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Year 2 > Genitourinary: Part 2 > Flashcards

Genitourinary: Part 2 Flashcards

1
Q

Define Aute Kidney Injury

A
  1. An abrupt sustained rise in serum urea and creatinine due to rapid decline in GFR causing failure to maintain fluid, electrolyte and acid-base homeostasis -usually but not always reversible or self-limiting
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2
Q

Define CKD

A

Long-standing and progressive impairment in renal function

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3
Q

What is the RIFLE classification of AKI

A

Describe three levels of renal dysfunction and two outcome measures (products increasing degree of renal damage and have a predictive value for mortality)

Risk
Injury
Failure
Loss
End-stage renal disease
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4
Q

What is the current staging system for AKI

A

Creatinine:

  1. Increase in 26 micro mol/L in 48Hr
  2. Increase in 2-2.9 x baseline
  3. Increase in 3 x baseline

Urine output:
Less than 0.5mL/Kg/h for > 6 consecutive hours

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5
Q

What condition is usually associated with AKI

A

Sepsis

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6
Q

What defines severe AKI

A

Creatinine greater than 500 micro mol/L

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7
Q

Symptoms of AKI

A
  1. Diarrhoea
  2. Haematuria
  3. Haemoptysis
  4. Hypotension
  5. Urine retention
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8
Q

Most common causes of AKI

A
  1. Ischaemia
  2. Sepsis
  3. Nephrotoxins
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9
Q

Pre-renal causes of AKI

A
  1. Renal hypo perfusion (hypotension drop in GFR)
  2. Hypovolaemia
  3. Hypotension without hypovolaemia - cirrhosis or septic shock
  4. Low CO 0 cardiac failure or cariogenic shock
  5. Renal hypoperfusio nay NSAIDs or ACEI
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10
Q

Intrinsic renal causes for AKI

A
  1. Renal parenchyma damage
  2. Acute tubular necrosis
  3. Vascular reasons
  4. Glomerular diseases
  5. Interstitial diseases
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11
Q

What are vascular causes for instrinc renal AKI

A
  1. Renal artery/vein thrombosis
  2. Cholesterol/thrombus emboli from angiography
  3. Vasculitis (SLE)
  4. Haemolytic uraemia syndrome (thrombotic microangiopathy/haemolytic anaemia + reduced platelets)
  5. Malignant hypertension
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12
Q

What are glomerular causes for AKI

A
  1. Glomerulonephritis or nephrotic syndrome

2. Du eto autoimmune (SLE, drugs or infections

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13
Q

Interstitial causes for AKI

A
  1. Drugs and infiltration following chemo
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14
Q

Post-renal causes for AKI

A
  1. Urinary tract obstruction at ureter, bladder or prostate
  2. Luminal: stones, clots or sloughed papillae
  3. Mural:
    - Malignancy
    - Benign prostate hyperplasia
    - Strictures
  4. Extrinsic compression from malignancy especially from pelvis or due to retroperitoneal fibrosis
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15
Q

Risk factors for AKI

A
  1. Age> 75 years
  2. Heart failure
  3. Peripheral vascular disease
  4. Chronic liver disease
  5. Sepsis
  6. Poor fluid intake/increased losses
  7. History or urinary symptoms
  8. Past history of AKI
  9. GFR <60
  10. Hpovolaemia
  11. Haematological malignancy
  12. Diabetes
  13. Prostate cancer
  14. Radioogical contrast use
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16
Q

Clinical presentation of AKI

A
  1. Palpable bladder, kidneys(polycystic disease), abdo/pelvic masses and rashes
  2. Oliguria (small amounts of urination) in early stage
  3. irregular heartbeats due to hyperaemia
  4. Symptoms of high urea:
    - Fatigue, weakness, anorexia, nausea and vomitinig
    - Pruritus and brusing
    - Confusion, seizures and coma
  5. Breathlessness rom anaemia and pulmonary oedema secondary to volume overload
  6. Pericarditis (pericardite rub)
  7. Postural hypotension
  8. Oedema
  9. Thirst - indicated fluid depletion and dehydration
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17
Q

Differential diagnosis of AKI

A
  1. Abdo aortic aneurysm
  2. Alcohol toxicity
  3. Alcoholic and diabetic ketoacidosis
  4. Chronic renal failure
  5. Dehydration
  6. GI bleed
  7. Herat failure
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18
Q

Diagnosis of AKI

A
  1. Establish if AKI is pre, renal, post
  2. Urine dipstick
  3. FBC
  4. Ultrasound
  5. CT-KUB
  6. ECG
  7. CXR
  8. Renal biopsy
  9. mid=stream Blood culture to exclude infection

