CARBOHYDRATES Flashcards
carbohydrates is composed of
Carbon
Hydrogen
Oxygen
carbohydrate contans what functional group
C=O
-OH
General Formula of carbohydrate
C6(H12O)6
Carbohydrates is stored in the body in the form of>
glycogen
Chemical Structure
-open chain form
-carbon are vertically conneected by solid lines
C-O and C-H horizontally connected
Fisher projection
Chemical structure
-cyclic form
Hayworth projection
Based on carbon chain size
3 carbon
4 carbon
5 carbon
6 carbon
Trioses
Tetroses
Pentoses
Hexoses
Smallest carbon chain found in the body
Glyceraldehyde
Also known as simple sugar
No further reduction in form
Monosaccharide
Monosaccharide is also known as
simple sugar
What are the 6 Hesoxes of Monosaccharide
Glucose
Fructose
Galactose
What are the Pentoses of Monosaccharide
Deoxyribose
Ribose
most common sugar in the body
D-glucose
-OH group on the right
D-glucose
-OH group on the left
L-glucose
Type of D-glucose predominant in starch
a-D-glucose
Type of D-glucose predominant in glycogen and cellulose
B-D-glucose
Consist of 2 monosaccharides joined by glycosidic linkage
Disaccharide
Disaccharide consists of 2 mmonosaccharides joined by??
glycosidic linkage
1st carbon atom of a monosaccharide is linked to 4th carbon of the other mmonosaccharide
1-4 glycosidic linkage
glucose+glucose=
maltose
glucose+galactose=
lactose
glucose+fructose=
sucrosehjy
hydrolize by enzyme lactase present in the intestine
Disaccharides
Composed of 3 to 10 monosaccharides some up to 20
Oligosaccharides
In the body they are called glycans (glycoprotein and glycolipids)
Oligosaccharides
What are Oligosaccharides called in the body?
Glycans (glycoprotein and glycolipids)
process of binding oligosaccharide to proteins or lipids
Glycosylation
Oligosaccharides that participate in immune responsee
cell recognition- cell receptors
auto antigens (RBC antigen)
The building block of A and B antigen in RBC
H-antigen
Consist of many units of monosaccharides linked together by glycosidic bonds
Polysaccharides
Serves as storage of energy in human and plants
Polysaccharides
Integral part of the cell and tissue structure
Polysaccharides
Exogenous Polysaccharides
Starch
Cellulose
Insulin
Chitin
storage form in plants (amylopectin annd amylose)
Starch
forms the cell wall of plants. also known as dietary fiber
Cellulose
Cellulose is also known as?
dietary fiber
also known as fructans (dietary fibers) found in plants. Used for Glomerular filtration rate estimation
Insulin
forms the cell wall of fungi and exoskeleton of arthropods
Chitin
Endogenous Polysaccharides
Glycogen
Hyaluronic acid
Heparin
storage form in human (liver)
Glycogen
lubricants of the joints
Hyaluronic acid
natural anticoagulant in the blood
Heparin
Major source of energy(glucose) in the body
Polysaccharide
Found as part of the cell membrane of the cell the glycoprotein and glycolipids
Polysaccharides
Forms the building block (oligosaccharides) of ABO antigen in the surface of RBCs
Polysaccharides
One of the major component of nucleotides (pentose)
Polysaccharides
starch and glycogen (polysaccharides) are broken down into Disaccharide in the mouth through?
salivary amylase
Limit dextrin and maltose (disaccharide)
In the small intestine hydolysis occur by the action of ______ to breakdown into monosaccharide
Pancreatic amylase, maltase, sucrase and lactase
From the duodenum and ileum monosaccharide is absorbed into the blood circulation for further metabolism
Glucose
Galactose
Fructose
Depending on the need of the body glucose can be?
Used as energy
stored in the form of glycogen
stored in the form of triglycerides
converted in protein, amino acids and keto acids
used for energy production through production of ATP, CO2 and H2O
GGlucose
3 process of energy production through ATP (glucose)
Glycolysis
TCA cycle (Krebs cycle)
Electron Transport Chain
The process of storing in the form of glycogen in the liver and peripheral tissues like skeletal muscle.
