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My ESA 3 > Urinary > Flashcards

Urinary Flashcards

1
Q

What are the 3 important characteristics of substances that can be used to measure GFR?

A

Must be freely filtered across the glomerulus
Must not be secreted, reabsorbed, or metabolised by the cells of the nephron
Must pass directly into the urine

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2
Q

What percentage of th embodies total blood flow goes to the kidney?

A

20-25%

~1200ml/min

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3
Q

At what spinal level are the kidneys?

A

T11/T12

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4
Q

What is the trigone?

A

The shape adapted by the empty bladder due to the 2 uretas and 1 urethra

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5
Q

What are the 4 major functions of the kidney (in order of importance)

A
  1. To maintain a stable internal environment to enable function in all parts of the body (controls conc of ions and small organic molecules)
  2. Excretion of waste products
  3. Endocrine (synthesis of renin, erythropoietin, prostaglandins)
  4. Metabolism (active form of Vit D, catabolism of insulin, PTH calcitonin)
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6
Q

Define osmolarity

A

Number of osmosis of solute per litre mmol/l

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7
Q

Define osmolality

A

Solute per kilogram of solvent milli-osmole

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8
Q

Do machines measure osmolarity or osmolality?

A

Osmolality (milli-osmole)

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9
Q

Relative to to ICF, what is the concentrations of Na+ and K+ in the ECF?

A

High Na+, low K+

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10
Q

What must kidneys do? (4 things)

A

Control volume
Control osmolarity
Help control pH
Excrete waste products

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11
Q

What is the functional unit of the kidney?

A

The nephron (1.5 million of them in each kidney!)

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12
Q

What percentages of components have been reabsorbed from the tubule by the end of the PCT?

A

~60-70% of Na+ and H2O
~80-90% of K+
~90% of bicarbonate
~100% of glucose and amino acids

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13
Q

How do reabsorbed materials leave the PCT?

A

Via the peritubular capillaries

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14
Q

What is the major function of the loop of henle?

A

Creating a gradient of increasing osmolarity in the medulla by counter current multiplication, allowing formation of concentrated urine (more conc. than plasma)

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15
Q

What is the distal convoluted tubule the major site for?

A

Site of variable reabsorption of electrolytes and H2O.
The fluid leaving the loop of henle is hypotonic, the DCT removes yet more Na+ and Cl-, and actively secretes H+. H2O may or may not follow electrolytes (if not large volume of urine)

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16
Q

How does the distal convoluted tubule function as the major site of variable reabsorption?

A

The fluid leaving the loop of henle is hypotonic, the DCT removes yet more Na+ and Cl-, and actively secretes H+. H2O may or may not follow electrolytes (if not large volume of urine)

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17
Q

What controls the Na+ recovery system/DCT/ECF volume

A

Renin angiotensin hormone system

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18
Q

What controls the recovery of water in the kidney/distal nephron?

A

ADH hormone system. Controls the permeability of DCT and collecting duct to H2O, controlling ECF osmolarity

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19
Q

What is in the cortex of the kidney?

A

Renal corpuscles

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20
Q

What is in the medulla of the kidney?

A

Tubules

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21
Q

What is in the terminal end of the renal artery/vein of the kidney?

A

Glomeruli, vasa recta

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22
Q

What is the renal corpuscle?

A

Glomerulus + bowmans capsule

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23
Q

What does the renal corpuscle do?

A

Produces the ultrafiltrate

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24
Q

Where are podocytes found, and what do they do?

A

Line the glomerulus, surrounding capillaries like a mesh, allowing filtration sites (spaces between podocyte processes)

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25
Q

What type of cells are in the proximal convoluted tubule?

A

Simple cuboidal epithelium with pronounced brush border

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26
Q

What are the 4 parts of the loop of henle?

A
  1. Pars recta
  2. Thin descending limb
  3. Thin ascending limb
  4. Thick ascending limb
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27
Q

What type of cells are in the thin descending limb of the loop of henle?

A

Simple squamous

No active transport occurring (looks like a capillary with no RBC)

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28
Q

What type of cells are in the thin ascending limb of the loop of henle?

A

Simple squamous

No active transport occurring (looks like a capillary with no RBC)

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29
Q

What type of cells are in the thick ascending limb of the loop of henle?

A

Simple cuboidal

Active transport occurs

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30
Q

What type of cells are in the distal convoluted tubule?

A

Simple cuboidal

Like PCT, but larger lumen and no brush border

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31
Q

What is the juxtaglomerular apparatus comprised of?

A

Macula densa of DCT
Juxtaglomerular cells (of afferent arteriole of glomerulus)
Extraglomerular mesangial cells (AKA lacis cells)

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32
Q

How does the collecting duct look hisiologically?

A

Continuation of DCT (simple cuboidal epithelium), similar to thick loop of henle, but lumen is larger and more irregular (rather than circular)

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33
Q

What is the renal pyramid?

A

A series of progressively larger ducts formed by merging collecting ducts. Empties at renal papilla.

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34
Q

What does the ureta look like histiologically?

A

Muscular tube with 2 layers of smooth muscle (and a 3rd layer in the lower third).
Lined by transitional epithelium

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35
Q

What other names might transitional epithelium go by?

A

Urinary epithelium

Urothelium

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36
Q

What does the bladder look like histiologically?

A

3 layers of muscle, outer adventitia, transitional epithelium.

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37
Q

What are the 4 types of epithelium in the male urethra?

A

Pre-prostatic
Prostatic
Membranous
Spongy

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38
Q

What is the passage of a RBC through the kidney?

A

Renal artery, One of the 5 segmental arteries, Interlobal arteries, Arcuate arteries, Cortical radiate artery , Afferent arteriole, Glomerulus, Efferent arteriole, Peritubular capillaries, Cortical radiate vein, Arcuate vein, Interlobal vein, Renal vein

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39
Q

Is the diameter of the afferent or efferent arteriole wider?

A

Afferent (creates hydronic pressure)

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40
Q

What are the 2 types of kidney nephrons?

A

Cortical

Juxtamedullary

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41
Q

Describe a cortical nephron

A

Superficial glomeruli, short loop of henle, next to outer cortex, high concentration of renin. Constitutes 80% of nephrons

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42
Q

Describe a juxtamedullary kidney nephron

A

Glomeruli very close to medullary border. Long loop of henle. Produces concentrated urine. Minimal renin conc. constitutes 20% of nephrons

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43
Q

What rate is the average glomerular filtration rate?

A

90-120mL/min/1.71m2

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44
Q

How much plasma delivered to the glomerulus is filtered out?

A

~20%

~1% leaves the body

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45
Q

What are the 3 main components to the filtration barrier?

A 
Capillary endothelium (permeable)
Basement membrane (acellular gelatinous layer of collagen/glycoproteins. Permeable to small proteins. Glycoproteins are negatively charged and repel Protein movement)
Podocyte layer (pseudopodia interdigitate, forms filtration slits)
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46
Q

Which molecules filter better through the glomerulus, positive or negatively charged ones?

A

Positive

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47
Q

What is the largest molecule that can diffuse through the glomerulus?

A

Insulin (5200molecular weight)

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48
Q

What are the 3 forces involved in the filtering if plasma?

A
  1. Hydrostatic pressure in capillary
  2. Hydrostatic pressure in bowmans capsule
  3. Oncotic pressure difference between capillary and tubular lumen
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49
Q

What is the main mechanism of autoregulation of the kidney?

A

Via changing diameter of afferent/efferent arterioles to control pressures and filtration rate in the glomerulus

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50
Q

What happens to the afferent arteriole when blood pressure increases?

A

Constriction (GFR is kept constant)

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51
Q

What happens to the afferent arteriole when when blood pressure decreases?

A

Dilation (GFR is kept constant)

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52
Q

What are the limits of BP where the kidney can compensate for to keep GFR constant?

A

80-180 mmHg

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53
Q

What is tubular glomerular feedback?

A

Changes in tubular flow rate as a result of changes in GFR changes the amount of NaCl that reaches the distal tubule.

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54
Q

What would the tubular glomerular feedback response to increased blood pressure be?

A

Increased Na+ and Cl- retention

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55
Q

What do MD cells in DCT respond to? What does this contribute to?

A

Changes in NaCl arriving in the DCT.

Contributes to regulation of arterial tone and therefore filtration rate

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56
Q

What can the juxtaglomerular apparatus release to reduce GFR?

A

Adenosine (vasodilator of efferent arteriole)

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57
Q

What can the juxtaglomerular apparatus release to increase GFR?

A

Prostaglandins (vasodilator of afferent arteriole)

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58
Q

What happens if NaCl increases?

A

GFR needs to decrease
Adenosine released (vasodilator of efferent arteriole)
This reduces pressure gradient across glomerulus and therefore slows GFR

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59
Q

What happens if NaCl decreases?

A 
GFR needs to increase
Prostaglandins released (vasodilator of afferent arteriole)
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60
Q

What is the relationship between GFR and distal salt concentration limited to?

A

Acute changes

Long standing primary disturbances in body fluid volume not regulated like this

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61
Q

Where does the majority of reabsorption take place?

A

PCT

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62
Q

On which membrane is the 3Na2KATPase located?

A

Basolateral

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63
Q

How does Na+ move across the apical membrane in the PCT?

A

Down a concentration gradient

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64
Q

How does water move into the PCT?

A

Down the osmotic gradient

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65
Q

What Na+ transporters are present in the PCT?

A

NaH antiporter

Na-glucose symporter

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66
Q

What Na+ transporters are present in the Loop of Henle?

A

Na-K-2Cl symporter

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67
Q

What Na+ transporters are present in the early DT?

A

NaCl symporter

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68
Q

What Na+ transporters are present in the late DT/CD

A

ENaC (epithelial Na+ channels)

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69
Q

What does SGlut transport?

A

2Na+ and 1 glucose

Against the glucose gradient,

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70
Q

On which membrane is SGlut found?

A

Basolateral membrane

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71
Q

What has normally been reabsorbed by the end of the PCT?

A 
100% filtered nutrients
80-90% filtered HCO3-
67% filtered Na+
65% filtered H2O
65% filtered Cl-
65% filtered K+
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72
Q

Where does the majority of drug metabolism take place?

A

Liver

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73
Q

Where does the majority of drug excretion occur?

A

Kidney

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74
Q

What does xenobiotic mean?

A

Foreign

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75
Q

What is clearance of a drug?

A

It’s rate of elimination by liver and kidney

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76
Q

What does half life describe?

A

The rate a drug is removed from the body

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77
Q

What is clearance rate proportional to?

A

The drugs free concentration in plasma

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78
Q

How does lipophilicity effect drug clearance?

A

The more lipophilic a drug is, the more easily it can diffuse back out of the lumen into the plasma

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79
Q

How does hydrophilicity effect drug clearance?

A

(Residual electrical charge)

The more charged a drug molecule is, the less easily it moves back out of the lumen.

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80
Q

How does the degree of binding to plasma protein effect drug clearance?

A

If lots, reduces the amount available for glomerular extraction

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81
Q

How does the degree of binding to tissue protein effect the clearance of a drug?

A

Effectively removes drug from the plasma, thus decreasing amount available for renal clearance

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82
Q

What is Vd?

A

The apparent volume of distribution

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83
Q

How is Vd calculated?

A

By measuring real plasma concentration of a drug (it’s impractical to measure drug concentration in all compartments of the body, so it’s generalised into a single number)

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84
Q

What’s it mean about a drug if Vd is high?

A

Lipohilic, leaves plasma

Reduces amount of drug available in plasma for excretion by kidney

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85
Q

What’s it mean about a drug if Vd is low?

A

Highly charged, confined to plasma

Increases amount of drug available in plasma for excretion by kidney.

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86
Q

What are xenbiotics?

A

Things the body sees as ‘foreign’ e.g. Drugs

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87
Q

What do the phase 1 and phase 2 enzyme systems work to achieve on xenobiotics?

A

Increase their ionic charge, therefore reducing lipophilicity, thus making it more difficult for the metabolised drug molecule to diffuse back out of tubular lumen and back into plasma

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88
Q

Why is reducing lipophilicity of xerobiotics beneficial?

A

Makes it more difficult for the metabolised drug molecule to diffuse back out of tubular lumen and back into plasma, thus increasing its secretion

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89
Q

What effect does acidic urine have on weak acidic anions?

A

Weak acidic anions more likely to be protonated - making them electrically neutral and therefore more lipophilic

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90
Q

What effect does alkaline urine have on weak acidic anions?

A

Weak acidic anions not protonated - more excreted.

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91
Q

What effect does alkaline urine have on weak bases?

A

Weak bases more likely to lose a proton, making them electrically neutral and more lipophilic (thus easier to cross nephron)

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92
Q

What effect does acidic urine have on weak bases?

A

Weak bases not deprotonated - more excreted

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93
Q

What effect will heart disease (or reduced renal vascular supply) have on the GFR?

A

Reduce GFR, and thus will reduce clearance

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94
Q

What effect does hepatic disease have on renal clearance?

A

Reduced drug metabolism, so reduced renal clearance
Reduced production of plasma proteins, so increases clearance of drugs bound to this (providing renal function is normal)

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95
Q

Define renal clearance

A

Volume of plasma required to ‘totally’ remove a given solute per unit time

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96
Q

What do you need to know before you are able to calculate renal clearance?

A

Conc. of physiological marker in plasma and urine

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97
Q

Give examples of good physiological markers

A

Inulin

Creatinine

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98
Q

What must physiological markers be in order to be of use?

A

Must not be synthesised, degraded or stored in the kidney

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99
Q

What are the 2 compartments in the body in which water is found? What separates them?

A

Intracellular fluid ICF
Extracellular fluid ECF
Separated by a cell membrane

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100
Q

Approximately how much water is in a 70kg male?

A

42 litres

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101
Q

Approximately how much water is ICF and ECF in a 70kg male?

A

28l ICF

14l ECF

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102
Q

What is the major osmotically active effective solute in the ECF?

A

Na+

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103
Q

What does concentration of Na+ in blood effect?

A

Effective circulatory volume

And therefore blood pressure

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104
Q

Other than via the kidneys, how else is Na+ lost from the body?

A

Sweat, Faeces

Although generally only small amounts

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105
Q

What do changes in osmotic pressure and hydrostatic pressure in peritubular capillaries alter?

A

Proximal tubule Na+ reabsorption (and hence water reabsorption)

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106
Q

What stimulates proximal tubule Na+ reabsorption?

