EDAIC/ FRCA MCQs from the daily-MCQ zone. Weekly free uploads by targetedaic (4).

A. administration of sodium bicarbonate
B. intravenous diazepam
C. aminophylline infusion
D. intubation and ventilation
E. nebulised salbutamol

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

INTERVENTIONS PROVEN TO BE HELPFUL IN THE MANAGEMENT OF CHILDREN WITH SEVERE ACUTE ASTHMA INCLUDE:

OXYGEN SUPPLEMENTATION: Different degrees of hypoxia are almost always present during an acute asthma attack, depending on the severity of the episode. Humidified oxygen therapy using a tight-fitting face mask or nasal cannula should be administered to children with a severe acute asthma attack and/or SpO2 < 92%. The given child with severe attack would need intubation to maintain the airway and mechanical ventilation support to treat hypoxia and hypercarbia.
BETA-2 AGONISTS: inhaled or intravenous beta-agonists are indispensable in the acute management of asthmatic attack. Inhaled short-acting ß2 agonists are the first-line treatment for an acute asthma attack in children. Salbutamol is a useful medication that can be used in children of all ages. In a severe attack, it should be administered frequently, up to 3 times every 20–30 min within the first hour.
Salbutamol could be administered intravenously (iv) in children with asthma attack not responding to initial therapy. The recommended dose is a single bolus of 15 μg/kg over 10 min, followed by a continuous infusion of 0.2 μg/kg /min. Higher doses (1–2 μg/kg/min up to 5 μg/kg/min) can be administered in unresponsive children. Intravenous salbutamol should be given in the ICU with continuous ECG and twice-daily electrolyte and lactate monitoring.
IPRATROPIUM BROMIDE: It induces a slower bronchodilator response than ß2 agonists, but combining the two medications produces a synergic effect. In a severe attack, the recommended nebulized dose is 125–250 μg/dose (in children < 4 years of age) to 250–500 μg/dose (in children ≥ 4 years of age), in combination with nebulized salbutamol. It should be administered frequently, up to 3 times every 20–30 min, within the first hour. After that, the ipratropium dose should be tapered to 4 to 6 hourly or discontinued. Once ipratropium bromide is discontinued, salbutamol dose should be tapered to one- to two-hourly thereafter according to clinical response.
STEROIDS: Systemic steroids (SS) have been reported to be effective in treating acute asthma attack in children, with no difference between oral or intravenously/intramuscular route of administration. Inhaled corticosteroids should not be used when the systemic route is used.
AMINOPHYLLINE use is not recommended in mild to moderate acute asthma attacks. It can be used in severe and life-threatening attacks under strict vigilance.
Sodium bicarbonate adds to the carbon dioxide burden and can worsen hypercarbia and acidosis, particularly in absence of effective ventilation. Assisting ventilation, maintaining oxygenation and carbon dioxide elimination are critical in managing asthma induced acidosis.
The child is already drowsy with depressed ventilation. diazepam use will exacerbate the respiratory depression and low GCS.

A. is associated with avascular necrosis of bone
B. is due to an alveolar oxygen deficit
C. is cured by breathing a mixture of oxygen and helium at atmospheric pressure
D. symptoms can occur four hours after the initial drop in pressure
E. is avoided if nitrogen is included in the inspired gas mixture

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

Decompression sickness also called generalized barotrauma or the bends refers to injuries caused by a rapid decrease in the pressure surrounding you (of either air or water). It occurs most commonly in scuba or deep-sea divers, although it also can occur during high-altitude or unpressurized air travel. However, decompression sickness is rare in pressurized aircraft, such as those used for commercial flights.
Decompression sickness is due to the supersaturation of the tissue with dissolved gas (breathed under pressure) and the subsequent evolution of gas bubbles when the isobaric surroundings are restored. Nitrogen makes up 70 per cent of the air we breathe. Large amounts of nitrogen are taken into the body’s tissues during a dive because the diver is breathing air at a higher pressure than at the surface. The more the nitrogen, the more the bubbling; hence avoiding/using low nitrogen in the inspiratory gas mixture (oxygen-helium mix, oxygen-helium-nitrogen mix) can help prevent bends. Breathing of oxygen or heliox (80/20) at 1 atm abs has a preventive effect on the development of DCS when compared with air-breathing; the effect of heliox seems to be superior to that of oxygen.
Symptoms of the Bends
• Joint pain
• Fatigue
• Itching and rashes
• Coughing and chest pain
• Dizziness and paralysis
• Unconsciousness
• Death
Dysbaric osteonecrosis is a type of avascular necrosis of the bone most commonly found in undersea divers and workers breathing compressed air or gas.
Most symptoms occur 24 hours after decompression but can occur up to 3 days after.
Prevention
• Ascending to the surface slowly (rate of 60 ft/min.)
• Spending time in a decompression chamber.
• Breathing a compressed air mixture of helium and oxygen with no nitrogen.
Treatment
• High flow oxygen, fluid and temperature management
• Recompression therapy (reinstating hydrostatic pressure/ hyperbaric conditions and slow/ graded decompression and breathing compressed oxygen-helium mix/Hyperbaric oxygen therapy.

