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2nd year medicine > Renal > Flashcards

Renal Flashcards

1
Q

How is glomerular filtration rate measured?

A

creatinine

* if elevated = kidney disease

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2
Q

Significance of proteinuria?

A

> 150 mg/day = significant glomerular damage

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3
Q

Normal kidney?
Microalbuminuria?
Clinical proteinuria?
Nephrotic?

A

Normal

  • dipstick = negative
  • PCR <15
  • total protein <0.150g
  • ACR <2.5 (M), <3.5 (F)

Microalbuminuria
* ACR = 2.5 - 30 (M), 3.5 - 30 (F)

Clinical proteinuria

  • 1+ or 2+ on dipstick
  • PCR = 45 - 449
  • Total protein = 0.45 - 1.49
  • ACR = >30

Nephrotic

  • 3+ on dipstick
  • PCR > 450
  • total protein > 4.5 g
  • ACR >30
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4
Q

Microalmbuminaemia?

Significance?

A

excretion of almbumin in abnormal quantities but still below limit of protein detection by dipstick
* earliest expression of diabetic nephropathy!!

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5
Q

Tubular function in oliguric patient?

A

Pre-renal failure i.e. tubules working

  • urine Na = <20
  • Urea = >10 (urine): 1 (serum)
  • osmolality = >1.5 (urine): 1 (serum)

Renal damage (tubules not working)

  • Na = >40
  • Urea = 3 (urine): 1 (serum)
  • osmolality = <1 (urine): 1 (serum)
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6
Q

what hormones does kidney release? (3)

A
  • Renin
  • 1, 25 dihydroxycholecalciferol (gut)
  • erythroprotein (bone marrow)
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7
Q

Function of kidney? (3)

A
  • maintain water and electrolyte balance
  • excrete toxic metabolic waste (urea + creatinine)
  • produces renin and erythroprotein
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8
Q

lobe of kidney?

A

each medullary pyramid

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9
Q

basic functional unit of kidney?

A

nephron

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10
Q

what is kidney nephron made up of?

A

renal corpuscle and renal tubules

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11
Q

function of renal corpuscle?

A

production and collection of glomerular filtrate

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12
Q

Order of nephron structures?

A
  • renal corpuscle: production and collection of glomerular filtrate
  • proximal convoluted tubule: reabsorption of water, proteins, amino acids, carbohydrates + glucose
  • loop of henle: creates hyperosmotic environment in medulla
  • distal convoluted tubule: acid-base and water balance
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13
Q

Bowman’s capsule?

A

simple squamous epithelium at blind end of nephron that capillaries invaginate into

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14
Q

podocytes?

A

specialised epithelium which seperates blood from glomerular filtrate (sit on top of glomerular capillaries)

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15
Q

mesangial cells?

A

produce connective tissue core called mesangium

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16
Q

Blood supply and drainage to renal corpuscle?

How do they enter/leave?

A 
supply = afferent arteriole
drain = efferent arteriole

(enter and leave thru bowman’s capsule)

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17
Q

Poles of renal corpuscle?

A
  • Vascular pole (bowman’s capsule)

* Urinary pole (opposite end - proximal convoluted tubule)

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18
Q

components of glomerular filter?

A

1) fenestrated endothelium of capillary wall
2) thick basement membrane (endothelium + podocyte)
3) filtration slits between pedicels

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19
Q

Function proximal convoluted tubule?

A

reabsorption of water, proteins, amino acids, carbs + glucose

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20
Q

significance of proximal tubule?

A
  • 70% of sodium + water reabsorbed
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21
Q

Function of loop of Henle?

A

creation of hyperosmotic environment in medulla

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22
Q

Blood supply to medulla?

A

Vasa recta

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23
Q

structure of loop of Henle?

A

1) thick descedning limb
2) thin descending limb which makes ahairpin turn and becomes thin ascending limb
3) transitions to thick ascending limb

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24
Q

What are thick limbs of loop of Henle lined with?

Thin limbs?

A 
Thick = simple cuboidal epithelium
Thin = simple squamous
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25
Q

Vasa recta?

A

loops of thin walled blood vessels that dip down into the medulla and then climb back up to the cortex

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26
Q

function of distal convoluted tubule?

A

acid-base and water balance

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27
Q

What is reabsorption of Na+ in distal convoluted tubule controlled by?

A

Aldosterone (results in greater Na+ and water reabsorption therefore increases blood pressure)

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28
Q

Function of collecting tubules and collecting ducts?

A

Reabsorption of water under the control of ADH

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29
Q

what are medullary rays?

A

proximal + distal tubules + collecting ducts running in parallel bundles

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30
Q

What hormone is active in collecting ducts?

A

ADH (vassopresin)

* results in concentrated urine as water is reabsorbed

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31
Q

what are conducting areas of the urinary tract lined with?

What is special about the luminal (i.e. facing the lumen) cells?

A

transitional epithelium/urothelium (renal papilla, minor calyx, major calyx, bladder, urethra)
* luminal cells are called umbrella cells because they are domed = highly impermeable barrier

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32
Q

what exists below urothelium?

A

lamina propria + 2-3 layers of smooth muscle

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33
Q

Explain structure of urethra?

A

Females

  • 3-5 cm
  • lined by transitional epithelium then transitions to stratified squamous

Males

  • 20 cm
  • prostatic urethra
  • membranous urethra (from prostate to bulb of penis) - it is at this point transitional epithelium changes to stratified columnar
  • penile urethra = stratified columnar becomes stratified squamous
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34
Q

What is osmolarity?

A

Concentration of osmotically active particles present in a solution

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35
Q

Units for osmolarity?

A

osmol/l or mosmol/l

mosmol/l for body fluids

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36
Q

How is osmolarity calculated?

A

1) molar concentration of solution
2) number of osmotically active particles present

e. g. 150 mM NaCl
* molar concentration = 150
* no. of osmotically active particles = 2 (Na+ and Cl-)
* osmolarity = 2(150) = 300 mosmol/l

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37
Q

Osmolarity of body fluids?

A

~300 mosmol/l

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38
Q

Tonicity?

A

Effect a solution has on cell volume

e.g. hypo, hyper, iso

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39
Q

Isotonic?

