The document discusses carbohydrate metabolism and diabetes. It begins by defining the different types of carbohydrates and outlining carbohydrate digestion and absorption. It then discusses glucose regulation and the hormones insulin and glucagon. Insulin helps regulate blood glucose levels by promoting glucose uptake and storage, while glucagon has opposing effects. The document also outlines the classification, causes, and characteristics of the main types of diabetes: type 1, type 2, and gestational diabetes. It concludes by mentioning some acute complications of diabetes like diabetic ketoacidosis.
1. Introduction to biochemistry: Cell and its biochemical organization, transport process across the cell membranes. Energy rich compounds: ATP, Cyclic AMP and their biological significance.
2. Biological oxidation: Coenzyme system involved in Biological oxidation. Electron transport chain (its mechanism in energy capture: regulation and inhibition): Uncouplers of ETC: Oxidative phosphorylation.
3. Enzymes: Definition: Nomenclature, IUB classification, Factor affecting enzyme activity, Enzyme action, enzyme inhibition. Isoenzymes and their therapeutic and diagnostic applications, Coenzymes and their biochemical role and deficiency diseases.
4. Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of carbohydrate metabolism (diabetes mellitus and glycogen storage diseases): Glucose, Galactose tolerance test and their significance, hormonal regulation of carbohydrate metabolism.
5. Lipid metabolism: Oxidation of saturated (-oxidation): Ketogenesis and ketolysis, biosynthesis of fatty acids, lipids, metabolism of cholesterol, Hormonal regulation of lipid metabolism. Defective metabolism of lipids (Atherosclerosis, fatty liver, hypercholesterolemia).
6. Protein and amino acid metabolism: protein turn over, nitrogen balance, Catabolism of Amino acids (Transamination, deamination & decarboxylation).Urea cycle and its metabolic disorders, production of bile pigments, hyperbilirubinemia, porphoria, jaundice. Metabolic disorder of Amino acids.
7. Nucleic acid metabolism: Metabolism of purine and pyrimidine nucleotides, Protein synthesis, inhibition of protein synthesis
8. Introduction to clinical chemistry:
a) Urine analysis (macroscopic and physical examination, quantitative and
semi quantitative tests).
b) Test for NPN constituents. (Creatinine /urea clearance, determination of
blood and urine creatinine, urea and uric acid).
c) Test for hepatic dysfunction-Bile pigments metabolism.
d) Test for hepatic function: test- Serum bilirubin, urine bilirubin and urine
urobilinogen.
e) Lipid profile tests: Lipoproteins, composition, functions. Determination of
serum lipids, total cholesterol, HDL cholesterol, LDL cholesterol and
triglycerides.
Solubility
Source
Classification
Important polysaccharide
Starch
Glycogen
Cellulose
Xantham
Pectin
Agar
Inulin
Chitin
Function of polysaccharide
Conclusion
1. Introduction to biochemistry: Cell and its biochemical organization, transport process across the cell membranes. Energy rich compounds: ATP, Cyclic AMP and their biological significance.
2. Biological oxidation: Coenzyme system involved in Biological oxidation. Electron transport chain (its mechanism in energy capture: regulation and inhibition): Uncouplers of ETC: Oxidative phosphorylation.
3. Enzymes: Definition: Nomenclature, IUB classification, Factor affecting enzyme activity, Enzyme action, enzyme inhibition. Isoenzymes and their therapeutic and diagnostic applications, Coenzymes and their biochemical role and deficiency diseases.
4. Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of carbohydrate metabolism (diabetes mellitus and glycogen storage diseases): Glucose, Galactose tolerance test and their significance, hormonal regulation of carbohydrate metabolism.
5. Lipid metabolism: Oxidation of saturated (-oxidation): Ketogenesis and ketolysis, biosynthesis of fatty acids, lipids, metabolism of cholesterol, Hormonal regulation of lipid metabolism. Defective metabolism of lipids (Atherosclerosis, fatty liver, hypercholesterolemia).
6. Protein and amino acid metabolism: protein turn over, nitrogen balance, Catabolism of Amino acids (Transamination, deamination & decarboxylation).Urea cycle and its metabolic disorders, production of bile pigments, hyperbilirubinemia, porphoria, jaundice. Metabolic disorder of Amino acids.
