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Y3 MedEd > Renal > Flashcards

Renal Flashcards

1
Q

Functions of the kidney (7)

A 
Regulation of blood volume
Regulation of blood pressure
Acid-base balance
Electrolyte balance
Production of Red blood cells
Synthesis of Vitamin D – Bone metabolism
Excretion of water-soluble waste products – Filter
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2
Q

Define AKI

A

“A rapid decline in renal function over hours or days”

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3
Q

How is AKI measured

A

Urea and creatinine

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4
Q

Easiest way to recognise AKI

A

You stop peeing

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5
Q

Main three ways AKI causes problems and what are they

A

Fluid  oliguria, volume overload
Electrolyte  hyperkalaemia
Acid-base  metabolic acidosis

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6
Q

Define CKD

A

Impaired renal function for >3 months based on
abnormal structure or function, or
GFR <60ml/min for >3m
+/- evidence of kidney damage

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7
Q

What is used to risk stratify AKI

A

KDIGO

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8
Q

Signs of AKI (5)

A

Hypertension
Distended bladder
Dehydration - postural hypotension
Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
Pallor, rash, bruising (vascular disease)

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9
Q

Main 4 symptoms of AKI

A 
Oliguria/anuria 
NOTE: abrupt anuria suggests post-renal obstruction 
Nausea/vomiting 
Dehydration 
Confusion
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10
Q

What is the pathological mechanism behind pre-renal AKI

A

Inadequate Perfusion

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11
Q

What are the 4 mechanisms that can cause prerenal AKI

A

Hypovolaemia
Systemic vasodilation
Decreased cardiac output
Intrarenal vasoconstriction

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12
Q

What can cause hypovolaemic AKI (7)

A

Renal loss from diuretic overuse, osmotic diuresis (e.g., diabetic ketoacidosis)
Extrarenal loss from vomiting, diarrhea*, burns, sweating, blood loss

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13
Q

What can cause systemic vasodilatory AKI (2)

A

Sepsis*, neurogenic shock

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14
Q

What can cause decreased CO AKI (2)

A

HF, MI

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15
Q

What can cause intrarenal vasoconstrictive AKI (3)

A

Cardiorenal syndrome, hepatorenal syndrome

ACEi with renal artery stenosis

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16
Q

What are the four main mechanisms behind renal AKI

A

Acute tubular necrosis
Glomerulonephritis
Interstitial nephritis
Vascular obstruction

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17
Q

What can cause renal AKI through acute tubular necrosis (3)

A

Ischemia, drugs, toxins (paracetamol, NSAIDs, ACE-I, contrast, myoglobinuria in rhabdomyolysis etc.)

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18
Q

Which drugs can cause renal AKI through acute tubular necrosis (3)

A

paracetamol, NSAIDs, ACE-I,

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19
Q

Which toxins can cause renal AKI through acute tubular necrosis (2)

A

contrast, myoglobinuria in rhabdomyolysi

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20
Q

Main way of getting glomerulonephritis?

A

Postinfectious

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21
Q

What can cause renal AKI through interstitial nephritis (3)

A

Drugs
Infection
Infiltration

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22
Q

What can cause renal AKI through vessel obstruction (3 (+3))

A

Thrombosis
vasculitis
haemolytic microangiopathy (HUS, TTP, DIC)

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23
Q

What are the 3 main mechanisms behind post-renal AKI

A

Luminal
Mural
Extrinsic compression

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24
Q

What can cause luminal post-renal AKI (2)

A

Stones, clots

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25
Q

What can cause mural post-renal AKI (3)

A

Malignancy (e.g. uteric, prostate, bladder), BPH,

strictures

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26
Q

What can cause extrinsic compression post-renal AKI

A

Retroperitoneal fibrosis

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27
Q

HUS is a microangiopathy characterised by what 3 things

A

Progressive renal failure - Kidneys
Microangiopathic haemolytic anaemia (MAHA) – Blood
↓ Platelets - Blood (thrombocytopenia)

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28
Q

Most common cause of HUS

A

E. coli O157:H7

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29
Q

Pathophysiology of HUS

A

Gastroenteritis (E.coli 90%)  toxin

Endothelial damage

Thrombosis, platelet consumption + fibrin strand deposition → ↓ Platelets

Destruction of RBCs – schistocytes, ↓ Hb

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30
Q

Ix for HUS

A

Raised urea and creatinine
Haematuria and proteinuria
Pain and bloody diarrhoea
Low Hb and platelets

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31
Q

What is the pentad of TTP

A 
Haemolytic anaemia
Thrombocytopenia
Uraemia
Fever
Neurological symptoms
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32
Q

