¤ 5–10% of cholecystectomies

¤ More fulminant than calculous cholecystitis; may present w/ gangrene, perforation, & empyema.

¤ Risk factors: sepsis, ICU, TPN, immunosuppression, major trauma,

burns, diabetes, infections, mechanical ventilation, opiates, CHD & CABG, prolonged fasting, childbirth, nonbiliary surgery, & AIDS rarely seen in systemic vasculitides due to ischemic injury to gall bladder.

¤ Insidious presentation in already critically ill pts.

¤ Elderly

¤ Male predominance (80%)

Signs & Symptoms:

¤ Clinical presentation variable, depending on predisposing conditions

¤ RUQ pain absent in 75% of cases

¤ Fever or hyperamylasemia may be only clue

¤ Unexplained sepsis w/ few early localizing signs.

¤ Half of patients already have experienced complication: gangrene,

perforation, abscess.

¤ RUQ pain, fever, & positive Murphy sign seen in minority.



¤ Leukocytosis w/ left shift in 70–85%

¤ Hyperamylasemia common

¤ Abnormal aminotransferases, hyperbilirubinemia, mild increase in serum alkaline phosphatase more common in acalculous than calculous cholecystitis.


¤ Plain x-ray: exclusion of a perforated viscus, bowel ischemia, or renal stones

¤ US: absence of gallstones, thickened gallbladder wall

° (>5 mm) w/ pericholecystic fluid, failure to visualize

° gallbladder, perforation w/ abscess, emphysematous cholecystitis; sensitivity of 36–96%; high false-negative rate.

° CT: thickened gallbladder wall (>4 mm) in absence of ascites or hypoalbuminemia, pericholecystic fluid, intramural gas, or sloughed mucosa; superior to US w/ sensitivity of 50–100%.

¤ Radionuclide cholescintigraphy (HIDA) scan: failure to opacify gallbladder; sensitivity almost 100%; false-positive rate of up to 40% in which gallbladder not visualized in spite of nonobstructed cystic

duct seen in severe liver disease, prolonged fasting, biliary sphincterotomy, hyperbilirubinemia; important not to allow test to delay treatment in very ill pts.

Differential diagnosis:

¤ Calculous cholecystitis, peptic ulceration, acute pancreatitis, rightsided pyelonephritis, hepatic or subphrenic abscess.


What to Do First

¤ CT: best test to exclude other pathology

¤ If suspect biliary sepsis, radionuclide study first; otherwise, CT first

General Measures:

¤ Blood cultures, IV broad-spectrum antibiotics

¤ Early recognition & intervention required due to rapid progression to gangrene & perforation.

Specific therapy:

¤ Cholecystectomy; both open & laparoscopic

¤ If evidence of perforation, then open cholecystectomy urgently; inflammatory mass may preclude successful laparoscopy.

¤ US-guided percutaneous cholecystostomy may be first choice in critically ill pts; success rate 90%; no surgery necessary if postdrainage

cholangiogram normal; catheter usually removed 6–8 wk.

¤ Transpapillary endoscopic drainage of gallbladder may be done when pt too sick for surgery & unsuitable for percutaneous drainage(massive ascites or coagulopathy).


¤ Routine post op. follow-up

complications and prognosis:

¤ <10% mortality in community-acquired cases.

¤ Up to 90% in critically ill pts.

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What is bacterial meningitis?

Meningitis is an infection of the membranes (meninges) that protect the spinal cord and brain. When the membranes become infected, they swell and press on the spinal cord or brain. This can cause life-threatening problems. Meningitis symptoms strike suddenly and worsen quickly.


¤ Increased risk with exposure to meningococcal meningitis or travel

to meningitis belt (sub-Saharan Africa), but most cases sporadic.

¤ Increased incidence with extremes of age, head trauma, immuno-suppression.

What are the causes of bacterial meningitis?

Several different bacteria can cause meningitis:

Streptococcus pneumoniae

Haemophilus influenzae

Neisseria meningitidis 

What are the symptoms of bacterial meningitis?

Painful, stiff neck with limited range of motion.


High fever.

Feeling confused or sleepy.

Bruising easily all over the body.

A rash on the skin.

Sensitivity to light.



¤ Prodromal upper respiratory tract infection progresses to stiff neck,fever, headache, vomiting, lethargy, photophobia, rigors, weakness,

seizures (20–30%).

¤ Fever, nuchal rigidity, signs of cerebral dysfunction; 50% with Neisseria meningitidis meningitis have an erythematous, macular rash that progresses to petechiae or purpura.

¤ Cranial nerve palsies (III, VI, VII, VIII) in 10–20%

¤ Elderly may to have lethargy or obtundation without fever, +/-meningismus.



¤ Basic Blood Tests:

° Elevated WBC

¤ Specific Diagnostic Tests:

° Blood cultures are often positive

° Typical cerebrospinal fluid (CSF) in bacterial meningitis (normal): opening pressure >180 mm H2O (50–150); color turbid (clear); WBC >1000/mm3 with polymorphonuclear cell predominance (5); protein >100 mg/dL (15–45); glucose <40 mg/dL (40–80); CSF/blood glucose ratio <0.4 (>0.6); Gram stain of CSF

shows organisms in 60–90%

° Culture of CSF is positive in 70–85%; community-acquired acute bacterial meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, Haemophilus

influenzae, Escherichia coli, group B streptococcus

° Antigen testing for specific pathogens appropriate when a purulent CSF specimen has a negative Gram stain and culture, sensitivity 80%

¤ Other Tests:

° Patients with evidence of ICP such as coma or papilledema or focal neurologic findings (seizures, cranial neuropathies) should have a noncontrast CT scan prior to lumbar puncture (LP); begin antibiotics before CT scan

Differential diagnosis:

¤ Bacteremia, sepsis, brain abscess, seizure disorder, aseptic meningitis (CSF WBC usually 100–1000/mm3, eventually with lymphocyte predominance), skull fracture, chronic meningitis, encephalitis,

migraine headache, rickettsial infection, drug reaction


What to Do First

¤ Medical emergency: do not delay appropriate antibiotic therapy

¤ Quick neurologic exam looking for focality or evidence of increased ICP.

¤ Blood culture × 2

¤ If increased ICP or focality, start empiric antibiotics based on patient’s age and circumstances and send for CT of head without contrast

¤ If CT nonfocal and safe for LP, proceed to lumbar puncture.

¤ If neurologic exam normal, LP and base therapy on STAT Gram stain of CSF

¤ If CSF consistent with bacterial meningitis and positive Gram stain, start specific antibiotics. If consistent with bacterial meningitis with a negative CSF Gram stain, start empiric antibiotics

General Measures:

¤ Rigorous supportive care

¤ Dexamethasone IV before antibiotics and q6h × 2 d for children >1 mo and consider for adults with increased ICP or coma

Specific therapy


¤ If strongly suspect meningitis, start IV antibiotics as soon as blood cultures drawn

Treatment options:

¤ Empiric antibiotics (1):

° Age 18–50: ceftriaxone or cefotaxime +/-vancomycin (2)

° >50 years: ampicillin + ceftriaxone or cefotaxime +/− vancomycin (2)

° Immunocompromised: vancomycin + ampicillin + cetazadime

° Skull fracture: ceftriaxone or cefotaxime +/− vancomycin (2)

° Head trauma, neurosurgery, CSF shunt: vancomycin + ceftazadime

¤ Positive CSF Gram stain in community-acquired meningitis (1):

° Gram-positive cocci: ceftriaxone or cefotaxime + vancomycin (1)

° Gram-positive rods: ampicillin or penicillin G +/− gentamicin

° Gram-negative rod: ceftriaxone or cefotaxime

(1) Modify antibiotics once organism and its susceptibility are known; organism must be fully sensitive to antibiotic used.

(2) If prevalence of third-generation cephalosporin-intermediate + resistant S. pneumoniae exceeds 5%, add vancomycin until organism proved susceptible; if intermediate or resistant to cephalosporins, continue vancomycin and ceftriaxone or cefotaxime for possible synergy; if penicillin-susceptible, narrow to penicillin G; if penicillin-non-susceptible. and cephalosporin-susceptible, narrow to third-generation cephalosporin

¤ If dexamethasone used with vancomycin, consider adding rifampin

to increase vancomycin entry into CSF.


