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Block 1 > Kidneys > Flashcards

Kidneys Flashcards

0
Q

Describe the surface anatomy of the kidneys

A

Between vertebral levels T11-L2/3, the right is lower and the hila sit around L1
Sit under 12th rib with the left under 11th & 12th rib

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1
Q

Name some anatomical relations of the kidneys

A 
Suprarenal glands
Liver
Transverse mesocolon
Jejunum 
Stomach 
Spleen 
Pancreas
2nd part duodenum 
Costodiaphragmatic recess 
Quadratus lumborum 
Psoas major 
12th rib
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2
Q

What is the renal angle?

A

Between 12th rib and lateral border of vertebral column extensor muscles

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3
Q

Describe the surface anatomy of the ureters

A

Run vertically inferior to pelvic cavity; follow tips of lumbar vertebrae
transverse processes

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4
Q

What protective layers cover the kidneys?

A

Perinephric fat
Renal fascia
Paranephric fat
Psoas fascia

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5
Q

Renal fascia is loose & kidneys can move with body position. What occurs if they move too much? And what can be a sign of this?

A

Nephroptosis

Blood in urine when running

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6
Q

What tissue type do kidneys derive from?

A

Metanephros - mesoderm

Ureteric bud

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7
Q

What can happen if the ureteric bud develops abnormally?

A

Bifid Ureter
Duplicated ureter
Absent

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8
Q

During what time frame do the kidneys ascend to their adult position?

A

Week 6-9
Start in pelvic cavity
Migrate superiorly
Receive new blood supply as they move upwards and take the ureters with them

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9
Q

What is a pelvic kidney?

A

One kidney never migrates and so remains in the pelvic cavity
If there is no impingement then it doesn’t matter

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10
Q

What is a horseshoe kidney?

A

Two kidneys fused and not ascended. Gets stuck on IMA, can block it so ischemic bowel

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11
Q

What is a polar renal artery?

A

Artery not running into hilum. Squash ureter so renal pelvis enlarges

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12
Q

What is the allantois?

A

Passes from cloaca to umbilicus

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13
Q

What is the adult remnant of the allantois?

A

Urachus

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14
Q

Name 3 remnants of the allantois that can cause clinical problems

A

Urachal fistula/patent - urine can leak out
Urachal cyst - can get infected
Urachal sinus - blind ended tract from umbilicus, cheesy discharge

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15
Q

Describe the blood supply to the kidneys

A

Renal arteries at L1/2 (listen for bruits)
Run posterior to renal vein & IVC
Segmental supply (4/5 end arteries)

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16
Q

Describe venous drainage of the kidneys

A

Right renal vein directly join IVC
Left veins receive gonadal & suprarenal veins
Left renal vein runs under SMA to join IVC

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17
Q

Describe nerve supply to the supra renal glands

A

Preganglionic sympathetic fibres (T10-L1)

Synapse directly with chromaffin cells in medulla

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18
Q

What arteries do the ureters receive blood supply from?

A 
Renal 
Gonadal 
Aortic 
Internal iliac  
Vesical/prostatic
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19
Q

Which direction should the ureters be displaced in order to prevent disrupting their blood supply?

A

Displace ureter medially in abdo cavity

Displace ureter laterally in pelvic cavity

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20
Q

What pain pattern occurs with renal calculi?

A

Shifting loin to groin pain T12-L1/2

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21
Q

What is the main differential concern for an elderly patient presenting with presumed left sided renal colic?

A

Dissecting aortic aneurysm

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22
Q

What are potential sites for stones?

A 
Renal tract (urolithiasis) 
Gallbladder/biliary tree (cholelithiasis)
Salivary glands (sialolithiasis) 
Appendix (faecolith) 
Prostate 
Veins (phleboliths)
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23
Q

How do stones form?

A

Increased concentration of solutes causing supersaturated solution
Stasis
Infection

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24
Q

What effects can stones have?

A

Block ducts: colic, jaundice, renal failure
Chronic inflammation: Cholecystits, cystitis, sialadenitis
Infection

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25
Q

Describe salivary stones

A 
Occur more in females
Usually Wharton’s duct
Pain and swelling of gland 
Idiopathic, infection, drugs 
Remove stone – open/endoscopic
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26
Q

Describe gallstones

A

Common (10%), more in females
GB stores & concentrates bile
Most stones cholesterol based due to high fat diets/hypercholesterolaemia
Pigment stones found in haemolytic disorders (high serum bilirubin)
Ratio of cholesterol:bile salts & lecithin

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27
Q

How do gallstones present?

A

Asymptomatic
Abdominal pain
Jaundice
Fever

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28
Q

How do you investigate gallstones?

A

Bloods – LFT, amylase
USS
ERCP (endoscopic retrograde cholangio pancreatography)/MRCP

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29
Q

Describe what factors can affect the likelihood of developing renal stones

A

Common (10%) Males > females
Varies with geography/climate
Age, Peak onset 20-30
Fluid intake, Family history, Affluence/diet/BMI

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30
Q

Describe how renal stones form pathophysiologically

A

Urine normally supersaturated but metastable
Crystal growth more than normal
Crystals aggregate to form small stones
Symptomatic stones require particle retention to enlarge

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31
Q

What different types of renal stones can form?

A 
Ca oxalate 60% - visible on xray
Ca phosphate 20% - visible on xray
Urate  7% - not visible on xray, but will show on USS and CT
Struvite 7%
Cysteine 2%
Others
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32
Q

Where do renal stones get stuck?

A

Pelvic ureteric junction (PUJ)
Pelvic brim
Vesicoureteric junction (VUJ)
Bladder urethra outlet

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33
Q

What can cause calcium oxalate stones to form?

A

Hypercalciuria: Idiopathic, Rare genetic disorders,Hyperparathyroidism, Malignancy, Sarcoidosis/TB
Hyperoxaluria: Primary hyperoxaluria, Secondary- Dietary, Enteric

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34
Q

Describe struvite stones

A

Triple phosphate
Urinary infection by urea-splitting bacteria (split urea to CO2 and ammonia) so alkaline urine
Proteus mirabilis, Klebsiella, Pseudomonas, Providentia
Even low colony numbers produce urease
Struvite stones cause most staghorn calculi

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35
Q

Describe the 2 types of staghorn calculi

A

Struvite stones cause most staghorn calculi
Partial staghorn – renal pelvis stone extending into at least 2 calyceal groups
Complete staghorn – renal pelvis stone extending into all major calyceal groups filling at least 80% of collecting system

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36
Q

What are risk factors for struvite stones?

A 
Risk factors all related to UTIs 
Female 
Indwelling catheters 
Neurogenic bladders 
Urinary tract abnormalities
Stagnant urine
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37
Q

Describe the formation of cysteine stones

A

Autosomal recessive disorder affecting dibasic amino acid transporter in tubule
Cystine not reabsorbed – crystalizes
Faintly radio-opaque, Often staghorn
Young, mulitple stones
5% get ESRF
Hard to manage; drink more, alkalinise urine

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38
Q

Describe uric acid stones

A 
Purine metabolism 
Associated with metabolic syndrome and acidic urine
Radiolucent 
Gout 
Some medications
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39
Q

How will a patient with renal stones present?

A 
Loin to groin pain (renal colic), Can’t get comfortable, Radiates to testicle 
Haematuria 
Vomiting 
Irritative voiding symptoms  
Exclude leaking AAA
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40
Q

What history information do you need from someone presenting with renal stones?

A 
No of stones passed 
Frequency of stone formation
Age at first onset 
Kidney(s) involved 
Stone type 
Previous interventions
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41
Q

What initial investigations would you perform on someone presenting with renal stones?

A

Urine dipstick (haematuria, pH)
Serum creatinine/electrolytes, calcium, urate
Urine microscopy & culture
Imaging: Urgent, Immediate if fever - pyonephrosis
KUB- Sensitivity 50% Ca>struvite>cystine>urate, USS- Sensitivity 60% (80% for obstruction), CT KUB

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42
Q

What is the initial management of a patient with renal stones?

A

Infected obstructed kidney requires immediate drainage

Need to remove them if: Pain/failure to pass, Recurrent infection, Renal impairment, Bleeding, Some jobs (airline pilot)

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43
Q

How can renal stones be removed?

A

Fragmentation: Extracorporeal shockwave lithotripsy (ESWL), Focussed shockwave
Removal: PCNL Percutaneous nephrolithotomy, surgery, laser

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44
Q

What are complications of Extracorporeal shockwave lithotripsy (ESWL)?