BIOPSY

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19
Q

FBC results:

A
  1. HIGH ESR
  2. Anaemia

Suggests myeloma and vasculitis as underlying cause

  1. High phosphate
  2. Low Ca
  3. High creatinine
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20
Q

When do we suspect CKF

A 
Small kidneys on ultrasound
Anaemia
Low ca
High phosphate 
ugh creatinine/low GFR
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21
Q

Urine dipstick results for CKD

A
  1. leucocyte and nitrile presence - Infection

2. Glomerular disease (blood and proteins)

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22
Q

Ultrasound results for CKD

A
  1. Give assessment on renal size
  2. Distinguish obstruction and hydronephrosis and look of abnormal cysts and masses

Corticomedullary differentiation

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23
Q

What would a CT-KUB show

A
  1. Obstructive cause
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24
Q

What usually causes urinary obstruction in males

A
  1. Elderly men usually Benign prostatic hyperplasia
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25
Q

What relives benign prostatic hyperplasia

A

Cathetisation

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26
Q

What should we do if cauterisation does not improve urinary obstruction

A

Suspect obstruction above prostate:
Urgent ultrasound to look for hydronephrosis
Urgent CT-KUB for obstructing masses/calculi or retroperitoneal fibrosis

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27
Q

Role of ECG in reCKD

A
  1. Hyperkalaemic hcnages
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28
Q

Role of CXR in CKD

A

Look for pulmonary oedema

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29
Q

When ar biopsies done

A

Interregnal causes for AKI

Done for unexplained AKI and normal kidneys

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30
Q

How is CKD treated pre-renally

A
  1. Correct volume depletion with fluids

2. Sepsis = antibiotics

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31
Q

How is CKD treated intrinsic renal

A

Refer to nephrology over tubulointerstitial or glomerular pathology

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32
Q

How is CKD treated post-penally

A
  1. Catheterise and consider CT or renal tract

2. Obstruction or hydronephrosis - cytoscopyy, retrograde stents or nephrostomy insertion - buys time for treatment

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33
Q

How is CKD treated for all causes

A
  1. STOP NEPHROTOXIC DRUGS
  2. Optimise fluid balance
  3. Hyperkalaemia:
    CALCIUM GLUCONATE - cardioprotective
    INSULIN + glucose to drive K into cells
    Use dialysis or haemofiltration
  4. Treat acidosis with sodium bicarbonate
  5. Treat pulmonary oedema with diuretics FUROSEMIDE or dialysis
  6. Renal replacement therapy
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34
Q

Name some nephrotoxic drugs

A

1> NSAIDS

  1. ACEI
  2. GENTAMYCIN
  3. AMPHOTERICIN
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35
Q

Diet to treat CKD

A
  1. NA / K restriction

2. Supply Vit D

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36
Q

What are indications for dialysis

A
  1. Symptomatic uraemia including pericarditis or tamponade
  2. Hyperkalaemia not controlled by conservative measures
  3. Pulmonary oedema
  4. Severe acids
  5. High K
  6. tall T waves, low flat p waves, broad QRS or arrhythmias on ECG
  7. Metabolic acidosis
  8. Fluid overload that is resistant to diuretics
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37
Q

Most common RRT

A

Haemofiltrtaion

Haemodialysis

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38
Q

Complications of RRT

A
  1. Cardiovascular disease (MI) due to hypertension or calcium/phosphate dysregulation
  2. Infection
  3. Amyloid accumulate sin long-term dialysis can cause carpal tunnel syndrome, arthralgia and fractures
  4. Malignancy is commoner in dialysis patients - may be due to cause of end-stage renal failure
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39
Q

Define glomerulonephritis

A

Broad term that refers to a group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

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40
Q

What is the consequence of glomerulonephritis

A

End stage renal failure

41
Q

How does glomerulonephritis effect the body

A
  1. HAEMATURIA and PROTEINURIA
  2. Damage to glomerulus restricts blood flow = compensatory HYPERTENSION
  3. AKI due to loss of filtration capacity
42
Q

In what four ways can glomerulonephritis present

A

1, Acute Nephritic Syndrome (Acute glomerulonephritis)

  1. Nephrotic syndrome
  2. Asymptomatic urinary abnormalities - haematuria, proteinuria or both
  3. CKD
43
Q

What causes acute nephritic syndrome

A

Immune response triggered by an infection

44
Q

What characterises Acute Nephritic Syndrome

A
  1. Haematuria - visible or non-visible (red cell casts seen on microscopy)
  2. Proteinuria (usually <2g in 24 hours)
  3. Hypertension and oedema (periorbital, leg or sacral)
45
Q