What neurological features can you get in TTP (4)

A

Seizures
Hemiparesis
↓ consciousness
↓ vision

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33
Q

What is the pathology behind TTP

A

Deficiency of protease (ADAMTS13) that cleaves cleave vWF 
Large vWF multimers form 
Platelet aggregation & fibrin deposition
Microthrombi

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34
Q

Typical population of TTP patients

A

Females between 10-50

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35
Q

Ix for glomerulonephritis (5)

A

BP: normal to malignant HTN
Urine dipstick: protein, blood
Renal function (urea and creatinine)

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36
Q

2 main mechanisms behind glomerulonephritis

A

Loss of barrier function - proteinuria and haematuria

Loss of filtering capacity - reduced toxin excretion

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37
Q

Common primary causes of nephritic glomerulonephritis (and which is the most common) (4)

A

IgA nephropathy (most common)
Henoch Schonlein purpura
Post-streptococcal GN
anti-GBM disease (Goodpasture’s disease)

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38
Q

Common primary causes of nephrotic glomerulonephritis (2)

A

Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

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39
Q

What is the triad in nephrotic syndrome

A

The nephrotic syndrome is a triad of:
• proteinuria >3g/24h (P:CR >300mg/mmol, A:CR >250mg/mmol, p294)
• hypoalbuminaemia (usually <30g/L, can be <10g/L)
• oedema.

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40
Q

What is the triad in nephritic syndrome

A

Hypertension + Haematuria + Oedema (+ Oligouria <400mL/day

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41
Q

What is the main cause of proteinuria

A

Injury to podocytes

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42
Q

What do red cell casts prove

A

Leakage is from the glomerulus

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43
Q

Common secondary causes of nephrotic syndrome (5)

A

Diabetes
SLE
Amyloid
HBV/HCV

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44
Q

Common secondary causes of nephritic syndrome (5)

A 
Post streptococcal 
Vasculitis
SLE 
Anti-GBM disease
Cryoglobulinaemia
45
Q

What is a common cause of glomerulonephritis in children

A

Minimal change disease

46
Q

Presentation (2) and what happens in IgA nephropathy

A

Days after URTI infection
↑IgA immune complex formation
Episodic haematuria

47
Q

Presentation (5) and what happens in IgA nephropathy

A

Haematuria

Purpuric rash extensor surfaces

Polyarthritis, Scrotal swelling , Abdo pain

Systemic variant IgA nephropathy

48
Q

Presentation (2) and what happens in anti-GBM disease

A

Haematuria

Haemoptysis

Auto-Ab to Type IV collagen (GBM & lung)

49
Q

Post streptococcal GN
Presentation (4)
What happens

A

1-12w after throat /skin infection: Strep Ag deposited glomerulus > immune complex formation

Nephritic syndrome: - consist of a TRIAD of
Hypertension + Haematuria + Oedema (+ Oligouria <400mL/day)

50
Q

What is the most common cause of glomerulonephritis

A

Pauci-immune

51
Q

Which antibody is associated with Pauci-immune

A

ANCA with negative immunofluorescence

52
Q

Mx of glomerulonephritis (50

A 
Refer specialist
BP management – <130/80 
ACE-I or ARB – reduce proteinuria and preserve renal function
Steroids/immunosuppression 
Treat underlying cause
53
Q

Ix for glomerulonephritis (6)

A

Bloods – FBC, U&Es, CRP, Complement, Autoantibodies
Urine MCS
Imaging - renal US/biopsy

54
Q

What is the most common cause of renal AKI

A

Tubular necrosis

55
Q

What can cause ischaemic tubular necrosis (6)

A

Hypovolaemia (haemorrhage/volume depletion/GI bleed/burns….etc)
Low CO
Systemic vasodilation – sepsis
DIC
Renal vasoconstriction
Impaired renal autoregulatory responses e.g COX inhibitors, ACE-I, ARBS

56
Q

What are the endogenous nephrotoxins (4)

A

myoglobinaemia (rhabdomyolysis), haemaglobinuria, crystals, myeloma

57
Q

What are the common exogenous nephrotoxins (3)

A

NSAIDs, cisplatin, aminoglycosides – gentamicin, streptomycin
Contrast agents
Anaesthetic agents

58
Q

3 phases of ischaemic acute tubular necrosis

A

INITIATION –acute ↓ GFR + ↑ Cr + ↑urea
MAINTENANCE – sustained ↓ GFR (~1-2w)  Cr + urea ↑
RECOVERY – tubular function regenerates  ↑urine volume + gradual ↓ urea + Cr

