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Year 3 - Medicine > Week 13 - Renal Disease > Flashcards

Week 13 - Renal Disease Flashcards

1
Q

What are the three groups of causes of AKI?

A

Pre-Renal (Hypovolaemia)
Renal
Post-Renal (Obstructive)

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2
Q

What causes 90% of AKIs?

A

Pre-renal (most common) or Post-renal causes

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3
Q

How is AKI staged?

A

By rise in serum creatinine or reduction in urine output.

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4
Q

What is the mortality of AKI Stage 3 in hospital?

A

30%

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5
Q

What is a pre-renal cause of AKI?

A

Inadequate blood supply to the kidney - can be due to
hypovolaemia,
decreased CO,
dehydration,
hypotension,
arterial occlusion (atherosclerosis, thromboembolic disease, renal artery dissection),
ACEIs, ARBs or NSAIDs,
renal vasoconstriction (NOR)

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6
Q

Which Ps are more at risk of AKI?

A
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7
Q

What are the intrinsic renal causes of AKI?

A

Glomerulonephritis
Small Vessel Vasculitis
Interstitial Nephritis
Acute Tubular Necrosis (Ischaemic or Nephrotoxic)
Renal Vascular Disease (rare)
Also -
Myeloma
Rhabdomyoloysis

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8
Q

What investigations should you do for an AKI assessment?

A

BP = are they hypo / hyper perfused?
Fluid status - dry / overloaded?
Urine dipstick - look for blood or protein - can indicate intrinsic cause
Imaging - USS or CT

Renal Screening -
Serum & Urine Electrophoresis - looking for amyloid
Immunoglobulins
Blood film - look for haemolysis
Calcium - Ps will often have high calcium
ANA, ANCA, GBM ABs
Complement levels - if you suspect lupus or infection
Cryoglobulins

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9
Q

Which guidelines are used for diagnosing and treating AKI?

A

STOP AKI

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10
Q

What is ANA antibody used to indicate?

A

Lupus

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11
Q

What disease is diagnosed with ANCA antibodies?

A

Vasculitis

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12
Q

What are the management steps you can take for AKI?

A

Fluid rehydration if pre-renal AKI

Stop nephrotoxic medications (ACEIs, ARBs, Abx = penicillin, gent, vanc, NSAIDs

Relieve obstruction if post-renal cause

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13
Q

What complications can result from AKI?

A

Hyperkalaemia
Fluid overload, HF, pul oedema
Metabolic acidosis
Uraemia -> encephalopathy or pericarditis

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14
Q

What can lots of blood but nothing else on dipstick indicate?

A

Post-renal obstruction or myoglobinuria (rhabdomyolysis)

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15
Q

What would a pre-renal cause of AKI show on urine dipstick?

A

No substantial blood or protein

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16
Q

How can you differentiate between glomerulonephritis and interstitial nephritis by dipstick?

A

GN = lots of blood and protein, no WBCs

IN = less blood + protein, WBCs present

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17
Q

What can cause lots of blood and protein but not WBCs on urine dipstick?

A

Glomerulonephritis
ANCA Vasculitis
Anti-GBM Lupus
Infections - Hep B/C, HIV

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18
Q

What is nephritic syndrome?

A

Symptoms of an inflamed kidney that has
- blood in urine (microscopic or macroscopic)
- protein in urine (less than 3g per 24hr)
- oliguria

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19
Q

What are the causes of glomerulonephritis?

A

Also minimal change disease
Goodpasture syndrome

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20
Q

What is a life threatening complication of vasculitis?

A

Pulmonary-renal syndrome - can get pulmonary haemorrhage and AKI

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21
Q

Which disease has anti-glomerular basement membrane antibodies that attack the glomerulus and pulmonary basement membranes? Can cause glomerulonephritis and pulmonary haemorrhage? - i.e. Acute AKI and haemoptysis

A

Goodpasture Syndrome

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22
Q

What will histology show for rapidly progressive glomerulonephritis?

A

Crescentic glomerulonephritis

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23
Q

Which antibody is associated with vasculitis?

A

ANCA antibody

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24
Q

What is an umbrella term for conditions that cause inflammation of or around the glomerulus.

