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Medicine Year 2 > Repro Topic 6 - Kidney > Flashcards

Repro Topic 6 - Kidney Flashcards

1
Q

How long is the PCT?

A

14 mm

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2
Q

What is the function of the PCT?

A
  • 70% reabsorption - microvilli increase surface area
  • Mostly active transport, almost everything moves with sodium (partially controlled by angiotensin II)
    • SGLT2 - active sodium and glucose reabsorption
    • Sodium and amino acid reabsorption
    • Sodium + sulphate/phosphate reabsorption
    • Sodium-hydrogen antiporter - sodium reabsorbed, hydrogen secreted
    • Basolateral Na+/K+ ATPase pumps sodium back into circulation
    • Aquaporin 1 - water movement due to osmotic gradient
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3
Q

How is H+ concentration maintained?

A
  • Acid-base balance
  • ECF and ICF equal, has to be kept within tight range
  • Typical western diet - net acid
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4
Q

How can kidney function be calculated?

A
  • MDRD formula used in labs
  • Cocheroft-Gault for prescribing - based on creatinine clearance
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5
Q

Describe the function of the kidney in erythropoietin production

A
  • Secreted from interstitial cells of the kidney
  • Filters blood, have cells sensitive to low pO2
  • Low pO2, increased EPO production, increased red blood cell mass, increased tissue pO2
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6
Q

What is the macula densa and what is its function?

A
  • Where thick ascending LH meets DCT - in contact with the glomerulus
  • Sensitive to sodium chloride concentration - increases blood flow in afferent arteriole and increases renein release from juxtaglomerular cells ( on afferent/efferent arterioles) if sodium chloride concentration is low
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7
Q

What triggers aldosterone release?

A

Angiotensin II or high serum K+ concentration

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8
Q

What causes metabolic alkalosis?

A

Low H+ or high bicarbonate

  • Volume depletion -
    • Gastric acid loss (vomiting)
    • Diuretics
  • Volume repleted type
    • Mineral corticoids
    • Hyperaldosteronism
    • Bartler’s syndrome
    • Cushing’s syndrome
    • Profoud K+ depletion
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9
Q

How does the kidney contrubite to acid-base balance?

A
  • Reabsorbs filtered bicarbonate - mostly in PCT (also thick ascending LH and DCT), carbonic anhydrase converts H+ and bicarbonate to H2O and CO2 to move into cells and be reabsorbed
  • Filters non-volatile acids e.g. sulphuric - uses PO4 or NH3 to fix H+, excreted into urine as H2PO4 or NH4
  • PCT synthesises ammonium, glutamine and amino acids
    • 1 bicarbonate ion returned to circulation for every H+ excreted as ammonium
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10
Q

How can uric acid stones be prevented?

A
  • Increase fluid consumption
  • Treat hyperuricaemia with xanthine oxidase inhibitors e.g. Allopurinol/rasburicase (gout treatment)
  • Alkalinise urine (pH > 6.0) - bicarbonate/citrate
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11
Q

Describe creatinine metabolism in the kidneys

A
  • Breakdown product of creatinine phosphate - muscle metabolism
  • Freely filtered at glomerulus
  • Not reabsorbed
  • Minimal tubular secretion
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12
Q

Describe the body fluid compartments

A

Intracellular fluid = 2/3

Interstitial and intravascular fluid (extracellular) = 1/3

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13
Q

What is the maximum/minimum urine production per day?

A

Minimum urine output = 0.4L per day

Maximum urine output = 12L per day

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14
Q

Why is maintenance of Ca2+ concentration important?

A

For normal muscle and nerve function

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15
Q

What are the causes of kidney disease?

A
  • Ineffective blood supply - low plasma volume (e.g. due to haemorrhage) or narrowed renal arteries
  • Glomerular disease
  • Interstitial disease - tubules
  • Obstructive uropathy
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16
Q

What is typically found on examination in renal stones?

A
  • Flank tenderness when balloting the kidneys
  • Signs of infection
  • Obesity
  • Hypertension
  • Gouty tophi - nodular masses, urate deposits
  • Diabetes mellitus
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17
Q

How is urine examined?

A
  • Visual inspection
  • Dipstick analysis
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18
Q

What are struvite renal stones composed of?

