Management of Acute Renal Failure

Posted by e-Medical PPT

Acute Renal Failure
Definition: Sudden deterioration in the ability of the kidneys to maintain fluid, solute or electrolyte homeostasis
Common in PICU patients (10-20%)
Greater than 50% mortality
ARF in PICU patients has an independent and significant impact on mortality

ARF: Causes and mortality
Primary renal disease: 33%
Hemolytic uremic syndrome: 88%
Obstructive uropathy
Renal vein/artery thrombosis
Primary glomerulonephritis (RPGN)

Overall mortality: 6%
Most primary renal diseases develop RF gradually and do not need emergent dialysis
Extrarenal causes of ARF: 67% of total

ARF: Risk factors for mortality
Multi-organ failure
Bacterial Sepsis
Fungal sepsis
Hypotension/vasopressors
Ventilatory support
Initiation of dialysis late in hospital course
Oliguria/anuria: with oliguric ARF, mortality is 50% compared to  20% with non-oliguric ARF

Best cure is to prevent
Have a high index of suspicion for reversible factors - volume depletion, decreasing cardiac function, sepsis, urinary tract obstruction
Be sure patient is well-hydrated when exposing patient to nephrotoxic drugs

Anticipate problems
Avoid worsening the ARF
Adjust medicines for renal insufficiency
Avoid nephrotoxins if possible
Avoid intravascular volume depletion (especially in third-spacing or edematous patients)


Introduction to Cardiac Auscultation

Posted by e-Medical PPT

Valvular Aortic Stenosis
Failure of valve to open normally during systole, requiring LV to develop excess pressure to overcome increased resistance.
Pressure gradient between LV and aorta may be as much as 100 mm Hg causes concentric hypertrophy
Symptoms of exertional chest pain, syncope, dyspnea
Mandate valve replacement to prevent sudden death
Murmur in AS is mid-systolic, crescendo-decrescendo.

Mitral Stenosis
Almost always rheumatic in origin
Murmur may be subtle, but high flow states cause increased pressure gradient, pulmonary edema
Classic presentation is during vaginal delivery. Tachycardia, straining, volume increase cause pulmonary edema
Patients eventually have exertional dyspnea, atrial fibrillation (often with thromboembolism), chest pain

Normal MVA 4-5 cm2
More than 2.5 cm2 asymptomatic
Less  than 1.5 cm2 may have sxs at rest
Stress which increases transmitral flow or decreases diastolic filling time will significantly increase gradient

Turbulent, high velocity flow occurs during diastole
murmur is therefore a DIASTOLIC, low frequency rumble heard at apex with stethoscope bell, patient in L lateral decubitus
requires quiet concentration, palpate carotid to time systole/diastole
Always look for MS in patient with new Atrial fibrillation
rate control, anticoagulation crucial


Type 1 Diabetes

Posted by e-Medical PPT

Diabetes mellitus type 1 is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas.The subsequent lack of insulin leads to increased blood and urine glucose.Type 1 is treated with insulin replacement therapy—either via subcutaneous injection or insulin pump, along with attention to dietary management.Pancreas and islet transplants have been used to treat type 1 diabetes; however, islet transplants are currently still at the experimental trial stage.
Most people who develop type 1 are otherwise healthy.The classical symptoms of type 1 diabetes include: polyuria,polydipsia,polyphagia,tiredness and weight loss.Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
    * Fasting plasma glucose level at or above 7.0 mmol/L (126 mg/dL).
    * Plasma glucose at or above 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load as in a glucose tolerance test.
    * Symptoms of hyperglycemia and casual plasma glucose at or above 11.1 mmol/L (200 mg/dL).
    * Glycated hemoglobin  at or above 6.5.
Type 1 can be distinguished from type 2 diabetes via a C-peptide assay, which measures endogenous insulin production.


Behçet disease

Posted by e-Medical PPT

Behçet disease is a rare, systemic, form of vasculitis that often presents with mucous membrane ulceration, and ocular involvements.As a systemic disease, it also involves visceral organs such as the gastrointestinal tract, pulmonary, musculoskeletal, and neurological systems. This syndrome can be fatal; death can be caused by complicated rupture of the vascular aneurysms, or severe neurological complications, and therefore immediate medical treatment is necessary.
The etiology is not well-defined, but it is primarily characterized by auto-inflammation of the blood vessels.
Nearly all patients present with some form of painful oral mucocutaneous ulcerations in form of aphthous ulcers or non-scarring oral lesions.The oral lesions are similar to those found in inflammatory bowel disease and can be relapsing.Painful genital ulcerations usually develop on the vulva and the scrotum and cause scarring in 75% of the patients.Inflammatory eye disease can develop early in the disease course and lead to permanent vision loss in 20% of the cases.Ocular involvement can be in form of posterior uveitis, anterior uveitis, or retinal vasculitis.Lung involvement is typically in form of hemoptysis, pleuritis, cough, fever, and in severe cases can be life threatening if the outlet pulmonary artery develops an aneurysm which ruptures causing severe vascular collapse and death from bleeding in the lungs.Arthralgia is seen in up to half of patients.
Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. High dose Corticosteroid therapy (1 mg/kg/d oral prednisone) is indicated for severe disease manifestationsAnti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease


Antiparkinsonian Drugs

Posted by e-Medical PPT

Parkinson’s Disease:Disease of the basal ganglia and related neuronal groups + neurotransmitter deficiencies “shaking palsy”
Bradykinesia – slowing down in the initiation and execution of movement
Rigidity – increased muscle tone
Tremor at rest
Impaired postural reflexes

Degeneration of dopamine-producing neurons in the substantia nigra of the midbrain
Disrupts the balance of:dopamine (DA) – neurotransmitter for normal functioning of the extrapyramidal motor system (control of posture, support, and voluntary motion)
Acetylcholine (Ach) in the basal ganglia
Symptoms do not occur until 80% of the neurons in the substantia nigra are lost