A

doesn’t mean water isn’t moving across membrane – just means no net movement of water

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40
Q

Hypotonic?

Hypertonic?

A 
Hypo = increase in cell volume (more water, less salt)
Hyper = decrease in cell volume
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41
Q

Osmolarity of cell <300?

>300?

A 
<300 = hypotonic
>300 = hypertonic
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42
Q

Difference between 300 mM urea and 300 mM sucrose on red blood cells?

A
  • Sucrose = isotonic (RBC impermeable)

* Urea = hypotonic

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43
Q

TBW males and females?

A
  • Male = ~60% of body weight

* Female = ~50%

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44
Q

Total body water compartments?

What is ECF composed of?

A
  • ICF = 67%
  • ECF = 33%

ECF

  • plasma (20%)
  • interstitial fluid (80%)
  • Lymph + transcellular fluid (negligible)
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45
Q

How are body fluid compartments measured?

Examples?

A

using “tracers”

  • TBW = 3H20
  • ECF = inulin
  • plasma = labelled albumin

TWB = ECF + ICF (so can calculate ICF if we know TBW and ECF)

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46
Q

Greatest loss of water from body?

Input and output?

A

Urine

Homeostasis
Input = output
i.e. 2500 = 2500

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47
Q

How is water balance increased?

A

Water balance is maintained by increased water ingestion. Decreased excretion of water by the kidneys alone is insufficient to maintain water balance

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48
Q

Ionic composition of ICF and ECF?

A

ICF = more K+, less Na, less Cl, less HCO3

ECF = less K+, more Na, more Cl, more HCO3 (think sea water!)

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49
Q

Main ions in ICF?

A

K+ and Mg2+

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50
Q

Osmotic concentrations of ICF and ECF?

A

Identical ~300 mosmol/l

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51
Q

Fluid shift?

A

Movement of water between the ICF and ECF in response to an osmotic gradient

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52
Q

What would happen to ECF and ICF volumes for the following situations:

1) if osmotic concentration of ECF increases
2) if osmotic concentration of ECF decreases

A

Increases

  • Would become hypertonic compared to ICF
  • Cell volume decreases

Decreases

  • ECF were to gain additional water but not salt
  • Would become hypotonic compared to ICF
  • Cell volume increases
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53
Q

ECF NaCL gain?

ECF NaCl loss?

A
  • Gain = increase ECF volume, decrease ICF volume

* Loss = decrease ECF, increase ICF

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54
Q

Effect of gain or loss of isotonic fluid on fluid osmolarity?
Example?

A

No change in fluid osmolarity
(change in ECF volume only!)
* e.g. 0.9% NaCL solution

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55
Q

What alters composition + volume of ECF?

A

Kidney

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56
Q

Why is it vital to regulate Na?

A

Major determinant of ECF volume

for ICF it is potassium

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57
Q

What can increase/decrease of K+ lead to? (2)

A

1) muscle weakness (paralysis)
2) cardiac arrest

(because it plays a major role in establishing membrane potential)

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58
Q

What is the key role of K+?

A

Establishing membrane potential

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59
Q

Function of kidney nephrons?

A
  • filtration
  • reabsorption
  • secretion
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60
Q

Blood supply to nephron?

A
  • Afferent arteriole drains into glomerular capillary (called glomerulus)
  • Then drains into efferent arteriole
  • Efferent arteriole drains into peritubular capillaries which eventually drain into renal vein
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61
Q

What is the fluid that flows through nephron?

End product?

A

Tubular fluid

* end product is urine

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62
Q

difference between juxtamedullary and cortical nephrons? (3)

A
  • Juxta = has much longer loop of henle
  • Cortical = have peritubular capillaries (juxtamedullary have vasa recta, single capillary), follows loop of henle
  • Juxta = able to produce much more concentrated urine
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63
Q

What are most nephrons?

A 
80% = cortical
20% = juxtamedullary
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64
Q

Function of macula densa?

A

salt sensitive cells, monitor level of salt in tubular fluid

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65
Q

Function of granular cells?

A

Production + secretion of renin

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66
Q

What percentage of plasma that enters glomerulus is filtered?

A

20%

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67
Q

Relationship between filtration, secretion, reabsorption and excretion?

A
  • Filtration + secretion = reabsorption + excretion

* Rate of excretion = rate of filtration + rate of secretion - rate of reabsorption

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68
Q

Rate of filtration =?

A

Rate of filtration = [X] in plasma x GFR

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69
Q

What is normally the value of GFR?

A

~125 ml/min
(plug in to equations)

so would be 0.125 l/min

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70
Q

Rate of excretion =?

A

Rate of excretion = [X] in urine x Vu

Vu = rate of urine production

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71
Q

Rate of reabsorption =?

A

rate of reabsorption = rate of filtration - rate of excretion

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72
Q

What if rate of filtration > rate of excretion?

A

Net reabsorption of that substance has occured

* rate of reabsorption = rate of filtration - rate of excretion

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73
Q

Rate of secretion =?

A

Rate of secretion of = rate of excretion – rate of filtration

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74
Q

What if rate of filtration < rate of excretion?

A

Net secretion of the substance has occured

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75
Q

Filtration barriers in glomerular filtration?

A

(1) Glomerular Capillary Endothelium (barrier to RBC)
(2) Basement Membrane (basal lamina) = plasma protein barrier)
(3) Slit processes of podocytes (plasma protein barrier)

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76
Q

Podocytes?

A

Make up inner membrane of bowman’s capsule

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77
Q

Which arteriole has larger diameter?

A

Afferent arteriole larger than efferent

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78
Q

what must fluid filtered from glomerulus into bowman’s capsule pass through?

A

three layers that make up glomerular membrane

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79
Q

why does basement membrane have a net negative charge?

fluid passes from capillary through endothelial cell -> basement membrane -> podocyte -> bowman’s capsule

A

Net negative charge – plasma proteins should be contained within the capillary (none should enter lumen of bowman’s capsule)

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80
Q

Forces that increase net filtration pressure? forces that compromise net filtration pressure?

so what is total net filtration pressure?

A

Increase

  • glomerular capillary blood pressure
  • bowman’s capsule oncotic pressure

Decrease

  • bowman’s capsule hydrostatic pressure
  • Capillary oncotic pressure

Net filtration pressure = 10 mm Hg

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81
Q

Starling forces?