A

Haematuria
UTI
Steinstrasse (stone fragments block ureter)
Tubular damage

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45
Q

What are the functions of the kidneys?

A 
Removal of toxins 
Electrolyte balance 
Acid base regulation 
Fluid and volume regulation
Endocrine functions
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46
Q

What cell types are found in the loop of Henle?

A

Thin - cuboid cells

Thick - columnar cells

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47
Q

What do cells in the distal convoluted tubule look like?

A

Virtually no brush border

Active cells with lots of cytoplasm

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48
Q

What type of cells are found in the ureters?

A

Transitional epithelium
Folded to allow stretch
Multiple layers for protection

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49
Q

Where do the kidneys sit in the abdomen?

A

Paired retroperitoneal organ located on posterior abdominal wall
Hilum at L1

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50
Q

What are the posterior relations of the kidneys?

A

Costodiaphragmatic recess
Quadratus lumborum
Psoas major
12th rib

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51
Q

What is the renal papilla?

A

Drainage point into calyxes

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52
Q

What is Psoas fascia?

A

Forms sheath down to hip region – infection can spread down this route; abscess can form under fascia

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53
Q

What is Thoracolumbar fascia?

A

Tough covering of intrinsic vertebral column muscles

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54
Q

What is Renal fascial space?

A

Communicates across midline, and serves as route for infection spread

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55
Q

What is nephroptosis?

A

Renal fascia is loose & kidneys can move with body position

Nephroptosis occurs if they move too much

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56
Q

What does the kidney develop from?

A

Metanephros (mesoderm) & ureteric bud

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57
Q

Describe the blood supply of the kidneys

A

Renal arteries at L1/2 (listen for bruits) behind IVC on right
Run posterior to renal vein & IVC
Segmental supply (4/5 end arteries)

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58
Q

Describe the venous drainage of the kidneys

A

Right renal vein directly join IVC
Left veins receive gonadal & suprarenal veins
Left renal vein runs under SMA to join IVC

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59
Q

Describe the blood supply to the supra renal glands

A

Left vein drains to renal vein

Right vein drains to inferior vena cava

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60
Q

Describe the nerve supply to the supra renal glands

A

Preganglionic sympathetic fibres (T10-L1)

Synapse directly with chromaffin cells in medulla

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61
Q

What do the ureters develop from?

A

Ureteric bud of mesonephric duct

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62
Q

Which arteries supply the ureters?

A 
Renal 
Gonadal 
Aortic 
Internal iliac 
Vesical/prostatic
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63
Q

What is the main differential concern for an elderly patient presenting with presumed left sided renal colic?

A

Dissecting aortic aneurysm

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64
Q

Which sensory nerves are involved in renal calculi pain?

A 
Renal plexus at renal pelvis
Abdomino-aortic plexus at pelvic brim 
Hypogastric plexus (superior) at vesico ureteric junction
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65
Q

What do the ureters cross to enter the pelvic cavity?

A

Iliac vessels

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66
Q

How much of an adult male is water?

A

60% so in 70kg male, 42 Litres

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67
Q

What are the 2 main compartments of ECF?

A

Interstitial fluid which surrounds the cells

Plasma which is non-cellular component of blood

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68
Q

What differences exist between Interstitial fluid and plasma?

A

Proteins which remain in plasma

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69
Q

What is osmosis?

A

Net diffusion of water across a selectively permeable membrane from a region of high water concentration to a region of low water concentration

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70
Q

What are osmoles?

A

Number of osmotically active particles in a solution

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71
Q

What are the endocrine functions of the kidney?

A

Production of EPO
Alpha hydroxylase production for vit D activation
RAAS system

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72
Q

What is EPO?

A

Erythropoietin, produced by interstitial cells in cortex & outer medulla
Growth factor, stimulates production of RBC precursors in bone marrow
Stimulus for its release is hypoxia
Kidneys are major source, disease can therefore result in anaemia (normochromic normocytic)

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73
Q

What is the functional unit of the kidney?

A

Nephron

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74
Q

What are the 3 main processes performed by the nephron?

A

Filtration
Reabsorption
Secretion

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75
Q

What is urinary excretion rate?

A

Filtration rate + Secretion rate – Reabsorption rate

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76
Q

What is renal blood flow rate? And what is renal plasma rate?

A

1 litre per min renal blood flow

600ml per min renal plasma flow

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77
Q

What make up the layers of the glomerular filtration barrier?

A 
Capillary endothelium (fenestrated) 
Basement membrane (negative charge) 
Epithelial cells (foot processes - podocytes & filtration slits)
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78
Q

How is the passage of substances limited across the glomerular filtration barrier?

A

By their size, shape and charge

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79
Q

What cells are excluded from glomerular filtrate?

A

Blood cells and plasma proteins

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80
Q

What effect do disease processes have on filtrate in the kidneys?

A

Alter the properties of barrier allowing protein to appear in the filtrate

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81
Q

What factors determine filtration?

A

Glomerular capillary filtration coefficient, Kf (leakiness of barrier)
Net filtration pressure (NFP)
GFR = Kf x NFP

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82
Q

What is glomerular filtration rate?

A

GFR

The volume of filtrate formed by all the nephrons in both kidneys per unit time

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83
Q

What is the glomerular filtration coefficient Kf?

A

Reflects:
Surface area available for filtration
Hydraulic conductivity (permeability) of the filtration barrier

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84
Q

How might Kf be affected in disease processes?

A

Reduced number of nephrons or processes which damage the filtration barrier will ↓surface area or ↓permeability & ∴decrease GFR

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85
Q

What is net filtration pressure?

A

Sum of pressures acting across the filtration barrier (Starling forces) Sum of the hydrostatic pressures
Sum of the colloid osmotic (oncotic) pressures
NFP = PG (glomerular hydrostatic) – PB (bowmanns capsule hydrostatic) – πG (glomerular colloid osmotic) + πB (bowmanns capsule colloid osmotic)
Typical is 10mmHg

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86
Q

What does glomerular hydrostatic pressure rely on?

A

Arterial pressure
Afferent arteriole resistance
Efferent arteriole resistance

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87
Q

How does most regulation of GFR occur?

A

Changes in glomerular hydrostatic pressure

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88
Q

How can you increase GFR?

A

Afferent arteriole dilation &/or Efferent Arteriole constriction

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89
Q

How can you decrease GFR?

A

Afferent Arteriole constriction &/or Efferent Arteriole dilation

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90
Q

What factors can cause Afferent Arteriole dilation and therefore lead to increased GFR?

A 
Prostaglandins
Kinins
Dopamine low dose
Atrial natriuretic peptide
Nitrous oxide
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91
Q

What factors can cause Afferent Arteriole constriction and therefore lead to decreased GFR?

A 
Angiotensin II high dose
Noradrenaline
Endothelin
Adenosine
Vasopressin
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92
Q

Describe the relationship between GFR and Arteriole resistance

A

Changes in AA resistance, effect on GFR is fairly linear
For EA resistance, effect on GFR is biphasic: Initial EA constriction causes ↑GFR by ↑glomerular hydrostatic pressure
Severe EA constriction slows down renal blood flow so that glomerular osmotic pressure rises more than hydrostatic & ∴GFR falls

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93
Q

What effect does angiotensin II have on GFR?

A

Preferentially constricts Efferent Arteriole – so increases glomerular hydrostatic pressure and therefore increases GFR

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94
Q

Which vasoactive substances dilate the Afferent Arteriole and therefore cause increased glomerular hydrostatic pressure and GFR?

A

Prostaglandins and atrial natriuretic peptide (ANP)

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95
Q

Which vasoactive substances constrict the Afferent Arteriole and therefore decrease glomerular hydrostatic pressure and GFR?

A

Noradrenaline (sympathetic nervous system), adenosine and endothelin

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96
Q

What occurs in the peritubular capillaries?

A

After leaving the glomerular capillaries and passing through the efferent arteriole the blood enters the peritubular capillaries
Changes in hydrostatic pressure and colloid osmotic pressure mean that absorption rather than filtration is favoured

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97
Q

Describe the autoregulation of GFR

A

GFR and renal blood flow relatively constant across a range of systemic blood pressures (~80–180 mm Hg)
Prevents large changes in renal excretion of water & solutes
Two mechanisms of autoregulation: Myogenic response and Tubuloglomerular feedback

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98
Q

What is Myogenic autoregulation of GFR?

