Medblr - Blog Posts
School’s about to start in two days, does anyone have any tips for taking notes?
A league of extraordinary people
MEDICINE & DARK ACADEMIA
If you know me based on what I was a year ago, you don't know me anymore. My evolution is constant.
We are moments of life and death in a universe in constant renewal.
Immunology | 21-10-2019
My second immunology exam is this Thursday. We are going to win this battle! ✨
Medicine + October
"Learning to defeat yourself is learning to live."
- Eliphas Levi
Anatomy | 26-09-2019
It's been a long time since I had devoted time to the elaboration of anatomical schemes.
I find fascinating their strident and complex beauty.
Is there an art more complex than that of the human body?
Medicine meets Dark Academia
"Vita brevis, ars longa, occasio praeceps, experimentum periculosum, iudicium difficile"
Recently, I have been working a lot in the dissection rooms, specialising myself, and discovering that the best way to learn Anatomy is in there. The human body is a book of knowledge, when we open it we discover its wisdom. I made some transparent templates that, when uniting, can show the epidemic layer, muscles and bones✨💉
MEDSCHOOL MOODBOARD
Cryptid & Distinguished, much prefer getting compliments on their intellect and hard work, obessive, well-versed…
It's been ages since I was here. I used to love the smell, the touch, the feeling of fascias separating...and now I remember why I loved both Anatomy and Surgery ❤️
Maybe when we chose this profession we were not very aware that not only were we going to study Medicine, but we had, as well, to become doctors. ✨⚕️
This is a drawing by Quaestor Valdemar that I did (before) Anatomy class a while ago~
Recently I returned to medical school with a more than fortunate situation. My effort paid off and it has encouraged me to give my best this year as well ✨ The dissections that I am now doing are not entirely like the ones I used to do last year, but I like them a little more. It is no longer simply to practice the surgical technique but really to see the Anatomy of all the organs ❤️
Cytochrome P450 Inducers & Inhibitors
The main ones can be remembered using "CRAP GPs spend all day on SICKFACES.COM".
Cytochrome P450 Inducers
These induce CYP450 activity, and thus reduce the concentration of drugs which are metabolised by this system.
Carbemazepine Rifampicin Alcohol (chronic use) Phenytoin Griseofulvin Phenobarbitone Sulphonylureas, St John's Wort, Smoking
Also topiramate.
Cytochrome P450 Inhibitors
These inhibit CYP450 enzyme activity and thus increase the concentration of drugs which are metabolised by this system.
Sodium valproate Isoniazid Cimetidine Ketoconazole Fluconazole Alcohol (acute use), Amiodarone, Allopurinol Chloramphenicol Erythromycin Sulfonamides, SSRIs Ciprofloxacin Omeprazole Metronidazole
Also grapefruit, cranberry juice, diltiazem, verapamil, clarithromycin.
Common Interactions
Medications which commonly interact with CYP450 inhibitors and inducers are:
Warfarin
Phenytoin
Combined Oral Contraceptive Pill (COCP)
Theophylline
Corticosteroids
Tricyclic antidepressants
Statins
Lamotrigine
Midazolam
Haemosiderin staining
"Haemosiderin staining" describes orange/red/brown skin hyperpigmentation caused by haemosiderin (an iron-containing pigment found in blood) leaking into the skin.
Causes:
Chronic venous insufficiency (in lower legs)
Skin inflammation
Trauma e.g. wound, fracture, surgery
Pigmented purpuric dermatoses
Haemochromatosis
Haemosiderin staining may be exacerbated by anticoagulant use as this increases extravasation (leakage) of red blood cells into the skin.
See an example here.
Causes of drug-induced lupus
SHIP
Sulfasalazine & Sulfonamide Hydralazine Isoniazid Procainamide & Phenytoin
This is by no means a definitive list (they are many!) but these are some of the most common causes.
Common ototoxic medications
"FAV Q&A"
Furosemide (and other loop diuretics) Aminoglycosides Vancomycin Quinine Aspirin
Hypokalaemia ECG changes
U have no pot and you have no T but you have a long PR and a long QT
Low potassium causes:
U waves (small deflection immediately after T wave)
Flattened/inverted T waves
Prolonged PR interval
Apparent prolonged QT interval (due to fusion of T and U waves)
Also:
Increased P wave amplitude
Widespread ST depression
Oedema - pitting vs non-pitting
Oedema is swelling due to excess fluids in tissues.
In pitting oedema, pressing on the affected area leaves an indentation (that persists after removing the pressure). In non-pitting oedema, the area feels firm to touch and does not form indentations.
