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Medical Finals 2020 > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

What is the clinical diagnosis needed for an AKI?

A

> 6hrs oliguria
Increase in creatinine by 25 from baseline
Increase in creatinine x1.5 from baseline

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2
Q

What is the difference between acute tubular necrosis and acute interstitial nephritis?

A

Acute tubular necrosis - ischaemia, either caused by renal injury or direct toxicity, there are granuloma casts

Acute interstitial nephritis - damage to the glomerulonephrons usually by penicillins, NSAIDs, rifampicin or allopurinol. There are white cell casts present, patients present with arthralgia or sterile pyuria

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3
Q

How do you manage haemolytic uraemic syndrome?

A 
Fluids
Blood transfusion
Dialysis
Plasma exchange
Eculizumab
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4
Q

What is a common cause of IgA nephropathy?

A

This is when IgA mesangial depositation resulting in haematuria and proteinuria. It is believed to be caused by autoimmune factors resulting in higher IgA levels.

This is NOT the same thing as post-streptococcal glomerulonephritis

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5
Q

What are the three features of nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema

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6
Q

Give some causes of nephrotic syndrome?

A

Minimal change disease
Focal Segment Glomerulosclerosis
Membranous nephropathy

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7
Q

Give some causes of nephrogenic DI?

A

Genetics
Hypercalcaemia, Hypokalaemia
Lithium
Pyelonephritis

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8
Q

What is reabsorbed in the proximal tubules?

A

Sodium (sodium, potassium pumps)
Glucose and amino acids (secondary active transport with sodium)
Bicarbonate

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9
Q

What is reabsorbed in the collecting duct?

A

Sodium (Potassium and H+ excreted through co-transporters)

Water is reabsorbed through aquaporin channels

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10
Q

What effect does hypotension have on the glomerular capillaries?

A 
Low BP
Decreased GFR
Decreased pressure
Afferent capillaries CONSTRICT
Efferent capillaries DILATE
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11
Q

How much is renal blood flow of normal cardiac output?

A

20%

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12
Q

What diuretics may result in low K+?

A

Loop diuretics

Thiazide diuretics

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13
Q

What cells in the kidney control renin release?

A

Macula densa cells int he juxtaglomerula apparatus detects low sodium causing renin release.
Renin is an enzyme that breaks down ngiotensinogen to Angiotensin I.

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14
Q

What risk does long-term corticosteroids hold?

A 
Thin skin
Increased appetite, weight gain
Bone thinning
GI symptoms
Immunosuppression
Impaired glucose regulation
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15
Q

What steroids have a predominantly glucocorticoid affect?

A

Prednisolone, Dexamethason

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16
Q

What steroids are primarily mineralocorticoid?

A

Fludrocortisone

Hydrocortisone

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17
Q

What part of the kidneys do each diuretic type act on? (3)

A

Loop diuretics - Loope of Henle
Thiazine - Distal convoluted tubule
Potassium sparing - aldosterone agonist

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18
Q

What are some side effects of thiazide diuretics?

A 
Low potassium, sodium, magnesium
Metabolic acidosis
High uric acid levels
Dehydration
Rarer - thrombocytopaenia, agranulocytosis, pancreatitis
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19
Q

What are the stages of CKD?

A 
1 - kidney damage with eGFR >90
2 - kidney damage with mildly lower GFR 60-90
3 - moderate decrease - 30-60
4 - severe decrease - 15-30
5 - kidney failure - <15
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20
Q

Give 5 causes of CKD?

A 
hypertension
diabetes
glomerulonephritis, IgA nephropathy
renal artery stenosis
obstruction
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21
Q

What are some clinical features in severe CKD?

A 
malaise, anorexia
Noctura, polyuria
Itching
N+V
Uraemic symptoms
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22
Q

How do you monitor the progression of kidney disease?

A

Blood pressure
Creatinine
Proteinuria

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23
Q

What are the DAMN drugs?

A

Diuretics
ACE-i
Metformin
NSAIDs

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24
Q

How can you manage proteinuria?

A

ACE-i
ARB
Lifestyle
Weight loss

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25
Q

What should be offered to all patients with CKD?

A

A statin, unless contraindicated

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26
Q

What complications can occur in CKD?