A

Glomerulonephritis

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25
Q

What is the term of inflammation of the space between the cells and the tubules within the kidney?

A

Interstitial nephritis

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26
Q

What is pathological scarring of the tissue in the glomerulus called?

A

Glomerulosclerosis

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27
Q

What can hyperkalaemia do to ECGs?

A

Can caused depressed ST segment, biphasic T waves, Tall Waves, Long PR interval and wide QRS duration

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28
Q

When should urgent treatment for hyperkalaemia be carried out?

A

K > 6 + ECG changes

OR

K > 6.5 regardless of ECG

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29
Q

In urgent hyperkalaemia what is the Rx that should be given?

A

First give calcium gluconate/chloride - is cardioprotective and stabilises the membranes of the heart cells.

Then give Insulin + Dextrose + Salbutamol - drives K into cells.

If acidotic - correct with bicarbonate

Stop any medications exacerbating the hyperkalaemia

Furosemide if overloaded

Dialysis

Can give K binders (Lokelma)

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30
Q

When should dialysis or haemofiltration be given for AKI?

A

If there is refractory hyperkalaemia (>7)

If ph <7.2 & bicarb <12

If pulmonary oedema & persistent anuria

If uraemia >30mmol

AEIOU
A = Acidosis (severe and not responding)
E = Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I = intoxication (OD certain medications)
O = oedema (severe and unresponsive pul oedema)
U = uraemia Sx - seizures or reduced consciousness

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31
Q

What is the definition of CKD?

A

Abnormal kidney function for >3m

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32
Q

Which Ps are at risk of CKD?

A

DM = biggest cause of CKD

HT = second largest cause of CKD

Age related decline
Glomerulonephritis
PKD
Meds - NSAIDs, PPIs, Lithium

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33
Q

Which is better for proteinuria measurement - ACR or PCR?

A

ACR - detects early stages of CKD better. Measures albumin:creatinine rather than protein:creatinine

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34
Q

What are possible S&S of CKD?

A

Normally asymptomatic and diagnosed incidentally.

Can also get
- itching
- loss of appetite
- nausea
- oedema
- muscle cramps
- peripheral neuropathy
- pallor
- HT

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35
Q

What are the different GFRs for staging CKD?

A

Stage 1 = >90
Stage 2 = 60-90
Stage 3a = 45-60
Stage 3b = 30-45
Stage 4 = 15-30
Stage 5 = <15

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36
Q

If a diabetic patient has diabetic retinopathy, what is it also likely that they have?

A

Diabetic nephropathy

This is because high levels of glucose passing through the glomerulus causes scarring (glomerulosclerosis).

=> Proteinuria - due to damage to the glomerulus allowing protein to pass through the barrier into the urine.

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37
Q

What are the possible complications of CKD?

A

Anaemia
Renal bone disease
CVD
Peripheral neuropathy

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38
Q

What are the aims of management of CKD?

A

Slow progression of disease
Reduce risk of CVD
Reduce risk of complications & treat any

Optimise diabetic control and hypertensive control if needed

Treat glomerulonephritis

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39
Q

What drug is used to treat metabolic acidosis?

A

Sodium bicarbonate

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40
Q

What is used to treat anaemia in CKD?

A

Iron supplementation + erythropoietin

EPO given because damaged kidney cells = drop in EPO production.

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41
Q

What is used to treat renal bone disease?

A

Vitamin D

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42
Q

How can renal bone disease show on Xray?

A

Can get sclerosis of the ends of vertebrae (denser white) and osteomalacia in the centre of the vertebra (rugger jersey spine)

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43
Q

What happens to P in CKD?

A

Can get high serum P due to reduced excretion

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44
Q

Why can CKD lead to secondary hyperparathyroidism?

A

Damaged kidneys = less Vit D converted => low serum calcium.

Parathyroid gland react to this (and the high P levels) by excreting more parathyroid hormone => inc osteoclastic activity.

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45
Q

What Rx can be given for renal bone disease?

A

Active forms of Vit D
Low P diet
Bisphosphonates can be used to Rx any osteoporosis.

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46
Q

What Sx does nephrotic syndrome usually present with?

