Injury to the axillary nerve during shoulder dislocation has been reported to be as high as 40%

Large-force trauma (eg, motor vehicle accidents, pedestrians struck by automobiles) are the most common causes of hip dislocations.[1, 2, 3, 4, 5] This type of injury is also associated with high-energy impact athletic events

Hip dislocations are either anterior or posterior, with posterior hip dislocations comprising the majority of traumatic dislocations

several classification systems are used to describe posterior hip dislocations.

The Thompson-Epstein classification is based on radiographic findings.

Type 1 – With or without minor fracture

Type 2 – With large, single fracture of posterior acetabular rim

Type 3 – With comminution of rim of acetabulum, with or without major fragments

Type 4 – With fracture of the acetabular floor

Type 5 – With fracture of the femoral he

Anterior hip dislocations may present in 2 different ways.

Superiorly displaced dislocations present with the affected hip extended and externally rotated.

The inferior type of anterior dislocations presents with the affected hip flexed, abducted, and externally rotated.

Patients with knee dislocation should undergo radiography and MRI, as well as angiography.

osterior hip dislocation most commonly appears shortened, internally rotated, and adducted.

neurovascular status of the injured leg is extremely important. Nerve injury, particularly neurapraxia, is not uncommon. The sciatic nerve and the common peroneal division of the sciatic nerve are most often injured in posterior dislocations

Many knee dislocations spontaneously reduce prior to ED presentation, m

Anterior: Anterior dislocation often is caused by severe knee hyperextension. Cadaver research has shown that approximately 30 degrees of hyperextension is required before dislocation will occur.

Posterior: Posterior dislocation occurs with anterior-to-posterior force to the proximal tibia, such as a dashboard type of injury or a high-energy fall on a flexed knee. The image below shows a radiograph of a posterior dislocation.

Posterior knee dislocation.

View Media Gallery

Medial, lateral, or rotatory: Medial, lateral, and rotatory dislocations require varus, valgus, or rotatory components of applied force. A lateral dislocation is illustrated in the image below.

MMore than half of all dislocations are anterior or posterior, and both of these have a high incidence of popliteal artery injury

o 50% of knee dislocations are reduced by the time of ED presentation and may not be obvious.

. DRF/distal radial fractures have a bimodal distribution, with a peak in younger persons (aged 18-25 years) and a second peak in older persons (aged >65 years). The mechanism of injury is unique to each group

Younger patients have stronger bone, and thus, more energy is required to create a fracture in these individuals. Motorcycle accidents, falls from a height,

Older patients have much weaker bones and can sustain a DRF from simply falling on an outstretched hand

Child programs

AgeVaccine

Birth

Hepatitis B (hepB)a

2 months

Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), Haemophilus influenzae type b, inactivated poliomyelitis (polio) (hepB-DTPa-Hib-IPV)

Pneumococcal conjugate (13vPCV)

Rotavirus

4 months

Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), Haemophilus influenzae type b, inactivated poliomyelitis (polio) (hepB-DTPa-Hib-IPV)

Pneumococcal conjugate (13vPCV)

Rotavirus

6 months

Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), Haemophilus influenzae type b, inactivated poliomyelitis (polio) (hepB-DTPa-Hib-IPV)

Pneumococcal conjugate (13vPCV)

Rotavirus b

12 months

Haemophilus influenzae type b and meningococcal C (Hib-MenC)

Measles, mumps and rubella (MMR)

18 months

Measles, mumps, rubella and varicella (chickenpox) (MMRV)

4 years

Diphtheria, tetanus, acellular pertussis (whooping cough) and inactivated poliomyelitis (polio) (DTPa-IPV)

Measles, mumps and rubella (MMR) (to be given only if MMRV vaccine was not given at 18 months)

School programs

AgeVaccine

10–15 years (contact your State or Territory Health Department for details)

Varicella (chickenpox) c

Human papillomavirus (HPV) d

Diphtheria, tetanus and acellular pertussis (whooping cough) (dTpa)

At-risk groups

Aboriginal and Torres Strait Islanders

AgeVaccine

12–18 months (In high risk areas) e

Pneumococcal conjugate (13vPCV)

12–24 months (In high risk areas) f

Hepatitis A

6 months to less than 5 years

Influenza (flu)

15 years and over

Influenza (flu)

Pneumococcal polysaccharide (23vPPV) (medically at risk)

50 years and over

Pneumococcal polysaccharide (23vPPV)

Other at-risk groups

AgeVaccine

6 months and over (people with medical conditions placing them at risk of serious complications of influenza)
Influenza (flu)
12 months (medically at risk) e       
Pneumococcal conjugate (13vPCV)
4 years (medically at risk)e       
Pneumococcal polysaccharide (23vPPV)
Pregnant women (at any stage of pregnancy)       
Influenza (flu)
65 years and over       
Influenza (flu)
Pneumococcal polysaccharide (23vPPV)

sure. Normal ABI is more than 1; a value less than 0.95 is considered abnor

treatment for cholysistitis

arious surgical techniques are now available and include 1) endoscopic retrograde cholangiopancreatography,[24, 25] 2) open cholecystectomy, and 3) laparoscopic cholecystectomy.[

Narcissistic personality disorder (NPD) is a personality disorder in which a person is excessively preoccupied with personal adequacy, power, prestige and vanity, mentally unable to see the destructive damage they are causing to themselves and others. It is

he Romberg test is used to investigate the cause of loss of motor coordination (ataxia). A positive Romberg test suggests that the ataxia is sensory in nature, that is, depending on loss of proprioception. If a patient is ataxic and Romberg's test is not positive, it suggests that ataxia is cerebellar in nature, that is, depending on localized cerebellar dysfunction instead.

romberg sign

The Committee continues to recommend the following from the from the October 2012 Update:

Occupational exposures require urgent medical evaluation. The Committee further emphasizes recommendations regarding the importance of initiating occupational PEP as soon as possible, ideally within 2 hours of exposure. A first dose of PEP should be offered while evaluation is underway. PEP should not be delayed while awaiting information about the source patient or results of the exposed worker’s baseline HIV test.

tpA indication

acute MI

pulmonary embilism

ischemicbstrock

centtal venus catheter occlusion

most significant lead exposure in adults usually occurs at the workplace, whereas for children, other forms of environmental exposure are more important.

