Year 2 > Genitourinary: Part 3 > Flashcards

Genitourinary: Part 3 Flashcards

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1
Q

What people are effected by minimal change disease

A

Boys under 5

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2
Q

What causes minimal change disease

A

Idiopathic

Atrophy and allergic reactions can trigger nephrotic syndrome

Drugs

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3
Q

What drugs can cause minimal change disease

A
  1. NSAIDs
  2. Lithium
  3. Antibiotics (CEPHALOSPORIN, RIFAMPICIN)
  4. Bisphosphonates
  5. Sulfasalazine
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4
Q

What disease is associated with minimal change disease

A

Hodgkins lymphoma

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5
Q

Pathophysiology of minimal change disease

A

NORMAL glomeruli on light microscopy

FUSION of foot processes of the podocytes on electron microscopy due to disrupted podocyte actin cytoskeleton

Immature differentiating CD35 stem cells are responsible

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6
Q

Clinical presentation of of minimal change disease

A
  1. Proteinuria
  2. Periorbital oedema
  3. Fatigue
  4. Frothy urine
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7
Q

Diagnosis of minimal change disease

A
  1. BIOPSY:
    - normal under light microscopy
    - Electron microscopy shows FUSED PODOCYTE FOOT PROCESSES
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8
Q

How is minimal change disease treated

A
  1. PREDNISOLONE (reverses proteinuria)

2. CYCLOPHOSPHAMIDE or CYCLOSPORIN for relapses

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9
Q

What can cause asymptomatic urinary abnormalities

A
  1. IgA nephropathy

2. Thin Membrane disease

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10
Q

How is IgA nephropathy treated

A

RAMIPRIL and CYCLOPHOSPHAMIDE

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11
Q

What is thin membrane disease

A

More likely to leak blood into urine

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12
Q

Define CKD

A

Long standing, progressive, impairment in renal function for more than 3 months

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13
Q

GFR threshold for CKD

A

GFR < 60mL/min/1.73 M^2 for more than 3 months with/without evidence of kidney damage

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14
Q

What gender is effected in CKD

A

FEMALES

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15
Q

What GFR threshold defines established renal failure

A

<15

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16
Q

What can cause CKD

A
  1. Diabetes
  2. Hypertension
  3. Atheroscloertic renal vascular disease
  4. Polycystic kidney disease
  5. Tuberous sclerosis
  6. Primary glomerulonephritides (IgA nephropathy)
  7. SLE
  8. Amyloidosis
  9. Hypertensive nephrosclerosis (common in black africans)
  10. Small and medium-sized vessel vasculitis
  11. Family history of stage 5 CKD or hereditary kidney disease
  12. Hypercalcaemia
  13. Neoplasma
  14. Myeloma
  15. Idiopathic
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17
Q

Risk factors for CKD

A
  1. Diabetes Mellitus
  2. Hypertension
  3. Old Age
  4. CVD
  5. Renal stones or benign prostatic hyperplasia
  6. Recurrent UTIs
  7. SLE
  8. Proteinuria
  9. AKI
  10. Smoking
  11. African, afro-caribbean or asian origin
  12. Chronic use of NSAIDs
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18
Q

What can CKD progress to

A

End-stage kidney disease

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19
Q

Factors effecting speed of decline in CKD

A

Underlying nephropathy and BP control

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20
Q

What happens in CKD

A
  1. Nephrons failed and burden of filtration falls on fewer functioning nephrons
  2. Functioning nephrons experience increased flow per nephron as blood flow has not changed, and adapt with glomerular hypertrophy and reduced arteriolar resistance
  3. Increased flow, increased pressure and increased shear stress set in motion a VICIOUS CYCLE of raised intraglomerular capillary pressure and strain which accelerates remnant nephron failure

PROTEINURIA

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21
Q

ROLE OF ANGIOTENSIN II

A

Produced locally, modulates intraglomerular capillary pressure and GFR, causing vasoconstriction of postglomerular arterioles and increasing the glomerular hydraulic pressure and filtration fraction

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22
Q

How does angiotensin II effect mesangial cells and podocytes

A

Increases pore size and impairs the size-selective function of the basement membrane for macromolecules - increased proteinuria

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23
Q

What molecules does angiotensin II up regulate

A

TGF-beta and PAI-1

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24
Q

Result of angiotensin II up regulating TGF-beta

A

Increases collagen synthesis and epithelial cell transdifferentiation to myofibroblasts that contribute to excessive matrix formation

