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Inflammation > Kidney disease and blood pressure > Flashcards

Kidney disease and blood pressure Flashcards

1
Q

How will glomerular disease present?

A 
Hypertension
Incidental microscopic haematuria
Incidental proteinuria
Nephrotic syndrome
Progressive renal impairment
AKI
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2
Q

What is nephrotic syndrome?

A

Heavy proteinuria > 3.5g a day
Hypoalbuminaemia
Oedema
Hyperlipidaemia

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3
Q

Most common cause of GD in children?

A

Minimal change disease

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4
Q

Why is it called minimal change disease?

A

Under the microscope the kidney tissue looks normal

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5
Q

What is renal bruits?

A

Stenosis

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6
Q

Blood investigations in glomerulonephritis?

A 
U+E
FBC
CRP
C3/4
Abs (IgA)
RF
Anti-NA, anti-dsDNA, ANCA
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7
Q

What are the primary glomerular causes of microscopic haematuria?

A 
IgA nephropathy
Alports
Thin BM disease
Post-infectious GN
Membranoproliferative GN
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8
Q

What are the secondary glomerular causes of microscopic haematuria?

A 
Henoch Scorlein Purpura (IgA vasculitis)
SLE
Haemolytic uraemic syndrome (HUS)
ANCA associated vasculitis
Sickle nephropathy
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9
Q

Presentation of ANCA associated vasculitis

A

Rapid decline in renal function

Rapidly progressing glomerulonephritis

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10
Q

Differentials between Henoch Scorlein Purpura and IgA nephropathy?

A

HSP affects small blood vessels in kidney, skin and gut
HSP is associated with a leucocystoclasic vasculitic rash
Extra-renal symptoms

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11
Q

Biopsy of IgA nephropathy findings?

A

Mesangial proliferation with IgA deposition

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12
Q

Primary causes of nephrotic syndrome:

A

Membranous nephropathy
FSGS
MCGN
Minimal change disease

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13
Q

Secondary causes of nephrotic syndrome:

A 
Diabetic nephropathy
SLE
Amyloidosis
Malignancy
Drugs
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14
Q

Complications of nephrotic syndrome:

A 
Protein malnutrition
Hypovolaemia
AKI
VTE - risk if albumin <20-25(DVT, PE, Renal vein thrombosis)
Infections
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15
Q

Pregnancy associated nephrotic syndrome?

A

Pre-eclampsia

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16
Q

Which nephrotic syndromes respond well to steroids?

A

Minimal change disease

Focal segmental glomerulosclerosis

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17
Q

Management of nephrotic syndrome:

A 
Diuretics
ACE
Anticoagulants
Statins
Renal biopsy
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18
Q

What is a paraneoplastic nephrotic syndrome of Hodgkin’s syndrome?

A

Minimal change disease

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19
Q

How will minimal change disease present?

A

Sudden onset oedema
(Periorbital in children)
(Peripheral in adults)

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20
Q

Drug causes of minimal change disease?

A 
NSAIDs
Lithium
Pellicinamine
Pamidronate
Sulfazolizine
Immunisations
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21
Q

MCD associated with?

A

SLE
T1DM
APKD
HIV nephropathy

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22
Q

What sets focal segmental glomerulosclerosis (FSGS) apart from other causes of nephrotic syndrome?

A

It is a lesion not a disease

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23
Q

Biopsy of FSGS?

A

Areas of mesangial collapse and sclerosis

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24
Q

Secondary causes of FSGS:

A 
HIV
Reflux nephropathy
Massive obesity
Scarring from previous insult (e.g. IgA, SLE, vasculitis)
Heroin
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25
Q

Symptoms of FSGS:

A

Proteinuria
Hypoalbuminaemia
High cholesterol
VTE risk

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26
Q

Most common cause of primary nephrotic syndrome in adults?

A

Membranous nephropathy

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27
Q

Pathology of membranous nephropathy

A

Glomerular BM thickening

Immune deposits in the glomerular BM

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28
Q

Idiopathic membranous nephropathy Ab?

