Nomenclature.

We use scientific terminology, classifications, and nomenclature, every day of our working lives. Often, we don’t pause to consider the layers of meaning behind these words.

What is a steroid?

The term “steroid” is used in connection with many things – corticosteroids, sex steroids, aminosteroids, cholesterol. We hear of illicit “steroids” being taken – what are they? Various “cortisone” containing preparations also come under the same umbrella.

So, what is a steroid? Before reading any further, look this up. You should look up both the chemical structure, and a definition in words.

Having done that, you should now appreciate how a steroid “backbone” can be used as the framework for many different molecules, because a vast array of different side chains can be added to the steroid core.

Which of the following drugs contains a steroid moiety?

T/F  hydrocortisone

T/F  vecuronium

T/F  digoxin

T/F  thyroxine

T/F  atracurium

Curare was the first neuromuscular blocking agent introduced into clinical use. But it is a benzylisoquinolone. To read a bit about the development of pancuronium, the first aminosteroid used clinically, click Brown_et_al-1997-Anaesthesia. This article should help you appreciate the key structure-activity relationships which were permitted by using a steroid core.

Now that the term “benzylisoquinolone” has been brought up, you are no doubt eagerly wondering what it really means. Apart from the neuromuscular blockers, what other drugs share this basic structure?

BT_PO 1.89 Outline the role of prostaglandins and other autocoids

T/F  an autocoid is a biological substance which acts like a local hormone, has a brief duration, and acts near the site of synthesis

T/F  examples of autocoids include: prostaglandins, histamine, serotonin, nitric oxide, and endothelins

T/F  all prostaglandins are derived from arachidonic acid (a fatty acid present in the phospholipids of cell membranes), and contain 20 carbon atoms, including a 5 carbon ring

T/F  cyclo-oxygenase 1 (COX 1) is expressed constitutively in most cells, and is responsible for the production of prostaglandins involved with homeostatic functions

T/F  prostacyclin (PGI2) is a vasodilator, and inhibits platelets

T/F  PGE2 plays a role in preventing gastric ulcertation, by increasing gastric mucus production and inhibiting gastric acid secretion

T/F  many drugs work by either inhibiting the synthesis of various prostaglandins, or mimicking their action

Fun Trivia
Why are prostaglandins called “prostaglandins”? What’s the significance behind the name?

BT_GS 1.19 Describe the mechanisms of drug interaction

Mechanisms of drug interaction can be classified as: pharmacodynamic, pharmacokinetic, and pharmaceutic.

T/F  the interaction between nitrous oxide and sevoflurane is an example of synergism because the combined effect is greater than would be predicted by simple addition

T/F  the interaction between propofol and remifentanil can be represented by a linear isobologram

T/F  in a patient using buprenorphine patches, morphine can have a reduced effect because buprenorphine is a partial antagonist

T/F  in a patient who has been reversed with neostigmine, but then needs to be urgently reintubated, suxamethonium would have a significantly reduced effect

T/F  cigarette smoking inhibits many of the cytochrome P450 enzymes, thereby slowing the metabolism of many drugs

T/F  competition for plasma protein binding sites between drugs, is a common reason for adverse drug effects in anaesthesia

T/F  if suxamethonium is injected into an IV port immediately after thiopentone, a precipitate will form in the line

Reference

Hemmings & Hopkins, Chapter 9 (Anesthetic drug interactions)

 

BT_PO 1.128 Describe the immunological basis and pathophysiological effects of hypersensitivity

Hedgerow by Angela Singer currently exhibited at Te Papa, Wellington

With the recent publication of the findings of the NAP6 audit, hypersensitivity (HS) is in the spotlight.

I have previously posted on anaphylaxis here but today we will stay a bit broader.

It may not be essential to know the exact Gell and Coombs classification of HS reactions, but it is not too complicated ( although I see that there have been some more recent amendements to it) and I think it does help with understanding of this reasonably common group of conditions

Power and Kam do this topic by far the best of the recommended texts in their chapter on the immune system. It would be reasonable for you to know the answer to the top 3.

BT_PO 1.128  Describe the immunological basis and pathophysiological effects of hypersensitivity

A single allergen may only produce a single type of HS reaction T/F

Type II hypersensitivity reactions, caused by antibodies binding to cell based antigens, include ABO incompatibility reactions T/F

A type I HS reaction can only occur after a prior exposure to the antigen T/F

I wouldn’t expect you to know the answer to these, but have a look if you are interested

Extrinsic allergic alveolitis is an example of Type III hypersensitivity caused by small immune complex deposition in tissues T/F
(as an aside the names of the causes of extrinsic allergic alveolitis are so descriptive . There is a list of some of them here – Hot Tub lung 😳)

Stevens-Johnson syndrome is a type of type IV hypersensitivity T/F

And one last thing. Blood is potentially a very immunogenic product. Have a think about the hypersensitivity reactions that can be caused by homologous blood. Then, have a think of what other immune mediated problems blood can cause.

BT_PO 1.81 Outline a physiological basis of classifying diuretics related to their site of action

It feels like I haven’t I haven’t been here for ages except for a few well wishes – I hope that everyone is in a good place…

Above is a dahlia (photo courtesy of Wikipedia). I once grew a tree dahlia which lost limbs every time a breeze blew. It was an amazing plant though – if you stuck the broken limb in the ground, more often than not, it would take root.

