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renal Flashcards

1
Q

What indicates poor prognosis with pancreatitis

A

Hypocalcaemia

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2
Q

Scoring systems for acute pancreatitis

A

Ransom
Glasgow
APACHE II

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3
Q

What medications makes renal function worse and should be stopped in acute kidney injury

A

ACEi
NSAIDs
Aminoglycosides
Angiotensin II receptor antagonists
Diuretics

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4
Q

Reasons for increasing incidence of AKI in high-income demographics

A

Drug use

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5
Q

definition of AKI

A

An abrupt (<48hours) reduction in kidney function defines as

An absolute increase serum creatinine by >26.4umol/l
OR
Increase in creatinine by >50%
OR
Reduction in UO

Refer to KDIGO staging classification

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6
Q

what is this

A

KDIGO classification for AKI

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7
Q

Risk factors for AKI

A

Old age
CKD
Diabetes
Cardiac Failure
Liver disease
PVD
Previous AKI

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8
Q

Exposure to what can make you more at risk to an AKI

A

Hypotension
Hypovoleamia
Sepsis
Deteriorating NEWS
Recent contact
Certain medications

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9
Q

Pre-renal causes of AKI

A

Hypovoleamia - haemorrhage, volume depletion

Hypotension - cardiogenic shock, distributive shock

Renal hypoperfusion - NSAIDs / COX-2 / ACEi / ARBs

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10
Q

Features of pre-Renal AKI

A

Reversible volumes depletion leads to oliguria and increase in creatinine

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11
Q

What percent of the kidneys receive cardiac output ?

A

20%

(But are overall 0.5% of body weight)

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12
Q

What happens if you leave pre-renal AKI untreated ?

A

Acute tubular necrosis

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13
Q

What is acute tubular necrosis

A

Commonest form of AKI

Due to usually decreased renal perfusion - other causes include sepsis and severe dehydration

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14
Q

Treatment of pre-renal AKI

A

Assess for hydration: clinical observations, JVP, CRT, oedema/pul. Oedema

Fluid challenge for Hypovoleamia:
Administer crystalloid (NaCl 0.9) or colloid (gelofusion)
DO NOT USE DEXTROSE
Give bolus of fluid then reassess and repeat as necessary

*if >1000mls IN and no improvement then seek help

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15
Q

What is renal AKI

A

A disease causing inflammation and damage to cells causing an AKI

Split by structures ie blood vessels, glomerular disease, interstitial injury and tubular injury

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16
Q

Causes of renal AKI

A

Vascular - vasculitis
Glomerular - glomerulonephritis
Interstitial nephritis - drugs (flucloxacillin, PPIs, NSAIDs), infection
Tubular injury - ischaemia, drugs (gentamicin), contrast, rhabdomyolysis

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17
Q

Signs and symptoms of AKI

A

Non-specifics = anorexia, wt loss, fatigue, lethargy
Nausea, vomiting, itch, fluid overload - oedema + SOB

Signs - fluid overload incl HTN, oedema, pulmonary oedema, effusions
Uraemia incl itch, pericarditis
Oliguria

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18
Q

Clues to renal cause

A

Sore throat - strept. = post strept. Gen
Rash = vasculitis , LUPUS
Joint pain = LUPUS, vasculitis
D&V = fluid loss
Haemoptysis = good pastures, GPA (anca)

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19
Q

Raised creatinine kinase ?

A

Rhabdomyolysis

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20
Q

Initial investigation for AKI

A

U&Es - look at K, is it high ?
FBC + coag. - abnormal clotting , anaemia
Urinalysis - haematoproteinuria
USS - obstruction / size (one kidney larger than the other ? Renal artery stenosis. Both kidneys are small? End disease.)
Immunology - ANA (lupus), ANCA (GPA), GBM (GoodPasture’s)
Protein electrophoresis & BJP - in an older person, rule out myeloma.

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21
Q

Hypercalcaemia, anaemia and bone pain in an older person with an AKI ?

A

Myeloma

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22
Q

Further management of AKI

A

Establish good perfusion pressure

Treat underlying cause

Stop nephrotoxics

Dialysis if they remain anuric and uraemia

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23
Q

What are the life-threatening complications of AKI

A

Hyperkalaemia
Fluid overload (pulmonary oedema)
Severe acidosis (pH <7.15)
Uraemia pericardial effusion
Severe uraemia (ur > 40 )

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24
Q

What is post renal AKI

A

OBSTRUCTION

AKI due to back flow > back pressure and thus loss of concentrating ability

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25
Q

*dilated renal pelvis on CT / USS

A

Post-renal AKI

Renal pelvis is dilated due to backflow of urine

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26
Q

Treatment of post renal AKI

A

Relieve obstruction

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27
Q

What is hyperkalaemia

A

Life threatening complication associated with cardiac arrhythmias

Hyperkalaemia > 5.5 ‘legs feel weak’ (muscle weakness)

Life threatening Hyperkalaemia = >6.5

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28
Q

ECG Changes in Hyperkalaemia

A
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29
Q

What does calcium gluconate do

A

Stabilises cardiac membrane

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30
Q

Medical treatment of hyperkalaemia

A

Cardia monitor and iv access

Protect myocardium - 10mls 10% calcium gluconate

Move K+ back into the cells - insulin with 50mls 50% dextrose
Salbutamol Neb.

Prevent absorption from the GI tract - calcium resonium

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31
Q

Urgent indications for dialysis

A

Hyperkalaemia >6.5 or >7

Severely acidotic pH <7.15

Fluid overload

Urea >40, pericardial rub/effusion

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32
Q

Is the prognosis for AKI good ?

A

NOOOO

AKI alone mortality = 10-30%
AKI w multi organ failure = 70-90%

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33
Q

40 year old male presenting with general malaise and haemoptysis (urea 28, creatinine 600, elevated anti-GBM)

What is the likely cause ?

A

GoodPasture’s

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34
Q

25 year old IVDA found collapsed at home - what is the likely diagnosis ?

A

Rhabdomyolysis

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35
Q

82 year old man admitted with: BP @ 70/30, Temp @ 39 degrees, pulse @ 140bpm , K+ 7.0, urea 48, Creatinine 789, CRP 250, CXR left basal consolidation

A
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36
Q

72 year old man presenting with difficulty passing urine and reduced urine output

A

Acute tubular necrosis

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37
Q

Which drugs cause Hyperkalaemia

A

Diuretics, ACEi, amiloride, beta-blockers can cause hyperkalaemia, NSAIDs

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38
Q

Can furosemide cause Hyperkalaemia ?

A

No it causes low potassium levels

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39
Q

80yr old male admitted with a 4-5 day history of diarrhoea. On admission BP 80/40, pulse 30bpm. Bloods phone back with Na 135, K+ 8.0, Urea 50, Cr 1000, bicarbonate 9

Which of the following drugs would you administer first ?

A

Calcium gluconate

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40
Q

What are indication for emergency dialysis

(4 things)

A

Pulmonary oedema (in context of AKI)
Life threatening hyperkalaemia
Uraemic pericarditis
Severe acidosis

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41
Q

What is this patient likely to have:

80yr old female presents with 3 days of diarrhoea
PMH = HBP, CKD, HF
Meds = ramipril, furosemide, spironolactone, ranitidine, amlodipine
BP = 80/40, HR 100, Temp = 36.5 degrees
Na 140, K 7.0, Bic 10, Urea 40, creatinine 450

A

Pre-renal AKI which has lead to acute tubular necrosis

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42
Q

What are the features seen in Nephritic syndrome

A

Haematuria - micro or macroscopic
Oliguria
Proteinuria - < 3g / 24 hours
Fluid retention

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43
Q

What are the features of nephrotic syndrome

A

Peripheral oedema
Proteinuria > 3g / 24 hours
Serum albumin < 25g / L
Hypercholesterolaemia

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44
Q

Most common cause of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

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45
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease

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46
Q

What would you seen in histology for IgA nephropathy

A

IgA deposits and glomerular mesangial proliferation

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47
Q

What is the antibody associated with Good Pastures?

