tag:blogger.com,1999:blog-76173699020821368092024-03-05T04:56:02.074-08:00Medical Powerpoint PresentationsFree Download Medical Powerpoint Presentations, Medical Flash AnimatedAnonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.comBlogger20125tag:blogger.com,1999:blog-7617369902082136809.post-20257835377235675912012-08-29T07:44:00.002-07:002012-08-29T07:44:53.237-07:00Evaluation of a Thyroid Nodule PPTIf you’re looking for <b>Evaluation of a Thyroid Nodule PPT</b> you can download <b>Evaluation of a Thyroid Nodule PPT</b> here. Download <b>Evaluation of a Thyroid Nodule PPT</b> from our website is simple and quick. If you have difficulty to download <b>Evaluation of a Thyroid Nodule PPT</b> read <b>How to Download</b> <b>Evaluation of a Thyroid Nodule PPT</b>.<br />
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<br />
<br />
Epidemiology – Thyroid Nodule<br />
Nodules common, whereas cancer relatively uncommon<br />
Goal is to <span class="IL_AD" id="IL_AD4">minimize</span> “unnecessary” surgery but not miss any cancer<br />
It increases with age.<br />
Higher in women <br />
Estimated 5-15% of nodules are cancerous<br />
Although cancer more common in women, a nodule in a man is more likely to be cancer<br />
<br />
Epidemiology – Pregnancy <br />
Pregnancy increases risk<br />
One study: u/s detection nodules –<br />
9.4% nulliparous women<br />
25% women previously pregnant<br />
Attributed to increased renal iodide excretion and <span class="IL_AD" id="IL_AD1">basal metabolic rate</span><br />
Rosen: Nodules presenting during pregnancy – 30 patients, 43% were cancer<br />
HCG may be growth promoter (TSH-like activity)<br />
<br />
Epidemiology – Radiation<br />
Appears to be dose-dependent<br />
ERR 7.7 at 100 cGy<br />
Maximum risk approximately 30 years later<br />
Nodule in radiated patient: 35-40% cancer<br />
Data suggest no more aggressive behavior over spontaneously-occurring cancers, but may be larger at presentation<br />
Only unequivocal environmental cause of thyroid cancer<br />
<br />
Epidemiology – Children<br />
Nodule more likely to be cancer than adults<br />
10% thyroid cancer age <21<br />
Thyroid ca 1.5-2.0% all pediatric malignancies<br />
More likely to present with <span class="IL_AD" id="IL_AD6">neck</span> metastasis<br />
Most common cause thyroid <span class="IL_AD" id="IL_AD3">enlargement</span> is chronic lymphocytic thyroiditis<br />
<br />
Medullary Thyroid <span class="IL_AD" id="IL_AD2">Carcinoma</span><br />
FMTC, MEN 2A, MEN 2B<br />
RET proto-oncogene (chromosome 10)<br />
Calcium / Pentagastrin stimulation<br />
Prophylactic thyroidectomy <span class="IL_AD" id="IL_AD5">recommended</span> age 2-6 <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com2tag:blogger.com,1999:blog-7617369902082136809.post-25532974421864111332012-08-29T07:32:00.003-07:002012-08-29T07:32:37.509-07:00Fluids, Electrolyte, and Nutrition Management in Neonates PPTIf you’re looking for <b>Fluids, Electrolyte, and Nutrition Management in Neonates PPT</b> you can download <b>Fluids, Electrolyte, and Nutrition Management in Neonates PPT</b> here. Download <b>Fluids, Electrolyte, and Nutrition Management in Neonates PPT</b> from our website is simple and quick. If you have difficulty to download <b>Fluids, Electrolyte, and Nutrition Management in Neonates PPT</b> read <b>How to Download</b> <b>Fluids, Electrolyte, and Nutrition Management in Neonates PPT</b>.<br />
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<br />
<br />
Things to consider: <br />
Normal changes in TBW, ECF<br />
All babies are born with an excess of TBW, mainly ECF, which needs to be removed<br />
Adults are 60% water (20% ECF, 40% ICF)<br />
Term neonates are 75% water (40% ECF, 35% ICF) : lose 5-10 % of weight in first week<br />
Preterm neonates have more water (23 wks: 90%, 60% ECF, 30% ICF): lose 5-15% of weight in first week<br />
<br />
Normal changes in Renal Function<br />
Adults can concentrate or dilute urine very well, depending on fluid status<br />
Neonates are not able to concentrate or dilute urine as well as adults - at risk for dehydration or fluid overload<br />
Renal function matures with increasing:<br />
gestational age<br />
postnatal age<br />
<br />
Insensible water loss (IWL)<br />
Insensible” water loss is water loss that is not obvious: through skin (2/3) or respiratory tract (1/3)<br />
depends on gestational age (more preterm: more IWL)<br />
depends on postnatal age (skin thickens with age: older is better --> less IWL)<br />
also consider losses of other fluids: Stool (diarrhea/ostomy), NG/OG drainage, CSF (ventricular drainage), etc <br />
<br />
Assessment of fluid and electrolyte status <br />
Lab evaluation:<br />
Serum electrolytes and plasma osmolarity<br />
Urine output <br />
Urine electrolytes, specific gravity (not very useful if the baby is on diuretics - lasix etc), FENa<br />
Blood urea, serum creatinine (values in the first few days reflect mom’s values, not baby’s)<br />
ABG (low pH and bicarb may indicate poor perfusion)<br />
<br />
Fluids and Electrolyte in common neonatal conditions<br />
RDS: Adequate but not too much fluid. Excess leads to hyponatremia, risk of BPD. Too little leads to hypernatremia, dehydration<br />
BPD: Need more calories but fluids are usually restricted: hence the
need for “rocket fuel”. If diuretics are used, w/f ‘lyte problems. May
need extra calcium.<br />
PDA: Avoid fluid overload. If indocin is used, monitor urine output.<br />
Asphyxia: May have renal injury or SIADH. Restrict fluids initially,
avoid potassium. May need fluid challenge if cause of oliguria is not
clear. <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-8480151772167148162012-08-19T20:25:00.001-07:002012-08-19T20:25:47.969-07:00Calcium Metabolism and Hypocalcemia PPTIf you’re looking for <b>Calcium Metabolism and Hypocalcemia PPT</b> you can download <b>Calcium Metabolism and Hypocalcemia PPT</b> here. Download <b>Calcium Metabolism and Hypocalcemia PPT</b> from our website is simple and quick. If you have difficulty to download <b>Calcium Metabolism and Hypocalcemia PPT</b> read <b>How to Download</b> <b>Calcium Metabolism and Hypocalcemia PPT</b>.<br />
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<br />
<br />
Calcium metabolism<br />
99% of total body calcium in the bone .<br />
1% in ICF ,ECF ,& cell membranes .<br />
Calcium weight is 400mg/kg in infant & 950mg/kg in adult .<br />
<br />
physiologic functions :<br />
1.blood coagulation .<br />
2.muscle contraction .<br />
3.neuromuscular transmission .<br />
4.Skeletal growth & mineralization<br />
Ionized Ca is physiologically important .<br />
<br />
Serum CA level is determined by net absorption (GI) & excretion (RENAL). <br />
Each components is tightly regulated-hormonally- to keep normal serum level .<br />