7. Nucleic acid metabolism: Metabolism of purine and pyrimidine nucleotides, Protein synthesis, inhibition of protein synthesis
8. Introduction to clinical chemistry:
a) Urine analysis (macroscopic and physical examination, quantitative and
semi quantitative tests).
b) Test for NPN constituents. (Creatinine /urea clearance, determination of
blood and urine creatinine, urea and uric acid).
c) Test for hepatic dysfunction-Bile pigments metabolism.
d) Test for hepatic function: test- Serum bilirubin, urine bilirubin and urine
urobilinogen.
e) Lipid profile tests: Lipoproteins, composition, functions. Determination of
serum lipids, total cholesterol, HDL cholesterol, LDL cholesterol and
triglycerides.
Solubility
Source
Classification
Important polysaccharide
Starch
Glycogen
Cellulose
Xantham
Pectin
Agar
Inulin
Chitin
Function of polysaccharide
Conclusion
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from which
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
lecture about diabetes mellitus for undergraduated student, master student
its include definition of diabetes, type 1 diabetes, type2, gestational, diagnosis criteria, complication, world day
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Excess of hyperglycemic hormones (glucagon, ete. ) obesity: ; cause relative insulin deficiency the β cells Tag behind
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Objectives
Review of CHO metabolism
Regulation of blood glucose
State the basic criteria for the diagnosis of diabetes
mellitus, including American Diabetes Association
guidelines.
Outline the procedure for administration of an oral
glucose tolerance test and interpret the results.
Lab tests for monitoring long-term glucose control in
people with diabetes mellitus.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
3. Introduction
Carbohydrates are widely distributed in plants
and animals, their function is ranging from
energy source to structural components.
According to its structure it classified into:
Monosaccharide: It contain 3, 4, 5, 6 or 7
carbon atom. Named tiroses, tetroses,
pentoses. Hexoses or heptoses.
Disaccharides: Two monosaccharide joined by
glycosidic bond.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
4. Maltose = Glucose – Glucose
Lactose = Glucose – Galactose
Polysaccharides: linkage of multiple
monosaccharide units results in the formation
of polysaccharides.
Starch in plants
Glycogen in animals
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
5. Break down of diet carbohydrates results in
glucose. Which maintained by regulatory
hormones.
When energy intake exceed the need of the body
it converted to fats which stored in the adipose
tissue and glycogen which stored in the liver &
muscle.
When the need of energy exceed the intake
endogenous formation of glucose occur.
Metabolism
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
6. Metabolism…con
The end metabolism of carbohydrates result
in:-
1- production of energy.
2- storage as glycogen and fats.
3- conversion to amino acids and proteins.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
7. CHO digestion:
CHO digestion started
in the mouth by salivary
amylase (occur little
digestion) then the food
mixed with salivary
amylase pass into
stomach where the acid
pH inhibit the amylase
action gradually.
In the duodenum where
the HCO3 & bile salt of
pancreatic juice make
the pH around 7 which
is suitable for the
pancreatic amylase to
continue the salivary
amylase action in the
hydrolysis of starch to a
maltose molecules.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
8. Contn....
Then the disaccharide molecules are hydrolyzed by
disaccharides enzymes (found in the small intestine)
into monosaccharide.
CHO absorption:
The absorption of the monosaccharide's occurs by an
active transport process which requires energy. They
are transported to the liver by portal vein of the liver.
Glucose is the only carbohydrate to be directly used
for energy or stored as glycogen. Galactose &
fructose must be converted to glucose before they can
be used. After the glucose enters the cell it will be
processed for production of energy.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
9. CHO catabolism:
Following absorption, they are transported to the
liver. Depending on the body need, the
monosaccharide are converted to glycogen or
metabolized to energy or they are converted to
triglycerides or proteins.
The raised level of glucose after a meal stimulates the
production of insulin from the pancreas. Insulin
reduce the glucose level by facilitates the entrance of
glucose inside the cells of the body except red cells,
hepatic cells and brain cells.
In the cells there are many processes can be take
place Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
10. 1-Glycolysis: metabolism of glucose to
pyruvate or lactate for production of energy.
2-Glycogenesis: Conversion of glucose to
glycogen for storage, occur in the liver and
muscle.
3-Glycogenolysis: Breakdown of glycogen to
glucose for use as energy.
4-Gluconeogenesis: formation of glucose from
noncarbohydrate substance (fat and protein).
5-Lipogenesis: Conversion of CHO to fatty
acids.
6-Lipolysis: Decomposition of fat.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
11. Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
12. Regulatory hormones
(A) Insulin secreted by β-cells of the pancreas in
form of proinsulin, converted to active insulin after
removal of peptide chain (C-peptide).
It is anabolic hormone tends to lower the blood
glucose concentration by enhancing glycogenesis.