A

Anti - GBM antibodies - (glomerular basement membrane)

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48
Q

Patient presents with acute renal failure and haemoptysis ?

A

GoodPasture’s or Granulomatosis with polyangiitis (Wegener’s)

GoodPasture’s = anti - GBM
Wegeners = anca

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49
Q

*epithelial crescents in the glomeruli

A

= rapidly progressive glomerulonephritis

They are crescent shaped scars

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50
Q

Definition of rapidity progressive glomerulonephritis

A

Is it a spectrum of conditions associated with severe glomerular injury
It is characterised by a nephritis picture associated with a rapid and progressive loss of renal function
Patients are often significantly oliguric

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51
Q

A 40 year old patient, started on penicillin, IV fluids, NSAIDs, and furosemides - for pneumonia (not all) the next day the nurse reports oliguria, fever and raised BP

There is a diffuse rash all over, and also proteinuria and raised eosinophils

What is the likely diagnosis

A

Drug induced interstitial nephritis

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52
Q

Drug induced nephritis

A

Presents acutely after the commencement of penicillins

> acute renal failure associated with fever, arthralgia, rash and eosinophils in blood and urine

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53
Q

Drug causes of acute interstitial nephritis

A

Antibiotics
NSAIDs
Diuretics
Rifampicin
Allopurinol
PPIs

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54
Q

What are all the conditions that can cause a nephritic picture (presence of haematuria and high BP)

A

SHARP AIM

SLE
Henoch-schonlein purpura
Anti - GBM (GoodPasture’s)
Rapidly progressive GN
Post - strept GN
Alport’s syndrome
IgA nephropathy
Membranoproliferative GN

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55
Q

Investigation for post-strept nephritis

A

1st = urinalysis, microscopy, culture and sensitive

Then: bloods and immunoglobulins

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56
Q

Gold standard investigation for suspected IgA nephropathy

A

Renal biopsy

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57
Q

Definitive diagnosis investigation for nephrotic syndrome

A

Renal biopsy

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58
Q

An 8-year-old boy is brought to the paediatric outpatient clinic with a two-day history of dramatic weight gain and swelling of his legs. His mother noted puffy eyes a few days ago, which did not subside even after giving him antihistamine syrup. He has no medical problems and is in the 50th percentile on all his growth charts. There is no significant family history of renal disorders. Urine analysis reveals marked proteinuria.

What is the most appropriate investigation to confirm his diagnosis?

A

Serum albumin

Proteinuria + = minimal change disease which nearly always presents as nephrotic syndrome (children)

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59
Q

What happens in nephrotic syndrome

A

Podocytes which prevent the excretion of protein into the glomerular filtrate are disrupted > resulting in excess protein excretion
The loss of proteins such as endogenous anti-coagulants like anti-thrombin III result in hypercoagulability, which can predispose patients to venous thromboembolic events ie DVT

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60
Q

A 30-year-old athlete presents to his GP with pain and swelling in his left leg. His past medical history is significant for Wilson’s disease, for which he takes regular Penicillamine. On examination, his left calf appears erythematous and oedematous, and is exquisitely tender when squeezed over the posterior aspect. He is noted to have significant peri-orbital oedema which has occurred over the past week. Additionally, the patient reports that his urine has been slightly more frothy during this time.

What is the most likely cause of his leg symptoms?

A

DVT - the nephrotic syndrome likely caused by Penicillamine use (copper-chelating agent in Wilson’s disease)

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61
Q

First line treatment for Minimal change disease

A

Oral corticosteroids - prednisolone

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62
Q

55 year old man comes in with 1 month history of gradually worsening swelling in his lower extremities. Frothy urine and has recently noticed puffiness around his eye. Has developed SEVERE LEFT SIDED FLANK PAIN* and complains of haematuria. Has T2DM and RA. There is periorbital oedema and pitting oedema bilaterally. He has a raised RR, and proteinuria. Light microscopy = prominent spike and dome pattern on silver staining.

What is the most likely diagnosis

A

Membranous glomerulopathy

*what happening here is renal vein thrombosis = severe flank pain - causing hyperventilation, and haematuria secondary membranous glomerulopathy

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63
Q

Features of membranous nephropathy

A

Associated with: cancers (Lung, colon, breast), infections (SLE, thyroid disease), Hepatitis B and drugs (penicillamine and gold)

Biopsy = subepithelial immune complex deposits

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64
Q

*haematuria, haemoptysis, hypertension (nephritic features)

A

= GoodPasture’s

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65
Q

Why do you get haemoptysis in GoodPasture’s

A

The autoantibodies (anti-GBM) are generated against type IV collagen - which is enriched in the lung and glomerular basement membrane > damage to these structures results in haemoptysis and haematuria respectively

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66
Q

*peripheral oedema in children

A

Nephrotic syndrome

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67
Q

Test for post-streptococcal glomerulonephritis

A

Anti-DNase antibody +

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68
Q

A 15 year old boy presents to the general practitioner with cola-coloured urine. He has no past medical history of note but reports suffering from a sore throat 3 weeks ago.

Physical examination reveals no abnormalities. Urine dipstick reveals 2+ blood and 1+ protein.

What is the likely diagnosis and which investigation will confirm diagnosis?

A

Post - strept. Glomerulonephritis

Positive anti-DNase antibody

(This typically presents 2-3 weeks after group A beta-haemolytic streptococcal infection - other investigation for this = red cell casts in urine and low C3/C4)

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69
Q

IgA nephropathy vs post-strept glomerulopathy

A

IgA nephropathy symptoms occurs much more quickly than post - strept. Glomerulopathy (2-3 weeks)

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70
Q

*saddle nose deformity

A

GPA

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71
Q

*recurrent sinusitis, haemoptysis, rapidly progressive glomerulonephritis

A

= GPA

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72
Q

What is GPA

A

A necrotising small-vessel vasculitis which often presents as recurrent sinusitis, haemoptysis, and rapidly progressive glomerulonephritis

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73
Q

What investigation is required to diagnose GPA

A

c-anca

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74
Q

MoA monoclonal antibodies

A

Block IL-2 receptor on CD4 T-cells
In this way they prevent activation of these cells therefore preventing rejection

*not useful if rejection has already started

Eg Basiliximab or Dacluzimab

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75
Q

MoA glucocorticoids

A

Inhibit lymphocyte proliferation, survival and activation

They suppress cytokines

*side effects = weight gain, diabetes, osteoporosis

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76
Q

MoA calcineurin inhibitors

A

Act by inhibiting activation of T-cells
They prevent cytokine release

*side effects = renal dysfunction, hypertension, diabetes, tremor

Eg tacrolimus and ciclosporin

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77
Q

MoA anti-metabolites

A

Blocks purine synthesis and suppression of proliferation of lymphocytes

Eg Azathioprine and mycophenolate mofetil

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78
Q

Contraindications to transplant

A

Malignancy
Active infection
Severe IHD (surgery)
Severe airways disease
Active vasculitis
Severe PVD
Hostile bladder

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79
Q

Why is tissue typing / HLA matching important so important for transplantation

A

Some alleles form epitopes that elicit strong antibody and cell-mediated immune response - mismatches for these alleles threaten the transplant

So good to know as drastically affects the outcome !

Good HLA match = better graft survival

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80
Q

What is a sensitising event

A

Things like: blood transfusion, pregnancy/miscarriage, previous transplant that lead to the formation of antibodies to non-self antigens making transplant rejection more likely

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81
Q

What is PTLD

A

Post - transplant lymphoproliferative disease

This occurs in all forms of transplantation and depends on the level of immunosuppressive

Usually related to EBV infection

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82
Q

A 59-year-old man is recovering on the colorectal ward following an elective right hemicolectomy four hours ago. On review by the junior doctor, the patient remains somewhat drowsy and appears to be in pain. His catheter bag contains approximately 100 ml of concentrated dark urine. His observations are: temperature 37.1, blood pressure 105/60 mmHg, heart rate 110 bpm, respiratory rate 18 bpm and a capillary refill time of five seconds. Measurement of serum urea and electrolytes show a Urea of 8.0 (2.5-6.7 mmol/L), Creatinine 230 (from a normal baseline), Sodium of 150 (135-145 mmol/L) and a Potassium of 4.8 (3.5-4.5 mmol/L). The patient weighs 90 kg.

