Carbohydrates

Almira Coleen · 28問 · 1年前

通報

問題一覧

Primary source of energy in most mammals

Carbohydrates

Glucose CF =

0.0555

Carbohydrate enzyme:

Amylase

Excess carbohydrates are stored in the liver as?

Glycogen

Too much carbohydrates intake and not used some will be stored on liver, some will be a?

Fat

Classification is based on? Hexa, Pentra, Tetra, Triose, Pentose, Hexose

Size of base carbon chain

Classification based on: Aldose, Ketose

Location of the CO function group

Monosaccharide, Polysaccharide

Number of sugar units

Structural Classification of Carbohydrates

Haworth Projection, Fisher Projection

Cyclical (closed chain form)

Haworth Projection

Straight (open chain form)

Fisher Projection

Glucose, Galactose, Fructose

Monosaccharides

Maltose, Lactose, Sucrose

Disaccharides

2-10 units Intermediate products of digestion

Oligosaccharides

More than 10 units (Starch and Glycogen) - storage form carbohydrates

Polysaccharides

Storage of plants and animals

Starch

Storage of animals

Glycogen

Breakdown of glucose: Pyruvate, Lactate (ATP) -> Energy

Glycolysis

Creation of glycogen Repacking of glucose -> glycogen Stored: Liver, Skeletal Muscle

Glycogenesis

Glycogen broken down into glucose Glycogen -> Glucose Strenuous activities, stressful situations

Glycogenolysis

Creation of new/Glucose products Come from lipids and amino acids Amino acids

Gluconeogenesis

Converting glucose into fat

Lipogenesis

Breakdown of fats Energy Dangerous: Ketone bodies (increase)

Lipolysis

Glucose to Glucose 6 Phosphate (Enzyme: Glycogen Synthase) to Glycogen to Liver

Glycogen Conversion Pathway

Non-nucleated cell (RBC) Pentose - Fructose 1,6 phosphate

Hexose Monophosphate Pathway

2 pyruvate - pyruvic acid

Embden Mayerhof Pathway

L, P -> Glucose

Gluconeogenesis

Glucose -> ATP

Electron Transport Chain: NADH

3ATPs

Electron Transport Chain: FADH

2 ATPs

Hormones That Regulate Glucose Metabolism:

Somatostatin, Insulin, Glucagon, Epinephrine, Cortisol, Growth Hormone, Thyroxine

Command center Delta cells of the pancreas Hyperglycemic agent Inhibits secretion of Insulin, Glucagon, and Growth Hormone

Somatostatin

Beta cells of pancreas Hypoglycemic agent Released when blood glucose is elevated Glucose cell entry Glycogenesis and Lipogenesis Prevents Glycogenolysis

Insulin

Alpha cells of pancreas Hyperglycemic agent Released when blood glucose is low Stimulate glycogenolysis and gluconeogenesis

Glucagon

Only hypoglycemic agent

Insulin

Adrenal medulla Hyperglycemic agent Stimulates glycogenolysis and lipolysis Inhibits insulin secretion

Epinephrine

Adrenal cortex Hyperglycemic agent Stimulates glycogenolysis, lipolysis and gluconeogenesis

Cortisol

Both are found in the adrenal glands

Epinephrine, Cortisol

- Also termed as adrenaline - Intense stressful situation - "flight/fight = survival instinct" - It needs energy for activities necessary for survival

Epinephrine

Usual stress Higher level in the morning, lower level in the morning

Cortisol

Cortisol hormone released by the pituitary gland?

ACTH

Anterior pituitary gland Hyperglycemic agent Stimulates glycolysis Prevents glucose cell entry

Growth Hormone

Thyroid gland Hyperglycemic agent Stimulates glycogenolysis and gluconeogenesis Increase intestinal absorption of glucose

Thyroxine

Only hypoglycemic agent

Insulin

Observe proper blood collection/phlebotomy procedure Blood additive:

Non-addictive/Anti-glycolytic -> Iodoacetate/oxidase

Anytime of the day

Random Blood Sugar

Random Specimen Considerations

Random Blood Sugar, Random Blood Glucose

Fasting Specimen Considerations

Fasting Blood Sugar, Fasting Blood Glucose

Fasting period:

8-10 hours

In centrifugation, you will separate _____ to decrease glycolysis

Serum

Glucose tolerance test: Adults

75g

Glucose tolerance test: Pregnant

100g

How many days for high carbohydrate diet before8-10hours fasting?