A

Oedema
Proteinuria - may get frothy urine - >3.5h of protein
Hypoalbuinaemia (<30g)

May get associated high cholesterol (as liver tries to produce more albumin) and inc tendency to thrombus

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47
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

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48
Q

What hereditary renal diseases can cause CKD?

A
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49
Q

What is the most common treatment for most types of glomerulonephritis?

A

Immunosuppression
Blood pressure control

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50
Q

What mechanisms in the body can CKD interfere with?

A

Sodium and water balance -> HT and HF

Potassium balance

Elimination of nitrogenous waste stopped = uraemia

Erythropoietin -> anaemia

Acid-base balance - no buffering = acidosis

Activation of Vit D & decreased P elimination = renal bone disease

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51
Q

What are the options for renal replacement therapy?

A

Transplantation
Peritoneal dialysis
Haemodialysis

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52
Q

At what GFR would you start looking at renal replacement therapy?

A

GFR <20

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53
Q

If you have hypoalbuminaemia but no proteinuria - what are the possible causes?

A

HF
Thyroid disease
Cirrhosis
Infections
IBD
Malnutrition

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54
Q

What are the associated features with nephrotic syndrome?

A
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55
Q

What are the most common causes of nephrotic syndrome in adults?

A

Glomerulosclerosis
Membranous Nephropathy

Can also be associated with AI conditions such as Lupus and Sarcoidosis

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56
Q

How is nephrotic syndrome treated?

A

ARBs or ACEIs
Statins
Diuretics
Treat infection

If albumin <35, dose with anticoagulation

May need high dose steroids / immunosuppressants

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57
Q

When should ACEIs be started in Ps with diabetic nephropathy?

A

Immediately = even if they have normal BP

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58
Q

What causes acute tubular necrosis?

A

Ischaemia or toxins - damage the kidney cells.

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59
Q

ATN can be reversible - how long does it take for cells to regenerate?

A

7-21 days

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60
Q

Which drugs are nephrotoxic and can cause ATN?

A

Contrast
Gentamicin
NSAIDs
Lithium
Heroin

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61
Q

How is ATN managed?

A

Same as any other AKI - fluids, stop nephrotoxic meds and treat complications

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62
Q

Which disease causes thrombosis in the small blood vessels in the body -> haemolytic anaemia, AKI & low platelet count (thrombocytopenia)?

What causes this?

A

Haemolytic uraemic syndrome

Caused by shiga toxin from E.coli 0157 or from shigella

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63
Q

When myocytes die in rhabdomyolysis - what is released into the blood stream?

A

Myoglobin (toxic to kidney -> AKI)
K (-> cardiac arrhythmias)
P
CK

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64
Q

What are the S&S of rhabdomyolysis?

A

Muscle aches and pain
Oedema
Fatigue
Confusion
Red-brown urine (from myoglobulin)

65
Q

What is the Rx of rhabdo?

A

IV fluids - encourage filtration of breakdown products

IV sodium bicarb - make urine more alkaline and reduce toxicity of myoglobin on kidneys

IV mannitol - can inc GFR and reduce oedema

66
Q

Why do ARBs cause pre-renal injury?

A

ARBs block the action of angiotensin II by binding to the angiotensin II type 1 (AT1) receptors.

Normally, angiotensin II constricts the efferent arterioles (the blood vessels exiting the glomeruli) more than the afferent arterioles (the blood vessels entering the glomeruli), which helps maintain glomerular filtration pressure and thus the glomerular filtration rate (GFR).

By blocking the effect of angiotensin II, ARBs cause dilation of the efferent arterioles. This can lead to a reduction in the intraglomerular pressure, thereby decreasing the GFR.
In patients with conditions that already compromise renal perfusion (e.g., dehydration, heart failure, or significant renal artery stenosis), this reduction in GFR can be substantial enough to precipitate pre-renal AKI.

In situations where renal perfusion is compromised, the body typically increases angiotensin II levels to help maintain GFR by preferentially constricting efferent arterioles.
When ARBs inhibit this compensatory mechanism, the kidneys’ ability to maintain adequate GFR in the face of reduced renal blood flow is impaired, leading to pre-renal AKI.

67
Q

What is the most common renal cause of AKI? (not pre or post renal cause)

A

ATN

68
Q

What is the most common causes of acute interstitial nephritis?

