Relationship between Organizational Behavior (OB) and Organizational Development (OD).

      Organization Behavior is defined as the study and application of knowledge about how people, individuals, and groups act in organizations. That is, it interprets people-organization relationships in terms of the whole person, whole group, whole organization, and whole social system. Its purpose is to build better relationships by achieving human objectives, organizational objectives, and social objectives. (Clar, 1998).

      In business science is the study of the way people interact within group ( (Investopedia ULC, 2011). Normally it is applied in an attempt to create more efficient business organizations. The central idea of the study of OB is that a scientific approach can be applied to the management of workers. These theories are used for human resource purpose to maximize the output from individual group of members.

      On the other hand Neilsen, pointed:

      Organizational Development is the attempt to influence the members of an organization  to expand their candidness with each other about their views of the organization and their experience in it, and to take greater responsibility for their own actions as organization members. The assumption behind OD is that when people pursue both of these objectives simultaneously, they are likely to discover new ways of working together that they experience as more effective for achieving their own and their shared goals, and that when this does not happen, such activity helps them to understand why and to make meaningful choices about what to do in light of this understanding. (1984).

     Based on the foregoing, and in revised the texts mentioned we can see the strongly relationship between both OD and OB, where  the   principal mission to improve the organization as a whole and to increase the capacity of the human being  to be productive, proactive and serve as an active component of the positive results of the organization. Work like teams is vital to the functioning of modern organizations. Members of teams bring different strings to the group such as leader, investigator, motivator, finisher, coordinator, thinker, negotiator or politician.   These roles are used at different stages of production when such role play becomes essential in the groups work. Teams take over from hierarchical systems where individuals are assumed to know everything depending on their level in the authority ladder. This system denies the organization the cumulative advantage of skills and strengths in different individuals.

      As shown us Wamwangi (2003) the Organizational Development is a change management strategy which has been in operation for the last forty years. It is based on the understanding of behavioral sciences and is concerned with how people and organizations function and how they can be made to function better through effective use of human and social process.

       Human behavior in organizations is unpredictable because it originates in needs and value systems deeply rooted in people. (Davis, 1999).There is no simple formulas and practices for working with people, nor is there an ideal solution to the problems of the organization. All we can do is to increase understanding and capacities to raise the quality of human relations at work. The goals are difficult to achieve, but are of great value. If you are willing to think of people as human beings can work effectively with them.

      In the today’s economic situation, the turbulence facing the modern man and organization is at a level that may not have been experienced before in human history, the modern change has changed in speed, depth and complexity bringing with it a new phenomenon in technological, social, political and economic pace adaptation to which becomes a fundamental condition of survival for individuals and organizations, that is why a change in approach and understanding of the behavior of individual, group or organization is vital to business development in these current conditions, where the participation of each other can help achieve the objectives of the company.

References:

Clar, D. (1998, march 19). Retrieved from Big Dog and Little Dog's Bowl of biscuits. Retrieved from http://www.nwlink.com/donclark/leader/leadod.html

Davis, K. &. (1999). Comportamiento Humano en el trabajo: comportamiento organizacional. Mexico city, Mx: McGraw-Hill companies.

Investopedia ULC. (2011, november 14). investopedia.com. Retrieved from

http:investopedia.com/terms/o/organizational-behavior.asp#axzz1dh9DFu1

Neilsen, E. (1984).Becoming an OD Practitioner. Englewood Cliffs, CA: Prentice Hall.

Wamwangi, K. (2003, October 21). info.worldbank.org. Retrieved from http://info.worldbank.org/etools/docs/library/114925/eum/docs/eum/tanzania/MODULEIIORGANIZATIONALDEVELOPMENTKINUTHIA.pdf

    

     

THANKS GIVING DAY:

In 1621, the Plymouth colonists and Wampanoag Indians shared an autumn harvest feast that is acknowledged today as one of the first Thanksgiving celebrations in the colonies. Governor William Bradford organized a celebratory feast and invited a group of the fledgling colony’s Native American allies, including the Wampanoag chief Massasoit. Now remembered as American’s “first Thanksgiving”—although the Pilgrims themselves may not have used the term at the time—the festival lasted for three days. While no record exists of the historic banquet’s exact menu, the Pilgrim chronicler Edward Winslow wrote in his journal that Governor Bradford sent four men on a “fowling” mission in preparation for the event, and that the Wampanoag guests arrived bearing five deer. Historians have suggested that many of the dishes were likely prepared using traditional Native American spices and cooking methods. Because the Pilgrims had no oven and the Mayflower’s sugar supply had dwindled by the fall of 1621, the meal did not feature pies, cakes or other desserts, which have become a hallmark of contemporary celebrations. For more than two centuries, days of thanksgiving were celebrated by individual colonies and states. It wasn't until 1863, in the midst of the Civil War, that President Abraham Lincoln proclaimed a national Thanksgiving Day to be held each November.[1]

 For many of us who do not know the tradition, no matter what the history, it is important that we practice gratitude every day, and in every aspect of our lives. Many references are found for "Thank" referred to the natural gift that makes it pleasant to anyone who has, or the expression of gratitude for the benefits, giving thanks is synonymous to recognize that something or someone has done a favor, someone provided us a benefit. The word "Thank" strengthens to who emitted it, whenever he expresses it with sincerity. Gratitude is the memory of the heart.[2]

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[1] (A&E Television Networks, LLC, 2011)

[2] (Guindi Lopata, 2011)

NEPHRITIC SYNDROME:

Nephritic is an older term used to clinically denote a child with hypertension, decreased renal function, hematuria, and edema, according to Fathallah-Shaykh (2011), nephritis suggest a noninfectious inflammatory process that involves the nephron; glomerulonephritis (GN) generally is a more precise term.

      Diseases that produce glomerulonephritis are usually classified as primary, where the kidney is the primarily affected organ, or secondary, in which systemic disorder involve the kidney in addition to other organs. (Fathallah-Shaykh, 2011).

      Essential of diagnosis. (Watnick & Morrison, 2005):

      Edema.

      Hypertension.

      Hematuria (with or without dysmorphic red cells, red blood cell casts).

      When, the inflammatory process involves glomeruli, it leads to hematuria and red blood cells casts in urine, associated with azotemia, oliguria, hypertension, and proteinuria < 3.5g/day.

      Medical care that Fathallah-Shaykh (2011) recommends for glomerulonephritis (GN) is usually divided into 2 major components: treatment of primary pathology and supportive care. In renal diseases, supportive care involves managing hypertension and fluid and electrolyte abnormalities and managing decreased renal function.

      The treatment of primary pathology ranges from watchful waiting, as in postinfectious GN, to treatment with immunosuppressive medication, such as steroids or cyclophosphamide in lupus; in the case of IgM nephropathy, no definitive therapy is known.

      Hypertension can be managed with antihypertensives, such as calcium channel–blocking agents, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor–blocking agents, peripheral vasodilators, and diuretics. The most common fluid abnormality, hypervolemia, is managed with fluid restriction and diuretics or with dialysis if renal function is too poor to respond to diuretics. Hyponatremia is usually dilutional and responds, at least partially, to removal of excess fluid. Hypocalcemia may respond to oral or IV calcium, depending on severity. Mild metabolic acidosis may be present but rarely requires primary treatment.

      Some recommend a short course of steroids or cyclophosphamide for tubulointerstitial nephritis (TIN). However, these drugs are usually not necessary. Most often, stopping the offending agent leads to recovery. (Fathallah-Shaykh, 2011).

      Acute poststreptococcal glomerulonephritis:

      Is a disorder most frequently seen in children, that can resolves spontaneously (Le, Bhushan, & Grimm, First AID fro the USMLE Step 1, 2011) characterized by sudden appearance of edema, peripheral and periorbital edema, hematuria, proteinuria, and hypertension; it is a representative disease of acute nephritic syndrome in which inflammation of the glomerulus is manifested by proliferation of cellular elements secondary to an immunologic mechanisms. (Bhimma, 2011) (Rodríguez-Iturbe B, Jun 2007).

      Rapidly progressive glomerulonephritis (RPGN).

