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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
What relives benign prostatic hyperplasia
Cathetisation
26
What should we do if cauterisation does not improve urinary obstruction
Suspect obstruction above prostate: Urgent ultrasound to look for hydronephrosis Urgent CT-KUB for obstructing masses/calculi or retroperitoneal fibrosis
27
Role of ECG in reCKD
1. Hyperkalaemic hcnages
28
Role of CXR in CKD
Look for pulmonary oedema
29
When ar biopsies done
Interregnal causes for AKI Done for unexplained AKI and normal kidneys
30
How is CKD treated pre-renally
1. Correct volume depletion with fluids | 2. Sepsis = antibiotics
31
How is CKD treated intrinsic renal
Refer to nephrology over tubulointerstitial or glomerular pathology
32
How is CKD treated post-penally
1. Catheterise and consider CT or renal tract | 2. Obstruction or hydronephrosis - cytoscopyy, retrograde stents or nephrostomy insertion - buys time for treatment
33
How is CKD treated for all causes
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
34
Name some nephrotoxic drugs
1> NSAIDS 2. ACEI 3. GENTAMYCIN 4. AMPHOTERICIN
35
Diet to treat CKD
1. NA / K restriction | 2. Supply Vit D
36
What are indications for dialysis
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
37
Most common RRT
Haemofiltrtaion | Haemodialysis
38
Complications of RRT
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
39
Define glomerulonephritis
Broad term that refers to a group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons
40
What is the consequence of glomerulonephritis
End stage renal failure
41
How does glomerulonephritis effect the body
1. HAEMATURIA and PROTEINURIA 2. Damage to glomerulus restricts blood flow = compensatory HYPERTENSION 3. AKI due to loss of filtration capacity
42
In what four ways can glomerulonephritis present
1, Acute Nephritic Syndrome (Acute glomerulonephritis) 2. Nephrotic syndrome 3. Asymptomatic urinary abnormalities - haematuria, proteinuria or both 4. CKD
43
What causes acute nephritic syndrome
Immune response triggered by an infection
44
What characterises Acute Nephritic Syndrome
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
What is the most common primary cause of acute glomerulonephritis
IgA neuropathy
46
How does IgA neuropathy cause acute glomerulonephritis
It accumulates in the glomeruli causing inflammation
47
What bacterial infections can cause Acute glomerulonephritis
MRSA, typhoid or secondary syphilis
48
What viruses can cause acute glomerulonephritis
Hep B and C
49
What worm can cause acute glomerulonephritis
Schistomiasis
50
How does Strep. pyogenes cause Acute Glomerulonephritis
1. Occurs in a child 1-3 weeks after streptococcal infection (pharyngitis or cellulitis) with a Lancefield group A beta-haemolytic streptococcus
51
When does strep. pyogenes occur
2 weeks after tonsillitis
52
How does strep. progenies cause acute glomerulonephritis
Bacterial antigen becomes trapped in the glomerulus leading to an act diffuse proliferative glomerulonephritis
53
How is acute glomerulonephritis
1. Antibiotics | 2. Supportive
54
What conditions can cause acute glomerulonephritis
1. Infective endocarditis 2. SLE 3. Systemic Sclerosis 4. ANCA associated vasculitis 5. Goodpastures disease 6. IgA neuropathy
55
Treatment of SLE
Immunosuppression: Cyclophosphamide | Rituximab
56
How is systemic sclerosis diagnosed
ANA positive, Anti-ro and Anti-la positive Severe hypertension Onion skin changes on renal biopsy
57
What is ANCA associated vasculitis
1. Multisystem small vessel vasculitis attack small vessels in kidney and the eye
58
How is ANCA associated vasculitis treated
1. IMMUNOSUPRESSION Cyclophosphamide Rituximab Plasma exchange
59
What is good pastures disease
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
How is good pastures disease treated
1. Remove antibody via plasma exchange 2. Immunosuppression 3. Steroids/cyclophosphamide
61
Most common cause of nephritic syndrome
IgA Nephropathy
62
Where does IgA deposit in the kidney
Mesangium (provides structural support to glomerulus) of kidneys and kidney get attacked
63
What condition is IgA nephropathy associated with
