High Yield Exam Cram Flashcards

1
Q

how do the kidneys sense blood pressure?

A

macula densa senses the sodium concentration of fluid in the tubule which is an indicator of blood pressure

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2
Q

Name the 2 compounds that can be used to assess eGFR

A

Inulin and CK

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3
Q

Explain where creatinine comes from

A

It is a muscle breakdown product

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4
Q

How is the anion gap calculated?

A

(Na+ + K+) – (Cl- + HCO3-) = Anion gap

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5
Q

What is a normal anion gap?

A

10-18

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6
Q

List the causes of a raised anion gap metabolic acidosis

A
  • M – Methanol
  • U – Uraemia
  • D – Diabetic ketoacidosis, starvation and alcoholic ketoacidosis
  • P – Paracetamol use (chronic)
  • I – Isoniazid
  • L – Lactic acidosis & shock
  • E – Ethylene Glycol
  • S – Salicylates
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7
Q

Which must be corrected first -calcium or phosphate?

A

Always correct phosphate before calcium

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8
Q

What 3 criteria can be used to diagnose AKI

A
  • 25 micromol/L rise in creatinine in 48 hours
  • 50% rise in creatinine in 7 days
  • <0.5ml/kg/hour urine output for 6 hours
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9
Q

Name the pre-renal causes of AKI

A

Cardiac failure
Haemorrhage
Sepsis
Vomiting and diarrhoea

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10
Q

Name the renal causes of AKI

A

Acute tubular necrosis
Glomerulonephritis
Vasculitis
Radiocontrast
Myeloma
Rhabdomyolysis
Drugs (e.g. NSAIDs and gentamycin)

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11
Q

Name the post-renal causes of AKI

A

Tumours
Prostate disease
Stones
Strictures

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12
Q

What are the immediately dangerous consequences of AKI?

A
  • Acidosis
  • Electrolyte imbalance
  • Intoxication & toxins
  • Overload of fluid
  • Uraemic complications
    (AEIOU)
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13
Q

Name 5 drugs that must be stopped in AKI

A
  • Angiotensin II receptor antagonists
  • Aminoglycosides
  • ACE inhibitors
  • Diuretics
  • Metformin (risk of lactic acidosis)
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14
Q

Which drugs should you consider stopping in patients with an AKI due to risk of accumulation and toxicity?

A

Lithium
Digoxin

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15
Q

Describe the steps involved in treating hyperkalaemia

A

Stabilise the myocardium (calcium gluconate)

Shift K+ intracellularly (salbutamol and insulin-dextrose)

Remove as much potassium as possible
(Diuresis, Dialysis, Potassium binders)

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16
Q

What is CKD?

A

Chronic reduction in kidney function over 3 months

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17
Q

What are the two biggest causes of CKD?

A

Diabetes and hypertension

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18
Q

What pathology within the kidney is caused by chronically high sugar levels?

A

Glomerulosclerosis

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19
Q

What pathology within the kidney is caused by chronically high blood pressure?

A

nephrosclerosis

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20
Q

What are the G and A scores for CKD based on?

A

G = eGFR
A= Albumin:creatinine ratio

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21
Q

How is proteinuria quantified?

A

Albumin:creatinine ratio

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22
Q

What is the BP target in patients <80 years with CKD?

A

130/80

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23
Q

Which drugs are used to slow the progression of CKD?

A

ACE inhibitors, SGLT-2 inhibitors

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24
Q

what additional drug should be stated in all patients with CKD to help prevent cardiovascular complications?

A

Statin

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25
Q

Why do patients with CKD become anaemic?

A

Due to lack of erythropoietin

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26
Q

How does the anaemia look in (CKD) - like what do the red blood cells look like?

A

Normocytic normochromic

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27
Q

What must be treated before erythropoietin can be given?

A

Iron deficiency

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28
Q

What impact does CKD have on calcium regulation

A

Causes low vitamin D because the kidneys aren’t able to activate it as well. This leads to low calcium

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29
Q

What is needed for a glomerulonephritis to be classed as nephrotic syndrome?

A

> 3g protein in the urine within 24 hours

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30
Q

What does nephrotic syndrome mean for the state of the kidney?

