Mnemonics: Asthma

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago

Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport)
Department of Allergy and Immunology
Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of
children (JACI, 2011). Prevalence of asthma is 8%, prevalence of AR is 3 times higher (24%). 40% of
patients with AR have asthma, 80% of patients with asthma have AR.
Classification of asthma - mnemonic
I'M MS ("I'm a Master of Science")
Intermittent
Mild persistent
Moderate persistent
Severe persistent
Number of controllers used in each stage of the classification of asthma - mnemonic:
I'M MS
0123
0 - SABA PRN (albuterol) only
1 - ICS or LTRA
2 - ICS/LABA or ICS plus LTRA
3 - ICS/LABA and LTRA, consider omalizumab (anti-IgE mAb)
Allergic Rhinitis and its Impact on Asthma (ARIA): Achievements in 10 years and future needs. ARIA has
reclassified AR as mild/moderate-severe and intermittent/persistent. This classification closely reflects
patients' needs and underlines the close relationship between rhinitis and asthma. http://buff.ly/QL1eYI
Pathogenesis of Asthma
Lymphocytes
CD4, Th2
Central effector cells
Cytokine release
Overview of adhesion molecules, 3 groups remembered by the mnemonic SIS:
Selectins
Integrins
Superfamily Ig
Mast cells are subdivided into 2 types based on proteinase content:

TC mast cells -- Tryptase and Chymase in granules

T mast cells -- Tryptase only granules
Mast cells
Mediator release
Mucosal inflammation
Mediators from eosinophils are remembered by the mnemonic CML EEE:
Cytokines
MBP
Lipid Mediators
EDN
ECP
EPO
Eosinophils
Emit
Eight mediators (at least 8, the first C in the mnemonic covers cytokines, chemokines and growth factors)
Overview of adhesion molecules, 3 groups remembered by the mnemonic SIS:
Selectins
Integrins
Superfamily Ig
There are 4 families of eicosanoids (PP-LT): prostaglandins (PG), prostacyclins (PGI), leukotrienes (LT)
and thromboxanes (TX).
Diagnosis of Asthma
A mnemonic to remember the different PFTs is SPIROMEtry:
Spirometry
PEFR
Inhalation tests:
Reversibilty of
Obstruction with beta-agonist
Metacholine challenge
Exhaled NO
The phases of spirometry can be remembered by the mnemonic BEIF:
Breath normally x 6 times
Exhale fully
Inhalation (deep)
Forceful exhalation for 6 seconds

FEV1/FVC
FEF 25-75
R
Regular (normal) or
Raised in
Restriction
FEV1
1ow in both obstructive and restrictive disease
Bronchodilation test: BB RR
Baseline spirometry
Beta-agonist
Repeat spirometry
Reversibilty of obstruction
Methacholine challenge test, remember the numbers: 5-25-20-5:
5 breaths
25 mg/mL metacholine
20% FEV1 reduction
5% of patients with asthma have a negative test, 95% react to the challenge
Test for Respiratory and Asthma Control in Kids (TRACK)
5
5 questions
5 year-old or younger (2-5 years)
Test for respiratory and asthma control in kids (TRACK) - mnemonic: 3S
Symptoms (3 questions)
SABA use
Steroid use
Test for respiratory and asthma control in kids (TRACK) - complete mnemonic: 3S
Symptoms - SPA: Symptoms - how often, Play, At night, past 4 weeks
SABA use, past 12 weeks (3 months)
Steroid use, past 12 months (1 year)
Time frame of TRACK:
Symptoms - 4 weeks (1 month)
SABA use - 12 weeks (3 months), quarter
Steroid use - 12 months (1 year)
References:

Test for Respiratory and Asthma Control in Kids (TRACK): A caregiver-completed questionnaire for
preschool-aged children. Kevin R. Murphy et al. JACI. Volume 123, Issue 4, Pages 833-839.e9 (April
2009).
Differential Diagnosis of Asthma
C
Children
Congenital conditions
CF
A
Adults
Acquired conditions
Asthma Classification: M MMS
Mild intermittent
Mild persistent
Moderate persistent
Severe persistent
Treatment
One can remember the stages by the number of controller medications a patient would need at each
stage:
I'M MS
0123
"Rule of 2s is used to determine level of control. If any of these are positive, consider a daily
controller medication:
- daytime symptoms more than 2 days/wk
- rescue 2 -agonist use more than 2 times per week
- nighttime symptoms more than 2 nights/mo
- more than 2 asthma exacerbations per year
- more than 2 rescue 2-agonist canisters/yr
Reference for rule of 2's: Audio: Asthma, noon conference. Muthiah Pugazhenthi. Podcasting Project for
the UT Internal Medicine Residency Program, 12/2006.
If asthma treatment is not working, check DAT:
Diagnosis - not asthma at all (VCD, CF, FBA), asthma plus AR, GERD
Adherence - compliance with medication

Technique - NEB, HFA with spacer, DPI, etc.

