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PHEOCHROMOCYTOMA causes,pathophysiology,clinical features,dx and treatment
PHEOCHROMOCYTOMA is a catecholamine secreting tumor of the adrenal gland originating from the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent. Extra-adrenal paragangliomas (often described as extra-adrenal pheochromocytomas) are closely related, though less common,
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PARALYTIC ILEIUS causes,pathophysiology,clinical features,diagnosis and treatment
ILEUS also known as paralytic ileus is a temporary arrest of intestinal peristalsis. It occurs most commonly after abdominal surgery, particularly when the intestines have been manipulated. Symptoms are nausea, vomiting, and vague abdominal discomfort. Diagnosis is based on x-ray findings and clinical impression. Treatment is supportive, with nasogastric suction and IV fluids. Etiology In addition to postoperative causes, ileus also results from intraperitoneal or retroperitoneal inflammation (eg, appendicitis, diverticulitis, perforated duodenal ulcer), retroperitoneal or intra-abdominal hematomas (eg, ruptured abdominal aortic aneurysm, lumbar compression fracture), metabolic disturbances (eg, hypokalemia), or drugs (eg, opioids, anticholinergics, sometimes Ca channel blockers). Ileus sometimes occurs in association with renal or thoracic disease (eg, lower rib fractures, lower lobe pneumonias, MI). Gastric and colonic motility disturbances after abdominal surgery are common. The small bowel is typically least affected, with motility and absorption returning to normal within hours after surgery. Stomach emptying is usually impaired for about 24 h or more. The colon is often most affected and may remain inactive for 48 to 72 h or more. classic colicky pattern present in mechanical obstruction. There may be obstipation or passage of slight amounts of watery stool. Auscultation reveals a silent abdomen or minimal peristalsis. The abdomen is not tender unless the underlying cause is inflammatory. Diagnosis • Clinical evaluation • Sometimes x-rays The most essential task is to distinguish ileus from intestinal obstruction. In both conditions, x-rays show gaseous distention of isolated segments of intestine. In postoperative ileus, however, gas may accumulate more in the colon than in the small bowel. Postoperative accumulation of gas in the small bowel often implies development of a complication (eg, obstruction, peritonitis). In other types of ileus, xray findings are similar to obstruction; differentiation can be difficult unless clinical features clearly favor one or the other. Water-soluble contrast studies may help differentiate. Treatment • NGT • IV fluids Treatment involves continuous nasogastric suction, npo status, IV fluids and electrolytes, a minimal amount of sedatives, and avoidance of opioids and anticholinergic drugs. Maintaining an adequate serum K level (more than 4 mmol/L) is especially important. Ileus persisting more than 1 wk probably has a mechanical obstructive cause, and laparotomy should be considered. Sometimes colonic ileus can be relieved by colonoscopic decompression; rarely, cecostomy is required. Colonoscopic decompression is helpful in treating pseudo-obstruction (Ogilvie's syndrome), which consists of apparent obstruction at the splenic flexure, although no cause can be found by contrast enema or colonoscopy for the failure of gas and feces to pass this point. Some clinicians use IV neostigmine (requires cardiac monitoring) to treat Ogilvie's syndrome
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What is peritonitis? Peritonitis is an inflammation of the membrane which lines the inside of the abdomen and all of the internal organs known as the peritoneum.... THANK YOU and don't forget to SUBSCRIBE to our channel ITS EAZZY MED for you to get update on various tutorials that will help you master medicine quicky and easily . The information provided is for learning and should not substitute medical advice. THANK YOU.
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ENDOCARDITIS causes,symptoms,pathophysiology,diagnosis and treatment
Endocarditis (infective endocarditis) is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as vegetations, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify. There are several ways to classify endocarditis. The simplest classification is based on cause: either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu-like feeling, cardiac murmur, heart failure, petechia of anterior trunk, Janeway's lesions, Infective endocarditis is an infection of the inner surface of the heart, usually the valves. Symptoms may include fever, small areas of bleeding into the skin, heart murmur, feeling tired, and low red blood cells. Complications may include valvular insufficiency, heart failure, stroke, and kidney failure. The cause is typically a bacterial infection and less commonly a fungal infection. Risk factors include valvular heart disease including rheumatic disease, congenital heart disease, artificial valves, hemodialysis, intravenous drug use, and electronic pacemakers. The bacterial most commonly involved are streptococci or staphylococci. Diagnosis is suspected based on symptoms and supported by blood cultures or ultrasound.
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FOURNIER GANGRENE causes,pathophysiology,features,diagnosis and treatment
Fournier gangrene, is a polymicrobial necrotizing fasciitis of the perineal, perianal, or genital areas Pathophysiology Localized infection adjacent to a portal of entry is the inciting event in the development of Fournier gangrene. Ultimately, an obliterative endarteritis develops, and the ensuing cutaneous and subcutaneous vascular necrosis leads to localized ischemia and further bacterial proliferation. Rates of fascial destruction as high as 2-3 cm/h have been described Signs & Symptoms Symptoms include fever, general discomfort (malaise), moderate to severe pain and swelling in the genital and anal areas (perineal) followed by rankness and smell of the affected tissues (fetid suppuration) leading to full blown (fulminating) gangrene. Rubbing the affected area yields the distinct sounds (crepitus) of gas in the wound and of tissues moving against one another (palpable crepitus). In severe cases, the death of tissue can extend to parts of the thighs, through the abdominal wall and up to the chest wall. This disease is commonly found in conjunction with other disorders (comorbidity), especially those that weaken the immune system. Some disorders that increase the predisposition to Fournier gangrene are diabetes mellitus, profound obesity, cirrhosis, interference with the blood supply to the pelvis, and various malignancies Causes Portals of entry for the bacteria, fungi, and/or viruses responsible for a particular case of Fournier gangrene are generally colorectal, urogenital or cutaneous in origin. Anorectal abscesses, urinary tract infections, surgical instrumentation and other contributing factors have all been implicated. Some cases continue to be of unknown cause (idiopathic). Why this process occasionally develops in individuals with common ailments is still not understood. There are many ways for the virulent microorganism to gain access to the host, where the compromised immunological system is unable to prevent the infection from taking hold. The virulence of the resulting disorder is thought to be enhanced by the toxins and enzymes produced by the combination of microorganisms (synergy).
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LEIOMYOMA (Fibroids)
What are leiomyomas? These are benign tumors that arise from the overgrowth of smooth muscle and connective tissue in the uterus...they are oestrogen dependent tumors that grow during the reproductive age
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Kidney function tests are group of investigations done to evaluate the function of thr kidneys. They can be classified to two categories A. Tests for glomerular function B.Tests for tubular function The tests that are part of the Kidney Function test panel are: (a) Urine examination (b) Serum Urea (c) Serum creatinine (d) Blood urea nitrogen (BUN) (e) Calcium (f) Phosphorus (g) Protein (h) Albumin (i) Creatinine clearance (j) Urea clearance (k) Inulin clearance (l) Dilution and Concentration test (l) Serum electrolyte levels URINE EXAMINATION Before we do a quantitative examination of urine a qualitative examination is necessary as it can provide excellent clues to the nature and location of the lesion in the renal system. This examination consists of a physical examination where the colour, odour, quantity, specifc gravity etc of the urine is noted. Microscopic examination of urine is done to rule out any pus cells, Rbc casts, Crystals. SERUM UREA Urea is the end product of protein catabolism. The urea is produced from the amino group of the amino acids and is produced in the liver by means of the Urea cycle. BLOOD UREA NITROGEN (BUN) Sometimes the Serum urea level is expressed as blood urea nitrogen. BUN can be easily calculated from the serum urea level A rise in blood nitrogen level is known as azotemia. SERUM CREATININE LEVEL Creatine is a small tripeptide found in the muscles. It stays in its phosphorylated form and releases energy for any burst of muscular activity. It is released from the muscles during regular wear and tear and is converted to creatinine (its internal anhydride). It is to be remembered that unlike urea, creatinine is not a toxic waste. It is simply used as a marker of renal function. Creatinine is freely filtered at the glomerulus and is also to a very small extent secreted into the tubules. So any problem with gromerular filtrations has a significant effect on the excretion of creatinine resulting in a much substantial rise in serum creatinine level. Normal serum creatinine level is 0.6 to 1.5 mg/dl. Serum creatinine is a better indicator of renal function and more specifically glomerular function than urea. For a particular individual the creatinine level is dependent on the muscle mass and muscle wear and tear. There may be significant difference in creatinine level of individuals with vastly differing muscle mass. For example a body builder or athlete will have higher creatinine levels than a sedentary desk worker. Similarly creatinine level will also increase in case of any muscle trauma or excessive wear and tear as seems in athletes and people involved in hard physical labor. Creatinine is most commonly measured in laboratories calorimetrically by Jaffe’s method. UREA CLEARANCE Urea clearance is the hypothetical amount of blood from which kidney clears urea in one minute. This is measured by measuring the concentration of urea in blood, concentration of urea in urine and amount of urine excreted over a one hour interval. Urea clearance is less than its glomerular filtration as some of the urea that is filtered at the glomerulus is reabsorbed at the tubules. To measure urea clearance first the patient is made to void urine and then the made to drink two glasses of water. Then the urine is collected after an hour and a blood specimen is also collected at the same time. Then the patients urine sample is collected after another hour. The urea level in the two urine samples and the blood sample is measured. The urine volume is calculated as urine output per minute. The functional unit of the kidney is called a nephron. It consists of two main parts, the glomerulus and the tubular system. The glomerulus is composed of a bowman’s capsule and a tuft of leaky blood vessels encapsulated by the bowman’s capsule. The primary purpose of the glomerulus is filtrations. The leaky vessels filter into the glomerulus almost all the water, electrolytes, small proteins, nutrients such as sugar
