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66 Cards in this Set
- Front
- Back
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Chronic renal failure,is
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persistent and usually progressive reduction in glomerular filtration rate (GFR; less than 60 mL/min/1.73 m2).
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Chronic renal failure,is
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persistent and usually progressive reduction in glomerular filtration rate (GFR; less than 60 mL/min/1.73 m2).
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Chronic renal failure,is
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persistent and usually progressive reduction in glomerular filtration rate (GFR; less than 60 mL/min/1.73 m2).
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As renal function declines, endocrine functions of the kidney, including
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ncluding synthesis of erythropoietin and vitamin D and catabolism of insulin, are impaired.
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As renal function declines, endocrine functions of the kidney, including
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ncluding synthesis of erythropoietin and vitamin D and catabolism of insulin, are impaired.
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As renal function declines, endocrine functions of the kidney, including
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ncluding synthesis of erythropoietin and vitamin D and catabolism of insulin, are impaired.
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The risk factors of CKD include
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increased body mass index, hypertension, smoking, diabetes, low high-density lipoprotein cholesterol, and lead exposure.
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The risk factors of CKD include
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increased body mass index, hypertension, smoking, diabetes, low high-density lipoprotein cholesterol, and lead exposure.
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The risk factors of CKD include
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increased body mass index, hypertension, smoking, diabetes, low high-density lipoprotein cholesterol, and lead exposure.
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The normal rate of decline in GFR in adults is about
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1 mL/year, with a GFR of about 70 mL per minute in males by the age 70 years. Albuminuria is a key adjunctive tool used to monitor CKD and response to treatment.
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The normal rate of decline in GFR in adults is about
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1 mL/year, with a GFR of about 70 mL per minute in males by the age 70 years. Albuminuria is a key adjunctive tool used to monitor CKD and response to treatment.
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The normal rate of decline in GFR in adults is about
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1 mL/year, with a GFR of about 70 mL per minute in males by the age 70 years. Albuminuria is a key adjunctive tool used to monitor CKD and response to treatment.
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stage 3 CKD
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GFR is 30 - 59 - refer to nephrologist to treat anemia, bone disease and malnutrition
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stage 3 CKD
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GFR is 30 - 59 - refer to nephrologist to treat anemia, bone disease and malnutrition
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stage 3 CKD
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GFR is 30 - 59 - refer to nephrologist to treat anemia, bone disease and malnutrition
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stage 4 CKD
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GFR is 15-29 - prep for dialysis and transplant
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stage 4 CKD
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GFR is 15-29 - prep for dialysis and transplant
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stage 4 CKD
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GFR is 15-29 - prep for dialysis and transplant
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stage 5 CKD
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gfr less than 15
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Metabolic acidosis is common in patients with advanced CKD. With advancing renal disease, net excretion of nonvolatile acids is limited to 30 to 40 mmol per day, which causes
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modest drop in the pH and plasma bicarbonate.his can usually be partially corrected by modest doses of NaHCO3 or sodium citrate. Hypocalcemia, hyperphosphatemia, and hyperkalemia are commonly present.
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Metabolic acidosis is common in patients with advanced CKD. With advancing renal disease, net excretion of nonvolatile acids is limited to 30 to 40 mmol per day, which causes
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modest drop in the pH and plasma bicarbonate.his can usually be partially corrected by modest doses of NaHCO3 or sodium citrate. Hypocalcemia, hyperphosphatemia, and hyperkalemia are commonly present.
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Metabolic acidosis is common in patients with advanced CKD. With advancing renal disease, net excretion of nonvolatile acids is limited to 30 to 40 mmol per day, which causes
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modest drop in the pH and plasma bicarbonate. his can usually be partially corrected by modest doses of NaHCO3 or sodium citrate. Hypocalcemia, hyperphosphatemia, and hyperkalemia are commonly present.
