Mnemonics Flashcards
Inputs of vomiting centre
CHILL - Barf Prep
CTZ, higher cortical centres, GIT, labyrinth, limbic system, baroreceptors, peripheral pain pathways
Liver functions
BSC SMID
Biotransformation, synthetic, capacitance, storage, metabolic, immunological, digestive.
Hypoxia
HASH
Hypoxic, anaemic, stagnant, histotoxic
Osmolality and osmolarity
OsmoLality in the Lab but not in Litres
Osmolality = osmoles/kg of solvent (more accurate as not temperature dependent) Osmolarity = osmoles/L of solution
Describing a drug
Physicochemical: chemical structure, presentation, storage
Indications, contraindications, dose, toxicity
PD: mechanism, effects by system
PK: ADME
Mechanisms of heat loss
RCECR
Radiation (40%), convection (30), evaporation (15), conduction (10), respiration (5).
Layers of adrenal cortex
GFR ACT
Glomerulosa, fasciculata, reticularis (outer to inner)
Aldosterone (mineralocorticoids), cortisol (glucocorticoids), testosterone (androgens) respectively
Medulla makes NA and A from chromaffin cells
Catecholamine synthesis
Paternity: Long Live DNA
Phenylalanine, L-tyrosine, L-dopa, dopamine, NA, A
Roles of endothelium
V SCOF BID
Vasomotor tone, secretion (ACE) coagulation (damage –> exposure of tissue factor), osmosis, filtration, barrier, inflammation, diffusion
Types: continuous (BBB), discontinuous (sinusoids), fenestrated (glomeruli)
Risks of transfusion
RIM(ember): Transfusion Has Its Downsides
Reactions (haemolytic, febrile), infection (bacterial, viral, parasite, prion), metabolic (low Ca, high K, acidosis if liver failure), TRALI/TACO/GVHD, hypothermia, iron overload, depletion of platelets/clotting factors (5 and 8).
RBC storage solutions
ACCS
ACD, CPD, CAPD, SAGM (in order of increasing RBC survival)
Coagulation: classical and cell based
XTF (“Cross the line To Finish”)
X to Xa, prothrombin to thrombin, fibrinogen to fibrin –> clot
Cell based: initiation, amplification, propagation
Oral hypoglycaemics
Big Tall Sugar Daddy Mega Increased Adiposity
Increase insulin sensitivity
- Biguanides (metformin)
- Thiazolidinediones (pioglitazone)
Increase insulin secretion
- Sulphonylureas (gliclazide)
- Dipeptidyl peptidase IV inhibitors (sitagliptin)
- Meglitinides (repaglinide)
- Incretin mimetics (exenatide)
Other
- Alpha glucosidase inhibitors (acarbose) - reduce carbohydrate absorption
Mechanisms of drug action
RENT-a-HIP
Receptors, enzymes, neurotransmitters, transport systems, hormones, ion channels, physicochemical.
Factors influencing drug absorption (and passage across placenta)
CLIPPR-M
Concentration gradient (Fick’s law), lipid solubility, ionisation and pKa, protein binding, route of administration, molecular weight (Graham’s law).
Extra factors for placenta:
- pH maternal blood and fetal blood (more acidotic fetus means more basic drugs will cross e.g. opioids and LAs –> ion trapping)
- placental blood flow
Also thickness of membrane and surface area.
Fentanyl/alfentanil comparison
DOC PIP VELD
Dose, onset, clearance, pKa, ionisation, protein binding, Vd, elimination t1/2, lipid solubility, duration.