A

Drugs - NSAIDs / penicillins
Infection - TB
Immune mediate - SLE, sarcoidosis

69
Q

What are the Sx of a pre-renal AKI?

A

Severe dehydration Sx

70
Q

Which antibody should you test for for Lupus?

A

Serum dsDNA antibody

71
Q

What is visible blood in the urine more indicative of?

A

A post renal AKI

72
Q

What do red casts on urine microscopy indicate?

A

Glomerular disease

73
Q

What can Coca Cola urine indicate?

A

Nephritic syndrome - protein and fat present in the blood

74
Q

What is the difference between nephrotic and nephritic syndrome?

A

Nephrotic syndrome = high proteinuria (>3.5g/day) + oedema + hypoalbuminemia + hyperlipidemia (The liver increases lipoprotein synthesis in response to hypoalbuminemia.)

Nephrotic syndrome results from damage to the glomerular filtration barrier, which includes the endothelial cells, glomerular basement membrane, and podocytes (specialized epithelial cells). This damage leads to increased permeability and excessive loss of proteins in the urine.

Causes = minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, DM, SLE, amyloidosis, infections (HIV & Hep B&C).

Nephritic syndrome = haematuria (Blood in the urine is a hallmark due to the rupture of glomerular capillaries), proteinuria (less than nephrotic), HT, reduced GFR.

Nephritic syndrome results from inflammatory damage to the glomeruli, leading to hematuria and a reduced glomerular filtration rate (GFR).

Causes inc post-infectious glomerulonephritis (often following strep - immune complexes deposit in the glomeruli), IgA Nephropathy (Berger’s disease), rapidly progressive glomerulonephritis (Goodpastures, systemic vasculitis), Lupus.

75
Q

How are podocytes in the glomerulus damaged?

A

Damage to podocytes can come from release of inflammatory mediators, pressure & immunoglobulin deposition

Damage by release of factors from T-cells causes effacement - the podocytes flatten out - barrier breaks down and allows proteins and RBCs to appear in Bowman’s capsule.

76
Q

What causes hypertensive nephropathy?

A

Atherosclerosis = arteries into kidney become thickened and narrowed - less blood reaches the glomerulus.

Over time - causes immune cells within mesangium (macs & foam) to secrete growth factors -> mesangial proliferation. Mesangial cells regress to mesangioblasts - secrete ECM (collagen etc) -> glomerulosclerosis

77
Q

How does diabetes affect the glomerulus?

A

Excess glucose in blood = non-enzymatic glycation

Glucose sticks to plasma proteins - causes toxicity and thickening of BM esp in efferent arteriole -> obstruction -> response is dilation of afferent arteriole - incs pressure in glomerulus -> over time leads to hyperfiltration injury.

Mesangial cells proliferate - secrete ECM - glomerulus becomes thickened and end up with nodular glomerulosclerosis.

Difference between hypertensive and diabetic glomerulonephropathy = diabetic is more nodular - doesn’t affect the whole of the glomerulus.

78
Q

What is the pathophysiology of ATN?

A

Cells die - end up with leakage of filtrate into substance of kidney - causes inflammatory reaction.

As the cells die = debris = obstruction to tubules - causes backleak into glomerulus and leakage from there into interstitium.

Inducting event = MI, bleed, - lowers BP - lowers GFR = hypoxic changes in tubules - extends by inflammatory response.

Corticomedullary nephrons affected the most - have the most precarious blood supply.

Maintenance = fix underlying problem, reverse hypoxia - give cells a chance to repair and proliferate - can restore renal function.

79
Q

What can cause interstitial nephritis?

A

Most common = drugs - NSAIDs, diuretics, ABx

80
Q

What are the stages of AKI in terms of creatinine baseline?

A

Stage 1 = Creatinine 1-2 x baseline
Stage 2 - 2-3
Stage 3 - >3

81
Q

When should you think about renal replacement therapy?

A
82
Q

How can you tell whether a P has acute or chronic CKD?

A

Acute - acidotic, unwell, normal Ca and normal kidney size

Chronic = well, low Ca, high PTH, small kidneys

83
Q

What lifestyle advice should Ps with CKD be given?

