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Year 6 > Renal > Flashcards

Renal Flashcards

1
Q

What are the functions of the kidneys?

A
  1. Water and salt balance
  2. acid base balance (buffers H+ ions with bicarbonate to maintain the body pH)
  3. Endocrine (EPO for RBCs, ACE/Angiotensin system for BP control, Vit D3 activation for calcium control)
  4. Excretion of waste products
  5. electrolyte homeostasis (monitors K+, phosphate, calcium, sodium)
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2
Q

How does CKD affect the functions (5) of the kidney and what presentations can this cause?

A

Water balance
-> Fluid overload /
hypervolaemia
-> Pleural effusions (SOB, cough), pedal oedema, sacral oedema, ascites (gut oedema), reduced urine output due to poor filtration

Electrolyte homeostasis
-> Hyperkalaemia
-> Cardiac dysrhythmias, palpitations

Excretion of waste
-> Uraemia
-> Pruritis, pericarditis, encephalopathy

Acid-base balance
-> Acidosis
-> Nausea, vomiting, tiredness

Endocrine
-> Normocytic anaemia
-> Hypocalcaemia
-> Hypertension
-> Tiredness, SOB, pallor, headaches, loss of consciousness, chest pain, weakness, signs of heart failure, Tetany, secondary hyperparathyroidism (eg. Brown’s tumour, adynamic bone turnover), osteomalacia /osteoporosis

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3
Q

What are the 2 ways to classify CKD?

A

via eGFR (G1-G5) and via albumin to creatinine ratio (ACR) (A1-A3)

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4
Q

What additional symptoms should you ask for when taking a history from a patient with renal disease?

A

SOB, tiredness, pedal swelling, reduced exercise tolerance

Reduced urine volume

Nausea, vomiting, itching

Palpitations, weakness, muscle twitching

-> symptoms associated with CKD

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5
Q

Most common causes (and some other causes) of CKD in the UK

A

Most common:
- diabetic nephropathy
- hypertensive nephropathy

Other:
- post-renal: e.g. prostate cancer, renal calculi
- PKD
- pyelonephritis
- glomerulonephritidies
- drugs (e.g. NSAIDs, lithium, allopurinol, aminoglycosides)

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6
Q

What are the risks associated with heamodialysis?

A

blood infection
thrombosis
bleeding (due to the added heparin/anticoagulant)

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7
Q

Risks of peritoneal dialysis

A

abdominal infections

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8
Q

What type of access can be used for haemodilaysis?

A

Tesio line or AV fistula

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9
Q

What is a Tesio line?

A

a double lumen central line that can be used for haemodialysis

one lumen enters the right atrium and the other lumen sits outside in the vena cava.

Different than other central lines because there are 2 lumens rather than one lumen and and a bifurcation.

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10
Q

What clinical findings indicate fistula patency?

A

the presence of a thrill and a bruit.

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11
Q

What are the two different types of peritoneal dialysis and what are their key features?

A

CAPD (continuous ambulatory PD) and APD (automated PD)

APD can be done during the night and requires the equipment is at home.
CAPD needs to be done multiple times during the day, every day, however the equipment is more portable.

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12
Q

What are causes of AKI?

A

STOP

Sepsis/dehydration
Toxins (NSAIDs, nephrotoxic drugs)
Obstruction in the urinary tracts
Parenchymal kidney disease

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13
Q

What is uremic encephalopathy?

A

an organic brain disorder seen in people with AKI or CKD.

Signs: seizures, somnolence (drowsiness from which a patient can be easily aroused), coma

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14
Q

What is the difference between haemofiltration and heamodialysis?

A

Haemodialysis removes solutes by diffusion. As such, it is relatively inefficient for solutes of high molecular weight as clearance by diffusion is inversely related to the molecular weight of the solute.

Haemofiltration removes solutes by convection. As such, efficiency remains more constant for all solutes able to cross the semi-permeable membrane.

The choice between haemodialysis and haemofiltration can be difficult.

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15
Q

Recommended diet for patients with low clearance?

A
  • low phosphate (avoid chocolate, shellfish, nuts)
  • low K+
  • fluid restricted
  • low salt

avoid alcohol, avoid too much tea/coffee/ avoid processed foods, avoid high K+ foods like chocolate and bananas, take phosphate binders if diet restriction alone does not succeed.

