middle cerebral atery infarction

Fx:

1.contralateral hemiparesis

2.contralateral hemisensory loss

3.hemianopia

4.aphasia: if the dominant hemisphere is involved;

may be expressive in anterior MCA territory infarction,

receptive in posterior MCA stroke, or global with extensive infarction

neglect: non-dominant hemisphere

even after total obstrutrition of middle meningial atery conciousness will not change

Area if the conciousness is in deep thalamus that bld supply by vertibal ateries

pinpoint pupils sug3st midbrain (specially pontine) leasion

fixed dialted pupils indicate high midbrain leasion

visual feild defect

central scotoma - Google Search

blind spot eye - Google Search

enlarge blindspot occur with papilo edema

homonymous hemianopsia - Google Search

homonymous hemianopsia - Google Search

The pyramidal tracts include both the corticospinal and corticobulbar tracts. These are aggregations of upper motor neuron nerve fibres that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in control of motor functions of the body.

anterior spinal artery compression - Google Search

upper motor signs - Google Search

how does increased tone with upper motor neuron lesion - Google Search

Hypertonia/ spasticity in the literature surrounding damage to the central nervous system, namely upper motor brain lesions.

 Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition.

These consequences result in abnormally increased muscle tone of symptomatic muscles.

Pathophysiology

Hypertonia is caused by upper motor neuron lesions which may result from injury, disease, or conditions that involve damage to the central nervous system.

. Motor neuronal hyperactivity occurs due to loss of inhibition of cells of the anterior horn of the spinal cord resulting from reticulospinal tract damage.

 Different patterns of muscle weakness or hyperactivity can occur based on the location of the lesion, causing a multitude of neurological symptoms, including spasticity, rigidity, or dystonia.

Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles, shock-like contractions of all or part of a group of muscles, and abnormal muscle tone.

 It is seen in disorders such as cerebral palsy, stroke, and spinal cord injury.

Rigidity is a severe state of hypertonia where muscle resistance occurs throughout the entire range of motion of the affected joint independent of velocity.

It is frequently associated with lesions of the basal ganglia. Individuals with rigidity present with stiffness, decreased range of motion and loss of motor control.

 Dystonic hypertonia refers to muscle resistance to passive stretching (in which a therapist gently stretches the inactive contracted muscle to a comfortable length at very low speeds of movement) and a tendency of a limb to return to a fixed involuntary (and sometimes abno

cervical spondylosis cause to compress anterior spinal atery and ischemia to the cortico spinal and related tract.

so upermotor neurone lesion cause to spasticity of bith upper limb and lower limb

Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia.

Vincrestine use to treat as a chemotherapy

vincrestine,Nutrofurantoin and Isonazide cause to peripheral neuropathy

polyateritis nodosa,sacoidosia and DM can cause mononeuritis multifex

Classic polyarteritis nodosa (PAN or c-PAN) is a systemic vasculitis characterized by necrotizing inflammatory lesions that affect medium-sized and small muscular arteries, preferentially at vessel bifurcations, resulting in microaneurysm formation, aneurysmal rupture with hemorrhage, thrombosis, and, consequently, organ ischemia or infarction.

tender ,firm,hyperpigmented ,subcutenious nodule might be first sign of Polyateritis nodosa

polyateritis nodosa

PAN, like other vasculitides, affects multiple systems and has protean manifestations, although it most commonly affects skin (see the image below), joints, peripheral nerves, the gut, and the kidney.[2]

The lungs are usually spared with PAN.

. A typical PAN patient might present with fever, night sweats, weight loss, skin ulcerations or tender nodules, and severe muscle and joint pains developing over weeks or months

The pathogenesis of polyarteritis nodosa (PAN) is unknown, and no animal model is available for study. H epatitis B virus (HBV) infection is strongly linked with PAN. Evidence for immune complex–induced disease is confined to HBV-related PAN

Fx if polyaterutis nodosa

Weight loss of 4 kg or more

Livedo reticularis

Testicular pain/tenderness

Myalgia or leg weakness/tenderness

Mononeuropathy or polyneuropathy

Diastolic blood pressure greater than 90 mm/Hg

Elevated blood urea nitrogen (BUN) or creatinine level unrelated to dehydration or obstruction

Presence of hepatitis B surface antigen or antibody in serum

Arteriogram demonstrating aneurysms or occlusions of the visceral arteries

Biopsy of small- or medium-sized artery containing polymorphonuclear neutrophils

cylophospomid and polyateritis nodosa are tge current Tx of Ploateritus nodosa

small muscle of the hand ( interossei,lumbrical,thena,hypothena) suply by T 1 nerve root.

