Can - Citrate

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!

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 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)

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.

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

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;

The renin-angiotensin system that helps regulate the constriction of blood vessels and blood pressure.

clearance = (urine concentration x urine volume passed over time) / plasma concentration

the only useful thing my prof ever taught me for the renal physiology portion of my physiology course is that clearance is calculated by the equation “pissing under the sun” ( C = UV/P)

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

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