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Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Nephrotic Syndrome:

  • there is massively increased what?
  • due to abnormalities of what?
  • what are the main 3 features?
A
  • increased filtration of macromolecules across the glomerular capillary wall
  • due to structural/functional abnormalities of the glomerular podocytes
  • hypoalbuminaemia, oedema and hypercholesterol/triglycerid-aemia
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2
Q

Podocyte dysfunction in nephrotic syndrome causes the triad of -hypoalbuminaemia, oedema and hypercholesterol/triglycerid-aemia, explain each.

A
  • hypoalbuminaemia: (<30g/L) due to heavy proteinuria (>3.5g/24hrs) and increased renal catabolism of filtered protein
  • oedema: due to sodium retention in CDs + increased capillary permeability, reduced circulating volume
  • high choles/TGs: common due to increased synthesis and impaired catabolism
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3
Q

Nephrotic Syndrome with ‘bland urine sediments’

-most common causes?

A

-membranous nephropathy and FSGS or minimal change in children

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4
Q

Nephrotic Syndrome with ‘bland urine sediments’ - caused by Membranous nephropathy

  • what is membranous n?
  • what are the most common causes?
A
  • IgG and C3 deposition along outer side of glomerular BM, BM expands as deposits slowly are resorbed
  • usually idiopathic or SLE/thyroiditis related, neoplasitc related, infection of sarcoid/sickle cell related or drug induced
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5
Q

Nephrotic Syndrome with ‘bland urine sediments’ - caused by Membranous nephropathy
-membranous (IgG and C3 deposition around BM) can be secondary to drugs or infections name 3 examples

A
  • drugs: penicillamine, gold, NSAIDs

- infections: hepatitis B and C, schistosomiasis, plasmodium malariae

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6
Q

Nephrotic Syndrome with ‘bland urine sediments’

  • is often caused by focal segmental glomerulosclerosis, what population is it more common in?
  • a similar histological appearance occurs in what?
A
  • black adults

- HIV

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7
Q

Nephrotic Syndrome with ‘bland urine sediments’

  • minimal change is a common cause in children (boys <5yrs mostly)
  • findings on light microscopy vs EM?
A

-glomeruli normal on light microscopy but on EM can see fusion of the podocytes (foot processes of epithelial cells)
NB: increase in glomerular permeability is suspected to be immunologically mediated

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8
Q

Nephrotic Syndrome with ‘bland urine sediments’

-Name 2 Causes that are NOT immune mediated?

A
  • associated with renal amyloid

- associated with diabetes

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9
Q

Nephrotic Syndrome with ‘active’ urine sediments (mixed nephrotic/nephritic)

  • can be primary or secondary glomerular disease causing this
  • suggest one primary cause that occurs with chronic infection (/idiopathic)
A
  • mesangiocapillary membranoproliferative glomerulonephritis (renal failure develops over years)
  • mesangial proliferative glomerulonephritis
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10
Q

Nephrotic Syndrome with ‘active’ urine sediments (mixed nephrotic/nephritic)

  • can be primary or secondary glomerular disease causing this
  • one primary cause is mesangial proliferative glomerulonephritis-describe it’s findings?
A
  • presents with heavy proteinuria, minimal changes on light microscopy
  • deposits of IgM and complement (IgM or C1q nephropathy) in the glomerular mesangium
  • some pts respond to steroids, others progress to renal failure
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11
Q

Podocyte dysfunction in nephrotic syndrome causes what clinical features and hence what 2 ddx’s may arise?

A
  • hypoalbuminaemia, oedema and hypercholesterol/triglycerid-aemia
  • ankle, genitals, abdo wall oedema (face/arms rarely)
  • ddx: CCF-but JVP would be raised whereas is low in/normal in nephrotic, cirrhosis
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12
Q

Investigations in Nephritic Syndrome Glomerular Disease:

  • baseline (4)
  • for diagnosis: -urine__?,-culture? -bloods?-
  • serum ix: what Igs and antigens
  • imaging?
A

baseline: eGFR, urine protein, U&Es, serum albumin
- diagnosis: urine microscopy, culture, serum U&E, albumin
- serum: ANA, anti-DNA Ig, ANCA, anti-GBM Ig, hepBsAg, hepCIg, HIV Ig, Cryoglobulins
- imaging: CXR, US kidneys, renal biopsy

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13
Q

What will you see on urine microscopy in a pt with nephrotic syndrome glomerulonephritis?
What may a throat swab come back positive with?
And blood glucose is checked because?

A
  • red cell casts
  • recent streptococcal infection + present
  • in case diagnosis of diabetes mellitus (RF for these renal diseases)
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14
Q

Wegener’s granulomatosis/Granulomatosis with polyangiitis can cause blood vessel inflamm. in nose, sinuses, throat, lung and kidney, what may be seen on CXR?

A

-Cavities

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15
Q

Complications of Nephrotic Syndrome name 3

A
  • Venous thrombosis
  • Sepsis
  • AKI
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16
Q

Why is there a predisposition for venous thrombosis in nephrotic syndrome? Presentation/diagnosis of this?

A
  • loss of clotting factors, in peripheral and renal veins
  • presents with renal pain, haematuria, and deteriorating renal function.
  • diagnose by US
17
Q

Why can sepsis arise as complication of nephrotic syndrome?

Why can AKI?