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PHENYTOIN: ADVERSE EFFECTS PHENYTOIN P-P-450 interactions H-Hirsutism E-Enlarged gums N-Nystagmus Y-Yellow-browning of skin T-Teratogenicity O-Osteomalacia I-Interference with B12 metabolism (hence anemia) N-Neuropathies: vertigo, ataxia, headache GYNAECOMASTIA-CAUSING DRUGS (DISCOS) D-Digoxin I-Isoniazid S-Spironolactone C-Cimetidine O-Oestrogens S-Stilboestrol K+ INCREASING AGENTS (K-BANK) K- K-sparing diuretic B- Beta blocker A- ACEI N- NSAID K- Ksupplement Amiodarone: action, side effects 6 P’s P-Prolongs action potential duration P-Photosensitivity P-Pigmentation of skin P-Peripheral neuropathy P-Pulmonary alveolitis and fibrosis P-Peripheral conversion of T4 to T3 is inhibited - hypothyroidis NICOTINIC EFFECTS (MTWTF) (DAYS OF WEEK): M-Mydriasis/ Muscle cramps T-Tachycardia W-Weakness T-Twitching H-Hypertension/ Hyperglycemia F-Fasiculation
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The external ear collects sound pressure waves and funnels them toward the tympanic membrane. The middle ear ossicles transmit the sound waves to the inner ear (cochlea). The middle ear acts to match the impedance difference between the air of the external environment to the fluid within the cochlea. This permits maximal sound transmission. The outer ear includes the portion of the ear that we see—the pinna/auricle and the ear canal. The pinna or auricle is a concave cartilaginous structure, which collects and directs sound waves traveling in air into the ear canal or external auditory meatus. The ear canal is 1.25 inches long and .25 inch in diameter. The inner two-thirds of the ear canal is imbedded in the temporal bone. The outer one-third of the canal is cartilage. the canal forms an elongated "s" shape curve. The ear canal directs airborne sound waves towards the tympanic membrane . The ear canal maintains the proper conditions of temperature and humidity necessary to preserve the elasticity of the tympanic membrane. Glands, which produce cerumen (earwax) and tiny hairs in the ear canal, provide added protection against insects and foreign particles from damaging the tympanic membrane. The tympanic membrane or eardrum serves as a divider between the outer ear and the middle ear structures. It is gray-pink in color when healthy and consists of three very thin layers of living tissue. The eardrum transmits the airborne vibrations from the outer to the middle ear and also assists in the protection of the delicate structures of the middle ear cavity and inner The middle ear cavity is located in the mastoid process of the temporal bone. The middle ear cavity extends from the tympanic membrane to the inner ear. The eustachian tube acts as an air pressure equalizer and ventilates the middle ear. Normally the tube is closed but opens while chewing or swallowing. When the eustachian tube opens, the air pressure between the outer and middle ear is equalized. The transmission of sound through the eardrum is optimal when the air pressure is equalized between the outer and middle ear The middle ear is connected and transmits sound to the inner ear via the ossicular chain. The ossicular chain amplifies a signal as it transfers signals from the tympanic membrane to the inner ear. The ossicular chain consists of the three smallest bones in the body: the malleus, incus, and stapes. The malleus is attached to the tympanic membrane. The footplate of the stapes inserts into the oval window of the inner ear. The incus is between the malleus and the stapes. Attached to the ossicular chain are two tiny muscles, the stapedius and tensor tympani muscles. These muscles contract to protect the inner ear by reducing the intensity of sound transmission to the inner ear from external sounds The inner ear is composed of the sensory organ for hearing—the cochlea, as well as for balance—the vestibular system. The systems are separate, yet both are encased in the same bony capsule and share the same fluid systems. The balance part of the ear is referred to as the vestibular apparatus. It is composed, in part, of three semicircular canals located within the inner ear. The vestibular system helps to maintain balance, regardless of head position or gravity, in conjunction with eye movement and somatosensory input. The semicircular canals are innervated by the VIIIth cranial nerve. Cochlea The hearing part of the inner ear is the cochlea The cochlea is composed of three fluid-filled chambers that extend the length of the structure. The two outer chambers are filled with a fluid called perilymph. Perilymph acts as a cushioning agent for the delicate structures that occupy the center chamber. It is important to note that perilymph is connected to the cerebrospinal fluid that surrounds the brain and the spinal column. The third fluid filled chamber is the center chamber, called the cochlear duct. The cochlear duct secretes a fluid called endolymph, which fills this chamber. The cochlear duct contains the Basilar membrane upon which lies the Organ of Corti. The Organ of Corti is a sensory organ essential to hearing. It consists of approximately 30,000 finger-like projections of cilia that are arranged in rows. These cilia are referred to as hair cells. Each hair cell is connected to a nerve fiber that relays various impulses to the cochlear branch of the VIIIth cranial nerve or auditory nerve. The "pitch" of the impulse relayed is dependent upon which areas of the basilar membrane, and hence, which portions of the Organ of Corti are stimulated. The apical portion of the basilar membrane (the most curled area of the cochlea) transfers lower frequency impulses. The basal end relays higher frequency impulses. The VIII cranial nerve carries the impulses generated from the Organ of Corti to the brainstem. From the brainstem, nerve pathways extend through numerous nuclei to the cerebral cortex in the temporal lobes of the brain.
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BROWN-SEQUARD SYNDROME causes,pathophysiology,clinical features  diagnosis and treatment
Brown-Séquard syndrome (Brown-Séquard's paralysis, hemiparaplegic syndrome) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. Brown-Séquard syndrome may be caused by injury to the spinal cord resulting from a spinal cord tumour, trauma [such as a fall or injury from gunshot or puncture to the cervical or thoracic spine], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis The hemisection of the cord results in a lesion of each of the three main neural systems: the principal upper motor neuron pathway of the corticospinal tract one or both dorsal columns the spinothalamic tract As a result of the injury to these three main brain pathways the patient will present with three lesions: The corticospinal lesion produces spastic paralysis on the same side of the body below the level of the lesion (due to loss of moderation by the UMN). At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion). The lesion to fasciculus gracilis or fasciculus cuneatus results in ipsilateral loss of vibration and proprioception (position sense) as well as loss of all sensation of fine touch. The loss of the spinothalamic tract leads to pain and temperature sensation being lost from the contralateral side beginning one or two segments below the lesion Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions Treatment is directed at the pathology causing the paralysis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.
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What is Pierre Robin Sequence? Pierre Robin Sequence is a group of congenital malformations characterized by a triad of micrognathia, glossoptosis and U-shaped cleft palate.
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PENICILLINS, classification,mode of action,indications ,side effects,pharmacokinetics.
Penicillins are bactericidal beta-lactam antibiotics that inhibit bacterial cell wall synthesis. A natural product, the penicillin structure has been modified to prepare a variety of semi-synthetic agents. The spectrum of antibacterial activity varies with each class of the penicillin family. The naturally occurring penicillins are generally effective against gram-positive organisms; the aminopenicillins against gram-positive and some gram-negative organisms; the carboxy and uriedopenicillins against gram-positive and gram-negative organisms, including pseudomonas; and the antistaphylococcal penicillins against staphylococcus and streptococcus. All of the penicillins have some anaerobic coverage, such as Clostridium infections, peptococcus, and peptostreptococcus. Penicillins are generally well-tolerated, with hypersensitivity being the major adverse effect. Penicillins are used to treat a variety of conditions including skin/skin structure infections, urinary tract infections, upper and lower respiratory infections, and endocarditis Mechanism of action Penicillins inhibit cell wall synthesis by interfering with formation of the peptidoglycan layer and are bacteriocidal. Specifically, penicillins bind to a transpeptidase enzyme whose function is to cross-link N-acetyl muramic acid and N-acetyl glucosamine (Fig. 4-3). This linkage provides bacteria with structural stability. This transpeptidase is one of several bacterial proteins that penicillin binds that are collectively referred to as penicillin-binding proteins (PBPs). Other PBPs that penicillins activate are autolysins that hydrolyze and destroy components of the cell as well as carboxypeptidases and endopeptidases that break peptide bonds.
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DEXAMETHASONE SUPPRESSION TEST: How it is done and interpretation of the findings
The dexamethasone suppression test (DST) is a test that is used to assess the function of adrenal glands by measuring how cortisol levels change in response to an injection of dexamethasone. It is used to diagnose Cushing's syndrome.....