During Treatment

¤ Look for contiguous foci (sinusitis, mastoiditis, otitis media) or distant infection (endocarditis, pneumonia) with S pneumoniae

¤ Narrow coverage as culture results and susceptibility data allow

¤ If patient on adjunctive corticosteroids and not improving as expected, or if pneumococcal isolate, repeat LP 36–48 hours after starting antibiotics to document CSF sterility.

¤ Treat close contacts of patients with N meningitidis to eradicate carriage. If not treated with a third-generation cephalosporin, the patient should receive chemoprophylaxis as well.

complications and prognosis:

A- Complications:

¤ Seizures, coma, sensorineural hearing loss, cranial nerve palsies, obstructive hydrocephalus, subdural effusions, CSF fistula (especially likely with recurrent meningitis), syndrome of inappropriate

antidiuretic hormone

¤ Consider placing ICP monitoring device

¤ ICP >15–20, elevate head to 30 degrees, hyperventilate adults

B- Prognosis:

¤ Average case fatality: 5–25%

¤ N meningitidis: 3–13%

¤ S pneumoniae: 19–26%

¤ L monocytogenes: 15–29%

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Actinic keratosis

Actinic keratoses are scaly spots or patches on the top layer of skin. With time they may become hard with a wartlike surface. An actinic keratosis is a rough, scaly patch on the skin that develops from years of sun exposure.

Actinic keratosis is an abnormal growth of cells caused by long-term damage from the sun,They are not cancerous, but a small fraction of them will develop into skin cancer. Because we don't know which ones will become cancer and which will not, dermatologists recommend treatment of these lesions.


¤ also called solar keratosis, senile keratosis

¤ This disorder is the earliest clinical manifestation of squamous cell carcinoma

¤ disease of the older adult with chronic sun-damaged skin

¤ risk factors: fair skin, blue eyes, red or blonde hair, years of ultraviolet radiation exposure through work (e.g., farmers, mail carriers, etc.) or through leisure activities (tanning bed use, tanning)

¤ Patients who are organ transplant recipients are prone to developing

many actinic keratoses, and malignant transformation (progression) is much more common in this setting.

¤ sun-exposed distribution most often on the head, neck, forearms or dorsal hands of men, and these areas plus the legs in women.

¤ poorly circumscribed erythematous macules, papules, or plaques,several millimeters to a centimeter in diameter

adherent, “sandpaper-like” scale

¤ may form a hypertrophic, verrucous surface and become a horn

¤ occasionally hyperpigmented

¤ may be tender


¤ The diagnosis is clinical.

¤ If the diagnosis is in question, a biopsy may be performed.

differential diagnosis

¤ Bowen’s disease (squamous cell cancer in situ)

¤ Squamous cell cancer

¤ Basal cell cancer

¤ Seborrheic keratosis – sharp demarcation, stuck on appearance,


¤ Suncreens, sun protective clothing and alteration of behavior lessen the chance of development of new lesions.

¤ Low-fat diet may also result in a lower rate of appearance of new lesions.

¤ Smoking cessation

specific therapy

¤ Liquid nitrogen application (destructive)

¤ Curettage with desiccation

¤ topical application

° 5-Fluorouracil

° imiquimod

° diclofenac

° tretinoin

¤ Photodynamic therapy


¤ 6–8 weeks after therapy the patient should be re-examined.

¤ 6 months to 1 year for treatment response and examination for new lesions

complications and prognosis:

¤ patient population is prone to develop new lesions despite avoidance of further ultraviolet exposure

¤ estimated 10% chance of at least one lesion developing into squamous cell cancer after 10 years if left untreated.

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¤ Enlargement of hands and feet

¤ Prognathism and loose teeth

¤ Increased sweating

¤ Sleep apnea and snoring

¤ Diabetes mellitus

¤ Coarsening change in facial appearance

¤ Frontal bossing

¤ Carpal tunnel syndrome

¤ Infertility

¤ Amenorrhea or oligoamenorrhea

¤ Family history of pituitary tumor

¤ Excessive linear growth (in children).

Signs & Symptoms:

¤ Headache

¤ Arthralgias

¤ Impotence

¤ Skin tags

¤ Decreased libido

¤ Visual field cut

¤ Hypopituitarism

¤ Galactorrhea in some women.



¤ Basic blood studies:

° Insulin-like growth factor-I (IGF-I) single best test

° growth hormone (GH) 1 h after 75-g glucose load: <5 ng/dL in normals

¤ Ancillary blood tests:

° LH, FSH, prolactin, free T4, TSH

° Testosterone

° Estradiol

° GH-releasing hormone

° Fasting serum glucose, HgA1c


¤ MRI of the pituitary to determine if there is pituitary mass.

differential diagnosis:

¤ GH-secreting pituitary tumor

¤ GH- and prolactin-secreting pituitary tumor

¤ GH- or GHRH-secreting neuroendocrine tumor (e.g., islet cell tumor of the pancreas).

¤ Acromegaloidism: acromegalic facies in patient with severe insulin resistance.


What to Do First:

¤ Assess size and resectability of tumor

specific therapy

¤ Surgical resection of tumor (usually transsphenoidal), esp. if there is visual field cut.

¤ Medical therapy:

° Somatostatin analog (octreotide or long-acting octreotide) given parenterally; can normalize serum IGF-I and GH; some tumor shrinkage

¤ Dopamine agonists (bromocriptine or cabergoline): may lower IGF-I and GH in some cases; often require high doses

¤ GH antagonists (pegvisomant) : very effective at lowering serum IGF-I; increases serum GH. Follow LFTs.

¤ Radiation therapy if surgery and medical therapy fail; may take up to 10 y to normalize serum IGF-I and GH; often causes hypopituitarism.

¤ Observation with repeated pituitary MRI to determine if tumor is growing

Treatment Goals:

¤ Normalize serum IGF-I level

¤ Normalize GH response to glucose load

¤ Diminish size of pituitary tumor

¤ Maintain normal pituitary function

¤ Fertility

¤ Cessation of galactorrhea

¤ Restoration of libido and potency.

Side Effects & Contraindications:

¤ Surgery and radiation: hypopituitarism

¤ Octreotide: gallstones and gastric upset

¤ Bromocriptine and cabergoline: gastric upset, nasal stuffiness,orthostatic hypotension with initial doses.


¤ Serum IGF-I postoperatively or 2 wks after changing dose of medicine

¤ Repeat pituitary MRI after 3–6 mo to assess pituitary growth.

complications and prognosis:

¤ Pituitary apoplexy (in patients with macroadenomas):

° Presents as very severe headache, altered consciousness, coma

° Requires emergent surgical intervention and resection of tumor

¤ Visual field changes signify tumor growth

¤ Patients require lifelong observation

¤ Increased risk of colonic polyps and perhaps colon cancer

¤ Osteoarthritis

¤ Increased risk of early mortality (cardiac) if not cured (normal IGF-I levels).

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¤ May exist transiently during neonatal period

¤ Commonly begins during early puberty with increased activity throughout the teens with spontaneous resolution thereafter (strong genetic influence recognized)

¤ May begin at or persist into later ages

¤ May result from exposure to various oils, greases, etc. found in cosmetics, pomades, or industry.

¤ May result from or be exacerbated by hormones - Polycystic ovary disease, insulin resistance, hyperandrogenism, Cushing’s disease.

¤ Complication of various drugs: corticosteroids, lithium, iodide/bromide, anticonvulsants.

Signs & Symptoms:

¤ Primary lesion = microcomedo (clinically unrecognizable = microscopic plugging of pilosebaceous unit).

¤ First clinically recognizable lesions are open comedones (“black-heads”) and/or closed comedones (“whiteheads”).

¤ Earliest stages most common on forehead and across nose and chin.

¤ Later stages of development include inflammatory papules (1–5 mm) and pustules.

¤ Most advanced lesions are cystic and/or nodular (> = 5 mm) with a predilection for lateral cheeks, chin and in more severe cases the chest and upper back (acne conglobata)

¤ Evaluate for signs of endocrinologic disease – hirsutism, striae, Cushingoid facies.