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25
What is PAI-1
Plasminogen activator inhibitor - 1
26
Role of PAI-1
Inhibits matrix proteolysis by plasmin - results in accumulation of excessive matrix and scarring in both the glomeruli and interstitium
27
Clinical presentation of CKD
1. Early symptomatic as kidney has a lot of reserve 2. Serum urea and creatinine are raised 3. Malaise 4. Anorexia and weight loss 5. Insomnia 6. Nocturne and polyuria due to impaired concentrating ability 7. Pruritus 8. Nausea, vomiting and diarrhoea 9. Symptoms due to salt and water retention (PULMONARY OEDEMA or peripheral oedema) 10. Amenorrhea in women and erectile dysfunction in men 11.
28
At what concentration do uraemic symptoms appear
40mmol/L
29
Complications of CKD
1. Anaemia 2. Bone disease 3. Neurological syndromes 4. CVD 5. Skin disease
30
What anaemia occurs in CKD
Normochromic normocytic anaemia due to decreased ERYTHROPOIETIN secretion
31
What bone diseases are associated with CKD
1. Bone pain 2. Renal osteodystrophy - osteomalacia, osteoporosis, hyperparathyroidism 3. Renal phosphate retention and impaired 1,25(dihydroxy) Vit D production = loss in ca and compensatory PTH = skeletal decalcification leading to bone disease
32
Neurological effects in CKD
1. Autonomic dysfunction = postural hypotension and disturbed GI motility 2. Polyneuropathy resulting in peripheral paraesthesiae and weakness 3. Advanced uraemia = depressed cerebral function (loss of consciousness) and myoclonic twitching and seizures
33
What CVD risk are there with CKD
1. MI, Cardiac failure, stroke 2. Increased frequency of hypertension , hyperlipidaemia and vascular calcification 3. Pericarditis and pericardial effusion due to ANAEMIA 4. Pericardial friction rub 5. Flow murmurs
34
Skin disease in CKD
1. Pruritus due to urea's nitrogenous waste product | 2. Brown discolouration in nails
35
Differential diagnosis of CKD
AKI
36
How can i distinguish between AKI and CKD
1. Duration of symptoms 2. History 3. Previous urinalysis 4. Normocytic anaemia, small kidneys on ultrasound and presence of renal osteodystrophy = CKD
37
Diagnosis of CKD
1. ECG for high K signs 2. Urinalysis 3. Urine microscopy 4. FBC 5. Immunology 6. Imaging
38
Urinalysis in CKD
1. Proteinuria 2. Haematuria 3. Mid-stream urine sample 4. Albumin to creatinine ratio OR protein to creatinine ratio
39
What would be seen in urine microscopy for CKD
1. White cells = bacterial UTI 2. Eosinophilia = allergic tubulointerstitial nephrotis/cholesterol emboli 3. Granular casts - active renal disease 4. Red cells = glomerulonephritis
40
FBC in CKD
1. Urea 2. Electrolytes 3. Bicarbonate 4. Creatinine HIGH 5. Low eGFR 6. Raised alkaline phosphatase due to renal osteodystrophy 7. Raised PTH if CKD is in stage 3 8. Anaemia 9. Fragmented red cells due to haemolysis 11. Raised viscosity
41
What conditions can cause CKD
1. Auto-antibody screening for SLE, scleroderma and good pastures 2. Hep B, C, HIV and streptococcal antigen tests
42
What imagine is used to diagnose CKD
1. Ultrasound 2. CT 3. Biopsy
43
Why is ultrasound used in CKD
1. Check renal size and exclude hydronephrosis
44
Why is CT used in CKD
1. Detect stones, retroperitoneal fibrosis and other causes of urinary obstruction
45
What is retroperitoneal fibrosis
Abnormal formation of tissue occurs behind cavity of perioenium, spreads to tubes that carries urine
46
3 main areas of treatment to CKD
1. Slow deterioration of kidney function 2. Reduce CVD risk 3. Treat complications (anaemia)
47
How do we identify and treat reversible causes of CKD
1. Relieve obstruction 2. Stop nephrotoxic drugs 3. Stop smoking and achieve healthy weight to deal with CVD risk 4. Tight glucose control in diabetics
48
How do we limit BP complications of CKD
1. ACEI - RAMPRIL 2. ARBs (CANESARTAN) 3. Diuretics (ORAL BENDROFLUMETHIAZIDE) 3. VERAPAMIL (calcium channel blocker)
49
In diabetes what drugs is given as first line treatment of BP
CANDESARTAN
50
How is bone disease caused in CKD treated
1. monitor PTh levels = restrict dietary phosphate 2. Give phosphate binders to decrease absorption 3. CALCITRIOL
51
How is CVD complications caused by CKD treated
SIMVASTATIN | ASPIRIN
52
How is anaemia treated
Iron/oflate
53
How is acidosis treated
Sodium Bicarbonaye
54
How is Oedema treated
Furosemide
55
What is the best form of renal replacement therapy
Transplantation
56
Indications for dialysis
1. Sympatic uraemia = pericarditis or tamponade 2. Hyperkalaemia not controlled by conservative measures 3. Severe acids 4. Pulmonary oedema not responsive to diuretics 5. Tall T waves, flat P waves, broad QRS complex or arrhythmias 6. Metabolic acidosis 7. Fluid overload resistant to diuretics
57
How does haemofiltration work
Achieves blood flow using a blood pump to draw and return blood from the lumen of a dual-lumen catheter placed in the jugular, subclavian or femoral vein Ultrafiltrate is continuously removed from patient combined with simultaneous infusion of replacement solution Less haemodynamic instability than haemodialysis