Total CA is usually measured & provides satisfactory assessment of ionized form .<br />
<br />
Calcium regulation :mainly by 3 common hormones :<br />
1}Parathyroid hormone <br />
2}Vitamin D <br />
3}Calcitonin <br />
Vitamin D<br />
Actions:<br />
1)increase Ca absorption from intestine.<br />
2) increase PO4 absorption from intestine.<br />
3) increase renal reabsorption of Ca &PO4.<br />
4) increase bone resorption from old bone &mineralize new bone{net resorption} .<br />
Overall effect :increase serum Calcium and Phosphate .<br />
<br />
PTH hormone<br />
Major hormone in regulation serum Ca .]<br />
Synthesis & secreted from chief cells of parathyroid gland .<br />
Actions :<br />
1)increase bone resorption..increase serum Calcium and Phosphate . <br />
2)increase renal Calcium reabsorption .<br />
3)increase Calcium absorption from intestine indirectly by increase VITD .<br />
4)decrease Phosphate reabsorption from proximal tubules …increase ionized Calcium .<br />
Overall effect :increase serum Calcium & decrease serum Phosphate.<br />
<br />
Hypocalcemia <br />
Causes of hypocalcemia<br />
Specific causes in neonates<br />
Early neonatal hypocalcemia:(within 48-72 hour of birth)<br />
Causes: 1- prematurity: poor intake, decrease response to Vit. D, increase calcitoni, decrease albumin.<br />
2- birth asphyxia: delayed introduction to feed, increase calcitonin, increased endogenous PO4 load, alkali therapy.<br />
3- infant of diabetic mother: functional parahypothyroidism induced by Mg defficiency has predominant role <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-21828171794764626362012-08-19T20:21:00.002-07:002012-08-19T20:21:40.359-07:00Dialysis Basics PPTIf you’re looking for <b>Dialysis Basics PPT</b> you can download <b>Dialysis Basics PPT</b> here. Download <b>Dialysis Basics PPT</b> from our website is simple and quick. If you have difficulty to download <b>Dialysis Basics PPT</b> read <b>How to Download</b> <b>Dialysis Basics PPT</b>.<br />
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<br />
<br />
Indications<br />
Pericarditis or pleuritis<br />
Progressive uremic encephalopathy or neuropathy (AMS, asterixis, myoclonus, seizures)<br />
Bleeding diathesis<br />
Fluid overload unresponsive to diuretics<br />
Metabolic disturbances refractory to medical therapy (hyperkalemia,
metabolic acidosis, hyper- or hypocalcemia, hyperphosphatemia)<br />
Persistent nausea/vomiting, weight loss, or malnutrition<br />
Toxic overdose of a dialyzable drug<br />
<br />
Modalities<br />
<b>Peritoneal dialysis</b><br />
<b>Intermittent hemodialysis</b><br />
<b>Hemofiltration</b><br />
<b>Continuous renal replacement therapy</b><br />
<br />
Decision of modality determined by catabolic rate, hemodynamic stability, and whether primary goal is fluid or solute removal<br />
<br />
Hemodialysis Apparatus<br />
Dialyzer (cellulose, substituted cellulose, synthetic noncellulose membranes)<br />
Dialysis solution (dialysate – water must remain free of Al, Cu, chloramine, bacteria, and endotoxin)<br />
Tubing for transport of blood and dialysis solution<br />
Machine to power and mechanically monitor the procedure (includes air
monitor, proportioning system, temperature sensor, urea sensor to
calculate clearance)<br />
<br />
Hemodialysis Access<br />
Acute dialysis catheter (vascular catheter, i.e. Quentin catheter)<br />
Cuffed, tunneled dialysis catheter (Permcath)<br />
Arteriovenous graft(AVG)<br />
Arteriovenous fistula (AVF)<br />
<br />
Complications of AVF and AVG<br />
Thrombosis<br />
Infection (10% for AVG, 5% for transposed AVF, 2% for non-transposed AVF)<br />
Seromas<br />
Steal (6% of B-C AVF, 1% of R-C AVF)<br />
Aneurysms and pseudoaneurysms (3% of AVF, 5% of AVG)<br />
Venous hypertension (usually 2/2 central venous stenosis)<br />
Heart failure (Avoid AVFs in pts with severely depressed LVEF)<br />
Local bleeding<br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-40998260857499414212012-08-19T20:16:00.002-07:002012-08-19T20:16:41.281-07:00SURGICAL EMERGENCIES IN THE NEWBORN PPTIf you’re looking for <b>SURGICAL EMERGENCIES IN THE NEWBORN PPT</b> you can download <b>SURGICAL EMERGENCIES IN THE NEWBORN PPT</b> here. Download <b>SURGICAL EMERGENCIES IN THE NEWBORN PPT</b> from our website is simple and quick. If you have difficulty to download <b>SURGICAL EMERGENCIES IN THE NEWBORN PPT</b> read <b>How to Download</b> <b>SURGICAL EMERGENCIES IN THE NEWBORN PPT</b>.<br />
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<br />
<br />
<b>Congenital Diaphragmatic Hernia</b><br />
Estimated Incidence to be between 1/2000 to 5000 live births<br />
Cause of CDH is unknown<br />
In most cases the defect is established by gestational week 12<br />
Classic left sided CDH features a 2-4 cm posterolateral defect<br />
Herniated contents often include the left lobe of the liver, the spleen, and almost the entire GI tract<br />
Long term compression of the developing fetal lungs results in pulmonary maldevelopment and lung hypoplasia<br />
<b>Alveolar development</b> is also severely affected<br />
<br />
<b>Esophageal Atresia</b> and <b>Tracheoesophageal Fistula</b><br />
EA and TEF are relatively common congenital anomalies<br />
Associated Anomalies:<b>VACTERL</b>: vertebral, anal, cardiac, TE, renal, limb<br />
<br />
<b>Congenital Intestinal Obstruction</b><br />
<b>Duodenal Atresia</b><br />
Most common site of neonatal intestinal obstruction<br />
Association with <b>Trisomy 21</b><br />
<br />
Radiologic studies<br />
Plain radiograph of the abdomen will generally confirm the diagnosis with a finding of the “<b>double bubble sign</b><br />
Upper GI series or barium enema may be helpful to differentiate from midgut volvulus<br />
<br />
<b>Meconium Ileus</b><br />
Almost always associated with <b>cystic fibrosis</b><br />
Reported to be the presenting symptom in 15-20% of cases<br />
Complicated meconium ileus<br />
In utero dilated proximal intestine volvulizes<br />
Early in gestation may cause one or more atresias<br />
Late in gestation infants may present with perforation -> meconium peritonitis <br />
<br />
Radiologic Studies – Simple Meconium Ileus<br />
Plain radiographs<br />
Varying sized loops of distended bowel<br />
Absence of air fluid levels<br />
<b>Soap bubble appearanc</b>e particularly in the right lower quadrant<br />
<br />
<b>Intestinal Malrotation</b> and <b>Volvulus</b><br />
Malrotation is when the normal process of rotation is arrested or deviated at various stages<br />
Anomalous fixation may also occur<br />
Dense fibrous bands extending from the cecum and right colon across the duodenum to the retroperitoneum may form – <b>Ladd’s Bands</b><br />
<br />
<b>Hirschsprung’s Disease</b><br />
