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Year 4 > Medicine - Nephrology > Flashcards

Medicine - Nephrology Flashcards

1
Q

What does glucose in urinalysis mean?

A

• Diabetes

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2
Q

What does blood in urinalysis mean?

A

• Menstruation
• Nephritis syndrome
• Stones
Infection

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3
Q

What does leukocytes in urinalysis mean?

A

• Infection/UTI

Nephritic syndrome

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4
Q

What does protein in urinalysis mean?

A

• Nephrotic/nephritis syndrome

Myeloma

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5
Q

What does nitrites in urinalysis mean?

A

UTI (nitrites are produced by coliform bacteria)

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6
Q

What does ketones in urinalysis mean?

A
  • DKA

* Pregnancy

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7
Q

What does bilirubin in urinalysis mean?

A

• Jaundice (hepatic/post-hepatic)

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8
Q

What does SG (specific gravity) in urinalysis mean?

A

• High solute concentration

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9
Q

Define AKI

A

Reduction in renal function following an insult to the kidneys
High urea and creatinine and low urine output over hrs/days
95% systemic and both kidneys affected

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10
Q

What are the aetiologies of AKI?

A

1) Pre-renal (issue with blood supply)
- sepsis
- NSAIDs/ACEi
- dehydration, bleeding, burns, D&V
- MI, cardiogenic shock
- renal artery stenosis
2) Renal (mixed)
- due to GN, vessels or tubular issues
- ATN, vasculitis, DIC, HUS, drugs, rhabdomyolysis, myeloma, sarcoidosis
3) Post-renal (obstructive)
- issue after the kidneys e.g. extrinsic compression, ureteric stone, BPH, hydronephrosis, external kidney compression

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11
Q

What are the three stages of an AKI? and its features

A

Stage 1 = serum creatinine 1.5-1.9x baseline
Stage 2 = serum creatinine 2-2.9x baseline
Stage 3 = serum creatinine >3x baseline

Features: reduced urine output, pulmonary and peripheral oedema, arrhythmias (electrolyte changes and increased K+ as the kidney are not excreting it!), uraemia (pericarditis, encephalopathies)

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12
Q

Describe the effect of NSAIDs and ACEi on the kidney

A

NSAID’s:

  • Stop COX pathways
  • No prostaglandin production
  • Prostaglandins are needed to dilate the afferent arteriole
  • NSAID’s result in reduced blood supply to the kidney = AKI!

ACEi:

  • Stop the production of AT1 -> AT2
  • AT2 causes the efferent arteriole to constrict to maintain BP within the kidney
  • No AT2 -> kidney hypotension = AKI
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13
Q

What investigations should be carried out in AKI?

A 
RENAL!
Rule out sepsis
Exclude obstruction
Note urinalysis
Assess fluid balance
Look at drugs

Bloods - FBC, U&E, DH, CK (rhabdo?), GN screen (ANCA/ANA)
Urinalysis (infection/rhabdo)
Renal USS (?obstruction)
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14
Q

What is the management for AKI?

A

Stop nephrotoxic drugs and give IV fluids
Depends on cause:
- pre-renal: correct volume depletion
- renal: ?biopsy if intrinsic disease
- post-renal: catheterise/nephrostomy
Correct any: hyperkalaemia, pulmonary oedema or hypoperfusion

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15
Q

What are indications for RRT in AKI?

A

Acidosis
Fluid overload (e.g. pulmonary oedema)
Uricaemia
Hyperkalaemia

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16
Q

Define CKD and its stages

A

Abnormal kidney structure/function (GFR <60) which is present for >3 months with implications for health

Stage 1 = eGFR >90
Stage 2 = eGFR >60
Stage 3a = eGFR 45-59
Stage 3b = eGFR 30-44
Stage 4 = eGFR 15-29
Stage 5 = eGFR <15
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17
Q

What are the causes of CKD

A 
Diabetic nephropathy
Ischaemia/renovascular disease
Glomerulonephritis
Pyelonephritis
ADPKD
Obstructive nephropathy
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18
Q

What are the signs and symptoms of CKD?

A

Signs: pulmonary oedema, peripheral oedema, pericardial rub, rash (due to toxins), HTN, tachypnoea, cachexia, pallor, yellow skin tinge

Symptoms: when eGFR<15, pruritis, weight loss, anorexia, nausea, fatigue, oedema (leg swelling, breathlessness), nocturia, joint/bone pain, confusion

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19
Q

What investigations should be carried out for CKD?

A

Bloods: U&E, eGFR, creatinine
Urinalysis: microalbuminaemia
Renal USS

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20
Q

How is CKD managed?

A

5 principles of management

1) nephro referral
2) slow the disease progression: BP control, good DM and glycaemic control, lifestyle measures (diet, smoking, cholesterol)
3) treat CKD complications (AFUS!)
4) treat non-CKD complications (anaemia, mineral bone disorder = ca and vitamin D replacement)
5) prepare for RRT

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21
Q

What are the complications of CKD?