59
Q

Define myeloma

A

Malignant disease of bone marrow plasma cells which results in a clonal expansion of plasma cells - monoclonal paraprotein production

60
Q

Features of myeloma (4)

A

Calcium – HIGH
Renal failure (acute or chronic) - ↑ urea ↑ Cr
Why? Hypercalcaemia, paraprotein deposition
Anaemia
Bone – osteolytic bone lesions – pain, fracture (risk cord compression)

61
Q

Symptoms of rhabdomyolysis

A

Muscle pain and swelling, dark urine (myoglobin)

62
Q

Ix for rhabdomyolysis (2)

A

Hyperkalaemia, High CK

63
Q

Causes of interstitial nephritis (5)

A 
Drugs
Infections 
Immune disorders e.g. SLE 
Lymphoma 
Tumor lysis syndrome following chemo
64
Q

What is the earliest sign of kidney damage in DM

A

detection of albumin in urine (elevated albumin:creatine ratio)

65
Q

Complications of AKI (6)

A 
Uraemia 
Volume overload - oedema
Hyperkalaemia 
Hyperphosphataemia 
Metabolic Acidosis 
Chronic progressive kidney disease
66
Q

What is the most common cause of nephrotic syndrome in adults

A

Membranous glomerulonephritis

67
Q

Define CKD

A

Progressive loss of kidney function over a period of months or years
Impaired renal function for >3 months based on abnormal structure or function

68
Q

Causes of CKD (6)

A 
Diabetes 
Hypertension 
Atherosclerosis
Chronic glomerulonephritis 
Infective or obstructive uropathy 
Adult polycystic kidney disease (APKD) is the commonest inherited cause of CKD
69
Q

RF of CKD (8)

A

DM, HTN, CVD, Structural renal disease, multisystem disorders involving kidney, FHx, recurrent UTI, vesicoureteric reflux

70
Q

Symptoms of severe CKD (9)

A 
Anorexia
Nausea and vomiting 
Fatigue
Pruritus
Peripheral oedema
Muscle cramps 
Pulmonary oedema 
Sexual dysfunction is common
71
Q

Main 5 consequences of CKD

A
  1. Progressive failure of homeostatic function
  2. Progressive failure of hormonal function
  3. Cardiovascular disease
  4. Uraemia and Death
72
Q

What does progressive failure of homeostatic function in CKD lead to (2)

A
  • Acidosis

- Hyperkalaemia

73
Q

What does progressive failure of hormonal function in CKD lead to (3)

A
  • Anaemia

- Renal Bone Disease - Osteomalacia

74
Q

What does progressive failure of CVD in CKD lead to (2)

A

Vascular calcification

-Uraemic cardiomyopathy

75
Q

What happens in renal osteodystrophy

A

Kidneys cant convert vitamin D3 into calcitriol = hypocalcaemia
Leads to secondary hyperparathyroidism
PTH stimulates bone resorption
Poor quality bones= osteomalacia: pain, fractures
Insufficient mineralization of bone osteoid

76
Q

What do you test for in the bloods of suspected CKD (8)

A

↓Hb (normocytic anaemia); U&Es (↑urea/Cr), glucose (DM), eGFR, ↓Ca2+, ↑PO43−, ↑ALP (in renal osteodystrophy) ↑PTH if severe CKD

77
Q

Ix for CKD not bloods (5)

A

Urine: dipstick, MC&S, Protein:Cr ratio
Imaging: USS to check size/anatomy/cortico-medullarly differentiation and eliminate obstruction – in CKD kidneys are small (<9cm) but may be enlarged in infiltrative disorders
CXR: Pericardial effusion or pulmonary oedema
Histology: consisted renal biopsy if rapidly progressing or unclear cause (C/I for small kidneys

78
Q

BP target in CKD and for diabetics

A

target <130/80 ( <125/75 is diabetic)

79
Q

Diet in CKD (3)

A

moderate protein, restrict K+, avoid high phosphate foods.

80
Q

Treatment for renal osteodystrophy

A

Calcichew - Ca supplement
Calcium acetate - phosphate binders
Cinacalcet (calcimimetic) – reduce PTH levels

81
Q

3 main ways CKD manifests and how to control them

A

Anaemia: Human EPO might be required

Acidosis: Consider sodium bicarbonate supplements for patients with low serum bicarbonate.

