Week 4 Flashcards

1
Q

Causes of acute kidney injury (AKI)

A
  • infection
  • sepsis
  • renal stones or obstruction
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2
Q

how does abnormal blood volume induce renal failure

A

poor renal blood perfusion

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3
Q

causes of chronic kidney disease (CKD)

A

hypertension
diabetes

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4
Q

factors affecting plasma creatinine levels

A

muscle mass and renal clearance.

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5
Q

models measuring GFR in chronic kidney disease (not AKI)

A

MDRD, CKD-EPI.

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6
Q

MDRD vs CKD-EPI

A

CKD-EPI is a more accurate measurement when GFR is 60-90

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7
Q

urea levels in CKD or AKI

A

reduced GFR or hypovolaemia will increase urea reabsorption.

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8
Q

urea raise and creatinine raise

A

obstructed renal flow will lead to increased urea reabsorption.
UREA is raised PROPORTIONALY higher than creatinine raise

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9
Q

what is a novel marker used to estimate GFR?

A

cystatin C

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10
Q

cystatin C predictive ability.

A

cystatin C is considered to be a sensitive marker for early changes in renal function.

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11
Q

What is a marker used in AKI?

A

NGAL - raised due to inflammation and kidney tissue damage.

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12
Q

overflow proteinuria

A

High concentrations of small proteins. Exceed tubule reabsorbing capacity.

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13
Q

tubular proteinuria

A

Decreased ability of tubule reabsorption.

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14
Q

glomerular proteinuria

A

Kidney damage (AKI or CKD), increased permeability.

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15
Q

is urinary protein test used for late or early/mild kidney disease?

A

more sensitive when it is towards the later stages of kidney disease.

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16
Q

overtly raised triglyceride

A

associated with acute pancreatitis.

17
Q

F

Familial hypercholesterolaemia

A

problem with PCSK9, LDLR and ApoB
PCSK9 - internalises LDL-R.

18
Q

what genetic factor could lead to hypertriglyceridaemia

A

LPL deficiency

19
Q

what could lead to HDL decrease?

A

Insulin resistance:
1. LPL decrease
2. overloading HDL with triglycerides via CETP, becomes VLDL
3. HDL filled with trig will be targeted by LPL.

20
Q

What does LPL decrease lead to??

A

increase in VLDL

21
Q

primary vs secondary prevention of cardiovascular disease

A

primary - individuals without disease
secondary - individuals with disease