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Phase 3 > Renal > Flashcards

Renal Flashcards

1
Q

Define Nephrotic Syndrome:

A

Criteria is:
*Proteinuria >3.5g/ 24hours

  • Hypoalbuminemia <30g
  • Oedema

[Must have all these!!]

additional features are:

  • hypogammaglobulinemia
  • Hypercoagulable
  • hyperlipidaemia
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2
Q

List some things that can effect creatinine levels:

A

Muscle mass

Concentration of plasma
- dehydration

Secretion of creatinine ~15% secreted

Diet
- high protein may increase it slightly

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3
Q

What things can effect urea levels?

A

G.I bleeds

Dehydration

Liver failure
- low urea

Increased tissue breakdown
- steroids

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4
Q

What does eGFR take into account?

A

Plasma creatinine
Age
Gender
Race

expressed as GFR expressed as ml/min 1.73m2

MDRD - the method used.

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5
Q

How much can kidney function drop by before the creatinine level rises?

A

50%

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6
Q

What does eGFR not take into account?

A

Acute injury to kidneys.

this is because muscle mass takes time to build up levels.

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7
Q

What are the stages of CKD?

A

Stage 1:
>90, with other abnormality

Stage 2:
60-89, with another abnormality

Stage 3:
30-59

Stage 4:
15-29

Stage 5:
<15

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8
Q

If a person has glomerulonephritis, will both kidneys be affected?

A

Yes.

but maybe not all of the kidney will be affected.

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9
Q

What is needed to make a diagnosis of glomerulonephritis?

A

Biopsy

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10
Q

What tests are done during biopsy?

A

Light microscopy
- glomerular and tubular structure

Immunofluorescence
- looking for IgG

Electron Microscopy
- deposits on membrane

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11
Q

What will be seen with Rapid Progressing Glomerulonephritis?

A

Crescent formation of the glomeruli membrane

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12
Q

List the stages that occur leading to glomerulonephritis, and the possible therapeutic strategies that can be done:

A
  1. Insult
    - infection
    - antibody
  2. Injury
    - Block Ab
  3. Response to Injury
    - Steroids
    - cytotoxics
  4. Outcome
    - dialysis
    - transplantation
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13
Q

What is the most common primary nephritis?

How does it present?

A

IgA nephropathy
- minor urinary abnormalities

  • Hypertension

Renal impairment

Can be rapidly progressing

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14
Q

What is IgA nephropathy?

A

Mesangial disease - proliferation leading to failure of the kidney.

there is deposits of IgA with complement activation.

often presents with Strep infection - Synpharyngitic infection.

its also associated with:

  • liver disease
  • coeliac disease
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15
Q

What is Membranous Glomerulonephritis?

A

Disease of adults - specifically caucasians.
Most common cause of nephrotic syndrome

Associated with:

  • lung cancer
  • prostate cancer

Due to [Anti- phospholipase A2 Receptor] located on the podocytes.

Immune complex deposition within the deposts.

Variable nature:

  • third spontaneous remission
  • Third progress to ESRF
  • third progress to persistent proteinuria

Treatment:
Primary:
- control blood pressure
- immunotherapy - steroids, cyclophosphamide, cyclosporin

Secondary
- treat underlying condition

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16
Q

What is minimal Change disease?

A

Commonest cause of nephrotic syndrome in children
- so common unlikely to biopsy because likely to be this.

Disorder of the podocytes. - where you get fusion of the podocytes.
T - cell mediated disease

Associated with:
- Hodgkin’s

Associated with:
- URTI

Relapsing disease

Treatment:
- steroids

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17
Q

Crescentic Disease:

A

Rapidly Progressive Glomerulonephritis
- group of conditions that cause crescents on kidney biopsy

ANCA Vasculitis - MPO 
Lupus 
Good Pastures disease  - anti GBM 
Infection Associated 
Henoch -Schonlein Purpura
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18
Q

What nodules are seen with diabetic nephropathy?

A

Kimmelstiel wilson nodules

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19
Q

Why are angiograms and contrast CTs not done in renal disease?

A

Due to the contrast agents which can contraindicate in renal disease.

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20
Q

Where does the hypoxia first occur in renal system in renal stenosis?

A

Cortex - most metabolically active part

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21
Q

What are the two ways you can lose albumin?

A

Renal

Bowels

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22
Q

What is the diagnostic tests for Amyloidosis:

A

Congo Stain

  • Apple green bifridgence
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23
Q

What is the treatment for lupus?

