Renal Flashcards

1
Q

What group of people are most affected by Acute Kidney Injury?

A

Elderly

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2
Q

What are Pre-Renal Causes of Acute Kidney Injury?

A

=Reduced renal function with no structural damage to the kidneys

Common examples:
-Haemorrhage
-Hypovolaemia
-SEPSIS
-Heart Failure
-Nephrotoxics
-Renovascular disease (e.g Renal Artery Stenosis)

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3
Q

Name 5 types of drugs that are Neprotoxic.

A

-ACE inhibitors
-Diuretics
-NSAIDs
-Aminoglycosides
-B Lactams

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4
Q

How are ACE inhibitors Nephrotoxic?

A

They dilate the efferent arterioles in the Kidney which DECREASES the Glomerular Filtration Rate.

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5
Q

What are Renal Causes of Acute Kidney Injury?

A

–>Acute Tubular Necrosis (ATN)
-Tubular cell death (either due to
-Ischaemia or Nephrotoxins)
-Ischaemia
-Nephrotoxins
–>Acute Interstitial Nephritis
-Mainly due to medication side effects

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6
Q

A patient comes in with Endocarditis. A few days later after treatment, they develop Acute Kidney Injury. What drug given was most likely responsible?

A

Aminoglycosides - Nephrotoxic!!
(e.g Gentamiacin)

(given in severe illness as it is a strong antibiotic targetting Gram-Negative bacteria - given to patients with infective endocarditis, sepsis, complicated intraabdominal infections)

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7
Q

Name the most common Aminoglycoside.

A

Gentamicin

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8
Q

What is the most common causes of Acute Kidney Injury?

A

Acute Tubular Necrosis (ATN)
-70% of cases

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9
Q

What is the prognosis of a patient with Acute Tubular Necrosis and why?

A

Good recovery.
=Just as the tubules of the kidney are most susceptible to damage due to their HIGH METABOLIC ACTIVITY AND REGULAR CELL RENEWAL, this also means that once the underlying condition is treated, they recover well!:)

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10
Q

What are the main causes Acute Intestinal Nephritis?

A

ALMOST ALWAYS DUE TO MEDICATION SIDE EFFECTS OF THE FOLLOWING:
-Beta Lactams (e.gPenicillins, Cephalosporins,Carbapenems)
-NSAID use

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11
Q

A patient presents with a gradual onset of fever and rash. Blood results show high Eosinophils. What does that indicate. What could have caused this?

A

High Eosinophils = Eosinophilia

~ Classic triad for Acute Intestinal Nephritis.

Persistent use of NSAIDs or use of Beta Lactams causing Acute Intestinal Nephritis

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12
Q

A patient has Acute Interstial Nephritis. What should be done to manage it?

A

-Withdraw causative agent
-Prescribe Steroids

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13
Q

What are Beta lactams and give some examples?

A

First choice for GRAM NEGATIVE BACTERIAL INFECTIONS
- Penicillin
- Carbapenems
- Cephalosporins

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14
Q

List some common Gram Negative infections.

A

-Pneumonia (Klebsiella pneumoniae)
-Peritonitis
-UTIs
-Meningitis
-Salmonella
-Shingles
-Typhoid Fever
-E.coli infections

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15
Q

A patient presents with a fever, general malaise, pruritus, palpitations and peripheral oedema. Patient was already in the hospital with Pneumonia. What seems most likely to have caused these symptoms?

A

Symptoms sound like Acute Kidney Injury
=caused by the Beta-Lactams given for the Pneumonia which has caused Acute Intestinal Nephritis

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16
Q

What are the Post-Renal causes of Acute Kidney Injury?

A

–>Obstruction to urinary outflow tract
-Tumours
-Clots
-Calculi
-Strictures

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17
Q

How does obstruction cause Acute Kidney Failure?

A

1.Build up of renal pressure
2.Causes atrophy of renal cells
3.Leukocyte infiltration and cytokine release

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18
Q

What are the complications of renal failure ?

A

1.Uraemia (high urea/ nitrogen from waste)
2.Hyperkalaemia
3.Acidosis
4.Fluid Overload

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19
Q

What is the presentation of Uraemia?

A

-General Malaise
-Pruritus
-Paraesthesia
-Altered Mental State
-Pericardial rub
-Pale Skin

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20
Q

What is the presentation of Hyperkalaemia?

A

Palpitations and Chest pain

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21
Q

What is the presentation of Acidosis?

A

Kussmaul breathing and Confusion

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22
Q

What is Kussmaul breathing?