¤ Laboratory – routine: none except when indicated for specific therapies

¤ Screening. Woman with severe or recalcitrant acne (or the onset or recurrence of acne beyond their late twenties) should have at least a measurement of their free testosterone and dehydroepiandrosterone sulfate levels to consider polycystic ovarian disease or Stein-Leventhal syndrome.

differential diagnosis:

¤ Pityrosporum or bacterial folliculitis more likely to occur on trunk, buttocks, and proximal extremities with follicular-based papules or pustules

¤ Acne keloidalis nuchae occurs as firm 2- to 5-mm papules on the occiput of African-American men

¤ Pseudofolliculitis barbae occurs as firm papules and occasionally pustules to beard areas of African-American men

¤ Hidradenitis suppurativa occurs within the axillae, under the breasts and the inguinal areas with larger cysts and sinus tract formation.

¤ Rosacea – more central facial and/or perioral, more common in adults, lack of comedones management.

What to Do First:

¤ Assess type and distribution of acne lesions – comedonal v. inflammatory v. cystic

General Measures:

¤ Keratolytic or antibacterial cleansers: salicylic acid, benzoyl peroxide, sulfur

¤ Topical vitamin A acid (and similar agents): tretinoin, Adapalene, tazarotene

¤ Topical antibiotics: erythromycin, Clindamycin, sulfacetamide preparations (both erythromycin and clindamycin may be combined with benzoyl peroxide).

¤ Oral antibiotics: Tetracycline, Doxycycline, or Minocycline

¤ Less commonly: sulfones, sulfamethoxazole-trimethoprim, Erythromycin, ampicillin or cephalosporins

¤ Oral retinoids: Isotretinoin 1 mg/kg/d for 16–20 weeks for severe cases

¤ Other Therapies

¤ Azaleic acid (topical), spironolactone, intralesional triamcinolone acetonide for individual inflamed lesions, very rarely oral corticosteroids.

¤ No role for dietary manipulation has been proven.

specific therapy:

¤ Keratolytic agents: Indicated for early acne forms, side effects may include irritation

¤ Topical vitamin A acid: indicated for early and more advanced acne stages. For pregnant patients discuss use with obstetrician.

¤ Topical antibiotics: Best for early papulopustular acne. Cream, lotion and gel bases

¤ should be matched with patient’s tolerance and preference, irritation possibly

¤ Oral antibiotics: Indicated for moderate to severe papulopustular acne and early stages

¤ of cystic acne.

° Minocycline use rarely complicated by pigment deposition, a lupus-like syndrome and reports of depression.

¤ Oral Retinoids

° Indication: Severe, recalcitrant nodulocystic acne +/− scarring.

¤ Laser/related modalities: limited by availability and cost restraints.


¤ Allow 6–8 weeks for topical or oral antibiotic therapies to take effect

¤ Expect gradual improvement over months with these agents

¤ Add to or alter these regimens at 6–8 week intervals

¤ Once control is established, may need to see patient only every 6–12 months

¤ With oral retinoid use, patients should be seen monthly with appropriate laboratory studies to include: CBC, liver function panel, lipid panel, +/− pregnancy test, +/− BUN and creatinine.

(Note: registration in the “iPLEDGE” program now mandatory for those prescribing, taking or dispensing Isotretinoin.)

¤ Standard course of Isotretinoin is 5 months, but may be repeated in selected individuals

complications and prognosis:


¤ Scarring: Occurs in nearly 100% of untreated cystic acne patients

° Occurs in approximately 25–50% of papulopustular patients (increased risk if lesions are excoriated or otherwise manipulated).

¤ Keloid formation: 10–20% of cystic patient, especially prominent on central chest and shoulders.

¤ Psycho-social considerations

° Depression or withdrawal occurs in a minority of patients.

° Does not necessarily correlate with severity of acne.

° Should be monitored for at each visit with early intervention, if indicated.


¤ Excellent with early, appropriate level of intervention.

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Pain can be categorized by location or syndrome. In most persons with the complaints described below, usually the pain, not the underlying pathology, prevents them from achieving a productive and satisfying lifestyle.

Low Back Pain:

Most persons receiving physical therapy for pain complain of low back pain (LBP).15 Approximately 3 to 7% of the population in Western industrialized countries experience chronic LBP. The impairment and disability associated with LBP often results in job absenteeism, loss of productive activity, and decreased participation.

The most common causes of LBP are injury or stress resulting in musculoskeletal and neurologic disorders in the lumbosacral region (e.g., disc lesions, muscle spasm, sciatica).

Pain may also result from infections, degenerative diseases, malignancies, and aging. Poor posture may cause spinal disk degeneration and thus lead to LBP. LBP tends to improve spontaneously over time.


Migraine and tension headaches are very common chronic pain complaints. Approximately 28 million Americans, roughly 18% of women and 6% of men, experience recurrent migraine headaches. Experimental evidence supports the role of serotonin in migraine. Stress, attention, and mood (e.g., anxiety) affect these headaches. In contrast, tension headaches are generally considered to be muscular in origin. There is not sufficient evidence, however, for a specific pathophysiology.

Myofascial Pain Syndrome:

Myofascial pain syndrome (MPS) refers to a large group of muscle disorders characterized by highly sensitive trigger

points within muscles or connective tissue. Myofascial pain is predominant and is perceived as a continual dull ache often located in the head, neck, shoulder, and low back areas. The trapezius muscle is one of the most commonly affected muscles. Myofascial pain may result from an acute strain caused by a sudden overload or overstretching of the muscle.


The prevalence of fibromyalgia ranges from 0.7 to 3.2% in the adult population. Fibromyalgia should not be confused with MPS. Although MPS and fibromyalgia may overlap clinically, they are two distinct pain syndromes. Skeletal muscles have been implicated as the cause of fibromyalgia, but no specific

abnormalities have been identified. Abnormalities of the neuroendocrine system, autoimmune dysfunction, immune regulation, sleep disturbances, and cerebral blood flow difficulties have also been suggested.

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history & physical

Risk Factors

¤ Family history of liver, neurologic, and/or psychiatric disease.

Symptoms and Signs

¤ Symptoms rare before 5 years of age

¤ Hepatic disease

° Asymptomatic with biochemical abnormalities

° Chronic hepatitis, with or without fatigue

° Cirrhosis with symptoms & signs of liver failure

° Fulminant hepatitis with or without intravascular hemolysis

¤ Neurologic disease

° Kayser-Fleischer rings in 90–100% with neurologic disease

° Dystonia with rigidity, contractures, bradykinesia, & cognitive impairment

° Tremors & ataxia

° Dysarthria, dyskinesia, & organic personality syndrome

¤ Psychiatric disease

° Symptoms present in almost all patients with neurologic disease

° Early symptoms: subtle behavioral changes, with deterioration of academic or work performance

° Late symptoms: emotional lability, depression, impulsive behavior, personality changes

° Rare: schizophreniform psychosis, anxiety, cognitive impairment

¤ Symptomatic arthropathy

¤ Azure lunulae (blue discoloration of fingernail base)

¤ Abdominal pain related to cholelithiasis.


Basic Tests: Blood

¤ Low serum ceruloplasmin in 90% of all patients & 65–85% of patients with hepatic manifestations with hepatic manifestations cirrhosis.

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Abscess and Fistula

Risk Factors

¤ Recent abdominal surgery

¤ Penetrating or blunt abdominal trauma

¤ Perforation of appendix or colonic diverticulum

¤ Perforation associated with intra-abdominal malignancy

¤ Crohn disease

¤ Chronic diseases, eg, cirrhosis, renal failure

¤ Drugs: corticosteroids & chemotherapy

¤ Prior radiotherapy.


¤ High spiking fevers w/ chills

¤ Abdominal pain

¤ Nausea & vomiting

¤ Hiccups

¤ Chest pain

¤ Dyspnea

¤ Shoulder pain.

Signs & Symptoms

¤ Tachycardia

¤ Abdominal tenderness

¤ Ileus

¤ Pleural effusion

¤ Basilar rales.


Basic Blood Tests

¤ Leukocytosis w/ left shift

¤ Anemia

¤ Non-specific elevation of bilirubin & liver enzymes.

Specific Diagnostic Tests

¤ Positive blood cultures

¤ Positive cultures from aspiration of abscess

¤ Most common aerobes: E coli & Enterococcus

¤ Most common anaerobes: Bacteroides.


¤ Plain abdominal & chest films: air-fluid levels in area of abscess , elevation of right diaphragm in subphrenic abscess.

