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43 Cards in this Set
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1. What changes are evident in kidney function in the elderly (see pages. 2 & 3 for figures 68.1 & 68.2). Add the following: decreased serum cystatin.
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Glomerulus: Decrease in Glomerular filtration rate
Decrease in effective renal plasma flow Proximal Tubule: Decreased tubular reabsorption of phosphate Decreased maximal excretion of glucose and PAH Distal Nephron: Inability to maximally excrete an acid load, impaired diluting ability, decreased maximal concentrating ability, impaired conservation of sodium |
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2. What is the relative change in plasma glucose, and glycosylated hemoglobin (GHb), as people age (see page 4 for figure 68.6).
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The fasting plasma glucose levels and glycosylated hemoglobin levels are increased with age
Glucose Intolerance: increased incidence as one ages of diabetes mellitus (10-30%) within the nondiabetic fraction of plder people fasting plasma and glycosylated hemoglobin both increase with age |
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3. Review changes that occur in endocrine function as one ages. In particular the loss of thyroid & gonad function. Also know the trend for TSH (increased), T3 (decreased), and T4 (unchanged) (see figure 29.4 on page 5)
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The two glands in the endrocrine function with the most notable changes are the thyroid and gonads.
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4. Review Pre-analytical, Analytical, and (Post-analytical) considerations related to lab testing in the elderly. (pages 6 & 7)
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Preanalytical considerations:
A.Specimen collection procedures and efficiency may have to be altered for the following reasons. • Phlebotomy is often more difficult in the elderly. • Preparation of the patients may be hindered (fasting samples may be difficult to get because or physical and/or psychological factors, patients may not understand sampling criteria • Sampling itself may lead to subsequent health problems ( a confused patient may remove bandages and open wound sites after phlebotomy) B. HMO and medicare coverage may dictate how and when tests can be performed Analytical Considerations • Samples may be inadequate in quantity and quality (inc. hemolyzed samples) • Elderly tend to have multiple drug therapies, drug interactions within the test itself is possible. |
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Review ((Pre-analytical, Analytical)) and Post-analytical considerations related to lab testing in the elderly. (pages 6 & 7)
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Post Analytical considerations:
• Less efficient utilization of results by healthcare providers ( nursing home residents often have periodic test which may or may not be followed up on. • Reduced ability of some elderly patients to utilize test result for improving health • Guidelines for interpreting lab results for such a WIDE range of people in elderly populations (nutritional status, level of exercise, and physiological status can be confusing. Table 29.5 Factors to consider: Exercise, Medications, Mobility, Nutritional status, Personal habits, Presence of multiple chronic and subclinical disorders, reference interval validity, specimen collection variables. |
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5. Review elderly-specific changes affecting TDM (see page 8)
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• Multidrug interaction
• Aging effects drug absorption (GI changes) • Aging effects drug distribution (decreased blood flow) • Aging effects drug metabolism (decrease in liver mass) • Aging effects drug excretion (kidney glomerular function is reduced) • Psychological factors altering compliance |
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1. Review bone remodeling theory. What is the function of osteoclasts and osteoblasts? What are the Four stages in normal remodeling ? Relate the following to the stages:
• What components are released? • Time periods • Net change in bone mass • % of healthy adult skeleton remodeled/year (in men and premenopausal women) |
4 stages in Normal Remodeling:
Phase 1: Osteoclasts attach to the bone surface, releasing bone collagen and minerals into the circulation Phase 2: Duration of bone pitting in resorption sites lasts on average 3 weeks; all the while releasing “altered bone collagen fragments” Phase 3: Osteoblasts are recruited to the newly resorbed area on the bone. New bone is laid down by osteoblasts as they deposit new collagen to fill the excavated pits (this processing phase typically lasts 2-4 months). Phase 4: In adults when resorption and formation are in balance, there is NO net change in bone mass. Before menopause, healthy adults are constantly turning over new bone, between 10% to 30% of the adult skeleton is remodeled each year. |
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2. What is the association of menopause and bone loss?
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Decrease in bone mass. Bone loss increases after menopause. Estrogen levels decrease which leads to osteoporosis because sex hormones maintain the rate of bone deposition. 1/3 of postmenopausal women develop osteoporosis.
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3. How is age related to bone mass?
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In healthy children and yourg adults bone remodeling is focused on the formation of new bone. Peak bone mass is achieved sometime in early adulthood, and is relatively stable for a long period of time (bone resorption = bone formation). Eventually the process of resorption occurs more rapidly than the formation of new bone resulting in bone loss. Osteoporosis occurs when loss of bone mass is to the extent that enhanced bone fragility and increased risk of fractures occurs.
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4. Review the risk factors that have been documented in increased risk of developing osteoporosis.
