CLM Chemistry 3 Renal/Cancer & Tumor Markers/Edocrine/Toxicology – Flashcards
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Primary Glucocorticoid produced and secreted by the adrenal cortex
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Cortisol
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Cortisol
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CHO, lipid and protein metabolism Suppression of inflammation Stimulates gluconeogensis Increases urine production Stimulates erythropoiesis Diurinal variation, highest in morning, lowest in evening
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Primary mineralocorticoid and produced by adrenal cortex
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Aldosterone
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Aldosterone
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Stimulates Na resorption in the DCT in exchange for K+ and H+ Regulated primarily by renin angiotensin system........... Regulates extracellular fluid volume Stimulates renal tubules to absorb H2O and to secrete K+ Targets distal renal tubules and large intestine
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Increased aldosterone secretion
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Primary - adrenal adenoma, bilateral cortex hyperplasia Secondary -(when the kidney thinks its being under per fused, so its response is to try and increase its perfusion. It does so by activating several things like ANGII and Aldosterone) -- renal vascular stenosis, hyponatremia, hypovolemia, malignant hypertension, CHF, nephrotic syndrome
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Catecholamines are made
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in the medulla part of the adrenals
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Catecholamines
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Products of the hydroxylation of tyrosine Mobilize energy stores by increasing BP, HR and glycogenolysis Neurotransmitter actions Released in response to pain and stress to mobilize organs 20% excreted into the urine as Metanephrine and Normetanephrine Vanillylmandelic acid (VMA)
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Renal Disorders
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Erythropoesis Calcium homeostasis Vitamin D
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Synthesized in the endothelial cells in the peritubular capillaries
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Erythropoietin
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Calcium homeostasis
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1-alpha-hydroxylase Synthesized in the proximal renal tubule cells Converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, the active form of Vitamin D
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Vitamin D
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Increases GI reabsorption of calcium and phosphorus Regulates serum calcium Promotes bone mineralization Increases the production of osteoclasts
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Role of kidney in concentration and dilution of osmolality
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...
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BUN
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Fairly good marker of what is being filtered into the kidney. End product: amino acid & pyrimidine metabolism Produced by the liver via urea cycle Filtered in the kidneys and partly reabsorbed in the proximal tubule (not a significant amount reabsorbed) Extrarenal sites of excretion (GI tract, lungs, skin) : < 5% of excretion
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BUN Serum levels dependent on:
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Glomerular filtration rate (GFR) Protein content in the diet Tissue metabolism Proximal tubule reabsorption which is dependent on GFR Functional status of the hepatic urea cycle
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INCREASED BUN
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CHF, Shock (hemorrhage), volume depletion (diuretics) High protein diet, TPN, blood in GI tract 3rd degree burns, Post-op states, wasting disease (HIV) Poststreptococcal glomerulonephritis Acute tubular necrosis, diabetic glomerulopathy Urinary tract obstruction
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DECREASED BUN
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Normal pregnancy, SIADH Cirrhosis, fulminant liver failure Starvation
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Is serum Creatinine a poor indicator of early renal disease?
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Yes
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Serum Creatinine
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End product: amino acid & pyrimidine metabolism Metabolic end product of creatine in muscle Filtered in the kidneys and not reabsorbed or secreted Serum concentration varies with age, gender, muscle mass
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INCREASED Creatinine
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Increased in renal disease, hypovolemia, acromegaly, hyperthyroidism & tissue necrosis
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Drugs and chemicals interfere with Creatinine
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Falsely increased with certain cephalosporins, trimethoprim, dronedarone Falsely increased in diabetic ketoacidosis Falsely decreased in hyperbilirubinemia
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What is elevated BUN and Cr?
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Azotemia
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***Prerenal BUN:Cr>20:1
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Reduced blood flow to kidney Reduced GFR Retention waste Volume depletion, CHF, Hemorrhage, pancreatitis
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***Renal (Acute renal failure) BUN:Cr <15:1
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Kidney is dysfunctional or damaged Glomerulonephritis or Acute tubular necrosis acute or chronic renal failure
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***Postrenal BUN:Cr >15:1
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Due to urinary tract obstruction Prostate hyperplasia obstructing the urethra Bladder/cervical CA obstructing ureters Blockage of ureters by stone (renal lithiasis)
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Creatinine Clearance
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Estimate of Glomerular filtration Annual decrease in CCr of 1mL/min beyond age 50
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CCr is useful in:
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Detecting renal dysfunction A change in >22 mL/min from previous in either direction is medically significant Calculating dose intervals for renally eliminated drugs, many of which are nephrotoxic Evaluating the effectiveness of therapy on progressive renal diseases Use of angiotensin-converting enzyme inhibitors in the treatment of diabetic glomerulopathy
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Equation that estimates CCr
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Cockroft-Gault Equation involving Age, Mass, Female factor
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Which of the following is a cause of acute kidney failure due to prerenal azotemia? A. Excessive diuresis B. Urinary tract obstruction C. Radiologic contrast media D. Aminoglycosides
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A. Excessive diuresis
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Urine Osmolality (Uosm)
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Evaluates the concentrating ability of kidney
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The first laboratory sign of tubular dysfunction?