Which of the following is the most appropriate management for this patient?

A

Intravenous bolus of 500mL crystalloid

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83
Q

What are features of AKI

A

Oliguria, raised serum UREA and Creatinine, hypotension and tachycardia

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84
Q

Why are people having recently undergone surgery more susceptible to pre-renal AKI ?

A

Nil-by-mouth pre-opt etc

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85
Q

What is AKI

A

A rapid and sustained reduction in renal function resulting in oliguria and a rise in serum urea and creatinine

AKI is usually reversible

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86
Q

What is the classification system for AKIs

A

KDIGO

Stage 1: creatinine rise of 1.5x compared to baseline OR urine output <0.5ml/kg/hour for 6hours
Stage 2: creatinine rise of 2x compared to baseline OR <0.5ml/kg/12hours
Stage 3: creatinine rise of 3x compared to baseline OR < 0.3ml/kg/24 hours OR serum creatinine > 354umol/dl

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87
Q

Renal causes for AKI

A

Dysfunction of glomeruli
Tubules
Interstitial
Renal vessels

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88
Q

Post renal causes of AKI

A

Caused by obstruction to urinary outflow : kidney stone , tumour , due to external compression

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89
Q

Pre - renal causes of AKI

A

Shock
Renovascular disease (Renal artery stenosis)

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90
Q

Management of AKI

A

DR ABCDE

Diagnosis what is the cause ie pre renal = IV crystalloid

Medication review - pretty much suspend lots of drugs

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91
Q

What would a raised creatinine kinase be suggestive of ?

A

Muscle damage ie rhabdomyolysis

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92
Q

What is rhabdomyolysis

A

Occurs when there is breakdown of skeletal muscle and myoglobin is released into the blood

This is nephrotoxic and causes AKI

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93
Q

Common causes of rhabdomyolysis

A

A long lie after a fall

Seizures

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94
Q

An 83-year-old man is brought into the emergency department after being found on the floor after a fall yesterday. He has no significant injuries but was unable to get himself up due to frailty. The patient’s main symptoms are nausea and weakness and he also mentions he has hardly passed any urine today. To monitor his urine output, he is catheterised and his urine is found to be dark brown in colour. Blood tests reveal an acute kidney injury and a very high creatinine kinase. What is the most likely diagnosis?

A

Rhabdomyolysis

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95
Q

Management of rhabdomyolysis

A

Supportive therapy ie IV fluids and management of hyperkalaemia

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96
Q

When would a fractional excretion of sodium investigation be appropriate

A

To differentiate between pre-renal AKI and acute tubular necrosis

A raised sodium indicates acute tubular necrosis
In pre-renal AKI there is reduced sodium in the urine as sodium is re-absorbed to maintain circulating blood volume

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97
Q

Why can Hypovoleamia cause GFR to drop

A

It causes vascoconstriction of renal arterioles leading to decreased blood flow to kidneys and subsequent decline in GFR

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98
Q

What colour is ureamic tinge

A

Greyish brown

Build of urea in kidneys (which normally excretes it)

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99
Q

What type of renal tubular acidosis is Fanoconi’s syndrome

A

Type 2

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100
Q

What is Fanconi’s syndrome

A

Disturbance of proximal collecting tubule function - leading to generalised impaired reabsorption of amino acids, K+, HCO3 phosphate and glucose

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101
Q

What is renal tubular acidosis

A

It is impaired acid excretion leading to hyperchoraemic metabolic acidosis > this leads to activation of the renin - angiotensin system leading to potassium wasting and hypokalaemia

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102
Q

What is the function of dialysis

A

Removal of toxins which build up in ESKD
:urea, creatinine, potassium, sodium

And allows for the infusion of bicarbonate

Does this via diffusion

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103
Q

What is haemodialysis

A

‘Artificial kidney’

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104
Q

What is the dialysis flow rate

A

500ml/min

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105
Q

What is ultrafiltration in dialysis

A

The movement of water, and all solutes dissolved in it - known as the convective solute drag - across a semi-permeable membrane in response to a pressure gradietn

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106
Q

Factors affecting haemodiafiltration

A

Water flux
Membrane pore size
The pressure difference
Viscosity of the fluid
Size shape and electrical charge (of each molecule)

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107
Q

What is the different between haemodialysis and haemodiafiltration

A

The replacement of extra-convective ultrafiltrate

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108
Q

What is high volume HDF (haemodiafiltration)

A

> 21 litres of replacement volumes

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109
Q

What is the gold standard for dialysis vascular access

A

The arteriovenous fistula

Pros = good blood flow, less likely to cause infection (compared to TCVC - tunnelled central venous catheter)

Cons = require surgery, can limit blood flow to distal arm ‘steal syndrome’

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110
Q

Types of peritoneal diffusion

A

Continuous ambulatory peritoneal dialysis (CAPD)

Automated peritoneal dialysis (APD)

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111
Q

what’s the main thing that can go wrong in peritoneal dialysis ?

A

Infection

Staph, strep, diptheroids
E.coli, klebsiella (gut infections)

And

Peritoneal membrane failure + hernias

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112
Q

What is peritoneal membrane failure

A

Inability to remove enough water&raquo_space; fluid overload

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113
Q

When to start dialysis (based on blood tests)

A

Resistant hyperkalaemia

EFGR <7ml/min

Urea > 40mmol

Unresponsive metabolic acidosis

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114
Q

When to start dialysis (based on symptoms)

A

Nausea
Vomitting
Anorexia
Profound fatigue
Itch
Unresponsive fluid overload

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115
Q

What is disequilibrium syndrome

A

When there is too rapid a correction of uraemic toxin levels

> > cerebral oedema confusion seizures sudden death

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116
Q

Definition of CKD

A

Reduction in kidney function
Structural damage

Or both

Present for more than 3 months with associated health implications

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117
Q

When to diagnose CKD ?

A

THE ASS

Transplant
Histological - abnormalities
Electrolyte imbalance
ACR > 3mg/mol
Sediment abnormalities in urine
Structural - abnormalities in imaging

And/or persisting reduction in renal function

EGFR < 60mL/min/1.73m2

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118
Q

Stages of CKD

A
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119
Q

What is the main cause of CKD

A
  1. Diabetes
  2. High blood pressure
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120
Q

What type of inheritance is poly cystic kidney disease

A

Autosomal dominant - the main one

Can also be autosomal recessive

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121
Q

What chromosomes is mutated in ADPKD (autosomal dominant poly cystic kidney disease) ?

A

16 and 4 (16 = common) PKD1 gene and PKD2 (respectively)

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122
Q

describe the pathology of ADPKD

A

Massive cyst enlargement - large kidneys

Epithelial lined cysts arise from a small population of renal tubules

A lot of patients with PKD develop ESKF and at a faster rate

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123
Q

What are the clinical features of ADPKD

A

Reduced urine concentration ability
Chronic pain
Hypertension
Haematuria
Cyst infection
Renal failure

Hepatic cysts
Intracranial-cranial aneurysms

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124
Q

Investigation for ADPKD

A

US - presence of multiple bilateral cysts, renal enlargement

Genetic - linkage analysis, mutation analysis

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125
Q

What disease is this ?

A

ADPKD

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126
Q

What are the odds of offspring of a parent with ADPKD having it too ?

