Proteins & Liver Function Flashcards

1
Q

Parts of an amino acid

A
  • Central carbon atom
  • Hydrogen
  • Amino group (-NH2)
  • Acidic carboxyl group (-COOH)
  • Organic side chain (R group)
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2
Q

Essential amino acids

A

Supplied by the diet in the form of proteins

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3
Q

Histidine (Amino Acid)

A

Help grow and repair body tissues

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4
Q

Methionine

A

Stabilize protein structure

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5
Q

Threonine (Amino Acid)

A

Needed for collagen, elastin and tooth enamel formation

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6
Q

Tryptophan (Amino Acid)

A

Metabolic precursor for melatonin and serotonin

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7
Q

Stomach enzyme

A

Gastrin —> HCl and pepsin —> denatures proteins

Pepsin breaks down proteins —> peptides

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8
Q

Small intestine enzymes

A

Secretin and cholecystokinin —> trypsin (proteolytic enzyme) —> breaks down proteins

Enzymes break peptides —> amino acids

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9
Q

Pancreatic enzymes

A

Hydrolyze polypeptides —> amino acids

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10
Q

Peptidase

A

Cleaves remaining peptide bonds —> free amino acids

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11
Q

Peptide bond

A

Links amino acids covalently

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12
Q

Polypeptide

A

Chain of amino acids linked by peptide bonds

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13
Q

Protein

A

large polypeptide

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14
Q

Primary structure of protein

A

Sequence of amino acids linked by peptide bonds

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15
Q

Secondary structure of protein

A

Hydrogen bonds - alpha-helix and beta-pleated sheet

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16
Q

Tertiary structure of protein

A

Overall conformation of the protein molecule

3D due to interaction of side chains

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17
Q

Quaternary structure

A

Interaction of more than one protein molecule

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18
Q

Protein denaturation by:

A
  • Heat
  • Hydrolysis by strong acid or base
  • UV light
  • Urea
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19
Q

Prealbumin (Plasma protein)

A
  • Transport protein for T4 and T3
  • Seen in CSF protein electrophoresis (not usually serum)
  • Migrates before albumin in serum protein electrophoresis
  • Negative acute-phase reactant (concentration decreases during inflammation)
  • Low conc: hepatic damage, tissue necrosis, poor nutritional status
  • Increased conc: steroid therapy, alcohol abuse or chronic renal failure
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20
Q

Albumin (Plasma protein)

A
  • Most abundant plasma protein
  • Maintains homeostasis
  • Negative acute-phase reactant
  • Decreased conc: inflammation, liver and kidney disease, malnutrition and malabsorption
  • Monitor efficacy of diabetes therapy
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21
Q

Globulins (Plasma Protein)

A

4 major types:
- alpha1
- alpha2
- beta
- gamma

Ex: haptoglobulin, transferrin, fibrinogen, CRP, immunoglobulins

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22
Q

Transferrin (Globulin)

A
  • Binds and transports iron
  • Iron status
  • Decrease: liver disease, insufficient dietary intake, iron overload
  • Increase: iron deficiency anemia
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23
Q

Fibrinogen (Globulin)

A

Thrombin —> fibrin clot
- Increases during inflammation and pregnancy

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24
Q

CRP (Globulin)

A
  • Increase: tissue inflammation, viral and bacterial infection, myocardial infarctions, rheumatic fever
  • Evaluate ateriosclerosis (plaque in arteries)
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25
Q

IgG

A
  • Blood plasma
  • Bacteria, fungi, viruses and foreign particles
  • Decrease: acquired immunodeficiency, hereditary deficiency, and protein losing states
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26
Q

IgA

A
  • Mucous secretions, tears, saliva, vaginal fluid, secretions from respiratory and GI mucosa
  • Protect mucosal tissues
  • Decrease: impaired protein synthesis and immunodeficiency
  • Increase: liver disease, infections and autoimmune diseases
27
Q

IgM

A
  • First antibody
  • Increase: bacterial infections, toxoplasmosis, biliary cirrhosis, cytomegalovirus, rubella, herpes, fungal diseases
  • Monoclonal spike: Waldenstrom’s macroglobulinemia
28
Q

IgE

A

Increase: allergic and anaphylactic reactions, autoimmune processes and parasitic infections

29
Q

Haptoglobin

A
  • Binds free hemoglobin
  • Increase: ulcerative colitis, acute rheumatic disease, acute myocardial infarction, severe infection
  • Evaluate hemolytic anemias: extravascular vs intravascular hemolysis
30
Q

Hemoglobin

A
  • Transport proteins and oxygen
  • Contains heme molecule (which reversibly binds oxygen)
  • Decreased: anemia
31
Q

Hemoglobinopathies

A
  • DNA mutations causing quantitative defects (inherited)
  • Structurally different form of hemoglobin
  • HbS = mutated form of HbA, causes sickle cell anemia
32
Q

Extravascular hemolysis

A

RBC lysis outside of the circulatory system
- Phagocytic cells/macrophages
- No free hemoglobin

33
Q

Intravascular hemolysis

A

Lysed RBCs —> creates:
- circulating free hgb
- haptoglobin and hemoplexin

  • Iron is reclaimed
  • Globin chains broken down —> amino acids recycled
  • Heme —> bilirubin and urobilinogen
34
Q

Bilirubin

A
  • Removal of heme waste products, excreted into bile by the liver
  • Albumin carries bilirubin to the liver
35
Q

Unconjugated bilirubin

A

Insoluble in water, so cannot be removed by the body until it’s conjugated, which requires UDPGT enzyme