A

Steroids
Cyclophosphamide
Rituximab

24
Q

Whats the gold standard for assessing renal scars?

A

DMSA

25
Q

What is MAG3 cystogram used?

A

Used for

Vesicoureteral Reflux

26
Q

Outline the grades of Vesicoureteral Reflux:

A

Grade 1:
- urine just makes it half way up ureter

Grade 2:
- Urine into the pelvis

Grade 3:
- dilatation of the pelvis

Grade 4:
- Torturous process of ureters and dilation

Grade 5:
- Massively tortuous and dilated.

27
Q

When can

Vesicoureteral Reflux be picked up?

A

In utero

After infection

28
Q

Whats the management for Vesicoureteral reflux:

A

Prophylaxis antibiotics

Surgery:

  • STING procedure
  • circumcision
29
Q

What is another common obstruction that can occur in children which involves faulty valves, and how does it present and how is it managed?

A

Posterior Urethral Valve

Presentation:

  • Antenatal Hydronephrosis
  • UTI
  • Poor Urinary Syndrome

Management:

  • Valve resection
  • antibiotic prophylaxis
  • CKD care

Outcome:
- Chronic renal failure

30
Q

Whats the most common cause of hydronephrosis in children?

A

Pelvi - Ureteric Junction Obstruction

Managed with:
- Pyeloplasty

31
Q

What is the most common congenital kidney disease?

A

Adult polycystic kidney disease
- Autosomal dominant condition

Caused by:

  • PKD1 - Chromosome 16
  • PKD1 - Chromosome 4

kidneys increases massively.

Diagnosed:
- Ultrasound

2 cysts need bilaterally in 15-30 years old.

Outcome:

50% risk of ESKD by 50 years

Cyst accidents - rupturing.

Management:

  • supportive
  • treat complications
  • Dialysis
  • Dialysis
  • Tolvaptan - reduces cyst formation
  • since its V2 antagonist they pass lots of water
32
Q

Name an inherited kidney disease that effects the collagen 4:

A

Alport’s syndrome

x-linked disease

Collagen 4 abnormalities

Symptoms:

  • renal
  • deafness
33
Q

Name an inherited kidney disease which effects storage defects;

A

Fabry’s disease

Angiokeratoma - associated skin pathology.

Alpha Gal A defect

34
Q

In someone with Minimal change disease what investigations would you carry out?

A

Urinalysis

  • high protein ++++
  • urine/ creatinine ratio

Serum albumin level

Coagulative factors
- often antithrombin is released

GFR

Serology

  • ANA
  • ANCA
  • Anti GBM

Renal ultrasound

  • not just checking for blockages
  • assessing kidney size
  • checking there is two kidneys

Chest - xray

  • pulmonary oedema
  • signs of hodgkins
35
Q

List some negative aspects of using eGFR:

A

Non- linear relationship but is expecnitional to kidney function.
- only starts to rise after 50% loss of kidney function

Overestimates kidney function in people with low muscle

Under estimates kidney function in people with large muscle mass

it is not useful for acute kidney failure
- there could be 0GFR and the creatinine would be normal until sufficient levels build up

It is inaccurate above eGFR >60. due to the studies it was conducted in

It is inaccurate in children - due to studies of people it was studied and developed in.

36
Q

What is some complication that can occur in people who are treated for glomerulonephritic conditions?

A

Infections - due to the high use of immunosupressants
namely - peritoneal infections in nephrotic patients.
*due to the movement of fluids

37
Q

What complications can occur in nephrotic syndromes?

A

Clots - due to lack of anti-thrombin III
- painful legs

Pulmonary Oedema - due to lack of Albumin to maintain oncotic pressure

Infections - Hypoglobulinemia

38
Q

In chronic kidney disease, why would you stop Thiazide diuretics?

A

Side effect is hyperuricaemia - thus in someone already prone to having high urea this could be dangerous

39
Q

Outwith direct analysis of the kidney, what other tests would you do to investigate someone with nephritic syndrome?

A

Chest - x- ray - checking for pulmonary edema

Sepsis check - these patients are hypoalbuminemic and predisposed to pneumococcal infections

Coagulation tests - loss of antithrombin III leaves these people predisposed to clots

Lipid tests - the liver secretes a high amount of lipids

40
Q

List some symptoms of AKI:

A

Oliguria

Oedema build up - around eyes and feet

Tachypnea

Confusion

Nausea

Chest pain

41
Q

List some medications associated with causing AKI:

A

Diuretics - dehydration

ACE and NSAIDs
- dysregulated autoregulation of the kidney

Gentamicin
- Acute tubular necrosis

Opiates
- blockage of the ureters

**usually it is a compensation or in the setting of damage kidneys already

42
Q

What is the Investigations in AKI:

A

Past medical history is absolutely key, to establish anything that may suggest hypovolemia or sorts.

