lab medicine

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Name 4 mechanisms of hemolysis: -hemolysis= rupture of RBCS -> release analytes found in RBCs into serum or plasma -4 mechanisms 1. Mechanical 2. Chemical or osmotic 3. Aging 4. Temp (both heat and cold)
Name some causes of hemolysis: 1. Blood drawing 2. Type of syringe or vacutainer 3. transfer of blood 4. transportation of blood 5. transportation in pneumatic automatic tube systems 6. Separation of red cels from plamsa or serum
What does refrigeration of whole blood do to it?: -it inhibits the Na/K ATPase pump -K+ lost from RBC into plasma -Na+ diffuses from plasma into RBC
Name the 5 types of interference: 1. Interference with chemical procedure 2. leakage of constituents of RBCs into plasma or serum 3. Dilution of plasma or serum contents 4. Interference of blood in other body fluids (ex CSF) 5. Drug interferences
Define interference: =effect of a component on the accuracy of a measurement of desired analyte Impt types: 1. Hemolysis -main type of hemolysis -causes type 1, 2, 3 interference -degree of hemolysis severity is impt 2. drugs
Why do we care what type of butterfly needles we use to draw blood: -B/c there are 2 types of butterfly needles: 1. The type to draw blood -used for kids, hard to draw people, IV drug users 2. The type to administer drugs -if use this type to draw blood, will cause hemolysis of the sample
How do you know if a blood sample has significant hemolysis?: -sample turns pink -> red
Name the major substances that hemolysis of a sample could affect the lab medicine: 1. K+ 2. folate 3. LDH 4. AST/ALT -these substances are all high in RBCs so hemolysis can elevate the levels measured in lab test
Define type 1 interference: =direct interference with a chemical procedure -hemolysis can cause this type of interference -includes: 1. spectrophotometric interference 2. participation of hemoglobin in the rxn through augmentation or inhibition -ex assay for total bilirubin -reagent will react with hemoglobin and not bilirubin -for some rxns, small hemolysis will cause huge suppression of rxns
Define type II interference: -when there is leaakge of analytes that are higher in RBCs into plasma/serum -caused by hemolysis -the analytes you need to worry about with hemolysis are ones with a huge difference between concentrations in RBC and plasma/serum -ex: 1. LDH 2. AST 3. folate 4. K+
Define type III interference: =when analytes are higher in concentration in plasma than in RBCs -hemolysis of RBCs results in dilution of analyte -includes: 1. Na 2. Cl 3. Lithium -this can or can't be a problem depending on degree of hemolysis
Define type IV interference: =the presence of blood in another fluid -includes: 1. CSF -spinal fluid protein 2. Amniotic fluid scan for bilirubin 3. L:S ratio in amniotic fluid -impt to assess fetal lung development
Name 4 analytes that show circardian rhythms in blood levels: 1. Cortisol -AM levels > PM levels 2. Growth hormone -elevated during sleep 3. Serum iron -AM levels > PM levels 4. Thyroxine -TSH, T4 - PM levels > AM levels (15%) -certain drugs (ex alcohol) can block diurnal variations
Name 3 major ways that drugs can cause interference: 1. In vivo effect -pharmacologic effects of the drug -interference can be due to intended/therapeutic effects OR side effects 2. Analytic/in vitro effects -drugs cause interference through methodological effects 3. Surreptitious -neither the physician nor pt knows why
Give some examples of drugs causing interference with in vitro/analytical procedures: -not due to pharmacologic effects of drugs but rather the drug effecting the methodology of a lab test 1. Alterations of chemical rxns -enhancement or inhibition 2. Causes of turbidity in the rxn system 3. interference with enzyme rxns 4. cross-reaction with Ab 5. radioactive interferences -due to in vivo use of radioactive compounds
Name some substances that can alter albumin chem values: Decreased levels 1. aspirin Increased 1. Heparin Bisalbuminemia 1. PCN -binds to albumin causes 2 peaks on serum electrophoresis 2. genetic
Name some substances that can alter alkaline phosphatase levels on chem panel: Decrease 1. Antiocoagulants Increase 1. Estrogens 2. Gentamaicin (hepatotoxicity) 3. Human albumin injections
Name some substances that can alter amylase levels on chem panel: Decrease 1. Anticoagulation -oxalate, citrate Increase 1. Opiates ->spasm sphincter of Oddi 2. OCPs
Name some substances that can alter levels of bilirubin on chem panel: Decrease 1. Daylight (30% per hr) 2. Barbiturates -induce glucuronyl transferase in newborns Increase 1. Any drug w/ liver toxicity or causes cholestasis 2. Methyldopa
Name some substances that can alter levels of Calcium on chem panel: Decrease 1. Diuretics (enhanced excretion) 2. Phenytoin Increased 1. Antacids (large amts) 2. Vit D
Name some substances that can alter XOL levels on chem panel: Decrease 1. Androgens (decrease synthesis) 2. Neomycin -forms salts w/bile acids in gut Increase 1. Bilirubin 2. Corticosteroids
Name some substances that can alter creatinine levels on chem panel: Decrease 1. marijuana 2. after meals Increase 1. Acetoacetic acid, acetone, ascorbic acid 2. glucose