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A. is characterised by dilated and hypertrophied LV
B. the pathogenesis involves rising wall stress and valvular regurgitation
C. is the leading cause of heart transplant in the elderly group
D. 1/3rd of all cases are idiopathic
E. can lead to systemic embolisation

DILATED CARDIOMYOPATHY
• It is the most common of all cardiomyopathies and, currently, the most common indication for cardiac transplantation in children and young adults.
Aetiology: 2/3rd are idiopathic.
• Genetic/ Familial cases follow the autosomal dominant pattern
• Myocarditis: coxsackievirus B infection
• Post-Ischemic/ hypertensive heart disease
• Others: peripartum, substance abuse, pheochromocytoma, Duchenne’s muscular dystrophy, chemotherapeutic drugs, radiation therapy.
Pathophysiology
An enlargement of the ventricular cavities without any increase in free wall thickness characterises DCMP (right/ left or a biventricular dilation). The dilation leads to forming a spherical shape and displacement of papillary muscles, which ultimately causes regurgitant lesions despite valve leaflets being normal(functional regurgitation).
Systolic dysfunction is the hallmark of DCMP. CO is initially maintained by increasing end-diastolic volume. As the disease progresses, marked LV dilatation occurs with normal or thinned out wall, causing valvular regurgitation and increased wall stress (as depicted by applying Laplace law)
CO falls as the disease progresses and circulatory failure ensues. The dilated ventricle becomes a nidus for blood stasis and thrombus formation.

A. sensitises the myocardium to adrenaline
B. is a butyrophenone derivative
C. is poorly soluble in water
D. causes bronchoconstriction
E. has a marked chronotropic effect

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

KETAMINE [2-(O-chlorophenyl)-2-methylamino cylohexanone] is a phencyclidine derivative.
• Has a chiral centre with two optical isomers (enantiomers), S(+) and R(-)
• Molecular weight: 238.
• The available solution has a pH: 3.5–5.5 with benzethonium chloride as a preservative
• Freely water-soluble
• pKa of 7.5.
• Ketamine has a high lipid solubility (5–10 times that of thiopental) and crosses the blood-brain barrier faster.
• It undergoes demethylation and hydroxylation of the cyclohexanone ring. The metabolites are conjugated and excreted in the urine. Norketamine has 20–30% of the activity of the parent compound.
CVS effects:
Ketamine produces a centrally mediated sympathetic response: tachycardia increased blood pressure and increased cardiac output. However, in the absence of autonomic control, ketamine has a direct myocardial depressant effect, which is usually overridden by this central response.
Respiratory effects
• A transient decrease in ventilation can occur after bolus administration.
• Ketamine is a bronchial smooth muscle relaxant, so it has a special role in intractable asthma. It improves pulmonary compliance and is as effective as halothane in preventing bronchospasm.
• Ketamine increases salivary secretions, which can produce potential problems in children by causing upper airway obstruction.
• Although swallowing, cough, sneeze, and gag reflexes are relatively intact with ketamine; silent aspiration can occur.

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• Infective endocarditis is most frequently caused by Staphylococcus aureus.
• Coagulase-negative staphylococci are the commonest bacteria isolated in the early prosthetic valve endocarditis.
• IV drug abuse is associated with a significant risk of IE.
• Infective endocarditis caused by Streptococcus bovis is associated with colonic cancer.
• Fungal infection is associated with large vegetations and negative blood cultures.

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

IE microbiology:
Bacterial
GRAM-POSITIVE ORGANISMS
Staphylococcus aureus (31–54%)
Methicillin sensitive staph aureus (MSSA): infects naïve valves, the main pathogen in community-acquired infection.
Methicillin-resistant staph aureus (MRSA): main pathogen in nosocomial infection, wound infection, permanent i.v. catheters, or surgical intervention in the previous 6 months. MRSA accounts for 23–31% of prosthetic-valve infections
Streptococcus viridens (17–26%)
Coagulase-negative Staphylococci: infects artificial valves, particularly within 6 months of surgery, accounting for 17% of prosthetic valve infections.
Streptococcus bovis (5-8%) common in bowel malignancy and mucosal lesions.
GRAM-NEGATIVE BACTERIA:
HACEK (Haemophilus parainfluenzae, Aggregatibacter aphrophilus, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) contribute towards 1.8-3% of cases, infecting native (2/3rd cases) and prosthetic valves (1/3rd) both.
Fungal infection (1-3%)
• Candida
• Aspergillus
More frequently seen in intravenous drug abusers, prosthetic valves and indwelling central venous catheters.
Fungal lesions are bulky with aggressive metastasis, perivalvular invasion, and embolization to large blood vessels. the blood cultures are frequently negative.
Less common pathogens
• Coxiella Brunetti
• Legionella
• Brucella
• Bartonella
• Chlamydia
Early-onset PVE is defined as that occurring within 60 days of surgery and it is usually a manifestation of healthcare-acquired infections. Staphylococcal aureus is the most common aetiology during this time period. Intermediate-onset PVE occurs from 60 to 365 days following valve replacement surgery overall, S. aureus is the most common pathogen
responsible for PVE, accounting for 23.0% of total cases. CoNS are the next most common group of organisms responsible for PVE, accounting for 16.9% of all cases, followed by enterococci at 12.8%.
Infective Endocarditis caused by Streptococcus bovis may usually be associated with gastrointestinal pathologies, particularly colon cancer. S. bovis endocarditis may cause higher rates of neurological complications and more extensive valvular destruction compared to other microorganisms

a. Diastole is an active, energy-consuming process
b. Diastolic time remains the same with increased heart rate
c. In the normal heart, only one-third of ventricular filling occurs before atrial
contraction
d. Atrial contraction is a part of diastole
e. Ventricular relaxation is a part of diastole

