A cholesteatoma consists of squamous epithelium that is trapped within the skull base and that can erode and destroy important structures within the temporal bone. Its potential for causing central nervous system (CNS) complications (eg, brain abscess, meningitis) makes it a potentially fatal lesion

3 types of cholesteatoma are identified:

Congenital cholesteatoma

Primary acquired cholesteatoma

Secondary acquired cholesteatoma

features of choleateatoma

Conductive hearing loss

Dizziness: Relatively uncommon

Drainage and granulation tissue in the ear canal and middle ear:

, cholesteatoma initially presents with symptoms of CNS complications, including the following:

Sigmoid sinus thrombosis

Epidural abscess

Meningitis

No laboratory tests or incisional biopsies are generally necessary for the diagnosis of cholesteatomas, because the diagnosis can be made based on physical examination and radiologic findings.

Computed tomography (CT) scanning is the diagnostic imaging modality

Virtually all cholesteatomas should be excised. The only absolute contraindications to the surgical removal of cholesteatomas are medical in nature.

A cholesteatoma consists of squamous epithelium that is trapped within the skull base that can erode and destroy important structures within the temporal bon

Secondary acquired cholesteatomas result directly from an injury to the tympanic membrane. This injury can be a perforation caused by acute otitis media or traum

Eliminating a cholesteatoma is almost always possible

Thiamine (vitamin B-1) deficiency can result in Wernicke's Encephalopathy

administration of dextrose in the setting of thiamine deficiency can be harmful because glucose oxidation is a thiamine-intensive process that may drive the insufficient circulating vitamin B-1 intracellularly, thereby precipitating neurologic injury

thiamine deficiency is characteristically associated with chronic alcoholism

wernicke enchepalopathy

average age at onset of WE is 50 years

Wernicke Encephalopathy

Presentation

History

The three components of the classic triad of WE are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction

disorders of the cerebellum caracteristically ruduce muscke tone.also reduce the reflexus.

pyramidal tract leasion or extrapyramidal involvemnt  cause increase the muscle tone.cortici spinal tract leasion cause to damge pyramidal tract and increse mucle rigidity.

basal ganglia disoder ( parkinsons D ) typically cause increse musvle rigidity

Atherosclerotic disease of the carotid artery may be associated with the following:

Amaurosis fugax (transient visual loss)

Transient ischemic attacks (TIAs)

Crescendo TIAs

Stroke-in-evolution

Cerebral infarction

Overview

Practice Essentials

Atherosclerosis is a diffuse, degenerative disease of the arteries resulting in plaques that consist of necrotic cells, lipids, and cholesterol crystals. These plaques can cause stenosis (see the image below), embolization, and thrombosis. Atherosclerosis has a predilection for certain arteries, including the extracranial carotid artery.

Arteriogram of a carotid stenosis.

View Media Gallery

Signs and symptoms

Atherosclerotic disease of the carotid artery may be associated with the following:

Amaurosis fugax (transient visual loss)

Transient ischemic attacks (TIAs)

Crescendo TIAs

Stroke-in-evolution

Cerebral infarction

See Overview for more detail.

Indications and contraindications for carotid endarterectomy

Indications

Indications for carotid endarterectomy (CEA) based on prospective randomized trials include the following:

Symptomatic patients with greater than 70% stenosis - Clear benefit was found in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) [1]

Symptomatic patients with greater than 50-69% stenosis - Benefit is marginal; appears to be greater for male patients

Asymptomatic patients with greater than 60% stenosis - Benefit is significantly less than for symptomatic patients with greater than 70% stenosis

Note: Available literature includes considerable overlap in the percentage of stenosis used as the threshold for CEA. Generally, symptomatic patients with greater than 50% stenosis and healthy, asymptomatic patients with greater than 60% stenosis warrant consideration for CEA.

Treatment of atherosclerosis of the carotid artery is dependent on the severity and degree of the disease.

