Exam 1 -Patho

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infammatory response

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infammatory response

bodies reaction to injury

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injury types

trauma irritant bacteria lack of oxygen lack of glucose necrosis toxins surgery cancer

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labs for inflammation

CRD ESR WBC count

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neutrophils

first responders

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eosinophils

allergy/parasite

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monocytes

phagocytes

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lymphocytes

increased if viral infection present (t and b cells)

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basophils

release histamine (inflammation)

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chronic inflammation

persistent inflammation/inhibits healing

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acute inflammation

rapid response/last hours to days

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3 outcomes of acute inflammation

complete resolution scarring becomes chronic

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bands

immature neutrophils

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if bands are present, what is happening?

overabundance need for neutrophils so body pushes them out before they are ready (war draft example)

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shift to the left

immature cell release

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why do lymph nodes become enlarged with inflammation

lymph nodes remove excess fluid that veins dont pick up

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colonization

no disease symptoms

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infection

disease symptoms - growth of pathogens

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virulence

agression level

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immunocompetence

immune system good against pathogens

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immunosuppression

immune system not good against pathogens

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opportunistic infection

infection seizes opportunity to take over once immune system is down

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nosocomial infection (HAI)

hospital acquired infections

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staphylococcal

s. aurus - leading cause of HAI's

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streptococcal

GABHS (group A beta hemolytic streptococcus)

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e.coli

found usually in colon / some strains more virulent

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c.diff

forms spores / ingested spores germinate in small/large intestine

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local signs of inflammation

redness/heat/swelling

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systemic signs of inflammation

lymphadenopathy/fever/lymphadenitis

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T cells types

killer (CD8) helper (CD4) suppressor

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T cells role

CD8- attack antigen CD4- activate other parts of of immune system

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B cells role

produce antibodies (immunoglobin)

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types of immunity

natural active artificial active natural passive artificial passive

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natural active immunity

history of disease

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artificial active immunity

vaccinations

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natural passive immunity

antibodies passed from mom to baby

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artificial passive immunity

antibodies rejected (sick person gets antibodies from healthy person)

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ways to boost immune system

eat healthy sleep 8-9 hours a night increased fluid reduce stress time outside

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main components of hypersensitivity

over response to antigen inflammation damages healthy tissue

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anaphylaxis causes

serums latex nuts, milk, eggs penicillin (most important)

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anaphylaxis symptoms

impending doom lump in throat stomach cramps swelling of tongue

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what is happening with autoimmune diseases?

body/immune system attack self

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remissions and exacerbations

periods of time where disease is less or more present in body (affecting signs and symptoms)

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causes of immunodeficiency

usually from single gene defect present at birth defective thymus development more than 70 types ID'd

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primary immunodeficiency groups

b-lymphocyte t-lymphocyte combined b&t complement phagocytic

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b-lymphocyte deficiencies

t-cells have to work overtime lower circulating immunoglobins

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t-lymphocyte deficiencies

yeast infections in mouth/genitals

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combined b&t deficiencies

SCID - sever combined immunodeficiency disease varying ranges

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complement deficiency

recurrent infections - w/ encapsulated bacteria

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phagocytic deficiency

unable to kill/remove bacteria effectively

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secondary immunodeficiency causes

pregnancy emotional trauma malnutrition burns malignancies

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HIV - what is happening

RNA converts DNA and replicates w/ CD4 DNA to spread virus

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HIV vs AIDS

HIV is a virus while AIDS is a condition (acute vs chronic)

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active AIDS symptoms

severe weight loss perineal lesions

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how is AIDS transmitted

blood/blood products intravenous drug abuse hetero and homosexual activity (most common) mom to baby during birth

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iron deficiency anemia

small RBC's with reduced hemoglobin

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iron deficiency anemia causes

blood loss of 2-4 mL/day most common anemia kids <2 (d/t iron needs with growth)

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pathological development of ID anemia

stage 1: body stores of iron are depleted stage 2: not enough iron transported to marrow stage 3: begins w/ small HGB deficient cells enter circulation in sufficient #'s and replace normal cells as they age and are removed from circulation

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ID anemia symptoms

HGB drops below 7-8 (normal 12-18) fatigue shortness of breath pale earlobes

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pernicious anemia

anemia related to B12 malabsorption and large RBC's

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pernicious anemia causes

congenital partial/complete removal of stomach chronic atrophic gastritis

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pernicious anemia symptoms

infections mood swings GI, cardiac, kidney ailments

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how are B12 and intrinsic factor associated with pernicious anemia

intrinsic factor is required for the absorption of B12 if intrinsic factor is absent or non functioning (as in pernicious anemia) absorption of B12 cannot occur

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sickle cell anemia

presence of abnormal HGB within RBC's

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sickle cell anemia causes

genetic mutation autosomal recessive disorder inherited

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sickle cell anemia symptoms

pallor fatigue jaundice irritability

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hemolytic anemia

premature, accelerated destruction of erythrocytes

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hemolytic anemia causes

acquired: caused by infection/drugs or toxins/liver disease hereditary: abnormalities of RBC membrane/present at birth

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hemolytic anemia symptoms

more hemolysis = more symptoms jaundice bone deformities from expansion of hematopoietic bone marrow

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aplastic anemia

normal sized RBC and HGB - just insufficient

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aplastic anemia causes

bone marrow hypoplasia pancytopenia 50% of cases - idiopathic

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aplastic anemia symptoms

pallor frequent mild infections petechiae nose bleeds excessive menstruation bleeding

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who is at risk for the various anemias?

sickle cell: African American's pernicious: English, Scandinavian, and Irish

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polycythemia vera

over production of RBC's

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what is happening with polycythemia vera?

increase in blood volume, viscosity, and hyper-coagulation

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polycythemia vera signs and symptoms

cyanotic or plethoric skin increased blood pressure tachycardia dyspnea headache unique: intense painful itching that appears to intensify with heat

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infectious mononucleosis

acute infection of B-cells has an incubation period of 30-50 days so it can be spread without knowing it

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infectious mononucleosis causes

spread through saliva (kissing disease) mostly caused by Epstein-Barr virus

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infectious mononucleosis symptoms

pharyngitis lymphadenopathy enlarged spleen dysphagia malaise

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leukemia

uncontrolled proliferation of leukocytes

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risk factors for leukemia

exposure to chemicals viral mutations ionizing radiation immunodeficiency disorders

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leukemia types

ALL AML CLL CML

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ALL acute lymphocytic leukemia

affects primarily children responds to therapy good prognosis

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AML acute myelogenous leukemia

affects primarily adults responds okay to treatment prognosis somewhat worse than ALL most common adult leukemia

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CLL chronic lymphocytic leukemia

responds poorly to treatment slow progression 2:1 males affects 70+

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