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CLINICAL CHEMISTRY 1 > CC1-LEC 4 - CARBOHYDRATES > Flashcards

CC1-LEC 4 - CARBOHYDRATES Flashcards

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1
Q

Most common monosaccharides:

A

glucose, fructose, and galactose

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2
Q

common disaccharides:

A

MALTOSE, LACTOSE & SUCROSE

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3
Q

Most common OLIGOSACCHARIDE:

A

STARCH & GLYCOGEN

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4
Q

To be a reducing substance, Carbohydrate must contain ________.

A

Ketone/ an aldehyde group

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5
Q

Examples of reducing substances:

A

glucose, maltose, fructose, lactose, and galactose.

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6
Q

MOST COMMON NONREDUCING SUGAR:

A

TABLE SUGAR/SUCROSE

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7
Q

PRIMARY SOURCE OF ENERGY FOR HUMANS

A

GLUCOSE

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8
Q

T or F
* Nervous tissue cannot concentrate or store carbohydrates

A

EURT

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9
Q

An enzyme released by the intestinal mucosa responsible for the digestion of nonabsorbable polymers to dextrins.

A

MALTASE

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10
Q

two other important gut-derived enzymes that hydrolyze sucrose to glucose and fructose and lactose to glucose and galactose

A

SUCRASE & LACTASE

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11
Q

act as an intermediate to couple glucose oxidation to the ETC (Electron Transport Chain) in
the mitochondria where much of the ATP is gained.

A

Nicotinamide adenine dinucleotide (NAD) in its reduced form (NADH)

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12
Q

What is the enzyme that catalyzes the conversion of glucose to G-D-P

A

HEXOKINASE

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13
Q

1ST PATHWAY:
-Glucose is broken down into two-and three-carbon molecules of pyruvic acid that can enter the tricarboxylic acid (TCA) cycle on conversion to acetyl-coenzyme A (acetyl-CoA).

A

Emnden- Meyerhof Pathway

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14
Q

2ND PATHWAY:
A detour of glucose-6-phosphate from the glycolytic pathway to become 6 phosphogluconic acid.

A

HEXOSE MONOPHOSPHATE SHUNT

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14
Q

Permits the formation of ribose-5-phosphate and NADP in its reduced form (NADPH)

A

HEXOSE MONOPHOSPHATE SHUNT

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15
Q

Is important to erythrocytes that lack mitochondria and are therefore incapable of the TCA cycle.

A

NADPH

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16
Q

3RD PATHWAY:
Glucose-6-phosphate is converted to glucose-1-phosphate, which is then converted to uridine diphosphoglucose and then to glycogen by glycogen synthase.

A

GLYCOGENESIS

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17
Q

Are capable of releasing glucose
from glycogen or other sources to maintain the blood glucose concentration.

A

HEPATOCYTES

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18
Q

WITHOUT this enzyme, glucose is trapped in the glycolytic pathway.

A

GLUCOSE-6-PHOSPHATASE

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19
Q

It is the process by which glycogen is converted back to glucose-6-phosphate for entry into the glycolytic pathway.

A

GLYCOGENOLYSIS

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20
Q

Metabolism of glucose molecule to pyruvate or lactate for production of energy.

A

GLYCOLYSIS

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21
Q

Formation of glucose-6-phosphate from noncarbohydrate sources

A

GLUCONEOGENESIS

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22
Q

Breakdown of glycogen to glucose for use as energy

A

GLYCOGENOLYSIS

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23
Q

Conversion of glucose to glycogen for storage

A

GLYCOGENESIS

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24
Q

Conversion of carbohydrates to fatty acids

A

LIPOGENESIS

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25
Q

Decomposition of fat

A

LIPOLYSIS

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26
Q

The principal pathway for glucose oxidation is through what pathway?

A

Embden-Meyerhof pathway

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27
Q

When the fasting period is longer than 1 day, glucose is synthesized from other sources through _____________.

A

gluconeogenesis

28
Q

Control of blood glucose is under two major hormones:

A

INSULIN AND GLUCAGON

29
Q

INSULIN AND GLUCAGON is produced by?

A

PANCREAS

30
Q

is the primary hormone responsible for the
ENTRY OF GLUCOSE into the cell.

A

INSULIN

31
Q

INSULIN is synthesized by what cells in the pancreas.

A

b-cells of islets of Langerhans

32
Q

When these cells detect an increase in body glucose, they release insulin.

A

b-cells of islets of Langerhans

33
Q

TRUE OR FALSE
* Insulin is normally released when glucose
levels are high and is not released when glucose levels are decreased.

A

EURT

34
Q

Ano ginagawa ni INSULIN if high ang glucose level?

A

It decreases plasma glucose levels by
increasing the transport entry of glucose in muscle and adipose tissue by way of nonspecific receptors.

35
Q

________ is the only hormone that decreases glucose levels and can be referred to as a hypoglycemic agent

A

INSULIN

36
Q

is the primary hormone responsible for
increasing glucose levels.

A

GLUCAGON

37
Q

GLUCAGON is synthsized by what cells in the pancreas and released during stress and fasting states.

