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1. CC 1 > CARBOHYDRATES > Flashcards

CARBOHYDRATES Flashcards

1
Q

carbohydrates is composed of

A

Carbon
Hydrogen
Oxygen

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2
Q

carbohydrate contans what functional group

A

C=O
-OH

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3
Q

General Formula of carbohydrate

A

C6(H12O)6

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4
Q

Carbohydrates is stored in the body in the form of>

A

glycogen

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5
Q

Chemical Structure
-open chain form
-carbon are vertically conneected by solid lines
C-O and C-H horizontally connected

A

Fisher projection

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6
Q

Chemical structure
-cyclic form

A

Hayworth projection

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7
Q

Based on carbon chain size
3 carbon
4 carbon
5 carbon
6 carbon

A

Trioses
Tetroses
Pentoses
Hexoses

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8
Q

Smallest carbon chain found in the body

A

Glyceraldehyde

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9
Q

Also known as simple sugar
No further reduction in form

A

Monosaccharide

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10
Q

Monosaccharide is also known as

A

simple sugar

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11
Q

What are the 6 Hesoxes of Monosaccharide

A

Glucose
Fructose
Galactose

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12
Q

What are the Pentoses of Monosaccharide

A

Deoxyribose
Ribose

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13
Q

most common sugar in the body

A

D-glucose

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14
Q

-OH group on the right

A

D-glucose

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15
Q

-OH group on the left

A

L-glucose

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16
Q

Type of D-glucose predominant in starch

A

a-D-glucose

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17
Q

Type of D-glucose predominant in glycogen and cellulose

A

B-D-glucose

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18
Q

Consist of 2 monosaccharides joined by glycosidic linkage

A

Disaccharide

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19
Q

Disaccharide consists of 2 mmonosaccharides joined by??

A

glycosidic linkage

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20
Q

1st carbon atom of a monosaccharide is linked to 4th carbon of the other mmonosaccharide

A

1-4 glycosidic linkage

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21
Q

glucose+glucose=

A

maltose

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22
Q

glucose+galactose=

A

lactose

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23
Q

glucose+fructose=

A

sucrosehjy

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24
Q

hydrolize by enzyme lactase present in the intestine

A

Disaccharides

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25
Q

Composed of 3 to 10 monosaccharides some up to 20

A

Oligosaccharides

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26
Q

In the body they are called glycans (glycoprotein and glycolipids)

A

Oligosaccharides

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27
Q

What are Oligosaccharides called in the body?

A

Glycans (glycoprotein and glycolipids)

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28
Q

process of binding oligosaccharide to proteins or lipids

A

Glycosylation

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29
Q

Oligosaccharides that participate in immune responsee

A

cell recognition- cell receptors
auto antigens (RBC antigen)

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30
Q

The building block of A and B antigen in RBC

A

H-antigen

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31
Q

Consist of many units of monosaccharides linked together by glycosidic bonds

A

Polysaccharides

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32
Q

Serves as storage of energy in human and plants

A

Polysaccharides

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33
Q

Integral part of the cell and tissue structure

A

Polysaccharides

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34
Q

Exogenous Polysaccharides

A

Starch
Cellulose
Insulin
Chitin

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35
Q

storage form in plants (amylopectin annd amylose)

A

Starch

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36
Q

forms the cell wall of plants. also known as dietary fiber

A

Cellulose

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37
Q

Cellulose is also known as?

A

dietary fiber

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38
Q

also known as fructans (dietary fibers) found in plants. Used for Glomerular filtration rate estimation

A

Insulin

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39
Q

forms the cell wall of fungi and exoskeleton of arthropods

A

Chitin

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40
Q

Endogenous Polysaccharides

A

Glycogen
Hyaluronic acid
Heparin

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41
Q

storage form in human (liver)

A

Glycogen

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42
Q

lubricants of the joints

A

Hyaluronic acid

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43
Q

natural anticoagulant in the blood

A

Heparin

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44
Q

Major source of energy(glucose) in the body

A

Polysaccharide

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45
Q

Found as part of the cell membrane of the cell the glycoprotein and glycolipids

A

Polysaccharides

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46
Q

Forms the building block (oligosaccharides) of ABO antigen in the surface of RBCs

A

Polysaccharides

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47
Q

One of the major component of nucleotides (pentose)

A

Polysaccharides

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48
Q

starch and glycogen (polysaccharides) are broken down into Disaccharide in the mouth through?

