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PATHOGENESIS OF
HYPEREMESIS
GRAVIDARUM
The etiology of hyperemesis in pregnancy is
multifactorial.
Usually seen in first trimester of pregnancy.
HORMONAL
BIOLOGICAL
ENVIRONMENTAL
HORMONAL:
Mainly related to high rising serum levels of
beta HCG.
During 8-12 weeks of gestation, beta HCG levels
are highest at that time and decline afterwards.
Also common in multiple pregnancies and
gestational trophoblastic disease due to very
high levels of beta HCG.
Hyper emesis
Also related to rising levels of other hormones
such as estrogen, progesterone, leptin,
placental growth hormones, prolactin and
adrenocortical hormones.
Metabolic,Biochemical and
Circulatory changes:
Metabolic:
Inadequate intake of food results in glycogen
depletion,hence the fat reserve is broken down
for energy supply.
Due to low carbohydrate,there is incomplete
oxidation of fat and accumulation of ketone
bodies in the blood.The acetone is ultimately
excreted through the kidneys and in
breath.There is also increase in endogenous
tissue protein metabolism resulting in excessive
excretion of non-protein nitrogen in the urine.
Water and electrolyte metabolism are seroiusly
affected leading to biochemial and circulatory
changes.
Biochemical:
 Loss of water and salts in the vomitus results in fall in
plasma sodium,potassium and chlorides.
 The urinary chloride may be well below the normal
5gm/dl or may even be absent.Hepatic dysfuction
results in acidosis and ketosis with rise in blood urea
and uric
acid;hypoglycemia,hyponatremia;hypovitaminosis and
rarely hyperbilirubinemia.
Circulatory:
There is hemoconcentration leading to rise in
hemoglobin percentage.
RBC count and hematocrit values.There is slight
increase in white cell count with increase in
eosinophils.
There is concomitant reduction of extracellular
fluid.
Changes in various organs:
 LIVER-Centrilobular fatty infiltration without necrosis.
 KIDNEYS-Fatty change in the cells of first convoluted
tubule.
 HEART-Small heart;Sub-endocardial hemorrhage.
 BRAIN-Small hemorrhages in the hypothalamic region
giving the manifestation of Wernicke’s
encephalopathy;Vitamin B1 defeciency.
REFERENCE:
Williams Obstetrics- 24th Edition
D.C.Dutta’s Textbook of Obstetrics

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Hyper emesis

  • 2. The etiology of hyperemesis in pregnancy is multifactorial. Usually seen in first trimester of pregnancy.
  • 4. HORMONAL: Mainly related to high rising serum levels of beta HCG. During 8-12 weeks of gestation, beta HCG levels are highest at that time and decline afterwards. Also common in multiple pregnancies and gestational trophoblastic disease due to very high levels of beta HCG.
  • 6. Also related to rising levels of other hormones such as estrogen, progesterone, leptin, placental growth hormones, prolactin and adrenocortical hormones.
  • 7. Metabolic,Biochemical and Circulatory changes: Metabolic: Inadequate intake of food results in glycogen depletion,hence the fat reserve is broken down for energy supply.
  • 8. Due to low carbohydrate,there is incomplete oxidation of fat and accumulation of ketone bodies in the blood.The acetone is ultimately excreted through the kidneys and in breath.There is also increase in endogenous tissue protein metabolism resulting in excessive excretion of non-protein nitrogen in the urine. Water and electrolyte metabolism are seroiusly affected leading to biochemial and circulatory changes.
  • 9. Biochemical:  Loss of water and salts in the vomitus results in fall in plasma sodium,potassium and chlorides.  The urinary chloride may be well below the normal 5gm/dl or may even be absent.Hepatic dysfuction results in acidosis and ketosis with rise in blood urea and uric acid;hypoglycemia,hyponatremia;hypovitaminosis and rarely hyperbilirubinemia.
  • 10. Circulatory: There is hemoconcentration leading to rise in hemoglobin percentage. RBC count and hematocrit values.There is slight increase in white cell count with increase in eosinophils. There is concomitant reduction of extracellular fluid.
  • 11. Changes in various organs:  LIVER-Centrilobular fatty infiltration without necrosis.  KIDNEYS-Fatty change in the cells of first convoluted tubule.  HEART-Small heart;Sub-endocardial hemorrhage.  BRAIN-Small hemorrhages in the hypothalamic region giving the manifestation of Wernicke’s encephalopathy;Vitamin B1 defeciency.
  • 12. REFERENCE: Williams Obstetrics- 24th Edition D.C.Dutta’s Textbook of Obstetrics