A

a-cells of islets of Langerhans

38
Q

acts by increasing plasma glucose levels by
glycogenolysis in the liver and an increase in gluconeogenesis. It can be referred to as a hyperglycemic agent

A

GLUCAGON

39
Q

produced by the adrenal medulla, increases plasma glucose by inhibiting Insulin secretion, increasing glycogenolysis, and promoting lipolysis.

A

EPINEPHRINE

40
Q

primarily cortisol, are released
from the adrenal cortex on stimulation by adrenocorticotropic hormone (ACTH).

A

GLUCOCORTICOIDS

41
Q

This hormone increases plasma glucose levels by increasing glycogenolysis, gluconeogenesis, and intestinal absorption of glucose.

A

THYROXINE

42
Q

produced by the d-cells of the islets of Langerhans of the pancreas, increases plasma glucose levels by the inhibition of insulin, glucagon, growth hormone, and other endocrine hormones.

A

SOMATOSTATIN

43
Q

is an increase in plasma glucose levels.

A

HYPERGLYCEMIA

44
Q

non–insulin-dependent
diabetes mellitus (NIDDM)

A

TYPE 2

44
Q

insulin-dependent diabetes
mellitus (IDDM)

A

TYPE 1

44
Q

a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.

A

DIABETES MELLITUS

45
Q

is a result of cellular-mediated autoimmune destruction of the b-cells of the pancreas, causing an absolute deficiency of insulin secretion.

A

Type 1 diabetes mellitus

46
Q

Is characterized by inappropriate hyperglycemia primarily a result of pancreatic islet b-cell destruction and a tendency to ketoacidosis.

A

Type 1 DIABETES

46
Q

includes hyperglycemia cases that
result from insulin resistance with an insulin secretory defect.

A

TYPE 2 DIABETES

47
Q

is characterized by hyperglycemia as a result of an individual’s resistance to insulin
with an insulin secretory defect.

A

Type 2 diabetes mellitus

48
Q
  • Most patients in this type are obese or have an increased percentage of body fat distribution in the abdominal region.
  • This type of diabetes often goes undiagnosed for many years and is associated with a strong genetic predisposition, with patients at increased risk with an increase in age, obesity, and lack of physical exercise.
A

TYPE 2 DIABETES

49
Q

DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS:

A
  1. HbA1c ≥ 6.5% using a method that is NGSP certified and standardized to the DCCT assaya
  2. Fasting plasma glucose ≥ 126 mg/dL (≥7.0 mmol/L)a
  3. Two-hour plasma glucose ≥ 200 mg/dL (≥11.1 mmol/L) during an OGTTa
  4. Random plasma glucose ≥ 200 mg/dL (≥11.1 mmol/L) plus symptoms of diabetes
50
Q

Normal fasting glucose

A

FPG 70–99 mg/dL
(3.9–5.5 mmol/L)

51
Q

Impaired fasting glucose

A

FPG 100–125 mg/dL
(5.6–6.9 mmol/L)

52
Q

Provisional diabetes diagnosis

A

FPG ≥126 mg/dL
(≥7.0 mmol/l)a

53
Q

involves decreased plasma glucose levels
and can have many causes—some are transient and relatively insignificant, but others can be life threatening.

A

HYPOGLYCEMIA

54
Q

The result of the deficiency
of a specific enzyme that causes an alternation of glycogen metabolism.

A

GLYCOGEN STORAGE DISEASES

55
Q

What is the most common congenital form of glycogen storage disease?
- is characterized by severe hypoglycemia that coincides with metabolic acidosis, ketonemia, and elevated lactate and alanine.

A

glucose-6-phosphatase deficiency type 1 (von Gierke disease)

56
Q

is characterized by severe hypoglycemia that coincides with metabolic acidosis, ketonemia, and elevated lactate and alanine.

A

von Gierke disease

57
Q

Other enzyme defects or deficiencies that cause hypoglycemia include:

A

glycogen synthase, fructose-1,6-bisphosphatase, phosphoenolpyruvate carboxykinase, and pyruvate carboxylase.

58
Q

a cause of failure to thrive syndrome
in infants, is a congenital deficiency of one of three enzymes involved in galactose metabolism, resulting in increased levels of galactose in plasma.

A

GALACTOSEMIA

59
Q

Glucose can be measured from:

A

serum, plasma, or whole
blood

60
Q

is the term used to describe
the formation of a hemoglobin compound produced when glucose (a reducing sugar) reacts with the amino group of hemoglobin (a protein).

A

GLYCOSYLATED HEMOGLOBIN

61
Q

the most commonly detected glycosylated
hemoglobin, is a glucose molecule attached to one or both N-terminal valines of the b-polypeptide chains of normal adult hemoglobin.

A

HbA1c

62
Q

is a more reliable method of monitoring long-term diabetes control than random plasma glucose. Normal values range from 4.0% to 6.0%.

A

HbA1c

63
Q

are produced by the liver through metabolism of fatty acids to provide a ready energy source from
stored lipids at times of low carbohydrate availability.

A

KETONES

64
Q

is defined as persistent albuminuria in two out of three urine collections of 30 to 300 mg/24 h, 20 to 200 μg/min, or an albumin–creatinine ratio of 30 to 300 μg/mg creatinine.

A

MICROALBUMINURIA

CLINICAL CHEMISTRY 1 (5 decks)

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