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Year 2 > Renal > Flashcards

Renal Flashcards

1
Q

At what vertebral level do the kidneys lie?

A

T12-L3

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2
Q

What surrounds the kidney?

A

a fibrous capsule which is covered in perinephric fat and then by perinephric fascia

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3
Q

What makes up the renal medulla?

A

Renal pyramids

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4
Q

Where are glomeruli found?

A

in the renal cortex

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5
Q

Where does the renal artery arise from

A

the aorta

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6
Q

is the ureter intraperitoneal or retroperitoneal?

A

Retroperitoneal

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7
Q

What vertebral levels innervate the bladder?

A

S2,3,4

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8
Q

Which type of nephron is more abundant?

A

Cortical (short loop)

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9
Q

What is erythropoietin and where is it found?

A

it is a hormone that causes stem cells in the bone marrow to be differentiated into RBC’s. It is made in the fibroblast like cells in the renal cortex

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10
Q

What is the function of mesangial cells?

A

provide a scaffold to support capillary loops and have contractile and phagocytic properties

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11
Q

How does blood enter the glomerular capillaries?

A

from an afferent arteriole and leaves by an efferent arteriole once filtration has occurred at the Bowmans Capsule

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12
Q

Why is there vasoconstriction of the efferent arteriole?

A

It creates a high hydrostatic pressure in the glomerular capillary forcing water, ions and small molecules through the filtration barrier into Bowmans space

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13
Q

What are the layers of the filtration barrier?

A

Endothelial cells (thin with pores and -ve charge), glomerular basement membrane (2 layers made of type IV collagen, -ve charge), epithelial cells of the bowmans capsule (has foot processes which join with others to give slit pores e.g. nephrin- pores are the key selective barrier in the filtration process and prevent the passage of larger molecules, also -ve charge)

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14
Q

What are podocytes?

A

cells in the bowmans capsule that wrap around capillaries of the glomerulus. They form a filtration barrier with endothelial cells and the GBM.

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15
Q

Where in the tubule does most of reabsorption occur?

A

Proximal tubule

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16
Q

What is the function of the loop of Henle on a basic level?

A

concentrates urine

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17
Q

What type of epithelium is Bowmans capsule?

A

thin squamous epithelial cells

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18
Q

What type of epithelium is in the tubules?

A

columnar epithelial cells which are specialised for transport processes

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19
Q

Which substances are reabsorbed in the proximal tubule?

A

Na2+, K+, Cl-, PO3, glucose, amino acids and water

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20
Q

Does water move with substances?

A

Yes- this keeps the filtrate diluted. Where salt goes, water goes

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21
Q

What is the juxtaglomerular apparatus?

A

it consists of the macula densa, extraglomerular mesangial cells and granular cells.

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22
Q

What is the function of the juxtaglomerular apparatus?

A

Regulates BP and monitor GFR

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23
Q

What do the efferent arterioles form in the juxtaglomerular nephron?

A

Vasa recta and peritubular capillaries

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24
Q

What is the function of the vasa recta?

A

it is the sole blood supply to the medulla of the kidney

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25
Q

Which hormones act on the kidney?

A

ADH, Aldosterone, natriuretic peptides and PTH

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26
Q

What effect does ADH have on the kidneys?

A

It promotes water reabsorption in the collecting ducts - concentrates urine

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27
Q

What effect does Aldosterone have on the kidneys?

A

Sodium reabsorption in the collecting ducts and excretion of potassium

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28
Q

What effect does natriuretic peptides have on the kidneys?

A

They are produced by the cardiac cells and promote sodium excretion in the collecting ducts

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29
Q

What effect does PTH have on the kidney?

A

it promotes renal phosphate excretion, calcium reabsorption and vitamin D production

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30
Q

What hormones are produced by the kidney?

A

Renin, Vitamin D, erythropoietin and prostaglandins

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31
Q

What is the effect of Renin?

A

It is released by the juxtoglomerular apparatus and results in the formation of angiotensin II which acts directly on the proximal tubules and via aldosterone on the distal tubules to promote sodium retention and vasodilates

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32
Q

When is renin released?

