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97 Cards in this Set
- Front
- Back
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Statistically, how does renal blood flow decrease as a person reaches age 80?
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Statistically it decreases 1200 ml/minute to 600 ml/minute
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Why might serum creatinine be normal but GFR be decreased?
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As patients age, they loose muscle mass and are thus producing less creatinine, so even though the GFR is decreased and the creatinine should be proportionally increased, the decreased muscle mass masks the problem by causing an overall normal or lowered creatinine level.
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How would you estimate creatinine clearance from a random creatinine level?
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Creatinine clearance = 140 -
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In diabetic patients with a compromised GFR and a normal creatinine level, would Metformin be recommended?
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Must first test whether they have a normal GFR - most certain test is a 24 hour creatinine clearance urine test.
Creatinine clearance can be masked in an elderly patient with reduced muscle mass |
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How does tubular function change as one ages?
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Proximal tubular function declines with age, including maximal excretion of p-aminohuppurate and maximal resorption of glucose.
Renal threshold for glucose decreases with age - less glycosurea in given level of blood glucose. |
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How are fluid and electrolyte balances affected by age?
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The ability to conserve sodium loss in Na+ deprivation is impaired
Ability to excrete Na+ in response to increased Na+ load is impaired Ability to excrete K+ is impaired partly due to decreased RAAS Ca++ absorption in the gut is less due to decreased hydroxylation of active vitamin D, but tubular reabsorption not normally affected. |
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What are renal disease states associated with aging?
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Renal vascular disorders
Acute glomerulonephritis Nephrotic syndrome Acute Renal Failure Chronic Renal Failure Urinary Tract Infections |
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What kinds of Urethral/Ureteral Obstructions are common in older patients?
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Prostate - BPH, neoplasm
Pelvic tumors - ovarian, uterine Urinary tract tumors Urolithiasis ----- Urosepsis may also occur |
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If an asymptomatic patient has a positive urine culture, how should it be treated?
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Watch the patient for UTI symptoms - do not treat until symptomatic, as people who are chronically infected have an even higher likelihood of developing ABx resistance
Also, treatment doesn't have a significant enough demonstrable effect. |
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What may increase the risk of urosepsis, particularly in older patients?
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Post-renal problems
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List some general categories of causes for acute interstitial nephritis.
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Drugs
Infection Idiopathic |
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List some general categories of causes for chronic tubulointerstitial disease.
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Hereditary renal disease
Exogenous toxins Metabolic toxins Autoimmune disorders Neoplastic disorders Miscellaneous |
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What are some of the basic functional consequences of tubulointerstitial disease?
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Reduced GFR - obliteration of microvasculature and obstruction of tubules
Hyperchloremic acidosis - reduced ammonia production, type 1 RTA, proximal bicarbonate wasting Tubular proteinuria - failure of proximal tubule protein reabsorption Polyuria - damage to medullary tubules and vasculature Hyperkalemia - potassium defects including aldosterone resistance Salt wasting - distal tubular damage with impaired sodium reabsorption Fanconi syndrome - damage to proximal tubular reabsorption of glucose, amino acids, phosphate, bicarbonate |
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How do drugs and toxins cause tubulointerstitial nephritis?
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May trigger an interstitial immunologic reaction, like acute hypersensitivity nephritis
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What is a classic example of a drug that triggers an interstitial immunologic reaction (acute hypersensitivity nephritis)?
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Methicillin
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How might a drug like cyclosporine cause acute renal failure?
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A potent immunosuppressive agent - can cause reduced renal blood flow, ischemia, and nephritis.
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What are some examples of drugs and toxins which, down the line, may cause slow cumulative damage to renal tubules?
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Lithium, cyclosporine, chinese herb nephropathy (those containing aristolochic acid)
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What are the clinical S/S for acute drug-induced interstitial nephritis?
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Start ~15 days after exposure
Fever, eosinophilia, rash, renal abnormalities (hematuria, mild proteinuria, leukocyturia, oliguria, elevated serum creatinine) |
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What are some of the most common drug culprits for acute drug-induced interstitial nephritis?
