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chemistry BOC deck Flashcards

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1
Q

Monosaccharides

A

Glucose – Broken down starch
Galactose – Dairy, sugar beets, jams, jelly
Fructose – Fruits, honey
Mannose – Plant polysaccharide, not starch

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2
Q

Disaccharides

A

Maltose – Barley, beer, cereals (glu + glu)
Lactose – Milk sugar (glu + gal)
Sucrose – Table sugar, sugar cane, maples (glu + fru)

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3
Q

Polysaccharides

A

Starch: plant made
Amylose shorter chains
Amylopectin longer chain with branching
Glycogen: animal made
Similar to amylopectin, but with more branching

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4
Q

What does glucose oxidase recognize?

A

β-D Glucose 36%

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5
Q

What does glucose form in sugars?

A

 Glucose forms ring structure in solution
 β-D Glucose 36%
 Glucose oxidase recognizes this
 α-D Glucose 64%

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6
Q

Which hormone lowers blood glucose?

A

Insulin
Secreted by β-islet cells of pancreas

Stimulates movement of glucose into cells

Second Messenger Duties:

1) INCREASE: Lipogenesis, protein synthesis & AA transport, glycogen synthesis

2) DECREASE: Lipase, protein breakdown, gluconeogenesis, glycogenolysis

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7
Q

Which three hormones raise blood glucose?

A

Glucagon, Epinephrine, Cortisol, GH, T4, ACTH, and somatostatin.

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8
Q

What is the primary hormone responsible for raising blood glucose levels?

A

Glucagon

Secreted by α-islet cell of pancreas

Stimulates glycogenolysis and gluconeogenesis

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9
Q

How does epinephrine raise blood glucose levels?

A

Catecholamine secreted by adrenal medulla

stimulates glucagon
release

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10
Q

How does cortisol raise blood glucose levels?

A

Secreted by adrenal cortex

Stimulates gluconeogenesis and glucagon release

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11
Q

How does growth hormone increase blood glucose levels?

A

Synthesized by Anterior Pituitary

Inhibits glucose uptake by cells

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12
Q

How does T4 increase blood glucose levels?

A

Least important, stimulates glycogenolysis

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13
Q

How does somatostatin increase blood glucose levels?

A

Secreted by δ-islet cells of pancreas, hypothalamus, and GI tract

Inhibits BOTH insulin and glucagon release

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14
Q

How does ACTH increase blood glucose levels?

A

Secreted by Anterior Pituitary
Stimulates cortisol, Insulin antagonist

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15
Q

What causes hyperglycemia?

A

High glucose
 Resolved by insulin

Pathology: Diabetes Mellitus

Type 1 Absolute Deficiency

Type 2 Resistance with secretory defect

Other
Pancreatic disease, drug/chemical induced etc.

Gestational
Metabolic and hormonal changes during pregnancy

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16
Q

Clinical Signs of Diabetes

A

Polyuria
Polyphagia
Polydipsia
Weight loss
Hyperventilation (acetone breath)

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17
Q

Polyuria

A

Renal threshold 160-180 mg/dL

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18
Q

Polyphagia

A

“Starvation in land of plenty”

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19
Q

Polydipsia

A
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20
Q

Weight loss

A

 “Starvation in land of plenty”

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21
Q

Hyperventilation (acetone breath)

A

High ketone level

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22
Q

What is the normal range for the fasting blood glucose (8-10 hrs)?

A

Normal 70-99 mg/dL

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23
Q

What is the impaied range for the fasting blood glucose (8-10 hrs)?

A

Impaired 100-125 mg/dL

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24
Q

What is the diabetes range for the fasting blood glucose (8-10 hrs)?

A

Diabetes ≥126 mg/dL

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25
Q

What is the normal range for the 2-hour Glucose Tolerance (OGTT) (8-10 hrs fast)?

A

 Normal ≤140 mg/dL

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26
Q

When do you see a peak in the 2-hour glucose tolerance test?

A

Usually time of peak after meal

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27
Q

What is the impaired range for the 2-hour Glucose Tolerance (OGTT) (8-10 hrs fast)?

A

Impaired 140-199 mg/dL

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28
Q

What is the diabetic range for the 2-hour Glucose Tolerance (OGTT) (8-10 hrs fast)?

A

Diabetes ≥200 mg/dL

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29
Q

What are the doses for the OGTT?

A

50g Gestational screen
75g 2 hr OGTT
100g Women who failed first gestational screen, 3 hour challenge

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30
Q

How does the three-hour challenge work if you fail the first gestational screen?

