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Angiotensin? Angio-tensing! – Endocrine essentials

Question.

Angiotensin II has all the following physiological effects EXCEPT which one?
a. Increased thirst
b. Arteriolar vasoconstriction
c. Renin release from the juxtaglomerular apparatus
d. Suppression of aldosterone release from the adrenal cortex
e. Stimulation of anti-diuretic hormone (ADH) release from the posterior pituitary

 

 

 

Answer.

The answer is d. Angiotensin II stimulates aldosterone release.

Explanation.

Renin is released from the juxtaglomerular apparatus of the kidney in response to sympathetic nervous activity, falling renal tubular flow and, in particular, renal hypoperfusion.

Renin cleaves circulating angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) in the lungs. Angiotensin II acts on angiotensin receptors (AT1R & AT2R) to exert the following physiological effects:
• Promotes thirst and consequent water intake
• Increases sympathetic activity
• Arteriolar vasoconstriction (remember angio-tensing!)
• Stimulates aldosterone secretion from the adrenal cortex. Aldosterone is a mineralocorticoid which promotes sodium and water retention by the kidney.
• Stimulates the anterior pituitary to secrete more anti-diuretic hormone (ADH). ADH increases the permeability of the collecting dusts to water and thereby promotes renal water retention.

Overall, these actions are all designed to increase blood pressure and blood volume and thereby restore renal perfusion.

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Angiotensin? Angio-tensing! – Endocrine essentials2021-02-17T17:22:54+00:00

Salicylate toxicity. – Core pharmacology

Question.

In a young patient symptomatic from aspirin (salicylate) overdose, which one of the following is true?

a. Activated charcoal is ineffective
b. Early symptoms are typically visual disturbance and haematemnesis
c. Mitochondrial oxidative phosphorylation is stimulated
d. Persistent respiratory alkalosis is a poor prognostic sign
e. Salicylate elimination is increased at higher urinary pH

 

 

Answer.

The answer is e. Urine alkalinisation (higher urine pH) enhances salicylate elimination through the kidney.

Explanation.

Salicylates (the active ingredient of aspirin) are markedly harmful in excess. Aspirin tablets often form concretions in the stomach which delay gastric absorption so that multiple doses or delayed administration of activated charcoal are still effective in reducing salicylate absorption.

 

Early features of salicylate overdose include:

  • Tinnitus, dizziness, nausea and vomiting (haematemesis is uncommon)
  • Toxic amounts of salicylates stimulate the respiratory centres and early on give rise to hyperventilation and respiratory alkalosis on the blood gas.

 

Delayed features in moderate and severe toxicity

  • Agitation, pyrexia and sweating. Confusion, convulsions and coma may occur in life threatening overdoses.
  • uncoupling of mitochondrial oxidative phosphorylation, leading to anaerobic respiration and development of metabolic acidosis, a hallmark of serious poisoning.
  • Intracellular glucose depletion and hypokalaemia may also occur

 

Aspirin has a Pk (acid dissociation constant) value of 3.5. Alkalization of urine therefore keeps aspirin in ionized form which inhibits its tubular reabsorption and enhances its elimination in urine.

 

Treatment of salicylate overdose is therefore with activated charcoal, intravenous sodium bicarbonate to alkalinise the urine and in severe poisoning consider haemodialysis – all guided by serial salicylate levels.

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Salicylate toxicity. – Core pharmacology2021-02-17T17:10:24+00:00

Core Anatomy: Blood supply to the face and scalp.

Question.

All the following arteries which supply the face and scalp with blood are branches of the external carotid artery EXCEPT which one?
a. Facial artery
b. Superficial temporal artery
c. Maxillary artery
d. Ophthalmic artery
e. Occipital artery

 

 

 

Answer.

The answer is d. The ophthalmic artery is a branch of the internal carotid artery not the external carotid.

Explanation.

