Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
53 Cards in this Set
- Front
- Back
|
Acute kidney injury: definition |
Acute reduction in renal blood flow => dec. GFR Etiology of AKI consists of 3 main mechanisms: prerenal, intrinsic, and obstructive. |
|
|
Acute tubular necrosis histology |
- Patchy or diffuse denudation of the renal tubular cells - Loss of brush borders - Flattening of the epithelium - Detachment of cells - Formation of intratubular casts - Dilatation of the lumen |
|
|
Principle behind urea:creatinine test |
Both urea & creatinine are freely filtered by the glomerulus; but urea reabsorbed by the tubules can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption). - Urea metabolite from dietary protein & tissue protein turnover. - Creatinine muscle creatine catabolism |
|
|
Causes increase urea:creatinine |
(drivers can GPS) - dehydration/prerenal failure - corticosteroids - GI haemorrhage - protein-rich diet - severe catabolic state |
|
|
Decreased urea:creatinine |
(Simple SR) - severe liver dysfunction - intrinsic renal damage - malnutrition - pregnancy - low protein diet - SIADH - rhabdomyolysis |
|
|
Urea:creatinine in post renal cause of AKI (also normal values) |
40-100:1 |
|
|
Intrinsic renal damage Urea:creatinine |
<40:1 – (urea unable to be reabsorbed, creatinine normally not reabsorbed-> ratio gets closer to 1) |
|
|
pre-renal AKI urea:creatinine |
>100:1 |
|
|
AKI ix |
- Urea and creatinine (elevated) - U:C ratio - CBE - USS: look at existing renal disease/obstruction of the urinary collecting system - Biopsy for intrarenal path - Serology for assoc. condit: eg. schistocytes in disorders such as hemolytic-uremic syndrome & thrombotic thrombocytopenic purpura - Aortorenal angiography: to diagnose renal vasc. diseases, such as renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, & certain cases of necrotizing vasculitis (eg, polyarteritis nodosa) |
|
|
AKI mgmt aims |
Maintenance of volume homeostasis and correction of biochemical abnormalities |
|
|
AKI MGMT |
- Frusemide for fluid overload - Correct severe acidosis w bicarb - Correct of hyperkalemia - Correction of haematologic abnormalities - Vasodilation with dopamine or fenoldopam |
|
|
Isosthenuria definition |
Excretion of urine whose specific gravity (concentration) is neither greater (more concentrated) nor less (more dilute) than that of protein-free plasma, typically 1.008-1.012. - reflects renal tubular damage/failure of renal medullary function. - Acute (ATN) or chronic renal failure - Happens in sickle cell trait (heterozygous sickle cell disease) |
|
|
Urinary Tract Infection definition |
- Sx suggestive of UTI + evidence of pyuria+ bacteriuria on urinalysis/MC&S - If asymptomatic + 100,000 CFU/mL = asymptomatic bacteriuria; only requires treatment in certain patients (e.g. pregnancy) |
|
|
Definition complicated UTI |
- Structural and/or functional abnormality - male patients - immunocompromised - diabetic - iatrogenic complication - pregnancy - pyelonephritis - catheter-associated |
|
|
Typical UTI organisms |
- E. coli (70% to 95% uncomp cases) - Staphylococcus saprophyticus (5-10% of cases) - E.coli 20-50% complicated cases, also caused by klebsiella, proteus, enterococci) |
|
|
Define focal, segmental, diffuse, proliferative |
Focal: some but not all the glomeruli contain thelesion Diffuse (global): most of the glomeruli (>75%)contain the lesion Segmental: only a part of the glomerulus is affected Proliferative: an increase in cell numbers due to hyperplasiaof one or more of the resident glomerular cells with or without inflammation. |
|
|
Primary causes of nephrotic syndrome |
- Minimal change disease - Membranous nephropathy - Focal segmental glomerulosclerosis (FSGS) - Mesangiocapillary GN (MCGN). |
|
|
Secondary causes of nephrotic syndrome |