A

When baroreceptors sense a drop in BP and when the macula densa senses a drop in salt

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33
Q

What is the metabolism of vitamin D?

A

It is metabolised int he kidney to the active form 1,25-dihydroxycholecalciferol

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34
Q

What is the function of vitamin D?

A

Promotes calcium and phosphate absorption from the gut

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35
Q

Where does erythropoeitin work on?

A

The stem cells in the bone marrow to differentiate them into RBC’s

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36
Q

What makes up the glomerular basement membrane?

A

collagen type IV, heparin sulfate proteoglycans and lamina

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37
Q

What are foot-like processes?

A

They are projected from podocytes (specialised epithelial cells) and interdigitate to form filtration slits

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38
Q

What is the importance of the foot like processes and podocytes?

A

They stop large anions from being filtrated

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39
Q

What factors of the substances affect filtration across the bowmans capsule?

A

weight and charge. Smaller substances cross easily, large ones don’t. Negatively charged ions are not filtered as freely as positively charged ions because the epithelium is negatively charged

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40
Q

What is the triad of symptoms of nephrotic syndrome?

A

Proteinuria, hypoalbuminaemia and oedema

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41
Q

What is fucked in minimal change disease?

A

Under a light microscope there is nothing to see but under electron microscope there is pathology of the podocytes. There is diffuse effacement of the foot processes of podocytes causing the widening of filtration slits

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42
Q

What are the 2 sections of the proximal convoluted tubule?

A

Para convolute (renal cortex) and pars recta (renal medulla)

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43
Q

What is the driving force for the reabsorption in the PCt?

A

Sodium, which is followed by chloride ions to keep electro-neurtality

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44
Q

What is transcellular transport?

A

Transporting solutes through a cell

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45
Q

What is paracellular transport?

A

Transporting solutes via the tight junctions between cells

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46
Q

What is the effect of the sodium-potassium pump?

A

Sodium out, potassium in

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47
Q

Where are SGLUT transporters found and what do they transport?

A

Found on the apical membrane of the PCT and transport sodium and glucose

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48
Q

How does glucose cross the basolateral membrane?

A

Facilitated diffusion

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49
Q

Which is the most common primary renal cancer?

A

Renal cell carcinoma

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50
Q

Where does RCC originate?

A

The PCT

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51
Q

What are the symptoms of renal cell carcinomas?

A

Mostly occurs in men and causes haematuria, flank pain, weight loss and fever

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52
Q

What is the cause of acute tubular necrosis?

A

It can be caused by ischaemia which usually occurs secondary to reduced renal blood flow (hypotension or sepsis)

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53
Q

Where are Na/K-ATPase channels found?

A

the basolateral membrane

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54
Q

What happens to SGLT channels when there is too much glucose?

A

When glucose exceeds the transport max, glucose spills into the urine and water follows.

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55
Q

Where is the primary site of sodium reabsorption in the loop of henle?

A

thick ascending limb

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56
Q

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

A

Thick ascending limb

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57
Q

How is sodium reabsorbed in the loop of Henle?

A

It is reabsorbed via the NKCC2 transporter on the thick ascending loop

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58
Q

What is the action of the NKCC2 transporter?

A

Moves sodium, potassium and 2 chloride ions

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59
Q

What is the action of the ROMK transporter?

A

Moves potassium back into the tubule to prevent toxins from building up

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60
Q

Is sodium reabsorbed in the thin ascending limb?

A

Yes- it moves paracellularly due to the difference in osmolarity between the tubule and interstitium

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61
Q

What is the effect on water of sodium reabsorption in the thin ascending limb?

A

It is reabsorbed from the descending limb- counter current multiplication

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62
Q

Is sodium reabsorbed in the thin ascending limb?

A

No

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63
Q

What is Bartter Syndrome?

A

It is a group of autosomal recessive conditions caused by genetic mutations in the genes that code for NKCC2 which causes Na to get reabsorbed in the distal tubule leading K to be excreted into the tubule leading to hypokalaemia and hypovolaemia

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64
Q

Which group of drugs work on the NKCC2 transporter?