Most of the blood supplied to the face and scalp comes from the external carotid artery, which after the carotid bifurcation gives off a series of branches supplying blood to the structures and skin of the anterior neck, face and scalp:

   1. Early branches include the superior thyroid artery and lingual artery which supply blood to the thyroid gland, the muscles of the anterior neck and
the tongue and mucous membranes of mouth and gums.

   2. Facial artery. This initially follows the inferior border of the mandible then passes upward to supplies most of the muscles and skin of the face from under the chin (submental artery) to the bridge of the nose (angular artery).

   3. Occipital artery passes posteriorly to supply blood to the scalp of the back of the head.

Further upward, and within the parotid gland just anterior to the ear, the external carotid divides into the maxillary artery and slightly smaller superficial temporal artery.

   4. Maxillary artery runs deep to the neck of the mandible and supplies blood to the deeper structures of the face and via it’s important branch – the middle meningeal artery (which enters the skull via the foramen spinosum) – the superficial meninges. Another branch, the inferior alveolar artery supplies the teeth and, via its terminal branch the mental artery (which exits the mandible through the mental foramen) the skin of the chin.

   5. Superficial temporal artery ascends in front of the ear to the temporal area where it supplies the muscles and skin of the fronto-lateral scalp. The superficial temporal artery, of course, may become inflamed in giant Cell arteritis (temporal arteritis).

The exception to the rule that the external carotid artery supplies the face and scalp, is the ophthalmic artery which supplies most of the structures of the orbit but also the nose (ethmoidal branches) , eyelids (medial palpebral arteries) and skin and muscles forehead (supraorbital artery which exits the cranium via the supraorbital foramen). The ophthalmic artery of course a branch of the internal carotid artery.

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Core Anatomy: Blood supply to the face and scalp.2020-11-18T11:19:03+00:00

Lower limb dermatomes. – Core anatomy


Question.

A middle aged man with back pain complains of pain and anaesthesia down the medial aspect of the lower leg. Which one of the following lower limb dermatomes corresponds best to the location of his symptoms?
a. L3
b. L4
c. L5
d. S1
e. S2

Answer. The answer is b. The skin of the medial lower leg is supplied by the L4 dermatome.  
Explanation. A dermatome is an area of skin supplied with afferent sensory fibres from a single spinal posterior nerve root. The dermatomes of the lower limb are derived from the lumbosacral plexus (L1 – S4), which has 3 main parts: one, the lumbar plexus (L1-L4 nerve roots with a contribution form T12 in around 50% of people); two, the lumbosacral trunk (L5 and usually including a branch from L4); and three, the sacral plexus (S1 – S4). In the limbs there is always some variation and overlap between dermatomes but in most the dermatomes of the lower limb are:
L1 – inguinal region
L2 – anterior and lateral upper thigh
L3 – anterior and medial lower thigh; front and sides of knee
L4 – medial ½ lower leg (front and back) below the knee
L5 – lateral aspect of the lower leg down over the anterior ankle and medial 2/3rds of the dorsum of the foot S1 – lateral ankle, lateral 1/3rd and sole of the foot
S2 – Posterior thigh and strip of skin over posterior calf; genitalia
S3 & S4 – perineal region
S5 perianal region (coccygeal plexus)  

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Lower limb dermatomes. – Core anatomy2021-02-17T17:04:17+00:00

Revision essentials: Ten useful FOAMED articles for your FRCEM primary revision!

Below is a list of ten educational modules from RCEM learning 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 can be found here. Modules take about an hour to complete and can be added to your CPD folder!

(more…)

Revision essentials: Ten useful FOAMED articles for your FRCEM primary revision!2021-02-17T16:53:37+00:00

Ventricular Tachycardia. VT or not VT? – Core physiology

Question.

A 56yr old man with previous cardiac disease presents with palpitations and a broad complex tachycardia on his ECG. Which one of the following electrocardiographic features would indicate that the rhythm is ventricular tachycardia as opposed to a supraventricular rhythm with aberrant conduction?

a. Absent concordance throughout the chest leads
b. J waves seen at the end of each QRS
c. Absence of visible p waves
d. Fusion beats and capture beats
e. Rate greater than 160 beats/minute

 

Answer.
The correct answer is d. The presence of fusion beats and capture beats indicates that a broad complex tachycardia is ventricular in origin (ventricular tachycardia).
 
