Sandstorms and downpours hit Egypt القاهرة

Egyptian scientists have used digital technology to peer inside the mummy of Amenhotep I - one of the few royal mummies that have not yet been deployed

A container ship that blocked the Suez Canal in March

left the waterway after the Egyptian authorities signed a compensation agreement with the owners and insurers.

Ever Given disembarked at about 11:30 local time and headed north toward the Mediterranean, accompanied by tugs.

The ship was arrested for three months near the city of Ismailia.

The terms of the deal were not disclosed, but Egypt demanded $ 550 million.

The 193km-long Suez Canal, which connects the Mediterranean with the Red Sea and provides the shortest sea link between Asia and Europe, was blocked when the 400-meter Ever Given ran aground due to strong winds. World trade has been disrupted by hundreds of ships stuck in traffic.

He was taken off the beach after a six-day rescue operation involving a flotilla of tugs and dredgers. One person died during the operation.

ACUTE ACALCULOUS CHOLECYSTITIS

History

¤ 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.

Tests

Laboratory

¤ 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.

Imaging

¤ 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.

Management:

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).

Follow-up

¤ 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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ACUTE BACTERIAL MENINGITIS

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.

History:

¤ 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.

Headaches.

High fever.

Feeling confused or sleepy.

Bruising easily all over the body.

A rash on the skin.

Sensitivity to light.

Nausea

Vomiting

¤ 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.

Tests:

Laboratory

¤ 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

Management:

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

Indications

¤ 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.

Follow-up

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.

History:

¤ 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

tests:

¤ 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,

management

¤ 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

follow-up

¤ 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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Acromegaly

History

¤ 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.

tests:

Laboratory

¤ 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

Imaging:

¤ 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.

management:

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.

follow-up:

¤ 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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Mahmoud Badawy

https://healthretrival.blogspot.com/2022/11/training-principles.html

Healthretrival.blogspot.com

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.

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