Absence of <b>ganglion cells</b> in the distal intestine is the hallmark of the disease<br />
Ganglion cells are absent in the submucosal plexus and intermuscular plexus<br />
Rectosigmoid region in ~80% of cases<br />
Aganglionosis is almost always continuous distally<br />
<br />
Diagnosis<br />
<b>Rectal biopsy</b> is the gold standard<br />
<br />
<b>Imperforate Anus</b><br />
Average incidence worldwide is believed to be 1 in 5000 live births<br />
Most common in females – rectovestibular fistula<br />
Most common in males – rectourethral fistula<br />
Imperforate anus without fistula 5% of patients and half of these patients have<b> Down’s syndrome</b> <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com1tag:blogger.com,1999:blog-7617369902082136809.post-63744156266508127572012-08-19T20:12:00.000-07:002012-08-19T20:12:46.704-07:00Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPTIf you’re looking for <b>Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPT</b> you can download <b>Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPT</b> here. Download <b>Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPT</b> from our website is simple and quick. If you have difficulty to download <b>Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPT</b> read <b>How to Download</b> <b>Endoluminal radiofrequency ablation and Endovenous laser therapy for the treatment of Varicose Veins PPT</b>.<br />
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<br />
<br />
Indications for <b>Endoluminal radiofrequency ablation</b> and <b>Endovenous laser therapy</b> <br />
Clinical <br />
C0: No visible or palpable signs of venous disease<br />
C1: telangiectases or reticular veins<br />
C2: <b>varicose veins</b><br />
C3: edema<br />
C4: skin changes ascribed to venous disease<br />
a. pigmentation or eczema <br />
b. <b>lipodermatosclerosis</b> or <b>atrophie blanche</b><br />
C5: skin changes as defined previously with healed ulcer<br />
C6: skin changes as defined previously with active ulcer <br />
Etiologic: congenital, primary, secondary or none<br />
Anatomic: superficial, perforator, deep or none<br />
Pathophysiologic: reflux, obstruction, both or none<br />
<br />
Endoluminal radiofrequency ablation (RFA) of the great saphenous vein: mechanism<br />
By directing resistive radiofrequency energy through a vein, a narrow <br />
rim of tissue less than 1mm is heated by an electrode.<br />
<br />
- The amount of heating is modulated using both a microprocessor and <br />
manual movement, resulting in controlled collagen contraction, <br />
thermocoagulation and absorption of the vein.<br />
<br />
Percutaneous access to the greater saphenous vein most commonly at the level of the knee under duplex ultrasound guidance <br />
1) A guidewire is then advanced to the saphenofemoral junction over which the closure catheter is passed<br />
2) catheter prongs are extruded to contact the intimal lining of the vessel wall<br />
3) radiofrequency generator allows the tip of the catheter and the prongs to attain a temperature of 85 degrees C.<br />
<br />
Results<br />
1) Vein occlusion at 1 week documented by venous ultrasound success rate of 98%<br />
2) None of the treated patients developed recanalization that was not seen at 6 weeks, with a successful outcome in 90%.<br />
3) At the 24 month follow-up, 19 of 21 patients had complete
disappearance of the treated saphenous vein,for a success rate of 90%.<br />
4) Side effects were minimal, and no skin burns or thromboses were observed<br />
<br />
Endovenous laser therapy (EVLT): mechanism<br />
Thermal reaction after laser exposure is essential.<br />
- Damages endothelial, intimal internal elastic lamina, and to some <br />
degree the media. Adventitia is rarely affected.<br />
- In vitro studies suggest that energy results in ‘boiling of blood’ and <br />
and generation of ‘steam bubbles’ that indirectly, homogenously <br />
affect the varicose vein. <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com1tag:blogger.com,1999:blog-7617369902082136809.post-35839142649073516472012-08-19T00:48:00.000-07:002012-08-19T00:48:00.425-07:00CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPTIf you’re looking for <b>CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPT</b> you can download <b>CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPT</b> here. Download <b>CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPT</b> from our website is simple and quick. If you have difficulty to download <b>CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPT</b> read <b>How to Download</b> <b>CHRONIC PULMONARY DISEASES_ASTHMA, EMPHYSEMA & CHRONIC BRONCHITIS PPT</b>.<br />
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<br />
Compare/contrast the difference between asthma, emphysema & chronic bronchitis<br />
List 3 anesthetic strategies in caring for this population<br />
Identify 3 pre operative tests desired for anesthesia screening<br />
Describe intraoperative planning for postoperative recovery in this population<br />
<br />
ASTHMA-what is it?<br />
Chronic, inflammatory disease<br />
Reversible obstruction (to a degree)<br />
Increased airway reactivity<br />
Most common chronic illness in children under 17 years<br />
Complex; involves inflammatory cells,mediators, cells&tissues residing in the airway<br />
<br />
ASTHMA-early response<br />
Immed bronchospasm on exposure<br />
Symptoms occur in 10-20 min<br />
Resolves in 60-90 min<br />
Antigen binds to IgE “coated” mast cells,bronchospasm . <br />
Reversible with B2 agonist inhalers<br />
<br />
ASTHMA-Late Response<br />
Onset 3-5 hrs after exposure<br />
Involves inflammation&inc. airway reactivity<br />
May begin cycles of exacerbation<br />
Chronic inflammation leads to airway remodeling, which limits reversibility degree<br />
<br />
CARDIAC ASTHMA<br />
Due to heart failure<br />
Chronic, nonproduct cough-becomes worse when supine(autotransfusion effect)<br />
Bronchospasm occurs b/o congestion of the bronchial mucosa<br />
<br />
EMPHYSEMA-what is it?<br />
Loss of lung elasticity, abnormal permanent enlargement of air spaces
distal to term bronchioles with distention of alveolar walls & <br />
<br />
capillary beds without obvious fibrosis<br />
Alpha1-antitrypsin normally protects lung against destruction caused by inflammatory cells-diminished in this disease<br />
<br />
CHRONIC BRONCHITIS or Blue Bloaters<br />
Inflammation of major & small airways. Edema & hyperplasia of
submucous glands with inc. mucous production. Chronic cough (3 mos)