Stages of Parkinson’s Disease
Flexion of affected arm - tremor / leaning toward unaffected side
Slow shuffling gate
Increased difficulty walking – looks for support to prevent falls
Further progression of weakness – assistance with ambulation
Profound disability – may be confined to wheelchair

Drug Therapy
Correcting the imbalance of neurotransmitters within the CNS
Dopaminergic – enhance release or supply of dopamine (DA)
Anticholinergic – antagonize or block the effects of overactive cholinergic neurons in the striatum
Monoamine Oxidase Inhibitor - Decreases MAO (the degradative enzyme for DA)
Results: DA levels are increased
Catechol-O-Methyl Transferase (COMT) Inhibitor
Betablocker
Antihistamine


Pathophysiology of Heart Failure

Posted by e-Medical PPT

Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by as diverse an array of conditions as myocardial infarction,hypertension and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen).Over time these increases in workload will produce changes to the heart itself:
* Reduced force of contraction, due to overloading of the ventricle. In health, increased filling of the ventricle results in increased force of contraction (by the Frank–Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.
* A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling – as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen).
* Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal arrhythmias.
* Hypertrophy of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and decreased ability to relax during diastole.
* Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.



Benign joint hypermobility syndrome

Posted by e-Medical PPT

Hypermobility syndrome, benign joint hypermobility syndrome describes joints that stretch abnormally.It can affect a single joint or multiple joints throughout the body.Hypermobility may also be symptomatic of a serious medical condition, such as Ehlers-Danlos syndrome, Marfan syndrome, rheumatoid arthritis, osteogenesis imperfecta, lupus, polio, Down syndrome, morquio syndrome, cleidocranial dysostosis or myotonia congenita.Hypermobility generally results from one or more of the following:
    * Misaligned joints
    * Abnormally-shaped ends of one or more bones at a joint
    * A Type 1 collagen or other connective tissue defect (found in Ehlers-Danlos Syndrome, Marfan syndrome) resulting in weakened ligaments, muscles & tendons.
Hypermobility syndrome is generally considered to comprise hypermobility together with other symptoms, such as myalgia and arthralgia. It is relatively common among children and affects more females than males.
People with hypermobility syndrome may develop other conditions caused by their unstable joints. These conditions include:
    * Joint instability causing frequent sprains, tendinitis, or bursitis when doing activities that would not affect the normal individual
    * Early-onset osteoarthritis
    * Subluxations or dislocations, especially in the shoulder
    * Knee pain
    * Back pain, prolapsed discs or spondylolisthesis
    * Joints that make clicking noises
    * Susceptibility to whiplash
    * Temperomandibular Joint Syndrome
    * Increased nerve compression disorders (i.e. carpal tunnel syndrome)
Joint hypermobility syndrome needs to be distinguished from other disorders that share many common features, such as Marfan syndrome, Ehlers-Danlos Syndrome, and osteogenesis imperfecta. Hypermobility is diagnosed using the Beighton Criteria.


Neurofibromatosis

Posted by e-Medical PPT

What is Neurofibromatosis?
The neurofibromatoses are genetic disorders of the nervous system that primarily affect the development and growth of neural (nerve) cell tissues. These disorders cause tumors to grow on nerves and produce other abnormalities such as skin changes and bone deformities. The neurofibromatoses occur in both sexes and in all races and ethnic groups. Scientists have classified the disorders as neurofibromatosis type 1 (NF1) and neurofibromatosis type 2 (NF2). Other or variant types of the neurofibromatoses may exist, but are not yet identified.

What is NF1?
NF1 is the more common type of the neurofibromatoses, occurring in about 1 in 4,000 individuals in the United States. Although many affected persons inherit the disorder, between 30 and 50 percent of new cases arise spontaneously through mutation (change) in an individual's genes. Once this change has taken place, the mutant gene can be passed on to succeeding generations. Previously, NF1 was known as peripheral neurofibromatosis (or von Recklinghausen's neurofibromatosis) because some of the symptoms--skin spots and tumors--seemed to be limited to the outer nerves, or peripheral nervous system, of the affected person. This name is no longer technically accurate because central nervous system tumors are now known to occur in NF1

What is NF2?
This less common of the neurofibromatoses affects about 1 in 40,000 persons. NF2 is characterized by bilateral (occurring on both sides of the body) tumors on the eighth cranial nerve. It was formerly called bilateral acoustic neurofibromatosis or central neurofibromatosis because the tumors, which cause progressive hearing loss, were thought to grow primarily on the auditory nerve, a branch of the eighth cranial nerve responsible for hearing. Scientists now know that the tumors typically occur on the vestibular nerve, another branch of the eighth cranial nerve near the auditory nerve. The tumors, called vestibular schwannomas for their location and for the type of cells in them, cause pressure damage to neighboring nerves. In some cases, the damage to nearby vital structures, such as other cranial nerves and the brainstem, can be life-threatening.


Gastroesophageal reflux disease (GERD)

Posted by e-Medical PPT

Gastroesophageal reflux disease (GERD) is chronic symptoms or mucosal damage caused by stomach acid coming up from the stomach into the esophagus.A typical symptom is heartburn.GERD is usually caused by changes in the barrier between the stomach and the esophagus, including abnormal relaxation of the lower esophageal sphincter, which normally holds the top of the stomach closed; impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia. These changes may be permanent or temporary ("transient").
The most-common symptoms of GERD are:
    * Heartburn
    * Regurgitation
    * Trouble swallowing (dysphagia)
    * Pain with swallowing (odynophagia)
    * Excessive salivation (also known as water brash)
GERD sometimes causes injury of the esophagus. These injuries may include:
    * Reflux esophagitis—necrosis of esophageal epithelium causing ulcers near the junction of the stomach and esophagus.
    * Esophageal strictures—the persistent narrowing of the esophagus caused by reflux-induced inflammation.
    * Barrett's esophagus— intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus.
    * Esophageal adenocarcinoma—a rare form of cancer.
A detailed historical knowledge is vital for an accurate diagnosis. Useful investigations may include ambulatory Esophageal pH Monitoring, barium swallow X-rays, esophageal manometry, and Esophagogastroduodenoscopy (EGD).The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and it also allows to monitor GERD patients in regards of their response to medical or surgical treatment.