Pitting oedema:
The excess fluid is mainly composed of water
Commonly caused by heart failure, venous insufficiency, or nephrotic syndrome
Non-pitting oedema:
The excess fluid consists of water WITH protein and salts
Usually indicates a condition of the thyroid / lymphatic system
Different types:
Lymphoedema is due to a build-up of lymphatic fluid (e.g. due to a tumour blocking lymphatic flow / after removal of lymph nodes).
Myxoedema occurs in hypothyroidism and often affected the pretibial or periorbital area.
Angioedema is localised swelling of the skin and is usually due to allergic reactions. It typically affects the face, tongue, larynx, abdomen, arms, and legs. When the larynx is affected, it may affect breathing, which is an emergency!
Lipoedema is when fat accumulates in subcutaneous tissues - it usually affects the legs/buttocks and almost exclusively occurs in postpubertal females (not the same as cellulite!)
If patients present with oedema, it's always important to test if it's pitting or non-pitting as this helps to determine the cause and correct treatment!
Causes of Acute Pancreatitis
In the UK and US, the main causes are gallstones and alcohol.
Use the mnemonic 'I GET SMASHED':
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps / Malignancy
Autoimmune
Scorpion stings
Hypercalcaemia / Hypertriglyceridaemia / Hypothermia
ERCP
Drugs (including azathioprine, mesalazine, bendroflumethiazide, furosemide, steroids, sodium valproate)
Branches of external carotid artery
Some Anatomists Like F*cking, Others Prefer S & M
Superior thyroid artery
Ascending pharyngeal artery
Lingual artery
Facial artery
Occipital artery
Posterior auricular artery
Superficial temporal artery
Maxillary artery
The superior thyroid, ascending pharyngeal, lingual and facial arteries are ANTERIOR branches.
The occipital and posterior auricular arteries are POSTERIOR branches.
The superficial temporal and maxillary arteries are TERMINAL branches.
“Some Anatomists Like F*cking, Others Prefer S & M”
is a mnemonic my professor just mentioned in class for the branches of the external carotid artery askjvb;askjbv;
Cranial nerves mnemonic
On, on, on, they travelled and found Voldemort guarding very ancient horcruxes.
Olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal.
On - Olfactory nerve (CN I)
On - Optic nerve (CN II)
On - Oculomotor nerve (CN III)
They - Trochlear nerve (CN IV)
Travelled - Trigeminal nerve (CN V)
And - Abducens nerve (CN VI)
Found - Facial nerve (CN VII)
Voldermort - Vestibulocochlear nerve (CN VIII)
Guarding - Glossopharyngeal nerve (CN IX)
Very - Vagus nerve (CN X)
Ancient - Accessory nerve (CN XI)
Horcruxes - Hypoglossal nerve (CN XII)
Distribution of calcium in the body
Bone calcium (99%)
Ca^2+ and PO4^3+ form hydroxyapatite
Plasma calcium
Diffusible pool
~50% of plasma calcium is free/unbound ionic Ca2+ (physiologically important form)
~10% of plasma calcium is complexed with small molecular weight compounds (citrate, phosphate)
Non-diffusible pool
~40% of plasma calcium is bound to calcium-binding proteins and plasma proteins (albumin)
The body utilises plasma albumin-bound calcium as a circulating reserve
Basic pharmacology of neuromuscular junction
ACh acts on N2 receptors (ligand-gated Na+/K+ receptors)
Block Na+ channels that propagate nerve impulse - local anaesthetics (lidocaine), tetrodotoxin
Inhibit ACh release - tetanus toxin, botulinum toxin
Competitive antagonists - vecuronium
N2 agonists - suxamethonium
Flaccid paralysis
Only cleared by plasma cholinesterase
Reversible anticholinesterases - edrophonium, neostigmine, physostigmine
Block activity of AChE
Diagnose and treat myasthenia gravis and treat glaucoma respectively
Irreversible anticholinesterases - organophosphates (pesticides, nerve gases)
Long-lived flaccid paralysis
Treat with pralidoxime within 10 minutes - cleaves OP-AChE complex
Management of acute MI
Reduce anginal pain
Morphine (+ anti-emetic)
Oxygen
Nitrate
Initiate reperfusion
Anti-platelet (aspirin, clopidogrel)
Thrombolytic (rtPA)
Primary angioplasty (PTCA)
Anticoagulant (heparin)
Protect myocardium
Beta-blocker
ACE inhibitor
Secondary prevention
Aspirin
Lipid-lowering (statin)
Lifestyle
Helpful mnemonic foe MI treatment.
Carpal bones mnemonic
So Long Till Pinky, Here Comes The Thumb
Scaphoid
Lunate
Triquetrum
Pisiform
Hamate
Capitate
Trapezoid
Trapezium
(going anti-clockwise in this diagram)