A

Magnesium ammonium phosphate

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19
Q

Describe the mechanism of action of Thiazide diuretics

A
  • Inhibits NCC (Na+/Cl- symporter), inhibits reabsorption of sodium and chloride ions from the DCT
  • Also increase reabsorption of calcium ions
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20
Q

What drives the movement of ions in the Loop of Henle?

A

Countercurrent exchange multiplier

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21
Q

What pathologies can CT of the kidneys show?

A

Trauma, stones, tumour, infection, renal stones (location and type)

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22
Q

Describe lactic acidosis

A
  • Pyruvate converted to lactic acid which is converted to lactate, metabolised in liver/kidney
  • Acidosis due to hypoperfusion, low hepatic clearance (sepsis) or drugs e.g. metformin
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23
Q

What is the cause of acidosis?

A

High H+ or low HCO3-

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24
Q

In what type of patients are loop diuretics the diuretic of choice?

A

Those with impaired renal function

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25
Q

How can cysteine stones be prevented?

A
  • Increase fluid intake
  • Low protein/sodium diet
  • Alkalinise - bicarbonate/citrate
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26
Q

How are renal stones in the ureter treated?

A
  • Small
    • Expectant management
    • Lower ureter - uteroscopic stone removal
    • Mid/upper - extracorporeal shock wave lithotripsy (ESWL)
  • Large (>7mm)
    • ESWL
    • Uteroscopic stone fragmentation
    • Open surgery
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27
Q

What is the effect of impaired renal function on drug excretion?

A

Drugs will be excreted very slowly

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28
Q

What is the function of the glomerulus/Bowman’s capsule?

A
  • Blood through afferent arteriole into the glomerulus at high pressure - controlled by sympathetic nervous system and prostaglandins
  • Blood flows through glomerulus tufts, fluid filtered into Bowman’s capsule to produce filtrate
  • Molecules and water pass through pass through glomerular basement membrane, negative charge repels proteins
  • Large molecules don’t get through
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29
Q

How is ureteric stenting used in the treatment of renal stones?

A
  • Allows drainage of obstructed kidney - alleviate pain
  • Dilate ureter - passage of stone?
  • Better ESWL and uteroscopic outcomes
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30
Q

How can calcium oxalate stones be prevented?

A
  • Increase fluid
  • Low oxalate diet
  • Citrate
  • Thiazide diuretic?
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31
Q

Describe urea metabolism in the kidney

A
  • Urea is by-product of amino acid metabolism in liver
  • Reabsorbed in inner medullary collecting ducts (passively)
  • Involved in countercurrent exchange and maintaining concentration gradient
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32
Q

Which drugs can cause renal papillary necrosis?

A
  • Aspirin
  • NSAIDs
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33
Q

Can a low calcium diet be used to prevent calcium containing renal stones?

A

No - no good evidence

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34
Q

What kind of ion channels are present in the thick ascending limb of the loop of Henle?

A
  • NKCC2 channel - active reabsorption of Na+, K+, Cl- (two chloride ions for every one sodium/potassium)
    • Blocked by loop diuretics - more Na+ excreted, more water excreted
  • Gradient maintained by basolateral Na+/K+ ATPase
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35
Q

What is the potential consequence of respiratory alkalosis?

A

Causes increased albumin binding to calcium, therefore lowers ionised calcium leading to tentany

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36
Q

What is the typical history of a patient with renal stones?

A
  • Renal colic (flank pain) - moves loin to groin
  • Passage of stones
  • Haematuria
  • Infection
  • Family history, diet
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37
Q

Describe the components of acid-base balance

A
  • Buffering
  • Ventilation - control of CO2
  • Renal regulation of HCO3- and H+ secretion/reabsorption
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38
Q

In which drugs does enhancement of adverse effects occur in renal impairement?

A
  • Digoxin
  • Potassium-sparing diuretics
  • Biguanides (metformin) - lactic acidosis
  • Sulphonylureas - hypoglycaemia
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39
Q

How does the kidney process lipid soluble drugs?