A

 3 hour challenge: 2 of these true for diagnosis
 FBS ≥95 mg/dL
 1 hr ≥180 mg/dL
 2 hr ≥155 mg/dL
 3 hr ≥140 mg/dL

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31
Q

5 hr GTT

A

Testing for reactive (postprandial) hypoglycemia

Will see large drop (40 mg/dL or more)

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32
Q

Which test reflects average glucose over 2-3 months

A

Hemoglobin A1c

Average lifespan of RBC 120 days

Test reflects average glucose over 2-3 months

Diabetes ≥6.5%

Hemoglobinopathies will interfere

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33
Q

Which test reflects average glucose over 2-3 weeks?

A

Fructoasmine

Glucose attaches to other proteins too!

2-3 week period, NO FRUCTOSE INVOLVED!

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34
Q

What is a product of insulin production?

A

C-peptide

A product of insulin production

Absent in type 1 diabetes

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35
Q

What is produced more in type 1 than type 2 diabetes?

A

Ketones

78% BHB, 2% acetone, 20% AAA

Produced more in type I diabetes (DKA)

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36
Q

Write out the hexokinase reaction.

At what wavelength does the absorbance increase at?

A

Hexokinase (reference)

Glucose + ATP
(HK, Mg2+)——->
Glucose−6−phosphate + ADP

Glucose−6−Phosphate + NADP
(G−6−PDH)———>
6−phosphogluconate
+ NADPH

 Increase in absorbance at 340 nm

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37
Q

What is used to measure the glucose oxidase reaction?

What does the glucose oxidase test measure?

Write out the reaction for glucose oxidase.

A

Glucose Oxidase

From here can measure with polarographic electrode

Measures O2 consumption, must sequester H2O2

β−D Glucose + O2
(GO)——–>
Gluconic Acid + H2O2

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38
Q

What is the trinder reation?

A

Trinder Reaction

H2O2+4−aninophenazone + phenol
(peroxidase)——->
Quinone Complex + 2 H2O

Many interferences

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39
Q

What is another method of measure glucose oxidase?

A

Chromogenic Oxygen receptor, or dye that changes color in presence
of H2O2

40
Q

Write out the glucose dehydrogenase reaction?

At what wavelength does the absorbance increase at?

A

Glucose Dehydrogenase

β−D Glucose+NAD
(GDH)——>
D−glucono δ lactone+NADH+H+

Patented Rxn, only 1% of labs use

Increase in absorbance at 340 nm

41
Q

Mutarose coverts?

A

If glucose is in the name, it is specific for β−D Glucose

 Mutarose coverts α to β

42
Q

Galactose

A

Galactosemia: failure to thrive

Deficiency in 1 of 3 enzymes for galactose metabolism

Usually galactose-1-phosphate uridyltransferase

Diarrhea, vomiting
Mental retardation (DD) and catarats if untreated

Screened for at birth

43
Q

Microalbumin

A

Diabetes causes damage to the kidney

Early sign is increase in urine albumin

Microalbumin is not a small molecule of albumin!

44
Q

Porphyrins

A
  • Chemical intermediates of heme synthesis
  • Hemoglobin, Myoglobin, Cytochromes
  • Iron captured to form heme
  • Heme + Proteins = hemoprotins
45
Q

What are the characteristics of porphyrins?

A
  • Stable compounds
  • Color
  • Red-violet, red-brown
  • Fluoresce when stimulated @ 400 nm
46
Q

3 clinically important compounds

A
  • Protoporphyrin- excreted in feces
  • Uroporphyrin-excreted in urine
  • Coproporphyrin- excreted in either!
47
Q

Reduced porphyrins are?

A

Porphyrinogens (the actual
building blocks)

48
Q

What are the characteristics of prophyrinogens?

A
  • Unstable
  • Colorless
  • No flourescence
  • Readily oxidized to porphyrins by light, O2 or oxidizing
    agents
49
Q

Why do we look for porphyrins over prophyrinogens?

A

porphrins are stable and prophyrinogens are unstable.

50
Q

Acquired or inherited enzyme deficiency

A
  • In Bone Marrow: Erythropoeitic
  • In Liver: Hepatic

Early precurors:

  • Abdominal pain
  • neuro-psych
  • vomiting
  • constipation
  • tachycardia
  • fever
  • leukocytosis
  • parastheia

Late precursors:
* Skin manifestations:
* blisters
* facial hair
* photosensitivity
* hyperpigmentation

51
Q

Inherited Porphyrias

A
  • Autosomal dominant inheritance
  • ADP and CEP are autosomal recessive
  • Decrease in enzyme activity leads to build-up of
    precursor molecule
  • The level of activity left is enough to make the heme
    needed to prevent anemia
52
Q