Name some substances that can alter digoxin levels on chem panel: Increase 1. Quinidine -releases digoxin from heart muscle -also decreases renal excretion of digoxin
Name some substances that can alter glucose levels on chem panel: Decrease 1. Ascorbic acid -interferes w/ glucose oxidase Increase 1. Ascorbic acid -interferes w/ procedures that utilize reduction
What substance can cause a false negative fecal occult blood test?: =Ascorbic acid -inhibits tetramethylbenzidine rxn
What substance can cause a false positive fecal occult blood test?: 1. large amounts of meat or undigested meat fiber 2. ASA -taking >3 g/day -causes bleeding into GI tract
What substance increases the level of phenobarbital on chem panel?: =valproic acid -inhibits renal excretion of phenobarbital
What causes a decrease in Na levels on chem panel?: =refrigeration of whole blood -via inhibition of Na/K ATPase
Name some substances that alters T4 levels on chem panel?: Decrease 1. Phenytoin 2. salicylates -both complete w/T4 for binding sites on TBG Increase 1. OCP -increase TBG
Name 3 substances that ascorbic acid can interfere with lab assays of:: 1. Glucose -both increases and decreases it 2. Occult blood -can cause false negative test 3. Creatinine -increases levels
True or false: smoking has little effects on analytes measured with a chem panel: -false -smoking has lots of effects -basically have different set of range values
Glucocorticoids can elevated levels of what substance?: -glucose
Name 3 substances that OCPs can cause elevated levels: 1. XOL 2. T4 3. Triglycerides
Name 3 substances that statins can cause altered levels: 1. ALT/AST increased 2. CPK 3. alkaline phosphate
How often does drug interference still result in a valid lab result? What is this related to?: -94% of time there is influence -this is due to in vivo effects of the drug (either intended or adverse effects) -lab result is valid 6% of time drug or a metabolite interferes in vitro -lab result is wrong
Name 3 non-Rx drugs that can affect lab values of various analytes on chem panel: 1. Amphetamines 2. Morphine 3. Cannabis
What substance is absent in newborns (hint pancreatic enzyme)?: -amylase
What are some reasons that pediatric chemistries can be so different?: 1. Immaturity of the liver -synthesis not at full capacity in newborns/children -ex less protein syntesis (ex albumin levels will be lower) -also, things the liver detoxifies tend to be higher b/c of immaturity of liver (higher bilirubin) 2. Values of IgA, IgM, and IgE are very low at birth 3. TSH levels elevated at birth and decrease to adult levels 2 weeks after birth -T4 levels also high but takes 10 years to normalize
Why do we need to ask pts about taking herbal remedies?: -b/c a lot of these can interfere w/ analyte levels in chem panel -classic ex: St. John's wart -herbal remedies can be spiked with pharmaceutical grade drugs (esp ones from China, SE Asia)
Name 2 drugs found in herbal remedies can cause aplastic anemia.: 1. phenylbuzatone 2. aminopyrine
Define Negative predictive value: =the fraction of negative values which are correct =true neg/(true neg + false neg) OR= (spec)(1-prev)/ [(spec)(1-prev) + (prev)(1-sens)]
Define Positive predictive value: =the fraction of positive values that are correct =true positives/(true pos + false pos) or= (prev)(sensitiv)/ [(Prev)(sens) + (1-prev)(1-sens)]
What does the sensitivity of a test mean?: =ability to detect a true positive =true positives/(true pos + false neg) -refers only to the diseased population
What does the specificity of a test mean?: =ability of a test to detect a true negative value =true neg/(true neg + false pos) -refers only to the healthy population
When do we care about the analytic variation of a lab test?: =observed differences in the value of an analyte after it has been prepared for analysis -when following the progression of a disease or assessing the impact of a treatment, we want to know whether the results of a lab test represent a real change in pt vs just analytic variation
Name some sources of variation in the lab values within the same individual.: 1. circadian rhythms 2. hydration 3. activity 4. stress 5. posture 6. food intake
True or false: the predictive value of a test does NOT change with disease prevalence: -false! Increased disease prevalence 1. Predictive value of positive test improves Decreased disease prevalence 1. Predictive value of negative test increases 2. Predictive value of positive test decreases
Define the efficiency of a test: =tells you the fraction of all subjects who are correctly classified by a test = (TP + TN)/ (TP + FN + TN + FP) -efficiency influenced by disease prev -as disease prev decreases, efficiency is approx specificity
Name 2 terms that describe the quality of a lab test: 1. Precision =reproducibility of a measurement 2. Accuracy =how close the measured value of analyte is to true value of analyte -accuracy influenced by many factors including precsion
Name 3 factors affecting the usefulness of a biomarker for ischemic cardiac damage: 1. Location -cytosolic components reach bloodstream faster 2. Size -smaller components reach bloodstream faster 3. Uniqueness -markers specific for cardiac tissue increase specificity of assay
