Everything You Need To Cover To Succeed As A Student

Cysteine Growth Requirements

MICROBIOLOGY MNEMONIC

BoyFriend Lost Penis

B rucella

F rancisella

L egionella

P asteurella

or….

The four sisters “Ella” worship in the “cystein” chapel

Brucella

Francisella

Legionella

Pasteurella

18/1/18 - Recent virology notes! Ignore the headings, I bought some new brush pens and I’m still getting used to them..

Innate Immunity - intro

First line of defence + first to act

A primitive response (exists in animals and some plants)

Non-specialised and without ‘memory’

Consists of:

Physical barriers (eg skin and mucosa//tight junctions, airflow)

Chemical barriers (eg enzymes, lung surfactant, antimicrobals)

Soluble mediators of inflammation (eg cytokines)

Microbal defence (eg commensal competition, secreted antimicrobals)

Cells (eg phagocytes)

Receptors to recognise presence of pathogen/injury - results in inflammation

Soluble Mediators

Complement Proteins

liver-derived 

circulate in serum in inactive form

activated by pathogens during innate response

functions include lysis, chemotaxis and opsonisation

Auxiliary Cells

Mediate inflammation as part of the immune response. The main auxiliary cells involved in the immune response are Basophils, Mast cells and Platelets.

Basophils 

Leukocyte containing granules 

on degranulation release histamine + platelet activating factor

causing increased vascular permeability and smooth muscle contraction

also synthesise and secrete other mediators that control the development of immune system reactions

Mast Cells

Also contain granules 

However they are not circulating cells - found close to blood vessels in all types of tissue especially mucosal and epithelial tissues.

rapidly release inflammatory histamine but this is IgE dependant so not innate

Platelets 

normally function in blood clotting

also release inflammatory mediators

Cytokines and chemokines

Produced by many cells but especially mØ (macrophages), initiate inflammatory response and act on blood vessels 

interferons - antiviral protection

chemokines - recruit cells

interleukines - fever inducing, IL-6 induces acute phase proteins 

IL-1 - encourages leukocytes to migrate to infected/damaged tissue

as does tumour necrosis factor (TNFa)

Acute phase proteins

Liver derived proteins 

plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation

called the acute-phase reaction 

triggered by inflammatory cytokines ( IL-1, IL-6, TNFα)

help mediate inflammation ( fever, leukocytosis, increased cortisol, decreased thyroxine, decreased serum iron, etc)

activate complement opsonisation 

Inflammation 

Cells

Cytotoxic Cells

Eosinophils/natural killer cells, cytotoxic T cells

kill target via release of toxic granules 

dendritic cell derived IL-12 helps activate NK cells

Phagocytes

mono-nuclear = long-lived; polynuclear = short-lived

engulf, internalize and destroy 

phagosome forms around microbe

enzyme filled with lysosomes fuses to form phagolysosome

organism is digested

fragments are either ‘presented’ or exocytosed

phagocytosis requires recognition of microbe via receptors for

PAMPs (pathogen associated molecular patterns - eg flagella or capsule) - recognised by toll-like receptors 

activated complement

antibody

The innate immune response primes for the adaptive 

B-cells are primed by activated complement

Th1 cell differentiation needs pro-inflammatory cytokines

BACTERIAL MENINGITIS Timeline, Organisms, Presentation

Sooo I’m studying microbiology 2:28 am because I’m a desperate bitch Microbiology + immunology = total final grade I got a 10 in my immunology test so I’m PRAYING for a 10 in microbiology so I can get a bIG BeauTiFul 10 on my final

hey! could you do a study tips post on studying w friends who aren't doing the same subjects? like, how to make good flashcards/questions and answers etc so they can quiz you and give you hints etc even if they don't know the content?

How to Effectively Study with Friends

Using Flash Cards

Oh easy peasy! Simply write examination style questions on your flashcards - that way when your friends read the questions out to you, you’ll be testing yourself in a way that might show up on the easier exam questions. Reason being that in order to cover all the topics, your questions will tend to be somewhat simple e.g. describe the different components of x, explaining how they related to y. Obviously, flash cards aren’t the best way to study more complex interrelationships between ideas/concepts, which should be explored more in a mind map fashion. For tips on mind maps, you can check out my briefing here. 

Using Your Existing Study Notes

Other than flash cards, if you intend to study in groups for most subjects, one of the best ways to do that is to use the Cornell Notetaking System (which you can read about with my personal tips here). Writing the questions out as you study saves you the trouble of writing out questions for your friends to test you on, and as well as that, means you can test yourself almost as well without them for any times when you’re studying solitary. 