A

Increase in arterial blood pressure
Increased renal blood flow and increased GFR
↑stretch of afferent arteriole smooth muscle which opens Ca channels Reflex contraction of AA smooth muscle, Vasoconstriction
↑Resistance to flow prevents changes in renal blood flow & GFR

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99
Q

What is a Myogenic response?

A

Inherent ability of smooth muscle in afferent arterioles to respond to
changes in vessel circumference by contracting or relaxing

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100
Q

What is the Tubuloglomerular feedback to maintain GFR when BP increases?

A

Mechanism links changes in [NaCl] in tubule lumen to control of afferent arteriole resistance
Utilises juxtaglomerular apparatus, Macula densa cells in initial part of
distal tubule sense [NaCl]
Arterial blood pressure increased, causes a transient ↑GFR which increases [NaCl] delivered to distal tubule
Release of paracrine factors (adenosine) by macula densa cells
Adenosine causes constriction of Afferent Arteriole smooth muscle
Vasoconstriction of AA so ↑Resistance to flow
Restores renal blood flow & GFR

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101
Q

What is the Tubuloglomerular feedback to maintain GFR when BP decreases?

A

Mechanism links changes in [NaCl] in tubule lumen to control of afferent arteriole resistance
Utilises juxtaglomerular apparatus, Macula densa cells in initial part of
distal tubule sense [NaCl]
Arterial blood pressure decreases, causes a transient ↓GFR which decreases [NaCl] delivered to distal tubule
Release of paracrine factors (renin) by macula densa cells
Renin causes release of Angiotensin II which causes constriction of Efferent Arteriole smooth muscle
Vasoconstriction of EA so ↑Hydrostatic pressure
Restores renal blood flow & GFR

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102
Q

What clinical disorders can occur if the kidneys dysfunction?

A

Failure of maintenance of fluid volume: Hypertension, Oedema
Failure of fluid composition: electrolyte and acid base disorders
Failure of excretion of waste: uraemia, drug toxicity
Failure of endocrine function: anaemia, renal bone disease

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103
Q

What investigations can be done relating to the kidneys? And what are you looking for?

A

Urine: What’s being filtered? What’s being excreted? e.g. protein, blood, glucose, leucocytes, osmolarity
Blood: Are waste products accumulating? Electrolyte abnormalities? Evidence of underlying cause? e.g. urea, creatinine, eGFR / GFR, sodium, potassium, pH, osmolarity, autoimmune diseases
Imaging: Any macroscopic structural abnormalities? Any functional abnormalities? e.g. ultrasound, plain X ray, CT, MRI, contrast studies, nuclear imaging
Biopsy: Any microscopic structural abnormalities?e.g. light microscopy, immunohistochemistry, electron microscopy

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104
Q

What are indicators of renal decline?

A

Proteinuria / albuminuria, Haematuria: Indicate damage
Estimated GFR / GFR, Serum creatinine /urea: Indicate function Calcium / phosphate homeostasis, Electrolytes /pH, Fluid balance / urine volume, Haemoglobin: Indicate function but not quantitative

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105
Q

What does proteinuria show about kidney function? And how can you detect it?

A

Indicates damage to the filtration barrier
Strong association between proteinuria and rate of disease progression in chronic kidney disease (CKD)
Can be detected by urine dipsticks
More sensitive methods include protein-creatinine ratio (PCR) and albumin creatinine ratio (ACR)

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106
Q

What is haematuria and what can effect its presence?

A

Blood can originate anywhere in urinary system
Beware menstrual bleeding and false positives on urine dipsticks e.g.
myoglobinuria
May be visible (frank / macroscopic) or non-visible (microscopic)
Age of patient an important factor in differential diagnosis

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107
Q

What is GFR?

A

Glomerular filtration rate (GFR)

The volume of filtrate formed by all the nephrons in both kidneys per unit time

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108
Q

What happens to GFR in disease states?

A

Directly related to function of nephrons & declines in all forms of progressive kidney diseases

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109
Q

What is the best overall index of kidney function in health &disease?

A

GFR

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110
Q

What is a normal GFR?

A

Linked to surface area of body ∴typical young male GFR = 120 ml/min/1.73m2

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111
Q

What factors effect the estimated GFR?

A

Age, sex and body size – declines with increasing age

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112
Q

What is renal clearance?

A

Volume of plasma from which a substance is completely cleared by the kidneys per unit time
Urine production x substance concentration in urine / substance concentration in plasma

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113
Q

Which substances have no renal clearance?

A

Proteins

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114
Q

Which substance is filtered and completely reabsorbed so has no renal clearance?

A

Glucose

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115
Q

Which substance is filtered but not reabsorbed or secreted and so gives an approximation of GFR?

A

Inulin

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116
Q

Which substance is filtered and partially reabsorbed?

A

Urea

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117
Q

Which substance is filtered and secreted?

A

Creatinine

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118
Q

For renal clearance of a substance to equal GFR, what properties must it have?

A 
Freely filtered across the glomerulus 
Glomerulus only route of excretion 
Not reabsorbed or secreted
Non-toxic 
Easily measured
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119
Q

What is creatinine and why is it used as an estimate for GFR?

A

Formed from breakdown of creatine, a skeletal muscle component
Produced at a steady rate for a given individual
Freely filtered at glomerulus & not reabsorbed
Small amount of secretion means clearance tends to overestimate GFR
Requires 24 hour urine collection – issues with compliance, time and reliability, Not suitable for a routine measure of renal function / GFR

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120
Q

Three tests used routinely to assess renal function, what are they?

A

Serum urea
Serum creatinine
Estimated GFR (eGFR)
Something normally filtered by kidneys builds up in the blood indicates ↓GFR and therefore ↓renal function

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121
Q

What is serum urea and what does it measure?

A

Nitrogen containing metabolic waste product of protein breakdown
Also known as: blood urea nitrogen (BUN)
Filtered but also partially reabsorbed
Levels typically rise in kidney disease as GFR falls
Serum levels reflect more than just GFR

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122
Q

What factors can increase serum urea?

A

Increase production: High protein diet, Increased catabolism (e.g.trauma, infection, surgery, cancer), Gastrointestinal bleed, Drugs e.g. corticosteroids, tetracyclines
Decreased elimination: Renal disease causing ↓GFR, Poor renal blood flow e.g.dehydration, hypotension

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123
Q

Why must a change in urea be compared to creatinine to see if there is a parallel change?

A

If both increased in parallel ie.both doubled, then a fall in GFR likely
If urea disproportionately higher than creatinine, need to consider:
Dehydration, High protein diet, GI bleed, Catabolic state

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124
Q

What factors can affect normal serum creatinine levels for that person?

A

Related to muscle mass: Age, sex, amputation, malnutrition, muscle wasting, ethnicity
Diet also affects creatinine levels (vegetarian diet vs. meat rich diet)

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125
Q

What happens to serum creatinine levels with diseased kidneys?

A

Increase as GFR is reduced

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126
Q

What happens to serum creatinine levels in a body builder with normal kidneys?

A

Levels will be high due to muscle mass and so will give impression of renal failure despite normal kidney function

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127
Q

What will serum creatinine levels be like in a elderly patient with diseased kidneys?

A

Levels may appear normal. Decreased GFR increases levels but decreased body mass decreases levels. Kidney disease may be masked and not detected

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128
Q

Why is serum creatinine not a useful measure in early kidney disease?

A

Can lose ~50% of renal function (GFR) and still appear to have a serum creatinine that lies within the ‘normal’ range

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129
Q

What is Estimated GFR (eGFR)?

A

Uses equations to calculate the GFR based on a single serum measurement of a substance
Incorporates clinical information along with a single serum measurement to generate an estimated GFR (eGFR)
Most use serum creatinine, age, sex and ethnicity to calculate
CKD-EPI equation (CKD Epidemiology) – recommended by NICE

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130
Q

Why do we need tubular processing?

A

Fine tune volume and composition of urine & to avoid huge fluid &
solute losses
Reabsorption more important than secretion for most substances

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131
Q

Describe the general mechanisms underlying tubular reabsorption

A

Utilises passive and active transport mechanisms to move fluid & solutes from tubule lumen to peritubular capillary
Luminal & basal surfaces of tubule epithelial cells have different transporters allowing concentration gradients to be established
Na+/K+ ATPase provides concentration gradient for reabsorption of many substances along the nephron
Water passively reabsorbed and linked closely to sodium reabsorption & permeability of the different parts of the nephron

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132
Q

Where does the majority of reabsorption occur?

A

Proximal convoluted tubule

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133
Q

Where does most fine tuning of solute concentrations occur?

