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General overview Flashcards

1
Q

Nephritic syndrome requirements

A 
Haematuria
Oliguria
Fluid retention
Proteinuria less than 3mg/l in 24 hours- any more and it becomes nephrotic syndrome
HIGH BP
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2
Q

Nephrotic syndrome

A

Peripheral oedema
Hypoalabuminaemia- less tha 24g/l
Proteinuria- more than 3mg/L
Hypercholesterolaemia

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3
Q

Pre-renal AKI causes

A

Hypovolaemia:
Renal loss from diuretic overuse, osmotic diuresis- DKA
Extrarenal loss from vomiting, diarrhoea, burns, sweating, blood loss
Systemic vasodilation- sepsis- neurogenic shock
Decreased cardiac output: HF and MI

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4
Q

Renal , cellular damage/intrinsic

A

Tubular: acute tubular necrosis- ischaemia, drugs, toxins, paracetamol, NSAIDs ACE-I contrast, myoglobinuria in rhabdomyolysis
GLOMERULONEPHRITIS, interstitial nephritis- TUMOUR LYSIS SYNDROME
VASCULAR vessel obstruction

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5
Q

Post-renal=obstruction

A

Luminal: stones, clots
Mural: malignancy- uretic, prostate, bladder, BPH, strictures
Retroperitoneal fibrosis

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6
Q

4 Places in the renal system where you can have damage

A

Tubular, glomerular, interstitial, vascular

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7
Q

Vascular causes of renal disease

A

Large vessel occlusion: renal artery/vein thrombus
Emboli

Small vessel- microangiopathy
Haemolytic uraemic syndrome (HUS)
Thrombotic Thrombocytopenic Purpura (TTP)
Disseminated Intravascular Coagulation (DIC)

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8
Q

Haemolytic Uraemic Syndrome

characterisations

A

1) Progressive renal failure- kidneys
Microangiopathic haemolytic anaemia (MAHA)
Decreased Platelet - blood

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9
Q

Most common cause of HUS?

A

E.coli

Toxin- endothelial damage- thrombosis- decreased platelets- destruction of RBCs, shistocytes- decreased HB

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10
Q

Presentation of patient with HUS?

A

Abdo pain, bloody diarrhoea, fever, seizures, lethargy

TREATMENT: Supportive- dialysis and plasmapheresis

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11
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Presentation and pathophysiology

A

Overlap with MAHA,
PENTAD of haemolytic uraemia, thrombocytopenia, uraemia, Fever, neurogenic symptoms
Seizures-, hemiparesis, decreased consciousness and decreased vision

Deficiency of protease- ADAMTS13 that cleaves vWF- multiform of vWF- platelet aggregation and fibrin deposition, microthrombi

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12
Q

Glomerulonephritis meaning

A

Inflammation of the glomeruli and nephrons

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13
Q

Glomerular inflammation:
Loss of barrier function presentation

Loss of filtering capacity presentation

A

Loss of barrier function Proteinuria- mild to nephrotic syndrome
Haematuria- mild to macrocytic

Filtering capacity- reduced excretion> accumulation of waste products- AKI

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14
Q

Causes of glomerulonephritis

A

IgA nephropathy- (days after UTI- increased IgA immune complex- episodic haematuria

Henoch-Shonlein Purpura (HSP)- systemic variant IgA nephropathy- purpuric rash -

Anti-GBM- Goodpastures- Auto Ab to Type IV collage (GBM and lung)- haemoptsis and haematuria

Post Streptoccocal GN- 1-12w after throat infection- nephritic syndrome

Pauci-immune - ANCA associated antibodies- bound to neutrophils- activation within glomerular capillary loops- vasculitis or limited to kidney

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15
Q

Link of oedema with nephrotic syndrome

A

Hypoalbuminaemia- liver tries to compensate and increases production of lipids- hyperlipidaemia > 10mmol/L

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16
Q

Underlying causes of Nephrotic syndrome

A

Minimal change glomerulonephritis- children (90%)<5 years

Membranous glomerulonephritis/DM- adults

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17
Q

What is berger’s disease

A

IgA nephropathy- most common cause of primary glomerulonephritis
NEPHRITIC SYNDROME

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18
Q

Common primary causes of nephrotic syndrome

A 
Membranous glomerulonephritis (ICM)
Minimal change disease (Non-ICM)
Focal segmental glomerulosclerosis (Non-ICM)
Mesangiocapillary glomperulonephritis (ICM/Non-ICM)
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19
Q

