Renal Med Flashcards

1
Q

What quantifies an AKI

A

Rise in creat more than 25micromol in 48 hrs

50% increase in creat in a week

Urine output less than 0.5ml/hr

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2
Q

What are the pre renal causes of AKI

A

Insufficient blood supply to kidneys

-Dehydration
-Shock- sepsis or blood loss
-HF

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3
Q

What are the renal causes of AKI

A

Intrinsic kidney disease
-Acute tubular necrosis
-Acute interstitial nephritis
-Haemolytic uraemia syndrome
-Rhabdomyolysis

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4
Q

What are the post renal causes of AKI

A

Outflow obstruction from kidneys
-Kidney stones
-Tumours
-Strictures/ ureters
-Benign prostatic hyperplasia
-Neurogenic bladder

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5
Q

What is acute tubular necrosis and what are it’s causes

A

Necrosis of epithelial cells of renal tubules
Most common renal cause of AKI

Caused by hypo perfusion and nephrotoxins (gentamicin or radio contrast)

Muddy brown casts on urinalysis

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6
Q

What is the management of acute tubular necrosis

A

Prevent by fluids and avoiding nephrotoxins

Treat with IV fluids and hold nephrotoxic drugs, reverse underlying cause/ relieve obstruction

Dialysis if needed

Stop ACE inhibit in AKI as they reduce filtration pressure

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7
Q

What is CKD and how does it present

A

Reduced kidney function over 3 months, eGFR below 60ml/min and urine:creatinine above 3

Diabetes, HTN, NSAID’s, Lithium,, glomerulonephritis, PKD

Fatigue, pruitis, oedema, HTN, peripheral neuropathy, nausea, pale, foamy urine

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8
Q

What are the scoring systems for CKD

A

G score- eGFR
G1- >90
G2- 60-89
G3a- 45-59
G3b- 30-44
G4- 15-29
G5- less than 15

A score- albumin:creatinine
A1 under 3
A2 3-30
A3 over 30

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9
Q

What referrals are made in CKD

A

Work out kidney failure risk equation- 5 yr risk of kidney failure

Refer to specialist if
eGFR less than 30
Urine ACR more than 70
Accelerated progression
5 yr risk over 5%
Uncontrolled HTN

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10
Q

What medications can be given in CKD

A

ACE inhibitors and statins
Want target BP under 130/80

Give ACE inhibit in
Diabetes + urine ACR over 3
HTN and urine ACR over 30
Anyone with Urine ACR over 70
Monitor serum potassium

SGLT2 inhibitors - Dapagliflozin
Given in diabetes and ACR over 30

Consider in diabetes and ACR 3-30
Non diabetes and ACR over 22.6

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11
Q

How does anaemia of chronic disease happen in CKD and how is it treated

A

CKD- not as much erythropoietin is made in the kidneys - normocytic anaemia

Treat with iron and erythropoietin

don’t blood transfuse - issues with immune reaction if transplant needed

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12
Q

How does renal bone disease occur in CKD and how is it treated

A

Reduced phosphate excretion causes high serum phosphate
Low vit D in serum ask kidneys can’t absorb it

Causes a secondary hyperparathyroidism - parathyroid glands secrete PTH in response to low fit d and high phosphate

PTH stimulates osteoclast activity to resorb and increase serum calcium

Causes osteomalacia and osteoclerosis (new bone formation due to osteoblasts but not properly mineralised)

Ruggery jersey spine

Treatment: Low phosphate diet, phosphate binders, active forms of fit D, adequate calcium intake

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13
Q

What is nephritic syndrome

A

Generic term for inflam of kidneys
Haematuria, oliguria, proteinuria, fluid retention

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14
Q

What is nephrotic syndrome

A

Basement membrane in glomerulus is permeable and causes proteinuriaa

Proteinuria more than 3g per 24hrs
Low serum albumin
Peripheral oedema
Hypercholesterolaemia

Oedema, frothy urine, predisposes to thrombosis , HTN and high cholesterol

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15
Q

What is the most common cause of nephrotic syndrome in children and in adults

A

Children- minimal change disease- idiopathic and treated with steroids

Adults- Membranous Neuropathy or local segmental glomerulosclerosis

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16
Q

What is IgA nephropathy (Berger’s)

A

Most common cause of glomerulonephritis in adults
Patient in 20s with haematuria, mesnagial cells in glomerulus and IgA deposits

17
Q

What is membranous neuropathy

A

Immune complexes in basement membrane - IgG and complement deposits

Can be idiopathic or caused by malignancy, SLE and NSAIDs

18
Q

What is membranoproliferative glomerulonephritis

A

Affects under 30s- immune complex deposits and mesangial proliferation

19
Q

What is post strep glomerulonephritis

A

Patients under 30 - 1-3 weeks after strep infection - tonsillitis or impetigo

20
Q

What is rapidly progressive glomerulonephritis

A

Acute severe illness but treats well - glomerular presents

21
Q

What is good pasture syndrome

A

anti-GBM antibodies attack glomerulus and pulmonary basement membranes- glomerulonephritis and pulmonary haemorrhage - in 20s or 60s

Acute kidney failure and haemolysis

22
Q

What systemic conditions can cause glomerulonephritis

A

Henoch Scholein purpura
Vasculitis - microscopic polyagnitis - pANCA
-granulomatosis with polyangitis cANCA
Lupus nephritis

23
Q

What is renal tubular acidosis

A

Metabolic acidosis due to pathology in kidney tubules- disrupted balance of hydrogen and bicarb ions

24
Q

What are the features of type 1 renal tubular acidosis

A

HYPOkalaemia
High urinary pH >6
Metabolic acidosis

Hydrogen ions can’t be excreted

Causes
Genetic, SLE, Sjogrens, primary biliary cholangitis, hyperthyroidism, sickle cell anaemia, Marfans syndrome

Failure to thrive in children, recurrencet UTI, bone disease, muscle weakness, arrhythmia

Treat with oral bicarb to correct acidosis and electrolyte imbalances

25
Q

What is type 4 renal tubular acidosis

A

Most common

HYPERkalaemia
Low urinary pH- low aldosterone function
metabolic acidosis

Low aldosterone activity due to
-Adrenal insufficiency
-Diabetic nephropathy
-ACE inhibit, spironolactone, epernone

Management
Treat underlying cause
Fludrocortisone in aldosterone def
Oral bicarb and treat hyperkalaemia

26
Q

What is type 2 renal tubular acidosis

A

High urine pH
Metabolic acidosis
Hypokalaemia

Inherited causes
Multiple myeloma and fonkoni’s syndrome

Treat with bicarb

Type 3 renal tubular acidosis is a mix of type 1 and 2

27
Q

What is haemolytic uraemia syndrome

A

thrombosis of small blood vessels due to shigella toxins

Gastroenteritis

Triad
Microangiopathic haemolytic anaemia
AKI
Thrombocytopenia (low plts)

Fever, abdo pain, reduced urine output etc, haematuria

Do a stool culture

Medical emergency
Hypovolaemia (IV fluids)
HTN
Severe anaemia
Severe renal failure

28
Q

What is rhabdomyolysis and how is it caused

A

Skeletal muscle breakdown where myoglobin, potassium, phosphate and creatine kinase are released

Treat hyperkalaemia first

Causes
Prolonged immobility
Extremely rigour exercise
Crush injuries
Seizures
Statins

Muscle pain. weakness, swelling, reduced urine output, red brown urine, fatigue, N&V, confusion

29
Q

how do you diagnose and treat rhabdomyolysis

A

CK needed for diagnosis
Myoglobinuria on dipstick
ECG- tall tented T- hyperkalaemia

Management
IV fluids
Treatment of hyperkalaemia
IV sodium bicarb
IV mannitol to increase urine output

30
Q

What are the causes and classifications of hyperkalaemia

A

AKI, CKD, rhabdomyolysis, adrenal insufficiency, Tumour lysis syndrome

Medication causes- ACE inhibit, ARBS, NSAIDs, aldosterone antagonists (spironolactone and eplereone)

Haemolysis can give false high K

Mild Hyperkalaemia - 5.4-6
Moderate 6-6.6
Severe - over 6.5

31
Q

What would a hyperkalaemia ECG show

A

-Tall tented t waves
-Flattened/ no p wave
-Prolonged PR interval
-Broad QRS complex

32
Q

What is the management of hyperkalaemia

A

Management
-Urgent treatment if
-EGC changes
-Serum K over 6.5

  1. insulin
  2. Dextrose
  3. Calcium glutinate

Nebulised salbutamol
Oral calcium resonium
Sodium bicarb
Dialysis if needed

33
Q

What are the main types of inheritance of polycystic kidneys

A

Autosomal dominant
PKD1 gene Chr 16 (most common)
PKD2 gene chr 4

Autosomal recessive
PKHD1 gene Chr 6 (more severe)

34
Q

What are the extra renal manifestations of PKD

A

Cerebral aneurysm - berry
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurg
Colonic diverticula

35
Q
A