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65 Cards in this Set
- Front
- Back
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What is Oedema?
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Oedema (which means swelling) is the subcutaneous (interstitial) retention of salt and water, and is seen in a variety of clinical conditions
LT1 |
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Where may oedema be located?
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periorbital
sacral ankle lungs ..anywhere LT1 |
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What are the most common causes of oedema?
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Congestive cardiac failure
cirrhosis of the liver nephrotic syndrome renal failure Others -- idiopathic cyclical oedema, pregnancy, endocrine, drug causes of fluid retention and DVT, lymphoedema, nephritic syndrome LT1 |
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How can lymphoedema be clinically differentiated from other swellings?
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beyond stage 1 --> this is NON-PITTING oedema
LT1 |
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What are the main components of ECF?
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Na
Cl Bicarbonate LT1 |
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When fluid enters the tissues from capillaries - How is it removed?
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Lymphatics
Or Further down the capillary (distal) where the hydrostatic pressure has decreased and the osmotic pressure has increased LT1 |
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What are some of the basic mechanisms which lead to oedema?
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Decreased PLASMA ONCOTIC PRESSURE hypoalbuminaemia due to nephrotic syndrome, cirrhosis, protein-losing enteropathy or malnutrition)
INCREASED VENOUS PRESSURE DVT, IVC obstruction/thrombosis, retroperitoneal neoplasia CARDIAC Disease Congestive cardiac failure, tricuspid regurgitations PULMONARY HYPERTENSION Cor pulmonale CAPILLARY LEAKINESS Sepsis, ischemia with endothelial damage Increases in TOTAL-BODY SALT renal failure, cardiac failure, liver cirrhosis LT1 |
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What forces prevent oedema in the physiological setting?
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lymphatic flow
plasma oncotic pressure negative interstitial pressure LT1 |
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What do Pts get oedema in end stage renal failure and even after starting dialysis?
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kidney's inability to excrete salt and water
LT1 |
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What are the common signs of nephritic syndrome?
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haematuria + RBC Casts
proteinuria - small fluid retention hypertension uremia oliguria Azotemia - elevated blood nitrogen LT1 |
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What are the common signs of Nephrotic syndrome?
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oedema - peripheral, periorbital, pleura effusion, ascites
heavy proteinuria hypoalbuminaemia hyperlipidaemia LT1 |
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Fluid and electrolyte homeostasis involves a number of mechanisms, what are some of these?
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Changes in blood volume can result in a number of corrective physiological responses.
'Volume' receptors, sensing vascular stretch in the carotid sinus and aortic arch, increase SNS activity in response to volume depletion, and maintain blood pressure by vasoconstriction and renal salt and water retention. Antidiuretic hormone (ADH) is also secreted in volume depletion and stress states and increases permeability at the distal nephron, resulting in oliguria ('antidiuresis'). Low arterial pressure, sensed by the renal juxtaglomerular apparatus, stimulates RENIN secretion and angiotensin II (AII) production, which maintains blood pressure via a direct vasoconstrictor action. AII stimulates Na reabsorption at the proximal nephron, and generates ALDOSTERONE which increases Na reabsorption at the distal nephron. In response to overhydration, right atrial stretch receptors release ATRIAL NATURETIC peptide or factor (ANP or ANF) which mediates an acute, corrective natriuresis. Its role in long-term volume regulation is less certain. Tubuloglomerular feedback --> Renin Reabsorption is proportional to GFR LT2 |
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What infection commonly precedes acute nephritic syndrome?
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streptococcal infection
Leads to - Post-streptococcal glomerularnephritis LT2 |
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What are the common causes of nephrotic syndrome?
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glomerulonephritis (minimal change GN, FSGS -focal-segemental-glomerulosclerosis and membranous GN), diabetic nephropathy, vasculitis or renal amyloidosis.
Results in proteinuria, oedema, hypoalbuminaemia LT2 |
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What causes oedema in Congestive Cardiac Failure?