A

Abnormal breathing pattern characterized by RAPID AND DEEP breathing at a consistent pace. It’s a sign of a medical emergency such as DKA or AKI.

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23
Q

What is the presentation of Fluid Overload?

A

Peripheral Oedema
Breathlessness
Raised JVP

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24
Q

What are contrast agents?

A

Agents used in imaging such as Xrays, CT, MRIs used to distinguish structures

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25
Q

A patient is required to take a contrast agent for their CT. What should be done to avoid WHAT emergency?

A

Aggressive Hydration
=AVOID AKI

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26
Q

What is the criteria for diagnosing AKI?

A

If any of the following are present:
–>Serum Creatinine rise
>26mmol/L within 48hrs
>50% rise within the past week of 1.5fold of baseline
–>Urine output decrease
<0.5ml/kg/hr for >6hrs in Adults and >8hrs in Children
–>eGFR decrease
>25% decrease in CHILDREN AND YOUNG PEOPLE

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27
Q

What in particular needs to be monitored in an AKI patient?

A

Their Serum Creatinine

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28
Q

What investigations into the underlying causes of AKI need to be done?

A

1.Medication review
2.Urinalysis
3.Blood tests (FBC, U&E, LFT, Glucose coagulation)
4.ECG
5.Fractional Excretion of Sodium
5.Urgent Renal ultrasound
6.Imaging

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29
Q

What does the Fractional Excretion of Sodium indicate about a patient with AKI?

A

<1% = Pre-Renal Cause
>2% =Most likely Acute Tubular Necrosis (ATN)

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30
Q

When would an AKI patient require a Urology / Nephrologist referral?

A

-If Post-Hepatic (Obstruction)
-Unresponsive to medical treatment
-If Renal replacement therapy is indicated

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31
Q

When is Renal Replacement therapy indicated in an AKI patient?

A

A HOPE
1.Acidosis
2.Hyperkalaemia
3.Oedema (general and pulmonary)
4.Pericarditis - Complications of uraemia
5.Encephalopathy (Complications of uraemia)

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32
Q

What 2 conditions can Uraemia cause?

A

-Pericarditis
-Encephalopathy

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33
Q

What is the treatment of an AKI?

A

–>Supportive
-Fluid balance monitoring (and daily weights)
-Review medications (may need to stop potentially nephrotoxic drugs)
-O2 if breathless
-Transfusion if anaemia
-Twice / daily U&Es

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34
Q

What is Rhabdomyolysis?

A

Skeletal Muscle breakdown releasing cellular contents that cause AKI and electrolyte abnormalities.

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35
Q

List common causes of Rhabdomyolysis.

A

1.Alcoholism
2.DKA
3.Infections
4.Ischaemia
5.Trauma (specifically crush injuries or burns)
6.Falls
7.Long lie (when a person has fallen and spends a prolonged period of time on the floor)
8.Compartment Syndrome
9.Seizures
10.Statin (small risk <1%)

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36
Q

What are the clinical features of Rhabdomyolysis?

A

-Reddish brown (tea coloured) urine
-Muscle swelling, pain or limb
paraesthesia
-Fever, Nausea, Vomiting
-Hyperkalaemia
-Hypocalcaemia

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37
Q

How would you diagnose Rhabdomyolysis?

A

-Urinalysis = Haematuria
-Hyperkalaemia, Hypocalcaemia and Hyperphosphataemia
-Creatinine is SIGNIFICANTLY elevated (5times baseline)

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38
Q

What is the management of Rhabdomyolysis?

A

-Aggressive Fluid therapy (and correction of electrolyte imbalance)

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39
Q

What is meant by a Long Lie?

A

When a person has fallen and spends a prolonged period of time on the floor = this can have devastating complications such as
-Pressure ulcers
-Pneumonia
-Rhabdomyolysis

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40
Q

What is Chronic Kidney Disease?

A

Kidney damage for 3 or more months that can be caused by structural functional disorders presenting with a low eGFR of <60ml/min/1.73m^2

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41
Q

What eGFR defines Kidney Failure?

A

<15 eGFR

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42
Q

What 2 measurements can indicate the prognosisof Chronic Kidney Disease?

A

Increased Albumin/Creatinine Ration and Decreased eGFR
=Poorer Outcome

IF THEY OCCUR TOGETHER THE RISK IS MULTIPLIED

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43
Q

What group of people may have a low eGFR than the average level?

A

Bodybuilders

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44
Q

Who would you more commonly see Chronic Kidney disease in?