3 C's of care - communication, continuity, concordance (finding common ground) are critical for asthma
management (http://goo.gl/8gJM6).
Medications
S
Singulair
Single daily dose
Suicude risk (potential)
LABA
M
Monotherapy
Masks inflammation
Mortality increase
Corticosteroids
C category during pregnancy
Budesonide
B category during pregnancy
Exercise-induced asthma treatment: CLIMB
Cromolyn
Leukotriene receptor antagonist
Inhaled steroids
Mast cell stabilizers other than cromolyn
Beta agonists
Leukotriene receptors
Leukotriene
B4
BLT 1, 2 receptors
Leukotriene
C4, D4, E4
CysLT 1, 2 receptors
Ciclesonide mnemonic
C
Ciclesonide
Converted to active form (des-CIC)

Carboxyl-esterases in bronchial epithelial cells

Clearance by liver

Asthma medical mnemonics

Asthma treatment medical mnemonic for USMLE and NCLEX takers.
Adrenergics
Steroids
Theophyllines(although not used as much now though)
Hydration
Mask

Asthma: precipitating factors for acute attack

DIPLOMAT:
Drugs

(aspirin,

NSAIDs,

beta

blockers,

Infections
Pollutants

etc)
(URTI/LRTI)

(at

home,

at

work)

Laughter(emotion)
Oesophageal
Mites

reflux

(nocturnal

asthma)

Activity

and

exercise

Temperature (cold)
Asthma

acute

attack:

life

threatening

signs

Silent

SHOCK:
chest

Hypotension
One

third

of

best/predicted

PFR

Cyanosis
Konfusion
Asthma:

management

Oxygen
Salbutamol

of
(high

(5mg

severe
dose:

via

Hydrocortisone
Ipratropium

acute

oxygen-driven
(if

S#!T:
>60%)

(or
bromide

nebuliser)
prednisolone)

life

threatening)

Theophylline (or preferably aminophylline-if life threatening)

Wheezing:

causes

ASTHMA

Asthma
Small

airways

Tracheal

obstruction

Heart
Mastocytosis

disease
failure

or

carcinoid

Anaphylaxis or allergy

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Asthma Treatment Mnemonic

I made this small and useful technique to remember the proper treatment of asthma. The
first two bullets are the pillars of asthma treatment.
A drenergics (beta 2)

S teroids
T heophylline
H ydration
M onoclonal antibodies (anti-IgE)
A ntagonists of LTs / Chromones
As a general reminder, intermittent asthma is treated with short-acting adrenergics.
Persistent asthma adds inhaled steroids. Severe persistent asthma can be treated with
oral steroids.
Theophylline, which has become widely unpopular, is beneficial against night symptoms.
Chromones and antagonists of LTs are beneficial against exercise-induced asthma.
Monoclonal antibodies (i.e. omalizumab) are the newest drug in asthma treatment.

Mnemonics: Allergic Rhinitis

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU
Prevalence of asthma is 8%, prevalence of AR is 3 times higher (24%). 40% of patients with AR have
asthma, 80% of patients with asthma have AR.
How the allergens change during the season: mnemonic TGR MI DC/DC ("a Tiger with an MI went
to DC")
"There's spring time, where you have the tree pollen. Summer time, where you have the grass pollens.
And then there's the fall time when you have the weed pollen.
This sequence is remembered by the mnemonic TGR MI DC/DC ("a Tiger with an MI went to DC").
Pollen calendar: TGR MI DC/DC
Tree pollens
Grass pollens
Ragweed and weed pollen
Mold spores
Indoor allergens - DC/DC - Dog/Cat and Dust mite/Cockroach

Pollen-producing plants (weeds and trees) in Omaha, Nebraska

References:

Characteristics of allergic sensitization among asthmatic adults older than 55 years: results from the
National Health Allergy Season Year Round. WTOC-TV Savannah.
Interactive Allergy Map by Greer Labs. Click your state to find region-specific, common airborne allergens
there.
Botanical sexism blamed for making life miserable for allergy sufferers as male trees fill city skies with
pollen http://goo.gl/cx5tH
Symptoms of Allergic Rhinitis: CS DIES
Congestion
Smell impairment
Discharge - watery nasal discharge
Itching
Eye symptoms
Sneeze
Samter's triad include asthma, aspirin sensitivity, and nasal/ethmoidal polyposis:
ASPirin
Asthma
Sensitivity to aspirin
Polyps
Treatment
Stepwise approach to treatment of allergic rhinitis: OASIS
Omit (avoid) allergens
Antihistamines (oral and topical)
Steroids (topical)
Immunotherapy (SCIT, SLIT)
Surgery
References: Clinical review: ABC of allergies, Perennial rhinitis. BMJ 1998;316:917, figure.
Medications
S
Steroids
Single best drug in AR for
Stuffiness (congestion)
F
Fexofenadine
Free of sedation at any dose

S
Singulair
Single daily dose
Suicude risk (potential)

Treatment Options for Allergic Rhinitis (AR) and Non-Allergic Rhinitis (NAR) (click to enlarge the image).
Allergic Rhinitis and its Impact on Asthma (ARIA): Achievements in 10 years and future needs. ARIA has
reclassified AR as mild/moderate-severe and intermittent/persistent. This classification closely reflects
patients' needs and underlines the close relationship between rhinitis and asthma. http://buff.ly/QL1eYI