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BRONCHIECTASIS etiology,pathophysiology,clinical features,diagnosis and treatment
Bronchiectasis is dilation and destruction of larger bronchi caused by chronic infection and inflammation. Common causes are cystic fibrosis, immune defects, and recurrent infections, though some cases seem to be idiopathic. Symptoms are chronic cough and purulent sputumexpectoration; some patients may also have fever and dyspnea. Diagnosis is based on history and imaging, usually involving high-resolution CT, though standard chest x-rays may be diagnostic. Treatment and prevention of acute exacerbations are with antibiotics, drainage of secretions, and management of complications, such as superinfection and hemoptysis. Treatment of underlying disorders is important whenever possible. Etiology Bronchiectasis may affect many areas of the lung (diffuse bronchiectasis), or it may appear in only one or two areas (focal bronchiectasis). Diffuse bronchiectasis develops in patients with genetic, immune, or anatomic defects that affect the airways. Cystic fibrosis is the most common cause. Immunodeficiencies may also cause diffuse disease, as may rare abnormalities in airway structure. Diffuse bronchiectasis is an uncommon complication of more common conditions, such as RAor Sjogren's syndrome. Allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to Aspergillus sp It occurs primarily in people with asthma and less commonly in people with cystic fibrosis and can lead to bronchiectasis. Focal bronchiectasis develops from untreated pneumonia or obstruction (eg, due to foreign bodies and tumors). Mycobacteria can cause focal bronchiectasis as well as colonize the lungs of patients with bronchiectasis due to other disorders Some cases have no readily apparent cause. Pathophysiology All the causative conditions impair airway clearance mechanisms and host defenses, resulting in an inability to clear secretions, which, in turn, predisposes patients to chronic infection and inflammation. As a result of frequent infections, most commonly with Haemophilus influenzae (35%), Pseudomonas aeruginosa (31%), Moraxella catarrhalis (20%), Staphylococcus aureus (14%), and Streptococcus pneumoniae (13%), airways become inspissated with viscous mucous containing inflammatory mediators and pathogens and slowly become dilated, scarred, and distorted. Histologically, bronchial walls are thickened by edema, inflammation, and neovascularization. Destruction of surrounding interstitium and alveoli causes fibrosis, emphysema, or both. Superinfection with multidrug-resistant organisms, including Mycobacterium tuberculosis, and mycobacteria other than M. tuberculosis can cause recurrent exacerbations and worsen airflow limitation on pulmonary function tests. Pulmonary hypertension and right-sided heart failure may ensue because functional lung tissue decreases. Symptoms and Signs Symptoms characteristically begin insidiously and gradually worsen over years. The major presenting symptom of bronchiectasis is chronic cough that almost always produces large volumes of thick, tenacious, purulent sputum. Dyspnea and wheezing are common. Hemoptysis, which can be massive, is due to neovascularization of the airways from the bronchial (as opposed to pulmonary) arteries. Acute exacerbations of disease due to new or worsened infection increase the extent of cough and the volume and purulence of sputum production. Low-grade fever may also be present and abnormal breath sounds, including crackles, rhonchi, and wheezing, are typical signs of disease. Finger clubbing may also be present. In advanced cases, hypoxemia and signs of pulmonary hypertension (eg, shortness of breath, dizziness) and right-sided heart failure can occur. Diagnosis • History and physical examination • Chest x-ray • High-resolution CT for confirmation • Pulmonary function tests for baseline function and progression of disease Treatment • Prevention of exacerbations with antibiotics and regular vaccinations • Measures to help clear secretions • Antibiotics for acute exacerbations • Sometimes surgical resection
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HEPATIC ENCEPHALOPATHY(portal systemic encephalopathy) causes,classification,features,dx and rx
HEPATIC ENCEPHALOPATHY (PORTAL-SYSTEMIC ENCEPHALOPATHY) Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. It most often results from high gut protein or acute metabolic stress (eg, GI bleeding, infection, electrolyte abnormality) in a patient with portal-systemic shunting As it progresses, confusion is followed by coma. Confusion needs to be differentiated from delirium tremens and Wernicke’s encephalopathy, and coma from subdural haematoma, which can occur in alcoholics after a fall Features include changes of intellect,personality, emotions and consciousness, with or without neurological signs Two broad categories of hepatic encephalopathy are covert (CHE) and overt (OHE) hepatic encephalopathy CHE is particularly associated with poor outcomes Hepatic encephalopathy is also classified into three types based on the disease state of the liver, as follows: Type A: Hepatic encephalopathy associated with acute liver failure Type B: Hepatic encephalopathy associated with portosystemic bypass with no intrinsic hepatocellular disease Type C: Hepatic encephalopathy associated with cirrhosis and portal hypertension or portosystemic shunts.
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WHAT IS ZOLLINGER ELLISON SYNDROME? -It is a severe peptic ulceration of the stomach caused by a gastrin-secreting pancreatic islet non beta-cell tumour (‘gastrinoma’). -in this tutorial you shall learn about the pathology behind it, clinical manifestations, investigations and treatment.
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Myositis ossificans (MO) is a benign process characterised by heterotopic ossification usually within large muscles. Its importance stems in large part from its ability to mimic more aggressive pathological processes. Myositis ossificans is one of the skeletal “don’t touch” lesions. There are some conditions that are related to, or share similar name to, myositis ossificans  myositis ossificans circumscripta: refers to new bone that usually appears after trauma myositis ossificans progressiva: a rare, inherited disorder characterised by fibrosing and ossification of muscle, tendon and ligaments of multiple sites that are disabling and ultimately fatal panniculitis ossificans: similar to MO but occurring in subcutaneous tissues fibro-osseous pseudotumour of the digits: variant of MO occurring in the fingers and toes Pathology Myositis ossificans is essentially metaplasia of the intramuscular connective tissue resulting in extraosseous bone formation (without inflammation).  It has a zonal organisation  peripheral, well-organised mature lamellar bone intermediate osteoid region central immature non-ossified cellular (fibroblasts) focus Unfortunately, the histologically of myositis ossificans can appear similar to osteosarcoma, and thus, can lead to inappropriate management.
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TOP 10 INCREDIBLE SELF SURGERIES (must watch for doctors)
Ever imagined of the feelings under the scalpel? or a surgeon cutting up himself? this video compilation is a MUST WATCH for all the medical doctors Self-surgery is the act of performing a surgical procedure on oneself. Sometimes it becomes necessity in extreme conditions to perform this act. This list includes 10 such individuals that because of great circumstances found it necessary to do so
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Caesarean section, also known as C-section, or caesarean delivery, is the use of surgery to deliver babies. A caesarean section is often necessary when a vaginal delivery would put the baby or mother at risk. This may include obstructed labour, twin pregnancy, high blood pressure in the mother, breech birth, or problems with the placenta or umbilical cord. A caesarean delivery may be performed based upon the shape of the mother's pelvis or history of a previous C-section. A trial of vaginal birth after C-section may be possible. The World Health Organization recommends that Caesarean section be performed only when medically necessary. Some C-sections are performed without a medical reason, upon request by someone, usually the mother. A C-section typically takes 45 minutes to an hour. It may be done with a spinal block, where the woman is awake or under general anesthesia. A urinary catheter is used to drain the bladder and the skin of the abdomen is then cleaned with an antiseptic. An incision of about 15 cm (6 inches) is then typically made through the mother's lower abdomen. The uterus is then opened with a second incision and the baby delivered. The incisions are then stitched closed. A woman can typically begin breastfeeding as soon as she is awake and out of the operating room. Often, several days are required in the hospital to recover sufficiently to return home. C-sections result in a small overall increase in poor outcomes in low-risk pregnancies. They also typically take longer to heal from, about six weeks, than vaginal birth. The increased risks include breathing problems in the baby and amniotic fluid embolism and postpartum bleeding in the mother. Established guidelines recommend that caesarean sections not be used before 39 weeks of pregnancy without a medical reason. The method of delivery does not appear to have an effect on subsequent sexual function
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NEPHROTIC SYNDROME causes,pathophysiology,diagnosis,features and treatment
Nephrotic syndrome is a collection of symptoms due to kidney damage. This includes (proteinuria) more than 3.5 g/day protein in the urine, low blood albumin levels (hypoalbuminemia), high blood lipids (hyperlipidemia) and significant swelling (edema) Other symptoms may include weight gain, feeling tired, and foamy urine. Complications may include blood clots (thrombosis), infections, and high blood pressure (hypertension). Causes include a number of kidney diseases such as focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease. It may also occur as a complication of diabetes or lupus. The underlying mechanism typically involves damage to the glomeruli of the kidney. Diagnosis is typically based on urine testing and sometimes a kidney biopsy. It differs from nephritic syndrome in that there are no red blood cells in the urine. Treatment is directed at the underlying cause. Other efforts include managing high blood pressure, high blood cholesterol, and infection risk. A low salt diet and limiting fluids is often recommended
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COOMBS TEST (antiglobulin test) made simple
Coombs test, as antiglobulin test or AGT is one of two tests used in immunohematology and immunology. The two Coombs tests are the direct Coombs test (DCT, also known as direct antiglobulin test or DAT), and the indirect Coombs test (also known as indirect antiglobulin test or IAT) The direct Coombs test is used to test for autoimmune hemolytic anemia In some conditions, an individual's blood may contain IgG antibodies that can specifically bind to antigens on the RBC surface membrane, and their circulating RBCs can become coated with IgG alloantibodies and/or IgG autoantibodies. Complement proteins may subsequently bind to the bound antibodies and cause RBC destructruction The direct Coombs test is used to detect the antibodies or complement proteins that are bound to the surface of red blood cells; a blood sample is taken and the RBCs are washed and then incubated with anti-human globulin "Coombs reagent". If this produces agglutination of RBCs, the direct Coombs test is positive, a visual indication that antibodies are bound to the surface of red blood cells. The indirect Coombs test is used in prenatal testing of pregnant women and in testing blood prior to a blood transfusion. It detects antibodies against RBCs that are present unbound in the patient's serum. In this case, serum is extracted from the blood sample taken from the patient. Then, the serum is incubated with RBCs of known antigenicity; that is, RBCs with known reference values from other patient blood samples. Finally, anti-human globulin is added. If agglutination occurs, the indirect Coombs test is positive
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DRUGS approved to treat erectile dysfunction are classified to three classes 1.PHOSPHODIESTEARASE 5INHIBITORS 2.VASODILATORS 3.ANDROGENS phosphodiestearase inhibitors include sildenafil
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What is yperosmolar hyperglycemic state? It is one of the two life threathening complications of diabetes mellitus that is characterized by hyperglycemia of more than 600mg/dl, hyperosmolarity more than320mOsm/l and very severe dehydration without ketoacidosis.....