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Risk factors are:
Small, thin frame Family history of osteoporosis Age and menopausal status Early or surgically-induced menopause Resorption-accelerating medication High level of bone resorption Low calcium diets Physical inactivity Smoking Excessive alcohol consumption High caffeine intake Excessive soft drink consumption |
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5. What biomolecules crosslinks collagen in new bone?
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c telopeptides and N telopeptides
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6. What is the difference between Primary Osteoporosis (type 1 & 2), and Secondary Osteoporosis? What are some known common conditions leading to secondary osteoporosis
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Primary Osteoporosis: Involutional osteoporosis which can be further classified as Type 1 (post menopausal) Type II (senile).
Secondary Osteoporosis: Loss due to certain diseases procedures and certain drugs (Glucorticoids-hydrocortisone andanticonvulsants). *Diseases: Hypogonadism, hyperthyroidism, chronic obstructive lung disease, hyperparathyroidism, insulin-dependent diabetes, rheumatoid arthritis, connective tissue disorders, proliferative disorders (multiple myeloma) |
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7. What markers can be used to measure bone formation? Also know the sample types and assay formats for these tests.
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Bone formation tests Sample Test Format
Osteocalcin Serum Immunoassay Bone alkaline Phosphatase Serum Enzymatic |
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8. What are the markers of bone resorption? The sample types and assays?
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Bone resorption Markers Test Sample Test Format
Crosslinked Ntx Urine Immunoassay Crosslinked CTx Urine Immunoassay Deoxyprydinole/pyridinole Urine HPLC, Immunoassay |
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9. Apart from collagen, which protein is at the highest concentration in the bone matrix? (osteocalcin) How does the level relate to such diseases such as Paget’s disease, acromegaly, hyperthyroidism, GH deficiency, etc
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Osteocalcin: highest non-collagen protein in bone (1%). Synthesized by osteoblasts during bone formation. They are increased in Pagets, acromegaly, hyperthyroidism, and GH deficiency.
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11. Review the relationship between NTx concentration & BMD. Relate your answer to fracture risk and treatment.
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NTx Bone Mass Density Risk Treat
High Low + + + YES! High Normal/High + + Yes Low Normal/High -- Consider for menopause Low Low + + Yes (same as above) |
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1. What are the definitions for: acute coronary syndrome, AMI, angina, atherosclerosis
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Acute coronary syndrome: A sudden cardiac disorder that varies from angina (chest pain on exertion with reversible tissue injury), to unstable angina (with myocardial injury) and to myocardial infarction (with extensive tissue necrosis).
Acute Myocardial Infarction (AMI): Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; almost always caused by atherosclerosis of the coronary arteries, on which coronary thrombosis usually is superimposed; commonly called “heart attack”. Angina: Chest pain often associated with a decrease in oxygen (ischemia) to the heart. Atherosclerosis: The disease process that causes plaque formation within large and medium-sized particles. |
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ischemia, plaque, reperfusion, unstable angina?
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Ischemia: Deficiency of blood flow to part of the heart caused by functional constriction or actual obstruction of a coronary artery.
Plaque: A pearly white area within the artery that causes the intimal surface to bulge into the lumen; composed of lipid, cell debris, smooth layer muscle cells, collagen, and sometimes calcium, with a fibroblast layer cap; also called atheromas. Reperfusion: The restoration of blood flow to an area of the heart after an AMI Unstable Angina: Angina that is increasing in severity duration, or frequency. Evident when no exertion is occurring (i.e. at rest). |
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2. Know the signs and symptoms associated with heart disease
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• Dyspnea (difficulty breathing; short of breath)
• Syncope (temporary loss of consciousness and posture, describe as “fainting” or “passing out”. It’s usually related to temporary insufficient blood flow to the brain). • Cyanosis (refers to the bluish coloration of the skin due to the presence of deoxygenated hemoglobin in blood vessels near the skin surface. • Pain • Palpitations • Fatigue • Edema (tissue fluid buildup most commonly of the legs and ankles, and sometimes the abdomen |
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3. What are the components and progression of plaque formation? (eg. initiation through full occlusion
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• initiation through full occlusion
• Plaque builds up on the wall of an artery • during stress or other stimulation • Plaque ruptures leading to activation of the coagulation cascade • which induces platelet aggregation and thrombus formation • Thrombus formation leads to partial or complete artery occlusion blocking blood flow and leading to the angina or AMI |
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4. What are the WHO, AMI diagnostic criteria? How many are needed for AMI diagnosis? What is STEMI? NSTEMI? How does elevated ST segment relate to AMI?
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WHO diagnostic AMI criteria:
1. Chest pain >20 minute duration 2. ECG (ST segment elevation infarct (STEMI) 3. Cardiac marker(s) elevation In theory the frist 2 WHO criteria might seem enough to diagnose AMI but lab markers are also very important due to: Silent AMI (pt. has no symptoms, especially important in the elderly and women) NSTEMI : non-ST segment elevation infarct |
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5. What is the serial blood collection schedule for possible AMI?
