BT_RT 1.5 Describe the systemic inflammatory response and its physiological effects

T/F  a systemic inflammatory response (of varying degrees) will occur in response to surgery or trauma

T/F  a patient with “systemic inflammatory response syndrome” (SIRS) may be hypotensive, but hypotension is not essential for the diagnosis

T/F  one element of the inflammatory response is mediated by cytokines, which are released from damaged tissues, and white blood cells

T/F  the main cytokine released is interleukin-6 (IL-6)

T/F  cytokines ramp up the immune response, and cause vasodilation, capillary leak, and fever

T/F  another element of the stress response is a neuro-endocrine response mediated by the hypothalamus, in response to nociceptive inputs reaching the brain

T/F  the neuro-endocrine response includes: increased ADH, increased ACTH (therefore cortisol**), and sympathetic nervous system activation

** what are the consequences of increased cortisol?

1. Hemmings & Hopkins. Foundations of anesthesia – basic sciences for clinical practice, 2nd ed, 2006, Chapter 72. (unfortunately not an on-line textbook).
2. there are bits and pieces in the online textbooks but nothing very satisfactory
3. Burton D etal. Endocrine and metabolic response to surgery. CEACCP, 2004; 4: 144-147. (a good summary article that you can access via the ANZCA library)

BT_PO 1.129 Outline the principles of tissue/organ transplantation and the mechanisms of rejection of allogeneic organs

An adequate coverage of this topic can be found on a single page in each of the 2 physiology texts listed below.

T/F  an “allograft” is tissue transplanted from one person to another; a “xenograft” is from one species to another

T/F  the most important antigens for causing graft rejection are the HLA antigens (human leukocyte antigens)

T/F  HLA’s are found on white blood cells, and on tissue cells

T/F  HLA’s are not found on red blood cells

T/F  there are about a trillion different possible combinations of HLA antigens – it is virtually impossible for 2 people to have exactly the same HLA match, except for identical twins

T/F  a hyperacute transplant reaction occurs within minutes of transplantation – it is mediated by pre-formed antibodies reacting to the HLA antigens on the transplanted cells

T/F  chronic rejection can occur over a period of months to years, and can be mediated by either a cellular or antibody immune response

T/F  cyclosporine blocks T cell activation – it can cause nephrotoxicity


  1. Kam & Power 3rd edition, p.320
  2. Guyton 12th edition, p.449-50
  3. Evers & Maze 2nd edition, Chapter 52.

BT_RT 1.6 Describe the physiological basis of anaphylactic and anaphylactoid reactions

Agasgal has previously posted on these topics.

She also mentioned NAP6

The UK National Audit Projects have provided us with some invaluable information courtesy of their size and widespread buy in by the UK anaesthetic community. This is particularly helpful when you look at important adverse outcomes which are quite uncommon. NAP6 looked at perioperative anaphylaxis and the results came out earlier this year. If you don’t look at anything else look at the one page infographic summary. NAP7 will look at perioperative cardiac arrest. Our College’s ANZAAG have developed an online module which can be done to complete the anaphylaxis activity for the emergency CPD module.

Although NAP6 is undoubtedly important it hasn’t made its way to any of the textbooks yet- but it will. I am going to be proactive and ask a few questions relating to its findings as well as the content of the ANZAAG module.

T/F anaphylaxis is the leading cause of death directly related to anaesthesia

T/F the incidence of anaphylaxis in NAP6 was 1 in 10,000 anaesthetics

T/F the single worst offender for causing anaphylaxis in the UK was teicoplanin

T/F IM adrenaline should be administered as first line therapy for low grade anaphylaxis responses

T/F tryptases should be taken at 1, 2 and 4 hours post event.

T/F Noradrenaline, vasopressin and glucagon are recommended for use in refractory anaphylaxis

The top three causes of anaphylaxis in Australasia are antibiotics, muscle relaxants and what?