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PATHOLOGY MNEMONICS Portal hypertension: features ABCDE: Ascites Bleeding (haematemesis, piles) Caput medusae Diminished liver Enlarged spleen Thrombosis and thrombocytopenia PARTNER together: Nephritic syndrome: glomerular diseases commonly presenting as nephritic syndrome Portal hypertension: features ABCDE: Ascites Bleeding (haematemesis, piles) Caput medusae Diminished liver Enlarged spleen Platelet count low Anemia (microangiopathic hemolytic) Renal failure Temperature rise Neurological deficits ER admission (as it is an emergency) MAKE PATHOLOGY SIMPLE AND FUN SUBSCRIBE TODAY
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IMMUNOGLOBULIN A NEPHROPATHY (Berger's disease) causes,pathophysiology,dx and treatment
Immunoglobulin A nephropathy, also known as Berger’s disease, is characterized by predominant IgA deposition in the glomerular mesangium. It is one of the most common causes of glomerulonephritisis and occurs when IgA deposits build up in the kidneys, causing inflammation that damages kidney tissues. IgA is an antibody—a protein made by the immune system to protect the body from foreign substances such as bacteria or viruses IgA nephropathy affects the kidneys by attacking the glomeruli. The glomeruli are sets of looping blood vessels in nephrons—the tiny working units of the kidneys that filter wastes and remove extra fluid from the blood. The buildup of IgA deposits inflames and damages the glomeruli, causing the kidneys to leak blood and protein into the urine. The damage may lead to scarring of the nephrons that progresses slowly over many years. Eventually, IgA nephropathy can lead to end-stage kidney disease, sometimes called ESRD, which means the kidneys no longer work well enough to keep a person healthy. When a person’s kidneys fail, he or she needs a transplant
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Cells require oxygen from the air to extract energy from glucose through respiration, which produces carbon dioxide and water as a waste product. Therefore, oxygen is vital for every part of normal cellular function, and oxygen deficiency can have severe pathological consequences. The respiratory system facilitates breathing. In the alveoli tissue of the lungs, the exchange of oxygen and carbon dioxide molecules between the air and the bloodstream occurs by passive transport, so that oxygen is taken in and carbon dioxide and water are removed. Passive diffusion (also called bulk flow) is the term for the movement of these gases between the air and bloodstream based on their relative concentration, with the gas with the greater concentration moving across to the area with the lower concentration. This process consumes no energy. The circulatory system is deeply connected with the respiratory system because it distributes the dissolved oxygen to the tissues of the body and the waste carbon dioxide to the lungs. The primary function of the respiratory system is gas exchange between the external environment and an organism’s circulatory system. In humans and other mammals, this exchange balances oxygenation of the blood with the removal of carbon dioxide and other metabolic wastes from the circulation. It shows a cutaway view of the pulmonary alveoli as the terminal ends of the respiratory tree, outcropping from either alveolar sacs or alveolar ducts, which are both sites of gas exchange with the blood. Bronchial anatomy: The pulmonary alveoli are the terminal ends of the respiratory tree, outcropping from either alveolar sacs or alveolar ducts, which are both sites of gas exchange with the blood. As gas exchange occurs, the acid-base balance of the body is maintained as part of homeostasis. If proper ventilation is not maintained, two opposing conditions could occur: respiratory acidosis (a life threatening condition) and respiratory alkalosis. At the molecular level, gas exchange occurs in the alveoli—tiny sacs which are the basic functional component of the lungs. The alveolar epithelial tissue is extremely thin and permeable, allowing for gas exchange between the air inside the lungs and the capillaries of the blood stream. Air moves according to pressure differences, in which air flows from areas of high pressure to areas of low pressure.
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ELECTROCARDIOGRAM waves and intervals explained
There are three main components to an ECG: the P wave, which represents the depolarization of the atria; the QRS complex, which represents the depolarization of the ventricles; and the T wave, which represents the repolarization of the ventricles.[6] It can also be further broken down into the following: O is the origin or datum point preceding the cycle P is the atrial systole contraction pulse Q is a downward deflection immediately preceding the ventricular contraction R is the peak of the ventricular contraction S is the downward deflection immediately after the ventricular contraction T is the recovery of the ventricles U is the successor of the T wave but it is small and not always observed During each heartbeat, a healthy heart has an orderly progression of depolarization that starts with pacemaker cells in the sinoatrial node, spreads throughout the atrium, passes through the atrioventricular node down into the bundle of His and into the Purkinje fibers, spreading down and to the left throughout the ventricles. This orderly pattern of depolarization gives rise to the characteristic ECG tracing. To the trained clinician, an ECG conveys a large amount of information about the structure of the heart and the function of its electrical conduction system. Among other things, an ECG can be used to measure the rate and rhythm of heartbeats, the size and position of the heart chambers, the presence of any damage to the heart's muscle cells or conduction system, the effects of heart drugs, and the function of implanted pacemakers
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MEN2 -is an autosomal dominant condition caused by mutation of the C-RET proto-oncogene The video describes MEN 2,causes,pathology,clinical manifestations,diagnosis and treatment
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BENIGN PROSTATIC HYPERTROPHY (BPH) pathology,features,diagnosis and treatment
Benign prostatic hyperplasia, a noncancerous enlargement of the prostate gland, is the most common benign tumor found in men. BPH produces symptoms by obstructing the flow of urine through the urethra. Symptoms related to BPH are present in about one in four men by age 55, and in half of 75-year-old men. However, treatment is only necessary if symptoms become bothersome. By age 80, some 20 to 30% of men experience BPH symptoms severe enough to require treatment. Surgery was the only option until the recent approval of drugs that can relieve symptoms either by shrinking the prostate or by relaxing the prostate muscle tissue that constricts the urethra. Diagram of an enlarged prostate gland, showing the prostate gland compressing the urethra and blocking the flow of urine from the bladder Signs and Symptoms The symptoms of BPH can be divided into those caused directly by urethral obstruction and those due to secondary changes in the bladder. Typical obstructive symptoms are: Difficulty in starting to urinate despite pushing and straining A weak stream of urine; several interruptions in the stream Dribbling at the end of urination Bladder changes cause: A sudden strong desire to urinate (urgency) Frequent urination The sensation that the bladder is not empty after urination is completed Frequent awakening at night to urinate (nocturia) As the bladder becomes more sensitive to retained urine, a man, may become incontinent (unable to control the bladder causing bed wetting at night, or inability to respond quickly enough to urinary urgency). Burning or pain during urination can occur if a bladder infection or stone is present. Blood in the urine (hematuria) may herald BPH, but most men with BPH do not have hematuria. Screening and Diagnosis The American Urological Association (AUA) Symptom Index provides an objective assessment of BPH symptoms that helps to decide on treatment. However, this index cannot be used for diagnosis, since other diseases can cause symptoms similar to those of BPH. A medical history will give clues to conditions that can mimic BPH, such as possible stricture, bladder cancer or stones, or abnormal bladder function (problems with holding or emptying urine) due to a neurologic disorder (neurogenic bladder). Strictures can result from urethral damage caused by prior trauma, instrumentation (for example, catheter insertion), or an infection, such as gonorrhea. Bladder cancer is suspected if there is a history of blood in the urine. Pain in the penis or bladder area may indicate bladder stones or infection. A neurogenic bladder is suggested when an individual has diabetes or a neurologic disease such as multiple sclerosis or Parkinson's disease, or describes a recent deterioration in sexual function. A thorough medical history should also include questions about previous urinary tract infections or prostatitis (inflammation of the prostate that may cause pain in to lower back and the area between the scrotum and rectum, chills, fever, and general malaise), and any worsening of urinary symptoms when taking cold or sinus drugs. The physician will also ask whether any over-the-counter or prescription medications are being taken, because certain varieties can make voiding symptoms worse in men with BPH. The physical examination may begin with the doctor observing urination to completion to detect any urinary irregularities. The doctor will manually examine the lower abdomen to check for the presence of a mass, which may indicate an enlarged bladder due to retained urine. In addition, a digital rectal exam (DRE) which allows the physician to assess the size, shape, and consistency of the prostate, is essential for proper diagnosis. This important examination involves the insertion of a gloved finger into the rectum, but is only mildly uncomfortable. The detection of hard or firm areas in the prostate raises the suspicion of prostate cancer. If the history suggests possible neurologic disease, the physical may also include an examination for neurological abnormalities that indicate the urinary symptoms result from a neurogenic bladder. A urinalysis, which is obtained in all patients with symptoms of BPH, may be the only laboratory test if symptoms are mild and no other abnormalities are suspected from the medical history and physical examination. A urine culture is added if a urinary infection is suspected. With more severe chronic symptoms of BPH, blood creatinine of blood urea nitrogen (BUN) and hemoglobin are measured to rule out kidney damage and anemia. Measuring prostate specific antigen (PSA) levels in the blood to screen for prostate cancer is recommended
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SIDE EFFECTS OF CYTOTOXIC DRUGS mnemonic (ABCDEFGHI) Alopecia Bone marrow suppression -Aplastic anemia -Thrombocytopenia -Agranulocytosis Carcinogenicity(secondary) Dermatitis Enteric disorders -Nausea, Vomiting, Hemorrhage, Xerostomia, Stomatitis Fetal death, abortion, terartogenicity Gonads: sterility, oligozoospermia, amenorrhea, mutagenesis Hyperuricemia: gout, urate, stones Immunosuppresion: opportunistic infections Kidney(nephro-)toxicity AND MANY MORE IN OUR PHARMACOLOGY VIDEOS LIKE AND SUBSCRIBE TO OUR CHANNEL
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CIRRHOSIS (causes,pathophysiology,features,diagnosis,treatment)