Pharmacotherapy

Medications used to manage atherosclerotic disease of the carotid artery include the following:

Antiplatelet agents (eg, aspirin, ticlopidine, clopidogrel)

Anticoagulants (eg, warfarin) - Note that use of warfarin in patients with noncardiac emboli is controversial

Surgery

Endovascular management of atherosclerotic disease of the carotid artery includes the following procedures:

Carotid angioplasty and stenting (CAS)

CEA

optic cotex supply posterior erebral atery which is terminal branch of vertebral atery.

Giant cell arteritis (GCA), or temporal arteritis, is a systemic inflammatory vasculitis of unknown etiology that occurs in older persons and can result in a wide variety of systemic, neurologic, and ophthalmologic complications.

Common signs and symptoms of GCA reflect the involvement of the temporal artery and other medium-sized arteries of the head and the neck and include visual disturbances, headache, jaw claudication, neck pain, and scalp tenderness. Constitutional manifestations, such as fatigue, malaise, and fever, may also be presen

Visual loss is one of the most significant causes of morbidity in GCA.

Acoustic neuromas are intracranial, extra-axial tumors that arise from the Schwann cell sheath investing either the vestibular or cochlear nerve. As acoustic neuromas increase in size, they eventually occupy a large portion of the cerebellopontine angle. Acoustic neuromas account for approximately 80% of tumors found within the cerebellopontine angle.

The vestibulocochlear nerve arises from the brainstem slightly posterior to the facial nerve

Acostic neuroma

Unilateral hearing loss is overwhelmingly the most common symptom present at the time of diagnosis and is generally the symptom that leads to diagnosis. Assume that any unilateral sensorineural hearing loss is caused by an acoustic neuroma until proven otherwise. The tumor can produce hearing loss through at least 2 mechanisms, direct injury to the cochlear nerve or interruption of cochlear blood supply.

Although tinnitus is most commonly a manifestation of hearing loss, a few individuals with acoustic tumors (

Acoustic neromas

vestibuler chocler nerve start at cerebeller pontine angle and tumour atart at that point.

patiebt present with hearing loss

vertigo is late sing

other ipilayeral cranial nerve may affect V.VI.IX and X

may show ipsilateral cerebeller signs

increasw ICP is a late sign

cochlear ... for hearing

vestibuler....for balance

vestibuler neronitis

abrupt onset sever vertigo

nausea

vomiting

may be due to viral virusin young guys

may be due to vasculer in old man

complete recovery in 3 to 4 weeks

reasure and sedate

VESTIBULER NEURITIS VALA HEARING LOSS EKAK NETHA.LEDE NAMENMA EKA KIYAVENAVA.VESTIBULER KOTASE VITHARAK UPSET EKA THIYENAVA KIYALA. TINITUS EKAKUTH NEE.. BUT Menier;s disease valA HEARING LOSS EKAK THIYANAVA.. RERURRENT  HEARING LOSS EKAK VENAVA. TINITUSS THIYENAVA.. EEETA MATHARAVA VERITO n AND v THIYANAVA.

PATHOLOGY EKA VENNE CHOCHLER EKE ENDOLYMP AND EXOLYMP MIX VELA.

Ramsay Hunt Syndrom

Monday, November 30, 2015

11:00 AM

herpetic eruption of external auditory meatus

ipsi lateral lover moter facial neave palsy

+_ defness

tinnitus

sever vertigo

vesicle in aricle... or anterior 2/3 of toung

Rt with antiviral and steroid

ramsay hunt syndrome - Google Search

ramsay hunt syndrome - Google Search

aminoglycoside and cause defness due ti auto toxicity

aminoglycosides: amikacin, gentamicin, kanamycin, neomycin,

Menieres disease

recurrent spontanious attack of vertigo- sever  and rotational

nausia and vomiting with vertiogo

tinitus

sense of aural fullness

senso neuronal hering loss whichbis fluctuate and progessive

VESTIBULER NEURITIS VALA HEARING LOSS EKAK NETHA.. ONLY VERIGO. NAUSIA AND VOMITING

Watch "Cranial Nerves (8 of 12): Vestibulocochlear Nerve -- Head and Neck Anatomy 101" on YouTube

