EDAIC 1 MCQs from the daily-MCQ zone. Weekly free uploads by targetedaic.

A. abdominal pain
B. COPD
C. ankylosing spondylitis
D. thoracic surgery
E. spinal anaesthesia

A. TRUE B. TRUE C. TRUE D. TRUE E. FALSE

The pathophysiology of post-op atelectasis is not fully understood. However, current theories suggest that airway collapse is due to a combination of airway compression, alveolar gas resorption intra-operatively, and impairment of surfactant production. The combination of general anaesthesia, supine positioning, opiates, and residual neuromuscular block reduces lung volumes and causes atelectasis in a spontaneously ventilating patient. This typically developing within 24 hours of surgical intervention.

The main risk factors for developing atelectasis in the surgical patient include:

1. Age > 60 years
2. Smoking, Lung pathologies
   1. COPD,
   2. Asthma
   3. ANKYLOSING SPONDYLITIS may result in fibrosis of the upper lobes, interstitial lung disease, ventilatory impairment due to chest wall restriction, sleep apnea, and spontaneous pneumothorax.
3. Obesity
4. Use of general anaesthesia, muscle relaxants, opioids, sedatives
   1. o SAB avoids all these predispositions towards post-op atelectasis. Unless the block is very high and impairs respiratory mechanics by weakening intercostal muscles, it is highly unlikely to result in atelectasis.
5. Duration of surgery > 2 hours
6. Type of surgery: upper abdominal, thoracic, laparoscopic, emergency
7. Pre-existing lung or neuromuscular disease
8. Prolonged bed rest (especially with limited position changes)
9. Poor post-operative pain control (resulting in shallow breathing)

The diagnosis of atelectasis is typically clinical, especially in the post-operative patient who has developed respiratory symptoms within 24hrs of surgery.

A CXR can reveal small areas of airway collapse. If inconclusive and warranting further investigation, CT imaging can have good sensitivity in identifying airway collapse and reduced airway volume (although they are rarely performed for such an indication)

Management

The most effective treatments for atelectasis are deep breathing exercises and chest physiotherapy. This ensures that the airways are opened maximally and coughing can be performed effectively.

As an adjunct, ensure that the patient has adequate pain control to allow them to deep breathe.

If no significant improvement is seen following physiotherapy, bronchoscopy may be required to aid in suctioning out pulmonary secretions, however, is not routinely performed.

A. salbutamol
B. ketamine
C. adrenaline
D. sodium cromoglycate
E. atropine

A. TRUE B. TRUE C. TRUE D. FALSE E. FALSE
Management of acute asthma includes

ABC should be assessed and actions are taken without further delay. Check for hypoxaemia, hypovolaemia, acidosis, and hypokalaemia.

OXYGEN
Keep SpO2 >92%. A FiO2 of 0.4–0.6 is often sufficient but, in general, start high and then titrate the FiO2 down.

NEBULIZED Β2 AGONISTS
Short-acting β2-agonists (e.g. salbutamol) should be given repeatedly in 5 mg doses or by continuous nebulization at 10 mg h−1 driven by oxygen. An alternative is a metered-dose inhaler, preferably with a spacer. 5-10 puffs should be given initially
Inhaled longer-acting β2-agonists have no role in the management of acute severe asthma and may increase mortality in this setting.

NEBULIZED IPRATROPIUM BROMIDE
This should be added to nebulized β2 agonists treatment for all patients with life-threatening asthma (500 µg 4 hourly) as it has been shown to produce significantly greater bronchodilation than β2 agonists alone. Side effects are minimal.
Many studies confirm the efficacy of atropine in reversing acute bronchoconstriction, but its routine use is limited due to side effects at required doses. Moreover, the addition of atropine adds no benefit over and above beta-agonists. Atropine though effective is not appropriate therapy for acute asthma.

STEROIDS
Systemic steroids (intravenous/oral) should be given to all patients with life-threatening asthma, as early as possible in the episode as this may improve survival. The intravenous route should be used (hydrocortisone 200 mg stat followed by 100 mg 6 hourly). Inhaled/nebulized steroids do not provide additional benefit.

INTRAVENOUS MAGNESIUM SULPHATE
A single intravenous dose of magnesium sulphate 1.2–2 g over 20 min has been shown to be safe and effective in acute severe asthma. However, hypermagnesaemia is associated with muscle weakness and may exacerbate respiratory failure in spontaneously breathing patients.

