Job Market Re: Australia

Hi :) I'm considering doing optom at unsw next year and I was wondering how the job prospects are currently? I've heard that it'll be a saturated job market in the next few years so I'm not if its a worthwhile investment, as I'm from WA and although I'm genuinely interested, a really big factor is the $ ahaha. Also I was wondering what the community life at the uni, since I'm a bit worried I wont make any friends lmaoo? Also how difficult is the workload as compared to year 12? Thanks so much <3

Job Market re: Australia

Hey! Keep in mind, this is what info I’ve been hearing from colleagues as well as some optometrists who are hiring. If you’re from WA, then I would say that you don’t have to worry about saturated job markets if you’re going to return to your home state after graduating. I’ve heard you can get $100K starting salary even relatively close to the city. Melbourne and Sydney though are probably closer to hitting saturation, but they’re capping university take ins next year, so again it could be a completely different ballgame by the time you get out in Sydney and Melbourne. WA though is totally safe, I believe they’re underserviced because there are no optometry schools there. And of course, anywhere that is regional or rural, regardless of state is underserviced, so if you’re cool with moving out to learn a bit more about using your therapeutic skills and ocular disease, then there should be absolutely no problem. Job prospects are only a bit riskier staying with Syd/Melb metro.

Student Life re: UNSW

Pretty friendly on the whole, I believe that because UNSW is one of the newer universities, even the aura here is a bit more cosmopolitan. We definitely have many international students, and also there are a lot of 1st years who are super bubbly because 1) it’s a new experience and they’re excited and 2) it’s a new environment and they’re apprehensive about making friends. So literally everyone feels the same way and as long as you make a little effort to get to know someone, it’ll be more than reciprocated. Just large cliques of high school friends may be trickier to break, because it’s difficult to broach friendship with someone who’s already 6 years deep in friendship with others and still not interested in making new friends.

Also, see these posts that I’ve written about making friends because I keep getting questions about it somehow LOL

Making Conversation - a guide for introverts!

Making Friends

Part 4 Extra-Curriculars

Part 6 Social Life

High School vs. University Workload

As a precursor, no matter what the degree, studying anything at a tertiary level is going to be a challenge, not necessarily difficult. Particular degrees might be easy/hard to particular people, etc. If you’d like to know more about university I have a whole series on it.

Read this for a summary: Transitioning from High School to University

Part 0 Choosing a Degree

Part 1 Administration

Part 2 Getting to Class - pros and cons of attending class, when you should choose not to attend, laptop and notebook recommendations, advice about choosing a backpack and other essential equipment.

> Laptop Considerations and Recommendations

Part 3 Studying

Part 4 Extra-Curriculars

Part 5 Exams

Part 6 Social Life

Part 7 Part Time Work

Part 8 Four Secrets The Uni Tells You

Part 9 Best Study Spots On Campus

Part 10 Saving Money 1 - Food, Transport, Entertainment

Part 10 Saving Money 2 - Textbooks, Tax, Scholarships

Part 11 Adapting to Uni Study popular!!

Part 12 How to Study From Textbooks in Uni

Part 13 Dealing with Lazy Group Members

But granted, I’m going to say that optometry is hard. Personally I would say, and I’ve also had someone describe to me, that it’s like doing 2 HSC exams every year because of the amount of info that you have to cram into 13 weeks of a semester. I’ve had a guest lecturer who was an ophthalmologist who originally graduated as an optometrist, worked for a while and then did the GAMSAT and post-grad medicine and he told us that optometry was more difficult than the generalist medical degree. I’ve also heard from numerous other people in the field, relatives, and also heard about families with children studying both optometry and medicine saying that optom undergrad is more difficult. This is most likely because the 5 year degree is meant to give you complete training, compared with medicine where you have a 6-7 year undergrad followed by the 3 year hospital training before another 5 years of specialisation.

Be prepared for hard work and long hours. I said this in a previous ask but at the end of the day, the job that you do as an optometrist requires you to keep an eye out for sight-threatening and life-threatening conditions, as well as to deal with common eye problems day to day, so you need to learn a lot about anatomy and physiology, anatomy of the eye/head/brain and the innervation/blood supply, as well as the diseases that can arise, and how to manage and treat them. Refraction and getting an actual prescription is a skill that needs a lot of practice and refinement too.

See these asks for more details about optometry:

Optometry Prerequisites and Difficulty (yes someone’s asked before :)

Why I Chose Optometry and Comparisons to Other Health Sciences

Entry Requirements at UNSW

Format of the Degree and 1st Year Contact Hours

+ general tag for all optometry related asks

Hope that helps! ^_^

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

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6 years ago

Tick vectors

Ixodes:

Lyme disease: Borrelia burgdorferi

Babesiosis: Babesia microti

Granulocytic Erlichiosis: Erlichia phagocytophila

Dermacentor:

Tularemia: Francisella tularensis

Rocky Mountain Spotted Fever: Ricketsia rickettsii

Colorado Tick Fever: CTFVirus (Reovirus)

Amblyomma (lone star tick)

Monocytic Erlichiosis: Erlichia chaffeensis

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6 years ago

Medically Important Fungi

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6 years ago

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

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6 years ago

Immunosupressants Drug Mnemonic

Bc everything’s better when I study with Harry Potter references.