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combination of renal hypoperfusion, increased sympathetic drive, increased renin-angiotensin-aldosterone activity and increased proximal reabsorption of sodium
This leads to Renal salt + water retention --> oedema LT2 |
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T/F
Fluid retention and oedema are common and harmless in pregnancy. |
TRUE
Due to - rogesterone and prostaglandins can block the effects of the renin-angiotensin and aldosterone axis, and a state of increased blood volume, peripheral vasodilatation from vascular smooth muscle relaxation, and increased renal blood flow and GFR is observed. BUT - PREECLAMPSIA - BAD Due to endothelial damage, fluid balance disturbances --> picture of vascular spasm and hypertension despite intravascular depletion, is accompanied by glomerular proteinuria and oedema, coagulation disturbances, abnormal liver function tests and fitting in extreme cases. LT2 |
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What drugs, hormones, or other may induce sodium retention and/or exacerbate oedema?
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NSAIDs + COXII inhibitors
Block renal prostaglandin synthesis --> stimulating Na reabsorption at Loop. Liquorice - sensitises to mineralocorticoid effects Oestrogens Antihypertensives Esp. Vasodilators LT2 |
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T/F
Haematuria indicates renal parenchyma disease. |
False
May be anywhere along the tract. This is true of proteinuria. LT3 |
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Proteinuria indicates what kind of disease?
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Renal parenchymal disease
LT3 |
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What is the normal level of protein in the urine?
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<150mg/day
<30mg Albumin/L most of this is secreted into the tubules * This level does NOT give a positive Dip Stick LT3 |
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At what level of proteinuria does a Dip Stick test become positive?
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>300mg/L
Note - The test measures concentration not Amount --> therefore the test will be more positive in concentrated urine than dilute The use of Urinary Protein/Creatinine ratio can be used to overcome this problem LT3 |
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What is microalbuminuria?
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30-300mg/24hr
May be an early sign of glomerular disease, but may also be raised with vigorous exercise. LT3 |
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What are the components of normal glomerular capillary barrier?
What factors allow the barrier function? |
Endothelium, glomerular BM, epithelial podocytes
Function depends on -- intercapillary haemodynamics (pressure + flow rate), Negative charge at epithelial slit pores (due to PG - heparan sulphate, sialic acid), Specific molecules - nephrin * changes that affect the function -- immunological damage in glomerularnephritis or elevation of intracapillary pressure LT3 |
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What is the different between tubular, selective and non-selective proteinuria?
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selective - albumin mainly
non-selective - other larger molecules are filtered (later) Tubular - impaired reabsorption of low molecular weight proteins or their loss from tubular cells --> usually <1mg/24H * Excess quantities of small proteins (such as myoglobin) rarely cause proteinuria LT3 |
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What is the normal level of RBCs in urine?
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<5x10^6
* may increase with vigorous exercise LT3 |
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At what level is haematuria detected?
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Microscopy - 0.5x10^6
Dipstick - 5x10^6 Visually - 5x10^9 * Haematuria needs to be distinguished from reddish urine due to certain foods or drugs (rare - neg micro, neg dipstick) + contamination (vaginal or intestinal bleeding) + Heme pigment (myoglobin, haemoglobin - neg micro, pos dipstick) LT3 |
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What are the characteristics of haematuria and pathology in different parts of the renal system?
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Urine is uniform in colour except - bladder outlet, prostate, urethral lesions
Renal parenchyma - haematuria + proteinuria + active sediment (granular + cellular casts) Isolate haematuria - renal pelvis, ureter, bladder, urethra LT3 |
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What is the difference between glomerular Vs non-glomerular when looking at RBCs on phase contrast microscopy?
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Glomerular -
high % of distored (dysmorphic) RBCs Ei. IgA disease + Thin glomerular basement disease Non-Glomerular Normal (eumorphic) biconcave RBCs Ie. - urinary tract sepsis (S&S cystitis, pyelonephritis), calculi (Pain), renal tract tumours (painless) LT3 |
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What is nephrotic syndrome?
