Archive for the Medicine Category

Mnemonics

Posted in Medicine on November 8, 2007 by dowite1588

Causes of acute Pancreatitis

BAD SHIT

Black scorpion bite
Alcohol ( or autoimmune : PAN )
Drugs ( tetracycline, azothioprin, sulfa, diuretics )
Stones ( gallstones or steroid )
Hyperlipidemia
Infection ( mumps )
Trauma

Small Bowel Obstruction

“SHAVIT”

S – Stone (gallstone ileus)
H – Hernia
A – Adhesions
V – Volvulus
I – Intussusception
T – Tumor

Non-GI Causes of Vomiting

ABC’s of Non- GI causes of vomiting

Acute renal failure
Brain (Increased ICP)
Cardiac (Inferior MI)
DKA
Ears (labyrinthitis)
Foreign substances (Tylenol, theo, etc)
Glaucoma
Hyperemesis Gravidarum
Infections (pyelonephritis, meningitis)

Extraintestinal manifestations of I. B. D. are A PIE SAC -
Aphthous ulcers, Pyoderma gangrenosum, Iritis, Erythema nodosum, Sclerosing cholangitis, Arthritis, clubbing.

Which I. B. D. has C-obblestones on endoscopy – C-rohn’s.

If QRS complex is wide, consider bundle branch block. LBBB causes a “W” pattern in V1-2 and a “M” pattern in V5-6. RBBB is the other way round. Remember as WiLLiaM MaRRoW.

Basal Systolic Murmur: Aortic Stenosis (AS)
-The mnemonic key is Arthur Shawcross (AS), a cannibalistic murderer, a key which immediately follows the symbol.

-Clinical:

Angina pectoris despite normal coronary arteries
Arthur Shawcross represents the Angel of death [Angina].

Exertional syncope
His victims Swooned [Syncope] with fear when they saw him.

Exertional dyspnea of congestive heart failure
Arthur Shawcross claims he left the crime scenes whistling Dixie [Dyspnea].

Sudden cardiac death
Arthur Shawcross causes Sudden Death.

-Physical findings

Loud, harsh, systolic ejection murmur at the upper right sternal border, usually
associated with a palpable systolic thrill.

Arthur Shawcross is a Base [Basal] Thrill-murderer [Thrill].
He is a Harsh Hardened criminal, who attributed his grotesque actions to
incest with his Sister [Systolic].

S4 gallop is common and represents left ventricular hypertrophy and increased
left ventricular pressure.
His ghoulish tales read like the Four [S4] Horsemen of the Apocalypse.

S3 when left ventricular failure is present.
As a child, AS displayed the classic homicidal Triad [S3]: animal torture,
fire-setting, and bed-wetting.

Delayed upstroke in the carotid pulse. Parvus et tardus carotid pulse.
His last victim still had a Small but palpable pulse. However, the ambulance was
Delayed [upstroke], and, it soon became too Little, too Late [Parvus et Tardus].

Paradoxical splitting of S2
AS sent his victims to Paradise [Paradoxical].

Apical Diastolic Murmur: Mitral Stenosis (MS)

-The mnemonic key is MicroSoft (MS), a key which immediately follows the symbol.

-Physical findings:

The thrill at the apex is the diastolic murmur.
>> Hopeful applicants at the Apex of their careers are Thrilled to be hired by
MicroSoft.

The left ventricle (LV) is of normal pressure and size, so the point of maximum impulse
is not displaced to the left.
>> MS owns a Healthy Windows [Vented: Normal LV] environment, and is Not willing
to be Displaced from its location.

High-pitched opening snap [OS] following S2, heard best between the second to
fourth left intercostal space.
>> The new Windows98 Operating System [OS] sold at a High-pitched pace.

S1 is loud and snapping.
>> MicroSoft 1-sound is Bill Gates [S1], who barks out Loud Snapping orders.

-Chest x-ray:

Kerley B lines (dilated interlobular septa or septal edema) are horizontal, nonbranching
lines at the peripheral lower lung fields.
>> The Curly-haired [Kerley B lines] computer geek…

The large left atrium straightens the left heart border and is suggested by a double
density right-heart border, by the posterior displacement of the esophagus, and
by an elevated left mainstem bronchus.
>> …stole Double Density [CXR] diskettes to be sold in Los Angeles [large LA].

-Catheterization:

The left atrial (LA) pressure pulse reveals a prominent “a wave (LA contraction
against the mitral valve).
>> Those trying to enter the ranks of MS had to show Prominent A grades ["a wave]
at the Apex [Apical diastolic murmur] of their class.

Symptoms of aortic stenosis are SAD or ASD – Syncope, Angina, Dyspnea.

For Causes of A-Fib/Flutter

H = cHf, other cardiomyopathies
E = Enlargement of the atria
A = Alcohol binge drinking
R = Rheumatic heart disease
T = hyperThyroid

Asystole
“3 Hypo’s & 3 Hyper’s”
Hypoxia
Hypothermia
Hypokalemia
Hyperkalemia
Hyper H (Acidosis)
Hyper Rx (Drugs/OD)
Submitted by Tag Filley, M.D.

Syncope
“HEAD, HEART and VESS’LS”
H – hypoglycemia hypoxia
E – epilepsy
A – anxiety [the "swoon"]
D – dysfunction of brain stem [i.e. brain stem TIA]
H – heart attack
E – embolism of pulmonary artery
A – aortic obstruction [ Aortic stenosis, myxoma, IHSS ]
R – rhythm disturbance
T – tachycardia esp VT
V – vasovagal
E – ectopic i.e. hemorrhage obvious or not
S – situational [micturation, defecation...]
S – subclavial steal
L – low SVR [eg: anaphalaxis]
S – sensitive carotid sinus
of M.I. is BOOMAR – Bed rest, Oxygen, Opiate, Monitor, Anticoagulate, Reduce clot size Proven MI.. should be met by M.O.N.A.

M = morphine
O = oxygen
N = nitrates
A = aspirin

suspected right ventricular MI suspected .. hold the Nitrates. submitted by Chris

Mnemonic for remembering antiarrhythmics

Class Drug Mnemonic Read as: Professor Quackers “dissed” – Lydia’s penny Mexican tacos. – Feeling profaned, – proper Bertha Butt – (amiable British socialite) – virtually dismembered ‘im. or Professor Quackers dissed Lydia’s Penny Mexican Tacos. Feeling profaned, proper Bertha Butt, (amiable British socialite), virtually dismembered ‘im.*Note: “Dissed” is used here as the slang term “dis” – from dismiss. I.e., “Don’t ‘dis’ me, man!”
Class IA Procainamide Professor
Quinidine Quackers
Disopyramide “dissed” *
Class IB Lidocaine Lydia’s
Phenytoin penny
Mexiletine Mexican
Tocainide Tacos
Class IC Flecainide feeling
Propafenone profaned
Class II Propranolol proper
Beta Blockers Bertha Butt
Class III Amiodarone amiable
Bretylium British
Solatol socialite
Class IV Verapamil virtually
Diltiazem dismembered ‘im
Atropine
Adenosine

Endocarditis
“FAME”
F – FEVER
A – ANEMIA
M – MURMUR
E – ENDOCARDITIS

Causes of pericarditis are CARDIAC RIND – Collagen vascular disease, Aortic aneurysm, Radiation, Drugs eg. hydralazine, Infections, Acute renal failure, Cardiac infarction, Rheumatic fever, Injury, Neoplasms, Dressler’s syndrome.

5 T’s of early cyanosis in congenital heart disease
• Tetralogy, Transposition, Truncus, Total anomalous, Tricuspid atresia
Sumbitted by Ben Humphreys

95% of hypertension is primary (idiopathic). 5% is secondary and causes include CHAPS – Cushing’s syndrome, Hyperaldosteronism (Conn’s syndrome) , Aorta coarctation, Pheochromocytoma, Stenosis of the renal arteries.

Takayasu’s disease is also called pulseless disease, therefore I can’t Tak’a ya’s pulse.

