PCL 8 A Big Night Out - tasks for this week

1. Component of blood, blood transfusion, units of blood & IV (Madhura)
2. Anatomy & Physiology of the kidney (gross) and nephron (detail) (John & Lawrence)

Kidney Failure
3. Causes/Pathophysiology - why kidneys stop working? effect of dramatic drop in renal perfussion during hypotension on the kidneys? (Ji Keon)
4. Signs & Symptoms - indication of kidney ceases function? normal urine output? decreased urine output? (Christine)
5. Investigations - ultrasound, kidney function tests and the significance of the results (Chris)
6. Management, Prognosis and Complications of end stage renal failure (Shanthini)
7. Urethral catheter - why? how? (Sri)

8. Spleen - physiology, effects of removal, management & follow up (Vivian)
9. Blood alcohol content effect on kidney function (Lawrence)

Announcement

The anatomy blog has been officially set up. Thus, all matters regarding anatomy sessions should now be directed and addressed at the new blog. This blog will be reserved specially for our PCL only.

Thanks.

Deep Facial Regions - Anatomy Tasks

This is just a reminder for the tasks that we are going to do on thursday, after the 2pm lecture.

1. Describe the temporomandibular joint. (Ji Keon)
2. Describe the muscles of mastication. (Shanthini)
3. Describe the maxillary artery and it's major branches. (Vivian)
4. Describe the maxillary and mandibular nerves. (Lawrence)
5. Describe the boundaries and contents of the temporal (John), infratemporal (Sree), and deep styloid regions (Madhura).
6. Group and list the foramina of these regions (temporal, infratemporal and deep styloid) ; describe contents. (Chris)
7. Demonstrate the surface anatomy of the regions and indicate clinical situations when this knowledge may be useful. (Christine)

John

CF - psychosocial issues

again not my area, but just my food for thought on the part D cliff hanger...

Issue in Pt D: Georgia (15y/o) has stopped her treatments and exercises.

Effect of CF on a adolescents:

• Adolescents will find it difficult to maintain a good social life due to their physical conditions and the fact that they are being controlled by their parents. Parents with children who have CF tend to be overprotective about their child doing certain things.
  These parents may fell that their chronically ill child is more susceptible to the dangers of the world.
• keeping up with school work can be difficult when you have to stay in the hospital for months at a time.
• If your friends have don't know you have Cystic Fibrosis, they will annoy you with questions about everything. They may wonder about your cough or all the pills you take.

this is a quote from the video i watched:

“Growing up has a lot of ups and downs when you have CF. The hardest thing for CF people (and me) I think, is that they want to be a normal person. No vitamins, aerosols, enzymes, Iv's, hospitalizations -- wouldn't that be great. It's hard for a lot of CF kids and even adults to remember that you have to do all those things to stay healthy. No matter what disease or problem you have, you still are a normal person. Another hard thing for me was not growing up as fast as everyone else. I'm not sure if that effects every CF person. But, for me, it sucked. In 8th grade, I only weighed 87 pounds. To me, I felt like a shrimp-- not just in 8th grade, up till about 10th grade. I didn't mature as fast as everyone else either. I hated that. I think I didn't have a lot of self confidence in myself at the time or maybe it wouldn't have mattered.
I always felt nervous taking my pills around other people. Even know when I go out to eat, I wonder what people think (It does not bother me as much now). I know it shouldn't matter, but I think every CF person wonders about it once in a while.”

Shantz

CF - clinical features

This wasn't really my area but I decided to post it up since I mentioned a couple of points during my presentation and just to expand a bit on what Vivian has done since Dr. Laksmi asked me to connect the pathophisiology with the signs and symptoms and complications...

So as mentioned earlier, the concentration of sodium and chloride within the ECF and ICF is disrupted because of the failure of opening of the chloride channel in response to elevated cAMP in epithelial cells (CFTR is a chloride channel). Consequences of this:

• In the sweat glands the chloride ions can not be reabsorbed from the sweat before it is expelled onto the skins surface, this also inhibits the reabsorbing of sodium ions. This results in significant loss of these ions, altering the overall balance within the body and which can cause abnormal heart rhythms.
• In the pancreas the inability to move chloride ions out of the cell and into the ducts also prevents the movement of water in the same fashion as the water normally followed the chloride ions via osmosis. These results in digestive enzymes not being carried out into the intestines through the water, the enzymes instead digest the pancreas triggering inflammation and mucus build up (90% of CF patients have pancreatic damage)
• The mutant CFTR also triggers mucous build-up in the lungs, causing the most noticeable symptoms of Cystic Fibrosis. The mucus can partially block parts of the lungs and most importantly is an excellent growing medium for bacteria, leading to chronic respiratory infections that inevitably result in lung damage.
• nutritional effects - malnutrition due to malabsorption and maldigestion
• delayed puberty and skeletal maturity
• males are always almost infertile owing to failure of development of the vas deferens and epididymis. Females are able to conceive but often develop secondary amenorrhoea as the disease progresses

~shantz~

Pathophysiology of CF

CF (Also known as mucoviscidosis or 65 roses)

• autosomal recessive inherited disorder (recap: both parents must be carriers; 25% chance for child to have the disease; 50% chance of being a carrier)


• single gene disorder


• gene mutation along long arm of chromosome 7 (7q21.3 to 7q22.1)


• There are at least 500 different genetic mutations associated with the disease, approximately 70% of the mutations are found to be deletion at position 508 (delta F508) in the amino acid sequence on chromosome 7, making it the most common CF mutation


• the gene codes for a membrane protein in epithelial cells which regulates chloride transport- cystic fibrosis transmembrane regulator (CFTR). Mutation results in defective CFTR


• In 20-30% of cases the secondary and tertiary structure of the protein is altered making the protein non-functional and leading to the chloride channels failing to open in the epithelial cells. The other 70-80% of cases involve the cells quality control processes destroying all the CFTR produced as it is ‘defective’, preventing the ion channels from even forming. Both result in an inability of the cell to control the concentration of ions in the intra and Extracellular fluid.
• So in summary (see diagram below):

xoxo~Shantz

source: Kumar and Clark and www.childsdoc.org

Tasks For Monday's PCL (Hot Summer's Night)

1. Function of kidney
2. Nephron (know how to draw)
3. Kidney function
- increase
- decrease
4. Urine output
- normal
- disease
5. Acute Renal Failure (ARF)
- alcohol - kidney function and urine output

(Posted by: Vivian)