for at least 2 consecutive years in the absence of other diseases <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-14598392396955541532012-08-18T00:44:00.000-07:002012-08-18T00:44:00.152-07:00Urinary Risk Factors for Bladder Cancer PPTIf you’re looking for <b>Urinary Risk Factors for Bladder Cancer PPT</b> you can download <b>Urinary Risk Factors for Bladder Cancer PPT</b> here. Download <b>Urinary Risk Factors for Bladder Cancer PPT</b> from our website is simple and quick. If you have difficulty to download <b>Urinary Risk Factors for Bladder Cancer PPT</b> read <b>How to Download</b> <b>Urinary Risk Factors for Bladder Cancer PPT</b>.<br />
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<br />
<br />
Bladder Cancer Incidence<br />
Most common type of urinary tract cancer <br />
More than 61,000 new cases of bladder cancer and approximately 13,000 deaths in 2005. <br />
Approximately 70% of new cases occur in men and 30% in women<br />
<br />
Types of Bladder Cancer <br />
Transitional cell carcinoma is the most common, followed by squamous cell carcinoma<br />
Cancer is staged by the layers of the bladder invaded and by cancer spread<br />
As cancer penetrates the layers, it has a higher chance to spread and becomes harder to treat<br />
<br />
Causes of Bladder Cancer <br />
Bladder cancer is believed to develop primarily as a result of environmental factors <br />
Chronic damage to the cells lining the bladder ultimately leads to DNA changes (Somatic Mutation)<br />
True inherited mutations are rare (Germline Mutation), although genetics raise other issues <br />
<br />
Cardinal Symptom: Hematuria <br />
Most common presenting symptom or sign for bladder cancer is hematuria<br />
Hematuria is a common symptom and sign with many causes that can range in clinical importance:<br />
insignificant, eg. urethral polyps <br />
significant requiring observation, eg. cystocele<br />
significant requiring treatment, eg. pyelonephritis <br />
life-threatening, eg. bladder cancer<br />
<br />
Gross hematuria is always cause for concern and requires intensive work-up<br />
30% of patients with gross hematuria are diagnosed with bladder cancer <br />
Microscopic hematuria may also require intensive work-up depending on degree<br />
greater numbers of bladder cancer patients present with microscopic hematuria<br />
Patients at high risk for bladder cancer have additional risk factors<br />
<br />
Risk Factor : Urinary Disorders <br />
Chronic inflammation of the bladder increases the risk of bladder cancer<br />
Irritative effect leads to cell damage over time <br />
Common history includes: <br />
repeated urinary tract infection, eg. cystitis<br />
recurrent kidney, ureter or bladder calculi<br />
chronic urinary retention requiring catheter (spinal cord injury or neurogenic bladder).. <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-75698388153422401162012-08-17T00:40:00.000-07:002012-08-17T00:40:00.250-07:00Benefits of Screening Colonoscopy PPTIf you’re looking for <b>Benefits of Screening Colonoscopy PPT</b> you can download <b>Benefits of Screening Colonoscopy PPT</b> here. Download <b>Benefits of Screening Colonoscopy PPT</b> from our website is simple and quick. If you have difficulty to download <b>Benefits of Screening Colonoscopy PPT</b> read <b>How to Download</b> <b>Benefits of Screening Colonoscopy PPT</b>.<br />
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<br />
<br />
<b>olorectal Cancer</b><br />
The third most common cancer in the U.S.<br />
148,810 new cases expected in 2008<br />
The second deadliest cancer<br />
49,960 deaths nationwide<br />
More than 1 million Americans living with colorectal cancer<br />
<br />
Colorectal Cancer Risk Factors<br />
Age-90% of cases occur in people 50 and older<br />
Gender-Slight male predominance, but common in both men and women<br />
Race/Ethnicity-African Americans have highest incidence and mortality
rate of all groups in U.S., Hispanics the lowest (with considerable
variation depending on <span class="IL_AD" id="IL_AD1">country of origin</span>).Increased rates also documented in Alaska Natives, some <span class="IL_AD" id="IL_AD5">American Indian</span> tribes, Ashkenazi Jews<br />
Increased risk with:Personal history of <span class="IL_AD" id="IL_AD2">inflammatory bowel disease</span>, adenomatous polyps, colon cancer, other conditions<br />
<br />
Risk Factors - <b>Polyps</b><br />
Different types<br />
<b>Hyperplastic</b>-Minimal cancer potential<br />
<b>Adenomatous-</b>Approximately 90% of colon and rectal cancers arise from adenomas<br />
<br />
<b>Benefits of Screening</b><br />
Cancer Prevention-Removal of <b>pre-cancerous polyps</b> prevent cancer (unique aspect <span class="IL_AD" id="IL_AD4">of colon cancer</span> screening)<br />
Improved Survival-Early detection markedly improves chances of long term survival<br />
<br />
<b>Colorectal Screening Rates</b><br />
Just 40% of colorectal cancers are detected at the earliest stage<br />
A little more than half of Americans over age 50 report having had a recent <span class="IL_AD" id="IL_AD3">colorectal cancer screening</span> test<br />
Slow but steady improvement in these numbers over the past decade (but all are not benefiting to the same degree)<br />
<br />
<b>CRC Screening Guidelines</b> What’s New?<br />
CRC <span class="IL_AD" id="IL_AD6">screening tests</span> are grouped into two categories:<br />
Tests that detect cancer and precancerous polyps<br />
Tests that primarily detect cancer<br />
* It is the strong opinion of the consensus guidelines group that colon
cancer prevention should be the primary goal of CRC screening.Exams that
are designed to detect both early cancer and precancerous polyps should
be encouraged if resources are available and patients are willing to
undergo an invasive test.If the full range of screening tests are not available, physicians should make every effort to offer at least one test from each category.<br />
Two new tests recommended:<br />
<b>Stool DNA (sDNA)</b> and<br />
<b>Computerized tomographic colonography (CTC)</b>-sometimes referred to as <b>virtual colonoscopy</b> <br />
<br />
<br />
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Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-86451626805566007772012-08-16T00:36:00.001-07:002012-08-16T00:37:16.806-07:00Acute Ano-rectal Conditions PPTIf you’re looking for <a href="http://medicppt.blogspot.com/2012/08/acute-ano-rectal-conditions-ppt.html" target="_blank"><b>Acute Ano-rectal Conditions PPT</b></a> you can download <b>Acute Ano-rectal Conditions PPT</b> here. Download <b>Acute Ano-rectal Conditions PPT</b> from our website is simple and quick. If you have difficulty to download <a href="http://medicppt.blogspot.com/2012/08/acute-ano-rectal-conditions-ppt.html" target="_blank"><b>Acute Ano-rectal Conditions PPT</b></a> read <b>How to Download</b> <b>Acute Ano-rectal Conditions PPT</b>.<br />
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<br />
<br />
Diagnosis of anal conditions which present with rectal bleeding<br />
