PATHOPHYSIOLOGY EXAM 1

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atrophy

decrease in cell size

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hypertrophy

increase in cell size

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hyperplasia

increase in number of cells

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metaplasia

cell type is replaced by another cell type

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dysplasia

deranged cell growth of tissue that results in cells that vary by size, shape, and organization

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changes that occur in cell with swelling

decreased activity of Na/K ATPase pump-->sodium ions increase in cell-->osmotic pressure increases--> water diffuses in cell causing swelling--> cell bursts

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reperfusion injury

reperfusion (large influx of O2)-->ischemic conditions-anaerobic metabolism-->oxidative enzymes produce reactive oxygen species (ROS)--> ROS damage cell membranes-liquid peroxidation-->cell death

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cell necrosis

occurs in irreversibly damaged cells, cell death

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benign tumors

grow slow well differentiated noninvasive do not divide do not metastasize surrounded by fibrous capsule

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malignant tumors

grow fast poorly differentiated invasive divide metastasis

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metastasis

The spread of cancer cells beyond their original site

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well differentiated vs poorly differentiated cells

well: looks like normal cells poor: do not look like normal cells

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how does cancer spread

direct invasion and extension, seeding of cancer cells into body cavities, metastatic spread through blood or lymph pathways

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Carcinogenesis

process by which carcinogenic agents cause normal cells to become cancer cells

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Carcinogenesis steps

initiation, promotion, progression

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initiation

Exposure of cells to a carcinogenic agent that causes them to be vulnerable to cancer transformation

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promotion

Allows for prolific growth of cells triggered by multiple growth factors and chemicals. Reversible if promoter substance is removed

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progression

Manifests when tumor cells acquire malignant phenotypic changes that promote invasiveness, metastatic competence, autonomous growth tendencies, and increase karyotypic instability

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physical carcinogens

tanning beds UV rays

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chemical carcinogens

Direct reacting agents or indirect reacting agents, alcohol, smoke

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viral carcinogens

HPV and Hepatitis B

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immune surveillance

  • Immune system plays a central role in resistance against the development of tumors

  • Provide a means for the detection, classification, and prognostic evaluation of cancers and as a potential method of treatment

  • Suggested that development of cancer might be associated with impairment or decline in surveillance capacity of immune system

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systemic manifestations of cancer

  • anorexia and cachexia

  • fatigue and sleep disorders

  • anemia

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tumor markers

  • Antigens expressed on the surface of tumor cells or substances released from normal cells in response to the presence of a tumor

  • Used for screening, establishing prognosis, monitoring treatment, and detecting recurrent disease

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systemic manifestations of inflammation

Acute-phase response. Alterations in WBCs Fever

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edema formation during inflammation

begins with momentary vasoconstriction followed rapidly by vasodilation mediated in part by lipid mediators and vasoactive products outpouring of protein rich fluid into extravascular spaces loss of proteins causes reduced capillary pressure

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macrophages

engulf large and great quantities of foreign material (more than neutrophils)

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neutrophils

attack and ingest bacteria and cellular debris

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phagocytosis

recognition and adherence, engulfment, intracellular killing

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cells of phagocytosis

neutrophils, monocytes, macrophages

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phases of wound healing

inflammatory, proliferative, remodeling

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inflammatory phase

the initial phase of wound healing in which bleeding is reduced as blood vessels in the affected area constrict

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proliferative phase

forms granulation tissue for scar tissue development key cell: fibroblast

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remodeling phase

scar tissue formed during healing

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factors that influence wound healing

malnutrition, impaired blood flow and oxygen delivery, impaired inflammatory and immune responses, infection, wound separation, foreign bodies, age effects

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labile cells

continue to divide and replicate throughout life (skin)

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stable cells

normally stop dividing when growth ceases (liver and kidney

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permanent or fixed cells

cannot undergo miotic division (nerve cells, cardiac cells)

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acquired immunity

Immunity that develops during your lifetime

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active immunity

acquired when host mounts an immune response to antigen

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natural active immunity

antibodies developed in response to infection

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artificial active immunity

antibodies developed in response to a vaccine

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passive immunity

transferred from another source

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natural passive immunity

acquired by a child through placenta and breast milk

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artificial passive immunity

antibodies received from a medicine, from a gamma globulin injection or infusion

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adaptive immunity

the ability to recognize and remember specific antigens and mount an attack on them

