BT_PO 1.66 Outline the endocrine functions of the kidney

And it will come as a surprise to no-one reading the posts this week to find I’ve been reading Ganong again.

Vitamin D is hydroxylated to calcitriol in the proximal tubules of the kidney     T/F

Calcitriol increases calcium reabsorption in the proximal tubules of the kidney     T/F

The O2 sensor to control erythropoietin production is probably a heme protein     T/F

Increasing catecholamines will stimulate erythropoietin production     T/F

Erythropoietin is also produced in the brain     T/F

 

BT_PO 1.82a Outline basic cellular physiology in particular The structure of the cell membrane and trans- membrane transport mechanisms The composition and regulation of intracellular fluid The generation of the trans-membrane potential Energy production by metabolic processes in cells

AKA read most of Ganong Chapters 1 and 2

The intracellular compartment contains about 5% of body water     T/F

Colligative properties are dependent upon the types of particles in a solution    T/F

The sodium/potassium pump prevents cellular oedema AND contributes to the membrane potential     T/F

Oxidative phosphorylation occurs in red blood cells     T/F

In some cells glucose crosses the cell membrane by secondary active transport     T/F

Bonus question (the answer can be worked out from material in chapter one) – the pH electrode has a semi-permeable membrane with the selective diffusion of hydrogen ions creating an electrical gradient which is measured. What equation is used to calculate the concentration of hydrogen ions from the electrical gradient?

And remember it’s the webinar today!

BT_PO 1.96 Discuss the significance of the blood brain barrier

Devilsadvocate has made a list of LOs we haven’t addressed yet and I’ll post on some of these orphans this week. I’ve used Ganong for this one but it should be in most of the basic texts.

Glucose passively diffuses into the brain     T/F

Circumventricular organs are within the blood brain barrier     T/F

Ions cross the blood brain barrier readily     T/F

Neurotransmitters cross the blood brain barrier readily     T/F

The blood brain barrier can be disrupted by acute severe hypertension     T/F

BT_RT 1.4 Discuss oxygen delivery and outline indicators of tissue oxygenation in resuscitation

Amazing sunrise this morning!

I though that this topic fit comfortably with yesterday’s post on the consequences of anaemia.

Oxygen delivery is an important issue for us. Knowing what happens as tissue oxygenation becomes impaired, will help you to understand the basis of the indicators we use.

Nunn’s Respiratory Physiology has a comprehensive chapter on Oxygen, Oh’s Manual of Intensive Care chapter on Oxygen Therapy (Ch 28) contains good information on measures of tissue oxygenation at the start of the chapter and here is an article from BJA Education (I think the CPT section is beyond the scope of the primary exam )

BT_RT 1.4 Describe oxygen delivery and outline the use of indicators of tissue oxygenation (base deficit, lactate, mixed venous oxygen saturation) in resuscitation

All the statements below are fairly core

In health, at rest, less than 30% of oxygen delivered to the tissues is used T/F

All organs have the capacity to increase their oxygen extraction ratio if oxygen supply is decreased T/F

Mixed venous blood can be sampled from a central line T/F

Lactate is only produced under anaerobic conditions  T/F

Base excess is positive with lactic acidosis T/F

 

 

BT_PO 1.110 Describe the physiological consequences of acute and chronic anaemia

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The plant above (photo courtesy of Jonny’s Seeds) is Amaranthus, or Love-lies-a-bleeding. Interestingly the seeds are a edible and very high in iron. How neat – the cause and cure for anaemia in one!

When I was in Copenhagen recently, I went to a very interesting set of talks regarding anaemia in the elderly and the implications for peri-operative management of these patients. Peri-operative management of anaemia has received a lot of interest in the literature in recent years as part of a patient blood management strategy. If you are interested in the topic, then you can have a look at this International Consensus Statement on Peri-operative Anaemia.

However the focus of this LO is more on the basic (patho)physiological consequences of anaemia.

BT_PO 1.110 Describe the physiological consequences of acute and chronic anaemia

There is a good chapter on anaemia in Nunn’s Applied Respiratory Physiology Ch 23 and here  is an article from BJA Education which covers the basic concepts.

These first statements cover core and important concepts

Oxygen delivery to the tissues is determined by both haemoglobin concentration and cardiac output T/F

PaO2 would be lower in the same patient at a Hb of 60g/dL compared with 13g/dL T/F

An increase in FiO2 from 0.21 to 0.5 will increase the oxygen content of the blood significantly in an anaemic patient T/F

Chronic anaemia decreases blood viscosity thereby reducing cardiac afterload T/F

Have a think about the next one, it is both true and false. You may need a calculator, but see if you can find some conditions where it is true

A doubling of cardiac output will compensate for a halving of Hb, with respect to oxygen delivery

I think this one is interesting, but not core (the answer lies in the first article I linked to in the introduction)

Iron deficiency is only detrimental if associated with anaemia T/F

 

BT_RT 1.13 Discuss factors leading to a loss of cerebral autoregulation

Nyhavn, Copenhagen

Last week I put up a post on regulation of cerebral blood flow.