A
  • sepsis as loss of Ig in urine increases susceptibility to infection (common cause of death)
  • AKI usually arises as consequence of hypovolaemia (esp. after diuretic therapy) or renal vein thrombosis
18
Q

Acute nephritic glomerulonephritis is characterised by what? (4)
NB: process is caused by an immune response that is triggered by disease/infection
e.g. post-streptococcal (group A beta-heamolytic) is a trigger in children
then bacterial antigen is trapped in glomerulus –> acute diffuse proliferative glomerulonephritis

A
  • haematuria (+red cell casts on microscopy)
  • proteinuria (<2g in 24hrs)
  • hypertension and oedema (periorbital/leg/sacral) caused by salt/water retention
  • oligouria
  • uraemia
19
Q

Acute nephritic glomerulonephritis
NB: process is caused by an immune response that is triggered by disease/infection
Suggest 5 diseases commonly associated?

A
  • e.g. post-streptococcal (group A beta-haemolytic) is a trigger in children - antigen is trapped in glomerulus –> acute diffuse proliferative glomerulonephritis
  • non-streptococcal post-infectious e.g. staphylococcus, mumps, legionella, hep B, hep C, schistosomiasis, malaria
  • Infective endocarditis
  • shunt nephritis
  • visceral abscess
  • SLE
  • Henloch-Schonlein syndrome
  • Cryoglobulinaemia
20
Q

Rx/management for nephritic syndrome:

e. g. post-streptococcal
- hypertension rx:
- fluid balance:
- in SLE/systemic vasculitis related:

A
  • e.g. post-streptococcal - supportive measures, spontaneously recovers
  • hypertension: treat with salt restriction, loop diuretics, and vasodilators
  • fluid balance: daily weights, input/output charts (if oliguric and overloaded must fluid restrict)
  • in SLE/systemic vasculitis related: immunosuppression e.g. prednisolone, cyclophosphamide, azathioprine or rituximab
21
Q

Rapidly progressive glomerulonephritis has 3 main causes:

A

-on background of acute nephritic syndrome
-anti-glomerular basement membrane disease (+lung involvement = Goodpasture’s)
-antineutrophilic cytoplasmic antibody (ANCA)-associated vasculitis
(treat the AKI and specific rx vs the cause)

22
Q

Reflux nephropathy aka chronic/atrophic pyelonephritis arises from what?
leading to what?

A

-childhood UTIs in combo with vesicourethral reflux (incompetent valve between bladder and ureter)
leading to progressive renal scarring presenting as HT or CKD in childhood/adult life

23
Q

Renal cysts are common with age, usually asymptomatic and incidentally found, occasionally what symptoms may occur?

A
  • pain

- haematuria

24
Q

ADPKD (autosomal dominant polycystic kidney disease) is a common 1:1000 condition due most commonly to a mutation in the ____ gene (short arm of chromosome __) which encodes for a protein “______1” - an integral membrane protein that regulates t____ and v____ development in kidneys and other organs.
(PKD2 mutation on chrsm 4 makes up rest of cases cause).

A
  • PKD1 gene (chrsm 16)
  • polycystin 1
  • regulates tubular and vascular development
25
Q

ADPKD (autosomal dominant polycystic kidney disease), due most commonly to a PKD1 mutation (chrsm 16) affecting tubular/vascular development causes what sort of disease/progression?

A
  • multiple cysts develop in both kidneys
  • cysts increase in size with age –> renal enlargement and progressive destruction of normal renal tissue
  • with gradual loss of renal function
26
Q

ADPKD (autosomal dominant polycystic kidney disease) 5 clinical features:
clue: pain-why?, 50% by 50yrs have …, cysts where else?, brain ? heart?

NB: presents any age from 20s

A
  • acute loin pain due to cyst haemorrhage/infection or urinary tract stone formation (uric acid)
  • abdo discomfort caused by renal enlargement
  • hypertension
  • progressive renal impairment (ESRF in 50% pts by 50yrs)
  • liver cysts, rarely cyst in pancreas/spleen/ovaries
  • subarachnoid haemorrhage - intercranial aneurysms common
  • mitral valve prolapse (20%)
27
Q

Diagnosis of ADPKD (autosomal dominant polycystic kidney disease) is definitively established by ?
Clinical exam demonstrates what?

A
  • US

- clinical exam: large irregular kidneys, hypertension +/- hepatomegaly

28
Q
  • in adults with a family hx of ADPKD (autosomal dominant polycystic kidney disease), diagnosis criteria by age of patient:
  • <30
  • 30-60
  • 60+
A

2+ unilateral renal cysts in pts <30yrs,
2 cysts in each kidney 30-60yrs and
4 cysts in each kidney 60yrs+

29
Q

Management or monitoring of polycystic kidney disease:

who should be offered screening in their 20s?

A
  • no rx slows progression or reduces cyst size
  • BP should be controlled
  • monitor disease progression by regular serum creatinine check ups
  • many will eventually need RRT by dialysis/transplant
  • offer children and siblings of pts with the disease screening with renal ultrasound
30
Q 
What is medullary sponge kidney ? 
Dilatation of ? in the ? +/- \_\_\_ change
What forms within the \_\_\_?
Pts present with renal \_\_\_ and \_\_\_\_\_
20% get h\_\_\_\_\_ or \_\_\_\_ \_\_\_\_ a\_\_\_
NB: Diagnosed by excretion urography
A
  • rare condition with dilatation of the CDs in the papillae +/- cystic change
  • in severe cases, the medullary area has a sponge-like appearance
  • small calculi form within the cysts
  • pts present with renal colic / haematuria
  • 20% get hypercalciuria or renal tubular acidosis

Medicine (10 decks)

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