Hypoglicemia-Endocrin 3

Hipoglikemia dan
Hiperglikemia pada DM
dr M Arman Nasution SpPD
www.freelivedoctor.com
Blood sugar and health

Sugar (glucose) is
an important source
of energy
What is eaten is
absorbed into
the blood
Insulin is produced
by the pancreas when
blood sugar is high
Insulin keeps blood

sugar level within
the normal range
for health
HYPOGLICEMIA
NORMAL PLASMA GLUCOSE LEVELS:
60-100 mgdl
NORMAL VALUES DEPEND ON:
SEX
FEED OR FASTING STATE
TIME OF FASTING
HYPOGLICEMIA
GLUCOSE CONTROL: INTERACTIONS
BETWEEN
INSULIN LEVELS
COUNTERRREGULATORY HORMONES
GLUCAGON
EPINEPHRINE
CORTISOL
GROWTH HORMONE
HYPOGLICEMIA
GLUCOSE CONTROL:
LIVER IS THE MAJOR GLYCOGEN
STORAGE ( 70 gr.), AND IS DEPLETED
AFTER 24 hrs. OF FASTING.
TO AVOID HYPOGLICEMIA IN STARVING
STATES, IT`S IMPERATIVE TO INCREASE
GLUCONEOGENESIS.
HYPOGLICEMIA
GLUCONEOGENESIS
THIS PROCESS IS CARRIED BY:
A DECREASE IN INSULIN LEVELS AND
INCREASE IN GLUCAGON
AN INTACT HEPATIC GLYCOGENOLYTIC
AND GLUCONEOGENIC ENZYMES
MOBILIZATION OF GLUCONEOGENIC
PRECURSORS ( A.A. & F.F.A.)
HYPOGLICEMIA
LACK OR DEFICIENCY OF INSULIN=
HYPERGLICEMIA
EXCESS OF INSULIN OR DEFICIENCY
OF COUNTER-REGULATORY
HORMONES= HYPOGLICEMIA
HYPOGLICEMIA
DEFINITION: CONDITIONS IN WHICH