A

indicates that the basement membrane has become so damaged that it is now permeable to the larger protein molecules

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31
Q

How does nephrotic syndrome present?

A

Frothy urine and oedema

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32
Q

What does nephrotic syndrome predispose patients to?

A

thrombosis, hypertension and high cholesterol

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33
Q

What are the distinguishing features of IgA nephropathy?

A

1-2 days after an infection
IgA deposits and mesangial proliferation

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34
Q

What are the distinguishing features of post-infective diffuse proliferative glomerulonephritis?

A

1-2 weeks after strep (tonsillitis or vitiligo)
Caused by IgG deposits

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35
Q

How is lupus nephritis managed?

A

Immunosuppressants and corticosteroids

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36
Q

What are the distinguishing features of Granulomatosis with Polyangiitis?

A

C-ANCA
Nosebleeds

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37
Q

What are the distinguishing features of good pastures?

A

Anti-GBM
Gomerulonephritis and pulmonary haemorrhage (AKI & Hameoptysis)
20s and 60s

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38
Q

What are the distinguishing features of Cresenteric / rapidly progressing glomerulonephritis?

A

Glomerular crescents
Acute severe illness

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39
Q

What are the distinguishing features of membranoproliferazive glomerulonephritis?

A

Patients under 30
Immune complex deposition and mesangial proliferation

40
Q

What are the distinguishing features of Membranous Glomerulonephritis (IgG)?

A

Underlying malignancy
IgG deposits

41
Q

What are the distinguishing features of Minimal change?

A

Children
Oedema

42
Q

What are the distinguishing features of Focal segmental glomerulonephritis?

A

Focal and segmental sclerosis

43
Q

What are the distinguishing features of diabetic nephropathy?

A

Hyperglycaemia causes damage to the glomerulus causing the leaking of albumin into the urine

Glomerulosclerosis and interstitial fibrosis also occurs

44
Q

How is glomerulonephritis diagnosed?

A

renal biopsy

45
Q

How is glomerulonephritis managed?

A

Supportive
Immunosuppression

For nephrotic syndrome:
* Reduce salt
* Loop diuretics
* Manage hypertension
* Heparin to reduce thrombus risk
* Pneumococcal vaccine
* Statins

46
Q

Which demographic tends to be affected by multiple myeloma?

A

Elderly

47
Q

What urine findings might indicate multiple myeloma?

A

Heavy proteinuria
Bence-jones proteins

48
Q

What causes damage to the kidneys in multiple myeloma?

A

Cast nephropathy

49
Q

How is multiple myeloma managed?

A

Immunotherapy and steroids

50
Q

What is acute tubular necrosis?

A

Damage and death of the epithelial cells of the renal tubules caused by ischaemia or nephrotoxins

51
Q

Explain the difference between the 4 different types of acute tubular necrosis

A

Type 1 = distal tubule cannot excrete hydrogen ions

Type 2 = proximal tubule cannot reabsorb hydrogen ions

Type 3 = mix of type 1 & 2

Type 4 = caused by reduced aldosterone

52
Q

What might you see on urinalysis in a patient with acute tubular necrosis?

A

Muddy brown casts

53
Q

How is acute tubular necrosis managed?

A

Oral bicarbonate

54
Q

What is acute interstitial nephritis?

A

An inflammatory reaction in the space between the tubes and the vessels (interstitum) caused by an immune reaction to drugs, infections or autoimmune conditions

55
Q

what blood test finding is associated with acute interstitial nephritis?

A

eosinophilia

56
Q

What is haemolytic uraemia syndrome?

A

Thrombosis in small blood vessels triggered by shiga toxins from E.coli or shigell

57
Q

Which demographic is commonly affected by haemolytic uraemia syndrome?

A

Children following a bout of gastroenteritis

58
Q

how should haemolytic uraemia syndrome be managed?

A

Give antibiotics and anti-motility medication (e.g. loperamide)

59
Q

How is the causative agent in haemolytic uraemia syndrome tested for?

A

Stool antigen test

60
Q

What is the inheritance pattern in polycystic kidney disease?

