Showing posts with label SGD. Show all posts
Showing posts with label SGD. Show all posts

Thursday, 22 March 2012

SGD: Concept of Compensation

At SGD a student asked questions about the nature of compensation:
  1. What is the meaning of compensation?
  2. What are the types of compensation?
  3. Why is the opposite of a condition taken as the compensation?
  4. Why is there 2 phases for compensation, acute and chronic phases?
  5. Which conditions have 2 phases for compensation?

There are 4 simple acid-base disorders: respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. 

Respiratory acidosis has a 2-phase compensatory mechanism - acute and chronic. Respiratory alkalosis has a 2-phase compensatory mechanism - acute and chronic. In respiratory conditions, the compensation is two-phase - acute and chronic. The acute phase involves correction by blood buffers and the chronic phase involves the kidneys. 

In respiratory acidosis, the chronic compensation involves mechanisms to conserve and increase the bicarbonate levels (this resembles metabolic alkalosis), and occurs by two means - regeneration of bicarbonate and reabsorption of bicarbonate.

In respiratory alkalosis, the chronic compensation involves mechanisms to reduce the levels of bicarbonate and to increase acids in the blood. The chronic compensatory phase involves excretion of bicarbonate and conservation/regeneration of acids.

Metabolic acidosis has a single phase compensation. Metabolic alkalosis has a single phase compensation. In metabolic conditions, the compensation is single phase. 

In metabolic acidosis, there is excess acids in the blood and the blood pH drops. The compensation in metabolic acidosis is to breathe fast (hyperventilate), which resembles the mechanism for respiratory alkalosis.

In metabolic alkalosis, there is loss of acids and excess bicarbonate exists in blood. The compensation in metabolic alkalosis is to breathe slowly (hypoventilate) or breathe into a paper bag and breathe the same expired air from the paper bag.


SGD: Compensation in Metabolic Acidosis

Questions asked by a student at SGD:

  1. Why in Metabolic Acidosis, the compensation has no acute phase? 
  2. Why is Respiratory Alkalosis single phase?
  3. Is the compensation acute or chronic?
  4. How long is the compensation in Metabolic Acidosis?

In Metabolic Acidosis, there is a marked drop in bicarbonate concentration, and pH falls considerably. The compensation is a steady (smooth hyperbolic) increase in PCO2. In the acute phase response or compensation, the blood buffers try to correct the change first and breathing slows down (becomes slower, hypoventilate). The slowed breathing continues past the 10-minute critical timeline and for up to 12 to 24 hours (approx. 1 day) whereby the body is able to retain sufficient CO2 to increase the PCO2 and the pH steadies to a higher level but never reaching 7.40. A rising pH and PCO2 are sufficient to tell us that compensation is taking place. When the PCO2 is high and pH near normal, then that is considered as complete compensation, and the patient should be breathing normally by 24 hours (one day observation).



SGD: Factors Affecting Plasma pH, PCO2 and HCO3

Please use the Henderson-Hasselbalch (HH) equation to answer Q2a-c.

In the HH equation, there are 3 terms which can be variable: pH, PCO2 and HCO3.

Since there are 3 variables, it means that if you know the values for 2 variables, you can work out the unknown variable.

pH - is controlled by HCO3 and PCO2

PCO2 - is controlled by pH and HCO3

HCO3 - is controlled by pH and PCO2


WHAT YOU MUST KNOW

For learning, assessment and exam purposes, you must remember that these 3 variables always work together. Disturbing any one variable will disturb the other 2, which will respond to the change. Thus, you have what is called compensation coming into play.

EXAMPLES OF CASES

In the conditions we get at the hospital (vomiting, diarrhoea, emphysema, coma, hysteria, ketoacidosis, poisoning, etc), usually pH is altered by the alteration of HCO3 or PCO2 (simple acid base disorders). We look at the physical state of the patient and we should know whether the respiratory system is held up or not.

HOW TO UNDERSTAND AND INTERPRET

If the main change (lesion) is due to respiratory causes, then it is more likely that the PCO2 changed, causing blood pH to change, and the compensation will be the corresponding change in the HCO3, which needs to correct and bring back pH towards normal.

If the main change is due to metabolic causes, then it is more likely that the HCO3 changed, causing blood pH to change, and the compensation will be the corresponding change in the PCO2, which needs to correct and bring back pH towards normal.

IS IT ACIDOSIS OR ALKALOSIS?

Whether it is acidosis or alkalosis depends on what the causative agent was and what the initial effect was on blood pH.