A

RAAS

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107
Q

What are the targets within the kidney nephron for the hormone aldosterone?

A

Principle cells of DCT and CD

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108
Q

How does the kidney nephron counteract an increase in renal artery BP?

A

Reduced number of Na-H antiporter
Reduced Na-K ATPase activity in proximal tubule
Reduced Na+ reabsorption in proximal tubule
Reduced water reabsorption in proximal tubule

This causes increased Na+ excretion and therefore increased H2O excretion - pressure diuresis
Decreases ECF volume

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109
Q

What effect does increased blood pressure have on the kidney nephron?

A

Increases peritubular capillary pressure
Increased renal interstitial pressure
Decreased fluid absorption
Independent of vasomotor activity

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110
Q

What effect does high ECF volume have on the renal nephron?

A

Increased renal artery pressure, large pressure natriuresis and diuresis

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111
Q

What effect does low ECF volume have on the kidney nephron?

A

Decrease in renal artery pressure, small pressure naturesis and diuresis

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112
Q

What drives Na+ reabsorption in the kidney nephron?

A

3Na+ - 2K+ - ATPase on basolateral membrane

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113
Q

What is reabsorbed along with Na+?

A

Cl-

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114
Q

Is Cl- absorption active or passive?

A

Both

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115
Q

What is Cl- reabsorption dependent on?

A

Na+ reabsorption - maintains electro-neutrality

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116
Q

What apical Na+ transporter is in the PCT of the kidney nephron?

A

Na-H antiporter
Na-Glucose symporter
Na-AA cotransporter
Na-Pi

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117
Q

What apical Na+ transporter is in the loop of Henle of the kidney nephron?

A

NaKCC symporter

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118
Q

What apical Na+ transporter is in the early DT of the kidney nephron?

A

NaCl symporter

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119
Q

What apical Na+ transporter is in the late DT and CD of the kidney nephron?

A

ENaC

Epithelial Na+ channel

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120
Q

What are the different possible types of apical Na+ transporter?

A 
Na H exchange
Co-transport with glucose
Co-transport with AA or carboxylic acids
CO-transport with phosphate
Aquaporin
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121
Q

What is the driving forever for reabsorption in the PCT?

A

Hydrostatic forces in interstitium
Oncotic forces in peritubular capillary (increased due to loss of 20% filtrate at glomerulus, but cells and Protein left in blood)

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122
Q

What are the mechanisms for glomerulotubular autoregulation?

A

Myogenic action - vasculature reacts to changes in BP

Tubulo-glomerular feedback - 2nd line of defence, alters Na+ excretion

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123
Q

What is the equation used to calculate filtered load?

A

Filtered load = GFR x Concentration

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124
Q

What occurs primarily in the descending limb of the loop of henle?

A

Water reabsorption

This concentrates Na+ and Cl- ready for active transport in the ascending limb

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125
Q

What primarily occurs in the thin ascending limb of the loop of henle?

A

Na+ reabsorption, passively

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126
Q

What primarily occurs in the thick ascending limb of the loop of henle?

A

Na+ reuptake, and therefore Cl- reuptake also
Na+ reuptake via NKCC2 transporter, powered by 3Na+/2K+ ATPase
K+ ions diffuse via ROMK back into lumen to maintain activity of NKCC3 and Cl- ions move into interstitium

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127
Q

Which part of the nephron is most sensitive to hypoxia?

A

Thick ascending limb as it is very energy dependent

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128
Q

What can the ascending limb also be known as?

A

They diluting segment

Absorbs NaCl but not H2O

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129
Q

Is tubule fluid leaving the loop of Henle hyper, hypo, or iso -osmotic?

A

Hypo

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130
Q

What Na+ transporter is present in the early DT and what type of diuretics is it sensitive to?

A

NCC transporter

Sensitive to thiazide diuretics

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131
Q

What form of diuretics are ENaC transporters sensitive to? Where in the nephron are they found?

A

Amiloride diuretics

Late DT and CD

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132
Q

Where is the major site for Ca2+ reabsorption in the kidney nephron?

A

DCT

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133
Q

What controls Ca2+ reabsorption in the kidney nephron?

A

Hormones - PTH, 1,25-dihydroxyvitamin D

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134
Q

What happens to cytosolic Ca2+ in DCT cells?

A

Immediately bound by calbindin to basolateral aspect of DCT cells
Then transported out by NCX (sodium calcium exchanger)

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135
Q

What is the collecting duct divided into?

A

Cortical and medullary regions

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136
Q

What are the 2 distinct cell types found in the cortical collecting duct?

A

Principle cells

Type B intercalated cells

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137
Q

What do principle cells in the CCD do?

A

Reabsorption of Na+ via ENaC

Comprise 20% of cells

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138
Q

What do type B intercalated cells in the CCD do?

A

Active reabsorption of Cl-. Secretion of H+ (AIC) or HCO3- (BIC) more in acids and bases

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139
Q

What are the 2 types of intercalated cells?

A

Acid secreting - AIC

Bicarbonate secreting - BIC

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140
Q

Where are intercalated cells found?

A

In cortical and outer medullary collecting duct

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141
Q

What does a principle cell do?

A

Absorption of Na+ via ENaC on apical membrane (powered by 3Na/2K ATPase

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142
Q

How is Cl- absorbed in the CD?

A

Principle cells reuptake of Na+ produces luminal (-Ve) charge, which is the driving force for Cl- reuptake via paracellular route

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143
Q

How is blood pressure regulated short term?

A

Adjustment of sympathetic and parasympathetic input to the heart to alter CO.
Adjustment of sympathetic input to peripheral resistance vessels to alter TPR.

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144
Q

What is the baroreceptor reflex?

A

Nerve endings in the carotid sinus and aortic arch are sensitive to stretch.
Increased BP causes stretch - activates afferent pathways - medulla - efferent pathways - activators to decrease BP activated

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145
Q

What is control of BP long term directed at?

A

Control of blood Na+ and thus extracellular fluid volume/plasma volume

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146
Q

What are the 3 parallel neurohumoral pathways used for long term regulation of BP?

A

Renin-angiotensin-aldosterone system (RAAS)
Sympathetic nervous system
Antidiuretic hormone (ADH)
Atrial natriuretic peptide (ANP)

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147
Q

Where is renin released from?

A

Granular cells of juxtaglomerular apparatus (JGA)

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148
Q

What stimulates renin release?

A

Reduced NaCl delivery to distal tubule
Reduced perfusion pressure in the kidney (detected by baroreceptors in afferent arteriole)
Sympathetic stimulation to JGA

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149
Q

How is angiotensin converted to angiotensin 2?

A

Angiotensin - angiotensin 1 (catalysed by renin)

Angiotensin 1 - angiotensin 2 (catalysed by angiotensin converting enzyme ACE)

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150
Q

What does Angiotensin 2 stimulate?

A 
Vasoconstriction
Na+ reabsorption at kidney
Stimulates aldosterone (from adrenal cortex)
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151
Q

How many types of angiotensin 2 receptors are there? What are they called?

A

2
AT 1 and AT2
(Most actions are via AT1)

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152
Q

What type of receptor is AT1?

A

G-protein coupled receptor

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153
Q

What is angiotensin 2s action at arterioles?

A

Vasoconstriction

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154
Q

What is angiotensin 2s action at the kidney?

A

Stimulates Na+ reabsorption

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155
Q

What is angiotensin 2s action at the sympathetic NS?

A

Increased release of NA

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156
Q

What is angiotensin 2s action at the adrenal cortex?

A

Stimulates release of aldosterone

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157
Q

What is angiotensin 2s action at the hypothalamus?

A

Increases thirst sensation (stimulates ADH release)

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158
Q

What are the direct actions of angiotensin 2 on the kidney?

A

Vasoconstriction of afferent and efferent arteriole

Enhanced Na+ reabsorption at the PCT (stimulates Na-H exchanger NHE3 in apical membrane)

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159
Q

Describe the action of aldosterone on the kidney

A

Acts on principle cells of collecting duct
Stimulates Na+ (and therefore water) reabsorption
Activates apical Na+ channel (ENaC) and apical K+ channel
Also increases basolateral Na+ extrusion via Na/K/ATPase

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160
Q

How does ACE further augmentate the vasoconstrictor effects of angiotensin 2?

A

ACE is also one of the kinase enzymes that breaks down the vasodilator bradykinin

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161
Q

What effect does high levels of sympathetic stimulation have on the kidney?

A

Reduces renal blood flow (Vasoconstriction of arterioles, decreased GFR, decreased Na+ excretion)
Activates apical Na/H exchanger and basolateral Na/K ATPase in PCT.
Stimulates renin release from JGcells, leading to increased angiotensin 2 levels and increased aldosterone levels (increased Na+ reabsorption)

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162
Q

What direct effects does sympathetic stimulation of kidney have?

A

Acts on arterioles to reduce renal blood flow
Stimulates granule cells of afferent arteriole to release renin (via RAAS axis)
Stimulates Na+ reabsorption from PCT

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163
Q

What is ADHs main role?

A

Formation of concentrated urine by returning water to control plasma osmolarity.
Increases H2O reabsorption in distal nephron

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164
Q

What stimulates ADH release?

A

Plasma osmolarity

Severe hypovolaemia

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165
Q

What is ADH also known as?

A

Arginine Vasopressin.

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166
Q

What do atrial natriuretic peptides ANP do?

A

Promote Na+ excretion

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167
Q

Where are atrial natriuretic synthesised/stored?

A

In atrial myocytes.

Released from atrial cells in response to stretch (low pressure/volume sensors in atria)

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168
Q

What effect does reduced effective circulation volume have on the release of ANP?

A

Inhibits release of ANP to support BP (reduced filling of heart, less stretch, less ANP released)

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169
Q

What are the actions of atrial natriuretic peptide ANP?

A

Causes vasodilation of the afferent arteriole
Increased blood flow increases GFR
Also inhibits Na+ reabsorption along the nephron
Acts in opposite direction to other neurohumoral regulators (causes natriuresis, loss of Na+ in urine)
If circulating volume is low, ANP release is inhibited, supports BP

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170
Q

What do prostaglandins act as?

A

Vasodilators

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171
Q

What effect can locally acting prostaglandins (mainly PGE2) have upon the kidney glomerulus?

A

Enhance glomerular filtration and reduce Na+ reabsorption

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172
Q

When is the vasodilator effects of prostaglandins important in the kidney?

A

When levels of angiotensin 2 are high; acts as a buffer to excessive vasoconstriction produced by SNS and RAAS. Helps to maintain renal blood flow and GFR in the presence of vasoconstrictors

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173
Q

What do NSAIDs do?

A

Inhibit cyclo-oxygenase (COX) pathway involved in the formation of prostaglandins.

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174
Q

When must you be careful of prescribing NSAIDs?

A

Administration of NSAIDs when renal perfusion is compromised can further decrease GFR - acute kidney failure

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175
Q

Where is dopamine used in the kidney formed?

A

Locally in the kidney from circulating L-DOPA.

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176
Q

Where in the kidney are dopamine receptors found?

A

Present on renal blood vessels and cells of PCT and TAL

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177
Q

What does dopamine cause in the kidney?

A

Vasodilation and increases renal blood flow

Reduces reabsorption of NaCl; inhibits NH exchanger and Na/K ATPase in principle cells of PCT and TAL

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178
Q

What is essential, or primary hypertension?

A

The cause is unknown (95% of cases)

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179
Q

What is secondary hypertension?

A

The cause can be defined e.g. Renovascular disease, aldosteronism, cushings, chronic renal disease
It’s important to treat the primary cause!

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180
Q

How may renovascular disease cause secondary hypertension?

A

Occlusion of renal artery (renal artery stenosis) causing a fall in perfusion pressure of that kidney. Decreased perfusion pressure leads to increased renin production, activation of RAAS. Vasoconstriction and Na+ retention at other kidney.

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181
Q

How may renal parenchymal disease cause secondary hypertension?

A

Earlier stage may be a loss of vasodilator substances. In later stages Na+ and H2O retention due to inadequate glomerular filtration (volume-dependent hypertension)

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182
Q

How might Conns syndrome cause secondary hypertension?

A

Conns syndrome - aldosterone secreting adenoma (hypertension and hypokalaemia)

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183
Q

How might Cushing’s syndrome cause secondary hypertension?

A

Excess secretion of glucocorticoid cortisol. At high concentrations, acts on aldosterone receptors, Na+ and H2O retention

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184
Q

How might a tumour of the adrenal medulla cause secondary hypertension?

A

Phaeochromocytoma - secretes catecholamines (noradrenaline and adrenaline)

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185
Q

What hypertension drugs target the RAAS?

A

ACE inhibitors. Prevent the formation of active angiotensin 2

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186
Q

What hypertension drugs target vasodilators?

A

L-type Ca2+ blockers

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187
Q

How do L-type Ca2+ channel blockers work to reduce hypertension?

A

Reduce Ca2+ entry to vascular smooth muscle cells - relaxation.

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188
Q

What diuretics are generally used for hypertension?

A

Thiazide diuretics

Inhibit Na/Cl CO-transporter on apical membrane of cells in distal tubule

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189
Q

Are beta blockers used to treat hypertension?

A

No
Will reduce effects of sympathetic output (decreasing HR and contractility). Would only be used if other indications such as previous MI

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190
Q

What proportion of total body fluids is ECF and ICF ?

A

1/3 ECF

2/3 ICF

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191
Q

Where is the majority of the K+ in the body?

A

ICF (98% - mainly in skeletal muscle cells, liver, RBC, bone)

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192
Q

What maintains the difference between ICF and ECF K+ levels?

A

Na+/K+ ATP ase

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193
Q

Why is maintaining ECF K+ conc so low so important?

A

Due to K+S effect on the resting membrane potential
And therefore it’s effects on excitability of cardiac tissue - life threatening arrhythmias with hyperkalaemia/hypokalaemia

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194
Q

What effect does low K+ level have on excitability?

A

Further to reach threshold potential - decreased excitability

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195
Q

What effect does high K+ level have on excitability?

A

Decreased distance to threshold potential - increased excitability

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196
Q

How is K+ immediately regulated?

A

By internal balance - moving K+ between ECF and ICF

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197
Q

How is K+ regulated longer term?

