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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
Q

What is the typical trio of drugs for immunosuppression regimens?

A

tacrolimus
prednisolone
mycophenolate

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26
Q

What is the definition of ‘kidney rejection’?

A

acute inflammatory state of the kidney, causing dysfunction and leukocyte infiltration
-> can lead to microthrombi formation

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27
Q

What is the definition of glomerulonephritis?

A

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

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28
Q

What are the causes of glomerulonephritis?

A

Primary - immune mediated, inflammatory, antibody deposition and immune complex deposition

Secondary - lupus, myeloma, infection, drugs, malignancy, amyloidosis, metabolic disorders (HTN, DM, thyroditis)

29
Q

Describe the 4 main congenital abnormalities of the kidneys:

A

1) VUR
2) BOU
3) PUJO
4) VUJO

30
Q

Describe ADPKD

A 
AD
PKD1/2 genes involved
Polycystin protein over-expressed
Progressive renal failure
Supportive treatment (BP, diuretics, limit H2O intake), RRT, ?tolvaptan (ADH antagonist)
31
Q

Describe VHL disease

A

AD
Multiple benign and malignant neoplasms form
Pts need annual screening: phaeos, renal tumours, brain tumours

32
Q

Describe tuberous sclerosis

A

AD
Benign hamartoma formation in various organs
CNS involvement, often co-associated with epilepsy

33
Q

Describe medullary cystic kidney disease

A

AD
Cysts form at the cortico-medullary junction
Small/normal sized kidneys
S/Sx of gout and increased uric acid

34
Q

Describe Alport’s syndrome

A

X-linked

Collagen mutations mean the GBM does not regenerate properly

35
Q

Describe Fabry’s disease

A

X-linked
alpha-galactosidase disorder and accumulation of Gb3 protein in glomeruli
Treatment = enzyme replacement therapy

36
Q

What are the 4 main systemic kidney diseases and how can they present?

A
  • diabetic nephropathy
  • amyloidosis
  • renal tubular stenosis
  • SLE

Present with: AKI, CKD, ESRF, nephrotic syndrome, nephritis syndrome

37
Q

Describe diabetic nephropathy

A

Disease of small kidney blood vessels
Presents w haematuria, proteinuria and renal failure
Eventually scarring, nodule formation, fibrosis and ESRF

38
Q

Describe amyloidosis

A

Extracellular protein deposition
AA = systemic amyloidosis
AL = light chain amyloidosis
Protein accumulation causes mesangial expansion

39
Q

Describe renal artery stenosis

A

part of systemic atheromatous vascular disease
reduced eGFR
Treatment: BP control, statins, lifestyle, angioplasty

40
Q

Describe SLE

A

Deposition of antibody complexes leading to inflammation and tissue damage
Tx: immunosuppression

41
Q

What are the functions of the kidney

A 
A-WET-BED
Acid/base balance
Water balance
Electrolyte balance
Toxin removal
BP control
EPO production
vitamin D metabolism (produces a-1-hydroxylase)
42
Q

What are the 4 classes of diuretics?

A

SGLT1/2 inhibitors (empagliflozin)
Loop diuretics (furosemide)
Thiazide diuretics (bendroflumethiazide)
K+ sparing diuretics (amiloride/spirololactone)

43
Q

Describe the difference between eGFR and creatinine clearance

A

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
Q

In rhabdomyolysis, why are there no RBC’s detected in urine microscopy, but the dipstick comes back blood +

A

This is because the haemoglobin is released causing the positive dipstick test, but there are no actual whole RBC’s in the urine

45
Q

What is dialysis?

A

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
Q

Describe haemodialysis and how it works

A

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
Q

Describe peritoneal dialysis and how it works

A

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
Q

What are the 5 most common reasons for someone needing a kidney transplant?

A 
CKD (due to DM, HTN, metabolic syndrome...)
Chronic infection
GN
ADPKD
Rarer (Allport's syndrome, cancer)
49
Q

Describe nephrotic syndrome

A
  • 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
Q

Describe nephritic syndrome

A
  • 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
Q

What is the treatment of nephrotic syndrome

A
  • dietary -> restrict Na intake
  • diuretics
  • avoid bedrest -> as high protein state means the pt is hypercoagulable
52
Q

Name the 3 nephrotic types of GN

A

minimal change disease
focal segmental glomerular sclerosis
membranous GN

53
Q

Name the 3 nephritic types of GN

A

IgA nephropathy
Post infectious GN
Rapidly progressive GN

54
Q

Which type of glomerulonephritis is most common in children?

A

Minimal change disease

55
Q

Which type of GN is associated with anti-phospholipase A2 receptor antibody?

A

Membranous GN (this antibody is seen in 70% cases)

56
Q

Which type of GN is the commonest in adults?

A

IgA nephropathy (also called Berger’s disease)

57
Q

How does IgA nephropathy present?

A 
Synpharyngeal presentation (sore throat and haematuria (usually macroscopic))
usually presents 24-48hrs post GI infection/UTI
58
Q

What type of infection normally causes post-infectious GN?

A

Usually a UTI (group A strep) and the GN presents weeks after the UTI

59
Q

Describe rapidly progressive GN

A

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
Q

How is GN investigated and generally treated?

A

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
Q

Name the 4 congenital abnormalities of the kidneys and urinary tract (CAKUT)

A
  • 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
Q

Describe ADPKD (autosomal dominant polycystic kidney disease)

A

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
Q

What is VHL

A

Von hippel lindau disease
AD
Multiple benign cysts and malignancy neoplasms
Annual screening for phaeochromocytomas/renal tumours/brain tumours

64
Q

Describe tuberous sclerosis

A

AD
Benign hamartoma formation of multiple systems (brain, heart, eyes, lungs…)
CNS involvement associated with epilepsy/CNS involvement

65
Q

Describe medullary cystic kidney disease

A

AD
cysts form at the cortico-medullary junction
presents with gout and hyperuricaemia

66
Q

Describe Alports syndrome

A

X linked (F carriers, M affected)
collagen mutations mean GMB does not regenerate properly
microscopic protenuria/haematuria
May need dialysis/transplant

67
Q

Describe Fabry’s disease

A

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
Q

Describe renal artery stenosis

A

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
Q

Describe kidney amyloidosis

A

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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