Henoch-Schonlein Purpura
“JARS”
J – Joints
A – Abdominal pain
R – Renal
S – Skin

Compartment Syndrome

“6 p’s”
pulselessness
pain
pallor
parasthesia
poikiolothermia
paralysis

Predisposing Conditions for Pulmonary Embolism TOM SCHREPFER
• T–trauma
• O–obesity
• M–malignancy
• S–surgery
• C–cardiac disease
• H–hospitalization
• R–rest (bed-bound)
• E–estrogen, pregnancy, post-partum
• P–past hx
• F–fracture
• E–elderly
• R–road trip

(Cot)Caught by Sin : Cottonà BySSinosis

Shortness of Breath

HAPISOCS

H: History of any pulmonary disease
A: Activity at onset
P: Pain upon inspiration
I: Infections fever/chills
S: Smoker years/packs
O: Orthopnea
C: Cough (Persistent)
S: Sputum Productive/color

Non-Cardiogenic Pulmonary Edema
“PONS”
P – Phosgene, paraquat, phenothiazines
O – Opioids/organophosphates
N – Nitrous dioxide
S – Salicylates

Treatment of acute pulmonary edema
As Easy as ‘LMNOP’ : Remember the mnemonic LMNOP when treating a patient with acute pulmonary edema
• Lasix¢ç (furosemide) intravenous (IV), one to two times the patient’s usual dose, or 40 mg if the patient does not usually take the drug.
• Morphine sulfate. Initial dose, 4 to 8 mg IV (subcutaneous administration is effective in milder cases); may repeat in 2 to 4 hours. Avoid respiratory depression. Morphine increases venous capacity, lowering left atrial pressure, and relieves anxiety, which reduces the efficiency of ventilation.
• Nitroglycerin IV, 5 to 10 ug/min. Increase by 5 ug/min q 3 to 5 minutes. Reduces left ventricular preload. Caution: may cause hypotension.
• Oxygen, 100% given to obtain an arterial PO2>60 mm Hg.
• Position patient sitting up with legs dangling over the side of the bed. This facilitates respiration and reduces venous return.

Beta-1 receptors are in the heart (you have 1 heart) and beta-2 receptors are in the lungs (you have 2 lungs).

Decreased Pleural fluid Glucose : “IRAN”
• I=Infections
• RA=Rheumatoid arthritis
• N=Neoplasia

Anterior Mediastinal Mass
“4 T’s”
T – Thymoma
T – Teratoma
T – Thyroid tumor/goiter
T – Terrible lymphoma

Middle Mediastinal Mass
“Habit5″
H – Hhernia, hematoma
A – Aneurysm
B – Bronchogenic cyst/duplication cyst
I – Inflammation (sarcoid, histo, coccidio, TB)
T5 – Tumors (lung, lymphoma, leukemia, leiomyoma, lymph node hyperplasia)

Bilateral Hilar Adenopathy
“Please Helen Lick My Popsicle Stick”
P – Primary TB
H – Histoplasmosis
L – Lymphoma
M – Metastases
P – Pneumoconiosis
S – Sarcoidosis

Sarcoidosis:

SARCOIDOSIS: G-E-R-M-A-N ACE “SCHAUMANN” B-O-E-K

G-Granulomas
E-Erythema nodosum
R-Restrictive lung defect (PFTs)
M-Multiple systemic manifestations
A-Asteroid bodies (inclusions)
N-Noncaseating granuloma, Negative TB test

ACE – Angiotensin converting enzyme levels monitor disease activity and response to therapy.

Schaumann’s bodies (inclusions)

B-Bell’s palsy, Bilateral hilar lymphadenopathy, Black females O-Optic nerve dysfunction is a common manifestation of neurosarcoid.
E-Eyes: uveitis
K-Kveim skin test

Rat Poisons

“RATS PANIC” I’m sure that you’ll easily remember this one!
R – Red squill
A – Arsenicals
T – Thallium
S – Strychnine
P – PNU/Phosphorus/zn Phosphide
A – Alpha naphtha thiurea (ANTU)
N – Norbormide
I – Indanediones
C – Coumadin/cholcalciferol

Anion Gap Acidosis:
“Mudpiles”
M – Methanol
U – Uremia
D – DKA/AKA
P – Paraldehyde/phenformin
I – Iron/INH
L – Lactic acidosis
E – Ethylene glycol
S – Salicylates

Normal Gap Acidosis
“HARDUP”
H – Hyperalimentation/hyperventilation
A – Acetazolamide
R – RTA
D – Diarrhea
U – Ureteral diversion
P – Pancreatic fistula/parenteral saline

Osmolar Gaps
“ME DIE”
M – Methanol
E – Ethanol
D – Diuretics (mannitol, sorbitol, glycerol)
I – Isopropanol
E – Ethylene glycol

Respiratory Alkalosis: Asthmatic Sally poisoned POPE’s HEN
• Asthma
• Salicylate poisoning
• PO= Pulmonary Oedema
• PE= Pulmonary Embolism
• HEN= Hepatic Encephalopathy

Hypoglycemia
“Reexplain”
R – renal failure
EX – exogenous
P – pituitary
L – liver failure
A – alcohol
I – insulinoma/infection
N – neoplasm

Hypoglycemia [By Sung Kim]

Hypoglycemia – H-U-N-G-E-R: B-E-S-T S-A-U-C-E I-S M-S-G

H-Hepatic failure (advanced), Hypothermia
U-Uremia/renal failure
N-Nausea, vomiting
G-Growth hormone deficiency
E-Ethanol metabolism blunts gluconeogenesis
R-Reye’s syndrome

B-Beta blockers
E-Enzyme defects (glycogen storage diseases)
S-Sepsis
T-Tumors: Islet beta cell tumors (pancreatic): Insulinomas
Non-islet cell tumors: Large mesenchymal tumors

S-Sulfonylureas
A-Adrenal insufficiency
U-Under 0.3 (insulin/glucose ratio) to make the diagnosis C-C-peptide measurement to rule out factitious hypoglycemia
E-Endocrine: Epinephrine, glucagon deficiencies (counterregulatory hormone deficiencies)

I-Immune disease with insulin or insulin receptor antibodies
S-Sarcomas: large retroperitoneal sarcomas

M-Maple syrup urine disease, severe Malaria
S-Salicylates in children
G-Galactosemia (with milk ingestion), disorders of Gluconeogenesis

Symptoms of hyperthyroidism
• Remember the following mnemonic when evaluating patients for hyperthyroidism:
S : Sweating
T : Tremor or Tachycardia
I : Intolerance to heat, Irregular menstruation, and Irritability N : Nervousness G : Goiter and Gastrointestinal (loose stools/diarrhea).

CUSHING’S
• DISEASE is
• Dependent on (Pituitary) and
• Depresses ( Cortisol) on
• Daddy Doses of Dexa(High doses of Dexamethasone).

Hypercalcemia
“SHAMPOO DIRT”
S – Sarcoidosis
H – Hyperparathypoidism, Hyperthyroidism
A – Alkali-milk syndrome
M – Metastases, myeloma
P – Paget disease
O – Osteogenesis imperfecta
O – Osteoporosis
D – Vitamin intoxication
I – Immobility
R – RTA
T – Thiazides

Hypercalcemia symptoms are Bones (pain), Stones (renal), abdominal Groans (pain) and psychic moans (confusion).

Multiple endocrine neoplasia
MEN I is 3 P’s (Pituitary, Parathyroid, Pancreas). MEN II is 2 C’s (Catecholamines ie. pheochromocytome, carcinoma of medulla of thyroid) and Parathyroid (IIa) or Mucocutaneous neuromas (IIb).

The most common thyroid carcinoma is P-apillary (P-opular). It also has P-sammona bodies on histology. It causes P-alpable lymph nodes (lymphatic spread).

The most common symptoms of PHEochromocytoma begin with the first 3 letters – Palpitations, Headache, Episodic diaphoresis (sweating).

Tumors that go to bone
“Kinds Of Tumors Leaping Primarily To Bone”
K – Kidney
O – Ovarian
T – Testicular
L – Lung
P – Prostate
T – Thyroid
B – Breast

Causes of joint pain are SOFTER TISSUE – Sepsis, Osteoarthritis, Fractures, Tendon/muscle, Epiphyseal, Referred, Tumour, Ischaemia, Seropositive arthritides, Seronegative arthritides, Urate, Extra-articular rheumatism (eg. polymyalgia).

Ossification centers of the elbow

There are two that I know of (most people use “CRITOE”):
C – Capitellum
R – Radial head
I – Internal (medial epicondyle)
T – Trochlea
O – Olecranon
E – External (lateral epicondyle)
These appear at 2, 4, 6, 8, 10, and 12 years of age in order and go away two years later.
The other mnemonic I know for the ossification centers is “Come Rub My Tree Of Love” where the “M” is medial epicondyle and the “L” is the lateral epicondyle.

Wrist Bones
“Never Loosen Tillies Pants, Mother Might Come Home”
Proximal row:
N – Navicular
L – Lunate
T – Triquetrium
P – Pisiform
Distal row:
M – greater Multiangular (trapezium)
M – lesser Multiangular (trapezoid)
C – Capitate
H – Hamate
Also: “Some Lovers Try Positions That They Can’t Handle”

Rotator Cuff Muscles
“SITS”
S – Supraspinatus
I – Infraspinatus
T – Teres minor
S – Subscapularis

The Salter Classification:
“SALTR”
S – Slip of physis
A – Above physis
L – Lower than physis
T – Through physis
R – Rammed physis

NEPHROTIC SYNDROME (NS) is characterized by the following: [By Shweta]

N = Na + water retention
This occurs due to several factors, including compensatory secretion of aldosterone in response to hypovolemia-mediated release of ADH.

