Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
405 Cards in this Set
- Front
- Back
- 3rd side (hint)
>=126 mg/dl |
Diagnostic value of FBS in hyperglycemia |
|
|
Carbohydrates |
Hydrates of aldehyde or ketone derivates based on location of CO functional group |
|
|
Types of carbohydrates |
Monosaccharides, disaccharides, oligosaccharides, polysaccharides |
MDOP |
|
Glycol aldehyde |
Simplest carbohydrate |
|
|
Glucose |
The only carbohydrate to be directly used for energy and stored as glycogen |
|
|
Blood glucose |
Brain is completely dependent on ????? for energy production |
|
|
Central nervous system |
2/3 of glucose utilization in resting adults occurs in???? |
|
|
Pyruvic acid, lactic acid, acetylcoenzyme A |
Intermediate products of glucose metabolism |
PLA |
|
Carbon dioxide, water, adenosine triphosphate |
Complete oxidation of glucose yields ...????? |
CWA |
|
Glucose, maltose, fructose, lactose, galactose |
Reducing substances/sugars |
GMFLG |
|
Double bond and negative charge |
present in enol anion that makes glucose an active reducing substance |
|
|
Sucrose |
Most common nonreducing sugar |
Fructose + glucose |
|
Pancreas |
It is both an endocrine and exocrine organ in the control of carbohydrate metabolism |
|
|
Pancreas as an endocrine gland |
Secretes the hormones: insulin, glucagon and somatostatin from different cells residing in islets of Langerhans in the pancreas |
|
|
Pancreas as an exocrine gland |
Produces and secretes enzymes: amylase (responsible for the breakdown of ingested complex carbohydrates) |
|
|
Pancreas |
Its main function is for carbohydrate metabolism |
An organ |
|
Insulin |
The primary hormone responsible for the entry of glucose into the cell |
|
|
Insulin |
Synthesized by the beta cells of the islets of Langerhans in the pancreas |
|
|
Insulin |
It is normally released when glucose levels are high |
|
|
Insulin |
It is the only hormone that decreases glucose levels; hypoglycemic agent |
|
|
Insulin |
It is stored from sources such as liver, fat, muscles |
|
|
Insulin |
It has a reciprocal relationship with glucagon |
A hormone |
|
Glycogenesis, lipogenesis, glycolysis |
Insulin promotes... ??? |
3 process involved in CHO metabolism |
|
Insulin |
It decreases glycogenolysis |
A hormone |
|
Membrane permeability |
Insulin enhances ...... to cells in the liver, muscle and adipose tissue |
MP |
|
Insulin-degrading enzyme |
Found in RBCs as well as in other tissues that is responsible for serum insulin measurements to be falsely low in the presence of hemolysis |
|
|
Glucagon |
It is primary hormone responsible for increasing glucose; hyperglycemic agent |
|
|
Glucagon |
Synthesized by the alpha-cells of the islets of Langerhans in the pancreas |
|
|
Glucagon |
It is released during stress and fasting states |
A hormone |
|
Catabolic functions |
Glucagon enhances ..... during fasting periods |
CF |
|
Glucagon |
A hormone that promotes glycogenolysis |
G |
|
25-50 pg/mL |
Normal value of fasting plasma glucagon concentrations |
|
|
Hyperglycemic hormones |
Other hormones that tend to increase glucose concentrations |
|
|
CCGTAS |
Hyperglycemic hormones |
|
|
Cortisol and corticosteroids (glucocorticoids) |
Primary promoter of gluconeogenesis |
Hyperglycemic hormone |
|
Cortisol and corticosteroids (glucocorticoids) |
Hormones that are secreted by the cells of the zona fasciculata and zona reticularis of the adrenal cortex |
|
|
Cortisol and corticosteroids (glucocorticoids) |
Hormones that decrease intestinal entry of glucose into the cell |
C and c |
|
Cortisol and corticosteroids (glucocorticoids) |
Hormones that promote gluconeogenesis and lipolysis |
|
|
Catecholamines |
Hormone that is released from the chromaffin cells of the adrenal medulla |
|
|
Catecholamines |
Hormone that inhibits insulin secretion and promotes glycogenolysis and lipolysis |
|
|
Growth hormone (somatotrophic) |
Hormones that is secreted by the anterior pituitary gland |
|
|
Growth hormone (somatotrophic) |
Hormone that decreases the entry of glucose into the cell |
|
|
Growth hormone (somatotrophic) |
Hormone that promotes glycogenolysis and glycolysis |
|
|
Thyroid hormones |
Hormone that promotes glycogenolysis, gluconeogenesis and intestinal absorption of glucose |
|
|
T3 and T4 |
2 thyroid hormones |
|
|
Adrenocorticotropic hormone (ACTH) |
Secondary promoter of gluconeogenesis |
|
|
Adrenocorticotropic hormone (ACTH) |
Hormone that stimulates release of cortisol from the adrenal cortex |
|
|
Adrenocorticotropic hormone (ACTH) |
Hormone that promotes glycogenolysis and gluconeogenesis |
|
|
Somatostatin |
Hormone that is produced by the delta cells of the islets of Langerhans in the pancreas |
|
|
Somatostatin |
Hormone that is synthesized in the paraventricular and arcuate nuclei of the hypothalamus |
|
|
Somatostatin |
A neuroendocrine hormone |
|
|
Somatostatin |
Hormone that primarily inhibits the action of insulin, growth hormone and glucagon |
|
|
Hyperglycemia and hypoglycemia |
Clinical conditions of carbohydrate metabolism |
|
|
Hyperglycemia |
A clinical condition which is an increase in blood glucose concentrations |
|
|
Hyperglycemia |