spondylosisat T1 level,apical Ca and cervucal rib can cause weekness of small muscle

ankle jerk =S1

knee jerk=L4

foot drop due to weekness of Tibialis anterior which is suply by L5 through common peroneal nerve

quadriceps mucsle suplly by L2 L3 L4 .(Predominatly L4)

blader function by lower sacral nerve

carbamazapine use for

1.complex partial seizure

2.trigeminal neuralgia

3.generalize tonic clinuc seizur

petit_mal seizue treated with ethosuximid and Na valpriate

trigeminal neuralgia - Google Search

Trigeminal neuralgia (TN), also known as tic douloureux, is a distinctive facial pain syndrome that may become recurrent and chronic. It is characterized by unilateral pain following the sensory distribution of cranial nerve V (typically radiating to the maxillary or mandibular area in 35% of affected patients) and is often accompanied by a brief facial spasm or tic

TN presents as attacks of stabbing unilateral facial pain, most often on the right side of the face. The number of attacks may vary from less than 1 per day to 12 or more per hour and up to hundreds per day.

very little stimulation make unbarebme pain... eg.. teayj brushing

The trigeminal nerve (cranial nerve V) can cause pain, because its major function is sensory. Usually,

cause for trigeminal neuralgia is stil contraversial..may be central or peripheral cause

Carbamazepine and oxcarbazepine are considered first-line therapy in trigeminal neuralgia (TN).

 Lamotrigine and baclofen are second-line therapy.

Other treatments are third line and the evidence for their efficacy is scant.

amitriptaline and gabapentine

stematil.=prochlorperazine

long term use cause to Tardive dyskinesia

Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications.eg.stematil

 People with schizophrenia and other neuropsychiatric disorders are especially vulnerable to the development of TDs after exposure to conventional neuroleptics, anticholinergics, toxins, substances of abuse, and other agents.

TDs are most common in patients with schizophrenia, schizoaffective disorder, or bipolar disorder who have been treated with antipsychotic medication for long periods, but they occasionally occur in other patients as well.

osteoporosis is usually asymptomatic and usually serum calcium level is normal

Gout and pseudogout are the 2 most common crystal-induced arthropathies. Gout (see the image below) is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate crystals and is more accurately termed calcium pyrophosphate disease.

Capture Dec 24, 2015

Thursday, December 24, 2015

3:33 PM

gout

Symptoms of gout or pseudogout include the following:

Podagra

 (initial joint manifestation in 50% of gout cases and eventually involved in 90%; also observed in patients with pseudogout and other conditions)

Arthritis in other sites –

 In gout, =ankle, wrist, finger joints, and knee;

in pseudogout, =large joints (eg, the knee, wrist, elbow, or ankle)

Monoarticular involvement most commonly, some time multiple joint involve.

In gout, attacks that begin abruptly and typically reach maximum intensity within 8-12 hours

; in pseudogout, attacks resembling those of acute gout or a more insidious onset that occurs over several days

Involvement of a single (most common) or multiple joints

Signs of inflamation

Fever (also consider infectious arthritis)

Migratory polyarthritis (rare)

Posterior interosseous nerve syndrome (rare)

Complications of gout include the following:

Severe degenerative arthritis

Secondary infections

Urate or uric acid nephropathy

Increased susceptibility to infection

Urate nephropathy

Renal stones

Nerve or spinal cord impingement

Fractures in joints with tophaceous

gout diagnosis

Joint aspiration and synovial fluid analysis

negatively bifringine cristal is diagnostic

Serum uric acid measurement (though hyperuricemia is not diagnostic of gout)

24-hour urinary uric acid evaluation

xray..ct..mri

Gout is managed in the following 3 stages:

Treating the acute attack

Providing prophylaxis to prevent acute flares

Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals

treatment for acute gout

1.Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin

2.Corticosteroids

3.Colchicine (now less commonly used for acute gout than it once was)

4.Adrenocorticotropic hormone (ACTH)

Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine, intra-articular steroids plus colchicine or NSAIDs)

Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled

Long-term management of gout is focused on lowering uric acid levels. Agents used include the following:

Allopurinol

Febuxostat

Probenecid

Nonpharmacologic measures for teat gout

Avoidance or restricted consumption of high-purine foods

Avoidance of excess ingestion of alcoholic drinks, particularly beer

Avoidance of sodas and other beverages or foods sweetened with high-fructose corn syrup

Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and desserts, as well as table salt

Maintenance of a high level of hydration with water (≥8 glasses of liquids daily)

A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the patient

Weight reduction in patients who are obese

scurvy - Google Search

high ALP and prominant costrochondrial junction can see in rickets

Colchicine is a medication most commonly used to treat gout. It is a toxic natural product and secondary metabolite, originally extracted from plants of the genus Colchicum

with cardiac tamponade tachycardia may occur.JVP may rise with inspirationdue ti increased venous return and fixed RV output.

systemic BP drip during the inspiration.