Allergic Rhinitis May Lead to Lower School Grades

Close functional link between mast cells and neurones might explain CNS symptoms during the
allergy season http://buff.ly/1ntpQqD

The study was a case-control analysis of 1800 teenage students sitting for national examinations in
the UK. On average, 40% of students reported symptoms of SAR. Seasonal allergic rhinitis (SAR) is
associated with a detrimental effect on examination performance in United Kingdom teenagers:
Case-control study. J Allergy Clin Immunol. 2007 Jun 7.
Symptomatic SAR and use of rhinitis medication were associated with a significantly increased risk
of unexpectedly dropping a grade in the examinations.
According to the study authors, this is the first time a relationship between SAR and poor
examination performance has been demonstrated.

Mind map for seasonal allergic rhinitis (SAR) from Allergy Cases.
Mnemonic for symptoms of SAR: CS DIES
Congestion
Smell impairment
Discharge - watery nasal discharge
Itching
Eye symptoms
Sneeze
Mnemonic for stepwise approach to treatment of allergic rhinitis: OASIS
Omit (avoid) allergens
Antihistamines (oral and topical)
Steroids (topical)
Immunotherapy
SCIT, SLIT, Surgery

You are here: Home ENT .

ATROPHIC RHINITIS (OZAENA)

Atrophic rhinitis is a chronic inflammatory disease of the nasal cavity that is characterised by atrophy of
turbinates and nasal mucosa with foul smelling crusts

It can be primary or secondary

PRIMARY ATROPHIC RHINITIS

Etiology (can be remembered with the mnemonic HERNIA)

Heriditary factors

Endocrine

Atrophic rhinitis is mostly seen in females, starts around puberty and decreases after puberty.

Hence a hormonal etiology is suggested

Racial more in whites and yellow races

Nutritional

Atrophic rhinitis is more seen in the developing nations

It is rarely seen in people belonging to higher socioeconomic status

Hence deficiency of vitamins and nutrients is believed to be a causative factor

Infective

Various bacteria Klebsiella ozaenae, streptococcus, staphylococcus, proteus and E.coli have
been isolated from the crusts

It is suggested that these bacteria are in fact secondary pathogens, responsible for the foul
smell

Autoimmune

Pathogenesis

The ciliated columnar epithelium is replaced by squamous epithelium

There is atrophy of the nasal mucosa and turbinates (with resorption of bone)

The venous sinusoids, the seromucinous glands and the nerves atrophy

Obliterative endarteritis of vessels occur

Arrested development of sinuses

Clinical features

Symptoms

Nasal obstruction even though the nasal cavity is roomy, there is deposition of crusts which
cause obstruction to air flow

Foul smell from nose Even though there is foul smell, the patient is unable to experience
this, hence called merciful anosmia

Epistaxis Occurs when the crusts get dislodged

Signs

Nasal cavity is filled with greenish / blackish crusts

On removal of crusts, there is bleeding and a roomy nasal cavity is revealed

Nasal mucosa is pale

Atrophy of turbinates, appear as ridges

Even the posterior wall of nasopharynx may be visible

Septal perforation and dermatitis of vestibule may be persent

Similar atrophic changes may be present in pharynx (atrophic pharyngitis) and larynx (cough
and hoarseness may be present)

Serous otitis media may be present due to eustachian tube dysfunction

Sinus may not be well developed (X ray)

Treatment

Medical

Removal of crusts with alkaline irrigation

Fluid for irrigation can be prepared by mixing one teaspoon full of powder (one part
sodium bicarbonate, one part sodium biborate, two parts sodium chloride) in 280ml of
water

The fluid can be introduced through one nostril and drained out through the other nostril

Care should be taken so that the fluid does not enter the eustachian tube or gets aspirated

Irrigation can be done initially 2-3 times a day, later decrease the frequency to 2-3 times
a week.

Hard to remove crusts can be removed by forceps once they are softened by irrigation

Painting the nasal mucosa with 25% glucose in glycerol helps prevent growth of bacteria so
that foul smell does not occur

Antibiotic sprays

Oestradiol spray to improve vascularity

Submucosal injection of placental extract

Streptomycin orally 1g/day for 10 days

Potassium iodide orally helps liquefy nasal secretion

Surgical

Youngs operation

Both the nostrils are surgically closed by raising flaps in the vestibule region

Aims to give rest to nasal mucosa so that it may revert back to ciliated columnar
epithelium

The nostrils are opened after 6 months

Modified youngs operation

In this, the nasal cavity is only partially closed

This is done to prevent the discomfort caused by complete nasal closure

It is also said to have same effect as that of youngs operation

Narrowing of the nasal cavity

Due to roomy nasal cavity, the air currents dry up secretions, causing crusting

Narrowing of nasal cavity aims to prevent crusting by decreasing the size of the airway

This can be done by the following techniques

Submucosal injection of teflon paste

Insertion of strips of cartilage, fat, bone or teflon

Medialisation of the lateral wall

SECONDARY ATROPHIC RHINITIS

This occurs secondary to certain conditions like

syphilis

lupus

leprosy

radiotherapy to nose

long standing purulent sinusitis

excessive surgical removal of turbinates

Unilateral atrophic rhinitis

This occurs in case of long standing septal deviation

The opposite side with the roomy nasal cavity is predisposed to development of crusts