A

-Older patients with
-Diabetes Mellitus
-Hypertension
-Afrocarribean and Asian populations

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45
Q

What are the symptoms of Chronic Kidney Disease?

A

=Asymptomatic until LATE STAGE :
-Pruritus
-Polyuria
-Oedema
-Fatigue
-Muscle weakness

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46
Q

Patients with Chronic Kidney Disease usually have Comorbidities. What are the common ones to be seen in CKI patients?

A

-Coronary Artery Disease
-Hypertension
-Dyslipidaemia
-Mineral and Bone Disorders

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47
Q

What investigations are to be done for a suspect Chronic Kidney Disease?

A

1.Assess Kidney Function
-eGFR
-Urine Albumin : Creatinine Ratio
2.Blood tests and dipstick
-Anaemia?
-Autoantibody testing (for underlying disease)
3.Renal Ultrasound if symptoms indicate:
-Obstruction
-Polycystic disease
-Visable/Microscopic Haematuria

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48
Q

When should a Renal ultrasound be done?

A

-Symptoms of Obstruction
-Accelerated progression of disease
-Family history of Polycystic Kidney Disease
-Visable/ Microscopic Haematuria

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49
Q

What blood test results would you expect from a patient with Chronic Kidney Disease?

A

Normochromic Normocytic Anaemia

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50
Q

What lifestyle advice would be given to a patient diagnosed with Chronic Kidney Disease?

A

-Stop smoking
-Diet: Lower calories, potassium, phosphate and salt intake
!DO NOT SUGGEST LOW PROTEIN DIET
-Avoid Nephrotoxic medications (e.g NSAIDs, Beta Lactams)

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51
Q

What is the target blood pressure for a patient with Chronic Kidney Disease?

A

<140/90
But if Albumin / Creatinine ratio is VERY high i.e >70
=<130/80

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52
Q

What are the 5 secondary consequences of Chronic Kidney Disease that need to be managed and how?

A

1.BP
=ACE inhibitors
2.CVD
=Statins and Antiplatelet agents
3.Anaemia
=Erythropoietic-stimulating agent
4.Oedema
=Loop Diuretic
5. Renal Bone Disease and Electrolyte abnormalities
-Measure calcium, phosphate, PTH and Vit D if eGFR is <30
-Bisphosphonates

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53
Q

Give examples of Erythopoietic Stimulating Agents.

A

Poetin, Darbepoetin

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54
Q

What drug given to patients with Chronic Kidney Injury cannot be given routinely to patients with Acute Kidney Injury?

A

Loop Diuretics (e.g Furosemide)

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55
Q

A patient has a eGFR of 18. What additional management will they have included?

A

1.End-stage disease indicated by low eGFR
Severe: 15-29
Kidney Failure: <15

=Renal Replacement Therapy

2.eGFR is <30 so check Calcium, Phosphates , PTH and VitD etc
= Bisphosphonates

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56
Q

Name 3 types of Glomerulonephritis.

A

1.Nephrotic Syndrome
2.Nephritic Syndrome
3.Mixed Nephrotic and Nephritic

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57
Q

Name 3 causes of Nephrotic Syndrome.

A

1.Minimal Change Nephropathy
2.Focal Segmental Glomerulosclerosis (FSGS)
3.Membranous Nephropathy

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58
Q

What is Nephrotic Syndrome characterised by?

A

1.Proteinuria
>3g/24hrs OR Urine/Creatinine Ratio >300mg/mol

2.Hypoalbuminaemia
<25g/L
-Associated with Hyperlipidaemia

3.Oedema

4.Hyperlipidaemia
(Xanthoma)

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59
Q

What is the most common cause of Nephrotic Syndrome in Children?

A

90% of cases
=Minimal Change Nephropathy

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60
Q

What is the cause/ pathophysiology of Minimal Change Nephropathy?

A

Idiopathic

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61
Q

What is the presentation of Minimal Change Nephropathy?

A

-Fatigue
-Peripheral or General Oedema
-Features of nephrotic syndrome (proteinuria, low albumin and hyperlipidemia)

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62
Q

What changes will be seen on microscopy of a patient with Minimal Change Nephropathy?

A

Normal Light Microscopy
BUT
-Podocyte fusion on electron microscopy

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63
Q

What is Focal Segmental Glomerulosclerosis?

A

Idiopathic disorder whereby part of the glomerulus is affected that causes Nephrotic Syndrome (accounts for 15% of cases)

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64
Q

Who is more likely to have Focal Segmental Glomerulosclerosis?