A
84
Q

When do Ps with ADPKD tend to become symptomatic?

A

30s - 40s

85
Q

When do Ps with ARPKD become symptomatic?

A

Infancy

86
Q

From which part of the kidney is classified as post-renal?

A

Anything beyond the nephron

87
Q

What is a dilated intrarenal collecting system called?

A

Hydronephrosis

88
Q

What causes hydropnephrosis and hydroureter?

A

Obstruction

89
Q

Why is urinary tract obstruction an emergency?

A

Because you get obstructive atrophy in a relatively short amount of time - which can lead to unrecoverable renal function.

Glomeruli can survive but the nephrons become scarred and non-functioning.

90
Q

What are the symptoms of urinary tract obstruction?

A
91
Q

Which mode of imaging is best for looking for stones?

A

CT

92
Q

What is dynamic renography of the kidneys called?

A

MAG3 Renography

93
Q

How is acute kidney obstruction treated?

A

Percutaneous nephrostomy

Radiologists pass needle to inside of kidney - can feed guide wire and leave tube hanging out - decompress kidney, let infection settle and let it recover.

94
Q

What can cause obstructions in the urinary system?

A
95
Q

What is the most common type of urinary tract stone?

A

Calcium oxalate and phosphate

96
Q

What composition are staghorn stones?

A

Ca, Mg & ammonium phosphate

97
Q

What are stones made from when associated with gout?

A

Uric acid

98
Q

What are the symptoms of ureteric colic?

A
99
Q

What is the commonest cancer of the bladder and ureter?

A
100
Q

What treatments can be given for urinary retention?

A
101
Q

What type of medication is tamsulosin?

A

α blocker

102
Q

What type of medications are finasteride and dutasteride?

A

5 α reductase inhibitors

inhibit further growth of BPH, reduce rate of growth by blocking conversion of testosterone.

103
Q

What procedures can be carried out for BPH?

A

HoLEP
TURP

104
Q

What are possible Sx of prostate cancer?

A

Haematuria
LUTS
Haematospermia
Bone pain if mets
Bladder outflow obstruction with AKI (rare)
Elevated PSA

105
Q

Do urethral strictures cause obstructive nephropathy?

A

Rarely

Can cause difficulty emptying but rarely cause high pressures in the bladder.

106
Q

What is the most common cause of end stage renal disease?

A

Diabetic nephropathy

107
Q

What term is used to define clinical conditions in which heart and kidney dysfunction overlap?

A

Cardio-renal syndrome

108
Q

How can dysfunction in the heart cause dysfunction in the kidney?

A

Type 1: Acute Cardio-Renal Syndrome
○ Primary Issue: Acute heart dysfunction (e.g., acute heart failure, acute myocardial infarction)
○ Secondary Effect: Acute kidney injury (AKI)
○ Mechanism: Reduced cardiac output leads to decreased renal perfusion, causing AKI. Additionally, high central venous pressure due to heart failure can increase renal venous pressure, impairing kidney function.

Type 2: Chronic Cardio-Renal Syndrome
○ Primary Issue: Chronic heart dysfunction (e.g., chronic heart failure)
○ Secondary Effect: Chronic kidney disease (CKD)
○ Mechanism: Chronic reduction in cardiac output leads to long-term decreased renal perfusion and progressive kidney damage. Neurohormonal activation (e.g., RAAS, sympathetic nervous system) exacerbates renal dysfunction.

109
Q

How can kidney dysfunction cause heart dysfunction?

A

Type 3: Acute Reno-Cardiac Syndrome
○ Primary Issue: Acute kidney injury
○ Secondary Effect: Acute heart dysfunction (e.g., acute heart failure, arrhythmias)
○ Mechanism: AKI leads to fluid overload, electrolyte imbalances (e.g., hyperkalemia), and increased levels of uremic toxins, all of which can adversely affect cardiac function.

Type 4: Chronic Reno-Cardiac Syndrome
○ Primary Issue: Chronic kidney disease
○ Secondary Effect: Chronic heart dysfunction (e.g., chronic heart failure)
○ Mechanism: CKD leads to chronic volume overload, hypertension, anemia, and mineral metabolism disorders, all of which can contribute to cardiac remodeling and heart failure.

