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

————————————————————

A patient came in E/R with C/O itching, redness and swelling of lips and gums giving the vague history of Insulin Allergy.He was known hypertensive and diabetic since years.

Vitals :

Pulse 100b/m

B.P  180/90 mmHg

Temp A/F        RBS 335mg/dL

What should we do?

1. First lower the B.P by Inj Furosemide 40mg and Captopril 25mg S/L

2. Then lower the blood glucose with Insulin S/C 4U.

3. After  that give Inj Pheniramine I/M or Inj Corticosteroid I/M for the allergic reaction.

An insulin allergy is an allergic response to an insulin medication. Insulin is a hormone normally produced by the pancreas that is taken via injection or other means by some people with diabetes. People whose bodies do not produce insulin or cannot use it properly may be prescribed insulin to regulate their glucose (blood sugar) levels.

Some people have an allergic response to insulin medication, although it occurs rarely.
An allergy occurs when the immune system identifies a harmless substance as being dangerous and produces antibodies to fight the substance. For some people with insulin allergies, the allergy goes undetected until they suffer an allergic reaction.
Insulin allergies occur because injectable insulin is not exactly the same as naturally produced human insulin. Insulin medication in the United States is almost exclusively a form that is genetically engineered to resemble natural human insulin. The chemical makeup of these human insulins is often modified slightly to change the duration of the insulin action. Rarely insulin from animal sources is used to treat diabetes. Allergic reactions are reactions to these differences, as well as the additives, bacteria and impurities that are present in synthetic human and animal-derived insulin. Insulin allergies are more common with insulin made from animals than with synthetic human insulin.

Allergic reactions associated with the use of insulin can be local (appearing around the injection site) or can affect two or more body systems (anaphylaxis). A local allergic reaction may cause itching, redness or swelling at the injection site. Anaphylaxis may cause breathing difficulty, rash and a drop in blood pressure. Without immediate emergency treatment, anaphylaxis can quickly progress to anaphylactic shock and become deadly.

Signs and symptoms of insulin allergy
Insulin allergies, although rare, are unpredictable and can occur at any time during treatment. Symptoms of an allergic reaction can be immediate or can appear after the patient has been taking the medication for longer than a week. Reactions can either be local or affect two or more body systems (anaphylaxis).
The signs and symptoms of a local allergic reaction to insulin include:

Dents under the skin at the injection site

Swelling at the injection site

Persistent or temporary redness at the injection site

Itching at the injection site

Clusters of small bumps that are similar to hives

Local reactions occur only in the area where the insulin was injected. These reactions usually appear within 30 to 60 minutes and usually disappear within a few days to a few weeks. Patients should contact their physician when they believe they are suffering a local allergic reaction to their insulin.

Early signs and symptoms include:

Severe itching of the eyes and face

Anxiety

Palpitations

Rapid or weak pulse

Swelling of the throat or tongue

Slurred speech

Difficulty swallowing

Coughing, choking, wheezing or difficulty breathing

Bluish tint to skin (cyanosis), including lips or nail beds

Nasal congestion

Red or swelling skin

Hives (including on the lips, eyelids, throat and tongue)

Abdominal cramps

Diarrhea

Nausea or vomiting

Drop in blood pressure

Without immediate emergency treatment, anaphylaxis can quickly progress to anaphylactic shock and become deadly. More advanced signs and symptoms include:

Collapse or loss of consciousness

Convulsions

Loss of bladder control

Shock

Stroke

Cardiac arrest

Respiratory arrest

Some of the typical approaches to an allergic reaction include administering an antihistamine, which may be given to relieve mild symptoms, such as itching and rash. Antihistamines are a group of drugs that block the effects of histamine, a chemical released during an allergic reaction.
Corticosteroid cream or tablets may be recommended when skin rashes fail to clear up. Corticosteroids are a group of anti-inflammatory and immunosuppressive drugs similar to hormones produced by the body. In patients with asthma-like symptoms, such as wheezing or cough, a bronchodilator may be prescribed. Bronchodilators are a group of drugs used to widen the lungs’ airways (bronchi).
In cases of anaphylaxis, treatment is frequently an injection of epinephrine. Epinephrine constricts the blood vessels, prevents fluid leakage, opens the airways and raises blood pressure. It also quickly relieves the itching and skin flushing that is part of most episodes of anaphylaxis.
Patients with a history of severe reactions may have a prescribed epinephrine injection kit to treat themselves in an emergency. These patients may be advised in advance by their physician to administer their shot while someone else calls for emergency help. Those who do not have access to epinephrine must seek emergency treatment immediately. Epinephrine may then be administered in an emergency room or by emergency personnel.
To diagnose an insulin allergy, a physician will ask patients about their medical history and perform a physical examination.
Symptoms and a history of allergies to medications are usually enough to diagnose an insulin allergy. A physician may order an allergy skin test to determine if any form of insulin can be tolerated. A variety of insulin types can be introduced to the skin. The test is positive if the skin shows a reaction.
When a patient reacts to all types of insulin, a physician may recommend desensitization. Desensitization is the process of reducing or eliminating a patient’s sensitivity to an allergen. This is accomplished over time by injecting the patient with small but increasing amounts of the allergen. Desensitization is a risky procedure and is considered only in cases when there are no alternative medications or therapies available.
The insulin type that triggered the smallest allergic reaction is usually used in the desensitization process. After the first dose is introduced, the patient is asked to wait a specific time period until the next dose. Increasing doses of insulin are given over a period of minutes or hours to days, until the usual therapeutic dose is tolerable. The patient is monitored for some time after each dose to ensure that a significant allergic reaction is not occurring. Allergic reactions can occur at any time, even when the previous doses did not trigger a reaction. Should allergy symptoms appear during the desensitization therapy, allergy medications (e.g., antihistamines, corticosteroids or epinephrine) may be administered to relieve the symptoms.
There is no known way to prevent the development of an insulin allergy. However, patients may be advised by their physician to avoid discontinuing insulin therapy because insulin allergies are more common in patients with a history of interrupted insulin therapy.

———————————————————–

Case # 2

————————————————————

A 60 year old man presents with worsening breathlesness, confusion and headache. Since 3 months ago he began to have progressive exertional dyspnea, aching in the legs and pain in the left arm (without chest discomfort) after 50 yards :

IgA 2.8 (0.5 - 4.0) g/l

IgG 7 (5 - 13) g/l

IgM 24 (0.3 - 2.2) g/l

ESR 90mm/hr

A. Monoclonal gammopathy of unknown significance
B. B cell lymphoma
C. Antiphospholipid syndrome
D. Multiple myeloma
E. Waldenstrom’s macroglobulinaemia

Answer: e) Waldenstrom’s macroglobulinaemia.
The diagnosis is likely to be Waldenstrom’s macroglobulinemia due to the high IgM levels. Waldenström’s macroglobulinemia is a malignant tumor of lymphocytic and plasmacytic cells that secrete IgM. Patients often present with hepatosplenomegaly and lymphadenopathy. Most of the clinical manifestations are due to the hyperviscosity syndrome. Common presentations are: fatigue (related to anaemia), serum hyperviscosity – causing mucosal and gastrointestinal bleeding, and retinal haemorrhage(not thrombosis); due to engorged vessels and platelet dysfunction , purpura , hepatosplenomegaly and lymphadenopathy (rare in multiple myeloma), bone involvement is rare, neurologic symptoms – alterations in consciousness, peripheral neuropathy, visual disturbance, nausea and vertigo.

————————————————————

The Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) trial

trial was designed to test the hypothesis that treatment with an ACE inhibitor combined with amlodipine would result in better cardiovascular outcomes than treatment with the same ACE inhibitor combined with a thiazide diuretic.

Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)/Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT)

Statins if added to ACEi/Thiazide/CCB then there is decreased event of CVA.

Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Trial

the primary cardiovascular outcomes (particularly stroke) with treatment with the angiotensin-receptor blocker losartan were better than those with atenolol therapy, even though there were similar reductions in blood pressure in the two groups.

———————————————————–

30 yrs of age Miss Farah resident of Shah Faisal Colony came through OPD with the complaints of :

Rt. Knee joint swelling for 6 months

According to the patient’s mother she was in her usual state of health uptil 3yrs of age then she developed fever and cough for 2 months, the fever was low grade, associated with paroxysmal unproductive cough, there is no H/O ear discharge, abdominal pain, abdominal distension, alternating diarrhea or constipation. She was diagnosed and treated for 9 months as pulmonary tuberculosis. When she was 14 yrs of age, she had low grade fever, associated with night sweats and weight loss for 3 – 4 months; then again she was evaluated and was given ATT for 9 months and the symptoms subsided. She remained symptom free for 5 to 6 yrs. when she noticed Rt. side neck swelling, she was evaluated, took ATT again for 9 months.

Now she presented with the C/O Rt. knee joint swelling for 6 months, started gradually, progressive, associated with mild joint pain-pain was aggravated by movement and relieved by rest.

Edema of feet, and later swelling of whole face was noticed. Edema initially started from feet for 2 months, gradual in onset and progressive over 15 to 20 days. During the same period, pt. also developed edema of face especially in the morning. Edema has subsided in part 1 month since starting treatment. The knee joint pain was neither related to any trauma to that knee, any movement, color change, morning stiffness nor any restriction of movement of that joint.

There is no H/O cough, hemoptysis, breathlesness, wheezing, chest pain, palpitation, PND, orthopnea, pain in flanks, dysuria, haematuria, frequency of micturition, polyuria, oliguria, nocturia, jaundice, nausea & vomiting, numbness, tingling, loss of consciousness, headache, blackouts, fits, visual loss, diplopia, rash, itch, coloured spots, polydypsia, heat or cold intolerance, wt. gain or loss, heart burn, diarrhoea or constipation, sweating or any contact with tubeculous patient, BCG vaccination, sexual contact or any blood transfusion.

Past Hx:

No H/O recurrent ear or urinary infections, sinusitis, HTN,DM,IHD,arthrits, travelling abroad.

Menstrual Hx:

Age of menarche: 13yrs.

cycle: regular

no associated pain or intermenstrual bleeding.

Drug Hx:

ATT thrice for 9 months.

Family History:

Parents are healthy. She has one brother who is healthy and there

is no any chronic illness in the family.

SocioecenomicHx:

Lives in well ventilated house of three rooms. Surroundings are clean.

Young female, average ht. and built, well oriented with time, place and person.

Pitting Pedal edema present

A, J, Cy, D, Cl, K not present

Lymph nodes not palpable

Thyroid not enlarged

JVP not raised

Fingers : No osler’s or heberden’s nodes, no joint swelling or any deformity.

Local Examination :

Rt. knee swelling, more on medial side, no discoloration of overlying skin, non-tender, no change in temperature as compared to the surrounding skin, no restriction of movement or crepitus.

Chest:

Inspection: R/R is 16/min. thoracoabdominal, shape is normal. No deformity, scar, prominent veins, pulsations visible. Apex beat couldn’t be visualized. Chest is moving equally on both sides with respiration.

Palpation: Trachea is central, Apex beat is in 5th ICS medial to midclavicular line, normal character. No tenderness or crepitus demonstrated. Chest expansion 5 cm. Vocal fermitus is equal on both sides.

Percussion: Upper border of liver is in 5th ICS, note is resonant and equal on both sides.

Auscultation: Vesicular breathing, no added sounds. Vocal Resonance is equal on both sides.

Abdomen:

Inspection: Shape is normal, moving with respiration. No pulsation or peristalsis visible. Umblicus is central and normal shape. There is no scar, striae, prominent veins. Hernial orifices are intact.