Oedema: loop diuretics, restriction of fluids

82
Q

What is the most common cause of a UTI

A

E coli

83
Q

What are the causes of a typical UTI (3)

A

Staphylococcus saprophyticus
Proteus mirabilis
Enterococci

84
Q

Define lower and upper UTI

A

Lower UTI - affecting the urethra (urethritis), bladder (cystitis) or prostate
Upper UTI - affecting the renal pelvis (pyelonephritis)

85
Q

Atypical causes of UTI and the population usually affected (3)

A

Klebsiella
Candida albicans
Pseudomonas aeruginosa

86
Q

Define UTI

A

The presence of a pure growth of > 105 organisms per mL of fresh MSU

87
Q

RF of UTI (9)

A 
FEMALE 
Sexual intercourse 
Exposure to spermicide 
Pregnancy 
Menopause 
Immunosuppression 
Catheterisation 
Urinary tract obstruction 
Urinary tract malformation
88
Q

S/s of cystitis (4)

A

Frequency
Urgency
Dysuria
Haematuria

89
Q

S/s of prostatitis (4)

A

Suprapubic pain
Flu-like symptoms
Low backache
Few urinary symptoms

90
Q

S/s of acute pyelonephritis (5)

A 
High fever 
Rigors 
Vomiting 
Loin pain and tenderness 
Oliguria (if AKI)
91
Q

General signs of UTI (5)

A 
Fever
Abdominal or loin tenderness 
Foul-smelling urine 
Distended bladder (occasionally) 
Enlarged prostate (if prostatitis)
92
Q

Mx of UTI (uncomplicated, pregnant, male, pyelonephritis)

A

Uncomplicated: Cefalexin 500mg PO BD 3/7 OR Nitrofurantoin 50mg PO QDS 7/7
If pregnant + BF: Cefalexin; Co-amoxiclav 62
Male: 7/7 course of Cefalexin OR ciprofloxacin 500mg PO BD 14/7 (if suspicion of prostatits)
Pyelonephritis/urosepsis: Co-amoxiclav 1.2mg IV ± amikaxin (CXH/HH) or gentamicin (SMH) first 1-2/7

93
Q

Define PCKD

A

fluid filled cysts grow on the kidney, 10% of ESRF

94
Q

Method of inheritance of PCKD

A

Autosomal dominant inheritance, onset at 30-60 years

95
Q

History of PCKD (6)

A

clinically silent for many years!
Acute loin pain, stone formation, abdominal discomfort
Sx of renal failure
FHx of SAH (berry aneurysms)

96
Q

Examination of PCKD (5)

A

HTN, renal enalregment, abdominal pain ± haematuria

97
Q

Ix of PCKD (5)

A

Haematuria, raised Hb, deranged U&E, abdominal USS, MRI angiography IF +ve 1st-degree SAH + ADPKD

98
Q

Classic triad of renal cell carcinoma

A

haematuria, loin pain, abdominal mass.

99
Q

Other presentations of renal cell carcinoma apart from the classic triad

A

Invasion of left renal vein compresses left testicular vein = varicocele
PUO, night sweats and rarely polycythemia

100
Q

When does a renal cell carcinoma cause varicocele

A

Invasion of left renal vein compresses left testicular vein

101
Q

Gender ratio of renal cell carcinoma

A

M:F = 2:1

102
Q

RF of renal cell carcinoma (6)

A

Age; Smoking; Obesity; HTN; Dialysis (15%); certain inherited syndromes (von Hippel-Lindau, tuberous sclerosis, familial papillary renal cell carcinoma)

103
Q

Which inherited syndromes cause renal cell carcinoma (3)

A

von Hippel-Lindau, tuberous sclerosis, familial papillary renal cell carcinoma

104
Q

Ix for renal cell carcinoma (7)

A 
Increased BP (renin), Polycythaemia or IDA (bleeding cysts), ALP (bone mets), RBCs in urine
CXR - Cannon ball metastasis, filling defect ± calcification (CT/MRI intravenous urogram IVU)
105
Q

Common metastases of renal cell carcinoma

A

Cannonball to lung

106
Q

4 causes of renal artery stenosis

A

Atherosclerosis (80%), fibromuscular dysplasia (10%, young F)

107
Q

Clues of renal artery stenosis (

A

↑ ↑ ↑ BP refractory to Tx (1-5% of HTN)
Worsening renal function after ACEi/ARB in bilateral RAS
Flash pulmonary oedema (sudden onset, without LV impairment on echo)
Abdominal ± carotid or femoral bruits, weak leg pulses

108
Q

Ix for renal artery stenosis (3)

A

Ultrasound measurement of kidney size (affected size is smaller)
CT Angiogram or MR Angiography: risk of contrast nephrotoxicity
Digital Subtraction Renal Angiography = GOLD STANDARD(but invasive)

Y3 MedEd (34 decks)

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