NOV2013

Treatment algorithms for lung disease: BLOP and RIPE

posted in Internal medicine
Happy November everyone! Today we focus on mnemonics for the treatment of dyspnea and tuberculosis.
BLOP is a cute mnemonic I learned from a staff physician to remember what to give your patient who is
presenting with dyspnea. Sometimes we cant be sure whether the cause of the shortness of breath is pulmonary or
cardiac. Therefore, you may end up treating for both and giving your patient some BLOP therapy:
B = B2-adrenergic agonist (e.g. salbutamol)
L = Lasix (aka furosemide)
O = Oxygen
P = Prednisone
We are now all aware that tuberculosis is not just a historical disease (I have seen a couple of cases myself) and the
first-line agents for its treatment are commonly remembered by the mnemonic RIPE:
R = Rifampin
I = Isoniazid (aka INH)
P = Pyrazinamide (aka PZA)
E = Ethambutol

Medical Mnemonic for COPD- 4 types and hallmark

Last updated: 29-Mar-2011 10:08 PM

All Mnemonics

ABCDE:
Asthma
Brochiectasis
Chronic bronchitis
Dyspnea [hallmark of group]
Emphysema
Alternatively: replace Dyspnea with Decreased FEV1/FVC ratio.

COPD Mnemonic

ABCDE:
Asthma
Brochiectasis
Chronic bronchitis
Decreased FEV1/FVC ratio
Emphysema

Cardiology Mnemonics
Anti-arrythmics: for AV nodes
"Do Block AV"
D igoxin
B -blockers
A denosine
V erapamil
Aortic regurgitation: causes
CREAM
C ongenital
R heumatic damage
E ndocarditis

Anti-arrythmics: for AV nodes

A ortic dissection/A ortic root dilation

M arfan's
Aortic stenosis characteristics
SAD
S yncope
A ngina
D yspnoea
Apex beat: abnormalities found on palpation
HILT
H eaving
I mpalpable
L aterally displaced
T hrusting/T apping
Apex beat: causes of impalpable apex beat
COPD
C OPD
O besity
P leural, P ericardial effusion
D extrocardia
Apex beat: differential diagnosis for impalpable apex beat
DOPES
D extrocardia (dont say this first!)
O besity
P ericarditis/P ericardial tamponade/P neumothorax
E mphysema
S hock/S inus inversus/S coliosis/S keletal abnormalities (e.g. pectus excavatum)
Arrhythmias
ARHYTHMIAL 3PC
A trial Myxoma
R h heart dis
HY pertension

Anti-arrythmics: for AV nodes

TH yrotoxicosis
M itral valve dis
I HD
AL cohol
P neumonia /PE / Pericardial eff
C ardiomyopathy
Atrial fibrillation: causes
PIRATES
P ulmonary: PE, COPD
I atrogenic
R heumatic heart: mirtral regurgitation
A therosclerotic: MI, CAD
T hyroid: hyperthyroid
E ndocarditis
S ick sinus syndrome
Atrial fibrillation: causes
A SHIT
A lcohol
S tenosis
H ypertension
I nfarction/I schemia
T hyrotoxicosis
Atrial fibrillation: causes
ARITHMATIC
A lcohol
R h fever
I HD
T hyrotoxicosis
H ypertension
M itral stenosis/M I /M yxoma (atrial)
A SD

Anti-arrythmics: for AV nodes

T oxins
I diopathic/I nfective endocarditis
C ardiomyopathy/Constrictive pericarditis
Atrial fibrillation: management
ABCD
A nti-coagulate
B eta-blocker to control rate
C ardiovert
D igoxin
Atropine use: tachycardia or bradycardia
"A goes with B"
Atropine is used clinically to treat Bradycardia
Beck's triad (cardiac tamponade)
3Ds
D istant heart sounds
D istended jugular veins
D ecreased arterial pressure
Beta-blockers: cardioselective beta-blockers
"Beta-blockers Acting Exclusively At Myocardium"
B etaxolol
A cebutelol
E smolol
A tenolol
M etoprolol
Beta receptor activity
"1 heart, 2 lungs"
Beta-1 receptors are primarily on the heart, and the airway is Beta-2 receptors
Bradycardia: regular
PAD HIM
P hysiological (athlete, sleep) /p aroxysmal
A V block (2II, 3)

Anti-arrythmics: for AV nodes

D rugs (beta, dig, amiodarone)

H ypothyroid /h ypothermia
I cteric (severe)
MI
Congestive heart failure: causes of exacerbation
FAILURE
F orgot medication
A rrhythmia/A naemia
I schemia/I nfarction/I nfection
L ifestyle: taking too much salt
U pregulation of CO: pregnancy, hyperthyroidism
R enal failure
E mbolism: pulmonary
Coronary artery bypass graft: indications
DUST
D epressed ventricular function
U nstable angina
S tenosis of the left main stem
T riple vessel disease
Coronary artery disease: risk factors
HOPEFULSSS
H TN
O besity
P VD
E levated LDL
F MH
U p glucose - DM
L ow HDL
S moking
S ex - male
S edentary life style

