Patho Inflamation/immune/hiv/aids

Front 1

Erythrocytes

Back 1

Red Blood Cells
Concave-->large surface-to-volume ratio, transport gases

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Erythropoietin

Back 2

low blood O2 levels-->kidneys produce erythropoietin (hormone)-->signals bone marrow-->RBC production

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Leukocytes

Back 3

White blood cells: Granulocytes, Monocytes, Basophils

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Granulocytes

Back 4

Neutrophils, Eosinophils, Basophils

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Lymphocytes

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B & T Cells - Antibodies; immune production; raise w/viral infections

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Neutrophils

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Protect against bacteria, fungal infections - die within 1-2 days

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Eocinophils

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Parasites, allergies; fight inflamation

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Basophils

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Histamine-->vasodilatation-->increased capillary permeability-->release Heparin & bradykinin.

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Agranulycytosis

Back 9

no granuloycytes due to drug suppression of bone marrow

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Thrombocytes

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Platelets; fragments of cells

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Anemia

Back 11

Decrease in quantity or quality of RBC's leading to hypoxia

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Causes of Anemia

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blood loss, damage or destruction (lysis) of RBC's -

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Signs/Symptoms of Anemia

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Decreased hematocrit & HBF,
Pallor, tachacardia, Angina, CHF, Dyspnia, Headache, Dizziness, Tinnitus, A-N-C-D, hypoxia

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Tachacardia

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Fast heart rate - more than 100
Normal is 60-100

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Angina

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Chest Pain

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CHF

Back 16

Congestive heart failure

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Dyspnea

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shortness of breath

Front 18

Three indications of decreased BF to CNS

Back 18

Headache, Dizziness, Tinnitus

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A-N-C-D

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Anorexia, Nausea, Constipation, Diarrhea

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Hypoxia

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Decreased oxygenation-->
Increases erythpoietin secretion-->bone pain in iliac crest or sternum

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ends in "cytic"

Back 21

refers to cell size

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ends in "chromic"

Back 22

refers to hemoglobin content (also color)

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microcytic

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below 81; normal is 81-96; iron deficient = small RBC

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macrocytic

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too large; deficient in Vit B-12

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hypo-chromic

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pale; too little hemoglobin

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hyper-chromic

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too much hemoglobin

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Slow chronic bleed

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continuous period; ulcers - too much aspirin

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megaloblasts

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Abnormally large stem cells-->erythrocytes too large in thickness & volume

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Newborn Anemia

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megaloblastic; B-12 deficiency, deficiency in intrinsic factor

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Intrinsic factor

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protein produced by parietal cells of stomach, needed to absorb Vit B-12

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Polycythemia

Back 31

Increase in number of RBC's

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Clinical manifestations of polycythemia

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Headache, Dizziness, Weakness, Increased BP, Itching/Sweating

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Primary polycythemia (vera)

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Cause unknown; increase in platelets & bone marrow cells
Benign tumor of marrow-->increased # of stem cells-->RBC's & spleenomeglia

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spleenomeglia

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enlarged spleen

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Secondary polycythemia

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chronic hypoxia-->overproduction of erythropoietin-->stimulates bone marrow-->development of thrombosis because of thick blood

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S/S secondary polycythemia

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Red complexion- ruddy face, bloodshot eyes, sense of fullness in head (more blood circulating), unable to concentrate, itching in fingers and toes (due to viscosity).

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Who is at risk for Secondary polycythemia?

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Persons in high altitudes, smokers, COPD patients, Congestive heart failure patients

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COPD

Back 38

two disease processes:
Chronic bronchitis and emphysema-->elevated HBG & HTC

Front 39

HbG

Back 39

Glycated hemoglobin (HbG) concentration is a retrospective measure of mean blood glucose

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HCT

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Hematocrit is a blood test that measures the number of red blood cells and the size of red blood cells. It gives a percentage of red blood cells found in whole blood. This test is almost always ordered as part of a complete blood count.