A

External balance - adjusting renal K+ excretion

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198
Q

Describe the events that follow K+ consumption

A

Intestine and colon absorb dietary K+
Blood K+ increases, potentially to dangerous levels
BUT 4/5 K+ moves into cells within minutes
After slight delay, kidneys begin to excrete K
Excretion complete in 6-12hrs

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199
Q

What mediates movement of K+ from ECF to cells?

A

Na+/K+ ATPase

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200
Q

What mediates the movement of K+ from cells to ECF?

A

K+ channels

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201
Q

List 3 factors that increase K+ uptake by cells

A

Hormones (act via Na+/K+ATPase) e.g. Insulin, aldosterone, catecholamines
Increased K+ conc. in ECF
Alkalosis (low ECF H+ conc)

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202
Q

List 5 factors that promote K+ shift out of cells

A 
Exercise
Cell lysis
Increased in ECF osmolality
Low ECF K+ conc
Acidosis (increased ECF H+ conc)
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203
Q

What does K+ in splanchnic blood stimulate?

A

Insulin secretion by pancreas

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204
Q

What effect does insulin have on K+ uptake by cells?

A

Increases, as increases activity of Na/K ATPase

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205
Q

How would you treat hyperkalaemia?

A

IV insulin and dextrose

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206
Q

What effect does K+ in blood have on aldosterone secretion?

A

Stimulates secretion

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207
Q

How does aldosterone stimulate K+ uptake?

A

Stimulates Na/K ATPase

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208
Q

How do catecholamines stimulate K+ uptake?

A

Act via beta2 adrenoreceptors, which stimulate Na/K ATPase and thus cellular uptake of K+

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209
Q

What is produced during high intensity exercise and trauma to offset high ECF K+ rise?

A

Increased catecholamines

Offset K+ rise by increasing K+ uptake by other cells

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210
Q

Describe how K+ is released during exercise

A

Net release of K+ during recovery phase of action potential, K+ leaves cell
Skeletal muscle damaged during exercise, releases K+
Increase in plasma K+ proportional to intensity of exercise

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211
Q

What prevents dangerously high ECF K+ levels during exercise?

A

K+ uptake by non-contracting tissues

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212
Q

Describe the effects of acidosis on potassium balance in a cell

A

Acidosis
H+ shift into cells
Reciprocal K+ shift out of cells

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213
Q

Describe the effects of alkalosis on the K+ balance of cells

A

Shift of H+ out of cells

Reciprocal K+ shift into cells

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214
Q

Does acidosis lead to hyper or hypo kalaemia?

A

Hyperkalaemia

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215
Q

Does alkalosis lead to hyper or hypo kalaemia?

A

Hypokalaemia

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216
Q

Describe the movement of K+ and H+ ions in hyperkalaemia

A

Hyperkalaemia, shift of K+ into cells
Reciprocal shift of H+ out of cells
Hyperkalaemia leads to acidosis

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217
Q

Describe the movement of K+ and H+ ions in hypokalaemia

A

Hypokalaemia, shift of K+ out of cells
Reciprocal shift of H+ into cells
Hypokalaemia leads to alkalosis

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218
Q

Where is K+ excretion monitored?

A

Late DT and cortical collecting ducts of kidney nephron

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219
Q

Describe what happens to K+ in the kidney

A

K+ freely filtered at glomerulus
K+ reabsorbed at proximal tubule (67%), thick ascending loop of henle (20%), distal tubule, cortical collecting duct (via intercalated cells), medullary collecting duct
K+ secreted at distal tubule & cortical collecting duct (principle cells)

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220
Q

Describe how K+ secretion occurs in principal cells in the distal tubule

A

Na/K ATPase activity in basolateral membrane increases intracellular K+, and decreases intracellular Na+
Na+ moves from lumen into cell down its conc. gradient (via apical ENaC), creating an electrical gradient
This together with high intracellular K+ creates a favourable electrochemical gradient for K+ secretion via apical K+ channels

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221
Q

What effect does aldosterone have on K+ secretion by principal cells of kidney?

A

Increases K+ secretion

Increases transcription of relevant proteins (increases Na/K ATPase, increases K+ channels, increases ENaC)

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222
Q

What effect does ECFs K+ concentration have on K+ secretion by principal cells of kidney?

A

Directly stimulates Na/K ATPase and increases permeability of apical K+ channels
Also stimulates aldosterone secretion

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223
Q

What effect does acidosis have on K+ secretion by principal cells of kidney?

A

Acidosis decreases K+ secretion (inhibits Na/K ATPase, decreases K+ channel permeability)

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224
Q

What effect does alkalosis have on K+ secretion by principal cells of kidney?

A

Increases K+ secretion

Stimulates Na/K ATPase, increases K+ channel permeability

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225
Q

What effect does increased distal tubular flow rate have upon K+ secretion?

A

Washes away luminal K+, increasing K+ loss

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226
Q

What effect does increased Na+ delivery to distal tubule have on K+ secretion?

A

More Na+ absorbed by principal cells, resulting in more K+ loss

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227
Q

How is K+ absorbed by intercalated cells?

A

Actively, via H+/K+ ATPase in apical membrane

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228
Q

Where are intercalated cells in the kidney?

A

Distal tubule

Cortical collecting duct

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229
Q

What can changes in ECF K+ concentration effect?

A

Alter cell membrane resting potential
Alter neuromuscular excitability
Resulting in arrhythmias, CA, muscle paralysis

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230
Q

What might cause hyperkalaemia?

A 
Increased K+ intake (unlikely unless inappropriate use of IV K+)
Decreased renal excretion (kidney injury, low aldosterone state, drugs blocking K+ excretion - ACE inhibitors, K+ sparing diuretics)
Internal shifts (diabetic ketoacidosis, cell lysis, metabolic acidosis)
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231
Q

What are the clinical features of hyperkalaemia?

A

Heart - altered excitability, arrhythmias, heart block
GI - neuromuscular dysfunction - paralytic ileus
Acidosis

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232
Q

What is the emergency treatment for hyperkalaemia?

A

IV calcium gluconate (reduce K+ effect on heart)
IV Glucose and insulin (shift K+ back into ICF)
Nebuliser beta agonists (salbutamol)
Remove excess K+ (dialysis)

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233
Q

What is the long term treatment for hyperkalaemia?

A

Treat cause
Reduce K+ intake
Measures to remove excess K+ (dialysis in acute or chronic kidney injury).
Oral K+ binding resins to bind K+ in gut

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234
Q

What may cause hypokalaemia?

A

Problems of external balance - excessive loss GI, diarrhoea, vomiting). Renal loss of K+ (diuretic drugs, osmotic diuresis, high aldosterone levels)
Problems of internal balance (shifts of K+ into ICF e.g. Metabolic alkalosis)

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235
Q

What are the clinical features of hypokalaemia?

A

Heart - altered excitability, arrhythmias
GI - neuromuscular dysfunction, paralytic ileus
Skeletal muscle - neuromuscular dysfunction, muscle weakness
Renal - unresponsive to ADH

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236
Q

What effect does hypokalaemia have on heart muscle excitability?

A

Hypopolarised RMP - more fast Na+ channels available in active form, heart more excitable

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237
Q

What is the treatment for hypokalaemia?

A 
Treat cause
Potassium replacement (IV/oral).
If due to increased mineralocorticoid activity (high aldosterone levels), K+ sparing diuretics, which block action of aldosterone on principal cells.
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238
Q

What are the ECG features of hyperkalaemia?

A

High T wave, depressed ST segment, prolonged PR interval, P wave absent (atrial standstill), intraventricular block, ventricular failure

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239
Q

What are the ECG features of hypokalaemia?

A

Low T wave, high U wave, low ST segments

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240
Q

What cells do K+ absorption at the collecting duct?

A

Alpha-intercalated cells

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241
Q

How is K+ absorbed in the kidney medulla?

A

Luminal and transcellular absorption

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242
Q

How is K+ absorbed in the PCT?

A

Paracellularly (solvent drag early, lumen - positive potential late)

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243
Q

How is K+ absorbed in the TAL?

A

Transcellular and paracellular (NKCC2, lumen positive potential K+ and Cl-)

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244
Q

Why does K+ absorption require such fast balancing?

A

Amount of K+ absorbed in the GI after a meal is approximately equal to the amount of K+ present in the ECF

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245
Q

What effect does adding HCO3- have on K+ absorption into the ICF?

A

Aids K+ to ICF absorption

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246
Q

What pH should the blood be at?

A

pH 7.35-7.45

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247
Q

What concentration of H+ ions should be in the blood?

A

44.5-35.5 nmol/l

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248
Q

What effect does alkalaemia have on Ca2+ ions? What are the consequences of this?

A

Lowers free Ca2+, causing Ca2+ ions to come out of solution. This increases neuronal excitability, can lead to paraethesia and tetany

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249
Q

What can Ca2+ ions coming out of solution lead to?

A

Increased neuronal excitability, can lead to paraethesia and tetany

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250
Q

How does acidaemia effect electrical excitability?

A

Increases plasma K+ conc

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251
Q

What effect may increased H+ conc have on proteins? What can this effect?

A

Denatures/disturbs them. Can effect muscle contractility, glycosis, hepatic function

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252
Q

At what pH is acidosis life threatening?

A

Below pH 7.0

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253
Q

How is plasma pH determined?

A

Ratio of the concentrations of HCO3-/pCO2 (via hendleson-hasselbalch equation)
Should be maintained at a 20:1 ratio CO2:O2

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254
Q

What ratio should CO2:O2 be in the blood?

A

20:1

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255
Q

What effect can hypoventilation have on plasma pH

A

Hypoventilation - hypercapnia - fall in plasma pH

Respiratory acidaemia

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256
Q

What effect can hyperventilation have on plasma pH?

A

Hyperventilation - hypocapnia - plasma pH rise

Respiratory alkalosis

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257
Q

What controls pCO2?

A 
Central chemoreceptors (change respiratory rate for disturbances in pCO2). Slower response, but account for ~80% of effect.
Peripheral chemoreceptors detect changes in pCO2 and pH of plasma. Respond rapidly but have overall smaller effect.
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258
Q

What can compensate for changes in pCO2?

A

Changes in HCO3-

Ratio = pH

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259
Q

What controls the concentration of HCO3- in the blood?

A

Kidneys (despite RBCs producing it)

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260
Q

What happens, with regard to HCO3-, to acid produced by tissues?

A

Reacts to form CO2, which is blown off at the lungs. This leads to a fall in HCO3-, therefore a decrease in pH
This can be compensated for by increasing ventilation.

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261
Q

What chemoreceptors detect a change in plasma pH?

A

Peripheral

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262
Q

When might plasma HCO3- levels rise?

A

E.g. After much vomiting

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263
Q

How might increases in plasma HCO3- be compensated for?

A

Decreasing ventilation

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264
Q

How can the kidney correct disturbances in pH?

A

Varying excretion of HCO3- (very easy to lose it)

Making more HCO3-

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265
Q

How do kidneys produce more HCO3-?

A

Have a very high metabolic rate, so produce lots of CO2, which then reacts with H2O, producing HCO3- (which enters plasma) and H+ (which is excreted in urine)
Kidney can also make HCO3- from amino acids (producing NH4+, which enters urine)

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266
Q

Where is 80% of HCO3- reabsorbed in the kidney nephron?

A

In the PCT

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267
Q

What drives HCO3- reabsorption in the PCT?

A

Na+ gradient (established by NaK ATPase)

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268
Q

Describe HCO3- recovery in the PCT

A

Na+ movement down gradient (established by NaK ATPase) drives H+ movement out of cells via NHE-3
H+ in lumen reacts with HCO3- to form CO2 (carbonic anhydrase is present on apical membrane and inside tubular cells)
CO2 moves into the cell and reacts with H2O to form more HCO3-, which moves across basolateral membrane to ECF (Na3HCO3- cotransporter)

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269
Q

Describe the creation of HCO3- in the proximal tubule. What happens to the products?

A

Glutamine is converted to alpha-ketoglutarate, producing HCO3- and ammonium NH4+
HCO3- enters ECF
NH4+ enters lumen

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270
Q

Describe the creation of HCO3- in the distal tubule

A

Metabolic activity produces CO2, so H+ ions need to be secreted and buffer to keep producing HCO3- (Na+ gradient not enough to drive secretion of H+), via H+ATPase.
H+ buffered by filtered HPO4+ and excreted NH4+

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271
Q

What is the lowest pH of urine?

A

pH 4.5

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272
Q

How is the lowest possible pH of urine (4.5) achieved?

A

No HCO3- is secreted (all has been recovered)

Some H+ buffered by phosphate, some has reacted with ammonia to form NH4+

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273
Q

Approximately how much H+ is secreted per day?

A

50-100mmol

Needed to keep the concentration of HCO3- normal

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274
Q

What controls H+ secretion?

A

Kidneys

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275
Q

What happens if ECF concentration of HCO3- is low?

A

More HCO3- moves out of cells to ECF, more H+ in cells

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276
Q

What is the kidney cellular response to acidosis?

A

Decreased pH enhances the activity of Na+/H+ exchanger
Decreased pH enhances ammonium production in proximal tube
Decreased pH enhances activity of H+ ATPase (proton pump) in distal tube
Increased capacity to export HCO3- from tubular cells to ECF

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277
Q

What is the anion gap?

A

Associated ion with metabolic acids (e.g. Lactic, keto…) left after H+ reacts with HCO3- to produce CO2 (exhaled).
Anion replaces HCO3-

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278
Q

How is the anion gap calculated?

A

The difference between the concentrations of
(Na+ + K+) - (Cl- + HCO3-)
Main cations - main anions

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279
Q

What is a normal value for the anion gap?

A

10-15mmol/l

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280
Q

What does an increased anion gap indicate?

A

HCO3- has been replaced by an anion other than Cl-

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281
Q

Do all metabolic acidosis create an anion gap?

A

Nope

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282
Q

What does a fall in pH stimulate in the kidney?

A

Acid secretion

HCO3- recovery

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283
Q

What does a rise in the pH of tubular cells lead to?

A

A fall in H+ excretion and reduction in HCO3- recovery

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284
Q

When is HCO3- excretion compromised?

A

If there is also volume depletion
Capacity to lose HCO3- is reduced because of high rate of Na+ recovery
Recovering Na+ favours H+ excretion and HCO3- recovery

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285
Q

What effect does hyperkalaemia have on HCO3-?