Discussion.
Broad complex tachycardia is frequently seen in the ED and is caused by either ventricular tachycardia (VT) or a supraventricular rhythm with new or pre-existing aberrant conduction (bundle branch block).  While as a rule, all broad complex tachycardia should be treated as ventricular tachycardia it can desirable to diagnose the underlying rhythm more accurately to give more focused management.

Electrocardiographic features indicating VT rather than SVT with aberrancy include:

– concordance of QRS polarity across the chest leads (figure. 1).
– AV-dissociation, visible P waves at sinus rate but with no relationship to the broad QRS complexes
– capture beats, an impulse from the SA node transiently captures the ventricle and intermittent narrow complex QRS complexes are seen
– fusion beats, a ventricular beat simultaneously triggered by both a sinus impulse and the ventricular tachycardia such that an occasional odd looking hybrid QRS complex is seen
– very broad complexes (>160ms)

Atrio-ventricular dissociation occurs in around half the episodes of VT where, despite the independent ventricular rhythm, the sinus node is still firing and sinus impulses are still reaching the ventricle via an intact atrioventricular conduction system. P waves, capture beats and fusion beats all provide evidence of A-V dissociation in a broad complex tachycardia and their presence indicate the underlying rhythm is VT.  Of course, the likelihood of a broad complex tachycardia being VT is also increased in those with structural heart disease, ischaemic heart disease and/or heart failure.

Figure.1 Ventricular tachycardia (VT) with positive concordance across the chest leads

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Ventricular Tachycardia. VT or not VT? – Core physiology2021-02-17T16:43:03+00:00

Mind the gap: excess anions to be aware of! – Clinical chemistry

Question.

All the following statements regarding the anion gap are true EXCEPT which one?

a. It may be calculated by the formula, anion gap (AG) =  ([Na+] + [K+]) − ([Cl] + [HCO3])
b. Normal anion gap is < 2 mEq/L
c. Ketoacidosis is a cause of raised anion gap
d. Hypoalbuminaemia may cause a falsely low anion gap
e. Excess paracetamol and aspirin are both causes of raised anion gap.

Answer.
The correct answer is b. The normal anion gap is less than 12 – 16mEq/L (depending on exact calculation method)
 
Discussion.
The anion gap is the difference between the measured cations (positive ions) and measured anions (negative ions) in the plasma. It is therefore calculated by subtracting the major plasma anions (CLand HCO3) from the major plasma cations (Na+ and K+) such that the anion gap (AG) =   ([Na+] + [K+]) − ([Cl] + [HCO3]).  The normal value of the anion gap calculated by the above formula is less than 16mEq/L (less than 12 mEq/L if the minor contribution of [K+] is excluded from the calculation).

A raised anion gap indicates the presence of unmeasured cations and in an unwell patient with a metabolic acidosis this may aid diagnosis. The most well-known mnemonic for remembering the causes of a high anion gap metabolic acidosis is MUDPILES:

M – methanol
U – uraemia (chronic renal failure)
D – diabetic ketoacidosis (and other causes of ketoacidosis – ethanol, starvation and metformin)
P – propyl alcohol
I – isoniazid, iron
L – lactic acidosis (sepsis, metformin)
E – ethylene glycol
S – salicylates (aspirin)

Other rare causes include cyanide and paracetamol (due to its metabolite, oxoproline).

A low anion gap most frequently arises from hypoalbuminaemia, where the loss of negatively charged albumin protein causes the retention of other anions (Cl and HCO3) to maintain electrical neutrality of plasma. Causes of hypoalbuminaemia include liver cirrhosis, nephrotic syndrome and congestive cardiac failure.      

 

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Mind the gap: excess anions to be aware of! – Clinical chemistry2021-02-17T16:29:27+00:00

Fascia iliaca compartment and beyond! – Core anatomy

Question.