A

50% risk

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127
Q

Mxm ADPKD

A

Symptomatic control ie Hypertension, hydration, proteinuria, cyst haemorrhage + infection

TOLVAPTAN

Renal failure = dialysis, transplant

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128
Q

What is Alports syndrome

A

Hereditary nephritis

X-linked inheritance

Mutation in COL4A5 gene > leads to deficient collagen opus matrix deposition

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129
Q

What type of collagen disorder is Alport’s

A

Type IV

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130
Q

What are the clinical features of Alports

A

Haematuria !
Proteinuria - seen later but confers a bad prognosis

Extra renal = sensorineural deafness, ocular defects, leiomyomatosis of oesophagus

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131
Q

Diagnosis of Alport’s

A

-microscopic haematuria +/- hearing loss
-renal biopsy shows glomerular basement membrane thickness

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132
Q

*thickness of GBM

A

Alport’s syndrome

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133
Q

Treatment of Alport’s

A

No specific tx
- HPT + proteinuria treated

  • dialysis, transplantation
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134
Q

What is Anderson-Fabrys disease

A

An inborn error of glycosphingolipid metabolism due to deficiency of a-galactosidase A

Is an X-linked disease, lysosomal storage disease

Affects kidneys, liver, lungs, erythrocytes

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135
Q

What are the clinical features of Anderson Fabrys ?

A
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136
Q

Diagnosis of Anderson Fabrys

A

Leukocyte a - GAL activity
Renal biopsy and skin biopsy

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137
Q

Treatment of Anderson Fabrys

A

Enzyme replacement (FABRYZYME)

+ management of complications

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138
Q

What type of inheritance is medullary cystic kidney

A

Autosomal dominant

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139
Q

Pathology of medullary cystic kidney

A

Morphologically abnormal renal tubules leading to fibrosis

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140
Q

At what age does medullary cystic kidney present

A

28

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141
Q

Diagnosis of medullary cystic kidney

A

Family history + CT

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142
Q

A 66 year old woman recently diagnosed with end-stage renal disease complains of decreased urination. She is currently taking medication for hypertension and type 2 diabetes mellitus. On examination, she has a temperature of 37.7 C, a pulse rate of 100 bpm, a blood pressure of 190/100 mmHg, and a respiratory rate of 26 breaths/min.

Results of arterial blood gas are as follows:

pH 7.15 (7.35-7.45)
Bicarbonate 15 mEq/L (22-26 mEq/L)
PaCO2 25 mmHg (35-45 mmHg)

What is the electrolytes abnormality observed ?

A

Hyperkalaemia

=common electrolyte abnormality in CKD characterised by oliguria and reduced EGFR
In renal failure there is low sodium delivery to the distal tubule leading to decreased renal excretion of potassium

Acidosis increases the plasma K concentration by inducing a net shift of K from the intracellular to the extracellular compartment in exchange for Hydrogen

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143
Q

A 40-year-old man recently diagnosed with hypertension now complains of painless haematuria and flank pain. Past medical history is significant for mitral valve prolapse. His father had a berry aneurysm. His blood pressure is 160/100 mmHg with a normal heart rate.

What is the single most likely diagnosis?

A

Adult poly cystic kidney disease

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144
Q

*flank pain and haemturia

A

= cyst rupture

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145
Q

*flank pain, haematuria, fever, urinary symptoms

A

=cyst infection

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146
Q

Mitral valve prolapse and aortic regurgitation is associated with what hereditary renal disease

A

Poly cystic kidney disease

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147
Q

What type of haemorrhage is associated with ADPKD

A

Subarachnoid haemorrhage

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148
Q

What drug can stop progression of microalbuminuria becoming nephropathy or CKD

A

If albumin:creatinine ratio >2.5mg/mol (Men) or >3.5 (women) then start on RAMIPRIL to slow progression

*microalbuminuria developed due to diabetic nephropathy

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149
Q

What do people with T1DM need to be screened for annually once they are over the age of 12

A

Spot urinary albumin

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150
Q

How is CKD diagnosed

A

Made when egfr is below 60 on 2 blood tests 3 months apart

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151
Q

If you have CKD what your most likely cause of death

A

CVD - CKD accelerates atherosclerosis

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152
Q

What is a complication of CKD

A

Hypocalcaemia

As the kidneys play a role in the activation of vit. D

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153
Q

Electron microscopy for post-strep glomerulo.

A

Subepithelial humps

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154
Q

What is the causative organism of HUS

A

E.coli O157

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155
Q

What is this

A

Glomerulus (healthy)

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156
Q

Nephritic vs nephrotic

A

Nephritic = haematuria + hypertension

Nephrotic = hyperlipidaemia, proteinuria

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157
Q

What investigation for glomerulonephritis

A

Renal biopsy - light microscopy, immunofluorescence, electron microscopy

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158
Q

what would glomerulonephritis look like on light microscopy

A

Sclerosis
Cellular crescents in Bowman’s (bad)
Vasculitis
Hyper-cellularity
Granulomas

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159
Q

What is this (crescent image glomerulonephritis)

A
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160
Q

What kind of antibodies are involved in glomerulonephritis

A

IgM, IgA, IgG

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161
Q

what is seen with glomerulonephritis on electron microscopy

A

Podocyte foot processes

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162
Q

What is anti-GBM disease

A

It is immune-mediated
IgG to a3 subunit of type IV collagen (found in basement membrane of glomerular and lung) (attacks antibody in Glomerulus)

Part of GoodPasture’s syndrome

Nephritic

Causes rapidly progressive GN

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163
Q

What will you seen on light microscopy of anti-GBM

A

Cellular necrosis and focal lesion(?)

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164
Q

Causes of membranous glomerulonephritis

A

infection = Hep B, malaria, syphillis,
Drugs = penicillamine, NSAIDs, gold, captopril
Malignancy = cancer

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165
Q

Features of membranous glomerulonephritis

A

Seen in adults

Nephrotic presentation

Sub-epithelial immune deposits

LM - thick membranes, membrane spikes

IF - granular deposits

Prognosis = 30% develop ESKF

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166
Q

IgA nephropathy features

A

Most common GN

Follows a cold/cough usually

Genetic defect > high IgA in serum > immune complexes gather in mesangium

Nephritic pattern
Mesangial hypercellularity
IgA deposits

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167
Q

MPGN - membranoproliferative GN features

A

Causes = idiopathic, secondary to infection, SLE

Immune complexes deposited under epithelial cells > new GBM forms overs them > reduplication of membrane

Nephritic + nephrotic pattern

Appearance = big lobulated hyper cellular glomeruli with thick membranes (tram tracks)

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168
Q

What are the 2 types of ANCA antibodies

A

MPO + PR3

> bind to granulocytes > damaged to epithelial cells > crescents

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169
Q

What is the ANCA associated with GPA

A

MPO ANCA

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170
Q

What is the ANCA associated with microscopic polyangiitis

A

PR3 ANCA

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171
Q

Minimal change features

A

Children

Nephrotic pattern

See : effacements of foot processes (loss of space)

Excellent prognosis with steroids

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172
Q

FSGS features ( focal segmental glomerulosclerosis )

A

Idiopathic - also associated with obesity

Nephrotic pattern

Can progress into ESKF

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173
Q

Diabetic nephrotic histology features

A

Expansion / thickening of GBM and mesangial matrix

Diffuse and nodular glomerulosclerosis

Nodules - Kimmelstiel Wilson lesions

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174
Q

*kimmelstein Wilson nodules

A

Diabetic nephropathy

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175
Q

What is the Bosniak score

A

How likely is a cyst being cancerous

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176
Q

Are acquired cysts scary

A

No

Very common - often seen on autopsy
Associated with long term dialysis
Nothing to worry about

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177
Q

ADPKD features

A

Kidney can become huge - mass effect symptoms

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178
Q

Haemorrhage associated with ADPKD

A

Subarachnoid haemorrhage

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179
Q

ADPKD

A

Smoother surface to ADPKD
Several subtypes all occurring in children

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180
Q

Wilm’s tumour

A

Renal tumour occurring in children

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181
Q

Common benign renal tumour

A

Oncocytoma:

Small, oval, circumscribed

Mahogany brown with a central, stellate scar

Microscopy = very pink and granular cytoplasm, central round nucleus

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182
Q

Chromophobe renal cell carcinoma

A

Uncommon

Malignant

Looks very similar to oncocytoma > raisin nuclei

Looks like plant cells

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183
Q

Papillary renal cell carcinoma

A

2nd most common type of renal tumour

Generally low grade

Papillary - finger like projections

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184
Q

Collecting duct carcinoma

A

Nasty

Least common - high grade

Poor survival

185
Q

Clear cell renal cell carcinoma

A

Most common tumour

Risk factors = obesity !! + genetic influence

Presenting complaint = haematuria, mass effect, hypertension

Features : often partly cystic, heterogenous surface, yellow/orange solid tumour areas

