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Phase 2a > Renal conditions > Flashcards

Renal conditions Flashcards

1
Q

Renal Colic - Description

A

Renal stones (calculi) made of crystal aggregates form in collecting ducts and then deposited anywhere from renal pelvis to urethra

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2
Q

Renal Colic - Epidemiology

A
  • More males
  • 10% lifetime risk
  • More in the Middle East
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3
Q

Renal Colic - Pathology

A
  • Solutes in urine become too concentrated → supersaturated → solvent precipitates → crystals form
  • Occurs when there is an increase in solute or a decrease in solvent (dehydration)
  • Crystals make stones which cause obstruction → hydronephrosis (obstruction and dilation of renal pelvis → lasting kidney damage)
  • Stones are made of: calcium oxalate (most common, in acidic urine), calcium phosphate (in alkali urine), calcium carbonate, uric acid, crystine, drug precipitants
  • Stones are most commonly found in pelviureteric junction (most common), pelvic brim, vesicoureteric junction
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4
Q

Renal Colic - Types

A
  • Upper urinary tract - renal stones, ureteric stones
  • Lower urinary tract - bladder stones, prostatic stones, urethral stones
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5
Q

Renal Colic - Causes (7)

A
  • Anatomical - congenital (horseshoe, duplex, pelviureteric junction obstruction, spina bifida) and acquired (obstruction, trauma, reflux)
  • Urinary - dehydration, too much solutes
  • Infection - UTIs with organisms that produce urease (Proteus, Klebsiella, Pseudomonas) produce specific types of stones called staghorn calculus
  • Hypercalciuria - increased urinary calcium excretion (caused by hyperparathyroidism - most common, hypercalcaemia, eating too much calcium, prolonged immobilisation - bone reabsorption)
  • Hyperoxaluria - increased oxalate means more clacium oxalate (eating too much oxalate, malabsorption, autosomal recessive enzyme deficiency)
  • Uric Acid Stones - patients with ileostomies as they loose more bicarbonate so have acid urine so uric acid is more soluble
  • Cystine stones - caused by an autosomal recessive condition, cystinuria
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6
Q

Renal Colic - Prevention (6)

A
  • Reduce dietary salt / sodium
  • Normal dairy intake
  • Healthy protein intake (50-100g/day)
  • Lose weight
  • Active lifestyle
  • Stop smoking
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7
Q

Renal Colic - Risk Factors (9)

A
  • Anatomical abnormalities
  • Hypercalciuria
  • Hypercalcaemia
  • Hyperparathyroidism
  • Family history
  • Hypertension
  • Gout
  • Immobilisation
  • Dehydration
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8
Q

Renal Colic - Differential Diagnosis (9)

A
  • Ruptured AAA
  • Diverticulitis
  • Appendicitis
  • Pylonephritis
  • Acute pancreatitis
  • Ectopic pregnancy
  • Ovarian cyst
  • Ovarian torsion
  • Testicular torsion
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9
Q

Renal Colic - Symptoms (6)

A
  • Asymptomatic
  • Loin pain, rapid onset, unable to get comfy, radiates to groin, N&V
  • UTI symptoms - dysuria (painful urinating), strangury (burining urinating), urgency, frequency
  • Shivering
  • Recurrent UTIs
  • Bladder distension
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10
Q

Renal Colic - Investigations (6)

A
  • History - excess Vit D consumption leads to hypercalcaemia, excess rhubarb or tea leads to high oxalate
  • X-Ray KUB (kidney, urethre, bladder) - first line
  • Non-contrast CT KUB - gold standard
  • Ultrasound - sensitive for hydronephrosis, good for pregnant or youth
  • Urine dipstick - blood traces
  • Bloods - FBC, U&E, Calcium, Uric acid, Creatinine
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11
Q

Renal Colic - Treatment (9)

