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Nephrology Flashcards

1
Q

How can we divide up the causes of AKI?

A

Prerenal
Lack of blood flow to the kidneys

Intrarenal
Intrinsic damage to the glomeruli, renal tubules or interstitium

Postrenal
Obstruction to the urine coming from the kidneys

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2
Q

What findings can be expected in AKI?

A

Reduced urine output (<0.5ml/kg/hour is termed oliguria)
Fluid overload
Rise in molecules that the kidney normally excretes/maintains balance of, e.g. potassium, urea and creatinine

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3
Q

Symptoms of AKI

A

Reduced urine output
Pulmonary/peripheral oedema
Arrhythmias (due to potassium levels)
Uraemia features (pericarditis/encephalopathy)

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4
Q

What should we test in all AKI patients?

A

U+Es

Urinalysis

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5
Q

When should we do a renal ultrasound in AKI?

A

If there’s no identifiable cause for the deterioration OR are at risk of a urinary tract obstruction

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6
Q

What commonly used drugs should be stopped in AKI?

A 
Metformin
Lithium
Digoxin
NSAIDs
Aminoglycosides
ACEi
Diuretics
Angiotensin II receptor antagonists
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7
Q

How should we treat hyperkalaemia should it arise in AKI?

A 
IV calcium gluconate
Combined insulin/dextrose infusion
Nebulised salbutamol
Loop diuretics
Calcium resonium
Dialysis (last line)
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8
Q

Blood supply of the kidneys?

A

Renal arteries + veins

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9
Q

What is the normal blood urea nitrogen (BUN):creatinine ratio?

A
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10
Q

Causes of pre-renal AKI

A

Decreased bloodflow due to:

Absolute loss of fluid -
Major haemorrhage
Vomiting
Diarrhoea
Severe burns

Relative loss of fluid -
Distributive shock
Congestive heart failure (blood pools in the venous system)

Local to the kidney -
Renal artery stenosis
Embolus

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11
Q

What is azotemia?

A

High levels of nitrogen containing blood

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12
Q

What happens to the RAAS system during AKI?

A

Kidneys activate the RAAS, causing adrenal glands to secrete aldosterone which tells the kidneys to reabsorb sodium

Sodium reabsorption results in increased water reabsorption AND urea reabsorption

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13
Q

Is urine more concentrated in pre-renal AKI?

A

Yes. There is more urea relative to water than usual

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14
Q

What is the BUN:creatinine ratio in pre-renal AKI?

A

> 20:1

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15
Q

What is the most common cause of intrarenal AKI?

A

Acute tubular necrosis:

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16
Q

What are causes of acute tubular necrosis?

A 
Ischaemia to the tubular cells
Nephrotoxins:
Aminoglycosides
Heavy metals (e.g. lead)
Myoglobin (from damaged muscle)
Ethylene glycol (anti-freeze)
Radiocontrast dye
Uric acid (tumour lysis syndrome during cancer treatment)
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17
Q

How can you prevent uric acid causing tubular necrosis during cancer treatment?

A

Make sure they stay well hydrated
Give medications: allopurinol, urate oxidase

Trying to reduce the effects of tumour lysis syndrome

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18
Q

What happens to the tubule during acute tubular necrosis?

A

For whatever reason there is cell death. These cells then go into the tubule lumen and plug the tubule. This increases the pressure and makes it harder for fluid to flow down the tubules, reduced eGFR

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19
Q

What do you get a build up of in the blood during acute tubular necrosis resulting in AKI?

A

Acid (metabolic acidosis)

Hyperkalaemia

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20
Q

What might you find in the urine of someone with an acute tubular necrosis?

A

Brown grannular casts (these are the clumps of dead cells from the necrosis)

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21
Q

What is glomerulonephritis?

A

Inflammation of the glomerulus causing a reduction in eGFR. It is often caused by the deposition of antigen-antibody complexes in glomerular tissue

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22
Q

What do the antigen-antibody complexes activate in glomerulonephritis?

A

The complement system. This then attracts macrophages and neutrophils to the site. These release lysosomal enzymes which then damage podocytes in the glomerulus

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23
Q

Function of podocytes

A

They are negatively charged and have small gaps in between them. As a result larger molecules cannot get through.

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24
Q

What happens when podocytes are damaged (e.g. by lysosomal enzymes from neutrophils etc.)

A

They allow larger molecules to pass through (e.g. proteins and red cells)
Fluid leakage also reduces pressure difference which means lower GFR
This causes fluid build up and therefore oedema and HTN

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25
Q

Which condition affecting the interstitium can cause AKI?