Bleeding but no pain:<br />
<b>Carcinoma of the Colon,Carcinoma of Rectum,hemorrhoids,colitis</b><br />
Bleeding + pain = <b>fissure or carcinoma of anal canal</b><br />
The most common causes of rectal bleeding in patients who visit <span class="IL_AD" id="IL_AD3">primary care physicians</span> are hemorrhoids, <span class="IL_AD" id="IL_AD5">fissures</span> and polyps. <br />
<br />
Careful history focusing on the nature of the pain and its relationship to defaecation<br />
The pattern <span class="IL_AD" id="IL_AD6">of pain</span> helps differentiate anal fissure from hemorrhoids and other conditions. (hemorrhoids and <span class="IL_AD" id="IL_AD4">rectal cancer</span> are usually not painful)<br />
<b>Anorectal pain</b> that begins gradually and becomes excruciating over a few days with localized are of tenderness is more likely to be <br />
abscess.<br />
A nagging, aching discomfort made worse by defecation could be due to piles.<br />
An occasional, severe, cramp-like pain deep in the anal canal, that often occur at night, lasting about half an hour <br />
proctalgia fugax. <b>Proctalgia fugax</b> pain is excruciating and may
be accompanied by sweating, pallor and tachycardia. Patients experience
urgency to defecate, yet pass no stool. <br />
A knife-like pain when you have your bowels open, and which may last for
10–15 minutes afterwards. often described like 'passing glass'. In
addition to the pain, some bright red blood on the toilet paper is
noticed.<b>Anal fissure.</b><br />
<br />
Diagnosis of anal conditions which present with pain<br />
Pain alone<br />
Fissure ( pain after defaction)<br />
Proctalgia fugax (pain spontaneously at night)<br />
Anorectal abscess<br />
Pain with bleeding<br />
Fissure<br />
Pain with a lump<br />
Perianal haematoma<br />
Anorectal abscess<br />
Pain, lump and bleeding<br />
Prolapsed <span class="IL_AD" id="IL_AD1">haemorrhoids</span>/rectum<br />
Carcinoma of the anal canal<br />
<br />
<b>Anorectal examination</b><br />
One of the most important examinations in a patient with abdominal disease.<br />
Still its the least popular segment of the entire physical <span class="IL_AD" id="IL_AD2">examination</span>.<br />
Should not be omitted from your examination, especially in middle-aged and older patient, why?<br />
risks missing an asymptomatic carcinooma <br />
Can be done in numerous positions:<br />
Left Lateral (Sims’) position. The usual position when the patient is
in bed. Turn patient on to left side with pelvis vertical. Ask patients
to draw knees up to chest with buttocks on the side of the couch<br />
The Knee-elbow position. Patient kneeling on couch, resting on elbows,
of particular use when palpating the prostate and seminal <br />
The Dorsal Position. This position with the patient lying on the back
with right leg flexed is useful when the patient is in severe pain, and
movement is contra-indicated. Enables assessment of rectovesical pouch
in abdominal emergencies.<br />
Lithotomy. best position for examination but not always available. <br />
<br />
<br />
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<br />
<br />
Objectives:<br />
- Colon and rectal cancer statistics in Canada.<br />
- Prevention and screening.<br />
- Medical management of localized and advanced stage cancer.<br />
<br />
Statistics:<br />
- An estimated 153,000 new cases & 70,000 deaths from cancer will occur in 2006 in Canada1.<br />
- An estimated 20,000 new cases & 8,500 deaths from colorectal cancer will occur in 2006 in Canada1.<br />
<br />
Risk factors:<br />
01.Sporadic (70%):<br />
- Age: Risk increases significantly b/w ages of 40 and 50, & in each succeeding decade thereafter1.<br />
- Lifetime incidence is about 5%.<br />
Inflammatory bowel disease (Pancolitis ,5-15 fold increased risk )1<br />
- Alcohol<br />
- Diabetes mellitus<br />
- Cigarette smoking.<br />
02.inherited (5-10%):<br />
(a) Germ line mutations.<br />
Polyposis syndromes:<br />
- Familial adenomatous polyposis.<br />
- Less than 1% of CRC.<br />
- Germ line mutations in APC gene on ch 5<br />
Non Polyposis syndromes<br />
- Hereditary nonpolyposis CRC.<br />
- Autosomal dominant.<br />
- More common than FAP1<br />
03.familial (20-25%):<br />
- Affected pts have family history, but pattern is different from inherited one. <br />
<br />
Diagnosis:<br />
* Presentation of metastatic disease:<br />
- 15-20% of pts have metastatic disease on presentation.<br />
- Common sites are LN, liver, lungs and peritoneum.<br />
<br />
Diagnostic procedures:<br />
- Colonoscopy.<br />
- Double contrast barium enema <br />
<br />
<br />
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<br />
<br />
Quick and Easy AXIS DETERMINATION<br />
Left axis deviation - negative QRS in lead AVF<br />
Right axis deviation - negative QRS in lead I<br />
Severe Right axis deviation negative QRS in BOTH lead I and AVF<br />
<br />
Why do we care about axis determination in the ER? <br />
Left axis deviation(LAD) : LBBB, LAFB, Mechanical shift due to ascites or elevated diaphragm, left atrial hypertrophy<br />
Right axis deviation(RAD) : RBBB, LPFB, right ventricular hypertrophy, dextrocardia, Pulmonary Embolism<br />
Both RAD and LAD can be caused by COPD, Hyperkalemia, MI, WPW <br />
<br />
Right Bundle Branch Block<br />
QRS more than 0.12 sec<br />
Predominantly positive rSR’ in V 1-2 <br />
Wide slurred S in lead I<br />
Left bundle branch block (Both fascicles are blocked)<br />
QRS more than 0.12 sec<br />
Deep S in V 1-3 <br />
Tall R and RsR’ in lateral leads: I, AVL, & V 5-6 <br />
<br />
AV-BLOCKS<br />
1st degree - PR > 0.2 sec<br />
2nd degree<br />
Mobitz I (Wenckebach) PR increases until a QRS is blocked<br />
Mobitz II - blocked QRS (2:1, 3:1, 4:1)<br />
PR interval is fixed and usually normal, then p-waves with dropped beats<br />
3rd degree - disassociation of PP and RR, the PP intervals and RR intervals are constant<br />
<br />
TYPES OF DYSRHYTHMIAS<br />
Re-entry (SVT, WPW)<br />
Two parallel pathways with different rates and refractory periods<br />
Something alters the refractory period and the alternative pathway becomes dominant<br />
This causes a unidirectional conduction block, and a circuitous conduction pathway forms. <br />
<br />
Enhanced or Triggered (PACs, PVCs, Afib, MFAT)<br />
Conduction cells act as Pacemaker cells <br />
Conduction cells can be enhanced and become dominant in the setting of ischemia, sepsis, electrolyte imbalance or toxins. <br />
Some dysrhythmias start with enhanced or triggered activity, but follow a
circuitous pathway seen in re-entry. (Atrial flutter, Vtach) <br />
<br />
<br />
