Chaotic Med Student

21 • PH • BSMLS/BSMT • 3rd year • Premed •Studying 3rd year Qualifying Examination•

[microscope-world]

This is non-pigmented human skin captured under the lab microscope at 40x.

[biomedicool]

Antimicrobial Resistance

(including antibiotic resistance) 

“this serious threat is no longer a prediction for the future, it is happening right now in every region of the world and has the potential to affect anyone, of any age, in any country.“  (x)

Antimicrobial resistance is the ability of a microbe (eg bacteria) to resist the effects of medication that could previously successfully treat it. These then require alternative medications or higher doses of antimicrobials, which can be more expensive, more toxic, and less effective. 

can be multidrug resistant (MDR).

Extensively drug resistant (XDR)/totally drug resistant (TDR)=“superbugs”

This makes the disease caused by the microbes ‘incurable’ as there are no drugs that can treat it.

All classes of microbe can become resistant through:

natural resistance 

genetic mutation

one species acquiring resistance from another

Preventive measures

Only using antibiotics when needed

Narrow-spectrum antibiotics -only target specific organism, avoiding creating resistnance in other types that happened to be present

Proper sanitation

Notable examples

Resistance to the treatment of last resort for life-threatening infections caused by a common intestinal bacteria, Klebsiella pneumoniae–carbapenem antibiotics–has spread to all regions of the world. K. pneumoniae is a major cause of hospital-acquired infections such as pneumonia, bloodstream infections, infections in newborns and intensive-care unit patients. In some countries, because of resistance, carbapenem antibiotics would not work in more than half of people treated for K. pneumoniae infections.

Resistance to one of the most widely used antibacterial medicines for the treatment of urinary tract infections caused by E. coli–fluoroquinolones–is very widespread. 

Treatment failure to the last resort of treatment for gonorrhoea–third generation cephalosporins–has been confirmed in Austria, Australia, Canada, France, Japan, Norway, Slovenia, South Africa, Sweden and the United Kingdom. An estimated 106 million people are infected with gonorrhoea every year.

Antibiotic resistance causes people to be sick for longer and increases the risk of death. For example, people with MRSA (methicillin-resistant Staphylococcus aureus) are estimated to be 64% more likely to die than people with a non-resistant form of the infection. 

[medlabscience]

This often occurs in people who prematurely stop taking their prescribed antibiotics. For example, if they’re prescribed a 10 day dose and feel better at day 9, they’ll not take the last one or two doses, which can let the bacteria live and the sickness lengthen!

Friendly reminder to always take medication as directed :)

[thechemteacher]

Nomenclature - Basics

Nomenclature is the method for naming chemical compounds, both inorganic and organic. It is a systematic method for naming compounds so that it’s structure can drawn according to its name, or named based off its structure. Usually, IUPAC rules are followed, and is used in most organic chemistry courses. Before learning the nomenclature for more complex structures, the parent names and some basic rules should be noted.

This is a list containing the parent names of organic compounds that contain up to 11 carbons. There are parent names for compounds containing more than 11 carbons, but most professors usually only require you to know the first 11 or so. You will need to memorize these.

If a chain of carbons is in a ring, ‘cyclo’ is placed before the parent name. So, a chain of 6 carbons in a ring will be cyclohexane.

The shape of the compound doesn’t change it’s parent name; molecules are always vibrating and rotating, so its conformation doesn’t influence its IUPAC name. The three drawings of hexane are conformational isomers, and represent the same compound.

To determine the parent chain of a compound, number it starting from the end. If its a ring, the numbering doesn’t matter unless there is a substituent or side chain hanging off of it, in which case, begin numbering where the side chain or substituent is attached to the ring.

In carbon chains, always number it so that you get the longest chain possible. Also, like numbering rings, number the compound so that any substituent or side chain has the lowest number. Thus, the correct way to name the compound on the left is 3-methylhexane, since a methyl group, a CH3, is attached to the 3rd carbon when correctly numbering the chain.

