Question

 

1. Diagnosis of Contraception initiation

a. Explain the pathophysiology of Contraception initiation

b. Therapeutic Regimen of Contraception initiation

c. What lab test is required to diagnosis the contraception initiation and explain why

2. Diagnosis Asthma

a. Explain the pathophysiology of Asthma

b. Therapeutic Regimen of asthma

3. Diagnosis bronchitis

a. Explain the pathophysiology of bronchitis

b. Therapeutic Regimen of bronchitis

c. Explain why the chest posteroanterior and lateral views are ordered for this diagnosis

4. Diagnosis esophageal atresia with G-tube

a. Explain the pathophysiology of esophageal atresia with G-tube

b. Therapeutic Regimen of  esophageal atresia with G-tube

d. Explain why EGD is ordered for this diagnosis

c. Explain why esophageal function study acid reflux is ordered for this diagnosis

Answer 1

1 a) pathophysiology of contraceptive initiation

Comprehension of hormonal regulation of normal menstrual cycle for contraception in women. The of menstruation begins with menarche usually around age 12 years and continue to occur in non pregnant women until menopause usually around 50 years of age. Factors such as body weight, medical condition and family history can effect the menstrual cycle. The cycle includes the vaginal discharge of sloughed endometrium called menses. The menstrual cycle has 3 phases a)follicular b)ovulatory c)luteal

b) Therapeutic regimen includes:

  progestine only pill

Emergency or post coital pill such as;

Levonorgestrol 0.75mg within 12 hours and second dose after 12 hours or levonorgestrol 1.5mg as single dose within 72 hours of sexual intercourse.

Combination of levonorgestrol (0.75mg) and ethinyl estradiol. Two doses at 12 hour interval within 72 hours.

Ulipristol 30mg as single dose as soon as possible.

Mefepristol 600mg as single dose taken within 72 hours or as early as possible after intercourse.

c) Laboratory tests:

  Before the contraception initiation, test for bp because oral contraceptives may increase the chance for hypertension and cardiovascular risk, glucose, lipids because of increased risk for CHD and there is chance for lipid and lipoprotein abnormalities, liver enzymes because it associated with one time or another with an increased risk of acute cholestasis, benign liver tumors, hepatocellular carcinoma, peliosis hepatis and hepatic vein thrombosis, thrombogenic mutations, cervical cytology, STD screening and HIV screening. But these tests does not contrinute substantially to safe and effective use method.

2 a) pathophysiology of asthma:

   Asthma can be classified as allergic and non allergic. Allergic asthma is caused due to allergents and is IgE mediated but non allergent asthma is caused due to other factors such as stress, exercise, viral infection etc. IgE antibodies are present on the surface of mast cell. When aperson is exposed to an allergent; the allergent binds to the IgE antibodies present on the durface of mast cell. For the first time there is no problem. On second exposure to the same allergent, the allergent binds with IgE antibody and there occurs the cross linking of adjacent antibodies and this results in degranulation of mast cell. This is followed by release of mediarors like histamine, leukotrienes, Eosnophilic chemotactic factor, Neutrophilic chemotactic factor.

Macrophages are also involved in inflammatory process. Macrophages release mediators such as thromboxaine, prostaglandin, PAF causing leakage of plasma from respiratory capillary resulting in mucosal edema.

PAF causes the accumulation of eosinophils in airways. They release mediators like leukotriene C4 etc. All these mediators together cause epithelial damage. Airways undergo structural changes due to hypertrophy and hyperplasia. This is called remodeling of airways. Hypertrophy of mucous glands leads to excess mucous secretion. But the mucocillary clearance remains normal and this results in accumulation of mucous in airways and cause broncho obstruction.

b) Therapeutic regimen of asthma:

Step 1: If patient shows mild symptoms, start the treatment with short acting beta 2 adrenergic agonist which is taken whenever necessary.

Step 2: If not controlled by SABA, then start short acting beta 2adrenergic agonist + low dose corticosteroids (maintenance dose)

Step 3: If not controlled by standard dose of corticosteroids, then start long acting beta 2adrenergic agonist + low dose corticosteroids or short acting beta 2adrenergic agonist + high dose corticosteroids.