In the pancreas, insulin is synthesized as pre-
proinsulin (inactive).
This form undergoes first cleavage forming pro-
insulin, then a second cleavage follows result in the
formation of insulin (active form) and a free short
peptide called C-peptide.
Both insulin and C-peptide are secreted in circulation.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
13. Brain, RBC, Liver, and Intestines are not insulin-
dependent
Muscles are the most important insulin-dependent
tissue.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
14. Hormones that regulates Plasma glucose Concentration:
1-Insulin:
1.released from pancreas (β-cells)
2.convert excess blood glucose into storage forms
–In liver and muscle:
–Stimulates glucose uptake (muscle)
–Stimulates glucose uptake (liver)
–Stimulates FAT synthesis (liver)
–Stimulates glycogen synthesis
–Inhibits glycogen breakdown
–Stimulates glycolysis, acetyl-CoA production
–In Adipose tissues:
–Stimulates triacylglycerol synthesis
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
15. The action of Insulin
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
17. 2. Glucagon:
Released from α-cells in pancreas;
raises blood glucose level
Mode of action: cAMP-dependent phosphorylations
In the liver: (primary target)
Stimulates glycogen breakdown
Inhibits glycogen synthesis
Inhibits glucose breakdown
Stimulates gluconeogenesis
In adipose tissues:
Stimulates fat mobilization
Dr Isse A, Mohamed/ BSc , MSc
in Clinical Chemistry
18. 3. Epinephrine:
A catecholamine secreted by the adrenal
medulla
Stimulates glycogen breakdown (glycogenolysis)
Stimulates glucagon secretion
Inhibits insulin secretion
Plays a key role in glucose counter regulatory when
glucagon is deficient.
Dr Isse A, Mohamed/ BSc , MSc
in Clinical Chemistry
19. 4. Growth hormone:
A polypeptide hormone secreted by the
anterior pituitary glands
Stimulates gluconeogenesis (During long
fasting)
Enhances lipolysis.
5. Cortisol:
Slow acting hormone, released from adrenal cortex
Counterbalances insulin effects
Stimulates gluconeogenesis (During long fasting)
Increase breakdown of protein & fat.
Dr Isse A, Mohamed/ BSc , MSc
in Clinical Chemistry
20. 6. Thyroxin : secreted by thyroid gland
Increases glucose levels by increasing glycogenolysis,
gluconeogenesis and intestinal absorption of glucose.
7. Somatostatin:
Produced by the δ-cells of the islets of Langerhans of
the pancreas.
Increases plasma glucose levels by the inhibition of
insulin, glucagon, growth hormone and other endocrine
hormones.
Dr Isse A, Mohamed/ BSc , MSc
in Clinical Chemistry
21. Things MUST remember
Normal range of fasting blood glucose: 75-115 mg/dL
Hypoglycemia: in adults: <50 mg/dl, in newborns <40 mg/dl
Serum glucose higher than whole blood glucose by 10-15%
(Plasma glucose = whole blood glucose x 1.15 + 6mg/dL)
Arterial or capillary blood glucose is higher than venous by
2-5 mg/dL
CSF glucose: 70% of FBS
CSF glucose MUST be analyzed immediately
Uncentrifuged whole blood: glucose decreases by 5-7%
each hour
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
22. Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
Carbohydrates metabolism disorders
24. Diabetes Mellitus
A group of metabolic disorders characterized by
hyperglycemia resulting from defect of insulin
secretion, insulin action or both of them.
WHO divides diabetes into:-
Type1 Insulin-dependent-diabetes mellitus (IDDM).
Type2 Noninsulin-dependent-diabetes mellitus
(NIDDM).
Other types a) Specific types of DM.
b) Gestational DM.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
25. Classification of Diabetes Mellitus
Type 1 Diabetes
This type is also known as Insulin Dependent Diabetes Mellitus
(IDDM). It is characterized as follows:
It occur in young children and young adults (< 35 years of age)
It accounts for 10-20% of all types of diabetes mellitus.
Patients with this disease have deficiency of insulin, and are
dependent on insulin injections.
Insulin deficiency is caused by an autoimmune disorder:
autoantibodies against islet cells, or against insulin itself.
Patients with type of diabetes are commonly prone to
Ketoacidosis.
Occurrence of complications in this type of diabetes mellitus,
are more common than that in type 2.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
26. Type 2 Diabetes
This type is also known as Non Insulin Dependent Diabetes
Mellitus (NIDDM).
It is the most common, and occur after age 40 years
More commonly seen in obese individuals
It has an inherited pattern
It accounts for 90% of all cases of diabetes mellitus.