INTRAVENOUS BRONCHODILATORS
Parenteral β2 agonists, in addition to nebulized β2 agonists, should be considered in ventilated patients and those with life-threatening asthma.
An additional or alternative intravenous bronchodilator is aminophylline. Some patients with life-threatening asthma gain benefit from its intravenous use (5 mg kg−1 loading dose over 20 min unless on maintenance oral therapy, then infusion of 0.5–0.75 mg kg−1 min−1). Concern and controversy about its use arise from its side effects (arrhythmias, restlessness, vomiting, and convulsions) related to a narrow therapeutic window. Trials showing little overall benefit in lesser degrees of asthma may not be relevant when faced with impending asphyxia. Plasma aminophylline concentrations should be monitored frequently (therapeutic range 10–20 µg ml−1).

EPINEPHRINE
The additional use of epinephrine (adrenaline) should be considered in patients not responding adequately to the measures outlined above via the subcutaneous (0.3–0.4 ml 1:1000 every 20 min for three doses), nebulized (2–4 ml of 1% solution hourly) or, in extremis, the intravenous route (0.2–1 mg as a bolus followed by 1–20 µg min−1).

INHALATIONAL ANAESTHETIC AGENTS
Volatile inhalational anaesthetic agents (e.g. isoflurane and sevoflurane) are effective bronchodilators. Prove an effective strategy when bronchospasm happens under GA. Usefulness in intensive care is limited by lack of expertise and non-availability of resources.

INTRAVENOUS ANAESTHETIC AGENTS
Most of the studies showed improved outcome with the use of ketamine in acute severe asthma unresponsive to conventional treatment. this is particularly helpful in resistant cases of spasm in children where ketamine is usually the preferred sedative agent owing to its excellent safety profile and bronchodilatory effect.

INTUBATION AND MECHANICAL VENTILATION WITH AID OF MUSCLE RELAXANTS MAY BE REQUIRED IN RESISTANT CASES.

EXTRA-CORPOREAL SUPPORT MAY PROVE LIFE-THREATENING IN TIDING OVER THE ACUTE CRISIS.
Sodium cromoglycate is a medicine used to prevent the symptoms of asthma. When it is used regularly, this medicine lessens the number and severity of asthma attacks by reducing inflammation in the lungs. Sodium cromoglycate is called a “preventer” medicine

A. congestive cardiac failure
B. pericardial effusion
C. mitral valve disease
D. hypertrophic subaortic stenosis
E. hiatus hernia

A. TRUE B. TRUE C. TRUE D. TRUE E. TRUE

Enlargement of the cardiac silhouette on a frontal chest x-ray can be due to several causes. Recognizing enlargement relies upon an understanding of the normal cardiomediastinal outline and normal cardiothoracic ratio. THE normal CT ratio is <2.

Differential diagnosis:

1. Cardiomegaly (most common cause by far)
   1. Congestive heart failure
   2. Valvular lesions (mitral regurgitation causes left atrioventricular enlargement while stenosis causes LA enlargement)
   3. Coronary artery disease
   4. Hypertension
   5. Kidney diseases
   6. infective conditions (HIV)
   7. Alcohol or cocaine abuse
   8. Peripartum cardiomyopathy – Heart enlarging in pregnant women at the time of delivery
   9. Genetic and inherited conditions
   10. Idiopathic dilated cardiomyopathy – No known cause
2. Pericardial effusion
3. Anterior mediastinal mass
4. Prominent epicardial fat pad
5. Expiratory radiograph
6. AP projection (e.g supine radiographs taken with a portable machine)

Chest radiographic findings In hypertrophic subvalvular aortic stenosis can vary from normal to an enlarged heart. Chest radiographs are more useful in identifying complications of cardiomyopathy, such as pulmonary oedema The typical radiograph is of a well-defined, rounded, retrocardiac opacity with an air-fluid level. They can even give the appearance of cardiomegaly. In this radiograph, the cardiac silhouette is distinctly visible within the confines of the hiatal hernia.

A. diminished venous return to the right heart
B. diminished left ventricular performance due to shift of the intraventricular septum
C. increased right ventricular afterload
D. decreased heart rate
E. carbon dioxide retention

A. TRUE B. TRUE C. TRUE D. FALSE E. TRUE

PEEP increases intrathoracic pressure, which is transmitted to central veins and the right atrium, decreasing right ventricular preload. The fall in the preload/ venous return (and subsequently right ventricular cardiac output) eventually manifests as a decrease in LV Cardiac output and systemic tissue oxygen delivery.