Name 3 major biomarkers for ischemic cardiac damage: 1. Cardiac troponin (I, T) 2. Creatine kinase MB isoenzyme -CKMB 3. Myoglobin -first to go up Biomarkers now key to def AMI: rise in troponin or CKMB with at least one other factor (ischemic sx, ECG changes, etc)
What influences how long cardiac troponins remain elevated following a heart attack?: =extent of damage -bigger MI, more leaks out b/c more cell death -> troponins remain elevated for longer -peak elevation is still 24-36 hrs post MI
Describe troponin: =regulatory protein complex located in thin filament of contractile apparatus in muscle -3 subunits: 1. Troponin T -binds tropomyosin 2. Troponin I -inhibits myosin ATPase 3. Troponin C -binds Ca -b/c specific cardiac isoenzymes, these make good biomarkers of AMI -impt to see both rise and fall of troponin levels in AMI
True or false: 60% of end stage renal failure on hemodialysis have elevated cardiac troponins: -true -does not represent AMI but is associated w/ future adverse cardiac events
Describe creatinine kinase: =enzyme responsible for conversion of creatine into phosphocreatine (energy source for muscle contraction) -3 diff isoenzymes found in diff proportions in various types of muscle 1. CKMM -SKM -Heart (also predominant form but increased proportion of CKMB) 2. CKMB -SKM and heart -heart has increased proportion of CKMB 3. CKBB -brain
What do we use the CK index for?: =to differentiate myocardial damage from SKM damage =(CKMB mass/total CK activity) x100 -normal: <2.5, with CKMB less than 10 ng/mL -cardiac: > 2.5 and CKMB > 10 ng/mL -SKM: <2.5 and CKMB greater than 10 ng/ML
True or false: elevations in CKMB are only caused by AMI: -false -CK index helps distinguish between cardiac and non-cardiac causes of elevated CKMB -other causes: 1. myocarditis 2. polymyositis 3. muscle trauma 4. muscular dystrophies 5. malignant hyperthermia 6. shock 7. cardiac surgery 8. severe angina 9. other surgery 10. drug induced rhabdomyolysis
Describe myoglobin: =small protein -> gets into serum rapidly after release from injured muscle -found in all SKM and cardiac muscle -involved in oxygen binding -cleared in urine -least specific of cardiac markers
Name 3 situations where myoglobin may be elevated.: 1. AMI -biomarker that appears early b/c small protein so gets into serum quickly 2. SKM injury -found in all SKM and cardiac muscle so not specific 3. Renal failure -usu cleared in urine -myoglobin should NOT be used as sole biomarker for AMI -if concentration has increased by at least 25% consistent w/early MI
What is the major biomarker for heart failure?: =BNP (B type natriuretic peptide) -synthesized as promolecule and later cleaved -released from left ventricle w/ increased LV dysfxn
Why are BNP levels helpful to assess CHF?: -b/c BNP levels correlate w/ severity of heart failure
Define microalbuminuria: =albumin levels in urine between 30-300g -normal is less than 20 -this is screening for low grade levels of albumin in urine that would NOT be picked up by urine dipstick -good screening tool for diabetic nephropathy -microalbuminuria not unique to diabetes -once over 300 g albumin in urine -> overt proteinuria
Why are serum creatinine measurements less reliable in the elderly?: -b/c they have less muscle mass
Where does the urea measured in serum urea nitrogen test come from: -urea is synthesized in liver as by-product of deamination of AA during protein catabolism -urea is freely filtered by glomeruli with variable amt of reabsorption (40-70%) -if GFR is decreased, SUN will be increased
True or false: serum urea nitrogen is a sensitive indicator of renal dysfxn: -false! -it's not sensitive b/c renal fxn must decrease by more than 50% to result in a rise of SUN
______ is a useful assessment of GFR. Clinically, creatinine clearance is used to estimate it.: =GFR -creatinine not a perfect estimate (it overestimates) -usu small amt secreted into urine by tubules (can be increased in chronic kidney disease or inhibited by drugs) -NOT a linear relationship between creatinine and GFR -As plasma creatinine doubles, GFR halves -Implication: can lose a lot of GFR before see changes in creatinine levels
True or false: urea levels are influenced by diet: -true -higher levels of protein intake -> more urea
When are serum urea levels increased? (BUN): 1. renal insufficiency 2. corticosteroids 3. high protein intake 4. amino acid infusions in hospitalized pts 5. GI bleeding -due to breakdown of cells
When are serum urea nitrogen levels decreased? (BUN): 1. Liver failure to synthesize 2. low protein intake 3. high urine flow rates
Name 4 factors influencing creatinine production: 1. body wt 2. muscle mass 3. gender 4. age Expect some people to have a low creatinine due to low muscle mass: 1. children 2. elderly 3. women 4. paralyzed 5. amputees
True or false: at steady state creatinine production = excretion: -true
True or false: creatine can be secreted by the kidney: -true -usu secreted in only small amounts -Amt secreted altered during: 1. chronic kidney disease -INCREASED secretion 2. certain drugs -DECREASED secretion (inhibition) -includes trimethoprim, cimetidine -> results in increased serum creatinine (but this does NOT reflect a loss of GFR)