Acute Abdomen

Posted by e-Medical PPT

Acute and severe abdominal pain, however, is almost always a symptom of intra-abdominal disease. It may be the sole indicator of the need for surgery and must be attended to swiftly: Gangrene and perforation of the gut can occur < 6 h from onset of symptoms in certain conditions (eg, interruption of the intestinal blood supply from a strangulating obstruction or an arterial embolus). 
Visceral pain comes from the abdominal viscera, which are innervated by autonomic nerve fibers and respond mainly to the sensations of distention and muscular contraction—not to cutting, tearing, or local irritation. Visceral pain is typically vague, dull, and nauseating. It is poorly localized and tends to be referred to areas corresponding to the embryonic origin of the affected structure. Common examples of referred pain are scapular pain due to biliary colic, groin pain due to renal colic, and shoulder pain due to blood or infection irritating the diaphragm.
Peritonitis is inflammation of the peritoneal cavity. The most serious cause is perforation of the GI tract which produces immediate chemical inflammation followed shortly by infection from intestinal organisms. Peritonitis can also result from any abdominal condition that produces marked inflammation (eg, appendicitis, diverticulitis, strangulating intestinal obstruction, pancreatitis, pelvic inflammatory disease, mesenteric ischemia). Intraperitoneal blood from any source (eg, ruptured aneurysm, trauma, surgery, ectopic pregnancy) is irritating and results in peritonitis. Rarely, spontaneous bacterial peritonitis occurs, in which the peritoneal cavity is infected by blood-borne bacteria. Peritonitis causes fluid shift into the peritoneal cavity and bowel, leading to severe dehydration and electrolyte disturbances. Adult respiratory distress syndrome can develop rapidly. Kidney failure, liver failure, and disseminated intravascular coagulation follow.


Electrical Therapies( Automated Electrical Defibrillators,Defibrillation, Cardioversion, Pacing)
Immediate CPR until defibrillator available
1-Shock vs 3-shock sequence
No studies humans/animals comparing the two
Animal studies: long interruptions in CPR assoc w/ post-resuscitation myocardial dysfunction and decrease survival
RCT: interruptions in CPR assoc with decreaseprobability of conversion of VF to another rhythm
3-Shock: 37 sec delay before 1st compression
1-Shock: efficacy of conversion more than 90% (biphasic defibrillators)

Monophasic vs Biphasic Defibrillators
1st-shock efficacy of monophasic less than 1st-shock efficacy of biphasic
Goal: delivery of current through chest to the heart to depolarize myocardial cells and eliminate VF/VT
Monophasic: delivers current of one polarity
1-shock 360J
Biphasic : less than 200J as safe and with higher efficacy than higher voltage in monophasic

Automated Electrical Defibrillators(AED)
Only useful for shockable rhythms
If implantable medical device (pacemaker, AICD) placed, this should place 1 inch away
Do Not place on transdermal medication devices as it causes burns, decrease energy to heart
If Individual wet/diaphoretic make him dry
For decreasing impedance we have to Shave chest hair and apply Conductive gel
Arched placement of AED in O2-rich environment can spark fires

Synchronized Cardioversion
Shock delivery timed with QRS complex
Indicated for Rx of unstable tachyarrhythmias associated with organized QRS complex and a perfusing rhythm
Rx unstable SVT -Reentry,Atrial Fibrillation ,Atrial flutter ,Unstable monomorphic VT
NOT effective in Junctional tachycardia,Ectopic/multifocal-atrial tachycardia (automatic focus)and Shocks to automatic focus can further increase HR


Acute disseminated encephalomyelitis (ADEM) is an immune mediated disease of the brain.It usually occurs following a viral infection but may appear following vaccination, bacterial or parasitic infection, or even appear spontaneously. As it involves autoimmune demyelination, it is similar to multiple sclerosis.Although it occurs in all ages, most reported cases are in children and adolescents, with the average age around 5 to 8 years old.The mortality rate may be as high as 5%, full recovery is seen in 50 to 75% of cases, while up to 70 to 90% recover with some minor residual disability.
ADEM produces multiple inflammatory lesions in the brain and spinal cord, particularly in the white matter. Usually these are found in the subcortical and central white matter and cortical gray-white junction of both cerebral hemispheres, cerebellum, brainstem, and spinal cord,but periventricular white matter and gray matter of the cortex, thalami and basal ganglia may also be involved.
ADEM has an abrupt onset and a monophasic course. Symptoms usually begin 1–3 weeks after infection or vaccination. Major symptoms include fever, headache, drowsiness, seizures and coma. Although initially the symptoms are usually mild, they worsen rapidly over the course of hours to days, with the average time to maximum severity being about four and a half days.Additional symptoms include hemiparesis, paraparesis, and cranial nerve palsies.
The widely accepted first-line treatment is high doses of intravenous corticosteroids,such as methylprednisolone or dexamethasone, followed by 3–6 weeks of gradually lower oral doses of prednisolone.Other antiinflamatory and immunosuppressive therapies have been reported to show beneficial effect, such as plasmapheresis, high doses of intravenous immunoglobulin (IVIg) and cyclophosphamide.


