Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease of Major Organs > Acute and chronic renal failure > Flashcards

Acute and chronic renal failure Flashcards

1
Q

What causes renal disease?

A

Inflammation, inherited (RTA, polycystic kidneys), metabolic disease (DM), obstruction (renal calculi, carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between CKD and AKI?

A

CKD develops slowly, whilst AKI have a rapid onset of kidney failure. CKD is irreversible whilst AKI isnt.
CKD is the progressive loss of glomerular and tubular function until end stage renal disease. CKD have significant morbidity and mortality, which is also true for AKI as it can be fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define CKD - lay terms

A

This is an abnormality of kidney function or structurepresent for >3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define CKD - Technical

A

GFR <60ml/min/1.73m2 on at least 2 occasion seperated by a period of at least 90 days, with ACR>3mg/mmol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

State some risk factors of CKD

A

Age, ethnicity, family history, DM, smoking, hypertension, obesity, structural renal disease/renal stones and cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some symptoms of early CKD?

A

Typical symptoms are changes in urinary quantity and frequency, but this tends to go unnoticed as technically you are asymptomatic to all other symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State the biochemical complications of CKD

A 
Increased serum creatinine and urea
Hyponatraemia 
Hyperkalaemia 
Metabolic acidosis
Hyperphosphataemia 
Hypocalceamia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does CKD affect glucose, lipid and red cell production?

A

Glucose - impaired glucose tolerance and decreased insulin secretion
Lipid - increased triglyceride, decreased HDL with significant effects to cardiovascular system
Red cell - decreased produciton, causing normocytic, normochromic anaemia because secretion of erythropoietin decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does protein loss affect a CKD patient?

A

Patient will become catabolic, meaning patient is breaking down or losing overall mass, both fat and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the main goal in treating CKD?

A

Aim to prevent or delay the progression and reduce the risk of complications and CVD. Also covers managing anaemia and hyperphosphatemia associated with CKD.

According to NG23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What population requires regular screening?

A

Risk population; DM, CVD, hypertension, multisystemic disease, family history, nephrotoxic drugs (some antibiotics and chemo). Incidental findings of proteinuria or haematuria require further testing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hows eGFR calculated?

A

CKD-EPI or CDK-MDRD formulas

EPI is the most accurate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What assay is used to determine serum creatinine?

A

An enzymatic assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What patient preparations are necessary ahead of a creatinine/eGFR test?

A

No meat 12hr before

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is creatinine an accurate measure of kidney function?

A

No becuase it is affected by muscle mass. A patient with a large body mass will have a really high creatinine which will be odd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

If ACR is 3-70mg/mmol we need to …

A

confirm by a subsequent EMU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If ACR is >70mg/mmol we need to …

A

Nothing required because its a clear indication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some investigation apart from eGFR and ACR to examine CKD presence?

A

Other investigations possible is urine sediment abnormalities, electrolyte, and other abnormalities due to tubular disorders, histology, imaging to detect structural abnormalities.

19
Q

What is necessary for patients in G3a/G3b?

A

We need to rule in or out CKD using a eGFRcystatinC

20
Q

When should the eGFR cystatin C be considered?

A. Symptomatic with eGFR creatinine of 85ml/min/1.73m2
B. Pregnancies
C. eGFRcreatinine of 45-59ml/min/1.73m2 sustained for at least 90 days and no proteinuria
D.eGFRcreatinine of 45-59ml/min/1.73m2 sustained for at least 90 days and presence proteinuria

A

C

21
Q

Is the MDRD formula validated for every patient group?

A

No it is not validated for use in children, AKI, amputees, pregnancies, malnourished, or muscle wasting disease

  • only validated for black ethnicities
22
Q

In a validated group when is MDRD and EPI most accurate?

A

MDRD underestimates GFR (>60), compared to EPI which is especially accurate for GFR>60

23
Q

Why are most CKD patients asymptomatic?

A

They are asymptomatic due to the large reserve capacity of the kidney. 50-60% loss of functioning kidney occurs before symptom/biochemical abnormalities seen

24
Q

Describe the progression of CKD

A

As the kidney begins to lose parts of its reserve the kidney adapts by hyperfiltrating other remaining nephrons. Hyperfiltration causes an inflammatory response involving cellular infiltration, T-cell activation, fibroblast activity increased leading to ECM synthesis (fibrosis), disruption to renal flow causing ischaemic damage

25
Q

Describe the current treatments administered to patients with CKD.