A

Think normal kidney functions, then what goes wrong:

Water balance - fluid overload
Electrolyte balance - hyperkalaemia
Toxin destruction - uricaemia
BP - HTN
EPO - anaemia
vit D production - OP
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22
Q

What are the indications for dialysis?

A

A-FUH

  • acidosis
  • fluid overloaded
  • uricaemia
  • hyperkalaemia
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23
Q

What are the pros and cons of transplantation of kidney?

A 
PROS:
more independence
fertility improved
life expectancy better
cost saving long term

CONS:
immunosuppression increases malignancy risk
infection
rejection
delayed graft function
post-transplant diabetes
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24
Q

What are the types of kidney donation?

A

1 - Living donor (altruistic (no relation, out of kindness) or allogenic (usually a relation))
2 - Deceased donor

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25
What is the typical trio of drugs for immunosuppression regimens?
tacrolimus prednisolone mycophenolate
26
What is the definition of 'kidney rejection'?
acute inflammatory state of the kidney, causing dysfunction and leukocyte infiltration -> can lead to microthrombi formation
27
What is the definition of glomerulonephritis?
renal disease characterised by inflammation and damage to glomeruli, which allows protein +/- blood to leak into the urine Rare, but can progress to CKD and ESRF
28
What are the causes of glomerulonephritis?
Primary - immune mediated, inflammatory, antibody deposition and immune complex deposition Secondary - lupus, myeloma, infection, drugs, malignancy, amyloidosis, metabolic disorders (HTN, DM, thyroditis)
29
Describe the 4 main congenital abnormalities of the kidneys:
1) VUR 2) BOU 3) PUJO 4) VUJO
30
Describe ADPKD
``` AD PKD1/2 genes involved Polycystin protein over-expressed Progressive renal failure Supportive treatment (BP, diuretics, limit H2O intake), RRT, ?tolvaptan (ADH antagonist) ```
31
Describe VHL disease
AD Multiple benign and malignant neoplasms form Pts need annual screening: phaeos, renal tumours, brain tumours
32
Describe tuberous sclerosis
AD Benign hamartoma formation in various organs CNS involvement, often co-associated with epilepsy
33
Describe medullary cystic kidney disease
AD Cysts form at the cortico-medullary junction Small/normal sized kidneys S/Sx of gout and increased uric acid
34
Describe Alport's syndrome
X-linked | Collagen mutations mean the GBM does not regenerate properly
35
Describe Fabry's disease
X-linked alpha-galactosidase disorder and accumulation of Gb3 protein in glomeruli Treatment = enzyme replacement therapy
36
What are the 4 main systemic kidney diseases and how can they present?
- diabetic nephropathy - amyloidosis - renal tubular stenosis - SLE Present with: AKI, CKD, ESRF, nephrotic syndrome, nephritis syndrome
37
Describe diabetic nephropathy
Disease of small kidney blood vessels Presents w haematuria, proteinuria and renal failure Eventually scarring, nodule formation, fibrosis and ESRF
38
Describe amyloidosis
Extracellular protein deposition AA = systemic amyloidosis AL = light chain amyloidosis Protein accumulation causes mesangial expansion
39
Describe renal artery stenosis
part of systemic atheromatous vascular disease reduced eGFR Treatment: BP control, statins, lifestyle, angioplasty
40
Describe SLE
Deposition of antibody complexes leading to inflammation and tissue damage Tx: immunosuppression
41
What are the functions of the kidney
``` A-WET-BED Acid/base balance Water balance Electrolyte balance Toxin removal BP control EPO production vitamin D metabolism (produces a-1-hydroxylase) ```
42
What are the 4 classes of diuretics?
SGLT1/2 inhibitors (empagliflozin) Loop diuretics (furosemide) Thiazide diuretics (bendroflumethiazide) K+ sparing diuretics (amiloride/spirololactone)
43
Describe the difference between eGFR and creatinine clearance
eGFR is calculated using MDRD formula and only calculates an accurate value if GFR is >60 Creatinine clearance is BETTER than eGFR as it takes into account body weight and SA CC = (140 - age/creatinine) x weight x 1.04/1.23
44
In rhabdomyolysis, why are there no RBC's detected in urine microscopy, but the dipstick comes back blood +
This is because the haemoglobin is released causing the positive dipstick test, but there are no actual whole RBC's in the urine
45
What is dialysis?
method of removing nitrogenous waste from the body and maintaining extracellular volume, maintaining normal electrolytes and correcting acidosis Blood filtration Types: haemodialysis, peritoneal dialysis, transplantation!
46
Describe haemodialysis and how it works
removes solute by diffusion and fluid by osmosis Blood passed over a semi-permeable membrane and the dialysis fluid on the other side of the membrane moves in the opposite direction Dialysate contains electrolytes Blood volume falls and dialysate can be discarded Home/hospital based for 4hrs 3x a week Needs carer, space, and is expensive
47
Describe peritoneal dialysis and how it works