Cirrhosis is defined as the presence of fibrous bands that divide the liver into regenerative nodules. Cirrhosis represents a late stage of progressive hepatic fibrosis MERCK MANUAL Professional Version Tap to switch to the Consumer Version ShareEmailLinkedInFacebookGoogle+Twitter Cirrhosis By Jesse M. Civan, MD, Assistant Professor and Medical Director, Liver Tumor Center, Thomas Jefferson University Hospital CLICK HERE FOR Patient Education Cirrhosis is a late stage of hepatic fibrosis that has resulted in widespread distortion of normal hepatic architecture. Cirrhosis is characterized by regenerative nodules surrounded by dense fibrotic tissue. Symptoms may not develop for years and are often nonspecific (eg, anorexia, fatigue, weight loss). Late manifestations include portal hypertension, ascites, and, when decompensation occurs, liver failure. Diagnosis often requires liver biopsy. Cirrhosis is usually considered irreversible. Treatment is supportive. Cirrhosis is a leading cause of death worldwide. The causes of cirrhosis are the same as those of fibrosis (see Table: Disorders and Drugs That Can Cause Hepatic Fibrosis). In developed countries, most cases result from chronic alcohol abuse or chronic hepatitis C. In parts of Asia and Africa, cirrhosis often results from chronic hepatitis B. (See table: Characteristics of Hepatitis Viruses for additional information on hepatitis B and C.) Cirrhosis of unknown etiology (cryptogenic cirrhosis) is becoming less common as many specific causes (eg, chronic hepatitis C, steatohepatitis) are identified. Injury to the bile ducts also can result in cirrhosis, as occurs in mechanical bile duct obstruction, primary biliary cholangitis, and primary sclerosing cholangitis. Pathophysiology There are 2 primary ingredients: Hepatic fibrosis Regenerating liver cells In response to injury and loss, growth regulators induce hepatocellular hyperplasia (producing regenerating nodules) and arterial growth (angiogenesis). Among the growth regulators are cytokines and hepatic growth factors (eg, epithelial growth factor, hepatocyte growth factor, transforming growth factor-alpha, tumor necrosis factor). Insulin, glucagon, and patterns of intrahepatic blood flow determine how and where nodules develop Angiogenesis produces new vessels within the fibrous sheath that surrounds nodules. These vessels connect the hepatic artery and portal vein to hepatic venules, restoring the intrahepatic circulatory pathways. Such interconnecting vessels provide relatively low-volume, high-pressure venous drainage that cannot accommodate as much blood volume as normal. As a result, portal vein pressure increases. Such distortions in blood flow contribute to portal hypertension, which increases because the regenerating nodules compress hepatic venules. The progression rate from fibrosis to cirrhosis and the morphology of cirrhosis vary from person to person. Presumably, the reason for such variation is the extent of exposure to the injurious stimulus and the individual’s response. It is a histological diagnosis and can be classified into micro and macronodular by the size of mm. Risk of developing Hepatocellular Carcinoma Chronic Viral Infection - HBV HCV Wilson's disease α-1 antitrypsin deficiency Alcohol Haemochromatosis NASH Alcohol and liver Steatosis - is reversible with alcohol abstention Alcoholic hepatitis - Mallory body Alcoholic cirrhosis - hobnail appearance Causes Chronic Hepatitis C infection (Alcoholic liver disease (AST more than ALT Elevated GGT) Chronic Hepatitis B infection (HBsAg HBeAg/HBV-DNA) Autoimmune liver disease (Raised Ig and Autoantibodies) Primary Sclerosing cholangitis (pANCA MRCP/ERCP) Primary Biliary cirrhosis (Anti Mitochondrial Ab) Hereditary Haemochromatosis (Ferritin high Transferrin saturation high, Genetics) Wilson's disease (Young, low Ceruloplasmin raised Urine copper, KF rings) Budd-Chiari syndrome (USS caudate lobe) Drugs - amiodarone, methotrexate, methyldopa Cystic fibrosis (genetics + sweat Cl) Alpha-1 antitrypsin (Young emphysema low serum AAT) Idiopathic - unknown Drugs that should be avoided in Cirrhosis These would include NSAIDs with their effects on kidneys and gastric mucosa. ACE inhibitors may be involved in hepatorenal syndrome and are best stopped. Codeine, Narcotics, Benzodiazepines and anxiolytics can all precipitate or worsen hepatic encephalopathy Complications Portal hypertension Liver failure Portosystemic Encephalopathy - always look for flap and assess mental state Variceal Bleeding formed from left gastric and short gastric veins to the oesophagus Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Osteoporosis Hepatocellular carcinoma Investigations U&E LFT's (low Na common) Prothrombin time and Albumin reflect liver synthetic functi
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CUSHING SYNDROME causes,pathophysiology,features,dx and treatment
Cushing’s syndrome results from excess cortisol secretion from adrenal adenoma and excessive activation of glucocorticoid receptors. It can be: Iatrogenic, due to prolonged administration of synthetic glucocorticoids such as prednisolone. Endogenous due to chronic over-production of cortisol by the adrenal glands, either as the result of an adrenal tumour or because of excessive production of ACTH by a pituitary tumour or ectopic ACTH production by other tumours. EPIDEMIOLOGY Male to female incidence ratio is 5:1 of cushing syndrome due to pituitary or adrenal tumor Ectopic ACTH production is more common in males than females because of higher incidence of lung tumors in men Peak incidence of cushing syndrome due to either adrenal or pituitary adenoma is in persons aged 25-40 years Ectopic ACTH production occurs in later life AETIOLOGY  ACTH DEPENDENT CUSHING SYNDROME -primary adrenal lesions A.Adrenal adenoma B.Adrenal carcinoma C.Macronodular or micronodular adrenal hyperplasia D. McCune-Albright syndrome -ectopic cortisol secretion from a case of ovarian carcinoma   ACTH INDEPENDENT CUSHING SYNDROME -ACTH producing pituitary adenoma Nelson syndrome -small cell lung carcinoma cause ectopic ACTH secretionAmongst endogenous causes, pituitary-dependent cortisol excess (byconvention, called Cushing’s disease) accounts for approximately 80% of cases. -Pseudo cushing can be due to hypercortisolism due to the following -Alcoholism -Depression -Obesity clinical features -Hair thinning -Acne plethora -Moon face -Hyperglycemia -Loss of height and back pain -Menstrual disturbance -Psychosis -Cataracts -Hypertension -Osteoporosis -hypokalemia Hypercalciuria Bufallo humps and truncal obesity -Decreased skin tickhness -Wasting and weakening of proximal thigh and extremities muscles(proteolysis) -Mild exophthalmos -Tendency to infections(immune suppression by inhibiting histamine release,intereukins and phospolipase A2) - poor wound healing -bruising -weight increase -metabolic alkalosis -hirsutism -striae(impared collagen synthesis)   Cushing disease is caused by a benign monoclonal pituitary corticotroph adenoma that secretes excess ACTH which in turn causes supraphysiological secretion of glucocorticoids from the adrenal glands. the excess circulating cortisol disrupts normal physiologic dunal variationin the cortisol levels and excerts a negative feedback inhibition on corticotrophin releasing hormone secretion from the hypothalamus. However the adenoma itself is resistant to inhibition by endogenous circulating cortisol. Consequently cushing disease is associated with suppressed secretion of CRH and elevated levels of ACTH in relation to the degree of cortisol production.   Endogenous excess cortisol overproduction that is independent of ACTH is usually due to an adenoma and rarely a carcinoma. . Ectopic cortisol secretion from a case of ovarian carcinoma is a cause of ACTH-independent Cushing syndrome. ACTH level in ACTH-independent Cushing syndrome is low due to the negative feedback to pituitary corticotroph cells from a high level of serum cortisol. ACTH-dependent Cushing syndrome is characterized by elevated ACTH levels. Elevated ACTH levels are usually due to an anterior pituitary tumor, which is classic Cushing disease Nonpituitary ectopic sources of ACTH, such as small-cell lung carcinoma , carcinoid tumor, medullary thyroid carcinoma, or other neuroendocrine tumors can result in high ACTH levels and sequentially hypercortisolism Ectopic corticotropin-releasing hormone (CRH) secretion leading to increased ACTH secretion comprises a very rare group of cases of Cushing syndrome Low dose dexamethasone suppression test (1 mg at 12 midnight and test serum cortisol the next day at 8 am) to differentiate btn cushing syndrome from pseudo cushing syndrome…in cushing cortisol level drops 24 hr urinary cortisol or serum cortisol at 8 am- in true syndrome levels will increase ACTH levels increases in pituitary adenoma and ectopic tumor but reduced in adrenal adenoma High dose dexamethasone suppression test to differentiate between pituitary adenoma and ectopic tumour) ACTH and cortisol levels remain high in ectopic but reduces in pituitary adenoma to locate the pituitary adenoma go for MRI but it isn’t confirmatory. Most accurate test to dx cushing disease is inferior petrosal sinus blood sample ACTH level . It the ACTH level in IPS/peripheral blood is more than 2 then its confirmatory TREATMENT AND MANAGEMENT The treatment for endogenous cushing syndrome is the removal of the pituitary, ectopic (usually in lung) or adrenal tumour if possible, coupled with corticosteroid replacement therapy. The primary therapy for cushing disease is transphenoidal surgery by an experienced neurosurgeon and the primary therapy for adrenal tumors is adrenalectomy Pituitary radiation therapy is useful if surgery fails to resolve the problem.Normalization of cormobidities
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DRUGS OF CHOICE -(Disease -drug correlation guide)
Drugs of choice for various conditions 1. Enuresis = imipramine 2. Rheumatic fever =penicillin 3. Paracetamol poisoning- :- - acetyl cysteine 4. acute bronchial- asthma :- salbutamol 5. acute gout :- NSAIDS 6. acute hyperkalemia:- calcium gluconate 7. severe DIGITALIS toxicity :-DIGIBIND 8. acute migraine :- sumatriptan 9. cheese reaction :- phentolamine 10. atropine poisoning :- physostigmine 11. cyanide poisoning :- amyl nitrite 12. benzodiazepine poisoning:- flumazenil 13. cholera :- tetracycline 14. KALA-AZAR :- lipozomal amphotericin- B 15. iron poisoning :- desferrioxamine 16. MRSA :- vancomycin 17. VRSA :- LINEZOLID 18. warfarin overdose :- vitamin-K (NIPER- 2009) 19. OCD - fluoxetine 20. alcohol poisoning :- fomepizole 21. epilepsy in pregnency :- phenobarbitone 22. anaphylactic shock :- Adrenaline 23. Malaria in Pregnancy-Chloroquine 24. Whooping Cough or Perteusis- Erythromycin 25. Kawasaki disease-IV Ig 26. Heparin Overdose-Protamine 27. Hairy Cell Leukemia-Cladirabine 28. Multiple Myeloma- Melphalan 29. CML-Imatinib 30. Wegner's granulomatosis-Cyclophosphamide 31. HOCM- Propranolol 32. Delirium Tremens-Diazepam 33. Drug Induced Parkinsonism-Benzhexol 34. Diacumarol Poisoning-Vit-K 35. Type-1 Lepra Reaction-Steroids 36. Type- 2 Lepra Reaction-Thalidomide 37. Allergic Contect Dermatitis-Steroids 38. PSVT- 1st-Adenosine, 2nd-Verapamil, 3rd-Digoxin 39. Z-E Syndrome- Proton Pump Inhibitor 40. Chancroid-Cotrimoxazole 41. Dermatitis Herpetiformis-Dapsone 42. Spastic Type of Cerebral Palsy-Diazepam 43. Herpis Simplex Keratitis-Trifluridine 44. Herpes Simplex Orolabialis-Pancyclovir 45. Neonatal Herpes Simplex-Acyclovir 46. Pneumocystis carinii Pneumonia- 47. Cotrimoxazole - Nodulo . 48. Trigeminal Neuralgia-Carbamezapine 49. Actinomycosis-Penicillin 50. Plague- Streptomycin 51. Opioid Withdrawal- Methadone 2nd-Clonidine 52. Alcohol Withdrawal- Chlordiazepoxide 2nd Diazepam 53. Post Herpetic Neuralgia- Fluphenazine 54. WEST Syndrome-ACTH 55. Diabetic Diarrhoea- Clonidine 56. Lithium Induced Neuropathy-Amiloride Communicable Disease: 57. Tetanus: PEN G Na; TETRACYCLINE; (DIAZEPAM 58. Diphteria: PEN G K; ERYTHROMYCIN 59. Pertusis: ERYTHROMYCIN; AMPICILLIN 60. Meningitis: MANNITOL (osmotic diuretic); DEXAMETHASONE (anti-inflammatory); DILANTIN/PHENYTOIN (anti-convulsive); PYRETINOL/ENCEPHABO L (CNS stimulant) 61. Amoebic Dysentery: METRONIDAZOLE 62. Shigellosis: CO-TRIMOXAZOLE 63. Typhoid: CHLORAMPHENICOL 64. Rabies: LYSSAVAC, VERORAB 65. Immunoglobulins: ERIG or HRIg 66. Malaria: CHLOROQUINE 67. Schistosomiasis: PRAZIQUANTEL 68. Felariasis: DIETHYLCARBAMAZINE CITRATE 69. Scabies: EURAX/ CROTAMITON 70. Chicken pox: ACYCLOVIR/ZOVIRAX 71. Leptospirosis: PENICILLIN; TETRACYCLINE; ERYTHROMYCIN 72. Leprosy: DAPSONE, RIFAMPICIN 73. Anthrax: PENICILLIN 74. Tuberculosis: R.I.P.E.S. 75. Pneumonia: COTRIMOXAZOLE; Procaine Penicillin 76. Helminths: MEBENDAZOLE; PYRANTEL PAMOATE 77. Syphilis: PENICILLIN 78. Gonorrhea: PENICILLIN 79. Cystic Acne -Retinoic aciddrug of choice -Retinoic
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POLYCYSTIC OVARIAN SYNDROME causes pathophysiology,signs and symptoms and treatment
WHAT IS POLYCYSTIC OVARIAN SYNDROME? Polycystic ovary syndrome (PCOS) is a set of symptoms due to elevated androgens (male hormones) in females. Signs and symptoms of PCOS include: signs of anovulation such as amenorrhea ,oligomenorrhea, excess body and facial hair... in this video you will learn of its pathophysiologyy, risk factors , clinical features,diagnosis and management....
