About Bromley Emergency

This author has not yet filled in any details.
So far Bromley Emergency has created 77 blog entries.

FRCEM Primary Revision Essentials: Five and five useful FOAMed articles for your FRCEM Primary revision!

frcem primary revision

FRCEM Primary Revision

Below is a list of ten educational modules, five from RCEM learning and five from Doctors.net.uk Education, which have a basic science focus and are useful for FRCEM primary revision. If you haven’t found RCEM learning before, it is a great free resource from the College and found at www.rcemlearning.co.uk/landing/.  Modules take about an hour to complete and can be added to your CPD folder! If you are not a member already you will need to register to view the Doctors.net.uk education modules. 

(more…)

FRCEM Primary Revision Essentials: Five and five useful FOAMed articles for your FRCEM Primary revision!2018-11-05T14:37:29+00:00

Core Physiology: A shunt too far.

Question.

Which one of the following statements is true regarding the pathophysiology of pulmonary shunts?

a. Alveolar ventilation and the alveolar–arterial (A-a) gradient are both increased
b. Alveolar ventilation and gas exchange are both reduced
c. Alveolar ventilation is decreased and dead space is increased
d. Alveolar ventilation is normal while perfusion is decreased
e. Alveolar ventilation and the alveolar–arterial (A-a) gradient are both unaffected.

 

 

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.

 

Core Physiology: A shunt too far.2018-11-05T14:41:50+00:00

Revision essentials: Five and five useful FOAMed articles for your FRCEM Primary revision!

FOAMed articles for your FRCEM Primary revision

Below is a list of ten educational modules, five from RCEM learning and five from Doctors.net.uk Education, which have a basic science focus and are useful for FRCEM primary revision. If you haven’t found RCEM learning before, it is a great free resource from the College and found at www.rcemlearning.co.uk/landing/.  Modules take about an hour to complete and can be added to your CPD folder! If you are not a member already you will need to register to view the Doctors.net.uk education modules. 

(more…)

Revision essentials: Five and five useful FOAMed articles for your FRCEM Primary revision!2018-11-02T17:29:54+00:00

Core Pharmacology: Understanding the adverse effects of Lithium.

Core Pharmacology lithium (Li)

Question.

Which one of the following statements regarding lithium (Li) is FALSE?

a. It has a narrow therapeutic range
b. Lithium levels are increased by drugs which induce cytochrome p450
c. Serum lithium levels for monitoring should be measured 12 hours after the last dose
d. Lithium inhibits the action of anti-diuretic hormone (ADH)
e. Hypothyroidism is a frequent adverse effect of lithium therapy

 

 

 

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.

Core Pharmacology: Understanding the adverse effects of Lithium.2018-11-02T17:25:54+00:00

Core physiology: When the pulse oximeter and blood gas disagree!

Question.

A normally well 17yr old woman is noted to have marked peripheral cyanosis. Pulse oximetry shows oxygen saturations of 79% though a follow up arterial blood gas records a normal Pa02. Which of the following conditions might explain the discrepancy between clinical signs, pulse oximetry and arterial PaO2?

a.

    1. Carbon monoxide poisoning

b.

    1. Methaemoglobinaemia

c.Red nail polish

d.Cyanide poisoning

e.Peripheral vasoconstriction

 

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!).

 

Core physiology: When the pulse oximeter and blood gas disagree!2018-11-02T17:19:03+00:00

Core Physiology: Hormones and renal blood flow

FRCEM Primary: Core Physiology: Hormones and renal blood flow

Question.

Renal blood flow is increased by which one of the following set of circulating hormones?

a.

    1. Dopamine and angiotensin II

b.

    1. Dopamine and renin

c.Angiotensin II and renin

d.Prostaglandins and angiotensin

e.Prostaglandins and dopamine

 

 

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.]

 

 

 

 

Core Physiology: Hormones and renal blood flow2018-11-02T17:21:32+00:00

Core pathology: Antigen and anaphylaxis.

Anaphylaxis Alert Wristband. Core Pathology Question

Question.

A young boy with known peanut allergy presents with an anaphylactic reaction after eating Thai food. Which one of the following statements is most true of the pathophysiology of this condition in this boy?

a.

    1. Antigen binding to surface IgM has triggered mast cell degranulation

b.

    1. Antigen binding to surface IgE has triggered mast cell degranulation

c.Antigen has directly stimulated neutrophil mediated inflammation

d.Antigen has directly stimulated mast cell degranulation

e.Antigen binding to surface Ig has triggered neutrophil degranulation

 

 

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.

 

 

Core pathology: Antigen and anaphylaxis.2018-11-02T17:11:19+00:00

Core Anatomy: Three heads with different moves.

Question.

Which of the following is true regarding the action of deltoid muscle?

a.

    1. It has two distinct parts

b.