Define urine osmolality: osmolality= concentration of osmotically active particles in solution -can vary widely in urine in healthy person (60-1250 mOsm/kg) -urine osmolality measures concentrating ability of the kidney -in chronic renal failure, loss of ability to concentrate urine -urine osmolality usu with in 50 mOsm or plasma osmolality
What does urine osmolality measure: =the concentrating ability of the kidney -loss of ability to concentrate urine is usu on of earliest signs of chronic renal failure -leads to polyuria (esp at night) -in chronic renal failure, urine osmolality within 50 mOsm of plasma osmolality
How are urine osmolality and urine specific gravity related?: =directly proportional -both are elevated by presence of glycosuria or proteinuria -also highly variable with fluid intake -these measurements are most useful when they are done repeatedly with fixed fluid intake
When do we use urine osmolality measurements?: 1. Distinguish prerenal azotemia from intrarenal causes of injury -prerenal: urine osmolality will be preserved 2. distinguish primary polydipsia from other causes hyponatriemia -if restrict water and becomes concentrated -> primary polydipsia -if restrict water and urine still dilute -> diabetes insipidus
Elevated WBC on CBC with urine analysis of bacteruria, WBCs in urine, and a dipstick positive for leukocyte esterase/nitrite suggests ___________.: =pyelonephritis -in addition to WBCs in urine, can also see: 1. casts 2. RBCs -usu SUN, SUN/Cre ratio are normal
Findings of proteinuria, oval fat bodies in urine, with low serum albumin and elevated serum lipids suggest _______.: =nephrotic syndrome -GFR may or may not be abnormal depending on the cause -can also get casts of epithelial cells (hyaline casts)
What are SUN/creatinine ratios used for?: 1. Evaluate cause of renal failure -prerenal azotemia ratio increases to 30/1 (normal ratio usu 12-20/1)
True or false: amorphous crystals in the urine are a sign of injury to the kidney: -false -these are granular, nonrystalline precipitate of salts -they have NO pathological consequence
Define cylinduria: =presence of casts in the urine
What are glitter cells?: =pale-staining, swollen, degenerated PMNs found in dilute urine -cytoplasmic granules that exhibit characteristic Brownian movement
What is a hyaline cast made up of?: =mucoprotein -transparent when found in urine
Name the 3 stages of urinanalysis: 1. macroscopic 2. chemical 3. microscopic
What are 3 things you assess for when doing macroscopic urine analysis?: 1. Color 2. Turbidity -how cloudy or clear the urine is 3. Odor
Name some things that can turn your urine red: 1. RBCs 2. hemoglobin 3. porphyrins 4. drugs 5. foods (beets, red candy) 6. myoglobin
If your urine is green to yellow-brown, what does this suggest?: =there may be bile in the urine -if you shake the urine and it's still yellow-brown, there is possibly bile in the urine
Name some things that can give you brown-black urine: 1. Old blood 2. hemosiderin 3. myoglobin 4. rhubarb 5. melanin 6. alkapton bodies 7. certain laxatives
Sweet smelling urine may be a sign of _______.: =ketosis -due to acetone in urine
Name some things we test for chemically during macroscopic urinanalysis: 1. Specific gravity -depends on hydration status 2. urine pH 3. Protein -note: dipsticks detect albumin only 4. Glucose 5. Ketone bodies -beta hydroxybutyrate NOT measured by dipsticks 6. Heme tests 7. Bile 8. Urobilinogen
What test can we do to detect total protein in urine?: =sulfosalicylic acid -total protein normally less than 150 mg/day -1/3: albumin -1/3: Tamm Horsfall -1/3: variety of proteins -also some radio-opaque dyes and light chains are detected
When do you want to check for the presence of Bence-Jones protein: =light chain immunoglobulin proteins in urine -can do immunofixation or electrophoresis to check for them -you want to do this when you have a dipstick negative for urine but a high total protein -Bence Jones protein present w/: 1. Multiple Myeloma 2. Waldenstrom macroglobulinemai 3. chronic lymphocytic leukemia 4. amyloidosis
What can interfere with a route glucose urine dipstick: =vitamin C -it can quench the rxn -> false negative result
What does microscopic urinalysis involve?: =screen wet, unstained urine for sediment 1. casts 2. parasites 3. ova 4. foreign bodies 5. RBCs, WBCs, epthelial cells -squamous epithelial: urethra, vagina -transitional epithelial: bladder -renal tubular cells 6. bacteria, yeast 7. crystals
Name some different types of casts that can be found in urine: 1. Hyaline casts -made up of Tamm Horsfall protein -normal excretion in small amts, increased in kidney diseases 2. WBC casts -pyelonephritis 3. RBC casts -acute glomerulonephritis, lupus nephritis, goodpastrue's syndrome, subacute bacterial endocarditis 4. renal epithelial casts -ATN/nephrotoxic drugs 5. granular casts -breakdown of cellular casts and Ig 6. waxy casts -severe chronic renal disease, amyloidosis 7. fatty casts -nephrotic syndrome 8. mixed cell casts
