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CARBOHYDRATES

 These are hydrates of aldehyde or ketone derivatives based on the
location of the CO functional group
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 IMPORTANCE OF CARBOHYDRATES
 Ribose and deoxyribose sugars form part of the structural framework
of RNA and DNA
 Provides a significant fraction of energy in the diet of most organism
 Serves as cell membrane components
 Provides the storage form of energy in the body
 Glucose, maltose, fructose, lactose and galactose – reducing
substances/sugars
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 Sucrose - most common non reducing sugar
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 NOMENCLATURE
GENERIC NAMES
3 CARBONS-triose
4 CARBONS-tetrose
5 CARBONS- pentose
6 CARBONS- hexose
7 CARBONS- heptose
9 CARBONS- nonose

EXAMPLES
GLYCERALDEHYDE
ERYTHROSE
RIBOSE, DEOXYRIBOSE
FRUCTOSE, GLUCOSE
SEDOHEPTULOSE
NEURAMIDIC ACID

 REGULATION OF BLOOD GLUCOSE LEVELS
1
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2
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The release of absorbed glucose for the cells’ immediate energy
needs: GLYCOLYSIS
B
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Conversion of excess glucose into glycogen for storage:
GLYCOGENESIS
D
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 As an endocrine gland, it produces and secretes the hormones
insulin, glucagon and somatostatin from different cells residing in
the islets of Langerhans in the pancreas
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It is synthesized by the β-cells of the islets of Langerhans in
the pancreas
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It is the only hormone that decreases glucose levels –
hypoglycemic agent
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 Glucagon
 Is the primary hormone responsible for increasing glucose –
hyperglycemic agent
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 It is released during stress and fasting states
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 OTHER HORMONES THAT TEND TO INCREASE GLUCOSE
CONCENTRATION
 Cortisol and corticosteroids (glucocorticoids)
 Secreted by the cells of the zona fasciculata and zona reticularis
of the adrenal cortex
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 It promotes gluconeogenesis and lipolysis
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 Inhibits insulin secretion and promotes glycogenolysis and
lipolysis
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 Decreases entry of glucose into the cell
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 Thyroid hormones
 It promotes glycogenolysis, gluconeogenesis and intestinal
adsorption of glucose
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 It promotes glycogenolysis and gluconeogenesis
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 It primarily inhibits the action of insulin and glucagon
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Hyperglycemia
 an increase in blood glucose levels
 Causes: stress, severe infection, dehydration or pregnancy,
insulin deficiency or abnormal insulin receptor
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 All adults older than 45 years should have a measurement of FBS
every 3 years unless the individual is diabetic
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Electrolyte imbalance
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Hypoglycemia
 It results from an imbalance between glucose utilization and
production
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 The warning signs and symptoms of hypoglycemia are related to
central nervous system
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 Diagnostic test-5-hour glucose tolerance test, (hypoglycemic dip
is often not seen until after 3 hours)
 Symptoms of hypoglycemia:
a
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Neuroglycopenic – dizziness, tingling, blurred vision, confusion,
behavioral changes
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 Glucosuria occurs when the plasma glucose level exceeds 18
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99 mmol/L) with normal renal function
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 The entire process of ketosis can be reserved by insulin
administration

 CRITERIA FOR THE DIAGNOSIS OF DIABETES MELLITUS
o Obesity
o Family history of diabetes in a first degree relative
o Hypertension (>140/90)
o Low HDL(<35mg/dL)
o Elevated triglycerides (>250 mg/dL)

 AN INBORN ERROR OF CARBOHYDRATES METABOLISM
1
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 It is cause by failure to thrive syndrome in infant
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Essential Fructosuria
 An autosomal recessive disorder characterized by fructokinase
deficiency
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 Diagnostic indicator: the presence of fructose in urine (Fructosuria)
3
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 Clinical features: irritability, lethargy, seizures and hepatomegaly
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Fructose-1,6-biphosphate deficiency
 A defect in fructose-1,6-biphosphate results in failure of hepatic
glucose generation by gluconeogenic precursors such as lactate and
glycerol
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5
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 It is an inherited autosomal recessive trait
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 80-90% reduction in the volume of the β-cells is required to induce
symptomatic type 1 diabetes
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Signs and Symptoms: polyuria, polydipsia, polyphagia, rapid weight
loss, hyperventilation, mental confusion and possible loss of
consciousness
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 Type 2 Diabetes
 Formerly known as:
o Non-insulin Dependent Diabetes Mellitus
o Maturity Onset Diabetes Mellitus
o Stable Diabetes
o Ketosis-Resistant Diabetes

 Is characterized by hyperglycemia due to an individual’s resistance
to insulin; there is relative insulin deficiency
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It has been described as a geneticist’s
nightmare
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 It has milder symptoms as compared to type 1, however, untreated
type 2 DM will result to nonketotic hyperosmolar coma –
overproduction of glucose (>500mg/dL) severe dehydration,
electrolyte imbalance and increased BUN and creatinine
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 Gestational Diabetes Mellitus (GDM)
 A disorder characterized by impaired ability to metabolize
carbohydrate usually caused by a deficiency of insulin, metabolic or
hormonal changes, occurring in pregnancy and disappearing after
delivery but, in some cases, returning years later
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 GDM is diagnosed if 2 plasma values or more of the above glucose
levels are exceeded
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 After giving birth, women with GDM should be evaluated 6 to 12
weeks postpartum
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 Impaired Fasting Glucose
 It is characterized by fasting blood glucose concentrations between
normal and diabetic values
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 METHODOLOGIES OF GLUCOSE
 Fasting glucose in whole blood is 15% lower than in serum or
plasma
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 ENZYMATIC METHODS
 Acts on glucose but not on other sugars and not on other reducing
substances
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Colorimetric glucose Oxidase Method
b
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 Hexokinase Method
 Most specific glucose method, reference method
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 Disadvantage: Hemolyzed samples can pose problem because
contents RBC’s may interfere with the stoichiometric relationship
between glucose and NAD(P)H accumulation
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 Dextrostics (cellular strip)
 Important is establishing correct insulin amount for next dose
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 TEST FOR KETONE BODIES
 Normal ratio of β-hydroxybutyrate and acetoacetic acid 1:1 (0
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0
mmol/L)
 The ratio of β-hydroxybutyrate to acetoacetate is greatly increased
in diabetic ketoacidosis (DKA) due to the altered redox state and
elevated levels of NADH in the hepatic mitochondria
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Gerhardt’s ferric chloride test – reacts only with acetoacetate
Nitroprusside test – 10x more sensitive to acetoacetate than to acetone
Acetest tablets – detects acetoacetate (lesser degree)
Ketosis – detects acetoacetate better than acetone

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