    1. It is supplied by musculocutaneous nerve

c.It initiates abduction of the shoulder

d.It acts with latissimus dorsi to extends the shoulder

e.Abduction more than 30 degrees requires rotation of the scapula

 

Answer.

The answer is d. The posterior fibres of deltod assist latissimus dorsi in extending the shoulder (moving the arm backwards from the resting position).

Explanation.

Deltoid muscle:

  1. Origin: Lateral third of clavicle, acromion process and spine of scapula.
  2. Insertion: Deltoid tuberosity of humerus.
  3. Nerve supply: Axillar nerve (C5,6)
  4. Action: Flexion, extension and abduction of shoulder.

Deltoid is a triangular muscle covering the rounded tip of the shoulder. It has three distinct sets of fibres (parts); the anterior, lateral and medial fibres. The three parts work together to abduct the shoulder. Individually the anterior and posterior fibres flex and extend the shoulder respectively.

Supraspinatus initiates abduction of shoulder up to about 15 degrees. The greater power of deltoid then takes over to further abduct the arm.  Lateral rotation of the scapula facilitates abduction beyond 90 degrees.

Core Anatomy: Three heads with different moves.2018-11-02T17:09:15+00:00

Microbiology essentials: Pelvic inflammatory disease

Question.

A young woman presents with a recurrence of her pelvic inflammatory disease (PID). Which one of the following is FALSE regarding this presentation?

a.

    1. Group B streptococcus is the most common cause

b.

    1. Chlamydia and gonorrhoea may be vertically transmitted

c.The risk of ectopic pregnancy is increased

d.She may also complain of right upper quadrant pain

e.Tubo-ovarian abscess is a complication

 

Answer.

The answer is a. Group B streptococcus is a rare cause of PID.

Explanation.

Pelvic inflammatory disease (PID) describes infection of the female upper genital tract (uterus, fallopian tubes and ovaries).

It results from ascending infection from sexually transmitted pathogens with Chlamydia trachomatis the most frequent causative pathogen; gonorrhoea is on the rise and becoming more common as a cause of PID. Many cases are polymicrobial.

Transmission of an infectious disease from mother to baby, either across the placenta or during childbirth is called vertical transmission. The classic vertically transmitted infections are the TORCH infections (though there are many more):

 

  • Toxoplasmosis
  • Other (chlamydia, gonorrhoea, Group B streptococcus)
  • Rubella
  • Cytomegalovirus, Chickenpox (VZV)
  • Herpes simplex virus

Scarring of the fallopian tubes from chronic PID increases the risk of both infertility and ectopic pregnancy. Other complications are tubo-ovarian abscess and sepsis.

An often overlooked complication of PID is transabdominal spread causing perihepatitis (the Fitz-Hugh-Curtis syndrome) which gives right upper quadrant pain and signs of systemic inflammation.

 

Microbiology essentials: Pelvic inflammatory disease2018-11-02T17:07:19+00:00

Core Physiology: The fast and slow of cardiac electrical activity.

Question.

Which one of the following statements is true of the spread of electrical activity through the heart?

a. Conduction velocity in atrio-ventricular (AV) node is 5 meters/second
b. Atrioventricular (AV) nodal delay gives ventricles time to fill before ventricular systole
c. Conduction of cardiac impulse is slowest in the bundle of His
d. Purkinje fibres transmit the cardiac impulse from the bundle of his to the left and right bundle branches
e.The right bundle branch is primarily responsible for septal depolarisation

 

 

Answer.

The answer is b.
 

Explanation.

Conduction velocity in cardiac tissues (meter/second):

SA node: 1m/s
Atrial pathway: 1m/s
AV node: 0.5m/s
Bundle of His: 1m/s
Purkinje fibres: 4m/s
Ventricular muscles: 1m/s

 

In sinus rhythm, the cardiac impulse begins at the sinoatrial (SA) node and passes via fast conducting internodal tracts (atrial pathway) to the atrioventricular (AV) node and via Bachmann’s bundle to the right atrium. The cells of both the sinoatrial (SA) and atrioventricular (AV) node are slow conducting. Of note, the time taken for the cardiac impulse to pass across the AV node is around 0.2 seconds (corresponding to the PR interval on the ECG). This built in nodal delay allows atrial contraction to take place (marked by the P-wave on the ECG) and ventricular filling to complete before the next ventricular systole (marked by the RS of the ECG)

From the AV node, the impulse passes across the non-conducting fibrous septum separating the atria and ventricles via the bundle of His and then on into the left and right bundle branches which pass through the interventricular septum. Depolarization of the septum starts on the left side and moves to the right across mid-portion of the septum. This generates a brief rightward and downward movement of the cardiac impulse seen as the physiological Q waves on the normal resting ECG.

Finally, from the bundle branches, the impulse is distributed tom the ventricular myocardium by the fast conducting Purkinje fibres.

 

Core Physiology: The fast and slow of cardiac electrical activity.2018-11-02T17:01:09+00:00