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Renal/Metabo Disease
MEDT 208 Renal & Metabolic Disease Correlation study objectives
| Question | Answer |
|---|---|
| What are the clinical features associated with glomerular disease? | Hematuria, Proteinuria, Oliguria, Azotemia, Edema, Hypertension |
| What factors affect the presence and severity of the clinical features of glomerular disease? | Number of glomeruli involved, Mechanism of injury, Rapidity of disease onset |
| Clinical presentation: Acute, fever, malaise, nausea, oliguria, hematuria, edema, hypertension. RBC, WBC, RTE, casts, (RBC, HGb, granular occasional WBC and renal cell) | Acute glomerulonephritis |
| Clinical presentation: Acute onset. Main cause of nephrotic syndrome. | Membranous glomerulonephritis |
| Clinical presentation: Proteinuria, Hematuria, ↓ GFR, Nephrotic syndrome | Focal segmental glomerulonephritis |
| Clinical presentation: Slow, progressive . Varied presentation: hematuria to nephrotic syndrome | Membranoproliferative glomerulonephritis |
| Clinical presentation: Hyalinized, acelular glomeruli. Slow and silent; hypertension, edema, proteinuria, azotemia. | Chronic glomerulonephritis |
| Clinical presentation: Fever, malaise, nausea, oliguria, hematuria, edema, hypertension. | Rapidly progressive glomerulonephritis |
| Clinical presentation: Loss of podocyte foot process in glomeruli. Nephrotic syndrome. Immune mediated. | Minimal Change disease |
| Clinical presentation: Glomerular inflammation, cellular proliferation, Nephritic syndrome. | Focal proliferative glomerulonephritis |
| Clinical presentation:Increased mesangial cellularity due to IgA deposits in mesangium; Slow + progressive; Recurrent hematuria + proteinuria. | IgA Nephropathy |
| What is the pathology of SLE? | Autoimmune disease causes lesions on glomerulus. |
| What is the pathology of diabetes mellitus? | Lack of insulin or insulin resistance causes glycosylation & sclerosis in glomerulus. |
| What is the pathology of amyloidosis? | Amyloid protein deposits in glomerulus causes sclerosis. |
| Presentation of systemic disease: Recurrent hematuria + Nephritic syndrome OR Nephrotic syndrome | SLE |
| Presentation of systemic disease: Proteinuria + Hyperglycemia | Diabetes mellitus |
| Presentation of systemic disease: Heavy proteinuria + Nephrotic syndrome +RTE casts/cells + Misc casts. | Amyloidosis |
| RTE's are seen in only what two conditions? | (1) Nephrotic Syndrome, (2) Glomerulonephritis |
| What are at least five clinical features that characterize the nephrotic syndrome? | (1) Heavy proteinuria >3.5 g/day, (2) Hypoproteinemia (3) Hyperlipidemia, (4) Lipiduria, (5) Edema |
| Which four glomerular inflammatory diseases are associated with nephrotic syndrome? | (1) Minimal Change Disease, (2) Membranous glomerulonephritis, (3) Focal Segmental Glomerulonephritis, (4) Membranoproliferative Glomerulonephritis |
| What is the clinical presentation of acute tubular necrosis (destruction of renal tubules)? | Oliguria + acute renal failure |
| Ischemic acute tubular necrosis means? | Destruction of renal tubules following a hypotensive event. |
| Toxic acute tubular necrosis means? | Destruction of renal tubules due to nephrotoxic agents. |
| The dysfunction in Fanconi's Syndrome is? | Loss of proximal tubular function (can't reabsorb stuff) |
| What are the clinical features of Fanconi's syndrome? | Low amino acids, Dehydration, Hypoglycemia, Hypophosphatemia, Hypokalemia , Hypo-calcium |
| What is the dysfunction in Renal Glycosuria? | Reduced tubular reabsorptive capacity (Tm) for glucose. |
| What are the clinical features of Renal Glycosuria? | Hypoglycemia, Normal Ca, Normal phosphate |
| What is the dysfunction in Renal Phosphaturia? | Rare hereditary disorder; Inability to reabsorb phosphate in the distal tubules; Decreased proximal tubular response to hypophosphatemia |
| What are the clinical features of Renal Phosphaturia? | Hypophosphatemia; Normal glucose; Normal Ca |
| What is the dysfunction in Renal Tubular Acidosis? | Tubules can't excreted H+. ; Type I - distal ; Type II - proximal; Type III - combined |
| What are the clinical features of Renal Tubular Acidosis? | Acidemia ; Urine pH > 5.3 |
| Acute Pyelonephritis is caused by an ascending infection characterized by flank pain, groin pain, dysuria, frequency, urgency, fever, nausea, headache, malaise, and mental confusion. What are the typically urinary findings? | Leukocytes, Inflammatory cells, Casts, Mild hematuria, Proteinuria, Low SG |