A clinical condition that is toxic to beta cell function and impairs insulin secretion |
|
|
SSD/PPHI |
Causes of hyperglycemia |
Stress, severe infection, dehydration/pregnancy, pancreatectomy, hemochromatosis, insulin deficiency or abnormal insulin receptor |
|
>=126 mg/dl |
Diagnostic value of FBS in hyperglycemia |
|
|
70-110 mg/dl |
Normal value of FBS |
|
|
Laboratory findings of hyperglycemia |
Increase glucose in plasma and urine; increase urine specific gravity; ketones in serum and urine; decrease blood and urine pH (acidosis); electrolyte imbalance (dec. Na+, inc. K+, dec. HCO3) |
IIKDE |
|
300-500mg/dl |
value of period of plateau of plasma glucose with normal renal function |
|
|
high serum osmolality |
as a result of hyperglycemia |
|
|
low sodium concentration |
due to polyuria and in part to a shift of water from cells because of hyperglycemia |
|
|
type 1 DM |
more likely to produce ketones opposed to type 2 DM |
type of DM |
|
ketoacidosis |
resulting from pH imbalance results from dehydration, electrolyte imbalance and acidosis |
|
|
Hyperkalemia |
It is almost always present as a result of the displacement of potassium from cells in acidosis |
|
|
Kussmaul-Kien respiration |
It usually decrease bicarbonate and total carbon dioxide |
Deep respirations |
|
Hypoglycemia |
A clinical condition that results from an imbalance between glucose utilization and production |
|
|
Hypoglycemia |
A clinical condition that involves decreased glucose levels |
|
|
Hypoglycemia |
A clinical condition that affects the CNS (warning signs and symptoms) and is asymptomatic |
|
|
Whipple's triad |
Low blood glucose concentration, typical symptoms and symptoms alleviated by glucose administration |
Hinimatay tapos pinainom ng juice (any sweet drinks) at biglang nagising |
|
5-hour GTT |
Diagnostic test of hypoglycemia |
Glucose tolerance test |
|
65-70 mg/dl |
Hypoglycemic value where glucagon and other glycemic hormones are released into the circulation |
|
|
<=60 mg/dl |
value that strongly suggest hypoglycemia (series of random fasting serum specimens) |
|
|
50-55 mg/dl (2.8-3.0 mmol/l) |
Value of observable symptoms of hypoglycemia appear |
|
|
55-60 mg/dl |
Hypoglycemic value of plasma glucose of healthy males |
|
|
40 mg/dl |
Hypoglycemic value of plasma glucose in healthy females |
|
|
Neurogenic and neuroglycopenic |
Symptoms of hypoglycemia |
|
|
Neurogenic |
Tremors, palpitations, anxiety, diaphoresis |
|
|
Neuroglycopenic |
Dizziness, tingling, blurred vision, confusion, behavioral changes |
|
|
Classification of hypoglycemia |
Drug administration, critical illness, hormonal deficiency, endogenous hyperinsulinism, autoimmune hypoglycemia, non-beta cell tumors, hypoglycemia of infancy AMD childhood, alimentary (reactive) hypoglycemia, idiopathic (functional) postprandial hypoglycemia |
DCHEANHAI |
|
Drug administration |
Insulin, alcohol, salicylates, sulfonamides, pentamidine |
Classification of hypoglycemia; IASSP |
|
Critical illness |
Hepatic failure, sepsis, renal failure, cardiac failure, malnutrition |
Classification of hypoglycemia; HSRCM |
|
Hormonal deficiency |
Epinephrine, glucagons, cortisol, growth hormone |
Classification of hypoglycemia; EGCG |
|
Endogenous hyperinsulinism |
Pancreatic beta cell disorders |
Classification of hypoglycemia |
|
Autoimmune hypoglycemia |
Insulin antibodies |
Classification of hypoglycemia |
|
Non-beta cell tumors |
Leukemia, hepatoma, pheochromocytoma, lymphoma |
Classification of hypoglycemia; LHPL |
|
Hypoglycemia of infancy and childhood |
Galactosemia, GSD, Reye's syndrome |
Classification of hypoglycemia; GGR |
|
Alimentary (reactive) hypoglycemia |
Post-gastric surgery |
Classification of hypoglycemia |
|
Idiopathic (functional) postprandial hypoglycemia |
Classification of hypoglycemia |
|
|
Diabetes mellitus |
It is a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion, insulin receptors or both |
DM |
|
>=126 mg/dl |
Diagnostic value of fasting plasma glucose concentration in DM |
|
|
Glucosuria |
It occurs when the plasma glucose level exceeds 180 mg/dl (9.99 mmol/l) with normal renal function |
|
|
Ketosis |
It develops in DM from excessive synthesis of acetyl-CoA |
|
|
6:1 |
In severe DM, what is the ratio of beta-hydroxybuterate to acetoacetate |
|
|
Insulin administration |
The entire process of ketosis can be reversed by.... |
|
|
Type 1 and Type 2 DM |
Classification of diabetes mellitus |
|
|
Type 1 DM |
Formerly known as Insulin Dependent Diabetes Mellitus (IDDM), Juvenile Onset Diabetes Mellitus, Brittle Diabetes, Ketosis-Prone Diabetes |
IJBK |
|
Type 1 DM |
It is a result of cellular-mediated autoimmune destruction of the Beta cells of the pancreas |
|
|
Type 1 DM |
A classification of DM where diabetic individuals have insulinopenia (absolute insulin deficiency) due to loss of pancreatic beta cells and depend on insulin to sustain life and prevent ketosis |
|
|
80-90% |
Percentage of reduction in the volume of the beta cells required to induce symptomatic type 1 DM |
|
|
Glutamic acid decarboxylase (GAD65) and insulin autoantibodies (IAA) |
Individuals at greater risk of developing type 1 DM have high titer of multiple autantiodies - .... and .... (Free diabetes markers) |