A

-Afro-Caribbean Populations
-HIV
-Drug abusers (heroin in particular)

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65
Q

What would a biopsy show for a patient with Focal Segmental Glomerulosclerosis?

A

IgM deposition

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66
Q

What is the treatment for Focal Segmental Glomerulosclerosis?

A

1.Steroids
2.Immunosuppressive agents if unresponsive to Steroids

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67
Q

What is the treatment for Minimal Change Nephropathy?

A

Prednisolone

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68
Q

What is the prognosis for Minimal Change Nephropathy?

A

Recover after 6-8weeks with Prednisolone but remission is frequent

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69
Q

What is the prognosis for Focal Segmental Glomerulosclerosis?

A

50% of patients progress, 50% experience remission

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70
Q

What is the most common cause of Nephrotic Syndrome in adults?

A

Membranous Nephropathy

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71
Q

What are the causes of Membranous Nephropathy?

A

-Idiopathic (majority)
-Malignancy (Lung and Colon)
-Autoimmune Diseases
-Penicillamine use (used in Willson’s and Rheumatoid Arthiritis)

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72
Q

What is used to diagnose Membranous Nephropathy?

A

Biopsy:
-IgG deposits (in a Spike and Dome patterned)

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73
Q

What is the treatment for Membranous Nephropathy?

A

Steroids and immunosuppressive drugs (Rituximab)

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74
Q

What is the prognosis for Membranous Nephropathy?

A

1/3 - Spontaneous Remission :)
1/3 - Respond to treatment
1/3 - Progress to End-stage disease

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75
Q

Describe examples of general oedema.

A

-Peri-orbital (eyes)
-Ascites
-Lower limb

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76
Q

What is the main difference between Nephrotic and Nephritic when diagnosing.

A

Nephrotic
Protein increase > Blood presence
+Prominent Creatinine increase and Hypertension

Nephritic
Blood presence > Protein increase
+Red cell casts

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77
Q

What is Nephrotic Syndrome characterised by?

A

-Haematuria
-Hypertension
-Associated proteinuria with oedema

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78
Q

What are the 5 causes of Nephritic Syndrome?

A

1.Thin Basement Membrane Disease
2.IgA Nephropathy (Berger Disease)
3.Post-streptococcal Glomerulonephritis (PSGN)
4.Rapidly Progressive Glomerulonephritis aka Crescentic GN
5.Granulomatosis with Polyangiitis

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79
Q

What is the most common cause of Nephritic Syndrome?

A

Most common: Berger Disease (IgA Nephropathy)
Common: Thin basement membrane disease

80
Q

What causes Thin basement membrane disease?

A

Autosomal Dominant

81
Q

How does Thin basement membrane disease usually present?

A

Asymptomatic Benign Haematuria

82
Q

What is the prognosis for Thin basement membrane disease?

A

EXCELLENT!

83
Q

How does IgA Nephropathy (Berger Disease) present?

A

-Frank Haematuria (usually in young adult)
-Proteinuria, albuminuria and haematuria

84
Q

What would a renal biopsy show for a patient with IgA Nephropathy (Berger Disease)?

A

Mesangial deposition of IgA confirms diagnosis

85
Q

What is the management for Berger Disease?

A

Nothing specific may use steroids

86
Q

What is the prognosis for Berger Disease?

A

Okay but 25% progress to end-stage disease.

87
Q

What is the presentation of Post-streptococcal Glomerulonephritis (PSGN) ?

A

Presents 1-2 weeks after initial infection
-Myalgia (muscle aches and pain)
-Headache
-Haematuria
-Proteinuria

88
Q

What clinical results could indicate Post-streptococcal Glomerulonephritis (PSGN) ?

A

-Increased Anti-Streptolysin O Titre
-Decreased C3 level

89
Q

What is the pathophysiology of Type1 Rapidly Progressive Glomerulonephritis aka Crescentic GN?

A

Autoantibody mediated damage to type VI collagen via Anti-GBM

90
Q

Who is more likely to be affected by Type 1 Rapidly Progressive Glomerulonephritis aka Crescentic GN?

A

Males

91
Q

How does Type 1Rapidly Progressive Glomerulonephritis aka Crescentic GN present?

A

-Haematuria
-Haemoptysis
-Pulmonary Haemorrhage

92
Q

What two organs are usually affected in Type 1 Rapidly Progressive Glomerulonephritis aka Crescentic GN?

A

-Kidneys
-Lungs

93
Q

How is Type 1 Rapidly Progressive Glomerulonephritis aka Crescentic GN diagnosed?