Common secondary causes of Nephrotic syndrome

A

Diabetes
SLE
Amyloid
HBV/HCV

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20
Q

Nephritic syndrome primary causes

A

IgA nephropathy

Mesangiocapillary Glomerulonephritis

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21
Q

Common secondary causes (systemic)

A

Post-streptococcal
Vasculitis
SLE
Anti-GMB disease- cryoglobulinaemia

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22
Q

Investigations and management of Glomerulonephritis

A

Bloods- FBC, U&Es, CRP, Complement, Autoantibodies
Urine
Imaging- renal US +/- renal biopsy

Management - Refer specialist
BP management <130/80
ACE-I or ARB- reduce proteinuria and preserve renal function
Steroids/immunosuppression

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23
Q

Tubular causes of AKI- ATN

A

ATN- most common cause of AKI
ischaemia, nephrotoxic agents
Exogenous drugs: NSAIDs, aminoglycosides, amphotericin b, contrast media, calcineurin inhibitors, cisplatin

Endogenous : myoglobinaemia (rhabdomyolysis) , haemoglobinuria, crystal, myeloma

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24
Q

Pathophys of Acute, tubular necrosis

A 
Hypovolaemia
Low CO- cardiac output
Systemic vasodilation-sepsis
DIC
Renal vasoconstriction
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25
Causes of ATN: ISCHAEMIA
Ischaemia- tubular cell injury, necrosis, obstruction of tubule by debris, reduced GFR 3 phases: Initiation- acute reduced GFR, increased Cr and increased UREA Maintenance of low GFR- increase in creatinine and urea Recovery- tubular function regenerates- increased urine volume and gradular decrease in urea and CR
26
Causes of ATN: myeolma
Malignant disease of bone marrow plasma cells- clonal expansion of plasma cells CRAB: Calcium- high Renal failure- increase Urea and increase Cr (hypercalcaemia and paraprotein deposition) Anaemia Bone- bone osteolytic bone lesions- pain fracture (risk cord compression)
27
Causes of ATN- nephrotoxic agents
``` Analgesics: NSAIDS Antibiotics: Aminoglycosides, gentamicin, streptomycin CONTRAST AGENTS Anaesthetic agents Chemotherapeutic agents ACE-I and ARBs Immunosuppressants- ciclosporin ```
28
Urine Exam- what to look for
``` pH Protein Blood Glucose Leucocyte esterases Nitrites Specific gravity Ketones Urobilinogen lab tests: Urine MCS Protein- creatinine 24 hour urine ```
29
Haematuria: what it indicates
``` Renal: Pyelonephritis Glomerulonephritis Carcinoma Trauma ``` ``` Extrarenal Cystitis/prostitis, urethritis Stones trauma Bladder cancer ```
30
Proteinuria indications
``` Nephrotic syndrome DM Amyloid HTN Multiple myeloma CCF ```
31
Glucose in blood
DM Renal tubular damage Pregnancy Sepsis
32
Urinobilinogen
Pre-hepatic jaundice
33
Ketones
Starvation DKA HMG
34
General management of AKI
Assess volume status- aim for euvolaemia Stop nephrotoxic drugs Monitoring and nutrition Treat underlying cause Pre-renal correct volume depletion and abx, inotropes Post renal - catheterise + imaging CTKUB+urology and reversal Intrinsic renal- nephrology
35
CKD symptoms
Anorexia, nausea and vomiting, fatigue, pruritis, peripheral oedema, musce cramps, pulmonary oedema, sexual dysfunction
36
CKD signs
``` Skin pigmenetation- uraemia excoriation marks- uraemia Pallor- anaemia of chronic disease hypertension Peripheral oedema Peripheral vascular disease Renal bone disease ```
37
Consequences of CKD
1) Progressive failure of homeostatic function - acidosis Progressive failure of hormonal function- anaemia Renal bone disease- osteomalacia Cardiovascular disease- vascular calcification Uraemia and death
38
Usual blood results for CKD
``` Decreased Hb- normocytic anaemia U&Es ( increased urea and creatinine) Glucose- DM eGFR Decreased calcium Increased phosphate Increased ALP- renal osteodystrophy Increased PTH if Severe CKD ```
39
Why do you need a CXR in these investigations?
Pericardial effusion or pulmonary oedema
40
Limiting progression/complications in CKD
BP target <30/80 (<125/75 if diabetic) Tight glucose control in DM Decrease CVS risk - stop smoking, lose wieght Diet- restrict K+, AVOID high phoosphate food
41
Renal osteodystrophy treatment