186
Q

Genetics involved with renal tumours

A

VHL - Von hippo landau
sporadic mutation of ccRCC > leads to inactivation of VHL protein > leads to accumulation of HIF > HIF promotes tumurogenesis

Renal cell
Cerebellar haemanigioblastoma

187
Q

What are staghorn calcului made up of

A

Struvite - magnesium ammonium phosphate

Super fast growing > so can get very large in size

Associated with recurrent UTIs

188
Q

Tenderness and dull percussion over the suprapubic region + oliguria
Confusion in a senior

What is the best investigation

A

Bladder scan first

189
Q

What is urothelium

A

Specialised epithelium lines the bladder

190
Q

What is cystitis

A

Inflammation of the bladder

Very common

Usually due to infection - UTIs (bacterial)

Not usually biopsied

191
Q

What is schistosomiasis

A

Water bourne infection > larvae penetrate skin and ova deposited in the bladder

Endemic in eastern Mediterranean and sub-Sahara Africa

Presents with haematuria

Untreated > hydronephrosis, renal failure, RCC

192
Q

What is interstitial cystitis

A

Symptoms = dysprosium, frequency

Persistently negative cultures and urinalysis

Almost always in middle-aged and older females.

193
Q

Cystitis cystica

A

A descriptive term
A reactive phenomenon involving in the infolding of bladder mucosa of cysts

Can mimic a carcinoma on histology

194
Q

Bladder diverticula

A

Outpouring of mucosa that penetrates muscle layer

= stagnant urine, infection stones and cancer

195
Q

Bladder obstruction

A

Muscle has to work harder with an obstruction > hypertrophy > eventual back pressure > back up the tract = kidney starts to dilate > renal parenchyma atrophy

(Hydronephrosis)

Obstruction can be a renal stone etc

196
Q

Urothelial neoplasia

A

Common
Middle aged and elderly population

Smoking !!

Beta-napthyline associated (used in dye industry)

197
Q

Big 3 bladder neoplasms

A

Urothelial carcinoma in situ - flat lesion

Papillary Urothelial carcinoma -
Non-invasive

Urothelial carcinoma - invasive, can develop from above 2

198
Q

Bladder adenocarcinoma

A

Can occur on a background of metaplasia
Difficult to distinguish between colonic cancer

199
Q

What is the urachus

A

Embryological remnant of urogenital sinus and allatois - connect bladder dome to umbilicus

Usually involutes - rarely some parts remain patent

Poor prognosis

200
Q

Squamous cell carcinoma in bladder

A

Can arise due to persistent inflammation > metaplastic change

201
Q

Benign prostatic hyperplasia

A

Enlarging prostate > increase in no. Of cells

Under hormonal influence

Affects central and transitional zones - obstructs the flow or urine

Treated by a transurethral resection

202
Q

Prostate cancer

A

At 70 years old 70% have prostate cancer (at 90 years 90%)

Many are low grade and slow growing

What causes it ? We are not sure - perhaps hormonal

203
Q

Types of prostate cancer can you get ?

A

Adenocarcioma (Acinar cells) (most common)
Ductal carcinoma
Small cell

204
Q

What is PSA

A

Prostate specific antigen

Glycoprotein enzyme - Kallikrein 3

Many things can raise PSA - so lacks specificity and sensitivity - therefore not a great indicate for prostate cancer but is used initially

Also high grade tumours do not even produce PSA (poorly differentiated)

205
Q

Diagnosis of prostate canc er

A

Core biopsies - can do a lot with these
Peripheral location
Transrectal US (TRUS)

206
Q

what is Gleason grading system

A

Histological pattern of the tumour of prostate - predicts - how bad is this tumour

207
Q

What is the appropriate management for a renal stone <2cm

A

Lithoscope thing - when you blast it with pressure to break it into smaller bits

208
Q

What is the appropriate management for a renal stone >4cm

A

Percutaneous nephrolithostomy

209
Q

Side effect of nitrofurantoin long-term

A

Precipitates restrictive lung disease

210
Q

How to treat GoodPasture’s / Anti-GBM disease

A

Early recognition = !!

High dose corticosteroids, cyclophosphamide, and plasmapheresis

211
Q

What is the function of = plasmapheresis

A

Removes circulating anti-GBM antibodies as well as other immunological mediators of injury

212
Q

What collagen type is GoodPasture’s / anti-GBM disease

A

IV

213
Q

Management of GoodPasture’s

A

Removing circulating antibody - plasmapheresis
Immunosuppression - high doses prednisolone or cyclophosphamide

214
Q

Penis anatomy :

A
215
Q

What is lichen sclerosus

A

A Chronic inflammatory condition that affects glans, coronal sulcus and foreskin
Usually occurs in middle aged men but can also occur in children

Can cause phimosis (inability to retract foreskin)

Is associated with squamous cell carcinoma

216
Q

clinical features of lichen sclerosis

A

White patches with petechia
Erosion
Ulceration
Pearly areas

217
Q

Microscopy of lichen sclerosus

A
218
Q

What is condyloma

A

Genital warts !!! = papillomatous proliferation of squamous epithelium
Occurs on glans, coronal sulcus, foreskin, meatus

219
Q

What causes condyloma

A

HPV infection - 16 and 18

Transmitted via direct skin contact

220
Q

*cauliflower like, papillary, exophytic growth

A

=genital warts

221
Q

*wrinkled nuclei, koilocytes, hyperkeratosis on microscopy

A
222
Q

Most common type of penis cancer

A

Squamous cell

223
Q

Where is sperm made ?

A

Seminiferous tubules

224
Q

Function of leydig cells

A

produce testosterone in response to LH

225
Q

Function of serotoli cells

A

Stimulated by FSH
Control environment within the tubules

226
Q

Inside the testes !

A
227
Q

What is a hydro elé

A

Accumulation of fluid around the testes

> unicystic, smooth and fluid-filled and so light will pass through

228
Q

What is a spermatocele

A

Cystic change within the epididymis

229
Q

What is a varicocoele

A

Varicose veins but in the penis - the venous plexus that drains into the testis

230
Q

*bag of worms appearance

A

Varicocele

231
Q

What can increase risk of testicular torsion

A

Bell clapper deformity

232
Q

Management of testicular torsion

A

EMERGENCY
>6 hours left untreated = poor prognosis
Requires surgery to detort and orchidopexy

233
Q

What is a seminoma

A

The most common germ cell tumour
Risk factor = undescended tests
Prognosis is very good

234
Q

What are the non-seminomatous GCTs?

A

Mature teratoma

Yolk sac tumour

Embryonal carcinoma

Choriocarcinoma - bizarre cells

235
Q

Histology of non-seminomatous GCTs

A
236
Q

Tumour marker for yolk sac tumour

A

AFP

237
Q

Tumour marker for hCG

A

Choriocarcinoma

238
Q

*berry aneurysm

A

Poly cystic kidney disease

239
Q

Define glomerular filtration rate

A

The volume of fluid filtered from the glomerular capillaries into the Bowman’s capsule per unit time

240
Q

Where is the majority of renin secreted from

A

Juxtoglomerular cells

241
Q

What does the posterior pituitary secrete

A

ADH
Oxytocin

242
Q

What is released in response reduced renal perfusion

A

Renin

243
Q

Effects of angiotensin II

A

Stimulates thirst, aldosterone and ADH release

Increases proximal tubule Na/H activity

Causes vasoconstriction of vascular smooth muscle > increased filtration fraction

244
Q

Function of aldosterone

A

Released by Zona glomerulosa

Causes retention of Na

245
Q

Where does furosemide act

A

Ascending loop of henle

246
Q

What is the lymphatic drainage of the testes

A

Para-aortic lymph nodes (level L2)

247
Q

Most common chromosome mutation on for ADPKD

A

16 (yes this was an actual question)

Chromosome 4 also but not as common

248
Q

What is the tracer marker used for measuring total body water ?

