Renal and urinary tract Flashcards

1
Q

What is the single most important factor to address to avoid future cardiovascular disease?

A

Blood pressure

Cholesterol, smoking, weight loss and diabetes are important, but not as statistically significant as BP

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2
Q

How do ACE-I and ARBs reduce proteinuria and albuminuria?

A

The reason that these proteins are getting through the glomerular threshold is because the glomerular pressure is too high.

ACE-I prevent the conversion of angiotensin 1 to angiotensin 2

ARBs prevent binding of angiotensin 2 to the angiotensin receptor

The angiotensin receptor acts on the efferent arteriole to constrict it, therefore ACE-I and ARBs prevent the increased glomerular hydrostatic pressure. This relieves the damage being done to the nephrons in CKD, slowing the progression.

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3
Q

How many people suffer from dry cough in ACE-I use?

A

Approximately 10%

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4
Q

Why must ACE-I and ARBs be stopped if AKI is suspected?

A

AKI is often due to pre-renal causes e.g. dehydration.

The kidney will be underperfused and so will use RAAS to increase perfusion, ACE-I/ARBs block this system and thereby block homeostasis.

This will exacerbate damage to the kidney.

Funny really: use ACE-I/ARBs in chronic but never acute kidney disease

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5
Q

WhY should serum creatinine be checked if a patient is put on ACE-I or ARBs?

A

Simply: These drugs have a potentially narrow therapeutic window if the patient has underlying cormorbidities

  1. Immediately after initiation - to check for rises of creatinine above 30% (increase of 25-30% is normal initially)
  2. Whenever the dose is changed

A small rise in serum creatinine is expected since we reduce glomerular perfusion pressure and therefore reduce creatinine excreted.

If serum creatinine significantly rises there may be renovascular disease or renal artery stenosis, since the drugs are reducing glomerular perfusion pressure too low - indicating further damage to the kidney

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6
Q

What warnings should you give a patient who is female and of child-bearing age when initiating ACE-I/ARBs?

A

In short: ACE-I/ARBs are contraindicated in the all trimesters of pregnancy.

Stop all ACE-I/ARBs within two days of positive pregnancy test.
They increase risk of congenital malformations: fetopathy, via inhibition of foetal renal function, and resultant anuria causing kidney malformations. (Not teratogenic)

Also cause: malformation of the cardiovascular system and the CNS.

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7
Q

What should be monitored in patients taking ACE-I/ARBs?

A

Serum Potassium - risk of hyperkalemia since angiotensin causes NaCl reabsorption and K secretion

Serum Creatinine - large rise may indicate underlying renovascular disease

States of diarrhoea or vomiting - hypovolaemia combined with ACE-I/ARBs can cause AKI, therefore medication must be temporarily stopped in these situations

Checked:

  1. Before starting treatment
  2. One week after start
  3. Whenever dose is changed
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8
Q

In a patient with resistant hypertension and chronic kidney disease, which medication are we particularly worried about, besides ACE-I/ARBs?

A

Spironolactone - sometimes given for resisting hypertension.

MOA: Binds aldosterone-dependent sodium potassium exchange sites in the DCT and increases NaCl excretion while decreasing potassium secretion.

This has the potential to cause hyperkalemia, especially in combination with ACE-I, since they stop the production of renin, and reduce the conc of aldosterone too.

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9
Q

Why are NSAIDs considered dangerous to the kidney?

A

Prostanoids facilitate renin release.

NSAIDs prevent renin release by decreasing prostanoid production.

This means they reduce aldosterone production and can cause hyperkalemia.

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10
Q

Which medications should a pregnant woman be given for hypertension?

A

Labetolol
Methyldopa
Nifedipine

NOT ACE-I/ARBs or chlorthalidone!

Note: targets are higher for BP in pregnant women with chronic HTN (150/100)

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11
Q

What is the treatment for secondary hyperparathyroidism in CKD?

A

Calcitriol or alphacalcidol - vitamin D analogues

In secondary hyperparathyroidism there is an excess of PTH released in response to hypocalcaemia, this is caused by the kidney failing to produce enough 1,25-dihydroxyvitamin D, which normally causes GI calcium uptake and bone mineralisation, and osteoclast activity (ups the bone turnover)

This simply replaces the vitamin D

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12
Q

What is the treatment for renal anaemia in CKD?

A

Erythropoietin and IV iron

Aim for a target ferritin >200

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13
Q

What is the treatment for metabolic acidosis in CKD?

A

Oral alkali - most often sodium bicarbonate

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14
Q

What is the treatment for hyperkalemia in CKD?

A

This is caused iatrogenically.

The treatment is dietary potassium restriction and then reduction of ACE-I if still necessary.

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15
Q

What is the treatment for fluid overload in CKD?

A

Fluid restriction
Salt restriction
Diuretics

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16
Q

What are the nutritional aspects to management of CKD?