A
  • Ureteric stones
    • Analgesia - diclofenac IV 75mg
    • Anti-emetics - metoclopramide
    • Allow 2 weeks for it to pass
    • Drainage if septic
    • ESWL (Extracorpeal Shock Wave Lithotripsy) - non invasive procedure breaks down stones, use if <1cm
  • Kidney stones
    • Analgesia - Diclofenac
    • Anti-emetics - Metoclopramide
    • ESWL - for stones 1-2cm
    • Surgical - uteroscopy, percutaneous nephrolithotomy, nephrectomy
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12
Q

Renal Colic - Complications (3)

A
  • Small stones migrate to ureter
  • Large stones occlude calyces or uteric pelvic junction
  • Chronic damage especially if it gets infected
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13
Q

AKI - Description

A

Abrupt deterioration (hours-days) in renal function (raised serum urea and creatinine) due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis. Usually reversible

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14
Q

AKI - Criteria for Diagnosis

A
  • Creatinine increased >26 micromol/L in 48 hours
  • Creatinine increased >50%
  • Urine output <o.5ml/kg/hr for more than 6 hours
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15
Q

AKI - Epidemiology

A
  • Associated with diarrhoea, haematuria, haemoptysis, hypotension, urine retention
  • Common in elderly
  • 25% with sepsis and 50% with septic shock have AKI
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16
Q

AKI - Causes

A
  • Pre-renal - reduced blood flow to kidney leading to reduced GFR
    • Shock, hypovolaemia, hypotension, Renal artery thrombosis, sepsis, renal hypoperfusion
  • Renal - kidney can’t filter blood properly, cells damaged so reabsorption and secretion impaired
    • Acute tubular necrosis, Nephrotoxins, Glomerulonephritis, Acute interstitial nephritis, Infection, Vasculitis, Malignant hypertension, Autoimmune disease
  • Post-renal - blockage of kidney reducing outflow
    • BPH, Kidney stones, Cancer, Blood clot
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17
Q

AKI - Risk Factors (8)

A
  • > 75
  • DM
  • HF
  • Sepsis
  • PVD
  • Family history
  • Drugs
  • Dehydration
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18
Q

AKI - Symptoms (11)

A
  • Asymptomatic in early stages
  • Oliguria (decreased urine output)
  • Anuria (no urine output)
  • Ddehydration
  • N&V
  • Tremor, weakness, fatigue, confusion
  • Breathlessness (anaemia and pulmonary oedema from volume overload)
  • Tachycardia
  • Peripheral oedema (from hypertension)
  • Poor tissue turgor
  • Postural hypotension (dehydration)
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19
Q

AKI - Investigations (5)

A
  • Urine dipstick - glomerulonephritis suggested by haematuria and proteinuria
  • Bloods - Anaemia and high ESR suggest myeloma or vasculitis
  • Renal ultrasound - shows obstruction, small kidney indicates CKD
  • Monitor urine output
  • KUB XR and non-contrast CT
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20
Q

AKI - Complication

A

Hyperkalaemia - when kidneys fail they go into cardiac arrest

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21
Q

AKI - Treatment (4)

A
  • Treat underlying cause - pre-renal (fluids, antibiotics), post-renal (catheteris, cystoscopy)
  • Stop nephrotoxic drugs - NSAIDs (aspirin, diclofenac, ibuprofen), ACEi (Ramipril), Gentamicin, Amphotericin
  • Treat complications - hyperkalaemia, pulmonary oedema, uraemia, acidaemia
  • Dialysis
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22
Q

CKD - Definition

A

Long standing, usually progressive abnormality of the kidney or a reduction of GFR to <60ml/min/1.73m2 for >3 months

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23
Q

CKD - Epidemiology

A
  • 6-11% incidence
  • Risk increases with age
  • More females
  • Highest mortality from cardiac complications
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24
Q

