Biochem Exam 1

Front 1

What does ALT stand for and what do increased levels of it suggest?

Back 1

Stands For: Alanine Aminotransferase
Increased levels suggest liver damage

Front 2

Diagnostic Enzymes Fixed On Cellulose Strips:

Back 2

1. Glucose Oxidase
Glucose + O2 + H2O --> D-gluconic acid+ H2O2

2. Peroxidase:
H2O2 + O-dianisidine --> O-dianisidine (oxidised) + H2O

Front 3

Immobilized Enzymes used in Diagnostic Tests

Back 3

1. Diagnostic Enzymes fixed on cellulose strips.

2. Immobilized urease, hexokinase, and amylase

3. ELISA

Front 4

How long after MI is a Troponin 1 assay useful?

When do levels peak?

Back 4

1. 4 hours to 5-9

2. Levels Peak at 12-16 hours following MI

Front 5

What level is indicative of myocardial damage?

Back 5

3. Levels above 1.5

Front 6

What test is useful for assaying for Cardiac Troponins?

Back 6

ELISA Assay

Front 7

Sickle Cell Anemia is the result of:

Back 7

Substitution of polar glutamate by non-polar valine in the 6th position in the beta subunit of hemoglobin.

Front 8

When does HbS onset occur?

Back 8

Symptoms occur after the first few months of life, when the HbF is replaced by HbA.

Front 9

Isozymes of Creatine Phosphokinase (CPK)

Back 9

CPK3 --> MM --> least electrophoretic mobility at pH 8.6 --> skeletal muscle

CPK2 --> MB --> Intermediate Mobility --> heart

CPK3 --> BB --> Maximum Mobility --> Brain

Front 10

pKa of Serine

Back 10

13

Front 11

pKa of Threonine

Back 11

13

Front 12

pKa of Aspartate

Back 12

4

Front 13

pKa of Glutamate

Back 13

4

Front 14

pKa of Histidine

Back 14

6

Front 15

pKa of Cysteine

Back 15

8

Front 16

pKa of Tyrosine

Back 16

10

Front 17

pKa of Lysine

Back 17

10.5

Front 18

pKa of Argenine

Back 18

12.5

Front 19

Testing for Toponin without reperfusion

Back 19

1-2 days until 7-9 days

Front 20

Testing for Troponin with repurfusion

Back 20

1-4 days

Front 21

Testing for CK-MB without repurfusion

Back 21

1-3 days

Front 22

Testing for CK-MB with repurfusion

Back 22

0-1 days

Front 23

To evaluate hepatocyte injury or necrosis in viral hepatitis, drug-induced hepatotoxicity, chlelithiasis, HELLP, AFLP:

Back 23

1. Aspartate aminotransferase (AST)

2. Alanine aminotransferase (ALT)

Front 24

In cholestasis and biliary obstruction

Back 24

1. Alkaline phosphatase

2. Gamma glutamyl transpeptidase

Front 25

LactaIsozymes of Lactate
Dehydrogenase (LDH)(LDH

Back 25

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

Front 26

Example of an extracellular protein that is stabilized by disulfide bonds:

Back 26

Albumin. What is albumin?

Hint 26

Albumin is a blood protein that functions as a transporter for a variety of molecules.

Front 27

What does it take to break a peptide bond non-enzymatically?

Back 27

Prolonged exposure to a strong acid or base in high temperature

Front 28

What causes Alzheimer's Disease?

Back 28

Amyloid Proteins that form plaques

Front 29

What causes Creutzfeldt-Jakob Disease?

Back 29

Prions

Front 30

Function of NO

Back 30

Vasodilation

Front 31

Regular HbS Symptoms

Back 31

1. Chronic Hemolytic Anemia wit associated hyperbillirubinemia

2. Increased susceptibility to infections

Front 32

Additional HbS Symptoms

Back 32

1. Acute Chest Syndrome

2. Stroke

3. Splenic and renal dysfunction

4. Bone changes due to marrow hyperplagia

Front 33

Lifetime of a sickle cell RBC

Lifetime of an HbA RBC

Back 33

HbS: 20 days

HbA: 120 days

Front 34

Sickle Cell Trait

Back 34

One HbA and one HbS

Normally asymptomatic and have a normal lifespan

Front 35

HbC

Back 35

Mutation on the 6th position of the beta chain where Glutamate is replaced by Lysine.

Front 36

Symptoms of HbC

Back 36

Relatively mild, chronic anemia.

No treatment is necessary.

Front 37

HbM Symptoms and Treatments

Back 37

Symptoms: Bownish-Blue skin and blood (chocolate cyanosis), anxiety, dyspnia, headache

Treatment: Methylene blue oxidizes to recuce Fe3+ to Fe2+

Front 38

Collagen Formation Sequence

Back 38

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.

Front 39

Where is AAT made?