A

Biopsy:
-Linear IgG deposits

94
Q

How do you treat Type 1 Rapidly Progressive Glomerulonephritis aka Crescentic GN?

A

Plasmapheresis, Steroids and Immunosuppression

95
Q

What diseases can cause Type 2 Rapidly Progressive Glomerulonephritis aka Crescentic GN?

A

-Systemic Lupus Erythematosus
-Post-Streptococcal Glomerulonephritis

96
Q

What are the characteristic features of Granulomatosis with Polyangiitis?

A

Nephritic Symptoms
+ELK:
ENT - Otitis, Epistaxis, Saddle shaped nose deformity, conjunctivitis,episcleritis
-Lungs - haemoptysis

-cANCA positive

97
Q
A
98
Q

What treatment is given to an asymptomatic patient with granulomatosis with polyangiitis

A

Methotrexate

99
Q

What treatment is given to an symptomatic patient with granulomatosis with polyangiitis

A

Cyclophosphamide with prednislone

100
Q

When would you switch therapy of cyclophosphamide for granulomatosis with polyangiitis and what to?

A
  • if poorly tolerated or unresponsive to therapy
    = rituximab
  • patient in remission
    =methotrexate/azathioprine
101
Q

Whate are the two causes of mixed nephrotic and nephritic syndrome?

A

Membranoproliferative glomerulo nephritis
Alport Syndrome

102
Q

What is the cause of Alport Syndrome

A

X-linked dominant inheritance

103
Q

How does Alport Syndrome present

A
  • hematuria
  • progressive proteinuria
  • neural deafness
  • lens abnormalities (eg. cataract)
104
Q

What is the typical age of presentation of Alport Syndrome when patient presents with sensorineural deafness?

A

Childhood (prior to renal disease presentation)

105
Q

What is the clinical management for Alport Syndrome?

A

Nothing specific but ACE inhibitors for blood pressure control

106
Q

Describe the pathophysiology of Alport Syndrome

A

X-linked dominant inheritance disorder causing Type IV collagen defect affecting the eyes, ears and kidney basement membrane; eventually leading to mixed nephrotic and nephritic syndrome

107
Q

What is meant by renal vascular disease?

A

Umbrella term to describe hypoperfussion in the kidney with vast majority of cases due to secondary artherosclerotic disease (hypertension).

108
Q

What is the key investigation for diagnosing renal vascular disease and what would the result be?

A
  • Renal ultrasound
  • ANGIOGRAPHY (GOLD STANDARD DIAGNOSTIC)
    = renal artery aneurism (beads on a string)
109
Q

What is the treatment for renovascular disease?

A
  • Not specific (optimize risk factors, avoid nephrotoxic agents and manage hypertension)
  • Angioplasty only when indicated
110
Q

When would a patient with renovascular disease need a angioplasty

A

OLNY IF STABLE:
- pulmonary oedema present
- refractory hypertension (uncontrollable hypertension despite medicine)

111
Q

What is haemolytic uraenic syndrome and who does it usually affect?

A
  • usually related to gastroenteritis infection which produces toxins that cause intravascular thrombosis and glomerular microvascular thrombosis leading to renal impairment
  • 90 % affects children
112
Q

How does a patient with haemolytic uraenic syndrome present?

A

Early stage:
- Bloddy diarrhoea
- Abdominal pain
Later stage:
+ Thrombocytopenia
+ Jaundice
+ Renal failure

113
Q

How would you diagnose haemolytic uraenic syndrome

A

Blood film
= Schistocytes (erythrocyte fragmentation)

114
Q

What is the prognosis for haemolytic uraenic syndrome?

A

Usually spontaneously resolves with management

115
Q

What complication is related to haemolytic uraenic syndrome

A

Renal cell carcinoma with metastasis to the lung

116
Q

In what group of people would an UTI warrant additional clinical suspicion?

A

Men

117
Q

List the risk factors for UTIs

A
  • Immunosuppression
  • Diabetes
    -Underlying renal tract abnormalities
118
Q

What is the presentation of UTIs?

A
  • Dysuria
  • Polyuria
    -Increased urgency to urinate
  • Foul-smelling urine

IN PATIENTS WITH UPPER UTI:
+ Fever
+ Loin pain
+ Back pain

119
Q

What is the key dipstick factor that is diagnostic of UTIs?

A

Nitrates
(with or without leukocytes)

120
Q

What is the treatment for UTIs in men?

A

Paracetamol and Trimethoprim

121
Q

When would you not prescribe trimethoprim and what should be prescribed instated?

