Biochemistry Exam - Week 1 PDF

BIOCHEMISTRY EXAM WEEK 1 Identify what false-positive and false-negative results are (sensitivity and specificity) False-positive: A test result that indicates a condition is present when it is not False-negative: A test result that indicates a condition is absent when it is present...

BIOCHEMISTRY EXAM WEEK 1 Identify what false-positive and false-negative results are (sensitivity and specificity) False-positive: A test result that indicates a condition is present when it is not False-negative: A test result that indicates a condition is absent when it is present Sensitivity: Frequency with which a test correctly identifies patients with the disease Specificity: How often healthy subjects are correctly identified IIdentify the 3 main parts of a routine urinalysis, the tests included in biochemical examination and their importance) The routine urinalysis has 3 main parts: Gross Appearance: Evaluates the urine's volume, color, and clarity. Microscopy: Examines the urine under a microscope for cells, casts, crystals, and bacteria Biochemistry: Analyzes the urine for various chemical components, including: pH: Reflects acidity or alkalinity of urine Osmolality: Measures the concentration of dissolved particles in urine Protein: Indicates possible kidney damage Urea: Indicates the body's ability to remove waste products from the bloodstream Creatinine: Indicates kidney function Glucose: Indicates possible diabetes Identify clinically relevant enzymes (e.g., their primary location, their clinical significance) Alanine aminotransferase (ALT):  Primary location: Liver and kidneys. Clinical significance: Elevated ALT levels primarily indicate damage to hepatocytes, suggesting liver disease such as hepatitis, cirrhosis, or liver cancer. However, ALT can also be elevated in conditions affecting the kidneys, such as infections or inflammation. Aspartate aminotransferase (AST): Primary location: Heart, liver, skeletal muscle, and kidneys. Clinical significance: Elevated AST levels are a marker of tissue damage, particularly in the liver, heart, and skeletal muscles. Increases in AST can occur in conditions like liver disease (hepatitis, cirrhosis), heart attack, muscular dystrophy, rhabdomyolysis, or hemolysis due to red blood cell breakdown. Creatine kinase (CK): Primary location: Mostly found in skeletal muscle, and heart muscle, with some presence in other tissues. Clinical significance: Elevated CK levels are primarily associated with muscle damage, indicating conditions like: Muscle dystrophy Rhabdomyolysis (breakdown of muscle tissue) Myocardial infarction (heart attack). Alkaline phosphatase (ALP): Primary location: Most organs, with highest concentrations in the liver, bones, small intestine, kidneys, and placenta. Clinical significance: Elevated ALP levels are associated with: Cholestatic liver disease (bile duct obstruction), which can be benign or indicative of more serious conditions like biliary cirrhosis, gallstones, or tumors. Osteoblast-mediated bone disease, including conditions like Paget's disease of bone, osteosarcoma, and bone metastases Growth spurts in children and adolescents Pregnancy, as ALP levels naturally increase during pregnancy. Gamma-glutamyl transpeptidase (GGT): Primary location: Kidney, liver, pancreas, and intestine, but in serum, primarily reflects liver origin. Clinical significance: Elevated GGT levels are a sensitive marker of liver disease, particularly in: Hepatocellular carcinoma Alcoholic hepatitis Chronic alcohol drinking  Amylase and Lipase: Primary location: Pancreas. Clinical significance: Elevated amylase and lipase levels are primarily associated with acute pancreatitis. However, they can also be elevated in other conditions affecting the pancreas, such as pancreatic cancer or obstruction of the pancreatic duct. Lactate dehydrogenase (LDH): Primary location: Present in various tissues, including heart, liver, red blood cells, kidneys, brain, lungs, and skeletal muscle. Clinical significance: Elevated LDH levels are non-specific, meaning they can be raised in various conditions affecting different organs. These conditions include: Myocardial infarction (heart attack). Pulmonary embolism (blood clot in the lung) Leukemia Hemolytic anemia (red blood cell breakdown) Liver and renal diseases Pernicious anemia (vitamin B12 deficiency) Megaloblastic anemia (vitamin B12 or folate deficiency) Certain cancers WEEK 2 The assessment of carbohydrates, lipids, proteins, vitamins and minerals and health maintenance Identify the different types of lipids, the classification of lipoproteins and their importance, and associate lipids and laboratory results (e.g., preanalytical factors, lipid panel) Types of Lipids: Fatty Acids: Essential for energy production 5 and can be linked to clinical conditions like uncontrolled diabetes mellitus 5 Triglycerides: Most prevalent fat in the diet; store excess carbohydrates 6  Phospholipids: Important for cell membrane structure 7 and act as lung surfactants 7 Cholesterol: Component of cell membranes 8, precursor for steroid hormones, vitamin D, and bile acids 8 Sphingolipids: Important for cell membranes and myelin sheath formation Fat-Soluble Vitamins: Include vitamins A, D, E, and K 9 Classification of Lipoproteins: Chylomicrons: Largest, least dense; transport dietary triglycerides 12 Very Low-Density Lipoprotein (VLDL): Synthesized in the liver; transport endogenously produced triglycerides 12 Intermediate-Density Lipoprotein (IDL): Formed from VLDL; rich in cholesterol 12 Low-Density Lipoprotein (LDL): Cholesterol-rich; carry cholesterol in the plasma 12 High-Density Lipoprotein (HDL): Smallest and densest; reverse cholesterol transport 12 Importance of Lipoproteins: Lipoproteins are essential for transporting lipids, including cholesterol, through the bloodstream. They play a significant role in cardiovascular disease, particularly atherosclerosis, which is linked to high LDL 10 and low HDL levels. HDL is considered “good cholesterol” due to its role in reverse cholesterol transport, helping remove cholesterol from arteries and delivering it to the liver for excretion. 12 LDL is considered “bad cholesterol” because high levels can accumulate in arteries, increasing the risk of atherosclerosis and heart disease. 12 Lipids and Laboratory Results: Preanalytical Factors: Diet/Lifestyle 16 Acute Illness 16 Plasma Appearance 16 (a 'creamy layer floating' indicates high levels of VLDL 16) Lipid Panel Analysis: A comprehensive blood test 16 used to determine the levels of total cholesterol, LDL, HDL, and triglycerides. Fasting for this test is essential 16. Used to identify potential risk factors for heart disease and inform treatment decisions. 16  Determine the levels of structure of proteins and their characteristics Primary Structure: The linear sequence of amino acids held together by peptide bonds. 17 Determines the overall shape and function of the protein. Like a string of beads, representing the basic building blocks of a protein. Secondary Structure: The local folding of the polypeptide chain into alpha-helices and beta-sheets. 17 Stabilized by hydrogen bonds between backbone atoms. 17 Gives the protein a more defined, three-dimensional shape. Imagine a string of beads being coiled up to form a helix or folded to form a sheet. Tertiary Structure: The overall three-dimensional shape of a single polypeptide chain. 