¤ Gallium scan: useful for smaller abscess not well seen on imaging.

¤ CT: imaging modality of choice for identification of abscess; also allows aspiration for culture.

¤ US: less sensitive for abdominal abscesses.

¤ Charcoal or methylene blue: oral administration with detection in drainage from fistula.

Differential diagnosis

¤ Necrotic tumors.


What to Do First

¤ Complete diagnostic studies, particularly imaging, for localization & aspiration.

General Measures

¤ Initiate general supportive care: fluid & electrolyte replacement, establish feeding (TPN if fistula present), oxygenation if needed.

¤ Swan-Ganz catheter, mechanical ventilation &/or vasopressors if unstable.

Specific therapy

¤ Adequate drainage of abscess either percutaneously or by surgery

¤ Surgery indicated if pt fails to respond to percutaneous drainage in 1–2 days.

¤ Establish adequate drainage of enterocutaneous fistulas, eg, open recent surgical excision, use of percutaneous catheters

¤ Surgery for complex fistulas or failure to resolve w/ external drainage & TPN

¤ Antibiotics: broad spectrum initially, & then based on culture results.


¤ Frequent clinical evaluation early after drainage

¤ Serial imaging when treated w/ catheter drainage to confirm catheter w/i abscess & abscess closed.

Complications and Prognosis


¤ Multiorgan failure leading to death

¤ Recurrent abscess

¤ Fistula formation

¤ Bowel obstruction

¤ Pneumonia

¤ Pleural effusion.


¤ Good with adequate drainage & response to antibiotic.



Human & Disease




¤ Most common during operative procedures involving major veins or cardiopulmonary bypass.

¤ Penetrating trauma to chest

(air from lung)

¤ Insertion or removal of large bore venous lines Carbon dioxide embolus from laparoscopic insufflation.

¤ Can occur with right to left shunt

(VSD, etc.)

¤ Source of air usually massive.


¤ Cardiovascular collapse

¤ Failure to respond to usual resuscitation



¤ EKG may show ischemic changes with coronary air embolus.

¤ If intraoperative TEE is in use, intracardiac air will be seen differential diagnosis.

¤ Pulmonary embolism

° Usually in ward patient with DVT

° Rarely occurs intraoperatively

¤ Stroke

° Intraoperative embolic stroke rarely causes cardiovascular collapse

¤ Myocardial Infarction

° Severe ischemia seen on EKG

¤ Traumatic cardiac tamponade

° Echocardiogram or surgical exploration

¤ Tension pneumothorax

° Hyper-resonant breath sounds

° Diagnose + treat with needle thoracostomy.



¤ Position patient head down, left side down

° Keeps air in apex of right ventricle where slow reabsorption occurs

¤ Cardiorespiratory support

° Intubation + mechanical ventilation

° 100% FiO2 to help reabsorption

(creates nitrogen gradient)

° Volume + pressors as needed

¤ Find and correct source of air embolism

° Close hole in vein

° Flush all lines

° Check bypass machine and connections.

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1. Nerve conduction studies (NCS) and needle electromyography (EMG) are the most useful diagnostic tests in determining the presence, type, severity, and chronicity of a suspected neuromuscular disorder.

2. Although the information collected during NCS and needle EMG testing is more objective and quantitative than that obtained by a standard clinical examination, there are many important technical factors that contribute to the collection of accurate data. Selection of a reputable or accredited laboratory and experienced electrodiagnostic consultant will help ensure the most accurate data and reliable interpretation.

3. Sensory NCS are the most useful way to distinguish preganglionic (radiculopathy) from postganglionic (peripheral neuropathy or plexopathy) processes that cause numbness.

4. NCS can help distinguish between demyelinating and axonal neuropathies. Demyelinating neuropathies have moderate to severe slowing of the nerve conduction velocities with relatively preserved compound muscle action potential (CMAP)/sensory nerve action potential (SNAP) amplitudes. On the other hand, axonal neuropathies have reduced CMAP/SNAP amplitudes with relatively preserved conduction velocities.

5. On EMG, the motor unit action potentials (MUAPs) in neurogenic disorders have characteristic large amplitudes with long durations and reduced recruitment. The MUAPs in myopathic disorders have small amplitudes with short durations and early recruitment.

¤ What is an EMG ?

It is a term used in two ways:

• As a general description of the combination of NCS and needle EMG testing.

• More specifically, to describe the needle electrode recording performed to assess the function of motor units.

¤ What is an NCS ?

NCS may be performed on either sensory or motor nerves. From the skin surface, a brief electrical stimulus is applied to the nerve of interest, and the evoked electrical signal is recorded distally from another point in the nerve in the case of a sensory nerve or from the innervated muscle in the case of a motor nerve; the evoked responses are known as SNAP or CMAP, respectively. Characteristics of the evoked action potentials such as amplitude, onset and/or peak latency, and conduction velocity provide information about axon and myelin components of the tested nerve.

¤ Some other types of electrodiagnostic tests :

• Repetitive stimulation studies are utilized for the evaluation of the neuromuscular junction (e.g., in myasthenia gravis).

• Somatosensory evoked potentials are used to evaluate conduction within the spinal cord and brain.

• Other less frequently used tests include single-fiber EMG, motor-evoked potentials, and nerve root stimulation.

¤ What is a motor unit ?

A motor unit includes the motor neuron found within the anterior horn of the spinal cord, its axon, the neuromuscular junction, and the associated muscle fibers supplied by the axon. The electrodiagnostic physician can utilize a combination of needle EMG, NCS, repetitive stimulation, and other electrophysiologic tests to assess

the individual components of the motor unit.

¤ What are the clinical indications for ordering an EMG ?

An EMG should be ordered to determine the localization and severity of a suspected neuromuscular disorder. The

NCS and needle EMG are almost always performed together in reputable laboratories. Testing can distinguish

between neurogenic (nerve or neuron-related), myopathic (muscle-related), and neuromuscular junction disorders.

In neurogenic conditions, testing can often distinguish between disorders primarily affecting myelin (i.e., demyelinating neuropathies) and axonal or neuronal disorders. An EMG is generally not useful in the assessment

of brain or spinal cord disease. In order to get the most useful information from the test, the requesting physician should indicate his or her clinical question or concern as specifically as possible. It is not usually necessary to request particular procedures (e.g., NCS, repetitive stimulation, needle EMG) as a qualified electrodiagnostic consultant can decide what is needed to answer the clinical question.

¤ What are some common disorders of nerve ?

Functionally, the peripheral nervous system starts in the vicinity of the spinal neural foramen where the sensory and motor fibers join. At its most proximal level, peripheral nervous system injury in the form of radiculopathy is caused by

an injury to a nerve root due to structural disease (e.g., herniated disc or trauma), inflammation, or other causes.

Plexus involvement by disease or injury may occur in the upper (brachial plexus) or lower extremity (lumbar or lumbosacral plexopathy).

Peripheral nerve conditions can be acquired or genetically mediated. Examples of genetic conditions

include the hereditary sensory and motor neuropathies (e.g., Charcot-Marie-Tooth disease). Acquired peripheral neuropathies can stem from conditions such as diabetes, toxins (medications or other exogenous substances), inflammatory disorders, or metabolic disturbances.

Focal neural entrapment can be seen in carpal tunnel syndrome (CTS), cubital tunnel syndrome, or tarsal tunnel syndrome, and few others.

¤ What are the three main types of nerve injury ?

Nerves sustain a gradient of injury, which was originally defined by Seddon:

1. Neurapraxia is the functional loss of conduction without anatomic change of the axon, usually due to focal demyelination. With remyelination, conduction returns to normal.

2. In axonotmesis, the axonal continuity is lost. With its loss, Wallerian degeneration occurs in the distal segment. Recovery, which is frequently incomplete, occurs as a result of axonal regrowth at a rate of 1- 3 mm/day in otherwise healthy individuals.

3. Neurotmesis results from separation of the entire nerve, including its supporting connective tissue. Regeneration frequently does not occur. Nerves with this degree of trauma may need surgical attention for recovery to


¤ Do these types of nerve injuries occur together ?