A

Distal parts of nephron under hormonal control

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134
Q

How much urine is produced per day?

A

1.5 litres

135
Q

Describe the function of the proximal convoluted tubule

A

Majority of sodium & water reabsorption occurs here
Brush border increases surface area
Mitochondria provide energy
Site of secretion of metabolic acids / bases, drugs etc.
Tubule fluid leaving PCT is isosmotic as epithelium is freely permeable to water
Essentially all glucose & amino acids reabsorbed
Co-transporters) linked to sodium reabsorption
Sodium glucose co-transporters (SGLT2 mainly) on luminal side move glucose against concentration gradient
Glucose transporters (GLUT) on basal side allow facilitated diffusion into interstitial fluid
Similar process for amino acids

136
Q

Which glucose transporters are present in the proximal convoluted tubule?

A 
Sodium glucose co-transporters (SGLT2 mainly) on luminal side move glucose against concentration gradient 
Glucose transporters (GLUT) on basal side allow facilitated diffusion into interstitial fluid
137
Q

What can lead to loss of glucose in the urine?

A

There are a finite number of SGLT transporters on tubule cells
Work fine within normal physiological limits of plasma glucose
If amount of glucose in filtrate increases, eventually reach a
transport maximum (Tm) where reabsorption cannot go any faster
This leads to loss of glucose in urine
Water is also retained in the tubule lumen and excreted along with the
glucose

138
Q

Describe the secretion of Na

A

Sodium reabsorption linked to secondary active transport of hydrogen ions into lumen (secretion)
Important for bicarbonate reabsorption
Na+/H+ exchanger, NHE (counter transporter)

139
Q

What are the 3 parts of the loop of Henle?

A

Thin descending limb
Thin ascending limb
Thick ascending limb

140
Q

Which part of the loop of Henle is permeable to water?

A

Thin descending limb

141
Q

What occurs in the thin descending limb of the loop of Henle?

A

Permeable to water

No active reabsorption or secretion ofsolutes

142
Q

What occurs in the thin ascending limb of the loop of Henle?

A

Impermeable towater

Essentially no active reabsorption or secretion of solutes

143
Q

What occurs in the thick ascending limb of the loop of Henle?

A

Impermeable to water
Active reabsorption of sodium (~25% filtered load) & other solutes
Dilutes the luminal fluid (hypo-osmotic) as solutes are removed but water cannot follow
Reabsorption from tubule lumen mediated by sodium, potassium 2-chloride co-transporter (Na+K+2Cl-)
Positive charge in lumen encourages paracellular reabsorption of cations (including Ca2+ and Mg2+)

144
Q

What occurs in the early distal convoluted tubule?

A

First portion contains the macula densa (sensitive to [NaCl]) part of juxtaglomerular apparatus involved with feedback control of GFR & blood pressure
Impermeable to water
Active reabsorption of sodium & water (~5% filtered load)
Sodium-chloride co-transporter on luminal side
Further dilutes the tubular lumen fluid

145
Q

What occurs in the Late distal & cortical collecting tubule?

A

Water permeability of this part of nephron under hormonal control by antidiuretic hormone (ADH): Water permeable when ADH present, Water impermeable when ADH absent

146
Q

What cell types are present in the cortical collecting duct?

A

Principal cells: sodium reabsorption & potassium secretion

Intercalated cells: potassium reabsorption & hydrogen ion secretion

147
Q

What are the functions of principal cells?

A

Na enters principal cells via epithelial Na channels (ENaC) on luminal side
Transported out of cells by Na+/K+ ATPase to maintain concentration gradient
Number of ENaC channels & activity of ATPase under hormonal control
by aldosterone
Important site of regulation & fine tuning of sodium reabsorption & potassium secretion

148
Q

Describe the Medullary collecting duct

A

Final site for urine processing, regulating urine concentration
Water permeability under hormonal control by ADH
Surrounded by medullary interstitium with high concentration of solutes
Urea permeability allows medullary interstitium to remain concentrated

149
Q

What effect does aldosterone have on the kidneys?

A

Acts on collecting duct and tubule
Increases NaCl & H20 reabsorption
Increases K secretion

150
Q

What effect does angiotensin II have on the kidneys?

A

Acts on proximal tubule, thick ascending limb, distal tubule and collecting duct
Increases NaCl & H2O reabsorption
Increases H secretion

151
Q

What effect does ADH have on the kidneys?

A

Acts on distal tubule and collecting duct

Increases H2O reabsorption

152
Q

What effect does atrial natriuretic peptide have on the kidneys?

A

Acts on distal tubule and collecting duct

Deceases NaCl reabsorption

153
Q

What effect does parathyroid hormone have on the kidneys?

A

Acts on proximal tubule, thick ascending limb and distal tubule
Decreases PO4 reabsorption
Increases Ca reabsorption

154
Q

What direct and indirect changes can receptors detect in the kidneys in regards to electrolyte balance?

A

Direct – [K+] has direct effect on release of aldosterone

Indirect – baroreceptors indicate ECF volume (marker of sodium)

155
Q

Describe Na regulation by the kidneys

A

Major osmotically active extracellular electrolyte, major determinant of ECF volume
Kidneys help maintain ECF volume by regulating Na excreted in urine
Na is lost – water will be lost and ECF volume will fall (and vice versa)
Normally reabsorb ~99.6% sodium that is filtered i.e. only excrete small
amount of daily filtered load in urine
Regulated by local, hormonal & neural factors

156
Q

Describe the role of the kidneys in Pressure diuresis / natriuresis

A

Ability of kidney to increase urine output / reduce sodium
reabsorption in response to increases in arterial blood pressure
Simple way of regulating extracellular volume / sodium
BP chronically elevated - mechanism even more sensitive
Maintain blood volume over a wide range of fluid (& sodium) intake

157
Q

What is the function of the juxtaglomerular apparatus?

A

Secrete renin in response to falls in extracellular volume / low sodium
Falls in ECF volume detected by baroreceptors around the body
Aim of response is to increase sodium reabsorption and therefore ∴water reabsorption

158
Q

What cells is the juxtaglomerular apparatus comprised of?

A

Macula densa cells
Extraglomerular mesangial cells
Granular cells (afferent arteriole)

159
Q

What are the main triggers to renin release? And which cells release it?

A

Released by granular cells of afferent arteriole:
Low afferent arteriole pressure
Activation of sympathetic nerves that supply JGA
Low [NaCl] in distal tubule
All markers of fall in blood pressure / fall in ECF volume

160
Q

Describe the RAAS system

A

Renin catalyses conversion of angiotensinogen to angiotensin I
Angiotensin converting enzyme (ACE) catalyses conversion of angiotensin I to angiotensin II
Angiotensin II causes release of aldosterone, vasoconstriction and Na and water reabsorption in the kidneys

161
Q

Where is angiotensinogen produced?

A

Liver

162
Q

Where is ACE produced?

A

Lungs

163
Q

Where is aldosterone produced?

A

Adrenal gland

164
Q

What is the function of the RAAS system?

A

Maintain extracellular volume and arterial pressure despite wide variations in dietary intake of sodium
Salt intake reduced leading to a fall in ECF volume – RAAS activity
increased
Salt intake increased leading to a rise in extracellular volume – RAAS activity reduced
RAAS also responds to situations where extracellular volume and
blood pressure falls independently of salt intake

165
Q

Describe angiotensin II and its functions

A

Formed from enzymatic cleavage of angiotensin I by ACE
Powerful vasoconstrictor
Direct and indirect actions on to promote sodium and water reabsorption: Direct effect on renal tubule cells to increase Na reabsorption by increasing activity of Na transporters
Indirect effects include promotion of thirst, release of antidiuretic hormone (ADH) and aldosterone

166
Q

Describe aldosterone and its functions

A

Increases Na reabsorption by its actions on principal cells in late distal / cortical collecting tubule
Secreted by adrenal cortex (zona glomerulosa) in response to increased angiotensin II or increased extracellular potassium concentration
Binds to intracellular mineralocorticoid receptors (MR)
Binds to nucleus & increases production of proteins, e.g. ENaC, Na+/K+ATPase, that increase ability of these cells to reabsorb sodium

167
Q

What is atrial natriuretic peptide and its functions?