A

Loop diuretics (furosemide) to increase excretion of NaCl in the urine

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65
Q

What is the role of the early distal convoluted tubule?

A

Reabsorption of Na, Cl and Ca

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66
Q

What is the channel on the early DCT?

A

Sodium-potassium pump. Na out and K in. And the NCC symporter- Na and Cl in from the urine

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67
Q

What are the cells of the late distal convuluted tubule?

A

Principal cells: involved in sodium and potassium exchange and intercalated cells: control hydrogen and bicarbonate ions

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68
Q

How does hydrogen move into the lumen?

A

By the K/H-ATPase antiporter. It then binds to ammonia or phosphate so that it cannot cross again and is excreted in the urine

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69
Q

How does ADH increase sodium reabsorption?

A

It acts on the kidney to increase the number of aquaporin 2 channels in the apical membrane of the tubular cells of the collecting duct.

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70
Q

Which water channels are on the basolateral membrane?

A

Aquaporins 3 and 4

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71
Q

What are the features of the descending loop of henle?

A

it is permeable to water but not to salt

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72
Q

What are the features of the ascending loop of henle?

A

it is impermeable to water but permeable to salt. NaCl is pumped out the thick ascending limb actively to dilute the filtrate since it gets really salty in the LOH.

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73
Q

Where is bicarbonate reabsorbed?

A

in the PCT then the remaining in the DCT

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74
Q

Where is urea reabsorbed?

A

It is reabsorbed in the collecting duct and can be recycled at the loop of henle for water reabsorption.

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75
Q

What does a lack of ADH do to the collecting duct?

A

This happens when a patient is overhydrated. This will make the collecting ducts impermeable to water so that it has to pass into the urine

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76
Q

What makes up the renal corpuscle?

A

Glomerulus and Bowmans capsule

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77
Q

What is Oncotic pressure?

A

Pressure exerted by plasma proteins on the walls of the compartment in which they are contained

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78
Q

What pressure is the major driving force for filtration?

A

Hydrostatic pressure of the glomerulus (forces fluid out of the capillary)

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79
Q

What are the forces involved in filtration at the bowmans capsule?

A

From capillary to bowmans capsule:
Glomerular capillary blood pressure 55mmHg
Bowmans capsule oncotic pressure 0mmHg
From bowmans capsule acting on the capillary:
Bowmans capsule hydrostatic fluid pressure 15mmHg
Capillary oncotic pressure 15mmHg
Think: Glomerular Blood (55+0) and Bowmans Capsule (15+30)

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80
Q

What is the net filtration pressure?

A

(55+0) - (15+30) = 10mmHg

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81
Q

What is the GFR?

A

The total amount of filtrate formed by all the renal corpuscles in both kidneys per minute

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82
Q

What are the factors that influence GFR?

A

Net filtration pressure, surface area available for filtration and permeability of the glomeruli

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83
Q

What happens if the afferent arteriole is constricted?

A

Then this causes the hydrostatic pressure of the glomeruli to decrease due to a reduction of blood available for filtration and therefore GFR will decrease

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84
Q

Why can water move passively in the descending loop of henle?

A

Because the medulla is so salty

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85
Q

How does countercurrent multiplication work?

A

Water is passively pumped out of the descending loop because it is a salty environment which dilutes the interstitial fluid but then in the ascending loop NaCl is pumped out. There is a gradient in place of a difference of 200mosmol/L

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86
Q

What is the function of the Na+/H+ exchanger (NHE3)?

A

To move sodium out and hydrogen in

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87
Q

How is secretion of H+ by the sodium/hydrogen exchanger balanced?

A

by the exit of bicarbonate

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88
Q

What is the net effect of NKCC2 and ROMK channels in the thick ascending loop?

A

NKCC2: 1 sodium, 2 chloride and 1 potassium leave
ROMK: 1 potassium in
Net: 1 sodium and 2 chloride leave

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89
Q

What channel reabsorbs sodium in the distal convoluted tubule?

A

The NCC channel

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90
Q

What drug acts on the distal tubule to prevent sodium reabsorption?