A

balance of hydrostatic pressure and osmotic forces

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82
Q

does glomerular filtration require energy?

Biggest driver of process

A

No, passive

* glomerular capillary blood pressure

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83
Q

glomerular filtration rate (GFR)?

Biggest determinant of GFR?

A

rate at which protein-free plasma is filtered from the glomeruli into the Bowman’s capsule
* glomerular capillary blood pressure

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84
Q

Equation GFR?

A

GFR = Kf x net filtration pressure

kf = filtration coefficient

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85
Q

Normal GFR?

A

125 ml/min

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86
Q

Regulation of GFR and renal blood flow?

A

Extrinsic
* baroreceptor reflex

Intrinsic

  • myogenic
  • tubuloglomerular feedback mechanism
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87
Q

Effect of increased arterial blood pressure on GFR?

A

GFR increases

if BP falls, then decrease

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88
Q

Vasoconstriction of afferent arteriole?

Vasodilation?

A 
Vasoconstriction = decreases blood flow to glomerulus (decrease GFR)
Vasodilation = increases (thus increase in GFR)
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89
Q

Baroreceptor reflex GFR?

A
  • fall in blood volume e.g. haemorrhage
  • decrease BP
  • baroreceptors increase sympathetic activity
  • cause vasoconstriction (incl. afferent arterioles)
  • decreased BPgc
  • decreased GFR
  • decreased urine production
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90
Q

Do slight changes in arterial BP cause changes in GFR?

A

No, renal blood blow and GFR protected over a wide range of MABP

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91
Q

Autoregulation (intrinsic) of GFR? (2)

A

Myogenic
* vascular smooth muscle constricts in response to stretching (i.e. increased BP)

Tubuloglomerular feedback
* if GFR rises, more NaCl flows into tubule causing constriction of afferent arteriole

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92
Q

what can cause increase in bowman’s capsule pressure?

What does this result in?

A

kidney stone

* decreased GFR

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93
Q

what can cause increase in capillary oncotic pressure?

What does this result in?

A

Diarrhoea

* decreased GFR

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94
Q

What causes decreased capillary oncotic pressure?

Resulting in?

A

Severe burns

* increased GFR

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95
Q

Plasma clearance?

A

A measure of how effectively the kidneys can ‘clean’ the blood of a substance (each substance will have a different plasma clearance value)

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96
Q

Plasma clearance equation?

Units?

A

clearance of X = rate of excretion of X/plasma concentration of X

otherwise written as
clearance = [X]urine x V(urine)/[X] plasma

Units = ml/min

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97
Q

Example of substance that clearance = GFR?

Why is this?

A

Inulin (creatinine can also be used)

* inulin is filtered but is NOT secreted or reabsorbed!

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98
Q

Example of substance for which clearance = 0?

Why?

A

Glucose

* it is filtered, COMPLETELY reabsorbed, and NOT secreted

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99
Q

Example of substance for which clearance < GFR?

Why?

A

Urea
* filtered, PARTLY reabsorbed, and NOT secreted

(

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100
Q

Example of substance for which clearance> GFR?

Why?

A

H+

* filtered, secreted but NOT reabsorbed

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101
Q

If clearance < GFR?
If clearance = GFR?
If clearance > GFR?

A
  • clearance < GFR = reabsorbed
  • clearance = GFR = substance is neither reabsorbed nor secreted
  • clearance > GFR = secreted
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102
Q

What is para-amino hippuric acid (PAH)?

Why?

A

Used to measure renal plasma flow

* it is fully secreted (not reabsorbed)

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103
Q

Normal value of renal plasma flow?

A

650 ml/min

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104
Q

Requirements of a GFR marker?

A RPF marker?

A
  • GFR marker = should be filtered but NOT secreted nor reabsorbed!!
  • RPF marker = should be filtered AND completely secreted!
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105
Q

Filtration fraction?
Value?
Remaining %?

A

fraction of plasma flowing that is filtered into the tubules

  • value = 20% filtered
  • remaining 80% enters efferent arteriole then peritubular capillaries
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106
Q

Renal blood flow value?

What % of CO do kidneys receive?

A

~1200 ml.min

* kidneys receive ~24% of CO

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107
Q

GFR?

A

125 ml/min

* 180 litres/day

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108
Q

How much fluid is reabsorbed in the proximal tubule?

So how much, therefore, flows into loop of Henle?

A

80 ml/min of filtered fluid

  • so 125 ml/min (GFR) - 80 ml/min = 45 ml/min
  • 45 ml/min flows into loop of Henle
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109
Q

Substances reabsorbed in proximal tubule? (5)

Secreted in proximal tubule? (7)

A

Reabsorbed
* sugars, amino acids, phosphate, sulphate, lactate

Secreted
* H+, hippurates, neurotransmitters, bile pigments, uric acid, drugs, toxins

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110
Q

Types of reabsorption? (2)

A
  • Transcellular (tubular)

* paracellular

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111
Q

How is glucose transported into cells? (2)

A

Either by

  • Facilitated diffusion
  • secondary active transport with Na+
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112
Q

What is essential for Na+ reabsorption?

A

NaKATPase carrier

active transport

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113
Q

How is Na reabsorbed in proximal tubule?

A

Due to:

  • osmotic gradient
  • oncotic pressure gradient
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114
Q

Glucose reabsorption in proximal tubule?

A

100% of glucose reabsorbed in proximal tubule

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115
Q

What do substances have to pass thru in reabsorption?

A

Tubular epithelial cell, interstitial fluid and peritubular capillary endothelium

116
Q

Transport maximum for glucose?

A

2 mmol/min

117
Q

What percentage of salt and water is reabsorbed in PT?

A

~67%

118
Q

What is Na reabsorption in proximal tubule driven by?

A

basolateral Na+-K+-ATPase

119
Q

What does Na reabsorption in proximal tubule drive?

A

Reabsorption of Cl through paracellular pathway

120
Q

What is tubular fluid described as once it leaves proximal tubule?

A

Iso-osmotic (i.e. 300 mosmol/l)

121
Q

Function of loop of Henle?