|
|
IAA |
A free marker that is more common in young children who develop type 1 DM |
|
|
GAD65 |
A free marker that is more common in adults |
|
|
Signs and symptoms of type 1 DM |
Polyuria, polydipsia, polyphagia, rapid weight loss, hyperventilation, mental confusion, possible loss of consciousness |
PPPRHMP |
|
Complications of type 1 DM |
Microvascular disorders: nephropathy, neuropathy, retinopathy |
|
|
Microalbuminuria test |
test if glucose level reached to 50-200 mg/dl per hour (diabetic nephropathy) |
|
|
Microalbuminuria test |
Earliest indication of glomerular dysfunction associated with type 1 DM |
|
|
Idiopathic type 1 DM |
A form of type 1 DM that has no known etiology; it is strongly inherited; it does not have beta cell autoantibodies and have episodic requirements for insulin replacement |
|
|
Type 2 DM |
Formerly known as Non-Insulin Dependent Diabetes Mellitus, Adult Type/Maturity Onset Diabetes Mellitus, Stable Diabetes, Ketosis-Resistant Diabetes, Receptor-Deficient Diabetes Mellitus |
NASKR |
|
Kidney |
First organ to be affected if you have type 1 DM; filters blood; glomeruli (filter) |
|
|
Type 2 DM |
It is characterized by hyperglycemia due to an individual's resistance to insulin; there is relative insulin deficiency |
|
|
Type 2 DM |
It is a classification of diabetes mellitus that is associated with strong genetic predisposition and not related to an autoimmune disease |
|
|
Nonketotic hyperosmolar coma |
Untreated type 2 DM will result to ????? due to overproduction of glucose (>300 mg/dl) accompanied by severe dehydration, electrolyte imbalance, increased BUN and creatinine |
|
|
Risk factors of type 2 DM |
Obesity, family history, advanced age, hypertension, lack of exercise, GDM, impaired glucose metabolism |
OFAHLGI |
|
45 and older; 3 years |
It is recommended that adults ages ??????? be screened for diabetes every ?????, but screening should be performed earlier or more frequently if the individual is at high risk |
|
|
Comparison between type 1 DM and type 2 DM is according to: |
Pathogenesis, incidence rate, onset, risk factors, c-peptide levels, pre-diabetes, symptomatology, ketosis, medication |
PIORCPSKM |
|
Beta cells destruction |
Pathogenesis of type 1 DM |
|
|
Beta cells destruction |
Pathogenesis of type 1 DM |
|
|
Insulin resistance |
Pathogenesis of type 2 DM |
|
|
5-10% |
Incidence rate of type 1 DM |
|
|
Autoantibodies (-) |
Pre-diabetes of type 2 DM |
|
|
Symptoms develop abruptly |
Symptomatology of type 1 DM |
|
|
Symptoms develop gradually (asymptotic) |
Symptomatology of type 2 DM |
|
|
Common; poorly controlled |
Ketosis of type 1 DM |
|
|
Rare |
Ketosis of type 2 DM |
|
|
Insulin absolute |
Medication of type 1 DM |
|
|
Oral agents |
Medication of type 2 DM |
|
|
Metformin |
Oral agents used for medication in type 2 DM |
|
|
90-95% |
Incidence rate of type 2 DM |
|
|
Any; most common to childhood/teens |
Onset of type 1 DM |
|
|
Any; most common with advancing age, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome |
ARHDP |
|
|
Genetic, autoimmune |
Risk factors of type 1 DM |
|
|
Genetic, obesity, sedentary lifestyle, polycystic ovarian syndrome, dyslipidemia and hypertension |
Risk factors of type 2 DM |
GOSPDH |
|
C-peptide |
Mainly differentiate type 1 and type 2 DM using fasting serum of 8-14 hours |
|
|
Decreased or undetectable |
C-peptide levels of type 1 DM |
|
|
Detectable |
C-peptide levels of type 2 DM |
|
|
Autoantibodies (+) |
Pre-diabetes of type 1 DM |
|
|
5-10% |
Incidence rate of type 1 DM |
|
|
Autoantibodies (-) |
Pre-diabetes of type 2 DM |
|
|
Symptoms develop abruptly |
Symptomatology of type 1 DM |
|
|
Symptoms develop gradually (asymptotic) |
Symptomatology of type 2 DM |
|
|
Common; poorly controlled |
Ketosis of type 1 DM |
|
|
Rare |
Ketosis of type 2 DM |
|
|
Insulin absolute |
Medication of type 1 DM |
|
|
Oral agents |
Medication of type 2 DM |
|
|
Metformin |
Oral agents used for medication in type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
A disorder characterized by impaired ability to metabolize carbohydrate usually caused by a deficiency of insulin, metabolic or hormonal changes |
|
|
90-95% |
Incidence rate of type 2 DM |
|
|
Any; most common to childhood/teens |
Onset of type 1 DM |
|
|
Any; most common with advancing age, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome |
ARHDP |
|
|
Genetic, autoimmune |
Risk factors of type 1 DM |
|
|
Genetic, obesity, sedentary lifestyle, polycystic ovarian syndrome, dyslipidemia and hypertension |
Risk factors of type 2 DM |
GOSPDH |
|
C-peptide |
Mainly differentiate type 1 and type 2 DM using fasting serum of 8-14 hours |
|
|
Decreased or undetectable |
C-peptide levels of type 1 DM |
|
|
Detectable |
C-peptide levels of type 2 DM |
|
|
Autoantibodies (+) |
Pre-diabetes of type 1 DM |
|
|
5-10% |
Incidence rate of type 1 DM |
|
|
Autoantibodies (-) |
Pre-diabetes of type 2 DM |
|
|
Symptoms develop abruptly |
Symptomatology of type 1 DM |
|
|
Symptoms develop gradually (asymptotic) |
Symptomatology of type 2 DM |
|
|
Common; poorly controlled |
Ketosis of type 1 DM |
|
|
Rare |