Watch "Vestibulocochlear Nerve Anatomy SIMPLIFIED" on YouTube

vestibulocochlear nerve - Google Search

cervical sympathatic trunk

cervical sympathetic chain - Google Search

cervical sympathatic  outflow

cervical sympathetic chain - Google Search

Myasthenia gravis (MG) is a relatively rare autoimmune disorder in which antibodies form against acetylcholine nicotinic postsynaptic receptors at the neuromuscular junction of skeletal muscles (see the image below).[1, 2] MG is sometimes identified as having an ocular and generalized form, although one is not exclusive of the other and the ocular form is considered an initial,

Bulbar muscles

Muscles of the mouth and throat responsible for speech and swallowing.

myasthenia gravs

1.

specific muscle group weakness rather than generalize weaknees

afected oculer mucsle comonly

ptosis  is 50%of cases at prasentation

bulber muscle weekness can see

limb weaness may be more sever in proximally than distally

weakness is typically least sever in the morning and worsning in evening

progresses from.mild to moderate

but

 exceserbation qnd remission could see

Diagnosis

The anti–acetylcholine receptor (AChR) antibody test for diagnosing MG has the following characteristics:

High specificity (up to 100% [4] )

Positive in as many as 90% of patients who have generalized MG

Therapy for MG includes the following:

Anticholinesterase (AchE) inhibitors

Immunomodulating agents_old age severe cases

Intravenous immune globulin (IVIg)

Plasmapheresis

Thymectomy_-when thymoma is there

AchE inhibitors

Initial treatment for mild MG

Pyridostigmine is used for maintenance therapy [6, 7]

Neostigmine is generally used only when pyridostigmine is unavailable

Corticosteroid therapy provides a short-term benefit

Azathioprine, usually after a dose of corticosteroids, is the mainstay of therapy for difficult cases

Cyclosporine A and occasionally methotrexate and cyclophosphamide are used for severe cases

muscular dystrophy

mʌskjələˈdɪstrəfi/

noun

a hereditary condition marked by progressive weakening and wasting of the muscles

dystonia myotonica

dystonia myotonica - Google Search

Mononeuritis multiplex is a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas.

Despite minor variations, all types of muscular dystrophy have in common progressive muscle weakness that tends to occur in a proximal-to-distal direction, although there are some rare distal myopathies that cause predominantly distal weakness.

type of heriditary musculer dystropy

Heritable MDs include the following:

Sex-linked MDs

Duchenne

Becker

Emery-Dreifuss

Autosomal dominant MDs

Facioscapulohumeral

Distal

Ocular

Oculopharyngeal

Autosomal recessive MD – limb-girdle for

In the X-linked forms of MD, such as the Duchenne and Becker dystrophies, the defect is located on the short arm of the X chromosome.

Duchchen musculer dystropy

no abnormality is noted in the patient at birth, and manifestations of the muscle weakness do not begin until the child begins to walk. T

Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem

pseudobulbar palsy describes impairment of function of cranial nerves IX-XII due to upper motor neuron lesions of the corticobulbar tracts in the mid-pons.

causes for bulber palsy

Causes

Genetic: Kennedy's disease, acute intermittent porphyria

Vascular causes: medullary infarction

Degenerative diseases: motor neuron disease (amyotrophic lateral sclerosis), syringobulbia

Inflammatory/infective: Guillain-Barré syndrome, poliomyelitis, Lyme disease

Malignancy: brain-stem glioma, malignant meningitis

Toxic: botulism

Autoimmune: myasthenia gravis

featues of bulber palsy

dysphagia (difficulty in swallowing)

difficulty in chewing

nasal regurgitation

slurring of speech

choking on liquids

dysphonia (defective use of the voice, inability to produce sound due to laryngeal weakness)

dysarthria (difficulty in articulating words due to a CNS problem)

Nasal speech lacking in modulation and difficulty with all consonants

Tongue is atrophic and shows fasciculations.

Dribbling of saliva.