A

Thiazide diuretics

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91
Q

What is the final stage of sodium chloride reabsorption?

A

In the collecting ducts, the principal cells have ENaC channels which lets sodium leave the cell. Chloride leaves the intercalated cells.

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92
Q

Which channel is most important for
a) the absorption of potassium
B) the secretion of potassium

A

A) Na/K ATPase

B) ROMK

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93
Q

What factors increase K+ secretion?

A

Increased luminal flow which can be caused by volume expansion, acidosis and diuretics

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94
Q

What effect does Aldosterone have on K+ secretion?

A

high aldosterone: increase Na reabsorption and increase K secretion. Does this through ENaC channels

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95
Q

What is the clearance of glucose?

A

0

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96
Q

What is hypotonic?

A

More water outside than inside so increase in cell volume

97
Q

What is hypertonic?

A

More water in the cell than outside so water moves out causing the cell to shrink

98
Q

What is a normal GFR?

A

90-120mL/min/1.73 squared

99
Q

What effect does an increase in glomerular capillary BP have on GFR?

A

Increased net filtration and increase GFR

100
Q

How may the glomerular capillary BP fall?

A

From vasoconstriction of the afferent arteriole

101
Q

What is autoregulation?

A

prevents short term changes in the systemic arterial pressure affecting GFR

102
Q

What is the function of the macula densa?

A

sence NaCl content of tubular fluid and cause the afferent arteriole to constrict

103
Q

What is inulin clearance?

A

It is a marker of GFr since it is freely filtered at the glomerulus, neither absorbed nor secreted, not metabolised by the kidney, not toxic and easily measured in urine and blood

104
Q

What is used as a marker for GFR?

A

Creatinine- it is approximate and easier to measure than inulin

105
Q

Where is glucose reabsorbed in the tubule?

A

PCT

106
Q

What is the tonicity of the filtrate in the loop of henle?

A

It is isoosmotic in the descending loop and hypoosmotic in the descending loop

107
Q

Where is the highest osmolarity? the Renal cortex or medulla?

A

Medulla

108
Q

What is the point in countercurrent multiplication?

A

to concentrate the medullary interstital fluid to enable the kidney to produce urine of different volumes and concentration according to the amounts of circulating ADH

109
Q

Why is the vasa recta a countercurrent exchanger?

A

Because as it dips down into the medulla water is lost and as it rises water is gained

110
Q

What is diabetes insipidus?

A

It is due to too little ADH or insufficient response to ADH

111
Q

What is the treatment of diabetes insipidus?

A

ADH replacement

112
Q

What are the effects of Angiotensin II?

A
  1. stimulates the adrenal cortex to release aldosterone to increase sodium reabsorption
  2. arteriolar vasoconstriction
  3. thirst
  4. Vasopressin (ADH)- increase water reabsorption
113
Q

What stimulates release of Renin?

A

Low salt, low ECF and a drop in BP

114
Q

Where is Renin released from?

A

It is released from granular cells near the macula densa

115
Q

When might RAAS be inappropriate in a falling BP?

A

Congestive heart failure

116
Q

What is the treatment for congestive heart failure?

A

Loop diuretic

117
Q

What is the mechanism of ACE inhibitors?

A

stop fluid and salt retention and arteriolar vasoconstriction- they lower BP

118
Q

What is the effect of ANP?

A

It is released in response to the heart stretching and causes increased excretion of sodium, vasodilation (increase in GFR), decrease in BP from a decrease in CO and TPR

119
Q

What are the mechanisms of micturation?

A

Micturation reflex and voluntary control

120
Q

What is the micturation reflex?

A

It causes involuntary emptying of the bladder by simultaneous bladder contraction and opening of both the internal and external urethral sphincters

121
Q

What does the Davenport diagram show?

A

Resp Acidosis metabolic acidosis
Metabolic acidosis resp acidosis

122
Q

What are causes of respiratory alkalosis?

A

low inspired PCO2 at altitude, hyperventilation, hysterical overbreathing

123
Q

What are causes of metabolic acidosis?