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16
Q

What are the indications for emergency dialysis?

A

AEIOU

acidosis
electrolyte imbalance (K+ of 6.5+ and refractory to medical management)
Intoxication (certain drugs require dialysis to clear the blood (BLAST: barbiturates, lithium, alcohol, salicylates, theophylline)
Overload of fluid (refractory, not responding to diuretics)
Uremic encephalopahty and pericarditis)

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17
Q

What risks are associated with renal transplants?

A

Can divide into surgical, anaesthetic, transplant, immunosuppression.

a. Surgical
– infection, bleeding, dehiscence, pain, reduced mobility, DVT, cosmetic etc.

b. Anaesthetic
–airway loss, death, coma, post-op nausea & vomiting etc.

c. Transplant
– failure or rejection

d. Immunosuppression related
–risks of being immunosuppressed (susceptible to
infections, certain cancers – SCC, lymphoma) and side effects of the drugs itself
(think steroids causing Cushingoid effects, methotrexate and lung fibrosis , Tacrolimus and hyperlipidaemia/fine tremor etc.)

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18
Q

What is the difference between transplant failure and rejection?

A

Failure
– organ fails to function. For kidneys, this me
and it does not produceurine clinically and creatinine level rises
-> Dialysis

Rejection
– body’s immune system recognises organ as foreign and attacks it
->Management depends on type of rejection

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19
Q

What is acute, chronic and hyperacute transplant rejection?

A

Hyperacute: occurs when there are pre-formed HLA antibodies in the recipients blood. Rct within 24h, pt v unwell. Mx: remove organ and put patient back on dialysis.

Acute: Cell-mediated rejection. usually within 6 months. pt becomes unwell, creatinine rises. mx: increase immunosuppression/steroids, plasma exchange works for some people.

Chronic: Ab and cell mendiated.

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20
Q

Which renal condition has a high rate of recurrence in transplant?

A

FSGS has a high rate of recurrence in transplant

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21
Q

Indications for medical kidney biopsies

A

delete

22
Q

What is the commonest inherited cause of chronic kidney disease?

A

ADPKD (1 in 1000)

23
Q

What medications can cause renal failure

A

CANDA

contrast media
aminoglycosides
NSAIDs
Diuretics
ACEi

also metformin

24
Q

What mutation in seen in ADPKD

A

PKD1 on chromosome 16 (85% of cases); polycystin-1 OR
PKD2 on chromosome 4 (15% of cases); polycystin-2

25
Q

Sx onset in ADPKD

A

Symptoms usually occur after 30 years of age, but the disease may also manifest during childhood.

26
Q

Onset of ADPKD and ARDKD

A

ARPKD onset is in infancy or childhood

27
Q

Sx of ADPKD

A

Renal manifestations
- Gross hematuria
- Flank or abdominal pain
- Recurrent UTIs
- Nephrolithiasis
- Kidneys might be palpable and enlarged on abdominal exam (they are usually normal at birth)
- Signs of CKD (e.g., HTN, fluid overload, uremia)

Extrarenal manifestations
- Multiple benign hepatic cysts
- Cysts may also occur in the pancreas
- Cerebral berry aneurysm (∼8%) [14]
- The risk is higher in patients with a FH +ve of ADPKD.
- the risk for growth and rupture is the same in patients with ADPKD as in the general population

Cardiovascular
- arterial HTN; through increased renin production
- mitral valve prolapse
- Colon diverticula (diverticulosis)

28
Q

Sx of ARPKD

A

Renal manifestations
- Protruding abdomen; bilateral renal enlargement and/or hepatomegaly
- Chronic renal failure: frequently hematuria, proteinuria, and oliguria
- Severe in-utero renal impairment → oliguria in utero → maternal oligohydramnios → Potter sequence

Extrarenal manifestation
- HTN
- Liver involvement: congenital hepatic and portal fibrosis → progressive liver failure and portal hypertension

29
Q

What subtype of polycystic kidney disease is associated with Berry aneurysms?

A

ADPKD

30
Q

Investigations in polycystic kidney disease

A

USS
CT -> only if US findings are unclear, this is not the method of choice.

Genetic testing for ADPKD1 and ADPKD2 mutations (often not necessary)

31
Q

What do you see on USS in ADPKD and in ARPKD?