Glycogenesis
Process of storing as triglyceerides in adipose tissues
Lipogenesis
Process that occurs in the skeletal muscle converted into keto-acids, amino-acids and protein
Cori cycle (glucose-alanine cycle)
Processes of glucose metabolismm
Glycogenesis
Glycogenolysis
Gluconeogenesis
Glycolysis
Lipogenesis
Lipolysis
Conversion of excess glucose to glycogen to be stored in the live and peripheral tissues
Glycogenesis
This process occur when cell is already met the energy requirement, glucose is stored as glycogen
Glycogenesis
Process of glucose metabolism that reduces blood sugar level
Glycogenesis
Stored glycogen in the liver is broken down into glucose for energy production
Glycogenolysis
This process occur during fasting state
Glycogenolysis
Process that is stimulated by glucagon and epinephrine
Glycogenolysis
This process is inhibited by insulin and increases blood sugar
Glycogenolysis
Formmation of Glucose-6-phosphate from non-carbohydrate source such as lactate, amino acids (keto acids) and glycerol
Gluconeogenesis
This process occurs in the liver, kidney, skeletal muscle, intestine, and brain
Gluconeogenesis
This process occur during prolong starvation and increases the blood sugar level
Gluconeogenesis
process where glucose is metabolized into pyruvate and lactate releasing energy (ATP) and this process reduces blood sugar level
Glycolysis
Conversion of glucose into fatty acids for storage in adipose tissues
Lipogenesis
This process occur when sufficient glycogen is already stored in the liver and it decreases blood sugar level
Lipogenesis
Fatty acids in adipose tissue is converted back to glucose to be used for energy production
Lipolysis
Triglycerides is broken down to FA and oxidized (B-oxidation) into Acetyl CoA to be used to generate ATP
Triglycerides
This process occurs during prolong starvation and it increases blood sugar level
Lipolysis
Processes that increase blood sugar level
Glycogenolysis
Gluconeogenesis
Lipolysis
Processes that decrease blood sugar level
Glycolysis
Glycogenesis
Lipogenesis
Also known as Hypoglycemic agent
Insulin
Produced by pancreas the beta islets of Langerhans.
Release when plasma glucose level increase thus lowering blood glucose.
Insulin
This hormonal regulation of blood sugar.
Actions include:
Increase glycolysis, glucogenesis and lipogenesis
Decrease glycogenolysis
Insulin
Also called Hyperglycemic agent
Glucagon
Produced by pancreas the alpha islets of Langerhans cells.
Release when plasma glucose decrease (stress and fasting state) therefore increasing blood glucose.
Glucagon
This hormonal regulation of blood sugar.
Actions include:
Increases glycogenolysis, gluconeogenesis and lipolysis.
Glucagon
Also called Regulator
Somatostatin
Produced by pancreas delta islets of Langerhans.
Somatostatin
This hormonal regulation of blood sugar.
Action
Inhibits the release of insulin and glucagon. Regulates the reciprocal relationship of these hormones.
Somatostatin
Growth hormone (GH)
Increases blood glucose level
Regulated by somatostatin produced by GIT, pancreas, CNS and somatomedins produced by liver.
Anterior pituitary gland
Release when cortisol level is low in the blood.
Increase blood glucose level through glycogenolysis and gluconeogenesis.
ACTH-adrenocorticotropic hormone
Thyroxine (T4)
Increase blood glucose thru glycogenolysis, gluconeogenesis and absorption of glucose in the GIT.
Thyroid gland
Increases blood glucose inhibiting insulin and increasing glycogenolysis.
Release during stress.
Epinephrine (adrenal medulla)
Stimulated by ACTH.
Increase blood glucose glycogenolysis, gluconeogenesis, and lipolysis.
Cortisol (adrenal cortex)
2 Adrenal Gland`
Epinephrine (adrenal medulla)
Cortisol (adrenal Cortex)
produce by the placenta
inhibits insulin activity
Human Placental Lactogen (HPL)
Hormone that Increase blood sugar
Glucagon
Growth hormone
ACTH
Thyroid hormone (thyroxine)
Epinephrine
Cortisol
Hormone that Decrease blood sugar
Insulin
Somatomedins
Abnormal blood glucose level (Hyperglycemia)
Diabetes mellitus (DM)
Pancreatic deficiency
Hyperadrenalism (Cushing’s syndrome)
Excessive growth hormone
Pheochromocytoma (tumor of the adrenal medulla)
Abnormal blood glucose level (Hypoglycemia)
Overdose of insulin
Hypothyroidism
Hypopituitarism
Hypoadrenalism (Addison’s disease – destruction of adrenal cortex)
Glycemic diseases
Hyperglycemia (Diabetes mellitus)
Hypoglycemia
Glycogen storage diseases
A group of metabolic disorder with hyperglycemia as the hall mark of the disease.
