Brainscape's Knowledge GenomeTM

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


See full index

Met > Acute/Chronic Kidney Disease > Flashcards

Acute/Chronic Kidney Disease Flashcards

1
Q

What is acute uraemia?

A

An acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output.
Abrupt (1-7 days) and sustained rise in serum creatinine x1.5 from baseline

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

What are the causes for acute renal failure?

A
  1. Pre-renal (mostly): Dehydration, circulatory collapse, bleeding, NSAID abuse, burns, vasculitis, myeloma
  2. Parenchymal (5%): Acute tubular necrosis, acute glomerulonephritis , acute cortical necrosis, renal vascular damage, necrotising papillitis, sepsis, rhabdomyolysis (myoglobin released is very irritant), ATN, Goodpasture’s syndrome, malignant hypertension
  3. Obstructive (10%): Intratubular, ureteral, urethral (clots, stones, enlarged prostate/bladder)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the surgical triad?

A

Infection, nephrotoxic drugs and post-operative volume depletion
It is the commonest cause of hospital-acquired AKI

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

Which drugs can increase risk of AKI?

A

• ACE inhibitors and angiotensin II blockers - efferent vasodilation
• NSAIDS - afferent vasodilation
- Do not give to dehydrated patients!!!
• PPIs - Interstitial nephritis
• Lithium
• Aminoglycosides: gentamycin
Contrast medium

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

What are some of the risk factors for AKI?

A

• Advanced age >75
• Renal disease
• Malignant hypertension (180/120)
• Diabetes mellitus (glycolisation of renal vessels leading to change in tunica media causing nephropathy)
• Liver disease
• Heart disease
• Use of nephrotoxins
• Radiology contrast media - iodide component
Increased risk if has sepsis, hypotension, high EWS, hypovolaemia

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

Which drugs cause vasodilation and vasoconstriction at the afferent arteriole?

A

Constriction - NSAIDS

Vasodilation - ANP, Prostaglandins

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

Which drugs cause vasodilation and vasoconstriction at the efferent arteriole?

A

Constriction - ANP, Angiotensin II, norepinephrine

Vasodilation - ACEI/ARBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why might a patient be acidotic?

A

→ Failure to remove acid from renal system
→ Overload of buffering system
→Production of other acids e.g. lactic acid from tissue hypoxia in severely ill

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

What would a urine dipstick show in a patient with AKI

A
  • Negative usually suggest pre-renal cause
      • protein and blood: glomerular disease
      • white cells is non-specific but may suggest infection or interstitial nephritis
    • People with catheters could get false + results
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What kind of ECG changes could occur with AKI?

A
  • Tenting of T waves
    • Widening QRS,
  • Disappearance of P waves
    Sine wave pattern
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is chronic kidney disease?

A

Progressive loss of nephrons resulting in permanent compromise of renal function. It is classified according to eGFR and ACR. Majority are asymptomatic.

Proteinuria or haematuria and/or reduced GFR for more than 3 months duration.

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

When is kidney damage at stage 1?

A

Stage 1 has to be GFR of >90 with evidence of kidney damage like microalbuminuria, proteinuria and haematuria. EVIDENCE OF KDINEY DAMAGE IS IMPORTANT

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

What is the ACR levels for the 3 CR categories?

A

A1 - <3
A2 - 3-30
A3 - >30

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

What is the ACR levels for the 3 CR categories?

A

A1 - <3 (only treat if have diabetes)
A2 - 3-30 (only treat if diabetes or hypertension)
A3 - >30

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

How does diabetes cause renal failure?

A

Estimated 30% of people will have CKD.

Hyperglycaemia -> oxidative stress -> matrix expansion -> increased vascular permeability -> inflammatory mediators

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

How can GFR be measured?

A

→ Using urinary clearance of an ideal filtration marker.
→ The gold standard of exogenous filtration markers is inulin.
- Inulin is a physiologically inert substance that is freely filtered at the glomerulus, and is neither secreted, reabsorbed, synthesized, nor metabolized by the kidney.
- in short supply, expensive, and difficult to assay.
→ The most common methods utilized to estimate the GFR are: measurement of the creatinine clearance; and the Cockcroft-Gault equation

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

What is the presentation of CKD?

A

→ Lethargy - anaemia is associated due to lack of erythropoietin produced in kidney
→ Concentration trouble
→ Nausea and pruritus - due to accumulation of toxic waste products
→ Poor appetite
→ Trouble sleeping
→ Muscle aches
→ Oedema - salt and water retention as the GFR declines
→ Dry, itchy skins
→ Polyuria
→ Foamy urine - proteinuria
→ Seizures - increase is neurotoxins that are not excreted in kidney
Orthopnoea & dyspnoea - due to pulmonary oedema due to reduced urine output

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

What is the pathophysiology of CKD?

A

→ Renal injury -> increase intra-glomerular pressure -> glomerular hypertrophy (adapting to nephron loss to maintain GFR)
→ Increase in glomerular permeability -> toxicity to mesangial matrix -> mesangial cell expansion, inflammation, fibrosis and scarring
Injury results in increased angiotensin II production -> increase TGF beta -> collagen synthesis -> renal scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What could be the differential diagnosis for CKD?