A

Hormone which inhibits sodium (and water) reabsorption by the kidney
Released by atrial muscle fibres in response to increased stretch of atria (as a result of excessive blood volume)
Causes small increases in GFR and decreases renal reabsorption
Levels can be raised in conditions where there is a pathological increase in extracellular volume e.g. cardiac failure

168
Q

Describe the importance of potassium regulation by the kidneys

A

Extracellular concentration of K tightly regulated as it is a major determinant of resting membrane potential – small changes can result in cardiac arrhythmias
Most potassium (98%) is located in intracellular compartment
Need rapid ways to regulate extracellular levels
Balancing overall intake and output is mainly done by the kidneys
Short term control of potassium levels can be achieved by moving
potassium between intracellular & extracellular compartments
Note: serum [K+] is not necessarily a good reflection of total body
potassium

169
Q

What factors shift K into cells and therefore decease extracellular K?

A

Na+/K+ ATPase activity: encourage cellular uptake of K with insulin (emergency treatment of hyperkalaemia)
Aldosterone: urinary excretion of potassium
Alkalosis (low extracellular [H+]) due to exchange of intracellular H+ for
extracellular K+
B adrenergic stimulation

170
Q

What factors shift K out of cells and therefore increase extracellar K?

A

Insulin deficiency, diabetes
Aldosterone deficiency, Addison’s disease
B adrenergic blockade
Acidosis: high extracellular [H+] due toexchange of extracellular H+ for
intracellular K+
Cell lysis: release of intracellular K from damaged cell membrane
Strenuous exercise
Increased extracellular fluid osmolarity: cellular dehydration. Increases intracellular [K+] and results in a larger concentration gradient to promote movement out of the cell

171
Q

Where is the majority of renal potassium excretion in the kidneys?

A

Secretion in late distal tubule / cortical collecting tubule

172
Q

What factors determine the rate of K+secretion?

A

Activity of Na+/K+ ATPase
[K+] gradient between blood, principal cell & lumen
Permeability of luminal membrane to K+

173
Q

What channels are involved in K excretion?

A

Na+/K+ ATPase moves K+ into principal cells creating a high
intracellular concentration
K+ passes through channels in luminal membrane into tubular lumen

174
Q

Which cells other than principal cells can reabsorb K during depletion?

A

Intercalated cells

175
Q

What factors regulate K secretion?

A

Plasma potassium concentration
Aldosterone
Tubular flow rate
H+ concentration

176
Q

What effect does an increasing plasma K level have on rate of K excretion?

A

Increased Na K ATPase activity
Increased K gradient from blood to lumen
Increased aldosterone release

177
Q

What effect does aldosterone have on K excretion?

A

Increased rate of potassium excretion

Due to increased NaKATPase activity and increased permeability of luminal membrane to K

178
Q

What is aldosterone release controlled by?

A

Plasma potassium levels

179
Q

What effect does increased tubular flor rate have on potassium levels?

A

Increased potassium excretion due to increased concentration gradient from principal cell to lumen

180
Q

What factors can increase tubular flow rate?

A

Volume expansion
High sodium intake
Diuretics

181
Q

What effect does increased H have on potassium levels?

A

Deceased rate of potassium excretion due to decreased NaKATPase activity

182
Q

What factors cause K increased excretion?

A 
Insulin
Adrenaline
Aldosterone
ADH
Plasma K levels
183
Q

What is the Normal range for extracellular [K+]?

A

3.5-5.3 mmol/L

184
Q

What are causes of hypokalaemia?

A

Reduced intake

Excessive losses e.g. diuretics, severe diarrhoea, aldosterone excess Altered body distribution

185
Q

What are symptoms of hypokalaemia?

A

Often asymptomatic
Muscle weakness
Cardiac arrhythmias

186
Q

What treatment is used in hypokalaemia?

A

Address underlying cause

Potassium supplementation

187
Q

What can cause Hyperkalaemia?

A

Excessive intake

Inadequate losses e.g. acute kidney injury, aldosterone deficiency Altered body distribution e.g. acidosis

188
Q

What are symptoms of Hyperkalaemia?

A

Often asymptomatic

Cardiac arrhythmias – ECG characteristic features e.g. tall T waves

189
Q

What is treatment for Hyperkalaemia?

A 
Address underlying cause 
Restrict intake 
Calcium gluconate (to stabilise myocardium) 
Insulin (along with glucose) to drive potassium into cells
Aid excretion – fluids, ion-exchange resins, dialysis
190
Q

What are the kidneys 2 roles in calcium and phosphate homeostasis?

A

Responding to PTH to increase calcium and decrease phosphate reabsorption
Activating vitamin D to enhance calcium absorption from GI tract

191
Q

Which part of kidney reabsorption of calcium is enhanced by PTH?

A

Distal tubule

192
Q

Why do patients with kidney disease get bone problems?

A

Kidney produces 1α-hydroxylase which converts inactive precursor into the active form of vitamin D
Develop renal bone disease due to failure to produce this enzyme so inability to absorb adequate calcium from diet

193
Q

What absorbs phosphate in the GI tract?

A

Sodium phosphate co-transporter which usually reaches Tm from dietary phosphate so excess phosphate spills over into urine

194
Q

What factors inhibit the sodium phosphate co transporter in the GI tract?

A

PTH & fibroblast growth factor-23 (FGF-23) inhibit the sodium phosphate co-transporter, thus reducing phosphate reabsorption

195
Q

What is the net effect of PTH?

A

Increase calcium and reduce phosphate reabsorption

196
Q

What can be consequences of fluid overload?

A

Oedema
Congestive heart failure - pulmonary oedema
Hypertension

197
Q

What are clinical features of hypovolaemia?

A 
Thirst   
Dizziness on standing
Confusion 
Low JVP 
Postural hypotension 
Weight loss    
Dry mouth  
Reduced skin turgor    
Reduced urine output
198
Q

What are clinical features of hypervolaemia?

A 
Ankle swelling 
Breathlessness, pulmonary oedema (crackles) 
Raised JVP 
Oedema 
Weight gain  
Hypertension
199
Q

What will a hypertonic solution cause a cell to do?

A

Shrink

200
Q

Where can total body water be lost from?

A

Lungs
Skin
Faeces
Urine

201
Q

What is the minimum fluid loss per day and therefore how much must we drink per day?

A

Total min. loss each day ~ 1400ml

Must drink >500ml

202
Q

What is the obligatory urine volume per day?

A

500ml

203
Q

How much is maximum urine production per day?

A

20 litres

204
Q

How much is normal urine production per day?

A

1500ml

205
Q

What is the normal urinary rate per minute?

A

1ml/min

206
Q

How do you calculate Osmoles excreted/day?

A

Urine osmolality (Osm/kg) x urine output (L/day)

207
Q

How much solute volume is excreted per day?

A

Average excretion 600 mOsm solutes/day
In 1500 ml urine, urine osmolality is 400 mOsm/kg (600 = 400 x 1.5)
If 3000ml urine, urine osmolality is 200 mOsm/kg (600 = 200 x 3)

208
Q

What is Maximum urine osmolality?

A

1200 mosmol/kg H2O

209
Q

What fluid balance issue is caused by diabetes?

A

High levels of solute cause a diuresis even if high levels of ADH present

210
Q

What is Polyuria?

A

High urine flow

211
Q

What can cause increase in solute excretion in the urine? And therefore an osmotic dieresis?

A

Glycosuria (diabetes mellitus)

Diuretics (failure to reabsorb sodium)

212
Q

What can cause an increase in water excretion?

A

Excessive water ingestion

Inability to concentrate urine (tubular damage, diabetes insipidus)

213
Q

What is oliguria?

A

Reduced urine volume

214
Q

What can cause oliguria?

A

Poor perfusion (dehydration / reduced volume)

215
Q

Where does most water reabsorption occur in the nephron?

A

Proximal convoluted tubule

216
Q

Describe Water reabsorption from collecting duct of nephron

A

Water reabsorption from collecting ducts is passive and requires:
Insertion of water channels (aquaporins), Regulated by ADH, release stimulated by: Cellular dehydration (increased plasma osmolality), Extracellular dehydration (decreased fluid volume)
An osmotic gradient: Generated by the countercurrent system

217
Q

Where is ADH produced?

A

Supraoptic & paraventricular nuclei of hypothalamus

218
Q

What is ADH?

A

Vasopressin

9 amino acid peptide

219
Q

Where is ADH transported too from the hypothalamus?

A

Transported to posterior pituitary (cleavage of precursor)
Packaged into storage granules
Released by exocytosis
Plasma half life 10-15 mins

220
Q

What are the two main functions of ADH?

A

Reduce water excretion

Stimulate vasoconstriction

221
Q

What are stimuli for ADH release?