<a href="https://www.box.com/embed/nylne0uxslcj5ze.swf" target="_blank"><b>Download ADVANCED ECG INTERPRETATION PPT</b></a>Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-14673161036109926702012-08-15T19:06:00.000-07:002012-08-15T19:07:12.379-07:00Minimally invasive endocrine surgery PPTIf you’re looking for <a href="http://medicppt.blogspot.com/2012/08/minimally-invasive-endocrine-surgery-ppt.html" target="_blank"><b>Minimally invasive endocrine surgery PPT</b></a> you can download <b>Minimally invasive endocrine surgery PPT</b> here. Download <b>Minimally invasive endocrine surgery PPT</b> from our website is simple and quick. If you have difficulty to download <a href="http://medicppt.blogspot.com/2012/08/minimally-invasive-endocrine-surgery-ppt.html" target="_blank"><b>Minimally invasive endocrine surgery PPT</b></a> read <b>How to Download</b> <b>Minimally invasive endocrine surgery PPT</b>.<br />
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<br />
<br />
Primary Hyperparathyroidism<br />
85 % - single <span class="IL_AD" id="IL_AD3">adenoma</span><br />
10% - multi gland disease, <span class="IL_AD" id="IL_AD1">hyperplasia</span><br />
4% - double adenoma<br />
1% - parathyroid carcinoma<br />
<br />
Diagnosis:<br />
Hypercalcemia with inappropriate high PTH level<br />
24 urine calcium (h/o kidney stone)<br />
<span class="IL_AD" id="IL_AD2">Bone density</span> study (h/o osteoporosis)<br />
Imaging has no role in making the Dx<br />
<br />
Indication for surgery:<br />
1) age < 50<br />
2) no ability for appropriate follow-up<br />
3) serum Ca > 1.0 mg/dL above normal<br />
4) urine Ca > 400 mg/24 hr<br />
5) 30% <span class="IL_AD" id="IL_AD6">decrease</span> in renal function<br />
6) complication of pHPT: nephrocalcinosis, osteoporosis ( T score <
2.5 SD 2 L-spine, hip or wrist) or sever psychoneurologic disorder)<br />
<br />
Surgery:Four gland exploration vs single gland-<span class="IL_AD" id="IL_AD4">minimally invasive</span> technique <br />
<br />
Minimally invasive techniques: <br />
Mid-neck focused approach<br />
Back-door approach<br />
Video-assisted parathyroidectomy<br />
Total endoscopic approach<br />
<br />
Advantages of minimally invasive technique: <br />
Ambulatory surgery (decrease hospital stay & coast)<br />
Local / regional anesthesia: <br />
- avoid risk of general anesthesia, <br />
- ability patient to talk during the surgery and assess<br />
r. laryngeal nerve function, <br />
- quicker recovery<br />
Small incision<br />
No drains<br />
Suture removed at the day of surgery right before d/c to home (skin glue)<br />
<br />
Benefits of videO-assisted minimally invasive technique:<br />
Better R. laryngeal nerve visualization and preservation<br />
No cutaneous flap – decrease postoperative scaring<br />
Faster healing with better cosmetic result<br />
Less pain<br />
<br />
Key Recommendations Regarding Diagnosis of Thyroid Nodules:<br />
Palpable nodule or Thyroid incidenteloma by US <br />
TSH level - normal or low (or high TSH with US suspicious features), cold on scintigraphy.<br />
Only nodule > 1 cm should be evaluated (unless suspicious US findings or high-risk history)<br />
FNA results:Inadequate, Malignant,Indeterminate,Benign<br />
<br />
Minimally invasive thyroid surgery<br />
Utilization of up-to-date knowledge and technology:<br />
video-endoscopic surgery, <br />
sutureless thyroid with LigaSure vessel-sealing systems ,<br />
intra – operative nerve monitoring for r.laryngeal and external branch of the superior laryngeal nerve<br />
Intraoperative flexible laryngoscopy for vocal cord evaluation <span class="IL_AD" id="IL_AD5">before and after</span> procedure <br />
<br />
<br />
<a href="https://www.box.com/embed/fsk5l2gh1ookzeg.swf" target="_blank"><b>Download Minimally invasive endocrine surgery PPT</b></a>Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-86266675499416442882012-08-15T18:59:00.000-07:002012-08-15T19:02:13.401-07:00Embryonic stem cell transplantation PPTIf you’re looking for <a href="http://medicppt.blogspot.com/2012/08/embryonic-stem-cell-transplantation-ppt.html" target="_blank"><b>Embryonic stem cell transplantation PPT</b></a> you can download <b>Embryonic stem cell transplantation PPT</b> here. Download <b>Embryonic stem cell transplantation PPT</b> from our website is simple and quick. If you have difficulty to download <a href="http://medicppt.blogspot.com/2012/08/embryonic-stem-cell-transplantation-ppt.html" target="_blank"><b>Embryonic stem cell transplantation PPT</b></a> read <b>How to Download</b> <b>Embryonic stem cell transplantation PPT</b>.<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhl71qSK_SuQak6YbS7vy_AIQe4uVV8oSeKZu93dZt1pGDF9IPPrMjZRTg_zCRhGJuVjF14ah8EBnhv7G6Y0xcsbdZCdl4dgCkcuw4bfZ4p6nhWlUt36H_SwWktXX7GnEcJwX3UVUVhMGLE/s1600/human-embryo-and-placenta.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="Embryonic stem cell transplantation PPT" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhl71qSK_SuQak6YbS7vy_AIQe4uVV8oSeKZu93dZt1pGDF9IPPrMjZRTg_zCRhGJuVjF14ah8EBnhv7G6Y0xcsbdZCdl4dgCkcuw4bfZ4p6nhWlUt36H_SwWktXX7GnEcJwX3UVUVhMGLE/s1600/human-embryo-and-placenta.png" title="Embryonic stem cell transplantation" /></a></td></tr>
<tr align="center"><td class="tr-caption">Embryonic stem cell transplantation</td></tr>
</tbody></table>
<br />
<br />
Embryonic stem cell lines are cultures of cells derived from the
epiblast tissue of the inner cell mass (ICM) of a blastocyst or earlier
morula stage embryos.Embryonic stem cell are pluripotent and they can
develop into each of the more than 200 cell types of the adult body when
given sufficient and necessary stimulation for a specific cell type.The
primitive stem cells located in the organs of fetuses are referred to
as fetal stem cells.Adult stem cells are undifferentiated cells, found
throughout the body after development, that multiply by cell division to
replenish dying cells and regenerate damaged tissues.<br />
<br />
Also known as
somatic stem cells.Pluripotent adult stem cells are rare and generally
small in number but can be found in a number of tissues including
umbilical cord blood.Most adult stem cells are lineage-restricted
(multipotent) and are generally referred to by their tissue origin
(mesenchymal stem cell, adipose-derived stem cell, endothelial stem
cell, dental pulp stem cell, etc.)The use of adult stem cells in
research and therapy is not as controversial as the use of embryonic
stem cells, because the production of adult stem cells does not require
the destruction of an embryo. Additionally, in instances where adult
stem cells are obtained from the intended recipient (an autograft), the
risk of rejection is essentially non-existent. <br />
<br />
There are currently no approved treatments using embryonic stem cells.
The first human trial was approved by the US Food and Drug
Administration in January 2009.However, the human trial was not
initiated until October 13, 2010 in Atlanta for spinal injury victims.
