Nephrology 2 Flashcards

1
Q

What are the subtypes of nephritis?

A

Glomerulonephritis

Interstitial nephritis/tubulo-interstitial nephritis

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2
Q

How does nephritis present?

A
Nephrotic syndrome
Nephritic syndrome
AKI
CKD
Renal pain and dysuria
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3
Q

What are the clinical features of nephritic syndrome?

A

Haematuria and proteinuria
Oliguria
Oedema
Uraemic symptoms

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4
Q

What symptoms suggest elevated levels of urea?

A

Anorexia
Pruritus
Lethargy
Nausea

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5
Q

What are some causes of nephritis?

A

Post Group A strep infection
EBV/Hep B infection
SLE/HSP

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6
Q

How is suspected nephritis managed?

A

Urine dipstick for protein and blood

Refer to secondary care

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7
Q

What is nephrotic syndrome?

A

A type of glomerulopathy where there is immunologically mediated injury to glomeruli

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8
Q

What are the 3 cardinal signs of nephrotic syndrome?

A

Large proteinuria (>3.5g/day)
Oedema
Hypoalbuminaemia (serum albumin <30g/L)

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9
Q

How do the signs of nephrotic syndrome come about?

A

Increased permeability of serum protein through the damaged basement membrane of the renal glomerulus

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10
Q

What are some other problems in nephrotic syndrome?

A

Dyslipidaemia
Coagulation/fibrinolysis abnormalities
Immunological disorders

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11
Q

What percentage of nephrotic patients progress to end stage renal failure?

A

25%

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12
Q

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

A

Focal segmental glomerulosclerosis

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13
Q

Name three secondary causes of nephrotic syndrome.

A

Diabetic nephropathy
SLE
Multiple myeloma

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14
Q

How does hyperlipidaemia occur in nephrotic syndrome?

A

In response to hypoalbuminaemia, the liver commences a compensatory mechanism, synthesizing proteins

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15
Q

Describe the oedema of nephrotic syndrome.

A

Children - facial/periorbital then spreads to whole body
Adults - starts with peripheral and spreads to whole body
Genital

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16
Q

Other than oedema, what are the other symptoms of nephrotic syndrome?

A

Frothy urine
Hypercoagulability
Fatigue etc
Xanthomata

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17
Q

How is nephrotic syndrome diagnosed?

A

Urine dipstick for haematuria and proteinuria, quantify using early morning urinary PCR or ACR
Renal biopsy and USS
eGFR
FBC and biochemistry

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18
Q

How is nephrotic syndrome managed?

A

Sodium and fluid restriction
High dose diuretics
PO prednisolone 6 months

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19
Q

What is the treatment of relapsed nephrotic syndrome?

A

Cyclophosphamide/ciclosporin

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20
Q

What are the different glomerulonephritides?

A
Minimal change
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis
Rapidly progressive glomerulonephritis
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21
Q

What is the cause of minimal change disease?

A

Idiopathic/infection/neoplasm

Loss of podocytes and fusion of foot processes

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22
Q

When is the peak incidence of minimal change disease?

A

2-3 years males

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23
Q

How do most glomerulonephritides present?

A

Nephrotic syndrome

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24
Q

What is the treatment of minimal change disease?