A

genereates cortico-medullary concentration gradient

* enables formation of hypertonic urine

122
Q

what is the opposing flow in the descending limb and ascending limb of loop of Henle called?

A

Countercurrent flow

123
Q

What term is used to describe function of loop of henle?

A

Countercurrent multiplier

124
Q

Compare ascending limb of loop of Henle to descending limb?

What is this important for?

A

THICK part of Ascending limb

  • Na and Cl are reabsorbed
  • impermeable to water

Descending limb

  • does not reabsorb NaCl
  • highly permeable to water

Selective permeabilities of the ascending and descending limbs of the Loop of Henle enable an osmotic gradient to be established in the medulla

125
Q

Where do loop diuretics act?

A

Loop diuretics block the NaKCL (triple) co-transporter in the thick ascending limb

126
Q

Explain processes in the loop of Henle

A
  1. Water leaves the descending limb by osmosis
  2. Fluid in the descending limb is concentrated
  3. Solute removed from lumen of ascending limb (water cannot follow)
  4. Tubular fluid is diluted and osmolality of interstitial fluid is raised
127
Q

How does the osmolaity differ at the start and the end of the loop of Henle?

A
  • Iso osmotic fluid leaves the proximal tubule

* Hypo osmotic fluid enters the distal tubule

128
Q

What is the purpose of countercurrent multiplication?

A

To concentrate the medullary interstitial fluid

* allows kidney to produce urine of different volume and concentration depending on ADH

129
Q

Normal Vu?

A

~1 ml/min

can be 0.3 - 25 ml/min

130
Q

What does vasa recta act as?

A

A countercurrent exchanger

131
Q

How does vasa recta prevent the loss of NaCl and urea?

A
  • Vasa recta capillaries follow hairpin loops
  • Vasa recta capillaries freely permeable to NaCl and water
  • Blood flow to vasa recta is low (few juxtamedullary nephrons)
132
Q

Chronic kidney disease classification?

End stage renal disease?

A

Chronic = CDK3 - 4

End stage = CDK5

133
Q

Renal replacement therapies? (3)

A
  • Haemodialysis (GFR = 7)
  • Peritoneal dialysis (GFR = 7)
  • transplant (GFR = 50)
134
Q

Contraindications to renal transplant? (8)

A
  • malignancy
  • active HCV/HIV infection
  • untreated TB
  • severe IHD
  • severe airway disease
  • Active vasculitis
  • Severe PVD
  • hostile bladder
135
Q

Which tissue types should e matched to avoid an immune reaction?

A

HLA type:

  • A
  • B
  • DR
136
Q

Sensitising events that can lead to pre-formed antibodies prior to transplant?

A
  • blood transfusion
  • pregnancy or miscarriage
  • previous transplant
137
Q

Explain process of kidney transplant?

A
  • Native kidneys stay in place
  • Transplant inserted in iliac fossa
  • Kidney grafted into iliac vein and artery
  • Ureter and bladder also grafted onto transplant
138
Q

What kind of procedure is kidney transplant?

A

Extra-peritoneal procedure

139
Q

Surgical complications of renal transplant?

A
  • Bleeding
  • Arterial stenosis
  • Venous stenosis / kinking
  • Ureteric stricture & hydronephrosis
  • Wound infection
  • Lymphocele
140
Q

Transplant function? (3)

A

Immediate graft function

  • good urine output
  • falling urea and creatinine

Delayed graft function

  • need haemodialysis
  • usually works within 10-30 days

Primary non-function
* transplant never works

141
Q

Types of transplant rejection? (3)

A

Hyperacute rejection

  • Due to preformed antibodies
  • Unsalvageable
  • Transplant nephrectomy required

Acute Rejection

  • Cellular or Antibody mediated
  • Can be treated with increased immunosupression

Chronic Rejection

  • Antibody mediated slowly progressive decline in renal function
  • Poorly responsive to treatment
142
Q

Immunosuppressive therapy for renal transplant?

A

Induction treatment
* basiliximab/dacluzimab

Prednisolone IV during operation

Maintenance tx

  • prednisolone, tacrolimus, MMF
  • prednisolone, ciclosporin, azathioprine
143
Q

Anti-rejection therapies? (5)

A
  • pulsed IV methylprednisolone
  • anti-thymocyte globulin
  • IV immunoglobulin
  • Plasma exchange
  • rituximab, eculizimab
144
Q

What should prophylaxis be given for following immunosuppression?

A

Pneumocystis jiroveci pneumonia (PJP)

145
Q

What is a common cause of morbidity in immunosuppressed patients in first 3 months of transplant?
Complications?
Tx?

A

Cytomegalovirus

  • renal and hepatic disease
  • oesophagitis, colitis
  • increased risk of rejection

Prophylaxis
* PO valganciclovir

Treatment
* IV ganciclovir

146
Q

What is the cause of BK virus nephropathy?

Tx?

A

Over-immunosuppression

Tx

  • there is no effective antiviral
  • tx is to reduce immunotherapy
147
Q

POST TRANSPLANT LYMPHOPROLIFERTIVE DISEASE (PTLD)?

A
  • Occurs in all forms of transplantation
  • Usually related to EBV infection

(leads to lymphoma)

148
Q

Tx for PTLD?

A
  • reduce immunosuppresion
  • chemotherapy

there is no role for antiviral therapy!!

149
Q

Examples of monoclonal antibodies?
Mechanism?
Why are they only used for prophylaxis?

A

Basiliximab or Dacluzimab

  • Block IL-2 receptor on CD4 T-cells
  • Not useful if rejection has already started
150
Q

Glucocorticoid mechanism?

A

Inhibit lymphocyte proliferation + suppress cytokines

151
Q

Examples of calcineurin inhibitors?
Mechanism?
Side effects? (4)

A

Tacrolimus & Ciclosporin
* inhibiting activation of T-cells

Side effects

  • Renal dysfunction
  • Hypertension
  • Diabetes
  • Tremor
152
Q

Anti-metabolites examples?
Mechanism?
Side effects? (3)

A

Azathioprine & Mycophenolate Mofetil (MMF)
* Block purine synthesis -> suppression of proliferation of lymphocytes

Side effects

  • leucopenia
  • GI upset
  • anaemia
153
Q

Glomerular disease classed as?