A 
K+ moves out of cells
H+ moves into cells
Favours H+ excretion
HCO3- recovery
More K+ reabsorption in distal nephron
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286
Q

What effect does hypokalaemia have on HCO3-?

A

K+ moves into cells
H+ moves out of cells
Favours HCO3- excretion (H+ recovery)
Less K+ reabsorbed in nephron

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287
Q

What value are most body fluids osmotically, so that they are isotonic to cells?

A

280-310mOsm/kg

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288
Q

Through what range can urine osmolarity go through?

A

50-1200 mOsm/kg

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289
Q

What approximate value is urine osmolarity in a normal hydrated person?

A

500-700mOsm/kg

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290
Q

What do disorders of water balance manifest as?

A

Changes in body fluid osmolarity

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291
Q

What detects changes in plasma osmolarity?

A

Hypothalamic osmoreceptors

292
Q

What are the 2 efferent pathways to effect plasma osmolarity?

A

ADH and thirst

Effects kidney and brain (behavioural), water excretion and water intake

293
Q

Where are osmoreceptors in the brain located?

A

Organum vasculosum of the lamina terminalis (OVLT), which is anterior and ventral to the third ventricle

294
Q

What feature of the organum vasculosum of the lamina terminalis (OVLT) aids its ability to detect plasma osmotic changes?

A

Fenestrated leaky endothelium, exposed directly to systemic circulation (on plasma side of blood brain barrier) - in direct contact with plasma

295
Q

What does the organum vasculosum of the lamina terminalis (OVLT) do?

A

Senses changes in plasma osmolarity, signals secondary responses - concentration of urine or thirst

296
Q

Under what conditions is ADH released?

A

Predominant water loss

297
Q

Where is ADH secreted from?

A

Posterior pituitary gland

298
Q

What controls ADH secretion?

A

Negative feedback loops

299
Q

Should ADH conc. ever reach zero?

A

Nope

300
Q

What is more important, blood osmolarity or volume?

A

Volume!
When faced with circulatory collapse, kidneys continue to conserve H2O even if this will reduce osmolarity of body fluids

301
Q

What is the analogue of thirst?

A

Salt ingestion

302
Q

Where is ADH produced?

A

Produced by neurosecretary cells in the hypothalamus

303
Q

What sort of peptide is ADH?

A

Small, 9 AA long

304
Q

What are some other names for ADH?

A

Vasopressin, argipressin, arginine vasopressin AVP

305
Q

What effect does ADH have on the kidney?

A

Increases permeability of collecting duct to water and urea

306
Q

What is diabetes insipidus?

A

When plasma ADH levels are too low

307
Q

What might cause diabetes insipidus?

A

Damaged hypothalamus or pituitary glands e.g. Brain injury (base of skull fracture), tumour, aneurism ect

308
Q

What is nephrogenic diabetes insipidus?

A

Kidney insensitivity to ADH (acquired)

309
Q

What effect does diabetes insipidus have on the kidney?

A

Water is inadequately reabsorbed from the collecting ducts, so a large quantity of urine is produced

310
Q

How can you manage diabetes insipidus?

A

ADH injections

ADH nasal spray

311
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

312
Q

What characterises SIADH?

A

Excessive release of ADH from PP gland or another source. Dilutional hyponatriemia, in which the plasma sodium levels are lowered and total body fluid is increased.

313
Q

What aquaporin channels are present in the proximal tubule?

A

AQP1

AQP7

314
Q

What aquaporin channels are present in the thin descending limb?

A

AQP1

315
Q

What aquaporin channels are present in the ascending limb?

A

None

316
Q

What aquaporin channels are present in the collecting duct?

A

AQP2
AQP3
AQP4
Mostly in medullary portion

317
Q

What happens in the kidney if there is little ADH present?

A

No aquaporin in basolateral membrane of latter DCT and collecting ducts
Therefore limited water reuptake in latter DCT/collecting ducts
Tubular fluid rich in water passes through the hyperosmotic renal pyramid with no change in water content
Loss of a large amount of hyposmotic urine - diuresis

318
Q

What happens in the kidney if ADH is present?

A

ADH causes insertion of aquaporin channels to basolateral membrane, enabling water to move out of collecting duct into hyperosmotic environment

319
Q

How is a counter current established in the kidney?

A

Juxtamedullary nephron - long loop of henle establishes gradient vertically, vasa recta helps maintain this osmotic gradient

320
Q

What effect does the thick ascending limb have on establishing the medullary gradient?

A

Removes solute without water, therefore increasing osmolarity of the interstitium

321
Q

Describe the action of loop diuretics

A

Block NaK2Cl transporters, medullary interstitium becomes isotonic and copious amounts of dilute urine is produced

322
Q

Describe the action of the descending limb with regards to osmolarity

A

Highly permeable to water (due to AQP1 channels), which are always open. Not permeable to Na+, so Na+ remains in descending limb and its concentration increases

323
Q

What is the maximum osmolarity at the tip of the loop of henle?

A

1200mOsm/kg

324
Q

Describe the action of the ascending limb with regards to osmolarity

A

Actively transports NaCl out of tubular lumen into interstitial fluid. Impermeable to water. Osmolarity decreases. Fluid entering DCT has a low osmolarity of 100mOsm/kg; it is hyposmotic

325
Q

What is counter current multiplication?

A

Active transport of Na+ out of ascending limb increases its concentration in the interstitial fluid surrounding the loop of henle. This is enabled by the vasa recta

326
Q

What enables counter current multiplication?

A

The vasa recta

327
Q

At what level is the osmolarity at the corticomedullary border?

A

Isotonic (~300mOsm/kg)

328
Q

What level of osmolarity is the medullary interstitium?

A

Hyperosmotic (up to 1200mOsm/kg at papilla)

329
Q

What aids osmotic gradient in the kidney?

A

Urea (not usually an effective osmole)

330
Q

What determines whether a substance is an effective osmolarity?

A

If a membrane enables certain solute to cross freely, then it is totally ineffective at exerting an osmotic force across the membrane

331
Q

Is urea hydrophilic or hydrophobic?

A

Hydrophilic

332
Q

Where is urea reabsorbed?

A

Medullary collecting duct

Cortical collecting duct cells are impermeable to urea

333
Q

What effect does ADH have on urea in the kidney?

A

Fractional excretion of urea decrease, and urea recycling increases

334
Q

What maintains the concentration gradient produced by the loop of henle?

A

The vasa recta, acts as a counter current exchanger

335
Q

What is bloodflow in renal medulla like?

A

Low (5-10% total RPF)

Needs to deliver nutrients and maintain medullary hyper-tonicity

336
Q

Has the vasa recta got any capacity for active transport?

A

Nope

337
Q

Describe osmotic stratification in medullary interstitium if ADH is present

A

Counter current multiplier give NaCl gradient

Also cortex to papilla gradient of urea

338
Q

Describe what happens in the descending limb of the vasa recta

A

Isoosmotic blood enters hyperosmotic mileu of medulla (high concentration of Na+ ions, Cl- ions, and urea)
Ions and urea diffuse into lumen of vasa recta
Osmolarity of blood in vasa recta increases as it reaches tip of loop

339
Q

Describe what happens in the ascending limb of the vasa recta

A

Blood ascending has higher concentration of solute than surrounding interstitium
Water moves in from the descending limb of the loop of henle

340
Q

Define ‘diuretic’

A

A drug/substance that promotes diuresis

Usually by increasing renal excretion of water and sodium, therefore causing a reduction of ECF volume

341
Q

When might diuretics be useful, in general?

A

Conditions where Na+ and H2O retention cause expansion of ECF volume e.g. HF, cirrhosis, nephrotic syndrome

342
Q

What are the stages in the formation of urine?

A

1 - Filtration
2 - Selective reabsorption of most of the solutes and water
3 - Secretion of substances

343
Q

How do diuretic generally work?

A

Blocking reabsorption of Na+ and H2O by the tubule fraction excretion (FE)

344
Q

What channel is common to all segments of the tubule?

A

Na+/K+ ATPase

345
Q

What channels are on the apical membrane of the proximal CT?

A

NaH Antiporter
Na-Glucose symporter
Na-AA symporter

346
Q

What channels are on the apical membrane of the loop of henle?

A

Na-K-2Cl symporter

347
Q

What channels are on the apical membrane of the early DT?

A

NaCl symporter

348
Q

What channels are on the apical membrane of the late DT and CD

A

ENaC

Epithelial Na+ Channels

349
Q

Describe tubular reabsorption of Na+ by principle cells of late DT and CD

A

Na-K-ATPase in basolateral membrane pumps out Na+
Na+ enters cells via ENaC on apical membrane
Na+ reabsorption favours K+ secretion by creating a luminal negative potential (secreted via K+ channels)

350
Q

What effect does aldosterone have on the expression of Na+ channels?

A

Increases expression of NaK ATPase, ENaC and K+ channels.

351
Q

What effects do diuretics blocking ENaC have on K+ secretion?

A

Diuretics blocking ENaC also reduces K+ secretion

352
Q

What are common sites of action of diuretics?

A

Loop of henle - loop diuretics
Distal convoluted tubule - thiazide diuretics
Collecting duct - potassium sparing diuretics
Aldosterone antagonists

353
Q

Give some examples of loop diuretics

A

Furosemide

Bumetanide

354
Q

Give some examples of thiazide diuretics

A

Metalozone
Indapamide
Bendroflumethiazide

355
Q

Give an examples of potassium sparing diuretics

A

Amiloride, trimterene

Aldosterone antagonists

356
Q

Give an example of an aldosterone antagonist

A

Spirolactone

357
Q

Describe the classification of diuretics

A

Loop diuretics - inhibitors of Na-K-2Cl symport
Thiazide diuretics - inhibitors of NaCl symport
K+ sparing diuretics - inhibitors of renal Na+ channels/aldosterone antagonists
Inhibitors of carbonic anhydrase
Osmotic diuretics

358
Q

Give an example of a diuretic that works via inhibiting carbonic anhydrase

A

Acetazolamide

359
Q

Give an example of an osmotic diuretic

A

Mannitol

360
Q

What are the 4 mechanisms via which diuretics may work?

A
  • By direct action on cells to block Na+ transporters in the luminal membrane (drug secreted into lumen in PCT, acts from within lumen on transporters)
  • By antagonising the action of aldosterone
  • By modification of filtrate content, osmotic diuretics (small molecules freely filtered at glomerulus, but not reabsorbed. Increase osmolarity of filtrate, reducing H2O and Na+ reabsorption throughout tubule)
  • By inhibiting activity of enzyme carbonic anhydrase in the PCT (interferes with Na and HCO3- reabsorption in PCT)
361
Q

Upon what transporters do diuretics acting on the loop of henle work on?

A

NaK2Cl transporter

362
Q

What proportion of filtered Na+ is absorbed in the loop of henle?

A

25%

363
Q

What helps drive absorption of Ca2+ and Mg2+?

A

K+ that has been carried across apical membrane drifts back via K+ channels, creating luminal positive gradient…

364
Q

Describe the action of loop diuretics

A

Secreted into lumen in the PCT and travel downstream to act on the loop of henle
Very potent diuretics (20-30% of filtered Na+ reabsorbed in the loop) - segments beyond have limited capacity to reabsorbed the resulting flood of Na+ and H2O

365
Q

How do loop diuretics get into the tubular lumen?

A

Secreted into lumen in the PCT via organic anion pathway

366
Q

When might you use loop diuretics?

A

Heart failure (diuretic effect = vaso/venodilation, decreases pre/afterload on heart)
Acute pulmonary oedema (furoseminide IV for rapid access)
Fluid retention and oedema in nephrotic syndrome, renal failure, cirrhosis of liver
Hypercalcaemia (impairs Ca2+ reabsorption, increasing urinary excretion of Ca2+)

367
Q

What sort of diuretics act on the early distal tubule?

A

Thiazides

368
Q

What channel do thiazide diuretics block?

A

NaCl transporter

369
Q

What effect can thiazide diuretics have on Ca2+ reabsorption?

A

Increased Ca2+ reabsorption

370
Q

Describe how thiazide diuretics work

A

Secreted into lumen in PCT, travel downstream to act at DCT
Block NaCl transporter in DCT
Increase Na+ (and H2O) loss in urine
Reduces Ca2+ loss in urine (increases Ca2+ reabsorption)

371
Q

How do thiazide diuretics get into the tubular lumen?

A

Secreted into lumen at PCT

372
Q

What potency do thiazide diuretics have?

A

Less than loop diuretics!
Only 5% Na+ reabsorption inhibited
Therefore ineffective in renal failure

373
Q

How much Na+ reabsorption is inhibited by thiazide diuretics?

A

~5%

374
Q

What are thiazide diuretics primarily used to treat?

A

Hypertension

375
Q

What diuretics act on the late DT and CD?

A

Inhibitors of epithelial Na+ channels

Aldosterone antagonists

376
Q

What are some features of diuretics acting on the late DT and CD?

A

Mild diuretics affecting only 2% of Na+ reabsorption
Reduce Na+ channel activity (directly or indirectly)
Reduce loss of K+
Risk of hyperkalaemia

377
Q

What is a risk of diuretics acting on the late DT and CD?

A

Can produce life-threatening hyperkalaemia, especially if used alongside ACE inhibitors, K+ supplements or in patients with renal impairment

378
Q

When would you use spironolactone? (An aldosterone antagonist)

A

Treatment of hypertension due to primary hyperaldosteronism (com’s syndrome - adrenal hypertension)
Treatment of ascites and oedema in cirrhosis
In addition to loop diuretics to in heart failure
As additional therapy in hypertension not controlled by ACE inhibitors ect

379
Q

What are ENaC blockers?

A

Mild diuretics with a K+ sparing effect

380
Q

When are ENaC blockers used?

A

In combination with K+ losing diuretics to minimise K+ loss

381
Q

Where is carbonic anhydrase found in the kidney?

A

Within the brush border of PCT cell

382
Q

What is a risk of using carbonic anhydrase inhibitors?

A

Can cause metabolic acidosis due to loss of HCO3- in urine

383
Q

When might you use osmotic diuretics?

A

Useful for cerebral oedema (IV)

384
Q

What are some possible consequences of using osmotic diuretics?

A

Can cause loss of H2O, Na+ and K+ in the urine

385
Q

How is K+ secreted in the DT and CD?