- Hepatitis B/C (usually membranous, hep C can cause MCGN) - SLE (class V lupus nephritis causes a membranous pattern) - Diabetic nephropathy - Amyloidosis - Paraneoplastic (usually membranous pattern) - Drug related (again usually membranous—NSAIDS, penicillamine, anti-TNF, gold). |
|
|
S/s nephrotic syndrome |
- Oedema (often severe and rapid onset in dependent areas eg. legs, periorbitally) - Ask about acute or chronic infections, drugs, allergies, systemicsymptoms suggestive of autoimmunity or malignancy. - Signs: Urine dip shows ++++protein, albumin is low, BP is usually normal or mildly increased, renal function is usually normal or mildly impaired. |
|
|
Most common cause of nephrotic syndrome kids |
- Minimal change disease (90% get better with steroid trial) - Avoid biopsy - Can be assoc w NSAIDs or paraneoplastic (commonly Hodgkin's lymphoma) - 20% of adult nephrotic |
|
|
Complications nephrotic syndrome |
• Susceptibility to infection (eg cellulitis, Strep infections+ spontaneous bacterial peritonitis) - Happens in up to 20% of adult px b/c of dec. serumIgG, dec. complement activity, dec. T cell function • Thromboembolism: (<40%): hypercoagulable state d/t inc. clotting factors + platelet abnormalities. • Hyperlipidaemia: inc. cholesterol+ triglycerides |
|
|
Histology Membranous nephrop |
- Thickened basement membrane - Effacement of pedicles - Ig and C3 deposition in subepithelium (granular and uniform) |
|
|
Histology MCD |
- Can only be seen on electron microscopy - Effacement of pedicles - Normalbasement memb |
|
|
Histology FSGS |
- Focal segmental sclerosis, affects juxtamedullary glomeruli first - Effacement of pedicles + focal areas of fusion - Discrete crescent shape IgM and C3 deposition |
|
|
Histology membranoproliferative type 1 |
- Thickening of basement memb w discrete deposits |
|
|
Histology membranoproliferative type 2 |
- Splitting of capillary memb. Enhanced lobulated appearance. Denser deposits - Denser deposits more visible IgA deposition - Deposits stain for C3 |
|
|
Nephrotic syndrome clinical def |
- Loss of 3g+/day of protein in urine OR on single spot urine collection, presence of 2 g protein per gram creatinine. + low serum albumin level and oedema You also get high cholesterol and wee out all your Igs + Hypocalcemia (d/t low albumin, but assoc w bone probs) |
|
|
Reason for hypercoagulability in nephrotic |
- Urinary loss of anticoagulant proteins, such as antithrombin III and plasminogen + increase in clotting factors, especially factors I, VII, VIII, and X. |
|
|
Membranous nephropathy |
- 20–30% of nephrotic syndrome inadults; 2–5% in children - Mostly idiopathic, but can be associated with malignancy, hepatitis B, drugs (gold, penicillamine, NSAIDS) and autoimmunity (thyroid,SLE). |
|
|
Mesangiocapillary GN patho immune complex mediated |
- driven by circulating immune complexes, whichdeposit in the kidney =>activate complement via the classical pathway. - underlying cause can be found in most cases, eg hepatitis C, SLE and monoclonalgammopathies |
|
|
Mesangiocapillary GN patho complement mediated |
- less common than IC med. - involves persistentactivation of the alternative complement pathway - Extra-renal manifestations, eg Drusen in the retina |
|
|
Histology mesangiocapillary GN |
- Biopsy: mesangial and endocapillary proliferation, a thickened capillary basement membrane, double contouring (tramline) of the capillary walls. - Immunfluorescence: Ig staining, complement staining or light chains depending on cause. - Electron microscopy shows electron dense deposits. |
|
|
FSGS |
- Primary - Secondary (vesicoureteric reflux, IgA nephropathy, Alport’s syndrome, vasculitis, sickle-cell disease, heroin use - HIV is associated with thecollapsing subtype (poor prognosis). ~50% have impaired renal function. |
|
|
Nephritic syndrome definition |
o Inflammatory alteration ofglomerulus resulting in nephritis.