A

Acute interstitial nephritis

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26
Q

Pathology of acute interstitial nephritis

A

Type I or type IV hypersensitivity reaction, usually in response to medications: NSAIDs, penicillins, diuretics.

These cause infiltration of immune cells (neutrophils, eosinophils) which cause inflammation of the interstium

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27
Q

Symptoms of acute interstitial nephritis?

A

Oliguria
Eosinophiluria
Fever
Rash

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28
Q

Complications of acute interstitial nephritis + cause?

A

If you don’t stop the medications causing interstitial nephritis, you can get renal papillary necrosis

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29
Q

Symptoms of renal papillary necrosis?

A

Haematuria

Flank pain

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30
Q

Causes of renal papillary necrosis?

A

Untreated acute interstitial nephritis
DM
Sickle cell disease
Pyelonephritis

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31
Q

What can cause obstruction to the outflow (postrenal AKI)?

A

Compression:
BPH
Intra-abdominal tumors

Blockage:
Kidney stones

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32
Q

Pathology of post-renal AKI?

A

Fluid backs up in post-renal AKI reducing the difference between the pressure between the tubule/glomerulus, thus reducing GFR

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33
Q

Longer-term effects of post-renal AKI?

A

Increased pressure in the renal tubule over time causes damage to the epithelial cells, reducing the amount of reabsorption of urea/sodium into the blood.
This then makes the urine higher in urea and thus the BUN:creatinine ratio falls
Damage to these epithelial cells also reduces the amount of water reabsorbed, and thus you start to produce less concentrated urine.

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34
Q

What are renal cysts?

A

Fluid filled sacs found in the kidney

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35
Q

How can we classify renal cysts?

A

Simple
Well-defined, homogenous features
Very common in older patients (50% prevalence over 50)

Complex
Complicated structures - thick walls, septations, calcification, heterogenous enhancement on imaging
Risk of malignancy

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36
Q

Risk factors for renal cysts?

A

Increasing age
Smoking
HTN
Male

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37
Q

What is polycystic kidney disease?

A

An autosomal dominant kidney caused by PKD1 or PKD2 genes. They result in individuals having multiple renal cysts

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38
Q

What is polycystic kidney disease associated with?

A

Berry aneurysm formation, leading to subarachnoid haemorrhage
Mitral valve disease
Liver cysts

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39
Q

Clinical features of renal cysts?

A

Usually asymptomatic
Can cause flank pain/haematuria if they rupture/become infected
Can also present with HTN/flank mass

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40
Q

What is the main differential of a renal cyst?

A

Renal cell carcinoma should be ruled out

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41
Q

How do we investigate renal cysts?

A

CT/MRI imaging both with and without IV contrast

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42
Q

What scoring system can we use for renal cysts?

A

Bosniak scoring system

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43
Q

Management of cysts?

A

If asymptomatic, no follow up required
Symptomatic simple renal cysts - simple analgesia +/- needle aspiration
Complex cyst - bosniak stage + continued surveillance/potential surgical intervention

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44
Q

Where do simple renal cysts originate from?

A

Renal tubule epithelium

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45
Q

Diagnostic criteria for autosomal dominant polycystic kidney disease?

A

US showing:
Two cysts (<30 y.o)
Two cysts in both kidneys (30-59 y.o)
Four cysts in both kidneys (aged >60)

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46
Q

Treatment for adpkd?

A

Tolvaptan (vasopressin receptor 2 antagonist)

47
Q

What typically causes pyelonephritis?

A

Ascending infection typically from e. coli

48
Q

Features of pyelonephritis

A 
Fever
Rigors
Loin pain
Vomiting
White cell casts in urine
49
Q

Management of pyelonephritis?

A

Broad-spectrum cephalosporin or quinolone (floxacins) for 10-14 days

50
Q

Investigations in pyelonephritis?

A

Mid-stream urine sample or catheter specimen of urine and culture
You can do a urine dip to check for leukocytes and nitrites though this isn’t that necessary

51
Q

Two names of kidney stones?

A

Urolithiasis (formation of stones in the urinary tract)
Nephrolithiasis (formation of stones in the nephron)

Guess renal calculi etc are also names

52
Q

Where are the sites of ureteric constriction (where stones can get lodged)

A

Periureteric junction
Pelvic brim
Vesicoureteric junction

53
Q

Formation of kidney stones?

A

Crystal like structures can be formed from electrolyte clusters. These usually pass in the urine but they can get larger and form a kidney stone which obstructs the tubule

54
Q

What is renal colic caused by?

A

Pressure from the kidney stone on the renal tubules, causing pain
Also from the inflammatory response to the renal stones

55
Q

Do you get a build up of pressure distal or proximal to the site of obstruction?