A
  • If symptoms don’t improve
    As it is associated with high rate of bacterial resistance
  • those that have used it before
  • older people in residential facilities

= Nitrofurantoin/Pivmecillinam/Fosfomycin

122
Q

What drugs cannot be prescribed to treat UTIs in pregnant women

A

Trimethropin (in 1st trimester as it can cause spina bifida)
- Nitrofurantoin (in 3rd trimester)

123
Q

What medications can be administered throughout a pregnancy to treat a UTI?

A
  • Amoxycillin (when sensitivities are known)
  • Cefalexin
124
Q

What is pylonephritis?

A

Infection of the renal pelvis which may be acute or chronic, usually due to E.Coli

125
Q

What group of people are susceptible to pylonephritis?

A

Women and elderly

126
Q

What are the risk factors of pylonephritis?

A
  • Urinary tract abnormalities
  • Diabetes mellitus
  • Vesicoureteric reflex
127
Q

What is the classic triad of symptoms for pylonephritis?

A
  1. Fever/rigors
  2. Loin pain
  3. Costovertebral angle tenderness
    - with or without nausea and vomiting
128
Q

What investigations are ordered for pylonephritis and state the expected result?

A
  • Ultrasound (1st line investigation)
  • Urinalysis (Haematuria, proteinuria and nitrites)
  • Blood tests (elevated blood inflammatory markers)
129
Q

Describe the managment of pylonephritis

A

IN HOSPITAL:
- Analgesia, fluid and antiemetics
- Empirical antibiotic therapy
- Cyproflozacin or co-amoxyiclav

130
Q

What is prostatitis and how does it present?

A

= Inflammation of the prostate
- fever, dysuria with urgency
- abdominal/pelvic pain
- pain on ejaculation

131
Q

What are the two types of prostatitis?

A

Bacterial or non bacterial chronic prostatitis

132
Q

What group are most affected by bacterial prostatitis?

A

Younger, sexually activemen

133
Q

What type of organism causes bacterial prostatitis?

A

Gram-negative

134
Q

What is the treatment for bacterial prostatitis?

A

Antibiotics for up to 8 weeks (eg. Fluoroquinolones)

135
Q

What causes non-bacterial prostatitis?

A

Idiopathic

136
Q

What is the presentation of non-bacterial prostatitis?

A

Pelvic or genital pain longer than 3 months and sometimes with pain on ejaculation

137
Q

What are the two types of polycystic kidney disease?

A

Autosomal dominant or autosomal recessive polycystic kidney disease?

138
Q

What are the genetic abnormalities of autosomal dominant polycystic kidney disease?

A

PKD1 or PKD2 or PKD2 mutations

139
Q

What are the typical presentations of a patient with autosomal recessive polycystic kidney disease?

A
  • loin pain
  • hypertension
  • elargemnet of the kidneys
  • haematuria
  • kidney stones
  • infection (UTI)
140
Q

What is associated with polycystic kidney disease?

A

Berry aneurisms

141
Q

What investigations should be ordered for a suspected autosomal recessive polycystic kidney disease and state expected results?

A
  • Urinalysis
    = haematuria
  • blood tests
    = polcythaemia vera (PV)
  • ultrasound (GOLD STANDARD DIAGNOSTIC)
    = cyst in kidneys
  • history taking
    = family history supports it
142
Q

What is the management for autosomal dominant polycystic kidney disease?

A

Advice:
- avoid contact sports
- reduce salt intake
Treatment:
- ACE inhibitors (for hypertension)
- NSAIDs )for pain relief for cysts)
- Consider surgical removal of cysts
- Transplant/dialysis if disease progresses

143
Q

At what age does autosomal recessive polycystic kidney disease present?

A

Infancy or childhood

144
Q

What is the presentation of autosomal recessive polycystic kidney disease?

A
  • Organomegaly
  • Kidney disease that progresses to end-stage in their teenage years
  • hepatic fibrosis
145
Q

At what age does autosomal dominant polycystic kidney disease usually present?

A

Usually between 30-40 but can begin in childhood

146
Q

What is the investigative choice for children vs infants in autosomal recessive polycystic kidney disease?

A

Infants
= Ultrasound
Children
= CT

147
Q

What treatment is recommended for infants with autosomal recessive polycystic kidney disease?

A

Monitoring in ICU with liver/renal transplants for long-term care

148
Q

What is Nephrolithiasis and Urolithiasis?

A

Calculi (stones) within the urinary tract (from Kidneys to Bladder)

149
Q

What group of people are more likely to be affected by Nephrolithiasis?