Exposure from lead-based paint was significant among children in the past.

led poisoning

With exposure to high levels of lead, patients develop lethargy, progressing to coma and seizures. Death is uncommon with appropriate medical management. Long-term sequelae depend on the duration, as well as the amount, of exposure. Acute lead nephropathy is usually completely reversible with chelation therapy. Deaths may result from the elevated intracranial pressure (ICP) associated with lead encephalopathy.

With chronic exposure to low or moderate levels of lead, subacute symptoms develop. Patients with chronic lead nephropathy may have a progressive decline in kidney function and eventually require renal replacement therapy.

lead poisoning

Currently, 3 forms of lead nephropathy are recognized.

The first is acute lead poisoning resulting from acute massive exposure to lead, which causes classic symptoms, including colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome

. The second is chronic lead nephropathy (see the image below), which is a slowly progressive interstitial nephritis resulting from excessive cumulative exposure to lead and is frequently associated with hypertension and gout.

The thirdis lead-induced hypertension.

CKD

legal ages of consent: Tasmanian Criminal Code

Children do not have the ability to consent to any sexual act, as they do not understand the implications of a sexual relationship and therefore cannot give ‘informed consent’.

The Tasmanian Criminal Code states:

Any person who has unlawful sexual intercourse with another person who is under the age of 17 years is guilty of a crime.

Unless:

(a) that person was of or above the age of 15 years and the accused person was not more than 5 years older than that person; or

(b) that person was of or above the age of 12 years and the accused person was not more than 3 years older than that person.

fibroma

Immunoglobulin A (IgA) nephropathy (also known as Berger disease)

] IgA nephropathy is the most common cause of glomerulonephritis in the world.[2, 3]

IgA nephropathy is highly variable, both clinically and pathologically. Clinical features range from asymptomatic hematuria to rapidly progressive glomerulonephritis (RPGN). IgA nephropathy is most often associated with microscopic hematuria or recurrent macroscopic hematuria, and spontaneously resolving acute kidney injury can occur. The condition can sometimes lead to chronic kidney disease as well.

IgA nephropathy, and is more commonly seen in children and adolescents.

Fibromas (or fibroid tumors or fibroids) are benign tumors that are composed of fibrous or connective tissue.

Keratoacanthoma (KA) is a relatively common low-grade tumor that originates in the pilosebaceous glands and closely resembles squamous cell carcinoma (SCC).

Keratoacanthoma is characterized by rapid growth over a few weeks to months, followed by spontaneous resolution over 4-6 months in most cases. Keratoacanthoma may progress rarely to invasive or metastatic carcinoma.

hypopyne after cateract surgery

yellowish extudate in the anterior compartment

Hypopyon is inflammatory cells in the anterior chamber of the eye.

It is a leukocytic exudate, seen in the anterior chamber, usually accompanied by redness of the conjunctiva and the underlying episclera

Chlamydial infection can cause disease in many organ systems, including the genitourinary tract. Chlamydiae are small gram-negative obligate intracellular microorganisms that preferentially infect squamocolumnar epithelial cell

C trachomatis is a sexually transmitted microorganism that is responsible for a wide spectrum of diseases, including cervicitis, salpingitis, endometritis, urethritis, epididymitis, conjunctivitis, and neonatal pneumonia. In chlamydial infection, unlike gonorrhea, most men and women who are infected are asymptomatic; thus, diagnosis is delayed until a positive screening result is obtained or a symptomatic partner discovered.

Dystocia of labor is defined as difficult labor or abnormally slow progress of labor.

Friedman's original research in 1955 defined the following three stages of labor[1] :

The first stage starts with uterine contractions leading to complete cervical dilation and is divided into latent and active phases. In the latent phase, irregular uterine contractions occur with slow and gradual cervical effacement and dilation. The active phase is demonstrated by an increased rate of cervical dilation and fetal descent. The active phase usually starts at 3-4 cm cervical dilation and is subdivided into the acceleration, maximum slope, and deceleration phases.

The second stage of labor is defined as complete dilation of the cervix to the delivery of the infant.

The third stage of labor involves delivery of the placenta.

Pertussis (whooping cough) is a respiratory tract infection characterized by a paroxysmal cough. The most common causative organism is Bordetella pertussis

persutis

The diagnosis of pertussis is made by isolation of B pertussis in culture. A polymerase chain reaction (PCR) test can also be performed

pertiusis tx

Pharmacologic therapy

Antimicrobial agents and antibiotics can hasten the eradication of B pertussis and help prevent spread

Erythromycin, clarithromycin, and azithromycin are the preferred agents for patients aged 1 month or older

The incidence of ExtraPyramidal side effects (EPS) and the subsequent risk for tardive dyskinesia is much lower with atypicals than with conventional antipsychotics

Olanzapine currently is the only approved atypical antipsychotic for the treatment of acute mania,

atypical antipsycotic side effecy

. Common side effects of olanzapine include somnolence, orthostatic hypotension, syncope, dry mouth, and increased appetite and weight gain. The latter symptoms of increased appetite and significant weight gain have been especially difficult for some patients, as the increase in weight can be significant (average of 27 pounds after one year according to study by the manufacturer[5]) and may lead to diabetes,[6] dyslipidemia, hypertension, and other components of the metabolic syndrome.[7]

Risperidone has recently been studied in the treatment of manic symptoms and has shown efficacy in this area.[8] Side effects of this medication include an increased incidence of EPS, mainly with higher dosages, increased prolactin levels, moderate weight gain, headache, and dizziness.

side effect of quetapine

The side effects of this medication include somnolence and occasional hypotension. Quetiapine has a placebo-level incidence of EPS and prolactin.

use treatment for dementia

 (donepezil hydrochloride) Tablets

ARICEPT (donepezil hydrochloride) is a reversible inhibitor of the enzyme acetylcholinesterase,

A Glucose Challenge Test (GCT) is a non-fasting screening test which measures the level of blood sugar after the patient has had a drink which contains a specific amount of glucose. An hour later a blood test is taken to check the blood sugar level.