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Sulfonamides, beta-lactams, vancomycin, quinolines, erythromycin, rifampin, NSAIDs, diuretics, anticonvulsants
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What is the likely pathogenesis behind acute drug-induced interstitial nephritis?
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Thought to be an idiosyncratic immune response that causes increased IgE in some patients, suggesting that late-phase reaction of IgE-mediated hypersensitivity may be involved.
Some cases suggest T cell-mediated delayed hypersensitivity reaction. |
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What are the typical symptoms of drug-induced acute interstitial nephritis?
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Acute intrinsic renal failure
Oliguria Malaise Anorexia N/V Mild-moderate proteinuria |
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What is the classic triad associated with drug-induced acute interstitial nephritis (in addition to acute renal failure)?
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Fever
Skin Rash Peripheral Blood Eosinophilia (Only in 10% of patients, however) |
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What may be seen in the urine sediment of a patient with acute interstitial nephritis (drug induced)?
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Hematuria
Often Pyuria (WBC, WBC casts) Eosinophils RBC casts are RARE |
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How does one visualize the kidney problem in acute interstitial nephritis (drug induced)?
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Renal ultrasound may show bilateral kidney enlargement
Biopsy is the gold standard - may not be needed if symptoms resolve after withdrawal of offending drug |
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How is drug-induced acute interstitial nephritis treated?
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Remove and/or treat underlying cause
Supportive measures - correct fluid and electrolyte abnormalities, symptomatic treatment of rash, fever, pain Consider corticosteroids - small studies have shown good improvement within 72 hours of starting treatment |
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What is analgesic nephropathy?
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A form of chronic renal disease caused by excessive intake of analgesic mixtures and characterized morphologically by chronic tubulointerstitial nephritis and renal papillary necrosis.
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What is the most common mixture of drugs causing analgesic nephropathy?
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Aspirin, Caffeine, Acetaminophen, and Codeine
Requires regular consumption of large quantities of at least 2 antipyretics. **Phenacetin (an analgesic that was withdrawn by the FDA) was the first drug noted to cause analgesic nephropathy** |
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What are the clinical S/S of analgesic nephropathy?
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Inability to concentrate the urine
Headache Anemia GI symptoms Hypertension Hematuria UTI - 50% of cases |
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What are some treatments for analgesic nephropathy?
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Screen at-risk patients
Discourage use of problematic medications Quit using the medications and correct fluid/electrolyte imbalances, consider corticosteroids. |
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How do acetaminophen (and phenacetin) cause analgesic nephropathy (papillary necrosis)?
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Renal cells are injured because the drugs deplete them of glutathione, and generate oxidative metabolites
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How does aspirin cause analgesic nephropathy (papillary necrosis)?
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Contributes by inhibiting the vasodilatory effects of prostaglandins, predisposing the papillae to ischemia
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What are some non-drug causes of papillary necrosis?
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Diabetes
Urinary tract obstruction Sickle cell disease Renal tuberculosis |
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Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Diabetes Mellitus.
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Male-to-Female 1:3
Time course - 10 years Infection - 80% Calcification is rare Several papillae are affected, all of same stage |
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Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Analgesic Nephropathy.
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Male-to-Female ratio - 1:5
Time course - 7 years of drug abuse Infection - 25% Calcification is frequent Almost all papillae are affected, at different stages of necrosis |
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Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Sickle Cell disease.
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Male-to-Female ratio - 1:1
Variable time course Infection may occur, may not occur Calcification is rare Few papillae are affected |
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Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae with Obstruction.
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Male-to-Female ratio - 9:1
Variable time course Infection - 90% Calcification is frequent Variable numbers of papillae are affected |
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What syndromes are included in NSAID nephropathy?
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Acute renal failure
Acute hypersensitivity interstitial nephritis Nephrotic syndrome (membranous nephropathy) Occurs mostly in patients who have already had some renal compromise, and take NSAIDs regularly May contribute to hyperkalemia in at-risk individuals |
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Describe the pathogenesis of NSAID nephropathy.