Name some common types of crystals that can be found in the urine: 1. Calcium oxalate crystals 2. uric acid crystals 3. cystine crystals may be associated with pathological states
Name 3 causes of respiratory acidosis: =retaining CO2 b/c of respiratory insufficiency 1. chronic lung disease 2. drug overdoses 3. head trauma/CNS abnormality affecting respiratory control centers -kidney compensates by retaining HCO3- and increasing renal acid excretion (slow compensation)
Define respiratory alkalosis: =decreased pCO2 by respiratory mechanisms -Causes: 1. fever 2. anxiety 3. high environmental temp 4. pregnancy 5. Underlying CHF 6. Pneumonias -could be alkalosis or acidosis 7. Pulmonary embolism -acute resp alkalosis 8. high altitude living at low PO2 -kidneys compensate by: 1. decrease HCO3- reabsorption 2. decrease ammonia production and excretion
Metabolic acidosis can be due to a loss of _________ or a gain in _______.: Loss of HCO3- Gain of H+ 1. overproduction of acid 2. decreased renal excretion of acid Features: 1. low serum HCO3- and low pH 2. compensation with respiratory alkalosis (breath off excess CO2) 3. can have normal or increased serum anion gap (with different causes of each)
Name 2 major causes of normal anion gap metabolic acidosis: 1. renal tubular acidosis 2. diarrhea
Metabolic alkalosis could be due to a loss of ______ or a gain in ______.: Loss of acid -vomiting Gain of HCO3- Causes: 1. vomiting 2. diuretic use 3. hyperaldo states Commonly associated with loss of K+ Compensation: hypoventilation
How can you tell a mixed acid/base disturbance?: -have abnormal bicarb or H+ levels but a normal pH
How do we distinguish acute vs chronic respiratory acidosis/alkalosis?: -we look to see whether there has been time for renal compensation to occur -renal compensation takes several days -compensation will return pH in general direction back to normal but usu does NOT return the pH back to normal
Name 4 renal acid/base compensation mechanisms: 1. Na/H ion exchange 2. ammonia production and net acid excretion 3. HCO3- reabsorption 4. hydrogen phosphate formation -when acid excretion increased -> all 4 mechanisms increase, serum HCO3- rises -when you suppress these processes, you get acid retention and serum HCO3- falls
Define achlorydia: =without hydrochloric acid =lack of acid production by stomach
What is the main test used to assess gastric fxn?: =measurement amt of HCl produced by stomach -measure at: 1. baseline -4 15 min samples 2. maximal stimulation w/pentagastrin -pentagastrin=synthetic peptide w/similar biologic activity as gastrin -inject pentagastrin -6 serial 15 min samples -calculate acid output based on 2 highest specimens -Results: 1. Achlorydia (no gastric acid secretion) 2. low gastric acid secretion 3. hyperacidity
What are some general trends with gastric acid secretion?: 1. young people > old 2. men > women 3. duodenal ulcers > controls 4. gastric ulcers < controls 5. gastric carcinoma < controls 6. jejunal ulcers > controls
If you have an elevated baseline gastric acid secretion on a gastric fxn test, you may suspect _________.: =Zollinger-Ellison syndrome -rare gastrin-secreting tumor of pancreatic islet cells ->overproduction of gastric acid -> fulminant ulceration of esophagus, stomach, duodenum, jejunum
Name some causes of achlorydia: =lack of hydrochloric acid (no gastric acid secretion) -can be assessed w/gastric fxn test measuring acid output at baseline and max stim Causes: 1. Pernicious anemia (all cases) 2. Advanced stomach cancer 3. Others -certain anemias, hypothyroidism
Name some causes of low gastric acid production on gastric fxn test: 1. gastric carcinoma 2. benign gastric ulcers 3. females 4. older people
Name some causes of hyperacidity on gastric fxn tests of HCl output.: 1. Duodenal ulcer -but lots of overlap w/normal range 2. extreme: Z-E
Name some different tests used to evaluate for H. pylori infection: 1. Biopsy -culture bacteria -detect urease enzyme 2. 13C breath test 3. Immunoassay for IgG antibody 4. Stool Ag test -very sensitive and specific for picking up current H. pylori infections
The 13C breath test is used to evaluate for the presence of _________.: =H. pylori infection -H. pylori have urease that can metabolize urea -> CO2 -pt ingests 13C labeled urea and measure expired CO2 for labeled 13C02 -peak levels 1.5 hrs after ingestion -test is very sensitive and specific for H. pylori -false negatives: if pt on PPIs, H2 blockers, antibiotics, bismuth (pt needs to come off meds before test)
Why would a pt have a negative 13C breath test but still be infected with H. pylori?: =b/c taking certain drugs will cause a false negative breath test 1. PPIs 2. H2 blockers 3. antibiotics 4. bismuth -pt needs to come of these medications before 13C breath test
Why is an immunoassay for IgG antibodies not as helpful as the 13C breath test or stool Ag test for H. pylori infection?: =b/c test may remain positive for several years, even after successful tx of H. pylori
Name the 5 main categories of diseases in the differential diagnosis of malabsorption syndrome: 1. Pancreatic diseases 2. Zollinger-Ellison syndrome 3. Live disease -due to blockage of bile flow 4. Intestinal diseases -major category 5. Resin tx -ex kayexolate