Laminar vs turbulent flow
LV has DTs
Laminar - viscosity most important
Turbulent - density most important
Paediatrics
WET FLAG
Weight = (age + 4) x 2 --> superseded Energy = 4J/kg Tube = uncuffed diameter = (age/4) + 4; length = (age/2) + 12 (or +15 for nasal) Fluids = 20ml/kg Lorazepam = 0.1mg/kg Adrenaline = 0.1ml/kg of 1:10:000; atropine = 20mcg/kg Glucose = 5ml/kg of 10%
BP = (age x 2) + 80 (median systolic value)
Fluid deficit: each % deficit means 10ml/kg deficit to be replaced over 48h
Receptor types
Let’s Go To India
Ligand gated ion channel (nAChR, GABA-A), G-protein coupled (opioid, adrenoceptors, mAChR), tyrosine kinase (insulin), intracellular (steroid, thyroxine)
In order of increasing time taken for response (ms, s, min, hours)
ICU daily review
FLATCHUG
Feed/fluids, lines/devices, analgesia/aperients/abx, thromboprophylaxis, communication, hydration/head up, ulcer prophylaxis, glycaemic control
Difficult BMV
OBESE
Obese, bearded, elderly (>55), snorers, edentulous
Surgical sieve
VITAMIN CDEF
V: vascular I: infective/Inflammatory T: traumatic A: autoimmune M: metabolic I: iatrogenic/idiopathic N: neoplastic C: congenital D: degenerative/developmental E: endocrine/environmental F: functional
Difficult LMA insertion
RODS
Restricted mouth opening, obstruction, distorted anatomy, stiff lungs or C-spine
Difficult front of neck access
SHORT
Surgery, haematoma, obese, radiation, tumour
Causes of PPH
4 Ts
Tone, tissue, trauma, thrombin
3 Es of APLS
Effort - WOB, RR, recession, grunting, flared nostrils, accessory muscles
Efficacy - air entry, chest expansion, exhaustion, SpO2
Effectiveness - heart rate/cardiovascular status, mental status
Valvular heart disease goals
Regurgitant: full, fast + forward
Stenotic (inc HCM, and PHTN): full, slow + tight
Cytotoxics
PASTA HAM
Platinum-based agents (cisplatin) - alter ca cell DNA
Alkaloids (vinca alkaloids) - block cell division
Steroids (dex) - damage lymphoma cells
Topoisomerase inhibitors (etoposide) - interfere with transcription/replication
Antitumour antibiotics (doxorubicin)
Hormones (tamoxifen, finasteride) - oestrogen receptor modulator, 5 alpha reductase inhibitor respectively
Antimetabolites (methotrexate) - mimic nitrogenous bases to stop cell division
Monoclonal antibodies (rituximab) - attach to ca cells to increase immune response
Example regimes
NHL: CHOP (cyclophosphamide, hydroxydaunomycin (doxorubicin), oncovin (vincristine), prednisolone
HL: ABVD (adriamycin, bleomycin, vinblastine, dacarbazine)
Immunosuppressants
SCAT
Steroids - methylpred - inhibit T cell lymphokine production; Cushing’s
Calcineurin inhibitors - ciclosporin, tac - prevent T cell activation/cell-mediated immune reactions; nephro/neurotoxic, HTN, DM, hyperkalaemia, enhance NMBs
Antiproliferative - MMF, aza - inhibit T/B cells; myelosuppression, antagonise NMBs, hepatotoxic
Target of rapamycin (TOR) inhibitors - sirolimus - prevent T/B cell activation; HTN, oedema, diarrhoea
All increase skin and lymphoproliferative malignancy and predispose to infection.
Types of sickle cell crisis
VASH
Vaso-occlusive - classic sickling, ischaemia, organ damage e.g. acute chest syndrome
Aplastic - acutely worsening anaemia - often caused by parvovirus B19, low retics
Sequestration - splenic, childhood, normal or high retics
Haemolytic - common with co-existent G6PD
Cholinergic side effects
Cholinergic (caused by anticholinesterases): DUMBBELS
Diarrhoea/diaphoresis Urination Meiosis/muscle weakness Bronchospasm Bradycardia Emesis Lacrimation Salivation
Nerves for scalp block
7 nerves: GGL SSAZ
From C2:
Greater auricular
Greater occipital
Lesser occipital
Trigeminal: Supraorbital (Vi) Supratrochlear (Vi) Auriculotemporal (Viii) Zygomaticotemporal (Vii)
ETT/ventilation problem
DOPES
Displacement Obstruction Pneumothorax Equipment Stomach
Diaphragm
Student Loans Company Loves My Money
Muscular portion
- Sternal (from xiphoid)
- Lumbar (R and L crura from vertebral bodies L1-3)
- Costal (cartilages of T6-12)
Arcuate ligaments
- Lateral (quadratus lumborum)
- Medial (psoas)
- Median (between crura)
Openings
T8 - IVC, R phrenic
T10 - oesophagus, vagi, gastric vessels
T12 - aorta, azygos vein, thoracic duct
Pacemakers
PSRRA
Pacing Sensing Response Rate modulation Anti-tachycardia pacing
Autoregulation theories
M and Ms Are Easily Hidden
Metabolic (K+/H+/lactate)
Myogenic (smooth muscle)
Autonomic (alpha 1/beta 2)
Endothelial (NO/PGI2 vasodilate vs. TXA2, endothelin vasoconstrict)
Hormonal (ANP vasodilates, angiotensin II vasoconstricts)
Response to blood loss
No Has Hamburger
Neuronal: vasoconstriction, venous reservoir constriction, baroreceptor activation
Hormonal: reduced RA stretch, ANP falls, ADH rises; RAAS activation
Haematological: dilutional anaemia from water resorption, increased epo production
MEN
1: pit, pan, para
2a: para, ad, thy
2b: ad, thy, Marfanoid
2a/2b and von Hippel Lindau get phaeos.
Trauma history
AMPLE
Allergies Medications Past medical history Last meal Events