A

salivary amylase

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49
Q

Limit dextrin and maltose (disaccharide)
In the small intestine hydolysis occur by the action of ______ to breakdown into monosaccharide

A

Pancreatic amylase, maltase, sucrase and lactase

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50
Q

From the duodenum and ileum monosaccharide is absorbed into the blood circulation for further metabolism

A

Glucose
Galactose
Fructose

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51
Q

Depending on the need of the body glucose can be?

A

Used as energy
stored in the form of glycogen
stored in the form of triglycerides
converted in protein, amino acids and keto acids

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52
Q

used for energy production through production of ATP, CO2 and H2O

A

GGlucose

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53
Q

3 process of energy production through ATP (glucose)

A

Glycolysis
TCA cycle (Krebs cycle)
Electron Transport Chain

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54
Q

The process of storing in the form of glycogen in the liver and peripheral tissues like skeletal muscle.

A

Glycogenesis

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55
Q

Process of storing as triglyceerides in adipose tissues

A

Lipogenesis

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56
Q

Process that occurs in the skeletal muscle converted into keto-acids, amino-acids and protein

A

Cori cycle (glucose-alanine cycle)

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57
Q

Processes of glucose metabolismm

A

Glycogenesis
Glycogenolysis
Gluconeogenesis
Glycolysis
Lipogenesis
Lipolysis

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58
Q

Conversion of excess glucose to glycogen to be stored in the live and peripheral tissues

A

Glycogenesis

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59
Q

This process occur when cell is already met the energy requirement, glucose is stored as glycogen

A

Glycogenesis

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60
Q

Process of glucose metabolism that reduces blood sugar level

A

Glycogenesis

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61
Q

Stored glycogen in the liver is broken down into glucose for energy production

A

Glycogenolysis

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62
Q

This process occur during fasting state

A

Glycogenolysis

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63
Q

Process that is stimulated by glucagon and epinephrine

A

Glycogenolysis

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64
Q

This process is inhibited by insulin and increases blood sugar

A

Glycogenolysis

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65
Q

Formmation of Glucose-6-phosphate from non-carbohydrate source such as lactate, amino acids (keto acids) and glycerol

A

Gluconeogenesis

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66
Q

This process occurs in the liver, kidney, skeletal muscle, intestine, and brain

A

Gluconeogenesis

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67
Q

This process occur during prolong starvation and increases the blood sugar level

A

Gluconeogenesis

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68
Q

process where glucose is metabolized into pyruvate and lactate releasing energy (ATP) and this process reduces blood sugar level

A

Glycolysis

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69
Q

Conversion of glucose into fatty acids for storage in adipose tissues

A

Lipogenesis

70
Q

This process occur when sufficient glycogen is already stored in the liver and it decreases blood sugar level

A

Lipogenesis

71
Q

Fatty acids in adipose tissue is converted back to glucose to be used for energy production

A

Lipolysis

72
Q

Triglycerides is broken down to FA and oxidized (B-oxidation) into Acetyl CoA to be used to generate ATP

A

Triglycerides

73
Q

This process occurs during prolong starvation and it increases blood sugar level

A

Lipolysis

74
Q

Processes that increase blood sugar level

A

Glycogenolysis
Gluconeogenesis
Lipolysis

75
Q

Processes that decrease blood sugar level

A

Glycolysis
Glycogenesis
Lipogenesis

76
Q

Also known as Hypoglycemic agent

A

Insulin

77
Q

Produced by pancreas the beta islets of Langerhans.
Release when plasma glucose level increase thus lowering blood glucose.

A

Insulin

78
Q

This hormonal regulation of blood sugar.
Actions include:
Increase glycolysis, glucogenesis and lipogenesis
Decrease glycogenolysis

A

Insulin

79
Q

Also called Hyperglycemic agent

A

Glucagon

80
Q

Produced by pancreas the alpha islets of Langerhans cells.
Release when plasma glucose decrease (stress and fasting state) therefore increasing blood glucose.