[meducalix-deactivated20221204]

Nephrolithiasis is the formation of kidney stones, which form when solutes precipitate out into crystals in the urine. The most common type of stones are calcium oxalate stones, though other types include uric acid stones and struvite stones.

Nephrolithiasis 是指肾结石的形成，即当溶质在尿液中沉淀成晶体时形成。草酸钙结石是最常见的类型，其他类型的结石有尿酸结石和感染性结石。

Meducal! Joint us at Osmosis

[medlabscience]

Calcium-derived urinary stones account for up to 75% of cases, and are formed from abnormal calcium metabolism.

Struvite stones at 15% may derive from urinary tract infection (UTI) complications.

Uric acid stones at 5% form alongside casss of hyperuricemia or gout.

Cystine stones at 1% are from errors within amino acid metabolism itself.

[biomedicool]

Immunohistochemistry

A section of tissue is taken as it would for Histology (see prev post)

The section is then treated with an antibody that recognises the marker we’re looking for. This is referred to as the primary antibody.

The primary antibody is then recognised by a secondary antibody that is linked to an enzyme, or several copies of the enzymes (conjugates).

Finally, the section is treated with a chromogen, a reagent that is acted upon by the enzyme, to deposit an insoluble coloured compound onto the cell, where the original primary antibody had bound.

A molecule that binds to, and is recognised by, an antibody, is called an antigen, 

In histology, antigens = markers, since they act as ways of recognising a particular cell. 

Many markers are designated by a CD number. 

EG different classes of lymphocyte appear virtually identical in size and shape (morphology), but they can be distinguished according to their surface markers. 

All T lymphocytes express CD3, 

Helper T cells and cytotoxic T cells express CD4 and CD8, respectively.

Therefore, a T cell lymphoma can be tracked in different tissues using these markers.

 Double immunolabelling of an islet of Langerhans in the pancreas identifies Insulin-producing cells (blue) and glucagon-producing cells (brown)

Another use for IHC is in guiding treatment. 

For example, many breast cancers require oestrogen to divide, but a drug called tamoxifen can bind to the oestrogen receptor on the cancerous cells, blocking this proliferative effect. 

[biomedicool]

Secretion - Breast

Breast

Structurally, the breast consists of a number of lobes connected by lactiferous (milk-carrying) ducts to the nipple. 

Each lobe is a compound gland 

branching into lobules and alveoli lined with epithelial cells

which are supported in a loose matrix of connective tissue. 

The connective tissue includes accumulations of adipocytes (fat cells).

During pregnancy the duct system and alveoli expand considerably (the epithelial cells lining the alveoli are responsible for milk secretion). 

connective tissue is correspondingly reduced

alveoli are surrounded by contractile cells (myocytes)

which put pressure onto the alveoli to promote milk secretion.

When the breast is stimulated, prolactin levels in the blood rise, peak in about 45 minutes, and return to the pre-breastfeeding state about three hours later. The release of prolactin triggers the cells in the alveoli to make milk. 

After weaning, when breast milk is no longer required, the alveoli regress, leaving just the duct system in place

[mm-medical]

[medlabscience]

Peripheral blood smear –> basophil, monocyte, lymphocyte, eosinophil, & neutrophil

[biomedicool]

Blood Typing - ABO

A blood type (also called a blood group) is a classification of blood, based on the presence and absence of antibodies and inherited antigenic substances on the surface of red blood cells (RBCs). 

inherited from both parents. 

A total of 36 human blood group systems exist - ABO and the Rh determine someone’s blood type (A, B, AB and O, with +, − or null denoting RhD status) 

Typing is essential for suitability in blood transfusion

Antibodies in an individual’s plasma are directed against blood group antigens that their own RBCs lack

(this is confusing, it’ll take a while before you can look at blood typing stuff without having to think)

The ABO blood group system involves two antigens and two antibodies found in human blood. 

antigen A and antigen B - on the RBCs

antibody A and antibody B - in the serum

All humans can be classified into 4 groups:

Antigen A with antibody B

Antigen B with antibody A

Antigen AB has no antibodies

Antigen nil (group O) with antibody A and B.