A

Passive process
Driven by electric-chemical gradient. Rate of K+ secretion depends on the concentration gradient across apical membrane, and the rate of Na+ absorption - inward movement of Na+ ions creates a favourable lumen negative gradient for K+ secretion

386
Q

What does the rate of K+ secretion in the DT and CD depend on?

A

Rate of K+ secretion depends on the concentration gradient across apical membrane, and the rate of Na+ absorption - inward movement of Na+ ions creates a favourable lumen negative gradient for K+ secretion

387
Q

List some things other than diuretic use which may contribute to hypokalaemia

A 
Excess diuresis reduces ECF volume
Activation of RAAS
Increased aldosterone secretion
Increased Na+ absorption and K+ secretion 
Hypokalaemia
388
Q

What effect do loop diuretics have on K+ excretion?

A

Increase Na+ absorption by principal cells, favourable electrical gradient for K+ excretion
(Also loop and thiazide diuretics - both increase Na+ and H2O delivery to late DT and CD)

389
Q

Describe effect of thiazide diuretics on K+ secretion

A

Faster flow rate of filtrate in tubule lumen, K+ secreted into lumen is washed away faster, lower K+ concentration in lumen. Favourable chemical gradient for K+ secretions

390
Q

What is particularly at risk of happening when K+ sparing diuretics are used?

A

Hyperkalaemia

Na+ reabsorption reduced, less K+ lost in urine

391
Q

What is it important to measure when using diuretic therapy?

A

Electrolyte Na/K levels

392
Q

When are diuretics used?

A

Conditions with ECF expansion and oedema

393
Q

How does congestive heart failure cause peripheral oedema?

A

Increases systemic venal pressure

394
Q

How does reduced renal perfusion lead to expansion of the ECF?

A

Activation of RAAS, Na+ and H2O retention

395
Q

What is nephrotic syndrome?

A

Glomerular disease - increase in GBM permeability to protein. Proteins are filtered and lost in urine, causes low plasma albumin, results in low plasma oncotic pressure - peripheral oedema.
Reduced circulatory volume - RAAS activated - expansion of ECF - more oedema

396
Q

Where is splanchnic circulation?

A

GI

397
Q

Is ascites transudate or exudate?

A

Transudate

398
Q

What might cause bladder stones?

A
  • Bladder outflow obstruction - urethral stricture, neuropathic bladder (doesn’t contract normally), prostate obstruction
  • Presence of foreign body - catheter, non-absorbable sutures
  • Some are passed down from upper urinary tract
399
Q

What are the consequences of bladder stones?

A

Can cause urine outflow obstruction. Anuria/painful bladder distension

400
Q

What are some other names for renal stones?

A

Kidney stone, renal calculus, nephrolith

401
Q

When do renal stones generally present?

A

30+yrs

2:1 male:female

402
Q

What can renal stones be made of?

A 
Calcium stones:
Calcium oxalate - usually with calcium phosphate (apatite)
Calcium phosphate alone 
Uric acid
Struvite 'infection stones', urease stones, triple phosphate stones (magnesium ammonium phosphate hexahydrate, from infection by bacteria that have urease)
Other types (rarer)
Cysteine stones
Drug stones
Ammonium acid rate stones
403
Q

What causes struvite ‘infection stones’ (urease stones, triple phosphate stones)

A

Magnesium ammonium phosphate hexahydrate, from infection by bacteria that have urease

404
Q

When are renal stones comprised of calcium phosphate alone seen?

A

Frequently in hyperparathyroidism and renal tubular disease

405
Q

When might cysteine stones occur?

A

Rare genetic disorder cystinuria

406
Q

Give some examples of kidney stones that occur as a result of drugs

A

Indinavir (treatment for HIV)
Triamterene (diuretic)
Sulphadiazine (sulphonamide antibiotic)

407
Q

Why do urinary stones form?

A

If there is urine supersaturation with minerals - solvent contains more solute than it can hold in solution. Seed crystals form by nucleation - 1st step is formation of a new structure by self assembly. A physical, not chemical reaction.

408
Q

In what circumstances might urinary stones form?

A

Decrease in water content - dehydration
Increase in mineral content - hypercalcaemia and hypercalciuria, hyperoxaluria, hyperuricaemia, hyperuricosuria, cysteinuria
Decrease in solubility of solute in urine - some solute more soluble at high pH and some at low pH

409
Q

What stones does acid urine favour the formation of?

A

Calcium oxalate and uric acid stones

410
Q

What stones does alkaline urine favour the formation of?

A

Calcium phosphate stones

411
Q

What renal tubular acidosis result in?

A

Persistently alkaline urine and decreased urinary citrate excretion

412
Q

What happens to calcium phosphate in alkali?

A

Precipitates

413
Q

What happens to calcium phosphate in acid?

A

Dissolves

414
Q

What happens if you put a bone in vinegar (ethanoic acid)?

A

Goes rubbery - calcium phosphate has dissolved away

415
Q

What is a likely cause of uric acid and cysteine stones?

A

Supersaturation

416
Q

How do calcium oxalate stones form?

A

75% grow like stalactites attached to exposed interstitial deposits of calcium phosphate ‘Randall’s plaque’ on the tips of renal papillae (composed of a core of calcium phosphate surrounded by calcium oxalate)
Otherwise, can form on plugs protruding from ducts of bellini or free in solution

417
Q

List some causative factors for urinary stones

A

Urine status - low urine flow, obstruction, infection
Genetic/congenital factors - primary metabolic disturbances e.g. Cystinuria, kidney abnormalities e.g. Polycystic kidneys, medullary sponge kidneys
Drugs

418
Q

Describe the presentation of calcium oxalate stones

A

5% associated with hypercalcaemia and hypercalciuria - treatable!
55% have hypercalciuria without hypercalcaemia - can be associated with hyperabsorption of calcium from the gut or impairment in renal tubular absorption of calcium
5% association with hyperoxaluria - hereditary or secondary to intestinal over absorption in patients with enteric disease

419
Q

What might cause calcium oxalate stones due to hypercalciuria and hypercalcaemia?

A

Hyperparathyroidism, diffuse bone disease, sarcoidosis

420
Q

Proportionally, how much Ca2+ is locked away in bone?

A

Over 99%
ECF conc 1000-10000 times lower than ICF
Cell membranes pump out Ca2+

421
Q

What regulates Ca2+ conc in the ECF?

A

PTH
Calcitriol
1,25 dihydroxy vitamin D
Calcitonin

Have effect in gut, kidney and bone

422
Q

Where are Ca2+ sensing receptors located in the body?

A

Parathyroid glands, kidney, brain and other organs

423
Q

How does PTH increase serum calcium?

A

Increases osteoclastic resorption of bone (rapid)
Increases intestinal absorption of Ca2+ (slow)
Increases synthesis of 1,25-(OH)2D3
Increases renal tubular resorption of Ca2+
Increases excretion of phosphate

424
Q

How does vitamin D effect Ca2+ levels?

A

Increases Ca2+ absorption in the gut

Increases calcification and resorption in bone

425
Q

Where is calcitonin produced?

A

Thyroid C cells

426
Q

How does calcitonin decrease serum Ca2+?

A

Inhibits osteoclastic bone resorption

Increases renal excretion of calcium and phosphate

427
Q

What is the most common metabolic abnormality in Ca2+ stone formation?

A

Hypercalciuria

428
Q

What might cause hypercalciuria?

A

Hypercalcaemia
Excessive dietary intake of Ca2+
Excessive resorption of Ca2+ from skeleton (prolonged immobilisation, weightlessness)
Idiopathic (increased absorption of Ca2+ from the GIT)

429
Q

What can be given to astronauts to help prevent them getting hypercalciuria due to resorption of unused skeletal bones?

A

Potassium citrate

430
Q

What are the possible causes of hypercalcaemia?

A 
Hypersecretion of PTH, resulting in increased bone resorption
Destruction of bone tissue
Other mechanisms (excessive Vit D ingestion, thiazide diuretics, sarcoidosis, milk-alkali syndrome - excessive Ca2+ intake)
431
Q

What is sarcoidosis?

A

Macrophages activate Vit D precursor

432
Q

What might lead to hypersecretion of PTH?

A

Primary - parathyroid hyperplasia or functional tumour
Secondary - to renal failure (which causes retention of phosphate and hence hypocalcaemia)
Ectopic - secretion of PTH related protein by malignant tumour (legal squamous cell carcinoma of lung)

433
Q

What might cause destruction of bone tissue (leading to hypercalcaemia)?

A

Primary tumour of bone marrow (e.g. Myeloma)
Paget’s disease of bone (accelerated bone turnover)
Immobilisation (reduces bone formation whilst reabsorption continues
Diffuse skeletal metastases

434
Q

What are the most common causes of hypercalcaemia?

A

Hyperparathyroidism and malignancies

435
Q

What are the main clinical signs of hypercalcaemia?

A

Bones, stones and moans.
Painful bones - fractures
Renal stones
Abdominal groans - constipation, peptic ulcers pancreatitis, gallstones
Psychic moans - depression, lethargy, seizures
Severe muscle weakness (opposite of tetany in hypocalcaemia!)

436
Q

What is hyperoxaluria?

A

Rare autosomal recessive genetic disorder of oxalate synthesis (primary hyperoxaluria types 1 and 2)
Increased intestinal oxalate absorption secondary to GI disease (England chrons disease) usually with an intestinal resection (increased absorption of oxalate from colon)
Dietary habits - high oxalate intake (spinich, rhubarb, tea, nuts)
Low calcium intake (increases GI absorption of oxalate)

437
Q

What type of stones are generally present with UTIs?

A

Struvite stones (mixed infection stones)

438
Q

What are struvite stones comprised of?

A

Magnesium ammonium phosphate with variable amounts of calcium

439
Q

What sort of infections usually produce struvite stones? Why?

A

Infection with organisms with the enzyme urease which hydrolyses urea to ammonium hydroxide (proteus species e.g. Proteus mirabilis)
Also production of mucoprotein from infection provides an organic matrix on which stones can form

440
Q

What are particularly large urinary stones called?

A

Staghorn calculus

441
Q

When are staghorn calculus predominantly seen?

A

In people predisposed to UTIs - spinal cord injury, neurogenic bladder, vesicoureteric reflux, obstruction uropathy

442
Q

When are uric acid stones seen?

A

In hyperuricaemia, and in people with tendency to have urine with pH of less than 5.5

443
Q

What is a key fact about uric acid stones?

A

They are radiolucent - can’t be seen on X-ray

444
Q

What is hyperuricosuria?

A

High uric acid in urine

445
Q

What is hyperuricaemia?

A

High uric acid in blood

446
Q

What is the endpoint of purine metabolism?

A

Uric acid

447
Q

When might hyperuricaemia be seen?

A

Seen in idiopathic gout
Secondary consequence of increased cell turnover (lympho or myeloproliferative disorders) after chemotherapy (tumour lysis syndrome)

448
Q

How do renal stones present?

A

Asymptomatic, but can be seen on radiography
Renal colic, dull ache on loins
Recurrent UTIs
Urinary tract obstruction
Haematuria
Renal failure
If urinary tract obstruction and fluid intake is increased, result is an increase in pain

449
Q

How long do renal bouts generally last?

A

20-60mins

450
Q

What causes bouts of renal colic?

A

Caused by peristaltic contractions or spasms of the ureter as it attempts to expel stone

451
Q

Where is the pain in renal colic felt?

A

Radiates from flank to iliac fossa and inner thigh (in distribution of 1st lumbar nerve)

452
Q

What often accompanies the pain felt in renal colic?

A

Nausea/vomiting, pallor, sweat, restlessness. Haematuria common.

453
Q

What generally happens to untreated renal colic?

A

Subsides in a few hours

454
Q

What is urolithiasis?

A

The formation of stony concretions in the bladder or urinary tract

455
Q

What does MSU stand for (with regards to urinary investigations)

A

Midstream specimen of urine

456
Q

What might you be looking for in a MSU (midstream specimen of urine)

A

RBCs, urinary casts, urinary crystals, culture, (cause or consequence of stones?)

457
Q

What might you be looking for in a serum test when investigating urinary stones?

A

Urea, creatinine, electrolytes, calcium levels

458
Q

What investigations might you do in urolithiasis?

A 
MSU (midstream sample of urine)
Serum
Plain abdominal x-ray
CT kidney, ureter and bladder
Pass urine through serve to catch calculi for chemical analysis
459
Q

Why aren’t x-rays the best way to look for calculi?

A

60% of stones are radiopaque (mostly Ca2+ containing stones). Uric acid stones are radiolucent

460
Q

Why is a CT of the kidney, ureter and bladder good for use in urolithiasis?

A

Better than USS - almost all stones can be seen. Ideally during pain.
Can see stones and dilated renal pelvis
Can see uric acid stones
Identifies any primary renal disease predisposing to stone formation

461
Q

What size urological stones can usually be passed (90%)?

A

<5mm diameter

462
Q

What size urological stones usually require intervention to be passed?

A

> 7mm diameter

463
Q

What are some possible complications of uric stones?

A

Acute pyelonephritis +- gram negative septicaemia
Pressure necrosis of the renal parenchyma
Urinary obstruction and hydronephrosis
Ulceration through the wall of the collecting system

464
Q

What are the possible treatments for renal colic?

A

Analgesia (IV diclofenac or pethidine), warmth to site of pain, bed rest
Ureteroscopy (usually for stones in lower ureter - like endoscopy…)
Percutaneous nephrolithotomy (surgery)
Extracorporal shock wave lithotripsy ESWL

465
Q

What does ESWL stand for?

A

Extracorporal shock wave lithotripsy

466
Q

When might you use ESWL (Extracorporal shock wave lithotripsy)?

A

Most commonly for renal stones near the pelvis

467
Q

How does ESWL (Extracorporal shock wave lithotripsy) work?

A

Lithrotriptor delivers external, focused, high intensity probes of ultrasonic energy. Takes 30-60 mins. Fragments stones, so they can then be passed spontaneously.

468
Q

How can you prevent getting urinary stones?

A

Keep hydrated!
Decrease excretion of Ca2+ or oxalate (thiazide diuretics)
Potassium citrate alkalinise urine - reduces risk of calcium oxalate, uric acid and cysteine stones. Also forms soluble complexes with Ca2+. Can induce phosphate stones

469
Q

What effect doe thiazide diuretics have on Ca2+ conc. in the urine?

A

Decreases such

470
Q

What percentage of women will have had at least 1 UTI by the age of 24?

A

~30%

471
Q

What are UTIs a common source of?