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

Diastole is a period of relaxation of the ventricles. It is divided into several sub-components
Isovolumetric relaxation
• Begins with the closure of Aortic and Pulmonary valves corresponding to S2 or second heartbeat.
• Atrioventricular valves (mitral and tricuspid) are closed.
• Ventricular pressure falls as ventricles relax after systole.
• Blood flows from SVC and IVC into the right atrium and pulmonary veins into the left atrium.
• Corresponds to steep downstroke in Ventricular pressure curve. The negative slope of the curve dp/dt denotes relaxation. It is increased by SNS stimulation/catecholamines (positive lusitropy)
• Cardiac relaxation is an active process requiring ATP for the active reuptake of calcium into SR. Incomplete reuptake causes diastolic dysfunction.
Rapid ventricular filling
• Begins with the opening of Atrioventricular valves.
• Blood flows rapidly from the filled atria into the ventricles causing the y descent in CVP trace due to rapid fall of atrial pressure.
• Ventricular pressures begin to rise.
At the onset of the cardiac cycle- Diastasis
➢ Atrial and ventricular pressures are both low: the whole heart is relaxed.
➢ Atrial pressures are still slightly higher and blood pours slowly from atria to ventricles across a small concentration gradient.
➢ Corresponds to: slow ventricular filling phase.
Late diastole: Atrial Contraction
• Corresponds to the P wave of ECG.
• Responsible for ⅕ of the ventricular filling (80% of ventricular filling has already passed into ventricles due to pressure gradient)
• Produces “a” wave in CVP trace (since there are no valves in SVC OR IVC, the atrial contraction reflects as a small pressure wave in the great veins)
• End diastolic pressure is <10mm Hg and is higher in the left than the right ventricle.
The diastolic time shortens with increased heart rate. The ratio of contraction time (systolic interval, SI) to relaxation time (diastolic interval, DI) increases as the heart rate increases. In a normal HR of 75/min, the period of contraction constitutes ∼34% of the cardiac cycle (RR interval). At 200 bpm, it increases to ∼53% of the cardiac cycle.

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a. Diastole is an active, energy-consuming process
b. Diastolic time remains the same with increased heart rate
c. In the normal heart, only one-third of ventricular filling occurs before atrial
contraction
d. Atrial contraction is a part of diastole
e. Ventricular relaxation is a part of diastole

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

Depolarising neuromuscular block
Depolarizing drugs are agonists at ACh receptors. Succinylcholine is the only depolarizing NMBD in clinical use. It is effectively two ACh molecules joined through the acetate methyl groups. The two quaternary ammonium radicals bind to the two α-subunits of one nicotinic receptor, and depolarization occurs. When voltage-sensitive sodium channels sense membrane depolarization (as a result of activation of the ACh receptors), they first open and thereafter close and become inactivated. The membrane potential must be reset before the sodium channels can be reactivated. This is a very rapid process with ACh (1 ms), as it is hydrolysed by acetylcholinesterase (AChE) within the synaptic cleft. However, succinylcholine is not metabolized by AChE, so a prolonged activation of the ACh receptors is produced. The sodium receptors at the end-plate and the prejunctional zone remain inactivated and junctional transmission is blocked. The muscle becomes flaccid.
Depolarization block is also called Phase I or accommodation block and is often preceded by muscle fasciculation. This is probably the result of the prejunctional action of succinylcholine, stimulating ACh receptors on the motor nerve, causing repetitive firing and release of neurotransmitter. Recovery from Phase I block occurs as succinylcholine diffuses away from the neuromuscular junction, down a concentration gradient as the plasma concentration decreases. It is metabolized by plasma cholinesterase (previously called pseudocholinesterase). Prolonged exposure of the neuromuscular junction to succinylcholine can result in (i) desensitization block or (ii) Phase II block.
Features of a depolarising block are:
• Non-competitive block.
• Absence of fade.
• Absence of post-tetanic facilitation.
• Not reversed by anticholinesterases.
• Prior use of a small defasiculating dose of NMDR can reduce fasciculations produced by Sch.
• Prior use of NDMR antagonises the block by decreasing the availability of Ach receptors.
Magnesium enhances the effect of non-depolarising muscle relaxants. High magnesium concentrations inhibit the release of acetylcholine from the presynaptic nerve terminal and enhance the effect of non-depolarizing neuromuscular blocking agents, while depolarization caused by Sch is by direct action on the post-synaptic cleft.