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Phase 2a Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Acute kidney injury

A

A significant deterioration in renal function occurring over hours or days. Severity is defined by 3 stages (1 to 3).

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2
Q

prerenal AKI

A

decreased perfusion to the kidney– hypoperfusion (sudden/severe drop in BP), atherosclerosis/ischaemia

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3
Q

Prerenal causes of AKI

A

Renal artery stenosis
Heart failure
Haemorrhage

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4
Q

Renal AKI

A

(intrinsic renal disease) – direct kidney damage, inflammation, infection, drug, autoimmune disease

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5
Q

4 causes of Renal AKI

A

Acute tubular injury
Glomerulonephritis
Acute interstitial nephritis
Renal vasculitis

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6
Q

postrenal AKI

A

obstruction to urine flow

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7
Q

postrenal causes of AKI

A

Benign prostatic hyperplasia
Kidney stones
Tumour

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8
Q

Pathology of Prerenal AKI

A

Low vascular volume
Decreased cardiac output
Systemic vasodilation
Renal vasoconstriction

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9
Q

pathology of renal AKI

A

Glomerular
Interstitial
Vessels

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10
Q

pathology of post renal AKI

A

Extrinsic compression

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11
Q

3 clinical manifestations of AKI

A

Oliguria (passing small volumes of urine)
Fatigue or tiredness
Shortness of breath

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12
Q

4 complications of severe AKI

A

pulmonary oedema, encephalopathy and pericarditis
hyperkalaemia

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13
Q

differential diagnoses for AKI

A

Chronic kidney disease
Hyperkalaemia/ hypernatremia
Acute tubular necrosis

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14
Q

First line investigations for AKI

A

Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine of >50% from baseline in 7 days
Urine output of <0.5ml/kg/hr for >6 hours
Determine cause: urea:creatinine ratio – pre-renal (>100:1), intrarenal (<40:1), post-renal (40-100:1)
Metabolic panel and urine output monitoring: raised serum creatinine, low urine output, raised potassium, metabolic acidosis (raised H+)
Urinalysis: leucocytes and nitrates (infection), proteinuria and haematuria (acute nephritis)

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15
Q

Gold standard investigations for AKI

A

Metabolic profile: U&E (GFR) and creatinine – raised serum creatinine, reduced urine output

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16
Q

management of AKI

A

Identification of risk factors
Dialysis may be needed whilst renal function improves
Manage complications
Dependent on the underlying aetiology

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17
Q

Management of Hypovolaemic AKI

A

fluid resuscitation;
Renal perfusion will improve with volume replacement
Give crystalloid

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18
Q

management of hypervolaemic AKI

A

Oxygen supplementation if required
Fluid restriction. Consider oral and IV volumes.
Diuretics – only in symptomatic fluid overload
Renal replacement therapy

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19
Q

Chronic kidney disease

A

abnormalities of kidney structure or function, present for >3 months, with implications for health. Irreversible loss of nephrons.

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20
Q

4 abnormalities of kidney function

A

Decreased glomerular filtration rate (GFR)
Increased albuminuria
Urinary sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders

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21
Q

4 main causes of CKD

A

Acute renal failure, hypertension, diabetes, kidney disease e.g. polycystic kidney disease

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22
Q

4 rarer causes of CKD

A

Dysplastic kidneys
Reflux nephropathy
Obstructive nephropathy
Infections/ drugs/ systemic diseases that affect the kidney

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23
Q

pathology of CKD

A

Injury may primarily affect glomeruli, vessels, or the tubulo-interstitium, but eventually it leads to reduction in nephron mass with reduction in renal function.
The reduction in nephron mass may then cause haemodynamic stress in remaining nephrons, leading to further nephron loss.

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24
Q

Manifestation of early CKD

A

asymptomatic and can only be picked up if GFR is measured in at-risk patients e.g. diabetics, hypertensives

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25
Q

Why do progressed CKD patients have bone pain

A

Bone decalcification due to metabolic acidosis

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26
Q

What is metabolic derangement

A

Increased sodium and water retention due to decreased GFR – vomiting and diarrhoea

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27
Q

differential diagnoses for CKD

A

Acute kidney injury
Diabetic nephropathy
Chronic glomerulonephritis

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28
Q

First line investigations for CKD

A

FBC (anaemia of CKD), U&E (raised creatinine, phosphate, potassium. Decreased eGFR), urinalysis (haematuria, proteinuria), raised urine albumin (albumin:creatinine >3mg/mmol), renal USS (bilateral renal atrophy)

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29
Q

Gold standard investigations for CKD

A

U&E for estimated GFR
(eGFR < 60mL/min/1.73m2 or, eGFR <90mL/min/1.73m2 + signs of renal damage)

