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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 0 1 2 3 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:

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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

0 1 2 3

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

0 1 2 3

"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 β2 -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 β2-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, etc)

Infections (URTI/LRTI)

Pollutants (at home, at work)

Laughter(emotion)

Oesophageal reflux (nocturnal asthma)

Mites

Activity and exercise

Temperature (cold)

Asthma acute attack: 5 life threatening signs SHOCK:

Silent chest

Hypotension

One third of best/predicted PFR

Cyanosis

Konfusion

Asthma: management of acute severe “O S#!T“:

Oxygen (high dose: >60%)

Salbutamol (5mg via oxygen-driven nebuliser)

Hydrocortisone (or prednisolone)

Ipratropium bromide (if life threatening)

Theophylline (or preferably aminophylline-if life threatening)

Wheezing: causes ASTHMA :

Asthma

Small airways disease

Tracheal obstruction

Heart failure

Mastocytosis or carcinoid

Anaphylaxis or allergy

Steps History: 1 + CK Posts: 73 Threads: 12 Thanked 80 Times in 38 Posts Reputation: 90

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

Young’s 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 young’s 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 young’s 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 can’t 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 (don’t 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 (2°II, 3°)

Anti-arrythmics: for AV nodes

D rugs (beta, dig, amiodarone)

H ypothyroid /h ypothermia

I cteric (severe)

M I

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 (prinzmetal’s)

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

M I

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

R A

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 "MR-

THEM 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 Cʼs

C Cough

C Caseation

C Calcification

C Cavitation