Bromley Emergency

Answer.

C

Explanation.

The anatomy of the larynx is complicated. It lies inferior to the hyoid bone, anterior to the lower pharynx and joins to the top of the trachea at C6 level.

 Three unpaired cartilages make up its external form:

(1) epiglottis (a flap of elastic cartilage covered by mucous membrane which is attached to the anterior thyroid cartilage)

(2) thyroid cartilage; and

(3) cricoid cartilage (most inferior and separated from the thyroid cartilage above by the cricothyroid membrane).

The three paired cartilages (the arytenoids, corniculate and cuneiform) are smaller, located posteriorly within the larynx, and function in movement of the vocal cords.

The extrinsic muscles of the larynx (infrahyoid, suprahyoid and stylopharangeus) move the larynx as a whole during swallowing. The intrinsic muscles (the arytenoids, cricoarytenoids, thyroarytenoids and cricothyroid) abduct, adduct, relax and tense the vocal cords during speech and respiration. The vocal cords are relaxed and abducted during respiration and adducted and tensed during phonation.

During swallowing the backward movement of the tongue and upward movement of the larynx forces the epiglottis down over the superior laryngeal opening to prevent swallowed matter from entering the trachea. 

The vagus nerve (CN X) provides motor and sensory innervation to the larynx via its superior laryngeal branch (motor to cricothyroid and sensory to the superior larynx above the vocal cords), and its recurrent laryngeal branch (motor to all the intrinsic muscles of the larynx except cricothyroid and sensory to the larynx below the vocal cords).

Answer.

The answer is b. Alveolar ventilation and gas exchange are both reduced in a pulmonary shunt, while the alveolar-arterial (A-a) gradient is increased.

Explanation.

A pulmonary shunt is a volume of lung with adequate perfusion but poor or absent ventilation. This creates regions of little or no gas exchange so that blood leaving the shunt remains de-oxygenated. When the deoxygenated blood from the shunt mixes with the oxygenated blood from rest of the lung, it lowers the overall arterial oxygen concentration (PaO₂) and if the shunt is large enough, cause systemic arterial hypoxia.  Shunts may be as small as a few alveoli in a tiny patch of atelectasis or large as an entire lung. A common cause of pulmonary shunting is pneumonia where the alveoli fill with inflammatory fluid (consolidation).

The alveolar-arterial (A-a) gradient is a measure of the difference between the alveolar concentration of oxygen (PAO₂) and the arterial concentration of oxygen (PaO₂): A-a gradient = PAO₂ – PaO₂. Now, the ‘ideal’ alveolar oxygen concentration (PAO₂) calculated by the alveolar gas equation is largely unaffected by pulmonary shunts while the arterial oxygen concentration (PaO₂) measured by blood gas analysis is markedly reduced, resulting in an increase in the A-a gradient.

Dead space refers to areas of lung that are ventilated but not perfused (the opposite of a shunt) and therefore shunts do not affect dead space.

Answer.

The answer is b. 

Explanation.

Lithium is a monovalent cation used in the treatment of bipolar disorder, depression and Schizoaffective disorders.

When administered orally it is fully absorbed from the gut with peak levels 4 hours after ingestion. It has a narrow therapeutic index and toxicity is common. Hence patients on lithium require monitoring with blood taken for serum lithium levels 12 hours after the last dose.

Lithium is not metabolised at all by the liver and so enzyme inducers and inhibitors have no effect on levels. It is, however, almost entirely eliminated via the kidneys so that pre-existing renal impairment as well as concomitant use of nephrotoxic drugs (diuretics, ACE inhibitors and NSAIDS) are causes of lithium accumulation and toxicity. Symptoms of lithium toxicity are mostly GI (nausea, vomiting and diarrhoea) and, with more serious poisoning, neurological (tremor, ataxia, confusion and coma).

Lithium inhibits the action of anti-diuretic hormone (ADH) in the collecting duct of the kidney and is a well-recognised cause of nephrogenic diabetes insipidus. It also causes hypothyroidism of varying degrees in around 1 in 5 patients.

Answer.

The answer is a. Methaemoglobinaemia

Explanation.