| Chronic Pyelonephritis is caused by reflux nephropathies characterized by persistent scarring and inflammation in the kidneys, hypertension & renal failure. What are they typical urinary findings? | LE +, Low SG, Moderate proteinuria, WBC, macropages; Casts: granular, waxy, broad, few WBC/renal cells |
| Lower UTI's are caused by bacteria from the GI tract entering the UT (usually E. coli). Characterized by cystitis , dysuria (Pain/burning), Urgency, Fever and Cramping. What are the typical urinary findings? | Increased WBC, Bacteria, RBC & Transitional epis. Chemical: Protein: small, Blood +, LE +, Nitrite + |
| Yeast infections are caused by fungus (Candida) proliferating after a disruption of normal flora (catheters). Causes itching, burning, urgency. What are the typical urinary findings? | Yeas + pseudohyphae |
| What is the effect of vascular disease on renal function? | Since renal function directly dependent on renal vasculature, any kidney-blood-supply altering diseases directly affect renal function, such as renal ischemia (insufficient blood flow), & hypertension. |
| What is the physiological mechanism of cystinosis? | Lysosomal storage disease: cellular deposition of lysosome of cells. Accumulated cystine crystallizes w/in cells, causes damages and disrupting cellular functions. |
| What are the clinical features of cystinosis? | Fanconi's syndrome, Growth retardation, Rickets, Polyuria, Polydispis, Dehydration, Acidosis, Light sensitivity |
| What urinalysis finding will diagnosis cystinosis? | Cystine crystals |
| What is the physiological mechanism of cystinuria? | Autosomal recessive disorder: nephrons unable to reabsorb aa's. |
| What are the clinical features of cystinuria? | Cystine excretion, AA excretion (arginine, lysine, ornithine), Renal calculi + |
| What urinalysis finding will diagnosis cystinuria? | Cystine crystals + pH < 8 |
| Homogentisic acid (alkaptonuria) is caused by? What color does urine turn? | Liver enzyme deficiency: excretion of large amounts of homogentisic acid. Black. |
| Describe the urine of a phenylketonuria patient? | Mousy, musty urine odor. |
| Phenylketonuria is caused by? | An enzyme deficiency resulting in increased urinary excretion of phenylpyruvic acid. |
| What are the clinical symptoms of phenylketonuria? | Severe mental retardation, aminoaciduria, delayed development, feeding difficulties, severe vomitng, light pigmentation |
| What is the cause of tyrosinuria? | Metabolic pathway defect. Large amounts of tyrosine in plasma. |
| What are the clinical symptoms of tyrosinuria? | High tyrosine levels, liver damage, renal disease, aminoaciduria, death in 1st decade |
| What is the preferred method for tyrosinuria diagnosis? | Ion exchange chromatorgraphy |
| Melanuria is caused by? | Inherited defective melanin production or malignant neoplasm. |
| What is the urinary indicator of melanuria? | Darkening of urine |
| What two mechanisms cause diabetes mellitus? | (1) Defective insulin production. (2) Defective insulin action. |
| What is diabetes mellitus? | Impaired ability to utilize glucose. |
| What are the clinical features of diabetes mellitus? | Chronic hyperglycemia, chronic glycosuria, polyuria, polydipsia, ketonuria, rapid weight loss |
| What is the characteristic urinary finding for diabetes mellitus? | Glucose in urine |
| What is galactosuria? | Galactose in urine caused by defective enzyme in galactose metabolic pathway. Leads to galactose accumulation in blood exceeding renal threshold. |
| What are the clinical symptoms of galactosuria? | Failure to thrive, vomitng, jaundice, liver disease, diarrhea, cataracts. |
| What is the purpose of urinary test for galactose? | Screening only |
| What is diabetes insipidus caused by? | Defective ADH production or response. Neurogenic is low ADH. Nephrogenic is normal ADH + defective renal tubular response. |
| What are the clinical features of diabetes insipidus? | Polyuria, glycosuria, polydipsia. |
| What are the urinary findings in diabetes insipidus? | Dilute specimen + low SG |
| What are porphyrins caused by? | Inherited or acquired enzyme deficiency or inhibition during heme biosynthesis. OR lead poisoning. |
| Are porphyrins are neurotoxins? | yes |