I’m reposting it, because I love this chart

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6 years ago

20 09 18

i feel as though i haven’t been as active these past couple of days. uni and work just drained the life out of me and i haven’t done anything but lay in bed when getting home.

on the bright side, i did force myself to get up and clean my room. so here are some low-light pics of my bedroom :)

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6 years ago

Antimicrobial Agents - Inhibition of DNA and Protein Synthesis

Bacterial chromosome replication

DNA replication

Bacterial Topoisomerases

maintain DNA in appropriate state of supercoiling

cut and reseal DNA

DNA gyrase (topoisomerase II) introduces negative supercoils

Topoisomerase IV decatenates circular chromosomes

these are the targets of the quinolone antibacterial agents

Quinolones

bind to bacterial DNA gyrase and topoisomerase IV after DNA strand breakage

prevent resealing of DNA

disrupt DNA replication and repair

bactericidal (kill bacteria)

Fluoroquinolone is particularly useful against

Gram +ves: Staphylococcus aureus, streptococci

Gram -ves: Enterobacteriacea; Pseudomonas aeruginosa

Anaerobes: e.g. Bacteroides fragilis

many applications e.g. UTIs, prostatitis, gastroenteritis, STIs

Adverse effects

Relatively well tolerated

GI upset in ~ 5% of patients

allergic reactions (rash, photosensitivity) in 1 - 2% of patients

Inhibition of Bacterial Protein Synthesis

Macrolides

in 1952: Erythromycin was isolated as the first macrolide (Streptomyces erythreus)

Newer macrolides: clarithromycin, azithromycin

Structurally they consist of a lactone ring (14- to 16-membered) + two attached deoxy sugars

Mode of action

bind reversibly to bacterial 50S ribosomal subunit

causes growing peptide chain to dissociate from ribosome → inhibiting protein synthesis

bacteriostatic (stops reproduction)

Macrolides’ spectrum of activity

good antistaphylococcal and antistreptococcal activity

treatment of respiratory & soft tissue infections and sensitive intracellular pathogens • e.g. Chlamydia, Legionella

Adverse effects

Generally well tolerated

nausea

vomiting

diarrhoea

rash

Aminoglycosides

large family of antibiotics produced by various species of Streptomyces (“mycin”) and Micromonospora (“micin”)

include: streptomycin, neomycin, kanamycin, gentamicins, tobramycin

Structure = linked ring system composed of aminosugars and an aminosubstituted cyclic polyalcohol

Mode of action of aminoglycosides

Bind irreversibly to 30S ribosomal subunit

disrupt elongation of nascent peptide chain

translational inaccuracy → defective proteins

bactericidal

Spectrum of activity

broad spectrum; mainly aerobic G-ve bacilli (e.g. P. aeruginosa)

used to treat serious nosocomial infections (hospital acquired infections)

First TB antibiotic

Used for cystic fibrosis

Adverse effects

all aminoglycosides have low Therapeutic Index (only a small amount needed to become toxic)

renal damage, ototoxicity, loss of balance, nausea

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6 years ago

Medically Important Bacteria: Clasification

Medically Important Bacteria: Clasification

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6 years ago

Rahul's Noteblog: What is an ELEK's Test?

Elek test to document toxi production of Corynobacterium diphteriae

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6 years ago

ANTIBIOTICS CHEAT SHEET :)

Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies

Warfarin: increases toxicity: bleeding

* Beta-lactamase (penicinillase) Suceptible:

Natural Penicillins (G, V, F, K)

Aminopenicillins (Amoxicillin, Ampicillin)

Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

* Beta-lactamase (penicinillase) Resistant:

Oxacillin, Nafcillin, Dicloxacillin

3°G, 4°G Cephalosporins

Carbapenems

Monobactams

Beta-lactamase inhibitors

* Penicillins enhanced with:

Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)

Aminoglycosides (against enterococcus and psedomonas)

* Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are "LAME“ bc they do not cover this organisms

L isteria monocytogenes

A typicals (Mycoplasma, Chlamydia)

M RSA (except Ceftaroline, 5°G)

E nterococci

* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

All 3°G cephalosporins cross the BBB except Cefoperazone.

All cephalosporins are renal cleared, except Cefoperazone.

Disulfiram-like effect

* Against Pseudomonas:

3°G Cef taz idime (taz taz taz taz)

4°G Cefepime, Cefpirome (not available in the USA)

Antipseudomonal penicillins

Aminoglycosides (synergy with beta-lactams)

Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

* Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T ion?

Q uinolones

Sulfonamides

T etracyclines