(M) Lec 2: Carbohydrates Flashcards

1
Q

The primary source of energy for the brain, erythrocytes, and retinol cells

A

Carbohydrates

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2
Q

The major food source and energy supply of the body as the cells depend on this

A

Carbohydrates

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3
Q

The general empirical formula “Cn(H2O)m” corresponds to what type of carbohydrate?

A

Monosaccharides

Note: Has the same proportion of H and O with that of water

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4
Q

Carbohydrates have been described as the “what” of carbon?

A

Hydrates

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5
Q

Depending on the location of the carbonyl functional group, carbohydrates are hydrates of the derivatives of what 2 functional groups?

A

Aldehydes and Ketones

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6
Q

Carbohydrates are indicated by what shorthand designation?

A

“CHO”

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7
Q

What 2 functional groups are carbohydrates made out of?

A
  1. Carbonyl (C=O)
  2. Hydroxyl (OH)
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8
Q

This is known as the simplest carbohydrate

A

Glycoaldehyde

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9
Q

Structures of carbohydrates can be depicted in 2 ways which are?

A
  1. Long-chain structure (Fischer projection)
  2. Ring structure (Haworth projection)
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10
Q

What are the 4 functions of carbohydrates?

A
  1. Energy
  2. Storage
  3. Structure
  4. Molecular Recognition

Acronym: M-E-S-S

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11
Q

Classification of Carbohydrates based on the Number of Sugar Units

  • Has one sugar unit (simple sugar unit)
  • e.g. Glucose, Fructose, and Galactose
A

Monosaccharides

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12
Q

Classification of Carbohydrates based on the Number of Sugar Units

  • Has 2 sugar units or 2 monosaccharides
  • Requires being split up by intestinal enzymes so they can be absorbed
  • e.g. Sucrose, Lactose, and Maltose
A

Disaccharides

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13
Q

Classification of Carbohydrates based on the Number of Sugar Units

  • Is made up of 2-10 sugar units
A

Oligosaccharides

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14
Q

Classification of Carbohydrates based on the Number of Sugar Units

  • Made up of more than 10 sugar units
A

Polysaccharides

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15
Q

What is the DISACCHARIDE?

Galactose + Glucose

A

Lactose

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16
Q

What is the DISACCHARIDE?

Glucose + Glucose

A

Maltose

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17
Q

What is the DISACCHARIDE?

Glucose + Fructose

A

Sucrose

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18
Q

Classification of Carbohydrates based on the Size of the Base Carbon

5 carbons

A

Pentose

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19
Q

Classification of Carbohydrates based on the Size of the Base Carbon

3 carbons

A

Triose

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20
Q

Classification of Carbohydrates based on the Size of the Base Carbon

6 carbons

A

Hexose

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21
Q

Classification of Carbohydrates based on the Carbonyl Location

Located on the TERMINAL end

A

Aldose

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22
Q

Classification of Carbohydrates based on the Carbonyl Location

Located on the middle (usually lands on C2)

A

Ketose

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23
Q

Reducing or Non-reducing Sugar?

  • A double bond is present
  • Can donate a free aldehyde or the ketone can be oxidized
  • e.g. Glucose, Maltose, Fructose, Lactose, and Galactose
A

Reducing Sugar

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24
Q

Reducing or Non-reducing Sugar?

  • There is no active ketone or aldehyde to be oxidized
  • e.g. Sucrose
A

Non-Reducing Sugar

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25
Q

The sugar present in fruits

A

Fructose

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26
Q

The sugar present in milk or in mammals

A

Lactose

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27
Q

Aside from lactose, this sugar is also present in milk

A

Galactose

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28
Q

The sugar known as “table sugar”

A

Sucrose

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29
Q

This is the only carbohydrate that is directly used as energy/converted to glycogen for storage

A

Glucose

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30
Q

What happens to glycogen when the body needs energy?

A

Converts back to glucose

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31
Q

Digestion of Carbohydrates

Carbohydrates are ingested as what 2 commonly ingested polysaccharides?

A

Starch and Glycogen

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32
Q

Digestion of Carbohydrates

This enzyme hydrolyzes starch to convert it into disaccharides in the duodenum

A

Amylase

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33
Q

Digestion of Carbohydrates

This type of amylase is present in the oral cavity

A

Salivary amylase

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34
Q

Digestion of Carbohydrates

This type of amylase is present in the pancreas

A

Pancreatic amylase

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35
Q

Digestion of Carbohydrates

After amylase hydrolyzes starch, it will be converted into what 2 products?