Neurapraxia and axonotmesis commonly occur as a result of the same injury. When compression is relieved from the involved segment of the nerve, two periods of healing typically occur. One is relatively immediate, from hours to weeks, as the neurapraxia resolves. A second period of healing, from weeks to months, may occur as a result of axonal regrowth.

¤ What is an innervation ratio ?

For each motor axon, there are a variable number of associated muscle fibers. Depending on the specific requirement of control, the ratio may be quite low or extremely high. The innervation ratio of the extraocular muscles is typically 1: 3, owing to the fine control required for binocular vision. Conversely, the innervation ratio of the gastrocnemius can be as high as 1: 2000 since most movements involving the plantar flexors of the ankle are relatively large motions requiring more force than accuracy.

¤ What are some common disorders of muscle ?

Muscle disease can be acquired or genetically mediated. Acquired muscle diseases such as inflammatory myopathies are most often proximal and symmetrical in distribution. A notable exception is inclusion body myositis, which has a predilection for the quadriceps and finger flexors and may be quite asymmetrical. Genetic myopathies or muscular dystrophies may also demonstrate specific patterns of muscle group involvement that may aid in diagnosis. In general, the degree of clinical weakness in a particular muscle correlates well with the severity of the findings on needle EMG examination.

¤ What are the components of a needle EMG evaluation ?

Insertional/spontaneous activity: An EMG needle inserted into a normal muscle should evoke brief electrical discharges of muscle fibers. Increased or prolonged electrical activity may indicate abnormalities of the muscle fibers or the nerves supplying them. Fibrillations, positive sharp waves, and complex repetitive discharges are electrical signals that represent abnormal spontaneous firing of muscle fibers due to nerve or muscle damage.

There should be no spontaneous activity in a healthy relaxed muscle. Motor unit analysis: When a patient slightly contracts a muscle, MUAPs can be recorded. The parameters of interest include the amplitude, duration, number of phases, and firing pattern of the MUAPs. Assessment of these parameters occurs in real time and is generally subjective. The quality of the interpretation depends on the skill and experience of the electromyographer, technical recording conditions, and patient cooperation.

Recruitment: When a patient contracts a muscle more forcefully, a large number of MUAPs can be recorded. How “full” this pattern of MUAPs is reflects the underlying health of the motor units and the ability of the patient to “recruit”

available motor units. In myopathic conditions, recruitment may be “early” because myopathic motor units generate less force than healthy ones. In neurogenic conditions, recruitment may be reduced as a result of axon or neuron loss.

¤ How do fasciculations, fibrillations, and positive sharp waves differ on needle EMG recording ?

A fasciculation potential is an involuntary firing of an entire motor unit, that is, single motor neuron and all its innervated muscle fibers. This is seen as a large electrical spike on needle EMG recording of a relaxed muscle. It is sometimes clinically visible in the patient as a brief, irregular twitch of the muscle. This can often be seen in normal individuals; however, if in excess, it may be a sign of a motor nerve or motor neuron disorder.

A fibrillation potential is an involuntary contraction of a single muscle fiber that usually indicates denervation or muscle damage. Unlike a fasciculation, a fibrillation usually does not cause clinically visible muscle movement.

Positive sharp wave potentials are similar to fibrillation potentials in that they represent abnormal muscle fiber firing from nerve or muscle damage. They are identified by their initial positive deflection from the baseline as opposed to the initial negative deflection of a fibrillation potential.

¤ How do normal EMG findings compare with the findings seen in a denervated muscle (neurogenic disorder) ?

Note that fibrillations and positive sharp waves are not seen in acutely denervated muscles until 7 to 14 days after the onset of axonal degeneration. Full reinnervation of denervated muscle, resulting in large, polyphasic MUAPs may take 3 to 4 months or more. In patients with reinnervation after nerve injury, muscles may be clinically strong and yet be very abnormal on needle EMG testing.

¤ How do normal EMG findings compare with the findings seen in a myopathic disorder ?

The weaker a patient with myopathy is, the more likely the needle EMG findings will be abnormal. In patients with very mild weakness or those with steroid myopathy, the needle EMG recording may appear normal.

¤ Is nerve conduction velocity the same throughout the length of a nerve ?

Nerve conduction velocities vary among nerves and along their lengths. Normally, proximal nerve conduction is faster than distal nerve conduction because of the increased temperature and larger diameter of the proximal nerve segments. For example, median nerve conduction velocity from wrist to palm should be faster than from palm to finger.

¤ Why is temperature recorded during the course of an electrodiagnostic examination ?

Nerve conduction velocities drop by 1.5 to 2.5 m/s per °C reduction in both sensory and motor nerves. These changes can be significant. Failure to warm the limb to a standard temperature, usually 30°C for the leg and 32°C for the arm, can result in false-positive studies, leading to a misdiagnosis.

¤ What is the F-wave? How is it clinically useful ?

The F-wave is a delayed motor potential recorded by stimulating a motor nerve in the distal extremity. As the electrical impulse travels backward along the nerve to the spinal cord, a small population of anterior horn cells is stimulated, resulting in small motor action potentials that can be recorded from the associated muscle. Abnormal F-waves can indicate proximal nerve disease such as radiculopathy or plexopathy. Absent F-waves are also early

findings in Guillain–Barré syndrome.

¤ How is the sensory portion of the peripheral nervous system tested ?

Sensory NCS are the primary means to test the integrity of the sensory nerves. The amplitude of SNAP, its point of onset, and its peak can be compared with standardized normal values and with those from the opposite extremity.

Sensory NCS are only abnormal in lesions distal to the dorsal root ganglia where sensory neurons reside.

Abnormal SNAPs can be an important way of distinguishing between peripheral neuropathies or plexopathies and radiculopathies. In the latter, SNAPs are usually normal even when a patient complains of numbness. Using the

complementary information obtained from needle EMG examination, an electromyographer can further localize the lesion to a particular spinal nerve root, portion of the plexus, or a particular peripheral nerve.

¤ How can a demyelinating peripheral neuropathy and an axonal peripheral neuropathy be differentiated by NCS and needle EMG?

Axonal loss and demyelination rarely occur in strict isolation, but some electrodiagnostic features may indicate

relatively more damage to myelin versus axons. The features of demyelinating neuropathies include moderate to severe slowing of conduction velocity, temporal dispersion of evoked sensory or motor action potentials, conduction block, and prolonged distal latencies. Axonal neuropathies show milder slowing of nerve conduction, with generally low sensory and motor amplitudes on NCS. The needle EMG shows denervation abnormalities early in axonal neuropathies and only later in demyelinating neuropathies when axons are secondarily affected.

¤ Which systemic diseases cause predominantly a demyelinating peripheral neuropathy ?

In most rheumatologic conditions where in neuropathy is present, the axons are primarily affected, though myelin is rarely completely normal. Demyelination may predominate in a few disorders, such as acute inflammatory demyelinating polyneuropathy (Guillain–Barré syndrome), chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, anti-myelin-associated glycoprotein antibody syndrome, and other paraproteinemias, and some hereditary neuropathies, such as Charcot–Marie–Tooth disease type 1A.

¤ How is EMG/NCS used in diagnosing CTS? Ulnar nerve entrapment at the elbow (cubital tunnel syndrome)

CTS or compressive median neuropathy at the wrist is the most common entrapment neuropathy, affecting 1%

of the population. CTS may show segmental nerve conduction slowing across the wrist. SNAP latencies of the

median nerve are delayed most often, but with increasing severity, motor latencies can be affected. Denervation of the thenar muscles seen on needle EMG indicates moderate to severe CTS. Clinical correlation is recommended for mild CTS as sometimes NCS/EMG studies are normal despite classic symptoms of hand pain/numbness in a median nerve distribution.




Oxygen and Free Radicals


one of the most important issues regarding aging is oxygen. Too much of it, or too little, and we age very fast. Most people are aware of oxygen’s benefits, but many people don’t realize its potential harm: the conversion of the stable O2 molecule to its very unstable and destructive cousin, the superoxide or free radical. When this occurs inside the body, it can lead to serious health problems.

Scientists now associate excess oxygen free radicals, also called oxidative stress, with every major chronic disease, including heart disease and cancer. Free radicals also play a major role in the aging process. Aging is the result of continuous reactions of the body’s cells with free radicals. It is important to become aware of these potentially harmful substances, what increases their production and how to control them, in order to reduce the devastating effects of disease and control the process of aging.