Ketosis of type 2 DM |
|
|
Insulin absolute |
Medication of type 1 DM |
|
|
Oral agents |
Medication of type 2 DM |
|
|
Metformin |
Oral agents used for medication in type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
A disorder characterized by impaired ability to metabolize carbohydrate usually caused by a deficiency of insulin, metabolic or hormonal changes |
|
|
Gestational diabetes mellitus (GDM) |
It occurs during pregnancy and disappears after delivery but, in some cases, returned years later |
|
|
90-95% |
Incidence rate of type 2 DM |
|
|
Any; most common to childhood/teens |
Onset of type 1 DM |
|
|
Any; most common with advancing age, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome |
ARHDP |
|
|
Genetic, autoimmune |
Risk factors of type 1 DM |
|
|
Genetic, obesity, sedentary lifestyle, polycystic ovarian syndrome, dyslipidemia and hypertension |
Risk factors of type 2 DM |
GOSPDH |
|
C-peptide |
Mainly differentiate type 1 and type 2 DM using fasting serum of 8-14 hours |
|
|
Decreased or undetectable |
C-peptide levels of type 1 DM |
|
|
Detectable |
C-peptide levels of type 2 DM |
|
|
Autoantibodies (+) |
Pre-diabetes of type 1 DM |
|
|
5-10% |
Incidence rate of type 1 DM |
|
|
Autoantibodies (-) |
Pre-diabetes of type 2 DM |
|
|
Symptoms develop abruptly |
Symptomatology of type 1 DM |
|
|
Symptoms develop gradually (asymptotic) |
Symptomatology of type 2 DM |
|
|
Common; poorly controlled |
Ketosis of type 1 DM |
|
|
Rare |
Ketosis of type 2 DM |
|
|
Insulin absolute |
Medication of type 1 DM |
|
|
Oral agents |
Medication of type 2 DM |
|
|
Metformin |
Oral agents used for medication in type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
A disorder characterized by impaired ability to metabolize carbohydrate usually caused by a deficiency of insulin, metabolic or hormonal changes |
|
|
Gestational diabetes mellitus (GDM) |
It occurs during pregnancy and disappears after delivery but, in some cases, returned years later |
|
|
90-95% |
Incidence rate of type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
It is a type of glucose intolerance with onset or first recognition during pregnancy (diabetic women who become pregnant are not included in this category) |
|
|
Any; most common to childhood/teens |
Onset of type 1 DM |
|
|
Any; most common with advancing age, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome |
ARHDP |
|
|
Genetic, autoimmune |
Risk factors of type 1 DM |
|
|
Genetic, obesity, sedentary lifestyle, polycystic ovarian syndrome, dyslipidemia and hypertension |
Risk factors of type 2 DM |
GOSPDH |
|
C-peptide |
Mainly differentiate type 1 and type 2 DM using fasting serum of 8-14 hours |
|
|
Decreased or undetectable |
C-peptide levels of type 1 DM |
|
|
Detectable |
C-peptide levels of type 2 DM |
|
|
Autoantibodies (+) |
Pre-diabetes of type 1 DM |
|
|
5-10% |
Incidence rate of type 1 DM |
|
|
Autoantibodies (-) |
Pre-diabetes of type 2 DM |
|
|
Symptoms develop abruptly |
Symptomatology of type 1 DM |
|
|
Symptoms develop gradually (asymptotic) |
Symptomatology of type 2 DM |
|
|
Common; poorly controlled |
Ketosis of type 1 DM |
|
|
Rare |
Ketosis of type 2 DM |
|
|
Insulin absolute |
Medication of type 1 DM |
|
|
Oral agents |
Medication of type 2 DM |
|
|
Metformin |
Oral agents used for medication in type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
A disorder characterized by impaired ability to metabolize carbohydrate usually caused by a deficiency of insulin, metabolic or hormonal changes |
|
|
Gestational diabetes mellitus (GDM) |
It occurs during pregnancy and disappears after delivery but, in some cases, returned years later |
|
|
90-95% |
Incidence rate of type 2 DM |
|
|
Gestational diabetes mellitus (GDM) |
It is a type of glucose intolerance with onset or first recognition during pregnancy (diabetic women who become pregnant are not included in this category) |
|
|
Last trimester or 6-7 months |
Stage of pregnancy where GDM occurs |
|
|
Any; most common to childhood/teens |
Onset of type 1 DM |
|
|
Any; most common with advancing age, race/ethnicity, hypertension, dyslipidemia, polycystic ovarian syndrome |
ARHDP |
|
|
Genetic, autoimmune |
Risk factors of type 1 DM |
|
|
Genetic, obesity, sedentary lifestyle, polycystic ovarian syndrome, dyslipidemia and hypertension |
Risk factors of type 2 DM |
GOSPDH |
|
C-peptide |
Mainly differentiate type 1 and type 2 DM using fasting serum of 8-14 hours |
|
|
Decreased or undetectable |
C-peptide levels of type 1 DM |
|
|
Detectable |
C-peptide levels of type 2 DM |
|
|
Autoantibodies (+) |
Pre-diabetes of type 1 DM |
|
|
24-28 weeks of gestation |
Screening should be performed between ????? (Without fasting) |
|
|
2-hour GCT (50g glucose load) |
Screening and diagnosis of GDM is performed by |
|
|
3-hour GTT (100g glucose load) (>140 mg/dl) with fasting |
Confimatory test of GDM |
|
|
FBS - >= 92-95 mg/dl Glucose administration 1hr GTT - >= 180 mg/dl (positive) 2hr GTT - >= 153-155 mg/dl (positive) 3hr GTT - >= 140 mg/dl (optional) CONFIRMATORY |
Diagnostic criteria for GDM |
|
|
2 criteria is met |
GDM is diagnosed if ???? |
|
|
Dilantin and pentamidine |