A

Type of parenchymal disease

154
Q

Types of glomerular disease? (4)

A

Diabetic Nephropathy
Glomerulonephritis (GN)
Amyloid/ Light Chain Nephropathy
Transplant Glomerulopathy

155
Q

Glomerulonephritis?

A

Immune-mediated disease of the kidneys affecting the glomeruli
(secondary tubulointerstitial damage)

156
Q

Pathogenesis of GN?

A
  • Humoral (antibody-mediated)
  • Cell-mediated (T-cells)
  • Inflammatory cells, mediators and complements
157
Q

Pathophysiology GN?

A

Disruption of glomerular capillary wall leads to haematuria/proteinuria

158
Q

Damage to endothelial/mesenagial cells?

Damage to podocytes?

A
  • Endothelial/mesangial = leads to proliferative lesion and RBCs in urine
  • Podocytes = non-proliferative lesion and protein in urine
159
Q

Why does damage to podocytes result in proteinuria?

What is different about this response compared to endothelial/mesangial damage?

A

Atrophies.
Loss of size/charge specific barrier so proteins leak out
* it is NON-INFLAMMATORY

160
Q

Result of damage to mesangial cells?

A

Proliferate and release angiotensin 2, chemokines + attract inflammatory cells

161
Q

Result of damage to endothelial cells?

A

Vasculitis (e.g. acute GN)

162
Q

24 year old man incidentally found to have ++ blood and + protein on dip, BP 148/92.
Protein quantified at 0.7g/day. Creat 72.
What glomerular cells are most likely to be injured?

A

Mesangial cells. High BP, protein and blood in urine.

163
Q

Dx of GN? (6)

A
  • Urinalysis - haematuria, proteinuria
  • Urine microsopy - RBC (dysmorphic), RBC & granular casts, lipiduria
  • Urine Protein: Creatinine Ratio/24 hour urine - quantify proteinuria
  • Kidney biopsy
  • Blood tests
164
Q

Clinical presentation glomerulonephritis? (5)

A
  • Haematuria (either asymptomatic microscopic haematuria or painless macroscopic)
  • Proteinuria
  • impaired renal function
  • hypertension
  • NephROTIC syndrome (if affects podocytes!)
  • NephRITIC syndrome (if affects endothelial cells)
165
Q

How is proteinuria classified?

A
  • Microalbuminuria (30-300mg albuminuria/day)
  • Asymptomatic proteinuria ( 1 g/day)
  • Heavy proteinuria (1-3 g/day)
  • Nephrotic syndrome (> 3 g/day)
166
Q

What is microabluminuria a sign of?

Tx??

A

Diabetic nephropathy - give an ACEI asap!!

167
Q

Urine microscopy of RBCs?

A

Microscopy can give a clue where red cells have come from

Red cells squeezed out of shape going through glomerulus so will be dysmorphic

168
Q

Red cell casts?

A

pathognomonic of glomerular bleeding

169
Q

NephrITIC syndrome indicative of?

S/s? (5)

A

Indicative of a proliferative process affecting endothelial cells

  • acute renal failure
  • oliguria (not peeing)
  • oedema/fluid retention
  • hypertension
  • haematuria!
170
Q

NephrOTIC syndrome indicative of?

S/s? (5)

A

Indicative of a non proliferative process affecting Podocytes

  • Proteinuria 3 g/day (mostly albumin, also globulins)
  • Hypoalbuminaemia (<30)
  • Oedema
  • Hypercholesterolaemia
  • Usually normal renal function (unlike nephritic syndrome)
171
Q

Complications of nephrotic syndrome?

A
  • Infections - loss of opsonising antibodies
  • Renal vein thrombosis (this would cause sudden decline of renal function which isn’t normal in nephrotic syndrome so watch out!)
  • Pulmonary emboli
  • Volume depletion (overaggressive use of diuretics) - may lead to acute renal failure (pre-renal)
172
Q

How does the presentation of GN differ from a non glomerular disease like Interstitial Nephritis?

A

Get proteinuria in glomerular disease, don’t get it in tubular disease

173
Q

Classification of GN?

A

1) Idiopathic - THE MAJORITY

2) caused by eg. infections, drugs, malignancies, ANCA, lupus, Goodpastures, HSP

174
Q

What is the use of immunofluoresence in GN?

A

IgG staining can indicate glomerulonephritis

175
Q

Histological classifications of GN?

A
  • Proliferative or non-proliferative (usually refers to presence or absence of proliferation of mesangial cells)
  • Focal/Diffuse (< or > 50% glomeruli affected)
  • Global/Segmental (all or part glomerulus affected)
  • Crescentic (presence of crescents - epithelial cell extracapillary proliferation eg. RPGN in vasculitis)
176
Q

Tx glomerulonephritis?

A

Non-immunosuppressive

  • anti-hypertensives (target BP <130/80, <120/75 if proteinuria)
  • ACEI/ARBs
  • Diuretics
  • Statins

Immunosuppressive

  • corticosteroids/azathioprine/ calcineurin inhibitors/ mycophenolate mofetil (MMF)
  • plasmapheresis (therapeutic plasma exchange)
  • antibodies
177
Q

Tx nephrotic patients?

A
  • Fluid restriction
  • Salt restriction
  • Diuretics
  • ACE Inhibitors/ ARBs
  • IV albumin (only if volume deplete)
  • immunosuppression (to achieve sustained remission)
178
Q

What is the goal of immunosuppression in GN?

A

To achieve sustained remission

  • complete remission (proteinuria <300 mg/day)
  • partial remission (proteinuria <3 g/day)
179
Q

What are the risks of immunosuppressing a patient who is nephrotic?

A

High risk of infection (they are already losing immunoglobulins i.e. protein)

180
Q

Main types of idiopathic GN?

A
  • MINIMAL CHANGE
  • FSGS (focal segmental glomerulosclerosis)
  • MEMBRANOUS
  • MEMBRANOPROLIFERATIVE
  • IgA NEPHROPATHY
181
Q

Minimal change disease?

A

Commonest GN in children
(EM pictures allow you to see where damage is)

DOES NOT CAUSE PROGRESSIVE RENAL FAILURE

182
Q

Tx minimal change nephropathy?