Removal of pericardial fluid is the definitive therapy for tamponade and can be done using the following three methods:

Emergency subxiphoid percutaneous drainage

Echocardiographically guided pericardiocentesis

Percutaneous balloon pericardiotomy

mitral valve prolapse is more commonnin famale. it may associate with late systelic murmur ot systolic click.

MVP does nit cause to Left ventticuler hypertropy

in VSD usually left to right shunt occur. but some time Pulmonary P. may gone up and R ventriculer  presure goes up..it cause to revers the shunt

Digoxin is occasionally used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication.

he most common indications for digoxin are atrial fibrillation and atrial flutter with rapid ventricular response, though beta blockers and/or calcium channel blockers are a better first choice

High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. T

Digoxin is no longer the first choice for heart failure, but can still be useful in people who remain symptomatic despite proper diuretic and ACE inhibitor treatmen

Digoxin is usually given orally, but can also be given by IV injection in urgent situations

Digoxin’s primary mechanism of action involves inhibition of the Na+/K+ ATPase, mainly in the

The reversal of this exchange causes an increase in the intracellular calcium concentration that is available to the contractile proteins. Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate.[20] Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential. This leads to increased contractility (the force of contraction) of the heart without increasing heart energy expenditure.

There is also evidence that digoxin increases vagal activity, thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node

thiazide diuratics has unfeverble side effect like.

1. decrese glucause tolarance

2.increse chleterol

using wafferin and asprin together  is cintraindicated .

AF

waffering reduce the riskof strok 85 %

Aspirin reducevthe risk 54%

thiazide diuratic not good for patient with metabolic syndrom as it cause to poose glucase intolarance and dislipidimia

Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic actions,[4] but have minimal effect on resting subjects.[citation needed] That is, they reduce excitement/physical exertion on heart rate and force of contraction,[46] and also tremor[47] and breakdown of glycogen, but increase dilation of blood vessels[48] and constriction of bronchi.[49]

, 20% or more of patients who receive ACE inhibitors develop a dry cough, sometimes severe enough to require discontinuation of the drug.

ACE inhibitor cough is thought to be linked to the suppression of ACE, which is proposed to result in an accumulation of substances normally metabolized by ACE: bradykinin or tachykinins (with the consequent stimulation of vagal afferent nerve fibers) and substance P.

cholestyramine, which binds bile in the gastrointestinal tract to prevent its reabsorption.

cholestyramine use to reduce bile acid reabsobtion.

cholesthyramin reduce digoxin absobtion tooo..

verapamin incresre half life of digoxin.

central chest pain radiating back ..1st DD is  aortic desection

thrombolytic theraphy has NO benificial effect on unstable angina.

only aspirin and heparin important

asbastose and silica not cause to asthma .

bronchial breathing is typically atbthe top of pleural effusion

also over the consolidated lung

clubbing and hypertropic pulmonary osteoatharopathy may seen in CA lung

Hypertrophic osteoarthropathy (also known as Hypertrophic pulmonary osteoarthropathy,Bamberger-Marie syndrome or Osteoarthropathia hypertrophicans) is a medical condition combining clubbing and periostitis of the small hand joints, especially the distal interphalangeal joints.

hypertrophic pulmonary osteoarthropathy definition - Google Search

90% ca lung is due to ciga smorning..

if non smorker develop a ca lung is due to adenocarcinoma.

small cell ca usually treated with combind chemotherapy( cyclophospomide...vincrestine...cisplatinum) and radiotheraphy

both small cell ca and non small cell ca produce hormone..

Small cell ca produce ACTH like syndrome

Non small cell ca produce parathhomormone like syndrome

pulmonary sacoidosis

B/L hyler LN enlagement

erythema nodosum over anterior surface of the leg is common

hypercalcemia is UNCOMMON complication

desirder usually resolve spontaniously  WITHOUT starting corticosteroid

idiopathic pulmonary fibrosis/fibrosing alveolitis

associate with clubbing ,fine end inspiratory crepitation

type 1 respuratory failiure

some time ANA & RF positive

fine end inspiratory crepitation

CXR....bilateral lower zone reticulo noduler shadows

advance Dx honeybcome apearance

Respiratory failure is inadequate gas exchange by the respiratory system, with the result that levels of arterial oxygen, carbon dioxide or both cannot be maintained within their normal ranges. A drop in blood oxygenation is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia.

