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Phase 3b > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

5 functions of the kidney

A

Acid-base control (pumps out H+, reabsorbs bicarb)

Regulates blood/fluid volume

Waste, toxin and drug excretion

Produces erythropoietin (stimulating red cell production)

Vitamin D metabolism (Vit D to 1-Hydroxyvit D)

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2
Q

How do we measure kidney function?

A

Creatinine:

Albumin:creatinine ration (mg/mmol)

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3
Q

CKD staging

A

1: >90 (+evidence kidney damage)
2: 60-89 (+evidence kidney damage)
3a: 45-59
3b: 30-44
4: 15-29
5: <15

Takes into account albuminuria (<3, 3-30, >30)

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4
Q

How does renal failure lead to anaemia?

A

Reduced erythropoietin production

Reduced hepcidin clearance (waste product from liver which impairs iron absorption by duodenum)

Therefore give iron supplements (IV as duodenum absorption reduced)

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5
Q

Nephrotic syndrome proteinuria threshold

A

> 3g protein excreted per 24 hours

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6
Q

CKD timescale

A

> 3 months

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7
Q

Which patients should be started on ARB/ACE-i?

What should their BP target be?

A

Diabetic and ACR >3mg/mmol

Hypertensive and ACR >30mg/mmol

ACR >70mg/mmol

Target of 130/80

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8
Q

Management of acute hyperkalaemia?

A

Calcium gluconate 10ml 10% (protects myocardium)

Followed by salbutamol, insulin and dextrose to drive potassium into cells

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9
Q

Role of vitamin D

A

Increases calcium absorption
Increases renal tubular reabsorption
Increases osteoclast activity (releasing calcium from bone)

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10
Q

Stages of vitamin D activation

A

Cholecalciferol to calcidiol by liver

Calcidiol to calcitriol by kidneys

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11
Q

What acid-base changes might occur in CKD?

A

H+ ion retention leading to acidosis - treated with sodium bicarbonate

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12
Q

Possible complications of CKD

A

Anaemia
Fluid overload
Mineral and bone disorders
Hyperkalaemia

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13
Q

What type of anaemia would you see in CKD and how would you manage?

A

Normochromic normocytic

Erythropietin-stimulating agents e.g. epoetin alfa

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14
Q

Indications for dialysis in AKI

A

Refracatory hyperkalaemia
Refractory pulmonary oedema
Severe metabolic acidosis (<7.1)
Severe uraemia (>60mmol/L or CXR)

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15
Q

Complications of AKI

A

Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemic complications (pericarditis and encephalopathy)

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16
Q

Rhabdomyolysis signs and symptoms

A

Muscle pain
Dark brown urine (myoglobinuria)
Raised CK levels

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17
Q

Nephrotoxic drugs

A 
ACE-i/ARBs
NSAIDs
penicillin 
Diuretics 
Furosemide 
Rifampicin 
Cephalasporins
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18
Q

Clinical definition of oliguria?

A

<0.5mls/kg/hr (35mls/hr in a 70kg patient)

If this persists >6hrs then is defined as AKI

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19
Q

How do NSAIDs adversely affect renal function?

A

Inhibition of COX1/2 leading to inhibition of prostaglandin synthesis. This causes constriction of afferent arterioles and reduced renal perfusion

Promotes natriuresis (sodium excretion in urine)

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20
Q

How is Stage 1 AKI diagnosed?

A

Serum creatinine (increase by >26umol/L in 48 hours or >1.5-1.9 in 7 days)

Urine output (<0.5mls/kg/hr over 6 hours)

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21
Q

Pre-renal causes of AKI and what can they lead to?