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BANDS

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immature neutrophils

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SEGS

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mature neutrophils

Front 43

left shift

Back 43

more bands=more "baby" white cells-->body is trying to fight off very active actue infection

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right shift

Back 44

more segs than bands = chronic infection

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Immune system

Back 45

responds to microroganisms; memory of encounter remains; subsequent encounter = quicker response

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Inflamatory system

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after injury or infection; benificial. Delivers WBC & platelet to tissue-->limit damage -->promote healing

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WBC functions

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protects-->infection, cancer; assist in healing

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WBC types

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Neutophils, basophils, eosinophils

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Neutophils

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1st to arrive-->begins phagocytosis in cells & debris

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Eosinophils

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appears at allergic response sites, protective, ends inflamatory reaction. Defends against parasitic reactions

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Basophils

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releases histamine, bradykinin, seratonin. vasodilation; secrets heparin, allergic responses-->simular to mast cells

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B - cell response to antigen

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B-cell binds-->matures-->becomes either plasma or memory cell

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plasma cell

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produces antibodies against antigens, detects in 6 months, 10 mil copies/hour, after primary exposure: 2 weeks to a year. Next exposure: immediate

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Antibodies=immunoglobins
5 specific

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IgG, IgM, IgA, IgE, IgD

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IgG

Back 55

IgG - most common (80%),crosses placenta-->transfers immunity

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IgG protections and deficeincies

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protects: bacteria, virus, toxins
deficiencies :URI, OM, sinusitis, pneumonia

Front 57

IgM

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largest antibody, produced first, higher concentration during 1st exposure; 1st MADE in newborn

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IgA

Back 58

secretions: saliva, breastmilk, vaginal mucus, GI, lung, semen

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IgM prevention

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local (not systemic), prevents attachement of virus, bacteria to epithelial cell

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IgA defiencies

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URI, GI infection, allergies, asthma, autoimmune, malignancies; self corrected by age 14

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IgE

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resposible for allergic reactions, stimulated during parasitic infection, combats inflammation. allergy binding of antigen-->histamine and other mediators. Activates mast cells and eosinophils.

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IgD

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function not clear, low concentration in plasma, elevated in cronic infections, serves as an antigen receptor-->initiating B cell differentiation

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memory cells

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B cells-->memory cells--> always circulates, new exposure to antigen-->immed. activation-->rapid immune response

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Direct immunoglobin destruction of a microorganism

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antigen binds via Fab portion antibody-->circulation;or to agglutinate with other complexes, Fab binding inactiviates antigen if site is same as micro-organism uses to bind to host

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Indirect immunoglobin destruction of a micro-organism

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Fc portion activated-->imflammatory reaction, complement and macrophage activity and phagocytosis

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histocompatibility(HLA)

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unique, fingerprint, inherited, same in twins, poor match=graft rejection.

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RBC antigens

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mismatch bet. mother and fetus, RBC lysis and anemia; Rh- mom Rh+, Rhogam

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Immune reactions against mismatch blood

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s/s inflammation, blood clotting (renal thrombosis), death; O=universal donor. AB=universal recipient

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Innate immunity

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species immunity, present at birth, physical barriers include-->skin, cough, mucus membranes.

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passive immunity

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short-term, IgG, transfered through placenta, IgA transferred through breast milk,

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active immunity

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aquired, cellular and humoral response, after exposure to micro-organsim or toxin(disease or immunization), memory in B and T cells.

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primary humoral immunity

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B lymphocytes-->plasma cells-->antibodies, when antigen introduced lag period before dectection of anitbodies

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secondary humoral immunity

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B lymphocytes-->plasma cells-->antibodies, rise in antibodies is rapid, higher level due to memory cells

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cell mediated immunity

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production against virus, cancer cells, T cell action, and macrophages,

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Complement system

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primary mediator, enables body to produce inflammation and localize infection

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immune status of fetus and newborn

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T cell immunity begins in utero, T cell immunodifieciency = Digeorge syndrome. antibody titler measured after 6 months=identification of true infection vs passive immunity, anit-HIV IgA indicates active immunity in non-breastfeeding infant

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inflammatory response=vascular

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injury/infection-->immediate, dialation=raised BF, raised BP, raised plasma -->interstitual place=swelling, release of histamine

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inflammatory response=cellular

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begins after rasided BF--> WBCs and platletes--> capallaries-->phagocytosis of dead cells-->clotting