17 Stabilized by interactions between side chains of amino acids, including hydrogen bonds, ionic interactions, hydrophobic interactions, and disulfide bonds. Gives the protein a more complex and functional shape. Like the final intricate and folded arrangement of a sculpture made from the beads. Quaternary Structure: The arrangement of multiple polypeptide chains (subunits) into a functional protein complex. 17 Stabilized by interactions between subunits. Creates a larger, multi-subunit protein structure. Imagine a complex structure formed by combining multiple sculptures. Identify common plasma proteins and their clinical importance Albumin: Clinical Importance: Maintains oncotic pressure in the blood, transports various molecules, and reflects nutritional status. 22 Decreased levels (hypoalbuminemia) can indicate inflammation, liver disease, malabsorption, or abnormal protein degradation. 23 Myoglobin:  Clinical Importance: Released into the bloodstream after muscle damage, with high levels indicating acute kidney injury or muscle damage. 24 Hemoglobin: Clinical Importance: Transports oxygen and carbon dioxide. Low levels can indicate iron deficiency or anemia. 25 Variations in hemoglobin structure can lead to hemoglobinopathies, such as sickle cell anemia. Immunoglobulins (Antibodies): Clinical Importance: Provide immune defense against pathogens. Abnormal immunoglobulin levels can indicate infections, autoimmune diseases, or immunodeficiency disorders. 26 Elevated immunoglobulin levels can be associated with polyclonal hyperimmunoglobulinemias or monoclonal immunoglobulinemia (paraprotein). 27 Coagulation Factors: Clinical Importance: Essential for blood clotting. Abnormalities can increase the risk of bleeding or thrombosis. 28 Other Plasma Proteins: Globulins (α, β, γ): Transport various substances, including hormones and enzymes. Increased levels in specific globulin fractions can indicate various conditions, such as inflammation or autoimmune disorders. 21 Determine the important of nutritional support and the different way patients can be fed Importance of Nutritional Support: Maintaining Health: Provides essential nutrients for growth, repair, and energy production, preventing deficiencies and supporting overall health. 34 Recovery from Illness: Essential for patients recovering from surgery, illness, or trauma to aid in tissue healing and recovery. 34 Preventing Complications: Minimizes complications associated with malnutrition, such as weakness, impaired immune function, and delayed wound healing. 34 Ways Patients Can Be Fed: Oral Feeding: The most common and preferred method, allowing patients to eat a balanced diet by mouth. 35 Enteral Feeding: Provides nutrition via a tube inserted into the stomach or small intestine, suitable for patients who can't swallow or have difficulty absorbing nutrients orally. 35  Parenteral Nutrition (TPN): Administration of a complete nutritional solution directly into a vein, ideal for patients unable to consume nutrients orally or enterally, but requiring long-term nutritional support. Identify clinically important tumour markers PSA (Prostate-Specific Antigen): Used for screening and monitoring prostate cancer. 38 CA 125: A marker for ovarian cancer, particularly useful for monitoring response to treatment and detecting recurrence. 40 CA 19-9: Used for detecting and monitoring colorectal and pancreatic cancers. 40 CEA (Carcinoembryonic Antigen): Particularly useful for detecting and monitoring colorectal cancer. 41 AFP (Alpha-Fetoprotein): Elevated in hepatocellular carcinoma, hepatoblastoma, and testicular germ cell tumors, specifically useful for monitoring treatment response and detecting recurrence of liver cancer. 41 hCG (Human Chorionic Gonadotropin): Primarily used in diagnosing and monitoring gestational trophoblastic disease and testicular cancer. 39 Calcitonin: Used as a marker for medullary thyroid cancer. 39 NSE (Neuron-Specific Enolase): A marker for several cancers, including small cell lung cancer, neuroblastoma, and pheochromocytoma. WEEK 3 The importance of water, sodium, and potassium balance Define osmolality and its clinical significance Osmolality: A measure of the total number of solute particles per kilogram of solvent (usually water) in a solution. 36 In simple terms, it's a measure of the concentration of dissolved substances in a fluid. Clinical Significance: Fluid Balance Regulation: Osmolality plays a crucial role in maintaining proper fluid balance in the body. Changes in osmolality can trigger shifts in fluid between compartments (intracellular, extracellular, and blood) to try and maintain balance.  Cellular Function: Osmolality affects the osmotic pressure of fluids, influencing cell function and volume. Abnormal osmolality can lead to cellular dehydration or swelling, affecting cell function. Kidney Function: The kidneys help regulate osmolality by controlling the concentration of electrolytes and water in urine. Measuring osmolality can provide information about kidney function or its ability to control fluid balance. Disease Evaluation: Abnormal osmolality can be a sign of various medical conditions, including dehydration, electrolyte imbalances, kidney disease, diabetes, and liver disease. Determine how osmolality is maintained by ADH regulation ADH (antidiuretic hormone) is released by the posterior pituitary gland. 8 The hypothalamus senses changes in the osmolality of the extracellular fluid (ECF). 8 Increased osmolality stimulates ADH release. 8 ADH acts on the kidneys to increase water reabsorption. 8 This leads to a decrease in urine volume and a restoration of ECF osmolality to a normal range. This is because reabsorbing water dilutes the ECF, reducing the concentration of solutes and therefore lowering osmolality. Low osmolality inhibits ADH release. 8 The interplay between ADH and osmolality ensures that water balance and osmolality within the body are maintained. Determine the causes of sodium and potassium imbalances Sodium: Hyponatremia (low sodium): Water retention: Kidney failure, heart failure [14, SIAD (syndrome of inappropriate antidiuresis), intake of excess water [12 Sodium depletion: Diuretics, vomiting, diarrhea, sweating Hypernatremia (high sodium): Excessive water loss: insufficient water intake, diabetes insipidus, dehydration, excessive sweating [16 Sodium gain: rarely occurs due to sodium intake; more common through direct IV sodium administration [16 Potassium:  Hypokalemia (low potassium): Increased losses: Diarrhea, vomiting, diuretics, metabolic alkalosis Redistribution: Shift of potassium into cells (e.g., insulin administration) Hyperkalemia (high potassium): Insufficient excretion: Kidney disease, hypoaldosteronism [20 Excessive intake: Supplements, high-potassium foods Shifting out of cells: Metabolic acidosis, cell damage, tissue injury Determine important clinical biochemistry pattern of AKI and CKD AKI (Acute Kidney Injury): Serum creatinine: Increased levels indicate a decrease in the kidney's ability to filter waste products. Urine output: Reduced urine output (oliguria) or complete absence of urine (anuria) are common indicators of AKI. Estimated glomerular filtration rate (eGFR): This measures the kidney's filtering capacity and is significantly reduced in AKI. CKD (Chronic Kidney Disease): Serum creatinine: Elevated levels reflect a gradual decline in kidney function over time. Urine output: May show decreased urine volume (oliguria) or normal output depending on the stage of CKD. Estimated glomerular filtration rate (eGFR): A progressively declining eGFR is a hallmark of CKD, indicating a loss of kidney function. Identify important biochemical tests that help diagnose renal dysfunction and Abnormalities ​Serum Creatinine: Indicates the kidney's ability to filter waste products. Elevated levels signal reduced kidney function. 