CKD - Classification/staging

A
  • Stage 1: >90ml/min - Normal GFR with evidence of renal damage
  • Stage 2: 60-89 - Slight decrease GFR with evidence of renal damage
  • Stage 3A: 45-59 - Moderate GFR decrease with or without evidence of renal damage
  • Stage 3B: 30-44 - Moderate GFR decrease with or without evidence of renal damage
  • Stage 4: 15-29 - Severe GFR decrease with or without evidence of renal damage
  • Stage 5: <15 - Established renal failure
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25
Q

CKD - Pathology

A
  • Progression of end-stage kidney disease (ESRF) with varying speed of decline
  • Many nephrons are failed so burden of filtration goes to functioning nephrons which experience hyperfiltration (increased flow per nephron as blood flow remains the same) → glomerular hypertrophy and reduced arteriolar resistance
  • Stress means increased failure of functioning nephrons and cycle continues
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26
Q

CKD - Pathology of bone disease

A

Increased renal phosphate and reduced 1,25-dihydroxyvitamin D → reduced serum calcium → compensatory increase PTH → skeletal decalcification

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27
Q

CKD - Pathology of Anaemia

A

reduced erythropoietin production → less RBCs → anaemia. reduced production and excretion of hepcidin builds up and inhibits iron absorption → anaemia

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28
Q

CKD - Pathology of Hyperkalaemia

A

less potassium excretion → build up in blood

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29
Q

CKD - Pathology of CVD

A

decreased filtration → renin release → increase BP → cardiomyopathy, pericarditis (uraemia), bleeding (urea stops platelet binding)

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30
Q

CKD - Causes (7)

A
  • Hypertension - walls thicken to withstand pressure → narrow lumen → less blood and O2 to kidney → ischaemic injury. Immune cells release TGF-B1 in damaged glomerulus → mesangial cells regress to immature mesangioblast and secrete extracellular matrix → glomerulosclerosis
  • DM - Excess glucose sticks to proteins making efferent arterioles stiff and narrow → obstruction for blood leaving glomerulus → hyperfiltration → supportive mesagnial cells secrete structural matrix → increased size of glomerulus → glomerulosclerosis
  • Glomerular disease - Nephrotic syndrome damages glomerular capillary call and decreases tubular protein reabsorption → renal tubular cell damage → inflammation → fibrosis of proximal tubular cells
  • PKD
  • SLE (Systemic Lupus Erythematosus
  • Obstructive uropathy
  • Nephrotoxic drugs
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31
Q

CKD - Risk Factors (9)

A
  • DM
  • Hypertension
  • Age
  • Female
  • CVD, IHD, PVD
  • SLE
  • Family history
  • UTIs
  • BPH
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32
Q

CKD - Symptoms (11)

A
  • Asymptomatic in early stages
  • Urinary - oliguria, haematuria, proteinuria, nocturia, polyuria
  • Non-specific - N&V, anorexia, itching, hiccups, lethargy, tremors, convulsions
  • Bone disease - osteomalacia, osteoporosis, osteosclerosis
  • Anaemia - pallor, lethargy, exertional breathlessness, bruising
  • Hyperkalaemia - cardiac arrhythmias/arrest, weakness/paralysis, metabolic acidosis
  • CVD - uraemic pericarditis, hypertension, PVD, HF
  • Neurological - confusion, coma, fits
  • Volume overload - pulmonary oedema, dyspnoea, ankle oedema
  • Sexual dysfunction
  • Increased skin pigmentation (yellow)
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33
Q

CKD - Investigations (2)

A
  • Ultrasound - bilaterally small kidneys, excludes obstruction
  • FBC - anaemia, raised creatinine, phosphate,PTH, K+, renin and urea, decreased Ca2+
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34
Q

CKD - Treatment (7)

A
  • Treat underlying cause
  • Manage BP (ABCD) - ACEi, Beta Blocker, Calcium channel blocker, Diuretic
  • Statins - if GFR <60
  • Lifestyle changes
  • Stop nephrotoxic drugs
  • Dialysis
  • Transplant
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35
Q