Pulse oximetry measures the ratio of oxygenated to de-oxygenated haemoglobin in arterial blood using their differential absorption of red and infrared light. It reports the result as a percentage oxygen saturation of a patient’s blood.

Pulse oximetry only measures oxygenated and deoxygenated haemoglobin and may give falsely high readings in the following circumstances:

• Methaemoglobinaemia (MetHb). MetHb contains an oxidised form of haemoglobin, ferric (Fe3⁺) Hb which cannot bind oxygen. In the presence of MetHb, therefore, the average haemoglobin oxygen saturation is reduced causing cyanosis and low saturations as measured by pulse oximetry. Arterial blood gas analysis does not take into account the presence of methaemoglobin and so shows high PaO₂ levels, reflecting the near full saturation of normal ferrous (Fe²⁺) Hb, even in the presence of cyanosis.
• Carbon monoxide has a much higher affinity for haemoglobin than oxygen, causing a cherry red appearance of the skin and falsely high pulse oximetry readings.
• Cyanide interferes with the dissociation of oxygen from haemoglobin in tissues, and while the high pulse oximeter readings in cyanide poisoning reflect the true state of haemoglobin oxygen saturation, they do not reflect at all the profound hypoxia occurring at the tissue level.

Falsely low pulse oximeter readings may arise from, motion artefact, venous congestion, tachycardia, poor tissue perfusion and opaque nail polish (of any colour!).

Answer.

The correct answer is e. Dopamine and prostaglandins both increase renal blood flow.

Explanation.

Renal blood flow is highly auto regulated and maintained at about 25% of cardiac output (or 1.2-1.3L/min for a 70kg adult). Renal blood flow depends on renal vascular resistance as well as on systemic arterial and venous pressures.

Circulating factors which increase renal blood flow include:

• Dopamine: Vasodilation of renal vessels
• Prostaglandins: Increases renal blood flow by vasodilating afferent* arterioles particularly at times of renal hypoperfusion (hence the nephrotoxic effect of NSAIDS which inhibit prostaglandin synthesis)
• Atrial natriuretic peptide (ANP) also vasodilates afferent renal vessels to promote promote glomerular filtration and reduce blood volume.

Those which reduce renal blood flow include:

• Angiotensin II: Vasoconstriction of both afferent and efferent arterioles*, though with greater effect on efferent vessels to increase glomerular filtration
• Norepinephrine: Vasoconstriction.

Local factors: CO₂, lactate, H⁺, K⁺, hypoxia all vasodilation renal vessels and increase renal blood flow.

[* afferent arterioles branch from the renal artery and supply blood to the glomerulus; efferent arterioles remove blood from the glomerulus and supply it to the capillaries of the renal medulla (vasa recta) and renal cortex.]

Answer.

The answer is b.

Explanation.

NICE Defines anaphylaxis as “a severe, life-threatening, generalised or systemic hypersensitivity reaction. It is characterised by rapidly developing, life-threatening problems involving: the airway (pharyngeal or laryngeal oedema) and/or breathing (bronchospasm with tachypnoea) and/or circulation (hypotension and/or tachycardia). In most cases, there are associated skin and mucosal changes.” It is a type I hypersensitivity reaction.

Anaphylaxis requires pre-sensitisation. During the initial exposure to an antigen, antigen specific IgE is produced and attached to the surface of mast cells. During  subsequent exposure(s), the antigen binds and crosslinks surface IgE triggering  mast cell degranulation and release of inflammatory mediators most notably histamine but also serotonin, bradykinin and others. This may occur locally and cause a local inflammatory condition (allergic rhinitis for example) or systemically where the inflammatory response causes the life threatening features of anaphylaxis.

Mast cells are produced by the bone marrow from where they migrate to many different body tissues. They are found in high number in sub-epithelial (sub-cutaneous and sub-mucosal) tissues and around blood vessels and nerves.  Hence, skin rashes (hives), swelling (angioedema), bronchospasm and vascular changes are prominent.

In many cases of anaphylaxis, an initial immediate reaction is followed by a late phase reaction, usually 2-8 hours after the initial exposure (rarely up to 24 hours). This late phase reaction happens due to the infiltration of tissues with eosinophils, basophils, neutrophils, monocytes and CD4+ T cells.