A

Glucagon

81
Q

This hormonal regulation of blood sugar.
Actions include:
Increases glycogenolysis, gluconeogenesis and lipolysis.

A

Glucagon

82
Q

Also called Regulator

A

Somatostatin

83
Q

Produced by pancreas delta islets of Langerhans.

A

Somatostatin

84
Q

This hormonal regulation of blood sugar.
Action
Inhibits the release of insulin and glucagon. Regulates the reciprocal relationship of these hormones.

A

Somatostatin

85
Q

Growth hormone (GH)
Increases blood glucose level
Regulated by somatostatin produced by GIT, pancreas, CNS and somatomedins produced by liver.

A

Anterior pituitary gland

86
Q

Release when cortisol level is low in the blood.
Increase blood glucose level through glycogenolysis and gluconeogenesis.

A

ACTH-adrenocorticotropic hormone

87
Q

Thyroxine (T4)
Increase blood glucose thru glycogenolysis, gluconeogenesis and absorption of glucose in the GIT.

A

Thyroid gland

88
Q

Increases blood glucose inhibiting insulin and increasing glycogenolysis.
Release during stress.

A

Epinephrine (adrenal medulla)

89
Q

Stimulated by ACTH.
Increase blood glucose glycogenolysis, gluconeogenesis, and lipolysis.

A

Cortisol (adrenal cortex)

90
Q

2 Adrenal Gland`

A

Epinephrine (adrenal medulla)
Cortisol (adrenal Cortex)

91
Q

produce by the placenta
inhibits insulin activity

A

Human Placental Lactogen (HPL)

92
Q

Hormone that Increase blood sugar

A

Glucagon
Growth hormone
ACTH
Thyroid hormone (thyroxine)
Epinephrine
Cortisol

93
Q

Hormone that Decrease blood sugar

A

Insulin
Somatomedins

94
Q

Abnormal blood glucose level (Hyperglycemia)

A

Diabetes mellitus (DM)
Pancreatic deficiency
Hyperadrenalism (Cushing’s syndrome)
Excessive growth hormone
Pheochromocytoma (tumor of the adrenal medulla)

95
Q

Abnormal blood glucose level (Hypoglycemia)

A

Overdose of insulin
Hypothyroidism
Hypopituitarism
Hypoadrenalism (Addison’s disease – destruction of adrenal cortex)

96
Q

Glycemic diseases

A

Hyperglycemia (Diabetes mellitus)
Hypoglycemia
Glycogen storage diseases

97
Q

A group of metabolic disorder with hyperglycemia as the hall mark of the disease.

A

Diabetes mellitus

98
Q

Signs and symptoms (3P’s)
Diabetes mellitus

A

Polyuria (excessive urination)
Polyphagia (excessive appetite)
Polydipsia (excessive thirst)

99
Q

Diabetes mellitus is due to?

A

Insulin secretion defects (insufficient insulin)
Impaired insulin action (insulin resistance)
Both

100
Q

excessive urination

A

Polyuria

100
Q

Excessive thrist

A

Polydipsia

101
Q

Excessive appetite

A

Polyphagia

102
Q

Diabetes mellitus complications (if left untreated) in the MICROVASCULAR COMPLICATIONS

A

Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathy

103
Q

Diabetes mellitus complications (if left untreated) in the MACROVASCULAR COMPLICATIONS

A

Circulatory problems
Diabetic foot

104
Q

Ophthalmic complications
Swelling retinal blood vessels and leakage of fluid.

A

Diabetic retinopathy

105
Q

Can lead to glaucoma and blindness.

A

Diabetic retinopathy

106
Q

damage in optic nerve due to high pressure in the eye.

A

Glaucoma-

107
Q

Glomerular sclerosis (scarring).

A

Diabetic nephropathy

108
Q

Thickening of the basement membrane resulting uremia and renal proteinuria.

A

Diabetic nephropathy

109
Q

high level of waste products in the blood such as urea and creatinine.

A

Uremia

110
Q

Can lead to Chronic kidney disease (CKD).