Drug or chemical inducers of beta cell dysfunction; anti-epileptic and anticonvulsant drugs |
|
|
Thiazides and glucocorticoids |
Substances that Impair insulin action |
|
|
Down syndrome, klinefelter's syndrome, rabson-mendengall syndrome, leprechaunism, huntington's chorea, Turner syndrome |
Genetic syndromes |
DKRLHT |
|
Cystic fibrosis, neoplasia, hemochromatosis |
Exocrine disorders |
CNH |
|
Venous plasma glucose |
Standard clinical specimen in glucose methodologies |
|
|
15% lower |
Fasting glucose in whole blood is ????? than in serum or plasma |
|
|
Within 30 minutes |
Fdd |
|
|
Respiratory distress syndrome, hypocalcemia and hyperbilirubinemia |
Infants born to diabetic mothers are at increased risk for ?????? |
RHR |
|
6-12 weeks postpartum |
After giving birth, women with GDM should be evaluated for how many weeks???? |
|
|
10 years in 30-40% of cases |
GDM converts to DM within ???? |
|
|
Pancreatic disorders/pancreatectomy, endocrine disorders, drug or chemical inducer of beta cell dysfunction, genetic syndromes, exocrine disorders |
Other specific types of diabetes |
PEnDGEx |
|
Cushing's syndrome, pheochromocytoma, acromegaly, hyperthyroidism |
Endocrine disorders |
CPAH |
|
Cushing's syndrome |
Increased cortisol |
|
|
Pheochromocytoma |
Increased catecholamines |
|
|
Acromegaly |
Increased growth hormone in adult |
|
|
Within 30 minutes; sodium fluoride |
A serum specimen is appropriate for glucose analysis if serum is separated from cells ????? But if serum is in contact with cells for longer than 30 minutes, a preservative such as ????? that inhibits glycolysis should be added |
|
|
7 mg/dl lower; tissue metabolism |
Venous plasma glucose is ????? than capillary blood due to ????? |
|
|
Oxidation-reduction method and condensation method |
Chemical methods |
|
|
Alkaline copper reduction method and alkaline ferric reduction method (hagedorn jensen) |
2 oxidation reduction methods |
|
|
Folin Wu method, Nelson Somogyi method, Neocuproine method (2,9 Dimethyl 1,10 Phenantroline Hydrochloride), Benedict's method (modification of Folin Wu) |
4 alkaline copper reduction methods |
|
|
Reduction of cupric ions to cuprous ions forming cuprous oxide in hot alkaline solution by glucose |
Principle of alkaline copper reduction method |
|
|
Arterial blood glucose |
Capillary blood glucose is same with ???? |
|
|
CSF glucose concentrations |
It should be approximately 60% of the plasma concentrations |
|
|
Peritoneal fluid glucose |
It is same with plasma glucose |
|
|
Fasting (2 mg/dl/decade) Postprandial (4 mg/dl/decade) Glucose challenge (8-13 mg/dl/decade) |
Plasma glucose levels increased with age |
|
|
Room temperature (20-25 deg C); 7 mg/dl/hour |
At ?????, glycolysis decreases glucose by ???? in normal uncentrifuged coagulated blood |
|
|
Refrigerated temperature (4 deg C); 1-2 mg/dl/hour |
At ????, glucose is metabolized at the rate of about ???? |
|
|
-20 deg C |
With long term specimen storage, even at ????, glucose values decrease significantly and progressively |
|
|
WBC and RBC |
They metabolize glucose resulting to decrease value in clotted, uncentrifuged blood |
|
|
Glycolysis |
Leukocytosis leads to ???? |
|
|
Hot alkaline solution |
Process on how to convert cupric to cuprous ions forming cuprous oxide |
|
|
Cuprous ions |
Alkaline copper tartrate using glucose and heat will yield to ????? |
|
|
Phosphomolybdic acid or phosphomolybdenum blue |
End product of folin wu method (cuprous ions + phosphomolybdate) |
|
|
Arsenomolybdic acid or arsenomolybdenum blue |
End product of nelson somogyi method (cuprous ions + arsenomolybdate) |
|
|
Cuprous-Neocuproine complex |
End product of neocuproine method (cuprous ions + neocuproine) |
|
|
Blue |
End color of Folin Wu method |
|
|
Blue |
End color of Nelson Somogyi method |
|
|
Yellow or yellow orange |
End color of neocuproine method |
|
|
Benedict's method |
Oxidation reduction method used for the detection and quantitation of reducing substances in body fluids like blood and urine |
|
|
Citrate and tartrate |
Stabilizing agent used in Benedict's method |
|
|
Alkaline ferric reduction method |
It involves reduction of yellow ferricyanide to a colorless ferrocyanide by glucose |
|
|
Alkaline ferric reduction method |
Also known as inverse colorimetry |
|
|
Ortho-toluidine (dubowski method) |
Only condensation method |
|
|
Glycosamine and Schiff's base |
End products of ortho-toluidine (dubowski method) |
|
|
Dubowski method |
Uses glucose and aromatic amines with glacial HAC and heat |
|
|
Enzymatic methods |
Method that acts on glucose ONLY but not on other sugars and not on other reducing substances |
|
|
Glucose oxidase method |
Enzymatic Method that measures the beta-D glucose |
|
|
Glucose oxidase method |
Enzymatic method that measures CSF and urine glucose |
|
|
Colorimetric enzymatic method |
Other term for glucose oxidase method |
|
|
Glucose oxidase method, hexokinase method, glucose dehydrogenase method, dextrostics (cellular strip), interstitial glucose measuring device |
Types of enzymatic method |
GHGDI |
|
Colorimetric glucose oxidase method (Saifer Gernstenfield Method) and polarographic glucose oxidase |