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NSAIDs inhibit cyclooxygenase-dependent prostaglandin synthesis
The selective COX-2 inhibitors affect the kidneys because COX-2 is expressed in human kidneys Inappropriate vasoconstriction and increased risk of renal ischemia are the potential outcomes NSAIDs also directly impair potassium secretion in the distal nephron |
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How does Lithium affect the kidneys?
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Induces tubular atrophy, interstitial fibrosis, tubular cysts, focal segmental glomerulosclerosis
Result: Chronic Renal Insufficiency May also induce nephrogenic diabetes insipidis - renal resistance to ADH - causing polyuria and polydipsia |
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How is Lithium nephropathy prevented?
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Regular renal function screenings in patients prescribed Lithium
Stop Lithium at the first sign of renal impairment and substitute another medication CKD may still progress even without Lithium |
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What is Cystic Kidney Disease?
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Cystic diseases are hereditary, developmental and acquired disorders
Important because they are fairly common, some forms are major causes of chronic kidney disease, and are important to differentiate from malignant tumors |
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Describe the epidemiology of Cystic Kidney Disease (adult).
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Autosomal dominant
Results in large multicystic kidneys 1/400-1000 births Caused by genetic mutations in chromosomes PKD1 and PKD2 |
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What are the associated risks of cystic kidney disease?
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Liver cysts
Berry aneurysm |
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What are the renal effects in cystic kidney disease?
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Hematuria
Flank pain Urinary tract infections Renal calculi Hypertension Typically results in CKD between ages 40 and 60 |
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What is the pathophysiology of cystic kidney disease?
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Renal cysts expand through the years, ultimately destroying the renal parenchyma, inducing interstitial inflammation and fibrosis along the way
It is thought that mutations in proteins related to mechanosensation by tubular cilia and calcium flux result in abnormal growth/differentiation of tubular epithelial cells, leading do abnormal ECM, cell proliferation and fluid secretion = cyst! |
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What are some causes of tubulointerstitial nephritis?
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Primary event in tubulointerstitium in absence of glomerular injury (proteinuria); In presence of tubular injury (WBC in urine)
Secondary to glomerular or vascular disease |
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What is the most common cause of tubulointerstitial nephritis?
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Drug induced - acute TIN, chronic, analgesic nephropathy
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What are some characteristics of acute tubulointerstitial nephritis?
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Eosinophilia
Rash, Edema Lymphocytes Positive skin test High IgE Not dose related Generalized interstitial edema by lymphocytes, plasma cells, macrophages, eosinophils |
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What are some clinical features of acute tubulointerstitial nephritis? Blood characteristics?
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Clinically - fever, hematuria
Blood - Azotemia, eosinophilia |
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What are some features of urine in acute tubulointerstitial nephritis?
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Hematuria
Pyuria Eosinophils Negative urine culture |
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What are some characteristics of chronic tubulointerstitial nephritis?
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Tubular atrophy
Fibrosis Mononuclear cells |
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What is a common cause of chronic tubulointerstitial nephritis?
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Analgesic nephropathy
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What kind of necrosis is caused in analgesic nephropathy?
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Renal papillary necrosis - dose related (Acetaminophine, Aspirin, Caffeine, Codeine)
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What are some clinical features of analgesic nephropathy?
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Chronic renal failure
Anemia Hypertension Increased risk of transitional cell carcinoma of the renal pelvis or bladder |
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What are some characteristics of acute pyelonephritis histologically?
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Acute neutrophilic exudate within tubules and interstitial inflammation
Tubules are filled with acute inflammatory cells with surrounding congestion |
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What is acute pyelonephritis?
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Acute inflammation of the pelvis, tubules, interstitium
Usually caused by ascending bacterial infection from the urinary bladder |
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What are some predisposing factors for acute pyelonephritis?
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Urinary obstruction (prostatic hypertrophy, uterine prolapse)
Vesicoureteral reflux Instrumentation Diabetes Neurological deficits |
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What is the most common causative organism behind acute pyelonephritis?
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Escherichia coli
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What are the gross morphological characteristics of a kidney with acute pyelonephritis?
