Week 1

Question 1

How is chronic kidney disease defined?

Answer 1

GFR < 60 mL/min/1.73m2 for >3 months with or without evidence of kidney damage (eGFR normally falls by 10mL/min per decade 40+ but a reduction is associated with increased CVD risk at all ages)

OR

Evidence of kidney damage (with or without decreased GFR) for >3 months:

• Microalbuminuria
• Proteinuria
• Glomerular haematuria
• Pathological abnormalities (e.g. on renal biopsy)
• Anatomical abnormalities (e.g. cysts on ultrasound)

Question 2

At what GFR do symptoms of chronic kidney disease usually present?

Answer 2

< 15ml/min (severe disease)

Question 3

How are the stages of CKD defined by eGFR?

Answer 3

Question 4

What conditions can give false proteinuria readings on urinalysis dipstick?

Answer 4

UTI

Sepsis

CCF

Strenuous exercise

Heavy protein intake

Menses

Question 5

What are the risk factors for development of CKD?

Answer 5

Stage

> 55

Diabetes

HTN

Target - < 130/80mmHg

< 125/75mmHg in proteinuria/diabetes

Smoker

Obese

1st degree relative with CKD

NOTE - HTN and proteinuria are the two most important modifiable risk factors for reducing progression of CKD

Question 6

What are the basic management principles for CKD?

Answer 6

Identify and treat underlying cause

Reduce progression - BP, lipid and glucose control

Manage metabolic complications - low calcium and phosphate, high PTH, acidosis

Cessation of nephrotoxic and renally excreted drugs

SNAP - smoking cessation, nutrition, alcohol reduction, physical activity

Renal replacement therapy (CKD 4-5)

Question 7

How does CKD cause anaemia?

Answer 7

Low EPO production - reduced stimulus for red blood cell production

Question 8

How does CKD cause hypocalcaemia?

Answer 8

Poor functioning kidneys - don’t get active form of vitamin D (calcitriol) - so don’t get aid for calcium absorption in the GIT

Question 9

How can CKD lead to osteoporosis?

Answer 9

Low calcitriol –> low calcium absorption –> osteclasts stimulated –> bone breakdown to maintain extracellular calcium levels

Question 10

Why does CKD cause low phosphate?

Answer 10

Reduce activation of vitamin D to calcitriol so reduced absorption of phosphate in the GIT

Question 11

How does CKD lead to hyperparathyroidism?

Answer 11

Low levels of calcium absorption (due to low levels of vitamin D activation in the kidneys) leads to hypocalcaemia - triggers activation of the parathyroid gland to secrete PTH to stimulate osteoclasts to breakdown bone to maintain extracellular calcium levels

Question 12

How does CKD lead to a metabolic acidosis?

Answer 12

Kidneys unable to filter properly so there is increased loss of bicarcbonate and decreased excretion of acids - leading to an acidosis

Question 13

When should renal replacement start?

Answer 13

GRF < 10ml/min or when symptoms dictate

Question 14

What is the major complication of CKD?

Answer 14

20x more likely to die from CVD event (before dialysis is even needed)

Question 15

How is APKD inherited and what is the typical presentation?

Answer 15

Autosomal Dominant

Abdo pain, haematuria, nocturia, flank pain, drowsy, clubbing, arthralgia

Question 16

How is APKD investigated?

Answer 16

US - renal cysts

CT - intracranial aneurysm

Question 17

What are the features of IgA nephropathy?

Answer 17

Few days post URTI - haematuria

Hypercellularity, fibrosis and inflammation

Question 18

What are the features of post-strep nephropathy?

Answer 18

1-4 wks post strep pyogenes infection - oliguria and haematuria

Diffuse and global with lots of polymorph nuclei

Question 19

What are the featrues of membranous nephropathy?

Answer 19

Nephrotic syndrome - proteinuria, oedema, high lipids, low albumin

Secondary to SLE, hep B, malaria

Thickened BM

Question 20

What is syncope?

Answer 20

Abrupt transient loss of consciousness, absence of postural tone with complete and rapid recovery, which is often complicated by injury

Question 21

18yo F, collapse after standing in hot crowded area, light headed and nauseous before collapse, quick recovery, no witnessed seizure, similar episode 6 months ago - what are the differentials and how can these be investigated?

Answer 21

Vasovagal syncope - hydration status, BG, temperature, hx, prodrome, FBE (anaemia)

Arrhythmia - ECG, echo, U&E

PE - CTPA (whole body contrast - don’t use in people with kidney disease or iodine allergy), ECG, V/Q scan (use in people who have contrast allergy or kidney disease - not a specific test (can’t tell whether PE is old or new - and it’s affected by other pathology))

Fixed output valve disease - echo, TOE

Question 22

What is the role of a spacer?

Answer 22

Increase lung deposition of medication and reduce oropharyngeal deposition

Useful in kids or elderly with poor metered dose inhaler technique and breath coordination

Question 23

How should a spacer be cleaned?

Answer 23

Clean before first use, wash in warm water with mild detergent and allow to air dry without rinsing, check regularly for cracks or splits and prime spacer before use

Question 24

What can cause prolonged QT interval?

Answer 24

High Mg, low K/Ca, sodium channel blockers, raised ICP, hereditary, hypothermia, drugs (SSRIs, antihistamine, amiodarone, tricyclics, antipsychotics)

Question 25

What is the first line treatment for long QT interval?

Answer 25

Beta blocker

Question 26

What is this ECG representative of, and what is the treatment?

Answer 26

Ventricular fibrillation (cardiac arrest) Shockable, adrenaline after 2nd shock, amiodarone after 3rd shock

Question 27

Is this a shockable rhythm?

Answer 27

This is ventricular tachycardia - this is only a shockable rhythm if the patient is unconscious - if conscious treat with amiodarone (or another anti-arrhythmic)