A
249
Q

T/F is the ascending loop of Henle impermeable to water

A

T - it is impermeable to water but actively reabsorbs salt

250
Q

T/F the descending loop of Henle is impermeable to water

A

F - the descending loop is permeable to water but does not actively or passively reabsorb salt

251
Q

Name the circled in red

A
252
Q

ARPKD is associated with a mutation on which chromosome ?

A

6

253
Q

What is the measure for total body water

A

3H2O

254
Q

What is insulin

A

The tracer marker for extra cellular fluid

255
Q

Albumin is the tracer marker for what ?

A

Plasma levels

256
Q

What is the gold standard imaging fro investigation local staging of cancer of transitional cell bladder cell cancer ?

A

MRI

257
Q

what mode of imaging would you use to see distal metastasis for transitional cell bladder cancer ?

A

CT

258
Q

What imaging would you use to see bladder wall tears?

A

Cystography

259
Q

At what point would you see an increase in creatinine and urea in contrast induced nephropathy ?

A

Would see renal function decrease 3 days post contrast (72-96 hours)

260
Q

What is found where ?

A
261
Q

Hyperventilation causes what pattern on ABG?

A

Respiratory alkalosis

262
Q

What are all the parasympathetic nerves

A

III
VII
IX
X

Also S2, 3, 4

263
Q

Gentamicin causing acute tubular necrosis is a what type of adverse drug reaction ?

A

Type A (dose dependent and predictable)

264
Q

A drug induced rash is what type of adverse drug reaction ?

A

Type B = dose dependent and unpredictable

265
Q

Long term steroid use causing Cushings is an example of what type of drug reaction ?

A

Type C = chronic effects

266
Q

Secondary malignancy post chemotherapy is what type of drug reaction

A

Type D = delayed effects

267
Q

Abrupt withdrawal of steroids causing Addisonian crisis is what type of drug reaction ?

A

Type E = end-of- treatment effects

268
Q

Bleeding right at the end of urination —> what structure affected ?

A

Bladder neck

269
Q

Bleeding during the start of urination —> what structure affected ?

A

Prostate or urethra

270
Q

Bleeding during the full length of urination —-> what structures involved ?

A

Kidney ureter or bladder

271
Q

First line imaging for suspected renal malignancy ?

A

US

272
Q

What structured is circled in red here ›

A

Transverse colon

273
Q

What structures is circled in red

A

Duodenum

274
Q

What are the consequences or uraemia ?

A

Encephalopathy
Nausea
Anorexia
Pericarditis
Neuropathy
Asterixis

275
Q

How are 5-alpha reductase inhibitors helpful in BPH

A

They shrink the prostate

276
Q

How are alpha-1 antagonists helpful in BPH

A

Relax the prostate

277
Q

How are anti-cholinergics helpful in BPH

A

Relax the bladder muscles

278
Q

What do thiazide diuretics block in the nephron

A

Na/Cl co transport

279
Q

What do diuretics block

A
280
Q

What organisms is cefalexin active against ?

A

Coliforms and staph aureus

281
Q
A

KDIGO for AKI

282
Q

What is inulin

A

An exogenous substance > must be injected into a patient > not easy to measure clinically

283
Q

Does Urea under or overestimate GFR ?

A

Underestimates GFR since it is reabsorbed in the renal tubule

284
Q

does creatinine under or overestimate GFR ?

A

Overestimates , it is secreted into the renal tubule

285
Q

Black triangle in BNF ?

A

Medication is no longer in use

286
Q

What happens in phase 1 of drug reactions

A

Oxidation, reduction, hydrolysis

Via cyp450 (adverse drug reaction are almost always phase 1)

287
Q

what happens in phase 2 drug metabolism

A

Conjugation - make water soluble

288
Q

*mahogany brown with central stellate scar ?

A

Oncocytoma

289
Q

*partly cystic, heterogenous surface, bright yellow Homer Simpson

A

Clear cell carcinoma

290
Q

*raisonoid nuclei + perinuclear haloes

A

Chromophobe

291
Q

*high grade , very desmoplastic stroma

A

Collecting duct carcinoma

292
Q

What is the equation fro calculating net filtration pressure ?

A
293
Q

What is the nerve supply of the structures within the perineum

A

Somatic motor fibres

(Levator ani, distal urethra, external urethral sphincter)

294
Q

What are the 2 indications for acute dialysis

A

Oliguria
pH at 7.15

295
Q

What is the blood supply to the scrotum ?

A

Internal pudendal and branches from external iliac artery

296
Q

What is the blood supply of the penis >

A

Deep arteries of the penis and branches of internal pudendal artery (from internal iliac)

297
Q

what hormone decreases sodium re absorption in the nephron ?

A

Atrial natriuretic hormone

298
Q

What effects of aldosterone on reabsopriton

A

Increases sodium re absorption and increases hydrogen and potassium secretion

299
Q

What does anti-diuretic hormone do?

A

Increase water reabsopriton

300
Q

What does parathyroid hormone do ?

A

Increase calcium reabsorption whilst decreasing phosphate reabsorption

301
Q

Pathway of urine drainage

A
302
Q

Difference between SGLT-1 and SGLT-2

A

SGLT-1 =. Expressed in intestine and kidney , reabsorbs only 10% of glucose , high affinity for glucose but low capacity

SGLT - 2 = expressed in kidney only, reabsorbs 90% glucose , low affinity for glucose but high capacity

303
Q

What are the most common type of nephrons ?

A

Cortical

304
Q

which nephrons have vasa recta instead of peritubular capillaries

A

Juxtamedullary nephrons

305
Q

which nephrons have a shorter loop of Henle

A

Cortical nephrons

306
Q

Benign renal tumours

A

Angiomyolipoma
Adenoma
Oncocytoma
Simple cysts

307
Q

Malignant type of renal tumour

A

Lymphoma

308
Q

What is myeloma due to

A

Collection of abnormal plasma cells

309
Q

‘Necrotising polyangiitis that affects capillaries, venues and arterioles’ describes what disease

A

Small vessel vasculitis

310
Q

Name a drug with a wide therapeutic index

A

Aspirin

311
Q

contraindication of omeprazole

A

Clopidogrel

312
Q
A

Just know

313
Q

Bactiruria in pregnant women in 3rd trimester

A

Trimethoprim

(Nitrofurantoin in 1st and 2nd)

314
Q

Where do carbonic anhydride inhibitors work?

A

Proximal convoluted tube + distal convoluted tube

315
Q

Where do loop diuretics act ?

A

Thick ascending loop of henle

316
Q

Where do thiazide diuretic act ?

A

Distal convoluted tubule

317
Q

Where do potassium sparing diuretics act ?

A

Collecting tubule and duct

318
Q

When must you fill out the yellow card scheme

A

When you experience a suspected or confirmed adverse drug reaction

319
Q

Which part of the prostate is felt in a digital rectal exam ?

A

Peripheral zone

(Also the area most common for cancer to develop)

320
Q

Which part of the prostate is BPH most likely to develop ?

A

Transition zone

321
Q

Gold standard for vascular access in dialysis

A

Arteriovenous fistula

322
Q

what CT scan best to see kidney stones ?

A

Non-contrast

323
Q

> in a contrast CT these are the best times to visualise certain pathologies

A
324
Q

What is 100% reabsorbed in kidneys

A

Glucose adn amino acids

325
Q

what is 99% reabsorpbed in kidneys ?

A

Fluid and Salt

326
Q

What is 50% reabsorbed in kidneys ?

A

Urea

327
Q

What % of creatinine is reabsorbed in kidneys ?

