the urine
  • this causes decreased ECF volume and so reduces hypertension
80
Q

what is the role of the alpha-intercalated cells in the late DT and CCD?

A
  1. H+ secretion

2. bicarbonate reabsorption

81
Q

what is transported at the basolateral membrane of the alpha-intercalated cell of the late DT and CCD?

A
  1. chloride channel
    - Cl- is reabsorbed/recycled and sets up electrochemical gradient to be exchanged for bicarbonate by AE1
  2. AE1: bicarbonate-chloride exchanger
    - bicarbonate is made inside the cell and is exchanged out of the cell, with Cl- entering the cell
    - bicarbonate is reabsorbed into peritubular capillary
82
Q

what is transported at the apical membrane of the principal cell of the late DT and CCD?

A
  1. Proton ATPase:
    - hydrolyses ATP to pump H+ against its conc gradient into tubular fluid
    - causes loss of H+ to urine
    - secretion
83
Q

what is the role of the beta-intercalated cells in the late DT and CCD?

A
  1. bicarbonate secretion
  2. H+ and Cl- absorption

(opposite of alpha ICs)

84
Q

what is transported at the basolateral membrane of the beta-intercalated cell of the late DT and CCD?

A
  1. proton ATPase

- protons are reabsorbed

85
Q

what is transported at the apical membrane of the beta-intercalated cell of the late DT and CCD?

A
  1. chloride channel
    - secretes Cl-
  2. AE1:
    - exchanges chloride for bicarbonate
    - chloride is absorbed into cell
    - bicarbonate is secreted into tubular fluid and into the urine
86
Q

what is the relationship between alpha and beta IC cells?

A
  • they are dynamic so can change formation depending on the function required
87
Q

what are the properties of the medullary collecting duct?

A
  • low Na+ permeability due to less ENaC

- high H2O and urea permeability in the presence of vasopressin due to trafficking of aquaporins

88
Q

what is acute renal failure and its symptoms?

A

fall in GFR over hours/days

symptoms:

  • hypovolaemia: oligura (low urine flow) due to low GFR and expansion of ECF volume
  • hyperkalaemia: lack of K+ secretion so increased plasma K+ -> affects cardiac excitability
  • acidosis: depression of CNS as more H+ accumulation due to low urine flow
  • high urea/creatinine: cannot remove nitrogenous waste
  • impaired mental functon
  • nausea and vomiting
89
Q

what causes acute renal failure and how can it be treated?

A

Causes:

  • impaired fluid and electrolyte homeostasis
  • accumulation of nitrogenous waste due to inability to excrete

lasts 1 week and is reversible

treatment: short term dialysis until kidneys gain function again

90
Q

what does the oligura of acute renal failure cause?

A
  • hypotension due to loss of blood volume, causes poor renal perfusion of blood
  • rhabdomyolysis (release of myoglobin from damaged muscle) has toxic effects on kidney tubules
  • compression damage causes release of ICF to ECF, so K+ enters ECF
  • tachycardia due to increased plasma K+ which had been released from damaged cells
  • low bicarbonate -> acidosis
91
Q

how is oliguria treated?

A
  • IV saline – treat hyperkalaemia and get blood volume and pressure back to normal for normal perfusion of kidneys for glomerular filtration
  • HCO3- - to bring level to normal
  • Rehydrate in this case – increase blood volume
  • Dialysis if oliguria persists

Physiology and Pharmacology (13 decks)

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