huyet van phan
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https://suzulan.wordpress.com/2009/03/26/100/

was learning leukotrien, And I think of Trien Chieu.
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-zumab
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Source: http://www.usmleforum.com/files/forum/2011/1/595872.php
if it ends with (mab)..> means antibody therapy.
if it has (ali) in the name..> means it binds to the receptors..

1- omalizumab...> (ali) means binds to receptors.... it got (m) on it..>binds to Mast(M) cell receptors( also IgE which look like m when you flip it)
2-adalimumab..>(ali) means binds to receptors...it got (D)on it..>binds to Dumor (tumor) necrotic factor receptors(TNF)
3-Infliximab..>it got (INF in the begining)..>binds to INF(TNF tumor necrotic factor)
4-Palvizumab..> it got (V) on it...> anti RSV (got V on it)
5- abciximab..>it got (ABC in the begining)..> binds to IIB/IIIA
6-Trustzumab..>(trust)..>binds to HER-2 (can you trust her?? )
7-dacLIzumab..>it got (LI) on it...> binds to IL-2

if you have more please add them to the list
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Asthma management mnemonics
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Source: http://allergycases.blogspot.com/2007/01/mnemonics-asthma.html

Mnemonics: Asthma

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport) Department of Allergy and Immunology

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (JACI, 2011). Prevalence of asthma is 8%, prevalence of AR is 3 times higher (24%). 40% of patients with AR have asthma, 80% of patients with asthma have AR.

Classification of asthma - mnemonic

I'M MS ("I'm a Master of Science")

Intermittent
Mild persistent
Moderate persistent
Severe persistent

Number of controllers used in each stage of the classification of asthma - mnemonic:

I'M MS
0 1 2 3

0 - SABA PRN (albuterol) only
1 - ICS or LTRA
2 - ICS/LABA or ICS plus LTRA
3 - ICS/LABA and LTRA, consider omalizumab (anti-IgE mAb)

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

Pathogenesis of Asthma

Lymphocytes

CD4, Th2
Central effector cells
Cytokine release

Overview of adhesion molecules, 3 groups remembered by the mnemonic SIS:Selectins
Integrins
Superfamily Ig

Mast cells are subdivided into 2 types based on proteinase content:
TC mast cells -- Tryptase and Chymase in granules
T mast cells -- Tryptase only granules

Mast cells
Mediator release
Mucosal inflammation

Mediators from eosinophils are remembered by the mnemonic CML EEE:

Cytokines
MBP
Lipid Mediators

EDN
ECP
EPO

Eosinophils
Emit
Eight mediators (at least 8, the first C in the mnemonic covers cytokines, chemokines and growth factors)

Overview of adhesion molecules, 3 groups remembered by the mnemonic SIS:Selectins
Integrins
Superfamily Ig

There are 4 families of eicosanoids (PP-LT): prostaglandins (PG), prostacyclins (PGI), leukotrienes (LT) and thromboxanes (TX).

Diagnosis of Asthma

A mnemonic to remember the different PFTs is SPIROMEtry:

Spirometry
PEFR
Inhalation tests:
Reversibilty of
Obstruction with beta-agonist
Metacholine challenge
Exhaled NO

The phases of spirometry can be remembered by the mnemonic BEIF:
Breath normally x 6 times
Exhale fully
Inhalation (deep)
Forceful exhalation for 6 seconds

FEV1/FVC
FEF 25-75
R
Regular (normal) or
Raised in
Restriction

FEV1
1ow in both obstructive and restrictive disease

Bronchodilation test: BB RRBaseline spirometry
Beta-agonist
Repeat spirometry
Reversibilty of obstruction

Methacholine challenge test, remember the numbers: 5-25-20-5:
5 breaths
25 mg/mL metacholine
20% FEV1 reduction
5% of patients with asthma have a negative test, 95% react to the challenge

Test for Respiratory and Asthma Control in Kids (TRACK) 

5
5 questions
5 year-old or younger (2-5 years)