CKD - Complications (8)

A
  • Hyperkalaemia
  • Osteoporosis - GFR <30 (give Bisphosphonates)
  • Vit D deficiency (give Cholecalciferol)
  • Anaemia
  • Metabolic acidosis
  • Pruritis
  • Pericarditis
  • Hypertension
36
Q

ADPKD - Description

A

Multiple cysts develop gradually resulting in renal enlargement, kidney tissue destruction and gradual renal failure

37
Q

ADPKD - Epidemiology

A
  • Most common inherited kidney disease
  • Presents 20-30
  • More male than female
  • Homozygous babies won’t survive
38
Q

ADPKD - Causes (2)

A
  • Mutation in PKD1 gene (85%) on chromosome 16 - more severe, earlier onset
  • Mutation in PKD2 (15%) on chromosome 4 - less severe, later onset
39
Q

ADPKD - Risk Factors (3)

A
  • Family history of APKD
  • End-stage renal failure
  • Hypertension
40
Q

ADPKD - Pathology

A
  • PKD1 encodes polycystin 1 which regulates tubular development in kidneys
  • PKD2 encodes polycystin 2 which functions as a calcium ion channel
  • Polycystin complex is in cilia responsible for sensing flow in the tubule
  • Disruption means reduced cytoplasmic Ca2+ → defective ciliary signalling and disorientated cell division in principal cells → cyst formation
  • Mechanical compression, apoptosis of healthy tissue and reactive fibrosis → loss of renal function
  • Rate of decline is dependent on growth and size of cysts
41
Q

ADPKD - Symptoms (7)

A
  • Acute loin pain
  • Abdominal discomfort
  • Nocturia
  • Haematuria
  • Hypertension
  • Bilateral kidney enlargement
  • UTIs and pyelonephritis
42
Q

ADPKD - Differential Diagnosis (4)

A
  • Acquired and simple cysts
  • ARPKD
  • Medullary sponge kidney
  • Tuberous sclerosis
43
Q

ADPKD - Investigations (3)

A
  • History - family history
  • Ultrasound - diagnostic if 15-39 years ≥ 3 cysts, 20-59 ≥ 2, >60 ≥ 4, <30 with family history at least 2
  • Genetic testing - PKD1 or PKD2
44
Q

ADPKD - Treatment (5)

A
  • Nothing slows progression
  • BP control with ACEi (Ramipril)
  • Laparoscopic removal to help pain
  • Nephrectomy
  • Renal replacement therapy for ESRF
45
Q

ARPKD - Epidemiology

A
  • Rarer than ADPKD
  • Disease of infancy
46
Q

ARPKD - Cause

A

PKHD1 mutation on long arm of chromosome 6

47
Q

ARPKD - Symptoms (3)

A
  • Mostly present in infancy with multiple renal cysts and congenital hepatic fibrosis
  • Can cause renal failure before birth → fetus has less urine → oligohydramnios (low amniotic fluid)→ potter sequence (developmental abnormalities e.g. clubbed feet, flattened nose)
  • 30% develop kidney failure
48
Q

ARPKD - Differential Diagnosis (4)

A
  • ADPKD
  • Multicystic dysplasia
  • Hydronephrosis
  • Renal vein thrombosis
49
Q

ARPKD - Investigations (3)

A
  • Ultrasound
  • CT and MRI to monitor liver disease
  • Genetic testing
50
Q

ARPKD - Treatment (6)

A
  • No treatment
  • BP control with ACEi or ARBs
  • Laparoscopic removal
  • Nephrectomy
  • Renal replacement therapy for ESRF
  • Liver transplant
51
Q

Renal Cell Carcinoma - Epidemiology

A
  • Malignant cancer of proximal convoluted tubular epithelium
  • Often asymptomatic and discovered incidentally
  • 25% have metastasis at presentation
52
Q