Inherited ALA Dehyratase Deficency Porphyria

A
  • Inherited ADP
  • 7 cases in the entire world, the ultimate zebra
  • Urinary ALA↑↑↑
  • PBG Norm
  • Coprophorphyrin III ↑-urine
  • Lead also decreases ALAD funtion
  • Adding dithiothreitol restores their ALA function
53
Q

Acute Intermittent Porphyria (AIP)

A
  • HMBS deficincy
  • Crisis often precipitated by drugs
  • Urine ALA ↑
  • Urine PBG↑
  • Urine turns red-brown on standing
  • Delayed by refrigeration, protection from light, pH
    preservation.
54
Q
  • Congenital Erythropoetic Porphyria (CEP)
A
  • Uroporphyrinogen III cosynthase deficiency
  • Appears shortly after birth
  • Red-brown urine staining diaper
  • Teeth fluoresce red under UV (stained red-brown)
  • Photosensitivity
55
Q
  • Porphyria cutanea tarda (PCT)
A
  • Deficiency of Uroporphyrinogen decarboxylase (UROD)
  • Most common porphyria
  • Blistering and fragility in light-exposed areas
  • Urine Uroporphyrin↑ hepatocarboxylic porphyrin↑
    isocoproporphyrin↑
  • Will be resolved with low dose chloroquine and iron
    depletion
  • Hepatoerythropoeitic porphyria more or less same
  • Has increased ZPP
56
Q

PCT type 1

A
  • Type I: Limited to liver no family history
57
Q

PCT type 2

A

*Type II: In all tissue, autosomal dominant

58
Q

Hereditary Coproporphyria (HCP)

A
  • Deficencey of coproporphyrinogen oxidase (CPOX)
  • Urine & Feces ↑↑Copro III
  • Can be precipitated by drugs, hormones, nutritional
    changes
  • Mild neurological and photosensitive symptoms
59
Q

Variegate Porphyria (VP)

A
  • Prevalent in South Africa thanks to two Dutch people
  • Protoporphyrinogen oxidase activity decreased
  • Neurologic dysfuntion
    And/Or
  • Photodermatitis
  • Fecal Copro↑ Proto↑↑
60
Q

Erythropoeitic Porphyria (EP/EPP)

A
  • Ferochelatase the enzyme that puts the iron in heme
  • Photosensitivity present from infancy
  • Burning, itching, pain on exposure
  • Liver concequences
  • RBCs Proto↑
  • Greatly varied presentation
61
Q

Watson-Schwartz & Hoesch screening tests

A
  • PGB forms red-orange when mixed with Ehrlich’s
    reagent
  • P-dimethylaminobenzaledhyde
62
Q

Watson-Schwartz uses chloraform or butanol extraction

A
  • If cherry-red remains in aqueous phase + for PBG
63
Q

Hoesch test

A

In Hoesch test there is no reaction with urobilinogen

64
Q

Why do porphyrins fluoresce better in acidic solutions?

A
  • After being extracted, ultraviolet light reveals pink or
    red fluorescence
  • They may be read quantitatively due to fluorescence
    peaks
  • 400-405nm and 594-598nm
  • Standards are used to calibrate curve
  • Each solvent has its own wavelengths in different
    solvents
65
Q
  • Zinc Protoporphyrin
A

Metabolite formed when Zn not Fe gets into
protoporphyin

  • If Iron cannot get into the ring, the zinc is used instead
  • Will also increase in iron-deficiency anemia
  • Whole amount not usually reported, usually in ratio to
    normal heme
66
Q
  • Heme synthesis interfered with
A

Similar symptoms
* Anemias, liver disease, lead, alcohol can cause

  • In 2º Porphyrias Urinary ALA↑ BUT PGB Normal
  • Lead poisoning will also have RBC ZPP ↑
  • Assay for lead is still better way to detect
67
Q

Draw out Porphyrin Synthesis. What is the rate controlling step?

A
68
Q

Evelyn Malloy

A

bilirubin combines with diazotized sulfanilic acid to
form azobilirubin (purple)

69
Q

How does the Jendrassik-Grof modify the evelyn Malloy test?

A

Jendrassik-Grof modifies this by shifting pH at end to make
azobilirubin blue

Only able to combine with water soluble bilirubin (direct)

Measuring all bilirubin requires solubilizing

Accelerant

70
Q

Direct Bilirubin

A

Water-soluble

Reacts readily
with diazo
reagent

71
Q

Indirect
bilirubin

A

Lipid-soluble

Reacts with
diazo after
adding
accelerant

72
Q

Total
Bilirubin

A

Assay with diazo
and accelerant

After doing total
and direct, can
calculate indirect

73
Q

Jaundice- Not a disease

A

 Yellowing due to high amounts of bilirubin, eye sclera/conjunctiva
first

74
Q

What causes pre-hepatic jaundice?