Embryonic stem cells, being pluripotent cells, require specific signals
for correct differentiation—if injected directly into another body, ES
cells will differentiate into many different types of cells, causing a
teratoma. Differentiating ES cells into usable cells while avoiding
transplant rejection are just a few of the hurdles that embryonic stem
cell researchers still face.<br />
<br />
Medical researchers believe that stem cell therapy has the potential to
dramatically change the treatment of human disease. A number of adult
stem cell therapies already exist, particularly bone marrow transplants
that are used to treat leukemia.In the future, medical researchers
anticipate being able to use technologies derived from stem cell
research to treat a wider variety of diseases including cancer,
Parkinson's disease, spinal cord injuries, Amyotrophic lateral
sclerosis, multiple sclerosis, and muscle damage, amongst a number of
other impairments and conditions. <br />
<br />
<br />
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<br />
<br />
Age Issues in Back Pain <br />
Osteoid osteoma in teenager<br />
Inflammatory bowel in 20 year old<br />
Multiple Myeloma in 70 to 80 year old<br />
Abdominal Aneurysm in 70 to 80 year old<br />
Sex Ratios in <span class="IL_AD" id="IL_AD4">Low back Pain</span><br />
Osteoporotic fractures > in women<br />
<span class="IL_AD" id="IL_AD1">Fibromyalgia</span> > in women<br />
<br />
Low Back Pain in the Elderly <br />
Due to a wide range of potential <span class="IL_AD" id="IL_AD2">causes of low back pain</span> in the elderly makes its diagnosis and management more challenging than in younger patients.<br />
<br />
4 Important Areas to Assess in the Elderly<br />
Characteristics of the pain<br />
Presence of malignancy<br />
History of non-spinal medical problems<br />
Psychosocial status<br />
<br />
<span class="IL_AD" id="IL_AD5">Causes of lower Back Pain</span> in Older patients<br />
Acute Low Back Pain<br />
Lumbar strain or sprain<br />
Vertebral compression fracture due to osteoporosis<br />
Abdominal aortic aneurysm<br />
Polymyalgia rheumatica<br />
<br />
<span class="IL_AD" id="IL_AD6">Chronic lower Back Pain</span><br />
Aging-related <span class="IL_AD" id="IL_AD3">degenerative</span> disk and joint disease<br />
Malignancy<br />
Paget disease<br />
Fibromyalgia<br />
Diffuse idiopathic skeletal hyperostosis <br />
<br />
Diagnostic Imaging Studies<br />
More cautious interpreting in older patients due to false-positive findings increase with age.<br />
Medical and psychosocial comorbidity increases significantly with age.<br />
<br />
<br />
<a href="https://www.box.com/embed/1uipoe2hbu70btz.swf" target="_blank"><b>Download Diagnosing Low Back Pain in the Elderly PPT</b></a>Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-42023597827646338212012-08-15T18:38:00.001-07:002012-08-15T18:54:53.257-07:00Polycystic Ovarian Syndrome & Hirsutism PPTIf you’re looking for <a href="http://medicppt.blogspot.com/2012/08/polycystic-ovarian-syndrome-hirsutism.html" target="_blank"><b>Polycystic Ovarian Syndrome & Hirsutism PPT</b></a> you can download <b>Polycystic Ovarian Syndrome & Hirsutism PPT</b> here. Download <b>Polycystic Ovarian Syndrome & Hirsutism PPT</b> from our website is simple and quick. If you have difficulty to download <b>Polycystic Ovarian Syndrome & Hirsutism PPT</b> read <b>How to Download</b> <b>Polycystic Ovarian Syndrome & Hirsutism PPT</b>.<br />
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<br />
Polycystic Ovarian Syndrome<br />
Formerly called Stein Leventhal Syndrome <br />
Characterized by:<br />
anovulatory bleeding/amenorrhea<br />
hirsutism, <br />
<span class="IL_AD" id="IL_AD3">obesity</span>, <br />
hyperinsulinemia/insulin resistance, <br />
bilateral ovarian enlargement & multiple cysts<br />
<span class="IL_AD" id="IL_AD1">Infertility</span><br />
Hyperandrogenemia & Hyperestrogenemia (due to peripheral conversion)<br />
<br />
Pathophysiology<br />
Incompletely understood<br />
Abnormally elevated LH levels<br />
Loss of mid cycle LH surge<br />
Excessive <span class="IL_AD" id="IL_AD2">androgen</span> production<br />
Atresia of ovarian follicles<br />
Ratio of LH:FSH markedly increased<br />
<br />
Affects 5% of reproductive age women<br />
Represents a leading cause of chronic anovulatory bleeding<br />
disorder of hypothalamic rhythmicity<br />
excessive LH production without mid cycle surge<br />
leads to overproduction of <span class="IL_AD" id="IL_AD4">testosterone</span> & Androstenedione<br />
Androgens converted to estrone which <span class="IL_AD" id="IL_AD5">causes</span> endometrial proliferation that results in irregular periods<br />
Serum concentrations of both estrogen and testosterone rise<br />
Insulin resistance once believed to be due to ovarian androgen overproduction<br />
Current <span class="IL_AD" id="IL_AD6">theory</span> is that Hyperinsulinism causes ovarian androgen overproduction<br />
Consequence of androgen overproduction<br />
hirsutism<br />
frank virilization<br />
Chronic unopposed estrogen stimulation leads to endometrial Hyperplasia, cellular atypia, and endometrial carcinoma <br />
<br />
<br />
<a href="https://www.box.com/embed/2fvxrr4pa0gva8b.swf" target="_blank"><b>Download Polycystic Ovarian Syndrome & Hirsutism PPT</b></a>Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-88062121938747565422012-08-15T08:34:00.002-07:002012-08-15T08:34:24.045-07:00Renal Tubular Disorders PPTIn this page you can download <titlle><b>Renal Tubular Disorders PPT</b>, If you have difficulty in downloading <b>Renal Tubular Disorders PPT</b><titlle>, please read <b>How to Download</b>.</titlle></titlle><br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEic6rXUTIblC1OY8ljnAYgs327Ss-1tJ31YTtTsJHYV76bIWvIRCRrUvaPIY8GU3J3riN2rxA9TWJTTSbCBJVMqg7vZl8-YsSdnYmKgdTDSf1QkQ_05Vn7nOn4NxTEXCDoFCYWIT2mNwqW2/s1600/Rickets+child_RTA.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="Renal Tubular Disorders PPT" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEic6rXUTIblC1OY8ljnAYgs327Ss-1tJ31YTtTsJHYV76bIWvIRCRrUvaPIY8GU3J3riN2rxA9TWJTTSbCBJVMqg7vZl8-YsSdnYmKgdTDSf1QkQ_05Vn7nOn4NxTEXCDoFCYWIT2mNwqW2/s1600/Rickets+child_RTA.jpg" title="Renal Tubular Disorders " /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Renal Tubular Disorders</td></tr>
</tbody></table>
<titlle><titlle></titlle></titlle><br />
Glomerulus produces an enormous volume of ultrafiltrate daily.<br />
Tubules modify the UF by selective reabsorption and secretion of various solutes to maintain body homeostasis.<br />
<br />
Classification of renal tubular disorders – Primary or Secondary<br />
PRIMARY – INHERITED OR SPORADIC<br />
CYSTIC DISEASES – PCKD (AR or AD), cortical cysts, nephronophthisis, medullary sponge kidney<br />
DYSPLASTIC DISEASES – Renal aplasia, dysplasia, MCDK (uni or bilateral)<br />
HEREDITARY DISEASES WITH TUBULAR TRANSPORT DEFECTS – Hartnup disease,
Fanconi syn, Lowe’s syn, Cystinosis, Wilson’s dis, Galactosemia, RTA
(many types), Vit D resistant rickets, Nephrogenic Diabetes Insipidus<br />
HEREDITARY DISEASES WITH INTRARENAL DEPOSITION OF METABOLITES – Fabry’s disease, Hurler syndrome<br />
HEREDITARY DISEASES WITH LITHIASIS – Hyperoxaluria, Xanthinuria, L- glyceris aciduria, Lesch- Nyhan syn, Cystinuria, Glycinuria<br />
MISCELLANEOUS – Sickle cell anemia, Bartter’s syndrome, Total and partial lipodystrophy<br />
<br />
Introduction to Renal Tubular Acidosis<br />
RTA is a clinical syndrome in which either an inherited or acquired
