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Clinical chemistry > Carbohydrates > Flashcards

Carbohydrates Flashcards

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1
Q

wha are the elements present in compond that are considered carbohydrates

A

Carbon, hydrogen and oxygen

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2
Q

Fuctional groups typically found in carbohydrates

A

Carbonyl and hdroxyl group

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3
Q

what does caboxyl grp contains

A

Carbon and oxygen connected by double bond

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4
Q

Hydroxyl grp contains

A

Oxygen that is covalently bonded to hydrogen atom

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5
Q

Compounds that can donate electrons during chemical reaction

A

Reducing substances

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6
Q

are all carbohydrates a reducing substaces?

A

No ; only some such as glucose and fructose which have free carbonyl grps

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7
Q

Reducing sbstance should contain?

A

Active aldehyde and ketone group

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8
Q

Enumerate the reducing substance

A
  • glucose
  • galactose
  • lactose
  • maltose
  • fructose
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9
Q

Enumerae the non reducin substance

A
  • sucrose or table sugar
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10
Q

Primary source of energy for humans

A
  • glucose
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11
Q

molecules / macromolecules that provide energy to the body

A
  • carbohydrates
  • amino acids
  • glycerol
  • lipids
  • ketones
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12
Q

carbohydrates provide energy to?

A

-erythrocytes
- brain
- human retinal cells

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13
Q

carbohydrates provide energy to?

A

-erythrocytes
- brain
- human retinal cells

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14
Q

What are the non carbohydrate sources?

A
  • amino acids
    -lipids
  • ketones
  • glycerol
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15
Q

carbs classification

A
  • size of the base of carbon chains
  • location of the CO function grp
  • number of sugar units
  • stereochemistry of the compound
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16
Q

Contains 3 carbons

A

Trioses

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17
Q

Contains 4 carbons

A

Tetrose

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18
Q

Contains 5 carbon

A

Pentoses

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19
Q

Contain 6 carbons

A

Hexoses

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20
Q

2 types of carbs based on the location of carboyl grp

A

Aldose and ketose

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21
Q

Location of carbonyl grp in the aldose

A

Terminal part (at the end of the carbon chain)

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22
Q

Location of the carbonyl grp in the ketose

A

Middle of the carbon chain

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23
Q

Example of aldose sugar?

A

Glucose

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24
Q

Example of ketose sugar?

A

Fructose

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25
Q

Simple sugar tha cannot be hydrolyzed into simpler forms

A

Monosaccharide

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26
Q

List the monosaccharides

A

Glucose, fructose, galactose

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27
Q

Joining of 2 carbohydrate molecules

A

Disaccharides

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28
Q

What links the 2 carbohydrate molecules

A

Glycosidic linkage

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29
Q

List the disaccharides

A

maltose, lactose, sucrose

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30
Q

Raffinose cosists of

A

1 glucose,1 galactose,1 fructose

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31
Q

stachyose consists of

A

2 galactose,1 glucose,1 fructose

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32
Q

Found in sugar bits (malasses) and whole rains

A

Oligosaccharide

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33
Q

Lists of polysaccharides

A

Starch and glycogen

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34
Q

Hydroxyl grp that is located on the right of fisher projection

A

Dextrorotatory

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35
Q

Hydroxyl grpthat is located on the left side of fisher projection

A

Leverotatory

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36
Q

Responsiblefor the digestion of the polymers such as starch and glycogen

A

Salivary and pancreatic amylase

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37
Q

His further hydrolyzed the polymers into monosaccharides

A

Maltase

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38
Q

sucrase will be further hydrolyzed into

A

Sucrose to glucose to fructose

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39
Q

Lactase will be further hydroyzed to

A

Lactose to glucose to galactose

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40
Q

What will happento monosaccharides after being hydrolyzed by maltase

A

Absorbed by the gut and transported to the liver by the hepatic portal venous blood supply

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41
Q

Monosaccharide such as glucose are transported to the liver through _____

A

Hepatic potal venous blood supply

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42
Q

3 possible metabolic pathways

A
  • embden meyerhof pathway
  • hexose monopphosphate shunt
  • glycogenesis
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43
Q