A

a. Diabetic kidney disease - a. history of poorly controlled diabetes
b. Hypertensive nephrosclerosis
c. Ischaemic nephropathy
d. Obstructive uropathy - more common in men [prostate enlargement]
e. Nephrotic syndrome
f. Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of hypercalcaemia?

A

Painful bones, renal stones, abdominal groans and psychic moans (low mood, confusion, insomnia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Can tertiary hyperparathyroidism occur due to CKD?

A

Yes, longstanding CKD is a common cause of tertiary hyperparathyroidism

This would differ from secondary hyperparathyroidism which would show high phosphate instead of low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Causes of persistent non-visible haematuria

A 
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

False haematuria causes - red/orange urine, where blood is not present on dipstick

A

foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does hypernatraemia present?

A

Symptoms of this include diarrhoea or vomiting, impaired thirst, weight loss, oliguria and other signs of hypovolemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does hyponatraemia present?

A

Mental status changes, including altered personality, lethargy and confusion. If the concentration falls lower, other signs can include hyperreflexia and seizures.

Na+ - <135

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does hypomagnesemia present?

A

Symptoms of this include nausea, vomiting, lethargy, weakness, tremor and muscle fasciculations, including Trousseau and Chvostek’s sign.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does hypocalcaemia present?

A

Symptoms of this include muscle cramps, and if over a long period of time it can cause symptoms of confusion, memory loss, delirium, and depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Trousseau’s sign?

A

Trousseau’s sign is a carpopedal spasm caused by inflating the blood-pressure cuff to a level above the systolic blood pressure in patients with hypocalcaemia

30
Q

What is Chvostek’s sign?

A

Chvostek’s sign is also seen in hypocalcemia; tapping over the facial nerve causes twitching of the facial muscles.

31
Q

How can CKD lead to osteomalacia?

A

High phosphate levels in CKD ‘drags’ calcium from the bones, resulting in osteomalacia

Alendronic acid is a bisphosphonate that reduces the rate of bone turnover and strengthens the bone.

32
Q

Difference between haemodialysis and peritoneal dialysis:

A

Haemodialysis:
Performed 3X a week, for four hours each time
Usually done in a hospital
Major food and fluid restrictions
Fatigue, hypotension and risk of septicaemia
Fistula is well concealed and easy to maintain

Peritoneal dialysis:
Performed daily, for shorter periods
Can be performed at home or when travelling
No food or fluid restrictions
Increased risk of peritonitis
Permanent catheter may be embarrassing
33
Q

What tests are performed to match donor and recipient compatability?

A

They are blood type, crossmatch and HLA testing.
1)Blood typing is the first step in identifying the level of compatibility
o Blood group O is the universal donor
o Blood group AB is the universal recipient
o Blood group A can receive from A and O
o Blood group B can receive from B and O
2) HLA typing is also called tissue typing – these are present on the plasma surface of the cells
 There are 6 main antigens that have been identified in playing a major role in rejection: A, B and DR (two antigens for each letter)
 You inherit HLAs from your parents (3 from each)
3)Crossmatch is a test done just prior to transplantation, to determine if the body already has antibodies against the
donor’s antigens – it is done by mixing the blood from the donor and recipient.

34
Q

What is the treatment for hypocalcaemia?

A

Usually treated with Vit D compounds
Remember role of Kidney in 1α-Hydroxylation as an essential step for activation of vitamin D alfacalcidol (1α-hydroxycholecalciferol)calcitriol (1,25-dihydroxyvitamin D3or 1,25-dihydroxycholecalciferol) – can be used in renal failure
colecalciferol (vitamin D3), ergocalciferol (vitamin D2) – need a functioning kidney

35
Q

How to treat hyponatraemia?

A

Risk of osmotic demyelination syndrome (cerebral oedema etc).

Need to check bloods every 24h and don’t want Na+ to rise/fall more than 10mmol/L

36
Q

What is tolvaptan?

A

Tolvaptanis a competitive antagonist at vasopressin V2 receptors. Its major action is in the renal collecting ducts to reduce water reabsorption and produce aquaresis without sodium loss, thus increasing free water clearance and correcting dilutional hyponatraemia

37
Q

How to treat hypercalcaemia

A

Bisphosphonates (IV alendronic acid)

IV fluids

38
Q

How can Rhabdomyolysis cause AKI?

A

Myoglobin released from muscle tissue is toxic to the kidneys and will produce acute kidney injury.

Raised creatinine kinase, and raised potassium levels are typical features of rhabdomyolysis.

39
Q

How would a Rhabdomyolysis typically present in the exam?

A

Patient who has fallen or had a prolonged epileptic seizure with AKI on admission

40
Q

How does haemodialysis work?

A

Involves regular filtration of the blood through a dialysis machine in hospital.

Most patients need dialysis 3 times per week, with each session lasting 3-5 hours.