E = Edema
Due to hypoproteinemia + Na, water retention. Edema is soft, pitting and starts in the periorbital region.

P = Proteinuria >3.5gm/1.74sq. ml/24hrs

H = Hypertension + hyperlipidemia (due to increased lipoprotein synthesis in liver, abnormal transport of circulating lipoproteins, decreased catabolism.)

R = Renal vein thrombosis

O = “Oval fat bodies” in the urine. Lipiduria follows hyperlipidemia. Albumin as well as lipoproteins are lost. Lipoproteins are reabsorbed by tubular epithelial cells and they shed along with degenerated cells- this appears as “oval fat bodies” in urine.

T = Thrombotic + thromboembolic complications owing to loss of anticoagulant factors (eg. anti-thrombin III )

I = Infection. These patients are prone to infection, especially with staphylococci and pneumococci. Vulnerability is due to loss of immunoglobulins.

C = hyperCoagulable state

Henoch-Schonlein Purpura
“JARS”
J – Joints
A – Abdominal pain
R – Renal
S – Skin

Causes of hematuria
• Use the mnemonic SITTT as an aid in evaluating the cause of hematuria:

S: Stone
I: Infection
T: Trauma
T: Tumor
T: Tuberculosis

Causes of secondary nephrotic syndrome ie. not of direct renal origin are DAVID – Diabetes mellitus, Amyloidosis, Vasculitis, Infections, Drugs.

Causes of acute and reversible forms of urinary incontinence The following mnemonic aids in remembering the causes of acute and reversible forms of urinary incontinence – DRIP

D: Delirium
R: Restricted mobility, retention
I: Infection, inflammation, impaction (fecal)
P: Polyuria, pharmaceuticals

Hereditary cystic disorders: Polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is associated with cysts in the kidneys and, in many cases, in the brain (berry aneurysms), liver, spleen, pancreas, and lungs.

¡°Halley Berry AKA Dorothy (Dandridge) Portrayed Carmen Jones.¡±

Halley ?Hematuria: Gross and microscopic
Berry -Berry aneurysms

AKA ?ADPKD

D-Dominant (autosomal) inheritance
O-Obstruction of the urinary tract by stones, blood clots R-Renal failure
O-Oxalate: calcium oxalate and uric acid stones
T-renal Tubular defects
H-Hemorrhagic cysts
Y-Year 1 – Most cases are diagnosed in the first year of life, presenting as bilateral abdominal masses.

Portrayed ?Polycystic: continued enlargement of the cysts often leads to progressive renal failure.

Carmen ?CT scanning: Enlarged kidneys with multiple bilateral cysts are diagnosed using ultrasound, IVP,
or CT scanning.
Jones – Juvenile nephronophthisis (JN) and medullary cystic disease (MCD) are in the DDx.

-Cardiac valvular disorders: Mostly mitral valve prolapse (MVP) and aortic regurgitation -Salt-wasting nephropathy, renal tubular acidosis (RTA) -Chronic flank pain due to the mass effect of the enlarged kidneys

Lusty Carmen Jones powdered her nose, using her Bivalve [MVP] mirror compact, ¡¦ -then she slowly raised her Salt-rimmed [Salt-wasting nephropathy] MargaRiTA [RTA], and seductively
placed her other hand on her Hip [Flank pain].

-Hyperchloremic acidosis
-Salt-wasting nephropathy causing hyponatremia

It was said that Dorothy was not allowed to swim in the hotels Chlorinated pool [Hyperchloremic acidosis].
When she defiantly swam in the pool, they Drained it [Salt-wasting nephropathy, Hyponatremia].

-Hypertension
-End-stage renal disease (ESRD)

Dorothy was forced to enter through the back door, even while she was contracted to sing under The Big
Tent [Hypertension].
Dorothy was only 41 when she was found DEAD [ESRD].

Review:

Dx: Positive family history (autosomal dominant inheritance)
Gross and microscopic hematuria
Ultrasound, IVP, or CT scanning detect the enlarged kidneys with multiple bilateral cysts

Renal Pathology Buzz words

Lupus = wire LOOP lesion (LUPUS=LOOP)

goodPASTURE = a pasture is FLAT so is the immunoflouresence for GP

Membraneous GN = spike and DOME appearance (think membrane = dome)
(held up by spikes)

Membranoproliferative GN = M P GN = Tram Track
think of MP’s (military police riding on Trams)

Post streptococcal GN= Lumpy Bumpy
think Strep aerobics
Lumpy people Bumping
around doing aerobics

WBC Count
“Never Let Mom Eat Beans” and “60, 30, 6, 3, 1″
• Neutrophils 60%
• Lymphocytes 30%
• Monocytes 6%
• Eosinophils 3%
• Basophils 1%

Hem – PT, PTT:

To remember the intrinsic and extrinsic pathways in relation to what blood test is affected:

PiTT (I for Intrinsic pathway) – PiTTsburgh
PeT (E for Extrinsic pathway)

Vitamin K-dependent proteins and warfarin sodium [by Sung Kim and S. Levine, MD, PhD.]

Warfarin sodium is a vitamin K antagonist.

-Vitamin K-dependent proteins C and S.
-Vitamin K-dependent clotting factors II, VII, IX, and X of the extrinsic pathway.

–> The Korean [vitamin K] War [Warfarin] was fought Outdoors [Extrinsic
--> pathway]. The American PT boats [PT, Protime, or prothrombin time],
–> whose access had been limited
by the rough Seas [protein C], quickly sent out SOS [protein S] messages.

Microcytic Anemia
“TICS”-
Thalasemia
Iron deficiency
Chronic disease
Sideroblastic anemia

Submitted by Jeff Rodgerson M.D.
HCMC Medical Center

Eosinophilia
“NAACP”
N – Neoplasm
A – Allergy
A – Addison’s
C – Cirrhosis, CVD
P – Parasite (visceral larva migrans), Periarteritis nodosa
Submitted by Tag Filley, M.D.

Thalassemia major is the most Severe ©-thalassemia [B-Beta-Bad].

-Major B-A-D M-A-F-I-A guys have the typical gangster appearance:
Short [Microcytic hypochromic anemia] and
Ugly [distortion of facial, skull, and long bones]

B-Basophilic stippling
A-Anemia, Anisocytosis
D-Deferoxamine

M?MCV is low
A-HbA is decreased
F-HbF is increased
I-Ineffective erythropoiesis
A?HbA2 is increased

Cooley’s anemia (beta-thalassemia major) is the homozygous state.

-The key is Denton A. Cooley, M.D., Texas Heart Institute (THI).

D-Deferoxamine therapy to prevent hemochromatosis
A-Anemia – In beta-thalassemia major or intermedia, anemia is due to a combination of ineffective erythropoiesis
and hemolysis of circulating cells. C-Congestive heart failure is a cause of death in the first years of life if the patient is not transfused.

M-MCV is low; Microcytic hypochromic anemia
D-Diagnosis, prenatal

T-Tower skull (also frontal bossing, chipmunk facies, and distortion of long bones) H-Hemolytic anemia with Hepatosplenomegaly in the first year of infant life I-Intermedia – Beta-thalassemia intermedia presents with abnormalities similar to those of thalassemia major.

Increased susceptibility to infections

Peripheral blood smear: Basophilic stippling
Helmet cells
Nucleated target cells
Anisocytosis (RBCs of different size/volume)

X-ray: Hair-on-end skull

Serum hemoglobin electrophoresis: HbA is decreased.
HbA2 is increased.
HbF is increased

–> Dr. Cooley performed Major surgery [thalassemia Major] as a
–> Cardiothoracic surgeon [Cardiac failure] live
on the Internet [Infections].

–> His skilled hands can perform Microsurgery [Microcytic hypochromic
--> anemia] on Fetuses [HbF].

–> His surgical cap [Helmet cells] fit loosely over his Crew cut
–> [Hair-on-end skull].

–> He proceeded to make an incision along the Blue Stippled line
–> [Basophilic Stippling] drawn on the skin.

–> Dr. Cooley’s Target [Target cells] academic score had always been an
–> A+ [HbA2 is increased].

–> He would Not accept a simple A [HbA is decreased].

–> The surgical staff is a close knit community, like a B-A-D M-A-F-I-A
–> (see below), quick to dispose of weak,
Ineffective [Ineffective erythropoiesis] residency candidates.