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30
Q

5 steps to management of CKD

A

Appropriate referral to nephrology
Treatment to slow renal disease progression
Treatment of renal complications of CKD
Treatment of other complications of CKD
Preparation for renal replacement therapy (dialysis/ transplant)

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31
Q

treatment to slow renal disease progression

A

Target to lower blood pressure
Offer treatment with renin-angiotensin system antagonist – ace inhibitors

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32
Q

Treatment of renal complications of CKD

A

Anaemia: treat underlying cause
Acidosis: consider sodium bicarbonate supplements
Oedema: restrict fluid and sodium intake
CKD bone mineral disorders: give vitamin D supplements

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33
Q

why does CKD increase risk of CVD

A

due to high blood pressure, vascular stiffness, inflammation, oxidative stress, and abnormal endothelial function.

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34
Q

treatment of CVD caused by CKD

A

Antiplatelets for CKD at risk of atherosclerotic events
Atorvastatin for primary and secondary prevention of CVD

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35
Q

Preparation for renal replacement therapy

A

Should begin in progressive CKD when the risk of renal failure is 10-20% within a year.
All suitable patients should be listed for a deceased donor transplant 6 months before the anticipated start of RRT.

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36
Q

main complication of CKD

A

High incidence of cardiovascular disease due to a combination of hypertension, vascular calcification, and hyperlipidaemia
Patients are much more likely to die of CVD than to need renal replacement therapy.

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37
Q

complications of calcium and phosphate metabolism derangement by CKD

A

leads to renal bone disease, which is a complex mixture of hyper-parathyroid bone disease, Osteomalacia and osteoporosis.

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38
Q

7 Symptoms of renal failure that lead to RRT being needed

A

Inability to control volume status, including pulmonary oedema
Inability to control blood pressure
Serositis
Acid-base or electrolyte abnormalities
Pruritus
Nausea/ vomiting/ deterioration in nutritional status
Cognitive impairment

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39
Q

Features of Haemodialysis

A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction.
A hydrostatic gradient is used to clear excess fluid as required (ultrafiltration).
Access is preferentially via an arteriovenous fistula which provides increased blood flow and longevity.
Haemodialysis is needed 3 times/week or more.

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40
Q

features of Peritoneal dialysis

A

Uses the peritoneum as a semi-permeable membrane.
Catheter is inserted into the peritoneal cavity and fluid infused. Solutes diffuse slowly across.
Ultrafiltration is achieved by adding osmotic agents to the fluid.
It is a continuous process with intermittent drainage and refilling of the peritoneal cavity, performed at home.

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41
Q

features of Haemofiltration

A

Water cleared by positive pressure, dragging solutes into the waste by convention.
The ultrafiltrate (waste) is replaced with an appropriate volume of clean fluid.
Low haemodynamic instability so used in critical care when HD not possible due to low BP.

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42
Q

3 complications of RRT

A

Cardiovascular disease: increased BP, calcium/phosphate dysregulation, inflammation
Renal bone disease: high bone turnover, renal osteodystrophy
Infection: uraemia causes granulocyte and T-cell dysfunction with increased sepsis-related mortality.

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43
Q

2 types of renal transplants

A

Living donor: best graft function and survival, especially if HLA matched.
Deceased donor

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44
Q

3 types of deceased donor renal transplant

A

Donor after brain death
Expanded criteria donor (an older kidney or from a patient with a history of CVA, BP or CKD)
Donor after cardiac death

45
Q

types of immunosuppressants

A

Monoclonal antibodies used at time of transplant e.g. daclizumab
Calcineurin inhibitors to inhibit T-cell activation and proliferation e.g. ciclosporin
Antimetabolites to prevent acute rejection and increase graft survival e.g. azathioprine
Glucorticosteroids to decrease transcription of inflammatory cytokines.

46
Q

surgical complications of renal transplant

A

bleed, thrombosis, infection, urinary leaks, lymphocele, hernia

47
Q

4 non-surgical complications of renal transplant

A

Delayed graft function
Rejection
Infection: increased risk of all infections
Malignancy: immunosuppression increases the risk of cancer

48
Q

Glomerulonephritis

A

GN is characterised by inflammation and damage to the glomeruli. This allows protein (+/- blood) to leak out into the urine.

49
Q

which conditions does the term glomerulonephritis encompass

A

Are caused by pathology in the glomerulus
Present with proteinuria, haematuria, or both
Are diagnosed on a renal biopsy
Cause CKD
Can progress to kidney failure (except minimal change disease)

50
Q

5 causes of Glomerulonephritis

A

IgA nephropathy
Systemic lupus erythematous nephropathy
Post-streptococcal glomerulonephritis
Goodpasture’s syndrome (rapidly progressing glomerulonephritis)
Haemolytic uraemic syndrome

51
Q

pathology of Glomerulonephritis

A

Damage to the glomerulus with leakage of protein and blood into the urine. There may be rupture of the glomerular basement membrane, with a cellular reaction in the Bowman’s space.