Test for respiratory and asthma control in kids (TRACK) - mnemonic: 3S

Symptoms (3 questions)
SABA use
Steroid use

Test for respiratory and asthma control in kids (TRACK) - complete mnemonic: 3S

Symptoms - SPA: Symptoms - how often, Play, At night, past 4 weeks
SABA use, past 12 weeks (3 months)
Steroid use, past 12 months (1 year)

Time frame of TRACK:

Symptoms - 4 weeks (1 month)
SABA use - 12 weeks (3 months), quarter
Steroid use - 12 months (1 year)

References:
Test for Respiratory and Asthma Control in Kids (TRACK): A caregiver-completed questionnaire for preschool-aged children. Kevin R. Murphy et al. JACI. Volume 123, Issue 4, Pages 833-839.e9 (April 2009).

Differential Diagnosis of Asthma

C
Children
Congenital conditions
CF

A
Adults
Acquired conditions

Asthma Classification: M MMS

Mild intermittent

Mild persistent
Moderate persistent
Severe persistent

Treatment

One can remember the stages by the number of controller medications a patient would need at each stage:

I'M MS
0 1 2 3

"Rule of 2s” is used to determine level of control. If any of these are positive, consider a daily controller medication:

- daytime symptoms more than 2 days/wk
- rescue β2 -agonist use more than 2 times per week
- nighttime symptoms more than 2 nights/mo
- more than 2 asthma exacerbations per year
- more than 2 rescue β2-agonist canisters/yr

Reference for rule of 2's: Audio: Asthma, noon conference. Muthiah Pugazhenthi. Podcasting Project for the UT Internal Medicine Residency Program, 12/2006.

If asthma treatment is not working, check DAT:

Diagnosis - not asthma at all (VCD, CF, FBA), asthma plus AR, GERD
Adherence - compliance with medication
Technique - NEB, HFA with spacer, DPI, etc.

3 C's of care - communication, continuity, concordance (finding common ground) are critical for asthma management (http://goo.gl/8gJM6).

Medications

S
Singulair
Single daily dose
Suicude risk (potential)

LABA
M
Monotherapy
Masks inflammation
Mortality increase

Corticosteroids
C category during pregnancy

Budesonide
B category during pregnancy

Exercise-induced asthma treatment: CLIMB

Cromolyn
Leukotriene receptor antagonist
Inhaled steroids
Mast cell stabilizers other than cromolyn
Beta agonists

Leukotriene receptors

Leukotriene
B4
BLT 1, 2 receptors

Leukotriene
C4, D4, E4
CysLT 1, 2 receptors

Ciclesonide mnemonic

C
Ciclesonide 
Converted to active form (des-CIC)
Carboxyl-esterases in bronchial epithelial cells 
Clearance by liver

Published: 01/24/2008
Updated: 11/27/2012
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lukast
Wonder Me!
"Zafir-luk-ast, Monte-luk-ast, Cina-luk-ast":
Anti-Lukotrienes for Asthma.
Dazzle your oral examiner: Zafirlukast antagonizes leukotriene-4.
http://www.presentmed.com/mnemonics/index.php/Zafirlukast,%20Montelukast,%20Cinalukast:%20mechanism,%20usage
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why i am the way i am
Wonder Me!
http://graphics.latimes.com/retirement-nomads/

And ppl wonder why I'm so young but already been planning for my retirements!!!!!  I've seen it all... the drudgery... the poverty....... 

 And that's why I don't do drugs, smoking, or anything that may affect health ------- I have a lot of years ahead of me to live... can't mess it up.... 

 Realizing that I belong to the working class, I know I need to work, save, and yes, I will enjoy.

 The older I get, the more I realize taking care of myself and my stuff is my duty. It's no longer optional. It's a duty. 