A

Cardiac output (cardiac failure)

Arteriolar changes (nephrotoxic drugs e.g. ACE-i or NSAIDs)

Systemic vasodilation (septic shock)

Reduced circulating volume (hypovolaemia)

This can lead to intrinsic damage due to prolonged ischaemia of renal parenchyma and development of acute tubular necrosis (ATN)

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22
Q

Intrinsic causes of AKI

A

Vascular:
Large vessel: atherosclerotic disease, thromboembolic disease, dissection, renal artery stenosis/thrombosis

Small vessel: vasculitides, malignant HTN, microangiopathic haemolytic anaemia (e.g. DIC), thromboembolic disease

Glomerular: primary or secondary. Can cause nephritic/nephrotic syndrome

Tubulointerstitial: acute tubular necrosis (ATN); acute interstitial nephritis (secondary to medication)

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23
Q

Post-renal causes of AKI

A

Obstructive uropathy (urolithiasis, malignancies, strictures and bladder neck obstruction)

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24
Q

Clinical features of pre-renal AKI

A

Evidence of dehydration/hypovolaemia:
Dry mucus membranes, reduced CRT, reduced urine output, low BP, reduced skin turgor, dizziness and thirst

Hypervolaemia (due to cardiac failure):
Pulmonary/peripheral oedema, orthopnoea, paroxysmal nocturnal dyspnoea, dyspnoea, raised JVP, ascites

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25
Q

Acute tubular necrosis clinical features

A

Brown muddy casts in urine (tubular cells)

AKI features

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26
Q

Clinical features of tubulointerstitial disease

A

Arthralgia
Rashes
Fever
Eosinophilia

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27
Q

Clinical assessment of patient with AKI

A 
Fluid assessment (urine output)
Urine osmolality and electrolytes
MSU 
Urine dipstick 
ECG

Bloods: FBC, U&Es, bone profile, blood gas
Complement, vasculitis screen (ANCA, ANA), clotting, CK, blood film, Ig

ULTRASOUND, CXR, renal doppler, MRA

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28
Q

When would you discuss an AKI patient with a nephrologist?

A

<30 GFR, or decrease by >15 in a year

ACR >70mg/mmol

Rare or genetic cause of CKD

Renal artery stenosis

Persistent HTN despite 4 anti-hypertensives

Diagnosis that may require specialist intervention (e.g. glomerulonephritis, systemic vasculitis)

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29
Q

Management of AKI

A

Regular assessment and monitoring of urine output (catheter), weight, creatinine levels compared with baseline

Hypovolaemia: IV fluids
Hypervolaemia: fluid restriction/diuretics

Hyperkalaemia: 10ml calcium gluconate 10%, 10 units ACTRAPID insulin in 20% dextrose, 2.5mg salbutamol

Acidosis: sodium bicarbonate

RRT: if refractory pulmonary oedema/hyperkalaemia, severe uraemia (leading to encephalopathy or pericarditis), metabolic acidosis

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30
Q

RENAL DRS 26

A 
Record baseline creatinine and regular U%Es
Obstruction excluded (USS)
Urinalysis +/- MSU
Nephrotoxic drugs stopped 
Dry (IV fluids) or wet (furosemide)
Urinary output monitoring 
Prescription review
26 (>26umol/L serum creatinine in 48 hours for diagnosis)
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31
Q

Triad of nephrotic syndrome (+ other features)

A
  1. Hypoalbuminaemia
  2. Proteinuria (>3.5g per day)
  3. Oedema (low oncotic pressure)

+ coagulopathy, sepsis, hyperlipidaemia, hypocalcaemia

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32
Q

Rapidly progressive glomerulonephritis features

A

Thrombosis and rupture of capillaries leading to glomerular crescent formation in >50% of glomeruli

50% reduction in GFR over 3 months

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33
Q

Primary and secondary causes of nephrotic syndrome

A

Caused by structural changes in the glomeruli

Primary: Minimal Change Disease (commonest in children), membranous GN (commonest in adults), focal segmental glomerulosclerosis (common in adults)

Secondary: SLE, diabetes mellitus, amyloidosis

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34
Q

Causes of nephritic syndrome?