A

Lipid soluble drugs passively reabsorbed by diffusion - not usually excreted in urine

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40
Q

List the functions of the kidney

A
  1. Removing metabolic waste from extracellular fluid - urea, acids
  2. Controlling volume of extracellular fluid (and therefore blood pressure)
  3. Maintaining optimal concentration of solutes in the extracellular fluid (Na+, K+, H+, Ca2+, Mg, Cl-, phosphate)
  4. Extra functions e.g. erythropoietin production
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41
Q

Describe the venous drainage of the kidneys

A
  • Left and right renal veins
  • Leave hilum anterior to arteries, drain to inferior vena cava
  • Left is longer, passes anterior to abdominal aorta
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42
Q

What causes calcium-containing stone formation?

A

Primary hyperparathyroidism

Hypercalcaemia

Idiopathic hypercalciuria

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43
Q

How can struvite stones be prevented?

A
  • UTI treatment
    • Bacteria increases urease enzymes - produce ammonium
    • E.g. proteous spp, staph spp, Klebsiella spp.
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44
Q
A
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45
Q

What is the function of the loop of Henle?

A

Reabsorbs 20% of Na+ and large amounts of water

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46
Q

Which drugs have decreased sensitivity in renal impairment?

A
  • Diuretics
  • Urinary antibacterials
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47
Q

What is the physiological response to acidosis?

A
  • Increased ventilation (shifts equilibrium)
  • Kidney - increased hydrogen secretion, increased bicarbonate reabsorption
  • Other buffers - haemoglobin, proteins, bone, PO4 - absorb H+
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48
Q

List the types of diuretics and give examples of each

A
  • Loop e.g. Bumetanide, Furosemide
  • Thiazide e.g. Bendroflumethazide, Indapamide
  • Potassium sparing e.g. Amiloride, spironolactone
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49
Q

How are renal stones within the kidney treated?

A
  • <2cm - expectant management or offer extracorporeal shock wave lithotripsy (ESWL)
  • >2cm or multiple - expectant management or percutaneous ultrasonic lithotripsy (PUL)
  • Large branched ‘staghorn’ stones - ESWL + PUL
  • Cysteine stones - PUL or open nephrolithotomy
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50
Q

What may be the consequence of maintaining [H+]?

A

May be at the expense of other abnormal blood chemistry e.g. [HCO3-], pCO2

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51
Q

Describe the release of anti-diuretic hormone

A

High serum osmolality and/or decreased stretch baroreceptors/atrial stretch causes increased ADH synthesis in the hypothalamus, released by the posterior pituitary

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52
Q

Describe secondary prevention of renal stones

A
  • If multiple stones in 10 years
  • Increase fluid intake, increase citrate, stone-type specific advice
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53
Q

How can the cause of metabolic acidosis be determined?

A
  • Use anion gap to identify likely cause
  • High anion gap - high acid production, chronic renal failure
  • Low anion gap - loss of bicarbonate = some cases of chronic renal failure, renal tubular acidosis
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54
Q

List drug induced glumerulonephropathies

A
  • Membraneous
    • Castopril, Gold salts, heavy metals, penicillamine, phenytoin
  • Minimal change
    • NSAIDs (stop synthesis of prostaglandin for vasodilation of afferent arteriole)
  • Acute nephritis - penicillin
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55
Q

Describe the typical dialysis regime of a patient with chronic kidney disease

A

3x per week, 4/5 hours per session

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56
Q

How do the kidneys interact with the circulation?

A
  • Baroreceptors (pressure) - carotid sinus, aortic arch, cardiac chambers, afferent arteriole of glomerulus
    • Detect changes, respond via sympathetic nervous system
    • If the ECF is depleted, baroreceptors detect change in BP, sympathetic stimulation causes afferent arteriole vasoconstriction to increase the volume of the ECF
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57
Q

What is the compensatory response to metabolic alkalosis?

A

Hypoventilation - increase pCO2

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58
Q

Define renal stones

A
  • Also called renal calculus or nephrolithiasis
  • Solid concretion of crystal aggregate formed within the urinary space
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59
Q

What problems does impaired renal function cause in drug therapy?

A

Toxicity due to increased sensitivity or ineffective treatment due to decreased sensitivity

  • Impaired absorption
  • Impaired elimination
  • Renal dysfunction effect on hepatic drug elimination
  • Increased tissue sensitivity
  • Protein binding
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60
Q

What is the physiological response to increased sensed volume?