Today I thought we would focus on another component of the same LO – factors that result in loss of autoregulation.

BT_RT 1.13  Describe the cerebral circulation, the regulation of cerebral blood flow and factors leading to the loss of autoregulation

Some of the mechanisms behind the loss of autoregulation are complicated. I think that a basic understanding of general principles would be sufficient for this part of the LO.

All the statements which follow fall into that category.

Miller and Hemmings and Egan, both have reasonable chapters on this stuff (they are very similar in terms of content and style as they have the same three authors…)

In a brain with significant cerebrovascular disease, vessels in areas of brain distal to an atherosclerotic narrowing will tend to be vasodilated to maximise flow T/F

Cerebral autoregulation is well preserved in traumatic brain injury T/F

Severe hypercapnoea will obliterate cerebral autoregulation T/F

If cerebral autoregulation is lost, and PaCO2 is normal, avoiding hypotension will help minimise the risk of ischaemia T/F

Cerebral autoregulation is preserved with propofol based anaesthesia T/F

Over at aGasgal I have attached links to a couple more articles on cerebral blood flow for those of you who are interested.

BT_RT 1.13 Describe the regulation of cerebral blood flow 

Louisiana Museum, about 45 minutes by train from Copenhagen – would strongly recommend you visit if you are ever in the vicinity (that’s Sweden in the distance)

I have recently been in Copenhagen at the Euroanesthesia meeting. I went to an interesting talk on hypotension, where the speaker made a joke regarding people being tortured by the cerebral blood flow autoregulation curve in their primary exams. It seems a shame to limit the “torture” to the exam setting…..

I have posted on the effect of cerebral blood flow on ICP  previously. You may find it useful to look at that post in conjunction with this one.

BT_RT 1.13  Describe the cerebral circulation, the regulation of cerebral blood flow and factors leading to the loss of autoregulation

The basics of this topic are covered in most physiology textbooks. However I think that Hemmings and Egan Ch 8  covers it better than most.

The first four statements cover important core material

Cerebral blood flow is autroregulated to maintain a constant flow in face of changing cerebral perfusion pressure T/F

Cerebral blood vessels are maximally dilated at the lower end of the autoregulation plateau T/F

As a general rule, the higher the cerebral metabolic rate, the higher the cerebral blood flow T/F

The most important factor in cerebral autoregulation is autonomic nervous system activity T/F

The speaker for the talk mentioned above was Adrian Gelb, from UCSF. Part of his talk referenced this article, which he authored, on the effect of CO2 on cerebral autoregulation. The article covers a lot of non core material, but I thought that his conceptualisation was very interesting, for those of you looking to explore the topic in more depth.

The last few T/F statements come from the article

Increased PaCO2 narrows the autoregulation range of blood pressures, by lowering the upper limit and elevating the lower limit T/F

The combination of hyopcapnoea and low normal BP may put the brain at risk of ischaemia T/F

The lower limit of autoregulation may be affected by the cause of the hypotension T/F

BT_PO 1.21 Discuss dead space, its measurement and apply the Bohr equation and alveolar gas equation

Core stuff and you should know the answers to all these questions. If you don’t then any physiology text will edify you.

The Bohr equation is used to calculate physiological dead space  T/F

End-tidal and mixed alveolar CO2 are very similar in the healthy subject  T/F

The Enghoff modification refers to substituting arterial CO2 for alveolar CO2  T/F

Anatomical dead space extends down as far as the fifteenth generation of airways  T/F

Intubation per se increases dead space  T/F

The PAO2 coming from the CGO of an anaesthetic machine with an FI02 of 40% can be calculated by the formula* = 0.4(760-47)- PaCO2/0.8  T/F

The calculated alveolar oxygen tension is altered depending on what you eat  T/F

ET CO2 decreases in hypotension because of increased anatomical dead space  T/F

*little tricky but nothing you can’t handle

BT_GS 1.2 Explain receptor activity with regard to: Ionic fluxes, Second messengers and G proteins, Nucleic acid synthesis, Evidence for the presence of receptors, Regulation of receptor number and activity

Signal transduction refers to the process by which receptors act to mediate their physiologic action  T/F

Important second messengers include cAMP, cGMP , Ca2+ and ITP        T/F

GPCRs have seven membrane-spanning alpha helices       T/F

Some receptors are intracellular             T/F

Receptors can be down-regulated by endocytosis and degradation by lysosymes     T/F

 

BT_RT 1.6 Describe the physiological basis of anaphylactic and anaphylactoid reactions

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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.

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

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 anaphylactic and anaphylactoid reactions T/F

The symptoms of 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 anaphylactoid, but not an anaphylactic reaction may be reduced by giving a drug slowly T/F

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