This blog post is to those who are doing Applied Animal Physiology.
We all know how much of struggle this subject has been. There is so much ambiguity, so much content…it is actually ridiculous.
This subject makes everything else seem like a breeze, even that Intro to blue planet subject which I was having problems with last semester. I’m faced with a question whether I should sacrifice my study time on my other 2 good subjects and work more on this crappy subject, and get somewhat balanced grades. OR, focus on the 2 good ones, do well on those 2, and do really bad on this one.
I’ve done the maths, and I need about 70% on this exam to pass.
I’ve come to a conclusion that there was no point in going through all the 12 weeks of lecture contents. I need to come up with a new (and smarter) way to approach to tackle this exam.
Seeing as time is running out (the exam is next tuesday), and there are quite a lot of past papers available – I thought I see if there are patterns in questions in these papers.
And, good news!
There ARE trends in the exam papers!
Looking at the 2011, 2010, 2008, 2007, 2006, 2005, 2003 past papers, I’ve noticed that they recycle the questions from past papers. The same kind of questions pop up in every paper – they would re-word it, put in new numbers for calculations…but essentially – the same types of questions!!
So I thought – hey, if they’ve been doing this for the past 10 years…there is a good chance that they’ll do it again this year! (I hope so…)
Disclaimer: I wouldn’t recommend this approach when studying for an exam, but desperate times call for desperate measures.
EDIT: Look at what I found on the LMS a week later
Mind you – there have been changes to the exam structure and format.
Format of our 2013 exam
This is the format of this year’s paper according to the coordinator on the discussion board
2 sections in the exam:
(1) 30 Multiple Choice worth 60 marks
(2) 5 written answers worth 90 marks (you get to choose out of 6 questions)
Bring your calculator – calculations may pop up in the paper.
Prac content is examinable – with the exception of the 2 pracs that we wrote up a lab report for.
What has changed?
Past papers had 3 sections – section A (multiple choice), section B and C (written). Now, there’s only 2.
Plus, the older papers went on for 3 hours, instead of 2. So just keep that in mind when you’re working on past papers.
What will I be doing in this blog post?
I’ve gone through all the past papers and noted down the patterns in the questions. I found some pretty interesting things looking at the old papers, and I thought that I should share them with the other people doing this horrendous subject.
Sharing is caring right?
Hopefully it will help us with the exam.
So, I’ve dissected the past exam papers and broken them down into these categories:
– Nervous system
– Muscle physiology
– Circulatory system
– Urinary system
– Respiration system
– Digestive system
– Endocrine system
And also, looking at the themes that pop up in the short answer section.
If you hover your mouse over the image, I’ve included the year of the paper that I’ve taken the question out of (just for reference).
The references to textbook are to the 2nd edition of Sherwood’s Animal Physiology: From genes to organisms.
The answers to the 2008 Multiple choice is available on the LMS
The highlighted answers are not 100% correct – I just quickly highlighted them as guesses, and I can’t figure out how to un-highlight them.
I know some of the pictures are tiny, wordpress gallery is just like that. You can click on the them to see the full size pic, and use the arrow keys to see the next image.
Here goes nothing.
These questions just change whether it’s sodium or potassium that is high/how in interstitial and plasma fluids.
Hyperpolarisation = making the membrane more negative than at resting potential
Hypopolarisation = making the membrane more positive
See page 122 of the textbook.
When I looked in the glossary of the textbook, astrocytes were defined as:
A type of glial cell in the vertebrate brain; major functions include holding the neurone tougher in proper spatial relationship and inducing the brain capillaries to form tight junctions important in the blood-brain barrier.
ADP and calcium levels contribute to muscle contraction, but magnesium?
From this article, I think it’s saying that magnesium reduces the rate at which calcium binds to something that causes contraction. Therefore increase amounts of magnesium = relaxed muscle? I think?
Do correct me if I’m wrong!
Haha, this one has been in almost every paper I’ve done. It varies whether it’s asked in a multiple choice or written answer format.
Here’s an example of a written response question:
And here it is in multiple choice format:
Some equations that will help you to do those calculations:
Tidal volume = Vital capacity – inspiratory reserve – expiratory reserve
Pulmonary ventilation (ml/min) = tidal volume x respiratory rate
Alveolar ventilation (ml/min) = (tidal volume – dead space) x respiration
Anatomical dead space is the volume of lung that doesn’t take place in gas exchange.
For example, looking at the 2008 MC question.
Tidal volume = 4,500 ml (vital capacity) – 3,000 ml (inspiratory) – 1,000 ml (expiratory) = 500 ml
Pulmonary ventilation = 500ml (tidal volume) x 15 (respiration rate) = 7,500 ml
See page 522-524 in the textbook for more info. I found the second diagram on pg 524 handy.