Disseminated intravascular coagulation (DIC)

D-I-S-S-E-M-I-N-A-T-E-D

D-Dx: D dimer
I-Immune complexes
S-Snakebite, shock, heatstroke
S-SLE
E-Eclampsia, HELLP syndrome
M-Massive tissue damage
I-Infections: viral and bacterial
N-Neoplasms
A-Acute promyelocytic leukemia
T-Tumor products: Tissue Factor (TF) and TF-like factors released by carcinomas of pancreas, prostate, lung,
colon, stomach
E-Endotoxins (bacterial)
D-Dead fetus (retained)

Characteristic features of multiple myeloma on X-ray are ABCDE – Asymmetry, Border irregular, Colour irregular, Diameter usually > 0.5cm, Elevation irregular.

Á¦ 9 Àå Á¾¾ç Áúȯ

Chronic lymphocytic leukemia (CLL) is a monoclonal malignancy, usually of B lymphocytes.

-Incidence: CLL is the most common adult leukemia in the United States.
Males>Females
50-70 years of age

Songwriter Phil CoLLins [CLL] is Male and probably over 50 years of age. He recently won an
Oscar for his “Tarzan” song.

Clinical and diagnosis

Lymphocytosis >15,000/mm3
Generalized lymphadenopathy

Tarzan can spring from Limb [Lymphocytosis] to Limb [Lymphadenopathy] above the tree
tops¡¦

Splenomegaly, hepatomegaly
Low serum immunoglobulins (immunosuppression)

–> where the Splendid [Splenomegaly] Moonlight [imMunosuppression]
–> streams through the
branches.

Diffuse bone marrow infiltration and replacement of cellular elements cause:
Anemia
Thrombocytopenia
Granulocytopenia

–> Walt Disney Pictures produced the Animated Animal [Anemia] adventure
–> “Tarzan”.

–> The “Tarzan” [Thrombocytopenia] song earned CoLLins an Oscar [Osteo,
--> bone marrow failure]
award for the best original song.

–> Tarzan had Little need for Plates [Platelets <100,000/¥ìL] in the
–> jungle.

–> Phil CoLLins is a Grammy [Granulocytopenia] Award-winning singer and
–> songwriter.

Occasionally extravascular hemolysis: warm-antibody autoimmune hemolytic anemia (AHA)

–> An African jungle [Autoimmune extravascular] APE [AHA] had Warmly
–> [Warm-antibody]
adopted baby Tarzan.

Differential diagnosis
Malignant lymphoma
Infectious mononucleosis

–> Tarzan is Lord [Lymphoma] of the Jungle and friend of the Monkeys
–> [Mononucleosis]. Phil CoLLins was born in London [Lymphoma].

Treatment
Chlorambucil (an alkylating agent), with or without prednisone
Fludarabine

–> Some may imagine a Ram [ChloRambucil] scrambling about, but others
–> will¡¦

–> recall that Clayton [Chlorambucil] is the villainous jungle guide
–> who was hired by
Professor [Prednisone] Porter, not knowing that¡¦

–> ¡¦Clayton [Chlorambucil] had his captured Prey [Prednisone]
–> immediately Flown
[Fludarabine] out for profit.

References:
1. Harrison’s Principles of Internal Medicine, 14/e Edition, McGraw-Hill, New York, 1998. 2. Maximum access to diagnosis and therapy (MAXX), Lippincott Williams & Wilkins, New York, 1999. 3. Scientific American Medicine (SAM-CD), Scientific American Inc, New York, 1997.

Hodgkin’s lyphoma classification – A = Asymptomatic, B = Bad.

Risk of underlying malignancy with dermatomyositis or polymyositis is 30% at age 30, 40% at age 40 etc.

Malignant Monoclonal Gammopathies: Multiple myeloma

-The mnemonic key for multiple myeloma (MM) is Marilyn Monroe (MM), a key which immediately follows the >> symbol.

-Clinical:

Weakness and fatigue due to normochromic normocytic anemia.
>> MM’s original name was Norma [Normochromic normocytic] Jean.

Bone pain and pathologic fractures: predominantly osteolytic tumors and osteoporosis.
>> MM’s name was illuminated in marquee Lights [osteoLytic], but she
>> secretly longed for
an Oscar award [Osteoporosis].

Susceptibility to bacterial infections.
>> MM was Susceptible to Toxic [infections] relationships.

Acute renal failure (ARF) due to the effects of filtered light-chain proteins,
hypercalcemia, and amyloid deposits in the kidney.
>> MM’s Lightly-Chained ARF dog barked when MM’s death was said to be
>> related to her
JFK Army-Lord [Amyloid].

-Laboratory

Hypercalcemia
>> MM fluffed White Talcum [hypercalcemia] powder on her delicate white
>> skin…

Hypergammaglobulinemia
>> …to protect it from the movie industry’s Large hot Camera
>> lights[hyperGammaglob].

Serum electrolytes: Low anion gap
>> MM wore gowns with Low [Low anion gap] revealing necklines.

Rouleaux on peripheral blood smear.
Occasionally Coombs(+) hemolytic anemia.
>> MM used hair Rollers [Rouleaux] and Combs [Coombs] to create her
>> famous hairdo.

Leukocyte alkaline phosphatase (LAP) staining reaction: High LAP score.
>> MM used her Great LAP to her advantage because….

Normal levels of Serum Alkaline Phosphatase (SAP)
>> …she was Not a SAP.

Antineoplastic agents & Adverse effects

Male testicular tumors: “S-E-C sac T-I-C-S¡±

S-Seminoma: most common
E-Embryonal carcinoma
C-Choriocarcinoma

Sac-Yolk sac tumor (endodermal sinus tumor)

T-Teratoma, Teratocarcinoma
I-C-Interstitial (Leydig) cell tumor
S-Sertoli cell tumor

Paraneoplastic syndromes and their associated cancers:

Your diagnosis can be “Highly S-C-R-A-M-B-L-E-D.”

Highly-Hypercalcemia (squamous cell carcinoma)

S-SIADH, hyponatremia (SCLC)
C-Clubbing (adenocarcinomas)
R-Retinal blindness (SCLC)
A-ACTH (SCLC)
M-Myasthenia gravis (thymoma)
B-Bone – hyperosteoarthropathy (adenocarcinomas)
L-Limbic encephalitis (SCLC)
E-Eaton-Lambert myasthenic syndrome (SCLC)
D-Dermatomyositis (cancer of the lung, ovary, breast, stomach; NHL)

SIADH: Syndrome of inappropriate antidiuretic hormone secretion
SCLC: Small cell lung cancer
NHL: non-Hodgkin’s lymphoma

Microbiology

The first two mnemonics are modifications of well-known mnemonics.

-Gram-positive, spore-forming, rods: Bacillus and Clostridium

Some love stay home forming spores:
Basically Claustrophilic (Bacilli and Clostridia)

-Other gram-positive rods:

Others love to belong: C-L-A-N

C-Corynebacterium
L-Listeria
A-Actinomyces
N-Nocardia

All species within the Enterobacteriaceae family are gram-negative enteric bacilli and are facultative anaerobes that can ferment glucose to acid.

When microorganisms compete with humans for glucose, they are Nasty CURSESS.”

Nasty-Neisseria (N. gonorrhoeae and N. meningitides)

C-Curved: Vibrio and C-Campylobacter species
UR-Urease-positive
SE-Serratia
SS-Salmonella, Shigella

Urease(+): Y. enterocolitica, Y. pseudotuberculosis, P. mirabilis, P. vulgaris, M. morgani

Clinically significant Anaerobes “A Closed Box For Pepsi.”

A-Actinomyces G+
C-Clostridia- G+
B-Bacteroides G-
For Fusobacterium G-
Pepsi Peptostreptococci G+

Bloody diarrhea

Bloody diarrhea may be caused by invasive bacteria or parasites, including:

Campylobacter, Shigella, Salmonella, Yersinia, and Trichuris (whipworm).

The Cutting edge of the Campbell’s [Campylobacter] soup can was Bloody.

The Shaggy [Shigella] surface was Abrasive [Bloody].

The Salmon [Salmonella] scales were Abrasive [Bloody].

The Jersey [Yersinia] sweatshirt was rough and Abrasive [Bloody].

The Bullwhip [Whipworm] drew Blood.

Bordetella pertussis: Whooping cough

Bordetella pertussis is the etiologic agent of whooping cough.

-Laboratory:

Absolute lymphocytosis in children (a reportedly recent USMLE Step 2 question).

>> Many crossed the Border [Bordetella] for their Green* cards [lymphocytosis].
*In our color-coding scheme of mnemonics, green will represent lymphocytes.

B-O-R-D-E-T-E-L-L-A

B-Bordet-Gengou agar culturing a nasopharyngeal swab is the standard diagnostic test ordered during the
first 2 weeks of onset.
O-whOoping cough
R-Rod: B. pertussis is a small, gram-negative pleomorphic rod

D-DFA – Direct fluorescent antibody test of nasopharyngeal secretions results in frequent false-positives.

