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Renal 500 SBA > REnal > Flashcards

REnal Flashcards

1
Q

What is Alport syndrome

A

A genetic defect in type IV collagen

synthesis. Mixed nephrotic and nephritic syndroms

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2
Q

what are the triad of synptoms in Alport syndrome?

A

Hereditary nephritis
Sensorineural hearing loss
Ocular abnormalities (cataracts, macular retinal flecks)

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3
Q

What is the renal abnormalities in Alport patients?

A

Proteinuria, haematuria, renal failure

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4
Q

What is thin basement membrname nephropathy?

A

a common cause of haematuria (asymptomatic)

good prognosis

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5
Q

what is IgA nephropathy?

A

the most common cause of glomerulonaphritis. and a cause of asymptomatic haematuria.

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6
Q

What is Wolfram syndrome?

A

a rare genetic disease that causes diabetes insipidus, diabetes
mellitus, optic atrophy and deafness

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7
Q

Do those with Downs have renal abnormalities?

A

The kidney tends to be spared in such patients

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8
Q

what type of cell lines the kidney to the urethra?

A

transitional cell epithelium

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9
Q

What are the risk facors of bladder cancer?

A

smoking
chemical dyes
aromatic amines

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10
Q

What is acute tubulointerstitial nephritis?

A

a drug hypersensitivity reaction most commonly to penicillin or NSAIDs

Fever, rash and painful joints.

Blood will have eosinophils (which in allergic responses such as asthma and drugs, and parastic infections)

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11
Q

What are the clinical features of Schistosomiasis?

A

can cause bladder cancer through chronic inflammation,
other symptoms include a local dermatitis at the area of penetration
while more systemic features include fevers, muscle pain and allergic rashes

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12
Q

What is acute tubular necrosis?

A

Commonly due to renal ischaemia

pharmacological toxicity (diuretics (volume depletion), redio-contrast dye)

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13
Q

What are the signs of acute tubular necrosis?

A

early oliguria followed by recovery of renal function with an increase in renal
output. GFR, however, may remain low due to tubular damage. Full renal
capacity is usually regained within 6 weeks of the initial stressor.

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14
Q

What is Haemolytic uraemic syndrome (HUS)?

A

AKI from RBC fragmentation due to thrombosis in the kidneys.

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15
Q

What are the triad of HUS?

A

heamolytic anaemia
thrombocytopeania
AKI

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16
Q

What is the cause of HUS?

A

E. coli bacterium, or shigalla.

The shiga toxin

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17
Q

Does SIADH cause hypokalaemia?

A

Nope

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18
Q

What does wegener’s granulomatosis do to the kidenys?

A

Antineutrophil cytoplasmic antibodies
(ANCAs) attack small to medium-sized blood vessels resulting in necrotizing
granulomatous inflammation.

REnal failure, patients can be asymptomatic to presenting with
renal failure on presentation

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19
Q

What is the histological finding of Wegener’s granulomatosis?

A

crescentic

necrotizing glomerulonephritis with the presence of RBC casts

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20
Q

What are the systemic features of minimal change nephropathy?

A

There is a high association with asthma and eczema

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21
Q

What is rapidly progressice glomerulonephritis?

A

Patients rapidly develop renal failure over

weeks and may have glomerular crescents on histology.

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22
Q

What are they types of rapidly progressive GN?

A

ANCA-associated glomerulonephritis, including Wegener’s granulomatosis,

Anti GBM antibody, Goodpasture’s disease

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23
Q

What is Goodpasture’s disease?

A

Goodpasture’s
disease (B) is due to a type 2 autoimmune reaction with antibodies attacking
the glomerular basement membrane and lung membrane. Patients often
present with upper respiratory tract complaints such as haemoptysis with renal
manifestations, such as anaemia and glomerulonephritis, occuring later.

24
Q

Whats is posr streptococcal GN?

A

usually associated with haematuria and hypertension
following a streptococcal infection which leads to an acute nephritis due to
deposition of immune complex

25
Q

what is the investigation for detecting diabetic nephropathy?

A

microalbumin in the urine

26
Q

Is serum creatinine an early or late marker of renal function?

A

Elevation in serum creatinine (C), which is usually excreted by the kidney, is a late marker of function renal impairment and not appropriate for early risk identification

27
Q

What do you find on electron microscopy in minimal change disease?

A

fusion of the podocyte foot process.

Pododcyte effacement

28
Q

Other than nephrotic syndrome what can minimal change disease present with?

A

eczema and asthema

29
Q

What can sustained hyperphosphataemia cause in the vascular structure?