Gluconic acid and peroxide (H2O2) |
End products of the first reaction in Saifer Gernstenfield method |
|
Oxidized chromogenic substance and water (H2O) |
End products of the second reaction in Saifer Gernstenfield method) |
H2O2 + chromogenic substance with peroxide will yield to |
|
Ascorbic acid |
It inhibits oxidized chromogenic substances and gives false decrease of glucose because it reacts on the second reaction |
|
|
Polarographic glucose oxidase |
A glucose oxidase method that measures rate of oxygen consumption which is proportional to glucose concentration |
|
|
Hydrogen peroxide |
Glucose oxidase in the reagent catalyzes the oxidation of glucose by oxygen under first order condition |
|
|
Consumption of oxygen on an oxygen-sensing electrode |
The enzymatic conversion of glucose is quantitated by ???? |
|
|
Molybdate, iodide, catalase, ethanol |
The hydrogen peroxide is prevented from re-forming oxygen by ?????? |
MICE |
|
CH3CHO (acetaldehyde) and 2H2O |
End products of hydrogen peroxide and ethanol (h2o2 + C2H5OH) using catalase |
|
|
I2 and 2H2O |
End products of H2O2 + 2H + 2I with molybdate |
|
|
Hexokinase method |
Enzymatic method which is the most specific glucose method; reference method |
|
|
Heparin, EDTA, fluoride, oxalate or citrate |
Tubes used in plasma collection for hexokinase method |
HEFOC |
|
Urine, CSF, and serous fluids |
Other samples used in hexokinase method |
UCS |
|
Nicotinamide Adenine Dinucleotide Phosphate (NADP) |
Acts a coenzyme in hexokinase method |
|
|
Glucose-6-phosphate dehydrogenase (G-6-PD) |
Most specific reagent for glucose in hexokinase method |
|
|
Glucose oxidase method and glucose dehydrogenase method |
2 enzymatic methods that use mutarotase |
|
|
Ascorbate, bilirubin, uric acid, glutathione, creatinine, l-cysteine, l-dopa, dopamine methyldopa and citric acid |
False decreased values of glucose in glucose oxidase method is due to what substances ????? |
ABUGCIIDMC |
|
Nicotinamide Adenine dinucleotide hydrogen (NADH) |
Increases the ability of RBC to consume glucose (cause of increase uptake of glucose in RBC); promotes glycolysis |
|
|
Presence of bleach |
Can cause false increase in glucose oxidase method |
|
|
Hemolysis and icterisia |
Can cause false decrease of plasma glucose in hexokinase method |
|
|
Hemolysis |
It is due to presence of hemoglobin that inhibits G6PD in hexokinase method |
|
|
> 0.5 hemoglobin/dl |
Hemolyzed samples containing ????? are unsatisfactory for hexokinase method because phosphate esters and enzymes released from RBCs interfere with the assay generating NADH |
|
|
Ascorbic acid and uric acid |
Hexokinase method is not affected by these substances???? |
|
|
NADH |
Reduced form of NAD |
|
|
Color change reaction |
Enzymatic conversion of glucose to product is quantitated by a ????? at the last of a series of coupled chemical reactions (kinetic analysis) |
|
|
Glucose Dehydrogenase Method |
In this enzymatic method, glucose is reduced to produce a chromophore that is measured spectrophotometrically or an electric current |
|
|
Glucose Dehydrogenase Method |
In this enzymatic method, the amount of NADH generated is proportional to the glucose concentration |
|
|
Glucose Dehydrogenase Method Method Method |
This enzymatic method provides results in close agreement with hexokinase procedures |
|
|
Mutarotase |
This substance is added to shorten the time necessary to reach equilibrium |
|
|
Beta-D glucose |
End product of alpha-D glucose + mutarotase (first reaction in glucose dehydrogenase method) |
|
|
D-gluconolactone + NADH |
End products of Beta-D glucose + NAD with Glucose Dehydrogenase (2nd reaction in Glucose dehydrogenase method) |
|
|
MTTH (blue color) + NAD |
End products of MTT + NADH with diaphorase (3rd reaction in glucose dehydrogenase method) |
|
|
Dextrostics (cellular strips) |
An enzymatic method that is important in establishing correct insulin amount for next dose |
|
|
Dextrostics (cellular strips) |
An enzymatic method that is effective in reducing the rate of development of diabetic complications |
|
|
>=140 mg/dl (7.8 mmol/L); fasting plasma glucose, HbA1c, or OGTT; venous samples |
In Dextrostics (cellular strips), an individual with a capillary glucose of ????? should be rescreened with a ?????? using ?????? |
|
|
Glucometer |
Example of Dextrostics (cellular strips) |
|
|
Interstitial Glucose Measuring Device |
An enzymatic method that is used for continuous monitoring of glucose levels in people with diabetes |
|
|
Interstitial Glucose Measuring Device |
An enzymatic method that uses electrochemical methods to automatically and frequently measure glucose levels in the interstitial fluid of dermis or subcutaneous fat tissue, and require repeated calibration to plasma or whole blood glucose levels |
|
|
Interstitial Glucose Measuring Device |
An enzymatic method that provides result that gives information about glucose patterns over hours to days |
|
|
7 mg/dl lower; tissue metabolism |
Venous plasma glucose is ????? than capillary blood due to ????? |
|
|
Oxidation-reduction method and condensation method |
Chemical methods |
|
|
Alkaline copper reduction method and alkaline ferric reduction method (hagedorn jensen) |