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Kidney has discreet patchy abscess
Yellow streaks (pus) extend from the pelvis to cortex on cross sections LM - inflammatory infiltrate within lumen and interstitium, edema in interstitium |
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What are some causes of Chronic Pyelonephritis?
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Vesico ureteric reflux
Lower Urinary Tract obstruction Prostatic Hyperplasia Renal Calculi |
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What are some histological / morphological characteristics of chronic pyelonephritis?
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Tubular atrophy
Dilated tubules Eosinophilic material is there, resembling thyroid tissue Chronic inflammation |
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What are some morphological characteristics of kidneys with chronic pyelonephritis?
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Blunt calyx
Uneven scarring Calyceal deformities |
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What are some causes for acute renal failure?
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Renal - acute tubular necrosis (toxic, ischemic - 50% of ARF), severe glomerular diseases, RPGN, acute (drug induced) interstitial nephritis
Prerenal - Ischemia Postrenal azotemia - urinary obstruction |
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What are some causes of renal azotemia (intrinsic renal failure)?
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Acute tubular necrosis (ischemia, toxins)
Diseases of small vessels and glomeruli - GN and vasculitis, HUS, TPP, malignant hypertension Diseases of large renal vessels - renal artery thrombosis Acute diseases of tubulointerstitium |
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What is the cause of acute tubular necrosis? What is happening pathologically and clinically?
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It is caused by ischemic or toxic injury, or as part of tubulointerstitial nephritis
Pathology - destruction of tubular epithelial cells Clinically - acute loss of renal function, oliguria and elevation of BUN and creatinine |
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Describe the pathogenesis of acute tubular necrosis.
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Increased afferent arteriolar resistance
Tubular obstruction Backleak of filtrate Decreased permeability of glomerular filtration membrane |
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Is acute tubular necrosis permanent?
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No, it is reversible - renal tubular epithelial cells have the capacity to regenerate - as long as there is intact basement membrane
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How does tubular cell injury result in acute tubular necrosis?
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Ischemia causes detachment of tubular cells
Renal tubular cell casts obstruct the lumen Increase in intratubular pressure Decreased GFR Oliguria |
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How does loss of polarity occur in Acute Tubular Necrosis?
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Na+K+ATPase enzyme moves from basolateral surface to luminal side
Increase in Na+ delivery to proximal tubules Feedback to glomeruli produces vasoconstriction and release of Renin-Angiotensin Overall results in a lower GFR |
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What are some microscopic features of acute tubular necrosis?
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Focal epithelial necrosis
Tubulorrhexis (detachment of tubular cells from basement membrane) Loss of proximal tubular brush border Hyaline casts Sloughing of epithelial cells Interstitial edema |
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Why are tubular epithelial cells so susceptible to ischemia?
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They have high metabolic rates, and are in a vulnerable position?
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In toxic acute tubular necrosis, where is the necrosis localized? What are the most common causes?
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Necrosis is prominent in the proximal tubules, while the tubular basement membrane is spared
Caused by drugs, amino glycosides, heavy metals, mushroom poisoning, pesticide, myoglobin, CCl4 |
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In ischemic acute tubular necrosis where is the necrosis localized? What are the most common causes?
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Necrosis - patchy, proximal tubules and ascending thick limb of the loop of Henle
Casts are in the DCT and collecting duct Causes include severe hemorrhage, hypotension, dehydration |
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Describe childhood polycystic kidney disease.
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Autosomal recessive
Childhood Progressive and fatal BIlateral enlarged kidneys May be associated with hepatic cysts |
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Describe adult polycystic kidney disease.
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Autosomal dominant
Asymptomatic Symptoms appear by age 40, presenting with renal insufficiency, intermittent hematuria, hypertension Bilateral Associated with Berry aneurysm, liver cysts |
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What are some histological / microscopic characteristics of autosomal dominant (adult) polycystic kidney disease?
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Cyst filled with desquamated cells and fluid
Surrounding tissue exhibits interstitial fibrosis and scattered chronic inflammatory cells |
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Describe a simple cyst (polycystic kidney disease).
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They may present as a single cyst or many. Confined to the cortex.
Present with hematuria and pain |
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How does a cyst in polycystic kidney disease (adult) present radiographically?
