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Renal > General overview > Flashcards

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
Q

Causes of ATN: ISCHAEMIA

A

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
Q

Causes of ATN: myeolma

A

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
Q

Causes of ATN- nephrotoxic agents

A 
Analgesics: NSAIDS
Antibiotics: Aminoglycosides, gentamicin, streptomycin
CONTRAST AGENTS
Anaesthetic agents
Chemotherapeutic agents
ACE-I and ARBs
Immunosuppressants- ciclosporin
28
Q

Urine Exam- what to look for

A 
pH
Protein
Blood 
Glucose
Leucocyte esterases
Nitrites
Specific gravity
Ketones
Urobilinogen 
lab tests: Urine MCS
Protein- creatinine
24 hour urine
29
Q

Haematuria: what it indicates

A 
Renal:
Pyelonephritis
Glomerulonephritis
Carcinoma
Trauma
Extrarenal
Cystitis/prostitis, urethritis
Stones
trauma
Bladder cancer
30
Q

Proteinuria indications

A 
Nephrotic syndrome
DM
Amyloid
HTN
Multiple myeloma
CCF
31
Q

Glucose in blood

A

DM
Renal tubular damage
Pregnancy
Sepsis

32
Q

Urinobilinogen

A

Pre-hepatic jaundice

33
Q

Ketones

A

Starvation
DKA
HMG

34
Q

General management of AKI

A

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
Q

CKD symptoms

A

Anorexia, nausea and vomiting, fatigue, pruritis, peripheral oedema, musce cramps, pulmonary oedema, sexual
dysfunction

36
Q

CKD signs

A 
Skin pigmenetation- uraemia 
excoriation marks- uraemia
Pallor- anaemia of chronic disease
hypertension 
Peripheral oedema
Peripheral vascular disease
Renal bone disease
37
Q

Consequences of CKD

A

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
Q

Usual blood results for CKD

A 
Decreased Hb- normocytic anaemia
U&amp;Es ( increased urea and creatinine)
Glucose- DM
eGFR
Decreased calcium
Increased phosphate
Increased ALP- renal osteodystrophy
Increased PTH if Severe CKD
39
Q

Why do you need a CXR in these investigations?

A

Pericardial effusion or pulmonary oedema

40
Q

Limiting progression/complications in CKD

A

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
Q

Renal osteodystrophy treatment

A

Calcichew- Ca supplement
Calcium acetate- phosphate binders
Cinacalecet- calcimimetic- reduce PTH levels

42
Q

Symptom control of:
Anaemia
Acidosis
Oedema

A

Sodium bicarbonate supplements for patients with low serum bicarbonate
Oedema- loop diuretics- restriction of fluids

43
Q

Renal replacement therapy

name 2 types

A

Haemodyalysis- vascular access requires

Transplanatation- gold standard treatment- major surgery

44
Q

Most common causative agent of an UTI

A

E.coli
Others- staphylococcus saprophyticus
Proteus mirabilis
Enterococci

45
Q

Risk factors for UTI

A 
Female
Sex
Exposure to spermicide
Pregnancy 
Menopause
Immunosuppression 
Catheterisation 
Urinary tract obstruction
46
Q

Cystitis symptoms

A

Frequency
Urgency
Dysuria
Haematuria

47
Q

Protatitis symptoms

A

Suprapubic pain
Flu-like symptoms
Low backache
Few urinary symptoms

48
Q

Acute pyelonephritis symptoms

A 
High fever
Rigors
Vomiting 
Loin pain and tenderness
Oliguria- AKI
49
Q

Investigations and management of UTIs

A

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
Q

Polycystic kidney disease

A

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
Q

Renal cell carcinoma

A

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
Q

Renal artery stenosis

A

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
Q

Membranous glomerulonephrits

A

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
Q

Causes of Membranous glomerulonephritis

A

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
Q

Features of Alport’s syndrome

A

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
Q

Features of Rhabdomyolysis

A

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
Q

Causes of rhabdomyolysis

A

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
Q

Management of Rhabdomyolysis

A

IV fluids to maintain good urine output

urinary alkalinization is sometimes used

59
Q

Causes of anaemia in renal failure

A

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
Q

Features of anaemia in patients with CKD

A

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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