Step 4: If not controlled, then start with short acting beta 2adrenergic agonist + high dose corticosteroids + addon therapy or long acting beta 2adrenergic agonist + low dose corticosteroids + addon therapy ( such as anti-cholinergics, oral bronchodilators, cromones)

Step 5: If not controlled by any of these, then go for long acting beta 2adrenergic agonist + low dose corticosteroids + oral corticosteroids or short acting beta 2adrenergic agonist + high dose corticosteroids + oral corticosteroids

3 a) pathophysiology of bronchitis:

  Chronic bronchitis is characterized with hypertrophy of mucous producing glands found in the lungs. There are several triggering factors that leads to bronchitis includes infectious agents such as virus and bacteria or non infectious agents such as smoking, environmental pollutions, dust can lead to wide spread inflammation in bronchial wall. Mucous lining of bronchi become irrant and swollen.

This leads to hypertrophy of globlet cells which thereby increase mucous secretion as a result stimulation of cough reflex. Also inflammation can lead to bronchial constriction as well so there occurs difficulty in breathing.

b) Therapeutic regimen of bronchitis:

First line:

Supportive; increased fluids ( cough results in increased fluid loss)

Antipyretic analgesics such as aspirin, acetaminophen, or ibuprofen

Decongestant if acaccompanied by sinus condition.

Cough suppressant for troublesome cough such as honey, benzonatate, guaifenesin with codeine or dextromethorphan. Not indicated in children age <6 years.

Mucolytic agents are not recommended.

Inhaled beta agonist (eg. Albuterol) or in combination with high dose inhaled corticosteroids for cough with bronchospasm in those with known airflow obstruction.

If influenza is highly suspected and symptom onset is <48 hours, then oseltamivir or zanamivir

Antibiotics only if treatable cause is identified. Such as;

Clarithromycin 500mg q12h or azithromycin

In patients with acute bronchitis of a suspected bacterial cause, azithromycin tends to be more effective in terms of lower incidence of treatment failure andbadverse events than amoxicillin.

Doxycycline: 100mg/ day × 10 days if Moraxella, Chlamydia, Mycoplasma suspected.

Quinolone for more serious infections or other antibiotic failure or in elderly or patients with multiple comorbidities.

Contraindication: Doxycycline and quinolones should not be used during pregnancy or in children.

Second line;

Other antibiotics if indicated by sputum culture.

c) The posteroanterior view are ordered for diagnosis so as to examine the lungs, mediastenum, bony thoracic cavity and great vessels.

The lateral view are ordered for diagnosis because to explore a retrostrenal or retrocardiac shadow or to confirm the presence of encysted fluid in the oblique fissure.

4 a) pathophysiology of esophageal atresia:

Esophageal atresia is characterized by incomplete formation of the esophagus. A fetus with esophageal Atresia cannot effectively swallow aminotic fluid.

Polyhydramnios leads to premature labour

If the baby is allowed to suck the aspiration of saliva or milk can lead to an aspiration pneumonitis. In baby with esophageal atresia and a distal TEF, the lungs may be exposed to gastric secretions. Also air from the trachea can pass down the distal fistula when the baby cries, strains, or receives ventilation. This condition can lead to over distention of abdomen which ultimately may cause gastric perforation which is often lethal.

b) Therapeutic regimen includes:

Preoperative management- The oropharynx should be cleared. The infants head should be elevated.

Oxygen therapy

IV fluids and nutrition

In infants with respiratory failure, endotracheal intubation should be performed.

Timing for surgical correction

a) Immediate primary repair;

An arterial PaO2>60mmHg in room air

Gap between proximal and distal esophageal pouch less than 2.5 cm.

b) Delayed surgical intervention

Severe prematurity

Associated with pneumonia, sepsis, or cardiac malformation

Gap between proximal and distal pouch is more than 2.5cm.

  

d) Esophagogastroduodenoscopy (EGD) is used to examine linings of esophagus, stomach, and upper part of small intestine inorder to identify esophagitis, intestial metaplasia, or gastric metaplasia.

c) Gastroesophageal acid reflux is extremely frequent in patients with esophageal atresia because of the serious structural and functional impairment. And it is often diagnosed after neonatal repair of this condition.