Tuesday, October 11, 2011

EOQ MODEL

The Economic Order Quantity (EOQ) is the number of units that a company should add to inventory with each order to minimize the total costs of inventory—such as holding costs, order costs, and shortage costs. The EOQ is used as part of a continuous review inventory system, in which the level of inventory is monitored at all times, and a fixed quantity is ordered each time the inventory level reaches a specific reorder point. The EOQ provides a model for calculating the appropriate reorder point and the optimal reorder quantity to ensure the instantaneous replenishment of inventory with no shortages. It can be a valuable tool for small business owners who need to make decisions about how much inventory to keep on hand, how many items to order each time, and how often to reorder to incur the lowest possible costs.
The EOQ model assumes that demand is constant, and that inventory is depleted at a fixed rate until it reaches zero. At that point, a specific number of items arrive to return the inventory to its beginning level. Since the model assumes instantaneous replenishment, there are no inventory shortages or associated costs. Therefore, the cost of inventory under the EOQ model involves a tradeoff between inventory holding costs (the cost of storage, as well as the cost of tying up capital in inventory rather than investing it or using it for other purposes) and order costs (any fees associated with placing orders, such as delivery charges). Ordering a large amount at one time will increase a small business's holding costs, while making more frequent orders of fewer items will reduce holding costs but increase order costs. The EOQ model finds the quantity that minimizes the sum of these costs.
The basic EOQ formula is as follows:
TC = PD + HQ/2 + SD/Q
where TC is the total inventory cost per year, PD is the inventory purchase cost per year (price P multiplied by demand D in units per year), H is the holding cost, Q is the order quantity, and S is the order cost (in dollars per order). Breaking down the elements of the formula further, the yearly holding cost of inventory is H multiplied by the average number of units in inventory. Since the model assumes that inventory is depleted at a constant rate, the average number of units is equal to Q/2. The total order cost per year is S multiplied by the number of orders per year, which is equal to the annual demand divided by the number of orders, or D/Q. Finally, PD is constant, regardless of the order quantity.
Taking these factors into consideration, solving for the optimal order quantity gives a formula of:
HQ/2 = SD/Q, or Q = the square root of 2DS/H.
The latter formula can be used to find the EOQ. For example, say that a painter uses 10 gallons of paint per day at $5 per gallon, and works 350 days per year. Under this scenario, the painter's annual paint consumption (or demand) is 3,500 gallons. Also assume that the painter incurs holding costs of $3 per gallon per year, and order costs of $15 per order. In this case, the painter's optimal order quantity can be found as follows: EOQ the square root of (2 3,500 15) /3 187 gallons. The number of orders is equal to D/Q, or 3,500 / 187. Thus the painter should order 187 gallons about 19 times per year, or every three weeks or so, in order to minimize his inventory costs.
The EOQ will sometimes change as a result of quantity discounts, which are provided by some suppliers as an incentive for customers to place larger orders. For example, a certain supplier may charge $20 per unit on orders of less than 100 units and only $18 per unit on orders over 100 units. To determine whether it makes sense to take advantage of a quantity discount when reordering inventory, a small business owner must compute the EOQ using the formula (Q the square root of 2DS/H), compute the total cost of inventory for the EOQ and for all price break points above it, and then select the order quantity that provides the minimum total cost.
For example, say that the painter can order 200 gallons or more for $4.75 per gallon, with all other factors in the computation remaining the same. He must compare the total costs of taking this approach to the total costs under the EOQ. Using the total cost formula outlined above, the painter would find TC PD HQ/2 SD/Q (5 3,500) (3 187)/2 + (15 3,500)/187 $18,062 for the EOQ. Ordering the higher quantity and receiving the price discount would yield a total cost of (4.75 3,500) (3 200)/2 (15 3,500)/200 $17,187. In other words, the painter can save $875 per year by taking advantage of the price break and making 17.5 orders per year of 200 units each.
Further Reading:
Krupp, James A. "Measuring Inventory Management Performance." Production and Inventory Management Journal. Fall 1994.
Piasecki, Dave. "Optimizing Economic Order Quantity." IIE Solutions. January 2001.
Weiss, Howard J., and Mark E. Gershon. Production and Operations Management. Boston: Allyn and Bacon, 1989.
Read more: http://www.answers.com/topic/economic-order-quantity#ixzz1Zk0T7Nh7
An inventory-related equation that determines the optimum order quantity that a company should hold in its inventory given a set cost of production, demand rate and other variables. This is done to minimize variable inventory costs. The full equation is as follows:  