A

The current treatments are to deal with the co-morbidities.
Statins are given to deal with hyperlipidaemia.
Anti-hypertensive drugs (ACEi, diuretics) are given for hypertension.
Diabetics will be given metformin.

This as well as lifestyle changes

26
Q

Match the lab monitoring associated with the stage of CKD.

A. All stages
B. G4
C. G5
D. G3b

  1. Calcium, phosphate, PTH
  2. U&E
  3. Hb
A

A 2
B1,3
C1,3
D3

27
Q

Which one of these statements needs to be true for AKI?

  • Serum creatinine rises by > 26umol/L within 48h
  • Serum creatinine rises > 1.5 fold from the reference value/baseline
  • Urine output is <0.5ml/kg/hr for >6 consecutive hours
A

One of them is sufficient

28
Q

How are AKIs classified?

A

Based on serum creatinine and urine output.

3 stages exist (serum creatinine):

  1. 1.5-1.9x baseline
  2. 2-2.9x baseline
  3. > 3x baseline
29
Q

What are some risk factors associated with AKI?

A

DM, CCF, CKD, age, albuminuria, hypovolaemia/hypotension, medication/iodinated contrast, sepsis/infection (big hospital risk), previous AKI, liver disease.

30
Q

State the causes of AKI

A

pre-renal
post-renal
intrinsic

31
Q

Describe the pre-renal causes of AKI

A

Associated with inadequate blood supply. This can be as hypovolaemia caused by haemorrhage, diuresis, GI fluid loss, burns, dehydration. Or the inadequate blood supply is due to reduced cardiac output, e.g. heart failure. Other causes of inadequate blood supply are sepsis, vasodilatory drugs (ACEi)

32
Q

Describe post-renal causes of AKI

A

Urinary obstructions, e.g. stones, bladder carcinoma,urethral stricture, prostate carcinoma, benign prostate hypertrophy

33
Q

Describ intrinsic causes of AKI

A

Tissue damage to glomerulus or tubular section.

  • Glomerular damage can be cause by glomerularnephritis, ANCA vasculitis, SLE and cryoglobulinaemia
  • Tubular damage can be caused by nephrotoxins, sarcoidosis, ischaemia, infection.
34
Q

What is a consequence of the pre-renal causes?

A

Acute tubular necrosis as the kidney is not supplied with enough oxygen. This will result in more of the intrinsic causes of AKI. Necrosis occurs due to ischaemia and nephrotoxins.

35
Q

Describe acute tubular necrosis

A

The ischaemia cause tubular cells to necrose. The tubular damage induces inflammatory and vasoactive mediators like NOx and endothelin, to further reduce

36
Q

What are some biochemical features of AKI?

A

Increased urea/creatinine
Hyponatraemia
Hyperkalaemia
Metabolic acidosis

37
Q

State some clinical features of AKI

A

muscle weakness, oligouria, anuria, cardiac arrythmias/arrest, nausea, vomiting, loss of consciousness, odema, ascites, pleural effusion

38
Q

What are the standardised tests for AKI?

A

U&E, blood gases, urinalysis, urine sodium, urine/serum osmolality, creatinine kinase, BJP/serum electrophoresis, blood/urine cultures, virology

39
Q

How do the pre-renal and intrisnic features differ?

A

Both show an increase in serum urea/creatinine. Pre-renal does not show proteinuria whilst intrinsic does.

40
Q

Diagnostic test to differ between pre-renal and intrinsic causes of AKI?

A 
Urine sodium
- Pre-renal <20mmol/L
- Intrinsic >40mmol/L 
Urine:plasma osmolality
- Pre-renal >1.5:1
- Intrinsic <1.1:1
41
Q

Treatment of AKI

A

Keep the patient hydrated, but not overhydrated as this will cause further damage. Stop nephrotoxic drugs

Treat metabolic complications e.g. hyperkalaemia

42
Q

When is renal replacement therapy considered?

A

should be the last treatment one should consider, but there are certain indications for commencing RRT. If the patient presents with hyperkalaemia, severe acidosis, uraemia, pulmonary oedema/neuropathy or stage 5CKD then these are indications for RRT

43
Q

Name some RTTs

A

Haemodialysis, hemofiltration, haemodifiltration, peritoneal dialysis, renal transplant.

Disease of Major Organs (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions