Renal Flashcards

1
Q

How is Acute Kidney Injury defined?

A

Rapid (<7 Days) and sustained (>24 Hrs) reduction in Renal Faiure resulting in Oliguria and a rise im serum Creatinine and Urea.

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2
Q

What are the effects caused by an AKI?

A

Fluid - Oliguria, Hypervolaemia

Electrolyte - Hyperkalaemia

Acid-Base - Metabolic Acidosis

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3
Q

How is Chronic Kidney Disease defined?

A

>3 Months

Abnormal structure or function

GFR <60ml/min for >3 Months

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4
Q

Which symptoms will a patient with an AKI typically present with?

A

Depends on Cause

Oliguria/Anuria

Nausea/Vomiting

Dehydration

Confusion

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5
Q

Which signs will a patient with an AKI typically present with?

A

HTN

Distended Bladder

Dehydration (Postural Hypo)

Fluid Overload (JVP, Oedema)

Pallor, Rash, Bruising

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6
Q

How would you classify the causes of an AKI?

A

Pre-Renal - Hypoperfusion

Renal - Cellular Damage

Post-Renal - Obstruction

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7
Q

What are the causes of a Pre-Renal AKI?

A

Hypovolaemia - Renal Loss (Diuretics, DKA), Extrarenal Loss (Vomiting, Diarrhoea, Bleeding etc.)

Systemic Vasodilation - Sepsis

Decreased Cardiac Output - Heart Failure, MI

Intrarenal Vasoconstriction - Cardiorenal/Hepatorenal Syndromes

Renal Artery Stenosis +- ACEi

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8
Q

What are the main causes of Renal AKIs?

A

Tubular - Acute Tubular Necrosis (Ischaemia, Nephrotoxic Agents)

Glomerular - Glomerulonephritis

Interstitial - Interstitial Nephritis

Vascular - Vessel Obstruction

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9
Q

What are the Post-Renal causes of an AKI?

A

Luminal - Stones

Mural - Malignancy

Extrinsic - Retroperitoneal Fibrosis

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10
Q

Which drugs can cause Renal AKIs?

A

Commonly

Paracetamol

NSAIDs

ACE Inhibitors

Aminoglycosides

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11
Q

What are the Vascular Causes of an AKI?

A

Large Vessel Occlusion - ie. Thrombosis

Small Vessel (Microangiopathy) - HUS, TTP, DIC

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12
Q

What is Haemolytic Uraemic Syndrome?

A

Microangiopathy characterised by:

Progressive Renal Failure

Microangiopathic Haemolytic Anaemia

Thrombocytopaenia

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13
Q

What causes HUS?

A

E.Coli 0157:H7 Gastroenteritis, typically in children

Endothelial Damage

Thrombosis, Platelet. Consumption, Fibrin strand deposition, Thrombocytopenia

RBC Destruction - Anaemia & Schistocytes.

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14
Q

What is Thrombotic Thrombocytopenic Purpura?

A

Disorder characterised by the formation of thrombi in small-vessels.

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15
Q

How does TTP typically present?

A

Pentad:

Haemolytic Anaemia, Uraemia, Thrombocytopenia (HUS)

+ Fever

+ Neurological Sx (Seizures, Hemiparesis, Decreased GCS, Vision Defects)

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16
Q

What is Glomerulonephritis?

A

Inflammation of the Glomerui and Nephrons.

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17
Q

How does Glomerulonephritis typically present?

A

No ‘Typical’ Presentation - Wide spectrum of disease

Loss of barrier function - Proteinuria, Haematuria

Loss of filtering capacity - Reduced Excretion.

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18
Q

How does Nephrotic Syndrome Present?

A

Proteinuria

Low Serum Albumin

Oedema

19
Q

Why does Hyperlipidaemia often occur in Nephrotic Syndrome?

A

Hypoalbuminaemia increases Lipid production in the Liver as a compensatory mechanism.

20
Q

What are the most common causes of Nephrotic Syndrome?

A

Adults - Membranous Glomerulonephritis / Diabetes Mellitus

Children - Minimal Change Disease

Also: SLE, Amyloidosis, HBV/HCV

21
Q

How does Nephritic Syndrome typically present?

A

Hypertension

Haematuria

Oedema

(Oliguria)

22
Q

What are the most common causes of Primary Glomerulonephritis?