52
Q

What can Glomerulonephritis cause

A

Damage to the filtration mechanism resulting in haematuria and proteinuria
Damage to the glomerulus restricts blood flow, leading to compensatory hypertension
Loss of the usual filtration capacity leads to acute kidney injury

53
Q

key presentations of Glomerulonephritis

A

Visible haematuria, proteinuria, hypertension, oedema (peripheral, pulmonary), oliguria (low urine output), uraemic signs

54
Q

symptoms of IgA nephropathy

A

visible haematuria, 1-2 days after viral infection

55
Q

symptoms of post-strep GN

A

visible haematuria, 2 weeks after strep infection

56
Q

Symptoms of Rapidly progressing GN (Goodpasture’s, Wegener’s)

A

Fatigue, SOB, cough, haemoptysis, acute kidney failure.

57
Q

first line investigations for GN

A

Urinalysis and microscopy (haematuria, proteinuria, dysmorphic RBCs), 24hr urine protein collection, bloods (anaemia, elevated liver enzymes, elevated creatinine)
Serology: anti-GBM (Goodpasture’s), anti-double-stranded DNA (SLE), antinuclear antibody (SLE), ANCA (Wegener’s vasculitis)
IgA: microscopy shows IgA complex deposition
Rapidly progressive GN: microscopy shows crescentic glomerulonephritis

58
Q

gold standard investigation for GN

A

Renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)

59
Q

cause of Acute nephritic syndrome

A

Caused by an immune response triggered by an infection or other disease
Most common primary cause is IgA nephropathy

60
Q

pathology of Acute nephritic syndrome

A

Kidney leaks blood from its basement membrane – podocytes develop large pores which allows blood and protein to escape into the urine.

61
Q

Distinguishing histological feature of Acute nephritic syndrome

A

Red cell casts are the distinguishing feature – formed in the nephrons and indicate glomerular damage

62
Q

symptoms of Acute nephritic syndrome

A

Haematuria – visible or non-visible
Proteinuria
Hypertension and oedema
Low volume of urine <300ml/day due to decreased renal function

63
Q

IgA nephropathy

A

Immune complex GN related to glomerular deposition of immune complexes containing IgA.

64
Q

primary causes of IgA nephropathy

A

incompletely understood; an abnormal mucosal immune system and the production of abnormally glycosylated IgA molecules play a role

65
Q

secondary causes of IgA nephropathy

A

IgA can be deposited in glomeruli, in association with liver disease, bowel disease and dermatitis herpetiformis

66
Q

pathological features of IgA nephropathy

A

IgA can cause a number of changes in the glomeruli, ranging from mild mesangial hypercellularity only to glocal glomerular hypercellularity.
Crescents may be seen in the most severe cases

67
Q

presentation of IgA nephropathy

A

Asymptomatic non-visible haematuria
Episodic visible haematuria
High BP

68
Q

investigation for IgA nephropathy

A

Renal biopsy: IgA deposition in mesangium.

69
Q

treatment of IgA nephropathy

A

ACE inhibitors – reduce BP and protein in the urine

70
Q

What is nephrotic syndrome

A

Proteinuria due to basement membrane pathology. Kidney leaks protein from its basement membrane

71
Q

triad of symptoms for Nephrotic syndrome

A

Proteinuria >3.5g/24 hours
Hypoalbuminemia
Oedema (oncotic pressure decreases due to hypoalbuminemia, meaning fluid moves out to surrounding tissues)

72
Q

What is a common complication of Nephrotic syndrome

A

Severe hyperlipidaemia is often present: liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol.

73
Q

primary renal causes of Nephrotic syndrome

A

minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN

74
Q

Secondary causes of Nephrotic syndrome

A

DM, lupus nephritis, myeloma, amyloid, pre-eclampsia.

75
Q

pathophysiology of Nephrotic syndrome

A

The filtration barrier of the kidney is formed by podocytes, the glomerular basement membrane (GBM), and endothelial cells.
Proteinuria results from podocyte pathology; abnormal function in minimal change disease or immune-mediated damage in membranous nephropathy.