A

-Men
-Those in hot, dry, tropical regions as DEHYDRATION is a key risk factor

150
Q

What are the 3 types of Renal stones?

A

1.Non-infective
2.Infective
3.Hereditary

151
Q

What is the most common type of renal kidney stone?

A

Calcium Oxalate (Non-Infective)

152
Q

Describe an Infective Kidney stone (what its made of, its characteristics and how it comes about).

A

-Magnesium Ammonium Phosphate (struvite)
-Calculi are described as ‘Staghorn’
-Caused by Urease-producing bacteria

153
Q

What are the 2 types of Hereditary Kidney Stones?

A

-Cystinuria
-Lesch-Nyhan Syndrome

154
Q

What is Cystinuria?

A

Autosomal Recessive condition characterised by impaired amino acid absorption causing saturated urine with Hexagonal Cysteine Crystals and therefore predisposes the patient to KIDNEY STONES.

155
Q

What are the risk factors for Nephrolithiasis?

A

-Dehydration
-Hyperparathyroidism
-Disturbed Oxalate metabolism
-Excessive fructose intake (e.g Honey)

156
Q

What the typical presentation of Nephrolithiasis / Urolithiasis?

A

-Sudden loin to groin pain
-Pain radiating to labia / scrotum
-Haematuria
-Dysuria
-Urinary retention

157
Q

What investigations are to be done for a suspect Kidney stone patient?

A

1.Non-Contrast CT
=GOLD STANDARD DIAGNOSTIC

2.Bloods, urine dipstick
=Haematuria
-Look for underlying cause : PTH (hyperparathyroidism), congenital disorders etc

158
Q

What is another name for Kidney stones?

A

Nephrolithiasis / Urolithiasis

159
Q

A pregnant woman presents to ER with sudden onset of loin to groin. She mentions painful urination as well. What is the likely diagnosis and what would be done?

A

Kidney Stones
=Pregnant women are offered UTERROSCOPY
-Passing a ureteric tube into urinary and renal tract to alleviate condition.

160
Q

What is the management for Kidney stones?

A

1.Analgesia (NSAIDs, Diclofenac; Morphine in extreme cases) and IV fluids

2.Intervention depending on stone size:

161
Q

What intervention is necessary for a kidney stone <0.5cm?

A

Resolve spontaneously, NO INTERVENTION

162
Q

What intervention is necessary for a kidney stone 0.5 - 1cm?

A

50% May resolve spontaneously, 50% may require Alpha blockers (TAMSULOSIN)

163
Q

What intervention is necessary for a kidney stone >1cm?

A

NEEDS INTERVENTION:
=Extra -Corporeal Shockwave Lithotripsy

164
Q

A patient requires Extra -Corporeal Shockwave Lithotripsy for removal of their Renal Stone. What is the main contraindication?

A

Pregnancy

165
Q

What intervention is necessary for a kidney stone >2cm?

A

NEEDS INTERVENTION
=Percutaneous Nephrolithotomy

166
Q

What is Renal Tubular Acidosis?

A

Impaired Kidney Excretion causes ACID ACCUMULATION which predisposes these patients to have Hypercholaraemic metabolic acidosis with a normal anion gap (loss of bicarbonate which can cause Urolithiasis if not corrected by supplements)

167
Q

Describe the pathophysiology of of Type 1 Renal Tubular Acidosis (RTA)?

A

Primary disorder or due to :
-Marfan’s, Ehlers-Danlos Syndrome
-Autoimmune (e.g Systemic Lupus Erythromosa SLE)

=Inability to acidify the urine at the DISTAL tubule

168
Q

What are the characteristics of Type Renal Tubular Acidosis?

A

-High Urinary pH
-Hypokalaemia
-Renal stones
-Progressive renal failure(if untreated)

169
Q

What is the management of Type 1 Renal Tubular Acidosis?

A

Oral bicarbonate

170
Q

What is Type2 Renal Tubular Acidosis?

A

Impaired bicarbonate resorption in the PROXIMAL TUBULE results in Acid accumulation.

NOTE: Usually presents with Fanconi Syndrome (low alkalis to neutralise acid i.e double whammy!)

171
Q

What are the characteristics of Type 2 Renal Tubular Acidosis?

A

-Hypokalaemia
-Polyuria
-Osteomalacia
-Rickets

172
Q

What is Fanconi Syndrome?

A

Defect in PROXIMAL TUBULE TRANSPOET which causes impaired absorption of Potassium, Amino Acids, Bicarbonate and Glucose.

173
Q

What is the treatment for Type2 Renal Tubular Acidosis?