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When proteinuria is severe enough to cause hypoalbuminaemia (liver cannot compensate for the protein losses) which leads to oedema
As the fluid leaves the intravascular space - this causes a drop in BV --> stimulates kidneys to retain Na + Water via SNS + Renin-ATII-Aldo --> leads to further oedema Oedema initially - subcutaneous -- then eventually serous sacs - pleura, peritoneal * glomerular damage is not always seen on microscopy - may be due to loss of Negative charge LT4 |
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What are the most common types of Nephrotic syndrome?
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Children
Minimal lesion disease Focal sclerosing glomerulonephritis Adults membranous glomerulonephritis focal sclerosing GN (primary or secondary to other renal damage such as vascular disease or chronic interstitial nephritis) LT4 |
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What are the complications associated with Nephrotic Syndrome?
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INFECTIONS - In large fluid filled collections
THROMBOEMBOLIC Disease: DVT, PE, Renal vein thrombosis) - (decreased zymogens, anti-thrombin3 + platelet hyperaggregability) LIPID Abnormalities: Raised Chol., LDL, VLDL, TAGs (if severe) - due to increased protein production in the liver (including lipoproteins) RENAL FAILURE: due to decreased circulating volume. CRF may be due to underlying disease process - (Rx -BP, Lipid control) LT4 |
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What are the Principle Treatments for Nephrotic syndrome?
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1) Treat the cause. - Need Renal biopsy in adults (children usually just treated with steroids, and only biopsied if no response(
2) restrict salt 3) Adequate protein intake (not excessive) 4) diuretics - Loop (1st choice) +/- others 5) Measures to decrease proteinuria -- A number of drugs are helpful including ACE inhibitors and Cyclosporin. Non-steroidal drugs decrease proteinuria by decreasing GFR and should only be used with great care with close observation of electrolytes and renal function. 6) Control of lipid abnormalities in severe cases 7) decrease thromboembolic risk with anticoagulants (if indicated) 8) prevent and avoid infections LT4 |
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What are the main findings in nephritic syndrome?
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impaired GFR
Hypertension Active urinary sediment (Red + white cells + cellular casts in urine) * usually following streptococcal infection LT4 |
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What is the Predominant mechanism of injury to the kidney in glomerulonephritis?
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Injury via components of the immune system
LT5 |
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List some diseases of the glomerulus, excluding types of glomerulonephritis.
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Vascular diseases - ie. hypertensive nephrosclerosis
Metabolic Disease - Diabetic glomerulosclerosis Dysproteinaemias (amyloidosis) Inheritied dieases - Alport's LT5 |
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Damage to the kidneys can lead to 3 main physiological problems. What are these?
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loss of filtration SA - impaired ability to secrete water soluble toxins (ie urea)
Excessive filtration of RBCs (glomerular haematuria) Inadvertent filtration of plasma proteins (proteinuria) LT5 |
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Because of the diverse components of the immune system and how they cause damage to the kidney - a variety of tests are done in Pt with suspected glomerulonephritis.
List some of these. |
1. look for triggering INFECTIONs - HepB, HepC, Streptococcus
2. Autoantibodies associated with immune system overactivity -- Anti-nuclear, anti-GBM, Anti-nuclear cytoplasmic Antibodies 3. Circulating Immune COMPLEXES + a depletion of serum COMPLEMENT as a result of complement activation 4. Ig + C deposition within glomerulus on a renal cortical biopsy These investigations may assist in Dx + Rx LT5 |
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What are the mechanisms of Glomerular Injury?
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1. Direct Ab mediated damage - Anti-GBM Abs - Goodpasture's Syndrome
2. Immune Complex mediated damage - Lupus - 3. Damage due to mesangial IgA deposition 4. Damage due to immune vascular inflammation ("vasculitis") - Wegener's Granulomatosis 5. Disruption of glomerular function due to production of soluble 'permeability factors' - Ie. minimal change GN, FSGS LT5 |
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what is Goodpasture's Syndrome?
