Dentistry yr 1 > Biochemistry > Flashcards

Biochemistry Flashcards

committee 2 exam prep (76 cards)

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1
Q

Macromolecules

A

carbohydrates, lipids, and proteins

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2
Q

Carbohydrates

A

monosaccharides, disaccharides, polysaccharides

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3
Q

Anabolic pathway

A

construction re-synthesis
requires energy

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4
Q

Catabolic pathway

A

releases energy
destruction (breakdown of large molecules)

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5
Q

What are the two main pathways used by the heart for energy and why?

A

Beta oxidation, Krebs cycle because the heart is highly aerobic, rich in mitochondria, and relies on fatty acids as a steady fuel source:
beta-oxidation –> acetyl coA –>krebs–> ATP

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6
Q

What pathways provide energy in the brain under normal conditions?

A

Glycolysis and krebs cycle
GLUCOSEEE

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7
Q

What does the brain use during prolonged fasting when glucose drops?

A

Ketone bodies from the liver

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8
Q

Why can’t the brain use fatty acids for energy?

A

Fatty acids cannot cross the blood-brain barrier, brain lacks beta-oxidation enzymes.

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9
Q

What happens to triglycerides in adipose tissue when fasting?

A

LIPOLYSIS –> fatty acids + glycerol

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10
Q

Where do fatty acids from adipose tissue go, and what pathway do they enter?

A

to the liver and muscle –> Beta oxidation

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11
Q

Why does lactate travel from muscle to liver?

A

liver converts lactate –> pyruvate –> glucose in the cori cycle

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12
Q

What fuels can muscle use according to the diagram?

A

fatty acids (beta oxidation), glucose (glycolysis), proteins (alanine)

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13
Q

When does muscle produce lactate?

A

During anaerobic glycolysis (low oxygen, EXERCISE)

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14
Q

How much metabolic water is produced during these rxns?

A

300-400ml of metabolic water

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15
Q

List of main energy sources

A
  1. GLUCOSE
  2. lipid
  3. proteins
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16
Q

Diabetic ketoacidosis

A

no insulin (no glucose entering krebs) to obtain energy fatty acid is used instead of glucose. high level of ketone bodies decreases blood PH and DKA occurs

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17
Q

Fasting blood glucose level

A

70-100 mg/dL

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18
Q

Oral glucose tolerance test

A

Blood glucoses reaches max level at end of first hour
then drops to reference value
at end of second hour
fatty acids follow the reversed version of this path

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19
Q

Glycogenesis

A

conversion of glucose to glycogen for storage in the liver

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20
Q

Glycogenolysis

A

conversion of liver glycogen to blood glucose (glucose formation)

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21
Q

Gluconeogenesis

A

synthesis of blood glucose by the liver (short term fasting)

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22
Q

Glycolysis

A

utilization of glucose by anaerobic oxidation

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23
Q

Citric acid cycle

A

Utilization of glucose by aerobic oxidation

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24
Q

pentose phosphate pathway

A

utilization of glucose ONLY NADPH
in cytosol
no ATP directly consumed or produced