OGTT

The reference range of serum or plasma glucose is less than 140 mg/dL at 2 hours after a 75-g glucose load.

oGTT

After baseline fasting plasma glucose testing, a glucose load is administered—either intravenously or, more commonly, orally—and plasma glucose is measured at specified intervals thereafter.

indications for oral GTT include the following:

Equivocal fasting plasma/random plasma glucose results

To screen for gestational diabetes mellitus at 24-28 weeks of gestation in all pregnant women not known to have diabetes

To screen for diabetes mellitus at 6-12 weeks postpartum in women with a history of gestational diabetes mellitus, using nonpregnant oral GTT criteria

OGTT

As stated above, diagnosis of GDM is made if any of the following plasma glucose values are exceeded after 75 grams Glucola is given:

Fasting of 92 mg/dL or higher (5.1 mmol/L)

1 hour of 180 mg/dL or higher (10 mmol/L)

2 hour of 153 mg/dL or higher (8.5 mmol/L

glucose challenge test is used to screen for gestational diabetes. The test is generally done between weeks 24 and 28 of pregnancy

Most patients with meningococcal meningitis, caused by the gram-negative diplococcus Neisseria meningitidis, recover completely if appropriate antibiotic therapy is instituted

meningococal meningitis treatment

initial empirical therapy until the etiology is established should include dexamethasone, a third-generation cephalosporin (eg, ceftriaxone, cefotaxime), and vancomycin. Acyclovir should be considered according to the results of the initial cerebrospinal fluid (CSF) evaluation. Doxycycline should also be added during tick season in endemic areas. A 7-day course of intravenous ceftriaxone or penicillin is adequate for uncomplicated meningococcal meningitis.

The traditional risk factors for coronary artery disease are high LDL cholesterol, low HDL cholesterol, high blood pressure, family history, diabetes, smoking, being post-menopausal for women and being older than 45 for men, according to Fisher. Obesity may also be a risk factor.

Autoantibody Tests for SLE

TestDescription

ANAScreening test; sensitivity 95%; not diagnostic without clinical features

Anti-dsDNA High specificity; sensitivity only 70%; level is variable based on disease activity

Anti-SmMost specific antibody for SLE; only 30-40% sensitivity

Anti-SSA (Ro) or Anti-SSB (La)Present in 15% of patients with SLE and other connective-tissue diseases such as Sjögren syndrome; associated with neonatal lupus

Anti-ribosomal PUncommon antibodies that may correlate with risk for CNS disease, including increased hazards of psychosis in a large inception cohort, although the exact role in clinical diagnosis is debated[90]

Anti-RNPIncluded with anti-Sm, SSA, and SSB in the ENA profile; may indicate mixed connective-tissue disease with overlap SLE, scleroderma, and myositis

AnticardiolipinIgG/IgM variants measured with ELISA are among the antiphospholipid antibodies used to screen for antiphospholipid antibody syndrome and pertinent in SLE diagnosis

Lupus anticoagulantMultiple tests (eg, direct Russell viper venom test) to screen for inhibitors in the clotting cascade in antiphospholipid antibody syndrome

Direct Coombs testCoombs test–positive anemia to denote antibodies on RBCs

Anti-histoneDrug-induced lupus ANA antibodies are often of this type (eg, with procainamide or hydralazine; p-ANCA–positive in minocycline-induced drug-induced lupus)

ANA = antinuclear antibody; CNS = central nervous system; ds-DNA = double-stranded DNA; ELISA = enzyme-linked immunoassay; ENA = extractable nuclear antigen; Ig = immunoglobulin; p-ANCA = perinuclear antineutrophil cytoplasmic antibody; RBCs = red blood cells; RNP = ribonucleic protein; SLE = systemic lupus erythematosus; Sm = Smith; SSA = Sjögren syndrome A; SSB = Sjögren syndrome B.

Ankylosing spondylitis (AS), a spondyloarthropathy, is a chronic, multisystem inflammatory disorder involving primarily the sacroiliac (SI) joints and the axial skeleton. The outcome in patients with a

led poisoning cause motor neuropathy usually proxymal

myxoedema can produce mixed sensorymotor neuropathy

Manganeese, Phenothiazine, methyldopa and CO poisoning cause dopamine like syndrome

best drug of choice for post herpetic neuralgia is tricyclic anti depressions such as amitripataline.

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause.

Capture Dec 11, 2015

Friday, December 11, 2015

11:00 AM

boutonniere deformity

RA investigations

No test results are pathognomonic; instead, the diagnosis is made by using a combination of clinical, laboratory, and imaging features. Potentially useful laboratory studies in suspected RA include the following:

Erythrocyte sedimentation rate

C-reactive protein level

Complete blood count

Rheumatoid factor assay

Antinuclear antibody assay

Anti−cyclic citrullinated peptide and anti−mutated citrullinated vimentin assays

Potentially useful imaging modalities include the following:

Radiography (first choice): Hands, wrists, knees, feet, elbows, shoulders, hips, cervical spine, and other joints as indicated

Magnetic resonance imaging: Primarily cervical spine

isease-modifying antirheumatic drugs (DMARDs

Overview

Practice Essentials

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. An external trigger (eg, cigarette smoking, infection, or trauma) that triggers an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals. See the image below.