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Liver function tests (LFTs or LFs) refers to a battery of blood tests that give information about the state of a patient's liver. USES Screening : They are a non-invasive yet sensitive screening modality for liver dysfunction. Pattern of disease : They are helpful to recognize the pattern of liver disease. Like being helpful in differentiating between acute viral hepatitis and various cholestatic disorders and chronic liver disease. (CLD). Assess severity : They are helpful to assess the severity and predict the outcome of certain diseases like primary biliary cirrhosis. Follow up : They are helpful in the follow up of certain liver diseases and also helpful in evaluating response to therapy like autoimmune hepatitis. LIMITATIONS Lack sensitivity: The LFT may be normal in certain liver diseases like cirrhosis, non cirrhotic portal fibrosis, congenital hepatic fibrosis, Lack specificity : They lack specificity and are not specific for any particular disease. Serum albumin may be decreased in chronic disease and also in nephrotic syndrome. Aminotransferases may be raised in cardiac diseases and hepatic diseases. Except for serum bile acids the LFT are not specific for liver diseases and all the parameters may be elevated for pathological processes outside the liver. Thus, we see that LFT have certain advantages as well as limitations at the same time. Thus, it is important to view them keeping the clinical profile of the patient in mind. CLASSIFICATION OF LIVER FUNCTION TESTS A. Tests of the liver’s capacity to transport organic anions and to metabolize drugs- Serum bilirubin, urine bilirubin, urobilinogen B. Tests that detect injury to hepatocytes (serum enzyme tests) – Aminotransferases, alkaline phosphatase, ã glutamyl transpeptidase, 5 nucleotidase, leucine aminopeptidase C. Tests of the Liver’s biosynthetic capacity- Serum proteins, albumin, prealbumin, serum ceruloplasmin, procollagen III peptide, a 1 antitrypsin, a feto protein, prothrombin time etc. Tests of the liver’s capacity to transport organic anions and to metabolize drugs These tests include prothrombin time (PT/INR), aPTT, albumin, bilirubin (direct and indirect), and others. The liver transaminases aspartate transaminase (AST or SGOT) and alanine transaminase (ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function. Most liver diseases cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance. This testing is performed on a patient's blood sample. Some tests are associated with functionality (e.g., albumin), some with cellular integrity (e.g., transaminase), and some with conditions linked to the biliary tract (gamma-glutamyl transferase and alkaline phosphatase). Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to detect the presence of liver disease, distinguish among different types of liver disorders, gauge the extent of known liver damage, and follow the response to treatment.
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HYPERTENSION,classification,pathophysiology,dx,features and rx
Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms. Long-term high blood pressure, however, is a major risk factor for coronary artery disease, stroke, heart failure, atrial fibrillation, peripheral vascular disease, vision loss, chronic kidney disease, and dementia. High blood pressure is classified as either primary (essential) high blood pressure or secondary high blood pressure. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors.lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, and alcohol use. The remaining 5–10% of cases are categorized as secondary high blood pressure, defined as high blood pressure due to an identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills. Blood pressure is expressed by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively. For most adults, normal blood pressure at rest is within the range of 100–130 millimeters mercury (mmHg) systolic and 60–80 mmHg diastolic. For most adults, high blood pressure is present if the resting blood pressure is persistently at or above 130/90 or 140/90 mmHg. Different numbers apply to children. Ambulatory blood pressure monitoring over a 24-hour period appears more accurate than office-based blood pressure measurement. Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. Lifestyle changes include weight loss, decreased salt intake, physical exercise, and a healthy diet. If lifestyle changes are not sufficient then blood pressure medications are used] Up to three medications can control blood pressure in 90% of people.The treatment of moderately high arterial blood pressure with medications is associated with an improved life expectancy.The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit and others finding unclear benefit. High blood pressure affects between 16 and 37% of the population globally.
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ACUTE BRONCHITIS causes,clinical features,diagnosis and treatment
Acute bronchitis is inflammation of the upper airways, commonly following a URI. The cause is usually a viral infection, though it is sometimes a bacterial infection; the pathogen is rarely identified. The most common symptom is cough, with or without fever, and possibly sputum production. In patients with COPD, hemoptysis, burning chest pain, and hypoxemia may also occur. Diagnosis is based on clinical findings. Treatment is supportive; antibiotics are necessary only for selected patients with chronic lung disease. Prognosis is excellent in patients without lung disease, but in patients with COPD, acute respiratory failure may result. Acute bronchitis is frequently a component of a URI caused by rhinovirus, parainfluenza, influenza Aor B, respiratory syncytial virus, coronavirus, or human metapneumovirus. Less common causes may be Mycoplasma pneumoniae, Bordetella pertussis, and Chlamydia pneumoniae. Patients at risk include those who smoke and those with COPD or other diseases that impair bronchial clearance mechanisms, such as cystic fibrosis or conditions leading to bronchiectasis Symptoms and Signs Symptoms are a nonproductive or minimally productive cough accompanied or preceded by URI symptoms. Subjective dyspnea results from chest pain or tightness with breathing, not from hypoxia, except in patients with underlying lung disease. Signs are often absent but may include scattered rhonchi and wheezing. Sputum may be clear, purulent, or, occasionally, bloody. Sputum characteristics do not correspond with a particular etiology (ie, viral vs bacterial). Mild fever may be present, but high or prolonged fever is unusual and suggests influenza or pneumonia. On resolution, cough is the last symptom to subside and often takes several weeks or even longer to do so. Diagnosis • Clinical evaluation • Sometimes chest x-ray Diagnosis is based on clinical presentation. Chest x-ray i necessary only if findings suggest pneumonia (eg, abnormal vital signs, crackles, signs of consolidation, hypoxemia). Elderly patients are the occasional exception. They may require chest x-ray for productive cough and fever in the absence of auscultatory findings (particularly if there is a history of COPD or another lung disorder). Sputum Gram stain and culture usually have no role. Cough resolves within 2 wk in 75% of patients. Patients with persistent cough should undergo a chest xray. Evaluation for pertussis, with a culture from nasopharyngeal secretions, and noninfectious etiologies, such as postnasal drip, allergic rhinitis, and cough variant asthma, may be needed. Treatment • Symptom relief (acetaminophen, hydration, possibly antitussives) • Inhaled β-agonist or anticholinergic for wheezing • Sometimes oral antibiotics for patients with COPD Acute bronchitis in otherwise healthy patients is a major reason that antibiotics are overused. Nearly all patients require only symptomatic treatment, such as acetaminophen and hydration. Antitussives should be used only if the cough is interfering with sleep Patients with wheezing may benefit from an inhaled β2-agonist (eg, albuterol) or an anticholinergic (eg, ipratropium) for 7 days. If cough persists for more than 2 wk because of airway irritation, some patients benefit from a few days of inhaled corticosteroids. Oral antibiotics are typically not used except in patients with pertussis or in patients with COPD who have at least 2 of the following: • Increased cough • Increased dyspnea • Increase in sputum purulence Drugs include amoxicillin 500 mg po tid for 7 days, doxycycline 100 mg po bid for 7 days, azithromycin 500 mg po once/day for 4 days, or trimethoprim/sulfamethoxazole 160/800 mg po bid for 7 days.