Catheter inserted into the peritoneum and dialysate inserted The peritoneal membrane acts as a semi-permeable membrane and solute/waste slowly diffuses from the abdominal capillaries into the peritoneal fluid Then the peritoneal fluid is emptied and replaced Needs draining and filling so risk of peritonitis, hernias Sclerosis and catheter dislodging can occur Best option for pts with some residual renal function
48
What are the 5 most common reasons for someone needing a kidney transplant?
``` CKD (due to DM, HTN, metabolic syndrome...) Chronic infection GN ADPKD Rarer (Allport's syndrome, cancer) ```
49
Describe nephrotic syndrome
- non-proliferative, lack of glomeruli cell proliferation - damaged podocytes lead to proteinuria and low serum albumin - increased risk of infections, and increased risk of venous thromboembolism due to increased lipidaemia FEATURES: oedema, low albumin, proteinuria, hyperlipidaemia
50
Describe nephritic syndrome
- proliferative, increased glomeruli cells, inflammatory damage - leads to haematuria - IF SCARRING occurs, also leads to proteinuria - DANGEROUS as can progress to ESRF FEATURES: PHHR - proteinuria - haematuria - HTN - renal impairment
51
What is the treatment of nephrotic syndrome
- dietary -> restrict Na intake - diuretics - avoid bedrest -> as high protein state means the pt is hypercoagulable
52
Name the 3 nephrotic types of GN
minimal change disease focal segmental glomerular sclerosis membranous GN
53
Name the 3 nephritic types of GN
IgA nephropathy Post infectious GN Rapidly progressive GN
54
Which type of glomerulonephritis is most common in children?
Minimal change disease
55
Which type of GN is associated with anti-phospholipase A2 receptor antibody?
Membranous GN (this antibody is seen in 70% cases)
56
Which type of GN is the commonest in adults?
IgA nephropathy (also called Berger's disease)
57
How does IgA nephropathy present?
``` Synpharyngeal presentation (sore throat and haematuria (usually macroscopic)) usually presents 24-48hrs post GI infection/UTI ```
58
What type of infection normally causes post-infectious GN?
Usually a UTI (group A strep) and the GN presents weeks after the UTI
59
Describe rapidly progressive GN
Nephritic type Breaks in the GBM allow inflammatory cells to enter the glomeruli and infiltrate bowmans capsule Type 1 -> anti-GBM disease (Goodpasture's syndrome), autoantibody made against type 4 collagen ``` Type 2 (vascuitics) a ->microscopic polyangitis b -> granulomatosis w. polyangitis ```
60
How is GN investigated and generally treated?
Inv. - bloods (check BM, ANCA, ANA, anti-phospholipid-A2R-Ab, bence jones protein) - biopsy (allows histological examination) - > light and electron microscopy and immunoflourescence! General treatment: steroids/immunosuppression
61
Name the 4 congenital abnormalities of the kidneys and urinary tract (CAKUT)
- VUR (vesico-ureteric reflux) = retrograde flow of urine from bladder -> ureters - VUJO (vesico-ureteric junction obstruction) = obstruction where ureters meet bladder - PUJO (pelvic-ureteric junction obstruction) = obstruction where ureters enter kidneys - BOU = bladder outlet obstruction = bladder outlet obstruction, due to BPH/neurogenic bladder
62
Describe ADPKD (autosomal dominant polycystic kidney disease)
AD (PKD1/2) Increased cyst growth, reduced kidney functional volume and reduced eGFR Normal kidney function until ~40yrs Presents as loin pain, haematuria, high BP, investigate with USS/CT/MRI Mainly supportive management, RRT or tolvaptan (ADH antagonist to prevent fluid reabsorption and reduce the stress on the kidneys)
63
What is VHL
Von hippel lindau disease AD Multiple benign cysts and malignancy neoplasms Annual screening for phaeochromocytomas/renal tumours/brain tumours
64
Describe tuberous sclerosis
AD Benign hamartoma formation of multiple systems (brain, heart, eyes, lungs...) CNS involvement associated with epilepsy/CNS involvement
65
Describe medullary cystic kidney disease
AD cysts form at the cortico-medullary junction presents with gout and hyperuricaemia
66
Describe Alports syndrome
X linked (F carriers, M affected) collagen mutations mean GMB does not regenerate properly microscopic protenuria/haematuria May need dialysis/transplant
67
Describe Fabry's disease
X-linked storage disorder a-galactosidase deficiency, resulting in accumulation of Gb3 protein in glomeruli = proteinuria and ESRF Patients also get cardiac neuropathy and angiokeratomas Treat with enzyme replacement!
68
Describe renal artery stenosis
Part of systemic atheromatous disease Progressing narrowing of the renal arteries with atheroma Reduced eGFR Irreversible kidney damage develops as cortical hypoxia leads to fibrosis of parenchyma Treat: BP control, statins, lifestyle, angioplasty
69
Describe kidney amyloidosis
extracellular protein deposition, due to pathological misfolding of proteins proteins can deposit in: - kidneys, liver, heart, gut 2 types: - AA (systemic amyloidosis) - AL (light chain amyloidosis) Protein causes mesangial expansion

Year 4 (28 decks)

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