Back 39

Made and secreted by the Liver

Front 40

Reactions in the Mitochondria

Back 40

1. TCA Cycle

2. Fatty acid oxidation

3. Oxidation of pyruvate

Front 41

Reactions in the Cytosol

Back 41

1. Glycolysis

2. HMP Pathway

3. Fatty acid synthesis

Front 42

Reactions in the Nucleus

Back 42

1. DNA and RNA Synthesis

Front 43

Reactions in the Lysosome

Back 43

1. Degradation of complex macromolecules

Front 44

Steady State Assumption

Back 44

Rate of production of ES is equal to the rate of degradation of ES.

Front 45

First order reaction

Back 45

Rate of reaction is dependent of Substrate concentration ([S] is less than Km)

Front 46

Zero Order Reaction

Back 46

Rate of reaction is independent of [S] because it is higher than Km

Front 47

What are Cofactors?

Back 47

Metal Ions

Front 48

What are coenzyme prosthetic groups?

Back 48

Coenzyme prosthetic groups are small organic molecules that associate permanently with an enzyme and are returned o their origin\al form on the enzyme;.

Front 49

What are coenzyme-co-substrates?

Back 49

Small organic molecules that associate transiently with an enzyme and leave the enzyme in a changed form.

Front 50

Electron Transport Chan (ETC) location

Back 50

Inner Mitochondrial Membrane

Front 51

Causes of Respiratory Acidosis (Clinical)

Back 51

1. Chronic Lung Disease

Front 52

Clinical Causes of Respiratory Alkalosis

Back 52

1. Head injuries

2. Drug-induced toxicity

Front 53

Clinical Causes of Metabolic Acidosis

Back 53

1. Increased ketogenesis

2. Diarrhea

3. Kidney Failure

Front 54

Clinical Causes of Metabolic Alkalosis

Back 54

1. Administration of salts of metabolic acids

2. Stomach Vomiting

Front 55

Ketoacidosis Etiology diagnosed by anion gap

Back 55

1. Increased hydroxybutyrate

2. Increased Acetoacetate

Front 56

Lactic Acidosis Etiology diagnosed by anion gap

Back 56

1. Circulatory Insufficiency (low O2)

Front 57

Drug Poisoning Etiology diagnosed by anion gap

Back 57

1. Excess Salicylate

2. Excess CH3OH

3. Excess Ethylene Glycol

-All of these lead to increased organic acids

Front 58

Base Excess

Back 58

Amount of base titrant needed to return blood pH to physiologic level (7.4)

Front 59

C-Reactive Protein (CRP)

Back 59

If there is arterial damage, CRP will be released and cause arterial damage

This is an issue in many arterial diseases such as diabetes

Front 60

Structure of Elastin

Back 60

Glycine, Valine, Alanine, Proline

Front 61

Dermal Fillers: Ways to Compensate for loss of subcutaneous collagen with age

Back 61

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

Front 62

Ehlers-Danlos Syndrome Etiology

Back 62

1. Mutations of Collagen Types I, III, IV

- Type 3 comes with vascular mutations

Front 63

How does Lead Poisoning work?

How is it treated?

Back 63

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

Front 64

How does Penicillin work?

Back 64

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.

Front 65

What tissue is damaged when you find AST?

Back 65

Liver

Front 66

What tissue is damaged when you find ALT?

Back 66

Liver

Front 67

What tissue is damaged when you find CPK-MB?

Back 67

Heart

Front 68

What tissue is damaged when you find LDH?

Back 68

Liver, Heart

Front 69

What tissue is damaged when you find GGT?

Back 69

Liver, Heart

Front 70

What tissue is damaged when you find Alkaline Phosphatase?

Back 70

Bone, Liver

Front 71

ETC Complex 1 Inhibitor:

Back 71

1. Amytal

2. Mercurials

3. Demerol

Front 72

ETC Complex 4 Inhibitor:

Back 72

1. Cyanide

2. Carbon Monoxide

3. Azide

Front 73

ETC Complex 5 Inhibitor:

Back 73

1. Oligomycin

Front 74

ETC ATP/ADP Transporter Inhibitor:

Back 74

1. Atractyloside

Front 75

ETC Complex Uncoupler:

Back 75

1. Thermogen (organic)

2. 2,4-dinitrophenol (synthetic)

Front 76

Tissue damage when Acid Phosphatase is found:

Back 76

Prostate

Front 77

Metabolic Syndrome Leads To...

Metabolic Syndrome is Treated by...

Back 77

1. Diabetes and Hypertension

2. Losing weight and removing fat from their diets

Front 78

TCA Cycle Products

Back 78

1. 3NADH - 3ATP each

2. 1FADH2 - 2ATP each

Front 79

What happens if there is inhibition of one of the complexes in the ETC?

Back 79

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)

Front 80

How do we form plaque in the blood vesels?

Back 80

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.