A

Proliferative: IgA nephropathy, membrano-proliferative GN, post-strep GN

Proliferative with crescents (rapidly progressing): anti-GBM, Wegener’s, microscopic polyangitis

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35
Q

Treatment for minimal change disease

A

Glucocorticoids

Immunosuppressants (cyclophosphamide) if not responding

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36
Q

Minimal change disease clinical features

A

Fusion of podocyte foot processes

Nephrotic syndrome
Normotensive
Highly selective proteinuria
PUFFY FACE

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37
Q

Causes of minimal change disease

A

Idiopathic (majority)
Drugs: NSAIDs or rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononeucleosis

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38
Q

Causes of membranous glomerulonephritis

A

Thickened basement membrane

Idiopathic: anti-phospholipase A2 antibodies
Infections: hepatitis B, malaria, syphilis
Malignancy: lung cancer, leukemia
Drugs: penicillamine, NSAIDs
SLE, thyroiditis, rheumatoid

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39
Q

Management of membranous glomerulonephritis

A

ACE-i/ARBs to reduce proteinuria
Immunosuppression (corticosteroid + cyclophosphamide)
Anti-coagulation if high risk

1/3 spontaneous remission
1/3 ongoing proteinuria
1/3 ESRF

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40
Q

Nephritic syndrome clinical presentation

A

Haematuria
Mild proteinuria
HTN
Oliguria

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41
Q

What is nephritic urinary sediment?

A

Urinary red cell casts
Leucocytes
Dysmorphic red cells
Sub-nephrotic proteinuria (>3.5g/day)

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42
Q

Most common cause of glomerulonephritis worldwide?

A

IgA nephropathy

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43
Q

What conditions are associated with IgA nephropathy and how might a patient present?

A

Alcoholic cirrhosis, coeliac disease/dermatitis herpetiformis, Henoch-Schonlein Purpura

Presentation: young male following URTI, recurrent episodes of frank haematuria

44
Q

Difference between IgA nephropathy and post-strep glomerulonephritis?

A

IgA is 1-2 days after URTI, post-strep 1-2 weeks

IgA young males with frank haematuria

Post-strep presents with proteinuria with haematuria less common

45
Q

Management of IgA nephropathy

A

ACE-i; Steroids/immunosuppressants

Up to 50% will have ESRF and need RRT

46
Q

Alport syndrome presentation

A 
Childhood 
Progressive renal failure 
Microscopic haematuria 
Sensorineural deafness
Ocular pathologies (lenticonus - protrusion of lens into anterior chamber)

Diagnosed by genetic testing (X-linked) and renal biopsy

47
Q

What antibodies are found in 30% of cases of anti-GBM?

A

ANCA (associated with better response to treatment)

48
Q

Anti-GBM management

A

Plasmapheresis (removes antibodies)
Corticosteroids
Cyclophosphamide

49
Q

Complicated UTIs

A 
Male 
Pregnant 
Diabetic 
Immunological abnormalities 
Catheter
Structural abnormalities
50
Q

Gram stain for E. coli

A

Gram negative bacillus

51
Q

Organisms other than E. coli that might cause UTIs

A

Staph saprophyticus
Klebsiella pneumoniae
Proteus

52
Q

What is urosepsis?

A

2 or more signs of systemic inflammatory response syndrome:

Temp: >38 or <36
HR: >90
RR: >20
WCC: >12 or <4

+ suspected urinary source of infection

53
Q

What would you expect to see on urinalysis for a UTI?

A

Nitrites (90% +ve)

Leucocytes (50% +ve)

54
Q

Bacteriuria definition

A

> 10^5 colony forming units/ml

55
Q

Which UTI bacteria are associated with poorer outcomes and require broad spectrum ABx?

A

Extended spectrum beta lactamase producing E. coli

Use carbapenems

56
Q

Which bacteria are more likely to lead haematogenous spread of UTI?

A

Staph aureus
Candida
Mycobacterium TB

57
Q

What signs might you see with a UTI

A 
Suprapubic tenderness 
Fever 
Rigors 
Costovertebral tenderness
Flank pain 
Confusion
58
Q

UTI diagnosis

A

In young, non-pregnant females usually clinical symptoms is enough, but you could also do a urine dip

Urine dip (leucocytes and nitrites) 
Urine microscopy, culture and sensitivity

FBC, U&Es, CRP

USS, CT (non-contrast) - abscesses, calculi, haemorrhages, obstruction

59
Q

Management of uncomplicated UTI

A

Nitrofurantoin/trimethoprim BD 3 days female, 7-10 days male

Uncomplicated pyelonephritis: don’t admit, treat with fluoroquinoline e.g. ciprofloxacin 12-hourly for 14 days

60
Q

Management of complicated UTI

A

Oral fluoroquinoline (e.g. ciprofloxacin)

IV co-amoxiclav if urosepsis or severe pyelonephritis

61
Q

Which Ig protects mucosal surfaces, and what does that include?