3 days

Factors that may affect glucose/tolerance tests in general:

Diet and Impaired Fasting, Alcohol, Smoking, Endocrine dysfunctions, Vomiting, Medication, Problems in the GIT

Fasting value:

70-110mg/dL

Fasting in 1 hour

200mg/dL

Fasting in 2 hrs

<140mg/dL

Normal glucose tolerance (2h PG)

140mg/dL (7.8mmol/L)

Impaired glucose tolerance:

140-199 mg/dL (7.8 - 11.1 mmol/L)

Provision diabetes diagnosis

200mg/dL (11.1mmol/L)

Glucose in the amine (valine) end of the hemoglobin Ideal for glucose monitoring (2-3 months)

Glycosylated Hemoglobin (HbA1c)

Range of fructosamine monitoring:

2-3 weeks

In the Glycosylated Hemoglobin, the only specimen used are?

EDTA Whole Blood

Glycosylated hemoglobin concentration is directly proportional to?

Plasma Glucose Determination

Glycosylated HbA1c Normal Value:

4-6%

Based on charge differences between Glycosylated and Non-glycosylated Hemoglobin:

Cation-Exchange Chromatography, Electrophoresis, Isoelectric Focusing

Based on structural characteristics of glycogroups on hemoglobin:

Affinity Chromatography, Immunoassay

An increase in plasma glucose levels.

Hyperglycemia

In healthy, patients, during a hyperglycemic state, ______ is secreted by the Beta cells of the pancreatic islets of Langerhans

Insulin

hyper to normal blood glucose level (hyperglycemia)

Insulin

This test is done to see how your body responds to sugar and starch after you eat a meal.

Post-Prandial Specimen

Actually a group of metabolic diseases characterized by hyperglycemia resulting from: Defects in insulin, secretion, insulin action

Diabetes Mellitus

Excretion of excess glucose through your urine

Polyuria

Hyperglycemia renal threshold

160-180mg/dL

160-180mg/dL excreted through urine to polyuria --> more likely to be dehydrated

Hyperglycemia renal threshold

Frequent fluid intake

Polydipsia

Frequent urination

Polyuria

Frequent feeling of hunger (inability of the cells to utilize glucose as source of energy it has something to do with the insulin action)

Polyphagia

Insulin dependent

Type 1 DM

Type 1 DM: Minimal amounts of insulin

Absolute insufficient deficiency

Type 1 DM: The way it utilize carbohydrate as a source of energy is different as usual since they lack insulin

Ketoacidosis

Type 1 DM: Three substances that causes the increase acidity of the blood

Acoacetate, Beta hydroxybutrate, Acetone

Type 1 DM: Carbs converted to fat and lipids to energy to produced a lot of ketone bodies -> causing acidosis or increasing acid ability of the blood pH

Ketoacidosis

Type 1 DM: Neutralizes the acidity which is done by the kidneys

Increased bicarbonate level

Type 1 DM: Decreased Carbon Dioxide due to _________ respiration (It is called hyperventilation)

Kusmaul kien

Increase fluid excretion because of polyuria removing a lot of fluid and electrolytes one of which is sodium

Hyponatremia

Potassium displacement

Hypokalemia

Autoimmune in origin (producing antibodies against your own cells or tissues)

Type 1 DM

The immune system will attack the insulin even before it is secreted the blood stream

Insulin Antibodies

Insulin production, if you don't have this enzymes your pancreas wont not be able to produce the hormone insulin

Glutamic acid decarboxylase, Thyrosine phosphatase IA-2, IA-2B autoantibodies

Blindness because of increase pressure toward the optic nerve

Retinopathy

Increase pressure towards the glomerulus which eventually destroys the nephron starts with micro albuminuria - early stage of chronic kidney disease, then little by little the albumin will increase level until it is a full blown proteinuria which is an indication now of chronic kidney disease

Neuropathy

- Rare (impediment of neural signals, attack peripheral and central nervous system) - Like hallucinations

Neuropathy

Insulin resistance and insulin secretion defect

Type 2 DM

Hyperinsulinemia with attenuated glucagon levels

Type 2 DM

Diabetic coma

Hyperosmolality

Genetic

Type 2 DM

More likely to experience diabetic trauma

Type 2 DM

Hypersplenismia (overactive spleen) with attenuated glucagon levels

Type 2 DM

100

• High insulin levels • The body is resistant to the defect of the insulin, no response to that stimuli

Hyperinsulinemia

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