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108 Cards in this Set
- Front
- Back
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Glomerular Structures That are targeted
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1. afferent arteriole; humoral, immune, thrombotic, pressure...
2. efferent arteriole 3. GBM; thich, thin, deposits 4. Mesangial cell and matrix; expansion, deposits 5. Endothelial cells; hypertrophy, proliferation, atrophy, necrosis 6. Epithelial Cell- visceral and parietal |
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Consequences of Glomerular Disease
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- red. GFR
- salt and water retention - hypertension - active urinary sediment - proteinuria |
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Nephrotic Syndrome
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1. proteinuria >3.5g/day
2. hypoproteinemia 3. edema - lyperlipidemia - dec. GFR - thromboembolic events - high ESR, infection |
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Nephritic Syndrome
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- hematuria
- proteinuria - hypertension - renal failure |
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Crescentric Glomerulonephritis
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- nephritis with rapidly progressive renal failure
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Immunofluroscents
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mesangial vs capillary wall
granular vs linear linear= Good Pastures |
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Light Microscope
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proliferative vs exudative
endocapillary vs extracapillary global vs segmental diffuse vs focal special stains |
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Electron Micrscope
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mesangium
GBM endothelial and epithelial cells EDD |
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1o Glomerulonephritis
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minimal change disease
focal sclerosing GN IgA disease membranous GN crecentic GN post-infectious GN |
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2o GN
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SLE
vasculitis |
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Misc. GN
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DM
dysproteinaemias (eg amyloid) HT - benign & malignant tubulointerstitial disease |
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Minimal Change Disease
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nephrotic syndrome
- Tc ? - minimal change on LM, loss of podcyte foot processes on EM Minimal change disease Treatment • empirical prednisolone • cyclophosphamide / CsA for relapse BJN L13e Nephrotic syndrome • childhood 90% (peak 2-4 y.o., males) • adults 15-25% Characteristics • selective proteinuria / nephrotic syndrome • benign urine sediment, normal S. creatinine |
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Focal Sclerosing GN
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nephrotic syndrome
- microscopic haematuria - CRF |
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Membranous GN
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immune complex
tumours SLE drugs- penicillamine, gold - infections- Hep B CRF |
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IgA Disease
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abnormal IgA regulation
? in response to envirnomental Ag CAUSES microscopic haematuria LEADING to CRF |
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Postinfectious GN
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NEPHRITIC syndrome
Ab vs Microbial Products |
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Diabetic Glomerulopathy
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hyperglycaemia
HT microalbuminuria proteinuria CRF |
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SLE
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EM only
Ab vs DNA diffuse proliferative membranous NEPHRITIC diffuse proliferative |
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Proteinuria Definitions
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>0.15g/d
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Tamm Horsfall Protein
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added into the urine from the tubules
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Effects of DEC. Glomerular permeability
- clinically |
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Urinary Losses and their effects
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Glomerular Injury
- IMMUNE |
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Glomerular Injury
- INFLITRATION |
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Hypoalbuminemia
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Oedema
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Starlings Forces
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Edema (underfill hypothesis)
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DDx Oedema of renal and cardiovascular origin
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renal is everywhere
CV is mainly in the legs |
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Pitting edema Causes
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Renal disease:
• nephrotic syndrome • renal failure Other causes: • CCF • liver disease • hypoalbuminemia • venous obstruction |
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Lipiduria: Fat in the urine
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Causes of proteinuria
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1. Glomerulonephritis
• membranous GN • FSGS • minimal change nephropathy • mesangiocapillary (MCGN) 2. Other • diabetic nephropathy • hypertension • amyloid, chronic renal failure |
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GN & urine sediment
- nephritic vs nephrotic |
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Pathogenesis of membranous GN
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Causes of membranous GN
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Causes of membranous GN
1. Idiopathic 2. Secondary • Neoplasia (lung, colon) • SLE • RA, penicillamine, gold therapy • Hep B, Hep C, syphilis • sarcoid, schistosomiasis (rare) |
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Stage I M-GN
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Stage 2 M-GN
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Stage 3 M-GN
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spikes upset the podcytes and proteinuria starts
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Stage 4 M-GN
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by this stage Immunosuppression Tx is useless
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Membranous GN: Spikes
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Progress of membranous GN
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Treatment of Membranous GN
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Non-nephrotic
• women, young & children (65% remission) • diuretics & wait 6 months BJN L13e Nephrotic or persistent proteinuria • steroids • cyclophosphamide or chlorambucil • ACEI & statins |
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Focal & segmental glomerulosclerosis
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Biopsy: glomerular nomenclature
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Focal and segmental glomerulosclerosis
NAMING |
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FSGS pathological variants
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Pathophysiology of FSGS
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Secondary FSGS
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MCD: Pathophysiology
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Capillary loops in MCD
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Diabetic nephropathy
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Amyloidosis
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Definition of glomerulonephritis (“nephritis”)
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Definition of glomerulonephritis (“nephritis”)
• intra-glomerular inflammation • cellular proliferation -> hematuria (dysmorphic & casts) -> nephritic syndrome (hematuria & proteinuria) Glomerulopathy • non-inflammatory, no cellular proliferation -> proteinuria / nephrotic syndrome |
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Mechanisms of GN
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Antibody & glomerular injury
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Post-Streptococcal GN
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Pathogenesis of PSGN
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PSGN: renal pathology
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PSGN:
Dx Course Tx |
Diagnosis
• acute nephritis • ASOT & anti-DNAse B titre • low C3 (+ve RF, CIC, ANF, cryoglobulins) Course • diuresis & recovery 1-3 wks • 5 - 15% mild persistent urinary abnormalities Treatment • diuretics, supportive, ± steroids |
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Goodpastureʼs Δ
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Autoimmunity to BM
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- ONLY linear IgG IF Stain
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Goodpasture's
1. Glomerulonephritis |
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Goodpasture's
2. Pulmonary Hemorrhage |
haemorraghe severe enough that the patients die infront of you.