Surgical Problems in Children

Posted by e-Medical PPT

* Bile-stained vomiting in neonates Malrotation - emergency referal.
* Constipation Soften with lactulose, stimulate with senna. Hirschprung's disease always has a neonatal history.
* Inguinal herniae Refer immediately for corrective surgery - high incidence of complications.
* Hydrocoeles Congenital hydrocoeles should resolve by age 1-2 years - refer if persistent.Newly-presenting hydrocoeles should be referred immediately (testicular tumours in older children).
* Painful red testis Torsion until proved otherwise - orchitis is rare in young children.
* Umbilical herniae No treatment required - resolve spontaneously by age 2. rarely may require surgical correction age 3. Periumbilical hernias do not resolve spontaneously, however.
* Undescended testes Should be discovered at birth or 6-week check. Retractile testes require NO action, so documentation of the presence of testes in the scrotum at birth is important. Refer at age 1 year.


Caesarean Section

Posted by e-Medical PPT

A Caesarean section is a surgical procedure in which one or more incisions are made through a mother's abdomen (laparotomy) and uterus (hysterotomy) to deliver one or more babies.Caesarean section is usually performed when a vaginal delivery would put the baby's or mother's life or health at risk(prolonged labor or a failure to progress,cord prolapse,placenta praevia, placental abruption,abnormal presentation,cord prolapse,fetal macrosomia ect) although in recent times it has been also performed upon request for childbirths that could otherwise have been natural.
There are several types of Caesarean section . An important distinction lies in the type of incision (longitudinal or latitudinal) made on the uterus, apart from the incision on the skin.
* The classical Caesarean section involves a midline longitudinal incision which allows a larger space to deliver the baby.
* The lower uterine segment section is the procedure most commonly used today; it involves a transverse cut just above the edge of the bladder and results in less blood loss and is easier to repair.
* An emergency Caesarean section is a Caesarean performed once labour has commenced.
* A crash Caesarean section is a Caesarean performed in an obstetric emergency, where complications of pregnancy onset suddenly during the process of labour, and swift action is required to prevent the deaths of mother, child or both.
* A Caesarean hysterectomy consists of a Caesarean section followed by the removal of the uterus. This may be done in cases of intractable bleeding or when the placenta cannot be separated from the uterus.


Lactic Acidosis

Posted by e-Medical PPT

Lactic acidosis is a physiological condition characterized by low pH in body tissues and blood  accompanied by the buildup of lactate especially D-lactate, and is considered a distinct form of metabolic acidosis.The condition typically occurs when cells receive too little oxygen (hypoxia), for example during vigorous exercise.If oxygen supply is inadequate (hypoxia), the mitochondria are unable to continue ATP synthesis at a rate sufficient to supply the cell with the required ATP. In this situation, glycolysis is increased to provide additional ATP, and the excess pyruvate produced is converted into lactate and released from the cell into the bloodstream, where it accumulates over time. While increased glycolysis helps compensate for less ATP from oxidative phosphorylation, it cannot bind the protons resulting from ATP hydrolysis. Therefore, proton concentration rises and causes acidosis.Lactic acidosis is characterized by lactate levels more than 5 mmol/L and serum pH less than 7.35.
The signs of lactic acidosis are deep and rapid breathing, vomiting, and abdominal pain—symptoms that may easily be mistaken for other problems.
Lactic acidosis may be caused by diabetic ketoacidosis or liver or kidney disease, as well as some forms of medication (notably the anti-diabetic drugs phenformin and metformin). Some anti-HIV drugs (antiretrovirals) warn doctors in their prescribing information to regularly watch for symptoms of lactic acidosis caused by mitochondrial toxicity. Heavy metal toxicity, including arsenic poisoning can raise lactate levels and lead to generalized metabolic acidosis as well.


Sepsis,Severe Sepsis and Septic Shock

Posted by e-Medical PPT

Sepsis is a potentially serious medical condition that is characterized by systemic inflammatory response syndrome or SIRS and the presence of a known or suspected infection.The body may develop this inflammatory response by the immune system to microbes in the body.Severe sepsis is the systemic inflammatory response, plus infection, plus the presence of organ dysfunction.Septicemiais a related medical term referring to the presence of pathogenic organisms in the bloodstream, leading to sepsis.
Severe sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor medications can be used. Mechanical ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed; measurement of other hemodynamic variables may also be used. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low-dose corticosteroids or activated drotrecogin alfa (recombinant protein C).


Pericardial Disease

Posted by e-Medical PPT

Pericarditis is an inflammation of the pericardium.Depending on the time of presentation and duration, it  is divided into "acute" and "chronic" forms. Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or even as a result of a myocardial infarction.Chronic type however is less common, a form of which is constrictive pericarditis.
It may be caused by viral, bacterial, or fungal infection.The most common worldwide cause  is infectious pericarditis with Tuberculosis.Other causes are systemic lupus erythematosus (more common among women) or rheumatic fever,Myocardial Infarction (Dressler's syndrome),Trauma to the heart, e.g. puncture, resulting in infection or inflammation,Uremia ect
Substernal or left precordial pleuritic Chest pain with radiation to the bottom portion of scapula on the back, which is relieved by sitting up and bending forward and worsened by lying down or inspiration,is the characteristic pain of pericarditis.Other symptoms  may include dry cough, fever, fatigue, and anxiety.
Pericarditis can progress to pericardial effusion and eventually cardiac tamponade. This can be seen in patients who present experiecing the classic signs of pericarditis but who will then obtundate, and progress to show signs of tamponade which include decresaed alertness and lethargy, pulsus paradoxus (decrease of at least 10 mmHg of the systolic blood pressure upon inspiration), hypotension (due to decreased cardiac index), elevated JVP, distant heart sounds on auscultation, and equilibration of all the diastolic blood pressures on cardiac catheretization due to the constriction of the pericardium by the fluid.