Left ventricular compliance is decreased by a leftward shift of the interventricular septum.

PEEP, by causing a dilatation of the right ventricle (as a result of increased right ventricular afterload) supposedly causes the interventricular septum to bulge into the left ventricle during diastole (because the LV end-diastolic pressure ends up being less than the RV end-diastolic pressure).

As a result, left ventricular preload is decreased even more, and cardiac output decreases.
PEEP modifies pulmonary vascular resistance (PVR), and thus RV afterload. It has a biphasic effect on the PVR and thus the RV afterload.

First, PEEP may reduce PVR by reducing increased pulmonary vasomotor tone due to hypoxic pulmonary vasoconstriction as PEEP recruits collapsed alveoli, thereby increasing regional alveolar pO2, hypoxic pulmonary vasoconstriction is reduced, the pulmonary vasomotor tone falls, and RV ejection will improve.

As lung volume increases from residual volume to FRC, PVR decreases and vascular capacitance increases. As lung volume continues to increase from FRC to total lung capacity, PVR increases and vascular capacitance decreases. Thus, RV afterload increases and output decreases.

Intra-alveolar vessels are compressed as lung volume increases, while extra-alveolar vessels are exposed to expanding forces when lung volume increases. At lung volumes below FRC, the effects on extra-alveolar vessels predominate and PVR decreases. As lung volume increases above FRC, effects on intra-alveolar vessels predominate and PVR rises again.
PEEP may lead to carbon dioxide retention and hypercapnic acidosis, which may adversely affect RV performance by inducing pulmonary arteriolar vasoconstriction.

Though PEEP has no remarkable effect on HR, and the fall in CO is entirely the result of the decreased preload and increased RV afterload along with deranged LV mechanics. Though, the irritation of alveolar wall receptors due to overstretching and compensatory reflexes due to hypotension may cause tachycardia.

A. lingual nerve
B. trigeminal nerve
C. lateral femoral cutaneous nerve
D. lumbar sympathetic nerve
E. femoral nerve

A. FALSE B. FALSE C. TRUE D. FALSE E. FALSE

Meralgia paresthetica meros (thigh) and algos (pain), also called Bernhardt-Roth syndrome, is a SENSORY MONONEUROPATHY characterized by tingling, numbness and burning pain in the patient’s outer thigh. The aetiology of meralgia paresthetica is compression/trapping/injury of the lateral femoral cutaneous nerve. The most common site is compression of the nerve below the inguinal ligament as it crosses the anterior superior iliac spine. The lateral femoral cutaneous nerve is purely a sensory nerve supplying the upper outer thigh and doesn’t affect muscle power or function directly.

Tight clothing (including pants, stockings, a belt, or girdle), Wearing a heavy tool belt, obesity or weight gain, and pregnancy are common causes of meralgia paresthetica. However, meralgia paresthetica can also be due to local trauma or a disease, such as diabetes.

SYMPTOMS: ARE MILD, TO BEGIN WITH, BECOMING SEVERE WITH THE PASSAGE OF TIME. USUALLY FELT UNILATERAL.

Pain, tingling, numbness, or burning in the outside of your thigh
Sensitivity to light touch rather than to firm pressure
High sensitivity to heat
Pain may be worse after you’ve been walking or standing for a time
Severe cases have frequent bursts of sharp, shooting pain that lack a predictable pattern.

TREATMENT:

Wearing looser clothing.
Losing excess weight.
Taking OTC pain relievers such as acetaminophen, ibuprofen.

IF SYMPTOMS PERSIST FOR MORE THAN TWO MONTHS OR YOUR PAIN IS SEVERE, TREATMENT MIGHT INCLUDE:

Corticosteroid injections.
Tricyclic antidepressants.
Gabapentin, phenytoin or pregabalin
Fluoroscopic or USG guided nerve block
Rarely, surgery to decompress the nerve is considered.
Download targetedaic course modules for a confusion-free and effective exam preparation. Our modules are based on syllabus and frequently asked questions in MCQ and viva examinations. The modules are designed to be one-point reference for all your study needs for a topic. Modules are available as separate chapters and combined system-based modules for your convenience and to suit your need. Feel free to contact us for any queries.