Which one of the following is correct regarding the anatomy of the fascia iliaca compartment?

a. Its roof is formed by the fascia lata
b. Its floor is formed by the fascia iliaca
c. The femoral artery and vein lie medial and deep to it
d. The femoral and lateral femoral cutaneous nerves lie within it
e. It is accessed by inserting a needle half way along and above the inguinal ligament

 

 

Answer.

The answer is d. The femoral nerve and the lateral femoral cutaneous nerve (at least for some of its course) lie within the fascia iliaca compartment.

 
Discussion.

The fascia iliaca compartment (FIC) is a potential space in the inguinal region just above the upper thigh (fig 1). It exists between the fascia iliaca above and the iliacus and psoas major muscles below. The femoral vessels – femoral artery and vein – lie outside and above the FIC, between the fascia iliaca and the more superficial fascia lata.

The fascia iliaca compartment (FIC) contains the femoral nerve and the lateral femoral cutaneous nerve. Since local anaesthetic injected into the FIC also often blocks the obturator nerve, this is also often included in its contents but anatomically both the anterior and posterior branches of the obturator nerve are separated from the main FIC by the psoas and pectineus muscles.  The femoral nerve and lateral femoral cutaneous nerve of the thigh arise from the lumbar plexus (L2, 3, 4) and supply sensation to the anteromedial surface and the lateral surfaces of the thigh respectively. Together, they also innervate the hip joint (Hilton’s law).

To access the FIC for fascia iliaca compartment block(FICB), a blunt needle is inserted 1cm below the junction of the medial two thirds and outer third of a line drawn from the anterior superior iliac spine to the pubic tubercle.  The needle passes through the skin, the fascia lata and then fascia iliaca (both identified by a pop feeling as the needle pierces the fascia itself) before entering the FIC.  A large volume of local anaesthetic is injected (typically 30-40ml of 0.25% bupivacaine; max dose 2mg/kg) which disperses within the compartment to reliably block the femoral and lateral femoral cutaneous nerves and often far enough to also block the obturator nerve. The resultant anaesthesia provides excellent pain relief for patients with either a neck of femur fracture or femoral fracture.

 

Fig 1. Anatomy of the fascia iliaca compartment.

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Fascia iliaca compartment and beyond! – Core anatomy2021-02-17T15:47:30+00:00

The ins and outs of fluid flow across the capillary endothelium. – Core physiology

Question.

Which one of the following statements is correct regarding the movement of fluid across the capillary endothelium?

a. Water and electrolytes are actively transported across the capillary endothelium
b. Capillary hydrostatic pressure is greatest at the distal end of the capillary
c. Interstitial oncotic pressure is greater than capillary oncotic pressure
d. Interstitial hydrostatic pressure increases 10-fold along the length of the capillary
e. Fluid reabsorption may occur at the venous end of the capillary

 

 

 

Answer.

The correct answer is e. In most capillary beds (but not all), fluid reabsorption occurs at the venous end of the capillary.

 
Explanation.

A series of hydrostatic and oncotic pressures, known as Starling’s forces (after the same Ernest Starling as discovered Starling’s law of the heart), control the bulk flow of water and accompanying solutes across the capillary endothelium.  The four Starling’s forces, and typical values for a skeletal muscle capillary, are;

– capillary hydrostatic pressure (Pc). Produced by the pressurized flow of blood into capillaries from the arterial system, this is the ‘water pressure’ pushing fluid out of the capillary. Pc is greatest, around 35mmHg, at the arteriolar end of a typical tissue capillary but falls to 25mmHg by the time blood reaches the venous end.

– capillary oncotic pressure (πc). Maintains fluid within the capillary attracted by the high concentration of plasma proteins. It remains roughly constant over the length of the capillary.

– interstitial hydrostatic pressure (Pi). This tends towards pushing fluid back into the capillary from the extracellular space. This pressure is negligible at the arterial end of the capillary but increases to a few mmHg as fluid passes out into the interstitium generating an increasing backpressure with distance along the capillary.