A

Raised plasma osmolality (hypertonicity)
Extracellular volume reduction
Angiotensin II (released if low BP/blood volume)
Nausea (precaution for expected vomiting and fluid loss)
Drugs e.g. nicotine & morphine

222
Q

Which cells can influence the release of ADH?

A

Osmoreceptors in hypothalamus detect cellular dehydration
Peripheral volume receptors: Low pressure sensors in atria, pulmonary
vasculature, High pressure sensors in carotid sinuses & aortic arch, Stretch receptors in afferent arterioles (via release of Ang II)
Cause an increase in thirst and ADH release

223
Q

Describe the process of restoring water balance from a low level

A

Water deficit -> increased osmolarity detected by osmoreceptors -> increased ADH secretion -> increased H2O permeability in distal tubule and collecting duct -> increased H2O reabsorption -> water volume restored

224
Q

What is thirst?

A

Conscious desire for water

225
Q

Where are thirst centres?

A

Hypothalamus

226
Q

What inhibits ADH release?

A

Reduction in plasma osmolality (hypotonicity)
Extracellular volume increase
Drugs e.g. alcohol

227
Q

Describe the cellular action of ADH

A

Binds to GPCR receptor which causes production of cAMP via Gs
This activates PKA which phosphorylates proteins
This leads to increased production of aquaporins and increased insertion of stored channels from vesicles into membrane thus increasing the permeability of the collecting duct to water

228
Q

Where are different aquaporins located?

A

AQP1: widely distributed (permeability of PT)
AQP2: collecting duct (apical membrane, uptake from lumen) regulated by ADH
AQP3+4: collecting duct (basolateral membrane) allows H2O reabsorbed from the lumen to enter interstitium
AQP5: primarily non-renal (brain, lungs, salivary glands)

229
Q

How can we form dilute urine?

A

Ascending limb of loop of Henle, tubule is relatively impermeable to
water in absence of ADH
Pumps move solutes out of tubule lumen, leave behind dilute tubular fluid which leads to dilute urine

230
Q

How can we form concentrated urine?

A

Distal & collecting tubules/ducts permeable to water in presence of ADH, water moves so osmotic equilibrium with surrounding interstitium which leads to concentrated urine
Note osmolality of medullary intersitium ~1200mOsm/kg/H2O

231
Q

What does ADH induced water movement require?

A

Osmotic gradient

232
Q

What does the Osmotic potential of kidney interstitium depend on?

A

Urea and NaCl

233
Q

Describe how the re circulation of urea contributes to our ability to concentrate urine

A

Filtered urea is recirculated & due to differing permeability along nephron becomes trapped at high concentration within medullary interstitium
Urea makes a key contribution to osmotic gradient
High protein diet improves ability to form a concentrated urine

234
Q

What does the countercurrent mechanism rely on?

A

Loop of Henle

Vasa recta

235
Q

What does the countercurrent mechanism result in?

A

A dilute filtrate entering distal nephron (allows water to move out of tubule to circulation by osmosis)
Generates an increase in [NaCl] in medulla, so contributing to increase in osmotic gradient (which allows osmosis of water)

236
Q

Describe water and NaCl permeability changes through loop of Henle

A

Thin descending: Permeable to H2O, Na+, Cl- (passive)
Thin ascending: Impermeable to H2O, Minimal Na+, Cl-
Thick ascending: Impermeable to H2O, Na+, Cl- reabsorption (active)

237
Q

What allows NaCl transport in the loop of Henle?

A

Na+, K+, 2Cl- (co-transporter) on luminal membrane driven by gradient generated by the Na+/K+-ATPase on basolateral membrane

238
Q

Describe what NaCl and water movement occurs in the thick ascending limb

A

Reabsorption from tubule lumen mediated by sodium, potassium 2-chloride co-transporter(Na+K+2Cl-)
Positive charge in lumen encourages paracellular reabsorption of cations (including Ca2+ and Mg2+)
As water cannot follow, the remaining tubular lumen fluid is diluted

239
Q

Describe countercurrent multiplication

A

NaCl pumps in thick ascending limb maintain 200 mOsmol difference to medullary intersitium
Water loss from thin descending limb to maintain osmolarity of medulla
Interstitial osmolarity always same as that in descending loop
Difference in osmolarities between descending and ascending limbs at any transverse level is only 200 mosmol/kg H2O

240
Q

What is the role of the vasa recta in countercurrent multiplication?

A

For countercurrent to work, salt released from loop of Henle must
remain in medulla, while most of water is removed
Vasa Recta are long thinned walled blood vessels that parallel loops of Henle - hairpin arrangement
Low blood flow ~5-10% renal blood flow (enough to provide nutrients) Hairpin arrangement allows nutrient delivery & water removal while minimising disruption to medullary concentration gradient
Constant flow urea and NaCl stops precipitation

241
Q

What are the consequences of countercurrent multiplication?

A

Filtrate hypo-osmotic relative to interstitium, water leaves by osmosis down a concentration gradient

242
Q

Give 2 examples of Disorders of water regulation

A

Too much ADH: Syndrome of inappropriate ADH (SIADH)

Too little ADH: Diabetes insipidus (cranial or nephrogenic)

243
Q

What is syndrome of inappropriate ADH? And what can cause it?

A

Excess ADH production
Causes: pneumonia, small-cell lung carcinoma, drugs, meningitis
Effects: Inappropriate water reabsorption leading to: Low plasma osmolality, Low serum [Na] (dilutional hyponatraemia), cerebral oedema, Urine inappropriately concentrated & high urinary [Na]

244
Q

What are treatment options for syndrome of inappropriate ADH?

A

Identify & treat underlying cause
Restrict fluid intake
Drugs that inhibit ADH e.g. demeclocycline or vasopressin V2 antagonists e.g. tolvaptan)
Avoid correcting hyponatraemia with saline infusions

245
Q

What is diabetes insipidus?

A

Inability to reabsorb water from distal nephron due to inadequate production (cranial DI) of ADH or insensitivity (nephrogenic DI) to ADH

246
Q

What can cause diabetes insipidus?

A 
Cranial DI (fail to produce/secrete ADH from hypothalamus/pituitary): head trauma, neurosurgery, tumours, infections 
Nephrogenic DI (renal tubules insensitive to circulating ADH): drugs (e.g. lithium), electrolyte abnormalities (↑[Ca2+]; ↓[K+])
247
Q

What are the effects of diabetes insipidus?

A

Large losses of water in urine: Polyuria (10-15 litres/day)
Thirst & polydipsia (need access to fluids to keep pace with losses)
Low urine osmolality (dilute)
High / high normal plasma osmolality & serum [Na]

248
Q

What investigations can be done to confirm diagnosis of diabetes insipidus?

A

Water/fluid deprivation test
Deprived of fluid so↑plasma osmolality should prompt release of ADH & concentration of urine if normal
Monitor plasma & urine osmolality, weight, BP
1st stage identifies if DI, 2nd stage differentiates cranial from nephrogenic. Administer synthetic ADH (desmopressin) to differentiate

249
Q

What is treatment for diabetes insipidus?

A

Identify & treat underlying cause
Ensure adequate fluid intake to match losses
Synthetic ADH (desmopressin) – cranial DI
Drugs to sensitise renal tubules to ADH – nephrogenic DI

250
Q

Why are the kidneys susceptible to drug induced acute kidney injury?

A

Highly vascular
Large surface area for binding & transport into blood
Reabsorption of water from kidneys concentrates drugs in nephron

251
Q

What is the important factor with drugs if the kidney is not functioning properly?

A

Accumulate to toxic levels if excreted through kidneys and renal function is impaired

252
Q

Which drugs should be avoided in renal disease?

A

Nephrotoxic drugs: consequences likely to be more serious when renal reserve is already reduced
Amoxicillin, ACE inhibitors, NSAIDs

253
Q

What are reasons for problems with medications in patients with impaired renal function?

A

Failure to excrete drug or metabolites:mreduce dose / frequency, Consider alternatives
Side-effects poorly tolerated by patients (e.g. increased potassium)
Drugs less effective when renal function is reduced (e.g. diuretics)

254
Q

What are dose adjustments in renal disease patients based on?

A

Severity of renal impairment
Proportion of drug eliminated by renal excretion
Toxicity of drug / ‘safety margin’

255
Q

What does the BNF say about drug dosing in renal disease patients?

A

Use eGFR values to guide, recognise limitations & situations where dosing needs more accurate measures of GFR e.g.
Toxic drugs
Patients at extremes of weight

256
Q

How does dialysis affect the analysis of dosing of patients with renal disease?