Using Essay or Long Response Questions

For long response essays, it’s better to use principles like the rubber duck method, i.e. explaining how concepts relate to each other as if the other person doesn’t know anything about it. So give your friends a list of essay questions and explain part by part in a logical sequential order how you would answer that question e.g. I would talk about the involvement of person A in event B, and explain their impact through examples C, D and E, etc. 

Choosing the Right Study Group 

Most of all, make sure you rally and encourage each other. Work with people who are like-minded, rotate between each other and have someone who will keep the others on task when you start getting too carried away when studying. Having a goal on what you intend to get finished during a group study session will make sure you always get more out of the session than studying alone!

Hope that helps! ^_^

(Day 4/100 days of productivity) - Haemophilus Influenzae card!

Today was mostly spent working on research, textbooks, but and making flashcards like this for microbiology!

What is Acute or Subacute Bacterial Endocarditis?

Acute or Subacute Bacterial Endocarditis is an infection of the heart’s endocardium. The endocardium is the inner lining of the heart muscle, which also covers the heart valves. Bacterial Endocarditis can damage or even destroy your heart valves. The difference between acute and subacute bacterial endocarditis is acute bacterial endocarditis is a sudden onset, whereas subacute bacterial endocarditis is a gradual onset.

Acute endocarditis most often occurs when an aggressive species of skin bacteria, especially a staphylococcus (staph), enters the bloodstream and attacks a normal, undamaged heart valve. Once staph bacteria begin to multiply inside the heart, they may send small clumps of bacteria called septic emboli into the bloodstream to spread the infection to other organs, especially to the kidneys, lungs and brain. Intravenous (IV) drug users are at very high risk of acute endocarditis, because numerous needle punctures give aggressive staph bacteria many opportunities to enter the blood.If untreated, this form of endocarditis can be fatal in less than six weeks.

Subacute endocarditis is caused by one of the viridans group of streptococci (Streptococcus sanguis, mutans, mitis or milleri) that normally live in the mouth and throat. Streptococcus bovis or Streptococcus equinus also can cause subacute endocarditis, typically in patients who have some form of gastrointestinal cancer, usually colon cancer. Subacute endocarditis tends to involve heart valves that already are damaged in some way, and it usually is less likely to cause septic emboli than acute endocarditis. If untreated, subacute bacterial endocarditis can worsen for as long as one year before it is fatal.

Nocardia

Gram+, aerobic, non-spore forming, non- motile, branching filamentous rod.

Partially acid fast

Immunocompromised pts, cancer pts.

DISEASES

Cavitary broncopulmonary Nocardiosis: > N. asteroides, fever, cough, dyspnea, localized or diffuse pneumonia (symptoms very similar to TBC) If spreads hematogenously => multiple brain abscesses.

Cutaneous, subcutaneous Nocardiosis: > N. brasiliensis,cellulitis => subcutaneous draining abscess with granules (mycetoma)

Most Common facts about infectious diseases

1. Most common cause of septic arthritis in a person less than 40 years old = Gonococcus 2. Most common cause of osteomyelitis in general population = S. aureus 3. Most common cause of osteomyelitis in Sickle Cell patients = Salmonella 4. Most common cause of osteomyelitis due to nail-puncture wounds = Pseudomonas (V.Imp!) 5. Most common parasitic infection of the brain = Neurocysticercosis 6. Most common cause of Encephalitis in USA = Herpes Simplex Virus (HSV) 7. Most common cause of dysentry in the USA = C. jejuni (undercooked poultry) 8. Second most cause of dysentry in the USA = Shigella (daycare centers) 9. Most common cause of pneumonia in nursing home residents = S. pneumoniae 10. Most common cause of malignant otitis externa = P. aeruginosa 11. Most common risk for contracting HIV in USA= Intravenous Drug Use 12. Most common presenting Manifestation of AIDs = P. carinii pneumonia 13. Most common cause of Menigitis in adolescents = N. Gonorhhaea 14. Most common cause of Meningitis in the USA = Streptococcus pneumoniae 15. Most common Neurological Manifestation of Lyme Disease = Facial Nerve palsy! 16. Most common Cardiac manifestation of Lyme Disease = AV Heart Block 17. Most Common viral STD in the USA = HPV ! 18. Most Common Complication of Mumps in Pre-pubertal Children = Encephalitis 19. Most Common Complication of Mumps in Pubertal and Post-Pubertal Adults (and Males) = Orchitis