23 Blood Urea Nitrogen (BUN): Reflects how well the kidneys are removing urea from the blood. Elevated BUN suggests decreased kidney function or dehydration. 26  Estimated Glomerular Filtration Rate (eGFR): Measures the kidneys' filtering capacity. A declining eGFR indicates a loss of kidney function, a feature of both AKI and CKD. [23 Urine Osmolality: Reflects the kidney's ability to concentrate urine. Abnormalities in urine osmolality may indicate impaired tubular function. 21 Uric Acid: Elevated levels indicate an inability of the kidneys to excrete uric acid efficiently. 26 Electrolytes: Abnormalities in electrolyte levels (such as sodium, potassium, calcium) can signal kidney dysfunction. 7 Urinalysis: This can reveal abnormalities in urine constituents, such as proteinuria (protein in urine), hematuria (blood in urine), and the presence of casts (cellular debris), which may indicate kidney disease. Determine how the urinalysis can contribute to the diagnosis of multiple myeloma diagnosis Urinalysis can help diagnose multiple myeloma by detecting the presence of Bence Jones proteins. 28 Bence Jones proteins are abnormal light chains of immunoglobulins that are produced by the cancerous plasma cells in multiple myeloma. 28 These proteins are small enough to be filtered by the kidneys and excreted in the urine. 28 Detecting Bence Jones proteins in the urine is a strong indicator of multiple myeloma. 28 WEEK 4 ❖ Acid-Base Balance and Oxygenation Identify important acid-base disorders (metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis), their concepts, causes and laboratory significance Metabolic Acidosis Concept: Decreased bicarbonate (HCO3-) in the extracellular fluid (ECF) 20. Causes: Increased H+ production, loss of H+, or direct loss of HCO3- 17 17. Laboratory Significance: pH < 7.35 22 Low bicarbonate levels 22 Decreased pCO2 (often compensated) 22  Anion gap can be normal or elevated 18 Metabolic Alkalosis Concept: Excess bicarbonate (HCO3-) in the ECF Causes: Loss of H+ (e.g., vomiting), ingestion of alkali, or potassium deficiency 24. Laboratory Significance: pH > 7.45 25 Increased bicarbonate levels 25 Elevated pCO2 (often compensated) 25 Respiratory Acidosis Concept: Increased CO2 levels due to hypoventilation, leading to increased carbonic acid 26 Causes: Depressed respiratory center (e.g., drugs), choking, asthma, or chronic respiratory conditions 28. Laboratory Significance: pH < 7.35 29 High pCO2 (> 45 mmHg) 29 High bicarbonate levels (often compensated) 28 Respiratory Alkalosis Concept: Decreased CO2 levels due to hyperventilation. Causes: Hyperventilation due to various factors (e.g., anxiety, high altitude) 31 Laboratory Significance: pH > 7.45 31 Decreased pCO2 31 Low bicarbonate levels (often compensated) Define anion gap, its significance and determine how it is calculated Definition: Anion gap (AG) is a calculated value that assesses acid-base conditions in the blood by comparing the sum of cations (positively charged ions) and anions (negatively charged ions) ? - [CI- + HCO3- ]|18]. 18 Significance: It helps to identify metabolic acidosis (particularly with an elevated AG) which is caused by increases in unmeasured anions 18. It aids in distinguishing different causes of metabolic acidosis.  A normal anion gap indicates a different cause for metabolic acidosis, such as a loss of bicarbonate 18 Calculation: Anion gap = [Na+ + K+] - [Cl- + HCO3-] ? - [CI- + HCO3- ]|18]. The normal reference range is typically between 8 and 16 mmol/L 18 WEEK 5 ❖ Assessing Laboratory Tests for Glucose Metabolism Disorders Identify important tests to help diagnose and monitor diabetes mellitus according to Diabetes Canada and their characteristics Fasting Plasma Glucose (FPG) Test 16 - Measures blood glucose levels after an overnight fast (8-12 hours). Random Plasma Glucose (RPG) Test 16 - Measures blood glucose levels at any time of day, regardless of the last meal. Oral Glucose Tolerance Test (OGTT) 16 - Involves drinking a sugary drink and then measuring blood glucose levels at intervals to assess how effectively the body regulates glucose. Glycated Hemoglobin (HbA1c) Test 16 - Measures the average blood glucose level over the past 2-3 months, providing a long-term picture of blood sugar control. Urine Ketone Test - Used for type 1 diabetes, especially when patients are unwell or hyperglycemic, to detect ketones in urine. 17 Identify important disorders of glucose metabolism (e.g., diabetes type 1 and 2, diabetic ketoacidosis, HHS), their characteristics and diagnoses Diabetes Mellitus (Type 1) Characteristics: Absolute insulin deficiency 10 Autoimmune destruction of beta cells in the pancreas 10 Prone to ketoacidosis 10 Usually develops before age 30 14 Often diagnosed in childhood or adolescence 11 Not usually obese 14 Diagnosis:  Fasting plasma glucose ≥7.0 mmol/L 16 Random plasma glucose ≥11.1 mmol/L 16 Oral glucose tolerance test (2-hour post-load glucose ≥11.1 mmol/L) 16 HbA1c ≥6.5% 16 Presence of symptoms (polyuria, polydipsia, weight loss, and fatigue) 12 May be asymptomatic 12 Confirmation through repeat testing or with other symptoms such as hyperglycemia Diabetes Mellitus (Type 2) Characteristics: Relative insulin deficiency 10 Insulin resistance 10 May have normal or high insulin levels (hyperinsulinemia) 10 Usually not associated with ketosis 10 Commonly linked to obesity and other factors 14 Usually develops after age 40 14 Often associated with hypertension and dyslipidemia 14 Diagnosis: Same testing criteria as Type 1 diabetes May be asymptomatic 12 Diabetic Ketoacidosis (DKA) Characteristics: A complication of type 1 diabetes 18 Occurs when the body cannot use glucose for energy and instead breaks down fat, producing ketones 19 Leads to metabolic acidosis 19 Symptoms include: High blood glucose (≥20-40 mmol/L) ? 20-40 mmol/L (hyperglycemia)|19] Dehydration 19 Fruity or acetone breath odor 19 Nausea and vomiting 19 Abdominal pain 18 Diagnosis: Blood glucose levels ≥14 mmol/L 21 Ketones in blood or urine 21  Arterial blood gas analysis showing metabolic acidosis (decreased pH and bicarbonate levels) 21 Electrolyte imbalances 21 Hyperosmolar Hyperglycemic State (HHS) Characteristics: A complication of type 2 diabetes 22 Extreme hyperglycemia (often exceeding 50 mmol/L) 22 Dehydration 22 No ketosis 22 Usually occurs in older adults or with prolonged illness 22 Often associated with impaired consciousness 22 Diagnosis: Blood glucose levels >50 mmol/L 22 Elevated osmolality 23 Dehydration 23 Lack of ketosis 22 May have altered mental status or coma 23 Similar laboratory testing as DKA, but ketones would be absent Treatment 23: Fluid replacement 23 Insulin in small doses 23 Monitor potassium levels 23 WEEK 6 ❖ Assessing the function of the endocrine system Compare and contrast primary, secondary and tertiary endocrine diseases Primary diseases involve direct pathology of the endocrine gland, leading to altered hormone levels. Secondary diseases arise from pituitary dysfunction, which impairs the ability of target glands to produce hormones. Tertiary diseases are due to hypothalamic failure, which impacts pituitary function and, in turn, affects hormone production by target glands. Identify disorders associated with