A

Some drugs removed by dialysis
Loss of therapeutic effect for some drugs
No longer worried about nephrotoxic effects

257
Q

What effect does urine pH have on drug excretion?

A

Alkaline urine, acidic drugs more readily ionised
Acidic urine, alkaline drugs more readily ionised
Ionised substances (polar) more soluble in water – easier to excrete via kidneys

258
Q

How can aspirin poisoning be rectified?

A

Aspirin is weak acid. Give them IV sodium bicarbonate so they excrete aspirin more quickly

259
Q

What is diuresis?

A

Formation of urine by the kidney

260
Q

What is a diuretic?

A

Substance that promotes the formation (excretion) of urine

261
Q

What is natriuresis?

A

Renal excretion of sodium

262
Q

What is a natriuretic?

A

Substance that promotes renal excretion of sodium

263
Q

What are diuretics used for?

A

Treat fluid overload: oedema, CHF, hypertension

264
Q

What are the 3 important and common classes of diuretics?

A

Loop diuretics
Thiazide diuretics
Potassium sparing diuretics

265
Q

What is Tolvaptan?

A

ADH antagonist
Licensed for use in SIADH they produce a water diuresis, as opposed to a natriuresis – important as have dilutional hyponatraemia

266
Q

Where do carbonic anhydrase inhibitors exert their effects?

A

Proximal convoluted tubule

267
Q

Which drugs exert their effects in the proximal convoluted tubule and descending limb of loop of Henle?

A

Osmotic diuretics

268
Q

Where do loop diuretics exert their effect?

A

Thick ascending limb of loop of Henle

269
Q

What is the mechanism of action of loop diuretics?

A

Block apical Na+K+2Cl- transporters

270
Q

Where do thiazide diuretics exert their effects and what is their mechanism of action?

A

Early distal convoluted tubule

Block apical Na+Cl- channels

271
Q

Which part of the nephron is sensitive to aldosterone?

A

Late distal convoluted tubule, early collecting duct

272
Q

What is spironalactone?

A

Aldosterone receptor blocker

273
Q

What is amiloride?

A

ENaC antagonist

274
Q

Which are the K sparing diuretics?

A

Spironalactone - aldosterone antagonist

Amiloride - ENaC antagonist

275
Q

Give an example of a carbonic anhydrase inhibitor and describe how it exerts its effect

A

Acetazolamide
Weak diuretic, Inhibits carbonic anhydrase in proximal tubule
CO2 + H2O -> H2CO3 -> H+ + HCO3-
HCO3- can’t be directly transported from lumen – needs carbonic
anhydrase (CA) & secreted H+
When CA is inhibited, HCO3- reabsorption is blocked, along with Na+ & accompanying water

276
Q

What can be a side effect of carbonic anhydrase inhibitors?

A

Prevents exchange and secretion of H+

Side effect can be metabolic acidosis

277
Q

What are uses of carbonic anhydrase inhibitors?

A

Not usually prescribed for diuretic effect
Reduce intraocular pressure (aqueous humour production requires HCO3- secretion): glaucoma, eye surgery
Mountain sickness
Given orally or intravenously

278
Q

Describe how osmotic diuretics work

A

Increase osmolality of filtrate: prevent water reabsorption

Act best where most osmotic reabsorption occurs (PT, descending loop of Henle)

279
Q

Name 2 osmotic diuretics and describe their use

A

Mannitol: ↓ intracranial pressure,↓ intraocular pressure (glaucoma)
Glucose (natural): Filtered and reabsorbed by transporters: if Tm exceeded (e.g. uncontrolled diabetes mellitus) glucose excreted in urine -> polyuria (->polydipsia)

280
Q

What is furosemide?

A

Loop diuretic

281
Q

Which are the most powerful diuretics?

A

Loop diuretics

282
Q

How do loop diuretics work?

A

↓ NaCl reabsorption in thick ALH causes ↓osmotic concentration in
medulla (so ↓ADH mediated H2O absorption)
Increase delivery of NaCl to distal collecting duct causes increased Na+ uptake there, so loss of K+ (& H+) - hypokalaemia

283
Q

Why are loop diuretics effective in renal disease patients? But less effective in nephrotic syndrome?

A 
Bind plasma proteins so not filtered, secreted directly into PT nephron 
Effective in renal impairment 
Nephrotic syndrome (large amounts of albuminuria) - bind to albumin in filtrate – may be less effective
284
Q

What are the main uses of loop diuretics?

A

Peripheral oedema in chronic heart failure
Acute pulmonary oedema
Resistant hypertension

285
Q

What are side effects of loop diuretics?

A 
Increased frequency of urination 
Hypovolaemia & hypotension (excessive Na+ and water loss)
Hypokalaemia 
Metabolic alkalosis can occur 
Ototoxicity (high doses)
286
Q

Give examples of thiazide diuretics

A

Bendroflumethiazide, indapamide, chlortalidone

287
Q

Describe the pharmacodynamics of thiazide diuretics

A

Weak/moderate diuresis (well tolerated), Usually given orally
Slower acting, but longer lasting than loop diuretics
Not so good in renal impairment (filtered and secreted)
Reduces calcium excretion in urine

288
Q

What are the main uses of thiazide diuretics?

A

Hypertension
Peripheral oedema in chronic heart failure
Reduces calcium excretion i.e. lower Ca2+ in urine so may see used to treat hypercalciuria

289
Q

What are side effects of thiazide diuretics?

A

Increased frequency of urination
Hypokalaemia / hyponatraemia / (metabolic alkalosis)
↑ plasma uric acid (gout) as it competes for uric acid transporter
Erectile dysfunction
Hyperglycaemia

290
Q

Why do thiazide and loop diuretics cause hypokalaemia?

A

Increase delivery of NaCl to distal nephron & decrease blood volume
Increases potassium secretion by:
Increasing tubular flow rate
↑activity of Na+/K+ATPase via↑[Na+] & activation of RAAS
(↑aldosterone)
Intercalated cells also stimulated to secrete H+ hence alkalosis

291
Q

Describe how potassium sparing diuretics work

A

Act on principal cells in late distal / cortical collecting tubule
Either inhibit ENaC or the mineralocorticoid receptor (MR)
Reduce K+ secretion

292
Q

How do ENaC antagonists work as diuretics?

A

Blocks epithelial sodium channels (competes for Na+ binding site) & decreases luminal permeability to sodium
Weak diuretic alone
Used in combination with thiazide or loop diuretics
Reduced potassium secretion into lumen ∴ potassium retained

293
Q

Describe how aldosterone antagonists work as diuretics

A

Aldosterone antagonist binds to mineralocorticoid receptor (MR)
Given orally and metabolised to active metabolite canrenone
Weak diuretic if used alone
Prevents synthesis of ENaC & Na+/K+ATPase activation & so reduced potassium secretion into lumen ∴ potassium retained

294
Q

What are the main uses of aldosterone antagonists?

A

Chronic heart failure
Peripheral oedema & ascites caused by cirrhosis
Resistant hypertension
Primary hyperaldosteronism (Conn’s syndrome)
Used in combination, prevent K+ loss from loop / thiazide diuretics

295
Q

What are side effects of potassium sparing diuretics?

A

Hyperkalaemia (care if prescribing with other agents that inhibit RAAS)
Gynaecomastia (aldosterone antagonists)

296
Q

What is Aliskiren?

A

Renin inhibitor

297
Q

What is Ramipril?

A

ACE inhibitor

298
Q

What are ARBs?

A

Angiotensin II receptor blocker /antagonist

Eg losartan

299
Q

What happens if thiazides and loop diuretics are combined?

A

Loop diuretics increase NaCl to distal nephron, increases efficiency of thiazides
Can cause large volume losses and K+ loss

300
Q

What effects occur if loop or thiazide diuretics are combined with K sparing diuretics?

A

Get good diuretic function without loss of K+

Take care with K+ retention

301
Q

What helps to determine GFR?

A

Balance of afferent (AA) and efferent arteriole (EA) resistances

302
Q

What effects do NSAIDs have on GFR?

A

NSAIDs inhibit prostaglandins which normally cause dilatation afferent arteriole flow
NSAIDs↓in GFR

303
Q

What effects do ACE inhibitors and ARBs have on GFR? So why are they used in CKD?

A

ACEI / ARB cause efferent arteriolar dilatation so↓in GFR

Initial fall in GFR but stabilises & renal function conserved long-term

304
Q

In which renal condition should ACE inhibitors not be given?