Rheumatoid changes in the hand. Photograph by David Effron MD, FACEP.

View Media Gallery

See Rheumatoid Arthritis: In and Out of the Joint, a Critical Images slideshow, to help identify the distinguishing features of RA as well as the signs of extra-articular manifestations of this disfiguring disease.

Signs and symptoms

In most patients with RA, onset is insidious, often beginning with fever, malaise, arthralgias, and weakness before progressing to joint inflammation and swelling.

Signs and symptoms of rheumatoid arthritis may include the following:

Persistent symmetric polyarthritis (synovitis) of hands and feet (hallmark feature)

Progressive articular deterioration

Extra-articular involvement

Difficulty performing activities of daily living (ADLs)

Constitutional symptoms

The physical examination should address the following:

Upper extremities (metacarpophalangeal joints, wrists, elbows, shoulders)

Lower extremities (ankles, feet, knees, hips)

Cervical spine

During the physical examination, it is important to assess the following:

Stiffness

Tenderness

Pain on motion

Swelling

Deformity

Limitation of motion

Extra-articular manifestations

Rheumatoid nodules

Guidelines for evaluation

2013 European League Against Rheumatism (EULAR) management guidelines

2010 American College of Rheumatology (ACR)/EULAR classification criteria [1]

2012 ACR disease activity measures [2]

2011 ACR/EULAR definitions of remission [3]

See Clinical Presentation for more detail.

Diagnosis

No test results are pathognomonic; instead, the diagnosis is made by using a combination of clinical, laboratory, and imaging features. Potentially useful laboratory studies in suspected RA include the following:

Erythrocyte sedimentation rate

C-reactive protein level

Complete blood count

Rheumatoid factor assay

Antinuclear antibody assay

Anti−cyclic citrullinated peptide and anti−mutated citrullinated vimentin assays

Potentially useful imaging modalities include the following:

Radiography (first choice): Hands, wrists, knees, feet, elbows, shoulders, hips, cervical spine, and other joints as indicated

Magnetic resonance imaging: Primarily cervical spine

Ultrasonography of joints: Joints, as well as tendon sheaths, changes and degree of vascularization of the synovial membrane, and even erosions

Joint aspiration and analysis of synovial fluid may be considered, including the following:

Gram stain

Cell count

Culture

Assessment of overall appearance

See Workup for more detail.

Management

Nonpharmacologic, nonsurgical therapies include the following:

Heat and cold therapies

Orthotics and splints

Therapeutic exercise

Occupational therapy

Adaptive equipment

Joint-protection education

Energy-conservation education

Guidelines for pharmacologic therapy

2013 EULAR management guidelines [4]

2012 updates to 2008 ACR recommendations for use of nonbiologic and biologic disease-modifying antirheumatic drugs (DMARDs)

2007 Agency for Healthcare Research and Quality (AHRQ) recommendations

Nonbiologic DMARDS include the following:

Hydroxychloroquine

Azathioprine

Sulfasalazine

Methotrexate

Leflunomide

Cyclosporine

Gold salts

D-penicillamine

Minocycline

Biologic TNF-inhibiting DMARDs include the following:

Etanercept

Infliximab

Adalimumab

Certolizumab

Golimumab

Biologic non-TNF DMARDs include the following:

Rituximab

Anakinra

Abatacept

Tocilizumab

Tofacitinib

Other drugs used therapeutically include the following:

Corticosteroids

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Analgesics

Surgical treatments include the following:

Synovectomy

Tenosynovectomy

Tendon realignment

Reconstructive surgery or arthroplasty

Arthrodesis

Antibodies directed against the Fc fragment of immunoglobulin G (IgG) are called rheumatoid factors (RFs).

Rheumatoid factor (RF) is used in the diagnosis of rheumatoid arthritis (RA). RF results are positive in approximately 75% of patients with RA, although RF is not etiologically related to RA.[6]

High RF titers indicate a poorer prognosis, as patients with higher RF levels tend to have more severe disease. Patients with nodules or clinical evidence of vasculitis usually have positive RF results.

Low levels of RF can even be found in healthy patients, and the test is positive in up to 20% of older individuals.

RF levels vary based on disease activity, though even patients with drug-induced remissions generally retain high titers of RF.

RF results may be positive in patients without RA who have the following conditions:

Systemic lupus erythematosus

Polymyositis

Tuberculosis

Syphilis

Viral hepatitis

Infectious mononucleosis

Influenza

Ankylosing spondylitis has a predilection for the axial skeleton, affecting particularly the sacroiliac and spinal facet joints and the paravertebral soft tissues. Extraspinal manifestations of the disease include peripheral arthritis, iritis, pulmonary involvement, and systemic upset

ankylosis spondylosis caise sacroilitis and finally fuse bith joints

Ankylosis S. treatm3nt

diagnosed by rediological immagine

1.NSAID

2.Sulfasalazine and methotrexate for peripberal atharutis

3.TNF .alfa natagonist .. infliximab

indomethazine is a good NSAID for AS.

sulfasalazin good pt who have IBD .

osteoatheritis most commonly affect interphalangial joint of the hand..not in metacarpophalangeal joint

oA

degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but the entire joint organ, including the subchondral bone and synovium

Ostioathritis

Stiffness during rest (gelling) - May develop, with morning joint stiffness usually lasting for less than 30 minutes...

in RA its more than 30 mins

Osteoarthritis of the hand

Distal interphalangeal (DIP) joints are most often affected

Proximal interphalangeal (PIP) joints and the joints at the base of the thumb are also typically involved

Pharmacologic therapy

For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends using one or more of the following:

Topical capsaicin

Topical nonsteroidal anti-inflammatory drugs (NSAIDs) - Including trolamine salicylate

Oral NSAIDs

Tramadol

For knee osteoarthritis, the ACR conditionally recommends using one of the following:

Acetaminophen

Oral NSAIDs

Topical NSAIDs

Tramadol

Intra-articular corticosteroid injections

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initial management:

Acetaminophen

Oral NSAIDs

Tramadol

Intra-articular corticosteroid injections

Polymyalgia rheumatica (PMR) is a relatively common chronic inflammatory condition of unknown etiology that affects elderly individuals.