Palpation: Upper border of liver is in 5th ICS. Abdomen is soft, non-tender, no rigidity. Liver is palpable 3 finger breadths below RCM, smooth border, non-pulsatile, with smooth, non-tender surface. Liver span is 16 cm.

Percussion: There is no shifting dullness or fluid thrill.

Auscultation: Bowel sounds are of normal intensity. No bruit or friction sound audible.

CNS:

Higher mental function: Normal

Speech: Normal

Cranial Nerves : Intact

Motor system : Intact

Sensory system : Intact

CVS:

S1, S2 audible. No added sounds or murmur.

Aspiration of Knee joint:

17/06/10

Gram stain: no microorganism seen

moderate-numerous pus cells

Culture: No growth. Anaerobes not isolated.

Synovial fluid :

RBC +

TLC 15800/mm3

Polymorph 90%

Lymphocytes 10%

Glucose 15mg/dL

Proteins 5500mg/dL

Aspiration of Knee joint:

29/09/10

Gram stain: no microorganism seen

few pus cells

Culture: No growth. Anaerobes not isolated.

AFB Smear: AFB not seen

AFB culture: negative for acid fast bacilli

Impression : TUBERCULOUS ARTHRITIS

————————————————————————————

63 years of age Mr. Yaqoob Ali resident of Federal B Area came through opd with the complaints of:

Pain in neck

Weakness in both hands

Difficulty during walking for 8-10 days

According to the patient, he was in his usual state of health 8-10days back then in one morning when he woke up he developed pain in neck, is sudden in onset, moderate in intensity, radiating to the arms , not progressive, continuous, aggravated by movements of neck and relieved by taking analgesics not associated with anxiety or depression. Weakness in both hands is sudden in onset, progressive , associated with numbness , tingling sensation and pain, having problems when grabbing something in his hand, buttoning his shirt. There is no H/O eating canned food, vomiting, headache, loss of consciousness, black outs, diplopia, visual disturbances, or fits. Difficulty during walking is sudden in onset, gets tired walking for some distance, tiredness is progressive and associated with the stiffness of legs and makes the patient to stop. There is no H/O breathlessness, palpitation, PND, chest pain, cough, wheezing, hemoptysis, nausea, vomiting, abdominal pain, diarrhoea or constipation, pain in the flanks, dysuria, urinary or faecal incontinence, rash, skin changes, joint pain, swelling, heat or cold intolerance, sweating, change in posture.

Past History

No H/O Hypertension, Diabetes mellitus, Ischemic heart disease, arthritis, TB, travel abroad.

Drug History

NSAIDs

Family History

Insignificant

Personal History

Appetite is normal, sleep is disturbed, Smoking 5-6 cigarettes / day for almost 30 to 40 yrs.

General Physical Examination

Elderly male average height and built, sitting comfortably on bed, well oriented with time, place and person.

Vital Signs :

Pulse – 82 b/m

B.P. – 130/80mmHg

Temp. 98.6F

R/R – 20/min.

A , J, CY, D, Cl, K , E not present

Systemic Examination :

CNS:

Higher Mental function:-

Appearance and behaviour – alert and co-operative

Orientation – well

Conscious level – normal

Memory – normal

Speech:- normal

Cranial Nerves :-

Olfactory – intact

Optic – intact

Oculomotor – intact

Trochlear – intact

Trigeminal – intact

Abducent – intact

Facial – intact

Vestibulocochlear – intact

Glossopharyngeal – intact

Vagus – intact

Accessory – The patient can bend the head downwards and sidewise against resistance but cannot shrug his shoulder against resistance.

Hypoglossal – intact

Motor System :- RUL           RLL            LUL        LLL

Tone                       INC              N                 INC         N

Bulk                         N                   N                N              N

Power                      DEC             N               DEC          N

Reflexes                INC                INC         INC      INC

Hoffman’s sign is positive

Inverse biceps reflex is positive

Inverse triceps reflex is positive

Sensory System :-

Touch, pain temperature, position, passive movements and vibration senses are decreased in upper limbs upto elbow and lower limbs upto the knees.