A

overwhelm liver processing

75
Q

What causes hepatic jaundice?

A

liver function impaired

76
Q

What causes post-hepatic-jaundice?

A

plumbing backs up

77
Q

Kernicterus

A

Unconjugated bilirubin overwhelms albumin

Lipid soluble, makes it to brain, damages newborn brain

Results in developmental disability, can be fatal

78
Q

Prehepatic
Jauncidce

A

Due to increased RBC turnover

Hemolytic anemias

Liver usually able to keep up

Keeps levels below harmful levels, <5 mg/dL

Circulating bilirubin is unconjugated (indirect)

79
Q

Hepatic
Jaundice

A

Bilirubin metabolism or transport is impaired

Bilirubin builds up, unconjugated (usually)

80
Q

Which disease is a partial loss of UDPGT?

A

Gilbert’s disease

81
Q

Total loss of UDPGT

A

Crigler-Najjar

82
Q

Which disease prevents secretion into canaliculi?

A

Dubin-Johnson syndrome

83
Q

Rotor syndrome

A

Unknown etiology, similar to D-J

84
Q

Post-Hepatic
Jaundice

A

Also known as obstructive jaundice

Gallstones, tumors, inflammation, even liver flukes may block bile
duct

Liver able to conjugate and secrete but it never gets past
gallbladder

No pigments in feces = clay colored stool

Backup causes regurgitation into bloodstream

Lots of conjugated/direct bilirubin present

85
Q

What is a key symptom/clinical sign of post-hepatic jaundice?

A

No pigments in feces = clay colored stool

86
Q

When is bilirubin a problem?

A

Phototherapy

87
Q

Typical testing patterns of pre-hepatic jaundice

A

Total bilirubin
Normal / Increased

Unconjugated
bilirubin
Increased

Urobilinogen
Increased

88
Q

Typical testing patterns of hepatic jaundice

A

Total bilirubin:
Increased

Conjugated bilirubin
Normal / Increased* /
?Decreased?

Unconjugated
bilirubin:
Increased

urine color:
Dark

Alkaline phosphate
levels:
Slight elevation

AST & ALT levels:
Increased

89
Q
A

Total bilirubin
Increased

Conjugated bilirubin
Increased

Urobilinogen:
?Decreased? /
Negative

Urine color:
Dark

Stool colour:
pale

Alkaline phosphate
levels:
increased

90
Q

Alkaline phosphate
levels

A

Hydrolase that breaks down starch and glycogen

– Requires Cl- and Ca2+ activators

– Acinar cells of pancreas and salivary glands are sources of amylase

■ Smallest enzyme, found in urine

■ Salivary amylase deactivated by stomach

– Acute pancreatitis

  • AMY rises in 5-8 hours, peaks @ 24, and normal at 3-5 days
91
Q

How do we measure amylase?

A

■ Somogyi Units
– Specifically amount of reducing sugar liberated (multiple products)

– U/L with our own ref. range

■ Measurement Methods
– Separate out salivary with
wheat germ lectin

– Immunoassay for specific
Isoenzymes

■ Macroamylasemia: benign

92
Q

Lipase (LIPA/LPS)

A

Hydrolyzes ester bonds to produce alcohol and fatty acids

– Specifically partially hydrolyzes triglyceride into 2-monoglyceride and 2 fatty
acids

– Pancreatic lipase is specific for the fatty acids at positions 1 & 2

■ Substrate must be emulsified to occur, bile salts and colipase accelerate

■ Lipase is primarily found in pancreas
– Specific for pancreas!
– Increases 4-8 hours after acute pancreatitis

– Peaks at 24 hours
– Normal at 8-14 days
■ Longer lasting marker for pancreatitis

93
Q

How do we measure lipase?

A

Assay
– Early method Cherry-Crandall used olive oil to measure
– Turbidimetric assay sees decrease in turbidity caused by fats
– Colorimetric also based on glycerol kinase coupled reaction

94
Q

Pancreatitis

A

Exocrine secretions digest foods
– Safeguards prevent activation of enzymes
– Intrapancreatic secretion and activation

■ “autodigestion”
■ Precipitated by alcohol abuse, gallstones, trauma, [extremely] high triglycerides
– Treatments usually supportive
– TPN only has given way to EN (Enteral Nutrition)

95
Q

Alkaline phosphatase (ALp)

A

Group of enzymes that catalyze hydrolysis of phosphomonoesters at
alkaline pH
– Liberates inorganic phosphate from organic molecule
– Production of alcohol as a result
– Optimal pH 9-10 but varies with substrate
■ Requires Mg2+ as activator
■ Present on most cell outer surfaces
– Liver, bone, spleen, intestine, placenta and kidneys are highest

Chemistry BOC PREP (2 decks)

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