A

Dextrin and Disaccharide

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36
Q

Digestion of Carbohydrates

The acidic pH of the stomach deactivates what enzyme?

A

Salivary amylase

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37
Q

Digestion of Carbohydrates

When passing through the pancreas, this enzyme will act on the disaccharides to produce another set of disaccharides

A

Pancreatic amylase

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38
Q

Digestion of Carbohydrates

Where are disaccharides further digested into monosaccharides through the enzymes: maltase, sucrase, or lactase?

A

Intestines

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39
Q

Digestion of Carbohydrates

Identify the enzyme that breaks these substances apart:

Maltose to 2 glucose units

A

Maltase

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40
Q

Digestion of Carbohydrates

Identify the enzyme that breaks these substances apart:

Sucrose to glucose and fructose

A

Sucrase

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41
Q

Digestion of Carbohydrates

Identify the enzyme that breaks these substances apart:

Lactose to glucose and galactose

A

Lactase

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42
Q

Digestion of Carbohydrates

What form of carbohydrates can be absorbed by the GIT before going to the liver where it will be circulated to the body?

A

Monosaccharides

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43
Q

These 3 pathways: PPP/HMP, EMP, and TCA, convert glucose into what?

A

Water and Carbon Dioxide

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44
Q

Aside from water and CO2, these 3 pathways: PPP/HMP, EMP, and TCA, convert glucose into what?

A

ADP and ATP

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45
Q

Glucose Metabolism

First step for all three pathways: Glucose, with the help of ATP, is coverted into what?

A

Glucose-6-phosphate (G6P)

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46
Q

Glucose Metabolism

These 2 pathways generate ATP from glucose

A
  1. EMP
  2. HMP
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47
Q

Glucose Metabolism

This pathway allows for the storage of glucose in the form of glycogen which usually occurs in the liver or muscles specialized in storing glycogen

A

Glycogenesis Pathway

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48
Q

Glucose Metabolism

In case the body needs glucose, what will the liver synthesize in order to convert glycogen into glucose?

A

Glucose-6-phosphatase (enzyme for G6P)

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49
Q

Glucose Metabolism

Only the liver is capable of synthesizing glucose-6-phosphatase in order to convert glycogen into glucose, what is its equivalent for the muscle if it cannot release the enzyme?

A

It directly releases glucose via muscle catabolism

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50
Q

Embden-Meyerhoff Pathway

Step 1: Glucose through the action of glucokinase is converted into what?

A

Glucose-6-phoshate (G6P)

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51
Q

Embden-Meyerhoff Pathway

Step 2: Glucose-6-phoshate (G6P) is converted into what?

pathway to glycogenesis

A

Glucose-1-phosphate (G1P)

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52
Q

Embden-Meyerhoff Pathway

Step 3: Glucose-1-phosphate (G1P) through the action of glycogen synthase is converted into?

A

Glycogen

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53
Q

Embden-Meyerhoff Pathway

Optional step: If glycogen is acted upon by glycogen phosphorylase, it will be converted back to what?

A

Glucose-1-phosphate (G1P)

This becomes glucose again later on

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54
Q

Embden-Meyerhoff Pathway

Step 4: Glucose-6-phosphate may also be converted to become what?

EMP

Clue: Another form of sugar

A

Fructose-6-phosphate

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55
Q

Embden-Meyerhoff Pathway

Step 5: Fructose-6-phosphate will be converted into what?

A

Phosphoenol pyruvate (PEP)

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56
Q

Embden-Meterhoff Pathway

Step 6: Phosphoenol pyruvate (PEP) through the action of pyruvate kinase will be converted to?

A

Pyruvate

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57
Q

Embden-Meyerhoff Pathway

Step 7: Pyruvate will be converted into what before entering the Tricarboxylic Acid Cycle (TCA)?

A

Acetyl CoA

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58
Q

Other Pathways involving Carbs

Conversion of glucose to pyruvate or lactate

A

Glycolysis

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59
Q

Other Pathways involving Carbs

Formation of glucose from non-carb sources (e.g. lipids and amino acids)

A

Gluconeogenesis

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60
Q

Other Pathways involving Carbs

From glycogen to glucose

A

Glycogenolysis

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61
Q

Other Pathways involving Carbs

From glucose to glycogen

A

Glycogenesis

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62
Q

Other Pathways involving Carbs

From carbs to fats

A

Lipogenesis

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63
Q

Other Pathways involving Carbs

The decomposition of fats

A

Lipolysis

64
Q

This cycle enables the production of glucose from amino acids, glycogen, glycerol, lactic acid/lactate, or ketone bodies

A

Tricarboxylic Acid/Citric Acid/ Krebs Cycle

65
Q

For cases of brief fasting, what organ is the source of glucose?