Lymph nodes are populated predominantly by macrophages, dendritic cells,B lymphocytes, and T lymphocytes. B lymphocytes are located primarily in the follicles and perifollicular areas, T lymphocytes are found primarily in the interfollicular or paracortical areas of the lymph node.In young children palpable lymphadenopathy is the rule who are continuously undergoing exposure to new antigens, In fact, the absence of palpable lymphadenopathy would be considered abnormal. In adults, lymph nodes larger than 1 to 2 cm in diameter are generally considered abnormal.

Generalized immune proliferation and lymphadenopathy can occur with a systemic disorder of the immune system,disseminated infection,or disseminated neoplasia. Malignancies of the immune system might be manifested as:localized or disseminated lymphadenopathy.

CAUSES OF LYMPHADENOPATHY
Infection
Bacterial (e.g., all pyogenic bacteria, cat-scratch disease, syphilis,tularemia)
Mycobacterial (e.g., tuberculosis, leprosy)
Fungal (e.g., histoplasmosis, coccidioidomycosis)
Chlamydial (e.g., lymphogranuloma venereum)
Parasitic (e.g., toxoplasmosis, trypanosomiasis, filariasis)
Viral (e.g., Epstein-Barr virus, cytomegalovirus, rubella, hepatitis, HIV)
Benign disorders of the immune system (e.g., rheumatoid arthritis, systemic lupus erythematosus, serum sickness)
Drug reactions such as to phenytoin,
Castleman's disease, sinus histiocytosis with massive lymphadenopathy, Langerhans'cell histiocytosis,
Kawasaki syndrome, Kimura's disease 
Malignant disorders of the immune system (e.g., chronic and acute myeloid and
lymphoid leukemia, non-Hodgkin's lymphoma, Hodgkin's disease, angioimmunoblastic-like
T-cell lymphoma, Waldenström's macroglobulinemia, multiple myeloma with amyloidosis, malignant histiocytosis)
Other malignancies (e.g., breast carcinoma, lung carcinoma, melanoma, head and
neck cancer, gastrointestinal malignancies, germ cell tumors, Kaposi's sarcoma)
Storage diseases (e.g., Gaucher's disease, Niemann-Pick disease)
Endocrinopathies (e.g., hyperthyroidism, adrenal insufficiency, thyroiditis)
Miscellaneous (e.g., sarcoidosis, amyloidosis, dermatopathic lymphadenitis)


Wegener's Granulomatosis

Posted by e-Medical PPT

Wegener's granulomatosis is a form of vasculitis  that affects the lungs, kidneys and other organs. Due to its end-organ damage, it is life-threatening and requires long-term immunosuppression.Wegener's granulomatosis is part of a larger group of vasculitic syndromes, all of which feature an autoimmune attack by an abnormal type of circulating antibody termed ANCAs (antineutrophil cytoplasmic antibodies) against small and medium-size blood vessels. Apart from Wegener's, this category includes Churg-Strauss syndrome and microscopic polyangiitis.

Initial signs are extremely variable, and diagnosis can be severely delayed due to the nonspecific nature of the symptoms. Rhinitis is generally the first sign in most patients.
Kidney: rapidly progressive glomerulonephritis (75%), leading to chronic renal failure
Nose: pain, stuffiness, nosebleeds, rhinitis, crusting, saddle-nose deformity due to a perforated septum
Oral cavity: strawberry gingivitis, underlying bone destruction with loosening of teeth, non-specific ulcerations throughout oral mucosa
Eyes: pseudotumours, scleritis, conjunctivitis, uveitis, episcleritis
Lungs: pulmonary nodules (referred to as "coin lesions"), infiltrates (often interpreted as pneumonia), cavitary lesions, pulmonary hemorrhage causing hemoptysis, and rarely bronchial stenosis.

Wegener's granulomatosis is usually suspected only when a patient has had unexplained symptoms for a long period of time. Determination of ANCAs can aid in the diagnosis, but positivity is not conclusive and negative ANCAs are not sufficient to reject the diagnosis. Cytoplasmic staining ANCAs that react with the enzyme proteinase 3 (cANCA) in neutrophils are associated with Wegener's.


Bell's palsy or idiopathic facial paralysis is a dysfunction of cranial nerve VII that results in inability to control facial muscles on the affected side. Several conditions can cause a facial paralysis, e.g., brain tumor, stroke, and Lyme disease. However, if no specific cause can be identified, the condition is known as Bell's palsy. Bell's palsy is the most common cause of acute facial nerve paralysis.
Bell's palsy is characterized by facial drooping on the affected half, due to malfunction of the facial nerve (VII cranial nerve), which controls the muscles of the face. Facial palsy is typified by inability to control movement in the facial muscles. The paralysis is of the infranuclear/lower motor neuron type.
Bell's palsy is defined as an idiopathic unilateral facial nerve paralysis, usually self-limiting. The trademark is rapid onset of partial or complete palsy, usually in a single day. It can occur bilaterally resulting in total facial paralysis in around 1% of cases.
It is thought that an inflammatory condition leads to swelling of the facial nerve. The nerve travels through the skull in a narrow bone canal beneath the ear. Nerve swelling and compression in the narrow bone canal are thought to lead to nerve inhibition, damage or death. No readily identifiable cause for Bell's palsy has been found.
Corticosteroids have been found to improve outcomes while anti-viral drugs have not.Early treatment is necessary for steroids to be effective. Most people recover spontaneously and achieve near-normal to normal functions. Many show signs of improvement as early as 10 days after the onset, even without treatment.