A

0%

328
Q

Development of hyperkalaemia ecg

A

Tall tented t waves > P wave depression > prolonged QRS > sine wave

329
Q

Define chronic kidney disease

A

Reduction in kidney function or structural kidney damage for more than 3 months with associated health problems

330
Q

Common causative organism of infection when on peritoneal dialysis

A

Strep. Epidermis

331
Q

Management for henoch-schonlein purpura

A

Painkillers

Usually self-liming

332
Q

What makes up the triad of HUS

A

Acute kidney injury
Microangiopathic haemolytic anaemia
Thrombocytopenia

333
Q

What is the main cause of HUS

A

Shiga toxin E.coli (0157:H7)

334
Q

Investigations for HUS

A

FBC
UE
Stool
( PCR )

335
Q

Treatment of HUS

A

Supportive = fluids

Plasma exchange ?

Eculizumab

336
Q

If a patient has a urine output of <0.5ml/kg/hr post-op what is the initial management ?

A

Fluid challenge —> administer 500mL fluid bolus

337
Q

What is preferred first : HD or PD

A

Usually PD but if the patient has something like Crohns then HD is better

338
Q

Use of 0.9% sodium chloride for fluid therapy in patients requiring large volumes can result in what ?

A

Hyperchloraemic metabolic acidosis

339
Q

ECG features of hypokalamia

A

Flattened t waves and u waves

340
Q

Symptoms of hypokalaemia

A

Weakness
Leg cramps
Palpitations secondary to arrhythmias
Ascending paralysis

341
Q

How to treat hypokalaemia

A

IV replacement - with cardiac monitoring

Ie transfer to high care area with cardiac monitoring , 3 x 1litres bags of 0.9% saline with 40mmol KCL per bag over 24 hours

342
Q

*poor response to fluid challenge

A

Acute tubular necrosis

343
Q

Most common cause of acute tubular necrosis

A

Haemorrhage

344
Q

Proteinuria of >3mg/mol ? What treatment

A

Commence ACEi

345
Q

eGFR categories

A
346
Q

Gold standard investigation for bladder cancer

A

Cytoscopy

347
Q

Management of ADPKD

A

Tolvaptan

348
Q

Investigation for anti-GBM

A

Renal biopsy = would show linear IgG deposits

349
Q

Management of anti-GBM

A

Plasmapheresis
Steroids
Cyclophosphamide

350
Q

What kidney diseases are worsened on administration of ACEi

A

Renovascular disease and renal artery stenosis

351
Q

*flash pulmonary oedema having started an ACEi

A

Bilateral renal artery stenosis

352
Q

What is the gold standard procedure of suspicion of bilateral renal artery stenosis

A

Renal angiography

353
Q

Management of Reno vascular disease / renal artery stenosis

A

Transluminal angioplasty +/- stunting

354
Q

T/F a creatinine level rise of 25% after starting an ACEi is ok ?

A

T - baseline creatinine is expected to rise about 30% after starting an ACEi before levelling out again , beyond 30% is a cause for concern

355
Q

Which blood test confirms rhabdomyolysis ?

A

Creatinine kinase - this is released by damaged muscle fibres and had a longer half life than myoglobin

356
Q

Why can CKD cause anaemia ?

A

In CKD there are reduced levels of erythropoietin which results in normocytic, normochromic anaemia

357
Q

How would you treat an elderly woman with CKD presenting with anaemia ?

A

Subcutaneous erythropoietin injection

358
Q

What are the causes of Acute tubular necrosis

A

ATN can occur after a prolonged ischaemic event
Hypotensive shock > hypoperfusion > post-ishaemic injury
(Increased creatinine)

Sepsis, nephrotoxins, radiological contrast, rhabdomyolsis as well are causes

359
Q

Treatment of Lupus nephritis

A

Rapid control with cyclophosphamide and methylprednisolone

360
Q

What can be seen on renal biopsy for post-strept. Glomerulonephritis

A

Subepithelial humps in the glomeruli

361
Q

Renal biopsy of anti-GBM

A

Linear deposition of antibodies along the glomerular basement membrane

362
Q

*basket weave appearance on renal biopsy

(Longitudinal splitting of lamina densa of the glomerular basement membrane)

A

Alports

363
Q

Renal biopsy of RPGN

A

Epithelial crescents in the glomeruli

364
Q

What is the most appropriate first line management for rhabdomyolysis

A

IV fluids

365
Q

Where is prostate cancer felt in a digital rectal examination

A

Peripheral zone

366
Q

Where does BPH occur in the rectum

A

Transition zone

367
Q

Which one part of the urinary tract found in the perineum

A

Distal urethra

368
Q

What is the serum creatinine criteria in KDIGO classification

A
369
Q

When would impairment from contrast induced nephropathy begin ?

A

3 days following intravascular administration of contrast medium

370
Q

Why are 5-alpha reductase inhibitors useful in the treatment of BPH

A

Shrinks the prostate

371
Q

What do alpha-1 antagonists do in BPH

A

Relax the prostate

372
Q

What do anti-cholinergics do in BPH

A

Relaxes the bladder muscle

373
Q

Where do potassium sparing diuretics act on in the nephron

A

Collecting tubule and duct

374
Q

Where do thiazide diuretics act

A

Distal convoluted tubule

375
Q

Where do loop diuretics act

A

Thick ascending limb of loop of Henle

376
Q

Where do carbonic anhydrase inhibitors work

A

Proximal convoluted tubule and distal convoluted tubule

377
Q

What is 100% reabsorbed by the kidney

A

Glucose and amino acids

378
Q

What is 99% reabsorbed by the kidney

A

Fluid adn salt

379
Q

What is 50% reabsorbed by the kidney

A

Urea

380
Q

What is 0% reabsorbed by the kidney

A

Creative

381
Q

Differences between SGLT-1 and SGLT-2 inhibitors

A

1 = reabsorbs 10% of glucose , found in distal 2/3rd of proximal tubule, has a high affinity for glucose but low capacity

2 = reabsorbs 90% of glucose, found in proximal 1/3rd of proximal tubule, has a low affinity for glucose but high capacity

382
Q

What are the benign renal tumours

A

Angiomyolipoma
Simple cysts
Adenoma
Oncocytoma

383
Q

Which structures within the perinuem are supplied by somatic motor fibres only

A

Levator ani
Distal urethra
External urethral sphincter

384
Q

What type of investigation is used to best visualise kidney stones

A

NON-CONTRAST CT SCAN

385
Q

What is the structure affected if a patient is bleeding at the end of urinaton

A

Bladder neck

386
Q

Which hormone decreases sodium reabsorption in the nephron

A

Atrial natriuretic hormone

387
Q

Which hormones increase sodium reabsorption in the nephron

A

Vasopressin / anti diuretic - increases water reabsorption
Parathyroid - calcium reabsorption increases while decreasing phosphate reabsorption
Aldosterone - increasing hydrogen and potassium

388
Q

What do thiazide diuretics block in the nephron

A

Na/Cl co transport

389
Q

Which are the most common type of nephrons

A

Cortical nephrons

390
Q

Cortical nephrons vs juxtamedullary nephrons

A

Cortical = short loop of henle, have peritubular capillaries

Juxtamedullary = long loop of henle, have vasa recta instead of peritubular capillaries

391
Q

1st line imaging for suspected renal malignancy

A

US

392
Q

Treatment of pregnant woman with bacteruria

A

Cefalexin to be used if also: trying to conceive or patient have a G6PD deficiency

393
Q

What antibiotics is active against coliforms and staph aureus

A

Cefalexin

394
Q

What is the gold standard imaging for local staging of transitional cell bladder cancer

A

MRI for local staging

(CT for distal metastasis
Cystography for bladder wall tears)

395
Q

Definition of CKD

A

Reduction in kidney function or structural kidney damage for more than 3 months with associated health problems

396
Q

When would you see a U wave

A

Hypokalaemia

397
Q

*muddy brown casts on urinalysis

A

Acute tubular necrosis

398
Q

What type of adverse drug reaction describes a dose dependant and predictable adverse effects

A

Type A

399
Q

Breaking out in rashes after administration of drug is what type of adverse drug reaction

A

Type B

400
Q

Long term steroid using causing someone to develop Cushings describes what type of adverse drug reaction

A

Type C

401
Q

What is a myeloma

A

A cancer due to a collection of abnormal plasma cells in the bone marrow / soft tissue

402
Q

What is the order in which drainage occurs in the kidney

A

Collecting ducts > renal papilla > minor calyx > major calyx > renal pelvis > ureter > bladder > urethra

403
Q

*partly cystic, heterogenous surface, bright yellow like Homer Simpson

A

Clear cell carcinoma

404
Q

*raisonoid, wrinkly nuclei and perinuclear haloes

A

Chromophobe

(Sounds like homophobe - someone who is ugly and wrinkly is a homophobe)

405
Q

*mahogany brown with a central stellate scar ?