A

Diabetic nephropathy

111
Q

test for diabetic nephropathy

A

Urine microalbumin and GFR

112
Q

Peripheral nerve damage mostly the feet and legs.
(numbness, tingling sensation, cramps, foot ulcers, bone and joint pain)

A

Diabetic neuropathy

113
Q

Loss of elasticity of blood vessels due to high blood sugar. Can lead to atherosclerosis.
Heart attack
Stroke

A

Circulatory problems.

114
Q

Diabetic complications wher damage to larger blood vessels

A

Macroangiopathy

115
Q

Diabetic complications where clogging of the blood vessels

A

Atherosclerosis

116
Q

Skeletal muscle damage

A

Diabetic foot

117
Q

infection of the bone.

A

Osteomyelitis

118
Q

bacterial infection (Group A strep.)

A

Cellulitis

119
Q

Beta cells of pancreas destruction.
classification of DM

A

Type 1

120
Q

Insulin resistance.
classification of DM

A

Type 2

121
Q

Impaired insulin action due to hormonal changes during pregnancy.
classification of DM

A

Gestational DM

122
Q

Insulin-dependent diabetes, type I diabetes, or juvenile-onset diabetes.

A

Immune-mediated diabetes (type I)

123
Q

10-20% of the cases of DM.

A

Immune-mediated diabetes (type I)

124
Q

Autoimmune destruction of β- cells of the pancreas resulting to absolute insulin deficiency

A

Immune-mediated diabetes (type I)

125
Q

β-cell include islet cell autoantibodies, autoantibodies to insulin, autoantibodies to glutamic acid decarboxylase (GAD)

A

Immune-mediated diabetes (type I)

126
Q

can also be predisposing factors. in Type 1 DM

A

HLA genes

127
Q

Hyperglycemia and ketoacidosis. type of DM

A

Type 1 DM

128
Q

3P’s, rapid weight loss, mental confusion, loss of consciousness and other complications of DM.

A

Type 1 DM

129
Q

Majority of cases of DM (90-95%).

A

Insulin resistance (Type 2 DM)

130
Q

Referred to as non-insulin-dependent diabetes, type II diabetes, or adult-onset diabetes.

A

Insulin resistance (Type 2 DM)

131
Q

Insulin resistance and usually have relative insulin deficiency.

A

Insulin resistance (Type 2 DM)

132
Q

Most are obese, microvascular and macrovascular complications develop.

A

Insulin resistance (Type 2 DM)

132
Q

Predisposing factors: genes, obesity, age, sedentary life style and nutrition.

A

Insulin resistance (Type 2 DM)

133
Q

Cause: excessive production of insulin due to excessive eating.

A

Insulin resistance

133
Q

Less ketoacidosis.
Treatment is hypoglycemic drugs (metformin).
Women with prior GDM has a higher risk.

A

Insulin resistance (Type 2 DM)

133
Q

Cells of the muscle, liver, and fat are not responding to insulin thus glucose is not uptake into the cell to be used for energy production. Therefore lead to hyperglycemia.

A

Insulin resistance

134
Q

Resistance to insulin starts to manifest at the of

A

35 or 40 years old.

135
Q

Type 1 DM (absolute insulin deficiency)
Age
Body structure
Ketoacidosis (ketosis)
Prevalence
Treatment
3p’s
Complications

A

Mostly young (juvenile)
Normal or thin
Present
Less (10%)
Insulin Injection or IV
Present
Macrovascular and microvascular

136
Q

Type 2 DM (Insulin resistance)

A

Mostly adult (>35 years old)
Mostly obese
Rare
More prevalent (90%)
Oral drugs (metformin)
Present
Macrovascular and Microvascular

137
Q

refers to accumulation of ketones bodies in the blood such as Acetoacetate, β-Hydroxybutyrate and acetone produced from the beta oxidation of fatty acids (lipolysis).

A

Ketoacidosis

138
Q

Due to metabolic and hormones (HPL)
Return to normal postpartum but has a higher risk of developing DM-2 later in life.

A

Gestational DM

139
Q

Development of glucose tolerance during pregnancy.