If a patient ingested (makan) a whole bottle of aspirin, that gives rise to metabolic acidosis.

If a patient has diarrhoea (cirit-birit) for 3 days, that gives rise to metabolic alkalosis.

If a chronic smoker has difficulty breathing, coughs a lot and has water in his lungs (emphysema), that is respiratory acidosis.

If a patient suffers from Duchenne Muscular Dystrophy (DSD), the breathing muscles are affected (usually the muscles for expiration), and if his respirator fails to operate, he should have respiratory acidosis.

BREATHING CHANGES

Breathing has significant effects on blood pH. Breathing rate affects blood pH. Breathing rate can be normal, fast or slow, depending on the state or condition a person is in.

Breathing fast is hyperventilation.

For example, this occurs after you dashed from your car into your house because you saw a burglar with a knife in your compound. When you are immediately inside the safe confines of your house, you are still panting and hyperventilating but that should cease within some 20 minutes when you can think properly.

Breathing slowly is hypoventilation.

For example, you are so full after eating 2 plates of nasi biryani from your favourite restaurant tepi jalan. The only thing you can do next is to sit back and breathe slowly cos even your lungs cannot expand properly cos your tummy is so tight and full, filled to the limits, that your lungs are slightly compressed. This slow breathing is dangerous as you tend to retain a lot of CO2 in your lungs and in the blood. Your blood pH drops as a result of high PCO2 in the blood. Now, when you have a lot of CO2 in blood, what comes next? What is the special property of CO2? I have told you in class that CO2 is a special gas that has a special property and that it can penetrate all parts of the body, diffuse everywhere and anywhere in the body but there is one location in the body that it likes to go to. Where is that? Yes, CO2 prefers to go to the brain. What does CO2 do to the brain? There are chemoreceptors in the brain that react to blood pH (from the reaction of CO2 with H2O). Essentially high CO2 tells the brain to go to sleep. And you will fall asleep after your nasi biryani feast, and also suffer from respiratory acidosis cos you can't breathe properly until that nasi biryani empties out of your tummy in 4 hours and your lungs can breath again.

RULES ABOUT BREATHING

Alveolar ventilation - hyperventilation reduces blood PCO2; hypoventilation increases blood PCO2

If the lungs are damaged (crushed or excised) - you can still live but with assisted respiratory support.

WHAT ABOUT BICARBONATE?

Bicarbonate is bicarbonate and never mention bicarbonate ion unless you failed chemistry in Form 5.

Bicarbonate is a negative ion or an anion with a negative one charge (-1).

You can write bicarbonate in full on exams but you can also just write HCO3 or HCO3-. Nobody cares whether you put a negative one for bicarbonate or not. It is clearly understood that bicarbonate has a negative one charge whether you write it or not.

What is special about bicarbonate?

The bicarbonate balance in blood deals with 2 things - regeneration and reabsorption. What is what?

Regeneration of bicarbonate means bicarbonate is generated once more. You start visualising at the glomerulus. I told you in class that blood bicarbonate concentration is the same as that in the glomerular filtrate because bicarbonate diffuses freely through the glomerulus. Now the problem is how to get back the bicarbonate from the renal tubules into blood. First you need to regenerate bicarbonate inside the tubular cells by combining bicarbonate with secreted protons to form carbonic acid, which instantaneously breakdown to H2O and CO2. Both H2O and CO2 diffuse and get inside the tubular cells. H2O goes to combine with cellular CO2 to form carbonic acid which dissociates to form proton and bicarbonate ... which can then exit the tubular cells into interstitial fluid and re-enters blood. This reabsorption is accompanied by sodium and water.

Reabsorption of bicarbonate means bicarbonate is absorbed and that the absorption process goes on until bicarbonate goes back where it belongs (blood). I have told you in class that of the many blood buffers, 70% of CO2 exists as bicarbonate in blood plasma. That process of bringing bicarbonate from the renal tubules back into blood plasma is referred to as reabsorption (serapan balik ke dalam darah semula).

If you study carefully you will see that the regeneration is the first part and reabsorption is the second part. Both processes are linked, and must occur in tandem, before bicarbonate reappears in blood.

EXCRETION

What is excreted and when does excretion occur?

Acidosis - excess protons are excreted in urine.

Alkalosis - excess bicarbonate is excreted in urine.

In acidosis, the urine is more acidic than normal but there is a limit to the acidity of urine. The acidity of urine stops at pH4.5 (round about that #) and it cannot be any lower. If you get a urine specimen and the pH says 3, I think there's something funny with that urine specimen. Probably it is a ghost urine (hantu jembalang).