A

Renal bone disease
Oedema
Heart disease

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27
Q

When do you offer haemodialysis?

A

eDFR 14-10

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28
Q

Give some causes of metabolic acidosis that cause a high or low anion gap?

A

High - lactate (sepsis, shock, hypoxia), DKA, alcohol, urate (renal failure)
Normal - GI bicarb loss (diarrhoea, fistula), drugs, Addison’s

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29
Q

What is membranous glomerulonephritis?

A

A cause of nephrotic syndrome, autoimmune association - SLE
Low total thyroxine levels may be seen
Puffy and swollen eyes
Fluid retention

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30
Q

What cancer are you at increased risk at post-renal transplant?

A

Melanoma and skin malignancy - SCC

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31
Q

What is HUS?

A

Haemolytic Uraemic Syndrome
Intravascular haemolysis with fragmentation that causes endothelial damage resulting in abdominal pain, blood diarrhoea and an AKI

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32
Q

What often causes HUS?

A

e.coli

Others include HIV, pneumococcal, SLE

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33
Q

What is the triad often seen in HUS?

A

AKI
Thrombocytopaenia
Microangiopathic haemolytic anaemia

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34
Q

How is HUS treated?

A

Supportive - fluids, blood transfusion and dialysis if required
Plasma exchange - in severe cases (not associated with diarrhoea)
Eculizumab

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35
Q

What is acute interstitial nephritis?

A

Drug-induced AKI
Caused by penicillin, rifampicin, NSAIDs, allopurinol, furosemide, SLE, sarcoidosis
Causes fever, rash, arthralgia, eosinophilia, mild renal impairment, HTN, sterile pyuria and WCC

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36
Q

What are risk factors for an AKI?

A

CKD
Dehydration
Age
Diabetes

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37
Q

What is seen on an ABG of someone with DKA?

A

Metabolic acidosis with a high anion gap

Hx may include high capillary blood glucose, tachy, dry mucous membranes, reduced skin turgor, fruity smell to breath

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38
Q

How much glucose is required per day in fluid therapy?

A

50-100g/day irrespective of weight

39
Q

Urea that is proportionally higher than creatinine rise may indicate?

A

GI bleed

Dehydration

40
Q

What is HSP?

A

Henoch-Schonlein Purpura
IgA mediated small vessel vasculitis
Seen in children following infection
Palpable purpuric rash, localed oedema, abdominal pain, polyarthritis, haematuria/renal failure

41
Q

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

A

Cytomegalovirus

Treat with Ganciclovir

42
Q

What does a raised anion gap suggest?

A

Increased production or reduced excretion of… lactic acid, urate, ketones or drugs/toxins (salicylates)

43
Q

What are some non-kidney associations of ADPKD?

A 
Mitral valve prolapse
Hepatomegaly (liver cysts)
Diverticulosis
Intracranial aneurysms
Ovarian cysts
44
Q

How do you treat minimal change disease?

A

Prednisolone

45
Q

What foods should be avoided in dialysis?

A

Tomatoes, bananas, coffee, chocolate, mushrooms and rhubarb - high potassium
Dairy, yoghurt, milk - phosphate

46
Q

Give 3 complications of haemodialysis

A

Access problems - blocked catheter, fistula inflammation
Hypotension, nausea, headaches
Infection

47
Q

What are the two types of peritoneal dialysis?

A

Continuous ambulatory peritoneal dialysis - manual drain of 2-3L of fluid, needs doing 3-4x a day
Automated peritoneal dialysis - machine overnight for 7hrs

48
Q

Give an advantage and disadvantage of haemodialysis

A

Better for those who live alone and need help managing
Better if previous abdominal surgery
Logistics of hospital visits 3 times a week

49
Q

Give an advantage of peritoneal dialysis

A

Better in severe HF

Useful for younger patients with work who want control of their care

50
Q

What is the biggest cause of death in dialysis patients?

A

Ischaemic heart disease

Mortality is very poor

51
Q

What is glomerulonephritis?

A

A parenchymal group of kidney diseases that involve inflammation of the glomerulus - usually immune mediated

52
Q

What is the classic triad in acute nephritis syndrome?

A

Haematuria
Proteinuria
Oedema

53
Q

What is IgA nephropathy and what do you see on biopsy?