where : 
S = Setup costs
D = Demand rate
P = Production cost
I = Interest rate (considered an opportunity cost, so the risk-free rate can be used) 
Investopedia Says:
The EOQ formula can be modified to determine production levels or order interval lengths, and is used by large corporations around the world, especially those with large supply chains and high variable costs per unit of production. 

Despite the equation's relative simplicity by today's standards, it is still a core algorithm in the software packages that are sold to the largest companies in the world.

INVENTORY

Mana 720                                      Septiembre 15, 2011
Tema: Inventario. Tipos y clasificaciones de inventario.

Reseña histórica de: Inventario.

Desde tiempos inmemorables, los egipcios y demás pueblos de la antigüedad, acostumbraban almacenar grandes cantidades de alimentos para ser utilizados en los tiempos de sequía o de calamidades. Es así como surge o nace el problema de los inventarios, como una forma de hacer frente a los periodos de escasez, que le asegurarán la subsistencia de la vida y el desarrollo  de sus actividades normales. Esta forma de almacenamiento de todos los bienes y alimentos necesarios para sobrevivir motivó la existencia de los inventarios.

Como es de saber; la base de toda empresa comercial es la compra y ventas de bienes y servicios;   de aquí viene la importancia del manejo de inventario por parte de la misma. Este manejo contable permitirá a la empresa mantener el control oportunamente, así como también conocer al final del periodo contable un estado confiable de la situación económica de la misma.

El inventario tiene como propósito fundamental proveer a la empresa de materiales necesarios, para su continuo y regular desenvolvimiento, es decir, el inventario tiene un papel vital para el funcionamiento acorde y coherente dentro del proceso de producción y de esta forma afrontar la demanda.

Inventario, Tipos y clasificaciones de Inventario

Inventario: Es una Técnica o procedimiento que nos permite llevar un control de las existencias a través de un conteo, con la finalidad de maximizar las operaciones de la empresa y minimizar los costos.
El inventario es el conjunto de mercancías o artículos que tiene la empresa para comerciar con aquellos, son bienes tangibles que se tienen para la venta en el curso ordinario del negocio o para ser consumidos en la producción de bienes o servicios para su posterior comercialización. Los inventarios comprenden, además de las materias primas, productos en proceso y productos terminados o mercancías para la venta, los materiales, repuestos y accesorios para ser consumidos en la producción de bienes fabricados para la venta o en la prestación de servicios; empaques y envases y los inventarios en tránsito.
Materia Prima: Materia extraída de la naturaleza que se transforma para elaborar materiales que mas tarde se convertirán en bienes de consumo (
Comprende los elementos básicos o principales que entran en la elaboración del producto. En toda actividad industrial concurren una variedad de artículos (materia prima) y materiales, los que serán sometidos a un proceso para obtener al final un articulo terminado o acabado. A los materiales que intervienen en mayor grado en la producción se les considera "Materia Prima", ya que su uso se hace en cantidades los suficientemente importantes del producto acabado.
La materia prima, es aquel o aquellos artículos sometidos a un proceso de fabricación que al final se convertirá en un producto terminado.
Productos en proceso: por sus siglas en ingles“WIP” (work in process).