Polymyalgia rheumatica (PMR) is a relatively common chronic inflammatory condition of unknown etiology that affects elderly individuals. It is characterized by proximal myalgia of the hip and shoulder girdles with accompanying morning stiffness that lasts for more than 1 hour. Approximately 15% of patients with PMR develop giant cell arteritis (GCA), and 40-50% of patients with GCA have associated

PMR.

treatment is law dose corticosteroid.. good prognosis is there

DRUG CLASS AND MECHANISM: Acetaminophen belongs to a class of drugs called analgesics (pain relievers) and antipyretics (fever reducers). The exact mechanism of action of acetaminophen is not known.J

for Osteoatharitis NSAIDS is not the first line drug.simple analgicis like panadol and acetominaphen  are the drug of choice..

3rd Heart sound

occur in diastalic phase

law pitch and best heard in bell

is a diastalic filling sound

occur with volume overload

not always pathological

may be normal up to the age if 30

avnormal if morebthan 40 years

implies ventriculer disease

ocuur with sever MR

contrictive pericarditis and CCF is rare cases

is not influence by AF

mitral stenosis

mid diastalic murmur(early systolic)

palpable loud 1st heart sound

opaning snap and law pitch

more prominent after exercise

systolic BP is the risk factor for strock.not diastolic BP

high right arial pressure and reised systemic venus pressure is a feature of pulmonary embolisum.

low CVP and lower atrial pressure is due to hypovolaemia

low cvp and low periperal venus pressure and low atrial pressure is dure to hypovolemic shock

high pulmonary venus pressure and pumonary edema dure to HF

10:35 AM

commonest sit eof aneurysm rupture is abdominal aota below the renal ateries

Emphysema and chronic bronchitis are airflow-limited states contained within the disease state known as chronic obstructive pulmonary disease (COPD).

Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis.

Pulsus paradoxus (PP), also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mm Hg. When the drop is more than 10 mm Hg, it is referred to as pulsus paradoxus. P

Pulsus paradoxus is a sign that is indicative of several conditions, including cardiac tamponade, pericarditis, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).[1]

ung fibrosis caused by the inhalation of dust containing silica.

mesothelium is a membrane composed of simple squamous cells that forms the lining of several body cavities: the pleura (thoracic cavity), peritoneum (abdominal cavity including the mesentery), mediastinum and pericardium (heart sac).

Mesothelioma (or, more precisely, malignant mesothelioma) is a rare form of cancer that develops from cells of the mesothelium, the protective lining that covers many of the internal organs of the body. Mesothelioma is most commonly caused by exposure to asbestos.[

sputum in asthma is typically thick

PaCO2 typically  law and if life thetning BA PaCO2 increase

repiratory

sequence of  assecing a patient

1.peak expiratory flor rate

2.ABG to checkbthe law PaCO2 level

3.CXR

PaCO2 more than 50 is a very riscky..may go to res arrest

streptococcal pneumoniae causing labar pneumonia

strapylococal and viras cause multipl site involving pneumonia

micoplasma cause dufuse changers in CXR

aspirin may induce asthma

Pneumocystis jiroveci pneumonia (PJP), formerly known as Pneumocystis carinii pneumonia (PCP), is the most common opportunistic infection in persons with HIV infection.

P jiroveci is now one of several organisms known to cause life-threatening opportunistic infections in patients with advanced HIV infection worldwide.

pneumocustic cariini While officially classified as a fungal pneumonia, PJP does not respond to antifungal treatmen

treted with  trimethoprium

Community-acquired pneumonia (CAP) is one of the most common infectious diseases and is an important cause of mortality and morbidity worldwide.

 Typical bacterial pathogens that cause the condition include Streptococcus pneumoniae (penicillin-sensitive and -resistant strains), Haemophilus influenza (ampicillin-sensitive and -resistant strains), and Moraxella catarrhalis (all strains penicillin-resistant). See the images below.

community acquried pneumonia

Atypical CAPs

The clinical presentation of atypical CAP is often subacute. In addition, patients with CAP due to atypical CAP pathogens present with a variety of pulmonary and extrapulmonary findings (eg, CAP plus diarrhea). Atypical CAP includes the following:

Psittacosis

Q fever

Tularemia

Mycoplasma pneumonia

Legionnaires disease

Chlamydophila ( Chlamydia) pneumonia

Extrapulmonary signs and symptoms seen in some forms of atypical CAP may include the following:

Mental confusion

Prominent headache

Myalgias

Ear pain

Abdominal pain

Diarrhea

Rash (Horder spots in psittacosis; erythema multiforme in Mycoplasma pneumonia)

Nonexudative pharyngitis

Hemoptysis

Splenomegaly

Relative bradycardia

community acquired pneumonia

CAP may be treated with monotherapy or combination therapy. Effective monotherapy antibiotics include macrolides(clarythro, azithro), respiratory quinolones, and, possibly, doxycycline

Combination therapy usually consists of (1) ceftriaxone plus doxycycline or azithromycin or (2) monotherapy with a respiratory quinolone for inpatient treatment of patients admitted to medical floor beds. I

mcroloide.... erythro..azithro..ect

quinolone.....cipro..levoflox

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia (CAP),

Mycoplasma pneumoniae has been identified with an increasing array of illnesses, such as acute hepatitis,[7, 8] immune thrombocytopenic purpura,[9] severe autoimmune hemolytic anemia,[10] Stevens-Johnson syndrome,[11, 12] arthritis,[13] and transverse myelitis.[1

mycoplasma infection

Antibiotic prophylaxis for exposed contacts is not routinely recommended. However, macrolide or doxycycline prophylaxis should be used in households in which patients with underlying conditions may be predisposed to severe mycoplasmal infection, such as those with sickle cell disease or antibody deficiencies.