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anemia seen in CKD is what
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normocytic normochromic
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anemia seen in CKD is what
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normocytic normochromic
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anemia seen in CKD is what
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normocytic normochromic
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Bleeding disorders may occur in what stages
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Bleeding disorders may occur in stage 4 or 5 CKD. Hemostatic abnormalities are prolonged bleeding time due to abnormal platelet function and impaired prothrombin consumption. These can be treated with cryoprecipitate, desmopressin, or conjugated estrogens if required.
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Bleeding disorders may occur in what stages
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Bleeding disorders may occur in stage 4 or 5 CKD. Hemostatic abnormalities are prolonged bleeding time due to abnormal platelet function and impaired prothrombin consumption. These can be treated with cryoprecipitate, desmopressin, or conjugated estrogens if required.
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Bleeding disorders may occur in what stagesstag
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Bleeding disorders may occur in stage 4 or 5 CKD. Hemostatic abnormalities are prolonged bleeding time due to abnormal platelet function and impaired prothrombin consumption. These can be treated with cryoprecipitate, desmopressin, or conjugated estrogens if required.
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Bone disease associated with CKD is called ...and includes
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one disease associated with CKD (renal osteodystrophy) includes osteitis fibrosa, which results from secondary hyperparathyroidism (Chapter 65), osteomalacia, or adynamic bone disease. The pathophysiology of secondary hyperparathyroidism (increased parathyroid hormone [PTH]), is related to abnormal calcium, phosphate, and vitamin D metabolism. Decreased GFR causes a decrease in inorganic phosphate excretion leading to a high phosphate level that stimulates PTH, suppressing calcium levels via decreased calcitriol production. Decreased calcitriol levels decrease gastrointestinal absorption of calcium, resulting in hypocalcemia, which will further increase PTH secretion. These bone diseases can lead to pain and increased risk of fractures. With progression of renal disease, the parathyroid mass increases and can lead to a pattern of diffuse hyperplasia, monoclonal nodular growth, or diffuse monoclonal hyperplasia. Abnormal Ca/PO4 metabolism can also lead to extraosseous calcifications in soft tissues and blood vessels, which may be contribute to increased cardiovascular mortality in CKD. Calciphylaxis is the severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
Secondary hyperparathyroidism and osteitis fibrosa are best prevented or treated by decreasing the phosphate levels to normal by dietary restriction, phosphate binders (e.g., calcium carbonate, calcium acetate, and sevelamer), and adding vitamin D as calcitriol or other preparations. Aluminium-based phosphate binders were used in the past but are generally avoided because of the risk of bone accumulation and resulting osteomalacia. |
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Bone disease associated with CKD is called ...and includes
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one disease associated with CKD (renal osteodystrophy) includes osteitis fibrosa, which results from secondary hyperparathyroidism (Chapter 65), osteomalacia, or adynamic bone disease. The pathophysiology of secondary hyperparathyroidism (increased parathyroid hormone [PTH]), is related to abnormal calcium, phosphate, and vitamin D metabolism. Decreased GFR causes a decrease in inorganic phosphate excretion leading to a high phosphate level that stimulates PTH, suppressing calcium levels via decreased calcitriol production. Decreased calcitriol levels decrease gastrointestinal absorption of calcium, resulting in hypocalcemia, which will further increase PTH secretion. These bone diseases can lead to pain and increased risk of fractures. With progression of renal disease, the parathyroid mass increases and can lead to a pattern of diffuse hyperplasia, monoclonal nodular growth, or diffuse monoclonal hyperplasia. Abnormal Ca/PO4 metabolism can also lead to extraosseous calcifications in soft tissues and blood vessels, which may be contribute to increased cardiovascular mortality in CKD. Calciphylaxis is the severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
Secondary hyperparathyroidism and osteitis fibrosa are best prevented or treated by decreasing the phosphate levels to normal by dietary restriction, phosphate binders (e.g., calcium carbonate, calcium acetate, and sevelamer), and adding vitamin D as calcitriol or other preparations. Aluminium-based phosphate binders were used in the past but are generally avoided because of the risk of bone accumulation and resulting osteomalacia. |
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Bone disease associated with CKD is called ...and includes