Calcichew- Ca supplement Calcium acetate- phosphate binders Cinacalecet- calcimimetic- reduce PTH levels
42
Symptom control of: Anaemia Acidosis Oedema
Sodium bicarbonate supplements for patients with low serum bicarbonate Oedema- loop diuretics- restriction of fluids
43
Renal replacement therapy | name 2 types
Haemodyalysis- vascular access requires | Transplanatation- gold standard treatment- major surgery
44
Most common causative agent of an UTI
E.coli Others- staphylococcus saprophyticus Proteus mirabilis Enterococci
45
Risk factors for UTI
``` Female Sex Exposure to spermicide Pregnancy Menopause Immunosuppression Catheterisation Urinary tract obstruction ```
46
Cystitis symptoms
Frequency Urgency Dysuria Haematuria
47
Protatitis symptoms
Suprapubic pain Flu-like symptoms Low backache Few urinary symptoms
48
Acute pyelonephritis symptoms
``` High fever Rigors Vomiting Loin pain and tenderness Oliguria- AKI ```
49
Investigations and management of UTIs
Urine dipstick MSU for urine MCS Microscopy Culture Bloods: FBC, Uand E, CRP Management- uncomplicated- cefalexin- 3/7 Nitrofurantoiin- 7/7 Mae- 7/7 cefalexin or ciprofloaxacin 14/7 if suspicious of prostatitis Pyelonephritis/urosepsis- co-amoxiclav 1-2/7
50
Polycystic kidney disease
fluid filled cysts grow on the kidney History acute loin pain, stones SAH (berry aneurysms) Examination- renal enlargement, abdo pain and haematuria, renal enlargement Investigate: haematuria, raised Hb, derranged Uand E, abdominal USS, MRI angiography, IF +ve 1st degree SAH and ADPKD
51
Renal cell carcinoma
Von-Grawitz tumour, hypernephroma arising from parenchyal cortex TRIAD: haematuria, loin abdom mass Ix: increased BP (renin) Polycythaemai or IDA, ALP- bone mets, RBCS, cannon ball mets CT/MRI-
52
Renal artery stenosis
Stenosis of renal artery Caused by atherosclerosis, fibromuscular dysplasia (10% young,) Increased BP refractory to Tx Worsening renal function after ACEi, ARB in bilateral RAS Flash pulmonary oedema Carotid or renal bruits Ix US measurement of kidney size CT angiogram- risk of cotrast enphotoxicity DIgital subtration renal angiography- GOLD STANDARD BUT INVASIVE
53
Membranous glomerulonephrits
Presents with nephrotic syndrome or proteinuria Renal biopsy: electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a 'spike and dome' appearance
54
Causes of Membranous glomerulonephritis
idiopathic: due to anti-phospholipase A2 antibodies infections: hepatitis B, malaria, syphilis malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia drugs: gold, penicillamine, NSAIDs autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
55
Features of Alport's syndrome
Alport's syndrome usually presents in childhood. The following features may be seen: microscopic haematuria progressive renal failure bilateral sensorineural deafness lenticonus: protrusion of the lens surface into the anterior chamber retinitis pigmentosa renal biopsy: splitting of lamina densa seen on electron microscopy
56
Features of Rhabdomyolysis
acute kidney injury with disproportionately raised creatinine elevated creatine kinase (CK) myoglobinuria hypocalcaemia (myoglobin binds calcium) elevated phosphate (released from myocytes) hyperkalaemia (may develop before renal failure) metabolic acidosis
57
Causes of rhabdomyolysis
seizure collapse/coma (e.g. elderly patients collapses at home, found 8 hours later) ecstasy crush injury McArdle's syndrome drugs: statins (especially if co-prescribed with clarithromycin)
58
Management of Rhabdomyolysis
IV fluids to maintain good urine output | urinary alkalinization is sometimes used
59
Causes of anaemia in renal failure
reduced erythropoietin levels - the most significant factor reduced erythropoiesis due to toxic effects of uraemia on bone marrow reduced absorption of iron anorexia/nausea due to uraemia reduced red cell survival (especially in haemodialysis) blood loss due to capillary fragility and poor platelet function stress ulceration leading to chronic blood loss
60
Features of anaemia in patients with CKD
Happens due to reduced EPO levels Normochromic, normocytic anaemia- beomes apparent when the GFR is less than 35ml/min Anaemia in CKD predisposes to LVH

Renal (6 decks)

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