2 oxidation reduction methods |
|
|
Folin Wu method, Nelson Somogyi method, Neocuproine method (2,9 Dimethyl 1,10 Phenantroline Hydrochloride), Benedict's method (modification of Folin Wu) |
4 alkaline copper reduction methods |
|
|
Reduction of cupric ions to cuprous ions forming cuprous oxide in hot alkaline solution by glucose |
Principle of alkaline copper reduction method |
|
|
Arterial blood glucose |
Capillary blood glucose is same with ???? |
|
|
CSF glucose concentrations |
It should be approximately 60% of the plasma concentrations |
|
|
Peritoneal fluid glucose |
It is same with plasma glucose |
|
|
Fasting (2 mg/dl/decade) Postprandial (4 mg/dl/decade) Glucose challenge (8-13 mg/dl/decade) |
Plasma glucose levels increased with age |
|
|
Room temperature (20-25 deg C); 7 mg/dl/hour |
At ?????, glycolysis decreases glucose by ???? in normal uncentrifuged coagulated blood |
|
|
Refrigerated temperature (4 deg C); 1-2 mg/dl/hour |
At ????, glucose is metabolized at the rate of about ???? |
|
|
-20 deg C |
With long term specimen storage, even at ????, glucose values decrease significantly and progressively |
|
|
WBC and RBC |
They metabolize glucose resulting to decrease value in clotted, uncentrifuged blood |
|
|
Glycolysis |
Leukocytosis leads to ???? |
|
|
Interstitial Glucose Measuring Device |
An enzymatic method that provides result that gives information about glucose patterns over hours to days |
|
|
Trend analysis |
In Interstitial Glucose Measuring Device, this can reveal useful findings for modifying treatment, such as unsuspected nocturnal hypoglycemia or postprandial hypoglycemia |
|
|
Only supplemental |
Interstitial Glucose Measuring Device used for glucose measurement is ????? - may supplement but cannot replace conventional home blood glucose monitoring |
|
|
Slow (5-30) equilibrium with capillary blood glucose |
Interstitial glucose is in ????? and therefore is not equal to blood glucose, except in stable systems |
how many minutes |
|
Random Blood Sugar (RBS) Fasting Blood Sugar (FBS) 2-hour Postprandial Blood Sugar (2-Hour PBBS) Glucose Tolerance Test (GTT) |
Samples for glucose measurement |
RF2G |
|
RBS |
Sample that is requested during insulin shock and hyperglycemic ketonic coma |
|
|
FBS |
It is a measure of overall glucose homeostasis |
|
|
NPO at least 8 hours (6-8hrs) before the test |
Requirement for FBS |
|
|
RBS value: >=160 mg/dl (8.9 mmol/L) FBS, HbA1c, 2-hour OGTT |
RBS value of suspected for diabetes mellitus; must undergo what tests ??? |
|
|
2-hour PBBS |
sample for glucose measurement without fasting (morning collection that evaluates hypoglycemia and hyperglycemia) |
|
|
>= 140 mg/dl - hyperglycemia <= 60 mg/dl - hypoglycemia |
2-hour PBBS value for hyperglycemia and hypoglycemia |
|
|
2-hour PBBS |
It measures how well the body metabolize glucose |
|
|
GTT |
It is used to determine how well the body metabolize glucose over a required period of time, same with 2-HPBBS |
|
|
GTT |
It should be performed to diagnose gestational diabetes |
|
|
GTT |
It is not generally recommended for routine clinical use in the diagnosis of diabetes (for DM and GDM) |
|
|
Thyrotoxicosis |
Caused by hyperthyroidism |
|
|
Papasa!!!!!! |
Papasa or papasa???? |
GANBATTE!!!!!! |
|
Papasa!!!!!! |
Papasa or papasa???? 💃🏿💃🏿💃🏿💃🏿💃🏿 |
GANBATTE!!!!!! |
|
Heres a pic of a buddha for goodluck charm |
Hi oliver!!! Hi mam twishhhh 💃🏿💃🏿💃🏿💃🏿💃🏿 |
GANBATTE!!!!!! |
|
Impaired glucose fasting |
It is characterized by fasting blood glucose concentration less than those required for the diagnosis of diabetes |
|
|
Impaired fasting glucose |
The OGTT is between normal and diabetic values (2nd hour OGTT = 140-199mg/dL |
|
|
True |
True or False: Normally, serum glucose levels rise and them fall within about a 2-hour period. |
|
|
True |
True or False:
If the glucose levels remain elevated, however, the diagnosis of diabetes mellitus may again be made. |
|
|
True |
True or False: If glucose is detected in the urine at any point, evidence for this condition is also obtained, although absence of urinary glucose does not in any way rule out DM. |
|
|
True |
True or False: If glucose is detected in the urine at any point, evidence for this condition is also obtained, although absence of urinary glucose does not in any way rule out DM. |
|
|
Glycosylated Hemoglobin |
Aso known as glycated hemoglobin. |
HbA1c |
|
Glycosylated Hemoglobin |
It is the largest subfraction of normal hemoglobin A in both diabetic and nondiabtletic individuals. |
|
|
Glycosylated hemoglobin |
It is the hemoglobin A that is irreversibly glycosylated at one or both N-terminal valines of the Beta chains of the tetramic hemoglobin molecule, including hemoglobin that may also (but not solely) be fly cost later on lysine residues. |
|
|
Glycosylated hemoglobin |
It represents a "weighted" average of glucose levels, with youngest erythrocytes contributing to a greater extent than older ones. |
|
|
Glycosylated hemoglobin |
It is a reliable method in the monitoring of long-term glucose control. |
HbA1c |
|
3-6 months |