Constituye un inventario inevitable en todo proceso de manufactura
El inventario de productos en proceso consiste en todos los artículos o elementos que se utilizan en el actual proceso de producción. Es decir, son productos parcialmente terminados que se encuentran en un grado intermedio de producción y a los cuales se les aplico la labor directa y gastos indirectos inherentes al proceso de producción en un momento dado. Al momento de llevar a cabo el recuento del inventario, parte de él estará en las máquinas otra parte estará en la fase de traslado de una máquina a otra, o en tránsito del almacén de materias primas a la línea de producción o de ésta, al almacén de artículos terminados.
Una de las características del inventarios de producto en proceso es que va aumentando el valor a medida que se es transformado de materia prima en le producto terminado como consecuencia del proceso de producción.
Si vamos a tener producción es inevitable tener inventarios en proceso.
Productos Terminados
Artículos transferidos por el departamento de producción al almacén de productos terminados por haber alcanzado su grado de terminación total y que a la hora de la toma física de inventarios se encuentren aun en los almacenes, es decir, los que todavía no han sido vendidos. El nivel de inventarios de productos terminados va a depender directamente de las ventas, es decir su nivel esta dado por la demanda

Mantenimiento, reparación y operaciones de inventario
Materiales, repuestos y accesorios para ser consumidos en la producción de bienes fabricados para la venta o en la prestación de servicios.
Inventario en Exceso y Obsoleto: (llamado Inventario ESO)
Contribuyen con costos adicionales para la empresa y además deteriora indicadores al bajar el índice de rotación de Inventario, reducir la capacidad de almacenaje y disminuir la capacidad de movilidad logística; no solo incluye el costo del inventario sino costos ocultos como el manejo del mismo, seguros, mantenimiento, espacio en almacenes y costo de administración logística y movilidad.
Conclusiones:
Los inventarios son un puente de unión entre la producción y las ventas.  Con él la empresa puede realizar sus tareas de producción y de compra economizando recursos, y también atender a sus clientes con más rapidez, optimizando todas las actividades de la empresa. Sin embargo, se presenta una desventaja: el costo de mantenimiento; ya que se debe considerar el costo de capital, el costo de almacenaje, el costo de oportunidad causando por inexistencia, y otros.
Por tanto, resulta de vital importancia el control de inventarios, dado que su descontrol representa mermas y desperdicios, pudiendo causar un fuerte impacto sobre las utilidades, por otro lado ayuda a la independencia de las operaciones, permite determinar condiciones económicas de aprovisionamiento, pudiendo alcanzarse una optima secuencia en el desarrollo y crecimiento de toda empresa.




Bibliografía:
Buffa, Elwood S, Dirección Técnica y Administración de la Producción, México, Editorial Limusa.
 Johnson, Robert w. Administración financiera, 1969
Starr, Martin K, foundation of production and operations management, 2007.



Just-in-time (JIT):

Conocido como la filosofía de gestión que se ha estado aplicando en la producción japonesa desde 1970-1980, dirigido por Taiichi Ohno, al cual se le considera el padre del JIT, aunque según el Ing. Industrial  Iván Escalona en su trabajo sobre gestión de calidad “Introducción al Just-in-Time”, publicado en Mayo-2004 este modelo comenzó a utilizar a principios de los años 50 con el propósito principal de eliminar todos los elementos innecesarios en el área de producción, que incluye desde el departamento de compras de materias primas, hasta el de servicio al cliente, pasando por recursos humanos y finanzas, etc. Siendo  utilizado para alcanzar reducciones de costos nunca imaginados cumpliendo con las necesidades de los clientes a los costos más bajos posibles.

Toyota fue capaz de responder a los desafíos cada vez mayores para la supervivencia a través de un enfoque centrado en las personas, instalaciones y sistemas. Toyota se dio cuenta de que JIT solo tendría éxito si cada individuo dentro de la organización se involucrara y estuviera comprometido con ella, si la planta y los procesos se organizaran con un máximo de rendimiento y eficacia, y si los programas de calidad y la producción se programaran para satisfacer las demandas con exactitud.