Agglutination (clotting) reaction occurs between similar antigen and antibody. This is a seriously dangerous reaction (essentially all your blood turns to jelly) - if a patient with A  antibody in their serum is given blood with A antigen on the surface, they could die.

Group O = universal donor –> has no antigens on the RBCs, can be given to anyone and no agglutination will occur because nothing to react with the antibodies in serum

Group AB = universal acceptor –> no antibodies in serum, so nothing to react with any antigens on RBCs that are introduced.

[medlabscience]

Great graphic/note to transfusion logic!

Quick note that these rulings apply to red blood cell donation, and that it’s a tad different for other blood products.

[0xygen]

Correct me if I’m wrong but an ABO is completely different than a TS.

[medlabscience]

If you’re referring to a type & screen, aka a T/S, that is different from an ABO in terms of the testing performed. A T/S is a test group that includes both a blood typing (so an ABORh) and a screen (an indirect antiglobulin test for antibody identification). This infographic covers the compatibility requirements of different blood types (and only ABO, not even getting into Rh) and does not touch on other clinically significant antibodies that can be discovered when performing the screen/IAT

[docinlimbo]

CML Mnemonic

CML also known as Chronic Myelogenous Leukemia. 

What do you find in the blood?

Well it’s called myleogenous leukemia. So obviously the leukocytes will be increased. But, what are myelocytes? They’re baby granulocytic cells, granulocytic cells create basophils and eosinophils. So look for increased white blood cells, granulocytes, and basophils. 

Break it down and you can figure out what you’re looking for! 

Photo from: http://www.hematocytologie.eu/wordpress/?page_id=209

What age group is most commonly affected?

It’s called CML, M stands for Middle Aged usually ages 13-40. 

Translocation?

BCR-ABL (9;22) aka the Philadelphia Chromosome. Remember Middle Aged People are ABLE to work in Philadelphia. 

Treatment? 

Imatinib, which inhibits. the BRR-ABL kinase. “I’m nibbling on the kinase”  (I know this one is a bit odd, but if it works.)

You also have to beware of blast crisis with CML 

[archenland]

Entamoeba histolytica

This little guy is the etiological agent of amebiasis.  E. histolytica is protozoan that is found worldwide. The highest prevalence of amebiasis is in developing countries where barriers between human feces and food and water supplies are inadequate.

E histolytica is transmitted via ingestion of the cystic form (infective stage) of the protozoa. Viable in the environment for weeks to months, cysts can be found in fecally contaminated soil, fertilizer, or water or on the contaminated hands of food handlers. Fecal-oral transmission can also occur in the setting of anal sexual practices or direct rectal inoculation through colonic irrigation devices.

Although most cases of amebiasis are asymptomatic, dysentery and invasive extraintestinal disease can occur. Amebic liver abscess is the most common manifestation of invasive amebiasis, but other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites.

[archenland]

Clostridium botulinum

Clostridium botulinum are rod-shaped bacteria. They are anaerobic, meaning they live and grow in low oxygen conditions. The bacteria form protective spores when conditions for survival are poor. The spore has a hard protective coating that encases the key parts of the bacterium and has layers of protective membranes. Within these membranes and the hard coating, the dormant bacterium is able to survive for years. C. botulinum is responsible for a disease called botulism.

Botulism is a life-threatening disease caused by the ingestion of a potent neurotoxin (called BTX or BoNT) produced during growth of the C. botulinum bacteria. This neurotoxin is among the most toxic substances known; even microscopic amounts can cause illness or death. There are two main commercial types: botulinum toxin type A and botulinum toxin type B.