A

-Bicarbonate supplements
-Correct Hypokalaemia
-Vit D supplementation

174
Q

What is Type 4 Renal Tubular Acidosis associated with?

A

-Lowered aldosterone
-ACEinhibitors
-Addisons’s Disease
-Diabetes

175
Q

What is the treatment for Type 4 Renal Tubular Acidosis?

A

-Fludrocortisone (aldosterone replacement)

176
Q

What is the most common type of tumour in the kidneys in adults?

A

Renal Cell Carcinoma

177
Q

What are the main risk factors for Real Cell Carcinoma?

A

-Smoking
-Hypertension
-Long term replacement therapy

178
Q

What are the main characteristics of Renal Cell Carcinoma?

A

1.Haematuria
2.Loin Pain
3.Flank Mass
4.PVC (high red blood cells)
5.Varicocele ( in men)

179
Q

What is a Varicocele?

A

Varicose Veins in the Spermatic Cord

180
Q

Where would Renal Cell Carcinoma most likely metastasise to?

A

Lungs

181
Q

What does treatment of Renal Cell Carcinoma involve?

A

Staging, Surgical Resection and Chemotherapy

182
Q

What illness is the most likely diagnosis until proven otherwise when a patient 45 yrs or older presents with frank haematuria?

A

Bladder Cancer

183
Q

What is the gold standard diagnostic for Bladder Cancer?

A

Cystoscopy and Biopsy

184
Q

For the most common type of Bladder Cancer, what is the management?

A

Transurethral Resection of bladder tumour
+Intravesical Chemotherapy

185
Q

A patient presents with Polyuria. What possible disorders could this be and what are their differentiating symptoms?

A

1.Diabetes Mellitus
+Polydipsia, Hyperglycaemia, Glucose in urine
-
2.Diabetes Insipidus
+Polydipsia, Low Specific Gravity, Increased serum osmorality
=Water deprivation and ADH test confirms

3.Nephrogenic Diabetes
+Dilute urine with low specific gravity
=ADH test confirms

-Psychogenic Polydipsia
=Normal serum sodium levels

-Diuretics

-Hypercalcaemia
+Dehydration and Increased serum calcium levels
-Chronic Kidney Disease
+elevated creatinine

-Primary Polyuria

-Hyperparathyroidism
+Dehydration, Elevated PTH and Calcium

-Hyperthyroidism
+Tachycardia, Elevated Metabolic Rate, Elevated t3 and t4
-Pregnancy

186
Q

What molecule is the basis of calculating the GFR?

A

Inulin (a prebiotic)

=Always filtered but never secreted/absorbed :)

187
Q

What is Posterior urethral valves?

A

Most common cause of Infravesical obstruction seen in boys
=After birth, the bladder has to develop high emptying pressures in utero, the child may develop renal parenchymal damage causing renal impairment.

188
Q

What is Infravesical obstruction?

A

Symptom seen in males:
-decrease in urinary flow rate
-increase in bladder pressure.

189
Q

What is the management for Posterior urethral valves?

A

Temporary:
Catheterisation

Permanent :
Endoscopic Valvotemy

190
Q

What is the key difference between Nephrotic and Nephritic Syndromes?

A

Nephrotic syndrome: occurs when glomeruli do not properly filter the protein ALBUMIN.
=HYPOALBUMINIA
-Oedema is everywhere including periphery
Nephritic syndrome occurs when glomeruli do not properly filter RBCs.
=HAEMATURIA (and Hypertension)
-Oedema is only see in periorbital and pulmonary

191
Q

What histological changes would you expect for a patient with Membranoproliferative Glomerulonephritis?

A

‘Tram-track’ appearance following periodic acid-Schiff stain indicates type 1

192
Q

A patient may have Renal Artery stenosis. What would be done to check the renal blood flow?

A

Para-aminohippurate (PAH) clearance

193
Q

What main red flag symptom in a young male would make you think of bladder cancer?

A

Frank Haematuria

194
Q

What main red flag symptom in a young male would make you think of testicular cancer?

A

Hydrocele

195
Q

What is the most common cause of AKI?

A

Renal tubular acidosis

196
Q

What is the presentation of Renal Tubular Acidosis?

A

Features of AKI: raised urea, creatinine, potassium
MUDDY BROWN CASTS IN URINE

197
Q

What are the 2 main causes of Renal Tubular Acidosis?

A

-Ischaemia:

shock
sepsis

-Nephrotoxins:

aminoglycosides
myoglobin secondary to rhabdomyolysis
radiocontrast agents
lead