What is the most common primary cause of acute glomerulonephritis

A

IgA neuropathy

46
Q

How does IgA neuropathy cause acute glomerulonephritis

A

It accumulates in the glomeruli causing inflammation

47
Q

What bacterial infections can cause Acute glomerulonephritis

A

MRSA, typhoid or secondary syphilis

48
Q

What viruses can cause acute glomerulonephritis

A

Hep B and C

49
Q

What worm can cause acute glomerulonephritis

A

Schistomiasis

50
Q

How does Strep. pyogenes cause Acute Glomerulonephritis

A
  1. Occurs in a child 1-3 weeks after streptococcal infection (pharyngitis or cellulitis) with a Lancefield group A beta-haemolytic streptococcus
51
Q

When does strep. pyogenes occur

A

2 weeks after tonsillitis

52
Q

How does strep. progenies cause acute glomerulonephritis

A

Bacterial antigen becomes trapped in the glomerulus leading to an act diffuse proliferative glomerulonephritis

53
Q

How is acute glomerulonephritis

A
  1. Antibiotics

2. Supportive

54
Q

What conditions can cause acute glomerulonephritis

A
  1. Infective endocarditis
  2. SLE
  3. Systemic Sclerosis
  4. ANCA associated vasculitis
  5. Goodpastures disease
  6. IgA neuropathy
55
Q

Treatment of SLE

A

Immunosuppression: Cyclophosphamide

Rituximab

56
Q

How is systemic sclerosis diagnosed

A

ANA positive, Anti-ro and Anti-la positive

Severe hypertension

Onion skin changes on renal biopsy

57
Q

What is ANCA associated vasculitis

A
  1. Multisystem small vessel vasculitis attack small vessels in kidney and the eye
58
Q

How is ANCA associated vasculitis treated

A
  1. IMMUNOSUPRESSION
    Cyclophosphamide
    Rituximab
    Plasma exchange
59
Q

What is good pastures disease

A

The co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage and the presence of circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung

Makes antibodies against glomerular basement membrane

60
Q

How is good pastures disease treated

A
  1. Remove antibody via plasma exchange
  2. Immunosuppression
  3. Steroids/cyclophosphamide
61
Q

Most common cause of nephritic syndrome

A

IgA Nephropathy

62
Q

Where does IgA deposit in the kidney

A

Mesangium (provides structural support to glomerulus) of kidneys and kidney get attacked

63
Q

What condition is IgA nephropathy associated with

A

Tonsilitis

64
Q

What treatment is needed for IgA nephropathy

A

BP control - ACEI, angiotensin receptor blockers

65
Q

Clinical Presentation of nephritic syndrome

A
  1. Haematuria
  2. Proteinuria (uaully less than 2g in 24 hours)
  3. Hypertension and oedema due to salt and water retention
  4. Oliguria (little urine)
  5. Uraemia and symptoms of it:
    - Anorexia
    - Pruritus
    - Lethargy and nausea
  6. Deteriorating kidney function
  7. Moderate-severe decrease in GFR
66
Q

Diagnosis of acute nephritic syndrome

A
  1. History
  2. eGFR, proteinuria, serum urea, electrolytes and albumin
  3. Culture - swab from throat and infected skin
  4. Urine dipstick to detect proteinuria and haematuria
  5. Renal biopsy if necessary
67
Q

How is Acute nephritic syndrome treated

A

Hypertension = loop diuretics ORAL FUROSEMIDE)

AMLODIPINE (calcium channel blocker)

68
Q

What defines nephrotic syndrome

A
  1. Proteinuria > 3.5g/24 hours
  2. Hypoalbuminaemia
  3. Oedema

Hyperlipidaemia

69
Q

Why is there hyperlipidaemia in nephrotic syndrome

A

Liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol

70
Q

Can you develop kindey failure with nephrotic syndrome

A

No but HUGE amounts of protein is leaking

71
Q

What is the most common secondary cause of nephrotic syndrome

72
Q

Primary cause of nephrotic syndrome

A
  1. Minimal change disease in kids
  2. Membranous neuropathy
  3. Focal segmental glomerulosclerosis
73
Q

What is minimal change disease

A

No deposits or changes to the mesangium yet there is proteinuria and widespread oedema = minimal change