A

ADPKD
- enlarged kidneys with multiple cysts bilaterally of varying sizes (anechoic masses)
- In children: evidence of cysts in combination with a +ve FHx of ADPKD
- Hepatic, pancreatic, and/or splenic cysts

ARPKD
- Enlarged kidneys with multiple cysts bilaterally of equal size
- Diffuse increased echogenicity, despite the presence of liquid-filled cysts (anechoic)
- Hepatic cysts

32
Q

Pathological findings in ADPKD and ARPKD

A

ADPKD
Progressive cystic dilatation of the kidney tubular system

ARPKD
Cystic dilatation of the collecting ducts

33
Q

Management of polycystic kidney disease

A

Treatment/prevention of renal dysfunction
- ACEi or ARBs: to prevent/treat HTN as well as to slow proteinuria and ESRD progression
- Tolvaptan: Slows down the growth of kidney cysts in ADPKD patients
- Avoid nephrotoxic substances
- Avoid ADH

In severe cases: e.g., ESRD
Kidney transplantation is the only curative option (see also “End-stage renal disease”).
dialysis whilst waiting for kidney

34
Q

What causes thin basement membrane nephropathy?

A

abnormalities in type IV collagen

35
Q

What are the different subtypes of thin membrane nephropathy?

A

Alport syndrome is generally a more serious version of TBMD

-> both have abnormalities in type IV collagen

36
Q

Sx and Ix findings in thin basement membrane disease

A
  • intermittent gross hematuria and flank pain
    -> often triggered by URTI or exercise
  • Urinalysis shows persistent microhematuria and sometimes proteinuria

Kidney biopsy is required for diagnosis, showing diffuse thinning of the glomerular basement membrane.

37
Q

What is the abnormality in thin membrane nephropathy?

A

Thin basement membrane nephropathy is a primary glomerulonephritis caused by abnormalities of type IV collagen and thinning of the glomerular basement membrane.

Kidney biopsy shows diffuse thinning of the glomerular basement membrane. progression.

38
Q

Mx and prognosis of thin basement membrane nephropathy

A

While the disease generally has an excellent prognosis and often does not require treatment, patients with proteinuria should be treated with ACE inhibitors to slow progression.

may also be on BP control (to help with proteinuria)

diuretics and low salt diet can reduce oedema

39
Q

How does IgA nephropathy generally present?

A

visible haematuria following a recent URTI

(immune complex deposition in the glomeruli)

40
Q

What is the commonest cause of glomerulonephritis worldwide?

A

IgA nephropathy (Berger’s disease)

41
Q

How long after URTI do you get post streptococcal glomerulonephritis?

A

7-14 days

42
Q

what acid base abnormality does diarrhoea cause?

A

normal anion gap metabolic acidosis

(due to GI loss of bicarbonate)

43
Q

drug used in renal patients to reduce blood phosphate levels (incl. MoA)

A

sevelamer (non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease)

44
Q

CKD mineral bone disease aetiology

A

1-alpha-OHase -> low activity -> low vitamin D

kidneys normally excrete phosphate -> CKD leads to high phosphate

-> high phosphate level drags calcium from the bones -> osteomalacia
-> low calcium due to lack of vitamin D and high phosphate
-> 2ndary hyperparathyroidism

45
Q

U&Es in dehydration vs AKI

A

in dehydration the urea is proportionally higher than the rise in creatinine

46
Q

What are the symptoms of HSP?

A

abdominal pain
haematuria
arthritis

purpuric rash over the buttocks and extensor surfaces of the arms and legs

47
Q

Commonest pathogens causing peritonitis in patients on PD?

A

coagulase -ve staphylococci (e.g. staphylococcus epidermidis)

also staphylococcus aureus

48
Q

Sx of fibromuscular disease

A

HTN
CKD or AKI e.g. secondary to ACEi
‘flash’ pulmonary oedema

49
Q

Tolvaptan - MoA

A

vasopressin receptor 2 antagonist

50
Q

List some risks of nephrotic syndrome

A

VTE (increased risk)
infections (increased risk)
cardiovascular complications
anaemia
acute renal failure
hypovolaemic crisis

51
Q

What skin cancer are post-transplant patients at particular risk of?

A

squamous cell carcinoma

52
Q
A

Year 6 (37 decks)

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