excess and deficiency of pituitary hormones (ADH and GH) and their associated laboratory findings Excess Pituitary Hormones Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Characterized by high levels of ADH without a stimulus, leading to water retention and hyponatremia. study_note Growth Hormone Excess: Causes gigantism in children and acromegaly in adults. study_note Hyperprolactinemia: Excessive prolactin production, often due to prolactinomas, leading to milk production in women and hypogonadism/erectile dysfunction in men. study_note Adrenocorticotropic Hormone (ACTH) Excess: Leads to Cushing syndrome, characterized by elevated ACTH stimulating glucocorticoid production. study_note Deficiency of Pituitary Hormones Diabetes Insipidus: Results from a deficiency of ADH, leading to the kidneys' inability to retain water. study_note Growth Hormone Deficiency: Diminished GH secretion causing growth failure and other symptoms in children and increased body fat and decreased muscle bulk in adults. study_note Explain the negative feedback in the hypothalamus-pituitary-thyroid axis The hypothalamic-pituitary-thyroid axis (HPT axis) uses negative feedback to regulate thyroid hormone levels, preventing them from becoming too high or too low. 1. Hypothalamus: The hypothalamus releases thyrotropin-releasing hormone (TRH). 2. Anterior Pituitary: TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH). 3. Thyroid Gland: TSH acts on the thyroid gland, stimulating the production and release of thyroid hormones (T3 and T4). Negative Feedback: Now, here's the crucial part- High Thyroid Hormone Levels: If thyroid hormone levels (T3 and T4) in the blood become too high, they act as a negative feedback signal to the hypothalamus and anterior pituitary.  Suppression of TRH and TSH: This inhibits further release of TRH from the hypothalamus and TSH from the anterior pituitary resulting in reduced stimulation of thyroid hormone production, bringing the levels back down. Low Thyroid Hormone Levels: If thyroid hormone levels fall too low, the negative feedback mechanism is reversed. This allows the hypothalamus to release more TRH and the anterior pituitary to release more TSH, stimulating the thyroid gland to produce more thyroid hormones to bring the levels back to normal. Identify disorders of the thyroid and their associated laboratory findings Hypothyroidism Primary Hypothyroidism: The thyroid gland fails to produce enough thyroid hormone. Laboratory Findings: Low free T4 (fT4) and T3 (fT3) levels and elevated TSH. Cause: Often autoimmune, Hashimoto's thyroiditis being the most common. Secondary Hypothyroidism: The pituitary gland fails to produce enough TSH. Laboratory Findings: Low free T4 (fT4) and T3 (fT3) levels and low TSH. Cause: Pituitary gland dysfunction (e.g., tumor, infection, trauma). Tertiary Hypothyroidism: The hypothalamus fails to produce enough TRH, leading to decreased TSH production. Laboratory Findings: Low free T4 (fT4) and T3 (fT3) levels, low TSH, and low TRH. Cause: Hypothalamic dysfunction. Hyperthyroidism Primary Hyperthyroidism: The thyroid gland produces too much thyroid hormone. Laboratory Findings: High free T4 (fT4) and T3 (fT3) levels and low TSH. Cause: Grave's disease (most common), toxic adenomas, thyroiditis. Secondary Hyperthyroidism: The pituitary gland produces too much TSH. Laboratory Findings: High free T4 (fT4) and T3 (fT3) levels and high TSH. Cause: Pituitary gland dysfunction.  Tertiary Hyperthyroidism: The hypothalamus produces too much TRH, leading to increased TSH and thyroid hormone production. Laboratory Findings: High free T4 (fT4) and T3 (fT3) levels, high TSH, and high TRH. Cause: Hypothalamic dysfunction. Other Relevant Tests: Thyroid antibodies: These can be present in autoimmune thyroid disorders like Hashimoto's disease and Grave's disease. Thyroid ultrasound: Can help evaluate the size and structure of the thyroid gland, identifying goiters or nodules. Identify disorders of the adrenal gland and their associated laboratory findings Adrenal Insufficiency Primary Adrenal Insufficiency (Addison's Disease): Cause: Autoimmune destruction of the adrenal cortex, leading to decreased cortisol and aldosterone production. Laboratory Findings: Low Cortisol: Often confirmed by a low cortisol level on an ACTH stimulation test. Low Aldosterone: Often confirmed by a low aldosterone levels. High ACTH: The pituitary gland attempts to compensate for the lack of cortisol by releasing more ACTH. High Potassium: Mineralocorticoid deficiency leads to increased potassium levels. Low Sodium: Mineralocorticoid deficiency leads to decreased sodium levels (hyponatremia). Secondary Adrenal Insufficiency: Cause: The pituitary gland fails to produce enough ACTH, resulting in insufficient cortisol production. Laboratory Findings: Low Cortisol: Often confirmed by a low cortisol level on an ACTH stimulation test.  Low ACTH: The pituitary gland is not releasing enough ACTH. Cushing's Syndrome (Adrenal Hyperfunction) Cause: Prolonged exposure to high levels of cortisol, often due to: Pituitary Adenoma (Cushing's Disease): A tumor in the pituitary gland produces too much ACTH, stimulating the adrenal cortex. Adrenal Adenoma or Carcinoma: A tumor in the adrenal gland itself produces too much cortisol. Iatrogenic Cushing's Syndrome: Cortisol excess due to prolonged steroid medication use. Laboratory Findings: High Cortisol: The cortisol level will be elevated, often with a suppressed ACTH level (in cases of adrenal tumor). High ACTH: High ACTH levels are observed in Cushing's disease (pituitary tumor). Low ACTH: Low ACTH levels would suggest adrenal tumor as the cause. Other Relevant Tests: Urine Free Cortisol: A 24-hour urine free cortisol test can measure cortisol levels over a longer period. Dexamethasone Suppression Test: This test helps differentiate between different causes by measuring cortisol levels after administering dexamethasone (a synthetic steroid). WEEK 7 ❖ Calcium, phosphate, magnesium and bone disease Identify the different forms of calcium, the relationship with albumin, and their relationship with acid/base changes Total calcium reflects both bound and unbound forms.  Ionized calcium is the biologically active form. Albumin binds to a significant portion of total calcium. Acidosis leads to increased ionized calcium, while alkalosis leads to decreased ionized calcium. Accurate assessment of calcium levels requires consideration of albumin levels and acid-base balance. Explain the importance of adjusted calcium calculation Adjusted calcium calculation is crucial for accurate assessment of calcium levels, especially in settings where albumin levels are abnormal. It helps determine the true amount of biologically active calcium in the body. By correcting for variations in albumin levels, adjusted calcium calculations help provide a more accurate picture of the patient's calcium status, leading to more informed treatment decisions. Identify disorders of calcium and their associated laboratory findings Hypocalcemia (Low Calcium) Causes: Parathyroid Gland Dysfunction (Hypoparathyroidism): The parathyroid glands don't produce enough parathyroid hormone (PTH), which is essential for calcium absorption from the gut and release from bones. Vitamin D Deficiency: Vitamin D is needed for calcium absorption in the gut. Chronic Kidney Disease: The kidneys play a role in calcium regulation, and impaired kidney function can lead to hypocalcemia. Hypoalbuminemia: Low albumin levels can lead