GLUCOSE PLASMA LEVELS FALL
BELOW NORMAL RANGES.
MECHANISM TO PRODUCE
HYPOGLICEMIA
ALTERED GLUCOSE UTILIZATION

ALTERED GLUCOSE PRODUCTION
HORMONAL CHANGES
ENZYMES DEFICIENCIES
GLUCOSE SUBSTRATE DEFICIENCIES
ETIOLOGY AND
CLASIFICATION
FASTING HYPOGLICEMIA: OCCURS
PRIMARILY IN THE ABSENCE OF
NUTRIENT INGESTION.
POST-PANDRIAL HYPOGLICEMIA:
PRECIPITATED BY NUTRIENT INGESTION,
ESPECIALLY CHO AND PROTEINS.
INDUCED HYPOGLICEMIA: INSULIN,
DRUGS, ORAL HYPOGLICEMIC AGENTS,
ALCOHOL, ETC.
FASTING HYPOGLICEMIA
COULD OCCUR BY ONE OR MORE OF THE
FOLLOWING MECHANISM:
EXCESS OF INSULIN OR INSULIN -LIKE
SUBSTANCES
DEFICIENCIES OF ANTI-INSULIN HORMONES
CONGENITAL OR ACQUIRED LIVER DISEASE
SUBSTRATE DEFICIENCY
FASTING HYPOGLICEMIA
HYPERINSULINISM
INSULINOMA: PANCREATIC BETA CELL
TUMOR.
90 % ARE BENIGN
10% ARE MALIGNANT (CANCER)
INSULINOMA DIAGNOSIS
INSULIN LEVELS > 20 U/ ml.
INSULIN/ GLUCOSE RATIO ( I/ G ratio)
I/G ratio > 0.4 is indicative of
relative hyperinsulinism.
CT scan and or ULTRASOUND
INSULINOMA TREATMENT
SURGERY
STREPTOZOTOCIN
HYPOGLICEMIA
NESIDIOBLASTOSIS:
INFANTS WITH HYPERINSULINISM
WITHOUT IDENTIFIABLE PANCREATIC
NEOPLASM.
NESIDIOBLASTOSIS
HISTOLOGY:
INCREASE IN BETA CELL MASS, DERIVED
FROM DUCTAL EPITHELIUM.
NESIDIOBLASTOSIS
TREATMENT:
PARTIAL OR TOTAL PANCREATECTOMY
DIAZOXIDE
HYPOGLICEMIA
EXTRAPANCREATIC TUMORS
ECTOPIC INSULIN PRODUCTION
INSULIN / LIKE SYNTHESIS
ACELERATED GLUCOSE CONSUMPTION
INHIBITION OF THE LIVER TO RELEASE
GLUCOSE (GLYCOGENOLISIS OR
GLUCONEOGENESIS)
HYPOGLICEMIA
MESENCHIMAL TISSUE DERIVED
TUMORS:
FIBROMAS
FIBROSARCOMAS
NEUROMAS
HYPOGLICEMIA
SOLID TUMORS:
HEPATOMA
ADRENAL CARCINOMAS
G.I. CARCINOMAS
COUNTER REGULATORY
HORMONES DEFICIENCY
GLUCAGON, EPINEPHRINE, CORTISOL,
GROWTH HORMONE.
INSULIN IS NORMAL OR EVEN DECREASE
HYPOPITUITARISM (ANY CAUSE)
ISOLATED DEFICIENCY OF G.H. OR A.C.T.H.
ADDISON`S DISEASE
HYPOGLICEMIA
LIVER DISEASES OR CONGENITAL
ENZYMES DEFICIENCY
DECRESED GLYCOGENOLISIS
DEPLETED GLYCOGEN STORAGE
DECREASED IN GLUCONEOGENESIS
ALTERED NEGATIVE FEED-BACK
GLUCOSE-INSULIN REGULATION
*INSULIN COULD BE NORMAL OR
INCREASED
HYPOGLICEMIA
SUBSTRATES DEFICIENCIES
ALANINE (PRIMARY AMINOACID)
FREE FATTY ACIDS
* IN NORMAL SUBJECTS THE RATE OF ALANINE
RELEASE FROM MUSCLE DETERMINES THE
RATE OF GLUCONEOGENESIS IN STARVATION
STATES.
INSULIN AUTOINMUNE
HYPOGLICEMIA
VERY RARE
IgG THAT BIND INSULIN IN PLASMA
HYPOGLICEMIA OCCURS WHEN
THERE IS A SUDDEN RELEASE OF
THE INSULIN BOUNDED TO IgG.
POST-PANDRIAL HYPOGLICEMIA
(REACTIVE)
ALIMENTARY TYPE:
G.I. SURGERY (RAPID GASTRIC
EMPTYING)
*DUMPING SYNDROME (DIARRHEA,
POOR ABSORPTION)
POSTPANDRIAL HYPOGLICEMIA
(REACTIVE)
SPONTANEOUS REACTIVE HYPOGLICEMIA
* 2 4 hrs. AFTER CHO MEAL
*GLUCOSE LEVELS < 60 mg/ dl BUT > 40 mg/dl
**THEORIES: ABNORMAL HYPERSECRETION
OF INSULIN IN RESPONSE TO
CHO
+EARLY TYPE II D.M.
FRUCTOSE INTOLERANCE
HYPOGLICEMIA
CLINICAL PICTURE
NEUROGLYCOPENIC SIGNS AND
SYMPTOMS
ADRENERGIC DISCHARGE SIGNS AND
SYMPTOMS
HYPOGLICEMIA
THE CLINICAL PICTURE DEPENDS ON:
RATE AND SEVERITY OF HYPOGLICEMIC
INSTALLATION
INTEGRITY OF SIMPATHETIC SYSTEM
HYPOGLICEMIA
NEUROGLYCOPENIC PICTURE:
HEADACHE
MENTAL DULLNESS
CLOUDING OF VISION
FATIGUE
CONFUSION
HALLUCINATIONS
BIZARRE BEHAVIOR
SEIZURES
COMA
IRREVERSIBLE BRAIN DAMAGE
HYPOGLICEMIA
REMEMBER
BRAIN VULNERABILITY: BRAIN USE
ONLY GLUCOSE AND KETONE BODIES
AS ENERGY SOURCES.
HYPOGLICEMIA
ADRENERGIC DISCHARGE PICTURE:
PALPITATIONS/ TACHYCARDIA
ANXIETY
SWEATING
TREMULOUSNESS
HUNGER
Diabetes Mellitus
Disease in which the body
doesnt produce or properly
use insulin, leading to
hyperglycemia.
Carbohydrate Digestion
Action of Insulin on the Cell