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one disease associated with CKD (renal osteodystrophy) includes osteitis fibrosa, which results from secondary hyperparathyroidism (Chapter 65), osteomalacia, or adynamic bone disease. The pathophysiology of secondary hyperparathyroidism (increased parathyroid hormone [PTH]), is related to abnormal calcium, phosphate, and vitamin D metabolism. Decreased GFR causes a decrease in inorganic phosphate excretion leading to a high phosphate level that stimulates PTH, suppressing calcium levels via decreased calcitriol production. Decreased calcitriol levels decrease gastrointestinal absorption of calcium, resulting in hypocalcemia, which will further increase PTH secretion. These bone diseases can lead to pain and increased risk of fractures. With progression of renal disease, the parathyroid mass increases and can lead to a pattern of diffuse hyperplasia, monoclonal nodular growth, or diffuse monoclonal hyperplasia. Abnormal Ca/PO4 metabolism can also lead to extraosseous calcifications in soft tissues and blood vessels, which may be contribute to increased cardiovascular mortality in CKD. Calciphylaxis is the severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
Secondary hyperparathyroidism and osteitis fibrosa are best prevented or treated by decreasing the phosphate levels to normal by dietary restriction, phosphate binders (e.g., calcium carbonate, calcium acetate, and sevelamer), and adding vitamin D as calcitriol or other preparations. Aluminium-based phosphate binders were used in the past but are generally avoided because of the risk of bone accumulation and resulting osteomalacia. |
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Bone disease associated with CKD is called ...and includes
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one disease associated with CKD (renal osteodystrophy) includes osteitis fibrosa, which results from secondary hyperparathyroidism (Chapter 65), osteomalacia, or adynamic bone disease. The pathophysiology of secondary hyperparathyroidism (increased parathyroid hormone [PTH]), is related to abnormal calcium, phosphate, and vitamin D metabolism. Decreased GFR causes a decrease in inorganic phosphate excretion leading to a high phosphate level that stimulates PTH, suppressing calcium levels via decreased calcitriol production. Decreased calcitriol levels decrease gastrointestinal absorption of calcium, resulting in hypocalcemia, which will further increase PTH secretion. These bone diseases can lead to pain and increased risk of fractures. With progression of renal disease, the parathyroid mass increases and can lead to a pattern of diffuse hyperplasia, monoclonal nodular growth, or diffuse monoclonal hyperplasia. Abnormal Ca/PO4 metabolism can also lead to extraosseous calcifications in soft tissues and blood vessels, which may be contribute to increased cardiovascular mortality in CKD. Calciphylaxis is the severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
Secondary hyperparathyroidism and osteitis fibrosa are best prevented or treated by decreasing the phosphate levels to normal by dietary restriction, phosphate binders (e.g., calcium carbonate, calcium acetate, and sevelamer), and adding vitamin D as calcitriol or other preparations. Aluminium-based phosphate binders were used in the past but are generally avoided because of the risk of bone accumulation and resulting osteomalacia. |
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Bone disease associated with CKD is called ...and includes
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one disease associated with CKD (renal osteodystrophy) includes osteitis fibrosa, which results from secondary hyperparathyroidism (Chapter 65), osteomalacia, or adynamic bone disease. The pathophysiology of secondary hyperparathyroidism (increased parathyroid hormone [PTH]), is related to abnormal calcium, phosphate, and vitamin D metabolism. Decreased GFR causes a decrease in inorganic phosphate excretion leading to a high phosphate level that stimulates PTH, suppressing calcium levels via decreased calcitriol production. Decreased calcitriol levels decrease gastrointestinal absorption of calcium, resulting in hypocalcemia, which will further increase PTH secretion. These bone diseases can lead to pain and increased risk of fractures. With progression of renal disease, the parathyroid mass increases and can lead to a pattern of diffuse hyperplasia, monoclonal nodular growth, or diffuse monoclonal hyperplasia. Abnormal Ca/PO4 metabolism can also lead to extraosseous calcifications in soft tissues and blood vessels, which may be contribute to increased cardiovascular mortality in CKD. Calciphylaxis is the severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
Secondary hyperparathyroidism and osteitis fibrosa are best prevented or treated by decreasing the phosphate levels to normal by dietary restriction, phosphate binders (e.g., calcium carbonate, calcium acetate, and sevelamer), and adding vitamin D as calcitriol or other preparations. Aluminium-based phosphate binders were used in the past but are generally avoided because of the risk of bone accumulation and resulting osteomalacia. |
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Calciphylaxis is
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severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
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Calciphylaxis is
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severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
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Calciphylaxis is
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severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
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severe form of soft tissue and vascular calcification, which can lead to skin and soft-tissue necrosis.
