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General practice > Renal > Flashcards

Renal Flashcards

1
Q

Effect of hyperventilation on pH

A

Hyperventilation –> reduced co2 –> increase in pH

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2
Q

Normal anion gap

A

10-20 mmol/L

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3
Q

How is anion gap calculated

A

Na+ - (Cl- + HCO3-)

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4
Q

What is high chloride in metabolic acidosis due to

A

Compensation for gastrointestinal bicarbonate loss(e.g., severe/prolonged diarrhoea)

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5
Q

Causes of metabolic acidosis with increased anion gap

A

MUDPILES!

M - Methanol 
U - Uremia(CKD) 
D - Diabetic ketoacidosis 
P - Paracetamol, propylene glycol 
I - Infection, iron, isoniazid 
L - Lactic acidosis
E - Ethylene glycol
S - Salicylates
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6
Q

How does kidney failure result in high anion-gap acidosis

A

Results in decreased acid excretion and increased bicarbonate excretion

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7
Q

Causes of metabolic acidosis with normal anion gap

A

Primary due to loss of bicarb or ingestion of H+

RTA 
Diarrhea 
Addison's disease 
Pancreatic fistula 
Drugs or toxins
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8
Q

Which drugs/toxins cause normal anion gap metabolic acidosis

A

Acetazolamide

Ammonium chloride

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9
Q

Causes of metabolic alkalosis

A

Vomiting
Hypokalaemia
Excessive alkali drugs(such as acid dyspepsia)
Burns

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10
Q

Acute causes of respiratory acidosis

A

Depression of central respiratory centre by cerebrovascular disease or drugs

Inability to ventilate adequately(myasthenia graves, amyotrophic lateral sclerosis, Guillain-barre)

Airway obstruction(asthma, copd exacerbation

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11
Q

Chronic cause of respiratory acidosis

A

COPD
Obesity
Hypoventilation syndrome
Neuromuscular disorders and restrictive ventilatory defects such as interstitial fibrosis or thoracic deformities.

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12
Q

Causes of respiratory alkalosis

A

Hyperventilation - eg, anxiety, stroke, meningitis, altitude, pregnancy (see the separate Hyperventilation article).

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13
Q

Definition of CKD

A

Is based on the presence of kidney damage (ie albuminuria) or decreased kidney function (ie glomerular filtration rate (GFR) <60 ml/minute per 1·73 m²) for three months or more, irrespective of clinical diagnosis.

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14
Q

Causes of CKD

A 
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease
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15
Q

CKD presentation

A 
Usually asymptomatic 
oedema: e.g. ankle swelling, weight gain
polyuria
lethargy
pruritus (secondary to uraemia)
anorexia
insomnia
nausea and vomiting
hypertension
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16
Q

1st line antihypertensives in CKD

A

ACE inhibitors(esp proteinic renal disease)

Furosemide is an alternative(added benefit of lowering serum K+)

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17
Q

How do CKD patients develop anaemia

A

Reduced EPO(normochromic normocytic anaemia)

Reduced absorption of iron

Anorexia/nausea due to uraemia

Reduced red cell survival

Blood loss due to capillary fragility and poor platelet function

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18
Q

Management of anaemia in CKD

A

Determination of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA).

Many patients, especially those on haemodialysis, will require IV iron

ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’

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19
Q

Factors which contribute to CKD bone disease

A

low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)

high phosphate(excretion normally by kidneys)

low calcium: due to lack of vitamin D, high phosphate
secondary

hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

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20
Q

Clinical manifestations of CKD bone disease

A

Osteitis fibrosa cystica
aka hyperparathyroid bone disease

Adynamic
reduction in cellular activity (both osteoblasts and osteoclasts) in bone
may be due to over treatment with vitamin D

Osteomalacia
due to low vitamin D

Osteosclerosis

Osteoporosis

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21
Q

How do high phosphate levels contribute to osteomalacia

A

High phosphate levels draw calcium from bones –> osteomalacia

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22
Q

Management of CKD mineral bone disease

A

reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases

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23
Q

What do NICE regard as clinically important proteinuria

A

ACR of 3mg/mmol or more

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24
Q

When do NICE advise referral to nephrologist in proteinuria

A

(ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated

a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection

consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease

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25
Q

Management of proteinuria in CKD

A

ACE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria

They should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol

if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure

26
Q

Drugs to avoid in renal failure

A

antibiotics: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin

27
Q

Drugs likely to accumulate in CKD which therefore need dose adjustment

A 
most antibiotics including penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
digoxin, atenolol
methotrexate
sulphonylureas
furosemide
opioids
28
Q

Which antibiotics are relatively safe in CKD

A

Erythromycin

Rifampicin

29
Q

What is pyelonephritis

A

Pyelonephritis refers to inflammation of the kidney resulting from bacterial infection. The inflammation affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue).