Respiratory failure

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic.

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD])

Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

Respiratory failure

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic.

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD])

Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased

Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable Pa CO2.

Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing

ABC inpatient with fibrosis Alviso is shows both hypoxia and hop ocarina as patient hyperventilate due to hypoxia.  so it is hypoxic type respiratory failure

Chronic bronchitis is defined clinically as cough with sputum expectoration for at least 3 months a year during a period of 2 consecutive years. Chronic bronchitis is associated with hypertrophy of the mucus-producing glands found in the mucosa of large cartilaginous airways. As the disease advances, progressive airflow limitation occurs, usually in association with pathologic changes of emphysema. This condition is called chronic obstructive pulmonary disease.

In Barrett esophagus, healthy esophageal epithelium is replaced with metaplastic columnar cells—the result, it is believed, of damage from prolonged exposure of the esophagus to the refluxate of gastroesophageal reflux disease (GERD). The inherent risk of progression from Barrett esophagus to adenocarcinoma of the esophagus has been established

chronic pain creators serum amylase normal or slightly increased.

acute pancreatic is greatly associated with cholilithisis and chronic pancreatic is greatly associated with alcoholism

condos a coma

chondrosacoma is not chemosesitive. sx is the treatment

Pseudomembranous colitis usually is associated with antibiotic use. In mild or moderate cases, supportive therapy alone is sufficient.

Pseudomembranous Colitis

The antibiotic-induced change in the balance of normal gut flora allows overgrowth of C difficile.[4] Colitis results from the bacterial production of large amount of toxins. The most important toxins are toxin A (enterotoxin) and toxin B (cytotoxin).

Clindamycin, lincomycin, ampicillin, and cephalosporin have been implicated in most of the reported cases, but any antimicrobial agent (including antifungal, antiviral, and metronidazole) could incite the disease, regardless of the amount administered or the route of administration.

C difficile, a gram-positive, spore-forming, anaerobic bacillus, is isolated in almost all of these cases.

normal mortality..2%

adulty motality 15 to 29%

toxic megacolon

toxic megacolon

spiranolactone and histamine H2 receptor antagonist cause to gynecomastia

Prolactinomas are the most common hormone-secreting pituitary tumors. Based on its size, a prolactinoma can be classified as a microprolactinoma (< 10 mm diameter) or a macroprolactinoma (>10 mm diameter).

microadenoma is very very common

rrised serum prolactine level can seen in patient with sever primary hypothyroidism.

mix type of pitiutary tumuor produce excesss prolactine and groth homone.prolactine cause to hypogonadism.

prolacine release can be inhibit by bromocriptine.

most common cause for addsion disease is auto immune adrenalitis.. thise days it was TB

primary adrenocortical insufficiency (Addison disease)

adrenal gland - Google Search

Addison disease (or Addison's disease) is adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex. It affects glucocorticoid and mineralocorticoid function. The onset of disease usually occurs when 90% or more of both adrenal cortices are dysfunctional or destroyed.

Morbidity and mortality associated with Addison disease usually are due to failure or delay in making the diagnosis or a failure to institute adequate glucocorticoid and mineralocorticoid replacement.[4]

If not treated promptly, acute addisonian crisis may result in death

Idiopathic autoimmune Addison disease tends to be more common in females and children.

adeson desease presentation

Patients usually present with features of both glucocorticoid and mineralocorticoid deficiency. The predominant symptoms vary depending on the duration of disease.

Patients may present with clinical features of chronic Addison disease or in acute addisonian crisis precipitated by stress factors such as infection, trauma, surgery, vomiting, diarrhea, or noncompliance with replacement steroids.

Presentation of chronic Addison disease

The onset of symptoms most often is insidious and nonspecific.

Hyperpigmentation of the skin and mucous membranes often precedes all other symptoms by months to years. It is caused by the stimulant effect of excess adrenocorticotrophic hormone (ACTH) on the melanocytes to produce melanin

Hyperpigmentation is usually generalized but most often prominent on the sun-exposed areas of the skin, extensor surfaces, knuckles, elbows, knees, and scars formed after the onset of disease. Scars formed before the onset of disease (before the ACTH is elevated) usually are not affected. Palmar creases, nail beds, mucous membranes of the oral cavity (especially the dentogingival margins and buccal areas), and the vaginal and perianal mucosa may be similarly affected.

Other skin findings include vitiligo, which most often is seen in association with hyperpigmentation in idiopathic autoimmune Addison disease. It is due to the autoimmune destruction of melanocytes

Almost all patients complain of progressive weakness, fatigue, poor appetite, and weight loss.