 Song of the day: I do it my way (Frank Sinatra)
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Osgood–Schlatter disease
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Osgood–Schlatter disease (OSD), also known as apophysitis of the tibial tubercle, or Lannelongue's disease,[1] is an inflammation of the patellar ligament at the tibial tuberosity.[2] It is characterized by a painful lump just below the knee and is most often seen in young adolescents. Risk factors include overuse (especially in sports involving running, jumping and quick changes of direction) and adolescent growth spurts.
The condition is named after Robert Bayley Osgood (1873–1956), an American orthopedic surgeon and Carl B. Schlatter, (1864–1934), a Swiss surgeon who described the condition independently in 1903.[1]

Signs and symptoms[edit]

25-year-old male with Osgood–Schlatter disease.
Male with Osgood–Schlatter disease
Osgood–Schlatter disease causes pain in the front lower part of the knee.[3] This is usually at the ligament-bone junction of the patellar ligament and the tibial tuberosity.[4] The tibial tuberosity is a slight elevation of bone on the anterior and proximalportion of the tibia. The patellar tendon attaches the anterior quadriceps muscles to the tibia.[5]
Intense knee pain is usually the presenting symptom that occurs during activities such as running, jumping, squatting, and especially ascending or descending stairs and during kneeling.[citation needed] The pain is worse with acute knee impact. The pain can be reproduced by extending the knee against resistance, stressing the quadriceps, or striking the knee. Pain is initially mild and intermittent. In the acute phase, the pain is severe and continuous in nature. Impact of the affected area can be very painful. Bilateral symptoms are observed in 20–30% of patients.[citation needed]

Diagnosis[edit]

Diagnosis is made based on signs and symptoms.[6]

Ultrasonography[edit]

This test can see various warning signs that predict if OSD might occur. Ultrasonography can detect if there is any swelling within the tissue as well as cartilage swelling.[5] Ultrasonography's main goal is to identify OSD in the early stage rather than later on. It has unique features such as detection of an increase of swelling within the tibia or the cartilage surrounding the area and can also see if there is any new bone starting to build up around the tibial tuberosity.

Types[edit]

Three types of avulsion fractures.
OSD may result in an avulsion fracture, with the tibial tuberosity separating from the tibia (usually remaining connected to a tendon or ligament). This injury is uncommon because there are mechanisms that prevent strong muscles from doing damage. The fracture on the tibial tuberosity can be a complete or incomplete break.
Type I: A small fragment is displaced proximally and does not require surgery.
Type II: The articular surface remains together and the fracture occurs at the junction where the secondary center of ossificationand the proximal tibial epiphysis come together (may or may not require surgery).
Type III: Total break (through articular surface) including high chance of meniscal damage that usually requires surgery.

Differential diagnosis[edit]

Sinding-Larsen and Johansson syndrome,[7] is an analogous condition involving the patellar tendon and the lower margin of the patella bone, instead of the upper margin of the tibia. Sever's disease is a similar condition affecting the heel.

Prevention[edit]

Example of how to stretch the quadriceps muscle.
One of the main ways to prevent OSD is to check the participant's flexibility in their quadriceps and hamstrings. Lack of flexibility in these muscles can be direct risk indicator for OSD. Muscles can shorten, which can cause pain but this is not permanent.[8] Stretches can help reduce shortening of the muscles. The main stretches for prevention of OSD focus on the hamstrings and quadriceps.[9]

Treatment[edit]

Treatment is generally conservative with rest, ice, and specific exercises being recommended.[10] Simple pain killers may be used if required such as acetaminophen (paracetamol) or ibuprofen. Typically symptoms resolve as the growth plate closes.[10] Physiotherapy is generally recommended once the initial symptoms have improved to prevent recurrence.[10] Surgery may rarely be used in those who have stopped growing yet still have symptoms.[10]

Physiotherapy[edit]

Recommended efforts include exercises to improve the strength of the quadriceps, hamstring and gastrocnemius muscles.[10]
Bracing or use of an orthopedic cast to enforce joint immobilization is rarely required and does not necessarily give quicker resolution. Sometimes, however, bracing may give comfort and help reduce pain as it reduces strain on the tibial tubercle.[11]

Surgery[edit]

Surgical excision may rarely be required in skeletally mature patients.[12] In chronic cases that are refractory to conservative treatment, surgical intervention yields good results, particularly for patients with bony or cartilaginous ossicles. Excision of these ossicles produces resolution of symptoms and return to activity in several weeks. After surgery, it is common for lack of blood flow to below the knees and to the feet. This may cause the loss of circulation to the area, but will be back to normal again shortly. A high pain may come and go every once in a while, due to the lack of blood flow. If this happens, sitting down will help the pain decrease. Removal of all loose intratendinous ossicles associated with prominent tibial tubercles is the procedure of choice, both from the functional and the cosmetic point of view.[13]

