Blog #5

DICTIONARY

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Words for the week:

• Pathogen-associated molecular patterns (PAMPs): can be defined as conserved molecular components on the surface of microbes, such as cell wall of fungi, parasite, virus and bacteria. They can be expressed whether or not the microbes are pathogenic.
• Pattern recognition receptors: Receptors that recognize PAMPs. They trigger phagocytosis of the specific microbe. 
• Opsonins: are phagocytosis-enhancing proteins that bind to conserved , repeating components on the surface of microbes such as sugar structures, lipopolysaccharides (LPS), and viral proteins. 
• Mucins: are glycoproteins which prevents pathogens attachment. Also, traps microbes and cilia propels microbes away. 
• Tumor Necrosis Family (TNF): can be defined as family of cytokines that regulates the production, effector function, and homeostasis of cells participating in the skeletal, neuronal, and immune systems. 

Little Knowledge

Encapsulated bacteria (bacteria with an outer covering) possess a polysaccharide coat with a unique chemical structure. Examples of E.B include--salmonella typhi, hemophilus influenzae type b, streptococcus, and many more. They are antiphagocytic and vulnerable to B cells. Therefore, patients with B cell deficiency are likely to have encapsulated bacterial infections. For instance, those who have gotten a splenectomy are more susceptible to these pathogens. In addition, children do not have the ability to create antibodies to polysaccharides and are therefore, more likely to be infected by these type of bacteria (especially kids who are not breastfed), they lack T cell independent response. Therefore, it is standard medical procedure to get vaccinations, so these vaccinations can produce an I.R in cases such as this. 

*immune response = I.R*

Works cited

• "Immunology Basics." Pinterest. N.p., n.d. Web. 26 Sept. 2016.
• Ambrosino, D. M., G. Schiffman, E. Gotschlich C., P. Schur H., G. Rosenberg A., G. Delange G., E. Loghem Van, and G. Siber R. "Correlation between G2m(n) Immunoglobulin Allotype and Human Antibody Response and Susceptibility to Polysaccharide Encapsulated Bacteria." Journal of Clinical Investigation 75.6 (1985): 1935-942. Web.

Life gives us so much to reflect on...but so little time!

Reflections

My Immunology class, so far, has been revealing. As a medical student who would like to pursue hematology/oncology, this class has been so informative on different topics on the structure and function of the immune system, innate and adaptive immunity.  

BASICS

The organs of the immune system are categorized. Primary organs include thymus and bone marrow. Secondary organs include spleen, lymph nodes, and mucosal tissues. Tertiary organs are liver, skin, lungs. First, the thymus produces what are called T cells--two types--CD4(helper t cell) and CD8(cytotoxic t cell). The helper t cells activate both the cytotoxic t cells (which are cells that kill infected target cells) and B cells (cells that secrete antibodies to destroy ingested microbes and are produced in the bone marrow). Second, the spleen is an organ that filters old RBCs & WBCs (macrophages and dendritic cells) are stored there. You may be wondering what happens when a person gets their spleen removed (splenectomy)? Well, I earned that there are other organs that can work as well as the spleen which are the liver and kidneys. These two will take over the role of a spleen. 

The diagrams and case studies make me think. It's awesome. Everything I have learned so far are important. One thing that is confusing would be placing each cell in either innate or adaptive or both category. I think a chart of both immunity would be helpful. Ex: Helper t cells are adaptive while NK cells are innate, because I confuse innate cells with adaptive cells.

As a future hematologist, I have been self-studying on various blood related disorders. It involves treating disease that affect blood and its components. But first, I would have to know the components of blood, types of blood, and blood proteins. And, comprehending these cells would truly assist me in diagnosing my patients and finding the best treatment for them. Recently, a friend of mine came down with a cold, presented with fever, headache, loss of appetite, and nausea; and as usual she bought some painkillers for her headache and 'supposedly' for the cold. During lunch, I noticed she took two pills and without any hesitation, I told her that antibiotics does not cure a common cold because a cold is a virus infection and antibiotics are antibacterial medications. I didn't expect her to believe me; and so I researched it and showed it to her then she put it away. As a medical student, it is my job to educate others.

Case Study: 

A case study of a 70 year old woman had a CC of lethargy and bronchitis. She had been treated for two months with  antibiotics for bronchitis. The patient noted increasing fatigue and a fever with night sweats. P.E showed splenomegaly and lymphadenopathy. After evidence of abnormal cells on the bone marrow examination, the patient was sent to a Cancer Institute where staging of this disease was done. Four months from diagnosis, she relapsed with CNS involvement. The spinal fluid showed 100% abnormal mononuclear cells. (www.polconsultant.com). 

I would need to know the WBC, hematocrit, Plt, Hgb, & RBC numbers by doing a laboratory examination. I would [of course] place her on chemotherapy. What is the probable diagnosis? Hint: 

WBC 12,600	Differential:
RBC 3.70	Segs 42%
Hgb 11.0	Lymphs 45%
Hct 34.5	Monos 10%
Plt 255,000	Eoso 3%
	Lymphocytes appear immature with cleaved nucleus.

a.  Hashimoto's disease
b.  Non-Hodgkin's disease
c.   Multiple Sclerosis




Happy blogging!