|
|
|
Nephritic syndrome s/s |
§ Overt haematuria: RBC casts and dysmorphic RBCs § Proteinuria § Hypertension § Renal failure § Dec. GFR § Azotemia (v increased nitrogen containing compounds (urea, creatinine) in blood) § Oliguria § Active urine sediment |
|
|
Types of nephritic syndrome |
§ Acute glomerulonephritis · Nephritis with short term renal failure § Crescentic glomerulonephritis · Nephritis with rapidly progressive renal failure § Chronic Glomerulonephritis § Chronic progression of renal failure |
|
|
Causes nephritic |
- Post-streptococcal glomerulonephritis – appears weeks after upper respiratory tract infection (URTI) - IgA nephropathy – appears within a day or two after a URTI. - Rapidly progressive glomerulonephritis (crescentic glomerulonephritis) - Goodpasture’s syndrome – anti-GBM antibodies against basal membrane antigens - Vasculitic disorder – Wegener’s granulomatosis / Microscopic Polyangiitis / Churg Strauss disease - Membranoproliferative glomerulonephritis – primary or secondary to SLE / Hepatitis B/C - Henoch-Schönlein purpura – systemic vasculitis – deposition of IgA in the skin & kidneys |
|
|
Rapidly Progressive/cresentic Glomerulonephritis definition |
• A subset of nephritic syndrome in which the clinical course proceeds over weeks to months • Clinical diagnosis, not histopathological • Any cause of GN can present as RPGN (except MinChange) • additional etiologies seen only as RPGN: Goodpasture’s syndrome and granulomatosis with polyangiitis (previously called Wegener's granulomatosis) |
|
|
IgA nephropathy definition/patho |
- Depositionof IgA polymers in the mesangium of the kidney due to aberrant glycosylation ofthe IgA1 molecule + dec liver clearance |
|
|
Polcystic Kidney Disease Autosomal dominant. epi and def APKD |
- 85% mutations in PKD1 (chrom 16), ESRF by age 50 - 15% have mutation PKD2 (chrom 4), ESRF by 70s |
|
|
Polcystic Kidney Disease Autosomal dominant. s/s |
- Can be silent for many years (family screening important) - renal enlargement w cysts - Abdo pain - Haematuria (haemorrhage into cyst) - Cyst infection - Renal calculi - Increased BP - Progressive renal failure Extrarenal: - Liver cysts - intracranial aneurysm=>SAH - Mitral valve prolapse, ovarian cysts, diverticular disease |
|
|
Autosomal recessive polycystic kids |
- Prevalence 1:40,000, chromosome 6. - Signs: Variable, many present in infancy with multiple renal cysts and congenital hepatic fibrosis. - There is currently no specific therapy. - Genetic counselling of family members is important. |
|
|
SLE nephropathy |
- Immune complex deposition |
|
|
Goodpastures |
- Lungs - Kidney disease - Kids - Autoimmune - Anti BM antibodies |
|
|
Medullary sponge kidney disease |
- Manifests in 30s - Genetic - recurrent UTI - Does not progress to ESRD - Haematuria - Stones - tx for sx - High fluid |
|
|
Medullary cystic disease |
- Cysts in collecting ducts=>blockage - ESRD |
|
|
"too late triad" RCC |
- Gross haematuria - Flank pain - Palpable mass |
|
|
RCC |
- 50% incidental finding - 30% already have mets at presentation - 20-30% more get them during course - Known for paraneoplastic syndromes |
|
|
Diabetic nephropathy. epi, histo |
- Diabetes responsible for 30-40% all ESRD (biggest cause) - Kidneys enlarge initially - Histo changes: *Mesangial expansion (glycation matrix proteins, earliest change) *Thickened GBM (also early change) *Glomerular sclerosis (hyaline narrowing of vessels around glom=>afferent artery dilation=>intraglomerular HTN) *Tubular atrophy - Interstitial fibrosis |
|
|
Criteria for diabetic nephropathy |
- Persistent albuminuria >300mg/d confirmed on 2 occasions >3months apart - Progressive decline in GFR - Elevated BP |
|
|
Who to expect diabetic nephropathy in |
• Passing of foamy urine - Have otherwise unexplained proteinuria - Diabetic retinopathy - Fatigue and foot edema secondary to hypoalbuminemia (if nephroticsyndrome is present) - Other associated disorders such as peripheral vascular occlusivedisease, hypertension, or coronary artery disease |
|
|
HTN nephropathy epi and diagnosis |
- 28% of px with ESRD, 2nd commonest cause in whites and commonest in blacks - Diagnosis based on clinical findings: *longstandinghypertension * htn retinopathy *LV dilation *minimal proteinurea (less than 0.5g/d) *progressive renal insufficiency |
|
|
HTN nephropathy patho |
- 2 mechs: 1. Tubular ischaemia *chronic HTN=>narrowing of preglomerulararteries and arterioles=>dec glom blood flow=>ischaemia 2. Glomerular hypertension andglomerular hyperfiltration * HTN =>someglomeruli become sclerotic. As compensation for loss ofrenal function, remaining nephrons vasodilate preglomerular arterioles=> inc in renal blood flow+glomerular filtration=>glom HTN+ hyperfiltration=>progressive glomerular sclerosis. - Also shown that there is a dec numberof pedicles |