Anti-arrythmics: for AV nodes

Cyanotic heart diseases
1-2-3-4-5-T's
Truncus Arteriosus (1 vessel)
Transposition of the 2 great vessels
Tricuspid atresia
Tetralogy of Fallot
Total anomalous pulmonary venous return (has 5 words)
ECG: causes of ST-segment depression
DEPRESSED ST
D rooping valve (MVP)
E nlargement of LV with strain
P otassium loss (hypokalemia)
R eciprocal ST-depression (in I/W AMI)
E mbolism in lungs (pulmonary embolism)
S ubendocardial ischemia
S ubendocardial infarct
E ncephalon haemorrhage (intracranial haemorrhage)
D ilated cardiomyopathy
S hock
T oxicity of digitalis, quinidine
ECG: left vs. right bundle block
"WiLLiaM MaRRoW"
W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W in V3-V6 is Right bundle block.
Note: consider bundle branch blocks when QRS complex is wide
ECG: T-wave inversion causes
INVERT
I schemia
N ormality [esp. young, black]
V entricular hypertrophy
E ctopic foci [eg calcified plaques]

Anti-arrythmics: for AV nodes

R BBB, LBBB
T reatments [digoxin]
ECG: dominant R wave in V1
WORD
W PW
O ld MI
R BBB
D extrocardia
ECG: ST elevation
ELEVATION
E lectrolytes
L BBB (Left Bundle Branch Block)
E arly Repolarization
V entricular hypertrophy
A neurysm
T reatment (eg pacemaker, pericardiocentesis)
I njury (AMI, contusion)
O sborne waves (hypothermia)
N on-occlusive vasospasm (prinzmetals)
ECG: pulseless electrical activity causes
PATCH MED
P ulmonary embolus
A cidosis
T ension pneumothorax
C ardiac tamponade
H ypokalemia/H yperkalemia/H ypoxia/H ypothermia/H ypovolemia
M yocardial infarction
E lectrolyte derangements
D rugs
ECG: exercise ramp contraindications
RAMP

Anti-arrythmics: for AV nodes

R ecent MI
A ortic stenosis
M I in the last 7 days
P ulmonary hypertension
EMD arrest
4Hs 4Ts
H ypothermia
H ypo & hyper-electrolytes
H ypovolaemia
H ypoxia
T oxic (including drugs)
T rauma
T amponade
T ension pneumothorax
Heart compensatory mechanisms that "save" organ blood flow during shock
"Heart SAVER"
S ymphatoadrenal system
A trial natriuretic factor
V asopressin
E ndogenous digitalis-like factor
R enin-angiotensin-aldosterone system
Heart sounds: 3rd heart sound
FIPPY
F ailure
I ncompetence (mitral/tricuspid)
P regnancy/Pill
P E/Pericarditis
Y outh
Heart sounds: 4th heart sound
SHIT
S tenosis (aortic/pulmonary)

Anti-arrythmics: for AV nodes

H ypertension/Heart Block
I schaemic HD
T amponade
Heart valves
LAB RAT
Left Atrium: Bicuspid
Right Atrium:Tricuspid
In case of high LDL
STArT with STATins
JVP: wave form
ASK ME
A trial contraction
S ystole (ventricular contraction)
K losure (closure) of tricusps, so atrial filling
M aximal atrial filling
E mptying of atrium
JVP: characteristics of
MOP HAIR
M ultiple wave form
O ccludable
P ostural changes
H epatojugular reflex
A bove (fills from)
I mpalpable
R espiratory changes
LVF: management
FOAM
F rusemide 40mg iv
O xygen
A trovent (& Ventolin) nebs
M orphine 2.5 5 mg

Anti-arrythmics: for AV nodes

Mitral stenosis: complications
PASTRI
P ulm BP up
A fib
S ystemic embolism
T ricuspid regurg
R ight heart failure
I nfective endocarditis
Mitral stenosis (MS) vs. mitral regurgitation (MR): epidemiology
MS is a female title (Ms.) and it is female predominant.
MR is a male title (Mr.) and it is male predominant.
Murmur attributes
IL PQRST ("Person has ill PQRST heart waves")
I ntensity
L ocation
P itch
Q uality
R adiation
S hape
T iming
Murmurs: questions to ask
SCRIPT
S ite
C haracter (e.g. harsh, soft, blowing)
R adiation
I ntensity
P itch
T iming
Myocardial infarction: complications
ABCDE x2
A rrhythmias/A neurysm

Anti-arrythmics: for AV nodes

B radycardia/BP lower
C ardiac failure/C ardiac tamponade
D resslers /D eath
E mbolism /E xtra (VSD, pap muscle rupture)
Myocardial infarction: treatment
INFARCTIONS
I V access
N arcotic analgesics (e.g. morphine, pethidine)
F acilities for defibrillation (DF)
A spirin/A nticoagulant (heparin)
R est
C onverting enzyme inhibitor
T hrombolysis
I V beta-blocker
O xygen 60%
N itrates
S tool softeners
Myocardial infarction: basic management
BOOMAR
B ed rest
O xygen
O piate
M onitor
A nticoagulate
R educe clot size
Myocardial infarction: symptoms
PULSE
P ersistant chest pain
U pset stomach
L ightheadedness
S hortness of breath