A

Starvation ketoacidosis, alcoholic ketoacidosis, DKA, paracetamol, increased urea, lactic acidosis, ethanol

124
Q

What are causes of metabolic alkalosis?

A

Vomiting, aldosterone production, ingestion of alkali

125
Q

What is stage 1 CKD?

A

GFR of >/= 90 with renal damage

126
Q

What is stage 2 CKD?

A

GFR of 89-60 with kidney damage

127
Q

What is stage 3 CKD?

A

GFR of 59-30

128
Q

What is stage 4 CKD?

A

GFR of 15-29

129
Q

What is stage 5 CKD?

A

GFR <15

130
Q

At what stage of CKD would you consider prepping for dialysis?

A

Stage 4, Have to have dialysis by stage 5

131
Q

What are the factors that may affect the creatinine level?

A

Age, sex, muscle mass, diet and race

132
Q

What is eGFR?

A

Estimated GFR based on the patients serum creatinine, age, sex and race

133
Q

What is proteinuria?

A

When there is more than 150mg/day in the urine which signifies significant glomerular damage

134
Q

What is microalbuminuria?

A

Moderate increase in the level of urine albumin. it occurs when the kidney leaks small amounts of albumin into the urine. it is still low enough to be undetected by urine dipstick

135
Q

What is ACR?

A

Albumin creatinine ration

136
Q

What is ACR used for?

A

detecting small amounts of protein in the urine

137
Q

What is PCR?

A

Protein creatinine ratio

138
Q

What is PCR used for?

A

It should be used rather than ACR in pregnancy and where non-albumin proteinuria is suspected

139
Q

What does an ACR of more than 30mg/mmol mean?

A

Proteinuria or nephrotic syndrome

140
Q

What is a normal ACR?

A

Around 3mg/mmol

141
Q

What causes a pre-renal AKI?

A

Reduced renal perfusion which can be caused by blood loss and hypovolaemia

142
Q

What causes a post-renal AKI?

A

Ureteric/urethral obstruction by stones or malignancy

143
Q

What causes a renal AKI?

A

intrinsic kidney tissue damage which can be due to GN or nephrotoxins

144
Q

What effect does AKI’s have on urea?

A

Urea is raised in kidney damage so the urine:serum urea ratio is much worse in renal AKI than pre-renal

145
Q

What is an AKI?

A

An abrupt (<48 hours) reduction in kidney function defined as:
An absolute increase in serum creatinine by >25.4 micromols/L
OR an increase in creatinine by >50%
OR a reduction in urine output
Can only be applied following adequate fluid resuscitation and exclusion/ obstruction

146
Q

What is a stage 1 AKI?

A

Increase >26 micromol/L or >50% increase in serum Cr (1.5-1.9x).
Urine: <0.5ml/Kg/hr for >6 consecutive hours

147
Q

What is a stage 2 AKI?

A

Increase >/= 2-2.9x reference serum Cr

Urine: <0.5ml/kg/hr for >15 hours

148
Q

What is a stage 3 AKI?

A

Increase in more than 3x reference serum Cr or increase to more than or equal to 354 micromol/L or need for RRT
Urine: <0.3ml/Kg/hr for >24 hours

149
Q

What is the normal creatinine level?

A

Women: 45-90
Men: 60-110

150
Q

What is the normal urine output?

A

1.5ml/kg/hr

151
Q

What are the causes of a pre-renal AKI?

A

Hypovolaemia (haemorrhage, volume depletion), hypotension (cardiogenic shock, anaphylaxis, sepsis) and renal hypoperfusion (NSAIDs, ACEi, ARBs, hepatorenal syndrome)

152
Q

What can untreated pre-renal AKI lead to?

A

Acute tubular necrosis

153
Q

What is acute tubular necrosis?

A

death of tubular epithelial cells that form the renal tubules. It is the most common cause of AKI. Often caused by sepsis and severe dehydration. Can also be caused by rhabdomyolysis and drug toxicity

154
Q

What is the treatment for pre-renal AKI?

A

Assess for hydration and give fluid challenge- crystalloid 0.9% NaCl and reassess

155
Q

What are the causes of renal AKI?