If patients

micoplasma inf3ction_ cold agglutinings are often seen in blood

acid fast bacilli in sputum highly sugestive of active TB but not pathognomic

pott disease

Symptoms of skeletal TB may include the following:

Back pain or stiffness

Lower-extremity paralysis, in as many as half of patients with undiagnosed Pott disease

11:29 PM

Miliary TB: Numerous small, nodular lesions that resemble millet seeds

Mantoux tuberculin skin test with purified protein derivative (PPD) for active or latent infection (primary method) ...positive  if more than 5mmm in 72 hour for HIV patients

Overview

Practice Essentials

Tuberculosis (TB) (see the image below), a multisystemic disease with myriad presentations and manifestations, is the most common cause of infectious disease–related mortality worldwide. Although TB rates are decreasing in the United States, the disease is becoming more common in many parts of the world. In addition, the prevalence of drug-resistant TB is increasing worldwide.

Anteroposterior chest radiograph of a young patient who presented to the emergency department (ED) with cough and malaise. The radiograph shows a classic posterior segment right upper lobe density consistent with active tuberculosis. This woman was admitted to isolation and started empirically on a 4-drug regimen in the ED. Tuberculosis was confirmed on sputum testing. Image courtesy of Remote Medicine (remotemedicine.org).

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See 11 Travel Diseases to Consider Before and After the Trip, a Critical Images slideshow, to help identify and manage infectious travel diseases.

Signs and symptoms

Classic clinical features associated with active pulmonary TB are as follows (elderly individuals with TB may not display typical signs and symptoms):

Cough

Weight loss/anorexia

Fever

Night sweats

Hemoptysis

Chest pain (can also result from tuberculous acute pericarditis)

Fatigue

Symptoms of tuberculous meningitis may include the following:

Headache that has been either intermittent or persistent for 2-3 weeks

Subtle mental status changes that may progress to coma over a period of days to weeks

Low-grade or absent fever

Symptoms of skeletal TB may include the following:

Back pain or stiffness

Lower-extremity paralysis, in as many as half of patients with undiagnosed Pott disease

Tuberculous arthritis, usually involving only 1 joint (most often the hip or knee, followed by the ankle, elbow, wrist, and shoulder)

Symptoms of genitourinary TB may include the following:

Flank pain

Dysuria

Frequent urination

In men, a painful scrotal mass, prostatitis, orchitis, or epididymitis

In women, symptoms mimicking pelvic inflammatory disease

Symptoms of gastrointestinal TB are referable to the infected site and may include the following:

Nonhealing ulcers of the mouth or anus

Difficulty swallowing (with esophageal disease)

Abdominal pain mimicking peptic ulcer disease (with gastric or duodenal infection)

Malabsorption (with infection of the small intestine)

Pain, diarrhea, or hematochezia (with infection of the colon)

Physical examination findings associated with TB depend on the organs involved. Patients with pulmonary TB may have the following:

Abnormal breath sounds, especially over the upper lobes or involved areas

Rales or bronchial breath signs, indicating lung consolidation

Signs of extrapulmonary TB differ according to the tissues involved and may include the following:

Confusion

Coma

Neurologic deficit

Chorioretinitis

Lymphadenopathy

Cutaneous lesions

The absence of any significant physical findings does not exclude active TB. Classic symptoms are often absent in high-risk patients, particularly those who are immunocompromised or elderly.

See Clinical Presentation for more detail.

Diagnosis

Screening methods for TB include the following:

Mantoux tuberculin skin test with purified protein derivative (PPD) for active or latent infection (primary method)

In vitro blood test based on interferon gamma release assay (IGRA) with antigens specific for Mycobacterium tuberculosis for latent infection

Obtain the following laboratory tests for patients with suspected TB:

Acid-fast bacilli (AFB) smear and culture using sputum obtained from the patient: Absence of a positive smear result does not exclude active TB infection; AFB culture is the most specific test for TB

HIV serology in all patients with TB and unknown HIV status: Individuals infected with HIV are at increased risk for TB

Other diagnostic testing may warrant consideration, including the following:

Specific enzyme-linked immunospot (ELISpot)

Nucleic acid amplification tests

Blood culture

Positive cultures should be followed by drug susceptibility testing; symptoms and radiographic findings do not differentiate multidrug-resistant TB (MDR-TB) from fully susceptible TB. Such testing may include the following:

Direct DNA sequencing analysis

Automated molecular testing

Microscopic-observation drug susceptibility (MODS) and thin-layer agar (TLA) assays

Additional rapid tests (eg, BACTEC-460, ligase chain reaction, luciferase reporter assays, FASTPlaque TB-RIF)

Obtain a chest radiograph to evaluate for possible associated pulmonary findings. The following patterns may be seen:

Cavity formation: Indicates advanced infection; associated with a high bacterial load

Noncalcified round infiltrates: May be confused with lung carcinoma

Homogeneously calcified nodules (usually 5-20 mm): Tuberculomas, representing old infection

Primary TB: Typically, pneumonialike picture of infiltrative process in middle or lower lung regions

Reactivation TB: Pulmonary lesions in posterior segment of right upper lobe, apicoposterior segment of left upper lobe, and apical segments of lower lobes

TB associated with HIV disease: Frequently atypical lesions or normal chest radiographic findings

Healed and latent TB: Dense pulmonary nodules in hilar or upper lobes; smaller nodules in upper lobes

Miliary TB: Numerous small, nodular lesions that resemble millet seeds

Pleural TB: Empyema may be present, with associated pleural effusions

Workup considerations for extrapulmonary TB include the following:

Biopsy of bone marrow, liver, or blood cultures

If tuberculous meningitis or tuberculoma is suspected, perform lumbar puncture

If vertebral ( Pott disease) or brain involvement is suspected, CT or MRI is necessary

If genitourinary complaints are reported, urinalysis and urine cultures can be obtained

See Workup for more detail.