Diabetes mellitus
Signs and symptoms (3P’s)
Diabetes mellitus
Polyuria (excessive urination)
Polyphagia (excessive appetite)
Polydipsia (excessive thirst)
Diabetes mellitus is due to?
Insulin secretion defects (insufficient insulin)
Impaired insulin action (insulin resistance)
Both
excessive urination
Polyuria
Excessive thrist
Polydipsia
Excessive appetite
Polyphagia
Diabetes mellitus complications (if left untreated) in the MICROVASCULAR COMPLICATIONS
Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathy
Diabetes mellitus complications (if left untreated) in the MACROVASCULAR COMPLICATIONS
Circulatory problems
Diabetic foot
Ophthalmic complications
Swelling retinal blood vessels and leakage of fluid.
Diabetic retinopathy
Can lead to glaucoma and blindness.
Diabetic retinopathy
damage in optic nerve due to high pressure in the eye.
Glaucoma-
Glomerular sclerosis (scarring).
Diabetic nephropathy
Thickening of the basement membrane resulting uremia and renal proteinuria.
Diabetic nephropathy
high level of waste products in the blood such as urea and creatinine.
Uremia
Can lead to Chronic kidney disease (CKD).
Diabetic nephropathy
test for diabetic nephropathy
Urine microalbumin and GFR
Peripheral nerve damage mostly the feet and legs.
(numbness, tingling sensation, cramps, foot ulcers, bone and joint pain)
Diabetic neuropathy
Loss of elasticity of blood vessels due to high blood sugar. Can lead to atherosclerosis.
Heart attack
Stroke
Circulatory problems.
Diabetic complications wher damage to larger blood vessels
Macroangiopathy
Diabetic complications where clogging of the blood vessels
Atherosclerosis
Skeletal muscle damage
Diabetic foot
infection of the bone.
Osteomyelitis
bacterial infection (Group A strep.)
Cellulitis
Beta cells of pancreas destruction.
classification of DM
Type 1
Insulin resistance.
classification of DM
Type 2
Impaired insulin action due to hormonal changes during pregnancy.
classification of DM
Gestational DM
Insulin-dependent diabetes, type I diabetes, or juvenile-onset diabetes.
Immune-mediated diabetes (type I)
10-20% of the cases of DM.
Immune-mediated diabetes (type I)
Autoimmune destruction of β- cells of the pancreas resulting to absolute insulin deficiency
Immune-mediated diabetes (type I)
β-cell include islet cell autoantibodies, autoantibodies to insulin, autoantibodies to glutamic acid decarboxylase (GAD)
Immune-mediated diabetes (type I)
can also be predisposing factors. in Type 1 DM
HLA genes
Hyperglycemia and ketoacidosis. type of DM
Type 1 DM
3P’s, rapid weight loss, mental confusion, loss of consciousness and other complications of DM.
Type 1 DM
Majority of cases of DM (90-95%).
Insulin resistance (Type 2 DM)
Referred to as non-insulin-dependent diabetes, type II diabetes, or adult-onset diabetes.
Insulin resistance (Type 2 DM)
Insulin resistance and usually have relative insulin deficiency.
Insulin resistance (Type 2 DM)
Most are obese, microvascular and macrovascular complications develop.
Insulin resistance (Type 2 DM)
Predisposing factors: genes, obesity, age, sedentary life style and nutrition.
Insulin resistance (Type 2 DM)
Cause: excessive production of insulin due to excessive eating.
Insulin resistance
Less ketoacidosis.
Treatment is hypoglycemic drugs (metformin).
Women with prior GDM has a higher risk.
Insulin resistance (Type 2 DM)
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.
Insulin resistance
Resistance to insulin starts to manifest at the of
35 or 40 years old.
