BT_PO 1.84 Discuss the factors that influence metabolic rate

Palm Cove, QLD

Just a short one from me today…

Guyton and Hall Texbook of Medical Physiology Ch 73 has a good chapter on metabolic rate

BT_PO 1.84 Discuss the factors that influence metabolic rate

Males have a higher metabolic rate than females for a given weight T/F

Basal metabolic rate declines with advancing age T/F

Environmental conditions have no effect on basal metabolic rate T/F

Eating a carbohydrate rich meal increases metabolic rate more than eating a protein rich meal T/F

Growth hormone and thyroxine both increase metabolic rate T/F

BT_PO 1.24 Describe the alveolar exchange of oxygen and carbon dioxide

T/F  oxygen and carbon dioxide are exchanged on a 1:1 basis across the alveolar-capillary membrane *

T/F  the diffusion of oxygen from alveoli to blood occurs down an average partial pressure gradient of approximately 110 mmHg (150 – 40)

T/F  the diffusion gradient for oxygen is greater in basal alveoli, compared with apical

T/F  carbon dioxide diffuses less readily than oxygen through the alveolar-capillary membrane, because its molecular weight is higher

T/F  at altitude, or with lung disease, the transfer of oxygen can become diffusion limited when the cardiac output increases

T/F  If an aircraft at 36,000 ft depressurised, the alveolar PO2 would be below mixed venous PO2 (i.e. the diffusion gradient for O2 would be reversed), so breathing would actually excrete oxygen from the body. Therefore, you should hold your breath until your oxygen mask is on.

* this statement was confidently made by an SRMO at an ALS course I attended

BT_PO 1.72 Phosphate

I wonder whether any of these potions contain phosphate? (Warner Bros Studios, UK)

We can’t let the cations have all the fun! Interestingly, phosphate it the only anion singled out in the LOs ( I thought chloride may have been there too…)

Again Chapter 59 in Miller’s Anaesthesia is good for this topic.

BT_PO 1.72 Describe the function, distribution and physiological importance of sodium, potassium, magnesium, calcium and phosphate ions

Phosphate is the most abundant intracellular anion T/F

The majority of phosphate is found within bone T/F

Phosphate is essential for the production of 2,3 DPG T/F

Phosphate is freely filtered at the glomerulus T/F

High parathyroid hormone levels enhance renal phosphate reabsorption T/F

The phosphate buffer system is more important in extracellular fluid than intracellular fluid T/F

The phosphate buffer system has a pKa of 6.8 T/F


Daylesford, Victoria – a place with abundant mineral springs, some high in Magnesium

I’m on an electrolyte role! Today, Magnesium – important both physiologically and pharmacologically.

The therapeutic benefits of Magnesium have been known for at least 400 years, when Epsom Salts (MgSO4) were first discovered to have a laxative effect!

Miller’s Anaesthesia Ch59 is an excellent resource on electrolytes.

BT_PO1.72 Describe the function, distribution and physiological importance of sodium, potassium, magnesium, calcium and phosphate ions

BT_PO 1.57 Describe the pharmacology of antiarrhythmic agents and their clinical applications including magnesium (and lots more)

SS_OB1.12 Describe the pharmacology of agents used for the treatment of pre-eclampsia including magnesium, hydralazine and labetolol

Magnesium is largely an extracellular ion T/F

Magnesium acts as a physiological calcium antagonist T/F

Magnesium is a co-factor for the production of ATP during oxidative phosphorylation T/F

Hypermagnesaemia predisposes patients to Torsades de Pointes T/F

A Mg2+ ion blocks the open NMDA receptor channel at normal RMP preventing ion flux T/F

Magnesium causes smooth muscle relaxation throughout the body T/F

Magnesium has class I and class IV anti-arrhythmic effects T/F

BT_GS 1.26 Fluoride

Flowing on from yesterday’s post on lithium, I thought I would focus on another element today, fluorine, or in particular the fluoride ion.

This little guy comes into its own in anaesthesia when thinking about the metabolism of volatile anaesthetic agents, and their toxicity, hence the LO which I have given it.

There has been a bit of debate between the authors of this blog about how much current trainees should know about methoxyflurane, no longer used as an anaesthetic agent, but still widely used in pre-hospital settings as an analgesic.