Management

Physical measures (if possible or practical) include the following:

Isolate patients with possible TB in a private room with negative pressure

Have medical staff wear high-efficiency disposable masks sufficient to filter the bacillus

Continue isolation until sputum smears are negative for 3 consecutive determinations (usually after approximately 2-4 weeks of treatment)

Initial empiric pharmacologic therapy consists of the following 4-drug regimens:

Isoniazid

Rifampin

Pyrazinamide

Either ethambutol or streptomycin [1]

Special considerations for drug therapy in pregnant women include the following:

In the United States, pyrazinamide is reserved for women with suspected MDR-TB

Streptomycin should not be used

Preventive treatment is recommended during pregnancy

Pregnant women are at increased risk for isoniazid-induced hepatotoxicity

Breastfeeding can be continued during preventive therapy

Special considerations for drug therapy in children include the following:

Most children with TB can be treated with isoniazid and rifampin for 6 months, along with pyrazinamide for the first 2 months if the culture from the source case is fully susceptible.

For postnatal TB, the treatment duration may be increased to 9 or 12 months

Ethambutol is often avoided in young children

mantaux tedt resding 48 to 72 hours

The reaction is read by measuring the diameter of induration (palpable raised, hardened area) across the forearm (perpendicular to the long axis) in millimeters. If there is no induration, the result should be recorded as "0 mm". Erythema (redness) should not be measured.

Clinical signs and symptoms for pulmonary embolism are nonspecific; therefore, patients suspected of having pulmonary embolism—because of unexplained dyspnea, tachypnea, or chest pain or the presence of risk factors for pulmonary embolism—must undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed

Pulmonary angiography is the historical criterion standard for the diagnosis of pulmonary embolism.

Ventilation perfusion scan

d dimer  not specific

50% increasing troponinenot specif8c

BNP not specific

non

The routine use of CT pulmonary angiography for the detection of pulmonary emboli has led to overdiagnosis of the condition, according to a recent study. Overdiagnosing pulmonary embolism has resulted in possible inappropriate treatment with anticoagulation, a leading cause of medication-related death

For acute PE, the ACCP guidelines recommend starting low–molecular weight heparin (LMWH) or fondaparinux, preferred over unfractionated heparin (UFH) (grade 2C for LMWH; grade 2B for fondaparinux) or subcutaneous heparin (grade 2B for LMWH; grade 2C for fondaparinux).[

pulmonary embolism treatment

Patients should have an oral anticoagulant (warfarin) initiated at the time of diagnosis, and they should have UFH, LMWH, or fondaparinux discontinued only after the international normalized ratio (INR) is 2.0 for at least 24 hours but no sooner than 5 days after warfarin therapy has been started (

omonilial esophagutis

maasthenia Gravis..

myasthenia gravis may cause dyspahgia when affect to upper 1/3 straied muscle

iron deficiancy  aneamia hypopharyngeal web

dysphagia due to motality disorder may presipitate vith cold fluid and reduce with Ca channel blockers.

solid liqvid dekatama enava

ocreotide is a long acting analog of somatostatin which inhibit  several GI hormon. use for veriveal bleeding....carcinoid T.....acromegally....ect

gluten enteropaty patients hv a risk of intestianl lymphoma

Wilson disease is a rare autosomal recessive inherited disorder of copper metabolism that is characterized by excessive deposition of copper in the liver, brain, and other tissues (see the image below). Wilson disease is often fatal if not recognized and treated when symptomatic.

Kayser-Fleischer rings

Formed by the deposition of copper in the Descemet membrane in the limbus of the cornea

more than 90 % of patient

its not pathognomic in wilson Dx

some time ut may apper in cholestatic disease

wilsoms disease test

serum ceruloplamins level low

urinary copper excretionnis high

live Bx

ect....

ttreatment for wilson disease

Features of treatment of Wilson disease are as follows:

The mainstay of therapy is lifelong use of chelating agents (eg, penicillamine, trientine)

Symptoms, particularly neurologic ones, may worsen with initiation of chelation

Surgical decompression or transjugular intrahepatic shunting (TIPS)

kaysar-fleiser ring

kayser fleischer ring - Google Search

Hepatitis B

compaierd to non carriers,carries hv 100 % increse risk  to hv heoato celluer CA

alpa interferon may efectively remove HepB Ag from blood .but Hep B SAg wil not be removed.

95% maternal fetal tensmission  occur at delevery..only 5 % in utero

if HBsAg positive mother deliver a baby we shoud inject hep B hyper immunuglobin andbthen vacinate the baby.

Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and altered bowel habits in the absence of a specific and unique organic pathology, although microscopic inflammation has been documented in some patients

Diagnosisof IBS

The Rome III criteria for the diagnosis of irritable bowel syndrome[3] require that patients have had recurrent abdominal pain or discomfort at least 3 days per month during the previous 3 months that is associated with 2 or more of the following:

Relieved by defecation

Onset associated with a change in stool frequency

Onset associated with a change in stool form or appearance

Supporting symptoms include the following:

Altered stool frequency

Altered stool form

Altered stool passage (straining and/or urgency)

Mucorrhea

Abdominal bloating

Enterotoxigenic Escherichia coli cause travellers diarrhoes

colonic CA

colonic cancer develop with colonic adenoma in most of the time

more common adenoma is villous adenoma

Colon cancer is the most common type of gastrointestinal cancer.