Renal dysfunction can lead to metabolic derangements -> systemic inflammation and microvascular dysfunction = can cause cardiomyocyte stiffening, hypertrophy and interstitial fibrosis.

110
Q

How is cardio-renal syndrome classified?

A

T1 - Acute cardiac
T2 - Chronic cardiac

T3 - Acute renal
T4 - Chronic renal

T5 - Systemic illness fucking both organs at once

111
Q

What can be the result of prolonged diuretic use?

A

Can lead to decrease in ANP + diuretic resistance - which requires higher doses of diuretics which Ps can resist

112
Q

Why can hyponatremia occur in severe HF?

A

Due to inc fluid levels in the body diluting the levels of Na in the serum

113
Q

How can ACEIs damage the kidney?

A

Stop AGTI to AGTII (potent vasoconstrictor).
AGTII - constricts the efferent arterioles (maintaining GFR) - thus ACEIs cause dilation of efferent arterioles - reducing glomerular pressure and GFR - can decrease kidney function - can be damaging if already have compromised kidney perfusion.

If Ps have renal artery stenosis - the kidneys rely on AGTII to maintain adequate perfusion - removing this with ACEIs can severely reduce renal BF = acute renal failure

ACEIs - can cause hyperkalaemia - by reducing aldosterone secretion (which normally promoted K excretion in the kidneys).

114
Q

When are ACEIs highly beneficial for protecting kidney function?

A

In Ps with DM or HT - they reduce proteinuria and slow progression of kidney disease.

115
Q

The kidney is very sensitive to nephrotoxic drugs when Ps have HF. Which drugs in particular should you you be wary of?

A

NSAIDs
ACEIs
Aminoglycosides

116
Q

How does liver cirrhosis affect the kidney?

A

Cirrhosis -> inc resistance in the portal system = portal hypertension = vasodilation in the abdominal circulation. This reduces circulating volume = activation of RAAS by the kidney which senses decreased volume.

RAAS -> inc aldosterone -> decreased excretion of Na. This causes hypernatremia -> water retention -> oedema and ascites.

117
Q

How does liver cirrhosis cause increased ANP?

A

Atrial Natriuretic Peptide (ANP) is a hormone produced by the atria of the heart that promotes natriuresis (excretion of sodium in the urine), diuresis (increased urine production), and vasodilation.

Patients with cirrhosis often have elevated levels of ANP. This is likely due to increased atrial stretch from hypervolemia and increased cardiac output commonly seen in cirrhosis.

118
Q

What is an important thing to control when managing ascites.

A

Sodium = needs restricting

119
Q

What is it called when both the liver and kidney are dysfunctional?

A

Hepatorenal syndrome

120
Q

What is hepatorenal syndrome?

A

Functional AKI - where there is severe renal vasoconstriction without evidence of structural kidney disease

121
Q

Why can the Cr be misleading as to kidney dysfunction in Ps with hepatorenal syndrome?

A

Ps with chronic liver disease - often have reduced muscle mass, lower protein intake - therefore Cr levels can be influenced by this and appear better than they would be with normal protein levels in the body.

122
Q

There are two types of hepatorenal syndrome - 1 and 2. What is the difference between them?

A

1 = Acute - oliguric with doubled creatinine within 2 weeks. Outcome poor (days-weeks).

2 = Chronic - diuretic resistant - less rapid deterioration in renal function - associated refractory ascites. Less poor but still crap survival (months).

123
Q

How is hepatorenal syndrome treated?

A

Mainly supportive - Na and H20 restriction.
Can give human albumin solution
Terlipressin (ADH analogue) - acts as a vasoconstrictor in the splanchnic circulation
TIPS procedure
Dialysis - only to support until transplantation if needed.

124
Q

Why can sepsis damage the kidneys?

A

Endotoxins are released in sepsis -> systemic vasodilation -> reduced renal perfusion = AKI

AKI in sepsis is very common

125
Q

How can systemic infections damage the kidney?

A

Can get immune complexes which stick in the kidney = immune complex nephritis -> post infectious glomerulonephritis

126
Q

Which is the most common infection to cause post infectious glomerulonephritis?