A

Gram negative septicaemia

472
Q

In whom do most UTIs occur?

A

Females (shorter urethra)
Obstruction - enlarged prostate, pregnancy, stones, tumours
Neurological problems - incomplete emptying, residual volume
Ureteric reflex - ascending infection from bladder especially in children

473
Q

What might cause a urinary tract obstruction at the PUJ?

A

Calculi

474
Q

What might cause a urinary tract obstruction at the ureta?

A

Calculi, Ca2+, retroperitoneal fibrosis

475
Q

What might cause a urinary tract obstruction at the bladder?

A

Neuropathic bladder

476
Q

What might cause a urinary tract obstruction at the VUJ?

A

Calculi

477
Q

What might cause a urinary tract obstruction at the bladder neck?

A

Hypertrophy

478
Q

What might cause a urinary tract obstruction at the prostate?

A

BPH/Ca2+

479
Q

What might cause a urinary tract obstruction at the urethra

A

Stricture

480
Q

What adaptations enables bacteria to colonise the urinary tract?

A

Fimbriae allow attachment to host epithelium. K antigen permits production of polysaccharide capsule. Haemolysins damage host membranes and cause renal damage. Urease breaks down urea creating a favourable environment for bacterial growth.

481
Q

What is cystitis?

A

Frequency and dysuria (lower UTI)

482
Q

What is acute pyelonephritis?

A

Upper UTI

483
Q

What is chronic pyelonephritis?

A

Renal inflammation and fibrosis due to recurrent and persistent renal infection, vesicoureteral reflux, or other cause of urinary tract obstruction

484
Q

When might asymptomatic bacteriuria become a problem?

A

If patient then becomes pregnant

485
Q

What are some clinical signs and symptoms of lower UTI?

A

Dysuria, frequency, urgency, sometimes low grade fever

486
Q

What are some clinical signs and symptoms of upper UTI (pyelonephritis)?

A

Fever, loin pain, may have dysuria/frequency

487
Q

What is an uncomplicated UTI?

A

‘An infection by a usual organism in a patient with a normal urinary tract and normal urinary function’

488
Q

What is a complicated UTI?

A

UTI when one or more factors present that predispose the person to persistent infection, recurrent infection, or treatment failure.

489
Q

Give some examples of when an UTI could be classed as ‘complicated’

A 
Abnormal urinary tract (e.g. Vesicoureteric reflux, indwelling catheter ect.)
Virulent organism (e.g. Staph aureus)
Impaired host defences (e.g. Poorly controlled diabetes, immunosuppression)
Impaired renal function
490
Q

IN PRACTISE, what is classed as an ‘uncomplicated’ infection?

A

Healthy, non-pregnant, woman of child bearing age.

All others are treated as ‘complicated’ (so culture urine)

491
Q

What is the clinical consequence of a UTI being classed as uncomplicated?

A

No need to culture urine

492
Q

How might you obtain a specimen collection for a UTI?

A 
MSU - cleansing not required in women 
Clean catch in children - no antiseptic
Collection bag (20% false positives)
Catheter sample
Supra-pubic aspiration
Transportation (4 degrees C, +- boric acid)
493
Q

What does dipstick testing analyse?

A

Leucocyte esterase
Nitrile
Haematuria
Proteinuria

494
Q

How is the turbidity of urine relevant to infection?

A

If urine is clear, infection is unlikely

495
Q

What is dipstick testing useful for?

A

Useful to exclude UTI in children >3yrs, men with mild/non-specific symptoms, elderly/institutionalised women

496
Q

When is dipstick testing not useful?

A

Acute uncomplicated UTI in women
Men with typical/severe symptoms
Catheterised patients
Older patients without features of infection (asymptomatic bacteriuria common)

497
Q

Why is culturing urine beneficial?

A 
Investigation of children, males, and other 'complicated' infections
Increased sensitivity 
Epidemiology of isolates
Susceptibility data
Control of specimen quality
498
Q

What would you analyse in a urine culture report?

A 
Clinical details again - symptoms, previous antibiotics (might decrease sample size)
Quality of specimen
Delays in culture
Microscopy (if available)
Organisms isolated
499
Q

What is urethral syndrome?

A 
Low-count bacteriuria
Fastidious organisms
Vaginal infection/inflammation
Sexually transmitted pathogens -urethritis
Mechanical, physical and chemical causes
500
Q

When is imagine of the urinary tract particularly useful?

A

In septic patients to identify renal involvement.

Considered in all children with UTI

501
Q

What might cause sterile pyuria?

A

Antibiotics, urethritis (chlamydia/gonococci), vaginal infection/inflammation, chemical inflammation, tuberculosis, appendicitis, fastidious organisms

502
Q

With whom is there a high prevalence of asymptomatic bacteriuria?

A

High prevalence in older people, particularly elderly females

503
Q

What is often associated with pyuria? What is a consequence of this?

A

Associated pyuria

Therefore positive dipstick/culture - so do not routinely dipstick/culture

504
Q

Is asymptomatic bacteriuria associated with increased risk of morbidity/mortality?

A

Nope

505
Q

When might asymptomatic bacteriuria require treatment?

A

In pregnancy and urological surgery

506
Q

What is the treatment for UTI?

A 
Increase fluid intake
Address underlying disorder
3 day course for uncomplicated UTI
5-7 day course for complicated UTI
CSU - only treat if systemically unwell
507
Q

What is the length of course for an uncomplicated UTI?

A

3 day course for uncomplicated UTI

508
Q

What is the length of course for an complicated UTI?

A

5-7 day course for complicated UTI

509
Q

What is the treatment for simple cystitis?

A

Uncomplicated infections can be treated with trimethoprim or nitrofurantoin.
3 day course just as effective as 5 or 7 days, but decreases risk of resistance

510
Q

What is the treatment for complicated lower UTI?

A

Trimethoprim, nitrofurantoin or cephalexin may be used - review susceptibility report. 5-7 day course. Post treatment follow up cultures in paediatric patients and pregnant women

511
Q

Why is amoxicillin not appropriate treatment for complicated lower UTI?

A

50% of isolates are resistant

512
Q

What is the treatment for pyelonephritis/septicaemia?

A

14 day course. Use agent with systemic activity (not nitrofurantoin). Possibly IV initially unless good PO absorption and patient well enough. Co-amoxiclav, ciprofloxacin, gentamicin.

513
Q

How is gentamicin administered?

A

IV only

514
Q

Is gentamicin nephrotoxic?

A

Yes

515
Q

When is prophylaxis used for UTI?

A

If 3 or more episodes in one year with no underlying testable condition

516
Q

What prophylaxis might be used for UTI?

A

Trimethoprim or nitrofurantoin

Single nightly dose, ensure all breakthrough infections are documented

517
Q

What nerve roots innervates the detrusor muscles?

A

S2, 3, 4 (keeps the piss off the floor)

Pelvic nerves

518
Q

What nerve roots control the urinary sphincter?

A

Pudendal nerve S2, 3, 4

519
Q

What normally happens as the bladder fills?

A

Compliance (receptive relaxation). Sensation of bladder filling, nodetrusor contraction

520
Q

What normally happens on voiding of the bladder?

A

Voluntary initiation, complete emptying

521
Q

What lower neurological problems might occur with bladder emptying?

A

Low detrusor pressure. Large residual urine +- overflow incontinence. Reduced perional sensation, lax anal tone.

522
Q

What upper neurological issues may occur with bladder emptying?

A

Constant contractions. High pressure, dilated ureters, thickened detrusor. Urine goes back up to kidneys, can damage them. Poor coordination with sphincter. Detrusor sphincter dyssunergia.

523
Q

List some storage symptoms of lower UTIs

A

Frequency, urgency, nocturia, incontinence

524
Q

List some voiding symptoms of lower UTIs

A

Slow stream, splitting/spraying, intermittency, hesitancy, straining, terminal dribble.

525
Q

List some post-micturition symptoms of lower UTIs

A

Post micturition dribble. Feeling of incomplete emptying

526
Q

What is stress urinary incontinence?

A

The complaint of involuntary leakage on effort or extortion or sneezing/coughing

527
Q

What is urge urinary incontinence?

A

The complaint of involuntary leakage of urine accompanied by or immediately proceeded by urgency

528
Q

What is mixed urinary incontinence?

A

The complaint of involuntary leakage of urine associated with urgency and also exertion, effort, sneezing or coughing

529
Q

What are the types of urinary incontinence?

A

Stress urinary incontinence
Urge urinary incontinence
Mixed urinary incontinence
Overflow incontinence

530
Q

What is overactive bladder syndrome?

A

Urgency, frequency, nocturia

Prevalence is much higher than that of urgency urinary incontinence

531
Q

What are the risk factors for urinary incontinence?

A

O&G: pregnancy/childbirth, pelvic surgery, pelvic prolapse
Predisposing: race, family predisposition, anatomical abnormalities, neurological abnormalities
Promoting: co-morbidities, obesity, age, UTI, drugs, menopause, increased infra-abdominal pressure, cognitive impairment

532
Q

How is the type of UTI categorised?

A

History

533
Q

How would one examine a patient with a UTI?

A

BMI, abdominal examination to exclude palpable bladder. Digital rectal exam - prostate (male), limited neurological exam. Females - external genitalia (stress test - cough). Vaginal exam

534
Q

What investigations would you do for a patient with urinary incontinence?

A

Mandatory: dipstick (UTI - haematuria, proteinuria, glucosuria)
Consider: basic non-invasive urodynamics, frequency - volume chart, bladder diary (>3days), post-micturition residual volume (in patients with voiding dysfunction)
Optional: invasive urodynamics (pressure - flow studies +-video). Pad tests. Cystoscopy

535
Q

How would you determine how to manage a patient with urinary incontinence?

A

Depends on symptoms, degree of bother, effects of treatment on other symptoms, previous other treatments.
Should be individualised, systematic approach

536
Q

Describe conservative management of urinary incontinence

A

Modify fluid intake, weight loss, stop smoking, avoid constipation, decrease caffeine intake, timed voiding (fixed schedule)

537
Q

How might you manage contained incontinence (for patients unsuitable for surgery who have failed conservative or medical management)?

A

Indwelling catheter (urethral or suprapubic), sheath device (adhesive condom attached to catheter tubing bag), incontinence pads

538
Q

What might pelvic floor muscle training be used for?

A

Stress urinary incontinence specific management.

8 contractions, thrice daily. At least 3 months duration

539
Q

What pharmacological treatments might be used for stress urinary incontinence?

A

Duloxetine - combined noradrenaline and serotonin uptake inhibitor. Increases activity in the striated sphincter during filling phase. Not recommended by NICE as 1st or 2nd line, but can be offered as an alternative to surgery.

540
Q

What surgical options are there for females with stress urinary incontinence?

A 
Permanent intention - low tension vaginal tapes (commonest), open retropubic suspension procedures, classical sling procedures.
Temporary intention (e.g. If further pregnancies are planned) - intramural bulking agents
541
Q

What surgical options are there for males with stress urinary incontinence?

A

Artificial urinary sphincter. Male sling procedure

542
Q

Describe urgency urinary incontinence specific management

A

Bladder training - schedule of voiding e.g. Every hr, must wait in between. Increase intervals by 15-30mins each week until 2-3hr interval has been reached. At least 6wks duration

543
Q

What pharmacological treatments are available for urge urinary incontinence?

A

Anticholinergics - acts on muscarinic receptors M2 M3
Oxybutynin
Beta3 adrenoceptor agonist mirabegron. Increases bladder capacity to store urine.

544
Q

What side effects occur with anticholinergics (act on muscarinic receptors)

A

Due to their effects on other M receptors at other sites
M1 - CNS, salivary glands
M2 - Heart smooth muscle
M3 - Smooth muscle (ocular and intestinal), salivary glands
M4 - CNS
M5 - CNS, eye

545
Q

Describe how botulinum toxin might be used to treat urge urinary incontinence

A

Potent biological neurotoxin. Inhibits release of ACh at pre-synaptic neuromuscular junction causing targeted flaccid paralysis. Mainly type A used clinically
Duration of action only 3-6months (needs to be redone)

546
Q

Describe how surgery may be used to treat urge urinary incontinence

A

Sacral nerve neuromodulation (probe inserted which disrupts the nerve signals from spinal cord)
Autoaugmentation, augmentation cytoplasy, urinary diversion (no bladder at all)

547
Q

What are the ‘compartments’ of the renal system that can go wrong?

A

Glomerular, tubular, interstitial, vascular

548
Q

What is nephrotic syndrome?

A

Filter can leak - proteinuria, haematuria. Swelling due to low blood albumin. (O for oedema!)

549
Q

What is nephritic syndrome?

A

Filter can block ‘renal failure’. Reduced renal function, acute kidney failure. Haematuria, hypertensive. Decreased eGFR

550
Q

What is a primary kidney injury?

A

Just effects the glomerulus

551
Q

What is a secondary kidney injury?

A

Systemic disease that effects kidneys, e.g. Diabetes

552
Q

What are the sites within the glomerulus where immune complex deposition (antigen-antibody complex/circulating factors) may occur?

A

Subepithelial (podocytes)
Within GBM
Subendothelial
Mesangial (and paramesangial)

553
Q

What is the likely site of kidney injury in nephrotic syndrome?

A

Podocytes/subepithelial damage

554
Q

What are they common primary causes of podocytes/subepithelial damage (causing nephrotic syndrome)

A

Minimal change glomerulonephritis
Focal segmental glomerulonephritis
Membranous glomerulonephritis

555
Q

What are they common secondary causes of podocytes/subepithelial damage (causing nephrotic syndrome)

A

Diabetes mellitus

Amyloidoses

556
Q

What is minimal change glomerulonephritis?

A

Heavy proteinuria or nephrotic syndrome. No foot processes on podocytes (only visible under electron microscope). Unknown cause. No immune complex deposition. Responds to steroids. May reoccur. Usually no progression to renal failure. Incidence increases with increasing age (usually presents in childhood/adolescence). Circulating factor damaging podocytes.

557
Q

What is FSGS spectrum (minimal change glomerulonephritis)?