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Loss of urine concentration
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Increased Urine Osmolality
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Syndrome Inappropriate ADH Secretion (SIADH) Dehydration Glycosuria Adrenal Insufficiency High protein diet
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Decreased Urine Osmolality
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Diabetes Insipidus Excessive hydration (oral or intravenous) Acute or chronic renal insufficiency Glomerulonephritis
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Hyperglycemic hyperosmolar state
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A stuporous patient with a history of type 2 DM is brought to the emergency room with a five day history of progressive lethargy and confusion along with polyuria and polydipsia. On examination the patient is dehydrated and is without Kussmaul respirations. Serum glucose: 1200 mg/dL (75-110) Serum NA+: 150 mEq/L (136-146) Serum pH: 7.5 (7.35-7.45) Serum osmolality: 320 mosm/kg (280-300 mosm/kg) Urinalysis reveals no ketones.
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Breast Cancer markers not to be used for screening: CA 15-3 CA 27.29
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Monitoring treatment <50% with localized breast CA have increased levels Metastatic breast dz 80% elevated CA 15-3 65% elevated CA 27.29
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Ovarian Cancer marker CA-125 that is elevated in >80% of woman w/ovarian cancer also Not effective for screening
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Extremely accurate marker for non-mucinous epithelial tumor High degree of sensitivity and specificity Used to determine response to therapy Used in post-treatment surveillance Increased in other cancers as well Ovary * Pancreas Nonovarian female genital tract Breast Colon Lung Lymphoma Peritoneal carcinoma
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Other markers:
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Beta-human chorionic gonadotropin (Beta-hCG)--prostate cancer Carcinoembryonic antigen (CEA)--colon cancer CA19-9 Alpha-fetoprotein (AFP) Prostate-specific antigen (PSA)
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Thyroid Panel
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TSH T4 Free T4 Free T3
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The most common cause of endocrine hypofunction?
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Auto-immune disease***
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The most common cause of endocrine gland hyperfunction?
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Benign adenoma***
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Levothyroxine
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synthetic T4 (less active than T3)
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Triiodothyronine
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(T3) is the most physiologically active
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Thyroxine (T4) the primary circulating thyroid hormone:
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is a prohormone and a reservoir for the active thyroid hormone (T3)
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Total T4 =
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bound and unbound fractions
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Free T4=
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: unbound metabolically active
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Elevated TBG (Thyroid Binding Hormone) corresponds to
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elevated T3 & 4
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TBG Elevated
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pregnancy, HRT, porphyria, infectious hepatitis, certain drugs (HRT, OCs, methadone
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TBG Decreased
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GI malabsorption, neprhotic syndrome, malnutrition, certain drugs (phenytoin, androgens, propranolol, steroids
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Primary hypothyroidism
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A 55 year-old female presents he clinic with lethargy, fatigue, constipation, and menorrhagia and depression. Physical examination reveals an enlarged thyroid, dry skin, and a heart rate of 50 bpm. Laboratory results show a decrease in free T4, and an elevation in TSH.
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Toxicology Specific tests:
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Acetaminophen Aspirin ETOH
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Toxicology Screen may include:
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Amphetamine Barbituate Benzodiazepine Cannabinoid Cocaine Opiates/Opioids Oxycodone Fentanyl Suboxone PCP
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Does Hemoglobin have a higher binding affinity for carbon monoxide than it does for oxygen?
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yes! 200-300x more
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carboxyhemoglobin
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bright red compound formed when hemoglobin combines with carbon monoxide
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Environmental Toxins
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Carbon Monoxide & Lead
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Carbon Monoxide Poisoning
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Based on carboxyhemoglobin May cause ischemic damage to skeletal and cardiac muscle
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Lead Poisoning
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Primarily children Levels >10 ug/dL consider lead poisoning treatment
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Do drugs of abuse have reference ranges?
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NO! Because the baseline is zero.
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When would therapeutic monitoring of drugs be necessary?
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Prescribed drug has a low margin of safety Decent relationship between drug in serum and either therapeutic or toxic effects Symptoms of underlying disease are difficult to distinguish from drug toxicity The treatment goal is not an objectively measured endpoint (such as blood pressure)
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Some drugs that typically require monitoring:
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Methotrexate Lithium Antibiotics (gent, tob, vanc) Tricyclic antidepressants Antiepileptics Older agents phenytoin, carbamazepine, phenobarbital Others: Digoxin Methadone Clonazepam
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A 22 year old woman had a generalized seizure. Her BP is 165/100, heart rate 119, temperature 100.9, respiratory rate 19, oxygen saturation 98% on room air, finger stick glucose 92 mg/dL. hallucinating her pupils are dilated to 6 mm bilaterally and reactive neck is supple tachycardia BUN 10 mg/dL Creatinine 1.0 mg/dL Glucose 103 mg/dL Sodium 109 mEq/L Potassium 3.5 mEq/L Chloride 83 mEq/L Bicarbonate 20 mEq/L WBC 12,000/mm3 HCT 49% Platelets 350/uL Which of the following substances did this patient most likely consume? A. Cocaine B. Heroin C. 3,4-Methylenedioxymethamphetamine D. Ketamine E. PCP
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C. 3,4-Methylenedioxymethamphetamine