In alkalosis, the urine is slightly more alkaline than normal and there is no limit to the alkalinity of urine, but of course the patient may pass out first. If the upper limit of blood pH is 7.45, you would expect urine from a dead person to be more than pH8. Next time you see a urine specimen with pH more than 8, let me know, I will bring kain kafan too.

SGD: Acid-Base Homeostasis, Fluid & Electrolyte Balance and Potassium Metabolism

I had finished my SGD when 2 students approached me and asked who was their SGD tutor. I asked them which group and they said Group 7. That time I didn't have this info (below) with me. I could not take them as I was already tired teaching my group but I asked the 2 girls to get in touch with the students in my group.

Next time ask the Block Coordinator for the names of tutors for all the groups, or ask Pejabat Akademik before the SGD. I have informed Pejabat Akademik that students must be informed of who their tutors are and this info should be printed on the time-table. For Phase 2, if they can print PBL tutors' names + Groups + Room #s, why can't they do the same for Year 1 SGDs?

This is the info that the Block Coordinator e-mailed to the lecturers (tutors) but the students were not informed for which they did not know who was taking them for SGD. I am not in-charge but I regret that your SGD tutor failed to show up for class.


from: Dr. Iskandar Zulkarnain Alias iskandarza@kb.usm.my
to: "A.Rashid, Faridah" <faridahar@gmail.com>,
 "Aini, Suzana" <ainiszn@kck.usm.my>,
 "Swamy, Dr" <mswamy@kb.usm.my>,
 soriani <soriani@kb.usm.my>,
 sirajuden <sirajuden@kb.usm.my>,
 "Julia, Omar" <julia@kb.usm.my>,
 "Hasnan, Nordin" <hans@kb.usm.my>,
 "Mar, Dr" <winmar@kb.usm.my>,
 "Iskandar, ZA" <iskandarza@kb.usm.my>
date: Sun, Mar 18, 2012 at 12:09 PM
subject: SGD Groups



Salam and good morning,


Here is a new grouping system for Chempath SGD provided by Academic.


SGD GROUPS YEAR 1 MEDICAL STUDENTS 2011/12. There are 18 groups totally.


1.      GROUP 1A & 1B – JOM
2.      GROUP 2A & 2B  – NSY
3.      GROUP 3A & 3B  – FAR
4.      GROUP 4A & 4B – KNSS
5.      GROUP 5A & 5B – IZA
6.      GROUP 6A & 6B – WMK
7.      GROUP 7A & 7B – HN
8.      GROUP 8A & 8B – MS
9.      GROUP 9A & 9B - ASA


Thank you
Dr. Iskandar ZA.

Tuesday, 25 October 2011

SGD: Energy Metabolism in Muscle - sources of energy for muscle contraction

Musculoskeletal Block, MD Phase I 2011/2012
Prepared by Dr Aini Suzana Adenan
17 October 2011

SGD
1. List the sources of energy that can be used for muscle contraction. Explain briefly how energy is derived from these energy sources.

SGD: Energy Metabolism in Muscle - plasma lactate rises after exercise

Musculoskeletal Block, MD Phase I 2011/2012
Prepared by Dr Aini Suzana Adenan
17 October 2011

SGD
2. Explain why plasma lactate level increases after prolonged and severe muscular exercise.

SGD: Energy Metabolism in Muscle - TCA cycle is aerobic pathway

Musculoskeletal Block, MD Phase I 2011/2012
Prepared by Dr Aini Suzana Adenan
17 October 2011

SGD
5. Give reasons why TCA cycle is an aerobic pathway even though oxygen is not involved directly in its reactions.

SGD: Energy Metabolism in Muscle - Chemiosmotic theory, oxidative phosphorylation, ATP generation

Musculoskeletal Block, MD Phase I 2011/2012
Prepared by Dr Aini Suzana Adenan
17 October 2011

SGD
6. Explain the chemiosmotic theory of oxidative phosphorylation in the generation of ATP.

SGD: Enery Metabolism in Muscle - Inhibitors and mutations of ETC proteins

Musculoskeletal Block, MD Phase I 2011/2012
Prepared by Dr Aini Suzana Adenan
17 October 2011

SGD
7. Inhibitors of the electron transport chain proteins and mutations in the mitochondrial and nuclear DNA that encodes them can cause reduced activity of the electron transport chain. Explain why impairment of the electron transport chain can cause lactic acidosis.