Name 8 nonspecific lab findings (biochemical) seen with malabsorption syndromes: Decreased 1. serum Ca++ 2. serum proteins 3. SUN 4. serum XOL 5. Vit A/D Increased 1. Serum alkaline phosphatase -due to Vit D def and hypocalcemia -> osteomalacia -> increase alkaline phosphatase 2. Prothrombin time -due to Vit K def Glucose tolerance test is flat -b/c defective glucose absorption
Why is serum Ca++ low in malabsorption syndromes?: 1. Decreased absorption -enterocyte damage -fat malabsorpt -> def in Vit D 2. Decreased serum albumin for Ca++ to bind to
Name 3 tests use to evaluation for carbohydrate malabsorption: 1. D-xylose absorption test -decreased 2. Dissacharidase test -increased 3. Breath hydrogen test -increased
Name 2 tests used to evaluate fat malabsorption.: 1. Fecal fat determination -increased 2. 14C triolein breath test -decreased
Describe the D-Xylose absorption test.: =test of enterocyte injury/malabsorption -D-xylose is a sugar that is passively absorbed that does NOT require pancreatic enzymes for its absorption -no metabolism in liver, gets excreted in urine -A low urine level of D-xylose suggests enterocytes damage but there could be other causes 1. If truly intestinal malabsorption, both plasma and urine levels will be decreased 2. renal dysfxn -nl/increase plasma level, decreased in urine 3. Myexedema (severe hypothyroidism) and baterial overgrowth -decreased plasma and urine -will mimic intestinal damage 4. incomplete urine collection -normal plasma level, decreased urine level
Describe the Dissacharidase test: This test is used to differentiate general malabsorption from specific disaccharidase def -individual disaccharides are given orally, blood glucose response measured every 30 min, 4 times -Abnormal test (increase in blood glucose < 20mg/dl) is followed by giving equivalent quantity of each monosaccharide -can identify: 1. lactase def 2. sucrase def 3. maltase def
Describe the H2 breath test: =test of carbohydrate intolerance -bacteria will release H2 when they ferment carbs -if have enzyme def for digesting sugars -> sugars pass through lumen unabsorbed -> in colon get fermented by bacteria -> increased H2 production
What is the best test confirm steatorrhea?: =fecal fat determination -Sources of fecal lipids 1. mucosal cells 2. GI flora 3. excretions into intestinal lumen 4. diet -in malabsorption, the fraction of unabsorbed dietary fat increases significantly -> increased fecal fat content -stool is collected for 3 days, specimens must be refrigerated -greater than 7g/24 hr suggest steatorrhea -does NOT tell you cause of malabsorption
Describe the 14C triolein breath test: =used to evaluate for fat malabsorption -give orally 14C labelled triglycerides -TG will get digested, absorbed, metabolized -some 14C will be released as CO2 -abnormal (+) will show a decrease in 14CO2 -the test is negative in ulcerative colitis -pt must be at rest and be fasting -not reliable in some pts (DM, obesity, thyroid disease, chronic resp insuff)
For whom is the 14C triolein breath test not reliable for?: =test to evaluate fat malabsorption 1. DM 2. obesity 3. thyroid disease 4. chronic respiratory insufficiency
Name some tests to work up a pt suspected of having Celiac disease.: 1.IgA antibodies against tissue transglutaminase 2. HLA typing -almost all celiac HLA DQ2 or DQ8 3. Biopsy of small bowel -villous atrophy, cyrpt hyperplasia, lymphocyte infiltration
Why would you get a negative test for IgA antibodies against tissue transglutaminase but still have Celiac disease?: =some people are IgA deficient -about 2% of Celiac pts will have low amts of IgA antibodies against TTG for this reason -so when ordering this test, should also get a total IgA count -if total IgA count is low, want to check for IgG anti-TTG
What does the Schilling test evaluate for?: =absorption of vit B12 -give orally 57Co-radiolabeled B12 -measure amts of radiolabeled B12 in serum, feces or urine -normal should excrete >8% of radiolabeled B12 in urine -If pernicious anemia, will excrete <7% in urine in 24 hrs
A sweat test for cystic fibrosis evaluates for high levels of ______ in the sweat: =chloride -in CF, chloride levels are 60-120mmol/L -normal is less than 60 -this test becomes positive in babies 3-5 weeks of age -Can get positive tests in other diseases (but they can be clinically distinguish from CF) -Put solution with pilocarpine on skin to induce sweating -> collect sweat with gauze pad -> weigh, elute, analyze for levels of Cl- and Na+
Define acute pancreatitis: =diffuse enzymatic autodigestive destruction of the pancreas -can assess damage with amylase levels
Define amylase: =enyzme that hydrolyzes polysaccharides into simple sugars -produced by pancreas but also by other organs (ex salivary glands) -amylase levels can be used to monitor for pancreatic damage -amylase is a small molecule -gets rapidly excreted in urine -levels go up and down rapidly (elevated levels normalize 2-3 days) -stable even at rom temp -can get elevated levels with: 1. increased entry amylase into the blood 2. decreased renal excretion