Requema Rodrigues y Vera Rios en su libro Contabilidad Interna nos plantean que para la puesta en marcha del proceso Just in Time se requiere que los proveedores suministren los materiales en el momento de su incorporación al proceso productivo. Para que ello sea posible, un mecanismo habitualmente empleado es el establecimiento de contratos a largo plazo con unos pocos proveedores capaces de suministrar los materiales con el nivel de calidad estipulado, en las cantidades y en el momento en el que son requeridos por la producción. El aumento en la frecuencia de las entregas, como consecuencia de la reducción del tamaño de los aprovisionamientos, no tiene por qué suponer un aumento de las actividades de recepción y control de calidad de los pedidos, pues en los acuerdos con los proveedores existen mecanismos que simplifican la ejecución.

JIT tiene la capacidad de fabricación, debidamente adaptada, para fortalecer la competitividad de la organización en el mercado sustancialmente por la reducción de residuos, la mejora de la calidad del producto y la eficacia de la producción.

Reduce los niveles de inventarios necesarios en todos los pasos de la línea productiva y, como consecuencia, los costos de mantener inventarios más altos, costos de compras, de financiación de las compras y de almacenaje.
Minimiza pérdidas por causa de suministros obsoletos. Permite el desarrollo de una relación más cercana con los suministradores. Esta mejor relación facilita acordar compras aseguradas a lo largo del año, que permitirán a los suministradores planearse
mejor y ofrecer mejores precios. El sistema es más flexible y permite cambios más rápidos.
Una definición del objetivo del Just-in-Time, encontrada en Foundation of P/OM de Martin K sería producir los elementos que se necesitan, en las cantidades que se necesitan, en el momento en que se necesitan.
El JIT persigue optimizar permanentemente los niveles de inventario, los tiempos de adaptación, los niveles de calidad, etc. Por lo que se puede decir que la producción ajustada es un sistema que se encuentra en una situación de permanente evolución, de mejora continua.
El sistema JIT implica un cambio cultural en la empresa, una filosofía sobre el manejo integral de la organización mediante valores y creencias que deben compartir sus integrantes.







Referencias:
Martin K, Starr. Foundation of P/OM. 2007. Capitulo 17.
 Cárdenas, Agustín. Administración con el Método Japonés, CECSA.1993
Requema Rodríguez, J.M y Vera Rios, S. Contabilidad Interna 2da ed. Ariel.
www.gestiopolis.com Escalona, Iván. Gestión de calidad. 05-2004
www.gestiopolis.com Lefcovich, Mauricio. Kaizen: Detección, prevención y eliminación de desperdicios .2004
www.monografias.com Lefcovich, Mauricio.  Matriz de Control Interno – 2003





Tuesday, August 9, 2011

CAMBIO DE BLOG

SOLO COMUNICARLES QUE HE CAMBIADO LA DIRECICION DEL BLOG, AHORA ESTARE EN DRALMANZA-MEMORIA.BLOGSPOT.COM, LOS VEO POR ALLA, GRACIAS

Tuesday, August 2, 2011

HYPERALDOSTERONISM

PRIMARY: caused by an aldosterone-secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma rennin.
Increased aldosterone secretion from adrenal, which results primary from 2 major subtypes:
1)      Unilateral aldosterone-producing adenoma (APA) or Conn’s syndrome, the most common subtype (50-60% of case), usually small <3 cm unilateral, and rennin-unresponsive. This means that aldosterone secretion is not affected by changes en posture. Rarely, the adenoma is rennin-responsive (aldosterone levels increase with standing).
2)      Idiopathic hyperaldosteronism (IHA) or bilateral adrenal hyperplasia. Aldosterone increases in response to postural studies. Rarely, patients are hyperplastic (primary adrenal hyperplasia), and the response of aldosterone to standing is similar to rennin-unresponsive APA

Other subtypes:
3)      Rennin-responsive adenoma
4)      Primary adrenal hyperplasia
5)      Glucocorticoids-remediable aldosteronism.

Aldosterone, by inducing renal distal tubular reabsortion of sodium, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, alkalosis.

Hypokalemia → fatigue, muscle weakness, cramping, headaches, and palpitations.
                            Polydipsia and polyuria from hypokalemia-induced nephrogeni diabetic insipidus.
Treatment: the goal of treatment is to prevent the morbidity and mortality associated with hypertension and hypokalemia. Appropriate treatment depends on the cause e.g. Conn’s syndrome vs. IHA (unilateral or bilateral adrenalectomy).
Medication: spironolactone (aldosterone antagonists).

