Hyperglycemia: Clinical Conditions of Carbohydrate Metabolism

Clinical Conditions of Carbohydrate Metabolism
1. Hyperglycemia
It is an increase in blood glucose concentration
Causes: Stress, severe infection, dehydration or pregnancy
Stress Adrenaline and/or cortisol hyperglycemic hormone
FBS (Fasting blood sugar): less than or equal to a 126 mg/dL
Laboratory findings:
Increased glucose in plasma and urine (renal threshold=160-180 md/dl)
Increased urine specific gravity (SG) (Urine SG= concentration of solute in urine)
Presence of ketones in serum and urine (increased glucose in the blood-glucose is not
present in the cell---glucose is used up by the cell as an energy source…(ketones—how? 
fat/ adipose tissue will undergo lipolysis  ketone release  energy source ng cell)
Decreased blood and urine pH ( presense of ketones ketone bodies (acetoacetic acid
and b-hydroxybutyrate)
Electrolyte imbalance (Increased Potassium, Decreased Sodium and Bicarbonate)
2. Hypoglycemia
It is a decrease in blood glucose concentration
s 60 mg/dL strongly suggest hypoglycemia (series of random fasting specimens)
50 to 55mg/dL — observable symptoms of hypoglycemia may appear
Diabetes Mellitus (DM)
Is a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin
secretion, insulin receptors or both
Fasting plasma glucose concentrations ? less than or equal 126 mg/dL on more than one testing
are diagnostic of DM
Glucosuria occurs when the plasma glucose levels exceed 180 mg/dL with normal renal
function
Triads of DM: Polyphagia, Polydipsia, Polyuria
Diabetes mellitus- increased blood glucose
Polyphagia- ( a lot + hunger/ eating)  adipose tissue sila yung nag undergo ng lipolysis ,
muscle tissue undergo protein protein breakdown which causes unexplained weight loss,
hence the patient tends to eat a lot)
Polyuria- ( a lot+ urine)—since meron kang excessive glucose sa blood , maeexcrete yun sa
urine. Pag naexcrete si glucose sa urine, sasama si water—which can lead to dehydration—
drink a lot (Polydipsia)
Glucose is osmotically active kaya may sumasama na water
In severe DM, the ratio of Beta-hydroxybutyrate to acetoacetate is 6:1
Classification of Diabetes Mellitus
1. TYPE 1 Diabetes Mellitus- destruction of the sourse of insulin/ destruction of insulin/ no insulin
 Formerly known:
Insulin dependent Diabetes Mellitus
(IDDM) Juvenile onset Diabetes Mellitus
Brittle diabetes
Ketosis-prone diabetes
PISO- POSTASSIUM INSIDE, SODIUM OUTSIDE

Characterized by Hyponatremia ( hypo+ natrium +emia) (Decreased Sodium) and
Hyperkalemia ( hyper + kallum + emia) (Increased Potassium)
Insulin stimulate Sodium potassium ATPase is to facilitate exchange of potassium into the
cell and sodium out of the cell
Destruction of Insulin insulin autoantibodies, Glutamic acid decarboxylase,
autoantibodies to beta cells( sinisira yung beta cells—sila po yung nagsysynthesize ng
insulin, HLA DR3-DR4
Autoimmune destruction of the Beta cells of the islets of Langerhans in the pancreas
Diabetic individuals have ingthaReS (absolute insulin deficiency) due to loss of pancreatic cells,
and depend on insulin to sustain life and prevent ketosis
Individuals at greater risk of developing this type of diabetes have high titers of multiple autoantibodies
— Glutamic acid decarboxylase (GAD6), more commonly seen in adults 8 Insulin
autoantibodies (IAA), more commonly seen in children
Idiopathic Type 1 Diabetes Mellitus: It is a form of diabetes that has no known etiology; it is strongly
inherited; it does not have Beta cells autoantibodies
2. Type 2 Diabetes Mellitus

Formerly known: Non-insulin dependent Diabetes Mellitus
Adult type/ Maturity onset Diabetes Mellitus
Stable diabetes
Ketosis-resistant diabetes
Receptor deficient Diabetes Mellitus
Receptor Deficient Diabetes Mellitus—insulin is present/enough
Defective yung insulin receptor sa cells
Receptor is needed para makapasok si glucose sa cell
It is characterized by hyperglycemia due to individual's resistance to insulin