Normally, the body produces free radicals to protect against harmful bacteria, viruses, chemical pollutants and even toxic substances produced within the body. However, in this chemical-saturated world, it is possible to produce too many free radicals. When this occurs, free radicals can react with and damage any cell in the body.

The most vulnerable part of the cell is the part containing unstable polyunsaturated fats, as these fats are easily destroyed by free radicals. This destruction is called lipid peroxidation and it’s associated with chronic inflammation. Together, this is the first step in the disease process. For example, before LDL cholesterol can be stored in the coronary arteries, damage from lipid peroxidation must first take place. Lipid peroxidation can produce toxins capable of traveling throughout the body, creating damage anywhere. These toxins are known to be carcinogenic and even have the potential to cause genetic mutations.

The damage from free radicals, oxidative stress, results in what we know as aging. The more of this damage, the more physiologically older we become. Fortunately, the body has an effective way to combat this problem. The antioxidant system controls free radicals by chemically changing them to harmless compounds. This system requires raw materials to function nutritional antioxidants from food and key places in the body to perform this task the aerobic muscle fibers. Too much free-radical activity, too little antioxidant activity, or both, speeds the aging process, sometimes significantly.

Antioxidants to the Rescue:

The importance of antioxidants(sometimes called free-radical scavengers). there are two key groups of them. The most common group of antioxidants includes vitamins A, C and E, beta-carotene, selenium, the bioflavanoids, and phytonutrients such as phenols. As powerful as these are, there’s a more potent antioxidant: glutathione.

Glutathione is not found in food and can’t be taken in a pill (it’s broken down in the stomach), although now intravenous and transdermal forms are being used. The best way to get enough glutathione is to give the body what it needs to make it certain other antioxidants. The most potent of these include the amino acid cysteine, found in animal protein (especially whey).

the phytonutrient sulphoraphan, high in cruciferous vegetables such as broccoli but very high in broccoli sprouts (before their leaves turn green); lipoic acid found in many dark vegetables and even beef (lipoic acid can also be produced in a healthy body); and both gamma-tocopherol and alpha-tocotrienol, parts of the vitamin E complex (however, too much alpha tocopherol, such as the typical 400 IU dose, can reduce levels of these other nutrients in the vitamin E complex).

The following is a list of the most potent antioxidants in order of their effectiveness the most powerful being those that help the body make glutathione. As you can see, some of the most popular nutrients, such as vitamins C and E, and especially the over-hyped quercetin and Co-Q10, are not the most potent. And, these are food sources of nutrients, not synthetic vitamins or unnatural doses and forms of nutrients that may not work as well.

- Sulforaphan Lipoic acid

- Cysteine Alpha-tocotrienol

- Gamma-tocopherol Alpha-

- tocopherol

- Vitamin C Lycopene

- Beta-tocopherol Beta-carotene

- Zeaxanthin Delta-tocopherol

- Lutein Canthaxanthin

- Astaxanthin Quercetin

- Co-Q10

It’s not necessary to remember the names of these antioxidants, but you do need to remember to eat as many antioxidant-rich foods as possible. Vegetables and fruits, berries, raw sesame seeds and almonds, extra-virgin olive oil, green and black tea, and red wine are excellent sources of antioxidants. Meats, especially grass-fed beef, contain significant amounts of certain antioxidants, as does whey. Of course there are now hundreds of antioxidant products available in pill, liquid, powder and other forms. If needed, be sure to take only supplements made from real, raw foods.

Signs and symptoms of a need for more antioxidants may include immune problems such as lingering cold or flu, frequent illness, sensitivity to chlorine or other chemicals, and chronic inflammation.

Exercise and Free-Radical Activity

A well-developed aerobic system is a key to making the antioxidant system work best. Even if you obtain all the best antioxidants, the body needs a place to put them to work. Improved circulation that accompanies aerobic fitness helps antioxidant activity. And, free-radical breakdown occurs in the mitochondria contained within aerobic muscle fibers. Therefore, people in better aerobic shape, those who have more aerobic muscle fibers and mitochondria, are more capable of controlling free radicals compared to those who are out of shape.

exercise itself produces free radicals :

Different levels of exercise intensity can produce varying amounts of free radicals. Easy aerobic exercise, especially at a moderate heart rate produces little or insignificant amounts of free radicals, and this smaller amount is most likely well controlled through the body’s natural defense system, especially if enough antioxidants are present. However, exercising at higher intensities or lifting weights any anaerobic exercise can have the opposite effect. Anaerobic activity can produce more oxidative stress some studies show a 120 percent increase over resting levels. This is the result of physical damage to muscles, lactic-acid production and higher oxygen uptake, which may increase tenfold during the activity.

Higher injury rates are also associated with increased free-radical production. In addition, the development of more anaerobic muscle fibers means less aerobic mitochondria for free-radical elimination.

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Mahmoud Badawy



Training Principles

1- Individuality:

Individuality refers to the fact that all athletes are not the same, and that heredity significantly influences the speed and degree to which a body adapts to a training regime. Therefore a training program should take account of individual needs.

2- Specificity:

Training adaptations are specific to the type of activity undertaken. Training for swimming is ideally performed in water rather than dry land, whilst a

cyclist is better suited to cycling as a mode of training rather than running.

3- Progressive overload:

The concepts of progression and overload are the foundation for all training. Progression means that as the training continues there is a need to increase the resistance in resistance training or produce a faster time in sets of running, swimming or cycling, whereas overload is where the muscles need to be loaded beyond which they are normally loaded.

4- Maintenance:

Once a specific level of adaptation has taken place, this level can be maintained by the same or a reduced volume of work.

5- Reversibility:

If an individual ceases training, the muscles (or cardiovascular system) become weaker, less aerobic or less powerful with time.

6- Warm-up and cool-down:

Although not essentially training principles per se, nonetheless warm-up and cool-down should play an integral part in any training program. Warm-up implies that as a result of appropriate activity the muscle temperature is elevated from that at rest. Cool-down occurs when appropriate activity following exercise is undertaken to gradually reduce muscle temperature and aid removal of waste products from muscle.

7- Individuality Heredity:

Individuality Heredity plays a significant role in determining how quickly and how much a body adapts to a training program. Other than identical twins, no two individuals have exactly the same genetic characteristics. Consequently, there can be large variations between individuals in cell growth and repair, metabolism, and regulation of processes by nerves and hormones. These individual variations may explain why some athletes can improve significantly on a certain training program whereas another may experience little or no change following the same training program. Appropriate training normally results in improvements in ,strength, flexibility, power, speed, aerobic power and so on, although the rates at which these changes occur vary between individuals in training principles.

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Denis James, known professionally by his stage name Lordboy Cmt, is a South Sudanese singer and EDM producer who currently resides in Cairo, Egypt. He has been associated with music since his school time. He was just a kick start to his career at the age of 15 Year's old.

He realized his bite; Capabilities; Decided to learn "MUSIC" and is now able to establish himself as a professional music producer. Learning new skills is not only an option, but a habit.

They can produce top genres like progressive EDM, trap, trance, hip-hop, rap and more. Undoubtedly, Lordboy Cmt is a golden genius from Central Equatorial state. He believes in reaching greater heights as he sees himself roaming all over the world and makes everyone dance to his tunes.

Lordboy Cmt created a YouTube channel YouTube in 2021, uploading the song that was the first remix song on that channel. But after some time, he made trap beats , the audience liked that music very much.

Now, if you search for him on YouTube, you will see that his channel is verified as a music artist. Now you might wonder why did YouTube verify its channel as a music artist or give it a music note verification badge?

Originally, Lordboy Cmt released its first soundtrack on Reverbnation in 2020, but after some time it officially released that track on Google Play Music, Hungama, Apple Music, YouTube Music, Spotify, JioSaavn, Napster, Deezer, Tidal , Released on music streaming platforms such as Resso, Boomplay, Amazon Music, Musixmatch, and many more.


What causes Vitamin D deficiency ?

Vitamin D2 and Vitamin D3:

Vitamin D is not a single nutrient, but rather a group of related nutrients. Vitamins D2 and D3 are the most popular dietary forms.The two types of vitamin D differ in their food sources and also in structure and function.Vitamin D3 is only available in animal-sourced meals, whereas D2 is mostly found in plant-based foods and fortified foods.