A

Vascular calcification

30
Q

how do you treat hyperphosphataemia?

A

phosphate binders–> sevelamer

it bind to phosphates in the Gut and lowers the serum phosphaste level

it also lowers calcium and cholesterol

31
Q

Why do we give phosphates bilders before Vitamin D in those with 2nd hyperparathyroidism?

A

Vitamine D increases calcium and phosphate reabsorption and so can
inadvertently exacerbate the patient’s symptoms.

32
Q

Can you get parechymal gas accumulation in pyelonephritis?

A

Parenchymal infection

results in gas accumulation which is identifiable on CT scan

33
Q

Does renal stone cause renal infections?

A

they are rarely
coincident with renal infection as suggested by the urine dipstick

But the obstruction can lead to infections

34
Q

what is Kimmelstiel-Wilson lesion associated ith?

A

Diabetic nephropathy; glomerulosclerosis

35
Q

What is a red cell cast

A

RBC that have gotten into the renal tubules. It is a strong indication of glomerular pathology

36
Q

Explain the pathophysiology of diabetic nephropathy

A

an initial increase in glomerular filtration rate and glomerular basement membrane
hypertrophy.

As the disease progresses, glomerulosclerosis occurs as a result of accumulation of extracellular matrix and destroying the filtering ability of the glomerular membrane. This allows protein leakage.

37
Q

clinial test results of renal failure?

A

oliguric

raised urea and creatinine

38
Q

UTI clinical test result?

A

dysuria
rised WBC
leucocytes and nitrites (bacterias convert nitrates to nitrites)

39
Q

Triad of nephrotic syndrome?

A

Proteinuria (>3g/24hrs)
hypoalbuminaemia (<25g/L)
hyperlipidaemia

40
Q

1st line treatment of nephrotic syndrome?

A

fluid restrict
sodium restriction
diuretic (furosemide)

41
Q

How does ACE-I protect against protinuria?

A

It reduces filtration pressure on the glomerular capillaries.

42
Q

The disadvantage of US KUB

A

KUB US scan is poor at differentiating different

stones and can often miss smaller stones.

43
Q

Symptons of tuberculosis on the kidneys?

A

Insidious symptoms.

Pain in the back, flank and suprpubic region

Haematuria, frequency and noicturia

Most patients with renal TB have sterile pyuria, which can be accompanied by microscopic hematuria.

44
Q

What is the classic presentation og bladder cancer?

A

Painless haematuria

45
Q

The triad of renal cell carcinoma?

A

haematuria,
flank pain
flank/abdo mass

weight loss, fever, malaise

Anaemia from impaired erythropoiesis (SOB, pallor)

46
Q

what is post streptococcal GN

A

part of the nephritic syndrome

Patients usually suffer from a streptococcal infection 1–3 weeks prior to presenting with the symptoms or signs of the nephritic syndrome. During this time, immune
complexes are formed and deposited in the glomeruli causing damage.

47
Q

Symptoms of hypercalaemia

A

abdo pain
depression
constipation

48
Q

Presentation of polycyctic kidney disease

A

loin or abdo pain

symptoms of renal failure

49
Q

What are vascular findings of PKD?

A

mitral valve prolapse

berry aneurysms

50
Q

what is a medullary sponge kidney?

A

a congenital disorder of the kidneys that
is characterized by the formation of cystic sacs within the papillary zone
of the kidney creating a sponge-like appearance.

51
Q

what does a medullaty sponge kidney predispose you to?

A

The cysts create an
obstruction that prevents the optimal flow of urine through the renal
tubules, predisposing to UTIs, haematuria and renal calculi.

hemihypertrophy, hypercalciuria and renal tubular acidosis

52
Q

what do hotse shoes kidney cause?

A

UTI, renal stones

53
Q

What is analgesic nephropathy?

A

From chronic NSAIDs consumption

Papillary necrosis and tubulointerstitial nephritis. Anaemia, UTI and haematuria

54
Q

Acute hyperuricaemice nephropathy

A

A result of hyperuricaemia, common in patients with increased cell turnover, such as those with myeloproliferative disorders after chemo.

Uric acid crystallizes within in the renal system causing obstructions–> flank pain, oliguria, hypertension and oedema.

55
Q

symptoms of hypoglycaemia?

A

sweating, tachycardia, palpitations and tremor.

56
Q

Triads of goodpasture’s disease?

A

glomerulonephritis, pulmonary haemorrhage and anti-GBM

a type 2 autoimmune reaction, attach on type 4 collagen of the lungd and glomerulus.

Renal 500 SBA (1 decks)

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