A

Anti-PLA2

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29
Q

Secondary membranous nephropathy causes?

A 
Hep B
Thyroiditis
Carcinomas
Penicillamine
Captopril
NSAIDs
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30
Q

Mesangiocapillary glomerulonephritis (MCGN) pathology?

A

Immune complex deposition

Complement dysregulation

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31
Q

Cryoglobulinaemia pathology?

A

Circulating complexes that precipitate out in the cold
Associated with rash - livedo reticularis
Arthralgia
Myalgia

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32
Q

Biopsy of cryoglobulinaemia findings?

A

MCGN

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33
Q

Pulmonary renal syndromes:

A

Anti-GBM disease
ANCA vasculitis
Lupus with pulmonary haemorrhage

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34
Q

What does GPA stand for in the context of ANCA +ve vasculitis?

A

Granulomatosis with polyangitis

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35
Q

ANCA +ve vasculitis biopsy findings?

A

Crescent formation

Rapidly progressing GN

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36
Q

ANCA stands for?

A

Anti-neutrophil cytoplasmic antibody

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37
Q

Presentation of ANCA +ve vasculitis?

A

Pulmonary haemorrhage with AKI

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38
Q

Symptoms of ANCA +ve vasculitis?

A

Joint pains
Rash
Upper respiratory tract symptoms
Nose bleeds

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39
Q

Nephritic syndrome associated diseases:

A

Post-streptococcal glomerulonephritis (post URTI)
IgA nephropathy
Crescentic, rapid GN - Goodpastures, vasculitis
Membranoproliferative GN
HSP
Rhabdomyolysis (myoglobin)

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40
Q

Pathology of Goodpastures syndrome?

A

Anti-glomerular BM Abs (crescent formation and rapid GN)

Anti-alveolar BM Abs (pulmonary haemorrhage)

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41
Q

Goodpastures presentation?

A

Pulmonary haemorrhage and AKI

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42
Q

Presentation of rhabdomyolysis?

A

Coca-cola coloured urine

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43
Q

What is rheumatoid factor?

A

Anti-bodies to the Fc portion of IgG (usually IgM)

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44
Q

Cancer test in glomerular disease?

A

Myeloma screen - Igs, electrophoresis and urine Bence-Jones proteins

45
Q

Life-threatening complications of glomerular disease?

A

Hyperkalaemia

Fluid overload

46
Q

Treatment for hyperkalaemia?

Need to normalise bicarbonate

A

Calcium gluconate (prevents arrhythmias)
Then dextrose
Then insulin

47
Q

When are ACE inhibitors contraindicated?

A 
Renal failure
Pregnancy/breastfeeding
Renal artery stenosis
Aortic stenosis (hypotension)
High dose diuretic therapy (>80mg furosemide)
Hereditary idiopathic angio-oedema
48
Q

Why are ACE inhibitors contraindicated in renal failure?

A

They lower the glomerular filtration pressure and thus GFR

49
Q

How do ACE inhibitors reduce the glomerular filtration pressure?

A

Vasodilate the efferent artery (angio II normally constricts it)

50
Q

Side-effects of ACE inhibitors?

A

Cough
Hyperkalaemia
Angio-oedema (year after starting)
First dose hypotension (especially in those on diuretics)

51
Q

Step 1 treatment for hypertension?

A

ACE inhibitor or CCB

52
Q

Step 2 treatment for hypertension?

A

ACE + CCB or ACE + Diuretic

53
Q

Step 3 treatment for hypertension?

A

ACE + CCB + Diuretic

54
Q

Step 4 treatment for hypertension and K is < or equal to 4.5?

A

Add spironolactone

55
Q

Step 4 treatment for hypertension and K is > 4.5?

A

Add alpha- or beta-blocker

56
Q

Which diuretics are potassium sparing and where do they operate?

A

Thiazides

Distal convoluted tubule blocking the NaCl symporter

57
Q

Which diuretics are used for reducing fluid overload in heart failure?