It is characterized by either decreased insulin secretion, or
increased resistance to insulin (decreased response to insulin)
Patients with this type are not prone to Ketoacidosis
Complications are les than that in type 1.
Classification of Diabetes Mellitus
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
27. Classification of Diabetes Mellitus
Gestational Diabetes
Occur during pregnancy: (2-5% cases of pregnancy
Caused by inability of pancreas to secrete sufficient amount of
insulin
Women who develop gestational diabetes during pregnancy,
mostly develop diabetes mellitus 20 years later.
Diagnosis: meet with two or more of the following criteria
Fasting plasma glucose >95mg/dL
A 1-hour plasma glucose>180mg/dL
A 2-hour plasma glucose>155mg/dL
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
28. Acute complications
1- Diabetic ketoacidosis.
2- Hyperosmolar nonketotic coma.
3- Hypoglycemia.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
29. Ketoacidosis
In uncontrolled diabetes the low insulin
concentration result in increase lipolysis and
increase plasma free fatty acids which
converted by liver to ketone bodies. Type I
DM has greater tendency to produce ketone
bodies than type II due to Insulin and
Glucagon concentration imbalance.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
30. Hyperosmolal non-ketotic coma
Hyperosmolality is due to hyperglycemia but
no detectable ketones or acidosis. Glycosuria
result in severe water and electrolyte depletion
with hypernatremia and uremia. Coma result
from cerebral cells dehydration.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
31. Hypoglycemia
It is decrease blood glucose below the fasting
value. In diabetics this is due to over dosage of
insulin.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
33. Signs & symptoms
Polydipsia “excessive thirst”.
polyphagia “increase food intake”.
polyuria “ excessive urine production”.
Weight loss.
hyperventilation.
mental confusion.
loss of consciousness
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
34. Diagnosis of DM
Normal levels
Normal plasma glucose concentration during
fasting ( 55 - 110 ) mg/dl.
And 2 hr post prandial ( 75 - 140) mg/dl.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
35. Positive findings
Any one of the followings is diagnostic:
– Symptoms of diabetes mellitus plus random
plasma glucose concentration >=200 mg / dL)
***or
– FBG >=126 mg / dL
***or
– 2hr post load BG >=200 mg /dl after 75-g glucose
load.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
36. Some individuals may not meet with the past
findings but have blood glucose level higher
than normal, those : -
either : Impaired fasting glucose
FBG ( 110 - 126) mg/dl.
Or: Impaired glucose tolerance
2hr after 75 grm g ( 140 - 200) mg/dl.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
37. GTT
Glucose tolerance test is used to diagnose
GDM or IGT and it is rarely used to
diagnose DM. to perform it : -
I. Patient should take diet rich in
carbohydrates three days before the test.
II. Performed after fasting for 10 to 16 hr.
III. Should not be done in hospital or during
severe illness.
IV. Pt Should not eat or smoke during the test.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
38. Monitoring DM
Glycosylated Haemoglobin
This test refers to the hemoglobin component formed
by interaction with glucose, since half life of RBCs is
approximately 120 days; a single HbA1c determination
can give information about glycemic control in the last
8-12 weeks.
Reference range:4-6%, effective treatment range<7%.
The levels of HBA1C are affected by:
Hemolytic anemia (falsely decreased)
HbS: falsely decreased
B12 or Macrocytic anemia: falsely increased
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
39. Fructosamine
Is a compound formed by attachment of glucose to
amino groups of proteins other than hemoglobin.
The concentration of glycated serum albumin reflects
glucose control over a period of 2 to 3 weeks.
It is evidence of both deterioration of control and
improvement with therapy, it is evident earlier than
with GHb.
Reference range:205-285 µmol/L
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
40. Microalbuminuria (MAU)
Microalbuminuria is defined as excretion of 30 – 300
mg of albumin /24 h.
MAU is the first warning signal to an impending
“Nephropathy”. Microalbumin is present in 25 per
cent of patients with type I disease and 36 per cent
patients with type II disease. Patients with
microalbuminuria have a greater risk for developing
renal failure, vascular damage and risk for
cardiovascular damage.
Dr Isse A, Mohamed/ BSc , MSc in
Clinical Chemistry
41. Diagnosis:
The types of investigations:
Fasting Blood Glucose (FBG)
2 hr postprandial Blood Glucose (2 hr PP)
Random Blood Glucose
Glucose Tolerance Test
Dr Isse A, Mohamed/ BSc , MSc
in Clinical Chemistry