– tissue oncotic pressure (πi). The force holding fluid in the extracellular space through its oncotic attraction to interstitial proteins. Due to the much lower protein concentration of the interstitium, πi is negligible.

In a typical tissue capillary, the net balance of the Starling forces at the arterial end of the capillary ([Pc-Pi] – [πc-πi]) is positive and fluid is driven from the capillary lumen into the tissue interstitium (fig 1). However, as blood flows along the capillary and more fluid leaves the capillary for the tissues, the outward hydrostatic pressure of the capillary falls while the hydrostatic pressure of the interstitium increases. This process continues down the length of the capillary until, toward the venous end, the balance of Starling’s forces reverses and fluid flows back across the capillary endothelium from tissue interstitium into the capillary lumen.

The amount of fluid filtering into the tissues in the proximal capillary always exceeds that re-absorbed at the venous end so that in all tissues, there is net movement of fluid from capillary to tissue. This excess tissue fluid, around 3L/day, is removed and ultimately returned to the vasculature by the lymphatic system.

Figure 1. The changing balance of Starling forces along the capillary.

 

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The ins and outs of fluid flow across the capillary endothelium. – Core physiology2021-02-17T16:09:42+00:00

Do you know a schizont from a hypnozoite! – Microbiology essentials.

Question.

A traveller returning from a tropical country attends the ED with recurrent fevers and at triage has a temperature of 39.8degC and rigors. He has a positive P. Falciparum antigen test. Which one of the following is responsible for the recurring fever in this man?
a. schizonts
b. sporozoite
c. merozoite
d. hypnozoites
e. trophozoites

 

 

 
Answer.

The answer is c. Recurrent fever of malaria is caused by successive waves of merozoite release from red blood cells.

 
Explanation.

Malaria is caused by Plasmodium species of protozoan parasites, transmitted from person to person by the bites of female Anopheles mosquitos. 

When a malaria carrying, mosquito bites a human, Plasmodium sporozoites enter the bloodstream with the mosquito saliva (fig 1). The sporozoites migrate to the liver, invade hepatocytes where they rapidly grow and multiply to form thousands of merozoites. After around 5-7 days the hepatocyte ruptures releasing merozoites into the circulation. Sporozoites of vivax and ovale malaria can enter a dormant stage within the liver – where they are known as hypnozoites –  with reactivation and hepatocyte rupture up to 5 years later (recurrent bouts of illness years apart therefore sometimes characterise these types of malaria).

Circulating merozoites invade red blood cells where they become trophozoites. The trophozoites initially enlarge through feeding on erythrocyte haemoglobin to form a multinuclear schizont. The schizont then asexually multiplies by several fold division to form new infective particles (more merozoites) in a process known as schizogeny.

After 2 – 3 days, red cell rupture releases even more merozoites into circulation (Figure 1), which go on to infect further red cells and the erythrocytic cycle repeats. The cyclical fever of malaria coincides with the synchronised release of merozoites into the blood stream. The proportion of red cells infected with malaria parasites is called the parasitaemia.  

Some trophozoites, instead of undergoing schizogeny, can transform into sausage-shaped structures known as gametocytes. These are infective to any mosquito that might bite the patient, and exist in male and female forms. Gametocytes undergo sexual reproduction within the mosquito gut to produce more sporozoites which migrate to the mosquito salivary glands and infect further humans during subsequent mosquito feeds.

P. falciparum is the most dangerous of the malaria parasites because the merozoites infect young red cells, and with each schizogeny the parasite count can rise higher and higher. The life-threatening complications of falciparum malaria – cerebral malaria, pulmonary oedema and renal failure (blackwater fever) – relate to schizogeny, during which infected red cells adhere to capillary walls, obstructing the microvasculature of the brain, lungs and kidney. Other serious complications include severe haemolytic anaemia (considered <5g/dL) and shock (algid malaria).

  • Figure 1. Plasmodium life cycle

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Do you know a schizont from a hypnozoite! – Microbiology essentials.2021-02-17T13:50:46+00:00

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