Cerebellar signs :-

Absent

Meningeal irritation :-

Absent

Chest

Normal Vesicular Breathing, no aded sounds.

CVS

S1 , S2 audible + 0

Abdomen

Soft, non tender, no visceromegaly, gut sounds audible.

CBC:

Hb 12.2g/dL

Hct 31.9 %

MCV 84fl

TLC 10.0/cmm

PLTS 132/cmm

Biochemistry

Sugar 96mg/dL                                Na 130.9mmole/L

Urea 26mg/dL                                  K 4.55mmole/L

Cr 1.0mg/dL

CXR P/A view

MRI Spine

Impression : CERVICAL SPONDYLOSIS 

——————————————————

John Murtagh (4th Ed.)

Internal Medicine on call (Australian Ed.2nd)

Oxford Handbook of Clinical Medicine

Oxford Handbook of Specialities

Gynaecology ( L. Johns – 8th Ed.)

Essential Paediatrics (Hull)

Practical Paediatrics (Robinson and Robertson)

Surgery (Scott)

Surgery (Churchill)

Psychiatry (General Practice by John Murtagh)

MCQS 

Annotated

Anthology

Past Papers www.aippg.com 

MRCP 

Phillip A. Kalra

Oxford Handbook of Medicine

Oxford Handbook of Specialities

Davidson/Pk

BCQS 

On Examination

Medical Master Class

Pastest Book Series

VSP Photostat shop near Hotel Jbees (Regal Sddar, Karachi) Mr. Fahim.  

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.
———————————————————–
MONITORING FOR
HEPATOTOXICITY DURING
ANTITUBERCULOSIS TREATMENT

GENERAL RECOMMENDATIONS
A consensus statement of
the Tuberculosis Control Coordinating Committee of
the Hong Kong Department of Health and
the Tuberculosis Subcommittee of
the Coordinating Committee in Internal Medicine of
the Hospital Authority, Hong Kong
April 2002

AUTHORS
TAM Cheuk-ming * FRCP(EDIN), FHKAM(Medicine)
YEW Wing-wai # FRCP(EDIN), FHKAM(Medicine)
LEUNG Chi-chiu * MRCP(UK), FHKAM(Medicine)
CHAN Yuk-choi @ FRCP(EDIN), FHKAM(Medicine)
* TB & Chest Service, Department of Health, Hong Kong SAR, China
# Department of Respiratory Medicine, Grantham Hospital, Hong Kong SAR, China
@ Department of Respiratory Medicine, Wong Tai Sin Hospital, Hong Kong SAR, China
Corresponding Author: TAM Cheuk-ming
Address: Wanchai Chest Clinic, 99 Kennedy Road, Hong Kong
April 2002
ACKNOWLEDGEMENT
This statement is prepared by a Working Group consisting of the above authors on behalf of
the Tuberculosis Control Coordinating Committee of the Hong Kong Department of Health
and the Tuberculosis Subcommittee of the Coordinating Committee in Internal Medicine of
the Hong Kong Hospital Authority. The authors would like to thank the members of the two
Committee/ Subcommittee. The members are: Dr. CK Chan, Dr. HS Chan, Dr. KS Chan, Dr.
WM Chan, Dr. WNK Chen, Dr. MT Cheung, Dr. K Choo, Dr. CM Chu, Dr. DLK Dai, Dr. SS
Ho, Dr. DSC Hui, Dr. KM Kam, Dr. CW Lam, Dr. CY Tam, Dr. KWT Tsang, Dr. ML Wong, Dr.
WKS Yee, Dr. WC Yu, and Dr. RWH Yung.
[Extracted from Annual Report (Suppl) 2002, TB & Chest Service, Department of Health, Hong Kong]