HbA1c levels should be performed every ??? in the individuals with diabetes to monitor glycemic control using certified method. |
12-24 weeks |
|
Glycosylated hemoglobin |
Traceable to diabetes Control and Complications Trial reference (DCCT) method. |
|
|
Diabetes Control and Complications Trial |
DCCT |
|
|
True |
True or False: Dietary status on the day of the test has no effect on HbA1c. |
|
|
Electrophoresis, Immunoassay, HPLC, Affinity Chromatography |
Measurement Methods for HbA1c |
EIHAC |
|
True |
True or False:
It is recommend that HbA1c be measured twice a year for patients who are meeting treatment goals, and quarterly for non-compliant patients. |
|
|
2-4 months or 2-6 months |
HbA1c Diagnostic Significance: It reflects the average glucose level over the previous ??? |
Even number. |
|
Carbohydrates |
Compounds that contain, hydrogen and oxygen |
|
|
Cx(H2O)y |
What is the general formula of carbohydrates? |
|
|
• provide energy to the body • part of the structural integrity of the cell membrane • determines blood type • essential component of nucleic acids |
What are the functions of carbohydrates? |
|
|
• glucose • galactose • fructose |
Examples of Monosaccharides |
GGF |
|
• Maltose = 2 glucose • Lactose = galactose + glucose • Sucrose = fructose + glucose |
Examples of Dissacharides |
MLS |
|
• starch • cellulose • glycogen |
Examples of Polysaccharides |
SCG |
|
Ptyalin |
Salivary amylase |
|
|
Mouth • Salivary glands produce salivary amylase (ptyalin) which digest carbohydrates in the mouth • Food goes to the esophagus • Food goes to the stomach (no carbohydrate digestion) • Food goes to the intestine (pancreatic amylase) is released from the pancreas and passes through the bile duct and into the intestines • Long chain of carbohydrates are degraded into glucose by the action of pancreatic amylase • Glucose is absorbed into the blood circulation (leading to hyperglycemia) • Hyperglycemia triggers release of insulin by the Beta cells odlf the pancreas • Insulin release leads to increased cellular uptake of glucose • Glucose enters the cell • Glucose in the blood decreases |
Pathway of Carbohydrate Metabolism |
10 |
|
• Glycolysis • Gluconeogenesis • Glycogenolysis • Glycogenesis • Lipogenesis • Lipolysis |
Process involved in Carbohydrate Metabolism |
GGGGLL |
|
Glycolysis |
Metabolism of glucose molecule to pyruvate or lactate |
|
|
Glycolysis |
Decrease blood glucose since glucose is consumed to produce lactate or pyruvate |
|
|
Gluconeogenesis |
Formation of glucose-6-phosphate from non-carbohydrate sources |
|
|
Gluconeogenesis |
Increase blood glucose since new glucoses are formed from other sources |
|
|
Glycogenolysis |
Breakdown of glycogen to glucose for use as energy |
|
|
Glycogenolysis |
Increases glucose since glycogen is degraded into glucose molecules |
|
|
Glycogenesis |
Conversion of glucose to glycogen for storage |
|
|
Glycogenesis |
Decreases glucose since excess glucoses in the body is stored in the liver and skeletal muscles as glycogen |
|
|
Lipogenesis |
Conversion of carbohydrates to fatty acids |
|
|
Lipogenesis |
Decreases glucose since carbohydrates are converted into fatty acids and stored as fats |
|
|
Lipolysis |
Decomposition of fats |
|
|
Lipolysis |
Increases glucose because fats are converted into consumable glucose |
|
|
Pancreas and Liver |
Organs involved in carbohydrate regulation |
PL |
|
Pancreas |
Has exocrine and endocrine function |
|
|
Pancreas as Endocrine gland |
Refers to the production of hormones |
|
|
Pancreas as Exocrine gland |
Leads to production of enzyme |
|
|
Glucagon |
Hormone that secreted by the alpha cells of the pancreas and leads to the increase in the blood glucose levels |
|
|
Glucagon |
Hyperglycemic agent |
|
|
Insulin |
Hormone secreted by the Beta cells of the pancreas and leads to the decrease in blood glucose levels |
|
|
Insulin |
Synthesized as proinsulin, in which the C-peptide in cleaved in order to convert it to the active insulin. |
|
|
Somatostatin |
Hormone secreted by the delta cells of the pancreas and causes inhibition of glucagon and insulin |
|
|
Pancreatic amylase |
Enzyme that degrades carbohydrates |
|
|
Lipase |
Enzyme that cleaves triglycerides |
|
|
Liver |
Functions in the production and regulation of carbohydrates, lipids and protein |
|
|
Liver |
Reposnsible for the formation of glycogen |
|
|
Diabetic ketoacidosis |
pH imbalance results from dehydration, electrolyte imbalance and acidosis |
|
|
Diabetic ketoacidosis |
Serious complication of diabetes that occurs when your body produces high levels of blood acid called ketones. |
|
|
Diabetic ketoacidosis |
It develops when your body is unable to produce enough insulin |
|
|
DM - increase specific gravity of urine DI - decrease specific gravity of urine |
Differentiate DM and DI based on urine specific gravity |
|
|
Vasopressin (antidiuretic hormone) |
DI lacks what hormone???? |
|
|
Diabetes insipidus |
A rare form of diabetes caused by a deficiency of the pituitary hormone vasopressin, which regulated the kidney function. |
|
|
Carbohydrates - without nitrogen (CHO) Protein - with nitrogen (CHON) |
Differentiate carbohydrates from proteins |
|
|
GTT |
It is a multiple blood sugar test |
|