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Calciphylaxis is
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leading cause of morbidity and mortality in patients with CKD and ESRD.
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Cardiovascular disease
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leading cause of morbidity and mortality in patients with CKD and ESRD.
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Cardiovascular disease
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leading cause of morbidity and mortality in patients with CKD and ESRD.
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Cardiovascular disease
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In patients with ESRD, pulmonary edema may be precipitated in the absence of volume overload due to
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increase in alveolar capillary membrane permeability.
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In patients with ESRD, pulmonary edema may be precipitated in the absence of volume overload due to
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increase in alveolar capillary membrane permeability.
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In patients with ESRD, pulmonary edema may be precipitated in the absence of volume overload due to
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increase in alveolar capillary membrane permeability.
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In patients with ESRD, pulmonary edema may be precipitated in the absence of volume overload due to
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increase in alveolar capillary membrane permeability.
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Hypertension needs to be treated
P.517 to a goal of what in patients with proteinuria |
125/75 mm Hg in patients with proteinuria and 130/85 mm Hg in patients without proteinuria. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) have a higher benefit in patients with proteinuria
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Hypertension needs to be treated
P.517 to a goal of what in patients with proteinuria |
125/75 mm Hg in patients with proteinuria and 130/85 mm Hg in patients without proteinuria. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) have a higher benefit in patients with proteinuria
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Hypertension needs to be treated
P.517 to a goal of what in patients with proteinuria |
125/75 mm Hg in patients with proteinuria and 130/85 mm Hg in patients without proteinuria. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) have a higher benefit in patients with proteinuria
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Hypertension needs to be treated
P.517 to a goal of what in patients with proteinuria |
125/75 mm Hg in patients with proteinuria and 130/85 mm Hg in patients without proteinuria. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) have a higher benefit in patients with proteinuria
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. Patients with polycystic kidney disease have a higher incidence of
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diverticulosi
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. Patients with polycystic kidney disease have a higher incidence of
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diverticulosi
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. Patients with polycystic kidney disease have a higher incidence of
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diverticulosi
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The history and physical examination is important to detect possible etiologies or initial symptoms and signs of uremia. Drugs of particular significance are analgesic use i.e.
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Drugs of particular significance are analgesic use (often ignored or underestimated by the patient), nonsteroidal anti-inflammatory drugs, antimicrobials, lithium, and ACE inhibitors.
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The history and physical examination is important to detect possible etiologies or initial symptoms and signs of uremia. Drugs of particular significance are analgesic use i.e.
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Drugs of particular significance are analgesic use (often ignored or underestimated by the patient), nonsteroidal anti-inflammatory drugs, antimicrobials, lithium, and ACE inhibitors.
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The history and physical examination is important to detect possible etiologies or initial symptoms and signs of uremia. Drugs of particular significance are analgesic use i.e.
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Drugs of particular significance are analgesic use (often ignored or underestimated by the patient), nonsteroidal anti-inflammatory drugs, antimicrobials, lithium, and ACE inhibitors.
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Physical examination should include
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blood pressure, fundoscopy, abdominal bruits, edema, neuropathy, asterixis, muscle weakness, prostatic masses in men, and pelvic masses in women.