A

Natruiretic peptides (ANP, BNP) - opposite effect to angiotensin II

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61
Q

What is the function of the collecting tubules and how is it regulated?

A
  • Collect and concentrate urine from the nephrons
  • Hormonal control - anti-diuretic hormone via AQP2 and aldosterone
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62
Q

What causes urate stone formation?

A

Hyperuricaemia

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63
Q

How is the action of rifampicin changed in impaired kidney function?

A

Metabolised by liver, half-life same in CKD

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64
Q

Which are the most common types of renal stones?

A

Calcium containing (phosphate or oxalate)

65
Q

What is the function of the juxtaglomerular apparatus?

A

Maintain glomerular filtration rate

66
Q

Describe the structure of the glomerular filtration barrier

A
  • Specialised capillary endothelium - fenestrated
  • Glomerular basement membrane is collagen based
  • Podocytes (foot processes)
67
Q

What is the first warning sign of acute tubular necrosis?

A

Oliguria

68
Q

What is ENaC?

A
  • Epithelial sodium channel - selectively permeable to sodium ions
  • Located in the apical membrane of polarised epithelial cells of the kidney, particularly in the collecting ducts
69
Q

What does proteinuria indicate?

A

Consistent = glomerular disease

One off = heavy exercise/infection

70
Q

What is the response of the juxtaglomerular apparatus to decreased tubular flow?

A

Juxtaglomerular cells produce renin

71
Q

Describe the acid-base balance equation

A

H+ + HCO3- <–> H2CO3 <–> H2O + CO2

HCO3- - buffer, absorbs H+, kidneys regenerate

CO2 exhaled

72
Q

List the ideal characteristics of drugs to be used in CKD

A
  • Predominant hepatic/biliary elimination
  • Less than 25% excreted unchanged
  • No active metabolites
  • Wide therapeutic margin
  • Disposition unaffected by protein binding changes or by fluid balance changes
  • Response unaffected by tissue sensitivity changes
  • Not nephrotoxic
73
Q

How is the tubular flow rate detected?

A

By the macula densa - detects changes in the DCT

74
Q

What is the physiological response to reduced sensed volume?

A

Oliguria, concentrated urine, decreased Na+ concentration, K+ excretion

75
Q

What is tested for in dipstick urinalysis?

A
  • Protein (albumin)
  • Haemoglobin (indicates presence of blood)
  • pH
  • Ketones
  • Glucose
  • Bilirubin
  • Leukocytes, nitrites (inflammation/infection)
76
Q

What are the clinical uses of thiazide diuretics?

A

Hypertension, oedema, hypercalcuria, nephrogenic diabetes insipidus

77
Q

Describe the mechanism of action of loop diuretics

A
  • Act on thick ascending loop of Henle - inhibits the NKCC2 channel
  • Inhibits sodium, potassium and chloride reabsorption - more water excreted
  • Acts by competing for the Cl- binding site
  • Also causes increased renin secretion, increased glomerular perfusion and so GFR
  • Inhibits magnesium and calcium reabsorption in the thick ascending limb
78
Q

What kind of junctions are present between the cells of the PCT?

A

Tight junctions

79
Q

What investigations should be done in suspected renal stones?

A
  • Imaging - ultrasound (see acoustic shadow)
  • Serum and urine biochemistry - dipstick for protein, blood, leukocytes
  • Composition of stone -
    • Cysteine - low density
    • Struvite - low density
    • Calcium - high density
80
Q

Describe examples of tubulo-interstitial diseases

A
  • Congenital - autosomal dominant polycystic kidney disease, reflux nephropathy/chronic pyelonephritis, medullary cystic kidney disease, nephropthiasis, salt losing nephropathies (e.g. Bartler’s syndrome)
  • Chronic nephrotoxic ingestion - analgesic nephropathy, lithium nephrotoxicity, chinese herb nephropathy, lead nephropathy
  • Autoimmune - sanoidosis, Sjogren’s syndrome
  • Other - chronic bilateral recurrent caliculi, nephrocalcinosis, myeloma
81
Q

What is respiratory acidosis?

A

High CO2 concentration, low pH

82
Q

How can calcium phosphate stones be prevented?