to a falsely low total calcium measurement, even if ionized calcium is normal. Laboratory Findings: Low Total Calcium: This can be misleading, especially if albumin levels are also low. Low Ionized Calcium: The active, unbound form of calcium will be low. High Phosphate: Low PTH levels can lead to an increase in phosphate levels. Low PTH: Parathyroid hormone levels are low in hypoparathyroidism. Hypercalcemia (High Calcium) Causes: Hyperparathyroidism: Overactive parathyroid gland, leading to excessive PTH production and increased calcium release from bones. Malignancy: Some types of cancer can cause the overproduction of parathyroid hormone-related protein (PTHrP), mimicking the effects of PTH. Vitamin D Toxicity: Excessive vitamin D supplementation can cause hypercalcemia. Sarcoidosis: This inflammatory disease can affect the body's ability to regulate calcium. Laboratory Findings: High Total Calcium: Usually indicates a problem with calcium regulation. High Ionized Calcium: This is the active, unbound form of calcium. Low Phosphate: High PTH levels lead to a decrease in phosphate levels. High PTH: Parathyroid hormone levels are high in hyperparathyroidism. Identify causes of phosphate disorders Hypophosphatemia (Low Phosphate) Decreased Intestinal Absorption: Vitamin D Deficiency: Vitamin D is essential for phosphate absorption in the gut. Malabsorption Syndromes: Conditions like celiac disease, Crohn's disease, and short bowel syndrome can impair phosphate absorption. Hypoparathyroidism: Parathyroid hormone (PTH) plays a role in phosphate reabsorption in the kidneys. Low PTH levels can lead to decreased phosphate reabsorption. Increased Renal Excretion: Hyperparathyroidism: High levels of PTH promote phosphate excretion in the urine. Fanconi Syndrome: A rare genetic disorder affecting the proximal tubules of the kidneys, leading to excessive excretion of phosphate.  Medications: Certain medications like diuretics, antacids, and some antibiotics can increase phosphate excretion. Alcohol Abuse: Chronic alcohol abuse can impair kidney function and increase phosphate excretion. Shifting of Phosphate from Extracellular to Intracellular Fluid: Insulin Administration: Insulin promotes glucose uptake into cells, which can also drive phosphate into cells, leading to low serum phosphate levels. Refeeding Syndrome: This can occur after prolonged starvation, where rapid refeeding leads to a shift of phosphate into cells. Hyperphosphatemia (High Phosphate) Decreased Renal Excretion: Chronic Kidney Disease (CKD): Impaired kidney function leads to decreased phosphate excretion. Hypoparathyroidism: Decreased PTH levels can impair phosphate excretion. Medications: Some medications like phosphate-binding agents, used for hyperphosphatemia in CKD patients, can reduce phosphate excretion. Increased Phosphate Intake: High Dietary Intake: Consuming a diet rich in phosphorus can lead to hyperphosphatemia. Intravenous Phosphate Administration: Infusion of phosphate-containing solutions can elevate serum phosphate levels. Shifting of Phosphate from Intracellular to Extracellular Fluid: Rhabdomyolysis: Muscle breakdown can release intracellular phosphate into the bloodstream. Tissue Necrosis: Cellular death releases phosphate. Tumor Lysis Syndrome: Rapid tumor breakdown can release significant amounts of phosphate into the bloodstream, often seen in cancer patients receiving chemotherapy. Identify metabolic bone diseases and important laboratory findings Osteoporosis Definition: A disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to increased bone fragility and fracture risk. Causes: Age-related bone loss Hormonal deficiencies (e.g., estrogen deficiency in women, low testosterone in men) Nutritional deficiencies (e.g., vitamin D deficiency, calcium deficiency) Medications (e.g., corticosteroids) Underlying medical conditions (e.g., celiac disease, inflammatory bowel disease) Laboratory Findings: Bone Mineral Density (BMD): Measured by DEXA scan - a standard tool for diagnosing osteoporosis. Serum Calcium: Generally normal, but may be low in severe cases or with vitamin D deficiency. Serum Phosphate: Usually normal but can be affected by vitamin D deficiency or other factors. Serum Alkaline Phosphatase: May be slightly elevated, reflecting bone turnover. Serum Parathyroid Hormone (PTH): May be mildly elevated in cases of secondary hyperparathyroidism (a complication of osteoporosis). Vitamin D Levels: Low levels may indicate vitamin D deficiency, a contributing factor to osteoporosis. Other Markers of Bone Turnover: Such as bone-specific alkaline phosphatase (BSAP) and N-terminal telopeptide of type I collagen (NTX) can assess bone resorption and formation. Osteomalacia Definition: A condition characterized by soft, weak bones due to inadequate mineralization of bone matrix, often caused by vitamin D deficiency. Causes: Vitamin D Deficiency: The most common cause. Malabsorption: Conditions that impair vitamin D absorption, like celiac disease or Crohn's disease.  Chronic kidney disease: Decreased production of active vitamin D by the kidneys. Laboratory Findings: Low Serum Calcium: Calcium absorption is impaired, causing low serum calcium. Low Serum Phosphate: Phosphate absorption is also affected, leading to low phosphate levels. High Alkaline Phosphatase: Elevated levels indicate increased bone turnover. Low Serum 25-Hydroxyvitamin D Levels: The most accurate measure of vitamin D deficiency. Rickets Definition: Similar to osteomalacia, but occurs in children and causes soft bones, bone deformities, bone pain, and delayed growth. Causes: Mostly due to vitamin D deficiency, leading to impaired calcium and phosphorus absorption, hindering bone mineralization. Laboratory Findings: Similar to osteomalacia, with low calcium, low phosphate, high alkaline phosphatase, and low vitamin D levels. Other Metabolic Bone Diseases Paget's Disease of Bone: This condition causes abnormal bone remodeling, with excessive bone formation followed by resorption, leading to deformed bones. Fibrous Dysplasia: A skeletal disorder where bone tissue is replaced by fibrous tissue, leading to bone weakening and deformity. Osteogenesis Imperfecta: A genetic disorder causing weak bones, recurrent fractures, and bone deformities. Determine useful laboratory tests to help diagnose rhabdomyolysis Creatine Kinase (CK): This is the most sensitive and specific marker for muscle damage. CK levels rise dramatically in rhabdomyolysis, often reaching 10-100  times the normal level. Measuring CK levels at multiple time points (e.g., 6, 12, and 24 hours) can help assess the severity and progression of muscle damage. Myoglobin: Myoglobin is a protein found in muscle cells. Its release into the bloodstream indicates muscle damage and is another sensitive marker for rhabdomyolysis. Myoglobin levels can be elevated even before CK levels rise. Lactate Dehydrogenase (LDH): LDH is an enzyme found in many tissues, including muscle. A significant elevation in LDH levels, along with CK and myoglobin, strengthens the diagnosis of rhabdomyolysis. Blood Urea Nitrogen (BUN) and Creatinine: These markers assess kidney function. Elevations in BUN and creatinine can suggest kidney injury, often secondary to rhabdomyolysis due to myoglobin accumulation in the kidneys. Electrolytes: Electrolyte imbalances can be present in rhabdomyolysis, especially with hyperkalemia (high potassium), hypocalcemia (low calcium), and hyperphosphatemia (high phosphate), due to muscle breakdown and