A

IgA

Intestines, resp tracts, oral mucosa, urothilium

62
Q

Who should you avoid trimethoprim in, and what adverse effects are there?

A

Pregnant women (or anyone with folate deficiency) - give nitrofurantoin instead

Nausea, vomiting, diarrhoea, rash, pruritis

63
Q

How does rhabdomyolysis lead to AKI?

A

Causes myoglobinuria

Myoglobin causes tubular cell necrosis - ATN

64
Q

When prescribing routine maintenance fluid, what is the normal requirement for chlorine, potassium and sodium?

A

1 mmol/kg/day

65
Q

What symptoms might come with Henoch-Schonlein Purpura?

A

Abdominal pain
Palpable rash
Arthritis

Usually children

66
Q

Pulmonary haemorrhage (chest pain/cough/haemoptysis) followed rapidly by haematuria - what is the disease and why does it present like this?

A

Goodpasture’s syndrome (anti-GBM)

Anti-GBM antibodies affect Type IV collagen found in lungs and kidneys leading to glomerulonephritis

67
Q

Risk factors and management of Goodpasture’s syndrome?

A

Smoking, LRTI, pulmonary oedema, hydrocarbon inhalation, young age (20-30)

Mx: renal biopsy (IgG deposits along basement membrane), raised transfer factor secondary to pulmonary haemorrhage

Plasma exchange (plasmapheresis), steroids, cyclophosphamide

68
Q

What do you use to prevent contrast-induced nephrotoxicity? When does it occur?

A

IV sodium chloride 0.9% 1ml/kg/hour for 12 hours pre- and post-procedure

Occurse 3-5 days post-procedure

69
Q

What antibodies would you see in Granulomatosis with polyangitis (Wegener’s)?

A

ANCA

Inflammation of blood vessels around the body

70
Q

Crystalloid vs colloid

A

Crystalloid: smaller molecules, immediate reuscitation, can cause oedema

Colloid: larger molecules, more expensive, quicker volume expansion in intravascular space but can cause allergic reactions, clotting disorders and kidney failure

71
Q

Treatment of Henoch-Schonlein?

A

Analgesia for arthralgia
Supportive therapy for nephropathy
Usually good recover, 1/3 have relapse

72
Q

What is Alport syndrome caused by

A

X-linked genetic defect in the gene which codes for type IV collagen (glomerular basement membrane)

73
Q

What can a failed renal transplant in an Alport patient lead to?

A

Goodpasture syndrome presentation (pulmonary haemorrhage and haematuria caused by anti-GBM antibodies)

74
Q

Potassium-sparing diuretics

A

Spironolactone

Eplerenone

75
Q

NICE guidelines for IV fluid resus

A

IV sodium chloride 0.9% 500mls over 15 mins

76
Q

SLE with proteinuria

A

Lupus nephritis

77
Q

What is the risk with using metformin in renal failure?

A

Build up of metformin as it is usually cleared by the kidneys
Can lead to lactic acidosis

78
Q

Use of aspirin in renal failure?

A

Has to be reduced to low dose (75mg per day)

79
Q

Features of autosomal dominant polycystic kidney disease

A 
HTN 
Abdominal pain and early satiety 
Recurrent UTIs 
Renal stones  
Haematuria 
CKD 
Liver cysts, berry aneyrsysm, pancreatic cysts, CV (mitral valve prolapse, aortic dissection, valve incompetence)
80
Q

Cause of diabetes insipidus and what might you see on biochemistry results?

A

Lack of ADH production from posterior pituitary (cranial) or reduced sensitivity of kidneys to ADH (nephrogenic)

High/borderline plasma osmolarity (making patients thirsty to reduce osmolarity)

Inappropriately low urine osmolarity

81
Q

How is DI diagnosed

A

Water deprivation test - leads to rise in plasma osmolarity and continued production of low urine osmolarity

In cranial DI, exogenous vasopressin will counteract this

In nephrogenic DI, exogenous vasopressin has no effect

82
Q

What drugs remove potassium from the body?