SECUNDARY: Due to: Renal artery stenosis
                                        Chronic renal failure
                                        CHF
                                        Cirrhosis
                                        Nephrotic syndrome
Kidney perception of low intravascular volume results in an overactive rennin-angioitensin system. Associated with high plasma rennin.

CUSHING SYNDROME

Cushing syndrome is caused by prolonged exposure to elevated levels of either endogenous glucocorticoids or exogenous glucocorticoids.

Etiologies include:
1)      Pituitary adenoma: classic Cushing’s disease (80%); ↑ ACTH.
2)      Adrenal hyperplasia/neoplasia: ↓ ACTH.
3)      Ectopic ACTH production e.g. oat cell carcinoma, small-cell lung carcinoma or carcinoid tumor. ↑ ACTH.
4)      Iatrogenic: most common etiology, chronic steroid use. ↓ ACTH.

Individuals with Cushing Syndrome can develop moon facies, facial plethora, supraclavicular fat pads, buffalo hump, truncal obesity, and purple striae. Often complain of proximal muscle weakness, easy bruising, weigh gain, hisutism, and, in children, growth retardation. Hypertension, osteopenia, diabetes mellitus, and impaired immune function may occur.

Exogenous steroids may cause suppression of the hypothalamus-pituitary-adrenal (HPA) axis, which can last for as long as a year after exogenous steroids administration has ended.

An individual with HPA axis suppression cannot increase steroids production appropriately during a medical illness or other stress, and would need to receive stress doses of steroids to avoid adrenal crisis. Thus, in an emergency, the potential for relative adrenal insufficiency should be considered in any patient with Cushing syndrome.

ADRENAL CRISIS

Adrenal crisis may occur in patients on steroids who stop taking their glucocorticoids or neglect to increase their steroid during an acute illness. It also may occur in patients who have recently undergone resection of an ACTH-producing or cortisol-producing tumor, or who are taking adrenal steroid inhibitors.
Finding: Hypotension, abdominal pain, vomiting, and mental confusion (secondary to low serum sodium or hypotension), hypoglycemia, hyperkalemia, hyponatremia, and metabolic acidosis.

Biochemical evaluation of Cushing syndrome.

Four methods are accepted for the diagnosis:
1)      Urinary free cortisol levels.
2)      Low-doses dexamethasone suppression test.
3)      Evening serum and salivary cortisol levels.
4)      Dexamethasone-corticopropin-releasing hormone test.


Treatment:
The Cushing syndrome treatment is directed by the primary cause of the syndrome.
A culprit tumor should be removed if possible.
For exogenous etiology a gradual withdrawal of glucocorticoids is the way.

Monday, August 1, 2011

THYROID PHYSIO-PATHOLOGY

Thyroid hormones: T3 (triiodothyronine)
                                T4 (tetraiodothyronine = thyroxine)

Both have systemic effects. Abnormal thyroid hormone levels lead to hypothyroid and hyperthyroid states. Inadequate thyroid hormone during the development leads to congenital hypothyroidism; also know as cretinism, with associated irreversible brain damage.

Source: Follicles of thyroid. Most T3 formed in blood.

Function: Bone growth (synergism with GH)
                Brain maturation.
                Beta-adrenergic effects: increases stimulation of β1 receptors in heart = ↑ CO, HR, SV, and contractility.
                Basal metabolic rate ↑ via ↑ Na/K-ATPase activity = ↑ 02 consumption, RR, body temperature.

Regulation: TRH (thyrotropin releasing hormone) from the hypothalamus stimulates TSH (thyroid stimulating hormone) in adenohypophysis, which stimulates follicular cells.


Hypothyroidism: Cold intolerance, hypoactivity, weigh gain, fatigue, lethargy, ↓ appetite, constipation, weakness, ↓ reflex, myxedema (facial/periorbital), dry, cool skin, and coarse, brittle hair.
↑ TSH (sensitive test for 1° hypothyroidism), ↓ total T4, ↓ free T4,↓ T3 uptake.