58
How does haemodialysis work
1. Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction, thus blood always meets a less-concentrated solution Blood is taken from artery and returned into a vein at atrioventricular fistula
59
Cons of haemodialysis
Larger solutes of not clear as effectively Time-consuming
60
Pros of haemodiyalysis
Allows good clearance of solutes in short periods but requires patient to be haemodynamically stable
61
IF a patient has an AV fistula how is haemodialysis done
A synthetic graft is used as you don't need to wait for a vein dilatation
62
Complications of haemodialysis
1. Hypotension/Cramps 2. Nausea/headache 3. Chest pain 4. Fever/rigors 5. Infected dialysis catheter
63
When is peritoneal dialysis used
CKD
64
How does peritoneal dialysis work
1. Uses peritoneum in the abdomen as a membrane which fluids and solutes are exchanged in the blood
65
When is peritoneal dialysis done
Home at night
66
Complications of peritoneal dialysis
1. Infection (peritonitis) 2. Abdo wall herniation 3. Intestinal perforation 4. Loss of membrane function over time
67
Complications of RRTs
1. MI 2. INFECTION 3. Amyloid accumulates in long-term dialysis = carpal tunnel syndrome, arthralgia nd fractures 4. Malignancy
68
When do renal cysts become more common
As age advances
69
When are kidney cysts found
Ultrasound examination
70
Types of kidney cysts
1. Simple cysts - benign 2. Polycystic 3. Hydronephrosis when ureter blocks 4. Dysplasia - when not formed properly 5. Medullary sponge - dilatation of collecting ducts 6. Acquired cystic disease - medullary uraemia, dialysis cystic
71
Types of kidney cysts
1. Simple cysts - benign 2. Polycystic 3. Hydronephrosis when ureter blocks 4. Dysplasia - when not formed properly 5. Medullary sponge - dilatation of collecting ducts 6. Acquired cystic disease - medullary uraemia, dialysis cystic
72
How does congenital renal cysts occur
1. Genetic mutation leaves predisposition 2. Increased abnormal cell hyper proliferation -> loss of planar polarity -> cysts initiation -> fluid secretion of epithelial cells -> cyst
73
How long does it take for renal simple cysts to form
Over time
74
What condition can cause cysts to form
CKD
75
What drug can cause CKD
Lithium
76
When is lithium given
Depression
77
What can cause renal cyst syndrome
Tuberous sclerosis
78
What is autosomal dominant polycystic kidney disease
Where multiple cysts develop, gradually and progressively thought the kidney eventually resulting in renal enlargement and kidney tissue destruction
79
When does ADPKD arise
Males in adulthood
80
Chance of transmission if one parent is effected with ADPKD
50%
81
In ADPKD, where does genetic mutations occur
Chromosome 16 (85%) Chromosome 4 (15%)
82
What gene does PKD1 code for
Plycystin 1 which is involved in cell-cell interactions - regulates tubular and vascular development of kidney
83
What protein does PKD2 code for
Polycystic 2 which functions as calcium ion channels
84
What is the role of polycystic complex that occurs in the cilia
Senses flow in tubule
85
Consequence of disruption of polycystic pathway
Reduced cytoplasmic ca in principal cells of collecting ducts, causes defective ciliary signalling and disorientated cell division = cyst formation
86
What causes progressive loss of renal function in ADPKD
progressive loss of renal function due to mechanical compression, apoptosis of healthy tissue and reactive fibrosis
87
What factors contribute to decline of renal function in ADPKD
Growth and size of cyst Rate of growth Patients with rapidly growing cysts on MRI lose function more rapidly
88
Clinical presentation of ADPKD
1. Asymptomatic (screening ended) until 20 2. Loin pain and haematuria from haemorrhage , cyst infection or stone formation 3. Excessive water and salt loss 4. Nocturne 5. Bilateral kidney enlargement 6. Renal colic due to clots 7. Hypertension 8. Renal stones (uric acid) 9. progressive renal failure 1
89
Extra renal presentation of ADPKD
1. Subarachnoid haemorrhage due to berry aneurysm rupture 2. Polycystic liver disease 3. Pancreatitis 4. Mitral valve prolapse 5. Ovarian cyst 6. Diverticular disease
90
Differential diagnosis of ADPKD
1. Simple cysts 2. Autosomal recessive PKD 3. Medullary sponge kidney 4. Tuberous sclerosis
91
How is ADPKD diagnosed
1. Family history 2. BP raised 3. ULTRASOUND
92
Diagnosis classification of ADPKD
1. 15-39 yrs > 3 cysts 2. 40-59 years < 2 cysts (each kidney 3. 60 years > 4 cysts in each kidney
93
When do you exclude ADPKD
greater than 40 and less than 2 cysts present
94
When can you not exclude ADPKD by ultrasound
Less than 30 years
95
How is ADPKD treated
1. BP control - RAMIPRIL 2. Treat stones + analgesia 3. Laparoscopic removal of cyst 4. Disease progression monitored by serum creatinine 5. Renal replacement therapy for ESRF 6. Children and siblings of patients with the disease should be offered screening by renal ultrasound in 20s 7. Counselling and support
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