20 09 18

ONE STEP AT A TIME: Free Printable

Hellooo! Yesterday I reached 15.000 followers (!!!!!!!!!!), which is so, so crazy. I would have never ever expected that when I first created this blog, so THANK YOU ALL SO MUCH <3 I love every single one of you.

To celebrate, I decided to make some printables yayyyy!! It’s a weekly planner that comes in the following options: blank, lined, graph and 2 columns (lined). Also I made portuguese versions yeahhh

Download links:

English: blank / lined / graph / 2 columns

Português: branco / pautado / quadriculado / 2 colunas

If you have any problem with it, please let me know. And also tag me if you use it! x

nov.21 | day 21 of @justjasminestudying‘s challenge

21. Show me some work/notes you’re most proud of

This picture was taken back when I was still in dental school and the subject was immunology. It was so complicated D: But at least I now know how to color code stuff lmao

song of the day : IU - Through the Night

Recurrente infections with catalase positive organisms in Chronic Granulomatose Disease (CGD)

https://www.instagram.com/studydiaryofamedstudent/

Medically Important Fungi

how am i always so behind in my work ??

(i do know the answer to this, it’s called procrastination lmao)

Leukocyes (WBCs) & Defence

A summary

Neutrophils -  non-specific defence against bacteria and fungi

Eosinophils -Defence against parasites; dampen allergic response

Basophils  - Anaphylactic & inflammation response

Monocytes - Mature into macrophages, engulf foreign substances;  remove aged RBCs and other debris

Lymphocyes - Recognise antigens, various roles

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

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.

20.1.18 // studygram: alimastudies

i don’t normally upload pictures of my homework because i don’t tend to spend a lot of effort or time on them as i know i won’t be using it again, but for this biology homework i thought i would do it nicely and use it for my future notes! i need to work on my handlettering oh dear god ahhh i used a crayola supertip for it