The Journal of Medical Student

19 year old mad medical students who loves science fiction and fantasy

[mad-med-stud]

I am a undergrad pre-med and I am trying to figure out what classes to take for next semester. Which class would be most helpful or better appreciated for med school Animal Development or Comparative Vertebrate Anatomy?

I think it’s all up to your interest :)

But i personally will choose animal development since it will explain the components and functions of key molecular genetic and signaling pathways, and also how they work to determine cell fate in selected organisms, and how their dysfunction causes human disease and malformation

[mad-med-stud]

Test for Thyroid Disease

RAIU (Radioactive Iodine Uptake Test) The RAIU test provides a useful assessment of thyroid function: in general, the higher the iodine uptake, the more active the gland. The most useful role of RAIU test is in determining the etiology of thyrotoxicosis. In "true hperthyroidism" - RAIU uptake will be high while thyrotoxic patients with thyroiditis or who abuse thyroid hormones will have a low RAIU (Thyrotoxicosis simply refers to excess thyroid hormone in the body and may be due to overactivity of the thyroid gland (hyperthyroidism), or other causes such as inflammation of the gland (thyroiditis) or ingestion of excess thyroid hormone)

In all Hyperthyroid, the TSH level will be low because of the high amount of thyroid hormon will give its feedback effect to hypothalamus, thus making the TSH low & the T3 T4 high

In Graves’ disease/toxic diffuse goiter, (autoimmune disease) the TSI is high because Thyroid-stimulating immunoglobulins (TSI) recognize and bind to the thyrotropin receptor (TSH receptor) which stimulates the secretion of thyroxine (T4) and triiodothyronine (T3). Thyroxine receptors in the pituitary gland are activated by the surplus hormone suppressing additional release of TSH in a negative feedback loop. The result is very high levels of circulating thyroid hormones and a low TSH level.

In Hypothyroid, higher TSH levels mean that your brain thinks the thyroid is not producing enough hormones and needs stimulation. But however the TSH level will be low if there’s pituitary abnormality, thus not stimulating the thyroid to produce TSH & T4

in Hashimoto’s disease/chronic lymphocytic thyroiditis, (autoimmune disease) Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors, although a small percentage of patients may have none of these antibodies present this is why there’s + result in antithyroid antibody

Source : http://www.auntminnie.com/index.aspx?sec=ser&sub=def&pag=dis&ItemID=55330

https://en.wikipedia.org/wiki/Graves'_disease

http://www.endocrineweb.com/conditions/hashimotos-thyroiditis/hashimotos-thyroiditis-diagnosis

[mad-med-stud]

Inflammatory Bowel Disease

http://www.ccfa.org/what-are-crohns-and-colitis/what-is-crohns-disease/Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine. Crohn's disease and ulcerative colitis are the principal types of inflammatory bowel disease.

Here’s the difference :

both of them are chronic & autoimmune disease, Normally, the cells and proteins that make up the immune system protect you from infection. In people with IBD, however, the immune system mistakes food, bacteria, and other materials in the intestine for foreign or invading substances. When this happens, the body sends white blood cells into the lining of the intestines, where they produce chronic inflammation and ulcerations.

and for the ulcerative colitis, there are 3 categories :

Source :

http://www.ccfa.org/what-are-crohns-and-colitis/what-is-ulcerative-colitis/

http://www.ccfa.org/what-are-crohns-and-colitis/what-is-crohns-disease/

[mad-med-stud]

Transverse Myelitis

Transverse myelitis is a neurological disorder caused by inflammation across both sides of one level, or segment, of the spinal cord. The term myelitis refers to inflammation of the spinal cord; transverse simply describes the position of the inflammation, that is, across the width of the spinal cord.

Symptoms of transverse myelitis include a loss of spinal cord function over several hours to several weeks. What usually begins  as a sudden onset of lower back pain, muscle weakness, or abnormal sensations in the toes and feet can rapidly progress to  more severe symptoms, including paralysis, urinary retention, and loss of bowel control.

four classic features of transverse myelitis emerge:

weakness of the legs and arms

 pain, The pain may be localized in the lower back or may consist of sharp, shooting sensations that radiate down the legs or arms or            around the torso.                                 

sensory alteration

bowel and bladder dysfunction.