A

Berger’s Disease (IgA Nephropathy)

Henoch-Schonlein Purpura

Anti-GBM (Goodpasture’s)

Post-Strep

23
Q

What are the most common causes of Nephritic Syndrome?

A

IgA Nephropathy

Post-strep

Vasculitis

SLE

Anti-GBM DIsease

24
Q

How does IgA Nephropathy typicallhy present?

A

Soon after URT Infection

Episodic Haematuria

25
Q

How does Henoch Schonlein Purpura typically present?

A

Purpuric Rash on Extensors

Haematuria

Polyarthritis

26
Q

How does Anti-GBM (Goodpasture’s) Disease typically present?

A

Haematuria

Haemoptysis

27
Q

How does Post-Streptococcal Glomerulonephritis typically present?q

A

1-2 weeks after a throat/skin infection.

Nephritic Syndrome

28
Q

How would you investigate Glomerulonephritis?

A

Bloods - FBC, U&Es, CRP, Complement, Autoantibodies (SLE)

Urine - Protein, Blood

Renal USS +/- Biopsy

29
Q

How would you manage a case of Glomerulonephritis?

A

Refer

Manage BP

ACE Inhibitors or Angiotensin Receptor Blockers

Steroids/Immunosuppression

Treat Cause

30
Q

What are the main causes of Acute Tubular Necrosis?

A

Ischaemia (Hypovolaemia, Low CO, Sepsis, DIC)

Nephrotoxic Agents (Drugs, Rhabdomyolysis, Myeloma)

31
Q

How does Myeloma present?

A

CRAB

HyperCalcaemia

Renal Failure - Raised Urea & Creatinine

Anaemia

Bone Lesions & Pain

32
Q

Which complications can occur as a result of an AKI?

A

Uraemia

Hypervolaemia

Hyperkalaemia

Hyperphosphataemia

Metabolic Acidosis

CKD

33
Q

How should you manage an AKI?

A

Volume Status

Stop Nephrotoxic Drugs

Treat the cause

Manage Complications

Renal Replacement Therapy (If complications are refractory to medical therapy)

34
Q

Which complications can occur as a result of CKD?

A

Acidosis

Hyperkalaemia

Anaemia

Osteomalacia

CVD

Uraemia

Death

35
Q

How should you manage a patient with CKD?

A

Limit Progression (BP, Glucose, CVS Risk Factors, Dietary)

Symptomatic - (EPO, Sodium Bicarbonate, Diuretics)

RRT (Transplant, Haemodialysis)

36
Q

How should you treat Renal Osteodystrophy?

A

Calcichew (Ca Supplements)

Calcium Acetate (Phosphate Binding)

Calcimimetic (Reduces PTH)

37
Q

Which organisms most commonly cause UTIs?

A

E.Coli

Staph saprophyticus

Proteus mirabilis

Enterococci

Klebsiella

Candida albicans

Pseudomonas aeruginosa

38
Q

What are the presenting symptoms of a UTI?

A

Cystitis - FUND HIPS

Prostatitis - Low Backache, Suprapubic Pain,

Acute Pyelonephritis - High Fever, Rigors, Vomiting

General - Fever, Abdo Pain, Foul-Smelling Urien

39
Q

How should you manage a patient with a UTI?

A

Cefalexin & Nitrofurantoin

Pregnant: Cefalexin & Co-Amoxiclav

Trimethoprim

40
Q

What is Polycystic Kidney Disease?

A

Fluid-filled cysts growing on the Kidneys

Autosomal Dominant

Clinically silent, eventually causes HTN, Calculus formation, Renal Failure, SAH

41
Q

How does a Renal Cell Carcinoma typically present?

A

Haematuria

Loin Pain

Abdominal Mass

42
Q

How should you investigate a possible Renal Cell Carcinoma?

A

BP (Increased renin release)

Polycythaemia (Bleeding)

Haematuria

‘Cannon-Ball Metastases’

CT/MRI

IV Urogram

43
Q

How does Renal Artery Stenosis typically present?

A

Hypertension refractory to treatment in younger people.

Decreased Renal Function after ACE inhibitor/ARb treatment.

44
Q

How should you investigate a possible case of Renal Artery Stenosis?

A

US Measurement of Kidney Size

CT/MRI Angiogram

Digital Subtraction Renal Angiography