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SHORT SYNACTHEN TEST (ACTH stimulation test) made simple
Standard Short Synacthen test for suspected adrenal failure Indication This is performed for the investigation of adrenal insufficiency. Contraindication The Synacthen test gives unreliable results within 2 weeks of pituitary surgery. Principle Adrenal glucocorticoid secretion is controlled by adrenocorticotrophic hormone (ACTH) released by the anterior pituitary. This test evaluates the ability of the adrenal cortex to produce cortisol after stimulation by synthetic ACTH (tetracosactide; Synacthen ). It does not test the whole pituitary-adrenal axis. The short test assesses the ability of the adrenal gland to respond to ACTH but is not reliable within 2 weeks of pituitary surgery. Preparation There are no dietary restrictions for this test. This test should be performed in the morning as the cortisol responses between the morning and late afternoon may differ by as much as 100 nmol/L at 30 min sample post Synacthen. Prednisolone should be stopped 24 hours before the Synacthen test. Requirements 2 plain tubes 250 microgram Synacthen (1 vial) the dose for children is 36 microgram/kg body weight up to a maximum of 250 micrograms Procedure 0900 take 3 mL blood for cortisol inject Synacthen iv or im 0930 take further sample for cortisol The above definition only defines adrenal insufficiency. The definition of normality is problematic since there is considerable variation in healthy individuals and a significant overlap with patients who have adrenal insufficiency. In ACTH deficiency the response to the short test may be normal or reduced. The response to Synacthen is not affected by obesity. There is no difference in cortisol response between iv & im administration. Baseline and incremental cortisol values do NOT apply to women taking oral contraceptives or to pregnant women. There is quite marked variation in the measurement of cortisol in the post-Syancthen samples by different laboratory methods Sensitivity and Specificity There are reports of patients with incipient adrenal failure with normal responses to Synacthen. The use of physiological doses eg 1 microgram may prove more useful at determining those subjects with poor responses than conventional (250 microgram) pharmacological doses. the standard test is better for diagnosing primary adrenal insufficiency. However, whilst there is no difference in diagnostic performance between the standard and low dose tests in cases of secondary adrenal insufficiency, neither test is recommended where there is a possibility of pituitary dysfunction
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FUNNY  MEMES COMPILATION 2018. Best medical school jokes and fun collection
BEST MEMES COMPILATION 2018. Best medical school jokes and fun collection. dont miss out
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Hodgkins lymphoma is a neoplasm of the immune system that is marked by the presence of a type of cell called the Reed-Sternberg cell. The two major types of Hodgkin lymphoma are classical Hodgkin lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma. Classic Hodgkin lymphoma Classic Hodgkin lymphoma (cHL) accounts for more than 9 in 10 cases of Hodgkin lymphoma in developed countries. The cancer cells in cHL are called Reed-Sternberg cells. These cells are usually an abnormal type of B lymphocyte. Enlarged lymph nodes in people with cHL usually have a small number of Reed-Sternberg cells with a lot of normal immune cells around them. These other immune cells cause most of the swelling in the lymph nodes. Classic HL has 4 subtypes: nodular sclerosis Hodgkin lymphoma or NSCHL: This is the most common type of Hodgkin disease in developed countries. It accounts for about 7 out of 10 cases. It's most common in teens and young adults, but it can occur in people of any age. It tends to start in lymph nodes in the neck or chest. Mixed cellularity Hodgkin lymphoma or MCCHL: This is the second most common type, found in about 4 out 10 cases. It's seen mostly in people with HIV infection. It's also found in children or the elderly . It can start in any lymph node but most often occurs in the upper half of the body. Lymphocyte-rich Hodgkin lymphoma: This sub-type isn't common. It usually occurs in the upper half of the body and is rarely found in more than a few lymph nodes. Lymphocyte-depleted Hodgkin lymphoma: This is a rare form of Hodgkin disease. It's seen mainly in older people and those with HIV infection. It's more aggressive than other types of HL and likely to be advanced when first found. It's most often in lymph nodes in the abdomen (belly) as well as in the spleen, liver, and bone marrow. Nodular lymphocyte-predominant Hodgkin lymphoma Nodular lymphocyte-predominant Hodgkin lymphoma accounts for about 5% of cases. The cancer cells in NLPHL are large cells called popcorn cells (because they look like popcorn), which are variants of Reed-Sternberg cells. You may also hear these cells called lymphocytic and histiocytic (L&H) cells. NLPHL usually starts in lymph nodes in the neck and under the arm. It can occur in people of any age, and is more common in men than in women. This type of HL tends to grow more slowly and is treated differently from the classic types. Symptoms include the painless enlargement of lymph nodes, spleen, or other immune tissue. Other symptoms include fever, weight loss, fatigue, or night sweats. Also called Hodgkin disease.
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HEMOSTASIS (blood clotting process, clotting factors,regulation and anticoagulants
Hemostasis is the natural process that stops blood loss when an injury occurs.It involves three steps: (1) vascular spasm ( vasoconstriction ); (2) platelet plug formation; and (3) coagulation. Vasoconstriction is a reflex in which blood vessels narrow to increase blood pressure. Next, platelet plug formation involves the activation, aggregation, and adherence of platelets into a plug that serves as a barrier against blood flow. Coagulation involves a complex cascade in which a fibrin mesh is cleaved from fibrinogen. Fibrin acts as a “molecular glue” during clot formation, holding the platelet plug together. Steps of Hemostasis Hemostasis includes three steps that occur in a rapid sequence: (1) vascular spasm, or vasoconstriction, a brief and intense contraction of blood vessels; (2) formation of a platelet plug; and (3) blood clotting or coagulation, which reinforces the platelet plug with fibrin mesh that acts as a glue to hold the clot together. Once blood flow has ceased, tissue repair can begin. Vasoconstriction Intact blood vessels are central to moderating blood’s clotting tendency. The endothelial cells of intact vessels prevent clotting by expressing a fibrinolytic heparin molecule and thrombomodulin, which prevents platelet aggregation and stops the coagulation cascade with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which causes platelet adherence during the initial formation of a clot. The vasoconstriction that occurs during hemostasis is a brief reflexive contraction that causes a decrease in blood flow to the area. Platelet Plug Formation Platelets create the “platelet plug” that forms almost directly after a blood vessel has been ruptured. Within twenty seconds of an injury in which the blood vessel’s epithelial wall is disrupted, coagulation is initiated. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes, the platelet plug is completely formed by fibrin. Contrary to popular belief, clotting of a skin injury is not caused by exposure to air, but by platelets adhering to and being activated by collagen in the blood vessels’ endothelium. The activated platelets then release the contents of their granules, which contain a variety of substances that stimulate further platelet activation and enhance the hemostatic process. When the lining of a blood vessel breaks and endothelial cells are damaged, revealing subendothelial collagen proteins from the extracellular matrix, thromboxane causes platelets to swell, grow filaments, and start clumping together, or aggregating. Von Willebrand factor causes them to adhere to each other and the walls of the vessel. This continues as more platelets congregate and undergo these same transformations. This process results in a platelet plug that seals the injured area. If the injury is small, the platelet plug may be able to form within several seconds. Coagulation Cascade If the platelet plug is not enough to stop the bleeding, the third stage of hemostasis begins: the formation of a blood clot. Platelets contain secretory granules. When they stick to the proteins in the vessel walls, they degranulate, thus releasing their products, which include ADP (adenosine diphosphate), serotonin, and thromboxane A2 (which activates other platelets). First, blood changes from a liquid to a gel. At least 12 substances called clotting factors or tissue factors take part in a cascade of chemical reactions that eventually create a mesh of fibrin within the blood. Each of the clotting factors has a very specific function. Prothrombin, thrombin, and fibrinogen are the main factors involved in the outcome of the coagulation cascade. Prothrombin and fibrinogen are proteins that are produced and deposited in the blood by the liver. When blood vessels are damaged, vessels and nearby platelets are stimulated to release a substance called prothrombin activator, which in turn activates the conversion of prothrombin, a plasma protein, into an enzyme called thrombin. This reaction requires calcium ions. Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long, insoluble fibers or threads of the protein, fibrin. Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot. This net of fibers traps and helps hold platelets, blood cells, and other molecules tight to the site of injury, functioning as the initial clot. This temporary fibrin clot can form in less than a minute and slows blood flow before platelets attach. Next, platelets in the clot begin to shrink, tightening the clot and drawing together the vessel walls to initiate the process of wound healing.
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pathophysiology of crohns disease
Pathophysiology Chronic inflammation from T-cell activation leading to tissue injury is implicated in the pathogenesis of Crohn disease. After activation by antigen presentation, unrestrained responses of type 1 T helper (Th1) cells predominate in Crohn disease as a consequence of defective regulation. Th1 cytokines such as interleukin (IL)-12 and TNF-α stimulate the inflammatory response. Inflammatory cells recruited by these cytokines release nonspecific inflammatory substances, including arachidonic acid metabolites, proteases, platelet activating factor, and free radicals, which result in direct injury to the intestine. In a study from 2012, investigators suggested that genetic predispositions for inflammatory bowel disease (IBD) lead to abnormal epithelial barrier integrity and homeostasis, deficits in autophagy, deficiencies in innate pattern recognition receptors, and problems with lymphocyte differentiation, especially in Crohn disease. Microscopically, the initial lesion starts as a focal inflammatory infiltrate around the crypts, followed by ulceration of superficial mucosa. Later, inflammatory cells invade the deep mucosal layers and, in that process, begin to organize into noncaseating granulomas The granulomas extend through all layers of the intestinal wall and into the mesentery and the regional lymph nodes. Colonic granuloma in patient with Crohn disease. H Colonic granuloma in patient with Crohn disease. Hematoxylin-eosin staining. Neutrophil infiltration into the crypts forms crypt abscesses, leading to destruction of the crypt and atrophy of the colon. Chronic damage may be seen in the form of villous blunting in the small intestine as well. Ulcerations are common and are often seen on a background of normal mucosa. Although granuloma formation is pathognomonic of Crohn disease, its absence does not exclude the diagnosis. Macroscopically, the initial abnormality consists of hyperemia and edema of the involved mucosa. Later, discrete superficial ulcers form over lymphoid aggregates and are seen as red spots or mucosal depressions These can become deep, serpiginous ulcers located transversely and longitudinally over an inflamed mucosa, giving the mucosa a cobblestone appearance. The lesions are often segmental, being separated by healthy areas, and are referred to as skip lesions. Colonoscopic image of a large ulcer and inflammati Transmural inflammation results in thickening of the bowel wall and narrowing of the lumen. As Crohn disease progresses, it is complicated by obstruction or deep ulceration leading to fistulization by way of the sinus tracts penetrating the serosa, microperforation, abscess formation, adhesions, and malabsorption. Bowel obstruction is caused initially by significant edema of the mucosa and associated spasm of the bowel. Obstruction is intermittent and can often be reversed by means of conservative measures and anti-inflammatory agents. With further disease progression, the obstruction becomes chronic because of fibrotic scarring, luminal narrowing, and stricture formation. Fistulae may be enteroenteral, enterovesical, enterovaginal, or enterocutaneous. The inflammation extending through the bowel wall may also involve the mesentery and surrounding lymph nodes. Creeping fat may be seen when the mesentery wraps around the bowel surface Serosal inflammation causes adhesions; thus, free perforations are less common in Crohn disease than in other inflammatory bowel conditions.