A

Adequate calorie intake (inc adequate protein intake!)

Salt restriction

Fluid management

Nutritional supplements

Weight management - independent risk factor

Lipid control - cardiovascular risk factor

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17
Q

What are the BP targets for patients with CKD?

A

<130/80 in all stages

<125/75 in proteinuric stages (urinary PCR >1g per day)

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18
Q

Why is gastroenteritis a danger in CKD?

A

CKD normally means treatment with ACE-I/ARBs, if the patient becomes hypovolaemic from vomiting or diarrhoea, they can develop AKI - this can damage their kidney further!

Must stop ACE-I/ARBs in hypovolaemia.

19
Q

What are the essential preparations before renal replacement? (stage 4 CKD is when preparations begin)

A

Immunisation:
Pnueumococcal
Influenza
Hepatitis B

Discuss choice of dialysis:
Conservative (If unsuitable or won’t benefit)
PD
HD
Transplant
Home CAPD
Home APD
Home HD

Patient will move between dialysis modes during their lifetime, it’s not a single one forever.

20
Q

What is the nominal treatment for each stage of CKD?

A

Stage 1+2 = treat cause and reduce CVS risk:
Smoking, exercise, cholesterol, BP
Medication: ACE-I/ARB

Stage 3 = ensure nutrition, immunise, monitor for acidosis/anaemia, and give supplements:
Medications: EPO, Alphacalcidol, bicarbonate and diuretic

Stage 4 = same as stage 3 but immunise again and prepare for renal replacement therapy

Stage 5 = renal replacement therapy and plan end of life care (-Liverpool care pathway for the dying patient)

21
Q

Which medications must we change in stage 4 CKD?

A

Stage 4 CKD = GFR <30:

Ramipril max dose is 5mg p/day
Metformin should be stopped entirely and replaced with something else.

22
Q

What are the six indications for dialysis aside from low GFR?

A

In short: ACIDIC, HYPERKALEMIC, FLUID O/L, TOXINS, CREATININE, URAEMIC PERICARDITIS

  1. pH <7.25
  2. Potassium >7mmol
  3. Fluid overload
  4. Toxins: SLIME - salicylate, lithium, isopropopanolol, magnesium and ethylene glycol
  5. Creatinine >400
  6. Uraemic pericarditis

Low GFR isn’t an absolute indication for dialysis, since some people do better with later dialysis.

23
Q

What is the management of patients with CKD who Rd approaching end stage renal failure?

A
  1. Patient has eGFR <15
2. Choose between:
Conservative Care
Transplant
Peritoneal dialysis
Haemodialysis
NOTE CONTRAINDICATIONS FOR EACH TYPE
  1. Haemodialysis chosen: must create AV fistula early
  2. Transplant possible: needs transplant before ESRF occurs
  3. Peritoneal dialysis chosen: must insert Tenckhoff catheter
  4. Start dialysis when symptomatic
24
Q

What are the absolute contraindications for peritoneal dialysis?

A
Active IBD
Ischemic bowel
Acute diverticulitis
Abdominal abscess
Pregnancy in the 3rd trimester

PD require you to learn a new skill and the ability to do this may be impaired by drugs, alcohol, cognitive issues (dementia) - this requires lots of help and education. Your abdomen may be contraindicated for peritoneal dialysis due to previous surgery or abdominal conditions.

25
Q

What are the absolute contraindications for haemodialysis?

A

Inability to achieve suitable vascular access - all AV fistula locations used up

26
Q

Side effects of haemodialysis and peritoneal dialysis?

A
Haemodialysis:
Fatigue
Hypotension 
Sepsis
Muscle cramps
Itchy skin between sessions
Others (sexual libido loss, dry mouth, arth/myalgia, insomnia)

PD:
Peritonitis (spontaneous bacterial)
Hernia
Weight gain

27
Q

What are the benefits of renal transplant over dialysis?

A

Regain the time lost to dialysis
No diet restrictions
No fluid restrictions
More able to work due to lack of restrictions and making them fitter/less fatigued
More freedom to travel (don’t need to plan dialysis abroad)

-98% of patients are alive after 5 years

28
Q

What are the two routes to access a kidney transplant?

A

Deceased donation (brain dead, often young and due to an accident) live donation (family, friend or altruistic or paired/pool donation)

29
Q

Which religion isn’t good for kidney donation numbers?

A

Shinto - belief is that it takes a few days for the spirit for leave the body, therefore low decreased donation.

30
Q

Where are the renal artery/vein and ureter of the donor kidney anastamosed in the patient’s body?

A

Kidney is placed in the iliac fossa, therefore local vessels are used:
Renal artery - common iliac artery

Renal vein - common iliac vein

Ureter - roof of bladder, in order to reduce reflux when urinating

31
Q

What are the absolute contraindications for renal transplant?