The mechanism of ethanol intoxication and withdrawal is complex. Most of the clinical effects can be explained by the interaction of ethanol with various neurotransmitters and neuroreceptors in the brain, including those interacting with gamma-aminobutyric acid (GABA), glutamate (NMDA), and opiates.Resulting changes in the inhibitory and excitatory neurotransmitters disrupt the neurochemical balance in the brain, causing symptoms of withdrawal.
In opioid or benzodiazepine addiction, chronic stimulation of specific receptors for these drugs suppresses endogenous production of neurotransmitters (endorphins or GABA, respectively). Removal of exogenous drug allows unopposed counter-regulatory effects to become clinically apparent. When the exogenous drug is precipitously removed, inadequate production of endogenous transmitters and the unopposed stimulation by counter-regulatory transmitters results in the characteristic clinical picture of withdrawal.
Alcohol withdrawal
Withdrawal symptoms appear within 6-12 hours after individuals cease or decrease alcohol intake and are usually relieved by consuming additional alcohol.
The hallmark of alcohol withdrawal is a continuum of signs and symptoms ranging from simple tremulousness to DT.

    * Mild withdrawal usually occurs within 24 hours of the last drink and is characterized by tremulousness (shakes), insomnia, anxiety, hyperreflexia, diaphoresis, mild autonomic hyperactivity, and GI upset.
    * Moderate withdrawal usually occurs 24-36 hours after the cessation of alcohol intake and includes intense anxiety, tremors, insomnia, and excessive adrenergic symptoms.
    * Severe withdrawal usually occurs more than 48 hours after a cessation or decrease in alcohol consumption. It is characterized by profound alteration of sensorium including disorientation, agitation, and hallucinations; along with severe autonomic hyperactivity including tremulousness, tachycardia, tachypnea, hyperthermia, and diaphoresis.
Opioid withdrawal
In general, opioid withdrawal does not directly cause life-threatening symptoms, seizures, or delirium.
Opioid withdrawal syndrome may resemble a severe flu-like illness. The syndrome is characterized by rhinorrhea, sneezing, yawning, lacrimation, abdominal cramping, leg cramping, piloerection, nausea, vomiting, diarrhea, and dilated pupils.


Secretory Diarrhea- Large volumes of water are normally secreted into the small intestinal lumen, but a large majority of this water is efficienty absorbed before reaching the large intestine. Diarrhea occurs when secretion of water into the intestinal lumen exceeds absorption.
Microvillus atrophy is the leading cause of secretory diarrhea in the first weeks of life.
The typical clinical presentation is watery profuse secretory diarrhea starting in the first hours of life. The peak age of onset is the early neonatal period. Although later-onset cases have been described, cases have never been described beyond the first 2-3 months of life.Three variants of the disease have been identified: congenital microvillus atrophy, late-onset microvillus atrophy, and atypical microvillus atrophy.In congenital microvillus atrophy, diarrhea starts in the first few days of life and is immediately life threatening. Oral alimentation in nutritionally significant amounts is impossible. In late-onset microvillus atrophy, diarrhea starts later in life, usually in the second month. Diarrhea tends to be less severe than in the other form, and some alimentation is possible. A few cases have been termed atypical microvillus atrophy, in which the onset can be congenital or late, but the histologic picture is different.
Microvillous inclusion disease, also known as Davidson's disease, congenital microvillous atrophy and, less specifically, microvillous atrophy, is a rare genetic disorder of the small intestine that is inherited in an autosomal recessive pattern.It is characterized by chronic, intractable diarrhea in new-born infants, starting in the first few days of life.This results in metabolic acidosis and severe dehydration.It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant. The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients.It is caused by a congenital lack of apical microvilli in the epithelial cells of the small intestine.


ContraindicatIons and Cautions for Fibrinolytic Used in Myocardial Infarction
Absolute Contraindications:
Previous hemorrhagic stroke at any time: other strokes or cerebrovascular events within one year
Known intracranial neoplasm
Active internal bleeding (does not include menses)
Suspect aortic dissection

Cautions / Relative Contraindications
Severe uncontrolled HTN on presentation (BP more than 180/110 mmHg)
History of prior CVA or known intra-cerebral pathology not covered in contraindications
Current use of anticoagulants in therapeutic doses (INR more than 2-3); no bleeding diathesis
Recent trauma (within 2-4 weeks) including head trauma
Noncompressible vascular punctures
Recent (within 2-4 weeks) internal bleeding
For streptokinase/anistreplase: prior exposure (especially within 5d-2 yrs) or prior allergic reaction
Pregnancy
Active peptic ulcer
History of chronic hypertension

Primary Percutaneous Transluminal Coronary Angioplasty Recommendations
Class I Recommendations
1. As an alternative to fibrinolytic therapy if:
ST segment elevation or new or presumed new LBBB
Within 12 hrs of symptoms or more than 12 hrs of persistent pain
In a timely fashion
By experienced operators
In appropriate environment
2. In cardiogenic shock patients less than 75 yrs or within 36 hrs of AMI and revascularization can be performed within 18 hrs of onset of shock
Class IIa Recommendations
1. As reperfusion strategy in candidates for reperfusion who have contraindications to fibrinolytic therapy
Class IIb Recommendations
1. In patients with AMI who do not present with ST elevation but who have reduced (< TIMI grade 2) flow of the infarct-related artery and when angioplasty can be performed within 12 hrs of onset of symptoms
Class III Recommendations
1. This classification applies to patients with AMI who:
undergo elective angioplasty in the non-infarct-related artery at the time of AMI
are beyound 12 hrs after the onset of symptoms and have no evidence of myocardial ischemia
have received fibrinolytic therapy and have no symptoms of myocardial ischemia
are fibrinolytic-eligible and are undergoing primary angioplasty by and unskilled operator in a laboratory that does not have surgical capability.