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Anti-GBM Abs cause direct damage to renal glomerulus (Ab's damage via complement activation)
* also causes haemorrhaging in the lungs Rx - plasmapheresis, immunosuppression LT5 |
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T/F
PT are usually symptomatic at 25ml/min/1.73m GFR |
False - they can be surprisingly asymptomatic.
Symptoms are universal at 10ml/min/1.73m LT6 |
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Uremia is due to the accumulation of urea.
T/F |
False
Although urea does build up - other substances also build up and and are important in causing symptoms - such at PTH, Beta2-microglobulin, organic phosphates LT6 |
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Renal failure Pts have a high incidence of heart disease. What factors are involved in the pathogenesis of heart disease.
And examples of heart diseases? |
Factors involved in the pathogenesis of heart disease include; fluid retention, anaemia, secondary hyperparathyroidism and metastatic vascular calcification, hyperlipidaemia, and the presence of an arteriovenous fistula.
Examples - ypertension, left ventricular hypertrophy, ischaemic heart disease, pericarditis and valvular heart disease LT6 |
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T/F
Gastrointestinal symptoms are unlikely to be associated with CRF. |
False
Usually associated with uraemia - anorexia, nausea, vomiting, weight loss + malnutrition (+ restricted diet), uraemic fetor, peptic ulceration LT6 |
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What is the Predominant mechanism of injury to the kidney in glomerulonephritis?
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Injury via components of the immune system
LT5 |
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List some diseases of the glomerulus, excluding types of glomerulonephritis.
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Vascular diseases - ie. hypertensive nephrosclerosis
Metabolic Disease - Diabetic glomerulosclerosis Dysproteinaemias (amyloidosis) Inheritied dieases - Alport's LT5 |
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Damage to the kidneys can lead to 3 main physiological problems. What are these?
|
loss of filtration SA - impaired ability to secrete water soluble toxins (ie urea)
Excessive filtration of RBCs (glomerular haematuria) Inadvertent filtration of plasma proteins (proteinuria) LT5 |
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Because of the diverse components of the immune system and how they cause damage to the kidney - a variety of tests are done in Pt with suspected glomerulonephritis.
List some of these. |
1. look for triggering INFECTIONs - HepB, HepC, Streptococcus
2. Autoantibodies associated with immune system overactivity -- Anti-nuclear, anti-GBM, Anti-nuclear cytoplasmic Antibodies 3. Circulating Immune COMPLEXES + a depletion of serum COMPLEMENT as a result of complement activation 4. Ig + C deposition within glomerulus on a renal cortical biopsy These investigations may assist in Dx + Rx LT5 |
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What are the mechanisms of Glomerular Injury?
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1. Direct Ab mediated damage - Anti-GBM Abs - Goodpasture's Syndrome
2. Immune Complex mediated damage - Lupus - 3. Damage due to mesangial IgA deposition 4. Damage due to immune vascular inflammation ("vasculitis") - Wegener's Granulomatosis 5. Disruption of glomerular function due to production of soluble 'permeability factors' - Ie. minimal change GN, FSGS LT5 |
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what is Goodpasture's Syndrome?
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Anti-GBM Abs cause direct damage to renal glomerulus (Ab's damage via complement activation)
* also causes haemorrhaging in the lungs Rx - plasmapheresis, immunosuppression LT5 |
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T/F
PT are usually symptomatic at 25ml/min/1.73m GFR |
False - they can be surprisingly asymptomatic.
Symptoms are universal at 10ml/min/1.73m LT6 |
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Uremia is due to the accumulation of urea.
T/F |
False
Although urea does build up - other substances also build up and and are important in causing symptoms - such at PTH, Beta2-microglobulin, organic phosphates LT6 |
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Renal failure Pts have a high incidence of heart disease. What factors are involved in the pathogenesis of heart disease.
And examples of heart diseases? |
Factors involved in the pathogenesis of heart disease include; fluid retention, anaemia, secondary hyperparathyroidism and metastatic vascular calcification, hyperlipidaemia, and the presence of an arteriovenous fistula.