Hyperthyroidism: Heat intolerance, hyperactivity, weigh loss, chest pain/palpitation, arrhythmias, diarrhea,reflex, warm, moist skin, and fine hair.
 ↓ TSH (if 1°), ↑ total T4, ↑ free T4, ↑ T3 uptake.

Hashimoto’s thyroiditis: Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture). Slow course, moderately enlarged, nontender thyroid. Lymphocyte infiltrate with germinal centers. Antimicrosomal and antithyroglobulin antibodies. Associated with Hürthle cells on histology.

Subacute thyroiditis (de Quervain’s): Self-limited hypothyroidism often following a flulike illness. Elevated ESR, jaw pain, early inflammation, and very tender thyroid gland. Histology shows Granulomatous inflammation.
May be hyperthyroid early in course. Lymphocytes subacute thyroiditis is painless.

Riedel’s thyroiditis: Thyroid replaced by fibrous tissue (hypothyroid). Presents with fixed, hard, and painless.

Cretinism: Due to several fetal hypothyroidism. Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine); sporadic cretinism is caused by defect in T4 formation or developmental failure in thyroid formation.
Finding: Pot-bellied, pale, puffy face child protruding umbilicus and protuberant tongue.

Graves’ disease: An autoimmune hyperthyroidism with thyroid-stimulating/TSH receptor antibodies. Ophthalmopathy (proptosis, extraocular muscle swelling), pretibial myxedema, diffuse goiter. Often presents during stress (e.g. childbirth).
Stress-induced catecholamine surge leading to death by arrhythmia. Seen as a serious complication of Graves’ and other hyperthyroidism disorder.
Graves’ is type II hypersensitivity.

Toxic multinodular goiter: Iodine deprivation followed by Iodine restoration. Causes release of T3 and T4. Nodules are not malignant.
Jod-Basedow phenomenon= thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

Thyroid cancer:
1)      Papillary carcinoma- most common, excellent prognosis, ground-glass nuclei (Orphan Annie), psammoma bodies, nuclear grooves. ↑ Risk with childhood irradiation.
2)      Follicular carcinoma-good prognosis, uniform follicles.
3)      Medullary carcinoma-from parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. Associated with MEN type 2A and 2B.
4)      Undifferenciated/anaplastic- older patients, very poor prognosis.
Lymphoma – associated with Hashimoto’s thyro

Thursday, July 28, 2011

CONGENITAL ADRENAL HYPERPLASIA

CONGENITAL ADRENAL HYPERPLASIA (CAH)

CAH is a familial autosomal recessive disorder of adrenal steroid biosynthesis in which one of enzyme necessary for cortisol production has defiant activity.
Decreased serum cortisol levels stimulate adrenocorticotropic hormone (ACTH) release via negative feedback. The adrenal glands undergo hypertrophy, apparently due to ACTH-stimulated production of insulinlike growth factor 2. Increased ACTH secretion also results in overproduction of both the adrenal steroids preceding the missing enzyme and those that do not require the missing enzyme.

Aldosterone (mineralocorticoid) synthesis and secretion is regulated via renin-angiotensin system (adrenal zone glomerulosa), which is responsive to the electrolyte balance state and plasma volume. Aldosterone secretion is also directly stimulated by high serum potassium concentrations.

Cortisol (glucocorticoid) synthesis and secretion is regulated by ACTH (adrenal zone fasciculate), which stimulates the enzyme P-450scc (20, 22 Desmolase) with subsequent increased production of all adrenal steroids.

Approximately 80-90 % of individuals with ACH have 21α-hydroxylase deficiency: ↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormone. Masculinization, female pseudohermaphroditism, hypotension, hyperkalemia, ↑ plasma rennin activity, and volume depletion. Salt wasting can be lead to hypovolemic shock in the newborn.