A
  • Increase fluid consumption
  • Citrate
  • Thiazide diuretic? - reduces calcium
83
Q

What is the kidney’s role in toxin metabolism?

A
  • Metabolism of:
    • Insulin
    • Beta-2-microglobulin
    • Medicines
84
Q

What kind of junctions are present between cells in the thin descending loop of Henle?

A

Loose junctions

85
Q

What does ultrasound of the kidneys show?

A

Size, shape, location, structure, drainage/obstruction, blood flow, cysts

86
Q

Describe the structure of the coverings of the kidney

A

Inner to outer:

  1. Renal capsule - fibrous
  2. Perirenal fat
  3. Renal fascia - around kidney and adrenal gland
  4. Pararenal fat
87
Q

List diseases of the renal arterial supply which affect the main renal arteries

A
  • Atherosclerotic renal artery disease
  • Fibromuscular dysplasia
88
Q

What are the consequences of kidney failure?

A
  • Excretion of solutes - high plasma concentration of urea/creatinine
  • Excretion of drugs - drug toxicity
  • Salt and water balance - extracellular fluid overload/depletion
  • BP control - hypertension
  • Electrolye balance - hyperkalaemia, hypokalaemia etc.
  • Acid-base balance - metabolic acidosis
  • Erythropoietin - anaemia
  • Vitamin D activation - hypocalcaemia and secondary hyperparathyroidism
89
Q

Which drugs have the potential to cause Fanconi’s syndrome?

A

Aminoglycosides, NSAIDs, paracetamol

90
Q

Why is the kidney vulnerable to toxicity?

A
  • Large blood flow
  • Drug and/or metabolites concentrate in renal medulla
  • Further concentration in tubular cells
91
Q

What produces aldosterone?

A

Zona glomerulosa of adrenal cortex

92
Q

What are the ‘rules’ which dictate the movement of ions/water in the loop of Henle?

A
  • Thick ascending loop is impermeable to water, actively transports Na+, K+ and Cl-, providing a concentration gradient (fluid in intersitium becomes more concentrated that in thick ascending LH)
  • Thin descending LH - freely permeable to salt and water
  • Interstitium becomes concentrated due to movement of ions out of thick ascending LH, water moves out of thin descending LH into interstitium
  • Specialised blood vessel - vasa recta - winds around loop to take water from interstitium, doesn’t wash away concentration gradient
93
Q

What are the clinical uses of loop diuretics?

A

Oedema, acute renal failure, hypertension, hypercalcaemia

94
Q

Describe the classification of chronic kidney disease

A
  1. Kidney damage with normal or raised GFR, GFR > 90
  2. Kidney damage with mildly impaired GFR, GFR 80-60
  3. Moderately impaired GFR, GFR 30-59
  4. Severely impaired GFR, GFR 15-29
  5. Established renal failure, GFR <15 or on dialysis
95
Q

List causes of metabolic acidosis

A
  • Extra acid - lactic acidosis, ketoacidosis
  • Failure to excrete acid - renal tubular acidosis
  • Loss of HCO3 - stool (diarrhoea) or urine (renal tubular acidosis)
96
Q

What is the function of the DCT?

A
  • 5% sodium reabsorption
  • Main channel = NCC
    • Active Na+ and Cl- reabsorption, maintained by basolateral Na+/K+ ATPase
    • Blocked by Thiazide diuretics - more Na+ excreted, more water secreted
  • No hormonal control
97
Q

How should drug prescription be altered if there is reduced elimination due to impaired renal function?

A
  • Modify dose - decrease dose or increase dose interval (in drugs with 50% renal clearance and low therapeutic index)
  • Loading dose?
  • Monitor drug concentration
98
Q

What are the effects of ADH?

A
  • Increased thirst
  • Collecting duct AQP2 channel insertion
  • Vasoconstriction
  • = increased fluid retention, decreased serum osmolality, increased BP
99
Q

Which organs contribute to drug metabolism?

A

Kidney and liver

100
Q

Give examples of drugs whose action is affected by renal impairment

A
  • Gentamicin, vancomycin
    • Antibiotics, metabolised fully in kidney
    • Toxicity and dosing altered in decreased kidney function
    • Take into accound gender, age, weight, height
101
Q

How is K+ concentration maintained?