Transverse myelitis may be either acute (developing over hours to several days) or subacute (usually developing over 1 to 4 weeks). (http://www.ninds.nih.gov/disorders/transversemyelitis/detail_transversemyelitis.htm)

[mad-med-stud]

Guillain-Barré syndrome

Guillain-Barré syndrome (GBS) is a disorder in which the body's immune system attacks part of the peripheral nervous system (http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024547/)

The mechanism of GBS is believed to be an inflammatory neuropathy due to cross reactivity between neural antigens and antibodies that is induced by specific infections. Infectious organisms, such as C. jejuni, express lipooligosaccharides in the bacterial wall similar to gangliosides.

The most common symptoms reported before onset of GBS are fever, cough, sore throat, and other upper respiratory symptoms.

The weakness typically reaches its peak by the second week, followed by a plateau of variable duration before resolution or stabilization with residual disability.

Facial, oropharyngeal, and oculomotor muscles may be affected because of cranial neuropathy, especially in the less common subtypes. Paresthesia in the feet and hands is common, but sensory symptoms are generally mild, except for in those patients with the acute motor-sensory axonal neuropathy subtype. Autonomic symptoms occur in about two-thirds of patients and include cardiac arrhythmias, orthostasis, blood pressure instability, urinary retention, and slowing of gastrointestinal motility.

Patients with GBS classically have increased protein levels and a normal white blood cell count (i.e., less than 10 per mm3 [10 × 106 per L]) in CSF. (http://www.aafp.org/afp/2013/0201/p191.html)

Intravenous immunoglobulin (IVIg) and plasma exchange are effective treatments in GBS; mainly for practical reasons, IVIg is the preferred treatment. 

[mad-med-stud]

Tumor Marker

A tumor marker is a biomarker found in the blood, urine, or body tissues that can be elevated in cancer, among other tissue types. Tumor markers can be produced directly by the tumor or by non-tumor cells as a response to the presence of a tumor. Most tumor markers are tumor antigens, but not all tumor antigens can be used as tumor markers.

Uses of tumor markers can broadly be classified as follows:

Screening for common cancers on a population basis.

Monitoring of cancer survivors after treatment. Example: elevated AFP in a child previously treated for teratoma suggests relapse with endodermal sinus tumor.

Diagnosis of specific tumor types, particularly in certain brain tumors and other instances where biopsy is not feasible.

There are 4 things that should be considered about a Tumor marker test:

Sensitivity, no Tumor marker test has 100 percent sensitivity, so some tumors are still not detected by a single Tumor marker test.

Specificity, only the M2-PK Tumor marker test for colorectal has up to 95 percent specificity.

False Negative, the result is negative, but in fact is positive.

False Positive, the result is positive, but in fact is negative.

[mad-med-stud]

The cell cycle - Canadian Cancer Society

Every cell in the body goes through a life cycle. Cells grow and divide to replace cells that are lost because of normal wear and tear or injury. Different cells grow and die at different rates

[mad-med-stud]

Molecular Basis of Cancer

Tumors developed as clonal progeny of a single genetically damaged progenitor cell. 4 classes or normal regulatory genes are the targets of genetic damaged :

Growth-promoting proto-oncogenes : Proto-oncogenes have many functions in a cell but they often code for proteins that stimulate cell division, prevent cell differentiation or apoptosis. If proto oncogenes mutated, they’ll become oncogenes. The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic methods of activation (to make proto-oncogenes to oncogenes) : deletion/point mutation in coding sequence, gene amplification & chromosome rearrangement

Growth-inhibiting tumor-suppressor genes : Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or apoptosis. Ex : p53, pRb

Genes that regulate apoptosis : Ex. BAX, BCl 2

Genes that regulate DNA repair

But what need to be remember if only one of those normal regulatory genes mutated, it will not become cancerous, because the other regulatory genes will compensate it.

[mad-med-stud]

Leukaemia

Leukaemia is a group of cancers that usually begins in the bone marrow and results in high numbers of abnormal white blood cells. These white blood cells are not fully developed and are called blasts or leukemia cells

FIRST CLASSIFICATION

Acute : rapid increase in the number of immature blood cells

Chronic : come from mature, abnormal cells. The cells thrive for too long and accumulate.The cells grow slowly.

SECOND CLASSIFICATION

lymphoblastic / lymphocytic leukemias : type of leukemia affects the lymphoid cells (lymphocytes), which form lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system. 

myeloid / myelogenous leukemias : This type of leukemia affects the myeloid cells. Myeloid cells give rise to red blood cells, white blood cells and platelet-producing cells.