These toxins are used in medicine for, among others, upper motor neuron syndrome, focal hyperhidrosis, blepharospasm, strabismus, chronic migraine and bruxism. It is also widely used in cosmetic treatments.

The injection of botulinum toxin, commonly known as Botox, has become very popular for reducing wrinkles and rejuvenating the aging face. The effects are only temporary, but the injections can be done quickly, require no recovery time, and are not as complicated as many other cosmetic procedures for the face.

Key characteristics: Gram(+), beta-hemolysis, motility(+), indole(-), catalase(v-), spores(+).

[medlabscience]

Microcytic Anemia

MCV <80 fL/cell

ATLIS (atlas)

Anemia of chronic disease (ACD)

Thalassemia

Lead poisoning

Iron deficiency anemia (IDA)

Sideroblastic Anemia

[medlabscience]

Complement Pathways

Components of complement pathways of the immune system. 

Classical Pathway: binds to the pathogen surface

C1 binds to phosphocholine on bacteria, which activates C1r to cleave C1s.

Activated C1s cleaves C4 to C4a and C4b.

C4b binds to the microbial surface and also binds C2.

C2 is cleaved to C2a and C2b by C1s, forming the C4bC2a complex.

The C4bC2a complex cleaves C3 to C3a and C3b.

C3b binds to the surface and causes opsonization.

MB-Lectin Pathway: uses mannin-binding lectin to bind to mannose-containing carbohydrates on the pathogen surface

Mannin-binding lectin (MBL) binds to the pathogen surface and activates MASP-2.

MASP-2 cleaves C4 to C4a and C4b.

C4b binds to the microbial surface and also binds C2.

C2 is cleaved to C2a and C2b by MASP-2, forming the C4bC2a complex.

The C4bC2a complex cleaves C3 to C3a and C3b.

C3b binds to the surface and causes opsonization.

Alternative Pathway: binds to the pathogen surface with spontaneously activated complement, amplifies C3b

C3b deposited by the C3 convertase binds to factor B.

Factor B is cleaved by factor D into Ba and Bb, forming the C3bBb complex.

The C3bBb complex cleaves C3 into C3a and C3b.

C3 spontaneously hydrolyzes to C3(H2O).

C3(H2O) binds to factor B, and factor D cleaves factor B.

Upon factor B cleavage, the C3(H2O)Bb complex is formed.

The C3(H2O)Bb complex cleaves C3 into C3a and C3b.

Factor B binds to C3b on the surface and is cleaved to Bb.

[microaerophilic-blog]

Pseudomonas aeruginosa on sheep blood agar.

a gram negative bacillus/cocci bacillus. some of of the standout characteristics of some pseudomonas are the metallic sheen of the colony morphology, and often a grape-like or musty corn tortilla odor (this had the latter).

pseudomonas is a cause of UTI’s, wound infections, ear infections, and can be a big issue for patients who are immunocompromised (especially patients with cystic fibrosis).

[medical-lab-minds]

Oxidase Positive too.

[palerlotus]

[mad-med-stud]

Anti-Platelet Drugs

ASA / Aspirin : inhibits the synthesis of thromboxane A2 ( thromboxane A2 is an arachidonate product that causes platelets to change shape, release their granules, and aggregate) by irreversible acetylation of the enzyme cyclooxygenase

Clopidogrel & Ticlopidine : reduce platelet aggregation by inhibiting the ADP pathway of platelets. These drugs are thienopyridine derivatives that achieve their antiplatelet effects by irreversibly blocking the ADP receptor on platelets.

Abciximab, Eptifibatide & Tirofiban : target the platelet IIb/IIIa receptor complex. The IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor. Activation of this receptor complex is the “final common pathway” for platelet aggregation.

Dipyridamole : vasodilator that inhibits platelet function by inhibiting adenosine uptake and cyclic GMP phosphodiesterase activity.

[eoile-deactivated20160716]

[medlabscience]

histo