First step of all 3 pathways

A

Glucose is converted to glucose 6 phosphate using ATP

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44
Q

Enzyme that converts glucoseinto glucose 6 phosphate

A

Hexokinase

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45
Q

Pathway where glucose is broken down into 2 to 3 carbo molecules of pyruvic acid -> convertd into acetyl coA and enter TCA

A

Embde meyerhof pathway

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46
Q

What type of pathway is EMF

A

Aerobic pathway

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47
Q

Substrates tha can enter EMF aside from glucose

A

Ketones, amino acids, fatty acids, and glycerol

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48
Q

The formation of glucose fronon carbohydrate sources

A

Gluconeogenesis

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49
Q

What is gluconeogenesis

A

The formation of glucose fro non carbohdrate sources such as glycerol

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50
Q

What is glycolysis

A

The process of breaking down of glucose into pyruvate to produce ATP

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51
Q

two products of hexose monophosphate shunt

A

ribose 5- phosphate and NADPH

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52
Q

first step of hexose monophosphate shunt

A

glucose 6 phosphate to 6 phosphogluconic acid

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53
Q

this pathway permits _____ to enter glycolytic pathway

A

pentoses ; hexose monophosphate shunt

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54
Q

function of NADP

A

protects the lipid bilayer and the other cell enzymes from destruction

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55
Q

first step of glycogenesis

A

glucose 6 phosphate is converted to glucose 1 phosphate

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56
Q

what happens after glucose 1 phosphate is formed?

A

converted to uridine diphosphoglucose

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57
Q

which enzyme is responsible for converting UDP- glucose to glycogen

A

glycogen synthase

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58
Q

glycogen primarily stored where?

A

muscle cells and liver

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59
Q

metabolism of glucose molecule to pyruvate or lactate for production of energy

A

glycolysis

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60
Q

formation of glucose 6 phosphate from noncarbohydrate sources

A

gluconeogenesis

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61
Q

breakdown of glycogen to glucose for use of energy

A

glycogenolysis

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62
Q

conversion of glucose to glycogen for storage

A

glycogenesis

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63
Q

conversion of carbs to fatty acids

A

lipogenesis

64
Q

decomposition of fat

A

lipolysis

65
Q

what happens to plasma glucose concentration during glycolysis

A

decreases

66
Q

effect of gluconeogenesis on plasma glucose concentration

A

increases

67
Q

how does glycogenolysis affect glucose concentration

A

elevates glucose

68
Q

effect of glycogenesis on plasma glucose concentration

A

decreases

69
Q

how does lipogenesis impact glucose concentration

A

decreases

70
Q

what happens to glucose concentration during lipolysis

A

increases

71
Q

hormones that control blood glucose

A

insulin and glucagon

72
Q

insulin is synthesized by?

A

beta cells of the islet of Langerhans

73
Q

when is insulin normally released

A

blood glucose is high

74
Q

primary role of insulin

A

responsible for the entry of glucose into the cells

75
Q

how does insulin regulate glucose levels

A

increasing:
-glycogenesis
-lipogenesis
-glycolysis

inhibit:
-glycogenolysis

76
Q

insulin is called?

A

hypoglycemic agent

77
Q

why is insulin called hypoglycemic agent

A

it decreases blood sugar levels by inhibiting glycogenolysis

78
Q

why is insulin called hypoglycemic agent

A

it decreases blood sugar levels by inhibiting glycogenolysis

79
Q

glucagon is synthesized where?

A

alpha cells of the islets of Langerhans

80
Q

when is glucagon released

A

during stress and fasting state

81
Q

how does glucagon regulate glucose level?

A

increasing:
- glycogenolysis
- gluconeogenesis

82
Q

glucagon is also called

A

hyperglycemic agent

83
Q

why is it called hyperglycemic agent

A

increases blood glucose levels

84
Q

what happens when blood glucose levels are high

A

insulin is released by the beta cells of the islets of Langerhans
- stimulating the cells to take up glucose and promoting storage as glycogen in liver and muscles

85
Q

primary function of glucagon in the body

A

stimulate liver cells to convert glycogen into glucose

86
Q

process in which glucagon stimulate to produce glucose from amino acids

A

gluconeogenesis

87
Q

Gluconeogenesis occurs in what organ?

A

liver

88
Q

what is epinephrine and where is it released from?