A
  • 1st line = oral steroids

* 2nd line = cyclophosphamide

183
Q

What does minimal change nephropathy appear like on EM?

A

podocytes are all fused together. Foot process fusion—fingers have retracted

184
Q

Focal segmental glomerulosclerosis (FSGS)?

Ax?

A

Commonest cause of nephrotic syndrome in adults

  • Idiopathic
  • type 2 = HIV, heroin use, obesity, reflux nephropathy
185
Q

Dx FSGS?

A

Renal biopsy = light miscoscopy with minimal Ig/complement deposition

186
Q

Tx FSGS?

A
  • Remission with prolonged steroids in 60%

* 50% progress to end stage renal failure after 10 years

187
Q

Membranous nephropathy?

Ax?

A

2ND commonest cause of nephrotic syndrome in adults

  • Idiopathic
  • infections (hepatitis B/ parasites)
  • connective tissue diseases (lupus)
  • malignancies (carcinomas/ lymphoma)
  • drugs (gold/penicillamine)
188
Q

Dx membranous nephropathy?

Tx?

A

Renal biopsy: immune complex deposition in the basement membrane
* Steroids/ Alkylating agents/B cell monoclonal Ab

189
Q

What is anti PLA2r antibody?

What does it cause?

A

Anti-podocyte antobody! (plasminogen lipase antigen 2 receptor)
It causes menbranous nephropathy (nephrotic syndrome)

190
Q

Histology membranous nephropathy?

A

Thickened basement membrane due to immune complex deposition

191
Q

IgA nephropathy?

S/s? (4)

A

Commonest GN in the world

  • asymptomatic microhaematuria
  • macroscopic haematuria after resp/GI infection
  • AKI/CKD
  • associated with henoch-schonlein purpura (arthritis/colitis/purpuric rash)
192
Q

Dx IgA nephropathy?

Tx?

A

Renal biopsy = mesangial cell proliferation + IgA deposits in mesangium (immunofluorescence)

Tx

  • BP control = ACEI + ARBs
  • Fish oil

(treatment is NOT immunosuppression)

193
Q

Pathogenesis IgA nephropathy?

A
  • IgA is abnormal
  • Immune complexes form in circulation
  • Immune complexes deposited in mesangium causing immune activation and injury
194
Q

Rapidly progressive glomerulonephritis (RPGN)?

S/s? (3)

A

A treatable cause of acute renal failure (affects endothelial cells)

  • Rapid deterioration in renal function over days/weeks
  • Active urinary sediment (RBC’s, RBC & Granular Casts)
  • May be part of systemic disease
195
Q

Dx rapidly progressive glomerulonephritis (RPGN)? (2)

A
  • Urinary sediment (RBCs, RBC casts)

* glomerular crescents on biopsy

196
Q

Systemic diseases associated with RPGN?

A

ANCA positive (systemic vasculitis)

  • GPA
  • microscopic polyangitis

ANCA negative

  • Goodpasture’s (anti-GBM)
  • Henoch scholein purpura
  • SLE
197
Q

Tx RPGN?

A

Strong immunosuppression with dialysis if needed!!

  • Steroids (IV methylprednisoone/oral prednisolone)
  • Cytotoxics (cyclophosphamide/azathioprine)
  • plasmapheresis
198
Q

74 year old woman. Hypoxic. Haemoptysis. creat 430. blood and protein on dip. Red cell casts on microscopy. Purpuric rash.

Cells affected?
Diagnosis?
Invetsigation?

A
  • Cells affected = endothelial cells (remember RBC = endothelial cells)
  • ANCA +ve vasculitis (RPGN)
  • Endothelial injury in lungs causes haemoptysis and hypoxia

Investigation
* blood test for ANCA

199
Q

Describe pathway and concentration of tubular fluid leaving the loop of Henle?

A
  • tubular fluid entering disal tubule is hypo-osmotic to plasma (100 mosmol/l)
  • surrounding interstitial fluid of renal cortext is 300 mosmol/l
  • empties into collecting duct
  • collecting duct bathes by increasing concentrtions of interstitial fluid (300 - 1200 mosmol/l)
200
Q

what % of ions are reabsorbed before filtrate enters the distal tubule?

A

95% (but residual load 700-1000 mmol NaCl is very important for salt balance!)

201
Q

How is ion and water balance regulated?

A

By hormones

  • ADH = increases water reabsorption
  • Aldosterone = increases Na reabsorption, and H+ and K+ secretion
  • Atrial natriuretic hormone = decreases Na reabsorption
  • Parathyroid hormone (PTH) = increases calcium reabsorption + increases phosphate secretion
202
Q

Distal tubule permeability?

Osmolality?

A

Low permeability to water and urea (therefore, urea is concentrated in tubular fluid)
* tubular fluid is hypo-osmotic (100 mosmol/l) to plasma

203
Q

2 segments of the distal tubule?

A

Early and late

  • Early: NaK2Cl transport (NaCl reabsorption)
  • Late: Calcium reabsorption, H+ secretion, Na and K reabsorption (aldosterone causes K secretion)
204
Q

2 segments of the collecting duct?

A

Early and late

  • Early collecting duct is similar to late distal tubule
  • Late collecting duct: low ion permeability, permeable to water and urea and influenced by ADH
205
Q

ADH secretion from the posterior pituitary?

A
  • Octapeptide (ADH) synthesised by the supraoptic and paraventricular nuclei in the hypothalamus
  • Transported down nerves to terminals where it is stored in granules in the posterior pituitary
  • Released into blood when action potentials down the nerves lead to Ca2+-dependent exocytosis
206
Q

Effect of ADH on water permeability of the collecting duct?

A
  • increase in intracellular cyclic AMP
  • Cyclic AMP initiates insertion of water channels into apical membrane of tubular cell (water reabsorption)
  • Aquaporins become internalised within intracellar vesicles once ADH level decreases
207
Q

High ADH?

Low ADH?

A
  • High ADH = high water permeability (more reabsorption) + thus hypertonic urine (1400 mosmol/l)
  • Low ADH = low water permeability thus hypotonic urine (<50 mosmol/l)
208
Q

In presence of maximal ADH?

Minimal ADH?