Diuretics are pretty dry topic (although patients on them might not think so…)

Some diuretics are particularly likely to cause certain electrolyte or acid base issues related to their site of action. It is worthwhile having some idea of what these particular issues are.

Here is an old article from BJA Education There have not been a lot of new developments in this field.

You will find a decent section of diuretics in any pharmacology textbook.

BT_PO 1.81 Outline a physiological basis of classifying diuretics related to their site of action

I have ranked these questions in order of difficulty, but I think it would be reasonable to know the answer to the top 5

Aldosterone antagonists act on the collecting ducts and are “potassium sparing” T/F

Loop diuretics block the Na+K+2Cl- co-transporter in the ascending LOH and are prone to cause hyponatraemia T/F

Thiazides diuretics are the most like to cause hyperkalaemia as they increase the amount of potassium presented to the Na/K exchanger in the DCT T/F

Loop diuretics causes effects the vasculature to produce vasodilation which precedes the diuretic effect T/F

Carbonic anhydrase inhibitors produce an alkaline diuresis, through action at the PCT, for the first 2-3 days of treatment T/F

Something to think about,

All natriuretics are diuretic but not all diuretics are natriuretic T/F

This one I didn’t know and it isn’t core, but it did make me think “What makes people try these things?”

Mannitol is derived from the tubers of dahlias T/F

BT_PO 1.8 Outline the anatomy of the pulmonary and bronchial circulations

T/F  oxygen and nutrients are supplied to all lung tissue including alveoli, via the bronchial circulation

T/F  the bronchial arteries usually arise from the aorta – there are 3 on the right and 2 on the left (one for each lung lobe)

T/F  all of the bronchial circulation returns via the pulmonary veins – thereby forming part of the ‘anatomical’ shunt

T/F  there are intrapulmonary arteriovenous anastomoses, which can open when the cardiac output increases

T/F  the flow through the pulmonary circulation is always identical to the systemic circulatuion

T/F  the pulmonary arteries and the pulmonary veins accompany and follow the same pattern of branching as the the bronchi and bronchioles

References

  1. Ellis, 9th edition, Anatomy for Anaesthetists, Ch 1
  2. Nunn’s Applied Respiratory Physiology, 8th edition, Ch 1

BT_PO 1.7 Outline the anatomy of the lower airways

T/F  the adult trachea is approx. 15 cm long

T/F  the trachea is supported by 16-20 individual complete rings of cartilage

T/F  the posterior wall of the trachea can be recognised during bronchoscopy, by the trachealis muscle, running longitudinally

T/F  the bracheocephalic artery runs anterior to the trachea – a tracheostomy tube may erode through the tracheal wall into this artery

T/F  the right main bronchus forms an angle of 45 degrees to the vertical, compared with 90 degrees on the left

T/F  the right upper lobe bronchus branches off the RMB at a 90 degree angle – occasionally, it arises directly from the trachea

Reference

Ellis, 9th edition, Anatomy for Anaesthetists, pp. 42-44, 63

 

 

 

T/F

SS_OB 1.8 Describe the anatomy and physiology of pain in labour and childbirth

T / F  Pain associated with the first stage of labour is visceral pain – dull, poorly localised, and felt in the lower abdomen or back. It is caused by cervical dilation, and increasing pressure in the lower uterine segment.

T / F  Nociception in the first stage occurs via A-delta and C fibres that travel with the sympathetic efferents. They eventually enter the neuraxis via the T10 – L1 nerve roots.

T / F  Pain associated with the second stage of labour is predominantly somatic pain – localised to the perineum. It is caused by stretching and tearing of the vagina and perineal skin.

T / F  Nociception in the second stage is transmitted via the pudendal nerves, which enter the neuraxis via the S2 – S4 nerve roots.

T / F  An epidural block to T10 would be adequate for labour, but needs to be extended to T4 for a Caesarian, in order to cover most of the peritoneal contents.

T / F  Ice is used to assess an epidural or spinal block, because input from thermoreceptors is transmitted via the same A-delta and C fibres that transmit pain.

References:
1. Macintyre etal. Clinical Pain Management: Acute Pain, 2nd edition 2008, Chapter 26.
2. Guyton 12th edition, Fig 46-6

 

BT_RT 1.23 Outline the anatomy of the cerebral and spinal cord circulation

T/F  The single anterior spinal artery is formed by branches of the vertebral arteries, and runs down the anterior midline of the spinal cord. It supplies the anterior 2/3 of the cross sectional area of the cord.

T/F  The two posterior spinal arteries are derived from the posterior inferior cerebellar arteries. They supply the posterior 1/3 of the cross sectional area of the cord.

T/F  This arterial supply is reinforced by segmental (radicular) arteries at all spinal levels below T4. They travel along the spinal nerve roots and enter via the intervertebral foramina.

T/F  An important segmental artery is called the artery of Adamkiewicz. It arises from lower intercostal arteries, or upper lumbar arteries (between T8 and L2) usually on the left.

T/F  The artery of Adamkiewicz contributes significantly to the blood supply of the lower spinal cord, so cross clamping the aorta can lead to spinal cord infarction.

T/F  Venous drainage of the spinal cord is usually via three anterior and three posterior spinal veins, which join the epidural venous plexuses.

 

References:
1. Anatomy for Anaesthetists 9th edition, p. 142-145
2. Moore’s Clinically Oriented Anatomy 7th edition, p. 502-504