A

Liver

66
Q

For cases of longer fasting times that last for more than a day, the body relies on what process?

A

Gluconeogenesis

67
Q

What 3 organs regulate carbohydrates?

A
  1. Liver
  2. Pancreas
  3. Endocrine Glands
68
Q

What are the 2 major hormones that control blood glucose?

A

Insulin and Glucagon

69
Q

This is both an endocrine and exocrine gland

A

Pancreas

70
Q

These glands are able to produce hormones

A

Endocrine glands

71
Q

These glands are able to produce enzymes

A

Exocrine glands

72
Q

What is the exocrine (enzyme) secretion of the pancreas?

A

Amylase

73
Q

What are the endocrine (hormones) secretions of the pancreas?

Clue: Remember the Islets of Langerhans

A
  1. Insulin
  2. Glucagon
  3. Somatostatin
74
Q

Islets of Langerhans

Alpha cells secrete what?

A

Glucagon

75
Q

Islets of Langerhans

Beta cells secrete what?

A

Insulin

76
Q

Islets of Langerhans

Delta cells secrete what?

A

Somatostatin

77
Q

Islets of Langerhans

Acinar and Duct cells (exocrine glands) produce what?

A

Amylase

78
Q

Islets of Langerhans

F cells secrete what?

A

Pancreatic polypeptides

79
Q

The most important hormone in the blood glucose concentration; the main hypoglycemic agent

A

Insulin

80
Q

The only hormone responsible for the entry of glucose into the cell

A

Insulin

81
Q

TOF: Insulin decreases the process of glycogenesis, lipogenesis, and glycolysis BUT increases glycogenolysis hence why it is a hypoglycemic agent

A

False (reverse the decrease and increase portions)

82
Q

Insulin is released when blood glucose levels are what?

A

High

Stimulates the entrance of glucose into tissue (decreases blood sugar)

83
Q

This is released during stressed and fasting stages; the main hyperglycemic agent

A

Glucagon

84
Q

This hormone increases the processes of glycogenolysis and gluconeogenesis

A

Glucagon

85
Q

Once insulin is released, the glucose in the blood goes to where?

A

Body cells (or muscles)

86
Q

TOF: Insulin production rates increase when glucose is absorbed by the muscles

A

False (because glucose is now in your body cells, not your blood, so there is nothing for insulin to counter)

87
Q

Insulin can stimulate what organ to take up glucose and store it as glycogen?

A

Liver

88
Q

Once glucagon is released in the blood, it stimulates the liver to break down what to become glucose?

A

Glycogen

89
Q

This is produced by the medulla of the adrenal glands (specifically chromaffin cells); it inhibits insulin making it a hyperglycemic agent as it increases the processes of glycogenolysis and lipolysis

A

Catecholamines

90
Q

TOF: Catecholamines are released with stress

A

True

91
Q

This is produced by the adrenal cortex (zona fasciculata and zona reticularis); it decreases glucose entry into the cell which increases the processes of gluconeogenesis, lipolysis, and glycogenolysis

A

Glucocorticoids

92
Q

This is the main promoter of gluconeogenesis in glucocorticoids

A

Cortisol (hyperglycemic hormone)

93
Q

Glucocorticoids are made up of what 2 substances?

A

Cortisol and Corticosteroids

94
Q

Hyperglycemic Hormones

Aka “somatotropic hormone” which causes decreased entry of glucose to cells

A

Growth hormone

95
Q

Hyperglycemic Hormones

Increases blood glucose by stimulating the release of cortisol from the adrenal glands

A

ACTH

96
Q

Hyperglycemic Hormones

A thyroid hormone that promotes glycogenolysis and gluconeogenesis (+ intestinal absorption of glucose)

A

Thyroxine

97
Q

Hyperglycemic Hormones

A hormone-inhibiting hormone

A

Somatostatin

98
Q

Clinical Conditions of Carbohydrate Metabolism

An increase in blood or plasma glucose levels

A

Hyperglycemia

99
Q

Clinical Conditions of Carbohydrate Metabolism

TOF: Insulin deficiency directly results to hyperglycemia

A

True

100
Q

Clinical Conditions of Carbohydrate Metabolism

A lack of this receptor prevents the passing of insulin through the cells which prevents the glucose from entering the cells, contributing to hyperglycemia

A

Insulin receptor

101
Q

Clinical Conditions of Carbohydrate Metabolism

With hyperglycemia, all adults older than how many years old should have their FBS checked every 3 years unless diabetic?