E-Erythromycin for therapy and prophylaxis.

T-Trimethoprim-sulfamethoxazole is an alternative antibiotic choice.

E-ELISA is the diagnostic test ordered after the first 2 weeks of onset.

L-Leukocytosis: 10,000 – 50,000 cells/uL with 50-75% mature lymphocytes

L-Lymphocytosis in children

A-Adult lymphocytosis is rare.

Organisms that Spread from Blood to Urine
CASH CML
C – candida
A – aureus staph
S – salmonella
H – histoplasma
C – cytomegalo virus
M – mycobacteria
L – leptospira
Submitted by Ousama Dabbagh M.D

Kawasaki’s

“scream fever”
S – sausage fingers
C – conjunctival redness
R – rash
E – extremity involvement
A – adenopathy
M – mucosal erythema
FEVER – fever

Causes of post op fever
Remember the following mnemonic when determining the possible cause(s) of fever in a patient who has recently undergone a surgical procedure: the 5 W’s (or 6 W’s)

Wind : the pulmonary system is the primary source of fever in the first 48 hours. ( Atelectasis, pneumonia ect.)
Wound : there might be an infection at the surgical site.
Water : check intravenous access site for signs of phlebitis.
Walk : deep venous thrombosis and pulmonay embolism can develop due to pelvic pooling or restricted mobility
Whiz : a urinary tract infection is possible if urinary catheterization was required.
Also Wonder drugs – drug fevers. (added by Calvin Lee)

Classification of hypersensitivity reactions
“ACID”
Type I Anaphylaxis
Type II Cytotoxic – mediated
Type III Immune – complex
Type IV Delayed hypersensitivity

Criteria for Lupus
SOAP BRAIN MD
Serositis (pleuritis, pericarditis)
Oral Ulcers
Arthritis
Photosensitivity
Blood (all are low – anemia, leukopenia, thrombocytopenia)
Renal (protein)
ANA
Immunologic (DS DNA etc.)
Neurologic (psyc, seizures)
Submitted by Mike Ritter, MD FAAEM, San Diego, CA

Risk of underlying malignancy with dermatomyositis or polymyositis is 30% at age 30, 40% at age 40 etc.

Blue Sclera: “MIXED”
• M = Marfans ,
• I = Imperfecta ( Osteogenesis )
• XE =(pseudo) Xanthoma elasticum
• ED = Ehlers Danlos
¯
Altered Mental Status
“AEIOU TIPS”
A – Alcohol/drugs
E – Endocrine
I – Insulin
O – Opiates
U – Uremia
T – Toxins/trauma
I – Infections
P – Psych/porhyria
S – SAH, shock, stroke, seizure, space occupying lesion

MIDAS : States to exclude as cause of coma.
• Meningitis
• Intoxication
• Diabetes
• Air – respiratory failure
• Subdural or subarachnoid hemorrhage.

Level of consciousness

“AVPU”
A – alert
V – resonds to verbal stimuli
P – responds to painful stimuli
U – unconscious

Vertebral/Basilar Ischemia
4Ds
dizziness (nystagmus)
diplopia (skew deviation)
dysarthria
dysphagia
Submitted by: Ronald H. Miller, OD, The Ohio State University

Cerebellar lesions lead to VANISHeD – Vertigo, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonic reflexes, Dysdiadochokinesia. ( or Dementia )

Marcus Gunn Pupil

Marcus Welby, M.D. “knows”. Robert Young was also in “Father Knows Best”.

D-R K-N-O-W-S

D-Deafferentation of the pupillary light reflex
R-Retrobulbar optic neuritis

K-Kan’t kick inward: afferent limb defect
N-No constriction to direct light stimulation
O-Optic nerve (CN II) damaged unilaterally
W-swinging flashlight test
S-consensual reflex intact

Subarachnoid hemorrhage (SAH): Rupture of an aneurysm releases blood directly into the cerebrospinal fluid (CSF) under arterial pressure.

Clinical manifestations:

CSF ~ FDR

F-D-R’s Last Words: O! CAN’T W-H-I-P ‘E-M

F-Focal signs: limb weakness, dysphagia, CN III palsy
D-Depression of consciousness with headache
R-Retinal (subhyaloid) hemorrhage

Last-Lucidity with headache is the usual pattern of onset.

Words-Warning leak sign of impending rupture (controversial sign).

O-(looks like eyes) CN III palsy

Can’t extend knees (Kernig’s sign)

W-circle of Willis
H-Headache: sudden onset of severe headache (“the worst headache of my life”)
I-Increased ICP
P-Papilledema

E-Epileptic seizures
M-Meningismus

Subarachnoid hemorrhage : Ruptured berry aneurysm

A-Adult polycystic kidney disease, Anterior communicating artery
B-Berry aneurysm
C-Circle of Willis
D-Danlos-Ehlers and Marfan’s syndromes

Causes of Syncope: F-A-D-E-O-U-T

F-Faint simple vasovagal fainting
A-Arrhythmia causing cardiac syncope
D-Drugs: alcohol, illicit drugs, nitrates, antihypertensives, sympathetic blockers
E-Eyeball pressure
O-Orthostatic hypotension: dysautonomias
U-Undiagnosed seizures
T-Takayasu’s arteritis: reduced cerebral blood flow due to involvement of the carotid and vertebral arteries.

Causes of Vertigo: revolving, P-I-V-O-T-I-N-G M-E-N

P-Petrositis, benign Positional vertigo
I-Ischemic attacks: transient vertebrobasilar ischemic attacks
V-Vestibular neuronitis
O-Other Otogenic causes: Otosclerosis, herpes zoster Oticus, Obstructed external auditory canal
T-Tumors of the middle ear, labyrinth, pons, cerebellopontine angle, CN VIII
I-Internal auditory artery occlusion
N-Neuronitis: acute vestibular neuronitis
G-Giant cell arteritis – internal auditory artery occlusion

M-Meniere’s disease
E-Ear: otitis media, labyrinthitis, barotrauma
N-Neuromas: acoustic neuromas

Headache: S-T-O-I-C M-P

S-Sentinel headache that precedes a major subarachnoid hemorrhage (SAH)
T-Temporomandibular joint dysfunction, Tension-type headache, Tumors
O-Other: pressure, traction, or displacement of extracerebral structures.
I-Indomethacin-responsive headache
C-Cluster headache

M-Meningitis, Migraine headache
P-Posttraumatic headache, Paranasal sinuses

____________________________________________________________________________________________

Intracerebral hemorrhage: T-I-P Ur H-A-T to M-Ds

T-Trauma
I-Idiopathic
P-Penia ? thrombocytopenia

Ur-Vasculitis

H-Hypertension
A-Amyloid angiopathy
T-Tumors associated with bleeding

M-Malformations: AV
D-blood Dyscrasias

Subdural hemorrhage: subconsciously dying¡±

-Elderly
-Slowly dying
-Alcohol
-Brain injury

____________________________________________________________________________________________

Cerebrovascular I-N-F-A-R-C-T-S

I-Infections: septic heart valve vegetations
N-Neoplasms; Nonbacterial thrombotic endocarditis
F-Fracture of the long bone
A-Atherosclerosis, Atrial fibrillation-related emboli
R-Reperfusion -> infarct -> hemorrhage
C-Carotid atheromas or mural thrombi
T-Thrombotic occlusions
S-Sylvan fissure: MCA is a particularly common site.

Lacunar infarct: “Lacunar” from the Latin for G-A-P or- D-I-S-P-A-R-I-T-Y

G-deep Gray matter: basal ganglia
A-Atherosclerosis
P-hyPertension

D-Dysarthria and a contralateral clumsy hand or arm due to infarction in the base of the pons or in the genu
of the internal capsule. (20%)
I-Internal Capsule: Lacunae in the posterior limb of the Internal capsule may cause pure motor hemiplegia
involving the face, arm, leg, foot. (60%)
S-Subcortical, capsular, or thalamic lacunae
P-Pontine lesions
A-Ataxic hemiparesis due to an infarct in the base of the pons
R-Rare: Lacunae in the anterior limb of the Internal capsule may cause severe dysarthria with facial weakness.
I-Ipsilateral ataxia (arm/leg) with leg weakness: Pontine lesion (rare)
T-Thalamus: Lacunae in the Thalamus may cause pure sensory stroke (10%)
y-V-Ventrolateral Thalamic lacunae

Anterior cerebral artery (A*C*A) occlusion:

*C*-Contralateral Crural (leg) monoplegia
*C*-Crest of Cerebral hemispheres and medial hemispheric walls represent the leg area of the motor strip

Middle cerebral artery (MCA) occlusion: “Difficulty with A-B-Cs in M-C-A”

A-Apraxia
B-Blindness in corresponding half of the visual field (contralateral homonymous hemianopsia)
C-Contralateral Clumsiness of arm, face. — Leg is somewhat spared.