A

Tubular fluid equilibrates with interstitium via aquaporins (small volume of concentrated urine)
* Minimal = Collecting duct is impermeant to water, so no water reabsorption (large volume of dilute urine)

209
Q

Diabetes insipidus classification?

A
  • Central diabetes insipidus (unable to secrete ADH)

* Nephrogenic diabetes insipidus (ADH production normal, problem with target cells)

210
Q

S/s diabetes insipidus? (2)

Tx?

A

Large volumes of dilute urine
Constant thirst

  • Tx = ADH replacement
211
Q

Most important stimulus for ADH release?

A 
Hypothalmic osmoreceptors
(less important = left atrial stretch receptors i.e. decreased atrial pressure = increased ADH release)
212
Q

Stimulation of stretch receptors in upper GI tract?

A

Feed-forward inhibition of ADH

213
Q

Drugs and substances increase/inhibit ADH?

A
  • Nicotine stimulates ADH release

* Alcohol + ecstacy inhibits ADH release

214
Q

Aldosterone?

When is it secreted?

A

Steroid hormone secreted by the adrenal cortex

Secreted in response to

  • rising K or falling Na in blood
  • activation of renin-angiotensin system
215
Q

Function of aldosterone?

A

Stimulates Na+ reabsorption and K+ secretion

Na retention contributes ot increased blood volume + pressure

216
Q

Effects of aldosterone on K+?

A
  • 90% K+ is reabsorbed in proximal tubule
  • When aldosterone absent the rest (10%) K+ reabsorbed in the distal tubule (therefore, no K+ is excreted in the urine)
  • Aldosterone stimulates the SECRETION of K+
217
Q

Direct and indirect secretion of aldosterone?

A
  • An increase in [K+] directly stimulates adrenal cortex

* decrease in plasma [Na+] = indirect secretion of aldosterone via juxtaglomerular apparatus

218
Q

Which cells release renin?

A

Granular cells in the juxtaglomerular apparatus

219
Q

What causes granular cells to release renin? (3)

A
  • Reduced pressure in afferent arteriole
  • If macula densa cells sense reduced NaCl in the distal tubule
  • Increased sympathetic activity as a result of reduced arterial blood pressure
220
Q

Effect on aldosterone on Na?

A

increases Na+ reabsorption in the distal and collecting tubule

221
Q

Pathophysiology renin angiotensin system?

Tx? (3)

A

Responsible of the fluid retention associated with congestive heart failure

Tx

  • low salt diet
  • diuretics
  • ACE inhibitors (stop salt and fluid retention)
222
Q

Atrial natriuretic peptide?
When is it released?
Effect?

A

Produced by the heart
* released when atrial muscle cells are stretched due to increased BP

Effect
* causes excretion of Na+ and diuresis lowering BP

223
Q

Micturition?

Controlled by?

A

Urination

  • micturation reflex
  • voluntary control
224
Q

When is micturation reflex triggered?

What kind of nerve reflex?

A

bladder can accommodate up to 250-400 ml of urine before stretch receptors in within its wall initiate the micturation reflex
* parasympathetic

225
Q

How is voluntary control of urination exerted?

A

Micturation can be voluntarily PREVENTED by deliberate tightening of the external sphincter and surrounding pelvic diaphragm

226
Q

PH equation?

A

pH = log 1/[H+]

227
Q

Is venous or arterial blood more acidic?

A

Venous - due to CO2

CO2 + H2O = carbonic acid

228
Q

pH of arterial blood?

Venous blood?

A 
Arterial = 7.45
Venous = 7.35
229
Q

How can fluctuations in [H+] affect the body? (4)

A
  • Acidosis = depression of CNS
  • Alkalosis = overexcitability of CNS
  • Changes in [H+} affect enzyme activity
  • changes in [H+] affect K+ levels
230
Q

HA [H+] + A-

What happens if [H+] is added?

A

Equilibrium shifts to the left, [HA] rises, [A- falls]

231
Q

Dissociation constant equation?

A

K = [H+][A-]/[HA]

pK = -log K

232
Q

Henderson-Hasselbalch equation?

A

pH = pK + log [A-]/[HA]

233
Q

Most important buffer system?

A

CO2-HCO3 buffer

234
Q

Mechanism of [HCO3] reabsorption in proximal tubule?

A

HCO3- disappears from the tubular fluid and appears in the interstitial fluid
* Unorthodox reabsorption – the same HCO3- ion does not cross the epithelium

235
Q

What happens when [HCO3] is low?

A

secreted H+ combines with the next most plentiful buffer in the filtrate…
phosphate

236
Q

What 3 things does H+ secretion by tubule allow? (3)

A
  • Reabsorption of HCO3
  • Formation of acid phosphate
  • Formation of ammonium ion
237
Q

Total H+ secretion/day?

Total H+ excretion?

A 
Secretion = 4360 mmol/day
Excretion = 60 mmol/day
238
Q

Acute urinary retention s/s?

Ax?

A
  • Inability to urinate
  • Painful urination

Usually complication of benign prostatic hyperplasia

239
Q

Tx acute urinary retention?

A
  • Catheter

* Alpha-blocker: alfuzosin, tamulosin

240
Q

Acute loin pain Ax?

A
  • Ureteric colic secondary to calculus

* AAA

241
Q

Tx ureteric colic?

A
  • NSAID/opiate
  • alpha blocker (for small stones that are expected to pass)
  • Surgical intervention if too large to pass
242
Q

Dx kidney stone?

A
  • Definitive test = non-contrast CT scan
243
Q

Surgical interventions for kidney stone? (3)

A
  • Ureteric stent
  • Stone fragmentation/removal
  • percutaneous nephrostomy for infected hydronephrosis
244
Q

Frank haematuria caused by?

A 
Infection
Stones
Tumours
Benign prostatic hyperplasia (BPH)
Polycystic kidneys
Trauma
Coagulation/platelet deficiencies
245
Q

Tx clot retention urinary system?

A

3-way irrigating haematuria catheter

246
Q

Ix haematuria?

A
  • CT urogram

* Cytoscopy

247
Q

S/s torsion of spermatic cord?
Examination?
Age group?

A

S/s

  • acute onset pain
  • nausea/vomiting
  • referral of pain to lower abdomen

Examination

  • testes high + transverse
  • absence of cremasteric reflex

Most common at puberty

248
Q

Ix torsion of spermatic cord?