A

Active malignancy

Concurrent or recurrent infection

Active, untreated HIV Infection or AIDS

  • basically anything with a life expectancy of under 2 years
32
Q

What are the treatments for hyperparathyroidism in CKD?

A

Parathyroidectomy - partial or total

Or Cinacalcet - mimics calcium, Binds sensors on the parathyroid gland and reduces PTH secretion.

33
Q

What is the management of nephrotic syndrome?

A
  1. Conservative measures:
    Salt restriction - dietician review, no salt diet
    Fluid restriction 1-1.5L per day
  2. Diuretics; oedema, max 500-700ml loss per day
  3. ACE-I or ARB
  4. Anticoagulation; loss of antithrombin 3, protein C and S
34
Q

What is the management for autosomal dominant polycystic kidney disease?

A
  1. Monitoring kidney size - the mainstay of treatment
  2. Blood pressure control from childhood: ACE-I/ARB or CCB
  3. If severe pain and poor function: Nephrectomy

There is no surgical or radiological role here, no decompression is possible.

35
Q

What is the management for Von Hippel-Lindau disease?

A

Direct therapy for ADPKD with CKD 1-4 who have evidence of rapid progression = Tolvaptan (Vasopression receptor antagonist)
Requirements:
- Annual MRI volume measurement of kidneys
- High fluid intake
- Regular blood tests for renal/hepatic function

  1. Treat hypertension: ACE-I/ARB/Amlodipine
  2. Treat UTIs: Trimethoprim or nitrofurantoin
  3. Treat infection of cysts: Quinolones
  4. Pain treatment: bed rest, paracetamol or opioids
  5. Adjuvant pain treatment: TCAs, gabapentin/pregabalin
  6. Renal stones (uric acid and calcium oxalate): potassium citrate, lithotripsy is more dangerous
  7. Polycystic liver: cyst drainage or liver resection if big enough
  8. Renal failure: Renal transplant or dialysis
36
Q

What is the treatment for AKI?

A
First exclude emergencies:
Check NEWS2
CXR for pulmonary oedema
U+E’s for potassium level
Basic obs

Treat hypovolaemia: Bolus 250/500ml crystalloid fluid challenge, then 2L If response, or with blood components if haemorrhage

Then SALFORD:
Sepsis - test for It, possible cause
ACEI/ARB - stop them
Labs - check serum creatinine every 24 hours
Fluid assessment - catheterise, watch urine output
Obstruction - perform USS, possible causes
Refer to Renal/ICU
Dip urine - look for bloods, proteins,possible causes

So, we’re looking for possible causes (Cultures, USS, urine dip), monitoring for progression (Serum creatinine, urine output) and treating (Referral and stopping ACEI/ARBs)

37
Q

In the treatment of AKI, what are the indications for dialysis? (Normally haemodialysis or haemofiltration)

A

Hyperkalemia (Recurrent or Severe or underlying pathology can’t be corrected)

Pulmonary oedema - fluid overload that is unresponsive to fluid resuscitation

Severe or prolonged acidosis

Uraemic encephalopathy (signs: confusion, myoclonic jerks and seizures)

Uraemic pericarditis (pericardial sac inflammation)

38
Q

What is the size threshold for indication for surgery to remove a renal stone?

A

8mm or more - considered large

Conservative management (fluids and painkillers) if:
Less than 5mm
Or lower ureter position
Or no obstruction occurring

39
Q

When do we opt for surgical intervention in ADPKD?

How do we manage ADPKD?

A

We do not, unless it is a total nephrectomy, and that is a last resort

Management:
Monitor size and kidney function
Screen family
Manage cardiovascular disease/RFs

40
Q

What is the treatment for pyelonephritis?

A

24-48 hour IV Gentamicin or temocillin
Then 10 day oral antibiotics

Make sure they treat e.coli - most common cause

41
Q

What is the treatment for simple UTI?

A

Non-pregnant female: 3 day treatment with oral trimethoprim/nitrofurantoin

Pregnant woman: Expert help needed

  • avoid trimethoprim in first trimester
  • avoid nitrofurantoin in third trimester

Man: 7 day treatment with oral trimethoprim/nitrofurantoin

42
Q

What is the treatment for complicated UTI?

Complicated: “anatomical or pathological abnormality (stones, reflux or stasis) that predisposes them to developing UTIs”

A

Cystoscopy and USS/CT - need to check why the UTI isn’t responding to normal treatment

Then same as simple UTI

43
Q

What is the treatment for bladder cancer?

A

First line: TURBT - if no bladder wall invasion has occurred, and regular cystoscopies

Some have bacillus calmette guerin (BCG) therapy (microbe is introduced to the bladder and induces an immune response to the tumour, inducing antitumour adaptive immunity), or cystectomy If:

  1. Superficial bladder wall invasion
  2. Grade 3 cancer

If deep muscle wall invasion: RADICAL CYSTECTOMY and RADIOTHERAPY