Ulcerative colitis (UC) is one of the 2 major types of inflammatory bowel disease (IBD), along with Crohn disease. Unlike Crohn disease, which can affect any part of the gastrointestinal (GI) tract, UC characteristically involves only the large bowel

ulcerative colitis

UC is associated with various extracolonic manifestations, as follows:

Uveitis

Pyoderma gangrenosum

Pleuritis

Erythema nodosum

Ankylosing spondylitis

Spondyloarthropathies

Other conditions associated with UC include the following:

Primary sclerosing cholangitis (PSC)

Recurrent subcutaneous abscesses unrelated to pyoderma gangrenosum [1]

Multiple sclerosis [2]

Immunobullous disease of the skin [3]

management of ulcerative colitis

Medical treatment of mild UC includes the following:

Mild disease confined to the rectum: Topical mesalazine via suppository (preferred) or budesonide rectal foam

Left-side colonic disease: Mesalazine suppository and oral aminosalicylate (oral mesalazine is preferred to oral sulfasalazine)

Systemic steroids, when disease does not quickly respond to aminosalicylates

Oral budesonide

After remission, long-term maintenance therapy (eg, once-daily mesalazine)

Medical treatment of acute, severe UC may include the following:

Hospitalization

Intravenous high-dose corticosteroids

Alternative induction medications: Cyclosporine, tacrolimus, infliximab, adalimumab, golimumab

Mesalazine (INN, BAN), also known as mesalamine (USAN) or 5-aminosalicylic acid (5-ASA), is an anti-inflammatory drug used to treat inflammatory bowel disease, such as ulcerative colitis and mild-to-moderate Crohn's disease.

Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days.

diarrhea in children

Use of child daycare (common pathogens: rotavirus, astrovirus, calicivirus; Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp]

causes for children diarhea

Use of child daycare (common pathogens: rotavirus, astrovirus, calicivirus; Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp])

diarrhea following travel

Travel history (common pathogens affect specific regions; also consider rotavirus and Shigella, Salmonella, and Campylobacter spp regardless of specific travel history, as these organisms are prevalent worldwide)

diarrhea

pH level: A pH level of 5.5 or less or the presence of reducing substances indicates carbohydrate intolerance, which is usually secondary to viral illness

culture following diarrhea

Cultures: Always culture for Salmonella, Shigella, and Campylobacter spp and Y enterocolitica in the presence of clinical signs of colitis or if fecal leukocytes are present; look for Clostridium difficile in those with diarrhea characterized by colitis and/or bloody stools; assess for Escherichia coli, particularly O157:H7, with bloody diarrhea and a history of eating ground beef; screen for Vibrio and Plesiomonas spp with a history of eating raw seafood or foreign travel

chlera is due to bacteria

Cholera is an intestinal infection caused by Vibrio cholerae

cholerae is a comma-shaped, gram-negative aerobic or facultatively anaerobic bacillus

cholera

After a 24- to 48-hour incubation period, symptoms begin with the sudden onset of painless watery diarrhea that may quickly become voluminous and is often followed by vomiting. The patient may experience accompanying abdominal cramps,

cholera watery diarrhea

Amebiasis is caused by Entamoeba histolytica (see the image below), a protozoan that is found worldwid

Amebic liver abscess is the most common manifestation of invasive amebiasis, but other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites.

amebiasis primarily affects migrants from and travelers to endemic regions,

E histolytica is transmitted via ingestion of the cystic form (infective stage) of the protozoa

ameabisis

Excystation then occurs in the terminal ileum or colon, resulting in trophozoites (invasive form). The trophozoites can penetrate and invade the colonic mucosal barrier, leading to tissue destruction, secretory bloody diarrhea, and colitis resembling inflammatory bowel diseas

Amebic liver abscess is the most common manifestation of invasive amebiasis, but other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites.

amebiasis primarily affects migrants from and travelers to endemic regions,

E histolytica is transmitted via ingestion of the cystic form (infective stage) of the protozoa

The presence of intracytoplasmic RBCs in trophozoites is diagnostic of E histolytica infection, though some studies have demonstrated the same phenomenon with E dispar.

shigellosis

Stool leukocytes may be found, but in fewer numbers than in shigellosis.

polymops leucocysts

Acute management of paroxysmal supraventricular tachycardia(PSVT) includes controlling the rate and preventing hemodynamic collapse. If the patient is hypotensive or unstable, immediate cardioversion with sedation must be performed. If the patient is stable, vagal maneuvers can be used to slow the heart rate and to convert to sinus rhythm. If vagal maneuvers are not successful, adenosine can be used in increasing doses. If adenosine does not work, atrioventricular (AV) nodal blocking agents like calcium channel blockers or beta-blockers should be used, as most patients who present with PSVT have AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT). These arrhythmias depend on AV nodal conduction and therefore can be terminated by transiently blocking this conduction.

Patients with symptomatic Wolff-Parkinson-White (WPW) syndrome should not be treated with calcium channel blockers or digoxin unless the pathway is known to be of low risk (long anterograde refractory period). This is because of the potential for rapid ventricular rates should atrial fibrillation or atrial flutter occur, which can result in cardiac arrest.

Pleural plaques are deposits of hyalinized collagen fibers in the parietal pleura. They are indicative of asbestos exposure and typically become visible twenty or more years after the inhalation of asbestos fibers, although latency periods of less than 10 years have been observed

plueral plaqs

The formal diagnosis of COPD is made with spirometry; when the ratio of forced expiratory volume in 1 second over forced vital capacity (FEV1/FVC) is less than 70% of that predicted for a matched control, it is diagnostic for a significant obstructive defect. Other studies, including laboratory studies and imaging, are particularly important during acute exacerbations of disease.

No blood-based biomarkers are accepted in COPD.

everal classes of antihypertensive agents may have a role in the treatment of CKD and HTN. Agents that target the renin-angiotensinaldosterone system (RAAS), such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), are generally considered first-line antihypertensive therapy for this patient population.[8,9,18] Table 2 provides guidance on recommended antihypertensive agents for patients with CKD with or without diabetes and with or without proteinuria.