Tonsilitis
64
What treatment is needed for IgA nephropathy
BP control - ACEI, angiotensin receptor blockers
65
Clinical Presentation of nephritic syndrome
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
Diagnosis of acute nephritic syndrome
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
How is Acute nephritic syndrome treated
Hypertension = loop diuretics ORAL FUROSEMIDE) AMLODIPINE (calcium channel blocker)
68
What defines nephrotic syndrome
1. Proteinuria > 3.5g/24 hours 2. Hypoalbuminaemia 3. Oedema Hyperlipidaemia
69
Why is there hyperlipidaemia in nephrotic syndrome
Liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol
70
Can you develop kindey failure with nephrotic syndrome
No but HUGE amounts of protein is leaking
71
What is the most common secondary cause of nephrotic syndrome
Diabetes
72
Primary cause of nephrotic syndrome
1. Minimal change disease in kids 2. Membranous neuropathy 3. Focal segmental glomerulosclerosis
73
What is minimal change disease
No deposits or changes to the mesangium yet there is proteinuria and widespread oedema = minimal change
74
Primary causes membranous neuropathy
Usually IDIOPATHIC
75
What is membranous neuropathy
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
Symptoms of membranous neuropathy
1. Asymptomatic preotinuria and microscopic haematuria, hypertension and renal impairment
77
Secondary causes of membranous neuropathy
1. Drugs (NSAIDs) 2. Autoimmune (SLE, thyroiditis) 3. infection (Hep B or C, schistomiasis) 4. Neoplasia (lung, colon,s stomach and breast)
78
Hows membranous neuropathy treated
IMMUNOSUPPRESION
79
What is focal segmental glomerulosclerosis
Where scar tissue develops on parts of the glomerulus that filter waste from blood
80
Pathophysiology of focal segmental glomerulosclerosis
CD80 in podocytes results in increased permeability in glomeruli and thus proteinuria and haematuria
81
Clinical presentation of focal segmental glomerulosclerosis
1. Secondary hypertension and renal impairment
82
How is focal segmental glomerulosclerosis treated
Corticosteroids and immunosuppressants: CYCLOPHOSPHAMIDE CICLOSPORIN
83
Secondary causes of nephrotic syndrome
1. Diabetes 2. Amyloidosis 3. Infections 4. SLE, RA 5. GOLD, NSAIDs, ACEI 6. Malignancy
84
Pathophysiology of nephrotic syndrome
Any diseases that cause injury to podocytes will cause loss of foot processes = proteinuria
85
Clinical presentation of nephrotic syndrome
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
Differential diagnosis of nephrotic syndrome
1. Congestive heart failure | 2. Cirrhosis
87
Why is nephrotic syndrome misdiagnosed for congestive heart failure
Oedema and raised Jugular venous pressure Nephrotic = low JVP
88
How is liver cirrhosis misdiagnosed and distinguished from nephrotic
1. Hypoalbuminaemia and oedema | 2. JAUNDICE, FEVER
89
How is nephrotic syndrome diagnosed
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
FBC results for nephrotic syndrome
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
Complications of nephrotic syndrome
1. Susceptibility to infection 2. Thromboembolism 3. Hyperlipidaemia
92
Why does nephrotic syndrome increase susceptibility to infection
1. Low serum IgG, decreased complement activity and T cell function IgG is being lost in urine and immunosuppressive treatment
93
Why does nephrotic syndrome cause thromboembolism
1. Hypercoaguable state due to increased clotting factors (produced by liver due to low albumin since liver goes into overdrive) and platelet abnormalities
94
How does nephrotic syndrome cause hyperlipidaemia
1. Increased cholesterol and triglycerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin
95
goals of treating nephrotic syndrome
REDUCE OEDEMA REDUCE PROTEINURIA REDUCE RISK OF COMPLICATIONS
96
How do we reduce oedema
1. IV FUROSEMIDE (IV as gut prevents absorption) 2. IV BENDROFLUMETHIAZIDE 3. Fluid and salt restriction
97
How do we reduce proteinuria
REMPIRIL CANDESARTAN Eat normal protein diet
98
How do we stop microvascular complications
Prophylactic anticoagulation with WARFARIN SIMVASTATIN Treat infections and vaccinate

Year 2 (155 decks)

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