At least 8 weeks before
treatment, the patient must undergo surgery to create an arteriovenous fistula, which provides the site for haemodialysis. Most commonly in the lower arm.

41
Q

How does peritoneal dialysis work?

A

Filtration occurs within the patient’s abdomen. Dialysis solution is injected into the abdominal cavity through a permanent catheter. The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum. After several hours of dwell time, the dialysis solution is then drained, removing the waste products from the body, and exchanged for new dialysis solution.

42
Q

List some of the complications of haemodialysis

A 
Infection
Endocarditis
Stenosis at side
Hypotension
Cardiac arrhythmia
Air embolus
Anaphylactic reaction
Disequilibrium syndrome
43
Q

List some of the complications of peritoneal dialysis

A 
Peritonitis - Staphylococcus Epidermidis (coagulase -) or Staph aureus
Catheter infection/ blockage
Constipation 
Fluid retention
Hyperglycemia
Hernias
Back pain
Malnutrition
44
Q

List some of the complications of renal transplantation

A 
DVT/PE
Graft rejection
Infection
Bone marrow suppression 
Recurrance of disease
Urinary tract obstruction 
CVD
45
Q

Causes of hypercalcaemia:

A
  1. Hyperparathyroidism
  2. Malignancy, melanoma, PTHpP from squamous cell lung cancer
  3. Sarcoidosis
  4. Vit D intoxication
  5. Thyrotoxicosis
  6. Milk-Alkali syndrome
  7. Drugs: Thiazides
  8. Addison’s disease
  9. Paget’s disease of the bone
46
Q

Example of corticosteroid with very high mineralocorticoid activity but low glucocorticoid activity

A

Fludrocortisone

47
Q

Example of corticosteroid with very high glucocorticoid activity but low mineralocorticoid activity

A

Dexamethasone

Betmethasone

48
Q

Example of corticosteroid with high mineralocorticoid activity and glucocorticoid activity

A

Hydrocortisone

49
Q

Example of corticosteroid with low mineralocorticoid activity and predominant glucocorticoid activity

A

Prednisolone

50
Q

Treatment for Rhabdomyolysis

A

Rehydration IV normal saline

Hartmann’s solution has potassium content which isn’t favorable in AKI

51
Q

What is the most common and important viral infection in solid organ transplant recipients?

A

Cytomegalovirus

52
Q

Which drugs can cause gynaecomastasia?

A 
Spironolactone (most common drug cause)
Cimetidine
digoxin
Cannabis
Finasteride
Gonadorelin analogues e.g. Goserelin, buserelin
Oestrogens, anabolic steroids
53
Q

eGFR can be inaccurate due to what reasons?

A

Increased muscle mass
Pregnancy
Eating red meat 12h prior to sample being taken

54
Q

Would calcium be low in chronic or acute kidney failure

A

Chronic rather than acute

55
Q

Patients who have received an organ transplant are at risk of developing what cancer?

A

Skin Cancer - particularly squamous cell carcinoma

Due to long term immuno

56
Q

How is hyperkalaemia managed?

A

IV Calcium gluconate (stabilises cardiac membranes)

57
Q

What is meant by acute-on chronic kidney injury

A

Decline in renal function with potential reversibility

58
Q

What is normal eGFR

A

80-120 (around 100)

59
Q

How can you have CKD but normal eGFR

A

If presence of proteinuria e.g. diabetic nephropathy

Polycystic kidney disease patients - genetic disease (might have CKD but normal eGFR for now)

60
Q

Common-est cause of post-renal kidney failure in patients not in hospital is:

A

BPH

61
Q

What would be the commenest pathology leading to a neurogenic bladder?

A

Diabetic neuropathy

This can lead to post-renal kidney failure

62
Q

Why is it not so common to see posterior urethral valves as a cause of post-renal failure

A

Picked up on neonatal screening so should have been surgically fixed

63
Q

What can cause pure acute tubular injury in a patient?

A

Gentamycin

64
Q

What is the commonestcause pure acute interstitial injury in a patient?

A

Drugs like amoxicillin, NSAIDS or PPIs

65
Q

Symptoms of uraemia

A 
Pruritus
Anorexia
Changes in cognitive function 
Confusion, coma
Myoclonic jerk 
Chest pain - due to pericarditis
66
Q

What is Nephrotic syndrome?

A

hypoalbuminaemia
•>3.5 g proteinuria/day
•dyslipidaemia
•salt and water retention, leading to oedema.

67
Q

Most common cause of nephrotic syndrome in children?

A

Minimal change GN

But cannot be diagnosed without biopsy - normally just given treatment and hoped for the best

Second most common: Focal segmental glomerular sclerosis

68
Q

Most common cause of nephrotic syndrome in adults?

A

Membranous nephropathy

Focal segmental GS

69
Q

What is Nephritic syndrome?

A

Haematuria
Oliguria
Hypertension
Oedema

70
Q

What is the complication of correcting hyponatraemia too rapidly?

A

Osmotic demyelination syndrome

71
Q

What is the complication of correcting hypernatraemia too rapidly?

A

Cerebral oedema

Met (7 decks)

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