renal tubular defect leads to failure to maintain a normal plasma
bicarbonate conc in the presence of a normal rate of acid production
from diet and metabolism<br />
Clinically, it is characterized by a normal anion gap (AG),
hyperchloremic metabolic acidosis (MA), bicarbonaturia, reduced urinary
excretion of titrable acid and ammonia and an elevated urinary pH.<br />
<br />
Types of Renal tubular acidosis (RTA) <br />
Type 1 RTA – Distal RTA – defect in hydrogen ion secretion by the distal tubule<br />
Type 2 RTA – Proximal RTA – defect in bicarbonate reabsorption by the proximal tubule<br />
Type 4 RTA – Hyperkalemic RTA – impaired distal nephron secretion of both H+ and K+ ions<br />
<br />
Distal RTA<br />
Distal renal tubular acidosis (dRTA) was recognized as a distinct entity
by Albright et al in 1946. The clinical syndrome described consisted of
hypokalemia, hyperchloremic metabolic acidosis, inability to lower
urine pH below 5.5, nephrocalcinosis, and nephrolithiasis. Additional
features included osteomalacia or rickets.<br />
<br />
In infancy-<br />
Failure to thrive, poor weight gain.<br />
Recurrent vomiting.<br />
May have episodes of life threatening metabolic acidosis precipitated by minor infections.<br />
In childhood- delayed physical milestones, short stature, rickets and bony deformities.<br />
Polyuria and polydipsia are constant features.<br />
Older children- myalgia, fatigue and muscle weakness.<br />
<titlle><titlle> </titlle></titlle><br />
<titlle><titlle><a href="http://adf.ly/BuuId" target="_blank"><b>Download Renal Tubular Disorders PPT</b></a></titlle></titlle>Anonymoushttp://www.blogger.com/profile/11064859817017095895noreply@blogger.com0tag:blogger.com,1999:blog-7617369902082136809.post-60199187031734016222012-08-15T08:28:00.002-07:002012-08-15T08:29:23.073-07:00Lupus Peritonitis PPTIn this page you can download <titlle><b style="color: black;">Lupus Peritonitis PPT</b>, If you have difficulty in downloading <titlle><b>Lupus Peritonitis PPT</b>, please read <b>How to Download</b>.</titlle></titlle><br />
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<br />
SLE-Disorder characterized by presence of autoantibodies and clinical
manifestations involving autoimmune inflammation that may affect nearly
every organ and tissue. <br />
<br />
GI manifestations of SLE<br />
Oral cavity ulcerations and Sjogrens<br />
Esophagitis and esophageal dysmotility<br />
PUD, especially if NSAIDs used<br />
Small vessel vasculitis affecting the large or small intestine<br />
Pancreatitis<br />
IBD: UC, Crohns, collagenous colitis<br />
Celiac disease<br />
Protein-losing enteropathy<br />
Fat malabsorption<br />
<br />
Lupus peritonitis<br />
Typically categorized under “serositis” however in some sources included under “GI manifestations of SLE”<br />
True prevalence unknown<br />
<br />
Serositis<br />
Inflammation of the serous membranes including the pericardium, pleura
and peritoneum which may lead to pain, fluid accumulation, adhesion and
even fibrosis.<br />
Pleuritis is the most commonly reported of the three<br />
<br />
Abdominal pain reported in 8-37% of SLE patients<br />
DDx for abdominal pain in lupus is broad and includes both disease-related and non- diseases-related entities.<br />
8-11% of SLE patients develop ascites <br />
Ascites may be due to causes other than lupus peritonitis
(hypoalbuminemia, R heart failure, hepatic vein thrombosis, malignancy,
infective peritonitis 2/2 bowel infarction, TB) <br />
Ascitic fluid: WBC 10-1630 with lymph/ mono predominance), SAAG< 1.1<br />
In laparotomy patients: peritoneum is hyperemic and thickened, nodular or adhesive, or normal<br />
<br />
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Osteoarthritis<br />
Typically affects people over the age of 50<br />
A biologic process which effects cartilage with subsequent inflammatory component<br />
Characteristically the major component of the clinical presentation is pain and decreased function<br />
>75% of people over the age of 75 have x-ray evidence of disease<br />
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> 75% of people over the age of 85 are symptomatic<br />
Probably affects 16-20,000,000 Americans<br />
<br />
OA Biology<br />
Slowly progressive disease<br />
Primarily initially affects cartilage<br />
Early cellular response: increased synthesis of proteoglycans and collagen followed by increased hydration<br />
Then later inability to keep up with repair process and failure to replace proteoglycans and collagen<br />
Consequent loss of cartilage, fissuring of cartilage, subchondral bone sclerosis and finally eburnation with “bone on bone”<br />
Subsequent inflammatory response to cartilage effects<br />
Clear synovial hypertrophy with consequent stimulus of inflammatory
cytokines (IL-1 and TNF alpha have been shown to be elevated in the
joint fluid)<br />
But these effects are more local: little increase in CRP, few signs and symptoms of systemic inflammatory disease<br />
<br />
Diagnosis of OA<br />
By imaging<br />
X-ray<br />
Presence of osteophytes (biologic evidence of an attempt to repair?)<br />
Progressive joint space narrowing which is a surrogate measure of cartilage thinning<br />
Now known not to be linear and some patients are rapid progressors while
others are slow progressors or somewhere in between; how to predict
which patient falls into which category<br />
Increased sclerotic change in subchondral bone<br />
When significantly progressive might reflect eburnation<br />
<br />
Radiographic Features of the Knee in OA<br />
Joint space narrowing<br />
Marginal osteophytes<br />
Subchondral cysts<br />
Boney sclerosis<br />
Malalignment<br />
<br />
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Classification of Seizures<br />
Partial: simple or complex<br />
Generalized: absence, tonic, clonic, tonic-clonic, myoclonic, febrile<br />
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<br />
Pathophysiology of Seizures<br />
The Interictal Spike (paroxysmal depolarization shift)<br />
Increased excitability <br />
Membrane depolarization, potassium buildup<br />
Increased excitatory (EAA, glutamate) input<br />
Decreased inhibitory (GABA) input<br />
<br />
Evidence for the Pathophysiology of Seizures<br />
Increased EAA<br />
Increased Excitatory Amino Acid Transmission<br />
Increased sensitivity to EAA<br />
Progressive increase in glutamate release during kindling<br />
Increased glutamate and aspartate at start of seizure<br />
Upregulation of NMDA receptors in kindled rats<br />
<br />
Decreased GABA<br />
Decreased binding of GABA and benzodiazepines<br />
Decreased Cl- currents in response to GABA<br />
Decreased glutamate decarboxylase activity (synthesizes GABA)<br />
Interfere with GABA causes seizures<br />
<br />
Strategies in Treatment<br />
Stabilize membrane and prevent depolarization by action on ion channels<br />
Increase GABAergic transmission <br />
Decrease EAA transmission<br />
<br />
Phenytoin – Toxicity and Adverse Events<br />
Acute Toxicity<br />
High i.v. rate: cardiac arrhythmias ± hypotension; CNS depression.<br />
Acute oral overdose: cerebellar and vestibular symptoms and signs:nystagmus, ataxia, diplopia vertigo.<br />
<br />
Chronic Toxicity<br />
Folate Deficiency - megaloblastic anemia<br />
Hypoprothrombinemia and hemorrhage in newborns<br />
Hypersenstivity Reactions – could be severe. SLE, fatal hepatic necrosis, Stevens-Johnson syndrome.<br />
Pseudolymphoma syndrome<br />
Teratogenic<br />
<br />
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