Weakness of the soft palate, examined by asking the patient to say aah.

The jaw jerk is normal or absent.

The gag reflex is absent.

Dystonia myotonica featues

Musculer dystropy and dystonia myotonica ara completely deferent  things.

Dystonia myotonica  Fx

Eyala shake hand karama atha galavaganna bee...SLOW HAND GRIP

Receding hairline kiyanne essaraha thatte

Weakness of facial and hand muscle

Weekness of facial and neck musle

Cateract

Nasal speach

Prolong QT interval

Cardio myopathies

causes for mononuritis multiflex

Diabetes mellitus [1, 3]

Vasculitis [4, 5, 6, 7]

Amyloidosis [8]

Direct tumor involvement - Lymphoma, leukemia [9, 10]

Polyarteritis nodosa [11]

Rheumatoid arthritis [12, 13]

Systemic lupus erythematosus [14, 15]

Paraneoplastic syndromes

hiv

leprasy

polymisitis

Polymyositis is an idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness; elevated skeletal muscle enzyme levels; and characteristic electromyography (EMG) and muscle biopsy findings (see the images belo

dermatomyositis

dermatomyositis is an idiopathic, inflammatory myopathy associated with

featues of polymiositis and dermatomyositis

The history of patients with polymyositis or dermatomyositis(cutenious manifestatiion are there) typically includes the following:

Symmetrical, proximal muscle weakness with insidious onset

Muscles usually painless (Myalgias occur in fewer than 30% of patients.)

Dysphagia (30%) and aspiration, if pharyngeal and esophageal muscles are involved

Arthralgias may be associated

Difficulty kneeling, climbing or descending stairs, stepping onto a curb, raising arms, lifting objects, combing hair, and arising from a seated position

Weak neck extensors cause difficulty holding the head up

Involvement of pelvic girdle usually greater than upper body weakness

Cardiac involvement may cause symptoms of pericarditis or cardiomyopathy

Characteristic rash of face, trunk, and hands seen in dermatomyositis only

diabetic (lumbosacral) amyotropy

Proximal neuropathy in diabetes mellitus (DM) is a condition in which patients develop severe aching or burning and lancinating pain in the hip and thigh. This is followed by weakness and wasting of the thigh muscles, which often occur asymmetrically. This disabling condition occurs in type 1 and type 2 DM

multiple sclerosis

Multiple sclerosis (MS) is an immune-mediated inflammatory disease that attacks myelinated axons in the central nervous system, destroying the myelin and the axon in variable degrees and producing significant physical disability within 20-25 years in more than 30% of patients. The hallmark of MS is symptomatic episodes that occur months or years apart and affect different anatomic locations.

Multiple slerosis

The relapsing/remittinv disorder consists of plaque of demylinations at site throught the CNS(but not periperal nerve)

female more than male 2 to 1

onset of age 30...remember u met a patient at ETU with relapsing

symptoms

unilateral optic neuritis

blind or bluringbif vision

pain during moving eyes

numbness limbs

leg weakness

barin stem or cerebeller sign such as diplopia or ataxia

sumptoms worst with hot barth

treatmet is  METHYL PREDISILON IV

Plasmaparisis and iv dexamethazone

Signs and symptoms of MS

Classic MS signs and symptoms are as follows:

Sensory loss (ie, paresthesias): Usually an early complaint

Spinal cord symptoms (motor): Muscle cramping secondary to spasticity

Spinal cord symptoms (autonomic): Bladder, bowel, and sexual dysfunction

Cerebellar symptoms: Charcot triad of dysarthria, ataxia, and tremor

Optic neuritis

Trigeminal neuralgia: Bilateral facial weakness or trigeminal neuralgia

Facial myokymia (irregular twitching of the facial muscles): May also be a presenting symptom

Eye symptoms: Including diplopia on lateral gaze (33% of patients)