74
Q

Primary causes membranous neuropathy

A

Usually IDIOPATHIC

75
Q

What is membranous neuropathy

A

Caused by immune complex formation (deposition of IgG and C3) in glomerulus by binding of antibodies to antigens in glomerular basement membrane = triggers a membrane attack complex on glomerular epithelial cells damaging them = leaky

76
Q

Symptoms of membranous neuropathy

A
  1. Asymptomatic preotinuria and microscopic haematuria, hypertension and renal impairment
77
Q

Secondary causes of membranous neuropathy

A
  1. Drugs (NSAIDs)
  2. Autoimmune (SLE, thyroiditis)
  3. infection (Hep B or C, schistomiasis)
  4. Neoplasia (lung, colon,s stomach and breast)
78
Q

Hows membranous neuropathy treated

A

IMMUNOSUPPRESION

79
Q

What is focal segmental glomerulosclerosis

A

Where scar tissue develops on parts of the glomerulus that filter waste from blood

80
Q

Pathophysiology of focal segmental glomerulosclerosis

A

CD80 in podocytes results in increased permeability in glomeruli and thus proteinuria and haematuria

81
Q

Clinical presentation of focal segmental glomerulosclerosis

A
  1. Secondary hypertension and renal impairment
82
Q

How is focal segmental glomerulosclerosis treated

A

Corticosteroids and immunosuppressants:
CYCLOPHOSPHAMIDE

CICLOSPORIN

83
Q

Secondary causes of nephrotic syndrome

A
  1. Diabetes
  2. Amyloidosis
  3. Infections
  4. SLE, RA
  5. GOLD, NSAIDs, ACEI
  6. Malignancy
84
Q

Pathophysiology of nephrotic syndrome

A

Any diseases that cause injury to podocytes will cause loss of foot processes = proteinuria

85
Q

Clinical presentation of nephrotic syndrome

A
  1. Normal-mild increase in BP
  2. Proteinuria >3.5g/day
  3. Normal-mild decrease in GFR
  4. Hypoalbuminaemia
  5. Pitting oedema of ankles, genital, abdo wall and face (periorbital)
  6. Frothy urine
86
Q

Differential diagnosis of nephrotic syndrome

A
  1. Congestive heart failure

2. Cirrhosis

87
Q

Why is nephrotic syndrome misdiagnosed for congestive heart failure

A

Oedema and raised Jugular venous pressure

Nephrotic = low JVP

88
Q

How is liver cirrhosis misdiagnosed and distinguished from nephrotic

A
  1. Hypoalbuminaemia and oedema

2. JAUNDICE, FEVER

89
Q

How is nephrotic syndrome diagnosed

A
  1. RENAL BIOPSY
  2. Urine dipstick for proteins
  3. CXR or ultrasound for pleural effusion or ascites
  4. Serum albumin low
  5. BP is increased or normal
  6. Renal function is normal
90
Q

FBC results for nephrotic syndrome

A
  1. Serum albumin low
  2. Serum creatinine, eGFR, lipids and glucose
  3. ANA positive, double-stranded DNA antibody, c3 and c4 = SLE
  4. Antiphospholipid A2 receptor antibody = membranous nephropathy
    Hep B surface antigens
91
Q

Complications of nephrotic syndrome

A
  1. Susceptibility to infection
  2. Thromboembolism
  3. Hyperlipidaemia
92
Q

Why does nephrotic syndrome increase susceptibility to infection

A
  1. Low serum IgG, decreased complement activity and T cell function

IgG is being lost in urine and immunosuppressive treatment

93
Q

Why does nephrotic syndrome cause thromboembolism

A
  1. Hypercoaguable state due to increased clotting factors (produced by liver due to low albumin since liver goes into overdrive) and platelet abnormalities
94
Q

How does nephrotic syndrome cause hyperlipidaemia

A
  1. Increased cholesterol and triglycerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin
95
Q

goals of treating nephrotic syndrome

A

REDUCE OEDEMA
REDUCE PROTEINURIA
REDUCE RISK OF COMPLICATIONS

96
Q

How do we reduce oedema

A
  1. IV FUROSEMIDE (IV as gut prevents absorption)
  2. IV BENDROFLUMETHIAZIDE
  3. Fluid and salt restriction
97
Q

How do we reduce proteinuria

A

REMPIRIL
CANDESARTAN
Eat normal protein diet

98
Q

How do we stop microvascular complications

A

Prophylactic anticoagulation with WARFARIN

SIMVASTATIN

Treat infections and vaccinate

Year 2 (155 decks)

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