HYPOGLICEMIA HYPOGLICEMIA “NORMAL” PLASMA GLUCOSE LEVELS: 60-100 mgdl “NORMAL VALUES “ DEPEND ON: – SEX – FEED OR FASTING STATE – TIME OF FASTING www.freelivedoctor.com
HYPOGLICEMIAHYPOGLICEMIA
“NORMAL” PLASMA GLUCOSE LEVELS: 60-100 mgdl
“NORMAL VALUES “ DEPEND ON:– SEX– FEED OR FASTING STATE– TIME OF FASTING
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HYPOGLICEMIAHYPOGLICEMIA
GLUCOSE CONTROL: INTERACTIONS BETWEEN– INSULIN LEVELS– COUNTERRREGULATORY HORMONES– GLUCAGON– EPINEPHRINE– CORTISOL– GROWTH HORMONE
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HYPOGLICEMIAHYPOGLICEMIA
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.
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HYPOGLICEMIAHYPOGLICEMIA
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.)
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HYPOGLICEMIAHYPOGLICEMIA
LACK OR DEFICIENCY OF INSULIN= HYPERGLICEMIA
EXCESS OF INSULIN OR DEFICIENCY OF COUNTER-REGULATORY HORMONES= HYPOGLICEMIA
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HYPOGLICEMIAHYPOGLICEMIA
DEFINITION: CONDITIONS IN WHICH GLUCOSE PLASMA LEVELS FALL BELOW “NORMAL” RANGES.
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MECHANISM TO PRODUCE MECHANISM TO PRODUCE HYPOGLICEMIAHYPOGLICEMIA
ALTERED GLUCOSE UTILIZATIONALTERED GLUCOSE PRODUCTIONHORMONAL CHANGESENZYMES DEFICIENCIESGLUCOSE SUBSTRATE DEFICIENCIES
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ETIOLOGY AND ETIOLOGY AND CLASIFICATIONCLASIFICATION
– 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.
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FASTING HYPOGLICEMIAFASTING 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
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FASTING HYPOGLICEMIAFASTING HYPOGLICEMIA
HYPERINSULINISM– INSULINOMA: PANCREATIC BETA CELL
TUMOR. – 90 % ARE BENIGN– 10% ARE MALIGNANT (CANCER)
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INSULINOMA DIAGNOSISINSULINOMA 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
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INSULINOMA TREATMENTINSULINOMA TREATMENT
SURGERY
STREPTOZOTOCIN
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HYPOGLICEMIAHYPOGLICEMIA
NESIDIOBLASTOSIS:
– INFANTS WITH HYPERINSULINISM– WITHOUT IDENTIFIABLE PANCREATIC
NEOPLASM.
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NESIDIOBLASTOSISNESIDIOBLASTOSIS
HISTOLOGY:
– INCREASE IN BETA CELL MASS, DERIVED FROM DUCTAL EPITHELIUM.
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NESIDIOBLASTOSISNESIDIOBLASTOSIS
TREATMENT:
– PARTIAL OR TOTAL PANCREATECTOMY
– DIAZOXIDE
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HYPOGLICEMIAHYPOGLICEMIA
EXTRAPANCREATIC TUMORS ECTOPIC INSULIN PRODUCTION INSULIN / LIKE SYNTHESIS ACELERATED GLUCOSE CONSUMPTION INHIBITION OF THE LIVER TO RELEASE
GLUCOSE (GLYCOGENOLISIS OR GLUCONEOGENESIS)
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HYPOGLICEMIAHYPOGLICEMIA
MESENCHIMAL TISSUE DERIVED TUMORS:
– FIBROMAS– FIBROSARCOMAS– NEUROMAS
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HYPOGLICEMIAHYPOGLICEMIA
SOLID TUMORS:
– HEPATOMA– ADRENAL CARCINOMAS– G.I. CARCINOMAS
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COUNTER REGULATORY COUNTER REGULATORY HORMONES DEFICIENCYHORMONES 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
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HYPOGLICEMIAHYPOGLICEMIA
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
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HYPOGLICEMIAHYPOGLICEMIA
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.
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INSULIN AUTOINMUNE INSULIN AUTOINMUNE HYPOGLICEMIAHYPOGLICEMIA
VERY RARE
IgG THAT BIND INSULIN IN PLASMA
HYPOGLICEMIA OCCURS WHEN THERE IS A SUDDEN RELEASE OF THE INSULIN BOUNDED TO IgG.
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POST-PANDRIAL POST-PANDRIAL HYPOGLICEMIA (REACTIVE) HYPOGLICEMIA (REACTIVE)
ALIMENTARY TYPE:G.I. SURGERY (RAPID GASTRIC
EMPTYING)*DUMPING SYNDROME (DIARRHEA,
POOR ABSORPTION)
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POSTPANDRIAL POSTPANDRIAL HYPOGLICEMIA (REACTIVE)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
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HYPOGLICEMIAHYPOGLICEMIA
CLINICAL PICTURENEUROGLYCOPENIC SIGNS AND
SYMPTOMS
ADRENERGIC DISCHARGE SIGNS AND SYMPTOMS
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HYPOGLICEMIAHYPOGLICEMIA
THE CLINICAL PICTURE DEPENDS ON:
– RATE AND SEVERITY OF HYPOGLICEMIC INSTALLATION
– INTEGRITY OF SIMPATHETIC SYSTEM
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HYPOGLICEMIAHYPOGLICEMIA
NEUROGLYCOPENIC PICTURE:– HEADACHE– MENTAL DULLNESS– CLOUDING OF VISION– FATIGUE– CONFUSION– HALLUCINATIONS– BIZARRE BEHAVIOR– SEIZURES– COMA– IRREVERSIBLE BRAIN DAMAGE
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HYPOGLICEMIAHYPOGLICEMIA
REMEMBER
BRAIN VULNERABILITY: BRAIN USE ONLY GLUCOSE AND KETONE BODIES AS ENERGY SOURCES.
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HYPOGLICEMIAHYPOGLICEMIA
ADRENERGIC DISCHARGE PICTURE:
– PALPITATIONS/ TACHYCARDIA– ANXIETY– SWEATING– TREMULOUSNESS– HUNGER
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