      RPGN have a poor prognosis with rapidly deteriorating renal function, days to weeks. The glomerular filtration rate (GFR) decreases at least 50% over a short period, from a few days to 3 months. The main pathologic finding is extensive glomerular crescent formation. ( Lohr, 2011).

      Rapidly progressive glomerulonephritis is classified pathologically into 3 categories (Lohr, 2011), as follows: (1) anti-GBM antibody disease (approximately 3% of cases), (2) immune complex disease (45% of cases), and (3) pauci-immune disease (50% of cases). Immunologic classification is based on the presence or absence of circulating antineutrophil cytoplasmic antibodies (ANCAs). The disorders are also classified based on their clinical presentation.

       Several disease processes may result in this pattern, including (Le, Bhushan, & Grimm, First AID for the USMLE step 1, 2011):

1)      Goodpasture syndrome: It is type II hypersensitivity; antibodies to GBM and alveolar basement membrane are presents.

2)      Wegener’s granulomatosis. (c-ANCA).

3)      Microscopie polyangiitis. (p-ANCA).

      Therapy for ANCA-associated disease consists of a combination of corticosteroids and cyclophosphamide. Treatment with steroids alone results in a 3-fold increase in the risk of relapse compared to combination therapy.

       Diffuse proliferative glomerulonephritis (DPGN).

       It the most common cause of death in SLE and MPGN, can also present as Nephrotic syndrome as explained Tao & at (2011), DPGN describe a distinct histologic form of GN common to various types of systemic inflammatory diseases, including autoimmune disorders, vasculitis syndromes, and infectious process. More than 50% of glomeruli show an increase in mesangial, epithelial, endothelial and inflammatory cells. The diagnosis is often suspected in a patient presenting with systemic inflammatory disease who manifests hematuria, proteinuria, and active urinary sediment or azotemia; histologic findings from kidney biopsy tissue are used to confirm the diagnosis. (Salifu, 2009).

      Early, aggressive therapy is indicated as regards Salifu (2009) because of the high risk of early-stage of renal diseases. Initiate the following as induction therapy: pulse methylprednisolone of 1 g daily for 3 days, followed by 1 mg/kg for 4-6 weeks and then tapered to 5-10 mg/d for maintenance therapy by 6 months. Alternatively, prednisolone 1 mg/kg (not to exceed 80 mg/d) can be started and tapered as above. Additional induction and maintenance therapy may be indicated, depending on the type of DPGN. Evidence suggests that mycophenolate mofetil (MMF) treatment benefits problematic patients who are refractory to conventional therapies for glomerulopathies (Sahin, Sahin, Kantarci, & Ergin, 2007).

      Berger’s diseases:

      Also know as Immunoglobulin A nephropathy is characterized by predominant IgA deposition in the glomerular mesangium, it is the most common cause of glomerulonephritis in the world. (Brake, 2010).

      Two common presentations of patients with IgA nephropathy are episodic gross hematuria and persistent microscopic hematuria. Recurrent macroscopic hematuria, usually associated with an upper respiratory tract infection, or, less often, gastroenteritis is the most frequent clinical presentation and is observed in 40-50% of presenting patients. In 30-40% of patients, the disease is asymptomatic, with erythrocytes (RBCs), RBC casts, and proteinuria discovered on urinalysis. Patients with IgA nephropathy can also present with acute or chronic renal failure, under what explains Brake (2010) currently, no cure exists for IgA nephropathy, but therapies that can delay the onset of need for dialysis and transplantation are available.

      Alport’s syndrome:

Due to a variety of gene defects resulting in abnormal type IV collagen, the most common form is X-linked recessive. Type IV collagen is an important structural component of the basement membrane of the kidney, ears, and eyes. The Alport’s syndrome presents as a progressive hereditary nephritic and deafness, may be associated with ocular disturbances (Le & at, 2011).

      No definite treatment exists for Alport’s syndrome. (Saxena, 2008).