This is what the coordinator said about this question.
S1= “lub” – this is the sudden block of blood because the valves contract (systole)
S2= “dub” – when the aortic and pulmonary valves closes after the blood has been pushed out (diastole)
S3 = de” – this is rare and indicates that there is an increased volume of blood in the ventricles
S4 = “pah” – blood if forced in the ventricles
Basically S1 and S2 = normal, S3 and S4 = rare.
(He covered this briefly in L9)
p.s. There was also a short answer question on heart sounds in the 2011 paper
Packed cell volume
In the 2006 and 2007 questions, this is how I got my answer: PCV = 7/11 = 0.64. (11 being the total)
And in 2008, if the PCV was 48%, then the plasma is 52%. So 52/10 = 5.2ml
More on PCV on page 388 in the textbook.
There are 3 steps in blood clotting.
1) Vascular spasm – releases chemicals to reduce blood flow and the skin surface are pressed together to seal off the damage vessels.
2) Formation of platelet plug – platelets attached to collagen, and continue to aggregate and build up via positive feedback. Note that it doesn’t continue to stick to the entire endothelial lining because of prostacyclin and nitric oxide.
3) Blood coagulation – transforming the blood into a gel to form a clot! This involves the conversion of fibrinogen to fibrin via thrombin. But to get thrombin in the first place, prothrombin is converted to thrombin via factor X. So there is this cascade of events to get clotting happening.
More info on page 394-397 in the textbook.
I ruled out C because looking at the equation for cardiac output…
Cardiac output (CO) = stroke volume x heart rate.
If you put a large number in there, cardiac output would be larger.
I’m going with the answer given in the 2008 paper (because they published the answer for that year), they said that cardiac output would decrease if end-systolic volume is increased. But I’m not sure why…more googling!
p.s. watch out for the wording of the question ;)
Increase in blood viscosity
It’s always an animal that is injected with something that increases/decreases blood viscosity, and you have to figure out what the impact is.
According to the textbook (pg. 420)
Higher viscosity creates higher resistance to flow
The 2008 paper says the answer is calcium…but I thought pacemaker cells leak potassium?
Cardiac cell contract
Page 409 of the textbook has a good diagram that summarises this.
The main difference between cardiac and pacemaker cells is that cardiac cells have a plateau in their action potentials.
Function of the spleen
Paraphrasing from the textbook (pg392)…
Spleens have 2 main roles: 1) Remove old blood cells and 2) as a reservoir for blood cells.
Look on page 393 for more info.
But basically – when the kidneys detect low oxygen in blood, it will secrete EPO into the blood. This stimulates erythropoiesis (the process of making more erthrocytes), and this occurs in the bone marrow. Then these extra erythrocytes increase the capacity of the blood to carry more oxygen.
Drop in CO2 to arterioles
This website says that: “the greater the carbon dioxide (CO2) concentration the less the extent of vasoconstriction (VCN). In other words, if there is a lot of carbon dioxide in the tissue a greater blood flow is needed to allow its diffusion into, and removal by, the blood.”
Page 585 textbook says that aquaporin “channels in the distal tubule and collecting duct are regulated by the hormone, vasopressin, which accounts for the variable H2O reabsorption in this region.”
In short, vasopressin is stored and released from the posterior pituitary when the hypothalamus tells it to. This causes the arterioles to contract (vasoconstriction). It also increases the water reabsorption from kidney tubules and collecting duct. I’m not 100% if my answer about hyper and hypo is correct (I always get them mixed up).
All I know is that
Hypertonic = urine more concentrated and less volume
Hypotonic = urine diluted and large volume
It should be hypertonic right? Seeing as water is reabsorbed, so urine is more concentrated?
Page 587 in the textbook:
Aldosterone increases Na+ reabsorption by distal tubules and collecting ducts
Renin is released from mammalian kidneys in response to a decrease in NaCI/ECF volume/arterial blood pressure; activates angiotensinogen.
FYI: I made a mistake in the sodium reabsorption question. The answer should be aldosterone.
Same question (except for the last one) in the papers.
Well the “latch phenomenon” or latch state” is defined as “a state of continuous contraction of smooth muscle that maintains tension.”
High protein levels in urine
Well…a quick google search about protein in urine said:
Although healthy people do pass small amounts of protein in the urine normally, above a certain level suggests that there may be damage to the filter mechanism (the glomeruli) or inflammation.
Don’t know about the horse one – will google later.
Gas transfer across alveolar membrane
The 2008 answers say that partial pressure is the answer…but, I don’t know. One thing I’ve learned in biology is that anything to do with diffusion is related to surface area. More googling for me.
