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56 Cards in this Set

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These are hydrated of aldehyde or ketone derivates -It is combination of carbon, hydrogen-oxygen

Carbohydrates

Disease states involved

hyperglycemia and hypoglycemia

-Sugar that cannot be hydrolyzed to a simpler form


-Sugar that contain 3, 4, 5, 6 carbon atoms (triose, tetroses, pentoses and hexoses, etc.)


-Examples include fructose, glucose, galactose

Monosaccharides or simple sugars

 Formed by interaction of two monosaccharides


 Examples


Maltose = glucose + glucose


Lactose = glucose + galactose


Sucrose = glucose + fructose

Disaccharides

 Linkage of many monosaccharide units Include starch, glycogen and cellulose

Polysaccharides

Pathways of Glucose Metabolism

Glycolysis


Gluconeogenesis


Glycogenolysis


Glycogenesis


Lipogenesis


Lipolysis

 Metabolism of glucose to lactate or pyruvate for production of energy

Glycolysis

-Formation of glucose-6-phosphate from non carbohydrate source

Gluconeogenesis

 Breakdown of glycogen to glucose for use as energy

Glycogenolysis

 Conversion of glucose to glycogen for storage

Glycogenesis

 Conversion of carbohydrates to fatty acids

Lipogenesis

 Decomposition of fat

Lipolysis

Regulation of Glucose Metabolism

1.Insulin


2.Glucagon


3.Epinephrine


4.Cortisol


5.Growth hormone


6.Thyroxine


7.Somatostatin


-Primary hormone responsible for decreasing blood glucose


-Synthesized by the β cells of the islets of Langerhan (pancreas)


- Regulates blood glucose by ↑ glycogenesis, glycolysis and lipogenesis; and ↓ glycogenolysis.

Insulin (Hypoglycemic agent)

-Primary hormone responsible increasing blood glucose


-Synthesized by the α cells of the islets of Langerhan (pancreas)


- Regulates blood glucose by ↑ glycogenolysis and gluconeogenesis.

Glucagon (hyperglycemic agent)


1. Produced by the adrenal medulla, ↑ blood glucose


2. Released during times of physical and emotional stress


3. Inhibits insulin secretion, ↑ glycogenolysis and lipolysis

Epinephrine

1.Produced by the adrenal cortex, in response to ACTH, ↑ plasma glucose


2. ↓ intestinal entry of glucose into the cell, ↑ gluconeogenesis, glycogenolysis and lipolysis

Cortisol (Glucocorticoids)

1. Produced by the anterior pituitary gland; ↑ plasma glucose


2. ↓ glucose entry to cells, ↑ glycolysis

Growth hormone

1. Produced by the thyroid gland; ↑ plasma glucose


2. ↑ glycogenolysis, gluconeogenesis and glucose intestinal absorption

Thyroxine

1. Produced by the Delta cells of the islet of Langerhans in the pancreasand hypothalamus


2. Increases plasma glucose by inhibition of insulin, glucagon, GH, etc.s

Somastostatin

Disease states in Glucose Metabolism

Hyperglycemia


Hypoglycemia

Increase in plasma glucose


Hyperglycemia

Metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both

Diabetes mellitus

Diabetes Mellitus Classification

1. Type 1 (IDDM)


2. Type 2 (NIDDM)


3. Other


4. Gestational

-10-20% of all cases of diabetes


-Occurs in childhood and adolescence


-Absence of Insulin with excess in glucagon

Type 1

Type 1.Sign and Symptoms


• Polydipsia (excessive thirst)


• Polyphagia (↑ food intake)


• Polyuria (excessive urine production)


•Rapid weight loss


•Hyperventilation


•Confusion and possible loss of consciousness

-90% of all cases of diabetesAdult onset


-Non Insulin dependendent

Type 2

Type 2 Milder symptoms than type 1


• Polydipsia (excessive thirst)


• Polyphagia (↑ food intake)


• Polyuria (excessive urine production)

HyperglycemiaLaboratory Findings


1.increase glucose in plasma and urine


2. Increase urine specific gravity


3. Ketones in serum and urine


4. Decrease oid and urine pH


5. Electrolyte imbalance

Result imbalance between glucose utilization and production

Hypoglycemia

HypoglycemiaLaboratory Findings

↓ glucose in plasma


↑↑↑ in patients with pancreatic β-cell tumors (insulinoma

-Glycogen build up in the liverdue to inhibition of hepatic glycogenolysis

Von Gierke Disease (glucose-6-phosphatase deficiency type 1)

Inhibition of glycogenolysis

Galactosemia (galactose-1-phosphate uridyl transferase dificiency)

Diagnosis of Glucose Metabolic Alterations


1. WB glucose concentration 11% lower than plasma


2. Serum or plasma must be refrigerated and separated from the cells within 1 hr


3. Sodium flouride (gray-top) can be used to inhibit glycolyticenzymes


4. FBG should be obtained in the morning after 8 to 10 hours fasting(not longer than 16 hours

-Copper reduction method (uses BaSO4 to remove saccharoids) Glucose + arsenomolybdic acid


arsenomolybdenum blue

Nelson Somogyi

-ferric reducion method (inverse colorimetry)


-Glucose + Ferricyanide (yellow)  Ferrocyanide (colorless)

Hagedorn jensen

-Condensation of carbohydrates with aromatic amines producing Schiff bases (green)

Ortho-toluidine (Dubowski)

Enzymatic Methods of Glucose Measurement


1. Glucose oxidase (Saifer Gernstenfield)


2. Hexokinase (reference method)


3. Clinitest

Self-Monitoring of Blood Glucose


1. Type 1 diabetes – 3 to 4 times/day

Polyclonal or monoclonal antibodies toward the glycated N-terminal group of the β chain of Hb

Immunoassays

Separated based on chemical structure using boronate group to bind glycosylated protein

Affinity Chromatography

Methods of HbA1C Measurement based on charge differences


-Cation-exchange Chromatography -Electrophoresis


-Isoelectri fucosing -HPLC

Positive-charge resin bed attaches to negatively charged hemoglobin

Cation-exchangechromatography

Separation is based on differences in charge

Electrophoresis

Type of electrophoresis using isoelectric point to separate

Isoelectric focusing

A form of ion-exchange chromatography Separates all forms of HbA1C (A1a, A1b, A1 c)

HPLC


Produced by the liver through metabolism of stored lipids

Ketone


3 ketone bodies


• Acetone (2%)


• Acetoacetic acid(20%)


• 3-β-hydroxybutyric acid (78%)

accumulation of ketones in blood

Ketonemia


accumulation of ketones in urine

Ketonuria


Mtds. of Ketone Measurement


-Gerhardt’s Test


-Nitroprusside


-Enzymatic

Acetoacetic acid + Ferric chloride


 Red color

Gerhardt’s Test


Acetoacetic acid + nitroprusside–alkaline pH


 Purple color

Nitroprusside


NADH + H+ + acetoacetic acid β-HBD NAD + β-hydroxybutyric

Enzymatic


Diagnosis at an early stage diabetic renal nephropathy and before the development of proteinuria

Microalbuminuria


Thank you 😊

Bastigue Via