Anti-arrythmics: for AV nodes

E xcessive sweating
Myocardial infarction: treatment of acute MI
COAG
C yclomorph
O xygen
A spirin
G lycerol trinitrate
Myocardial infarction: therapeutic treatment
ROAMBAL
R eassure
O xygen
A spirin
M orphine (diamorphine)
B eta blocker
A rthroplasty
L ignocaine
Occlusive arterial disease
6Ps
P ain
P allor
P ulseless
P arasthesia
P aralysis
P erishing with cold
Pericarditis
DRUMSTICX
D resslers
R h fever /R A
U raemia
MI
S LE

Anti-arrythmics: for AV nodes

T rauma
I diopathic
C oxsackie
X ray
Postural hypotension
HANDI
H ypovolaemia / hypopituitarism
A ddisons
N europathy (autonomic)
D rugs (vasodilators / TCADs, diuretics, antipsychotics)
I diopathic
Rheumatic fever: Jones major criteria
CASES
C arditis
A rthritis (migratory)
S ubcut nodules
E rythema marginatum
S yndenhams chorea
Rheumatic fever: Jones major criteria
JONES
J oints (migrating polyarthritis)
O bvious, the heart (carditis, pancarditis, pericarditis, endocarditis or valvulits)
N odes (subcutaneous nodules)
E rythema marginatum
S ydenham's chorea
Rheumatic fever: Jones minor criteria
4PA
P yrexia
P rolonged PR
P ast Hx
P ositive (ie ?)ESR/CRP

Anti-arrythmics: for AV nodes

A rthralgia
Rheumatic fever: Jones minor criteria
CAFE PAL
C RP increased
A rthralgia
F ever
E levated ESR
P rolonged PR interval
A namnesis of rheumatism
L eucocytosis
Splinter haemorrhages
TRIP SAM
T rauma
RA
I nfective Endo
P AN
S LE / Sepsis
A naemia (profound)
M alignancy (haematological)
Supraventricular tachycardia: causes
SNAP
S inus tachy
N odal tachy
A fib
P aroxysmal atrial tachy
Supraventricular tachycardia: treatment
ABCDE
A denosine
B eta-blocker
C alcium channel antagonist
D igoxin

Anti-arrythmics: for AV nodes

E xcitation (vagal stimulation)

Ventricular tachycardia: treatment
LAMB
L idocaine
A miodarone
M exiltene/ Magnesium
B eta-blocker
Secondary Causes of Hypertension (courtesy of Brian Dalton)
TRACKPADS
T hyroid disease (hyper-)
R enovascular disease (renal artery stenosis)
A orta, coarctation of
C ushing syndrome
K idney disease, chronic
P heochromocytoma
A ldosteronism (hyper-)
D rugs (e.g. oral contraceptives, decongestants, NSAIDS)
S leep apnea

CARDIOLOGY
MNEMONICS
Aortic stenosis characteristics SAD:
Syncope
Angina
Dyspnoea
MI: basic management BOOMAR:
Bed rest
Oxygen
Opiate
Monitor

Anticoagulate
Reduce clot size
ECG: left vs. right bundle block "WiLLiaM MaRRoW":
W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W in V3-V6 is Right bundle block.
Note: consider bundle branch blocks when QRS complex is wide.
Pericarditis: causes CARDIAC RIND:
Collagen vascular disease
Aortic aneurysm
Radiation
Drugs (such as hydralazine)
Infections
Acute renal failure
Cardiac infarction
Rheumatic fever
Injury
Neoplasms
Dressler's syndrome
Murmurs: systolic types SAPS:
Systolic
Aortic
Pulmonic
Stenosis
Systolic murmurs include aortic and pulmonary stenosis.
Similarly, it's common sense that if it is aortic and
pulmonary stenosis it could also be mitral and tricusp regurgitation].
MI: signs and symptoms PULSE:
Persistent chest pains
Upset stomach
Lightheadedness
Shortness of breath
Excessive sweating

Heart compensatory mechanisms that 'save' organ blood flow

during shock "Heart SAVER":
Symphatoadrenal system
Atrial natriuretic factor
Vasopressin
Endogenous digitalis-like factor
Renin-angiotensin-aldosterone system
In all 5, system is activated/factor is released
Murmurs: right vs. left loudness "RILE":
Right sided heart murmurs are louder on Inspiration.
Left sided heart murmurs are loudest on Expiration.
If get confused about which is which, remember LIRE=liar which will
be inherently false.
ST elevation causes in ECG, ELEVATION:
Electrolytes
LBBB
Early repolarization
Ventricular hypertrophy
Aneurysm
Treatment (eg pericardiocentesis)
Injury (AMI, contusion)
Osborne waves (hypothermia)
Non-occlusive vasospasm
Beck's triad (cardiac tamponade) 3 D's:
Distant heart sounds
Distended jugular veins
Decreased arterial pressure
MI: therapeutic treatment ROAMBAL:
Reassure
Oxygen
Aspirin
Morphine (diamorphine)