A

More common in adults/older patients. Nephrotic. Less responsive to steroids. Glomerulosclerosis (scarring). Circulating factor damaging podocytes. Progressive to renal failure. Collagen deposition in glomerulus

558
Q

Describe membranous glomerulonephritis

A 
Immune complex deposits, probably autoimmune. May be secondary (associated with other pathologies e.g. Lymphoma). Immune complexes deposited near podocytes. Complex activation leads to cell injury IgG. Antigen either already on podocytes or gets there separately (complex can't get through BM!). Attracts antibody.
Rule of 1/3s
1/3 Get better
1/3 Stay the same
1/3 Progress to renal failure
559
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

560
Q

How does diabetes effect the kidneys?

A

Progressive proteinuria. Progressive renal failure. Microvascular. Mesangial sclerosis –> nodules. Basement membrane thickening.

561
Q

Describe IgA Nephropathy

A

Commonest glomerulonephritis. Classically presents with visible/invisible haematuria. Relationship with mucosal infections. Variable histological features and course. +- proteinuria. Significant proportion progress to renal failure. No effective treatment (only ways to support renal function).

562
Q

Is there a cure for IgA nephropathy?

A

No effective treatment (only ways to support renal function).

563
Q

Does IgA progress to renal failure?

A

Significant proportion progress to renal failure.

564
Q

Where is a particularly easy target, in the kidney, for IgA and antigen?

A

There is no BM/filtering system between the blood and mesangium

565
Q

What might cause hereditary nephropathy?

A 
Thin GBM nephropathy
Benign familial nephropathy
Isolated haematuria
Thin GBM
Benign course
Alport syndrome
X-linked
Abnormal collagen 4
Associated with deafness
Abnormal appearing GBM
Progression to renal failure
566
Q

What is the glomerular basement membrane primarily comprised of?

A

Collagen 4

Hence any abnormalities in collagen 4 will cause issues

567
Q

What can you use to look for hereditary nephropathies?

A

Electron microscope

568
Q

Describe goodpasture syndrome (anti GBM)

A

Relatively uncommon, though clinically important. Rapidly progressive GN. Acute onset nephritic syndrome. Classically described associated to pulmonary haemorrhage (smokers). Autoantibody to collagen 4 in BM, but BM is ubiquitous. Treatable by immunosuppression and plasmaphoesis if caught early. Replace patients plasma with donor - rapidly get rid of antibody. Cannot be seen on electron microscopy (just antibody)

569
Q

What causes goodpasture syndrome?

A

Autoantibody (usually linked to collagen 4) suddenly starts to attack glomerulus

570
Q

What is vasculitis?

A

A group of systemic disorders. No immune complex/antibody deposition. Associated with anti neutrophil cytoplasmic antibody (ANCA) - activates neutrophils, attack cells e.g. Endothelial cells as line blood vessels, inflammation of blood vessels. Nephritic presentation (RPGN). Treatable if caught early. Urgent biopsy service. Endothelial target.

571
Q

What does ‘focal’ mean, with regards to kidney disease?

A

Involving <50% of the glomeruli on light microscopy

diffuse>50%

572
Q

What does ‘diffuse’ mean, with regards to kidney disease?

A

Involving >50% of the glomeruli on light microscopy

Focal <50%

573
Q

What does ‘segmental’ mean, with regards to kidney disease?

A

Involving part of the glomerular tuft

574
Q

What does ‘global’ mean, with regards to kidney disease?

A

Involving the entire glomerular tuft

575
Q

What does ‘membranous’ mean, with regards to kidney disease?

A

Thickening of the glomerular capillary wall

576
Q

What does ‘proliferative’ mean, with regards to kidney disease?

A

Increased number of cells in glomerulus, cells can be either proliferating glomerular cells or infiltrating circulating inflammatory cells

577
Q

What does ‘crescent’ mean, with regards to kidney disease?

A

Accumulation of cells (mostly mononuclear cells) within bowman space. Often compress capillary tuft, associated with more severe disease

578
Q

What does ‘glomerulosclerosis’ mean, with regards to kidney disease?

A

Segmental or global capillary collapse - presumed there is little filtration across sclerotic area

579
Q

What does ‘glomerulonephritis’ mean, with regards to kidney disease?

A

Any condition associated with inflammation in glomerular tuft

580
Q

List some risk factors associated with malignancy of the urinary tract

A

Increased age, family history, BRCA 2 gene mutation, ethnicity (black>white>Asian)

581
Q

What are the issues for PSA (prostate specific antigen) screening?

A

Over diagnosis, over treatment, quality of life (comorbidities of established treatments), cost effectiveness, other causes of raised PSA (infection, inflammation, large prostate)

582
Q

What is the clinical presentation of urinary malignancy?

A

Usually asymptomatic, or urinary symptoms (benign enlargement of prostate/bladder overactivity +- CaP), bone pains. Sometimes haematuria (if advanced CaP)

583
Q

What is the typical diagnostic pathway of a urinary malignancy?

A

Digital rectal examination, serum PSA (prostate specific antigen), TRUS (transracial ultrasound, guided biopsy of prostate), lower UTI symptoms, transurethral resection of prostate TURP

584
Q

What factors would influence treatment of a urinary malignancy?

A

Age, DRE (localised, T1/T2), locally advanced (T3), advanced (T4). PSA level. Biopsies (Gleason grade, extent). MRI scan and bone scan (nodal and visceral metastases)

585
Q

If a urinary malignancy is local, what treatment might you use?

A

Established Rxs. Surveillance. Robotic radical prostatectomy. Radiography. External beam, low dose brachytherapy.

586
Q

What treatment might you use for metastatic CaP? With regards to urinary malignancy

A

Hormones +- chemotherapy. Surgical/medical castration, LHRH agonists. Palliation single dose radiotherapy. Bisphosphonates (zoledronic acid). Chemotherapy (docetraxel). New treatments?

587
Q

Below what PSA (prostate specific antigen) level is bone metastases highly unlikely ?

A

<10ng/ml

588
Q

How would bone metastases appear on a bone scan?

A

Sclerotic (osteoblasts) ‘hotspots’ on bone scan

589
Q

How might you treat locally advanced CaP (with regards to urinary malignancy)?

A

Surveillance, hormones, hormones + radiotherapy

590
Q

What are the classifications for haematuria?

A

Visible

Non-visible (symptomatic and asymptomatic)

591
Q

What are the different types of cancer for urinary malignancies?

A

Renal cell carcinoma, upper tract transitional cell carcinoma TCC, bladder cancer, advanced prostate carcinoma

592
Q

What might cause symptoms similar to a urinary malignancy?

A

Stones, infection, inflammation, benign prostatic hyperplasia (large)

593
Q

What investigations might you do for a urinary malignancy?

A

Blood - FCB, U&Es
Urine - culture and sensitivity (cytology)
Radiology - ultrasound (tumour, stone, blockage)
Endoscopy - flexible cystoscopy

594
Q

How does bladder cancer Presentation differ from men to women?

A

Less common in woman, but usually more advanced on presentation

595
Q

What is the most common type of cancer in bladder cancer?

A

90% transitional cell carcinoma TCC

596
Q

List some risk factors for bladder cancer

A

Smoking, occupational exposure, schistosomiasis

597
Q

Exposure to what sort of occupational things might increase risk of bladder cancer?

A

Rubber/plastics manufacture, arylamines, carbon, crude oil, polyaromatic hydrocarbons, painter, mechanic, hairdresser ect….

598
Q

Is chemotherapy alway systemic?

A

No, e.g. TUR bladder tumour treatment

599
Q

What treatment might be used for bladder cancer?

A

Low risk non muscle invasive TCC (G1, G2, Ta) - check cystoscopies +- invasive chemotherapy
High risk non muscle invasive TCC (G3, Tis, T1) - check cystoscopies. Intravesical immunotherapy.
Muscle-invasive TCC. Neoadjuvant chemotherapy + radical cystectomy or radiotherapy

600
Q

What sort of carcinoma are most upper urinary tract tumours?

A

Renal cell carcinoma RCC (95%)

601
Q

What increases a persons risk of getting renal cell carcinoma?

A

Smoking, obesity, dialysis

602
Q

Where does renal cell carcinoma frequently spread to?

A

Lymph nodes, IVC to right atrium, perinephric spread

30% metastases on presentation

603
Q

What is the treatment for renal cell carcinoma?

A

Surveillance, radical nephrectomy, partial nephrectomy, developmental ablation.
Palliative - molecular therapies targeting angiogenesis (new 1st choice), poorly responsive to chemo/radiotherapies

604
Q

Are upper urinary tract malignancies common?

A

No, only ~5%

605
Q

What increases a persons likelihood of getting upper urinary tract malignancies?

A

Smoking, phenacetin abuse, balking nephropathy

606
Q

What is the standard treatment for upper urinary tract malignancy ?

A

Nephro-ureterectomy (kidney, far, ureter, cuff of bladder)

607
Q

What sort of cancer is in the upper urinary tract malignancies?

A

Upper tract transitional cell carcinoma

608
Q

What initial inveatigations would you do for upper urinary tract malignancies?

A

USS, hydronephrosis, UT urogram, filling defects ureteric structure, retrograde pyelogram, ureteroscopy, biopsy, washings for cytology

609
Q

What are the functions of the kidney?

A

Excretion - salt and electrolytes, water, acid, other metabolites, waste solutes
Glomerular permselectivity
Tubular functions - urine concentration/dilution, bicarbonate reclamation, NH4 secretion
Hormonal/vitamins - vitamin D, renin, erythropoietin

610
Q

What might the symptoms of a failure of kidney excretion be?

A 
Hyperkalaemia
Na+ overload paralleled by H2O overload (oedema, peripheral and pulmonary, hypertension)
Acidosis - acidotic breathing
Lethargy and fatigue
Uraemic syndrome
611
Q

How might an error in glomerular permselectivity present?

A

Proteinuria

Haematuria

612
Q

How might impaired tubular function present?

A

Impaired concentrating ability - frequency of urine, altered diurnal urine concentrating ability. Nocturia
Contributes to acidosis
May result in glycosuria with normal blood glucose

613
Q

How might impaired kidney hormonal function present?

A

Metabolic bone disease
Anaemia
Hypertension

614
Q

How is most kidney disease detected?

A

Opportunistically through screening at risk populations (hypertension, heart disease, diabetes, UT obstruction, systemic disease)

615
Q

Describe asymptomatic microscopic haematuria

A

Common, may be due to urinary infection, polycystic kidneys, renal stones, renal/bladder tumours ect….
Increased likelihood of micro haematuria associated with proteinuria and/or hypertension of glomerular disease
Patients over 45yrs require cystoscopy alas first investigation

616
Q

What colour is the urine in episodic macroscopic haematuria usually?

A

Brown/smokey rather than red

617
Q

What might cause red or brown urine?

A

Haemoglobinurea, myoglobinuria, consumption of food dyes, macroscopic haematuria

618
Q

What are the symptoms of (heavy) proteinuria?

A

Frothy urine, reduced plasma oncotic pressure (oedema), loss of immunoglobulins (infection), imbalanced regulators of the coagulation cascade (thromboembotic risk increased)

619
Q

What is the normal urine protein excretion level?

A

Less than 150mg/24hrs (10-30mg albumin)

620
Q

What is microalbinuria?

A

30-300mg albumininuria in 24hrs

Important prognostically in diabetes

621
Q

What is non-nephrotic proteinuria?

A

Defined as protein excretion of less than 3.5g/24hrs

622
Q

What sort of kidney disease is usually associated with proteinuria?

A

Glomerular

623
Q

What is the classical triad of findings in nephrotic syndrome?

A

Proteinuria (usually over 3.5g/24hrs)
Hypoalbuminaemia
Oedema
+ hyperlipidaemia

624
Q

Describe the clinical presentation of nephrotic syndrome

A

Muehrckes bands (fingernails)
Xanthelasma
Fat bodies in urine
Oedema

625
Q

What does classical nephrotic syndrome accompany in children?

A

Post-streptococcal glomerulonephritis

626
Q

Describe the manifestation of nephrotic syndrome

A 
Rapid onset
Oliguria
Hypertension
Generalised oedema
Haematuria with smoky brown urine
Normal serum albumin
Variable renal impairment
Urine contains blood proteins and red cell casts
627
Q

Compare the onset of symptoms in nephrotic and nephritic syndromes

A

Nephrotic - insidious

Nephritic - abrupt

628
Q

Compare the onset of oedema in nephrotic and nephritic syndromes

A

Nephrotic - ++++

Nephritic - +

629
Q

Compare the BP in nephrotic and nephritic syndromes

A

Nephrotic - normal

Nephritic - raised

630
Q

Compare the jugular venous BP in nephrotic and nephritic syndromes

A

Nephrotic - ++++

Nephritic - ++

631
Q

Compare presence of haematuria in nephrotic and nephritic syndromes

A

Nephrotic - +/-

Nephritic - +++

632
Q

Compare the presence of red cell casts in nephrotic and nephritic syndromes

A

Nephrotic - absent

Nephritic - present

633
Q

Compare the serum albumin in nephrotic and nephritic syndromes

A

Nephrotic - low

Nephritic - normal/slightly reduced

634
Q

What is rapidly progressive glomerulonephritis?

A

Describes a condition/clinical situation in which glomerular injury is so severe that renal function deteriorates over days. Patient may present as a uraemic emergency with evidence of extrarenal disease

635
Q

When do symptoms of chronic kidney disease appear generally?

A

Once eGFR is over 30ml/min
Even then symptoms are mild and non-specific
Most patients start dialysis with eGFR 8-10ml/min

636
Q

Describe some symptoms of advanced kidney disease

A 
Tiredness and lethargy
Breathlessness
Nausea and vomiting
Aches and pains
Sleep reversal
Nocturia
Restless legs
Itching
Chest pains
Seizures and coma
637
Q

What is the clinical presentation of acute kidney injury ?

A

Abrupt decline in actual GFR (days-weeks). Upset of ECF volume, electrolyte and acid/base homeostasis. Accumulation of nitrogenous waste products.

638
Q

What are the measurements that can be used to define acute kidney injury?

A

Increase in serum creatinine by >26.5umol/l within 48hrs
Increase in serum creatinine by >1.5 times baseline within 7 days
Urine volume <0.5ml/kg/h for 6hrs

639
Q

What is the serum creatinine criteria for stage 1 AKI?

A

Increase of SCr >26umol/l

Increase of SCr >150-200% (1.5-2fold) from baseline

640
Q

What is the serum creatinine criteria for stage 2 AKI?

A

Increase of SCr >200-300% (>2-3 fold) from baseline

641
Q

What is the serum creatinine criteria for stage 3 AKI?