Type 1 DM (absolute insulin deficiency)
Age
Body structure
Ketoacidosis (ketosis)
Prevalence
Treatment
3p’s
Complications
Mostly young (juvenile)
Normal or thin
Present
Less (10%)
Insulin Injection or IV
Present
Macrovascular and microvascular
Type 2 DM (Insulin resistance)
Mostly adult (>35 years old)
Mostly obese
Rare
More prevalent (90%)
Oral drugs (metformin)
Present
Macrovascular and Microvascular
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).
Ketoacidosis
Due to metabolic and hormones (HPL)
Return to normal postpartum but has a higher risk of developing DM-2 later in life.
Gestational DM
Development of glucose tolerance during pregnancy.
Gestational DM
Autosomal inherited pattern, mutation in chromosome 12 (Hepatocyte nuclear factor) and chromosome 7 (glucokinase) these are glucose sensor.
type of other specific DM
Genetic β cells defect
Occurs at young age (before 25), characterized by insufficient insulin production.
type of other specific DM
Genetic β cells defect
Dysfunction of glucose sensors can lead to insufficient insulin secretion therefore can lead to hyperglycemia.
type of other specific DM
Genetic β cells defect
Other genetic diseases
Other specific type of DM
Cystic fibrosis
Down’s syndrome
Klinefelter’s syndrome
Turner’s syndrome.
Pancreatic carcinoma, pancreatitis, pancreatotomy, trauma or infection.
Pancreatic disease
Endocrine diseases
Acromegaly- growth hormones
Cushing’s syndrome- cortisol
Glucagonoma- glucagon
Pheochromocytoma- epinephrine
Thyroid diseases- Thyroxine
These hormones inhibits the action of insulin.
Acromegaly- growth hormones
Cushing’s syndrome- cortisol
Glucagonoma- glucagon
Pheochromocytoma- epinephrine
Thyroid diseases- Thyroxine
Drug- or chemical-induced diabetes
Nicotinic acid
Glucocorticoids
α-interferon
Vacor (a rat poison)
Pentamidine
affects insulin secretion and sensitivity, destruction of pancreatic cells or increased production of glucose.
Drug- or chemical-induced diabetes
Production of anti-insulin receptor thereby blocking the binding of insulin to its receptor in target tissues.
Insulin receptor deficiency (autoimmune disease)
These autoantibodies are usually seen in SLE.
Insulin receptor deficiency (autoimmune disease)
The body compensate: increase secretion of glucagon, epinephrine, cortisol, GH increases to raise the blood glucose level.
Hypoglycemia
Types of Hypoglycemia
Rapid fall of plasma glucose
Gradual fall in plasma glucose
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.
Rapid fall of plasma glucose
Not accompanied by epinephrine release; causes impairment of CNS function such as confusion, lethargy, seizure, and loss of consciousness.
Gradual fall in plasma glucose
severe hepatomegaly due to deficiency of glucose-6-phosphate
Von gierke’s disease
Causes of hypoglycemia
Excessive pancreatic insulin
Hypothyroidism
Hypoadrenalism
Von gierke’s disease
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.
Glycogen storage diseases
Enzyme Defect
Glucose-6-phosphate dehydrogenase
Clinical Feature
Hepatomegaly, hypoglycemia, ketosis, hyperlipidemia
Type I: Von Gierke
(most common)
Enzyme Defect
Alpha 1.4 glucosidase
Clinical Feature
Cardiorespiratory failure
Type II: Pompe
Enzyme Defect
Amylo-1-6 glucosidase
Clinical Feature
Like type I but milder
Type III: Cori
Enzyme Defect
Phosophorylase
Clinical Feature
Like type I but milder
Type VI: hers
Enzyme Defect
Alpha 1-4 and alpha 1-6
Clinical Feature
Liver cirrhosis
Type IV: Andersen
Enzyme Defect
Phosphofructokinase
Clinical Feature
Mild hepatomegaly and hypoglycemia
Type VIII
Enzyme Defect
Phosphorylase
Clinical Feature
Limited physical activity due to muscle cramps
Type V: Mcardle
For early detection to provide clinical intervention thus minimizing signs and symptoms.
Newborn screening (NBS)
Enzyme Defect
Phosphofructokinase
Clinical Feature
Like type V
Type VII