A
  • Low plasma volume or increased plasma K+- renin-angiotensin system activated, K+ excreted
  • High or low potassium affects muscles and nerves - cardiac arrhythmias/paralysis
102
Q

Why does hypocitraturia cause renal stone formation?

A
  • Citrate is protective - prevents stone formation
  • Inhibits stone formation - increased by low Na+ diet, decreased by acidosis
  • Forms complexes with calcium
  • Increases activity of macromolecules which inhibit CaOx aggregation
  • Alkalinising effect - inhibits urate and cysteine stones
103
Q

Where is aspirin secreted in the nephron?

A

PCT - weak acid (salicylic acid)

104
Q

Define medullary sponge kidney

A

Congenital disorder of kidneys characterised by cystic dilation of collecting tubules of one or both kidneys - predisposes to stone formation

105
Q

Describe the distribution of ions across the body fluid compartments

A

Sodium, calcium, chloride, bicarbonate = mostly ECF

Potassium, magnesium, phosphate, sulphate = mostly ICF

106
Q

What is the physiological response to respiratory acidosis?

A

Renal retention of HCO3-

107
Q

What urinary environment predisposes to renal stones?

A

Renal tubular acidosis (type 1 diabetes)

Hypocitraturia

108
Q

Which drugs can cause interstitial nephritis?

A
  • DCT and CT
    • NSAIDs
    • Penicillins
    • Sulphonamides
    • Thiazides
    • Vancomycin
109
Q

What effect do NSAIDs have on renal function?

A
  • Inhibit prostaglandins - for afferent arteriole dilation (maintenance of glomerular capillary pressure)
  • Present with fluid overload (oedema) and renal failure
110
Q

What is the compensatory response to respiratory alkalosis?

A

Renal secretion of HCO3-

111
Q

Which drugs can cause nephrogenic diabetes insipidus?

A

Lithium (affects CTs)

112
Q

What are the clinical uses of potassium sparing diuretics?

A

K+-conservation, oedema, hyperaldosteronism, hypertension

113
Q

What is the normal appearance of the kidneys on ultrasound?

A
  • <9cm is abnormal, >1cm cortex normal
  • Should be less echobright than liver
  • Blood flow - renal artery/vein
114
Q

What is metabolic acidosis?

A

Low bicarbonate ion concentration - low pH

115
Q

What is the typical life-long effects of chronic kidney disease?

A
  • Dialysis, transplant
  • Transplant can eventually fail so require dialysis again until new transplant can be found
  • Increasing cardiovascular risk (strokes, MI) throughout life, even with transplant
116
Q

Where is the highest osmotic gradient in the loop of Henle?

A

Tip of the loop - increases down descending then decreases up ascending

117
Q

Which drugs can cause renal tubular acidosis?

A
  • Proximal CT - acetazolamide
  • Distal CT - amphotericin B, lithium
118
Q

How can you tell that the kidneys are not functioning?

A

Low estimated glomerular filtration rate (eGFR) - below 60ml/min

High creatinine within eGFR >60ml/min range

119
Q

What is the term for blood in the urine at what does it indicate?

A
  • Haematuria
    • Visible (frank/gross) haematuria or microscopic haematuria
  • Source can be anywhere in urinary tract
120
Q

Describe examples of glomerular diseases

A
  • Diabetic glomerulopathy - thickening of tubules, damage to glomerular basement membrane, protein gets through
  • Acute glomerular disease - inflamed tissue, basement membrane damage
  • Cresentic glomerulonephritis e.g. antiglomerular basement membrane disease
121
Q

What effect do ACE inhibitors have on renal function?

A
  • Associated with reduced renal function
    • Bilateral renal artery stenosis
    • Especially with NSAIDs, diuretics or when dehydrated/septic
  • Prevent Angiotensin II production - unable to maintain glomerular capillary pressure (no vasoconstriction of efferent arteriole)
122
Q

What is the volume of extracellular fluid dependent on?

A

Salt intake, water intake, salt and water losses

123
Q

Describe examples of obstructive uropathy

A
  • Bladder outflow - prostate hyperplasia, urethral stricture
  • Vesico-ureteric junction - bladder/cervical cancer
  • Uterus - ureteric calculi, retroperitoneal fibrosis
124
Q

What causes respiratory acidosis?