Background
Treatment of tuberculosis (TB) involves several drugs in combination for six
or more months. An updated set of guidelines has been published by a working
group of the Tuberculosis Control Coordinating Committee/ Tuberculosis & Chest Subcommittee of the Department of Health and the Hospital Authority
(TBCCC/TBSC).1 In view of the concern about the risk of hepatotoxicity, this short paper has been prepared to address the issue in greater depth.
Many of the commonly used anti-TB drugs are associated with significant
potential of causing hepatotoxicity. While the occurrence of drug-induced hepatitis is difficult to predict, it has been observed that certain patients are at higher risk of developing drug-induced hepatitis during the course of anti-TB chemotherapy.
These include patients with pre-existing liver diseases, particularly those associated with chronic viral infection due to Hepatitis B, Hepatitis C, and HIV, the alcoholics, the elderly and the malnourished.2-4
The exact role of regular monitoring of liver function tests in patients
receiving antituberculosis drugs remains controversial. Certain guidelines only emphasize the need of clinical monitoring without mentioning regular biochemical monitoring,5,6 while a number of authorities recommend routine biochemical monitoring among the high risk groups.7-9
Transient changes in alanine transaminase and bilirubin levels are relatively
common during antituberculosis chemotherapy and do not signify true hepatotoxicity.
However, progressive rise in alanine transaminase and bilirubin levels is much more ominous. Existing data do not allow reliable prediction of the exact clinical course of asymptomatic patients with moderate degree of biochemical derangement.
Opinions therefore differ as at what cut-off level of liver dysfunction should
modification of treatment regimen be initiated. For the alanine transaminase level, some recommend stopping the hepatotoxic drugs three times or above that of normal,8-12 while others recommend five times.6,7,13 The recommendations regarding the level of bilirubin are also not uniform.13
Furthermore, opinions on the frequency and duration of biochemical
monitoring also differ. While more frequent testing may be more likely to pick up those cases with rapid progression, cost-effectiveness and patient acceptance are practical issues among those without clinical symptoms. Whether monitoring should be performed throughout the whole course of anti-TB treatment, or just during the initial treatment phase also requires deliberation. More recently, a number of fatal cases of drug-induced hepatitis have been
reported during the course of treatment of latent TB infection (LTBI) since the publication of the guidelines for the treatment of LTBI by ATS/CDC.14 Although the absence of data on the denominator precludes an accurate assessment of the risk, an updated statement has been promulgated recommending more vigilant measures in liver function and clinical monitoring.13
A recent study in Hong Kong showed that among patients treated with
anti-TB drugs, the incidences of liver dysfunction and symptomatic hepatitis were
rather high among Hepatitis B carriers compared with non-carriers2 (Table 1).
Another local study also quoted a significant rate at 12% of clinically symptomatic
hepatic dysfunction among 1,181 hospital patients who received rifampicin, isoniazid
with or without pyrazinamide and other drugs.15 Although the definitions employed
for those hepatitic reactions are not exactly similar, the rates of liver dysfunction
found in these local studies are clearly higher than those reported elsewhere.16,17
Recommendations
Basing on the available clinical information, international guidelines, and
experiences from local experts, a consensus statement has been prepared by a working
group of the TBCCC/TBSC on clinical and biochemical monitoring of hepatotoxicity
during anti-TB treatment in the local setting:
(a) For all patients undergoing treatment with potentially hepatotoxic anti-TB drugs,
health education should be provided to alert them of the symptoms suggestive of
hepatitis, which include loss of appetite, nausea, vomiting, fever, and jaundice.
They should be advised to report such symptoms promptly to the nursing or
medical staff should these arise.
(b) During medical consultations in the course of anti-TB treatment, all patients
should be assessed clinically for symptoms and signs suggestive of hepatitis.
(c) Directly observed treatment (DOT), apart from ensuring treatment adherence,
also allows health care workers to monitor the patients closely for such
symptoms and signs.
(d) Patients developing symptoms suspicious of hepatitis should have liver function
tests checked, and in the case of clinical suspicion of significant hepatitic