Heat intolerance

Constitutional symptoms: Especially fatigue (70% of cases) and dizziness

Pain: Occurs in 30-50% of patients at some point in their illness

cervical spondylosis

Tuesday, December 1, 2015

1:03 AM

comlression of the cervical spinal cord(myelopathy)and nerve root(radiculopathy) causing progressive spastic quadriparesis with sensory loss below the neck.

symotoms..

neck pain and stiffness

arm oain(brachialgia)

spastic leg weakness+/- ataxia

sign

limited painful neck movement

crepituss

arm-LMN sign atbthe levelnof compress cordor rootUMN sign below that.

atropybof hand and forarm muscle

sensory loss for specialy pain and twmperature

leg

spasticuty,weakness....brick reflex+/-planter extense

position and vibreasion sense reduce

??sensory level

root compression .. radiculopathy

Tuesday, December 1, 2015

1:07 AM

pain of arm and fingers

diminished  r3flexes

dermotomal sensory disterbance

Capture Dec 1, 2015

Tuesday, December 1, 2015

1:08 AM

The 2 major neuropathologic findings in Parkinson disease are loss of pigmented dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neurites

clincal diagnosis of PD

Clinical diagnosis requires the presence of 2 of 3 cardinal signs:

Resting tremor

Rigidity

Bradykinesia

pakinsonism and parkinson s disease

parminsonism is a syndromenof tremor,rigidity,bradykinesia and losss of postural reflexus..

treamor most marked at rest

cerebeller tremor

pill rollingbof thumb

lead pipe rigidity

unlike spastisity rigidity is present bith flexers and extensers

monitonus speach

expressionless face

dribbling

shirt

 shuffing steps with flex trunk

festinate gate

feet frozen to ground

parkinsons disease

PD is onebcause if parkinsonisom

due to degeneration of subtensia nigra doperminergic nurons

pathalogicallbhallmarknis Lewy bidies

symptoms syary at age of 60

The goal of medical management of Parkinson disease is to provide control of signs and symptoms for as long as possible while minimizing adverse effects.

Symptomatic drug therapy

Usually provides good control of motor signs of Parkinson disease for 4-6 years

Levodopa/carbidopa: The gold standard of symptomatic treatment

Monoamine oxidase (MAO)–B inhibitors: Can be considered for initial treatment of early disease

Other dopamine agonists (eg, ropinirole, pramipexole): Monotherapy in early disease and adjunctive therapy in moderate to advanced disease

Anticholinergic agents (eg, trihexyphenidyl, benztropine): Second-line drugs for tremor only

PD management

drugs should bebstart when the d8sease seriously affect the life.

L-dopa effect will wear off with time

explain the patient and offer him to choose the time2 start drugs

L-dopa

dopa decarboxylase inhibitors

dopamin agonis-pergolide and bromocriptine

subcutineous apimorphine

new dopamine agonist- ropinirole and pramipexole are better tolarated

entacapone will decrese peripheral L-dopa metabolisam by inhibiting COMT

dor tremer-strat anticholinergic like Benzhexol

Levodopa, coupled with carbidopa, a peripheral decarboxylase inhibitor (PDI), remains the gold standard of symptomatic treatment for Parkinson disease. Carbidopa inhibits the decarboxylation of levodopa to dopamine in the systemic circulation,

for PD

Monoamine oxidase (MAO)-B inhibitors can be considered for initial treatment of early disease.

Dopamine agonists (ropinirole, pramipexole) provide moderate symptomatic benefit and delay the development of dyskinesia compared with levodopa

Guillain-Barré syndrome (GBS) can be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes.

asensing weakness

Most patients complain of paresthesias, numbness, or similar sensory changes. Paresthesias generally begin in the toes and fingertips, progressing upward but generally not extending beyond the wrists or ankles.