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(admission, followed by 4-8 hour interval blood sample collection in serial with ECG performance
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6. What are the present day AMI lab markers? Know the kinetics for each
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Myoglobin,, CK-MB (very sensitive but not used by all labs)
Troponin I and Troponin T |
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7. What are the troponins? Which are useful for AMI evaluation? Compare Troponins I &T (specificity problems, kidney failure interference, etc.)
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Troponin I heart isoform has never been shown to be expressed in normal, regenerating, or diseased skeletal muscle. CONs: It has numerous manufacturers making the components and they have unequal overlapping reference ranges and standards which can be a problem when comparing data from different labs with different analyzers.
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8. Which formats are used for the lab markers discussed in class? (immunoassays for all, with the exception of IMA using the colorimetric ACB test
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8. Which formats are used for the lab markers discussed in class? (immunoassays for all, with the exception of IMA using the colorimetric ACB test
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9. Which formats are used for the lab markers discussed in class? (immunoassays for all, with the exception of IMA using the colorimetric ACB test How is successful reperfusion reflected in CK-MB kinetics (see page 7). Why is CK-MB best as a reperfusion marker?
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CK-MB is better in reperfusion detection. Its levels drop at 0 after 80 hours from onset of infarction, whereas troponins lasts for more that 160 hours.
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10. What are the uses for AMI indicator markers? Why is Troponin I or T best for revealing older AMI events (ie. 5-14 days previous to admission or evaluation)
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Uses for AMI indicator markers:
• Risk stratification (i.e. risk of death) • Success of reperfusion using thrombolytics • Determination of infarct size (direct relationship) • Reinfarction detection : CK-MB is better for this than Troponins • Detection of potential heart damage that occurred during major surgery (Heart and non-heart tissues) |
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11. Why is rise or fall of AMI markers important? What condition is indicated by an unchanging troponin value through the serial time point periods? (remember what happens in some kidney failure patients)
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The rise and fall of AMI is important because they can help assess the damage done and if there is a reinfarction. An unchanging troponin value throughout several time periods indicates or is caused by chronic renal disease.
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12. What are the 2 negative AMI prediction scenarios related to myoglobin determination
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2 Negative AMI predictor situations:
• Myoglobin levels less than URL within 2-4 hours after onset of symptoms is 100% certainty of non-AMI scenario. • Increased myoglobin above URL in peak followed by lower serial values, but no increase in troponins or CK-MB values within the first 12 hours of the onset of symptoms indicates skeletal muscle damage only. |
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13. What is “Ischemia Modified Albumin” , and how is it related to ischemia or AMI? What is the ACB test
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? IMA are produced at the site of plaque inflammation or rupture due to increased Oxygen radicals near ischemic tissues. It increases much earlier than the other Cardiac markers. ACB detects IMA.
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14. What is Heart Failure (HF)? (include causes and symptoms)
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A condition in which the heart cannot pump enough oxygenated blood to the body (i.e. decreased ventricle efficiency). It can be acute of chronic.
The causes are: Heart valve disease, high blood pressure, infection (endocarditis), previous AMI (healed), coronary artery disease, congenital heart disease, irregular heartbeat, chronic lung disease/pulmonary embolism, drug-induced heart failure, diabetes, anemia/severe blood loss. The symptoms are: Shortness of breath (even during rest), weight gain, swelling of legs/ankles and occasionally abdomen, fatigue/weakness, loss of appetite, persistent cough, reduced urination (decreased kidney function) |
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15. What is BNP? NT-proBNP? How does there measurement relate to HF?
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BNP is the hormone produce by the ventricles of the heart, a useful lab test related to the diagnosis or monitoring of HF. It is on e of 4 known natriuretic peptide (ANP, BNP, CNP, DNP)
BNP: Dilates arteries and veins, Decreases levels of vasoconstricting and sodium-retaining neurohormones, Promotes diuresis and natriuresis (water and sodium output is increased in conjunction with ANP. BNP (or NT-proBNP) levels are used to : Help determine the presence of HF; Grading the severity of HF/prognosis; Impact of treatment with synthetic BNP (tradename Nesiritide) (a good outcome is shown by a decrease in the levels of natural BNP or NT-proBNP. |
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16. What is the relationship of troponin, myoglobin, & IMA in conjunction with ECG to “Rule-Out AMI
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16. What is the relationship of troponin, myoglobin, & IMA in conjunction with ECG to “Rule-Out AMI
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1. What are the fat-soluble vitamins? Water-soluble vitamins? (Table 28.1) Also review case study 28.3 related to fat malabsorption.
