GIT disorders Flashcards

1
Q

What are the causes of hyperemesis gravidarum?

A
  • high HCG
  • estrogen & thyroid hormone may be involved

associated with
- multiple pregnancy
- molar pregnancy
- clinical hyperthyroidism

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2
Q

What is the clinical picture of hyperemesis gravidarum?

A
  • > 5% pre pregnancy weight loss
  • dehydration: pallor, hypotension, tachycardia
  • electrolyte imbalance: metabolic alkalosis
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3
Q

What are the effects of hyperemesis gravidarum on pregnancy?

A

on MOTHER
- Mallory Weiss tear
- VTE
- Wernicke’s enecephalopathy + Korsakoff psychosis

on BABY
- low birth weight
- fetal death

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4
Q

What is the cause of Wernicke’s encephalopathy?

A

Vitamin B1 thiamin deficiency

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5
Q

What are the sign & symptoms of Wernicke’s encephalopathy?

A

Symptoms
- blurred vision
- confusion
- unsteadiness
- memory problem

Signs
- nystagmus
- opthalmoplegia
- hyporeflexia

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6
Q

How is Wernicke’s encephalopathy diagnosed?

A

Clinically but can be confirmed by MRI

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7
Q

What are the investigations done for hyperemesis gravidarum?

A

Blood test
- CBC: leucocytosis, hemoconcentration
- electrolytes: hyponatremia, hypokalemia, metabolic alkalosis
- Liver Function Tests: abnormal in 50%
- Thyroid Function Tests: abnormal in 66%

Ultrasound
- gestational age
- number of fetuses
- exclude molar pregnancy

Urine
- ketonuria

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8
Q

How is hyperemesis gravidarum managed?

A

1- Emotional support & reassurance that it resolves by 20 weeks
2- Rehydration: IV normal saline solution with potassium chloride
3- Anti-emetics: H1 receptor antagonist, phenothiazine’s, dopamine antagonist (Metoclopramide), seretonin inhibitors (Odansetron
4- Steroids incase of vomiting refractory for treatment
5- thromboprophylaxis with LMWH
6- termination of pregnancy if not treated with anything

all women admitted with prolonged vomiting should be on thiamine supplementation

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9
Q

What is the management of hyperemesis gravidarum according to classification?

A

Mild
- small frequent meals
- ginger extract
- B6 (pyridoxine)

Moderate
- promethazine
- metoclopramide
- ondansetron
- prochlorperazine

Severe
- IV hydration with thiamine
- Parenteral: metoclopramide, ondasetron, promethazine

Intractable
- Chlorpromazine
- Methylprednisolone
- Enternal nutrition

LAST RESORT
- termination of pregnancy

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10
Q

What are the symptoms of intrahepatic cholestasis?

A

In second half of pregnancy
- pruritus without rash
- jaundice
- anorexia
- malaise

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11
Q

What is the mechanism of intrahepatic cholestasis?

A

increase in cholestatic effect of estrogen in genetically predisposed patients
- positive family history is found in 35%

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12
Q

What investigations should be done for intrahepatic cholestasis?

A
  • LFT: increased serum bile acids > 10 fold, increased AST, ALT, increased direct bilirubin
  • Coagulation profile: PT, APTT, INR
  • Liver ultrasound: exclude other causes (stones)
  • Viral serology: exclude HCV, HBV, CMV, HEV
  • Liver autoantibodies: exclude antimitochondrial, antismooth muscle antibodies

exclude all other causes of jaundice first

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13
Q

How is intrahepatic cholestasis managed?

A
  • for pruritis -> ursodeoxyxholic acid (UDCA)
  • enterohepatic circulation -> cholestyramine to decrease it
  • weekly LFT
  • Vitamin K for women with prolonged PT
  • fetal wellbeing monitoring
  • induce labor at 37 weeks
  • intensive monitoring during labor
  • neonate should receive vitamin K

fully reversible postpartum within 1-2 weeks

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14
Q

What are the effects of intrahepatic cholestasis on pregnancy?

A
  • fetal growth restriction
  • fetal death
  • preterm birth
  • fetal intracranial hemorrhage
  • postpartum hemorrhage
  • recurrence risk is 90%
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15
Q

What is the pathophysiology & prognosis of acute fatty liver in pregnancy?

A

dysfunction of fatty acid oxidation
- more in primigravida’s & male fetuses

life threatening third trimester complication
- 20% maternal mortality

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16
Q

What is the clinical presentation of acute fatty liver?

A

presents after 30 weeks with gradual onset of
- vomiting
- jaundice 2 weeks after symptom onset & fever
- epigastric pain
- hypertension
- acute kidney injury
- fulminant hepatic failure
- coagulopathy & encephalopathy

17
Q

What investigations are preformed for acute fatty liver?

A
  • increased liver enzymes
  • rule out other diagnosis
  • HYPOGLYCEMIA & INCREASED SERUM AMMONIA (characteristic)
  • hyperuricemia
  • coagulopathy
  • proteinuria
18
Q

How is acute fatty liver managed in pregnancy?

A

1- ICU with acute IV hydration & monitoring
2- immediate delivery
3- coagulopathy treated with FFPs (acute) & vitamin K (maintenance)
4- glucose containing solutions 10% or 50% to treat hypoglycemia
5- low threshold for antibiotic therapy to guard against sepsis
6- liver transplant in patients with fulminant hepatic failure

19
Q

What is the cause of gallstones in pregnancy?

A

increased estrogen hormone
- 3 - 8% form stones during pregnancy
- occur in multiparous women 19% & in 8% of nulliparous

20
Q

What is the clinical picture of acute cholecystitis?

A
  • acute upper abdominal pain in the epigastric or right hypochondrial region
  • pain radiates to tip of right shoulder
  • positive Murphy’s sign
  • nausea
  • vomiting
  • indigestion
  • fever
21
Q

How is acute cholecystitis diagnosed?

A
  • ultrasound -> detects stones & thickening of gallbladder wall
  • FBC -> high TWBCs
  • abnormal liver function test
  • mildly elevated amylase level
22
Q

How is acute cholecystitis managed?

A

Conservative
- NPO, nasogastric aspiration
- IV fluids, antibiotics & analgesics
- 75% resolve

Surgery
- laparoscopic cholecystectomy -> second trimester