GBS

Unlikebother neuropathies proximal muscle are more affected.and trunk,repiratory andvcranial nerve may bebaffected

Ix.   NCT and EMG

        vital capacity 4 hourly

    CSF protine increase 10g /L

The pathophysiologic mechanism of an antecedent illness and of GBS can be typified by Campylobacter jejuni infections

Miller-Fisher syndrome

Miller-Fisher syndrome (MFS), which is observed in about 5% of all cases of GBS, classically presents as a triad of ataxia, areflexia, and ophthalmoplegia.[19] Acute onset of external ophthalmoplegia is a cardinal feature.[12] Ataxia tends to be out of proportion to the degree of sensory loss. Patients may also have mild limb weakness, ptosis, facial palsy, or bulbar palsy. Patients have reduced or absent sensory nerve action potentials and absent tibial H refl

In several studies, C jejuni was the most commonly isolated pathogen in GBS. Serology studies in a Dutch GBS trial identified 32% of patients

Mononeuritis multiplex is a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas. Multiple nerves in random areas of the body can be affected.

EBV cause to inf3ctious mononuckeosis

EBV is transmitted via intimate contact with body secretions, primarily oropharyngeal secretions.

EBV is transmitted via intimate contact with body secretions, primarily oropharyngeal secretions. EBV infects the B cells in the oropharyngeal epithelium.

Circulating B cells spread the infection throughout the entire reticular endothelial system (RES), ie, liver, spleen, and peripheral lymph nodes

INDICATIONS FOR THE TREATMENT OF HELICOBACTER PYLORI INFECTION

The indications for H. pylori eradication according to the latest international consensus conference (Maastricht III) are listed below:

Nonulcer dyspepsia.

Duodenal and gastric ulcer.

Atrophic gastritis.

Gastric MALT lymphoma.

Uninvestigated dyspepsia for populations with a prevalence of H. pylori greater than 20%.

After gastric cancer resection.

First-degree relatives of patients with gastric cancer.

Unexplained iron-deficiency anemia and idiopathic thrombocytopenic purpura.

Patients on long-term NSAIDs therapy, who have gastrointestinal bleeding and/or peptic ulcer.

Patients' wishes (after explanation of risks and benefits).

Capture Dec 2, 2015

Achalasia is a primary esophageal motility disorder characterized by the absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES) in response to swallowing. T

acalasia cardia fx

Symptoms of achalasia include the following:

Dysphagia (most common)

Regurgitation

Chest pain

Heartburn

Weight loss

acalasia cardia

Barium swallow demonstrating the bird-beak appearance of the lower esophagus

bird beak sign - Google Search

rat tail appearance - Google Search

5:16 PM

intermittant dyspagia for both solid and liqvids a feature if acalasia

methotrexate

Wednesday, December 2, 2015

5:19 PM

Indicated for management of severe, active rheumatoid arthritis (RA) in adults who have had an insufficient response or intolerance to an adequate trial of first-line therapy including full dose NSAIDs

Capture Dec 2, 2015

Wednesday, December 2, 2015

5:30 PM

GUIDELINE STATEMENTS

Guideline Statement 1: The Panel recommends against PSA screening in men under age 40 years. (Recommendation; Evidence Strength Grade C)

In this age group there is a low prevalence of clinically detectable prostate cancer, no evidence demonstrating benefit of screening and likely the same harms of screening as in other age groups.

Guideline Statement 2: The Panel does not recommend routine screening in men between ages 40 to 54 years at average risk. (Recommendation; Evidence Strength Grade C)

For men younger than age 55 years at higher risk (e.g. positive family history or African American race), decisions regarding prostate cancer screening should be individualized.

Guideline Statement 3: For men ages 55 to 69 years the Panel recognizes that the decision to undergo PSA screening involves weighing the benefits of preventing prostate cancer mortality in 1 man for every 1,000 men screened over a decade against the known potential harms associated with screening and treatment. For this reason, the Panel strongly recommends shared decision-making for men age 55 to 69 years that are considering PSA screening, and proceeding based on a man's values and preferences. (Standard; Evidence Strength Grade B)

The greatest benefit of screening appears to be in men ages 55 to 69 years.

Guideline Statement 4: To reduce the harms of screening, a routine screening interval of two years or more may be preferred over annual screening in those men who have participated in shared decision-making and decided on screening. As compared to annual screening, it is expected that screening intervals of two years preserve the majority of the benefits and reduce overdiagnosis and false positives. (Option; Evidence Strength Grade C)

Additionally, intervals for rescreening can be individualized by a baseline PSA level.