Have you thought about why it is no longer used as an anaesthetic, given that it is both hypnotic and analgesic – a combination which is hard to find and highly sought after?

Miller’s Anaesthesia Ch 26 covers this topic well and I would think all the statements below could be examined. 

BT_GS 1.26 Describe the toxicity of inhalational agents

All modern volatile anaesthetic agents contain fluorine atoms T/F

Approximately 70% of methoxyflurane is metabolised, with the kidney being a significant site of metabolism T/F

Plasma concentrations of fluoride ions following prolonged sevoflurane anaesthesia do not approach levels seen with methoxyflurane T/F 

Peak plasma concentrations of fluoride ions following inhalational anesthesia correspond well with the risk of renal failure T/F

High intra-renal levels of fluoride due to renal metabolism are the likely reason for the high incidence of nephrotoxicity with methoyflurane T/F

The renal failure caused by fluoride ions is oliguric T/F

The risk of renal failure with methoxyflurane is negligible after 1MAC hour T/F

Did you know that the “Green Whistle” is actually an Australian development? (thanks to Slowlywaving, for pointing this out) 

BT_PO 1.99 Lithium

The Hubble Space Telescope’s image of the star V838 Monocerotis 

On the way to work today I listened to a fascinating podcast about an Australian psychiatrist, John Cade, who discovered the benefit of using Lithium in the treatment of bipolar mood disorder. Apparently Lithium was one of the three elements created in the Big Bang along with H and He

Lithium is not a drug we encounter commonly in our anaesthetic practice, although it is still the gold standard treatment for severe bipolar mood disorder and has some interesting toxic effects. As such, I thought it was worthy of a post. None of this is particularly examinable, but still good to know.

Lithium is covered well in Katzung Basic and Clinical Pharmacology (Ch 29)

BT_PO 1.99 Outline the pharmacology of anti-depressant, anti- psychotic, anti-convulsant, anti-parkinsonian and anti- migraine medication

Lithium can mimic the actions of sodium in the generation of membrane potentials T/F

Lithium produces a nephrogenic diabetes insipidus which does not respond to vasopressin T/F

Patients on lithium often exhibit T wave flattening on their ECG T/F

Lithium is completely renally cleared T/F

Leukocytosis is almost universal in patients receiving lithium therapy T/F


BT_PO 1.111 Outline the major haemoglobinopathies and their clinical significance

T/F  methaemoglobin has the iron in the ferric (Fe3+) rather than the ferrous (Fe2+) state – this renders it completely unable to bind with oxygen

T/F methaemoglobin is normally present in trace amounts – but metHb can increase to toxic levels with certain drugs (e.g. prilocaine, nitrates) especially in people with methaemoglobin reductase deficiency

T/F  carboxyhaemoglobin (COHb) has CO bound to the terminal amino groups on each of the 4 globin chains – this renders the Hb unable to bind O2

T/F  CO binds to Hb with 250 times greater affinity than O2

T/F  the binding of CO to Hb instead of O2 is the sole mechanism by which carbon monoxide leads to hypoxia

T/F  sickle cell disease is a genetic disorder leading to a single nucleotide substitution on the B globin chain of Hb (valine instead of glutamic acid) – this reduces the affinity of HbS for O2

T/F  a sickle cell crisis can be treated with IV methylene blue

Guyton, Nunn


BT_PM 1.25 Describe in detail pharmacology of paracetamol including mode of action, clinical utility, metabolism and toxicity, advantages and disadvantages of different routes of administration

T / F  paracetamol inhibits both COX-1 and COX-2

T / F  paracetamol is a prodrug – the active metabolite is para-aminophenol

T / F  the oral biovavailability of paracetamol is about 90%

T / F  paracetamol is metabolised by CYP2E1 to NAPQI (N-acetyl-p-benzoquinonamine) which is hepatotoxic – NAPQI is then further metabolised by conjugation with glutathione (this step renders NAPQI non-toxic)

T / F  the above is the only metabolic pathway for paracetamol

T / F  in paracetamol overdose, depletion of glutathione leads to NAPQI accumulation

1. Hemmings & Egan
2. Goodman & Gilman

Discussion Question

Do you use IV paracetamol? Can you justify its use with reference to any good quality evidence, and/or any niche situations?