A

Blood vessels: Vasculitis, renovascular disease
Glomerular: GN
interstital injury: drugs, infection (TB), systemic (sarcoid)
Tubular injury: Ischaemia, drugs (gentamicin), contrast, rhabdomyolysis

156
Q

What are the signs of a renal AKI?

A

anorexia, weight loss, fatigue, lethargy, N&V, itch, fluid overload (oedema, SOB), Oligiuria, uraemia

157
Q

What is the treatment for Renal AKI’s?

A

good perfusion, fluid resuscitation, dopamine/epinephrine/vasopressin. May require uregnat dialysis

158
Q

What are the complications of an AKI?

A

Hyperkalaemia, fluid overload, severe acidosis, uraemic pericardial effusion, severe uraemia

159
Q

What is a post-renal AKI?

A

AKI due to obstruction of urine flow leading to back pressure (hydronephrosis) and then loss of concentrating ability

160
Q

What are the causes of a post renal AKI?

A

Stones, cancers, strictures, extrinsic pressures

161
Q

What is the treatment of a post renal AKI?

A

Relieve obstruction, ureteric stenting, catheter

162
Q

What are the ECG changes associated with hyperkalaemia?

A

Peaked T waves, flattened P wave, QRS prolonged, sine wave

163
Q

What is the treatment for hyperkalaemia?

A

Calcium gluconate, insulin, dextrose, nebulised salbutamol, calcium resonium

164
Q

What management protects the myocardium in hyperkalameia?

A

Calcium gluconate

165
Q

What management moves potassium back into the cells?

A

Insulin, salbutamol

166
Q

What drug prevents K+ absorption from the digestive tract?

A

Calcium resonium

167
Q

What are urgent indications for haemodialysis?

A

Hyperkalaemia (>7), severe acidosis, fluid overload, urea >40, pericardial effusion

168
Q

How do you treat pulmonary oedema?

A 
sit up and give high flow oxygen
venous vasodilator e.g. diamorphine
furosemide
haemodialysis 
Consider CPAP
169
Q

What are the sick day rules?

A

if there is V&D or fevers, sweats or shakes for more than 24 hours then stop taking the tablets until the patients feel well enough.

170
Q

Which medications should be stopped in the sick day rules?

A

NSAIDs, ACEi, ARBs, Diuretics, diabetic medication

171
Q

What may low platelets in AKI may indicate?

A

haemolytic uraemic syndrome

172
Q

What is bence jones protein? and What is the test for this?

A

Protein electrophoresis and it is indicative of myeloma

173
Q

Does the risk of CKD increase with age?

A

Yes

174
Q

What is needed to make a diagnosis of CKD?

A

2 samples 90 days apart

175
Q

How bad is the prognosis based on eGFR and ACR?

A

The lower the eGFR and the higher the ACR the worse the prognosis

176
Q

How is the stage of AKI done?

A

using creatinine and urine output

177
Q

How long do you monitor patients for CKD after they have had an AKI?

A

2-3 years after

178
Q

What accounts for an accelerated progression of CKD?

A

Decrease in serum Cr of 25% per year or 15ml/min/1.73 squared

179
Q

When should someone be referred for a CKD?

A 
CFR <30
ACR >70
ACR >30 with haematuria
decrease in GFR by 25% yearly
decrease in GFR by 15ml/min/1.73squared yearly
poorly controlled hypertension after use of 4 hypertensives
known genetic causes of CKD
suspected renal artery stenosis
180
Q

What is the BP aims in those with CKD?

A

SBP below 140 and DBP below 90

181
Q

What is given as a prophylaxis of CVD in those with CKD?

A

Atorvastatin

182
Q

What are the causes of CKD?

A

Diabetes, hypertension, GN, renal artery stensosis, vasculitis, acute interstitial nephritis, ADPKD, calculi, prostatic, bladder malignancy, ureteric stricture

183
Q

What are signs of advanced urea?

A

lemon yellow, uraemic frost (crystallised urea deposits), twitching, encephalopathic flap, confusion, pericardial rub, kassmaul breathing

184
Q

What are the complications of CKD?