Define chronic pancreatitis: =chronic inflammation of the pancreas -generally irreversible -replacement by fibrous tissue -loss of both exocrine and endocrine pancreatic fxn
Define lipase: =enzyme that cleaves fatty acid from triglycerides -produced by pancreas and other organs -lipase levels can be used to monitor for pancreatic damage
Name some major causes of pancreatitis: 1. Alcohol 2. Obstructive -gallstones, sphincter of Oddi, tumor of head of pancreas -block pancreatic duct -> inflammation -> cells leak enzymes -> autodigestion 3. Pharmacologic drugs (2%) 4. biochemical -hyperTG
What lab tests are useful to assess for acute pancreatitis: 1. Serum amylase and isoenzymes -usu 5x's upper limit (ex 5x 150) 2. Serum lipase -usu 3-5x upper limit (3-5x 250) 3. effusion fluids amylase -b/c acute pancreatitis can cause pleural effusions -amylase should not normally be present in pleural fluids
Describe the serum changes of enzymes and metabolites that are characteristic of acute pancreatitis: 1. elevated serum amylase 2. elevated serum lipase 3. if pleural effusion, amylase present in it 4. decreased serum calcium 5. increased serum bilirubin (esp if obstructive) 6. increased serum methalbumin 7. increased TG 8. increased plasma glucose
Name some conditions associated with increased serum amylase levels: 1. acute and chronic pancreatitis 2. DKA (pancreas injured by acidosis) 3. intestinal inflammation -intestinal obstruction, perotinitis, etc 4. ectopic pregnancy, salpingitis 5. macroamylasemia 6. sialitis (salivary amylase) 7. mumps 8. post-traumatic
Define macroamylasemia: =benign condition in which normal amylase forms macromolecular complexes with immunoglobulins or exists as a large polymeric aggregate -these large complexes get stuck together and are not cleared by the kidney as normal -cause of elevated serum amylase level
True or false: lipase activity is normally detectable in the urine: -false -lipase is resorbed by the kidney, therefore activity not detected in urine
When do we suspect non-pancreatic causes of an elevated serum amylase level?: =when serum amylase is elevated but serum lipase level is normal
When do we want to use a urinary amylase level?: 1. determine if pt has macroamylasemia -level should be low b/c aggregates can't be cleared by the kidney 2. pt who presents with clinical picture of pancreatitis but normal serum amylase
When do you use a amylase/creatinine clearance ratio?: 1. Distinguish between pancreatitis vs macroamylasemia -pancreatitis: elevated (5-20%) -macroamylasemia: depressed (less than 1%) -this is a helpful measure b/c it corrects for differences in renal fxn -in pancreatitis, there will increased renal excretion of amylase
True or false: a high amylase value found in an effusion fluid supports a dx of pancreatitis: -true -amylase can get in b/c it's a small molecule
What electrolyte is used as a prognostic indicator in pancreatitis?: = serum Ca -decreased values below 7mg/dl -> poor prognosis -decrease in Ca by a variety of mechanisms 1. forms soap with fatty acids 2. increased CT in pancreatitis 3. hypoalbuminemia (b/c 50% of Ca usu bound to albumin) -Ca levels remain low despite infusions
True or false: pancreatitis is associated with hyperbilirubinemia: -true -even when no evidence of biliary obstruction
True or false: acute pancreatitis is associated with hyperglycemia: -true -only transient b/c pancreatic inflammation impairs ability to produce insulin and glucagon appropriately
Are the lab findings in chronic pancreatitis the same as in acute pancreatitis?: -Not necessarily -chronic pancreatitis lab values may level depending on severity and stage of disease -ex amylase may be elevated, normal, or decreased
SGPT and SGOT refer to ____ and _______ respectively.: 1. ALT 2. AST -liver enzymes commonly used to detect hepatocellular damage
Define GGT: =gamma glutamyl transferase -enzyme whose levels are useful to help determine if elevations of alkaline phosphatase are due to bone or liver (b/c GGT NOT found in the bone) -very sensitive indicator of EtOH induced liver disease -also produced by the pancreas, kidney
Does indirect bilirubin move freely in the blood?: -indirect=has not been conjugated with glucuronic acid (not as water soluble) -usu bound to albumin
Name 3 tests used to assess for hepatocellular damage: 1. AST 2. ALT 3. Bilirubin (conjugated and total)
Name 3 tests of biliary tract disease: 1. Alkaline phosphatase 2. GGT 3. Bilirubin (conjugated and total)
Name some useful tests to establish the cause of liver disease: 1. Hepatitis virus antigens 2. Hepatitis virus antibodies 3. alpha fetoprotein (tumor) 4. immunoglobulins 5. autoantibodies (antimitochondrial, smooth muscle, antinuclear) 6. iron, transferrin, ferritin (hemochromatosis) 7. copper, ceruloplasmin (Wilson's disease)
Name 2 factors that can affect the accuracy of a bilirubin level: 1. hemolysis 2. being left out in the light for too long -b/c bilirubin is light sensitive
Name the normal values for: a. conjugated bilirubin b. total bilirubin: a. conjugated bilirubin N: less than 0.2 mg/dl 2. total N: less than 1.2 mg/dl
Name some causes of elevated unconjugated bilirubin: 1. hemolytic disorders 2. Hyperbilirubinemias -Gilbert's, Crigler-Najjar, etc 3. immaturity of the newborn liver -common