M-Memorization difficulties
C-Calculation difficulties
A-Aphasia with language-dominant hemispheral involvement.

Posterior cerebral artery (PCA) occlusion: P-O-S-T

P-Proximal fling movements
O-Occipital lobe infarction results in contralateral homonymous hemianopsia which may be complete
S-Speech and Spelling maintained, but unable to read fluently
T-Thalamic syndrome

____________________________________________________________________________________________

A well-known mnemonic regarding occlusion of the vertebral-basilar circulation: 4D

-Dizziness
-Diplopia
-Dysarthria
-Dysphagia

____________________________________________________________________________________________

Types of Stroke

Stroke “H-I-T” you!

H-Hemorrhagic
I-Ischemic
T-TIA (Transient Ischemia Attack)

T.I.A (Transient Ischemic attack)

Patients often describe it as a shade being pulled over their eyes: S-H-A-D-E-D

S-Sensory loss; TIA may herald a stroke
H-Hypertension, Hyperlipidemia
A-Amaurosis fugax (transient monocular blindness)
D-DDx: seizures, neoplasms, migraine, vertigo
E-Extrinsic factor is monitored for warfarin administration; E-Endarterectomy
D-Diabetes

Root values of reflexes are 1,2,3,4,5,6,7,8 – S1-2 ankle, L3-4 knee, C5-6 biceps/supinator, C7-8 triceps.

Argyle Robertson Pupil
• Accomodation Reflex Present – Pupillary Reflex Absent.

Neurosyphilis [By jsara]

-Symptomatic Neurosyphilis: The small, irregular Argyll Robertson pupil reacts to accommodation but
not to light.
-Tabes dorsalis:
Argyl-Robertson Pupil (ARP) in syphlis – Accomodation Reflex Present (ARP)
but the light reflex is absent, so ARP=ARP.
-General paresis: P-A-R-E-S-I-S*
P-Personality
A-Affect
R-Reflexes are hyperactive
E-Eye: Argyll Robertson pupils
S-Sensorium: illusions, delusions, hallucinations
I-Intellect: decrease in recent memory, orientation, calculations
S-Speech

Reference:
*From Harrison Principles of Internal Medicine, 14/e Edition, McGraw-Hill, New York, 1998.

Pattern of Weakness in UMN lesions
• FLUE weakness FUELs Contractures
• F=Flexion,L=Lower Limb,U=Upper Limb E= Extensors

Normal Pressure Hydrocephalus
• Demented (Memory Loss)
• Dribbles (Urinary Incontinence)
• Disbalanced (Gait disorder)

TRAP to identify parkinson’s disease
• Tremor at rest (pill-rolling tremor)
• Rigidity
• Akinesia
• Posture typical of a Parkinson’s patient

Progressive Cerebellar Ataxias: Bassen-Kornzweig Acanthocytosis (Abetalipoproteinemia)

Abetalipoproteinemia is a rare autosomal recessive disorder that occurs primarily in Ashkenazi
Jews during their childhood years (6-12 years of age).

-The key is Bette [aBeta] Midler, who is Jewish [Ashkenazi Jews] by birth, but hardly shy or
Recessive.

-Clinical:

Lack of intestinal apolipoprotein B causes mild malabsorption (notably of fat-soluble
vitamins A, D, E, K), steatorrhea, and low serum chylomicrons, VLDL, IDL, and LDL.

- Did you know that Bette is computer-savvy? Know that she created her own web page
on a PC, and Not on an Apple [No Apolipoprotein-B] computer.

Progressive neuromuscular disease of the peripheral nervous system (PNS) and of the
cerebellum (ataxia of gait, trunk, and limbs).

- Bette wanted to be featured on serious PBS [PNS] television, but instead her trash
with flash persona was interviewed for E! Celebrity [Cerebellum] Profile.

- Bette paid heavy Taxes [aTaxia] after starring in “That Old Feeling” [sensory ataxia] with
Dennis Farina.

- The concert tour: As the tail-wagging mermaid, Bette motored around the stage in a
Wheelchair [muscle weakness].

Retinitis pigmentosa
-Then she donned her mermaid Goggles [retinitis pigmentosa] and grinned.

-Diagnosis:

Ataxia plus acanthocytes in peripheral blood smear. The low cholesterol gives rise to
deformed or spiky red blood cells called acanthocytes.
Low apolipoprotein B, low vitamin E
Low plasma triglyceride (TG) and cholesterol levels

- The Jewish Cantor [aCanthocytosis] disapproved of the bawdy stiletto Spike [Spiky
RBC] heels she wore to holy day services.

Small bowel biopsy: Foamy epithelial cells and lacy villus tips.
- The mermaid character was set in a Foamy [epithelial cells] sea backdrop.
- Under her Lacy [Lacy villus tips] mermaid costume, Bette had to wear a tightly laced
corset. She was still No Twiggy [low TGs].

-Treatment:

Low fat diet, fat-soluble vitamins such as vitamins A and E.
- Bette tried to lose weight on a Low Fat Diet in preparation for her A&E [vitamins A and
E] interview.

Radiopaque Ingestants
“Chipes”
C – Cocaine condoms/ chloral hydrate/ calcium
H – Heavy metals
I – Iron/ iodides
P – Psychotropics (TCA, phenothiazines)
E – Enteric coated/BA
S – Solvents (CCl4)

Drugs that can go into an ET tube

“lane”
L – lidocaine
A – atropine
N – naloxone
E – epi
Some like NAVEL, which includes Valium. Others have commented that valium should not go in an ET tube.

History taking in EMS

“sample”
S – signs/symptoms
A – allergies
M – medications
P – past medical history
L – last oral intake
E – events leading to injury or illness

Pain scale:

“OPQRST”

O – onset
P – provocation
Q – quality
R – radiation
S – severity
T – time

Pain Scale (Revisited)
PQRSTAPPP
P – palliates/provokes
Q – quality
R – region/radiation
S – severity (on a 1-10 scale)
T – timing (onset, frequency, duration)
A – associated symptoms
P – prior
P – persists
P – progression (stable, better, worse)
Submitted by Omar A. Blanco

More on Pain Evaluation
LOCI” (Latin for places) and the “Daughters of the American Revolution”
L – Location
O- Onset
C- Character
I- Intensity
D- Duration
A- Aggravation
A- Alleviation
A – Association
R – Radiation

One More Pain Mnemonic
P – period of pain
A – area of pain
I – intensity of pain
N – nullify ( what makes pain go away, if any)
Submitted by Greg Van Hook

Concretions:
“Big Mess”
B – Barbituates
I – Iron
G – Glutethemide
M – Meprobamate
E – Extended release theophylline
SS – Salicylates

X linked
• Bleeder, Blind, Becker and Duch, B cell
• others : G6PD,NDI,SCID,CGD

Medicine

Posted in Medicine on August 1, 2007 by dowite1588

Markers of Tuberculosis in Pleural Effusion :-

Interferon gamma > 140 IU
Adenosine deamylase > 40
PCR

Roth Spots :-

seen in the retina of Myeloproliferative, Lymphoproliferatie disorders and Infective endocarditis.

Spiral CT scan :-

for pulmonary embolism

Addison’s disease :-

The patients have microcardia (small heart).

Kikuchi’s disease :-

Mostly in Japan, in young girls, bilateral lymphadenopathy with high grade fever is seen in this disease.

The National Institute for Health and Clinical Excellence (NICE) and the National Collaborating Centre for Chronic Conditions, in conjunction with the British Hypertension Society (BHS) have today (Wednesday 28 June) launched the keenly awaited updated clinical guideline on the management of hypertension:-

The updated recommendations in the guideline include the following:

• In hypertensive patients aged 55 and over, or Black patients* of any age, first choice of initial therapy should be either a calcium channel blocker or a thiazide-type diuretic.

* Black patients are those of African or Caribbean descent, and not mixed race, Asian or Chinese patients

• In hypertensive patients younger than 55, first choice initial therapy should be an ACE inhibitor (or an Angiotensin receptor blocker if an ACE inhibitor is not tolerated).

• If initial therapy was with a calcium channel blocker or thiazide-type diuretic and a second drug is required, add an ACE inhibitor (or an Angiotensin receptor blocker if an ACE inhibitor is not tolerated). If initial therapy was with an ACE inhibitor, add a calcium channel blocker or a thiazide-type diuretic.

• If treatment with three drugs is required, the combination of ACE inhibitor (or an Angiotensin receptor blocker if an ACE inhibitor is not tolerated), calcium channel blocker and thiazide-type diuretic should be used.