It has been described as a geneticist's nightmare
(hindi maintindihan)
Also characterized by Hyponatremia (Decreased Sodium), Hyperkalemia (Increased
Potassium), Increased Creatinine and BUN levels
3. Gestational Diabetes Mellitus (GDM) – merong increased glucose levels in pregnants

during their third trimester
It is a disorder characterized by impaired ability to metabolize carbohydrate usually caused by
deficiency of insulin, metabolic or hormonal changes
It occurs during pregnancy and disappears after delivery, but, in some cases, returned years
later ( 10 years into DM--- RESPIRATOTY DISTRESS SYNDROME ( pwedeng magsuffer
ditto si baby)
Screening should be performed between 24 and 28 weeks of gestation
The screening and diagnosis of GDM is by performance of OGTT (Oral glucose tolerance test)
using 75g glucose load
Inborn Errors of Carbohydrate Metabolism
A. Galactosemia
It is caused by failure to thrive syndrome in infants
It is a congenital deficiency of one of three enzymes involved in galactose metabolism. 3
enzymes:
a.Galactose-1-phosphate taWyj transferase (most common deficiency)
b. Galactokinase (GALK)
c.Uridine diphosphate galactose-4-epimerase (GALE)
Laboratory features: Elevated blood and urine galactose
Clinical features: Jaundice, Hepatomegaly, Galactosuria, Sepsis (cause by Escherichia coli),
Cataract, Hypotonia, Sensory neural deafness and Easy bruisability
B. Essential Fructosuria
It is an autosomal recessive disorder characterized by Fructokinase deficiency
C. Hereditary Fructose Intolerance

It is a defect of Fructose-1-6-biphosphate aldolase B activity in the liver, kidney and intestine
Clinical features: Irritability, Lethargy, Seizures and Hepatomegaly
D. Fructose-1,6-biphospahe deficiency
It is a defect in Fructose-1,6-biphospahe resulting in failure of hepatic glucose generation by
gluconeogenic precursor such as lactate and glycerol
Clinical features: Hypoglycemia, Lactic acidosis, Convulsions and Coma
E. Glycogen Storage Disease (GSD)

It is an inherited autosomal recessive trait
The disease is a consequence of inherited deficiencies of enzymes that control the synthesis
or breakdown of glycogen
Cause liver damage: Type I, III, IV, VI, IX, 0 (Symptoms: Hypoglycemia, Hepatomegaly)
Cause muscular defect: Types V, VII (Symptoms: Muscle cramps, exercise intolerance, fatigue
and weakness)
Von Gierke disease is the most common GSD and it associated with Hyperlipidemia
 most common GSD in the world
Pome- most common GSD in the phil.
Key terms
Gluconeogenesis: formation of glucose from other substrate
Glycogenesis: conversion of glucose to glycogen
Glycolysis: breakdown of glucose into pyruvate and 2 ATPs
Glycogenolysis: breakdown of g ycogen to glucose
Mnemonics: VP CORY AQUINO MADE HER TITS FALL
TYPE OF SYNONYMN ENZYME DEFICIENT CLINICAL FEATURES

GSD (Tissue affected)
la Von Gierke Glucose-6- Hepatomegaly, retarded growth.

Phosphatase seizures
lb Glucose-6- Recurrent bacterial infections
Phosphatase
translocase
ll Pompe 1,4-Glucosidase Cardiomegaly, infantile death
llla Cori Forbes De brancher (Liver & Hepatomegaly, muscle weakness,
C-D muscle) retarded growth, cardiomyopathy
lllb De brancher (Liver) Same as IIla except muscle
weakness
IV Anderson Brancher Cirrhosis, esophageal varices,
A-B ascites
Mc Ardle
V M-M Muscle Phosphorylase Myoglobinuria, muscle cramps
Hers Hepatomegaly, hypoglycemia

VI Liver Phosphorylase
Her-ver
VII Tarul Phosphofructokinase Pain and stiffness on exertion
VIII Adenyl kinase Urinary excretion of
catecholamines
IXa Phosphorylase kinase Hepatomegaly, hypoglycemia,
(Liver) delay in motor development
IXb Phosphorylase (Liver Hepatomegaly, retarded growth,
and muscle) muscle hypotonia
X Cyclic AMP-dependent Hepatomegaly
kinase
Fanconi-
XI Glucose transporter-2 Hepatomegaly, rickets
Bicket
0 Glycogen synthetase No hepatomegaly, hypoglycemic
symptoms om morning, growth
delay
Lipolysis: breakdown of fats to form ketone bodies

Lipogenesis: formation of fat from acetyl coenzyme A
CSF (Cerebrospinal Fluid) Glucose

It is about 40 to 60% of the blood plasma glucose level
Increased: Diabetes mellitus
Decreased: Bacterial meningitis, Tuberculosis, Fungal and amoebic meningitis subarachnoid
hemorrhage, systemic hypoglycemia

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Clinical Conditions of Carbohydrate Metabolism

Diabetes Mellitus (DM)

PISO- POSTASSIUM INSIDE, SODIUM OUTSIDE

2. Type 2 Diabetes Mellitus

It is characterized by hyperglycemia due to individual's resistance to insulin

3. Gestational Diabetes Mellitus (GDM) – merong increased glucose levels in pregnants

Inborn Errors of Carbohydrate Metabolism

C. Hereditary Fructose Intolerance

E. Glycogen Storage Disease (GSD)

TYPE OF SYNONYMN ENZYME DEFICIENT CLINICAL FEATURES

la Von Gierke Glucose-6- Hepatomegaly, retarded growth.

Hers Hepatomegaly, hypoglycemia

Lipolysis: breakdown of fats to form ketone bodies

CSF (Cerebrospinal Fluid) Glucose

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