| What are the clinical symptoms of porphyrin? | Light sensitivity + neurologic symptoms |
| What are the urinary findings in porphyrins? | Porphyrins + red blood |
| Which of the following is a characteristic feature of type 2 diabetes mellitus? | usually presents first in adults |
| Diabetes insipidus is not characterized by _________ | increased vasopressin |
| Testing for reducing substances in infants is important to detect a carbohydrate disorder with galactosemia. These infants may present with all of these features except ______________ | polyuria |
| Galactose is a metabolic product of ____? | lactose |
| What condition results in the accumulation homogentisic acid? | Alkaptonuria |
| A urine sample exposed to air developed a brown-black color. This indicates the sample may contain ? | melanin |
| Which of the following are related to tyrosine metabolism or production? Tyrosinuria, melanuira, phenylketonuria, alkaptonuria. | All of them |
| Which of the following can lead to severe mental retardation if not detected early in life? Phenylketonuria, Maple syrup disease, glactosuria, alkaptonuria. | Phenylketonuria, Maple syrup disease, glactosuria. |
| Which of the following regarding porphyrins and their precursors is true? (1) porphyria can be inherited or induced; (2) Porphyrin precursors are neurotoxins; (3) Porphyrins can be dark red or purple; (4) Porphyrin precursors cause skin photosensitivity. | (1) porphyria can be inherited or induced; (2) Porphyrin precursors are neurotoxins; (3) Porphyrins can be dark red or purple; |
| What specific characteristic of the organism causing Acute post streptococcal glomerulonephritis is causing sore throat? | M protein |
| What is the significance of dysmorphic RBCs? | Glomerular bleeding |
| What is the prognosis of acute post-streptococcal glomerulonephritis? | Full recovery with treatment |
| Which laboratory result is most helpful in diagnosing IgA Nephropathy? | Serum IgA level |
| A positive result for urine glucose generically means? | tubular damage |
| What are waxy casts associated with? | Chronic tubular damage with oliguria |
| What physiologic mechanism causing massive proteinuria? | Basement membrane injury |
| What is the relationship between proteinuria and edema? | Decreased capillary oncotic pressure |
| What mechanism produces oval fat bodies? | Tubular reabsorption of filtered lipids |
| State two additional procedures that can be performed to verify the presence of the ovalfat bodies and the fatty casts. | Polarized microscopy and Sudan III staining |
| Minimal change disease usually presents in ? | children |
| What two population are most at risk for developing cystitis? | Pregnant women and female children |
| What disorder will develop if cystis is not treated? | acute pyelonephritis |
| RTE cells indicate? | tubular damage |
| Crenated RBCs will appear in urine with a low SG or high SG? | High SG |
| The most common crystal in renal calculi is? | Ca oxalate |
| Identify the disorder:A patient with severe lower back pain and microscopic hematuria is scheduled for lithotripsy. | Renal calculi |
| Identify the disorder: A patient who tested positive for human immunodeficiency virus exhibits mild symptoms resembling the nephrotic syndrome. | Focal segmental glomerulonephritis |
| Identify the disease: A 40-year-old patient diagnosed with systemic lupus erythematosus develops macroscopic hematuria, proteinuria, and the presence of RBC casts in the urine sediment. | Rapidly progressive glomerulonephritis |
| Identify the disease:A 50-year-old patient diagnosed with systemic lupus erythematosus exhibits symptoms of gradually declining renal function and increasing proteinuria | membranous glomerulonephritis |
| Identify the disease: A patient who has taken outdated tetracycline develops glycosuria and a generalized aminoaciduria | Fanconi's syndrome |
| Identify the disease: A patient known to form renal calculi develops oliguria, edema, and azotemia | Acute renal failure |
| Identify the disease: A patient has a normal blood glucose and mild glucosuria | Nephrogenic diabetes insipidus |
| What are the four morphological changes in glomeruli during glomerular damage? | (1) Cellular proliferation, (2) Leukocyte infiltration, (3) Glomerular basement membrane thickening, (4) Hyalinization (sclerosis) of glomeruli |
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