Beta blocker
Arthroplasty
Lignocaine
CHF: causes of exacerbation FAILURE:
Forgot medication
Arrhythmia/ Anaemia
Ischemia/ Infarction/ Infection
Lifestyle: taken too much salt
Upregulation of CO: pregnancy, hyperthyroidism
Renal failure
Embolism: pulmonary
Murmurs: systolic vs. diastolic PASS: Pulmonic
& Aortic Stenosis=Systolic.
PAID: Pulmonic & Aortic Insufficiency=Diastolic.
Murmurs: systolic vs. diastolic Systolic murmurs: MR AS:
"MR. ASner".
Diastolic murmurs: MS AR: "MS. ARden".
The famous people with those surnames are Mr. Ed Asner and Ms.
Jane Arden.
Mitral stenosis (MS) vs. regurgitation (MR): epidemiology MS is a
female title (Ms.) and it is female predominant.
MR is a male title (Mr.) and it is male predominant.
Pericarditis: EKG "PericarditiS":
PR depression in precordial leads.
ST elevation.
Jugular venous pressure (JVP) elevation: causes HOLT: Grab
Harold Holt around the neck and throw him in the ocean:
Heart failure
Obstruction of venea cava
Lymphatic enlargement - supraclavicular
Intra-Thoracic pressure increase

Depressed ST-segment: causes DEPRESSED ST:

Drooping valve (MVP)
Enlargement of LV with strain
Potassium loss (hypokalemia)
Reciprocal ST- depression (in I/W AMI)
Embolism in lungs (pulmonary embolism)
Subendocardial ischemia
Subendocardial infarct
Encephalon haemorrhage (intracranial haemorrhage)
Dilated cardiomyopathy
Shock
Toxicity of digitalis, quinidine
Murmurs: innocent murmur features 8 S's:
Soft
Systolic
Short
Sounds (S1 & S2) normal
Symptomless
Special tests normal (X-ray, EKG)
Standing/ Sitting (vary with position)
Sternal depression
Murmur attributes "IL PQRST" (person has ill PQRST heart waves):
Intensity
Location
Pitch
Quality
Radiation
Shape
Timing
Murmurs: locations and descriptions "MRS A$$":
MRS: Mitral Regurgitation--Systolic
A$$: Aortic Stenosis--Systolic

 The other two murmurs, Mitral stenosis and Aortic regurgitation, are
obviously diastolic.
Betablockers: cardioselective
betablockers "Betablockers Acting Exclusively At Myocardium"
Cardioselective betablockers are:
Betaxolol
Acebutelol
Esmolol
Atenolol
Metoprolol
Apex beat: abnormalities found on palpation, causes of
impalpable HILT:
Heaving
Impalpable
Laterally displaced
Thrusting/ Tapping
If it is impalpable, causes are COPD:
COPD
Obesity
Pleural, Pericardial effusion
Dextrocardia
MI: treatment of acute MI COAG:
Cyclomorph
Oxygen
Aspirin
Glycerol trinitrate
Coronary artery bypass graft: indications DUST:
Depressed ventricular function
Unstable angina
Stenosis of the left main stem
Triple vessel disease

Peripheral vascular insufficiency: inspection criteria SICVD:

Symmetry of leg musculature
Integrity of skin
Color of toenails
Varicose veins
Distribution of hair
Heart murmurs "hARD ASS MRS. MSD":
hARD: Aortic Regurg = Diastolic
ASS: Aortic Stenosis = Systolic
MRS: Mitral Regurg = Systolic
MSD: Mitral Stenosis = Diastolic
Mitral regurgitation When you hear holosystolic murmurs, think "MRTHEM ARE holosystolic murmurs".
Sino-atrial node: innervation Sympathetic acts on Sodium channels
(SS).
Parasympathetic acts on Potassium channels (PS).
Supraventricular tachycardia: treatment ABCDE:
Adenosine
Beta-blocker
Calcium channel antagonist
Digoxin
Excitation (vagal stimulation)
Ventricular tachycardia: treatment LAMB:
Lidocaine
Amiodarone
Mexiltene/ Magnesium
Beta-blocker
Pulseless electrical activity: causes PATCH MED:
Pulmonary embolus
Acidosis
Tension pneumothorax

Cardiac tamponade
Hypokalemia/ Hyperkalemia/ Hypoxia/ Hypothermia/ Hypovolemia
Myocardial infarction
Electrolyte derangements
Drugs
Sinus bradycardia: aetiology "SINUS BRADICARDIA" (sinus
bradycardia):
Sleep
Infections (myocarditis)
Neap thyroid (hypothyroid)
Unconsciousness (vasovagal syncope)
Subnormal temperatures (hypothermia)
Biliary obstruction
Raised CO2 (hypercapnia)
Acidosis
Deficient blood sugar (hypoglycemia)
Imbalance of electrolytes
Cushing's reflex (raised ICP)
Aging
Rx (drugs, such as high-dose atropine)
Deep anaesthesia
Ischemic heart disease
Athletes
Rheumatic fever: Jones criteria Major criteria: CANCER:
Carditis
Arthritis
Nodules
Chorea
Erythema
Rheumatic anamnesis
Minor criteria: CAFE PAL:
CRP increased
Arthralgia