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25
Uronic acid pathway
synthesis of glucuronic acid (detoxification process)
26
Hyperglycemia
High amount of glucose present in the blood <126 mg/dl
27
Hypoglycemia
Low amount of glucose present in the blood less than 70 mg/dl (sometimes because of excess insulin or insulin resistance)
28
What bond links multiple monosaccharides?
Glycosidic linkages/bonds
29
lactose
galactose + glucose
30
sucrose
glucose + fructose
31
maltose
glucose + glucose
32
Salivary alpha amylase
during mastication: it acts briefly on dietary starch and glycogen, hydrolyzing random random alpha(1-4) bonds
33
pancreatic alpha amylase
when the acidic stomach contents reach the small intestine, it is neutralized by bicarbonate secreted by the pancreas and this enzyme continues the process of digestion.
34
Intestinal disaccharides
final digestive process occurs primarily at the mucosal lining of the duodenum and upper jejunum
35
Intestinal absorption of monosaccharides
SGLT-1 sucks in sugar with sodium: GLUT-5 ferries fructose: GLUT-2 sends all 3 out
36
Abnormal degradation of disaccharides
Lactose intolerance
37
GLUT-1
RBC'S Blood brain barrier
38
GLUT-2
Liver Kidney pancreatic beta cells Bidirectional glucose sensor
39
GLUT-3
Neurons
40
GLUT-4
Muscle and adipose tissue INSULIN DEPENDENT
41
GLUT-5
Fructose transporter (intestine and testes)
42
Na+/K+ ATPase
pump that SETS up the gradient
43
SGLT-1
the cotransporter that USES the gradient to bring glucose into enterocyte
44
hexokinase (in most tissues)
high affinity, works at low glucose, inhibited by G6P
45
glucokinase (liver and beta cells)
low affinity, works only when glucose is high, not inhibited by G6P helps liver store glucose
46
Phosphofructokinase-1
main control point inhibited by ATP and citrate activated by AMP commits glucose to glycolysis
47
PFK-1 fed state
insulin HIGH glucagon low PFK-2 dephosphorylates glycolysis ON gluconeogenesis OFF
48
PFK-1 fasting test
Glucagon HIGH insulin low PFK-2 phosphorylates glycolysis OFF gluconeogenesis ON
49
Arsenic
stops ATP production in glycolysis
50
Flouride
inhibits enolase, means less bacterial acid, fewer cavities
51
2,3 bisphosphoglycerate
made in RBC's to help release oxygen to tissues
52
energy phase
1,3-BPG and PEP steps make ATP
53
Pyruvate Kinase
irreversible step producing pyruvate and ATP
54
Lactic acidosis
high lactate in the blood and low PH usually happens when there is a collapse in the circulatory system.
55
Anaerobic glycolysis
net 2 molecules of ATP for each molecule of glucose converted to two molecules of lactate
56
Aerobic glycolysis
2 NADH Net 2 ATP
57
Type 1: Von Gierke Disease
Cannot release glucose from liver b/c G6Pase is missing no response to glucagon or epinephrine causes severe fasting hypoglycemia and glycogen accumulation.
58
Type 2: Pompe's disease
deficiency of lysosomal acid alpha glucosidase, leading to glycogen accumulation in lysosomes and resulting in cardiomyopathy, severe hypotonia, muscle weakness, and respiratory failure.
59
Type 3: limit dextrinosis
caused by debranching enzyme deficiency, leading to accumulation of limit dextrins and resulting in hypoglycemia, muscle weakness, hepatomegaly.
60
Type 4: myophosphorylase deficiency or mcardles disease
deficiency of muscle glycogen phosphorylase causing exercise intolerance, no rise in lactate after exercise, muscle glycogen accumulation. BUT normal blood glucose levels.
61
NADPH uses
Reductive biosynthesis Hydrogen peroxide reduction Antioxidant chemicals
62
G6PD deficiency
hereditary condition, by hemolytic anemia caused by the inability to detoxify oxidizing agents. could appear as neonatal jaundice (increased production of unconjugated bilirubin)
63
Favism
Hemolysis episode caused by fava beans
64
Insulin
most imp hormone stimulates 2nd messenger cAMP NEED TO USE GLUCOSE ANABOLIC
65
Adrenaline and noradrenaline
block release of insulin from pancreas, bc of this it raises blood sugar
66
Hyperthyroidism
metabolism INC weight loss high blood sugar
66
Glucocorticoids
raise blood sugar by increasing gluconeogenesis, inc amino acid breakdown, reducing glucose use in tissues, working AGAINST insulin.
67
Hypothyrdoidism
metabolism DEC weight gain low blood sugar
68
lipids storage and water
high energy compounds hydrophobic, do not retain water and take very little space
69
Lipids insulation
low thermal conductivity high heat capacity can absorb shocks
70
simple lipids
fatty acids, triglycerides, waxes
71
complex lipids
phospholipids glycolipids lipoproteins
72
isoprene derived lipds
terpenes and steroids
73
fatty acids
terminal carboxyl hydrocarbon chain saturated: no double bond unsaturated: one double bond polyunsaturated: multiple double bonds
74
solubility and melting point of FA's
solubility: decreases as chain length increases melting point: decreases as chain length decreases, decreases as the number of double bonds INC
75
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