A

Renal artery stenosis

ACE inhibitors will precipitate a continuing fall

305
Q

What are the functions of the kidney?

A

Homeotasis: Fluid, electrolytes and acid base balance
Hormone production: Renin / angiotensin, Vitamin D metabolites, Erythropoietin
Excretion of metabolites: Organic acids, Phosphates, Urea / creatinine

306
Q

What is the RIFLE criteria?

A

Risk: 1.5x↑ creatinine,↓ 25% GFR, 4 weeks

ESRD (established renal disease): Need RRT for>3 months

307
Q

What is the AKIN criteria?

A

Stage 1: 1.5-2x ↑creatinine, 3x ↑ creatinine, <0.3ml/kg urine for 24h or anuria for 12h

308
Q

What is the definition of acute kidney injury?

A

Significant deterioration in renal function, potentially reversible, over a period of hours or days

309
Q

Where can the causes of acute kidney injury come from?

A

Pre-renal failure: Renal hypoperfusion, Systemic hypotension (Hypovolaemia, Sepsis), Renal artery stenosis, Drugs- ACE inhibitors, NSAIDs
Intrinsic renal failure
Post-renal failure: obstruction

310
Q

How would you diagnose obstruction causing post renal failure?

A

Ultrasound scan

Anatomically: Where? In lumen, wall, Outside wall

311
Q

What are the categories of intrinsic renal failure?

A

Primary renal disease: Glomerulonephritis
Secondary renal disease: Diabetes, SLE, myeloma
Interstitial nephritis: Usually caused by drugs
Secondary acute tubular necrosis: Established after pre-renal failure

312
Q

What are the most common causes of acute kidney injury?

A

Pre-renal failure 85%: Hypoperfusion
Intrinsic renal failure 5%: Many causes, ATN
Post-renal failure 10%: Obstruction

313
Q

What is important in a history for renal issues?

A 
Rate of onset 
Precipitating factors 
Urinary symptoms 
Chronic symptoms 
Systemic features of autoimmune disease: Myalgias, rash, ENT symptoms, haemoptysis 
Relevant PMH/FH 
CKD, DM, vascular disease 
Drug history
314
Q

What are important features to look for on examination with renal issues?

A

Fluid status: Tissue turgor, Mucous membranes/tongue, Pulse rate, rhythm and volume, Lying and standing blood pressure, JVP, Peripheral perfusion, Peripheral oedema
Signs of sepsis: Fever, Tachycardia/bounding pulse, Tachypnoea, Warm peripheries, Local signs of sepsis
Cardiac: Pericardial rub
Respiratory: Pulmonary oedema/effusion
Abdominal: Ascites/masses/bladder
CNS: Drowsiness/confusion
Skin: Rashes

315
Q

What blood tests can be done to test renal function?

A

Biochemistry: Creatinine, eGFR, Na/K, Bicarbonate, Ca/Phos/PTH, CRP, CK
Haematology: Hb
Immunology: ANA, ANCA, anti-GBM, complement (C3, C4), electrophoresis (IgA/G/M)

316
Q

What urine tests can be performed to look at renal function?

A 
Urine dipstix: protein, blood 
ACR/PCR: quantify protein 
24h creatinine clearance 
Urine output 
MSU: check for infection 
Urine creatinine/electrolytes/calcium
317
Q

What radiological studies can be done to test for renal issues?

A 
Renal tract USS 
CT renal angiogram
CT KUB 
Plain AXR KUB 
IVP 
Renogram 
CXR
318
Q

What is the initial management of acute kidney injury?

A

Keep the patient alive: Hyperkalaemia, Fluid overload, Hypotension, Acidosis, Uraemia
Generic management of AKI: Fluids, Stop nephrotoxins
Diagnose cause of AKI (& treat)

319
Q

What ECG changes might be present with Hyperkalaemia?

A 
Peaked “tented” T waves
Prolonged P-R interval 
Prolonged QRS duration 
Loss of P waves 
VF/asystole
320
Q

What management can be performed for Hyperkalaemia?

A

Stabilise myocardium: Ca Gluconate
Shift K+ into cells: Insulin+Dextrose, Salbutamol, NaBic if acidotic
Treat ARF, treat cause
Dialysis

321
Q

What would be subsequent management strategies for acute kidney injury?

A

Close observation: BP, pulse, Daily weight, Fluid balance assessment, resp function (Sats, RR, O2 requirement)
Daily U&E
Review medications (nephrotoxins/dose adjustment)
Manage underlying cause

322
Q

When might ICU need to be informed and involved with acute kidney injury management?

A

Hypotensive secondary to sepsis
Hypotensive and fluid overloaded
Hypotension is not responding to fluid resuscitation
If >1 organ failure

323
Q

When might a renal specialist registrar need to be involved in the care of a patient with acute kidney injury?

A

Pre-renal AKI not rapidly resolving with supportive therapy
Doubt about cause of AKI
Blood/protein in urine or other reason to suspect intrinsic AKI
Life-threatening complications (HyperK, fluid overload)

324
Q

What are mortality rates with acute kidney injury?

A

10% in uncomplicated AKI

>50% in AKI with multi-organ failure

325
Q

What were the NCEPOD summary recommendations on acute kidney injury management?

A

Emergency admissions should have risk assessment for AKI and electrolytes checked on admission and appropriately thereafter
Predictable avoidable AKI should not occur
Acute admission receive senior review (consultant within 12 hours)
Sufficient critical care and renal beds to allow rapid step up care
Undergraduate medical training should include recognition of acutely ill patient and prevention, diagnosis and management of AKI
Postgraduate training in all specialties should include training in detection, prevention and management of AKI

326
Q

What are the stages of chronic kidney disease?

A

Stage 1: kidney damage with normal GFR, over 90
Stage 2: kidney damage with mild decrease GFR, 60-89
Stage 3: moderate decrease in GFR, 30-59
Stage 4: severe decrease in GFR, 15-29
Stage 5: kidney failure, GFR <15, for dialysis

327
Q

What can be complications of chronic kidney disease?

A 
Cardiovascular disease 
Hypertension 
Anaemia 
Bone-mineral metabolism 
Poor nutritional and functional status
Progression of CKD 
AKI
328
Q

What tests can be used to measure chronic kidney disease?

A

Tests for renal excretory function: Creatinine, Cystatin C, eGFR
Urinalysis: haematuria
Urine protein: 24h urine collection, Urine albumin:creatinine ratio (sensitive at low levels, recommended in diabetes), Urine protein:creatinine ratio
Tests for complications: Hb, K+, sBic, cCa, PTH
Diagnostic blood tests: ANCA, electrophoresis, Glc
Radiological tests: USS, CT, DMSA

329
Q

What is the relationship between creatinine levels and kidney function?

A

Creatinine levels remain fairly constant until a large loss of function so may not be an accurate measurement of normal function. Good measure for relatively end stages CKD

330
Q

What is significant progression of CKD?

A

Sustained decline in GFR of 25% or more and a change in category in within 12 months
Or sustained decline in GFR of 15ml/min/1.73m2 per year

331
Q

What risk factors are associated with progression of CKD?

A 
Hypertension 
Diabetes mellitus 
Albuminuria 
Cardiovascular disease
Smoking 
Ethnicity 
NSAIDS
332
Q

What are the consequences of late presentation of CKD?

A

Higher mortality, morbidity, hospital stay, cost
Due to poorer clinical state at presentation, lack of vascular access
No possibility of pre-emptive transplantation

333
Q

What is established renal failure?

A

Stage of chronic kidney disease where renal replacement therapy is required to safely sustain life

334
Q

What is the treatment of established renal failure?

A

Dialysis: Haemodialysis (hospital, satellite, home), Peritoneal dialysis (CAPD, APD)
Transplantation: Deceased-donor transplant, Living-donor transplant (including pre-emptive)
Conservative care

335
Q

What are Considerations when discussing RRT modality?

A

Physical & social factors: Eyesight & manual dexterity, Mobility and functional status, Family and social support, Work
Medical factors: Abdominal surgery, Vascular disease, Hypotension/left ventricular dysfunction
Geographical factors: Distance from haemodialysis unit, Space/cleanliness of house

336
Q

What are pros and cons of renal replacement therapy?

A

Pro-RRT: Increased survival, Decreased uraemic symptoms

Con-RRT: 3x4h/week (+travel), Dialysis access procedures & complications,mdoes not cure other comorbidities

Block 1 (17 decks)

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