Name some causes of simultaneous elevation unconjugated AND conjugated bilirubin: usu related to cholestasis 1. hepatitis 2. cirrhosis 3. posthepatic obstruction 4. dubin-johnson syndrome -liver pigmentation, excretory defect 5. Rotor syndrome -no liver pigmentation, excretory defect 6. drug-induced cholestasis
Define delta bilirubin: =third type of bilirubin that is formed when high amts of conjugated bilirubin around for a long time -> forms covalent bond with albumin -direct reacting with test reagent -b/c bound to albumin, prob responsible for persistent hyperbilirubinemia once sx have resolved -the body can't get rid of it until it replaces the current albumin proteins in the plasma
What color is urine containing an increased amt of bilirubin?: =yellowish green -if swirl it, you'll get a green/brown foam -Vit C levels can interfere with appropriate urinanalysis
True or false: pts with elevated unconjugated bilirubin levels have bilirubinuria: -false -b/c unconjugated can't be excreted in urine
Urobilinogen is a breakdown product of _________.: =conjugated bilirubin -conjugated bilirubin excreted in bile -> broken down by bacteria in the gut colorless chromogens (ex urobiliogen) and their colored oxidation products -partially reabsorbed and re-excreted through bile, some excreted in urine -urobilinogen normally found in urine -absent from urine if complete biliary obstruction (will also get chalky white stools)
When are urinary urobilinogens absent? Increased?: Absent -complete biliary obstruction -also see chalky white stools Absent -hemolytic anemia (greater amts of bilirubin excreted by liver) -early liver damage (re-excretion impaired)
Bilirubin is the end product of ______ catabolism.: =heme catabolism -conjugated in liver and excreted in bile -most of bilirubin in blood is in unconjugated form bound to albumin
True or false: fecal urobilinogens are normally present: -false
Name 3 organs systems that when diseased can result in hypoalbuminemia.: 1. liver disease -decreased synthetic capacity 2. renal disease -destruction of glomerulus -increased renal excretion 3. GI disease -increased loss of albumin
True or false: severe cirrhosis can lead to elevated amino acid levels in the blood and urine: -true -b/c impaired handling of amino acids by liver (normally breaks them down and forms them from other things) -associated w/increased amts in urine that can precipitate and form crystals
What is the connection between the liver and ammonia levels in the blood?: =the liver normally removing ammonia from the blood -increased blood levels with significant loss of liver fxn -can also see elevated ammonia blood levels congenitally if have defects in urea cycle or unable to process some modified AAs
Between AST and ALT: which is more sensitive of liver injury? Elevations of which persist longer?: ALT 1. more sensitive 2. elevations persist longer
When is AST higher than ALT?: =DeRitis ratio < 1 (ALT/AST) 1. cirrhosis 2. MI 3. metastatic carcinoma 4. progressive muscular dystrophy
When is ALT higher than AST?: =DeRitis ratio > 1 (ALT/AST) 1. acute hepatic necrosis 2. intrahepatic cholestasis 3. infectious mono
What is the LDH isozyme found in the liver? Is it found anywhere else?: =LD5 -also found in skeletal muscle -LDH released during liver cell injury
Define alkaline phosphatase: =enzyme present in high [] in lining of biliary system -gets into bloodstream when lining cells are affected by inflammation, necrosis, obstruction -elevations of alk phos are sensitive for: 1. biliary problem 2. liver cell damage -in general the higher the alk phos, the more likely its due to posthepatic obstruction -there are other sources of alk phos (bones, GI, etc) -isoforms found in liver are more heat stable than those found in bone
Name 3 causes of a decreased serum anion gap: 1. hypoalbuminemia -decrease in negative charge 2. hemodilution 3. paraproteins that increase unmeasured cations, due to positive charge -ex multiple myeloma
Name some major causes of increased serum anion gap: =MUD PALES M=methanol U=uremia D=diabetic ketoacidosis P=paraldehyde A=alcoholic ketoacidosis L=lactic acidosis E= ethylene glycol S=salicylates
How do we convert to osmoality for nondissociable water-soluble substance?: rule of thumb= MW/10=mg/dL yielding 1 mosmol/kg -good for: glucose, urea, ethanol -for urea: don't forget 2 Nitrogens/urea -> 28
How is osmolality measured?: osmolality=# of particles of solute dissolved in a kg of water -measure freezing pt depression of water due to solutes in solution -freezing pt linearly related to solute [] -more osmols of solute will lower the freezing pt more -osmolality usu measured on serum NOT plasma
Name some major causes of hyperosmolality: 1. dehydration 2. hyperglycemia/ketoacidosis 3. DI (serum osmolality high but urine osmolality low) 4. uremia 5. ethanol ingestion 6. improper specimen collection -ex use of anticoagulants
Name some major causes of hyposmolality: 1. overhydration 2. SIADH -serum osmolality low but urine osmolality high 3. polydipsia

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Number of cards 179

Created By kwithers