Fever
Elevated ESR
Prolonged PR interval
Anamnesis of rheumatism
Leucocytosis
JVP: wave form ASK ME:
Atrial contraction
Systole (ventricular contraction)
Klosure (closure) of tricusps, so atrial filling
Maximal atrial filling
Emptying of atrium
See diagram.
Coronary artery bypass graft: indications DUST:
Depressed ventricular function
Unstable angina
Stenosis of the left main stem
Triple vessel disease
Exercise ramp ECG: contraindications RAMP:
Recent MI
Aortic stenosis
MI in the last 7 days
Pulmonary hypertension
ECG: T wave inversion causes INVERT:
Ischemia
Normality [esp. young, black]
Ventricular hypertrophy
Ectopic foci [eg calcified plaques]
RBBB, LBBB
Treatments [digoxin]
Rheumatic fever: Jones major criteria JONES:
Joints (migrating polyarthritis)

Obvious, the heart (carditis, pancarditis, pericarditis, endocarditis

or valvulits)
Nodes (subcutaneous nodules)
Erythema marginatum
Sydenham's chorea
Myocardial infarctions: treatment INFARCTIONS:
IV access
Narcotic analgesics (eg morphine, pethidine)
Facilities for defibrillation (DF)
Aspirin/ Anticoagulant (heparin)
Rest
Converting enzyme inhibitor
Thrombolysis
IV beta blocker
Oxygen 60%
Nitrates
Stool Softeners
Atrial fibrillation: causes PIRATES:
Pulmonary: PE, COPD
Iatrogenic
Rheumatic heart: mirtral regurgitation
Atherosclerotic: MI, CAD
Thyroid: hyperthyroid
Endocarditis
Sick sinus syndrome
Atrial fibrillation: management ABCD:
Anti-coagulate
Beta-block to control rate
Cardiovert
Digoxin
Anti-arrythmics: for AV nodes "Do Block AV":
Digoxin

B-blockers
Adenosine
Verapamil
Murmurs: systolic MR PV TRAPS:
Mitral
Regurgitation and
Prolaspe
VSD
Tricupsid
Regurgitation
Aortic and
Pulmonary
Stenosis
Apex beat: differential for impalpable apex beat DOPES:
Dextrocardia
Obesity
Pericarditis or pericardial tamponade
Emphysema
Sinus inversus/ Student incompetence

Treatment of MDR tuberculosis mnemonic

Hi everyone!

This is a complicated mnemonic. Too many drugs but hopefully it will help you write a SAQ on it :)

Before I get to the mnemonic, here are some general principles.

4 drugs to which the mycobacteria are susceptible should be used.

6 months intensive phase is followed by a continuation phase for 18-24 months.

An injectable drug like kanamycin or streptomycin is dropped in the continuation phase.

1st group:
High-dose isoniazid, pyrazinamide, and ethambutol are thought of as an adjunct for the treatment of MDR
and XDR tuberculosis.

2nd group: Fluoroquinolones, of which the first choice is high-dose levofloxacin.

3rd group are the injectable drugs:

Capreomycin, amikacin, kanamycin.
Mnemonic: CAKe

4th group:
Cycloserine, aminosalicylic acid (PAS), thioamides (Ethionamide).
Mnemonic: CAT

If susceptibility to drugs is not available:

Give KEEPQ for 6 months and then PEEQ for 18 months (Drop the injectable, remember?)
Kanamycin
Ethionamide
Ethambutol
Pyrazinamide
Quinolone

If resistant to Rifampin and Isoniazid:

Give PEQS for 6 months and then PEEQ for 18 months.
Pyrazinamide
Ethambutol
Quinolone
Streptomycin
And then replace injectable Streptomycin with Ethionamide

If resistant to all first line drugs:

Quinolone + any one from CAKe + any two from CAT

That's all!

-IkaN

Updated on 16th February, 2015:

Mnemonic for drug resistance in MDR TB:

HeR multi drug resistance.
Resistance to H (Isoniazid) and R (Rifampin) is defined as MDR TB.

Mnemonic for XDR TB:

Her extra fluorescent cake.
Resistance to H (Isoniazid), R (Rifampin), any fluoroquinolone and one of the three second line injectable
drugs (Capreomycin, Amikacin & Kanamycin) is defined as XDR or extensive drug resistance.

Related post:
Antitubercular drugs mnemonic
Tuberculosis treatment regimen mnemonic!

TB mostly affects your RESPIration

RESPIration
Rifampicin
Ethambutol
Streptomycin
Pyrazinamide
Isoniazid

TB treatment:
mnemonic RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
two phase:
1.intensive>RIPE for 2 month.
2.continuation>RI for 4 month.
Note:details in Davidson's

Features of Tuberculosis (TB)

Mnemonic: 4 Cs
C Cough
C Caseation
C Calcification
C Cavitation