A

Proximal

56
Q

What is hyperperistalsis?

A

This is where you get oedema proximal to the site of obstruction
The tubule then contracts more vigorously to try get rid of the stone

57
Q

Risk factors for developing a renal stone?

A 
High protein diet
High salt intake
Obesity
Dehydration
Drugs (antacids)

These all result in urine saturation with products that are used to make these crystals (stones)

58
Q

Give 2 examples of stone formation inhibitors?

A

Citrate

Magnesium

59
Q

Name the 5 types of renal calculi

A 
Calcium oxalate (80%)
Calcium phosphate
Uric acid
Struvite
Cystine
60
Q

Investigations in renal calculi?

A 
FBC
CRP
Magnesium calcium phosphate levels
Urinalysis
24hr urine electrolyte etc. levels (calcium, oxalate, urate, cystine etc.)
X-ray
Ultrasound
CT
61
Q

What might you see on ultrasound in renal calculi?

A 
Acoustic shadowing (blocks out part of the wall with a shadow)
Hydronephrosis if it is in the ureter (backflow of urine proximally)
62
Q

Acute management of renal calculi?

A

Analgesia
Antiemetic
IV fluids

<0.5cm
Passes spontaneously

Surgical

63
Q

What is percutaneous nephrostomy?

A

Placement of a catheter into the kidney to drain urine out if there’s obstruction (this is symptomatic relief)

64
Q

What is ureteric stent insertion?

A

Rod up through the urethra, up through bladder/ureter up to the point of obstruction. Can then put in a stent to help urine bypass the obstruction

65
Q

What is percutaneous nephrolitheotomy?

A

Removal of the stone from the kidney through a puncture wound

66
Q

What is extracorporeal shock wave lithotripsy?

A

This uses focused shock waves to allow easy passage of the stone out through the urine.

67
Q

What are bladder stones?

A

Small mineral deposits that can form in the bladder, usually only when the urine is very concentrated or when one is dehydrated

68
Q

How do bladder stones present?

A

Lower abdo pain (can refer to back)
Painful urination
Blood in the urine
Nausea/vomiting/chills

69
Q

What is the management of bladder stones?

A

Usually just drink lots of fluids to facilitate passage

If larger, may need to be fragmented by: laser lithotripsy or ultrasonic energy. Can sometimes need open cystotomy

70
Q

What is cystolithotomy?

A

A treatment for bladder stones in which an incision is made and the stone is removed

71
Q

What are jackstone calculi?

A

Urinary calculi that are almost always made of calcium oxalate. Located in the bladder, they have the appearance of jack toys

72
Q

CKD stages

A 
1 - >90ml/min
2 - 60-90ml/min
3a - 45-59ml/min
3b - 30-44ml/min
4 - 15-29ml/min
5 - <15ml/min (this is the level for dialysis/kidney transplant)
73
Q

What causes CKD?

A 
HTN
Chronic pyelonephritis
Chronic glomerulonephritis
Diabetic nephropathy
Adult polycystic kidney disease
74
Q

How do we manage CKD?

A

Lifestyle changes
Drugs (to manage associated symptoms)
Dialysis
Kidney transplant

75
Q

Lifestyle changes in CKD

A 
Stop smoking
Restrict salt intake
Exercise (150 mins/week)
Limit alcohol
Lose weight
76
Q

Medicines in CKD

A

BP control drugs (ACEi are first line, can use furosemide as well)
Statins (hyperlipidaemia)
Iron/erythropoetin/darbepoetin (for anaemia)
Calcium carbonate/acetate (to reduce blood phosphate)
Vitamin D (colecalciferol)

77
Q

What are the 3 types of renal replacement therapy?

A

Haemodialysis
Peritoneal dialysis
Renal transplant

78
Q

What is required for haemodialysis?

A

Creation of an arteriovenous fistula at least 8 weeks before treatment

79
Q

What is peritoneal dialysis?

A

This is where filtration occurs within the patient’s abdomen
Dialysis solution is injected into the abdomen via a permanent catheter
High levels of dextrose in the cavity draws waste products from the blood into the abdominal cavity
After several hours, the fluid is then drained.

^ This describes CAPD

80
Q

What are the two types of peritoneal dialysis?

A

Continuous ambulatory peritoneal dialysis (CAPD)

Automated peritoneal dialysis (APD) - a machine fills and drains the abdomen whilst the patient sleeps

81
Q

Where is the site/what is the blood supply in a renal transplant?

A

Inserted into the groin

Renal vessels connect to the external iliac vessels

82
Q

What must patients have for life following a renal transplant?