A

Gestational DM

140
Q

Autosomal inherited pattern, mutation in chromosome 12 (Hepatocyte nuclear factor) and chromosome 7 (glucokinase) these are glucose sensor.
type of other specific DM

A

Genetic β cells defect

141
Q

Occurs at young age (before 25), characterized by insufficient insulin production.
type of other specific DM

A

Genetic β cells defect

142
Q

Dysfunction of glucose sensors can lead to insufficient insulin secretion therefore can lead to hyperglycemia.
type of other specific DM

A

Genetic β cells defect

143
Q

Other genetic diseases
Other specific type of DM

A

Cystic fibrosis
Down’s syndrome
Klinefelter’s syndrome
Turner’s syndrome.

144
Q

Pancreatic carcinoma, pancreatitis, pancreatotomy, trauma or infection.

A

Pancreatic disease

145
Q

Endocrine diseases

A

Acromegaly- growth hormones
Cushing’s syndrome- cortisol
Glucagonoma- glucagon
Pheochromocytoma- epinephrine
Thyroid diseases- Thyroxine

146
Q

These hormones inhibits the action of insulin.

A

Acromegaly- growth hormones
Cushing’s syndrome- cortisol
Glucagonoma- glucagon
Pheochromocytoma- epinephrine
Thyroid diseases- Thyroxine

147
Q

Drug- or chemical-induced diabetes

A

Nicotinic acid
Glucocorticoids
α-interferon
Vacor (a rat poison)
Pentamidine

148
Q

affects insulin secretion and sensitivity, destruction of pancreatic cells or increased production of glucose.

A

Drug- or chemical-induced diabetes

149
Q

Production of anti-insulin receptor thereby blocking the binding of insulin to its receptor in target tissues.

A

Insulin receptor deficiency (autoimmune disease)

150
Q

These autoantibodies are usually seen in SLE.

A

Insulin receptor deficiency (autoimmune disease)

151
Q

The body compensate: increase secretion of glucagon, epinephrine, cortisol, GH increases to raise the blood glucose level.

A

Hypoglycemia

152
Q

Types of Hypoglycemia

A

Rapid fall of plasma glucose
Gradual fall in plasma glucose

153
Q

Triggers release of epinephrine which account for the following signs and symptoms attributed to hypoglycemia : weakness, shakiness, sweating, nausea rapid pulse, hunger and epigastric discomfort.

A

Rapid fall of plasma glucose

154
Q

Not accompanied by epinephrine release; causes impairment of CNS function such as confusion, lethargy, seizure, and loss of consciousness.

A

Gradual fall in plasma glucose

155
Q

severe hepatomegaly due to deficiency of glucose-6-phosphate

A

Von gierke’s disease

156
Q

Causes of hypoglycemia

A

Excessive pancreatic insulin
Hypothyroidism
Hypoadrenalism
Von gierke’s disease

157
Q

Inherited metabolic disorder (rare).
Commonly seen in infants and young children
Deficiency in enzymes due to genetic cause.
Impaired glucogenesis or glycogenolysis.
Causes severe hypoglycemia, hepatomegaly and mental retardation.

A

Glycogen storage diseases

158
Q

Enzyme Defect
Glucose-6-phosphate dehydrogenase

Clinical Feature
Hepatomegaly, hypoglycemia, ketosis, hyperlipidemia

A

Type I: Von Gierke
(most common)

159
Q

Enzyme Defect
Alpha 1.4 glucosidase

Clinical Feature
Cardiorespiratory failure

A

Type II: Pompe

160
Q

Enzyme Defect
Amylo-1-6 glucosidase
Clinical Feature
Like type I but milder

A

Type III: Cori

161
Q

Enzyme Defect
Phosophorylase

Clinical Feature
Like type I but milder

A

Type VI: hers

161
Q

Enzyme Defect
Alpha 1-4 and alpha 1-6

Clinical Feature
Liver cirrhosis

A

Type IV: Andersen

161
Q

Enzyme Defect
Phosphofructokinase

Clinical Feature
Mild hepatomegaly and hypoglycemia

A

Type VIII

161
Q

Enzyme Defect
Phosphorylase

Clinical Feature
Limited physical activity due to muscle cramps

A

Type V: Mcardle

161
Q

For early detection to provide clinical intervention thus minimizing signs and symptoms.

A

Newborn screening (NBS)

162
Q

Enzyme Defect
Phosphofructokinase

Clinical Feature
Like type V

A

Type VII

1. CC 1 (4 decks)

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