A

Loop diuretics

58
Q

Common side effects of thiazide diuretics:

A 
Dehydration
Postural hypotension
Hyponatraemia, hypokalaemia, hypercalcaemia
Gout
Impaired glucose tolerance
Impotence
59
Q

Rare side effects of thiazide diuretics:

A

Thrombocytopaenia
Agranulocytosis
Photosensitivity rash
Pancreatitis

60
Q

Indications for loop diuretics?

A 
Heart failure
Resistant hypertension (particularly in patients with renal impairment)
61
Q

Adverse effects of loop diuretics?

A

Hypotension
Hyponatraemia, hypokalaemia, hypomagnesaemia
Hypochloraemic alkalosis
Ototoxicity
Hypocalcaemia
Renal impairment (from dehydration + direct toxic effect)
Hyperglycaemia (less common than with thiazides)
Gout

62
Q

Dietary advice for a patient with chronic kidney disease

A

Low protein
Low potassium
Low phosphate
Low sodium

63
Q

Kidney cancer in children?

A

Wilms’ tumour (abdominal pain and painless haematuria)

64
Q

Cause fo oxalate nephropathy?

A

Vitamin C overdose

65
Q

MACHINE mnemonic for causes of hyperkalaemia:

A 
M - Medications: ACE, NSAIDs
A - Acidosis: metabolic and respiratory
C - Cellular destruction: burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake (excessive)
N - Nephrons (renal failure)
E - Excretion (impaired)
66
Q

Hyperkalaemic ECG changes:

A

Tall tented t waves
Small p waves
Widened QRS leading to sinusoidal pattern and asystole

67
Q

Why is metabolic acidosis associated with hyperkalaemia?

A

H and K ions compete for eachother for sodium ions across cell membranes and in the distal tubule

68
Q

Drug causes of hyperkalaemia:

A 
Potassium sparing diuretics
ACE inhibitors
Angiotensin 2 receptor blockers
Spironolactone
Ciclosporin
Heparin
Beta blockers (can interfere with K transport into cells and can cause hyperkalaemia in renal failure patients - treat with salbutamol)
69
Q

Disease causes of hyperkalaemia:

A

Addison’s disease
Rhabdomyolysis
Massive blood transfusion

70
Q

Drug causes of hypokalaemia:

A 
Beta agonists (temporary)
Calcium resonium (temporary)
Thiazide diuretics
Loop diuretics 
Acetazolamide
71
Q

Which type hypersensitivity is Goodpastures syndrome?

A

Type 2

72
Q

Does oliguria in acute tubular necrosis respond to IV fluids?

A

No because the damage is within the kidneys rather than there being fluid depletion

73
Q

Wilms’ tumour is an example of what?

A

Nephroblastoma

74
Q

What is the most common form of AKI?

A

Acute tubular necrosis

75
Q

How can a fall cause AKI?

A

Rhabdomyolysis from the fall (myoglobin release from damaged muscle) causes ischaemia and acute tubular necrosis in the kidney

76
Q

Diabetic nephropathy histology findings?

A

Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)
Hyaline arteriosclerosis
BM thickening

77
Q

What is the histological finding in amyloidosis?

A

Apple green birefringence in polarised light

78
Q

What does the histological finding of apple green birefringent crystals in the kidney suggest?

A

Amyloidosis

79
Q

When is the histological finding of wire looping of the capillaries in the glomeruli found?

A

SLE - a diffuse proliferative glomerulonephritis

80
Q

When is the histological finding of presenting found?

A

Rapidly progressive glomerulonephritis

81
Q

Pathophysiology of diabetic nephropathy?

A

Increase in the glomerular capillary pressure

Glycosylation of the basement membrane

82
Q

Associations with renal cell carcinoma?

A

Middle aged man
Smoking
Tubular sclerosis
Von Hippel-Lindau syndrome

83
Q

Potential endocrine secretions of a renal cell carcinoma?