Works Cited

• AG, Donna. "Reflection Perfection: 60 Photos That Show You How It’s Done." Hongkiatcom. Laura Williams, n.d. Web. 22 Sept. 2016.
• "Case Studies." Hematology. Western Tennessee Healthcare, n.d. Web. 22 Sept. 2016.

Blog #3 HOUSE.MD.

House, M.D. S2:E22 "Forever" 

In this episode, a woman suffered seizures while bathing her baby and almost drowned her baby. Her husband throwing up in a separate bathroom calls for her and with no response, he goes to check on her and dials 9-1-1. 

 (In the hospital)

EMT:  Four year old infant submerged in the bathtub.
           Don't know how long. Not responsive to the scene.

            (baby continues crying)

EMT #2: Caucasian, female, 32
               Tonic-cloning seizure in the bathroom.

First (False) Diagnosis: Colic Disease: Excessive crying in babies. Causes include constipation, GERD, lactose intolerance, anal fissures, subdural hematomas, and infantile migraine. The baby showed signs of intestinal gas, and allergy to the vitamins used for treatment. The baby experienced burning feeling in the thoracic cavity, pain, and tightness, dyspnea which led the doctors to think that he had chemical pneumonitis. In addition, the mother had multiple contractions in the chest which also led them to think that whatever the baby has, he got from the mother.

Actual Diagnosis: Celiac Disease aka Gluten-sensitive Enteropathy--genetic immune disease that results in the damage of the lining of the small intestine due to a sensitive reaction to gluten proteins. Celiac can be triggered by all kinds of stress--bills, childbirth, marriage, etc. The small intestine becomes damaged, less able to absorb vitamins and minerals into her bloodstream. Her body couldn't absorb niacin which caused pellagra, her body couldn't absorb vitamin K, which caused the bleeding.

My Immunology thoughts on Celiac Disease

A.A = Amino Acid(s)

So gluten is a protein, and proteins are long chains of amino acids. There are 20 various kinds of amino acids which of course would have 20 different kinds of linked long chains. These A.A are broken down to simpler compounds in our gut cell, proteins are secreted from the pancreas into the Ileum. (enterocytes = intestinal cells) and then transferred to our bloodstream. These A.A are created into a genetic sequence (AUG, GUU, GAA...) to make them into a protein. According to gi.org, "Gluten has two large numbers of glutamine and proline. We don't have the enzymes to break these amino acids apart. Rather than breaking the long chain into peptides, it stops at a peptide, a short chain." Therefore, gluten protein breaks down into a number of various peptides. In people with celiac disease, it's like each peptide causes a problem that increases the autoimmune reaction of other peptides.  I think the gluten peptide passes through the stomach cells where they are recognized as "foreign invaders."

Comment for more questions!

Works Cited

Chawla, Anupama. "Diagnosis and Management of Celiac Disease." Clinical Nutrition INSIGHT 36.1 (2010): 1-4. Web.

Blog #2 Investigation

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When I was searching up more information about the bone marrow, a condition came up during one of my researches called Amyloidosis. Amyloidosis is a condition where abnormal proteins called amyloid builds up in the tissue or organs. These proteins are produced in the bone marrow. Due to this build up, that affects their shape and function. My sources explains the types of amyloidosis, which are: Primary (AL) amyloidosis--seen in people with blood cancer and affects the kidneys, liver, heart, and certain nerves. Secondary (AA) amyloidosis--results from another chronic diseases such as lupus, rheumatoid arthritis, Crohn's disease. Familial Amyloidosis--this is passed down from families. It is caused by abnormal amyloid transthyretin (TTR) protein made in the liver. Dialysis-related amyloidosis--mostly occurs in the elderly that have been in dialysis for more than 5 years.
Although, some types of amyloid proteins have been linked to Alzheimer's disease but the brain is rarely involved in systemic amyloidosis. I have a lot of questions involving this disorder. Since it's produced in the bone marrow, why isn't it autoimmune? People with this condition, do they make enough CD4 cells & B cells? What is/are the main purpose(s) of amyloid proteins? What are they intended for? So many questions! I'm still researching on this topic...Amyloidosis Pt. 2 coming soon! :)

Works Cited

• "Amyloidosis: Symptoms, Treatments, Prognosis, Causes." WebMD. WebMD, 16 Apr. 2005. Web. 09 Sept. 2016.
• Tanzi, R. E., A. Mcclatchey I., E. Lamperti D., L. Villa-Komaroff, J. Gusella F., and R. Neve L. "Protease Inhibitor Domain Encoded by an Amyloid Protein Precursor MRNA Associated with Alzheimerʼs Disease." Alzheimer Disease & Associated Disorders 2.4 (1988): 383. Web.