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humoral immunity

mediated by antibodies produced by B lymphocytes

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cellular immunity

immune response that relies on T cells to destroy infected body cells

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innate immunity

body's first line of defense

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innate immunity cells

neutrophils macrophages DCs NK cells phagocytes monocytes

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adaptive immunity cells

B and T cells macrophages DCs NK cells

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IgG

responsible for protection of newborn only one that crosses placenta

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IgA

protects mucous membranes

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IgM

forms natural antibodies such as those for ABO blood antigens activates complement

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IgD

needed for maturation of B cells

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IgE

allergic reactions

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classification of immune disorders

primary secondary hypersensitive autoimmunity

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primary

congenital or inherited as sex linked, autosomal dominant, or autosomal recessive traits

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secondary

develop later in life because of other pathophysiologic states such as malnutrition, disseminated cancers, infection of cell of immune system (HIV)

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hypersensitive

abnormal and excessive response of the activated immune system that causes injury and damage to host tissues

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autoimmunity

heterogenous group of disorders that occur when the body's immune system fails to differentiate "self" from "nonself" and mounts an immunologic response against host issues

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pathophysiologic mechanisms in HIV

takes over CD4 T cells

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Type 1 hypersensitivity

  • IgE mediated

  • Onset within 1 hour

  • Ex: Anaphylaxis

  • Allergies

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Type 2 hypersensitivity

  • IgG or IgM cytotoxic mediated

  • Onset in hours to days

  • Ex: Hemolytic anemia

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Type 3 hypersensitivity

  • Immune complex mediated

  • Onset within 1-3 weeks

  • Ex: serum sickness SLE

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Type 4 hypersensitivity

  • T cell mediated

  • Onset from days to weeks

  • Ex: Rash SJS

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components of host defense

skin and mucous membranes

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host

any organisms capable of supporting the nutritional and physical growth requirements of another

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factors affecting host defense

  • Weakened by illness, malnutrition, or medical therapy

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symptom production in neutropenia

decreased neutrophil count first signs are skin lesions, pharyngitis, diarrhea

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Acute Lymphocytic Leukemia (ALL)

most common in children structural changes in chromosomes of leukemic cells

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Acute Myelocytic Leukemia (AML)

mainly in older adults affects myeloid precursor cells in bone marrow

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Chronic Lymphocytic Leukemia (CLL)

immune incompetent B cells due to failure of apoptosis

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Chronic Myelocytic Leukemia (CML)

overgrowth of mature granulocytes in bone marrow specific chromosome abnormality: Philadelphia chromosome

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Non-Hodgkin's Lymphoma manifestations

slow growing: painless lymphadenopathy more aggressive: fever, weight loss, night sweats

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Hodgkin's lymphoma manifestations

painless enlarged lymph nodes, chest discomfort, fevers, chills, night sweats, weight loss, fatigue, anemia

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hemostasis

stoppage of blood flow

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mechanisms of hemostasis

vascular constriction, platelet plug formation, coagulation

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manifestations of thrombocytopenia

  • History of bruising, bleeding from gums, epistaxis, melena, and abnormal menstrual bleeding in those with moderately reduced platelet counts

  • Splenic enlargement may occur

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effect of vascular disorders on hemostasis

  • Bleeding resulting from vascular disorders is sometimes referred to as nonthrombocytopenic purpura.

  • May occur from structurally weak vessel walls or because damage to vessels by inflammation or immune responses

  • Easy bruising or petechia and purpura of skin

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manifestations of anemia

  • Impaired oxygen transport, compensatory mechanisms, decrease in HGM and RBC indices, weakness, chest pain, cold hands and feet, headache, lightheaded

  • Causes: loss of RBCs from bleeding, destruction (hemolysis) of RBCs, defective RBC production, inadequate RBC production from bone marrow failure

  • Compensatory mechanisms

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TNM best

Tis N0 M0

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TNM worst

T4 N4 M4

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T

tumor

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N

nodes

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M

metastasis

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B-12 deficiency anemia

cause: pernicious anemia which causes failure to absorb B12

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iron deficiency anemia

anemia caused by inadequate iron intake

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apoptosis

programmed cell death

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When does HIV become AIDS?

when the CD4 count goes below 200

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opportunistic infection

occur as immune system becomes severely compromised

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sickle cell anemia screening

made on the basis of clinical findings and hemoglobin solubility results newborn screening

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anemia that handles bone marrow

aplastic anemia

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petechiae

small, pinpoint hemorrhages

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multiple myeloma

B-cell malignancy of terminally differentiated plasma cells

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