The decision not to recommend Beta-blockers for first line therapy is based on evidence that suggests that they perform less well than other drugs, particularly in the elderly, and the increasing evidence that the most frequently used Beta-blockers at usual doses carries an unacceptable risk of provoking type 2 diabetes. The guideline also makes recommendations beyond a 3-drug combination, where, although the evidence is less certain, the GDG took into account existing guidelines and constructed recommendations most compatible with current good practice.

Hypertensive Crisis:-
Only HTN.

Hypertensive Emergency:-
With Complications.

Accelerated Hypertension:-
End Organ Damage.

The young patient with paroxysm of palpitations:-

at rest —-> mostly its paroxysmal svt

after exercise —-> rvot – vt.

Side effects of captopril:-

Angioedema.

Mechanical Valves induce haemolysis.

Regarding contraceptive when a male patient is on thalidomide , the answer is a single barrier method:-

Because of the known human teratogenicity of thalidomide, thalidomide is contraindicated in women who are or may become pregnant and who are not using the two required types of birth control or who are not continually abstaining from heterosexual sexual contact. If thalidomide is taken during pregnancy, it can cause severe birth defects or death to an unborn baby. Thalidomide should never be used by women who are pregnant or who could become pregnant while taking the drug. Even a single dose [1 capsule (regardless of strength)] taken by a pregnant woman can cause birth defects. If pregnancy does occur during treatment, the drug should be immediately discontinued. Under these conditions, the patient should be referred to an obstetrician/gynecologist experienced in reproductive toxicity for further evaluation and counseling. Any suspected fetal exposure to THALOMID® (thalidomide) must be reported to the FDA via the MedWatch program at 1-800-FDA-1088 and also to Celgene Corporation at 1-888-423-5436.

Because thalidomide is present in the semen of patients receiving the drug, males receiving thalidomide must always use a latex condom during any sexual contact with women of childbearing potential. The risk to the fetus from the semen of male patients taking thalidomide is unknown.

————————————————————

Inducers of the P450 system include

antiepileptics: phenytoin, carbamazepine

barbiturates: phenobarbitone

rifampicin

St John’s Wort

chronic alcohol intake

griseofulvin

smoking (affects CYP1A2, reason why smokers require more aminophylline)

Inhibitors of the P450 system include

antibiotics: ciprofloxacin, erythromycin

isoniazid

cimetidine, omeprazole

amiodarone

allopurinol

imidazoles: ketoconazole, fluconazole

SSRIs: fluoxetine, sertraline

ritonavir

sodium valproate

acute alcohol intake

quinupristin
————————————————————
Young people with septic arthritis – gonococcus; older people – Staph aureus
————————————————————

Using Beta Blockers in Patients with Heart Failure

Compelling evidence now exists to support the safety and efficacy of beta-blocker therapy in patients with heart failure. Guidance on the implementation of beta-blocker therapy in these patients is provided in the following sections.
Beta-blocker therapy is appropriate in patients with New York Heart Association class II or class III symptoms resulting from left ventricular systolic dysfunction.Patient Selection
Beta blocker therapy is appropriate in patients with NYHA class II or class III symptoms resulting from left ventricular systolic dysfunction. Unless contraindicated, beta blockers should be considered a mainstay of therapy in these patients to improve symptoms and mortality and to decrease hospitalizations.

None of the trials described in this article tested the use of beta blockers in patients with NYHA class I disease. Many asymptomatic patients with left ventricular dysfunction have had a myocardial infarction sometime in the past. Data on the administration of beta blockers subsequent to myocardial infarction are compelling enough to justify the use of these agents, if tolerated, in patients with NYHA class I disease. Many of these patients have other comorbid conditions, such as hypertension or angina, for which beta blockers may also be indicated.
When beta blockers are used in patients with heart failure, they should be considered disease-modifying agents rather than “rescue” agents. Their utility lies in blocking the neurohormonal cascade that leads to progression of the disease, not in providing immediate symptomatic relief.

None of the published trials have included sufficient numbers of patients with NYHA class IV symptoms to justify the safety or efficacy of beta blockers in this group. BEST was designed to better address this issue, but the trial included relatively few patients with NYHA class IV symptoms and was stopped early. The COPERNICUS trial may provide guidance once data become available. Pending release of the COPERNICUS trial results or other data, beta blockers should not be used in patients with NYHA class IV symptoms; however, these agents may be started or resumed once NYHA class IV symptoms resolve and patients are hemodynamically stable.

When beta blockers are used in patients with heart failure, they should be considered disease-modifying agents rather than “rescue” agents. Their utility lies in blocking the neurohormonal cascade that leads to progression of the disease, not in providing immediate symptomatic relief. Thus, patients should be hemodynamically stable when beta-blocker therapy is initiated. This approach provides certain pragmatic difficulties in dealing with patients who may already be taking a number of medications and may be resistant to the thought of adding another medication at a time when they seem well. In this setting, however, the risks of polypharmacy seem to be justified when compared to the mortality benefit of beta-blocker therapy.

Beta blockers appear to be effective irrespective of the etiology of the heart failure. Similarly, no age-specific phenomena have been reported. Preliminary data from BEST imply that racial differences may exist in the response of patients with heart failure to beta blockers; however, conclusions about this issue must await release of the trial results.

Carvedilol is the only agent labeled by the FDA for use in patients with heart failure. It is also the only agent that is available in the appropriate starting dosage (3.125 mg twice daily). The starting dosages for metoprolol tartrate, metoprolol succinate and bisoprolol require that the tablet in the smallest available dose size be split into fourths, which may be a cumbersome task for some patients. In addition, dividing the metoprolol succinate tablet into fourths may disrupt the delivery system, although it is not known if tablet division would have an adverse clinical impact. Metoprolol tartrate and bisoprolol are the least expensive of these agents (Table 6).

Once the patient has tolerated the starting dosage of the selected beta blocker, the dosage should be doubled every two to four weeks as tolerated. While the dosage is being titrated, the patient should be monitored for signs of worsening heart failure, hypotension or bradycardia. If symptoms develop, the dosage may need to be held at the current level or decreased; in some patients, the drug may need to be stopped. Otherwise, the dosage should be increased until the target dosage is achieved or the patient is receiving the maximal tolerated dosage, if below the target level. Once the desired dosage has been reached, no further adjustments need to be made. Even if the patient’s symptoms stabilize or the ejection fraction normalizes, most experts recommend continuing beta-blocker therapy indefinitely.

Other Pharmacologic Therapy
In all of the published mortality trials, beta blockers were added to background therapy with ACE inhibitors, diuretics and, sometimes, digoxin (Lanoxin). All patients for whom beta-blocker therapy is indicated should also be taking an ACE inhibitor as tolerated, unless contraindications exist. Diuretics should be titrated as needed for symptoms of volume overload. Digoxin may be used to improve symptoms, but it has never been shown to improve mortality. Spironolactone (Aldactone) has recently been shown to improve mortality in heart failure and its use is indicated in patients with systolic dysfunction who have symptoms at rest or a recent history of symptoms at rest.13

The long list of potential medications poses challenges for both the physician and the patient. Close surveillance for volume, electrolyte and hemodynamic changes is essential. The frequency of office monitoring is based on the characteristics and needs of the individual patient.

Contraindications to Beta Blockers
Beta blockers should not be administered to patients with heart failure who have bradycardia, heart block or hemodynamic instability. Patients hospitalized for heart failure may receive beta blockers only after they have been stabilized. Patients with severe asthma should not be given beta blockers, although those with milder symptoms may be able to tolerate these medications.

Members of various medical faculties develop articles for “Practical Therapeutics.” This article is one in a series coordinated by the Department of Family Medicine at the University of Michigan Medical School, Ann Arbor. Guest editor of the series is Barbara S. Apgar, M.D., M.S., who is also an associate editor of AFP.

Long-term benefits of using Beta blowckers :-

• improved survival

• improved control of heart failure

• reduced need for hospitalisation

• improved quality of life

• improved left ventricular ejection fraction

Mechanism of action

The benefit of beta blockers almost certainly depends on blockade of beta-1 receptors. This action is consistent with the large body of data documenting high plasma catecholamines in severe heart failure, and more sophisticated studies demonstrating increased cardiac sympathetic activity and catecholamine release. Possible mechanisms for beta receptor blockade improving survival include:

• antiarrhythmic action

• anti-ischaemic action

• attenuation of catecholamine toxicity

• reduced cardiac remodelling.

Metoprolol and bisoprolol are both cardioselective beta blockers acting primarily on beta-1 receptors. By comparison, carvedilol is a non-selective beta blocker with additional alpha-receptor blocking and antioxidant properties. Based on the unequivocal treatment benefits seen in the CIBIS2 and MERIT3 studies, the principal mechanism by which these drugs improve outcome in heart failure is likely to be via their beta-1 receptor blocking action. We will not know if the additional properties of carvedilol are important, and whether carvedilol actually produces a larger benefit than standard beta blockers, until the results of current head-to-head comparisons are reported.