A

Loop diuretics
Calcium resonium
Dialysis

83
Q

What conditions lead to bilaterally enlarged kidneys?

A

Diabetic nephropathy
HIV-induced nephropathy
Amyloidosis
Autosomal-dominant polycystic kidney disease

84
Q

Most common cause of viral infection following organ transplant, and what is the treatment?

A

Cytomegalovirus

Ganciclovir

85
Q

Best way of distinguishing pre-renal uraemia from ATN?

A

Pre-renal: <20mmol/L urinary sodium

ATN: >40mmol/L

86
Q

Maintenance fluid calculation for non-neonates

A

100ml/kg/day for first 10kg
50ml/kg/day for every kg from 10-20kg
20ml/kg/day for all weight after

87
Q

Features of renal cell carcinoma

A

Triad: haematuria, loin pain, abdo mass

Pyrexia

Left varicocele (due to occlusion of left testicular vein)

Can secrete EPO (polycythaemia), PTH (hypercalcaemia), renin, ACTH

88
Q

Chlamydia features

A

Majority asymptomatic

Urinary leucocytes and blood
Dysuria, cervicitis (discharge and bleeding)
Men: discharge and dysuria

89
Q

Causes of haematuria

A 
Persistent, non-visible: 
Cancer (bladder, renal, prostate)
Prostatitis 
Cervicitis 
Stones 
Renal - IgA nephropathy, thin basement membrane 
Sudden onset:
Menstruation 
Sexual intercourse 
UTI 
Vigorous exercise

Spurious:
Rifampicin, doxorubicin
Beetroot

90
Q

Indications for urgent referral

A

> 45 AND unexplained visible haematuria in absence of UTI or after successful treatment of UTI

> 60 AND unexplained nonvisible haematuria with either dysuria or raised WCC

91
Q

Indications for non-urgent referral

A

> =60 with persistent UTIs

no referral needed if normotensive, normal renal function and no proteinuria

92
Q

Test to assess diabetic nephropathy in a patient

A

Early morning ACR

93
Q

Causes of haemolytic uraemic syndrome

A

E.coli
HIV
Pneumococcus
Cancer

94
Q

Diagnosis and management of HUS

A

FBC (thrombocytopaenia, anaemia), U&E (AKI), stool culture

Management: Fluids, blood transfusion and dialysis if severe, eculizumab

95
Q

Stage 2 AKI

A

2-2.9 baseline creatinine

96
Q

Most common causes of acute interstitial nephritis

A

Drugs: rifampicin, penicillin, NSAIDs, allopurinol, furosemide

SLE

Sarcoidosis

Staph

97
Q

Features of acute interstitial nephritis

A

Arthralgia
Rash
Fever

Eosinophilia
Mild renal impairment
Hypertension

98
Q

Diagnosis of acute interstitial nephritis

A

Sterile pyuria

White cell casts

99
Q

Features of tubulointerstitial nephritis with uveitis

A

Young women
Painful red eye
Weight loss
Fever

Urinalysis: leucocytes and protein

100
Q

Indication for MRI in renal failure

A

Renal artery occlusion

101
Q

Indication for abdo X-ray in renal failure

A

Renal stones

102
Q

Maintenance fluid calculation for adults

A

25-30ml/kg/day

1mmol/kg/day of electrolyte

50-100g/day glucose

103
Q

Recommended fluid challenge for patients with no signs of heart failure

A

500ml 0.9% saline STAT

104
Q

Rhabdomyolysis treatment

A

IV saline to perfuse kidneys

105
Q

Treatment for nephrogenic DI

A

Chlorothiazide (promotes sodium release into the urine)

106
Q

EPO side effects

A 
Flu-like symptoms 
HTN leading to encephalopathy 
Bone aches 
Skin rashes 
Pure red cell aplasia 
Increased risk of thrombosis
107
Q

What abx can cause AKI

A

Gentamicin

Phase 3b (18 decks)

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