A

catecholamine ; adrenal medulla

89
Q

epinephrine effect

A

-inhibits insulin secretion
- increase glycogenolysis
- increases lipolysis

90
Q

what hormone is released by the adrenal cortex and its effect on glucose metabolism

A

glucocorticoids (cortisol) ;

  • decreases the glucose uptake by the cells (less glucose is absorbed into the bloodstream)
  • increases gluconeogenesis
  • lipolysis
91
Q

function of ACTH (adrenocorticotropic hormone)

A
  • stimulates the adrenal cortex to release cortisol
    -glycogenolysis
    -gluconeogenesis
92
Q

hormone released by thyroid gland and its effect

A

thyroxine (T4);

-glycogenolysis
-gluconeogenesis
-intestinal absorption of goucose

93
Q

function of somatostatin and where is it released from?

A

inhibits:
-insulin
-growth hormone
-glucagon
-endocrine hormones

released from:
-delta cells of the islet of Langerhans

94
Q

group of metabolic diseased characterized by hyperglycemia resulting from defects in insulin secretion or action

A

diabetes mellitus

95
Q

old classification of type 1 IDDM and type 2 NIDDM is classified according by?

A

National diabetes group

96
Q

IDDM MEANING

A

insulin dependent diabetes mellitus

97
Q

NIDDM meaning

A

non insulin dependent diabetes mellitus

98
Q

old classification of type 1 and type 2 is classified according by?

A

International expert committee

99
Q

new categories of diabetes is by?

A

-american diabetes association
-world health organization

100
Q

type 1 IDDM is also known as

A
  • insulin dependeng
  • juvenile on set
  • brittle
  • ketosis prone diabetes
101
Q

type 1 DM is usually diagnosed to?

A

-children
-teen
-young adults

102
Q

unpredictable swings of blood glucose levels

A

brittle diabetes

103
Q

unpredictable swings of blood glucose levels

A

brittle diabetes

104
Q

production of ketone bodies coming from fat bodies

A

ketosis prone diabetes

105
Q

causes of type 1 DM?

A

results from the cellular-mediated autoimmune destruction of the beta cells of the islet of Langerhans - leading to absolute insulin deficiency

106
Q

antibodies that destroy the beta cells of the pancreas in type 1

A
  • islet cells autoantibodies
    -insulin autoantibodies
    -glutamic acid decarboxylase autoantibodies
  • tyrosine phosphatase IA2 and IA-2B autoantibodies
107
Q

Type 1 dm constitutes

A

10 to 20% of all cases of DM

108
Q

risk factors for developing type 1 dm?

A

-genetic
-autoimmune
-environmental

109
Q

characteristics of type 1 DM?

A

abrupt onset, insulin dependence, ketosis tendency

110
Q

signs and symptoms of type 1 dm

A

-polydipsia
-polyphagia
-polyuria
-rapid weight loss
-hyperventilation
-mental confusion
-loss of consciousness

111
Q

microvascular complications associated with type 1

A

nephropathy
retinopathy
neuropathy

112
Q

type of administration is required for type 1 dm

A

Parenteral administration of insulin

113
Q

no known etiology, strongly inherited, lacking beta cell autoimmune, requiring insulin replacement

A

idiopathic type 1 diabetes

114
Q

type 2 dm is also known as

A

-non insulin dependent
-maturity onset/ adult
-ketosis resistant
-receptor deficient
-stable diabetes

115
Q

causes of type 2 dm

A

insulin resistance and insulin secretory defects

116
Q

characteristics of type 2 dm

A

-adult onset
-milder symptoms
-ketoacidosis

117
Q

risk factors for type 2

A

-genetic
-obesity
-race
-sedentary lifestyle
-PCOS
-dyslipidemia
-hypertension

118
Q

signs and symptoms of pcos

A

-irreg menstruation
-hirsutism (excessive hair growth)
-oilness skin
-acne

119
Q

microvascular and microvascular complications associated with type 2

A

macro:
-coronary heart disease
-cardiovascular dxs

micro:
-nephropathy
-retinopathy
-neuropathy

120
Q

type of medications used to manage type 2

A

-oral agents or hypoglycemic agents such as metformin

121
Q

any degree of glucose intolerance with onset of first recognition during pregnancy

A

gestational diabetes mellitus

122
Q

risk for infants born to mothers with gestational diabetes

A

-respiratory distress syndrome
-hypocalcemia
-hyperbillirubinemia

123
Q

causes of respiratory distress syndrome in infants

A

breathing difficulty due to immature lungs - increased glucose delay the development of the lungs

124
Q

what is hypocalcemia and what causes it in infants?