D3 is found in fatty animal-sourced foods like fish oil and egg yolk. It is also produced by your skin in response to sunshine or UV radiation.Surprisingly, vitamin D3 appears to be more effective at increasing vitamin D levels in the blood.

What Does Vitamin D do ?

Vitamin D received from sunlight, meals, and supplements is physiologically inactive and require two hydroxylations in the body to be activated.

The first hydroxylation takes place in the liver and transforms vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as "calcidiol."

The second hydroxylation takes place largely in the kidney and results in the physiologically active 1,25-dihydroxy vitamin D [1,25(OH)2D], also known as "calcitriol"

  • The first hydroxylation takes place in the liver and transforms vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as "calcidiol."
  • The second hydroxylation takes place largely in the kidney and results in the physiologically active 1,25-dihydroxy vitamin D [1,25(OH)2D], also known as "calcitriol"

Importance of Vitamin D:

Low vitamin D levels have been shown in studies to increase your risk for several diseases. A lack of vitamin D may also lead to poor bone health. Much recent contradictory research now demonstrates a link between vitamin D insufficiency and cancer, cardiovascular disease, diabetes, autoimmune illnesses, and depression.

There are many health benefits associated with getting enough vitamin D each day including:

  • Helping manage weight effectively
  • Lowering blood pressure
  • Reducing inflammation
  • Protecting against infections like influenza
  • Preventing cancer
  • Reducing inflammation
  • Protecting against infections like influenza
  • Reducing the risk for heart disease and stroke
  • Improving insulin sensitivity
  • Promoting healthy pregnancy outcomes
  • Absorb calcium and phosphorus, which are crucial for bone
  • health and strong teeth.

Recommended Vitamin-D Intakes:

RDAs (Recommended Dietary Allowance) for vitamin D were developed by an FNB (Food and Nutrition Board) committee to identify daily vitamin D doses that are sufficient to preserve bone health and appropriate calcium metabolism in healthy persons.

Is vitamin-D needed daily ?

If you’re following the latest recommendations, you might be falling short.

According to the National Institutes of Health, adults should get at least 600 international units (IU) of vitamin D per day to maintain bone and muscle health, boost immune function, and reduce the incidence of a variety of cancers Unfortunately, many people.....

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Posture and Metabolism

There are twelve of body systems: skeletal, muscular, nervous, integumentary (skin), circulatory, respiratory, reproductive, digestive, urinary, lymphatic, endocrine (hormones), and immune. Each of them is subject to stimulation-reaction-response.

Musculoskeletal dysfunction triggers (stimulates) a reaction and response in each of the eleven other systems. When the tape broadcasts the news that something is happening, it's not a warning as such-stimulus is initially regarded as neither good nor bad. But the news that important major muscle groups are not engaging needs to be known by all systems because, for starters, it's going to affect the metabolic process.

Does Posture affect metabolism?

One of the body's most complex biochemical operations, metabolism is the way the body provides fuel to its cells. Muscles play an important role in at least three ways. First, by creating heat from the friction of contracting and relaxing. The heat helps to essentially cook the food, oxygen, and water that we consume until they break down and recombine into substances that can be converted by the cells into usable energy. The more work the muscles do, the more fuel is available to the cells. And the reverse is true: the less work the muscles do, the less fuel for the cells.

The second metabolic role for the muscles is that of being a major metabolic consumer. Large, active muscles have many muscle cells to fuel. This appetite serves to create an expanded metabolic capacity in order to meet muscular demand. But the metabolic supply isn't exclusively used by the muscles, though. When we rest or sleep, our muscles are relatively (and temporarily) inactive, and the fuel that's not needed by the muscles is diverted to other tissue and organs.

That's why poor posture-slumping, misaligned dysfunctional posture-indicates a metabolic dysfunction. Notice that I didn't call it a symptom. Poor posture is actually a cause of metabolic dysfunction. Once the deep muscles-the ones closest to the bones and joints-disengage, the metabolism backs off because the body's monitoring system tells it there are fewer cellular mouths to feed and reduced means to do the feeding. The other eleven organ systems immediately lose.

The benefit of a revved up, efficient, fully functional metabolism. The energy they need to carry out basic functions is no longer as abundant. It puts a strain on every organ in the body and the roughly 75 trillion metabolically dependent individual cells.

Will My Posture Improve If I Lose Weight?

The third important metabolic role played by the muscles is this: reduced muscular engagement means reduced oxygen intake and distribution. Oxygen is the combustion agent that the metabolic process uses to refine the fuel (primarily glucose, amino acids, and enzymes) needed for the operation of the body's cells. Disengaged and dysfunctional major muscle groups mean that the primary vehicle for getting oxygen into and around the body isn't in optimal condition. But suppose circumstances require optimal metabolism. A sudden demand for physical exertion, the effects of stress, or severe illness all call for extra energy to support extra work from the body's organ systems. They depend on the support of a fully functional metabolic process. Since muscular action is involved with drawing oxygen into the lungs and assisting the heart and circulatory system in moving oxygenated blood throughout the body, the disengagement of major posture muscles hinders this work. As a result, fuel production is compromised, as is cell function.

Conceivably, the body could cope with the problem simply by doing less work with less metabolism. After all, our environment is not as rough-and-tumble as it once was. But one system in particular is working as hard as ever-maybe harder.

The immune system is like a network of fire stations scattered strategically throughout the body. The T-cells and various anti-bodies are the fire fighters, ready to deploy, when the alarm sounds, to battle invading viruses, toxins, and other conflagrations. An immune system undermined by an inefficient metabolism cannot respond as quickly or effectively. It just doesn't have enough available energy for aggressive fire fighting, as if many of the fire trucks are out of gas and their crews understaffed.

That's why we're seeing the rise of the new "epidemics" -diabetes, asthma, allergies, virulent but heretofore unknown strains of TB, some types of cancer, and the like. This alarming trend coincides with another epidemic-chronic back pain, headaches, bad hips, knee injuries, hurting wrists, and other musculoskeletal disorders.

I believe the link between this epidemic and the others is visible all around us. If millions of people do not have the strength to stand up straight, to hold their shoulders square and their heads high and level, and to move smoothly without stiffness or pain, how do we expect them to have the strength to fight off disease?

Without adequate musculoskeletal support for the metabolic process, they simply cannot. Around us, the very embodiment of health is crumbling.

I'm painting this gloomy picture not to spread pessimism but to inspire faith. We need to regain our faith in the strength of the human body. After all, it got us through two or three million years of BS-Before Suburbia. Rediscovering it can yield a cure for these epidemics.

By recognizing our strength and its source in muscle and bone, we can escape from the modern delusion that health comes only from experts and technology that soon will be crushingly expensive and beyond the reach of all but a few. Down that road lies misery and future epidemics, the horror of which we can't even begin to imagine.

All of us can afford the price of a genuine miracle cure. We were born with potentially strong, aligned bodies. We were therefore born rich... posture and metabolism.




Osteoarthritis is a pathology associated with inflammation in the joints of the body. In the case of hand osteoarthritis, the arthritis and inflammation most commonly associated with a loss of carpal, MC, or phalanges glenoid cartilage leading to hand pain.

Osteoarthritis is a term derived from the Greek word“osteo”meaning “of the bone,”“arthro”meaning“joint,”and“itis”meaning inflammation even though the amount of inflammation present in the joint can range from excessive to little or no inflammation.


• Hand arthritis

• Hand degenerative joint disease


( What Causes Hand Osteoarthritis? )

• The wearing down of the hyaline cartilage leads to an inflammatory response. There is thickening and sclerosis of the subchondral bone and development of osteophytes or bone spurs. This leads to a narrowing of the joint space, loss of shock absorption, and ultimately pain.

• Daily wear and tear in combination with various injuries sustained throughout life is the most common cause of the breakdown of healthy tissue.

• Degeneration of the cartilage and resultant arthritis can also be the result of other factors such as trauma or joint injury....

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What is the Big Fat Lie ?

- What is The Bad Fat ?

- What does fat do for you ?

The Big Fat Lie:

For decades, fat has been seen as the “bad” component of the diet. Low- and no-fat has become synonymous with being healthy. These ideas, of course, are untrue. In fact, fat is one of the most beneficial substances in your diet, and is often the missing ingredient in developing and maintaining optimal health and human performance. But an ongoing, well-financed misinformation campaign against fat has misled the public to an epidemic of fat phobia. Just think of the billions of dollars spent each year on low-fat and fat-free foods and you’ll understand why you might not have been told the whole truth about fat.