30
Q

Risk factors for pyelonephritis

A

Female sex
Structural urological abnormalities
Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children)
Diabetes

31
Q

Causes of pyelonephritis

A

E.coli(most common)
Klebsiella pneumoniae
Enterococcus
Pseudomonas aeurginosa

32
Q

Pyelonephritis presentation

A 
Fever
Loin or back pain (bilateral or unilateral)
Nausea/vomiting 
Similar to LUTS(dysuria, suprapubic discomfort, increased frequency) 
Systemic illness 
Loss of appetite 
Haematuria 
Renal angle tenderness
33
Q

Ix for pyelonephritis

A

Urine dip
MSU for microscopy, culture and sensitivity
Blood tests
Imaging(ultrasound or CT)

34
Q

Abx for pyelonephritis

A

NICE guidelines (2018) recommend the following first-line antibiotics for 7-10 days when treating pyelonephritis in the community:

Cefalexin
Co-amoxiclav (if culture results are available)
Trimethoprim (if culture results are available)
Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)

35
Q

Mx of pyelonephritis

A

Oxygen to maintain oxygen saturations of 94-98% (or 88-92% in COPD)
Empirical broad-spectrum IV antibiotics (according to local guidelines)
IV fluids
Sepsis 6 if suspected

36
Q

What should be considered in patients with pyelonephritis with significant symptoms or not responding to treatment

A

Renal abscess

Kidney stone obstructing the ureter, causing pyelonephritis

37
Q

What is chronic pyelonephritis

A

Chronic pyelonephritis presents with recurrent episodes of infection in the kidneys.

Recurrent infections lead to scarring of the renal parenchyma, leading to chronic kidney disease (CKD). It can progress to end-stage renal failure.

38
Q

Ix in recurrent pyelonephritis

A

Dimercaptosuccinic acid (DMSA) scans involve injecting radiolabeled DMSA, which builds up in healthy kidney tissue.

When imaged using gamma cameras, it indicates scarring or damage in areas that do not take up the DMSA. They are used in recurrent pyelonephritis to assess for renal damage.

39
Q

Most common place for renal stones

A

Vesico-ureteric junction

40
Q

Two key complications of kidney stones

A

Obstruction leading to acute kidney injury

Infection with obstructive pyelonephritis

41
Q

Most common type of kidney stones

A

Calcium-based stones

42
Q

Risk factors for calcium stones

A

raised serum calcium (hypercalcaemia) and a low urine output

43
Q

Which kidney stones are not visible on x-ray

A

Uric acid

44
Q

What are cystine kidney stones associated with

A

Associated with cystinuria, an autosomal recessive disease

45
Q

What are struvite kidney stones produced by

A

Bacteria, therefore, associated with infection

46
Q

What is a stag horn calculus

A

A staghorn calculus is where the stone forms in the shape of the renal pelvis, giving it a similar appearance to the antlers of a deer stag. The body sits in the renal pelvis with horns extending into the renal calyces. They may be seen on plain x-ray films.

47
Q

Which stones most commonly cause stag horn calculus

A

Struvite stones

In recurrent upper urinary tract infections, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite.

48
Q

Presentation of renal colic

A

Renal colic is the presenting complaint in symptomatic kidney stones. Renal colic is:

Unilateral loin to groin pain that can be excruciating (“worse than childbirth”)
Colicky (fluctuating in severity) as the stone moves and settles

49
Q

Symptoms of renal colic

A

Patients often move restlessly due to the pain.

There may also be:

Haematuria
Nausea or vomiting
Reduced urine output
Symptoms of sepsis, if infection is present

50
Q

Ix for renal colic

A

Urine dip
AXR
Non-contrast CT KUB
Ultrasound

51
Q

Mx of renal stones

A 
NSAIDs(IM diclofenac) 
Antiemetics 
Antibiotics 
Watchful waiting if less than 5mm 
Tamulosin 
Surgical intervention
52
Q

Surgical interventions for kidney stones

A

Extracorporeal shock wave lithotripsy(ESWL)

Ureteroscopy and laser lithotripsy

Percutaneous nephrolithotomy(PCNL)

Open surgery

53
Q

General advice for recurrent stones

A

Increase oral fluid intake (2.5 – 3 litres per day)

Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones)

Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation)

Reduce dietary salt intake (less than 6g per day)

Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones)

54
Q

Dietary advice for calcium stones specifically

A

Reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea)

55
Q

Dietary advice for uric acid stones specifically

A

reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)

56
Q

Which medications may be used to reduce the risk of kidney stone recurrence

A

Potassium citrate in patients with calcium oxalate stones and raised urinary calcium

Thiazide diuretics (e.g., indapamide) in patients with calcium oxalate stones and raised urinary calcium

57
Q

Prevention of oxalate stones

A

cholestyramine reduces urinary oxalate secretion

pyridoxine reduces urinary oxalate secretion

58
Q

Risk factors for renal stones

A

dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure

59
Q

Risk factors for urate stones

A

gout

ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

60
Q

Drug causes of renal stones

A

drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline

thiazides can prevent calcium stones (increase distal tubular calcium resorption)

General practice (26 decks)

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