A

Autosomal dominant

61
Q

What is the gene and chromosome affected in polycystic kidney disease

A

PKD1 gene on chromosome 16

62
Q

What additional complications are those with polycystic kidney disease at risk of?

A

Liver cysts
Subarachnoid haemorrhage
Mitral regurgitation

63
Q

What medication can slow the development of cysts in polycystic kidney disease

A

Tolvaptan

64
Q

What is the best imaging modality for detecting renal stones?

A

Non contrast CT KUB

65
Q

What are most renal stones made from?

A

Calcium oxalate

66
Q

Which renal stones don’t show up on X-ray?

A

uric acid

67
Q

What are stag horn calculi made from and what produces this compound?

A

Struvite (made by bacteria)

68
Q

How are renal stones managed?

A
69
Q

How are renal stones prevented?

A
  • High fluids
  • Low protein, low salt
  • Thiazide diuretics
70
Q

What is the difference between acute and chronic urinary retention?

A

Acute = painful inability to void with a palpable and percussible bladder

Chronic = painless, palpable and percussible bladder after voiding

71
Q

How do alpha blockers (tamsulosin) work?

A

Causes smooth muscle relaxation

72
Q

How do 5-alpha reductase inhibitors work (finasteride)?

A

Blocks the hormone responsible for converting testosterone to its active form. This slows prostatic growth.

73
Q

What type of cancer is prostate cancer?

A

Adenocarcinoma

74
Q

Where in the prostate does cancer most commonly grow?

A

Peripheral zone

75
Q

What grading system is used for prostate cancer/

A

Gleason

76
Q

name the two most common types of bladder cancer and their causes

A

Aromatic amines in dye and rubber cause transitional cell carcinoma

Schistosomiasis causes squamous cell carcinoma of bladder

77
Q

What is the biggest risk factor for bladder cancer?

A

smoking

78
Q

what characteristic metastasis is associated with renal cell carcinoma?

A

Cannon ball lung mets

79
Q

How is hydronephrosis managed?

A

Percutaneous nephrostomy or an antegrade ureteric stent

80
Q

What antibiotic can be used to treat a UTI in pregnancy?

A

amoxicillin or nitrofurantoin (up to 37 weeks)

81
Q

How many days should a UTI be treated for in men, pregnant women and women with a complicated UTI?

A

7 days (and send an MSSU!!)

82
Q

What is the treatment for an asymptomatic UTI in a catheterised patient?

A

No treatment

83
Q

What is the treatment for pyelonephritis?

A

7-10 days of cefalexin

84
Q

What is the management for stress incontinence

A
  • Pelvic floor exercises
  • Duloxetine (SNRI)
85
Q

What is the management for urge incontinence

A
  • Bladder retraining
  • Oxybutynin (Anti-muscarinic)
86
Q

What is the difference between nephrogenic and cranial diabetes insipidus?

A

Nephrogenic = lack of response to ADH.

Cranial =Lack of ADH production.

87
Q

How can cranial and nephrogenic diabetes insipidus be differentiated?

A

Water depravation test

88
Q

How is cranial diabetes insipidus treated?

A

Desmopressin

89
Q

How is nephrogenic diabetes insipidus managed?

A

Conservative

90
Q

What are the indications for renal replacement therapy?

A
  • A – acidosis
  • E- electrolyte abnormalities
  • I – intoxication
  • O – oedema
  • U – uraemia symptoms such as seizures or reduced consciousness
91
Q

What is the most common osmotic agent for ultrafiltration of fluid in peritoneal dialysis?

A

Glucose

92
Q

How long does an AV fistula need to mature before it can be used

A

4-16 weeks

93
Q

Which viruses pose a major risk o kidney transplant recipients?

A

Cytomegalovirus and EBV

94
Q

What is the standard immunosuppressant regimen following kidney transplant?

A
  • Induction with Basilximab
  • Maintenance with Tacrolimus, Mycophenolate and steroids
95
Q

How are donors and recipients matched for renal transplant?

A

matched based on the human leukocyte antigen (HLA ) A, B & C on chromosome 6. The closer the match, the less chance of rejection

96
Q
A