A

decreased blood calcium due to low parathyroid hormone

125
Q

what contributes to hyperbilirubinemia in infants?

A

prematurity and polycythemia

126
Q

screening for gestational diabetes performed

A

between 24 to 48 weeks of gestation

127
Q

specific types of diabetes associated with secondary conditions?

A

-genetic defects of beta cells function
-pancreatic dxs
-endocrine dxs
-drug or chemical induced
-insulin receptor abnormalities
- genetic disorders

128
Q

increased levels of growth hormone

A

acromegaly

129
Q

increased production of cortisols

A

Cushing’s syndrome or hypercortisolism

130
Q

lab finding of glycosuria?

A

presence of glucose in urine

131
Q

laboratory findings in hyperglycemia?

A

-increased glucose in plasma and urine
-increased urine specific gravity
-ketones in urine and serum
-decreased blood and urine ph
-electrolyte imbalance

132
Q

electrolytes imbalance due to hyperglycemia

A

low sodium concentration and high potassium concentration

-sodium due to polyuria

133
Q

ADA recommendation for diabetes testing in adults (age, year, and using)

A
  • starting the age of 45
  • every 3 years
  • using: HbA1c, fasting plasma glucose, 2 hour 75 mg oral glucose tolerance test
134
Q

who should be tested for Diabetes outside of the age of 45 recommendation?

A

overweight and have additional risk factors

135
Q

hyperpigmentation of the skin, dark areas in the armpits.or groins

A

acanthosis nigricans

136
Q

asymptomatic children be tested for type 2 dm when?

A

-begin at age 1/onset puberty
-follow up testing every 2 years

137
Q

asymptomatic children be tested for type 2 dm when?

A

-begin at age 1/onset puberty
-follow up testing every 2 years

138
Q

risk factors that when present with being overweight indicate the need for diabetes testing in children

A

-family history of type 2
-race or ethnicity
-signs of insulin resistance
-GDM

139
Q

test used to diagnose GDM

A

2 hour OGTT using 75 g glucose load

140
Q

fasting requirement for 2 hr OGTT

A

8-10 hours but not more than 16 hours

141
Q

at what plasma glucose level do glucagon and other glycemic factors get released

A

65-70 mg/dL (3.6-3.9 mmol/L)

142
Q

at what plasma glucose level is associated with observable symptoms of hypoglycemia?

A

50-55 mg/dl (2.8 to 3.1 mmol/L)

143
Q

laboratory findings that are associated with hypoglycemia

A

-decreased plasma glucose levels
-extremely elevated insulin levels in patients with pancreatic beta cell tumors

144
Q

result from the deficiency of specific enzymes that alter glycogen metabolism

A

glycogen storage diseases

145
Q

what is von gierke disease and what enzyme is deficient?

A

-type 1A glycogen storage dxs ;
-caused by deficiency of glucose 6 phosphatase

146
Q

von gierke dxs leads to?

A

serve hypoglycemia

147
Q

symptoms of liver forms of glycogen storage dxs

A

hepatomegaly
hypoglycemia

148
Q

symptoms of galactosemia

A

-failure to thrive
-diarrhea
-vomiting

149
Q

primary enzyme deficiency in galactosemia

A

galactose 1 phosphate uridyltransferase

150
Q

other enzymes that may be deficient in galactosemia

A

-galactokinase
-uridine diphosphate galactose 4 epimerase

151
Q

laboratory test used to confirm the enzyme deficiency in galactosemia

A

-erythrocyte galactose 1 phosphate uridyltransferase activity test

152
Q

enzyme deficiency associated with essential fructosuria?

A

fructokinase deficiency

153
Q

defect in hereditary fructose intolerance

A

defect in fructose 1,6 biphosphate aldolase B activity

154
Q

causes the fructose 1,6 biphosphate deficiency

A

fructose 1,6 biphosphatase

155
Q

What is glycolysis

A

The process of breaking down of glucose into pyruvate to produce ATP

Clinical chemistry (2 decks)

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