Hypoglicemia

HYPOGLICEMIAHYPOGLICEMIA

“NORMAL” PLASMA GLUCOSE LEVELS: 60-100 mgdl

“NORMAL VALUES “ DEPEND ON:– SEX– FEED OR FASTING STATE– TIME OF FASTING

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GLUCOSE CONTROL: INTERACTIONS BETWEEN– INSULIN LEVELS– COUNTERRREGULATORY HORMONES– GLUCAGON– EPINEPHRINE– CORTISOL– GROWTH HORMONE

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.

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.)

LACK OR DEFICIENCY OF INSULIN= HYPERGLICEMIA

EXCESS OF INSULIN OR DEFICIENCY OF COUNTER-REGULATORY HORMONES= HYPOGLICEMIA

DEFINITION: CONDITIONS IN WHICH GLUCOSE PLASMA LEVELS FALL BELOW “NORMAL” RANGES.

MECHANISM TO PRODUCE MECHANISM TO PRODUCE HYPOGLICEMIAHYPOGLICEMIA

ALTERED GLUCOSE UTILIZATIONALTERED GLUCOSE PRODUCTIONHORMONAL CHANGESENZYMES DEFICIENCIESGLUCOSE SUBSTRATE DEFICIENCIES

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.

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

FASTING HYPOGLICEMIAFASTING HYPOGLICEMIA

HYPERINSULINISM– INSULINOMA: PANCREATIC BETA CELL

TUMOR. – 90 % ARE BENIGN– 10% ARE MALIGNANT (CANCER)

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

INSULINOMA TREATMENTINSULINOMA TREATMENT

SURGERY

STREPTOZOTOCIN

NESIDIOBLASTOSIS:

– INFANTS WITH HYPERINSULINISM– WITHOUT IDENTIFIABLE PANCREATIC

NEOPLASM.

NESIDIOBLASTOSISNESIDIOBLASTOSIS

HISTOLOGY:

– INCREASE IN BETA CELL MASS, DERIVED FROM DUCTAL EPITHELIUM.

NESIDIOBLASTOSISNESIDIOBLASTOSIS

TREATMENT:

– PARTIAL OR TOTAL PANCREATECTOMY

– DIAZOXIDE

EXTRAPANCREATIC TUMORS ECTOPIC INSULIN PRODUCTION INSULIN / LIKE SYNTHESIS ACELERATED GLUCOSE CONSUMPTION INHIBITION OF THE LIVER TO RELEASE

GLUCOSE (GLYCOGENOLISIS OR GLUCONEOGENESIS)

MESENCHIMAL TISSUE DERIVED TUMORS:

– FIBROMAS– FIBROSARCOMAS– NEUROMAS

SOLID TUMORS:

– HEPATOMA– ADRENAL CARCINOMAS– G.I. CARCINOMAS

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

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

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 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.

POST-PANDRIAL POST-PANDRIAL HYPOGLICEMIA (REACTIVE) HYPOGLICEMIA (REACTIVE)

ALIMENTARY TYPE:G.I. SURGERY (RAPID GASTRIC

EMPTYING)*DUMPING SYNDROME (DIARRHEA,

POOR ABSORPTION)

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

CLINICAL PICTURENEUROGLYCOPENIC SIGNS AND

SYMPTOMS

ADRENERGIC DISCHARGE SIGNS AND SYMPTOMS

THE CLINICAL PICTURE DEPENDS ON:

– RATE AND SEVERITY OF HYPOGLICEMIC INSTALLATION

– INTEGRITY OF SIMPATHETIC SYSTEM

NEUROGLYCOPENIC PICTURE:– HEADACHE– MENTAL DULLNESS– CLOUDING OF VISION– FATIGUE– CONFUSION– HALLUCINATIONS– BIZARRE BEHAVIOR– SEIZURES– COMA– IRREVERSIBLE BRAIN DAMAGE

REMEMBER

BRAIN VULNERABILITY: BRAIN USE ONLY GLUCOSE AND KETONE BODIES AS ENERGY SOURCES.

ADRENERGIC DISCHARGE PICTURE:

– PALPITATIONS/ TACHYCARDIA– ANXIETY– SWEATING– TREMULOUSNESS– HUNGER

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