A

haemorrhage, haematuria, proteinuria, impaired salt balance, hypertension, acid base disturbance, electrolyte disturbance, end stage renal disease

185
Q

What effect does kidney dysfunction have on mineral bone disease?

A

there is insufficient mineral homeostasis. Beginning in CKD3 the kidneys cannot excrete phosphate leading to hyperphosphataemia, increased PTH, decreased vit D. Vitamin D metabolism is impaired reducing calcium and increasing PTH

186
Q

What is the treatment for CKD-MBD?

A

Alfacalcidol, phosphate binders, cinacalet

187
Q

Which membrane do diuretics act on?

A

The apical membrane

188
Q

How do diuretics enter the filtrate?

A

glomerular filtration, secretion by organic anion and cation transporters

189
Q

Where do loop diuretics act?

A

e.g. furosemide actons on the NKCC2 transporter on the thick ascending limb to prevent reabsorption of Na, Cl and K (causes K loss due to ROMK)

190
Q

What are the side effects of loop diuretics?

A

hypokalaemia, metabolic alkalosis and hypovolaemia

191
Q

What are examples of thiazide diuretics?

A

Bendroflumethiazide

192
Q

Where do thiazide diuretics work?

A

They work on the DCT to inhibit the NaCl transporter causing decrease salt and water reabsorption

193
Q

What is an example of potassium sparing diuretics?

A

Spironolactone

194
Q

Where do potassium sparing diuretics work?

A

They work on the late distal tubule and inhibit the action of aldosterone and block sodium channels decreasing potassium excretion and increasing sodium excretion

195
Q

Where do osmotic diuretics (mannitol) work?

A

On the PCT to increase water excretion

196
Q

Where do carbonic anhydrase inhibitors work (acetazolamide)?

A

Proximal tubule by increasing secretion of HCO3, Na, K, and H2O

197
Q

What are the symptoms of nephrotic syndrome?

A

proteinuria, hypoalbuminuria, hypercholesterolaemia and oedema

198
Q

What are the symptoms of nephritic syndrome?

A

proteinuria and haematuria

199
Q

Does nephrotic or nephritic syndrome have a worse GFR?

A

Nephritic

200
Q

What are the types of GN that cause nephrotic syndrome?

A

membranous, minimal change, focal segmental glomerulosclerosis, mesangiocapillary, SLE, amyloid, diabetes, hepatitis

201
Q

What types of GN cause nephritic syndrome?

A

IgA nephropathy, mesangiocapillary, post strep, vasculitits, SLE, Anti-GBM, cyroglobulinaemia

202
Q

What is the most common GN?

A

IgA nephropathy

203
Q

What are the features of IgA nephropathy?

A

microscopic haematuria, increased IgA which forms immune complexes and deposits on mesangial cells of IgA and C3

204
Q

What blood pressure medication is okay to take with IgA nephropathy?

A

ACEi

205
Q

What is Henoch Schonlein purpura?

A

systemic variant of IgA nephropathy causing a small vessel vasculitis. Features are purpuric rash on extensor surfaces, polyarthritis, abdominal pain and nephritis

206
Q

How do you confirm the diagnosis of HSP?

A

IgA and C3 on immunofluoresence

207
Q

What are the classifications of SLE GN?

A

Class I: minimal mesangial lupus nephritis
Class II: mesangial lupus nephritis
Class III: focal proliferative lupus nephritis (<50%)
Class IV: diffuse proliferative lupus nephritis (>50%)
Class V: membranous lupus nephritis

208
Q

What is Goodpastures syndrome?

A

When there is anti-GBM antibobies to the type IV collagen of the basement membrane

209
Q

How does goodpastures syndrome present?

A

Haematuria and nephritic syndrome

210
Q

What is the treatment of goodpastures syndrome?

A

plasma exchange, steroids and cytotoxics

211
Q

What is post streptococcal GN?

A

a diffuse proliferative GN that occurs 1-12 weeks after a sore throat or skin infection. A streptococcal antigen is deposited on the glomerulus causing a host reaction and immune complex formation.