release of these substances. Urine Studies: Myoglobin in Urine: The presence of myoglobin in urine (myoglobinuria) is another indicator of rhabdomyolysis Urine Creatinine Kinase: Increased levels in urine can also support the diagnosis. Urine Color: Dark, reddish brown urine, due to myoglobinuria, is a characteristic sign of rhabdomyolysis. Other Considerations: Complete Blood Count (CBC): May show elevated white blood cell count, indicating inflammation. Liver Function Tests: Liver enzymes may be elevated in severe cases. **Arterial Blood Gases: ** Might show signs of acidosis if significant muscle damage has occurred. WEEK 8 ❖ Blood Disorders and Diagnostic Tests Identify the types of leukemias and important biochemical tests that aid in Diagnosis Types of Leukemia Leukemia is a type of cancer that affects blood-forming cells in the bone marrow, leading to an overproduction of abnormal white blood cells. These abnormal cells can crowd out healthy cells and impair the body's ability to fight infections. Leukemias are classified based on: Cell Type: Acute Lymphoblastic Leukemia (ALL): This type affects immature lymphocytes (a type of white blood cell). It is more common in children and young adults. Acute Myeloid Leukemia (AML): This type affects immature myeloid cells (a type of white blood cell that gives rise to other blood cells, such as neutrophils, basophils, eosinophils, monocytes, and red blood cells). AML is more common in adults. Chronic Lymphocytic Leukemia (CLL): This type involves mature lymphocytes; it is more common in older adults. Chronic Myeloid Leukemia (CML): This type affects mature myeloid cells and is more common in adults. Rate of Progression: Acute Leukemias (ALL, AML): These types are characterized by a rapid accumulation of abnormal cells. Chronic Leukemias (CLL, CML): These types are characterized by slower progression, but they can eventually become acute. Important Biochemical Tests for Diagnosis Complete Blood Count (CBC): This test evaluates the number and types of blood cells. In leukemia, we often see: High White Blood Cell Count (WBC): Although not always present, since some leukemias have a low WBC count. Blast Cells: These are immature white blood cells, and their presence is a hallmark of acute leukemia. Anemia: Red blood cell count and hemoglobin levels can be low. Thrombocytopenia: Low platelet count, which can cause bleeding problems.  Peripheral Blood Smear: Examines the blood cells under a microscope to evaluate their morphology. It can help identify leukemia cells and their features, such as abnormal size or shape. Bone Marrow Aspiration and Biospy: This procedure involves extracting a sample of bone marrow. It is the most important test for diagnosing leukemia; it helps: Determine the Type of Leukemia: Identifying the cell type and whether the cells are acute or chronic. Assess the Percentage of Blast Cells: Helps determine the severity and stage of leukemia. Identify Genetic Abnormalities: Important for prognosis and treatment planning. Immunophenotyping: This test uses antibodies to identify the specific type of leukemia cells based on their surface markers. It helps distinguish between different types of leukemia (e.g., ALL, AML, CLL) and is often used to guide treatment decisions. Cytogenetic Analysis: Examines the chromosomes of leukemia cells to identify specific genetic abnormalities (e.g., Philadelphia chromosome in CML) which helps in treatment planning and prognosis. Molecular Testing: Tests for specific gene mutations or translocations relevant to leukemia diagnosis and treatment. Additional Tests: Lumbar Puncture (Spinal Tap): To check if the leukemia cells have spread to the central nervous system (CNS). Imaging Studies (e.g., CT scan, PET scan): To assess for the spread of leukemia (metastasis) and monitor response to treatment. Compare and contrast leukemia and lymphoma Leukemia affects the bone marrow and blood, 6 while lymphoma involves the lymphatic system. 14 Leukemia is characterized by abnormal white blood cells circulating in the blood. 6 Lymphoma involves abnormal B or T cells that originate in the lymphatic system.  Determine the main types of anemias and useful biochemical tests to help in diagnosis Iron-deficiency anemia: This is the most common type of anemia. It's caused by a lack of iron in the blood, which is needed to make hemoglobin. 24 Biochemical tests: Iron levels, Total Iron Binding Capacity (TIBC), Ferritin. 24 Pernicious anemia: This anemia is caused by a lack of vitamin B12, which is needed for the production of red blood cells. 25 Biochemical tests: Vitamin B12 levels, Methylmalonic acid (MMA), Homocysteine. Sickle cell anemia: This anemia is caused by a genetic defect that affects the shape of red blood cells. 27 Biochemical tests: Sickling tests and electrophoresis. 27 Thalassemia: This anemia is caused by a genetic defect that affects the production of hemoglobin. 28 Biochemical tests: Hemoglobin electrophoresis, Genetic testing. 28 Anemia of chronic diseases: This type of anemia is caused by chronic inflammation or infection and leads to a decrease in red blood cell production. 29 Biochemical tests: Erythropoietin levels. WEEK 9 ❖ Cardiovascular Diseases and Evaluation Tests Identify important biomarkers that help diagnose MI, and their timeline of appearance in the blood Troponin I and T: These are highly specific markers for myocardial injury. They rise within a few hours 10 and remain elevated for several days 10. Troponin I is the most specific marker 11. Myoglobin: This marker rises early, usually within 2-3 hours 12 after damage, but its specificity is low. Creatine kinase MB (CK-MB): This enzyme is involved in cellular energy metabolism and is found in various tissues 13. Levels rise within 3 to 4 hours after an MI 13. CK-MB is less sensitive than troponins 13  Identify important changes of MI on the ECG Q waves: These are a sign of transmural MI, meaning the entire thickness of the heart wall is affected 16. ST-segment elevation: This is a hallmark of STEMI (ST-segment elevation myocardial infarction) 16. T wave inversion: This may indicate ongoing injury and can be seen in both STEMI and NSTEMI (non-ST-segment elevation myocardial infarction) 16. Abnormal rhythm: The heart may beat irregularly, making diagnosis more complex. Compare and contrast characteristics of endocarditis, myocarditis, and pericarditis that can be helpful in diagnosis Endocarditis is characterized by systemic infection and fever, with specific findings like heart murmurs, Janeway lesions, and positive blood cultures. Myocarditis presents with chest pain and heart failure symptoms, and is diagnosed with elevated cardiac biomarkers, ECG changes, and echocardiogram showing signs of myocardial injury. Pericarditis often features pleuritic chest pain relieved by sitting up, a friction rub on auscultation, and diffuse ST-segment elevation on ECG, with a pericardial effusion on echocardiography. Determine key characteristics of congestive heart failure and identify biochemical tests that may aid in diagnosis Progressive disease: CHF worsens over time, with the heart becoming less efficient at pumping blood. 26 Decreased ability to pump blood: The heart cannot adequately pump blood, leading to fluid buildup. 26 Causes: MI, hypertension, heart valve disease, cardiomyopathies 26 Stasis in blood vessels: Blood flow slows, leading to fluid leaking into surrounding tissues (lungs, extremities). 26 Symptoms: Shortness of breath, fatigue, peripheral edema (swelling). 