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Physical examination should include
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blood pressure, fundoscopy, abdominal bruits, edema, neuropathy, asterixis, muscle weakness, prostatic masses in men, and pelvic masses in women.
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Physical examination should include
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blood pressure, fundoscopy, abdominal bruits, edema, neuropathy, asterixis, muscle weakness, prostatic masses in men, and pelvic masses in women.
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Physical examination should include
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blood pressure, fundoscopy, abdominal bruits, edema, neuropathy, asterixis, muscle weakness, prostatic masses in men, and pelvic masses in women.
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The most useful imaging study in the initial evaluation of patients with CKD i
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renal ultrasound. It can verify the presence of two kidneys, renal size including presence or absence of disparities between sides, renal masses, and obstruction. Symmetric small kidneys imply renal scarring and chronic irreversible renal disease, although normal-sized kidneys may be present in patients with polycystic kidney disease, amyloidosis, diabetes, and human immunodeficiency virus–associated renal disease. Asymmetric renal size implies a unilateral process, either developmental or chronic. Renal vascular imaging may be done through renal Doppler or magnetic resonance angiography to evaluate the feasibility of revascularization. Spiral computed tomography without contrast may be useful in evaluating renal stones.
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The most useful imaging study in the initial evaluation of patients with CKD i
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renal ultrasound. It can verify the presence of two kidneys, renal size including presence or absence of disparities between sides, renal masses, and obstruction. Symmetric small kidneys imply renal scarring and chronic irreversible renal disease, although normal-sized kidneys may be present in patients with polycystic kidney disease, amyloidosis, diabetes, and human immunodeficiency virus–associated renal disease. Asymmetric renal size implies a unilateral process, either developmental or chronic. Renal vascular imaging may be done through renal Doppler or magnetic resonance angiography to evaluate the feasibility of revascularization. Spiral computed tomography without contrast may be useful in evaluating renal stones.
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The most useful imaging study in the initial evaluation of patients with CKD i
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renal ultrasound. It can verify the presence of two kidneys, renal size including presence or absence of disparities between sides, renal masses, and obstruction. Symmetric small kidneys imply renal scarring and chronic irreversible renal disease, although normal-sized kidneys may be present in patients with polycystic kidney disease, amyloidosis, diabetes, and human immunodeficiency virus–associated renal disease. Asymmetric renal size implies a unilateral process, either developmental or chronic. Renal vascular imaging may be done through renal Doppler or magnetic resonance angiography to evaluate the feasibility of revascularization. Spiral computed tomography without contrast may be useful in evaluating renal stones.
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The most useful imaging study in the initial evaluation of patients with CKD i
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renal ultrasound. It can verify the presence of two kidneys, renal size including presence or absence of disparities between sides, renal masses, and obstruction. Symmetric small kidneys imply renal scarring and chronic irreversible renal disease, although normal-sized kidneys may be present in patients with polycystic kidney disease, amyloidosis, diabetes, and human immunodeficiency virus–associated renal disease. Asymmetric renal size implies a unilateral process, either developmental or chronic. Renal vascular imaging may be done through renal Doppler or magnetic resonance angiography to evaluate the feasibility of revascularization. Spiral computed tomography without contrast may be useful in evaluating renal stones.
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For patients with diabetes or hypertension and chronic disease preevntion and early treatment includes
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Prescribe angiotensin converting enzyme inhibitor or angiotensin receptor blocker to protect kidney function
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For patients with diabetes or hypertension and chronic disease preevntion and early treatment includes
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Prescribe angiotensin converting enzyme inhibitor or angiotensin receptor blocker to protect kidney function
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For patients with diabetes or hypertension and chronic disease preevntion and early treatment includes
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Prescribe angiotensin converting enzyme inhibitor or angiotensin receptor blocker to protect kidney function
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For patients with diabetes or hypertension and chronic disease preevntion and early treatment includes
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Prescribe angiotensin converting enzyme inhibitor or angiotensin receptor blocker to protect kidney function
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