Inflammatory Renal Disorder Typically Wcu Pathoph

Inflammatory Renal Disorder Typically Wcu Pathoph

This week, compose a 1–2 paragraph response to ONE of the following questions. Click on the discussion forum and choose the question you wish to answer. Explore the other questions/answers when you respond to your peers.

  1. Alterations in Immune Function
    1. How do type 1, 2, 3, and 4 hypersensitivity reactions differ according to mechanism of action?
    2. What are the clinical features of the common immunodeficiency disorder?
  2. Malignant Disorders of White Blood Cells
    1. How do the various types of leukemia, lymphoma, and plasma cell myelomas differ based on malignant transformation?
    2. Why are malignant disorders of white blood cells commonly associated with bone marrow depression?
  3. Alterations in Oxygen Transport
    1. How are history and clinical manifestations used to differentiate the various forms of anemia and polycythemia?
  4. Alterations in Hemostasis and Blood Coagulation
    1. What findings from the patient history, physical examination, or lab studies would indicate a possible bleeding disorder?
    2. What are the common causes of platelet dysfunction due to quantity and quality?
    3. What are the common causes of inherited and acquired coagulation disorders?
  5. Alterations in Blood Flow
    1. What are the clinical consequences of acute and chronic arterial obstructions and how do they develop?
    2. What are the causes and clinical consequences of superficial and deep venous obstructions?

comment 1

A.) How do the various types of leukemia, lymphoma, and plasma cell myelomas differ based on malignant transformation?

Leukemia – Is the cancer from the blood or bone marrow. Leukemia usually starts when the blood has a problem with cell production.

Lymphoma – Is when the cancer starts in the infection fighting cells of the immune system. These cells are located in the lymph nodes, spleen, bone marrow, thymus and can be found in the other parts of the body.

Plasma cell myelomas – Is when the cancer is produce in the plasma cells. Plasma cells make the antibodies that help the body fight infection and disease. More antibodies are made when the number of multiple myeloma cells increase. Multiple myeloma can also and damage and weaken bones.

For malignant transformation they need the properties of the cancer in order to process its cells (rapid dividing tumor cells).

Overall, leukemia, lymphoma, and plasma cell myelomas differ from malignant transformation because they are common neoplastic disorders of the bone marrow and lymphoid tissues. Whereas, malignant transformation needs the cancer properties to help rapidly divide the tumor cells into a number of specific subtypes.

B.)Why are malignant disorders of white blood cells commonly associated with bone marrow depression?

The reason that malignant disorders of white blood cells are associated with bone marrow depression because of the insufficient amounts of normal red blood cells (RBC), platelets, and white blood cells (WBC) that is the result from leukemic infiltration.

Reference:

Banasik J. L. & Copstead, L. C. (2019). Pathophysiology (6th ed.). Elsevier, Inc.

comment 2

How do type I, II, III, IV hypersensitivity reactions differ according to mechanism of action?

  • Having a hypersensitivity means that someone’s immune system has reacted to something abnormally in such a way that it ends up damaging them instead of protecting them. Hypersensitivity reactions are classified into four types: hypersensitivity types I, II, III, and IV.
    • Hypersensitivity type I rely on immunoglobulin E, or IgE antibody. IgE is the principle-mediating antibody. Hypersensitivity type I is also known as immediate hypersensitivity because the reaction is immediate and occurs 15-30 minutes after exposure to antigen/allergen. Most allergic reactions are IgE-mediated. The mechanism of action is initiated when IgE binds to Fc receptors on mast cells. The exposure of mast cells with cross-linked IgE-Fc receptors binding to antigen causes the release of proinflammatory mediators such as prostaglandins, interleukins, leukotrienes, and histamine. Histamine is the most important mediator that causes increased vascular permeability, vasodilation, hypertension, and bronchoconstriction. Clinical manifestations of a hypersensitivity type I reaction vary in severity and intensity. Mild symptoms include hives and seasonal allergies. More problematic symptoms include throat constriction, localized edema, and tachycardia. In a very small number of highly allergic individuals, the reaction can be expressed as a life threatening reaction known as anaphylaxis.

    • Hypersensitivity type II is known as tissue-specific, cytotoxic, or IgG/IgM mediated hypersensitivity. The mechanism of action is initiated when antibodies attack antigens on the surface of particular cells or tissues, which cause cell destruction or lysis. Examples include blood transfusions. This is when an individual received blood from someone with a different blood type. The recipient of the blood transfusion has antibodies to the donor’s RBC antigens.
    • Hypersensitivity type III is known as immune complex mediated hypersensitivity. It occurs when immune and phagocytic systems fail to effectively remove antigen-antibody complexes. The mechanism of action begins with interaction between a circulating soluble antigen and soluble antibody or between an insoluble antigen and a soluble antibody. Most immune complexes are removed before then can cause injury, however, in hypersensitivity type III the immune complexes are not removed. This causes an inflammatory response leading to tissue injury. Immune complex glomerulonephritis is an example of hypersensitivity type III. It is an inflammatory renal disorder typically occurring 10 to 14 days after infection with Streptococcus or staphylococcal bacterial strain.
    • Hypersensitivity type IV is also known as delayed hypersensitivity reaction is cell-mediated and does not require antibody involvement. The cell-mediated response involves the interaction of T-cells, monocytes, and macrophages. The mechanism of action is caused when CD4+ T helper (Th1) cells recognize foreign antigen in a complex with the MHC class II on the surface of antigen presenting cells, mediating the reaction by releasing a cascade of cytokinases. Overreaction of the helper T cells and overproduction of cytokinases damages tissues causes inflammation, and cell death.

What are the clinical features of the common immunodeficiency disorder?

  • Deficient immune responses result from functional decrease in components of the immune system that can affect lymphocytes, antibodies, phagocytes, and complement proteins. Two types of immune deficiency are: primary and secondary immunodeficiency disorders.
    • Primary immunodeficiency disorder weakens the immune system, allowing infections and other problem to occur more easily. They may be congenital or acquired. An example is HIV/AIDS.
    • Secondary immunodeficiency disorders occurs when the immune system is compromised due to an environmental factor. Diseases may be caused by excessive or defective neuroendocrine responses, and other non-immune system disorders that suppress the immune system.

Question for the class: Hemolytic disease of the newborn is what type of hypersensitivity?

Reference:

Banasik J. L. & Copstead, L. C. (2019). Pathophysiology (6th ed.). Elsevier, Inc.