A

Post streptococcal infection = post-streptococcal glomerulonephritis

MRSA or S. aureus are also becoming more common

127
Q

What are the most common viral causes of nephrotic syndrome or glomerulonephritis?

A

HIV
Hep B
Hep C

128
Q

Which cancers can affect the glomerulus?

A

Lymphoma
Leukaemia
Myeloma
Lung, GI, Uterine, Prostate carcinomas

129
Q

What is haemolytic uraemic syndrome?

A

Thrombosis of small blood vessels throughout the body

Triad of
- Haemolytic anaemia
- AKI
- Thrombocytopenia

130
Q

What often triggers HUS?

A

Shiga toxin - E Coli 0157 most common

Also produced by shigella

131
Q

What are the S&S of HUS?

A

Initially brief gastroenteritis, often + bloody diarrhoea

5 days later
- reduced urine output
- haematuria / dark brown urine
- abdominal pain
- lethargy and irritability
- confusion
- HT
- bruising

132
Q

What is the management of HUS?

A

Supportive treatment - but medical emergency - 10% mortality.

Anti-hypertensives
Blood transfusions
Dialysis if needed

70-80% make a full recovery

133
Q

What are the most common causes of glomerular disease?

A

DM
HT
Genetic conditions
Malignancy
Recent infection - streptococcus
Drugs/toxins - NSAIDs, heroin

134
Q

How much protein does a normal kidney excrete in a day?

A

<150mg

135
Q

What is the definition of nephrotic syndrome in terms of proteinuria?

A

Proteinuria >3.5g/1.73m2 body surface area / day

136
Q

What is greater in the urine - blood or protein - in
1) nephrotic syndrome
2) nephritic syndrom?

A

Nephrotic = excess protein in the urine

Nephritic = excess blood in the urine

137
Q

What can nephrotic syndrome cause?

A

Low albumin
Oedema
High lipids (hyperlipidaemia)
Vascular thromboses

138
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease (Minimal Change Glomerulonephritis)

139
Q

What can cause nephrotic syndrome in adults?

A

Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis

140
Q

What are secondary causes of nephrotic syndrome?

A

DM
SLE
Amyloidosis

141
Q

What are the clinical signs of nephritic syndrome?

A

Haematuria
HT
Decreased urine output
Oedema

142
Q

What are the biggest cause of nephritic syndrome?

A

IgA nephropathy

143
Q

What systemic causes can cause nephritic syndrome?

A

Vasculitis
Goodpastures Syndrome
SLE

144
Q

What is AKI?

A

Sudden decline in GFR over days

145
Q

What is pyonephrotis?

A

Pus in the collecting system of the kidney

146
Q

When should US be done in the following situations:

  • Suspected pyonephrosis
  • No idenfied cause of AKI
  • At risk of urinary tract obstruction
A

Within 6 hours

2&3 = Within 24 hours

147
Q

If there is an upper urinary tract obstruction - how should a nephrostomy or stent be done?

A

Within 12 hours

148
Q

What is hydronephrosis?

A

Dilation of the renal collecting system - caused by obstruction of the kidney.

149
Q

What imaging is used for AKI to determine whether there is an obstructive cause?

A

CT KUB

150
Q

What imaging is used for CKD?

A

Ultrasound

151
Q

What imaging is used for diagnosing renal artery stenosis?

A

Renal angiogram

152
Q

What rare reaction can occur with gadolinium contrast?

A

Nephrogenic Systemic Fibrosis - fibrosis of skin, joints, eyes and internal organs

153
Q

How long can it take to develop Sx of NSF?

A

Hours - Years

154
Q

Which Ps are more likely to get an AKI from contrast?

A

Those with existing renal impairment

155
Q

How is renal obstruction treated?

A

Nephrostomy

156
Q

What is pyelonephritis?

A

Acute infection of the upper urinary tract

157
Q

What does streaky or wedge shaped enhancement in the kidney on CT mean?

A

Pyelonephritis

158
Q

What is the difference between renal or peri-nephric abscesses?

A

Peri-nephric = pus filled collection around the kidney resulting from unresolved pyelonephritis

Renal abscess = pus fulled collection within the kidney

Year 3 - Medicine (15 decks)

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