L34.5 CKD and AKI

1

Choose the incorrect statement about Acute Kidney Injury (AKI).

1

Choose the incorrect statement about chronic kidney disease (CKD)

1

NZ has higher rates of sepsis, post infectious glomerulonephritis and HUS causing AKI compared with other countries in the developed world.

1

Reduced renal blood flow (❌) initiates AKI. It can be as a result of infection (❌), medications, disease, or trauma. The medication combination likely to cause AKI is the ‘triple whammy’; concurrent use of an ❌ inhibitor or an ARB, with a ❌.
AKI is largely ❌ and late diagnosis of injury is common.

ischemia

sepsis

diuretic and an NSAID

ACE

asymptomatic

1

Pathogenesis of AKI:
1. Disruptions of the glycocalyx and ❌ monolayer in renal tubule
2. Upregulation of ❌ molecules
3. Enhanced ❌ interactions
4. Formation of ❌
5. Inflammation causing ❌ overload, ❌ imbalances

endothelial

adhesion

leukocyte-endothelium

microthrombi

fluid

electrolyte

1

CKD Pathogenesis"
1. Nephrons atrophy with time
2. Worsened by genetic & environmental factors – ❌
3. Fewer nephrons cause an increase in ❌ size, ❌ can’t cope & detach – loss of barrier function and impaired filtration - ❌
4. Inflammation, which leads to fibrosis & ❌ formation
5. Leads to ❌

hypertrophy

nephron

podocytes

proteinuria

scar

ischaemia

1

Which of these is not a systemic effect of CKD?

PHCY310 Test sobre L34.5 CKD and AKI, creado por Mer Scott el 16/04/2019.

L34.5 CKD and AKI

L34.5 CKD and AKI

Choose the incorrect statement about Acute Kidney Injury (AKI).

Choose the incorrect statement about chronic kidney disease (CKD)

NZ has higher rates of sepsis, post infectious glomerulonephritis and HUS causing AKI compared with other countries in the developed world.

Pathogenesis of AKI: 1. Disruptions of the glycocalyx and ❌ monolayer in renal tubule 2. Upregulation of ❌ molecules 3. Enhanced ❌ interactions 4. Formation of ❌ 5. Inflammation causing ❌ overload, ❌ imbalances

Which of these is not a systemic effect of CKD?

Pathogenesis of AKI:
1. Disruptions of the glycocalyx and ❌ monolayer in renal tubule
2. Upregulation of ❌ molecules
3. Enhanced ❌ interactions
4. Formation of ❌
5. Inflammation causing ❌ overload, ❌ imbalances