A

45 years old

102
Q

Clinical Conditions of Carbohydrate Metabolism

TOF: Ketones are decreased in the serum and urine when a patient is hyperglycemic

A

False (increased)

103
Q

Clinical Conditions of Carbohydrate Metabolism

Why is blood and urine pH decreased when the patient is experiencing hyperglycemia? What urinary tract event is experienced when blood glucose levels are high?

A

Polyuria = decreases urine pH

104
Q

Clinical Conditions of Carbohydrate Metabolism

A decrease in blood or plasma glucose levels which is usually a warning sign for CNS-related disorders

A

Hypoglycemia

105
Q

Clinical Conditions of Carbohydrate Metabolism

What is the characteristic sign and symptom of hypoglycemia?

A

Whipple’s Triad

  1. Hypoglycemic symptoms
  2. Low blood glucose concentration
  3. Immediate relief after glucose administration
106
Q

Clinical Conditions of Carbohydrate Metabolism

TOF: The Whipple’s Triad is used to diagnose patients that have diabetes

A

False (no diabetes)

Hypoglycemia

107
Q

Clinical Conditions of Carbohydrate Metabolism

What glucose level indicates that glucagon and other hyperglycemic hormones are being released by the endocrine gland?

A

65 to 70 mg/dL

108
Q

Clinical Conditions of Carbohydrate Metabolism

Hypoglycemia symptoms are observable at what glucose level?

A

50-55 mg/dL

109
Q

Clinical Conditions of Carbohydrate Metabolism

What is the diagnostic glucose level for hypoglycemia?

A

Less than 50 mg/dL

110
Q

Classifications of Hypoglycemia can be Based on:

“Whether administered with insulin, alcohol, or salicylates”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

A. Drug Administration

111
Q

Classifications of Hypoglycemia can be Based on:

“Those with hepatic failure, renal failure, or sepsis”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

B. Critical Illnesses

112
Q

Classifications of Hypoglycemia can be Based on:

“Deficiency of GH or cortisol deficiency”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

C. Hormonal Deficiency

113
Q

Classifications of Hypoglycemia can be Based on:

“Wherein there is a pancreatic beta cell disorder”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

D. Endogenous Hyperinsulinism

114
Q

Classifications of Hypoglycemia can be Based on:

“There is a production of insulin autoantibodies”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

E. Autoimmune Hypoglycemia

115
Q

Classifications of Hypoglycemia can be Based on:

“Such as leukemia or hepatoma”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

F. Non-Beta Cell Tumors

116
Q

Classifications of Hypoglycemia can be Based on:

“Cases of post-gastric surgery”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

H. Alimentary Hypoglycemia

117
Q

Classifications of Hypoglycemia can be Based on:

“Cause is unknown”

A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia

A

I. Idiopathic Postprandial Hypoglycemia

118
Q

A group of metabolic disorders characterized by hyperglycemia

A

Diabetes Mellitus

119
Q

This condition is caused by defects in insulin secretion, insulin receptors, or both

A

Diabetes Mellitus

120
Q

This is exhibited when the plasma glucose level exceeds 180 mg/dL with a normal renal function

A

Glucosuria

121
Q

This condition is also exhibited in Diabetes Mellitus but may be reversed by insulin administration

A

Ketosis

122
Q

TOF: Ketone bodies are frequently found in patients with severe uncontrolled diabetes

A

True

123
Q

Endocrine disorders such as Cushing’s Syndrome, Acromegaly, or Pheochromocytoma have an increased release of hormones that (increase/decrease) blood glucose levels

A

Increase

124
Q

Types of DM:

Aka insulin dependent DM, juvenile onset DM, brittle diabetes, or ketosis-prone diabetes

A

Type 1

125
Q

Types of DM:

Caused by the cellular mediated autoimmune destruction of B cells in the pancreas

A

Type 1

126
Q

Types of DM:

Manifested by insulinopenia wherein there is absolute insulin deficiency due to the loss of pancreatic B cells which resuts to the dependency in insulin to sustain life and prevent ketosis

A

Type 1

127
Q

Types of DM:

There is a genetic association with HLA DR3 and DR4 located on Chromosome 6

A

Type 1

128
Q

Types of DM:

There is a presence of multiple autoantibodies (glutamic acid decarboxylase and insulin autoantibodies)

A

Type 1

129
Q

Types of DM:

This type is rare, has no known etiology, strongly inherited, no B-cell autoantibodies, episodic insulin requirements, and is prone to developing ketosis

A

Idiopathic Type 1 DM

130
Q

Types of DM:

What are the 3 signs and symptoms of type 1 DM?

Clue: 3Ps

A
  • Polyuria
  • Polydipsia
  • Polyphagia
131
Q

Types of DM:

Aka non-insulin dependent DM, adult type/maturity onset DM, stable diabetes, ketosis-resistant DM, or receptor-deficient DM

A

Type 2

132
Q

Types of DM:

This is a relative-type of insulin deficiency as opposed to the other type with absolute deficiency

A

Type 2

133
Q

Types of DM:

This is caused by a resistance to insulin due to a deficiency in insulin receptors

A

Type 2

134
Q

Types of DM:

This is a geneticist’s worst nightmare because of its genetic predisposition

A

Type 2

135
Q

Types of DM:

Results to non-ketotic hyperosmolar coma (overpopulation of glucose) plus a notable increase in BUN and creatinine

A

Type 2

136
Q

Types of DM:

This type has no presence of ketoacidosis

A

Type 2

137
Q

Types of DM:

In this type, insulin is present but there is no receptor that is why the C-peptide is linked to be present (C-peptide is produced with insulin)

A

Type 2

138
Q

Types of DM:

What are the 3 signs and symptoms of Type 2 DM?

Clue: 3Ps

A
  • Polyuria
  • Polydipsia
  • Polyphagia
139
Q

This is characterized by a deficiency in ADH or vasopressin with normoglycemia, severe polyuria, and polydipsia (decreased SG but increased urine volume)

A

Diabetes Insipidus

140
Q

Diabetes Mellitus Table (Type 1 or 2)

Incidence Rate: 10-15%

A

Type 1

141
Q

Diabetes Mellitus Table (Type 1 or 2)

Incidence Rate: 90-95%

A

Type 2

142
Q

Diabetes Mellitus Table (Type 1 or 2)

Onset: Any (childhood/teens)

A

Type 1

143
Q

Diabetes Mellitus Table (Type 1 or 2)

Onset: Over 40 years old

A

Type 2

144
Q

Diabetes Mellitus Table (Type 1 or 2)

Risk Factors: Genetic/Autoimmune

A

Type 1

145
Q

Diabetes Mellitus Table (Type 1 or 2)

Risk Factors: Genetics, obesity, and lifestyle

A

Type 2

146
Q

Diabetes Mellitus Table (Type 1 or 2)

C-Peptide Levels: Decreased or undetectable

A

Type 1

147
Q

Diabetes Mellitus Table (Type 1 or 2)

C-Peptide Levels: Detectable

A

Type 2

148
Q

Diabetes Mellitus Table (Type 1 or 2)

Pre-diabetes: (+) for autoantibodies

A

Type 1

149
Q

Diabetes Mellitus Table (Type 1 or 2)

Pre-diabetes: (-) for autoantibodies

A

Type 2

150
Q

Diabetes Mellitus Table (Type 1 or 2)

Symptomatology: Symptoms develop abruptly

A

Type 1

151
Q

Diabetes Mellitus Table (Type 1 or 2)

Symptomatology: Symptoms develop gradually (some are asymptomatic)

A

Type 2

152
Q

Diabetes Mellitus Table (Type 1 or 2)

Ketosis: Common and poorly controlled

A

Type 1

153
Q

Diabetes Mellitus Table (Type 1 or 2)

Ketosis: Rare

A

Type 2

154
Q

Diabetes Mellitus Table (Type 1 or 2)

Medication: Insulin absolute

A

Type 1

155
Q

Diabetes Mellitus Table (Type 1 or 2)

Medication: Oral agents

A

Type 2

156
Q

TOF: Genetic syndromes such as Down’s syndrome or Klinefelter syndrome can also have an increased chance to manifest diabetes mellitus

A

True