212
Q

What can be seen on immunofluoresence of streptococcal GN?

A

IgG and C3

213
Q

What is rapidly progressive GN?

A

proliferative GN characterised by acute deterioration of kidney function associate with cresent formation around the glomerulus. Most aggressive forms of GN

214
Q

What are the 3 categories of rapidly progressive GN?

A

Immune complex disease: post-infectious, SLE, IgA/HSP
Pauci-immune disease- Vasculitis related
Anti-GBM disease

215
Q

What is the presentation of rapidly progressive GN?

A

AKI with systemic features such as fever, myalgia, weight loss, haemoptysis, pulmonary haemorrhage

216
Q

What is the treatment of rapidly progressive GN?

A

Aggressive immunosuppression with high dose steroids IV and cyclophosphamide +/- plasma exchange

217
Q

What is the main cause of proteinuria?

A

injury to the podocyte

218
Q

What is the most common cause of GN in children?

A

Minimal change

219
Q

What is the treatment of Minimal change GN?

A

a trial of steroids or can resolve spontaneously

220
Q

Do you biopsy patients with GN?

A

Yes in adults but not in children

221
Q

Generally, what is the treatment of nephrotic syndrome?

A

Reduce oedema with loop diuretics, reduce proteinuria with ACEi, reduce risk of complications with statins and treat the underlying disease

222
Q

What are the features of minimal change disease?

A

Normal biopsy, electron microscopy shows effacement of the podocyte foot processess. they have nephrotic syndrome and frothy urine.

223
Q

What causes membranous nephropathy?

A

Usually idiopathic but can be due to malignancy, hep B, drugs (gold, penicillin, NSAIDs) and autoimmunity

224
Q

What does biopsy in membranous nephropathy look like?

A

diffusely thickened GBM with IgG and C3 subepithelial deposits

225
Q

What antibodies are found in those with idiopathic membranous nephropathy?

A

anti-PLA2

226
Q

What is mesangiocapillary GN?

A

Can be immune complex mediated or complement mediated.
Immune complex:driven by circulating immune complexes which deposit in the kidney and activate complement via the classical pathway
Complement: less common and involves persistent activation of the alternative complement pathway e.g. C3 nephritic factor

227
Q

What can be seen on biopsy in mesangiocapillary GN?

A

mesangial and endocapillary proliferation, a thickened capillary basement membrane, double contouring of the capillary walls

228
Q

What is FSGS?

A

Segments of glomeruli develop sclerosis. presents with nephrotic syndrome. 50% progress to renal failure

229
Q

What is seen on immunofluoresence of FSGS?

A

IgM and C3

230
Q

What is the treatment of FSGS?

A

Corticosteroids or cyclophosphamide or ciclosporin if resistant

231
Q

What is tubulointerstitial nephritis?

A

inflammation of the renal interstitium

232
Q

What causes acute interstitial nephritis?

A

immune reaction to drugs, infections or autoimmune disorders e.g. NSAIDs, antibiotics, diuretics, allopurinol, omeprazole, phenytoin, staph/strep, SLE, sarcoid

233
Q

What is the treatment of interstital nephritis?

A

stop the drug, conservative treatment and if not improved in a week then consider starting prednisolone

234
Q

What things are nephrotoxic?

A

Gentamicin, NSAIDs and contrast

235
Q

What is Rhabdomyolysis?

A

results from skeletal muscle breakdown with release of its contents into the circulation including myoglobin, potassium, urate and CK

236
Q

How does rhabdomyolysis cause AKI’s?

A

Myoglobin is filtered by the glomeruli and precipitates obstructing renal tubules

237
Q

What are the features of rhabdomyolysis?

A

muscle pain, swelling, tenderness and red-brown urine

238
Q

What confirms the diagnosis of rhabdomyolysis?

A

CK >1000, tea coloured urine, urinalysis +ve for blood

239
Q

What is the treatment of rhabdomyolysis?

A

Urgent treatment for hyperkalaemia, IV fluid rehydration is a priority to prevent AKI and sodium bicarbonate to alkalinse the urine

Year 2 (10 decks)

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