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80 Cards in this Set
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- Back
- 3rd side (hint)
What does ALT stand for and what do increased levels of it suggest?
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Stands For: Alanine Aminotransferase
Increased levels suggest liver damage |
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Diagnostic Enzymes Fixed On Cellulose Strips:
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1. Glucose Oxidase
Glucose + O2 + H2O --> D-gluconic acid+ H2O2 2. Peroxidase: H2O2 + O-dianisidine --> O-dianisidine (oxidised) + H2O |
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Immobilized Enzymes used in Diagnostic Tests
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1. Diagnostic Enzymes fixed on cellulose strips.
2. Immobilized urease, hexokinase, and amylase 3. ELISA |
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How long after MI is a Troponin 1 assay useful?
When do levels peak? |
1. 4 hours to 5-9
2. Levels Peak at 12-16 hours following MI |
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What level is indicative of myocardial damage?
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3. Levels above 1.5
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What test is useful for assaying for Cardiac Troponins?
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ELISA Assay
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Sickle Cell Anemia is the result of:
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Substitution of polar glutamate by non-polar valine in the 6th position in the beta subunit of hemoglobin.
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When does HbS onset occur?
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Symptoms occur after the first few months of life, when the HbF is replaced by HbA.
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Isozymes of Creatine Phosphokinase (CPK)
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CPK3 --> MM --> least electrophoretic mobility at pH 8.6 --> skeletal muscle
CPK2 --> MB --> Intermediate Mobility --> heart CPK3 --> BB --> Maximum Mobility --> Brain |
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pKa of Serine
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13
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pKa of Threonine
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13
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pKa of Aspartate
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4
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pKa of Glutamate
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4
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pKa of Histidine
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6
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pKa of Cysteine
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8
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pKa of Tyrosine
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10
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pKa of Lysine
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10.5
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pKa of Argenine
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12.5
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Testing for Toponin without reperfusion
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1-2 days until 7-9 days
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Testing for Troponin with repurfusion
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1-4 days
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Testing for CK-MB without repurfusion
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1-3 days
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Testing for CK-MB with repurfusion
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0-1 days
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To evaluate hepatocyte injury or necrosis in viral hepatitis, drug-induced hepatotoxicity, chlelithiasis, HELLP, AFLP:
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1. Aspartate aminotransferase (AST)
2. Alanine aminotransferase (ALT) |
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In cholestasis and biliary obstruction
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1. Alkaline phosphatase
2. Gamma glutamyl transpeptidase |
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LactaIsozymes of Lactate
Dehydrogenase (LDH)(LDH |
electrophoretic
mobility subunits at pH 8.6 tissue of origin LDH-1 H4 fastest heart LDH-2 H3M1 faster RBC LDH-3 H2M2 fast brain LDH-4 H1M3 slow liver LDH-5 M4 slowest skeletal muscle |
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Example of an extracellular protein that is stabilized by disulfide bonds:
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Albumin. What is albumin?
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Albumin is a blood protein that functions as a transporter for a variety of molecules.
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What does it take to break a peptide bond non-enzymatically?
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Prolonged exposure to a strong acid or base in high temperature
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What causes Alzheimer's Disease?
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Amyloid Proteins that form plaques
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What causes Creutzfeldt-Jakob Disease?
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Prions
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Function of NO
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Vasodilation
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Regular HbS Symptoms
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1. Chronic Hemolytic Anemia wit associated hyperbillirubinemia
2. Increased susceptibility to infections |
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Additional HbS Symptoms
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1. Acute Chest Syndrome
2. Stroke 3. Splenic and renal dysfunction 4. Bone changes due to marrow hyperplagia |
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Lifetime of a sickle cell RBC
Lifetime of an HbA RBC |
HbS: 20 days
HbA: 120 days |
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Sickle Cell Trait
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One HbA and one HbS
Normally asymptomatic and have a normal lifespan |
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HbC
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Mutation on the 6th position of the beta chain where Glutamate is replaced by Lysine.
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Symptoms of HbC
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Relatively mild, chronic anemia.
No treatment is necessary. |
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HbM Symptoms and Treatments
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Symptoms: Bownish-Blue skin and blood (chocolate cyanosis), anxiety, dyspnia, headache
Treatment: Methylene blue oxidizes to recuce Fe3+ to Fe2+ |
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Collagen Formation Sequence
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Signals on the pro-collagen direct it to the RER.
It is released to the Golgi and then the vesicles fuse with the cell membrane. They are cleaved extracellularly and form collagen fibrils. |
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Where is AAT made?