Tx HIGH dose steriods |
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Pulmonary hemorrhage
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Glomerular immune injury
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Clinical syndromes of glomerular Δ
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Asymptomatic proteinuria
Nephrotic syndrome Hematuria (asymptomatic or macroscopic) Acute glomerulonephritis (nephritis ± short term renal failure) Rapidly progressive glomerulonephritis (crescentic GN with renal failure) Chronic glomerulonephritis |
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Diseases & clinical syndromes
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Clinical Patterns of Hematuria
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IgA nephropathy
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Pathogenesis of IgA nephropathy
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more IgA in corculation and doesnt clear as well causing damage (proliferation of mesangial cells)
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Pathology of IgA Nephropathy
- under the microscope |
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Clinical IgA Nephropathy
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BJN L13f
• recurrent macroscopic hematuria “synpharyngitic” with viral LRTI or gastroenteritis • microscopic (glomerular) hematuria • chronic GN (hematuria ± proteinuria) • hypertension • ↓ renal function • CRF |
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Infections and Hematuria
( 2 cases) |
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Hematuria; IgA GN
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IgA nephropathy
- Dx - Course - Tx |
Diagnosis
• inferred in isolated glomerular hematuria • renal biopsy (if clinically severe) Natural history • usually benign • 10-20% CRF after 20 years (30% after 30yrs) • worse nephrotic, HT, ↑ creatinine, old male Treatment: control BP (no way to contral the IgA primarily) |
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Henoch Schonlein Purpura
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With kidney involvement, there may be a loss of small amounts of blood and protein in the urine, but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as pharyngitis.
HSP is a systemic vasculitis (inflammation of blood vessels) and is characterized by deposition of immune complexes containing the antibody IgA; the exact cause for this phenomenon is unknown. It usually resolves within several weeks and requires no treatment apart from symptom control, but may relapse in a third of the cases and cause irreversible kidney damage in about one in a hundred cases. |
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Thin membrane glomerulopathy
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Rapidly-progressing GN
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Rapidly-progressing GN
• relentless ↑ S. Cr (subacute or ARF) • active urinary sediment: blood & protein, red-cell casts • normal sized kidneys on US • Bx. crescentic GN • active treatment required Examples: Goodpastures, RPGN, Wegener's granulomatosis, microscopic polyangitis NB: crecentric pattern can be found in more than one disease pattern |
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Cresentic glomerulonephritis
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- the crecent squashes the glom. eventually killing it
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Vasculitis ;
Systemic Vascular Inflammation |
Clinical features
1. Constitutional symptoms • fever • arthralgia, weight loss, myalgia 2. Localised ischemia • claudication, mesenteric ischemia, bruits 3. Arterial tenderness • e.g. temporal arteritis |
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Renal vasculitis
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Small vessel vasculitis
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Classification of small vessel vasculitis
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SLE GN
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SLE Nephritic or Nephrotic?
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SLE Deposits in...
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SLE IF
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Clinical approach to hematuria
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Aim:
• distinguish glomerular vs. urological bleeding By: • urine analysis RBC morphology, proteinuria & cytology • imaging (± cystoscopic examination) Isolated hematuria -> exclusion of neoplasia • risk analysis for neoplasia (age, APC intake) • differential diagnosis USUALLY: Haematuria + proteinuria = GN |
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Is it hematuria?
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A. Is it urinary?
• or contamination from menses, perineal or urethral lesions B. Is it blood? • dipstick • microscopy |
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Other causes of reddish urine
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Drugs:
• metronidazole, nitrofurantoin, rifampicin, amitryptiline, adriamycin, α methyl-dopa phenytoin, sulphasalazine Aperients: • cascara, senna, anthroquinones Foods: • beetroot, rhubarb |
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Detection of Haematuria
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Hematuria by dipstick
False positives |
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Urine Microscopy
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Normal Individuals and RBC in urine
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1 - 2,000,000 RBC / day
< 8,000 RBC / ml 0 - 5 RBC / HPF < 10 RBC x 106 / L Glomerular hematuria (100% dysmorphic) |
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Red cell Morphology
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Categorisation of hematuria
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Normal urinary sediment
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Urinary cells
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Cellular casts
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Types:
• red cell cast • white cell cast • bacterial or mixed • epithelial BJN L13f • cellular elements incorporated within matrix formed in distal tubule & collecting ducts • Tamm-Horsfall protein & filtered proteins Types: • red cell cast (ONLY ONES THAT ARE ALWAYS PATHOLOGICAL) • white cell cast • bacterial or mixed • epithelial |
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RBC Casts
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Formation of RBC casts
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• glomerular damage & urinary bleeding
• addition of Tamm-Horsfall protein • release of red cell cast into urinary stream • modification of cast with passage |
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RBC casts: Stages of degeneration
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Leukocyte casts
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Bacterial casts
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Epithelial cell casts
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Basic work-up of persistent hematuria
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• MSU - MC&S, urine RBC morphology
• spot urine protein / creatinine • S. creatinine • sickle cell preparation (African, Indian, Arab) • IVP & bladder-renal U/S or spiral CT (kidneys / prone bladder / KUB) • urine cytology x 3 (may miss grade I TCC) • cysto-urethroscopy (if > 50 y.o.) |
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Renal biopsy stains
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Patterns of immunofluorescence
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