In addition, this anti-fat campaign has contributed to actual deficiencies in fat that have contributed to various diseases. The bottom line on dietary fat: Too much or too little is dangerous. It’s simply a question of balancing your intake.

First, let’s define fat a term that also includes oil. Fats are found in concentrated forms such as vegetable oils, butter, egg yolk, cheese and other naturally occurring foods, and in less concentrated forms that make up the content of almost all natural foods. And some foods contain very small fat components that are as essential as all other nutrients.

Virtually all natural fats are healthy. As noted above, eating a balance of fats is most important. In general, eating too much of one type of fat, such as too much saturated fat from dairy products or too much omega-6 fat from vegetable oil, is an example of a fat imbalance that can adversely affect health. In addition, eating “bad” fats those that are artificial and highly processed, such as trans fat and overheated fats in fried foods, can cause serious health problems. Foods such as chips, French fries and fried chicken, to name just a few, are examples of those containing bad fat.

Dietary fats have been a staple for humans throughout evolution.Ironically many people are learning of the true importance of fats in the diet only since the low-fat trend of the last few decades. This is not news, really. Scientists have known of the importance of fat in the diet since the discoveries in 1929 by researchers who demonstrated the necessity of dietary fat. Before discussing these issues which fats are best and how can they be balanced let’s highlight some of the many healthy functions of fat.

Disease Prevention and Treatment:

Certain dietary fats consumed in balanced proportions can actually help prevent many diseases. For instance, we now know that dietary fats are central to controlling inflammation,which is the first stage of most chronic diseases. And, selectively increasing certain dietary fats has been shown to reduce the growth or spreading of cancer and improving recovery in heart disease. Many brain problems, including cognitive dysfunction such as Alzheimer’s disease, can also be treated with fats. A healthy brain is more than 60 percent fat.


The aerobic system depends on fat as the fuel for the aerobic muscles, which power us through the day. Fat produces energy, and prevents excessive dependency upon sugar, especially blood sugar. Fat provides more than twice as much potential energy as carbohydrates do, 9 calories per gram as opposed to only 4 calories.....

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Mahmoud Badawy



Few people in industrialized societies have true calcium deficiencies,regardless of what the advertisements tell us. The bigger problem is that most people are unable to utilize the calcium they already have in their bodies. Poor calcium metabolism, rather than deficiency, is almost at epidemic proportions. The end result is that not enough calcium gets into the cells, including the bones, muscles and other tissues, with the remaining excess calcium depositing in the joints, tendons, ligaments or even the kidneys as stones. Plaque that clogs the arteries can also contain calcium.

In order for your body to properly metabolize calcium, and more effectively absorb calcium from food, you must have sufficient vitamin D. This nutrient is free and plentiful, yet most people don’t have enough. That’s because it comes from the sun and the public is told that the sun is dangerous. This issue is so important that it’s discussed s in this article. Just remember that without sufficient vitamin D, calcium cannot be properly regulated, and that most problems of insufficient calcium are really due to low levels of vitaminD.

Another important issue regarding calcium is to consume enough

calcium-rich foods; this is easily done without supplementation through good dietary practices. And it does not necessarily mean eating a lot of dairy foods.

Consider the high amounts of calcium in the following single servings of non-dairy foods:

• Salmon: 225 mg

• Sardines: 115 mg

• Almonds: 100 mg

• Seaweed: 140 mg

• Rainbow trout: 100 mg

• Spinach: 135 mg

• Green beans: 100 mg

• Collards: 125 mg

Two other important issues regarding calcium are absorption (the most important part is also having sufficient vitamin D), and getting the calcium into the bones and muscles once it’s absorbed.

Absorption is the first step to utilizing calcium in the body. In general, smaller amounts are better absorbed than larger amounts, whether from food or supplements. If a small amount of calcium is present in the intestine, 70 percent may be absorbed, for example, while a larger amount of calcium may have only a 30 percent absorption rate. If you’re taking calcium supplements, it may be best to take a lower dose several times a day rather than a large dose once daily.

Even though vegetables contain smaller amounts of calcium, larger percentages are absorbed compared to milk. So in some situations, a serving of broccoli may result in more calcium getting into the body than a serving of milk.

The stomach’s natural hydrochloric acid is also very important in making calcium more absorbable. Neutralizing stomach acid has a negative effect on calcium absorption, and a serious impact on digestion and absorption of all nutrients. Once absorbed, calcium is utilized best when the body is in a slightly acidic state. Otherwise, calcium that is absorbed may be more easily deposited in joints, muscles or arteries rather than inside the cells where it’s needed. The cells that are calcium-starved cause symptoms such as muscle tightness and irritability, identical to those of calcium deficiency. Morning stiffness which loosens up only after moving around for a while, is one of the most common symptoms of this calcium problem. Signs of an advanced problem include so-called bone spurs (a deposit of calcium in the ligament) or kidney stones. Rather than needing more calcium,these people need more acidity (and vitamin D) to utilize the calcium.

Two teaspoons daily of apple-cider vinegar may help maintain the proper pH to help calcium work properly. This can be taken as part of your salad dressing, or even mixed into a 4-ounce glass of water. Excess phosphorus intake can be very detrimental for calcium utilization, pulling it out of bones and muscles. Most soft drinks contain large amounts of phosphorus and the people who drink them risk significant calcium loss from their teeth and bones.

The type of calcium supplement may be associated with absorbability. For example, calcium carbonate is more poorly absorbed than calcium lactate or calcium citrate. This is due to the alkaline nature of carbonate, and the acid nature of lactate and citrate.

Taking too much calcium in supplement form can disturb the body’s complex chemical makeup. For example, too much calcium can reduce magnesium. Most people may be in need of more magnesium than calcium it’s necessary for most enzymes to work, including the ones important for fat metabolism. And the best sources of magnesium are vegetables.

What causes Osteoporosis ?

Osteoporosis is usually a multifactorial problem, meaning there’s hardly ever just one cause. We know that a lack of calcium is usually not the cause, nor is low estrogen. Methods that are effective in treating or preventing osteoporosis in one person may have very different results in someone else. In addition, osteoporosis may not be as much of a problem as it has been made into, as Susan Brown, Ph.D., author of “Better Bones, Better Body” emphasizes:

• Osteoporosis itself doesn’t cause bone fractures; half of those with osteoporosis never get fractures.

• Severely osteoporotic vertebrae are strong enough to withstand five times the normal weight-bearing.

• Menopause does not cause osteoporosis, and only 15 percent of a woman’s bones are affected by estrogen.

• Zinc and magnesium may be as important as calcium for bones.

• Up to 80 percent of all hip-fracture patients may have a vitamin D deficiency.



Jersey/Rugby Finger Syndrome


• Rupture or avulsion of the flexor digitorum profundus (FDP).

• Classification is based on how far the tendon retracts,which in turn will affect the success of surgical repair.

 A type I injury retracts all the way to the palm.The vincula brevis and longus are ruptured and blood supply is interrupted. Extensive scarring can develop within the tendinous sheath,therefore surgical repair is indicated within 7 to 10 days.

Type II retracts to the PIP joint.The long vinculum may still be intact, and a small chip of bone may be avulsed with the tendon.The avulsed end may become entrapped at the flexor digitorum superficialis (FDS) chiasma, causing a flexion contracture.

Type III occurs when a bony fragment is avulsed and remains attached to the tendon,which isthen unable to retract through the pulley.The tendon remains in the synovial sheath.


• FDP avulsion

• Rugby finger


• Rupture or avulsion of the FDP tendon can occur during activities that require sustained digital flexion against forceful or unexpected resistance, resulting in hyperextension of the DIP joint and rupture of the FDP tendon.

• Rupture of the FDP tendon commonly occurs when an athlete’s finger catches on another player’s clothing in sports such as football.



Ring finger (fourth digit) is the most common involvement. It is the weakest and accounts for 75% of all cases.


• Forceful passive extension of the digit while the FDP is in maximal contraction.

• The injury causes forced extension of the DIP joint during active flexion...

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Finger Dislocation