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Made and secreted by the Liver
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Reactions in the Mitochondria
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1. TCA Cycle
2. Fatty acid oxidation 3. Oxidation of pyruvate |
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Reactions in the Cytosol
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1. Glycolysis
2. HMP Pathway 3. Fatty acid synthesis |
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Reactions in the Nucleus
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1. DNA and RNA Synthesis
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Reactions in the Lysosome
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1. Degradation of complex macromolecules
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Steady State Assumption
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Rate of production of ES is equal to the rate of degradation of ES.
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First order reaction
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Rate of reaction is dependent of Substrate concentration ([S] is less than Km)
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Zero Order Reaction
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Rate of reaction is independent of [S] because it is higher than Km
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What are Cofactors?
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Metal Ions
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What are coenzyme prosthetic groups?
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Coenzyme prosthetic groups are small organic molecules that associate permanently with an enzyme and are returned o their origin\al form on the enzyme;.
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What are coenzyme-co-substrates?
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Small organic molecules that associate transiently with an enzyme and leave the enzyme in a changed form.
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Electron Transport Chan (ETC) location
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Inner Mitochondrial Membrane
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Causes of Respiratory Acidosis (Clinical)
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1. Chronic Lung Disease
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Clinical Causes of Respiratory Alkalosis
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1. Head injuries
2. Drug-induced toxicity |
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Clinical Causes of Metabolic Acidosis
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1. Increased ketogenesis
2. Diarrhea 3. Kidney Failure |
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Clinical Causes of Metabolic Alkalosis
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1. Administration of salts of metabolic acids
2. Stomach Vomiting |
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Ketoacidosis Etiology diagnosed by anion gap
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1. Increased hydroxybutyrate
2. Increased Acetoacetate |
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Lactic Acidosis Etiology diagnosed by anion gap
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1. Circulatory Insufficiency (low O2)
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Drug Poisoning Etiology diagnosed by anion gap
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1. Excess Salicylate
2. Excess CH3OH 3. Excess Ethylene Glycol -All of these lead to increased organic acids |
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Base Excess
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Amount of base titrant needed to return blood pH to physiologic level (7.4)
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C-Reactive Protein (CRP)
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If there is arterial damage, CRP will be released and cause arterial damage
This is an issue in many arterial diseases such as diabetes |
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Structure of Elastin
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Glycine, Valine, Alanine, Proline
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Dermal Fillers: Ways to Compensate for loss of subcutaneous collagen with age
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1. Human Collagen - does not require compatibility testing
2. Hyalyronic Acid - expands by binding water (ground substance GAG) 3. Autologous Fat - take fat from one part of the body and put it into another |
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Ehlers-Danlos Syndrome Etiology
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1. Mutations of Collagen Types I, III, IV
- Type 3 comes with vascular mutations |
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How does Lead Poisoning work?
How is it treated? |
1. There are 2 points in the process of heme synthesis where lead can inhibit the production of Protoporphyrin IX.
2. Heavy metals are removed with Kylation |
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How does Penicillin work?
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1. Penicillin is a competitive inhibitor of cell wall synthesis in bacteria.
2. It binds to the Serine at a portion of the glycopeptide transpeptidase and change the configuration, preventing the bacteria from forming cell walls. |
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What tissue is damaged when you find AST?
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Liver
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What tissue is damaged when you find ALT?
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Liver
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What tissue is damaged when you find CPK-MB?
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Heart
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What tissue is damaged when you find LDH?
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Liver, Heart
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What tissue is damaged when you find GGT?
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Liver, Heart
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What tissue is damaged when you find Alkaline Phosphatase?
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Bone, Liver
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ETC Complex 1 Inhibitor:
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1. Amytal
2. Mercurials 3. Demerol |
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ETC Complex 4 Inhibitor:
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1. Cyanide
2. Carbon Monoxide 3. Azide |
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ETC Complex 5 Inhibitor:
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1. Oligomycin
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ETC ATP/ADP Transporter Inhibitor:
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1. Atractyloside
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ETC Complex Uncoupler:
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1. Thermogen (organic)
2. 2,4-dinitrophenol (synthetic) |
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Tissue damage when Acid Phosphatase is found:
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Prostate
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Metabolic Syndrome Leads To...
Metabolic Syndrome is Treated by... |
1. Diabetes and Hypertension
2. Losing weight and removing fat from their diets |
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TCA Cycle Products
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1. 3NADH - 3ATP each
2. 1FADH2 - 2ATP each |
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What happens if there is inhibition of one of the complexes in the ETC?
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NADH level builds up and then the body goes into anaerobic metabolism so that the NAD+ can be restored and used for glycolysis
Lactic acid builds up (metabolic acidosis) |
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How do we form plaque in the blood vesels?
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LDL cholesterol becomes oxidized and combines with macrophages. The macrophage becomes a "foam cell".
The foam cell settles inside the lining of the blood vessels and aggregates, forming plaques. |
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