MAJOR TYPES

[mad-med-stud]

Hodgkin & Non-Hodgkin Lymphoma

Above, is the basic difference of Hodgkin & NHL, as we know the basic characteristic to differentiate Hodgkin & NHL is knowing whether there's Reed Stenberg cell or not, but by the latest update it is known that some of NHL (rarely) have RS cell, but what makes them different with Hodgkin RS's cell is their antigen.

In most instances, Hodgkin lymphoma appears to spread or grow by contiguous extension (spreading from one lymph node to adjacent nodes or to extranodal tissue). Non-Hodgkin's lymphomas tend to be less defined in their growth pattern, commonly being diffuse, without evidence of contiguous spread. How does this happen? It is known that Hodgkin distributed by lymphatic spread while NHL spread by hematogenous spread, so this is also explain why in most cases, Hodgkin have shplenomegaly while NHL have hepatomegaly.

Meanwhile, in Hodgkin there's B symptom which is Pel-Ebstein Fever ( fevers which cyclicly increase then decrease over an average period of one or two weeks.), weight loss, and night sweats. This all is caused by Reed Sternberg cell, which realease some chemical mediators.

[mad-med-stud]

Pathogenesis of Cancer (Genetic Factors)

The 23 pairs of human chromosomes contain the genetic material of the cell made up of unique sequences of DNA base pairs, which code for the amino acid building blocks of proteins responsible for all the basic metabolic processes that enable the individual cells to survive, reproduce and express properties characteristic of their tissue of origin. Subtle changes in the genes comprising the chromosome may lead to a malignant tumour characterized by loss of the normal cellular mechanisms responsible for control of proliferation, cell differentiation, programmed cell death (apoptosis), cellular organization and cellular adhesion. The uncoupling of the usual balance between cell loss and multiplication leads to growth of the tumour and its subsequent invasion both locally and at distant sites.

Activated Oncogenes : These are genes which, when expressed, code for a protein that in some way is related to the proliferative cycle of cells or cell differentiation. They are activated during the intense cell proliferation and differentiation of embryogenesis but, in the mature cells, are suppressed by regulating genes at other points along the chromosome. The activation of oncogenes involves genetic changes to cellular protooncogenes. The consequence of these genetic alterations is to confer a growth advantage to the cell. Three genetic mechanisms activate oncogenes in human neoplasms: (1) mutation, (2) gene amplification, and (3) chromosome rearrangements. 

Tumor Suppresor Genes : Each cell has one of a pair of tumour-suppressor genes on each homologous chromosome, and both must be inactivated for the cancer to develop. This means that individuals from a ‘cancer family’ with only a single gene inherited owing to a ‘germ line’ mutation have a normal phenotype, act as a carriers, but will develop cancer if the second gene is lost owing to a somatic mutation or other form of genetic mis-coding. Normal individuals must lose both genes by a somatic mutation for a sporadic cancer to develop. Thus tumour-suppressor genes cause cancer not by amplification or overexpression

Source : Clinical Oncology 4th ed, Neal Anthony J.

[mad-med-stud]

Prognosis for Life

Ad vitam (life) : medical opinion as to whether the disease can lead to death of the individual or not.

Sanam (healthy)

Bonam (good)

Malam (bad)

Dubia (doubtful)

Dubia ad sanam/bonam (doubtful, tend to good)

Dubia ad malam (doubtful, tend to bad)

Ad functionam (function)

Ad sanationam (healthy)

[mad-med-stud]

This text has nothing to do with medics but i just wanted to say that, i'm finally in 'Neoplasm' class! It almost about 7 years ago when Samuel told me that he want me to be an Oncologist so i can cure & help a lot of people like him, time really fly so fast :')

well, if you heard me, i'm trying really hard to get an A in this class, hehe, i have a really big interest in this subject!

[mad-med-stud]

Enneking Classification of Musculoskeletal Tumor

What to know :

G : The grade of the tumor

G1 : Low-grade tumor cells look more like normal cells and are less likely to grow and spread quickly,

G2 : High-grade tumor cells look more abnormal.