Acute Glomerulonephritis

Posted by e-Medical PPT

Acute nephritic syndrome is the most serious and potentially devastating form of various renal syndromes. Acute glomerulonephritis is characterized by the abrupt onset of hematuria and proteinuria, often accompanied by azotemia (ie, decreased glomerular filtration rate and renal salt and water retention.

Causes of Acute Glomerulonephritis (AGN)

In diffuse glomerulonephritis (GN), all of the glomeruli are aggressively attacked, leading to acute renal failure (ARF). Disorders that attack several organs and cause diffuse GN are referred to as secondary causes. Secondary causes of diffuse GN include the following:
    * Cryoglobulinemia
    * Goodpasteur’s syndrome (membranous antiglomerular basement membrane disease)
    * Lupus nephritis
    * Schönlein-Henoch purpura
    * Vasculitis (e.g., Wegener's granulomatosis, periarteritis nodosa)
Primary diseases that solely affect the kidneys and cause AGN, include the following:
    * Immunoglobulin A nephropathy (IgA nephropathy, Berger’s disease)
    * Membranoproliferative nephritis (type of kidney inflammation)
    * Postinfectious GN (GN that results after an infection)
Patients with acute glomerulonephritis (AGN) have an active urinary sediment. This means that signs of active kidney inflammation can be detected when the urine is examined under the microscope.
The goal of treatment is to stop the ongoing inflammation and lessen the degree of scarring that ensues. Depending on the diagnosis, there are different treatment strategies. Often the treatment warrants a regimen of immunosuppressive drugs to limit the immune system’s activity. This decreases the degree of inflammation and subsequent irreversible scarring.


Henoch–Schönlein purpura

Posted by e-Medical PPT

Henoch–Schönlein purpura is a disease of the skin and other organs that most commonly affects children.In the skin, the disease causes palpable purpura;often there are joint pains and abdominal pain. When there is kidney involvement there may be loss of small amounts of blood and protein in the urine,the kidney involvement proceeds to chronic kidney disease.HSP is often preceded by an infection, such as pharyngitis.
HSP a systemic vasculitis and is characterized by deposition of immune complexes containing the antibody IgA; the exact cause for this phenomenon is presently unknown.
Purpura, arthritis and abdominal pain are known as the classic triad of Henoch–Schönlein purpura.The purpura typically appear on the legs and buttocks, but may also be seen on the arms, face and trunk. The abdominal pain is colicky in character, and may be accompanied by nausea, vomiting, constipation or diarrhea. There may be blood or mucus in the stools.The joints involved tend to be the ankles, knees, and elbows but arthritis in the hands and feet is possible; the arthritis is non-erosive and hence causes no permanent deformity.Forty percent have evidence of kidney involvement, mainly in the form of hematuria , but only a quarter will have this in sufficient quantities to be noticeable without laboratory tests.
The diagnosis is based on the combination of the symptoms, as very few other diseases cause the same symptoms together. Blood tests may show elevated creatinine and urea levels (in kidney involvement), raised IgA levels (in about 50%[7]), and raised C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) results; none are specific for Henoch–Schönlein purpura.
Overall prognosis is good in most patients.In adults, kidney involvement progresses to end-stage renal disease (ESRD) more often.


Endocrine Emergencies

Posted by e-Medical PPT

Hypoglycemia is the medical term for a state produced by a lower than normal level of blood glucose.It can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose to the brain, resulting in impairment of function (neuroglycopenia). Effects can range from vaguely "feeling bad" to seizures, unconsciousness, and (rarely) permanent brain damage or death.
The most common forms of hypoglycemia occur as a complication of treatment of diabetes mellitus with insulin or oral medications. Hypoglycemia is less common in non-diabetic persons, but can occur at any age, from many causes.
Hypercalcaemia is an elevated calcium level in the blood.(Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L).It can be due to abnormal parathyroid gland function(primary hyperparathyroidism), disorders related to high bone-turnover rates(Paget's disease of the bone,multiple myeloma),vitamin-D metabolic disorders(hypervitaminosis D),Increased intestinal calcium absorption, or decreased renal calcium excretion.
Malignant or critical thyrotoxicosis, thyroid storm, is a life-threatening medical emergency in which excessive concentrations of thyroid hormone produce organ dysfunction.Symptoms include thermoregulatory dysfunction (high fever, diaphoresis), neurologic manifestations (seizure, coma, psychosis,hyperreflexia), cardiovascular dysregulation (atrial fibrillation, tachycardia, hypertension, congestive heart failure), respiratory distress and gastrointestinal dysfunction (diarrhea).
Acute adrenal crisis is a life-threatening condition that occurs when there is not enough cortisol, a hormone produced by the adrenal glands.In adrenal crisis, patients need an immediate injection of hydrocortisone through a vein (intravenous) or muscle (intramuscular). You may receive intravenous fluids if you have low blood pressure.You will need to go to the hospital for treatment and monitoring. If infection caused the crisis, you may need antibiotic therapy.


Addison’s disease (also chronic adrenal insufficiency) is a rare, chronic endocrine disorder wherein the adrenal glands produce insufficient steroid hormones (glucocorticoids and often mineralocorticoids).
The symptoms of Addison's disease develop insidiously, and it may take some time to be recognized. The most common symptoms are fatigue, lightheadedness upon standing or while upright, muscle weakness, fever, weight loss, difficulty in standing up, anxiety, nausea, vomiting, diarrhea, headache, sweating, changes in mood and personality, joint and muscle pains. Some have marked cravings for salt or salty foods due to the urinary losses of sodium.Affected individuals may note increased tanning since adrenal insufficiency is manifested in the skin primarily by hyperpigmentation.
In suspected cases of Addison's disease, one needs to demonstrate that adrenal hormone levels are low even after appropriate stimulation (called the ACTH stimulation test) with synthetic pituitary ACTH hormone tetracosactide .he short test compares blood cortisol levels before and after 250 micrograms of tetracosactide (IM/IV) is given. If, one hour later, plasma cortisol exceeds 170 nmol/L and has risen by at least 330 nmol/L to at least 690 nmol/L, adrenal failure is excluded.
Treatment for Addison's disease involves replacing the missing cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol.