Examples - ypertension, left ventricular hypertrophy, ischaemic heart disease, pericarditis and valvular heart disease LT6 |
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T/F
Gastrointestinal symptoms are unlikely to be associated with CRF. |
False
Usually associated with uraemia - anorexia, nausea, vomiting, weight loss + malnutrition (+ restricted diet), uraemic fetor, peptic ulceration LT6 |
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What causes lethargy + tiredness in CRF Pts>?
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anaemia due to reduction in EPO
Also due to iron, folate deficiency, occult bleeding, shortened RBC survival, uraemia --> also contribute to anaemia LT6 |
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What are the haematological problems/consequences from CRF?
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Anaemia - reduced EPO + other factors
Bleeding Diathesis (propensity to bleed) due to abnormal platelet function --> ecchymoses + purpura LT6 |
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What causes the itch/pruritis in CRF?
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Hyperparathyroidism due to phosphate retention and decreased activation of Vit D
LT6 |
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What are some of the main complications of chronic renal failure
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CARDIO
hypertension, left ventricular hypertrophy, ischaemic heart disease, pericarditis and valvular heart disease GIT Anorexia, N&V, weight loss, malnutrition, peptic ulcers HAEMATOLOGICAL Anaemia, bleeding diathesis BONE Abnormal bone turnover - osteitis fibrosa + osteomalacia HORMONAL hyperparathyroidism - Pruritis NEUROLOGICAL apathy, anorexia, altered sleep patterns, restlessness -- due to a central encephalopathy associated with uraemia - may progress to stupor, coma OTHER growth retardation in children, impaired immune response, thyroid dysfunction + sexual dysfunction LT6 |
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What are the signs of Uraemic encephalopathy ?
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flapping tremor, twitching, fasciculations, asterixis and convulsions, peripheral neuropathy (including restless legs, burning feet, paraesthesia, muscle weakness and autonomic neuropathy)
LT6 |
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What are the main metabolic problems associated with CRF?
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Accumulation of toxic metabolites - urea, guanido compounds, acidosis
Accumulation of nitrogenous compounds - due to failure of excretion + failure of catabolism by the kidney Impaired metabolism --> problems with ion transport, carbs, lipids, proteins, AA metabolism Insulin resistance Hyperlipidaemia Increased protein catabolism LT7 |
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T/F
A protein restricted diet can significantly help elevate the symptoms of uraema. |
True
- must be careful - do not want the Pt to be Protein malnourished LT7 |
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What are the common causes of CRF?
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*Glomerulonephritis
*Diabetic renal diseases Polycystic renal disease Reflux renal disease *Hypertension *Analgesic Renal disease *Obstructive Nephropathy * - These/ some forms of these disease may be treatable or preventable LT8 |
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What causal factors for CRF are preventable?
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early onset of diabetes
early onset of chronic infection both urinary and general sepsis early onset of hypertension vascular disease LT8 |
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What strategies have been implemented to modify causal factors of CRF?
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education
Lifestyle change urinary screening for infection + protein early intervention with reno-protective therapies (such as ACEi +AT2R blockers) LT8 |
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What are the pathological processes that occur in established renal failure (+ when function<30%), regardless of aetiology?
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There is an increase in intrarenal vascular resistance with development of intimal and medial hypertrophy, glomerular hypertension, tubular cell injury and the development of progressive interstitial inflammation and fibrosis.
This will lead to progressive impairment LT8 |
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Which causes of renal failure are potentially treatable or preventable?
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Diabetic renal disease
Hypertensive diseases Rapidly progressive glomerulonephritis cause by focal necrotizing or cresentic glomerulonephritis (Vasculitis, Goodpastures, Wegeners Granulomatosis, and polyarteritis nodosa) Drug-related interstitial nephritis Drug toxicity (cyclopsorin, penicillamine) Obstructive uropathy Possibly membranous GN LT8 |