36
Q

UDPGT enzyme

A

Conjugates bilirubin

Conjugated bilirubin —> urobilinogen —oxidized—> urobilin —> excreted in feces

37
Q

Prehepatic jaundice

A
  • Caused by a problem prior to liver metabolism
  • Hemolytic anemia —> increased bilirubin
38
Q

Hepatic jaundice

A
  • Defects of liver
  • Gilbert’s disease: mutation in UGT1A1 gene
  • Dubin-Johnson syndrome: deficiency of protein MDR2/cMOAT
39
Q

Posthepatic jaundice

A

Gallstones or tumors (conjugated by liver but cannot leave because something is physically obstructing the way)

40
Q

Neonatal hyperbilirubinemia

A

UDPGT enzyme deficiency —> buildup of unconjugated bilirubin —> hernicterus (brain damage)
- Tx: phototherapy

41
Q

Total bilirubin measurement

A

Jendrassik-Grof

Bilirubin + diazotized sulfanilic acid + ACCELERATOR/CAFFEINE —> azobilirubin

42
Q

Conjugated bilirubin measurement

A

Diazo reaction

Bilirubin + diazonized sulfanilic acid —> azobilirubin

43
Q

Unconjugated bilirubin measurement

A

TBIL - conjugated

44
Q

Myoglobin

A
  • Oxygen carrying protein
  • Reversibly binds oxygen
  • My-oh-mi — myoglobin transports oxygen to mitochondria
  • Striated muscle damage - released myoglobin into blood
  • Increase: acute myocardial infarction, damaged skeletal muscle (progressive muscular dystrophy, crush injuries, rhabdomyolysis), renal failure (impaired glomerular filtration)
  • Myoglobin elevation in urine/myoglobinuria —> reddish-brown
45
Q

Myoglobinuria measurement

A

Urine dipstick
- Positive for heme
- No RBCs

46
Q

Porphyria

A
  • Metabolic disorder
  • Loss/gain of function mutation in enzymes responsible for heme biosynthesis (rare disorder that is caused by a buildup of porphyrins)

Affects heme metabolism

47
Q

Acute porphyrias

A

Neurological symptoms and acute attacks of abdominal pain

Urine tested for PBG and prophyrins

Wet diaper —> UV light —> fluorescence

48
Q

Cutaneous porphyria

A

Photosensitization from exposure to sunlight

49
Q

Prophyrinuria

A

Disorder associated with increased excretion of urinary porphyrins

  • Liver diseases: hepatitis, cirrhosis
  • Bilirubin metabolism disorders: Dubin Johnson, Rotor, Gilbert syndromes
  • Heavy metal poisoning: lead toxicity
  • Insufficient iron stores —> RBC protoporphyrin assimilate zinc —> zinc protoporphyrin (ZPP)
  • Lead interferes with: enzyme formation of porphobilinogen (PBG) and insertion of ferrous iron into heme
50
Q

Fetal Fibronectin (fFN)

A

Short term risk of premature delivery

51
Q

Cystatin C

A

Glomerular/kidney function

52
Q

Hypoproteinemia

A

Serum or plasma total protein concentration is below the reference range

Renal disease, malnutrition, maldigestion, malabsorption, digestive system inflammation, blood loss

53
Q

Hyperproteinemia

A

Excessive production of proteins

  • Dehydration
  • Addison disease
  • Diabetic acidosis
54
Q

Total protein - Method of Analysis

A
  • No hemolyzed samples
  • TP: lower at birth, adult levels around 3 yo
  • Biuret reaction: cupric (Cu2+)
  • Purple color = (+)
55
Q

Monoclonal spike

A

M- protein or M- spike
- Detected in blood and/or the urine
- Waldenstrom’s macroglobulinemia, Multiple myeloma

56
Q

Albumin - Method of Analysis

A

Dye binding procedures: bromocresol green (BCG) or bromocresol purple (BCP)

  • BCG affected by LIH (lipemia, icterus, hemolysis)
  • BCP affected by I (icterus)
57
Q

Serum protein electrophoresis

A

Separates protein based on: charge and density
Smaller proteins move faster than larger proteins

58
Q

Capillary electrophoresis

A

Separation of molecules inside a silica capillary

Heat is dissipated

59
Q

Immunofixation electrophoresis

A

Anti-seras (anti-IgA, IgM, etc) added to form antigen-antibody complexes

Identifies M protein/monoclonal spike present

60
Q

Proteinuria

A

Causes:
- Protein overflow from plasma
- Increased permeability of the glomeruli
- Decreased tubular reabsorption
- Increased synthesis of renal proteins
- Renal inflammation

Bence Jones proteins: Multiple myeloma or Waldenstrom’s macroglobulinemia

61
Q

Proteins in CSF

A

Increased permeability of the blood brain barrier
- Meningitis, traumatic lumbar puncture, multiple sclerosis, neoplasm, disk herniation, cerebral infarction

Compare CSF albumin with measured serum albumin

Reference protein: albumin

Value > reference range = damage to blood brain barrier

62
Q

Proteins in CSF

A

Increased permeability of the blood brain barrier
- Meningitis, traumatic lumbar puncture, multiple sclerosis, neoplasm, disk herniation, cerebral infarction

Compare CSF albumin with measured serum albumin

Reference protein: albumin

Value > reference range = damage to blood brain barrier

63
Q

Isoelectric focusing

A

Isoelectric point
- Polyacrylamide or agarose gel

  • Genetic variants of enzymes and hemoglobins
  • Detect paraproteins in serum, oligoclonal bands in CSF, isoenzyme determinations
64
Q

Bence Jones protein

A

Multiple myeloma
Waldenstroms macroglobulemia