A

Erythropoeitin - polycythaemia
Parathyroid hormone - hypercalcaemia
Renin
ACTH

84
Q

Hepatic paraneoplastic syndrome of renal cell carcinoma?

A

Stauffer syndrome - cholestastis/hepatosplenomegaly

(thought to be secondary to increased levels of IL-6

85
Q

What is acute kidney injury?

A

Syndrome arising from a rapid decline in GFR
Serum creatinine > (or equal to) 26.5 umol/L
OR raise of 1.5 fold or over in 7 days AND urine output <0.5ml/kg/h for 6 hours

86
Q

KDIGO stage 1 AKI:

A

Serum creatinine 1.5-1.9 x baseline

87
Q

KDIGO stage 2 AKI:

A

Serum creatinine 2.0-2.9 x baseline

88
Q

KDIGO stage 3 AKI:

A

Serum creatinine 3 x baseline

89
Q

Pre-renal causes of AKI:

A

Hypovolaemia
Cardiac failure
Hepatorenal syndrome

90
Q

Renal artery causes of AKI:

A

Renal artery occlusion

Large/medium vessel vasculitis

91
Q

Small vessel causes of AKI:

A

Thrombotic microangiopathy
Renal atheroembolism
Small vessel vasculitis

92
Q

Glomerular disease causes of AKI:

A 
Anti-GBM disease (Goodpastures)
Lupus nephritis
Post-infective GN
Infective endocarditis
Membranoproliferative GN
Cryoglobulinaemia
IgA nephropathy/HSP
93
Q

Causes of acute tubular necrosis (AKI):

A 
Amphotecerin
Aminoglycosides
Antiretrovirals
Cisplatin
Acetaminophen
Radiocontrast
Organic solvents
IV immunoglobulin
94
Q

Causes of acute interstitial nephritis (AKI):

A

Drugs
Infection
Systemic disease

95
Q

Intra-tubular obstruction causes of AKI:

A

Cast nephropathy
Drugs
Crystalluria

96
Q

Post-renal obstruction causes of AKI:

A 
Papillary necrosis
Tumours
Retroperitoneal fibrosis
Renal calculi
Urinary retention
97
Q

What can AKI cause?

A

Hyperkalaemia

98
Q

ECG change with serum K 5.5-6.5 mmol/l

A

Peaked T waves

Prolonged PR segment

99
Q

ECG change with serum K 6.5-8 mmol/l

A

Loss of P wave
Prolonged QRS
ST elevation
(ectopic beats and escape rhythms)

100
Q

ECG change with serum K >8 mol/l

A

Sine wave
Wide QRS
(ventricular fibrillation, asystole, bundle branch blocks, axis deviation, fascicular blocks)

101
Q

What does the kidney have receptor sites for?

A

ADH
Aldosterone
ANP
PTH

102
Q

What doe the kidney produce?

A 
Urine
Erythropoetin
Prostaglandins
Vitamin D
Renin
(also has a role in gluconeogenesis)
103
Q

Features of metabolic acidosis?

A

pH<7.3
Low PaCO2
Normal-high PaO2
Low bicarbonate

104
Q

Symptoms of metabolic acidosis?

A

Breathless
Tachypnoea
Nausea
Non-specifically unwell

105
Q

Features of uraemia?

A 
Waste retention so higher blood levels of:
Sulfate
Urea
Ammonia
Creatinine
Phosphate
106
Q

What does uraemia lead to?

A

Pericarditis
Pleurisy
Encephalopathy, coma, death

107
Q

RRT may be needed for severe complications of AKI such as…

A 
Life threatening pulmonary oedema
Severe metabolic acidosis
Severe hyperkalaemia with ECG changes
Uraemia pericarditis
Uraemic encephalopathy
108
Q

Bone disease:

A

High bone turnover due to hyperparathyroidism
OR low bone turnover causing osteoporosis
Vertebral fracture occurs in 21% of harm-dialysis patients

Inflammation (9 decks)

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