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Fat Soluble vitamins: A, D, E, K
Water Soluble : B1, B2, B4, Niacin , Folic Acid, B12, Biotin, Pantothenic acid, Vitamin C, Carnitine |
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2. Compare the heterogeneous and homogeneous tesating formats for folate measurement (pg 4) Why do endogenous binders have to be dealt with before assaying? (to release bound folate, so it can be measured in the assay -- boiling or elevated pH of 12-13 for a short period will release the bound forms)
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Heterogenous assay: Tpyically labeled folate (acridinium ester-labeled folate) competes for binding to a folate binding protein (like beta-galactoglobulin from cows milk) reagent with sample, unlabeled folate. The binder/folate complexes are specially removed, the supernatant is then measured for remaining chemiluminenscen from remaining unbound (free) acridinium ester-folate molecules.
Homogenous assay: Similar to heterogenous assay except no separation is needed because measurement is by fluorescence polarization. **Both assays requires that endogenous binders be removed or inactivated |
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3. What are some of the non-protein lab markers that can be used to assess malnutrition status? (hematology --- reduced hemoglobin/hematocrit, low WBC [especially if lymphopenia is evident]; chemistry -- low triglycerides and low cholesterol levels
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Hematology: Reduced RBC components like hemoglobin, white cell count, hematocrit
Immunology Assays: Reduced lymphocyte levels, delayed or decreased immune functions, increased TDT levels (inc. of immature T lymphocytes) , Cytokine levels IL-1 and IL-2 if fat soluble and B complex vitamins are adequate. Chemistry: Ind vit. Analysis, fecal fat, Urine BUN/Creatinine , cholesterol and triglyceride levels, mineral levels. |
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4. What are the typical analytes that are tested in a routine panel to assess TPN success in a patient that relies on this feeding format for an extended time period (weeks to years
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Adults: CBC, Prothrombin Time, Glucose, Electrolytes, Ca++, Mg++, Phosphate, Cu++, Zn, Tranthyretin
Newborns: CBC, Prothrombin time, Glucose, BUN, Electrolytes, Ca++, Mg++, Phosphate, Aspirate aminotransferase, Bilirubin, Alkaline phosphatase, Triglycerides, Cholesterol, Transthyretin. |
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5. Review the use of B12 and folate testing for the differentiation of megaloblastic anemia. Which test is used to measure B12 deficiency due to intrinsic factor deficiency (either secretion or autoimmune related) (pags. 8 – 12)
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Schillings test provides a measure of a person’s ability to secrete viable intrinsic factor and absorb orally administered labeled (e.g. Co-labeled B12). Parenteral B12 is given simultaneously to saturate endogenous protein binding sites. Serum and urine are collected at intervals, and labeled B12 is measured in the specimens. Patient who cannot absorb B12, cannot absorb the labeled B12, and so have low levels in blood and urine.
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6. What are the criteria tht is good for choosing a protein marker for nutritional status? Which markers have been used? Which appears to be the best (transthyretin) (pgs. 8 – 12)
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Criteria for choosing a protein marker:
• Easily and cheaply measured • Rapid turnover (short half-life) • Should correlate with poor nutritional status, and should directly correlate with improvement in nutritional status • Rapid rate of synthesis • Not or minimally affected by non-nutritional factors • Relatively low vascular concentration level, and low extra-vascular levels (small body pool) |
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7. How can CRP and transthyretin be used in conjunction for abetter assessment of nutritional status/change (figures pg 12)
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Using a plasma marker like transthyretin in conjunction with an acute phase reactant like CRP can be very useful
If: • The CRP level is normal a low transthyretin level indicates protein malnutrition • The CRP level is significantly increased in the presence of low transthyretin there might be a false decrease (related to protein nutrition status) in transthyretin ( a negative acute phase reactant) • During monitoring, patients with decreasing levels of CRP and increasing levels of transthyretin, indicates an improving protein nutrition status. |
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, Analytical, ((and Post-analytical)) considerations related to lab testing in the elderly. (pages 6 & 7)
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Analytical Considerations
• Samples may be inadequate in quantity and quality (inc. hemolyzed samples) • Elderly tend to have multiple drug therapies, drug interactions within the test itself is possible. |
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What is atherosclerosis
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Atherosclerosis: The disease process that causes plaque formation within large and medium-sized particles
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Troponin T vs Troponin I
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Troponin T heart isoform has been shown to be present in fetal developing skeletal muscle, and in regenerating or diseased skeletal muscle (e.g. muscular dystrophy), as well as small percentage of chronic renal disease patients. CONs: It is prone to increases in non-AMI pathologies; especially in some chronic renal failure patients. These patients can be easily seen in serial troponin assays (same elevated value each time; instead of a rise or fall as seen with AMI patients.
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