Metabolism
Natural History of Type 2 Diabetes

Normal
Insulin
resistance
Insulin
secretion
After meal
glucose
Fasting
glucose
Prediabetes
Type 2 diabetes
Increasing insulin
resistance
Hyperinsulinemia,
then islet cell failure
Abnormal
glucose tolerance
High sugar levels
Adapted from International Diabetes Center (IDC), Minneapolis, Minnesota.
What goes wrong in

diabetes?
Multitude of mechanisms
Insulin
Regulation
Secretion
Uptake or breakdown
Beta cells
damage
38
39
40
Carbohydrate
Metabolism
Carbohydrates are metabolized in the body
to glucose.
CNS uses glucose as its primary energy
source. This is independent of insulin.
Glucose is taken by the muscle to produce
energy (insulin required).
Glucose is stored in the liver as glycogen
and in adipose tissues as fat.
Insulin is produced and stored by the cells of the pancreas
41
Carbohydrate Metabolism
(Contd)
Postprandial glucose metabolism in normal
individuals:
After food is ingested, blood glucose concs
rise and stimulate insulin release.
Insulin action:
glucose uptake by the tissues
liver glycogen formation and glycogen
breakdown
lipid synthesis and inhibits fatty acid
breakdown to ketone bodies
Promotes protein synthesis
42
Carbohydrate Metabolism
(Contd)
Fasting glucose metabolism in normal
individuals:
In the fasting state, insulin release is inhibited.
Hormones that promote an increase in blood glucose
are released:
Glucagon, epinephrine, growth hormone,
glucocorticoids, and thyroid hormones.
Glycogenolysis
Gluconeogenesis: AA are transported from muscle to
liver and converted to glucose.
TG are broken down into free FAs as an alternative
fuel source.
43
Action of Insulin on Carbohydrate, Protein

and Fat Metabolism
Carbohydrate
Facilitates the transport of glucose
into muscle and adipose cells
Facilitates the conversion of glucose
to glycogen for storage in the liver
and muscle.
Decreases the breakdown and
release of glucose from glycogen by
the liver

and Fat Metabolism
Protein
Stimulates protein synthesis
Inhibits protein breakdown;
diminishes gluconeogenesis

and Fat Metabolism
Fat
Stimulates lipogenesis- the transport
of triglycerides to adipose tissue
Inhibits lipolysis prevents excessive
production of ketones or ketoacidosis
Type I Diabetes
Genetic component to disease
Type II Diabetes
Insulin levels may be normal,
elevated or depressed
Characterized by insulin resistance,
diminished tissue sensitivity to insulin,
and impaired beta cell function (delayed
or inadequate insulin release)
Often occurs >40 years
Diagnostic Criteria
Any one test should be confirmed with a second

test, most often fasting plasma glucose (FPG).
This criteria for diagnosis should be confirmed by
repeating the test on a different day.
50
51
Self Monitoring Test

Self-monitoring of blood glucose
Extremely useful for outpatient monitoring specially for
patients who need tight control for their glycemic state.
A portable battery operated device that measures the
color intensity produced from adding a drop of blood to
a glucose oxidase paper strip.
e.g. One Touch, Accu-Chek, DEX, Prestige and
Precision.
52
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Terima kasih
ASS WR WB

Hypoglicemia-Endocrin 3

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Hipoglikemia dan

Blood sugar and health

Insulin keeps blood

DEFINITION: CONDITIONS IN WHICH

ALTERED GLUCOSE UTILIZATION

Action of Insulin on the Cell

Natural History of Type 2 Diabetes

Adapted from International Diabetes Center (IDC), Minneapolis, Minnesota.

What goes wrong in

Action of Insulin on Carbohydrate, Protein

Action of Insulin on Carbohydrate, Protein

Action of Insulin on Carbohydrate, Protein

Often occurs >40 years

Any one test should be confirmed with a second

Self Monitoring Test

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