Rehabilitation[edit]

Straight leg raises help strengthen the quadriceps without the need to bend the knee. The knee should be kept straight, legs should be lifted and lowered slowly, and reps should be held for three to five seconds.
Rehabilitation focuses on muscle strengthening, gait training, and pain control to restore knee function.[14] Nonsurgical treatments for less severe symptoms include: exercises for strength, stretches to increase range of motion, ice packs, knee tape, knee braces, anti-inflammatory agents, and electrical stimulation to control inflammation and pain. Quadriceps and hamstring exercises prescribed by rehabilitation experts restore flexibility and muscle strength.
Education and knowledge on stretches and exercises is important. Exercises should lack pain and increase gradually with intensity. The patient is given strict guidelines on how to perform exercises at home to avoid more injury.[14] Exercises can include leg raises, squats, and wall stretches to increase quadriceps and hamstring strength. This helps to avoid pain, stress, and tight muscles that lead to further injury that oppose healing. Knee orthotics such as patella straps and knee sleeves help decrease force traction and prevent painful tibia contact by restricting unnecessary movement, providing support, and also adding compression to the area of pain.

Prognosis[edit]

This graph represents the total amount of subjects that were discharged from the hospital with OSD within the years of 2008 and 2011. 100% of patients admitted were discharged, and each year showed that males obtained the disease more frequently than females.
The condition is usually self-limiting and is caused by stress on the patellar tendon that attaches the quadriceps muscle at the front of the thigh to the tibial tuberosity. Following an adolescent growth spurt, repeated stress from contraction of the quadricepsis transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple subacute avulsion fracturesalong with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump which can be very painful, especially when hit. Activities such as kneeling may also irritate the tendon.
The syndrome may develop without trauma or other apparent cause; however, some studies report up to 50% of patients relate a history of precipitating trauma. Several authors have tried to identify the actual underlying etiology and risk factors that predispose Osgood–Schlatter disease and postulated various theories. However, currently it is widely accepted that Osgood–Schlatter disease is a traction apophysitis of the proximal tibial tubercle at the insertion of the patellar tendon caused by repetitive micro-trauma. In other words, Osgood–Schlatter disease is an overuse injury and closely related to the physical activity of the child. It was shown that children who actively participate in sports are affected more frequently as compared with non-participants. In a retrospective study of adolescents, old athletes actively participating in sports showed a frequency of 21% reporting the syndrome compared with only 4.5% of age-matched nonathletic controls.[15]
The symptoms usually resolve with treatment but may recur for 12–24 months before complete resolution at skeletal maturity, when the tibial epiphysis fuses. In some cases the symptoms do not resolve until the patient is fully grown. In approximately 10% of patients the symptoms continue unabated into adulthood, despite all conservative measures.[12]

Long-term implications[edit]

OSD occurs from the combined effects of tibial tuberosity immaturity and quadriceps tightness.[5] There is a possibility of migration of the ossicle or fragmentation in Osgood-Schlatter patients.[4] The implications of OSD and the ossification of the tubercle can lead to functional limitations and pain for patients into adulthood.[9]
Of people admitted with OSD, about half were children who were between the ages of 1 and 17. In addition, in 2014, a case study of 261 patients was observed over 12 to 24 months. 237 of these patients responded well to sport restriction and non-steroid anti-inflammatory agents, which resulted in recovery to normal athletic activity.[16]

Epidemiology[edit]

Osgood–Schlatter disease generally occurs in boys and girls aged 9–16[17] coinciding with periods of growth spurts. It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. It has been suggested that difference is related to a greater participation by boys in sports and risk activities than by girls.[18]

Society and culture[edit]

Steven Gerrard, Rafael Nadal, Paul Scholes, Danny Welbeck and Stephen Ireland are sportsmen who have recovered from this condition.[19] The French tennis player, Gaël Monfils wears patella bands in an attempt to combat the condition.[20]
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pinguecula
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A pinguecula is a common type of conjunctival degeneration in the eye. 