reactions, the anti-TB drugs may have to be stopped even before the availability
of the test results.
5
(e) Patients at risk of developing drug-induced hepatitis should be identified at the
beginning of the treatment course. Patients with pre-existing liver diseases, the
alcoholics, the elderly and the malnourished constitute the most clearly defined
risk groups. Liver function tests should therefore be checked before the start of
anti-TB treatment.
(f) For those who belong to the risk groups as mentioned in (e), it would be
desirable to monitor liver function tests once every two weeks during the initial
two months of treatment, or more frequently as clinically indicated.
(g) In view of the high Hepatitis B carrier rate and the high incidence of
drug-induced hepatic dysfunction among them locally, it is also desirable to
check the HBsAg status of patients who need to receive anti-TB treatment.
Close clinical and biochemical monitoring should also be considered for
hepatitis B carriers as in (f).
(h) Regarding the cut-off levels of liver dysfunction for withholding potentially
hepatotoxic anti-TB drugs in patients without symptoms, the followings are
recommended:
(i) Alanine transaminase level rising to three times or above the upper limit of
normal;
(ii) Bilirubin level rising to two times or above the upper limit of normal.
Discussion and conclusions
Biochemical monitoring is not a replacement for close clinical monitoring.
Clinical heterogeneity dictates that each case should be assessed individually with the
monitoring procedures tailored accordingly. More frequent and intensive
biochemical monitoring may be indicated in situations where the patient’s condition
or the liver enzyme levels change rapidly. If the anti-TB drugs are given for the
treatment of latent TB infection, the standard for safety monitoring is clearly higher
than that for the treatment of active disease.18
Not uncommonly, mildly elevated pretreatment liver enzymes are
encountered among TB patients without any other evidence of liver disease. When
these patients are given the full treatment regimen,1 their enzyme levels are often
observed to revert to normal and this phenomenon is presumably related to the
6
resolution of hepatic TB microgranulomas. However, for those patients with
evidence of underlying chronic liver diseases, anti-TB drugs should be started
carefully. Depending on the nature of the underlying liver problem, it may be
necessary to begin with a potentially less hepatotoxic combination of drugs, and then
modify the regimen according to tolerance.
If significant drug-induced hepatitis develops, careful balance of all factors
is required to decide on when and how to resume treatment. In case of doubt,
experts in the field should be consulted. It should be noted that patients with active
TB disease would develop detrimental consequences if the TB is left untreated,
particularly if the disease is extensive. Hence, the decision on when to resume
treatment with anti-TB drugs should be made not only by the time the liver function
tests reverting to the normal or pretreatment level, but also on the rate of TB disease
progression and the disease severity. Sometimes, a regimen with less hepatotoxic
drugs or a combination of drugs without potential hepatotoxicity may have to be tried
first, with the more potent but potentially hepatotoxic drugs added subsequently one
after the other (Table 2). It is generally desirable to include both isoniazid and
rifampicin in the final regimen whenever possible, so that the duration of treatment
does not need to be excessively prolonged. During resumption of the treatment, the
liver chemistry should be closely monitored, and the frequency of monitoring usually
depends on the severity of the liver dysfunction that has had occurred and the drugs
on trial. It has to be noted that the cause of that hepatitis, apart from being
drug-induced, could be due to alternatives such as viral infections, or induction by
other drugs used at the same time. Resumption of treatment utilizing the original full
drug regimen may rarely be possible.
Although there has been substantial progress in the treatment of certain liver
diseases, like chronic viral hepatitis, the implications of these advances on the
treatment of tuberculosis have not yet been fully clarified. The above guidelines and
recommendations need to be reviewed periodically with the availability of future
updates in scientific data and medical literature, as well as further accumulation of
local experience.
7
Table 1. Rate of liver dysfunction and symptomatic hepatitis among patients given
anti-TB drugs, among HBV carriers as compared with non-carriers, and among HBV
carriers not given anti-TB drugs2