Bibliography

Lohr, J. (2011, June 8). Medscape references. Retrieved from Rapidly Progressive Glomerulonephritis : http://emedicine.medscape.com/article/240457-overview

Bhimma, R. (2011, september 21). Medscape. Retrieved from Acute Poststreptococcal Glomeruloneph: http://emedicine.medscape.com/article/980685-overview

Brake, M. (2010, Mar 23). Medscape references. Retrieved from IgA Nephropathy: http://emedicine.medscape.com/article/239927-overview

Fathallah-Shaykh, S. (2011, june 29). Medscape references. Retrieved from http://emedicine.medscape.com/article/982811-overview

Le, T., Bhushan, V., & Grimm, L. (2011). First AID for the USMLE step 1. USA: McGraw Hill.

Le, T., Bhushan, V., & Grimm, L. (2011). First AID fro the USMLE Step 1. USA: McGraw Hill.

Rodríguez-Iturbe B, B. S. (Jun 2007). Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. In Kidney Int (pp. 71(11):1094-104.).

Sahin, G., Sahin, S., Kantarci, G., & Ergin, H. (2007). Mycophenolate mofetil treatment for therapy-resistant glomerulopathies. Nephrology (Carlton). June:12 (3):285-8.

Salifu, M. O. (2009, may 11). Medscape references. Retrieved from Glomerulonephritis, Diffuse Proliferative : http://emedicine.medscape.com/article/239646-overview

Saxena, R. (2008, september 8). Medscape references. Retrieved from Alport Syndrome Treatment & Management: http://emedicine.medscape.com/article/238260-treatment

Watnick, S., & Morrison, G. (2005). Kidney. Glomerulonephropathies. In L. M. Tierney, S. J. McPhee, & M. A. Papadakis, Current Medical Diagnosis & Treatment (p. 885). USA: McGraw Hill.

ACID-BASE DISTURBANCES

ACID-BASE DISTURBANCES[1]

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ACIDEMIA    pH< 7.4			ALKALEMIA  pH> 7.4
P CO₂ > 40mmHg	P CO₂ < 40mmHg		PCO₂ <40mmHg		PCO₂ >40mmHg
pH↓PCO₂↑HCO₃↑	pH↓PCO₂↓HCO₃⁻↓		pH↑PCO₂↓HCO₃⁻↓		pH↑PCO₂↑HCO₃↑
Respiratory Acidosis	Metabolic Acidosis		RespiratoryAlkalosis		MetabolicAlkalosis
Hypoventilation .airway obstruction .acute lung disease .chronic long disease .opioids, narcotics, sedatives .weakening of respiratory muscles	Check anion gap [(Na⁺-(Cl⁻+HCO₃⁻)] Normal=12[2]		Hyperventilation (Early high altitude exposure) Aspirin ingestion(early)		Diuretic use Vomiting Antacid use Hyperaldosteronism
	↑anion gap .methanol(formic acid) .uremia .diabetic ketoacidosis .paraldehyde or phenformin .iron tablets or INH(isoniazid) .lactic acidosis .ethylene glycol .salicylates Normal anion gap .diarrhea .glue sniffing .renal tubular acidosis .hyperchloremia
COMPENSATORRY  RESPONSE
↑ renal HCO₃⁻ reabsorption		hyperventilation		↓renal HCO₃⁻ reabsorption	hypoventilation

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[1] (Le, Bhushan, & Grimm, 2011)

[2] (© 2009 mdcalc.com, 2011)

ELECTROLYTE DISTURBANCES

	SERUM CONCETRATION
ELECTROLYTE	LOW	HIGH
Na⁺	Disorientation, stupor, coma	Neurologic irritability, delirium, coma
Cl⁻	2ᵈᵃ to metabolic alkalosis, hypokalemia, hypovolemia, ↑aldosterone	2ᵈᵃ to non gap anion acidosis
K⁺	U waves on ECG, flattened T waves, arrhythmias, paralysis.	Peaked T waves, wide QRS, arrhythmias
Ca²⁺	Tetany, neuromuscular irritability	Delirium, renal stones, abdominal pain, not necessarily calciuria
Mg²⁺	Neuromuscular irritability, arrhythmias	Delirium, ↓DTRs, cardiopulmonary arrest
PO₄ᶟ⁻	Bones loss, Osteomalacia	Renal stones, metastatic calcifications

References:

Le, T., Bhushan, V., & Grimm, L. (2011). First AID for the USMLE STEP 1. USA: McGraw-Hill.