Rhythmicity of respiration rate
On page 547, the textbook says
Vertebrate breathing is regulated by a rhythmic neural program in the medullar respiratory centre in the brain stem
I couldn’t find anything useful about pleural cavities in the textbook p 510. So I turned to wikipedia.
Wikipedia says that “Normally, the pressure within the pleural cavity is slightly less than the atmospheric pressure.” And IF the pressure is equal to atmospheric pressure, that means that the cavity is damaged.
Textbook (page 550) says that “the two most obvious signals to increase ventilation are a decreased P02 or an increased arterial PCO2”.
It later goes on and says that the receptors respond “most strongly to H+, but also to O2”. (No mention of CO2). And it also says that “chemoreceptors of air breathers are moderately sensitive to reductions in arterial PO2.”
Page 542 textbook:
Hypoventilation = excess CO2 in the arterial blood. Aka too much CO2 in your system.
Changes in blood CO2 concentration primarily affect acid-base balance. Results in elevated production of carbonic acid. Excess H+ produces respiratory acidosis.
Page 521 of the textbook says that surfactant provides 2 benefits:
(1) It increases pulmonary compliance, thus reducing the work of inflating the lungs
(2) It reduces the lungs’ tendency to recoil so that they do not collapse as readily
Okay…St John’s wort is poisonous in large doses and this reduces albumin levels. Albumin is a plasma protein and is important for the transportation of stuff in the bloodstream. According to this website, decreased albumin “allows fluid to leak out from the interstitial spaces into the peritoneal cavity, producing ascites.” So I picked B.
Unique feature of GI system
Well…contractions are caused by action potentials and are influenced by nervous activity – so that’s rules two of the options out.
Wasn’t sure about the other 2 options…Wikipedia says that:
The basal electrical rhythm allows the smooth muscle cell to depolarize and contract rhythmically when exposed to hormonal signals
Page 678 of the textbook
Basically there are 3 phases in gastric secretion: cephalic, gastric and intestinal
Cephalic = secretions BEFORE the food ever reaches the stomach
Gastric = secretions when the food is in the stomach
Intestinal = secretions when the food leaves the stomach
Page 684 of the textbook: “The primary stimulus for secretin release is acid in the duodenum”
I haven’t looked into this yet.
Enterogastric reflex, secretin and cholecystokinin all inhibit gastric mobility whereas gastrin doesn’t. See page 672/3 in textbook.
See page 686-689 of the textbook.
When a large fat droplet is broken up into smaller fat droplets by intestinal contractions, bile salts adsorb on the surface of the small droplets, creating shells of negatively charged, water-soluble bile salt components that cause the fat droplets to repel from one another. This emulsifying action holds the fat droplet apart and prevents them from recoalescing, increasing the surface area of exposed fat available fro digestion by pancreatic lipase – pg 689
Page 322 ” Thyroid hormone regulation of basal metabolism is important for fuel homeostasis”
Fat absorption through micelle formation
Glossary of the textbook define bile salts as:
Cholesterol derivatives secreted in vertebrate bile that facilitate fat digestion through their detergent action and facilitate fat absorption through their micellar formation
Movement of food
Page 668: “Peristaltic waves push the food through the esophagus”
Plus, a bolus is equivalent to a ball of food. Unnecessary fancy-pants term.
Amino Acid absorption in small intestine
Page 697-8 of the textbook: “Amino acids are absorbed into the epithelial cells by means of NA+ and energy-dependent secondary active transport via a symporter”
In regards to simple diffusion – “amino acids enter the blood by simple diffusion,” not absorbed.
Wikipedia: It is both an endocrine gland producing several important hormones, including insulin, glucagon, somatostatin, and pancreatic polypeptide, and a digestive organ, secreting pancreatic juice containing digestive enzymes that assist the absorption of nutrients and the digestion in the small intestine.
Antagonism of hormones
Page 278: “Antagonism occurs when one hormone causes the loss of another hormone’s receptors, reducing the effectiveness of the second hormone”
Yep – epinephrine is secreted by the medulla and is involved in the “fight or flight” response.
Permissiveness of hormones
Wikipedia: Permissiveness is a biochemical phenomenon in which the presence of one hormone is required in order for another hormone to exert its full effects on a target cell.
Also – check this out on page 278 of the textbook.
Stepping away from the multiple choice section now…I also found that the questions in the short answer were quite predictable.
Themes spotted in short answer sections
Change in movement and its impact
Feeding animals with high sodium
Anterior vs posterior pituitary gland
Carbohydrates and fat digestion
Types of hormones
So that’s that. I hope that you have found this post somewhat useful – and good luck with the studying!