Prominent gastrointestinal symptoms may include nausea, vomiting, and occasional diarrhea.

Dizziness with orthostasis due to hypotension occasionally may lead to syncope. This is due to the combined effects of volume depletion, loss of the mineralocorticoid effect of aldosterone, and loss of the permissive effect of cortisol in enhancing the vasopressor effect of the catecholamines.

Myalgias and flaccid muscle paralysis may occur due to hyperkalemia

Impotence and decreased libido may occur in male patients, especially in those with compromised or borderline testicular function.

Female patients may have a history of amenorrhea due to the combined effect of weight loss and chronic ill health or secondary to premature autoimmune ovarian failure.

Presentation of acute Addison disease

Patients in acute adrenal crisis most often have prominent nausea, vomiting, and vascular collapse. They may be in shock and appear cyanotic and confused.

Abdominal symptoms may take on features of an acute abdomen.

Patients may have hyperpyrexia, with temperatures reaching 105° F or higher, and may be comatose.

In acute adrenal hemorrhage, the patient, usually in an acute care setting, deteriorates with sudden collapse, abdominal or flank pain, and nausea with or without hyperpyrexia.

The most common cause of Addison disease is idiopathic autoimmune adrenocortical insufficiency resulting from autoimmune atrophy, fibrosis, and lymphocytic infiltration of the adrenal cortex, usually with sparing of the adrenal medulla. This accounts for more than 80% of reported cases. Idiopathic autoimmune adrenocortical atrophy and tuberculosis (TB) account for nearly 90% of cases of Addison disease.[10, 11]

summury of the lab test for adesons disease

The diagnosis of adrenocortical insufficiency rests on the assessment of the functional capacity of the adrenal cortex to synthesize cortisol. This is accomplished primarily by use of the rapid ACTH stimulation test (Cortrosyn, cosyntropin, or Synacthen).

Performing the rapid adrenocorticotrophic hormone test

nterpreting the rapid adrenocorticotrophic hormone test [

In acute adrenal crisis, where treatment should not be delayed in order to do the tests, a blood sample for a random plasma cortisol level should be drawn prior to starting hydrocortisone replacement.

A random plasma cortisol value of 25 mcg/dL or greater effectively excludes adrenal insufficiency of any kind. However, a random cortisol value in patients who are acutely ill should be interpreted with caution and in correlation with the circumstances of each individual patient. Random cortisol levels should also be interpreted cautiously in critically ill patients with hypoproteinemia (serum albumin < 2.5 g/dL). Approximately 40% of these patients will have baseline and cosyntropin-stimulated cortisol levels below the reference range even though the patients have normal adrenal function (as evidenced by the measurement of free cortisol levels

other than above test lot of test are doing

treatmet for adrenal crisis

In patients in acute adrenal crisis, IV access should be established urgently, and an infusion of isotonic sodium chloride solution should be begun to restore volume deficit and correct hypotension. Some patients may require glucose supplementation. The precipitating cause should be sought and corrected where possible.

Administer 100 mg of hydrocortisone in 100 cc of isotonic sodium chloride solution by continuous IV infusion at a rate of 10-12 cc/h.

also 300 to 400mg of hydroctzone in 1 litter of saline can infuse over 24 hour

Clinical improvement, especially blood pressure response, should be evident within 4-6 hours of hydrocortisone infusion. Otherwise, the diagnosis of adrenal insufficiency would be questionable.

After 2-3 days, the stress hydrocortisone dose should be reduced to 100-150 mg, infused over a 24-hour period, irrespective of the patient's clinical status. This is to avoid stress gastrointestinal bleeding.

As the patient improves and as the clinical situation allows, the hydrocortisone infusion can be gradually tapered over the next 4-5 days to daily replacement doses of approximately 3 mg/h (72-75 mg over 24 h) and eventually to daily oral replacement doses, when oral intake is possible.

As long as the patient is receiving 100 mg or more of hydrocortisone in 24 hours, no mineralocorticoid replacement is necessary. The mineralocorticoid activity of hydrocortisone in this dosage is sufficient.

Thereafter, as the hydrocortisone dose is weaned further, mineralocorticoid replacement should be instituted in doses equivalent to the daily adrenal gland aldosterone output of 0.05-0.20 mg every 24 hours. The usual mineralocorticoid used for this purpose is 9-alpha-fludrocortisone, usually in doses of 0.05-0.10 mg per day or every other day.