The second most common types of ACH is the 11β-hydroxylase deficiency, it has an incidence of about 1 in 100.000.
Finding: ↓ cortisol, ↓ Aldosterone and Corticosterone, ↑ sex hormones
Masculinization, hypertension (like Aldosterone, 11-deoxycorticosterone is a mineralocorticosteroids and is secreted in excess).

17α-hydroxylase deficiency is probably even more rare genetic disorder of steroid biosynthesis that causes decreased production of glucocorticoids and sexual steroids, and increased synthesis of mineralocorticoids precursors.
Finding: ↓ sex hormone, ↓ cortisol, ↑ mineralocorticoids.
Hypertension, hipokalemia.
XY: ↓ Dihydrotestosterone → pseudohermaphroditism (external phenotypic female, no internal reproductive structure).
XX: external phenotypic female with normal internal sex organs, but lacking secondary sexual characteristics (sexual infantilism).

Hypogonadism occurs as a result of deficient sex steroid production. Deoxycorticosterone mineralocorticoid activity causes sodium retention, plasma volume expansion, hypertension, hipokalemia, and decreased renin and Aldosterone levels in most untreated patients with 17α-hydroxylase deficiency.

Exogenous glucocorticoid therapy is the treatment of choice.
All congenital adrenal enzyme deficiencies are characterized by an enlargement of adrenal glands due to an ↑ in ACTH stimulation because of the ↓ levels of cortisol.






Wednesday, July 20, 2011

CARDIOVASCULAR PATHOLOGY (vasculitis small-medium-large vessels).

Telangiectasia
Dilated vessels on skin and mucous membrane.
Osler-Weber-Rendu Syndrome
(autosomal dominant inheritance-nosebleeds and skin discoloration)
Affects small vessels
Raynaud’s disease
Decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress.
Most often in the fingers and toes.
Small vessels
Wegener's granulomatosis
Necrotizing vasculitis.
Necrotizing granulomas in the lungs and upper airway.
Necrotizing glomerulonephritis.
(Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dysnea, hemoptysis, hematuria).
*c-ANCA
Treatment: Cyclophosphamide and corticosteroids.

Small vessels
Microscopic polyangeitis
Like Wegener’s but lacks granulomas
*p-ANCA
Small vessels
1º pauci-immune crescentic glomerulonephritis 
Limited to the kidneys
Small vessels
Churg-Strauss syndrome
Granulomatous vasculitis with eosinophilia.
Involves lungs, heart, skin, kidneys, and nerves.
Often seen in atopic patients.
*p-ANCA


Small vessels
Sturge-Weber disease
Congenital vascular disorder.
Port-wine stain on face and leptomeningeal angiomatosis (intracerebral AVM)
Small vessels



Henoch-Schönlein purpura
Most common form on childhood.
Skin rash on buttocks and legs, arthralgia, intestinal hemorrhage, abdominal pain, and melena.
Follows with URIs.
Associates with IgA nephropathy.
Lesions at the same age
Small vessels.
Common triad
-skin
-joints
-GI
Buerger’s disease
(thromboangiitis obliterans)
Idiopathic, segmental, thrombosing vasculitis.
Seen in heavy smokers.
Intermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynaud’s phenomenon), severs pain in affected part. May lead to gangrene and autoamputation digits.
Treatment: smoking cessation
Small and medium vessels.
Cause thrombosis/
Infarction of arteries.

Kawasaki disease
Acute, self-limiting disease of infants/kids.
May develop coronary aneurysms.
Fever, congested conjunctiva, strawberry tongue, lymphadenitis.
Necrotizing vasculitis of small and medium vessels.
Polyarteritis nodosa
Fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, neurologic dysfunction, cutaneous eruption.
Hepatitis B + in 30 %
Aneurysms and constrictions on arteriogram.
Treatment: corticosteroids, Cyclophosphamide.
Necrotizing immune complex inflammation of medium sized muscular arteries. Lesions at different ages.
Takayasu’s arteritis
(pulseless disease)
Asian females <40 years old.
Fever, arthritis, night sweats, myalgia, skin nodules, ocular disturbances, weak pulse in upper extremities.
Granulomatous thickening of aortic arch and
/or proximal great vessels.