A

Autoimmune nephrophathy
Biopsy: mesangial proliferation, IgA and C3 deposits on immunofluorescence

Cause of glomerulonephritis, occurs post URTI, causes haematuria

54
Q

What is HSP?

A

Henoch-Schonlein Purpura
Systemic vasculitic variant of IgA nephropathy
Presents with abdominal pain, GI bleeding, nephritis, purpuric rash on extensor surfaces

55
Q

What is Goodpasture’s Disease and what other organ can it affect?

A

Anti-glomerular basement membrane, autoantibodies to type IV collagen
Haematuria, nephritic syndrome, AKI
Can affect the lungs
Treat with plasma exchange

56
Q

What is the difference between nephrotic and nephritic syndrome?

A

Nephritis - haematuria, proteinuria, oedema

Nephrotic - low albumin, proteinuria, oedema

57
Q

By what increase in creatinine defines an AKI?

A 
>50% increase
or
>26.4 from baseline
or
oliguria
58
Q

How are the causes of an AKI divided up and give 3 causes for each.

A

Pre-renal - dehydration, burns, infection, hamorrhaging (to do with volume), renal artery stenosis
Renal - glomerulonephritis, acute tubular necrosis, nephrotic syndrome, nephrotoxic drugs (damage to kidneys)
Post-renal - obstructive causes, renal stones, tumours, BPH

59
Q

How might an AKI result in complications?

A 
Hyperkalaemia
Metabolic acidosis
Pulmonary oedema
Hypernatraemia
Hypocalcaemia
60
Q

What actions should be taken to manage an AKI?

A

Stop ACE-i, diuretics, metformin, anti-hypertensives, NSAIDs
Optimise fluid balance
Monitor
Dialysis

61
Q

What is rhabdomyolysis and what are risk factors for it?

A

It is inflammation and breakdown of skeletal muscles resulting in chemical release.
Occurs after prolonged falls, crush injuries, post-ischaemia, drugs and statins

62
Q

What are clinical features and symptoms of rhabdomyolysis?

A 
Malaise
Dark coloured urine
Muscle swelling, pain and weakness
Hyperkalaemia
AKI
63
Q

Give the name of 5 nephrotoxic drugs that should be stopped in an AKI

A 
NSAIDs
Gentamicin
ACE-i
Metformin
Acyclovir
Diclofenac
LMWH
64
Q

What is transluminal angioplasty used in the treatment of?

A

Renal vascular disease

65
Q

What is HUS?

A

Haemolytic uraemic syndrome - microangiopathy, intravascular haemolysis with endothelial fragmentation
Presents with AKI, abdo pain, blood diarrhoea, usually post-e.coli infection
Treat with plasma exchange or dialysis

66
Q

What is TTP?

A

Thrombotic Thrombocytopenic Purpura
Fragmental and endothelial damage resulting in platelet aggregation
Ix: low platelets, anaemia, fragmental RBC
Treat with plasma exchange and steroids
Monoclonal antibodies - eculizumab

67
Q

What are clinical features of polycystic kidney disease (autosomal dominant)?

A

Renal enlargement
Cysts on USS (black spaces)
Increased BP
Abdominal pain, haematuria

68
Q

What are associations of Horseshoe kidneys?

A

Gout, hypomagnesia, abnormal LFTs, abnormal genital tract development

69
Q

What is Alport syndrome and it’s main association?

A

A problem with T4 collagen production

Glomerular basement membrane problems, sensorineural deafness, eye abnormalities

70
Q

Give 3 diseases that have systemic renal manifestations.

A

Amyloidosis
Multiple myeloma
Diabetes

71
Q

What happens when the kidneys stop working (AKI)?

A 
Reduced urine output
Fluid overload
Raised in potassium, urea and creatinine
(potassium - arrythmias)
(uraemia - pericarditis, encephalopathy)
72
Q

Mixed symptoms of weakness, dyspnoea, hepatomegaly and worsening renal function may indicate?

A

Amyloidosis
Typically diagnosed between 50-65
High levels of proteinuria

73
Q

What would a desmopressin test result look like for cranial DI?