A

Oncocytoma

406
Q

*high grade, very desmoplastic stroma

A

Collecting duct carcinoma

407
Q

Which drug has a wide therapeutic index

A

Aspirin

408
Q

What is the equation for therapeutic index

A

LD50/TD50

409
Q

What is the tracer marker used for measuring total body water

A

3H2O

410
Q

What medications could cause drug to drug interaction if co-prescribed with omeprazole

A

Clopidogrel, theophylline, macrolide abx, statins, fibrates, tricyclic antidepressants with type 1 anti-arrhythmic drugs, ACEI, sulphonylureas

411
Q

What are the parasympathetic nerve fibres

A

CN III VII IX X
S2 S3 S4

412
Q

*sterile pyuria in person moved to UK from India

(Presence of white cells in the urine but negative culture)

A

Most likely diagnosis = renal tuberculosis

413
Q

Investigation for suspected renal tuberculosis

A

3x early morning urine samples

(Mid - stream urine will not likely reveal TB)

414
Q

Given the biopsy - what is the likely disease

A

Nodular (diabetic) glomerulosclerosis

Red stuff = Kimmelstiel-Wilson nodules

415
Q

Investigation for suspected acute tubular necrosis

A

Fractional exertion of sodium in urine

(Findings would be high ie >1%)

416
Q

What is post-operative urinary retention (POUR)

A

Acute n painful inability to void after surgery

417
Q

First line investigation for POUR

A

Bladder scan OR US

Then catheterisation can be performed to relieve the retention

418
Q

What is the characteristic triad of symptoms for acute interstitial nephritis

A

Rash
Fever
Oesinophilia

419
Q

Common drug cause of acute interstitial nephritis

A

PPIs ie omeprazole

420
Q

What is the abx of choice in someone who is trying to conceive and also has a G6PD deficiency ?

A

Cefalexin

421
Q

What is the abx of choice for non-pregnant woman aged 16 years + for lower UTI

A

Nitrofurantoin

If resistant then second line = a penicillin

422
Q

Management of pyelonephritis

A

Patient should be admitted for IV abx - broad spectrum (gentamicin/cephalosporin)

423
Q

Gold standard for Goodpastures

A

Renal biopsy

424
Q

Diagnostic ivx. For anti-GBM/ good pastures

A

Anti-GBM antibodies

425
Q

Management of good pastures

A
  1. Remove any circulating anti-GBM (plasmapheresis)
  2. Immunosuppression of individual (high dose prednisone)

If severe enough —> dialysis

426
Q

Man with resistant hypertension despite being on 4 different medication and reduced salt intake - has CKD 3 - what can you do ?

A

Refer to nephrology - seems like need to target RAAS system as not related to atherosclerosis apparently

Could be renal artery stenosis etc

427
Q

*headache followed by sudden loss of consciousness on examination there are palpable masses over both flanks

A

Subarachnoid haemorrhage due to ADPCKD

Berry aneurysms rupture —> haemorrhage and ‘thunderclap headache’ and rapid neurological deterioration

428
Q

What is included in the renal screen

A

Protein electrophoresis
C3 C4
ANA
DsDNA
ANCA
Anti-GBM
Immunoglobulins

429
Q

Which malignancies can occur secondary to immunosuppresion in renal transplant

A
  1. Squamous cell carcinoma
  2. Lymphoma ( EBV - reactivation )
430
Q

What fall under the RPGN type IIs ?

A

Immune complex deposition disease ie post. Strep. Lupus, IgA nephropathy , Henoch Schonlein

431
Q

Biopsy of post-strep - what does it look like ?

A

IgG and C3 subepithelial deposition / subepithelial humps

432
Q

Biopsy of minimal change - what does it look like ?

A

Effacement of podocyte foot processes

433
Q

What is likely going on here ?

A

Renal artery stenosis due to atherosclerosis of renal arteries

*renal artery stenosis due to atherosclerosis is characterised by refractory hypertension and rapidly worsening renal function after starting an ACEi or ARB

These medications result in efferent arteriolar dilation , resulting in a fall in glomerular filtration pressure . In healthy individuals - to compensate for this fall in GFR - the kidneys vasoconstrict its afferent arteriolar to maintain GFR

However in Renal artery stenosis the arteries are already narrowed

434
Q

*schistocytes on blood film

A

HUS

435
Q

How does HUS present ?

A

Classic triad of:

Microangiopathic haemolytic anaemia —> causing fragmentation of red blood cells (schistocytes)
Thrombocytopenia
AKI

436
Q

Causes of HUS

A

E.coli O157 From undercooked meat
Or petting farms

437
Q

*normal or low calcium
Raised PTH
Raised phos.

A

Secondary hyperparathyoridism
(Triggered by hypocalceamia)

438
Q
A

Keep them on the Iisinopril 10mg - in the initial phases of ACEi use there is a rise in creatinine

439
Q

Starting an ACEi - what is expected to rise and to what extent is acceptable ?

A

Creatinine is expected to rise and up to 30% baseline is acceptable

  • ACEi leads to differential vasodilation of efferent and afferent arterioles of glomeruli which reduces glomerular hypertension —> nephroprotective
    However reducing GF pressure means that less creatinine is filtered (as seen in a rise)
440
Q

Common drug cause of AKI

A

NSAIDs (ibuprofen)

441
Q

Common drug that induces acute interstitial nephritis

A

PPIs ( omeprazole )

442
Q

Mnemonic to remembering all nephritic pictures

A

SHARP AIM

S-SLE
H-henoch
A-Anti-GBM
R-rapidly progressive glomerulonephritis
P-post strept.

A-alports
I-IgA nephropathy
M-membranoproliferative

443
Q

Which substance abused drug can cause thickening of the bladder wall

A

Ketamine

444
Q

What drugs should definitely be stopped in AKI due to hypovolaemia

A

ACEi
Diuretics

445
Q

Which bacteria is routinely screened for before renal transplant

A

Mycobacterium TB

446
Q

What are the different types of graft for renal transplant

A

Cadaveric
No heart - beating donor
Live - related
Live - unrelated

447
Q

What is hyperacute rejection

A

(Within minutes)

Caused by ABO incompatibility - presents with graft thrombosis / SIRS

Managed by immediate graft removal

448
Q

What is acute graft rejection

A

Within 6 months
Cause by cell-mediated autoimmunity

Managed with additional immunosuppressive therapy

449
Q

What is chronic graft rejection

A

After 6 months

Characterised by interstitial fibrosis and tubular atrophy

450
Q

What is the most common:
Infection secondary to immunosuppression
Malignancy

A
  1. CMV - ganciclovir
  2. Squamous cell carcinoma
451
Q

What is needed for a diagnosis of CKD

A

EGFR <60
Or eGFR of 60 with electrolyte abnormalities , persistent haematuria etc or histologically ie biopsy proven chronic glomerulonephritis

452
Q

*diffuse glomerular basement membrane thickening

A

Anti-GBM

453
Q

*tea coloured urine

A

PSGN

454
Q

Biopsy of PSGN

A

Subepithelial humps

455
Q

What would CKD show on USS

A

Bilateral shrunken kidneys

456
Q

Electrolyte imbalance associated with long term CKD

A

Hypocaleamia - kidneys play a role in the activation of vitamin D

457
Q

*Anti-DNase antibody

A

PSGN

458
Q

Which: 1. Antibiotic 2. Antihypertensive can cause a rise in creatinine

A
  1. Trimethoprim - competes with creatinine for secretion
  2. ACEi - reduces filtration pressure

everything (29 decks)

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