26 Biochemical tests used to diagnose CHF: Echocardiogram: Measures blood volume, assesses heart function. 27 Chest x-ray: Detects fluid buildup around the heart. 27 ECG: Evaluates heart's electrical activity, identifies origin of CHF. 27 BNP (B-type natriuretic peptide): Elevated levels indicate increased pressure in the ventricles. 27  Electrolytes: High sodium (Na) and low potassium (K) are common, suggesting kidney involvement. 27 Kidney function tests: BUN and creatinine levels are checked, as reduced blood flow to the kidneys is common. WEEK 10 ❖ Liver Disorders Identify the importance of the liver in the metabolism of carbohydrates (e.g., gluconeogenesis, glycogenolysis) The liver plays a central role in carbohydrate metabolism by regulating blood glucose levels. 3 Important processes: Gluconeogenesis: The liver produces glucose from non-carbohydrate sources like amino acids and glycerol when blood glucose is low. 3 Glycogenolysis: This process involves the breakdown of glycogen (stored glucose) in the liver to release glucose into the bloodstream when needed. 3 Glycogenesis: The liver also stores excess glucose as glycogen for later use. 3 Identify the liver function tests, their importance in diagnosing liver conditions, and when they are released into blood 1. Alanine Aminotransferase (ALT) Importance: ALT is a key enzyme involved in protein metabolism. It is primarily found within liver cells, but can also be found in smaller quantities in other tissues, such as the kidneys and heart. Elevated ALT levels in the blood indicate damage to liver cells, suggesting inflammation, hepatitis, or other liver injuries. Release into blood: ALT is released into the bloodstream when liver cells are damaged or destroyed. 2. Aspartate Aminotransferase (AST)  Importance: Similar to ALT, AST also participates in protein metabolism and is primarily found in liver cells, but other organs like the kidneys and muscles can also contain it. While elevated levels can indicate liver damage, AST is less liver-specific than ALT. Its presence in the blood can suggest damage to various tissues, including the liver. Release into blood: AST is released into the bloodstream when liver cells are damaged or destroyed. 3. Alkaline Phosphatase (ALP) Importance: ALP is an enzyme primarily associated with the cells lining bile ducts. Although found in bone, intestine, and placenta, increased ALP levels in the blood often signify problems related to the liver, particularly those associated with bile flow, known as cholestasis. Release into blood: ALP is released into the bloodstream when bile ducts are blocked or damaged, or when there's inflammation or obstruction in the bile ducts. 4. Bilirubin Importance: Bilirubin is a byproduct of red blood cell breakdown. The liver processes and eliminates bilirubin. Elevated levels can indicate a problem with liver function, such as impaired processing of bilirubin, or even hemolysis (destruction of red blood cells). Release into blood: Two types of bilirubin are tested - unconjugated (indirect) and conjugated (direct). Elevated unconjugated bilirubin can indicate hemolysis or impaired liver function, while elevated conjugated bilirubin might suggest problems with bile flow. 5. Albumin Importance: Albumin is a major protein synthesized by the liver, critical for maintaining blood volume, transporting substances, and for coagulation. It's a good indicator of liver function, and its levels can drop significantly during liver disease, particularly in chronic conditions. Release into blood: Albumin is constantly produced and released by the liver into the bloodstream. 6. Prothrombin Time (PT) Importance: PT is a crucial test for assessing the liver's ability to synthesize proteins involved in blood clotting. It is measured in seconds and is primarily affected by the liver's production of several clotting factors. Release into blood: Prothrombin is synthesized by the liver and released into the bloodstream. 7. Gamma-Glutamyl Transpeptidase (GGT) Importance: GGT is a very sensitive marker of liver disease, especially in conditions like cholestasis, as well as alcohol abuse. GGT is elevated in various liver conditions, but its primary use is to help determine the cause of elevated ALP. Release into blood: GGT is released into the bloodstream when liver cells are damaged or when there's inflammation or obstruction in the bile ducts. Explain the bilirubin metabolism from the breakdown of red blood cells to the transport of unconjugated bilirubin and conversion to conjugated bilirubin 1. Breakdown of Hemoglobin: When red blood cells reach the end of their lifespan, they are broken down in the reticuloendothelial system, primarily within the spleen. 6 This process releases heme, which is further converted to bilirubin, a yellow pigment. 6 2. Unconjugated Bilirubin: The newly formed bilirubin is initially unconjugated (also called indirect bilirubin), which means it is not water-soluble and cannot be excreted in urine. 6 It binds to albumin, a protein found in the blood, for transport. 6 3. Transport to the Liver: The albumin-bound unconjugated bilirubin is carried to the liver, where it is taken up by liver cells (hepatocytes). 6 4. Conjugation in the Liver: Inside the hepatocytes, unconjugated bilirubin is conjugated with glucuronic acid, making it water-soluble. This is a vital step for bilirubin’s excretion. 6 5. Excretion in Bile: Once conjugated (also called direct bilirubin), bilirubin is secreted into the bile produced by the liver. 6 Bile then enters the small intestine, where bilirubin is further metabolized by bacteria, ultimately excreted as stercobilinogen in feces, giving it its characteristic color. 6  Identify the main causes of jaundice (e.g., pre-hepatic, hepatic and post- hepatic) Pre-hepatic Jaundice: This type of jaundice occurs before the bilirubin reaches the liver. It's caused by excessive breakdown of red blood cells (hemolysis) leading to a high concentration of unconjugated bilirubin in the bloodstream. Example: Hemolytic anemia, transfusion reactions, certain medications. Hepatic Jaundice: This type results from problems within the liver itself, affecting the ability of the liver to process and conjugate bilirubin. Example: Hepatitis, cirrhosis, drug-induced liver injury, certain genetic disorders like Crigler-Najjar Syndrome. Post-hepatic Jaundice: This type occurs due to blockage or obstruction in the biliary system, preventing the flow of conjugated bilirubin from the liver to the intestine. Example: Gallstones, pancreatic cancer, tumors in the bile duct, strictures (narrowing) of the bile duct. Identify important liver diseases discussed in class and their key laboratory Findings Disease Key Laboratory Findings Gilbert Syndrome Reduced activity of glucuronyl transferase; high levels of unconjugated bilirubin. Crigler-Najjar Type I: Lack of glucuronyl transferase; severe unconjugated bilirubinemia. Type II: Syndrome Decreased glucuronyl transferase; chronic bilirubinemia; normal liver enzymes. Dubin-Johnson Conjugated hyperbilirubinemia; dark pigmentation in the liver; increased serum Syndrome bilirubin.  