Renal Cell Carcinoma - Types

A
  • Clear cell (80%)
  • Papillary (15%)
  • Chromophobe (5%)
53
Q

Renal Cell Carcinoma - Symptoms (5)

A
  • Vagure loin pain
  • Haematuria
  • Abdo mass
  • Varicocele
  • Anaemia
54
Q

Renal Cell Carcinoma - Investigations (3)

A
  • Ultrasound - 1st line
  • Renal biopsy - diagnostic
  • CT chest/abdo/pelvis - more sensitive than ultrasound
55
Q

Renal Cell Carcinoma - Treatment

A

Nephrectomy or partial nephrectomy if bilateral - 1st line

56
Q

Renal Cell Carcinoma - Complications (4)

A

Paraneoplastic changes - polycythaemia, hypertension, hypercalcaemia, Cushing’s

57
Q

Nephrotic Syndrome - Description

A

Protein leaks due to inflammation of podocytes

58
Q

Nephrotic Syndrome - Pathology

A

Inflammation from immune cells (IgG) → damage of podocytes → protein leakage (albumin) → increased liver activity to increase albumin → consequential increase in cholesterol and coagulation factors → reduced oncotic pressure → oedema → blood volume decrease, RAAS stimulation, exacerbation

59
Q

Nephrotic Syndrome - Symptoms (5)

A
  • Proteinuria (>3.5g/day) - damaged glomerulus is more permeable → more protein from blood into nephron
  • Hypoalbuminaemia - albumin leaves blood
  • Oedema (periorbital and arms) - oncotic pressure falls due to less protein in blood → lower osmotic pressure → water driven out of vessels into tissues
  • Hyperlipidaemia - loss of protein = less lipid synthesis → more lipid in blood → more in urine
  • Breathlessness
60
Q

Nephrotic Syndrome - Causes (10)

A
  • Primary - membranous glomerulonephritis (GN), minimal change disease, focal segmental glomerulosclerosis, membranoproliferative GN
  • Secondary - diabetic nephropathy, SLE, amyloidosis, Hep B/C, myeloma, drugs
61
Q

Nephrotic Syndrome - Investigations (4)

A
  • Urine dipstick - haematuria, proteinuria
  • Bloods - FBC, ESR, U&Es, creatinine
  • Renal ultrasound
  • Needle biopsy and microscopy - gold standard
62
Q

Nephrotic Syndrome - Treatment (3)

A
  • Steroids in children
  • Diuretics for oedema
  • ACEi/ARBs for proteinuria
63
Q

Nephrotic Syndrome - Complications (4)

A
  • Infections
  • Thromboembolism
  • Hypercholesterolaemia
  • Chronic renal failure
64
Q

Nephritic Syndrome - Description

A

Blood vessels inflamed → blood leaks out

65
Q

Nephritic Syndrome - Symptoms (7)

A
  • Haematuria - can be visible or non-visible
  • Reduced GFR - hypercellular glomeruli → decreased blood flow and leaks BM → reduced filtration
  • Oliguria
  • AKI symptoms
  • Proteinuria - <2g in 24hrs
  • Oedema - periorbital, leg and sacral
  • Hypertension
66
Q

Nephritic Syndrome - Causes (8)

A
  • Primary - IgA Nephropathy (most common cause), mesangiocapillary GN, diffused proliferative GN
  • Secondary - post-streptococcal GN, vasculitis, SLE, Goodpasture’s, Cryoglobulinaemia
67
Q

Nephritic Syndrome - Investigations (4)

A
  • Urine dipstick - haematuria, proteinuria and RED CELL CLASTS (differentiates nephritic and nephrotic)
  • Bloods - FBC, ESR, U&Es, creatinine
  • Renal biopsy
  • Renal ultrasound
68
Q

Nephritic Syndrome - Treatment (2)

A
  • Corticosteroids
  • Hypertension treated with ACEi, salt restriction, loop diuretics (oral furosemide) and CCB (amlodipine)
69
Q