HBV carriers given
anti-TB drugs Non-carriers given
anti-TB drugs
HBV carriers not
given anti-TB                                                                                                                                              drugs
Total number 43                               276                                       86

Liver dysfunction * 15 (34.9%)    26 (9.4%)                     7 (8.1%)

Symptomatic
hepatitis #
7 (16.3%)                        13 (4.7%)                    1 (1.2%)
* Liver dysfunction is defined as an increase in ALT levels to 1.5 times above the upper limit of
normal on at least 2 consecutive occasions within 4 weeks. For patients with increased
pretreatment ALT, the elevation in ALT had to be greater than 1.5 times the baseline level.
# Symptomatic hepatitis is defined as the presence of malaise, nausea, vomiting, lethargy and/or
right upper quadrant discomfort together with the presence of liver dysfunction irrespective of the
severity of the biochemical abnormality.
Table 2. Anti-TB drugs and potential for hepatotoxicity
Potentially hepatotoxic drugs
Isoniazid
Rifampicin, Rifabutin
Pyrazinamide
Ethionamide, Prothionamide
Para-aminosalicylic acid

Drugs with much lower or little                                                                                              potential for  hepatotoxicity
Streptomycin, Kanamycin, Amikacin, Capreomycin
Ethambutol Ofloxacin, Levofloxacin, Ciprofloxacin
Cycloserine

1. is a fixed, false, firm belief.

2. held on inadequate grounds.

3. cannot be shaken by the contrary evidence.

4. cannot be explained by social, religious, cultural or educational ground.

If anyone of these pillars is missing, then it is not delusion.

Reactive Depression

• Psychological symptoms present
• Psychotherapy and SSRIs work

Indogenous Depression

• Biological symptoms(sleep, weight loss, anorexia, sexual dysfunction)  present
• Tricyclic antidepressents work

Benzodiazepines

should be used for 2 weeks because of psychological dependence (drug dependence) which happens if used more than 2 wks.

Cannabinnoids

Urinary canabinnoid can come upto 1 month after leaving its use because it is lipophylic, deposits in the lipid of the body and slowly comes in circulation. Blood cannabinnoid is not measured.

T1/2 is 48hrs in the body.

Drives and Motives

The internal factors compelling one to perform some activity are

called Drives. While the external environment compelling one to 

perform some activity is called Motive.

–Tricyclic antidepressants have anticholinergic effect (constipation, dry mouth).

Physiological Drug Dependence

The receptors are formed n the brain due to the use of drug, and when these receptors are empty withdrawal symptoms take place. e.g; heroin and diazepam dependence.

Psychological Drug Dependence

There is no receptor mechanism in this dependence and instead the patient himself thinks that he is dependent on the drug. e.g ; cannabinoids dependence.

Claustrophobia

Claustrophobia is an anxiety disorder that involves the fear of enclosed or confined spaces. Claustrophobes may suffer from panic attacks, or fear of having a panic attack, in situations such as being in elevators, trains, boxes or aircrafts.

Conversely, people who are prone to having panic attacks will often develop claustrophobia. If a panic attack occurs while they are in a confined space, then the claustrophobe fears not being able to escape the situation. Those suffering from claustrophobia might find it difficult to breathe in closed auditoriums, theatres, and elevators. Like many other disorders, claustrophobia can sometimes develop due to a traumatic incident in childhood.

Claustrophobia can be treated in similar ways to other anxiety disorders, with a range of treatments including cognitive behavior therapy and the use of anti-anxiety medication. Hypnosis is an alternative treatment for claustrophobia.

Delirium and Dementia

Global impairment of cognitive functions is called delirium ( acute) and dementia (chronic).

In Delirium consciousness is not present while in Dementia it is present.

Epilepsy Psychosis

Try to give the drugs which don’t aggravate anticholinergic effect e.g; SSRIs and Tricyclic antidepressants increase the anticholinergic effect, so avoid it’s use in the seizures of Psychosis.