A

High dose prednisolone

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25
What is the name of infection within the renal pelvis/parenchyma?
Pyelonephritis
26
What are the risk factors for chronic pyelonephritis (from repeated attacks of acute pyelonephritis)?
Vesicoureteric reflux Diabetes Structural renal tract anomalies
27
Which organisms cause pyelonephritis?
The same as for lower UTI: E.coli, klebsiella, proteus, enterococcus.
28
What are risk factors for acute pyelonephritis and cystitis?
``` Female Children and elderly Abnormalities of the renal tract Calculi Immunocompromised Incomplete bladder emptying ```
29
How does pyelonephritis present?
``` Loin/suprapubic/back pain Fever and rigors V+D, malaise, anorexia LUTS Tenderness without guarding ```
30
Name some LUTS.
Frequency Hesitancy Dysuria Gross haematuria
31
What is found on urinalysis in pyelonephritis?
Urine cloudy with offensive smell Dipstick positive for blood, protein, leukocyte esterase, nitrite Pyuria in MCS
32
What are other investigations in pyelonephritis?
Raised CRP and WCC +ve cultures USS in men, children, and recurrent cases
33
Which antibiotic is recommended for pyelonephritis?
Ciprofloxacin or co-amoxiclav | If culture confirms sensitivity then trimethoprim.
34
Which bacteria are sensitive to trimethoprim?
``` E.coli Proteus Klebsiella Enterococcus HIB Strep.pneumoniae ```
35
What are three complications of pyelonephritis?
Pyonephrosis Perinephric/renal abscess Sepsis
36
Which types of E.coli are associated with pyelonephritis, and cystitis?
Pyelonephritis - type p fimbriae (PapG adhesin) | Cystitis - type 1 fimbriae (FimH adhesin)
37
When is a UTI a relapse, and a reinfection?
Relapse: same organism, within 7 days Reinfection: same or different organisms, after 14 days
38
How is UTI diagnosed?
Nitrites and leukocyte esterase on dipstick | MCS - leukocytes
39
How is UTI treated?
Trimethoprim or nitrofurantoin | 3d women, 7d men
40
From where does renal cell carcinoma arise?
Proximal tubule epithelium
41
What is the most common type of RCC?
Clear cell
42
Where does RCC spread?
Adrenal glands, liver, spleen, colon, pancreas Most common site of metastases - lungs, cannon ball secondaries
43
What are the risk factors for RCC?
Smoking and obesity Renal disease Von Hippel Lindau syndrome (AD inheritance, multiple tumours developed)
44
What is the classic triad of RCC?
Haematuria Loin pain Loin mass But often asymptomatic
45
How may a left sided varicocele develop in RCC?
If the tumour has invaded the left renal vein, the left testicular vein is obstructed.
46
Why might hypertension occur in RCC?
Tumour secretes renin
47
30% RCC patients have paraneoplastic symptoms such as...
``` Neuromyopathy Anaemia Polycythaemia Amyloidosis Hypercalcaemia ```
48
What is the best investigation initially for RCC?
Abdominal CT with contrast
49
What is the gold standard treatment of RCC?
Laparoscopic partial nephrectomy
50
What is the gold standard treatment of metastatic RCC?
Tumour nephrectomy with IFN-alpha chemotherapy
51
What is the syndrome of inappropriate ADH secretion?
Excess release of ADH from posterior pituitary or ectopic source
52
Why is ADH released normally?
In response to hyperosmolality.
53
What is the function of ADH?
Increases the amount of water reabsorbed in the kidney | Constricts arterioles, which increases peripheral vascular resistance and arterial blood pressure
54
What is the pathophysiology of SIADH?
Patient drinks water, plasma osmolality decreases, but ADH continues to be released, leading to a hypo-osmolar state
55
Which tumours may secrete ADH?
GI Lung small cell GU Lymphoma
56
Which conditions may increase ADH secretion?
CNS infection, mass, or bleed Hydrocephalus MS Pneumonia or asthma
57
Which drugs may increase ADH secretion?
Diuretics SSRIs PPIs ACEIs
58
How does SIADH present?
Stems from water retention and hyponatraemia: - Confusion, coma, seizures - Nausea - Muscle weakness and ataxia - Cheyne Stokes respiration
59
How is SIADH diagnosed?
Serum hypoosmolality<275mOsm/kg (low) | Urine osmolality>100mOsm/kg and sodium>30mmol/L (high)
60
What should be excluded in SIADH investigations?
Hypothyroidism | Addison's disease
61
Which formula should be used to calculate electrolyte free water clearance?
Furst formula
62
What are the principles of management of SIADH?
Fluid restriction in most cases | Increase sodium levels
63
What drug can be used for SIADH?
Tolvoptan or demeclocycline
64
What are the symptoms of IgA nephropathy?
Recurrent episodes of macroscopic haematuria, 1-2 days after URTI
65
How does IgA nephropathy differ from post-strep glomerulonephritis?
Post-strep occurs weeks after URTI
66
What is the treatment of ascites in patients with chronic liver disease?
Aldosterone antagonists - spironalactone
67
How do you calculate anion gap?
(Na + K) - (Cl + HCO3)
68
What is the normal range for anion gap?
8-16mEq/L
69
How can you differ dehydration from AKI?
In dehydration, the urea is proportionally higher than a rise in creatinine
70
What is the management of acute clot (urinary) retention?
Continuous bladder irrigation via a 3 way urethral catheter
71
What is the usual first line option of renal replacement therapy?
Peritoneal dialysis
72
How does autosomal dominant polycystic kidney disease present?
Usually in 3rd to 4th decade ``` Haematuria/hypertension Polycythaemia Liver cysts Berry aneurysms MV prolapse ```
73
How does autosomal recessive polycystic kidney disease present?
In childhood Haematuria/HTN Hepatic fibrosis and portal hypertension
74
Name three chronic metabolic complications of haemodialysis treated end stage renal failure.
Amyloidosis Secondary or tertiary hyperparathyroidism Dyslipidaemia