Temporal arteritis
(giant cell arteritis)
Most common vasculitis that affects medium and large arteries, usually branches of carotid artery.
Focal, Granulomatous inflammation. Affects elderly females.
Unilateral headache, jaw claudication, impaired vision.
↑ ESR, systemic involvement and polymyalgia rheumatic.
Treatment: high doses of steroids.
Medium and large arteries.


Monday, July 18, 2011

INFECTIVE ENDOCARDITIS (IE).

Infective endocarditis is a microbial infection on the endothelial surface of the heart, which includes one or more heart valve, the mural endocardium or septal defect. IE produce a wide variety of systemic signs and symptoms through a several mechanisms, including both sterile and infected embolic and various immunological phenomena.

IE generally occur as a consequence of nonbacterial thrombotic endocarditis, which result s from turbulence or trauma to the endothelial surface of the heart. A transient bacteriemia then seeds the sterile platelet/fibrin thrombus, which IE as the end result. Pathologic effects due to infection can include local tissue destruction and embolic phenomena. In addiction, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur.

Endocarditis can be broken down into the fallowing categories:
.Native valve endocarditis: Acute (Staphylococcus aureus, high virulence, large
                                            vegetation on previously normal valves). 
                                            Subacute (Streptococcus viridans, low virulence,
                                            smaller vegetation on congenitally abnormal or diseased
                                             vales.
                                             Sequela of dental procedures. More insidious onset)
.Prosthetic valve endocarditis, early and late.
.Intravenous drugs abuse endocarditis.

Other types include.
_Pacemaker IE.
_Nosocomial IE.

Endocarditis may also be nonbacterial secondary to malignancy or hypercoagulable state (marantic/thrombotic endocarditis).
Streptococcus bovis is present in colon cancer and staphylococcus epidermidis on prosthetic valves.

Mitral valve is most frequently involved, closely fallowed by the aortic valve, the combined mitral and aortic valve, the tricuspid valve (associated with intravenous drugs abuse), and, rarely, the pulmonic valve.

General finding:
Fever (most common symptom).
Roth’s spots (round white spot on retina surrounded by hemorrhage).
Osler’s node (tender raised lesions on finger or toes pads)
New murmur (caused by valvular damage)
Janeway lesions (small erythematous lesion on palm or sole)
Anemia.
Splinter hemorrhages on nail bed.
Signs of neurological disease: Embolic stroke with focal neurologic deficit is the most common etiology.
Signs of systemic septic emboli are due to left heart disease and are more common associated with mitral valve vegetation. Multiples embolic pulmonary infections or infarction are due to right heart disease.
Signs of congestive hear failure.

Diagnosis considerations.
The clinical criteria for definitive infectious endocarditis (Duke Criteria) include 2 major, 1 major and 3 minor, or 5 minor.

Major criteria.
Positive blood culture: 2 separate cultures for a typical endocarditis microorganism, persistently positive cultures, or evidence of infection with a Coxiella organism and/or Q fever.
Positive echocardiography finding: oscillating mass and/or vegetation, paravalvular abscess, or dehiscence of prosthetic valve.
New valvular regurgitation.

Minor criteria.
Predisposition: history of IV drug use or congenital heart disease).
Fever with a temperature of more than 38 º C.
Vascular phenomena (arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions).
Immunologic phenomena (glomerulonephritis, Osler node, Roth spots, a positive result for rheumatoid factor).
Positive blood culture findings without meeting the criteria above or serologic evidence of active infection consistent with endocarditis.

Treatment: Antibiotic are the mainstay of treatment. Goals to maximize treatment success are early diagnosis, accurate microorganism identification, and reliable susceptibility testing, prolonged intravenous administration of bactericide antimicrobial agents, proper monitoring of potentially toxic antimicrobial regimens, and aggressive surgical managements of correctable mechanical complications.

Prognosis largely depends on whether or not complications develop. If left untreated, IE is generally fatal. Early detection and appropriate treatment of this uncommon disease can be lifesaving.