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31 Cards in this Set
- Front
- Back
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name the drugs that are associated with chronic TIN
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analgesics (acetaminophen, aspirin), herbal medicine (aristolochic acid), cisplatinum (for testicular cancer), lithium (for bipolar disorder)
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what is the mechanism for analgesic nephropathy of aspirin, caffeine?
of acetaminophen? |
Aspirin and caffeine lead to chronic vasoconstriction of renal vasculature renal ischemia
Chronic Acetaminophen leads to increased oxidative stress on kidneys --> ischemia of renal papilla/medulla |
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what is the normal progression of ischemia in the kidneys due to chronic analgesic usage?
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Aspirin and other NSAIDs are inhibitors of the cyclooxygenases. In the kidney, this inhibition results in decreased PGE2 concentration causing a reduction in blood flow. Because blood flow to the kidney first reaches the renal cortex (outside) and then the renal medulla (inside), the deeper structures of the kidney are most sensitive to decreased blood flow. Thus the innermost structures of the kidney, called the renal papillae, are especially dependent on prostaglandin synthesis to maintain adequate blood flow. Inhibition of cyclooxygenases therefore rather selectively damages the renal papillae, increasing the risk of renal papillary necrosis.[2]
This kidney damage may lead to progressive chronic renal failure, abnormal urinalysis results (pyuria), high blood pressure, and anemia. A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease. In chronic tubulointerstitial nephritis, the most serious long-term effect is kidney failure. When the proximal tube is injured, sodium, potassium, bicarbonate, uric acid, and phosphate intake may be reduced or changed, resulting in low bicarbonate, known as metabolic acidosis, low potassium, low uric acid known as hypouricemia, and low phosphate known as hypophosphatemia. Damage to the distal tubule may cause loss of urine-concentrating ability and polyuria. |
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what viruses can cause chronic TIN?
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EBV
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what hematopoietic dz's can cause chronic TIN?
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S-hemoglobinopathies (Sickle cell, sickle trait) - can cause necrosis of medulla, myeloma (light chains are directly toxicity to tubular cells)
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what heavy metal can cause chronic TIN?
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lead
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how would you differentiate acute and chronic interstitial nephritis from other causes of renal failure
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based on urinary findings:
1. urine sediment active in ACUTE inflammation (ie. acute interstitial nephritis or acute pyelonephritis) - pyuria, white cell casts, bacteriuria (with infection) 2. chronic tubulointerstial dz will tend to have bland urinary findings that reflect interstitial fibrosis and tubular atrophy |
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hematuria and red cell casts are commonly seen in _______nephritis
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glomerulo
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"muddy brown" epithelial cells and epithelial tubular cell and granular casts seen in urine sediment are characteristic of what dx?
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acute toxic tubulopathies (ie. aminoglycoside-induced ARF)
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what are different features b/w acute and chronic TIN in terms of clinical manifestations?
kidney size? |
acute = sudden dec in kidney fxn
chronic = slow dec in kidney fxn acute= normal to large kidneys chronic = small kidneys |
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which will present with cellular infiltration, edema, and normal glomeruli?
a. acute TIN b. chronic TIN |
A
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which will present with tubular atrophy, fibrosis, cellular infiltrates, and glomerulosclerosis?
a. acute TIN b. chronic TIN |
B.
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in acute tubulointerstitial nephritis, acute tubular cell insult leads to release of ______and ______ _____. this leads to what three things?
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cytokines; growth factors
1. edema (due to increased vascular permeability) 2. interstitial infiltration (due to inc recruitment of antigenically activated cells) 3. initiation of fibrosis (due to inc fibroblasts and matrix deposition) THESE ALL EVENTUALLY LEAD TO TUBULAR DYSFUNCTION, DECREASED CAPILLARY PERFUION AND ULTIMATELY, ACUTE LOSS OF RENAL FXN |
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what are some common etiology of acute TIN due to infections?
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bacterial - strept
viral - EBV, CMV fungal - candida, herpex simplex |
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what are the most common drugs that can cause acute interstitial nephritis (AIN...aka. ATIN)
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penicillins, sulfa drugs, NSAIDs (remember, onset of ATIN will be due to hypersensitivity rxns to these drugs acutely)
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acute drug-induced interstitial nephritis is due to a __________ rxn.
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hypersensitivity rxn
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common systemic manifestations that you will see with drug-induced acute TIN
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fever, rash, eosinophilia, flank pain
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what will the urine show with NSAID-induced acute TIN?
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pyuria (WBCs in the urine); microhematuria
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name some important metabolic disorders that can lead to acute TIN
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excessive urate, oxalate, calcium, heavy metals
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how would you diagnose acute TIN...
- for big kidneys? - for cellularity? - diagnostic gold standard |
ultrasound
gallium scan kidney biopsy |
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what are the tx options fo r acute TIN?
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- discontinue offending drug
- supportive measures - steroids (short, tapered course) - inform patient that they have hypersensitivity rxn |
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T or F. all chronic TIN begins as acute TIN.
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true...therefore, if you detect and tx ATIN early, you can prevent progression to chronic TIN.
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what is the main difference b/w acute and chronic TIN in terms of pathogenesis?
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fibroblasts ----> myofibroblasts (this increases deposition of fibrous tissue)
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infiltrating macrophages and fibroblasts have crosstalk via ____
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TGF-beta
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how will tubular dysfunction in chronic TIN affect the reabsorption and secretion of Na, bicarb, glucose, phosphate
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decrease reabsorption proximally and distally (of Na, bicarb, glucose, phosphate)...so you get natriuresis, acidemia, renal glucosuria, etc
decrease secretion (of hydrogen, potassium) so you get acidemia and hyperkalemia ***Big problem is the inability to reabsorb Na. and a bunch of other things like urea, glucose, phosphate, etc and they end up in the urine |
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TIN is primarily a defect of _____ reabsorption
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sodium
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which is more likely to be associated with hypertension?
a. glomerular dz b. TIN |
A. HTN doesn’t show up much in TIN until GFR goes below 25 (around renal failure). This is bc TIN is a defect of sodium reabsorption (so volume overload is not as much of a problem).
pts with glomerular dz will more likely have sodium retention |
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in what part of the kidneys are analgesic drugs concentrate the most?
a. papilla b. medulla |
A
The drugs are concentrated in the urine, in the papilla where max conc occurs. So people who sweat a lot are more prone to sustain analgesic nephropathy. |
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what are the 4 most common clinical conditions associated with renal papillary necrosis?
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DM
urinary tract obstruciton analgesic abuse S-hemoglobinopathy |
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pt comes in with a history of recurrent UTIs in childhood, now presenting with slowly progressive loss of kidney fxn.
dx? |
pt has reflux nephropathy due to combination of VUR (vesiculoureteric reflux) and chronic pyelonephritis (CPN), beginning in childhood.
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what is the final common pathway of CKD
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chronic TIN (glomerulosclerosis, tubular atrophy, fibrosis)
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