Guideline Statement 5: The Panel does not recommend routine PSA screening in men age 70+ years or any man with less than a 10 to 15 year life expectancy. (Recommendation; Evidence Strength Grade C)

Some men age 70+ years who are in excellent health may benefit from prostate cancer screening.

Capture Dec 2, 2015

Wednesday, December 2, 2015

5:49 PM

brest cancer screening

Women ages 40 to 44 should have the choice to start annual breast cancer screening with mammograms (x-rays of the breast) if they wish to do so.

Women age 45 to 54 should get mammograms every year.

Women 55 and older should switch to mammograms every 2 years, or can continue yearly screening.

Screening should continue as long as a woman is in good health and is expected to live 10 more years or longer.

colonic cander screening guidline

Colon and rectal cancer and polyps

Starting at age 50, both men and women should follow one of these testing plans:

Tests that find polyps and cancer

Flexible sigmoidoscopy every 5 years*, or

Colonoscopy every 10 years, or

Double-contrast barium enema every 5 years*, or

CT colonography (virtual colonoscopy) every 5 years*

Tests that mostly find cancer

Yearly guaiac-based fecal occult blood test (gFOBT)**, or

Yearly fecal immunochemical test (FIT)**, or

Stool DNA test (sDNA) every 3 years*

* If the test is positive, a colonoscopy should be done.

** The multiple stool take-home test should be used. One test done in the office is not enough. A colonoscopy should be done if the test is positive.

cervical cancr screening

Cervical cancer

Cervical cancer testing should start at age 21. Women under age 21 should not be tested.

Women between the ages of 21 and 29 should have a Pap test done every 3 years. HPV testing should not be used in this age group unless it’s needed after an abnormal Pap test result.

Women between the ages of 30 and 65 should have a Pap test plus an HPV test (called “co-testing”) done every 5 years. This is the preferred approach, but it’s OK to have a Pap test alone every 3 years.

Women over age 65 who have had regular cervical cancer testing in the past 10 years with normal results should not be tested for cervical cancer. Once testing is stopped, it should not be started again. Women with a history of a serious cervical pre-cancer should continue to be tested for at least 20 years after that diagnosis, even if testing goes past age 65.

A woman who has had her uterus and cervix removed (a total hysterectomy) for reasons not related to cervical cancer and who has no history of cervical cancer or serious pre-cancer should not be tested.

All women who have been vaccinated against HPV should still follow the screening recommendations for their age groups.

Colon and rectal cancer and polyps

Starting at age 50, both men and women should follow one of these testing plans:

Tests that find polyps and cancer

Flexible sigmoidoscopy every 5 years*, or

Colonoscopy every 10 years, or

Double-contrast barium enema every 5 years*, or

CT colonography (virtual colonoscopy) every 5 years*

Tests that mostly find cancer

Yearly guaiac-based fecal occult blood test (gFOBT)**, or

Yearly fecal immunochemical test (FIT)**, or

Stool DNA test (sDNA) every 3 years*

* If the test is positive, a colonoscopy should be done.

** The multiple stool take-home test should be used. One test done in the office is not enough. A colonoscopy should be done if the test is positive.

The tests that can find both early cancer and polyps should be your first choice if these tests are available and you’re willing to have one of them. Talk to a health care provider about which test is best for you.

If you are at high risk of colon cancer based on family history or other factors, you may need to be screened using a different schedule. Talk with a health care provider about your history and the testing plan that’s best for you.

important

post-tubal ligation syndrome -- a range of symptoms including hot flashes, heavier periods, mood swings, depression, anxiety, insomnia, vaginal dryness, mental confusion, and fatigue -- has not been studied,  treatment is OCP

contra cepative during lactation.