Von Hippel-Lindau - Description

A

Rare genetic disorder - mutation of tumour suppressor gene VHL (chrom 3) 20% are de novo mutations (recent mutation)

Benign tumours and cysts in many organs and malignant tumours in certain locations

70
Q

Von Hippel-Lindau - Pathology

A

VHL normally regulates hypoxia inducible factor (HIF) which promotes transcription of PDGF and VEGF

71
Q

Von Hippel-Lindau - Tumour Locations (6)

A
  • CNS (haemangioblastoma)
  • Liver
  • Lungs
  • Pancreas (malignant neuroendocrine)
  • Adrenals (phaeochromocytoma)
  • Renal cell carcinoma (in 70% with VHL mutation)
72
Q

Von Hippel-Lindau - Symptoms (4)

A
  • Renal cell carcinoma - haematuria, flank pain, abdominal mass
  • B symptoms - weight loss, fever, fatigue, night sweats
  • CNS - ataxia, headaches, N&V
  • Phaeochromo - headaches, sweating, palpitations, hypertension
73
Q

Von Hippel-Lindau - Investigations (5)

A
  • Screening - annual BP and abdo ultrasound
  • CT head, chest and abdo
  • MRI - baseline scan, tumour staging
  • Bloods - FBC, U&Es, LFTs
  • Renal biopsy - histology of tumour
74
Q

Von Hippel-Lindau - Treatment (2)

A
  • Surgery - once renal cell carcinoma >3cm
  • Nephrectomy
75
Q

Wilm’s Tumour - Description

A
  • Affects kidneys in children (usually <5 years)
  • Early tumours have 90% cure chance, worse if its metastatic
76
Q

Wilm’s Tumour - Symptoms (7)

A
  • Abdo mass
  • Abdo pain
  • Haematuria
  • Lethargy
  • Fever
  • Hypertension
  • Weight loss
77
Q

Wilm’s Tumour - Investigations (3)

A
  • Ultrasound - 1st line
  • CT/MRI - staging
  • Biopsy - diagnostic
78
Q

Wilm’s Tumour - Treatment (2)

A
  • Nephrectomy 1st line
  • Chemo or radiotherapy if that doesn’t work
79
Q

IgA Nephropathy - Epidemiology

A
  • Most common cause of nephropathy worldwide
  • Usually presents in childhood during GI or respiratory infection
80
Q

IgA Nephropathy - Pathology

A
  • IgA depositis in mesangium of kidney → kidney attacked by anti-glycan autoantibodies → complement pathway activation → release of pro-inflmmatory cytokines and macrophages
  • Type of type III hypersensitivity so inflammation occurs as deposition site not site of formation
81
Q

IgA Nephropathy - Symptoms (7)

A
  • Haematuria
  • Proteinuria
  • Hypertension
  • Oedema
  • Oliguria
  • Uraemia
  • Decresed GFR (moderate-severe)
82
Q

IgA Nephropathy - Investigations (3)

A
  • Biopsy - diffuse mesangial IgA deposits, sub-endothelial and sub-epithelial deposits
  • Light microscopy - mesangial proliferation
  • Urine dipstick
83
Q

IgA Nephropathy - Treatment (2)

A
  • Supportive - BP control, diet, lower cholesterol
  • Immunosuppression - steroids with cyclophosphamide (in induction) or azathioprine (in remission)
84
Q

Minimal Change Disease - Pathology

A

Cytokines attack foot processes of podocytes, shrinkage/blunting of podocytes leads to protein leakage. Most common in children

85
Q

Minimal Change Disease - Investigations (2)

A
  • Renal biopsy
  • Electron microscopy
86
Q

Minimal Change Disease - Treatment (2)

A
  • Corticosteroids and Cyclophosphamide
  • Cyclosporine rather then Cyclophosphamide for frequent relapses

Phase 2a (15 decks)

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