Indications other than systolic heart failure

There are two other types of heart failure where use of beta blockers provides clear benefits and little risk.

Atrial fibrillation

In some patients, atrial fibrillation with rapid ventricular response is a major factor which worsens the severity of their heart failure. In this situation, controlling the ventricular response alone can produce a major improvement in heart failure. Digoxin is usually effective in this situation. Beta blockers are also effective in slowing the ventricular rate, and rarely worsen the situation providing ventricular systolic function is reasonably well preserved.

Diastolic heart failure

Possibly as many as one third of patients with heart failure have normal ventricular systolic function. In these patients, the primary cardiac abnormality leading to heart failure is an abnormality of ventricular filling. They have so-called ‘diastolic heart failure’. In this situation, beta blockers can also produce improvement with little risk of the patient deteriorating. The drugs slow the heart rate and allow a longer period for diastolic filling, particularly if atrial fibrillation is also present. Patients with mitral stenosis are the best example. Beta blockers can also facilitate diastolic filling by improving abnormal myocardial relaxation, for example in patients with diastolic failure due to severe left ventricular hypertrophy. This is generally in patients with severe, long-standing, poorly-controlled hypertension.

Clinical trials in systolic heart failure

Patients with primarily systolic heart failure with low ejection fraction may deteriorate when given a beta blocker. Paradoxically, it is this very group of patients that had unequivocal long-term benefits in recent trials (see box).

Carvedilol trials

In the meta-analysis of beta blockade1, there were eight trials of carvedilol, with a total of 1657 patients. Carvedilol appeared to reduce total mortality by 49%. However, only one of the eight individual carvedilol trials produced a statistically significant reduction in total mortality. This trial markedly influences the overall estimate of the treatment benefit of carvedilol. The ANZ trial was the largest of the carvedilol trials (415 patients). Although it found a 27% reduction in total mortality and a 30% reduction in hospitalisation, neither result was statistically significant. None of the carvedilol trials were sufficiently powered to be able to detect a significant difference in these end-points.

It was pooled data from a number of relatively small trials of carvedilol which convinced the Therapeutic Goods Administration to approve carvedilol for systolic heart failure in 1998. Carvedilol requires an authority prescription under the Pharmaceutical Benefits Scheme.

CIBIS-II

CIBIS stands for Cardiac Insufficiency Bisoprolol Study.2 Bisoprolol is a beta-1 selective blocker not available in Australia. A total of 2647 patients, mostly in Class III heart failure, had either bisoprolol or a placebo added to optimal therapy. (Most patients were taking a loop diuretic and ACE inhibitor in reasonable doses, and 50% were taking digoxin.) The trial was stopped early because of an unequivocally statistically significant reduction in total mortality of 34%. There were also significant reductions in sudden death (44%) and in hospitalisation for congestive cardiac failure (20%).

MERIT-HF

MERIT-HF stands for Metoprolol Randomised Intervention Trial in Heart Failure.3 Metoprolol is a beta-1 selective blocker which has been available in Australia for many years. However, this trial used a slow-release formulation not currently available in Australia. A total of 3991 patients, with predominantly Class III heart failure, were randomised to have either a placebo or metoprolol, added to the optimal conventional therapy of a loop diuretic and ACE inhibitor. The trial was stopped early because of an unequivocally statistically significant reduction in total mortality of 34%. There was also a significant reduction in sudden death (41%).

COPERNICUS

This stands for Carvedilol Prospective Randomized Cumulative Survival Trial. This trial compared carvedilol with placebo in 2289 patients with severe Class III/IV heart failure and ejection fraction of less than 25%. Carvedilol or placebo was added to optimal conventional therapy for heart failure. The trial has been stopped prematurely because of a beneficial effect of carvedilol on the primary end-point of all cause mortality. The results have been presented at an international meeting, but have not yet been published. Carvedilol was associated with a 35% reduction in total mortality.

In COPERNICUS, the annual mortality in the placebo group (18.6%) was higher than in either the MERIT (11.0%) or CIBIS (13.2%) studies. This reflects a generally sicker group of patients in COPERNICUS with more severe heart failure. As a result, the same relative risk reduction has resulted in a larger absolute mortality benefit and a smaller number needed to treat. However, the relative risk reduction was similar between the three studies.

Unresolved issues

Severity of heart failure

Both the CIBIS and MERIT trials enrolled predominantly patients with Class III heart failure. The number of patients with more severe Class IV heart failure was small (17% and 3% respectively) and the treatment benefit was not statistically significant in this sub-group. Nevertheless, on average, the magnitude of benefit was not different in the patients with more severe failure. The COPERNICUS study enrolled more patients with Class IV heart failure, yet produced virtually the same relative reduction in total mortality. It must be emphasised that patients with very severe heart failure are a much more difficult group in which to start beta blockers because of the risk of exacerbating their already severe heart failure.

Co-medication

Digoxin

Approximately 50% of patients in both the CIBIS and MERIT studies were taking digoxin. Randomisation was not performed in relation to digoxin, but there was no difference between the treatment benefit from beta blockade in those taking and those not taking digoxin. Given that there is no mortality benefit from digoxin4, it seems logical to recommend that patients in sinus rhythm should have a beta blocker added to optimal therapy before digoxin is introduced. However, this recommendation is not based on any definitive data.

Spironolactone

In the recently published RALES trial5 there was a highly significant 30% reduction in total mortality when a low dose of spironolactone (25 mg daily) was added to conventional therapy in patients with very severe heart failure. Only 10% of the patients were taking beta blockers. The patients in this study had much more severe heart failure than in most of the beta blocker studies. As a result of this trial, many physicians are now including low dose spironolactone as part of ‘optimal conventional therapy’ in patients with very severe heart failure before introducing a beta blocker.

Antiarrhythmics

There is no consensus on the role of conventional antiarrhythmics in severe heart failure. What is clear is that the beta blocker trials have shown a clear reduction in the very substantial risk of sudden death. This is assumed to be because they prevent ventricular tachyarrhythmias. It seems logical to recommend that, in the absence of documented sustained ventricular tachycardia, beta blockers should be used before any consideration of antiarrhythmic drug therapy.

Recommendations

A beta blocker should be considered for all patients with systolic heart failure who are stable on optimal doses of a diuretic and ACE inhibitor. If patients are not stable on optimal treatment, then digoxin and perhaps spironolactone should be added before a beta blocker.

Which beta blocker to use?

Both carvedilol and standard beta-1 blockers appear to be effective. There are currently multiple trials in progress of carvedilol in various different groups of heart failure patients. The results should tell us if carvedilol is more effective than standard beta-1 blockers. Carvedilol has the advantage of a lower dose formulation for starting treatment. However, carvedilol is also much more expensive than standard beta blockers (up to 10 times the cost of the standard form of metoprolol).

What dose for starting therapy?

Starting a beta blocker can make heart failure worse, so low doses are used. For most patients you can cautiously start with carvedilol 3.125 mg twice a day or metoprolol 12.5 mg twice a day. Patients with very severe heart failure should probably start on only a morning dose.

How rapidly can the dose be increased?

The dose can be doubled every 2-4 weeks providing the patient is stable. If the heart failure has deteriorated, the doses of diuretic, ACE inhibitor or digoxin should be adjusted first before any further increase in beta blocker. The dose of beta blocker may need to be reduced, particularly if there is undue bradycardia or worsening cardiac conduction.

What is the target dose?

For carvedilol, the target dose is 25 mg twice a day. For metoprolol it is 100 mg twice a day. Many patients will not reach these doses. Substantial benefits are almost certainly achieved with doses which are lower than these targets.

What about patients who are already taking a beta blocker?

Some patients who have been taking beta blockers long term for other indications such as angina or hypertension will develop heart failure. The clinician must first determine why the patient has developed heart failure (for example, new atrial fibrillation, silent myocardial infarction). Both the underlying cause and the heart failure must be treated appropriately. In many patients the degree of heart failure may not be too severe, and the beta blocker will be able to be continued. In other patients it may be necessary to either reduce the dose or even withdraw the beta blocker completely until the heart failure is under control. Once this has been achieved, the beta blocker should be cautiously reintroduced.

Who should manage the patient?

These patients are extremely fragile and difficult to treat. Occasional patients will deteriorate markedly after starting a beta blocker and may even require intensive or coronary care with intravenous beta agonist support. In Australia carvedilol can only be started in hospital patients. General practitioners should always consider involving a physician or cardiologist before starting or changing beta blocker therapy.
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