Acute vs Chronic
- e-alert changes

FBC:

  • signs of anaemia
  • Hypocalcaemia
  • these are suggestive of long standing renal failure

U&Es
- specifically K+ levels - lack of excretion of K+ can lead to hyperkalemia

Urine output

Urine analysis

Osmolality of blood and urine

ABGs
- looking for acidosis - which can be common due to lack of filtration and excretion of H+

Underlying diagnosis

  • ANCAs
  • ANAs
  • IgA
  • volume stasis

Ultrasound
- establish post renal causes

ECG
- for hyperkalemia

43
Q

What is your management of AKI?

A

ABCS

Pre-renal:
- fluid - hartmann’s or saline

Remove causes

  • sepsis treat
  • drug causes - remove drugs

Remove obstructions

  • *treat hyperkalemia
  • this is what is likely to kill

Dialysis if not improving

  • refractory hyperkalemia
  • Refractory pulmonary oedema
44
Q

What features would you expect to see that suggest hyperkalemia and how would this be treated:

A

Tall T waves

Flattening of P waves

Prolongation of P- R interval

Broad QRS
- late component

Treatment:
- Calcium resonium
(stops absorption in the G.I)

  • Insulin - actarapid
    +/-
  • Glucose
  • Calcium gluconate
    (protects Membrane, less likely to be activated by K+

Treat Acidosis
- bicarbonate
(patients are likely to become acidotic in AKI due to failure of H+ secretion and HCO3- reabsorption - acidosis increases K+ build up)

Dialysis
- if needed

45
Q

What drugs are associated with tubular necrosis and should be stopped immediately in AKI?

A

Gentamicin

NSAIDs

ACE

Contrast

Poisons

**note some of these cause necrosis through dysregulation of blood flow and some cause it through direct toxicity

46
Q

What biochemical marker will be elevated in Rhabdomyolysis?

A

Serum Creatinine

47
Q

What side effect may Sulphonylureas or Insulin therapy have in CKD?

A

Kidneys play a role in insulin metabolism - therefore drugs increasing their level the person more predisposed to developing hypoglycemia

48
Q

Name some common causes of CKD:

A

Vascular:

  • HTN
  • Renal sclerosis
  • Diabetes

Congenital:

  • Polycystic kidney disease
  • Congenital Obstructive Uropathy

Glomerular disease:

  • Lupus
  • Amyloidosis
  • Wegner’s

Tubulointerstitial disease:

  • drug toxicity
  • TB

Urinary Tract obstruction

  • Calculus disease
  • Prostatic disease
49
Q

List some symptoms of CKD and why are these?

A

Symptoms usually refer to the build up of toxic metabolites:

  • malaise
  • Loss of appetite
  • nocturia (due to impaired ability to concentrate urine)
  • itching
  • nausea
  • restless legs

Advance stages:

  • Pericardial rub (urea irates the pericardium)
  • Encephalopathy
50
Q

What is the management of CKD:

A

Control of Blood pressure

Diabetic control

51
Q

Overview some common lab abnormalities seen in CKD:

A

Hyperkalemia
- lack of excretion and acidosis

Hypocalamia
- no Vit D activation and Increased Phosphate

Anemia
- No EPO drive

52
Q

CKD can cause bone destruction due to secondary hyperparathyroidism, what is this referred to as?

A

Renal Osteodystrophy

53
Q

What drug can be used as a synthetic EPO?

A

Darbepoetin Alfa

54
Q

What may cause a false positive for haematuria in the setting of AKI?

A

Rhabdomyolysis

it is myoglobin from muscle break down that is found in the urine and is nephrotoxic.

55
Q

Why is albumin lost during nephrotic disease?

A

There is loss of the negatively charged basement membrane

56
Q

What is a drug that can elevate the creatinine and how does it do this?

A

Trimethoprim

blocks excretion of creatine in DCT

57
Q

In pre renal AKI, what would you expect the urine osmolality to be?

A

HIgh - the kidneys will be concentrating the urine as much as possible

Phase 3 (50 decks)

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