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OSTEOMYELITIS causes,pathophysiology,classification,clinical features,diagnosis and treatment
Osteomyelitis is inflammation of the bone and the bone marrow caused by an infecting organism. Although bone is normally resistant to bacterial colonization, events such as trauma, surgery, the presence of foreign bodies, or the placement of prostheses may disrupt bony integrity and lead to the onset of bone infection. Osteomyelitis can also result from hematogenous spread after bacteremia. When prosthetic joints are associated with infection, microorganisms typically grow in biofilm, which protects bacteria from antimicrobial treatment and the host immune response. Early and specific treatment is important in osteomyelitis, and identification of the causative microorganisms is essential for antibiotic therapy. The major cause of bone infections is Staphylococcus aureus. Infections with an open fracture or associated with joint prostheses and trauma often must be treated with a combination of antimicrobial agents and surgery. When biofilm microorganisms are involved, as in joint prostheses, a combination of rifampin with other antibiotics might be necessary for treatment.
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ACUTE GASTROINTESTINAL BLEEDING causes,features,diagnosis and treatment
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool. Small amounts of bleeding over a long time may cause iron-deficiency anemia resulting in feeling tired or heart-related chest pain Other symptoms may include abdominal pain, shortness of breath, pale skin, or passing out. Sometimes in those with small amounts of bleeding no symptoms may be present. Bleeding is typically divided into two main types: upper gastrointestinal bleeding and lower gastrointestinal bleeding. Causes of upper GI bleeds include: peptic ulcer disease, esophageal varices due to liver cirrhosis and cancer, among others. Causes of lower GI bleeds include: hemorrhoids, cancer, and inflammatory bowel disease among others. Diagnosis typically begins with a medical history and physical examination, along with blood tests. Small amounts of bleeding may be detected by fecal occult blood test. Endoscopy of the lower and upper gastrointestinal tract may locate the area of bleeding Medical imaging may be useful in cases that are not clear. Initial treatment focuses on resuscitation which may include intravenous fluids and blood transfusions. Often blood transfusions are not recommended unless the hemoglobin is less than 70 or 80 g/L. Treatment with proton pump inhibitors, octreotide, and antibiotics may be considered in certain cases. If other measures are not effective, an esophageal balloon may be attempted in those with presumed esophageal varices Endoscopy of the esophagus, stomach, and duodenum or endoscopy of the large bowel are generally recommended within 24 hours and may allow treatment as well as diagnosis.
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ACUTE RHEUMATIC FEVER Causes, pathophysiology,symptoms,diagnosis and treatment
Acute rheumatic fever (ARF) is an autoimmune inflammatory process that develops as a complication of untreated strep throat (caused by a group A streptococcal infection). It can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves. Rheumatic fever may occur following an infection of the throat by the bacterium Streptococcus pyogenes. If the infection is untreated rheumatic fever can occur in up to three percent of people. The underlying mechanism is believed to involve the production of antibodies against a person's own tissues. Due to their genetics, some people are more likely to get the disease when exposed to the bacteria than others. Other risk factors include malnutrition and poverty. Diagnosis of RF is often based on the presence of signs and symptoms in combination with evidence of a recent streptococcal infection. Treating people who have strep throat with antibiotics, such as penicillin, decreases the risk of developing rheumatic fever. In order to avoid antibiotic misuse this often involves testing people with sore throats for the infection, which may not be available in the developing world. Other preventive measures include improved sanitation.In those with rheumatic fever and rheumatic heart disease, prolonged periods of antibiotics are sometimes recommended. Gradual return to normal activities may occur following an attack. Once RHD develops, treatment is more difficult. Occasionally valve replacement surgery or valve repair is required. Otherwise complications are treated as per normal.
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ANAEMIA causes,classification,clinical features,treatment
Anaemia is a decrease in the RBC count, HGB and/or HCT values as compared to normal reference range for age and sex. Functionally defined as the inability of haemoglobin to supply the tissues with adequate oxygen.....hypoxia. ‘True’ anemia….decreased RBC mass and normal plasma volume. Pseudo or dilutional anemia….normal RBC mass and increased plasma volume . An increase in plasma volume may cause a dilutional or pseudo anemia (with low Hgb & HCT values) even though the RBC mass is normal ....can occur during pregnancy or caused by volume overload (IVs), congestive heart failure. 1. Classification of Anemia I. Etiologic Classification • Impaired RBC production • Excessive destruction • Blood loss II. Morphologic Classification • Macrocytic anemia • Microcytic hypochromic anemia • Normochromic normocytic anemia 2. Impaired RBC Production 1. Abnormal bone marrow • Aplastic anemia • Myelophthisis : Myelofibrosis, Leukemia, Cancer metastasis 2. Essential factors deficiency • Deficiency anemia : Fe, Vit. B12, Folic acid, etc • Anemia in renal disease : Erythropoietin 3. Stimulation factor deficiency • Anemia in chronic disease • Anemia in hypopituitarism • Anemia in hypothyroidism 3. Excessive Destruction of RBC Hemolytic anemia Intracorpuscular defect ;- • Membrane : Hereditary spherocytosis Hereditary ovalocytosis, etc. • Enzyme : G-6PD deficiency, PK def., etc. • Hemoglobin : Thalassemia, Hemoglobinopathies Extracorpuscular defect • Mechanical : March hemolytic anemia MAHA (Microangiopathic HA) • Chemical/Physical • Infection : Clostridium tetani • Antibodies : HTR, SLE • Hypersplenism Blood Loss • Acute blood loss : Accident, GI bleeding • Chronic blood loss : Hypermenorrhea, Parasitic infestation II. Morphologic Classification Macrocytic AnemiaMegaloblastic dyspoiesis • Vit. B12 deficiency: Pernicious anemia • Folic acid deficiency: Nutritional megaloblastic anemia, Sprue, Other malabsorption • Inborn errors of metabolism: Orotic aciduria, etc. • Abnormal DNA synthesis: Chemotherapy, Anticonvulsant, Oral contraceptives Microcytic Hypochromic AnemiaFe deficiency anemia: Chronic blood loss, Inadequate diet, Malabsorption, Increased demand, etc. • Abnormal globin synthesis: Thalassemia with or without Hemoglobinopathies • Abnormal porphyrin and heme synthesis: Pyridoxine responsive anemia, etc. • Other abnormal Fe metabolism: Normocytic Normochromic Anemia Blood loss • Increased plasma volume: Pregnancy, Overhydration • Hemolytic anemia: depend on each cause • Hypoplastic marrow: Aplastic anemia, RBC aplasia • Infiltrate BM: Leukemia, Multiple myeloma, Myelofibrosis, etc. • Abnormal endocrine: Hypothyroidism, Adrenal insufficiency, etc. • Kidney disease/Liver disease/Cirrhosis Hemolytic Anemia What is Hemolysis • Premature destruction of red cells. • Caused by hereditary and acquired disorders. Hemolysis occurs at two sites: Intravascular • Hemolysis occurs within systemic circulation. • Hemoglobin is released into plasma. • Hemoglobin is lost through kidneys or catabolized in the liver. Extravascular • Trapping of red cells in spleen or liver sinuses. • Lyses of trapped red cells. • Release of lysed hemoglobin and catabolism within the sequestering organ. Classification of Hereditary Hemolytic Anemia • Based on side effect: • Metabolic defect • Membrane defect • Hemoglobin defect A) Metabolic defect: • Defect in hexose monophosphate shunt: G-6-PD deficiency. • Defects of glycolysis: pyruvate kinase def., glucose phosphate isomerase deficiency. • Defects in red cell nucleotide metabolism: pyrimidine-5-nucleotidase def. B) Membrane defect: • Hereditary spherocytosis • Hereditary elliptocytosis • Hereditary pyropoikilocytosis C) Hemoglobin defect:  Thalassemias  Sickle cell anemia  Hemoglobin C disease  Hemoglobin E disease  Unstable hemoglobin
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Appendicitis is an acute inflamation and infection of the vermiform appendix... in this video we will discuss the causes,pathology, signs and symptoms of appendicitis, Alvaro score , diagnostic tests and treatment.
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The complement system consists of a series of heat-labile serum proteins that are activated in turn. The components normally exist as soluble inactive precursors; once activated, a complement component may then act as an enzyme , which cleaves several molecules of the next component in the sequence. Each precursor is cleaved into two or more fragments. The major fragment has two biologically active sites: one for binding to cell membranes or the triggering complex and the other for enzymatic cleavage of the next complement component . Control of the sequence involves spontaneous decay of any exposed attachment sites and specific inactivation by complement inhibitors. The classical pathway was the first to be described. It is activated by a number of substances, the most widely recognized being antigen–antibody complexes where the antibody is either IgM or IgG (Fig. 1.21). The reaction of IgM or IgG with its antigen causes a conformational change in the Fchregion of the antibody to reveal a binding site for the first component in the classical pathway, C1q. C1q reacts with Fc via its globular heads; attachment by two critically spaced binding sites is needed for activation. The Fc regions of pentameric IgM are so spaced that one IgM molecule can activate C1q; in contrast, IgG is relatively inefficient because the chance of two randomly sited IgG molecules being the critical distance apart to activate C1q is relatively low. IgA, IgD and IgE do not activate the classical pathway. Once C1q is activated, C1r and C1s are sequentially bound to generate enzyme activity (C1 esterase) for C4 and C2 splitting both molecules into “a” and “b” fragments. The complex C b b4 2 is the classical pathway C3 convertase. Other fragments released are C4a, C2a and a vasoactive peptide released from C2. C4b2b cleaves C3 into two fragments, C3a possessing anaphylotoxic and chemotactic activity and C3b that binds to the initiating complex and promotes many of the biological properties of complement. The C4b2b3b complex so generated is an enzyme, C5 convertase which initiates the final lytic pathway
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WHAT IS ENDOMETRIAL CARCINOMA? endometrial carcinoma is a malignancy that arises from endometrial hyperplasia..... In this tutorial you shall learn on the subtypes, risk factors,clinical features, pathology , diagnosis and treatment approaches.
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