Tx?

A

Doppler USS

Tx

  • If testis necrotic, remove
  • MUST fix contralateral side (bell clapper deformity)
249
Q

S/s torsion of testicular appendage?

A
  • Can be identical to torsion of cord
  • “blue spot” sign
  • Cremasteric reflex is present!
250
Q

Epididymitis difficult to distinguish from?

A

Testicular torsion

  • dysuria/pyrexia more common
  • Hx of UTI, urethritis, catheterisation
251
Q

O/E epididymitis?

A
  • absent cremasteric reflex
  • pyuria
  • doppler = swollen epididymis
252
Q

Ax epididymitis?

A

Associated with chlamydia

253
Q

Tx epididymitis?

A
  • Analgesia

* Ofloxacin 400mg/day for 14 days

254
Q

Idiopathic scrotal oedema?

S/s?

A
  • self-limiting, unknown cause

S/s

  • tender
  • pruritis
  • no fever (unlike epididymitis)
255
Q

Paraphimosis?

Ax?

A

Painful swelling of the foreskin distal to a phimotic ring
* Often happens after foreskin retracted for catheterization or cystoscopy and staff member forgets to replace it in its natural position

256
Q

Tx paraphimosis?

A
  • Iced glove
  • granulated sugar for 1-2 hrs
  • punctures in oedematous skin
  • manual compression
  • dorsal slit
257
Q

Priapism?

Ax?

A

Prolonged erection (> 4hrs), often painful and not associated with sexual arousal

Ax

  • Papaverine injetion for ED
  • Trauma
  • Sickle cell
258
Q

Classification priapism? (3)

A
  • Ischaemic
  • Vascular stasis (compartment syndrome)
  • Corpora cavernosa (rigid and painful)
259
Q

Dx priapism?

A
  • Aspirate blood (in low flow, will have low O2 and high CO2)
  • Colour duplex USS - low flow = absent flow in cavernosal arteries (normal flow in non-ischaemic priapism)
260
Q

Tx priapism?

A

Ischaemic

  • aspiration
  • alpha-agonist e.g. phenylephrine
  • surgical shunt

Non-ischaemic
* may resolve spontaneously

261
Q

Fournier’s gangrene?

S/s? (4)

A

necrotizing fasciitis of the male genitalia

  • starts as cellulitis - swollen, erythematous, tender, fever
  • crepitus of scrotum
  • dark purple areas
262
Q

Tx fournier’s gangrene?

A

Antibiotics + surgical debridement

263
Q

Emphysematous pylonephritis?

Risk factors?

A

Infective emergency!!

  • acute necrotizing parenchymal and perirenal infection caused by gas-forming uropathogens, usually E coli
  • risk factor = diabetes
264
Q

S/s emphysematous pylonephritis?
Dx? (2)
Tx?

A

S/s

  • fever
  • vomiting
  • flank pain

Dx

  • gas on KUB
  • CT

Tx = nephrectomy

265
Q

Perinephric abscess?

S/s? (5)

A

Usually results from rupture of an acute cortical abscess into the perinephric space

  • flank mass
  • not usually pyrexial
  • high WCC
  • high creatinine
  • pyuria
266
Q

Ix perinephric abscess?

TX?

A 
Ix = CT
Tx = antibiotics + percutaneous surgical drainage
267
Q

Indications for imaging?

Ix?

A
  • Frank haematuria

Ix = CT contrast (unlike non-contrast CT for kidney stone)

268
Q

Bladder injury associated with?

S/s? (5)

A

Associated with pelvic fracture

  • abdominal pain
  • inability to void
  • lower abdominal bruising
  • guarding
  • diminished bowel sounds
269
Q

Ix bladder injury?

Tx?

A

Ix = CT cystography

Tx

  • large-bore catheter
  • antibiotics
270
Q

Urethral injury associated with?

S/s? (5)

A

often associated with fracture of pubic rami

  • blood at meatus
  • inability to urinate
  • full bladder (palpable)
  • “high-riding” prostate
  • BUTTERFLY perineal haematoma!
271
Q

Ix urethral injury?

Tx?

A

Retrograde urethrogram

Tx
* suprapubic catheter

272
Q

Penile fracture?

S/s?

A

Typically happens during intercourse – buckling injury when penis slips out of vagina and strikes pubis
* Cracking or popping sound followed by pain, rapid detumescence, discolouration and swelling

273
Q

Tx penile fracture?

A

Circumcision incision with degloving of penis to expose all 3 compartments

274
Q

Testicular injury Ix?

A

USS to assess integrity / vascularity

275
Q

Infective inflammation of the kidney?

Non-infective inflammation of the kidney?

A
  • Infective = pyelonephritis

* Non-infective = glomerulonephritis

276
Q

What does bowman’s space contain?

A

Urine

277
Q

What is glomerulus held together by?

A

Mesangial cells

278
Q

Which glomerulonephritis involves a direct attack of the glomerulus?

A

Good pasture’s syndrome (lung + renal)

279
Q

Types of vasculitis? (2)

A
  • cANCA = GPA

* pANCA = microscopic polyangiitis

280
Q

Classification of glomerulonephritis? (2)

A
  • Nephritic syndrome

* Nephrotic syndrome

281
Q

Difference between nephritic and nephrotic syndrome?

A

Nephritic
* haematuria, hypertension

Nephrotic

  • proteinuria (protein loss = immunosuppression due to loss of antibodies)
  • Oedema
  • hyperlipidaemia
  • renal vein thrombosis
282
Q

Crescents histology?

Granulomas?

A
  • Crescents = RPGN (poor prognosis)

* granulomas = GPA or sarcoid

283
Q

Dx goodpasture’s?

A

Immunofluorescence = linear IgG

284
Q

Minimal change glomerulonephritis? (4)

A
  • Kids
  • nephrotic
  • appearance = duh, not much to see
  • prognosis = very good (usually resolves with steroids)
285
Q

Focal segmental glomerulosclerosis?

A
  • obesity, HIV, sickle cell, IV drug users (heroin)
  • adults
  • nephritic
  • appearance - duh, segmented sclerosis (appears pink)

2nd year medicine (24 decks)

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