Acute: Anti-HAV IgM, HBAg, anti-HBc IgM, anti-HCV (depending on type). Chronic: Elevated liver enzymes (ALT, AST), bilirubin, anti-hepatitis B core antibodies (if Hepatitis related to Hepatitis B), anti-hepatitis C antibodies (if related to Hepatitis C). May also see decreased albumin and prolonged PT. Serum iron, ferritin, transferrin saturation (TSAT)- 70% or greater, elevated liver Hereditary enzymes (ALT, AST, ALP), total protein, albumin, glucose levels. Note: Genetic Hemochromatosis testing can confirm the diagnosis. Low serum copper, high urine copper, decreased ceruloplasmin, elevated AST, ALT, Wilson Disease GGT, and bilirubin (extent of disease), Kayser-Fleischer rings. While not a definitive diagnosis, evidence includes: elevated liver enzymes, prolonged prothrombin time (PT), decreased albumin, elevated bilirubin, high Cirrhosis ammonia levels, and abnormalities in the liver function tests. Golden Standard is a biopsy. Elevated liver enzymes, elevated bilirubin, prolonged prothrombin time, decreased Acute Liver Failure albumin, high ammonia levels, elevated blood glucose levels, and decreased urine output. Golden Standard is a biopsy. Identify important antigen/antibodies utilized to diagnose hepatitis B Hepatitis B surface antigen (HBsAg): Indicates the presence of the virus in the blood, suggesting active infection. 32 Anti-hepatitis B surface antigen (Anti-HBs): The presence of this antibody indicates immunity to Hepatitis B, either from vaccination or previous infection. 32 Hepatitis B core antigen (HBcAg): Found within the hepatitis B virus. It's not usually tested directly but is used to detect antibodies to it (anti-HBc).  Anti-hepatitis B core antigen (Anti-HBc): This antibody indicates past or current infection with Hepatitis B. 32 Anti-hepatitis B core antigen IgM (Anti-HBc IgM): This antibody is specifically IgM, which is a type of antibody produced early in an infection. Its presence suggests a recent infection. 32 WEEK 11 ❖ Pancreatic Disorders Identify key laboratory findings of acute pancreatitis Elevated serum amylase levels 6 Elevated serum lipase levels 7 Elevated trypsinogen activation peptide (TAP) levels Identify important laboratory tests utilized to help diagnose pancreatic insufficiency (e.g., fecal fat, fecal pancreatic elastase 1, etc.) and their expected results Fecal Fat Test: Measures fat in stool 14 Expected Result: Elevated levels, indicating malabsorption 14 Fecal Pancreatic Elastase 1 Test: Measures elastase 1, an enzyme produced by the pancreas 15 Expected Result: Low levels, indicating pancreatic insufficiency 15 Secretin-Cholecystokinin Test: Assesses pancreatic response to secretin and cholecystokinin 16 Expected Result: Decreased response, indicating pancreatic insufficiency Trypsinogen Test: Measures trypsinogen levels in blood 18 Expected Result: Low levels, indicating pancreatic insufficiency WEEK 12 Gastrointestinal Disorders  Determine the causes and characteristics of GI ulcers and laboratory tests that help in diagnosis Peptic ulcers are breaks in the stomach or duodenal mucosa 4. They are commonly caused by Helicobacter pylori 4 bacteria. H. pylori stimulates the inflammatory process 4 and increases hydrochloric acid production 4, as well as producing urease 4. This leads to irritation and damage to the stomach or duodenal lining. Ulcers can also be caused by long-term use of NSAIDs, smoking, alcohol consumption, and stress. Gastroscopy: This involves examining the stomach and duodenum with a flexible, lighted tube (endoscope) 5. Tissue samples 5 are taken for further examination, which may include a rapid urease test 5 (using phenol red to detect color changes), microbiological cultures 5, and histologic tests 5. Urea breath test: This noninvasive test 5 uses urea labeled with carbon-13 5to detect Helicobacter pylori. Pathogenic H. pylori produces urease 5, an enzyme that breaks down urea and releases CO2 5. Elevated levels of labeled CO2 5 in the breath indicate an active H. pylori infection. Stool antigen tests: These are reliable, convenient, and noninvasive tests 6that detect H. pylori antigen in the stool. They are highly sensitive and specific 6 for active or recent infections. Serological tests: These blood tests 6 detect antibodies (IgM, IgA, IgG) against H. pylori. They can indicate past or present infections but may not distinguish between active and inactive infections. Compare and contrast IBD Characteristic Ulcerative Colitis Crohn's Disease Anywhere in the digestive tract, Location Rectum and colon only commonly terminal ileum and colon Limited to the inner lining (mucosa) of the Can affect all layers of the intestinal Inflammation colon wall (transmural)  Frequent, watery diarrhea with blood and Loose, semiformed stools; may Stool mucus alternate with diarrhea Continuous inflammation; the entire colon is Patchy inflammation; "skip lesions" Appearance involved are common Fistulas, obstruction, bowel Rectal bleeding, dehydration, colon perforation, Complications narrowing, malnutrition, anemia malabsorption Medications (anti-inflammatories, Medications (similar to ulcerative Treatment immunosuppressants) and in some cases colitis) and often surgery surgery Determine the cause and consequences of celiac disease Celiac disease is an autoimmune disorder triggered by gluten, a protein found in wheat, barley, and rye 16. When people with celiac disease eat gluten, their immune system mistakenly attacks the lining of their small intestine 16. This damage can lead to a variety of symptoms and health problems, including: Malabsorption: The damaged intestinal lining can't absorb nutrients effectively. Diarrhea: Undigested food and fluid pass through the intestines more quickly, causing loose, watery stools. Weight loss: The inability to absorb nutrients can lead to weight loss and malnutrition. Abdominal pain and bloating: Inflammation and gas can cause abdominal discomfort. Anemia: Insufficient iron absorption can lead to anemia. Fatigue: Low energy levels due to poor nutrient absorption. Other symptoms: Celiac disease can also cause bone pain, skin problems, seizures, and infertility. WEEK 13 ❖ Biochemical Toxicology Diagnosis of poisoning Diagnosis of poisoning is usually made based on clinical findings, like the patient's symptoms, rather than solely on lab results. 3 Important information includes the date and time of exposure and details about the patient's physical condition and symptoms. 3 Each poison can cause a specific toxic syndrome (toxidrome), but symptoms can sometimes overlap, making identification difficult. Compare and contrast acute and chronic toxicity Acute toxicity happens quickly from a single or few exposures, while chronic toxicity develops over a longer time from repeated exposure. Determine the importance of ethanol poisoning and identify the biochemical tests that help in diagnosis Ethanol poisoning is important because it is a frequent cause of overdose and can be life-threatening. 16 The biochemical tests for diagnosis include blood ethanol measurement, plasma osmolality, and osmol gap. Determine the usefulness of anion gap and osmol gap in toxicology and how they are calculated The anion gap and osmol gap are useful tools in toxicology for identifying potential poisoning. Anion Gap: An increased anion gap indicates an increase in unmeasured anions such as those from toxins like methanol, ethylene glycol, or salicylates. 22 The formula for calculating anion gap is: (Na+ + K+) - (Cl- + HCO3-) = Anion Gap The normal range is 8 to 16 mmol/L. Consider the importance of toxicity of common medications Toxicity of common medications is important because many people take them for long periods. Many medications have side effects, and even therapeutic doses can become toxic at times. 23 Common causes of poisoning include salicylates and acetaminophen (paracetamol).