76
Q

presentations of Nephrotic syndrome

A

Generalised, pitting oedema of ankles, genital, abdominal wall which can be rapid and severe
Hypoalbuminemia
Frothy urine (due to the protein)
Systemic symptoms e.g. joint, skin
Consider malignancy and chronic infection

77
Q

differential diagnoses of nephrotic syndrome

A

Congestive heart failure
Where there is oedema and raised jugular venous pressure
Cirrhosis
Where there is oedema and hypoalbuminemia

78
Q

investigations for nephrotic syndrome

A

Establish cause via renal biopsy
Urine dipstick shows very high protein
Serum albumin is low

79
Q

management of nephrotic syndrome

A

Reduce oedema
Fluid and salt restriction. Diuretics with loops diuretics
Treat underlying cause
Adults need a renal biopsy to discover cause
Reduce proteinuria
ACEi/ ARB reduce proteinuria

80
Q

complications of nephrotic syndrome

A

Thromboembolism
Infection
Hyperlipidaemia

81
Q

pathology of minimal change disease

A

loss of podocyte foot processes, vacuolation and appearance of microvilli in the glomerulus = three hallmarks
Podocyte losses may account for proteinuria

82
Q

diagnosis of minimal change disease

A

biopsy, electron microscope of biopsy shows abnormal podocytes

83
Q

clinical presentation of minimal change disease

A

like nephrotic syndrome

84
Q

natural history of MCD

A

has a relapsing – remitting course

85
Q

Does MCD progress to renal failure

A

NO

86
Q

treatment of MCD

A

steroids (prednisolone). For frequent relapses or steroid dependent cases second line treatment is with cyclophosphamide or cyclosporine

87
Q

presentation of focal segmental glomerulosclerosis

A

Presents as nephrotic syndrome

88
Q

causes of FSGS

A

Can either be primary (genetic mutations) or secondary (HIV/ reflux nephropathy)

89
Q

investigations for FSGS

A

Specific segments of certain glomeruli develop sclerosed lesions
Antibody tests are all negative

90
Q

treatment of FSGS

A

Salt restriction and diuretics – reduce oedema
Antihypertensives
Statins – treat hyperlipidaemia
Transplant

91
Q

presentation of Membranous glomerulonephritis

A

Presents with nephrotic syndrome
Slowly progressive

92
Q

cause of Membranous glomerulonephritis

A

Usually idiopathic but can be associated with Hepatitis B/ Malaria/ Penicillamine/ SLE
Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins.

93
Q

investigations for membranous glomerulonephritis

A

Microscopic analysis shows thickened glomerular basement membrane
Immunofluorescence shows diffuse uptake of IgG

94
Q

treatment of Membranous glomerulonephritis

A

Steroids if disease begins to progress

95
Q

prognosis of Membranous glomerulonephritis

A

: 1/3 have chronic membranous glomerulonephritis, 1/3 go into remission, 1/3 progress to end-stage renal failure.

96
Q

What is Polycystic kidney disease

A

An inherited disorder in which clusters of cysts develop primarily within your kidneys, causing your kidneys to enlarge and lose function over time.

97
Q

cause of Adult PKD

A

an inherited mutation in the PKD1 gene on chromosome 16

98
Q

pathology of Adult PKD

A

Defects in the function of the PKD1 protein lead to cystic change in renal tubules and loss of normal renal tissue

99
Q

presentation of adult PKD

A

May be clinically silent unless cysts become symptomatic due to size/haemorrhage.
Loin pain
Visible haematuria
Cyst infection
Renal calculi
High BP
Progressive renal failure

100
Q

Extra renal manifestations of adult PKD

A

liver cysts and berry aneurysms.

101
Q

First line and gold standard investigations for PKD

A

Kidney ultrasound (enlarged bilateral kidneys with multiple cysts). Age 15-39 (at least 3 cysts unilateral or bilateral), 40-59 (at least 2 in each kidney), 60+ (at least 4 in each kidney)

102
Q

treatment of PKD

A

Water intake 3-4L/day may suppress cyst growth
High BP should be treated to target <130/80mmHg
1st line ACE-i/ ARB
2nd line thiazide-like
3rd line β-blocker
Treat infection
Persistent/ severe pain may need cyst decompression

103
Q

Infantile PKD

A

A rare, inherited condition causing bilateral polycystic kidneys and congenital hepatic fibrosis.

104
Q

Cause of infantile PKD

A

mutations in the PKHD1 on chromosome 6p which encodes a component of the cilia on collecting duct epithelial cells

105
Q

complications of infantile PKD

A

Severe cases cause neonatal death from pulmonary hypoplasia.
Children with less severe renal disease who survive, suffer from;
Congenital hepatic fibrosis
Complications of portal hypertension

106
Q

treatment of infantile PKD

A

Poor prognosis if neonatal respiratory distress. No specific therapy.
Continuous renal replacement therapy needed

107
Q

Renal colic

A

a type of pain you get when urinary stones block part of your urinary tract

108
Q

features of Renal colic

A

Rapid onset – woken from sleep
Pain that results from upper urinary tract obstruction
Excruciating ureteric spasms – patient is writhing in pain
Pain is from loin to groin
Associated with nausea and vomiting
Worse with fluid loading
Radiates to groin and ipsilateral testis/labia
Often cannot lie still

Phase 2a Medicine (10 decks)

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