Patients may need to be advised to increase salt intake in hot weather.

uring surgical procedures, 100 mg of hydrocortisone should be given, preferably by the IM route, prior to the start of a continuous IV infusion

A pheochromocytoma (see the image below) is a rare, catecholamine-secreting tumor that may precipitate life-threatening hypertension. The tumor is malignant in 10% of cases but may be cured completely by surgical removal. Although pheochromocytoma has classically been associated with 3 syndromes—von Hippel-Lindau (VHL) syndrome, multiple endocrine neoplasia type 2 (MEN 2), and neurofibromatosis type 1 (NF1)—

Classically, pheochromocytoma manifests as spells with the following 4 characteristics:

Headaches

Palpitations

Diaphoresis

Severe hypertension

Diagnostic tests for pheochromocytoma include the following:

Plasma metanephrine testing: 96% sensitivity, 85% specificity [1]

24-hour urinary collection for catecholamines and metanephrines: 87.5% sensitivity, 99.7% specificity [2]

Test selection criteria include the following:

Use plasma metanephrine testing in patients at high risk (ie, those with predisposing genetic syndromes or a family or personal history of pheochromocytoma)

Use 24-hour urinary collection for catecholamines and metanephrines in patients at lower risk

when thyroxine take exogenously it cause mark reduction if TSH and T3

high dose of oestrogen containing OCP cause to increase DVT /strock ,migrain and small rise in BP

both congestive CF and polysithemia rubravera cuse typically law ESR

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 remaining 20% are principally meningiomas.

autosomal dominent Dx

neurofibromatosis type 2

congenital sperocytosis

polycystic kidney Dx

G6PD deficiency _x link recesive

alfa 1 antitripsine deficiency =autosomal recesive

imobilisazion cause to hypercalcemia

hydated disease

it is only by ingestion the egs released by the tapeworm in the dog faeces thst hydated disease can develop in tha itermediate host( human or sheep)

the tape worm infected pigs is Taenia solium in this instance human contact the disease by eating infected pork and develop an intestinal tape wotm as ptimary host

hydatid disease - Google Search

side effects

levodopa=visual halusination, confusion

amantadine=visual halusination

proponalol= nightmare

haloperidol/butyrophenon like drugs=  Tardive diskinaesia

Chlorpromazin=pakinsonism like syndrom

effect of digitalis potentiated by both hypokaleamia and hypocalceamia

persistant dry cough and angio edema(welling over toung and skin) are side effect of ACE inhibitor

short term side effect of steroid are

mood disorxer

 hypokaleamia

high dose of prednislone cause to avasculer necrosis of  bone. minaralocoricoid effect of prednislone cause to Na and water retention .

Amphotericin B is an antifungal drug often used intravenously for serious systemic fungal infections and is the only effective treatment for some fungal infectio

side effect of IV ampoteracine B

hypokalemia,anemia,increase sCr

long term immosupretiom therapy( azythioprin,cylophosphamid,sterid) cause to

1,skin cance

2.asepic bone necrosis

3.lens cateract

neurological manifestation of HIV infection

1.Gullian Barre sundrom

2.dementia

3.pheriperal neuropathy

ITP associate with some drugs like heparin,penicillin and quinine

ITP is common betweenn20 to40 years old women

destruction of plt by IV gMma globulin

Malignant melanoma (see the image below) is a neoplasm of melanocytes or a neoplasm of the cells that develop from melanocytes.

Surgery is the definitive treatment for early-stage melanoma, with medical management generally reserved for adjuvant treatment of advanced melanoma.

hx of melanoms

Signs and symptoms

The history should address the following:

Family history of melanoma or skin cancer

Family history of irregular, prominent moles

Family history of pancreatic cancer or astrocytoma

Previous melanoma (sometimes multiple; patients have reported as many as 8 or more primary melanomas)

Previous sun exposure

Changes noted in moles (eg, size, color, symmetry, bleeding, or ulceration)

History or family history of multiple nevus syndrome

Physical examination includes the following:

Total-body skin examination, to be performed on initial evaluation and during all subsequent visits

Serial photography, epiluminescence microscopy

Early melanomas may be differentiated from benign nevi by the ABCDs, as follows:

A - Asymmetry

B - Border irregularity

C - Color that tends to be very dark black or blue and variable

D - Diameter ≥ 6 mm

If a patient is diagnosed with a melanoma, examine all lymph node groups

Procedures to be considered in the workup include the following:

Complete excisional biopsy of a suggestive lesion

Surgical excision or reexcision after biopsy

Elective lymph node dissection (ELND) for patients with clinically enlarged nodes and no evidence of distant disease

Sentinel lymph node biopsy (SLNB; see Sentinel Lymph Node Biopsy in Patients With Melanoma)

melanoma staging

Breslow classification (thickness) is as follows:

0.75 mm or less

0.76-1.5 mm

1.51-4 mm

4 mm or more

Histologic types of melanoma

There are five different forms, or histologic types, of melanoma:

Superficial spreading melanomas

Nodular melanomas

Lentigo maligna melanomas

Acral lentiginous melanomas

Mucosal lentiginous melanomas

Superficial spreading melanomas

Approximately 70% of cutaneous malignant melanomas are the superficial spreading melanoma (SSM) type. Many SSMs arise from a pigmented dysplastic nevus, often one that has long been stable. Typical changes include ulceration, enlargement, or color changes

A tophus (Latin: "stone", plural tophi) is a deposit of uric acid crystals, in the form of monosodium urate crystals, in people with longstanding hyperuricemia (high levels of uric acid in the blood). Tophi are pathognomonic for the disease gout.

common site... 1st meta taso phalangial joint of foot

 1st distal interpalangial joint of 1st finger

achelees tendon

anterior helix of the ear

gouty tophi - Google Search

Transvaginal ultrasonography, or endovaginal ultrasonography, can be used to visualize an intrauterine pregnancy by 24 days postovulation or 38 days after the last menstrual period (about 1 week earlier than transabdominal ultrasonography)

Salpingitis is the inflammation of the fallopian tube, most commonly caused by an infection. Acute salpingitis is often used synonymously with pelvic inflammatory disease (P

Clinical presentation of ectopic pregnancy occurs at a mean of 7.2 weeks after the last normal menstrual period, with a range of 4 to 8 weeks. L

Hydrops fetalis (fetal hydrops) is a serious fetal condition defined as abnormal accumulation of fluid in 2 or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin edema.

n some patients, it may also be associated with polyhydramnios and placental edema.

vulvovaginitis  Fx

vaginal discharge

erythema

soreness

prjritus

duysuria

Vulvovaginal candidiasis

Acute vulvovaginal candidiasis

In acute vulvovaginal candidiasis, vulvar pruritus and burning are the main symptoms. Patients commonly complain of both symptoms after intercourse or upon urination.

In lewy body demential withing one year of dementia  parkinsonm symptoms wil be apper..sometimes both comes together

Hypochondriasis also known as hypochondria, health anxiety or illness anxiety disorder, refers to worry about having a serious illness.

This debilitating condition is the result of an inaccurate perception of the condition of body or mind despite the absence of an actual medical condition

An individual suffering from hypochondriasis is known as a hypochondriac.

Hypochondriasis", as a somatoform disorder[4] and one study has shown it to affect about 3% of the visitors to primary care settings.[5] The newly published DSM-5 replaces the diagnosis of hypochondriasis with the diagnoses of "Somatic Symptom Disorder" and "Illness Anxiety Disorder".[6]

Pregnant women (at any stage of pregnancy)
Influenza (flu

if b score more than 9 good for normal labour

bishop scord - Google Search

ischeamic limb pain

the condition is often partially or fully relieved by placing the extremity in a dependent position, so that perfusion is enhanced by the effects of gravity.

Current standard of care for the prevention of MTCT of HBV infection is treatment of the newborn with HBIG and HBV vaccination (Table 3). At-risk neonates who received HBV vaccine alone at birth had a 26 to 36% chance of MTCT of HBV infection,[47] whereas administration of HBIG alone at birth decreased the rate of perinatal HBV transmission to 15 to 20%

There has been little evidence that cesarean delivery prevents HBV transmission, and current guidelines do not recommend cesarean section to decrease the risk of MTCT in pregnant women with chronic HBV infection.[21] Cesarean section would have to be performed before the onset of labor or before the rupture of membranes to be effective.

Although breast milk contains HBsAg,[66] breastfeeding does not increase the risk of MTCT of HBV

amniocentiyis and fetal scalp bldcsmpling iare the highest risk to infect the baby with matoer who has hep

Who Should Have a Bone Density Test?

According to National Osteoporosis Foundation guidelines, there are several groups of people who should consider bone density testing:

All postmenopausal women below age 65 who have risk factors for osteoporosis.

All women aged 65 and older.

Women with medical conditions associated with osteoporosis. Your health care provider can tell you if you have a medical condition associated with osteoporosis.

Men age 70 or older.

Men ages 50-69 with risk factors for osteoporosis or medical conditions associated with osteoporosis.

Tibial torsion is inward twisting of the tibia (shinbone) and is the most common cause of intoeing.

Capture Dec 30, 2015

Wednesday, December 30, 2015

5:36 PM

Metastases to the ovaries are relatively frequent; the most common are from the endometrium, breast, colon, stomach, and cervix. See the image below.

Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is a chronic disorder of the digestive tract that results in an inability to tolerate gliadin, the alcohol-soluble fraction of gluten. Gluten is a protein commonly found in wheat, rye, and barley.

celiac disease

At the time of diagnosis, further investigations may be performed to identify complications, such as iron deficiency (by full blood count and iron studies), folic acid and vitamin B12 deficiency and hypocalcaemia (low calcium levels, often due to decreased vitamin D levels). Thyroid function tests may be requested during blood tests to identify hypothyroidism, which is more common in people with coeliac disease.[13]

Osteopenia and osteoporosis, mildly and severely reduced bone mineral density, are often present in people with coeliac disease, and investigations to measure bone density may be performed at diagnosis, such as dual-energy X-ray absorptiometry (DXA) scanning, to identify risk of fracture and need for bone protection medication.[12][13]

Dyspepsia/GORD also known as indigestion, is a condition of impaired digestion.

Weight loss

Iron-deficiency anaemia

GI bleeding

Persistent vomiting

Difficulty swallowing

Epigastric mass

Commonly encountered alarm symptoms include: dysphagia (difficulty swallowing); odynophagia (painful swallowing); gastrointestinal bleeding or anemia; weight loss; and chest pain. Dysphagia in combination with GERD usually signifies a peptic stricture, but can also be present in esophageal malignancies.

breach presentation

Women with a  breech  presentation  at  term, Grade and reference with to E CV,  should be  informed  about  ECV no  contraindications ,  the  likely  success  rate Consensusand offered  it  if  clinically  appropriate. Recommendation 4 based recommendation 10 Grade ECV  is  inappropriate  where a  caesarean  section  is  indicated  on  othe

Forms of HRT

HT can be prescribed as local (creams, pessaries, rings) or systemic therapy (oral drugs, transdermal patches and gels, implants). Hormonal products available in such preparations may contain the following ingredients:

Estrogen alone

Combined estrogen and progestogen

Selective estrogen receptor modulator (SERM)

Gonadomimetics, such as tibolone, which contain estrogen, progestogen, and an androgen

The estrogens most commonly prescribed are conjugated estrogens that may be equine (CEE) or synthetic, micronized 17β estradiol, and ethinyl estradiol. The progestins that are used commonly are medroxyprogesterone acetate (MPA) and norethindrone acetate.

The various schedules of hormone therapy include the following:

Estrogen taken daily

Cyclic or sequential regimens: Progestogen is added for 10-14 days every 4 weeks

Continuous combined regimens: Estrogen and progestogen are taken daily

1. Patient Summary

The main use of menopausal hormone therapy (MHT) is the relief of menopausal symptoms, such as hot

flushes. However, there may be other benefits including reducing the risk of fractures of the hip, wrist, and

spine. Because there may be some potential risks associated with use of MHT, it is important the women

using, or planning to use, MHT should be carefully assessed and have treatment individualised to their

needs and general health status. As women’s health may change over time, regular reassessment by a

doctor experienced in use of MHT is important.

2. Summary of recommendations

Recommendation1 Grade

The primary indication for the use of MHT is the alleviation of distressing

menopausal vasomotor symptoms.

Consensus-based

recommendation

Recommendation 2 Grade

In women with primary ovarian insufficiency MHT should be continued until the

normal age of the menopause.

Consensus-based

recommendation

Recommendation 3 Grade

MHT is also effective and appropriate for the prevention of osteoporosis related

fracture in at risk women within 10 years of the menopause.

Consensus-based

recommendation

Recommendation 4 Grade

The risk of VTE and stroke increases with oral MHT but the absolute risk is rare

before age 60.

Consensus-based

recommendation

Recommendation 5 Grade

In women within 10 years of the menopause MHT does not increase the risk of

coronary heart disease.

Consensus-based

recommendation

Recommendation 6 Grade

Combined MHT use for more than 5 years may be associated with an increased

risk of breast cancer. This risk appears to be related to the use of a Progestogen

and duration of therapy.

Consensus-based

recommendation

Recommendation 7 Grade

Oestrogen only MHT does not increase risk of breast cancer. Consensus-based

recommendation

Recommendation 8 Grade

Current safety data do not support the use of MHT in breast cancer survivors. Consensus-based

recommendation

Recommendation 9 Grade

Oestrogen only therapy is appropriate for women who have undergone.

Hysterectomy.

Consensus-based

recommendation

Recommendation 10 Grade

Oestrogen plus Progestogen should be used in women with an intact uterus. Consensus-based

recommendation

Recommendation 11 Grade

The dose and duration of therapy should be consistent with treatment goals. Consensus-based

recommendation