A

Immunosuppressants

83
Q

What complications might you see in haemodialysis?

A 
Site infection
Endocarditis
Stenosis at the site
Hypotension
Cardiac arrhythmia
Disequilibrium syndrome
84
Q

What is dialysis disequilibrium syndrome?

A

Occurrence of neurological signs and symptoms shortly after dialysis (papilloedema, focal neurological deficits)

Treatment of this is avoidance (i.e. no dialysis)

Make sure dialysis is a gradual process to lower risk of disequilibrium syndrome

85
Q

What are complications of peritoneal dialysis?

A 
Peritonitis
Sclerosing peritonitis
Catheter infection
Catheter blockage
Constipation
Fluid retention
Hyperglycaemia
Hernia
Back pain
Malnutrition
86
Q

What are the complications of renal transplants?

A

Graft rejection
Opportunistic infections
Malignancy (lymphona/skin cancer)
DVT/PE (surgery, duh)

87
Q

What is nephritic syndrome?

A

Haematuria (red cell casts - indicating glomerular damage)
Proteinuria (less than 3.5g/24hrs though)
HTN
Low urine volume <300ml

88
Q

What is nephrotic syndrome?

A

Massive proteinuria >3.5g/day
Hypoalbuminaemia <30g/L
Hyperlipidaemia
Oedema

89
Q

Which glomerulonephridites cause nephrotic syndrome?

A

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis
Membraneous glomerulonephritis

90
Q

Which conditions can cause a secondary nephrotic syndrome?

A 
SLE
Hep B and C
HIV
DM
Malignancy
91
Q

What is the pathophysiology of nephritic syndrome?

A

Inflammatory response WITHIN the glomeruli causing glomerular basement membrane disruption

92
Q

What is the pathophysiology of nephrotic syndrome?

A

Structural damage to the glomerular filtration barrier causing massive renal loss of protein

93
Q

What are the glomerulonephridites that cause nephritic syndrome?

A

Poststreptococcal glomerulonephritis
IgA nephropathy (Berger’s disease)
Rapidly progressive glomerulonephritis (crescentic)

94
Q

Other conditions that cause nephritic syndrome?

A 
Goodpasture's
Wegener's granulomatosis
Churg-strauss
Henoch-schonlein purpura
Alport syndrome
95
Q

What is the most common type of renal cancer?

A

Renal cell carcinoma

96
Q

What are renal cell carcinomas?

A

An adenoma of the renal cortex

They make up 85% of all renal malignancies

97
Q

Symptoms of renal cell carcinoma?

A

Haematuria (50%)
Loin pain (40%)
Mass (30%)

98
Q

Investigations in renal cell carcinoma?

A

CT scan

99
Q

Treatment for renal cell carcinoma?

A

If <7cm (i.e. T1), partial nephrectomy

If >7cm (i.e. T2), radical nephrectomy

100
Q

What is a transitional cell carcinoma?

A

A cancer that typically occurs in the lower urinary tract - makes up 90% of all lower urinary tract cancers
It can affect the kidney, but only makes up 10% of these

101
Q

Presentation of transitional cell carcinoma

A

Painless haematuria in 80% of cases

102
Q

How do we diagnose transitional cell carcinoma?

A

CT IVU (intravenous urogram)

103
Q

Treatment for transitional cell carcinoma?

A

Radical nephroureterectomy

104
Q

What is renal tubular acidosis?

A

This is a condition in which the kidneys fail to adequately acidify the urine

105
Q

What are the two ways in which we can acidify the urine?

A

Reabsorption of bicarbonate in the proximal tubule

Secretion of hydrogen ions in the distal tubule

106
Q

Is the problem usually proximal or distal in RTA?

A

Classically it is distal (i.e. can’t secrete enough H+ into the urine)

107
Q

What are the 4 types of RTA?

A

Type I - Distal
Type II - Proximal
Type III - Combined
Type IV - Aldosterone related

108
Q

How do we treat type I RTA?

A

Correct hypokalaemia

Chronic - oral bicarbonate

109
Q

What is hydronephrosis

A

Swelling of the kidney due to urine failing to drain from kidney to bladder

110
Q

Causes of unilateral hydronephrosis

A 
PACT
Pelvic-ureteric obstruction
Aberrant renal vessels
Calculi
Tumours
111
Q

Causes of bilateral hydronephrosis

A 
SUPER
Stenosis of urethra
Urethral valve
Prosatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis
112
Q

Investigations in hydronephrosis

A

Ultrasound

CT Intravenous urogram - assess position of obstruction

113
Q

Management of hydronephrosis

A

Remove the obstruction
Nephrostomy tube
Ureteric stent

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