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;
25 Cards in this Set
- Front
- Back
|
What are the Five Types of Renal Disease? |
1. Pre-Renal |
|
|
What are the Common Causes of Pre-Renal Disease? |
- Volume depletion due to GI / renal / skin losses - Congestive heart failure - Hepatic Chirrosis - Renal Artery Steriosis - Shock due to sepsis / fluid loss |
|
|
What are the Most Common Causes of Post Renal Disease? |
- Malignancy - Renal Calculi - Congenital Abnormalities - Prostatic Disease |
|
|
What are the Most Common Causes of Glomerula Renal Disease? |
- Glomerulonephritis - Nephrotic Syndrome |
|
|
What are the Most Common Causes of Tubular Renal Disease? |
- Acute tubular Necrosis - Kidney Myeloma - Hypercalcaemia - Polycystic Kidneys |
|
|
What are the Most Common Causes of Interstitial Renal Disease? |
- Acute drug induced interstitial nephritis - Infection - Analgestic abuse |
|
|
How is Acute and Chronic Renal Disease Distinguished? |
- Knowledge of duration of the disease is important -Accuracy relies on previous information - Progressive rise in plasma creatinine levels is indicative of chronic disease whereas a sudden rise is indicative of acute - Disease is classifies on the rate at which the damage occurs - GFR and other information is also required |
|
|
What is Acute Renal Failure / Kidney Injury? |
- Rapid decline (few hours / days) of renal functioning / excretory functions of the kidneys
- Sharp rise in serum creatinine concentration, electrolyte disturbances and metabolic acidosis - Accounts for 5% of hospital admission- very common - May occur as a consequence of medical treatment |
|
|
What are the causes of ARF? |
Prerenal: Dehydration, fluid loss & hemorrhage Intrinsic Renal: Glomerulanephritis, Good Pastures & renal calculi Postrenal: Obstruction due to malignancy or prostate disease |
|
|
What is Chronic Renal Disease? |
- Kidney damage for at least 3 months - Markers include: Abnormal blood / urine tests and imaging studies - Classified into 5 stages - Usually only see symptoms around stage 3 and stage 5 involves kidney failure and GFR > 15 ml/min |
|
|
What is the Leading Cause / Contributor to End Stage Renal Disease? |
Diabetic Nephropathy: - Found in 33% of deaths - Overall risk for ESRD with diabetic nephropathy is 12 fold higher than in the general population |
|
|
What is Diabetic Nephropathy? |
- Chronic Microvascular Disease - Development related to the duration of diabetes / degree of hyperglycaemia - Develops in five stages - 40% with diabetes develop nephropathy |
|
|
What are the Stages of Diabetic Nephropathy? |
1. Early: Hyperglycaemia leads to an increase in kidney filtration and increased GFR with enlarged kidneys 2. Developing: Silent phase, continued hyperfiltration and hypertrophy. There is a progression to microalbuminuria 3. Overt: Damage progresses to clinical microalbuminurea 4. Late: Increased glom damage, protein in urine, plasma and creatinine levels increases, hyperfiltration decreases 5. End: GFR > 10 mil/min - renal replacement therapy required |
|
|
What is the Pathogenesis of Diabetic Nephropathy? |
- Not much known - thought to be genetic predisposition - Supported by fact some well controlled diabetics still get nephropathy and less well controlled individuals dont - Glomerula hyperfiltration leads to hypertrophy accelerating glomerula cell failure. |
|
|
What are Metabollic Pertubations of Diabetic Nephropathy? |
- Oxidants - Non-enzymatic glycosylation - Basement membrane thickening |
|
|
How is Diabetic Nephropathy Diagnosed? |
- Monitoring of urinary protein and BP - Specific tests for urinary albumin - Ratio of albumin: creatinine is most useful - Microalbuminurea: 30-300 ug / mg |
|
|
What is the Treatment for Diabetic Nephropathy? |
Improved glucose control: To reduce incidence of microalbuminuria Reduce Hypertension: Using ACE Inhibitors |
|
|
What is Glomerula Disease? |
- Glomerula contains small and large pores - Glomerula disease leads to a decrease in GFR and and increase in albumin / other large molecules being filtered |
|
|
What are Abnormalities of Glomerula Disease? |
- Nephrotic Syndrome - Protein Urea - Hypertension - Odema - Haematuria |
|
|
What are the Laboratory Investigations for Glomerula Disease? |
- Urinary Protein excretion - Serum creatinine levels - GFR - Glucose Conc - Urinary excretion of bence jones - Autoantibodies |
|
|
What Happens in Patients with Nephrotic Syndrome, and how is this Investigated? |
- Excretion of fewer smaller molecules due to a loss of filtration S/A - Increase in excretion of larger molecules due to an increase in larger pores Investigation: Given different sized molecules to assess the molecular sieving properties of the kidneys an increase in higher MW end is indicative of disease |
|
|
What is Tubulointerstitial Disease? |
- Injury to the Kidneys affecting the tubulointerstitium - Characterised by alterations in tubular fuction - Can be acute or chronic - Caused by: UTIs, drug tox and hypersensitivity |
|
|
What is Renal Tubular Acidosis? |
-Affects the proximal / distal tubules |
|
|
What is the Classification of type I, II and IV tubular acidosis? |
Type I: Occurs in distal tubules, severe acidosis, hypopotemia, caused by failure to secrete H+ Type II: Occurs in prox tubules, acidosis is present, hypopotaemia, caused by failed bicarbonate reabsorption by proximal cells. Type IV: Occurs in adrenal, acidosis is mild is present, hyperpotaemia, caused by a deficiency in aldosterone / resistance in its effects |
|
|
What are Renal Calculi / Stones? |
- 5-10% experience stones by age of 70 - More common in males - Made of substances which are poorly soluble and likely to crystallise e.g. calcium oxalate, magnesium ammonium phosphate, calcium phosphate, urate and cystine. |