T : The extent of the main (primary) Tumor

T1 : intracompartmental, meaning it has basically remained within the bone

T2 : extracompartmental, meaning it has extended beyond the bone into other nearby structures

M : If the tumor has spread to nearby lymph nodes / other organs

M0 : no metastasis

M1 : metastasis happen

[mad-med-stud]

Allergic Bronchopulmonary Aspergillosis (ABPA)

What is ABPA?  Allergic bronchopulmonary aspergillosis is a form of  lung disease that occurs in some people who are allergic  to Aspergillus. With ABPA, this allergic reaction causes  the immune system to overreact to Aspergillus leading  to lung infammation (This is why in the blood test, you'll find immunoglobulin E (IgE) level increased. This level is increased  with any type of allergy. Many people with asthma  have higher than normal IgE levels. In ABPA however, the IgE level is extremely high (more than 1000 ng/ ml or 417 IU/ml)) ABPA also causes bronchospasm  (tightening of airway muscles) and mucus buildup  resulting in coughing, breathing diffculty and airway obstruction.

Diagnosis

A sputum culture (mucus coughed up from theairway) can be done to see if Aspergillus is growing in the airway but is not always reliable. Many people will have Aspergillus in their airway secretions (sputum) but not have ABPA. On the other hand, even if the culture is negative, a person can still have ABPA.

Chest X-rays are often not helpful in diagnosing ABPA. A CT scan (computed tomography) however, is a more detailed view of your lungs and therefore can be very helpful. The bronchiectasis is kind of a curve to the reader.

A blood test can be done to measure sepcifc IgE to Aspergillus. There are some other blood tests that also can help with the diagnosis

Pathophysiology

So basically, ABPA occurs in persons with asthma and those with cystic fibrosis (CF) but it's also possible for a normal person to have it. Aspergillus spores are small and can penetrate deep into the respiratory system to the alveolar level. In healthy people, innate and adaptive immune responses are triggered by various immune cells drawn to the site of infection by numerous inflammatory cytokines and neutrophilic attractants. In this situation, mucociliary clearance is initiated and spores are successfully phagocytosed, clearing the infection from the host. So if there's any condition that allowed Aspergillus spores to enter the lung & persist in pulmonary tissues, it permits successful germination which leads to hyphae growing in mucus plugs. From this, it will react to hypersinsitivity response, both a type I response (atopic, with formation of immunoglobulin E, or IgE) and a type III hypersensitivity response (with formation of immunoglobulin G, or IgG). The reaction of IgE with Aspergillus antigens results in mast cell degranulation with bronchoconstriction and increased capillary permeability. Immune complexes (a type III reaction) and inflammatory cells are deposited within the mucous membranes of the airways, leading to necrosis and eosinophilic infiltration.

Symptoms

A person with ABPA will have some or all of the following symptoms: • Coughing frequently • Coughing up mucus plugs that may be brown in color. You may also cough up blood (hemoptysis). • Diffculty exercising • Wheezing • Shortness of breath or feeling like it is difficult to get air into or out of your lungs. • Chest pain or tightness • Fever that goes away then comes back • Fatigue

Source. American Academy of Allergy, Asthma & Immunology, American Thoracic Society, Medscape

So that's basically what's happening right now, but i still have a few question to ask, How is the mechanism of leukopenia in ABPA patient? Is it the same as in sepsis patient? (First, proinflammatory mediators work and then a compensatory anti-inflammatory response soon ensures that the effects of these proinflammatory mediators do not become destructive *which is why in the sepsis patient, most of them have leukocytosis in acute-phase and leukopenia in chronic phase)

Anyone?

[mad-med-stud]

Rare Case #3 : The Ability to see UV light

In this case, we can use Claude Monet as example.

Late in his life, Claude Monet developed cataracts. As his lenses degraded, they blocked parts of the visible spectrum, and the colors he perceived grew muddy.  He agreed at age 82 to have the lens of his left eye completely removed.With his lens removed, Monet continued to paint. Flowers remained one of his favorite subjects. Only now the flowers were different. When most people look at water lily flowers, they appear white. After his cataract surgery, Monet's blue-tuned pigments could grab some of the UV light bouncing off of the petals. He started to paint the flowers a whitish-blue.

I still didn't know what's this condition called, anyone?

[mad-med-stud]

Rare Case #2 : Tetrachromacy

Tetrachromacy is the condition of possessing four independent channels for conveying color information, or possessing four types of cone cells in the eye. The normal explanation of tetrachromacy is that the organism's retina contains four types of higher-intensity light receptors (called cone cells in vertebrates as opposed to rod cells which are lower intensity light receptors) with different absorption spectra.

So Short said, he/she can see more colours than we can see right now. An example is Concetta Antico