A

After water deprivation - 240mOsmol/kg
After desmopressin - 850 mOsmol/kg

High sodium

74
Q

What are some causes of cranial DI?

A

Post-head injury, pituitary surgery/tumour (craniopharyngiomas)
Haemochromatosis (raised RBCs)

75
Q

What are some causes of nephrogenic DI?

A

Genetic
Hypercalaemia, hypokaelaemia
Lithium
Pyelonephritis, tubulo-interstitial disease

76
Q

What do fused podocytes on light microscopy indicate and what symptoms might this patient present with?

A 
Minimal change disease
Children
Scrotal swelling, leg swelling, eye swelling
Fatigue, frothy urine
Cough
77
Q

What is your first line management in cranial and nephrogenic diabetes insipidus?

A

Cranial - desmopressin

Nephrogenic - thiazide diuretic, chlorothiazinde, low salt/protein diet

78
Q

What do muddy brown casts on urine microscopy indicate?

A

Acute tubular necrosis

79
Q 
What is the difference between the following kidney diseases?
Acute interstitial nephritis
Acute tubular necrosis
Glomerulonephritis
IgA nephropathy
Thin basement membrane
A

Acute interstitial nephritis - drug toxicity, NSAIDs, rifampicin, allopurinol, penicillin, furosemide
Acute tubular necrosis - muddy brown casts, myoglobinuria, worsening renal function
Glomerulonephritis
IgA nephropathy
Thin basement membrane - autosomal dominant, persistant microscopic haematuria, no worsening of renal function

80
Q

What is acute interstitial nephritis?

A

Acute kidney injury caused by drugs (penicillin, NSAIDs, rifampicin, allopurinol, furosemide), SLE, sarcoidosis, Hanta virus, staphyclocci
There is marked intersitial oedema on histology with intersitial infiltrate in the connective tissue between renal tubules
Features: fever,r ash, arthralgia, eosiophilia, mild renal impairment, HTN
Ix: sterile pyuria, white cell casts

81
Q

Give the name of two alpha blockers and explain their mechanism of action.

A

Tamsulosin
Alfuzasin
Sympathetic fibre innervation, muscle relaxation

82
Q

What are finasteride and dutasteride?

A

5-alpha reductase inhibitors

83
Q

What is the classic three symptoms of pyelonephritis and how is it treated?

A

Loin pain
Fever
Dysuria

Co-amoxiclav or IV cefuroxime if bad

84
Q

Give 8 side effects of PO steroids.

A

Osteoporosis, central obesity, impaired glucose tolerance, fatigue, fluid retention, headache,

85
Q

What structures arise from the ectoderm?

A 
CNS
Brain
Peripheral nerves
Melanocytes
Nails
Sweat glands
Sebaceous glands
Hair
Tooth
Breast
86
Q

What structures arise from the mesoderm?

A 
Muscle
Bone
Cartilage
Dermis
Connective tissue
Kidneys
Ovary
Testis
Heart
Blood cells
Spleen
87
Q

What structures arise from the endoderm?

A 
Stomach
Intestine
Liver
Pancreas
Bladder
Epithelial lining of bladder and urethra
Thyroid
Tonsils
Parathyroids
88
Q

What is your first line management of high phosphate?

A

Reduce dietary intake of phosphate
Bisphosphates
Vitamin D: alfacalcidol, calcitriol
May require parathyroidectomy

89
Q

What are your investigations for a renal vein thrombosis?

A

Doppler ultrasound

90
Q

What are some complications of nephrotic syndrome and post-strep glomerulonephritis?

A

Renal vein thrombosis
Sepsis
Hyperlipidaemia

91
Q

Why is there a delay in infection before presentation with nephrotic syndrome?

A

Time requires for immunocomplexes to form, attach to basement membrane and cause resulting damage to basement membrane

92
Q

What cause would you suspect in a child with swollen eyes and frothy urine post-sore throat?

A

Post-streptococcus proliferative glomerulonephritis
Lancefield group A beta-haem strep
Strep pyogenes
(cause infections of throat, ear and skin)

93
Q

What are some potential causes of a low urine output post-surgery?

A
  • dehydration
  • blocked catheter
  • retention

Give fluids and see if patient responds, if they don’t then consider haemorrhage

Medical Finals 2020 (25 decks)

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