A

SCr >354umol/l with an acute rise of >44umol/l in less than 24hrs
Increase in SCr >300% (3 fold) from baseline or initiated on RRT (irrespective of stage at time)

642
Q

What is the urine output criteria for stage 1 AKI?

A

<0.5ml/kg/hr for over 6hrs

643
Q

What is the urine output criteria for stage 2 AKI?

A

<0.5ml/kg/hr for over 12hrs

644
Q

What is the urine output criteria for stage 3 AKI?

A

<0.3ml/kg/hr for 24hr

Anuria for 12hr

645
Q

What are the 3 types of AKI?

A

Pre-renal failure
Intrinsic renal failure
Post-renal failure

646
Q

What is pre-renal AKI?

A

Actual GFR is reduced due to decreased renal blood flow.
No cell damage, so kidneys work hard to restore blood flow. Avidly reabsorption of salt and water (aldosterone and ADH release). Responds to fluid resuscitation

647
Q

How does kidney autoregulation help prevent prevent pre-renal AKI?

A

Intrarenal prostacyclin high to reduce afferent tone. Effect tone high due to circulating vasoconstrictors. Of overwhelmed, AKI occurs.

648
Q

What effect can NSAIDs have on kidney autoregulation?

A

Inhibit prostaglandins, so inhibit vasodilation of afferent artreriole

649
Q

What effect can ACE inhibitors have on the kidney autoregulation?

A

Inhibit angiotensin 2 production, so inhibit vasoconstriction of efferent arteriole.

650
Q

What are the 2 causes of pre-renal AKI?

A

Reduced effective extracellular fluid volume

Impaired renal autoregulation

651
Q

What might develop if the causes of poor renal perfusion is not recognised and treated promptly?

A

Acute tubular necrosis

652
Q

Why is ‘acute tubular necrosis’ a misnomer?

A

Generally not necrosis, but cells damaged therefore cannot be immediately reversed. The damaged cells cannot reabsorbed salt and water efficiently, or expel excess water

653
Q

What might cause acute tubular necrosis?

A

Ischaemia (depletion of cellular ATP)
Nephrotoxins
Sepsis

654
Q

Describe the sequence of blood vessels in renal bloodflow

A

Interlobar arteries - afferent arterioles - glomerular capillaries - efferent arterioles - peritubular capillaries - interlobar veins

655
Q

List some endogenous nephrotoxins

A

Myoglobin, urate, biliruben

656
Q

List some exogenous nephrotoxins

A

X-ray contrast
Assume every drug given to patient with ATN is nephrotoxic is until proven otherwise
Drugs e.g. ACE-I, aminoglycosides, NSAIDs, ect.

657
Q

What is rhabdomyolosis?

A 
Due to muscle necrosis - release of myoglobin ('crash injury e.g. Drug users/elderly who can't move, earthquakes/disasters ect). Myoglobin is filtered at the glomerulus and toxic to tubule cells, can cause obstruction. Very dark urine.
Give forced (alkaline) diuresis
658
Q

What is acute glomerulonephritis?

A

Immune disease affecting the glomeruli. Can be primary or secondary.

659
Q

Describe primary acute glomerulonephritis

A

Disease only affects kidneys e.g. IgA nephropathy

660
Q

Describe secondary acute glomerulonephritis

A

The kidneys are involved as part of a systemic process e.g. vasculitis

661
Q

What is acute pyelonephritis?

A

Toxin induced - many drugs but commonest are antibiotics, NSAIDs, PPIs or bacterial infection that travels up the urinary tract.

662
Q

Describe post-renal failure

A

5-10% AKI. More common in elderly. To cause AKI, obstruction must block both kidneys, or a single functioning kidney.
Obstruction with continuous urine production causes a rise in intraluminal pressure - dilation of renal pelvis (hydronephrosis) - decrease in renal function

663
Q

How might the causes of post-renal kidney failure be grouped?

A

Within the lumen (kidney, ureter, bladder) e.g. Stones, blood, tumour
Within the wall (usually causes CKD, nor AKI) e.g. Congenital megaureter, stricture post TB
Pressure from outside e.g. Enlarged prostate, tumour, aortic aneurism

664
Q

To cause AKI, what just stones be in?

A

Both renal pelvis or ureters
Obstruction of a single kidney
Neck of bladder
Urethra

665
Q

Above what size will ureteric stones usually not be able to pass?

A

10mm

666
Q

When might you use a USS for the urinary system?

A

Perform within 24hrs of presentation if obstruction is suspected as cause or AKI, or if cause is unclear
Do not need USS if cause is pre-renal/ATN unless not improving

667
Q

When might you use a CXR for the renal system?

A

To look for fluid overload +- infection

668
Q

When might you obtain a kidney biopsy?

A

Pre-renal and post-renal AKI ruled out
A confident diagnosis of ATN cannot be made
Systemic inflammatory symptoms/signs are present

669
Q

How is AKI prevented?

A 
Identify risk factors
Monitor 'at risk' patients
Ensure adequately hydrated
Avoid nephrotoxins
Detect early and identify cause
670
Q

List some indications for dialysis

A

High K+ refractory to treatment
Metabolic acidosis where NaHCO3 not appropriate
Fluid overload refractory to diuretics
Presence of a dialysable nephrotoxin e.g. Aspirin OD

671
Q

What are the signs of uraemia?

A

Pericarditis, reduced consciousness, intractable N&V

672
Q

What is the prognosis of uncomplicated ATN?

A

Generally recovered within 2-3 wks if no superimposed insults. But hypertension on dialysis can cause additional ischaemic lesions and prolong recovery.
Mortality 30-80% (dependent on stage)

673
Q

Define chronic kidney disease

A

The irreversible and sometimes progressive loss of renal function over a period of months to years.
Renal injury causes renal tissue to be replaced by extracellular matrix in response to tissue damage

674
Q

Describe the parameters of GFR category G1

A

GFR >90

Termed normal or high

675
Q

Describe the parameters of GFR category G2

A

GFR 60-89

Termed mildly decreased

676
Q

Describe the parameters of GFR category G3a

A

GFR 45-59

Termed mildly to moderately decreased

677
Q

Describe the parameters of GFR category G3b

A

GFR 30-44

Termed moderately to severely decreased

678
Q

Describe the parameters of GFR category G4

A

GFR 15-29

Termed severely decreased

679
Q

Describe the parameters of GFR category G5

A

GFR <15

Termed kidney failure

680
Q

Define the parameters of ACR category A1

A

ACR <3mg/mmol

Termed normal to mildly increased

681
Q

Define the parameters of ACR category A2

A

ACR 3-30mg/mmol

Termed moderately increased

682
Q

Define the parameters of ACR category A3

A

ACR >30mg/mmol

Termed severely increased

683
Q

At what point does does mortality start to increase with regards to normal renal function?

A

25% less than normal renal function

684
Q

What is the normal range for GFR?

A

80-120ml/min

685
Q

What is the normal range for serum creatinine?

A

80-120umol/l

686
Q

What percentage of renal function can be lost, and still have creatinine levels within normal range?

A

Up to 60%

687
Q

What determines creatinine conc.?

A

Renal function and muscle mass (age, sex, race)

688
Q

If kidneys are normal in size and cause of CKD is not obvious, what should be considered?

A

A renal biopsy

689
Q

What complications might acidosis have on CKD?

A

May affect muscle, bone, renal function progression (makes kidneys worse).
Not generally a problem until eGFR is <20, so only in serious kidney disease

690
Q

How might you treat acidosis in CKD?

A

Oral NaHCO3 tablets

691
Q

What are some complications of anaemia in CKD?

A

Decreased erythropoietin production, resistance to erythropoietin, decreased RBC survival. Blood loss.

692
Q

Describe the effect of CKD on phosphate levels, and the consequences of this.

A

Decreased GFR causes an increase in blood phosphate levels (as phosphate is usually excreted at the kidney). This increase in phosphate leads to a decrease in serum calcium, thus causing an increase in PTH

693
Q

What usually happens to phosphate at the kidney?

A

Excretion

694
Q

What effect does an increase in phosphate in the blood have on serum calcium?

A

Decrease in serum calcium (stimulating PTH production)

695
Q

What effect does decreased GFR have on active Vit D, and the consequences of this?

A

Decrease in levels of active Vit D, which can lead to osteomalacia

696
Q

What are some signs of osteodystrophy found in an X-ray?

A

‘Rugger jersey’ spine (dark stripe in X-ray of vertebrae due to loss of Ca2+)
Erosion of terminal phalanges and bone cysts
Non bone calcification

697
Q

How might you prevent or delay progression of mineral and bone disorders in CKD?

A 
Lifestyle (smoking, obesity, lack of exercise)
Treat diabetes (if present)
Treat blood pressure
ACE inhibitors/ARBs in proteinuria
Lipid lowering
698
Q

When is renal replacement therapy required?

A

When native renal function declines to a level no longer adequate to support health. Usually when eGFR 8-10ml/min (normal ~100ml/min)

699
Q

Give some indications for initiating dialysis

A 
Uraemic symptoms
Acidosis
Pericarditis
Fluid overload 
Hyperkalaemia
700
Q

What are the forms of renal replacement therapy?

A

Dialysis - haemodialysis, peritoneal dialysis

Renal transplant

701
Q

When would you start renal replacement therapy?

A

When death is likely without it

eGFR <15mls/min

702
Q

What are the symptoms of end stage renal disease

A

Tiredness - overwhelming fatigue. Physically and mentally incapacitated. Feelings of guilt and ineptitude at needing rest.
Difficulty sleeping
Difficulty concentrating
Symptoms and signs of volume overload (SoB, oedema)
Nausea and vomiting/reduced appetite (eat less meat)
Restless legs/cramps
Pruritus (itchy skin)
Sexual dysfunction/reduced fertility
Increased infections (reduced cellular and humoral immunity)

703
Q

What does the amount of water produced depend upon?

A

GFR

ADH

704
Q

What effect does reduced GFR have upon urine production?

A

Loss of the ability to maximally dilute and concentrate urine. Small glomerular filtrate but same solute load causes osmotic diuresis. Noctururia. Low volume of filtrate reduces maximum ability to excrete urine therefore maximum urine volume much smaller.

705
Q

What bone diseases might occur as a result of kidney disease?

A

Hyperphosphataemia
Low 1-alpha-calcidiol
Generally asymptomatic in pre-dialysis patients (some have muscle and bone pains)

706
Q

Why is there an increased tendency to bleed in anaemia?

A

Reduced platelet function

707
Q

What effect does accumulation of waste products have in CKD?

A

Contributes to uraemia symptoms - reduced appetite, nausea and vomiting, pruritus

708
Q

What might happen to dosing in a patient with ESRD/CKD?

A

Dose alteration required due to reduced metabolism/elimination. Drug sensitivity can be increased even if elimination is unimpaired, meaning side effects more likely e.g. Statins

709
Q

Describe the passage of bloodflow in haemodialysis

A

Arterial blood - pressure monitor - pump - +anticoagulant - pressure monitor - dialyzer - airtrap & detector/pressure monitor - vein

710
Q

What is the principles behind what goes on in a dialyzer?

A

Blood and dialysate move in opposite directions (countercurrent) to maximise clearance of solute through dialysis membrane

711
Q

How often does a person on haemodialysis require dialysis?

A

3 times a week, 4hrs on the machine, in a designated slot.

712
Q

What are some good points of haemodialysis?

A

Less responsibility than other renal replacement therapies

You get days off treatment

713
Q

What are some not so good points of haemodialysis?

A

Travel time/ waiting
You’re tied to your allocated dialysis times
Big restrictions of food and fluid intake
Requires a fistula, which can be unsightly
~19 pills a day!

714
Q

What are some contra-indications for haemodialysis?

A

Failed vascular access
Coagulopathy
Heart failure (can’t deal with loss of blood into machine)

715
Q

What are some possible complications of haemodialysis?

A

Lines - infections, thrombosis, venous stenosis
AVF - thrombosis, bleeding, access failure, steal syndrome
CVS instability
Feel chronically unwell
Accumulate morbidity (CVS, bone ect.)

716
Q

Describe the principles of peritoneal dialysis

A

Peritoneum is filled with dialysate fluid. Waste products cross the semipermeable membranes (from capillaries) into the perineal space. The fluid here is then replaced. Approx 4-5 bags throughout the day, but overnight dialysis is also an option.

717
Q

Give some positives of peritoneal dialysis

A

Self-sufficient/independence
Generally less fluid/food restrictions
Fairly easy to travel
Renal function may be better preserved initially

718
Q

Give some negatives of peritoneal dialysis

A

Frequent daily exchanges or overnight

You are responsible for your own care

719
Q

Give some contraindications of peritoneal dialysis

A

Failure of peritoneal membrane
Adhesions, previous abdo surgery, hernia, stoma
Patient (or carer) unable to connect/disconnect
Obese or large muscle mass
~10 pills a day (significantly less than haemodialysis)

720
Q

Give some possible complications of peritoneal dialysis

A 
Peritonitis, exit or tunnel site infections
Ultrafiltration failure 
Leaks (scrotal, diaphragmatic)
Development of hernia
~10 pills a day
721
Q

Talk about home dialysis

A 
Allows more dialysis hours
Better large molecule clearance
Patients often feel better
Patients often need fewer medications
Home HD requires someone at home with you
722
Q

What are the benefits of transplant?

A

Reduced mortality and morbidity compared to dialysis

Better quality of life

723
Q

What are some drawbacks of transplant?

A

Peri-operative risk (mortality risk greatest for first 3 months)
Malignancy risk
Infection risk
Risk of diabetes/hypertension from meds

724
Q

What are the different types of kidney transplant available?

A

Live donor (related or not)
Deceased after brain death (DBD)
Deceased after circulatory death (DCD) or non-heart beating

725
Q

Is dialysis better for everyone?

A

No - patients who choose conservative care can survive a substantial length of time achieving similar numbers of hospital-free days to patients who choose haemodialysis.
Dialysis prolongs survival for elderly patients with ESRD and significant comorbidity by ~2yrs
Heart disease is especially associated with poor outcomes on dialysis

726
Q

List some S ymptoms with ESRD with end of life care

A 
Pain - related to ESRD (bone pain, dialysis-related pain). Not related (neuropathy, musculoskeletal)
Constipation
Fatigue
Nausea/lack of appetite
Pruritus
Cramps/restless legs
Sleep disturbance

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