Presentation[edit]

It is seen as a yellow-[1] white deposit on the conjunctiva adjacent to the limbus (the junction between the cornea and sclera). (It is to be distinguished clinically from a pterygium, which is a wedge shaped area of fibrosis that may grow onto the cornea.) A pingueculum usually does not cause any symptoms. It is most common in tropical climates and there is a direct correlation with UV exposure.
Histologically, there is degeneration of the collagen fibers of the conjunctival stroma with thinning of the overlying epithelium and occasionally calcification.[2] Actinic exposure of the thin conjunctival tissue is thought to cause fibroblasts to produce more elastin fibers, which are more twisted than normal elastin fibers and may lead to the degradation of the collagenfibers.[3] Alternatively, it has been postulated that the sub-epithelial collagen fibers undergo degradation and assume the qualities of elastic tissue while fragmenting and twisting in a different configuration from their normal state.[4]
It is thought that the high reflectvity of the solid white scleral tissue underlying the conjunctival tissue may result in additional UV exposure to the back side of the tissue.[5]The side of the nose also reflects sunlight on to the conjunctiva. As a result, pingueculae tend to occur more often on the nasal side of the eye. While most pingueculae are found in people over the age of 40, they are not uncommon in 20 and 30 years old adults who spend significant time in the sun.
The surface of the conjunctival tissue overlying a Pingueculum interferes with the normal spreading of the tear film. The tear ferning test reveals abnormalities of the mucous component of the tear film, making it useful as a predictor of a person's tolerance of hydrophilic soft contact lenses.[6] Contact lens intolerance can also result from the elevation of the peripheral edge of the contact lens if it overlies a pingueculum.
The plural form of pinguecula is pingueculae. Pinguecula is derived from the Latin word "pinguis" for fat or grease.[7]

Prognosis and treatment[edit]

Pingueculae may enlarge slowly over time, but are a benign condition, usually requiring no treatment. Artificial tears may help to relieve discomfort, if it occurs. If cosmesis is a concern surgical excision is sometimes done. Occasionally a pinguecula may become inflamed, a condition called pingueculitis. The cause of pingueculitis is unknown but there are no known infectious agents associated with it. If an inflamed pinguecula is causing discomfort or cosmetic concerns it may be treated with an anti-inflammatory agent, such as prednisolone drops.

Associated conditions[edit]

A pinguecula is one of the differential diagnoses for a limbal nodule. It may have an increased prevalence in Gaucher's disease.

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hiatal hernia
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A hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through the esophageal hiatus because of a tear or weakness in the diaphragm. Hiatus hernias often result in heartburn but may also cause chest pain or pain with eating.[1]
The most common cause is obesity. The diagnosis is often by endoscopy or medical imaging.[1]
A hiatus hernia may be treated with lifestyle changes such as raising the head of the bed, weight loss, and adjusting eating habits. Medications such as H2 blockers or proton pump inhibitors may help. If the symptoms do not improve with medications the surgery known as laparoscopic fundoplication may be an option.[1]

Treatment[edit]

In most cases, sufferers experience no discomfort and no treatment is required. If there is pain or discomfort, 3 or 4 sips of room temperature water will usually relieve the pain. However, when the hiatal hernia is large, or is of the paraesophageal type, it is likely to cause esophageal stricture and discomfort. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals. If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided. Antisecretory drugs like proton pump inhibitors and H2 receptor blockers can be used to reduce acid secretion.
Where hernia symptoms are severe and chronic acid reflux is involved, surgery is sometimes recommended, as chronic reflux can severely injure the esophagus and even lead to esophageal cancer.
The surgical procedure used is called Nissen fundoplication. In fundoplication, the gastric fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus in the diaphragm and the reflux of gastric acid. The procedure is now commonly performed laparoscopically. With proper patient selection, laparoscopic fundoplication recent studies have indicated low complication rates, quick recovery, and relatively good long term results.[6][7][8][9][10]
Complications include gas bloat syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely, achalasia. The procedure sometimes fails over time, requiring a second surgery to make repairs.



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