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Smooth contour
Avascular In ultrasound - Fluid-filled |
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How do you approach a patient with unilateral flank pain and hematuria?
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History and Physical where appropriate
Urine analysis Imaging if appropriate, as needed |
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What are the different renal imaging modalities and relative costs?
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Plain X-Ray - KUB, IVP, flat plate ($100)
Computed Tomography (CT) - with or without contrast ($1000) Magnetic Resonance Imaging - with or without contrast ($2000) Ultrasound (USN) - imaging or vascular ($500) Nuclear medicine - flow, function, reflux ($1000) |
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What are some risks associated with IV iodine contrast?
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Allergy
Renal toxicity Acute renal injury (acute tubular necrosis) Prevention is best policy - serum creatinine > 1.5; GFR < 60 ml/1.73m^3; Avoid NSAIDs, risk factors like DM, MM; Avoid volume depletion - hydrate pre- and post-procedure |
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What are the main symptoms of urinary obstruction?
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Pain - Flank with radiation to anterior and down to perineum or genital area
Severe, onset relatively acute, history of previous similar symptoms Physical/lab - Flank tenderness, Hematuria |
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What are some intrinsic causes of urinary obstruction?
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Calculi
Tumor Blood clot |
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What are some extrinsic causes of urinary obstruction?
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Crossing vessels
Tumor Strictures |
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What are some radiographic signs of obstruction?
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Delayed excretion of contrast
Dense nephrogram Blunting of Forniceas - calyx Dilatation of ureter, pelvis Decreased or absent peristalsis in ureter No contrast beyond point of obstruction |
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What us the UPJ?
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Ureteropelvic junction
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What are some characteristics of obstruction of the UPJ?
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Most common congenital anomaly of the GU system in neonates
20% are bilateral Intrinsic, 80% - defect in circular muscle Extrinsic, 20% - crossing renal vessels Treatment - pyeloplasty |
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What are some characteristics of renal calculi? Epidemiology?
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5% of population, 20% at autopsy
50% recurrence of stone disease Calcium oxalate, calcium phosphate, struvite calculi (magnesium ammonium phosphate - Infection stones) Non-opaque - uric acid (gout, myeloproliferative disease) Staghorn calculus |
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What are some radiographic features of renal calculi.
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Most quickly and cheaply seen on KUB
Radiopaque calculus best on Non-contrast CT Radiolucent best seen on IVP/non-contrast CT Renal calculi can be seen on USN |
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What are the three most common locations of renal calculi?
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UPJ - ureteropelvic junction
At crossing of pelvic vessels UVJ - insertion of ureter into bladder |
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What are staghorn calculus?
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They occupy nearly the entire collecting system
Association with Xanthogramulomatous Pylonephritis (XGP) Increased chance of squamous cell cancer Treatments include extra corporeal shock wave lithotripsy (ESWL), percutaneous removal (nephrostomy), open surgical stone removal or nephrectomy |
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What is a renal parenchymal tumor?
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Renal cell adenocarcinoma - 80% of cases
Adenoma (early RCC) < 2 cm in size Oncocytoma (epithelial cells of proximal tubule) WIlms tumor - 5% (pediatrics) |
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What is a mesenchymal tumor?
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Angiomyolipoma - contains fat, smooth muscle, and blood vessels - usually no calcifications
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What are renal pelvis tumors?
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Transitional cell tumors - 40-80% have associated bladder tumors
Squamous cell - associated with chronic irritation (XGN) |
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What are bladder/ureter tumors?
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Transitional cell tumors
Squamous cell-chronic irritation |
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What are some characteristics of renal cell carcinomas?
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Most frequent renal parenchymal tumor, origin from tubular epithelium
Spread locally to hilar lymph nodes Spread to renal vein and then to IVC and to right atrium Distal metastasis to lung, bone, brain, everywhere. Very vascular - possible bleeding |
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What are some characteristics of uroepithelial tumors?
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Transitional cell
Squamous cell - relationship to chronic irritation, infection, stone, XGN, pyelonephritis Location - Calyces, Pelvis, Ureter, Bladder |