BT_PO 1.127 Outline the effects of anaesthesia and surgery on immune function

Nozawa Onsen

UPDATE: 26/9/18 for those who are interested, here is a relevant fairly recent article from BJA Education. It has opioids in the title but also talks about the impact of other anaesthetic agents. Interestingly it also discusses anti-nocioception (another tricky one…)

As a group, the participants in this blog (I can’t bring myself to says bloggers!) have been trying to address those LOs which are yet to receive a post – some of the remaining ones are quite unattractive ….

I don’t think this one is necessarily unattractive. It is an area that I suspect with continue to receive increasing attention in coming years as a target to improve peri-operative outcome.

It isn’t however a straightforward topic and not one that jumps out at you to learn – I suspect that is why is has been neglected.

Primer for the Primary Exam has this topic as low in importance, so don’t spend too long on it.

It is hard to find good simple information on this topic. Miller’s Anesthesia, in the chapter Nutrition and Metabolomics, covers the stress response to surgery and the effects of anaesthesia well. It also has a bit on the immune effects. The chapter is located beyond page 3000, perhaps giving us all a hint….

BT_PO 1.127  Outline the effects of anaesthesia and surgery on immune function

Immune cells express receptors (eg GABA-A) that are known targets of anaesthetic drugs T/F

It is likely that anaesthesia and surgery affect immune function T/F

It is too early to make definitive statements regarding the best anaesthetic combination to maintain a competent immune system T/F

Avoidance of hypothermia is known to assist in the maintenance of immune competency T/F

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_RT 1.6 Describe the physiological basis of anaphylactic and anaphylactoid reactions


Relatives of the little guy hiding in the poppy, are big culprits in this department…

Anaphylaxis – arrgghh! I think this is one of the most awful complications associated with anaesthesia – its idiosyncratic nature mades it hard to avoid even with careful practice and, although rare, despite gold standard treatment a few patients will have a terrible outcome.

Anaphylaxis is obviously not a normal physiological response and hence tends not to be covered in physiology textbooks. Of those books on the reading list, Hemmings and Egan Ch 6 Adverse Drug Reactions and Miller Ch 34 Anaesthetic Implications of Concurrent Disease, both discuss it. Here  is and article from BJA Education and the Australian and New Zealand Anaesthetic Allergy Group have a wide range of resources especially for management of suspected anaphylaxis.

UPDATE SEPT 2018: following the comments after this post was originally published, I have amended the nomenclature of the statements. Unfortunately the LO remains as it is for now….

BT_RT 1.6 Describe the physiological basis of anaphylactic and anaphylactoid reactions

The first four of these statements are core and the answers and be found in the textbook references above

Allergic anaphylaxis is a Type 1 hypersensitivity reaction T/F

Following initial exposure to an allergen, IgE anitbodies are generated with circulate in the plasma until a repeat exposure T/F

Products of mast cells may be released en masse with both allergic and non-allergic anaphylactic reactions T/F

The symptoms of allergic anaphylaxis can all be attributed to histamine T/F

These two require a bit more thought (although the answer to the first in the books 😉 )

The severity of an non allergic but not allergic anaphylactic reaction may be reduced by giving a drug slowly T/F

Immediately after a life threatening allergic anaphylactic reaction, the same drugs may be given without risk if the same response T/F

2017.2 SAQ 11

Describe the immunology, mediators and pathophysiology of anaphylaxis. Do not discuss management.

Anaphylaxis continues to be a major cause of anaesthetic morbidity and mortality. Understanding the pathophysiology is essential in order to comprehend the management of this complex, challenging emergency.

T / F  histamine is released from MAST cells during anaphylaxis – it causes bronchospasm via H1 receptors

T / F  anaphylaxis to muscle relaxants can occur due to prior sensitisation from exposure to some cosmetics, or pholcodeine cough mixture

T / F  MAST cell degranulation occurs when an allergen binds to IgG on the MAST cell surface

T / F  histamine, leukotrienes and platelet activaing factor all increase vascular permeability during anaphylaxis – many litres of IV fluid can be needed during resuscitation

T / F  patients with anaphylaxis will reliably show a rash or urticaria

T / F  if you suspect a penicillin allergy, 100 mg of cephazolin can be given IV to determine if it is safe to give that drug