A

Hypoventilation, leads to build up of CO2

125
Q

How does ADH cause AQPII activation?

A
  • ADH binds to V2 receptor
  • Activates cAMP on vesicles containing pre-formed AQPII
  • AQPII inserts on membrane - pure water channel, water pumped back into circulation via AQPI
126
Q

Describe the structure of the nephron

A
  • Afferent arteriole into glomerulus, surrounded by Bowman’s capsule
  • Proximal convoluted tubule
  • Loop of Henle
    • Thick descending, thin descending
    • Thin ascending, thick ascending
  • Distal convoluted tubule
  • Collecting duct
127
Q

What causes reduced sensed volume by the juxtaglomerular apparatus?

A
  • ECF depletion
  • Haemorrhage
  • Vasodilation
  • Heart failure
128
Q

How is proteinuria quantified?

A

Using creatinine:protein ratio in urine

129
Q

What pathologies can be seen on MRI of the kidneys?

A

Tumour, infection, cysts, renal vasculature, fistulas, stenosis

130
Q

What effect does aldosterone have?

A
  • ENaC insertion in cortical collecting duct, sodium reabsorption and potassium excretion (maintained by basolateral Na+/K+ ATPase)
  • Uses renal outer medullary potassium channel (ROMK) to pump potassium out
  • Site of action of potassium sparing diuretics - blocks mineralocorticoid receptor that aldosterone binds to - no ENaC insertion = water loss, high K+ as not excreted
131
Q

How long is the DCT?

A

1mm

132
Q

What kind of channels are present in the thin descending loop of Henle?

A

AQP1 - no hormonal control

133
Q

What is the response of the juxtaglomerular apparatus to increased tubular flow?

A
  • Produces adenosine
  • Efferent arteriole constriction, Na+/water reabsorbed
134
Q

What is the action of each class of diuretics in renal failure?

A
  • Loop = effective
  • Thiazide = ineffective
  • K-sparing = dangerous
135
Q

What causes respiratory alkalosis?

A

Hyperventilation - low pCO2

136
Q

Describe the anatomical position of the kidneys

A
  • Retroperitoneal, T12-L3
  • R lower due to liver
  • Adrenal glands immediately superior
  • Morrison’s pouch between R kidney and liver
137
Q

Describe the mechanism of action of potassium-sparing diuretics

A
  • Block ENaC, more sodium ion excretion so more water excretion
  • Antagonist for aldosterone - prevents synthesis of proteins produced in response to aldosterone
    • Prevents sodium reabsorption and potassium/hydrogen ion secretion in the late distal tubule and collecting duct
138
Q

How are renal stones classified?

A
  • By location
    • Kidney - nephrolithiasis
    • Ureter - ureterolithiasis
    • Bladder - cystolithiasis
  • By composition
    • Calcium phosphate
    • Calcium oxalate
    • Urate
    • Cysteine
    • Struvite
    • Uric acid
    • Mixed
139
Q

What are the side effects of Thiazide and Loop diuretics?

A
  • Non-specific - GI upset (nausea, vomiting), hypersensitivity reactions (rash), thrombocytopaenia
  • Metabolic - hypokalaemia, urate retention, glucose intolerance
  • Specific - ototoxicity (high dose loop)
140
Q

What does radiosotope scanning of the kidneys show?

A

Structure, perfusion

141
Q

Define acute and chronic kidney disease

A

Acute - 1-2 weeks

Chronic - 3+ months

142
Q

How is CT of the kidney enhanced?

A
  • Contrast enhanced - perfusion/excretion
    • Potentially nephrotoxic, weigh up risk vs benefit
    • Avoid if GFR < 30mL/min
    • Risk lowered by pre-hydration
143
Q

Which drugs can cause damage to the PCT, loop of henle and collecting ducts?

A

Methotrexate, sulphonamides, omeprazole

144
Q

Describe the systemic effects of metabolic acidosis

A
  • Symptoms related to cause
  • CVS - arrhythmias, reduced cardiac contractility, vasodilation
  • Respiratory - increased ventilation (Kussmaul’s breathing)
  • Metabolic - protein wasting, resorption of Ca2+ from bone
145
Q

What is the functional unit of the kidney?