1.condom

2.IUCD..mirena..progestrone contain

3..minipill..lwa dose progesterone tablet

4.birth control implant contain progestrol

depoprovera..... if you want u can take..but furtility wil be late..

uiu cant give oestrogen during lactation

MDMA....=Ectasy

ectacy will increase theblevel of 3 neuroransmitter in brain

1seratonine ..2 dopamine.and 3.norepineprine

common sitw cor endometrial deposit

The following sites are, in descending order, the most common sites of involvement found during laparoscopy:

Ovaries

Posterior cul-de-sac

Broad ligament

Uterosacral ligament

Rectosigmoid colon

Bladder

Distal ureter

Endometriosis is defined as the presence of normal endometrial mucosa (glands and stroma) abnormally implanted in locations other than the uterine cavity

endometriosis remain asymptomatic.[1] When they do occur, symptoms, such as the following, typically reflect the area of involvement:

Dysmenorrhea

Heavy or irregular bleeding

Pelvic pain

Lower abdominal or back pain [2]

Dyspareunia

Dyschezia (pain on defecation) - Often with cycles of diarrhea and constipation

Bloating, nausea, and vomiting

Inguinal pain

Pain on micturition and/or urinary frequency

Pain during exercise

treatment of endometriosis

Combination oral contraceptive pills (COCPs)

Danazol

Progestational agents

Gonadotropin-releasing hormone (GnRH) analogues

Impulse control disorder (ICD) is a class of psychiatric disorders characterized by impulsivity – failure to resist a temptation, urge or impulse that may harm oneself or others

impilse control disorder

Five behavioural stages can prove to be the symptoms of ICD: an impulse, growing tension, pleasure from acting, relief from the urge and finally guilt which may or may not arise.

Manifestations of local anesthetic toxicity typically appear 1-5 minutes after the injection, but onset may range from 30 seconds to as long as 60 minutes.[1] Initial manifestations may also vary widely. Classically, patients experience symptoms of central nervous system (CNS) excitement such as the following:

Circumoral and/or tongue numbness

Metallic taste

Lightheadedness

Dizziness

Visual and auditory disturbances (difficulty focusing and tinnitus)

Disorientation

Drowsiness

Although cardiac toxicity classically does not occur without preceding CNS toxicity, numerous published case reports describe episodes limited to cardiovascular manifestations. In these cases, onset of symptoms was delayed by 5 minutes or more.

deep peroneal nerve supplies muscular branches to the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus (propius), and an articular branch to the ankle-joint. After its bifurcation past the ankle joint, the lateral branch of the deep peroneal nerve innervates the extensor digitorum brevis and the extensor hallucis brevis, while the medial branch goes on to provide cutaneous innervation to the webbing between the first and second digits.

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l schistosomiasis caused by S mansoni occurs in 52 nations, including Caribbean countries (ie, Saint Lucia, Antigua, Montserrat, Martinique, Guadeloupe, Dominican Republic, Puerto Rico), eastern Mediterranean countries, South American countries (ie, Brazil, Venezuela, Surinam), and most countries in Africa.[23]

Obstruction of the SVC may be caused by neoplastic invasion of the venous wall associated with intravascular thrombosis or, more simply, by extrinsic pressure of a tumor mass against the relatively thin-walled SVC. Complete SVC obstruction is the result of intravascular thrombosis in combination with extrinsic pressure. I

Nonmalignant conditions that can cause SVCS include the following:

Mediastinal fibrosis

Vascular diseases, such as aortic aneurysm, vasculitis, and arteriovenous fistulas

Infections, such as histoplasmosis, tuberculosis, syphilis, and actinomycosis

Benign mediastinal tumors such as teratoma, cystic hygroma, thymoma, and dermoid cyst

Cardiac causes, such as pericarditis and atrial myxoma

Thrombosis related to the presence of central vein catheters

More than 80% of cases of SVCS are caused by malignant mediastinal tumors

The characteristic physical findings of SVCS include venous distention of the neck and chest wall, facial edema, upper extremity edema, mental changes, plethora, cyanosis, papilledema, stupor, and even coma. Bending forward or lying down may aggravate the symptoms and signs.