Pharmacology of Antipsychotics

Posted by e-Medical PPT

Dopamine Hypothesis
Drugs that increase dopamine will enhance or produce positive psychotic symptoms
E.G. Cocaine, amphetamine
All known antipsychotics drugs capable of treating positive psychotic symptoms block the dopamine receptors

Dopamine Pathways
Mesolimbic
Projects from brainstem to limbic areas.
Overactivity produces delusions and hallucinations.

Nigrostriatal
Projects from the substania nigra to the basal ganglia
A part of the extrapyramidal system
Thus side effects are called “extrapyramidal”
Controls movements
Types of movement disorders caused by this pathway include:
Akathisia,Dystonia,Tremor, rigidity, bradykinesia
Drug-induced Parkinsonism

Mesocortical
May be associated with both positive and negative symptoms
Blockade may help reduce negative symptoms of schizophrenia
May be involved in the cognitive side effects of antipsychotics “mind dulling”

Tuberoinfundibular - Blockade produces galactorrhea


Localized fibrous tumor of the pleura

Posted by e-Medical PPT

From visceral pleura.
On a stalk, project into pleural space.
May inward growth into lung parenchyma.
Occasionally within fissure.
May from mediastinal, diaphragm, costal portion of parietal pleura— Often malignant.
Solitary, ovoid round.
Histology— Fibroblastlike cell and connective tissue.
Lack keratin reactivity and positive CD34 antigen– Differentiates fibrous tumor from mesothelioma.
Equal frequency in both sex.
Common in 5th to 8th decades.

Clinical Features
Half asymptomatic,
Chronic cough,Chest pain – Most lesion arise from parietal pleura, Dyspnea
Hypertrophic pulmonary osteoarthropathy (20%)– Stiffness of the joint, edema of ankle, arthralgia, pain of long bone (especially the tibia).
Gynecomastia.
Clubbing finger.
Hypoglycemia (3-4%)– Tumor production insulin like growth factors or somatomedins.
Galactorrhea.


Irritable Bowel Syndrome

Posted by e-Medical PPT

What is Irritable Bowel Syndrome(IBS)?
A group of functional bowel disorders
Chronic abdominal complaints without a structural or biochemical cause
Constitutes a major health problem with gastrointestinal (GI) symptoms
The cause of IBS is unknown.
Affects up to ~20 % adults in the industrialized world
The condition is more frequent in women.
The direct medical costs of IBS are ~ $ US 8 billion in the US each year.

Symptoms of IBS
Abdominal discomfort and pain
Bloating, mucous in stools, diarrhea, constipation, or alternating diarrhea and constipation
Depression, anxiety or stress
IBS can be subdivided into
Diarrhea-predominant (IBS-D)
Constipation-predominant (IBS-C)
Alternating diarrhea and constipation

Subclassification of patients
Supportive symptoms of IBS
  1. Fewer than 3 bowel movements a week
  2. More than 3 bowel movements a day
  3. Hard or lumpy stools
  4. Loose or watery stools
  5. Urgency
  6. Feeling of incomplete bowel movement
  7. Passing mucus during a bowel movement
  8. Abdominal fullness, bloating or swelling
Diarrhea-predominant IBS (IBS-D) - One or more of 2, 4 or 6 and none of 1, 3 or 5
Constipation-predominant IBS (IBS-C) - One or more of 1, 3 or 5 and none of 2, 4 or 6


NaHCO3 administration during CPR
Should not be used until other proven interventions (ET tube, defibrillation, cardiac compression, adrenaline)
Estimated that this interventions required at least 10 min.

Guideline for NaHCO3 administration during CPR
Known preexisting metabolic acidosis with or without hyperkalemia
Known hypercalcemia
Doasage
1 mEQ/kg then no more than half for subsequent dose
No more frequently than every 10 min
Postresuscitation phase, guideed by arterial blood gas

Alternate buffer agents during CPR
THAM (tromethamine), potent amine buffer
DCA (Dichloroacetate), stimulating pyruvate dehydrogenase (oxidative enzyme in step of lactate to pyruvate)
However, no alternate buffer agents improve survival during CPR


Pediatric Surgery

Posted by e-Medical PPT

Congenital Abnormality
Defects in the abdominal wall (diaphragmatic hernia, gastroschisis, omphalocele)
Neurological system(brain, spinal cord, etc.)
Cardiovascular and pulmonary abnormality
Malformation of digestive system
Malformation of urological and reproductive system
Limbs and vertebra abnormality

Congenital Posterolateral Diaphragmatic Hernia (CDH)
One of most severe conditions of neonate
Defect in diaphragm during early fetal development
Left side most commonly affected

Pathophysiology
1、Hypoplasia of the lung
Pulmonary weight (ipsilateral+contralateral)↓
Alveoli number↓
Hypertrophy of the media of pulmonary arteriole
Resistance of the vessels↑

2、Pulmonary hypertension
Abdominal viscera into the thoracic cavity → compression of the lung, PaO2↓PaCO2↑→ acidosis, hypoxemia(PH less than 7.30)→pulmonary vessels spasm →vessel resistance↑, right to left shunting through patent ductus arteries and foramen ovale↑→aggravate acidosis and hypoxemia in the body circulation (fetal circulation syndrome)

Diaphragmatic hernia clinical manifestations:
1,Severe respiratory distress,cyanosis, vomit
2,Breath sounds: diminished on the side of hernia
3,Heart sounds: deviated to the contralateral
chest
4,Scaphoid abdomen

Share Medical Presentations