A

Nephron

146
Q

List the processes which occur in the nephron

A
  1. Glomerular filtration - blood filtered to glomerular filtrate
  2. Tubular reabsorption (into the blood)
  3. Tubular secretion - blood to tubular fluid
147
Q

How do the kidneys compensate for ineffective blood supply?

A
  • Baroreceptors detect low blood supply, causes sympathetic outflow
  • Efferent arteriole constriction due to reduced sensed bloodflow at macula densa
  • Renin production by juxtaglomerular cells - conversion of angiotensin to angiotensis I to angiotensin II (by angiotension converting enzyme - ACE), constriction of afferent arteriole, increased aldosterone production by the adrenal cortex (lowers potassium concentration)
  • Baroreceptors cause ADH production in hypothalamus, release in posterior pituitary - thirst and renal water reabsorption
148
Q

List diseases of the renal arterial supply affecting small renal arteries

A
  • Hypertension
  • Nephrosclerosis
  • Accelerated phase hypertension
  • Vasculitides
149
Q

List abnormal urine characteristics which can be seen on visual inspection and what they indicate

A
  • Frothy = protein
  • Red = blood, drugs (e.g. rifampicin)
  • Brown = myoglobin
  • Cloudy = infection
150
Q

Describe the arterial supply of the kidney

A
  • Right and left renal arteries, from the abdominal aorta (L1-L2, just below the origin of the superior mesenteric artery)
    • Right is longer, crosses the inferior vena cava posteriorly
  • Within the kidneys:
    • Renal arteries
    • Segmental arteries
    • Interlobar arteries
    • Arcuate arteries
    • Interlobular arteries
    • Afferent arteriole
    • Capillary network (glomerulus)
  • Efferent arteriole form peritubular network - supplies nephron tubules
  • Inner 1/3 of cortex and medulla supplied by vasa recta
151
Q

Define acidaemia and acidosis

A

Acidaemia = high [H+]

Acidosis = H+ normal, other ion imbalances e.g. HCO3-

152
Q

Describe the gross structure of the kidney

A
  • Parenchyma = outer cortex and inner medulla
    • Medulla forms medullary pyramids - apex of pyramids drains to the minor calyces via the renal papillae
    • Minor calyces drain to major calyces, which drain to the renal pelvis
  • Renal hilum = where the vessels and ureters enter/exit
153
Q

What causes oxalate stone formation?

A

Primary/secondary hyperoxaluria

Hypocitraturia

154
Q

Which drugs have increased sensitivity in impaired renal function?

A
  • CNS depressants - opiates (respiratory depression)
  • Antihypertensives
155
Q

What is the normal response to low serum Calcium?

A
  • Increased parathyroid hormone (PTH) secretion
    • Increased calcium ion reabsorption in the kidneys
    • Increased hydroxylated vitamin D - increased GI calcium absorption
    • Calcium ion release from bone resorption
156
Q

How can renal stones be distinguished by pH?

A

Calcium >7.0

Struvite >7.0

Uric acid/cysteine <6.0

157
Q

What are the risk factors for renal stones?

A
  • Gender - male
  • Family history
  • High BMI
  • Immobile/sedentary
  • Dehydration
  • Urinary tract infections
  • Protective factors - vegetarian, diet high in fruit/fibre
158
Q

List the disorders of renal ion channel dysfunction and how they are treated

A
  • PCT - Fanconi’s syndrome, use acetazolamide diuretic (carbonic anhydrase inhibitor)
  • NKCC2 - Bartler’s syndrome, use loop diuretics
  • NCC - Gitelman’s syndrome, use thiazide diuretics
  • ENaC - Liddle’s syndrome, use amiloride (potassium-sparing) diuretics
159
Q

Describe the functions of the parts of the nephron in terms of drug excretion

A
  • Glomerulus - filtration of all LMW drugs
  • PCT - active tubular secretion of acid, bases and digoxin
  • DCT - passive tubular reabsorption
  • CT - water soluble drugs and metabolites
  • Drugs very heavily bound to plasma proteins e.g. albumin not filtered out - only free fraction filtered

Medicine Year 2 (41 decks)

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