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release of histamine and bradykinin

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raised capallary permablilty=endothelial cells surrounding capalliries pull apart, vasodiliation, bronchiolar constriction to smooth muscles and causes itching

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mast cell

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inflammation due to rupture cell releases histamine

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prostaglandins

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raises BF and capallary permeabilty, stimulates pain receptors. synthesis blocked by non-steroidal anti-inflammatory drugs including ASA-->too much= renal damage

Front 82

leukotrienes

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raises vascular permeability

Front 83

inflammatory exudates

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serous=plasma, fibrinous=fibrogen/thick mesh like, membranous=necrotic cells in fibrinopurulent exudate

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bradykinin

Back 84

pain, acts like histomine and prostoglandins

Front 85

cytokines

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regulates immune response aka immunotransmitters, released by WBCs, act as hormones-->stimulation of other immune cells-->increase/activate during infection/inflammation

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interleukin-1

Back 86

cytokine that mediates inflammation, 2nd signal in CD-4 activiation; tumor necrosis factor

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interleukin-2

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cytokine needed for proliferation and function of T helper, Cytotoxic T, B, and NK cells

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interferrons

Back 88

cytokine; proteins released by cells that are infected by virus, protects other cells-->interfer with viral replication-->activate immune system

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Tumor necrosis factor

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cytokine; induces fever, sleep. responsible for tissue wasting during cronic inflammation.

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Local characteristics of inflamation - 5 signs

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Redness - raised BF
Heat - raised BF
Swelling - raised cap. perm.
Pain - stretching of nerves due to swelling
Altered function - because of pain/swelling

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Fever - Systemic characteristics

Back 91

elevation of set point-->hypothalamus-->shivering-->raised BMR (interluekin 1 released by neutrophils, macrophages & injured cells)

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Interleukin-1
Systemic characteristics

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prostaglandin-->hypothalamus-->fever. ASA & NSAIDS-->inhibit prostaglandins-->block fever

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Leukocytosis

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raised WBC's. Prolonged infection-->immature neutrophils (myloid cells)-->left shift; righ shift when infection lowers and mature cells released

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Chronic inflamation

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Longer than 2 weeks following acute, unresolved infection; wound. Infections walled off (TB, leprosy)-->granuloma

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Factors affection inflamation and healing

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poor circulation - diabetes
persistent infection
bone depression (lower WBC)
immuno-depressed patients
steroids
nutritional deficiencies

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Type 1 hypersensitivity

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allergic - IgE antigen-->histamine-->vasodilation-->swelling-->bronchial constriction

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Type 1 hypersensitivity symptoms

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specific to tissue:
nose-->congestion, hay fever, allergies hives.
GI-->darrhea, vomiting

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type 1 hypersensitivity - severe anaphlactic reaction

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exposure to antigen-->rapid IgE-->histamine-->vasodilation-->lower BP-->tissue perfusion-->closure of respiratory.
Itching, abdominal cramps, flushing, GI upset.

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Type 2 hypersensitivity

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Cytotoxic Autoimmune reactions
IgG or IgM-->edema-->lysis-->phagocytosis

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Autoimmune Hemolytic anemia

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Type 2 hypersensitivity
against thyroid

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Autoimmune hemolytic anemia

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Type 2 hypersensitivity against RBC's
Transfusions against donor cells

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Autoimmune thrombcytopenic purpura

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Type 2 hypersensitivity against platelets = bleeding

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Good pasteur's syndrome

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type 2 hypersensitivity against renal/lung tissue; associated w/flu, smoking.

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hemoptysis

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coughing up blood

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Type 3 reactions

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Immune complex - occurs when antibody-antigen precipitate out of BV-->activates mast cells

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Serum Sickness

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Type 3 reaction - eg: IV drug use-->injection of foreign material-->antibodies form-->inflammation

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Vasculitis

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Type 3 reaction --> inflammation of vascular bed; seen in SLE (systemic lupis) - Acute glomerulonephritis

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Glomerulonephritis

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Type 3 reaction - Antigen-antibody complex-->deposits in vascular bed, joints, kidneys, in response to infection (usually strep)

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Systemic Lupus Erythematosus (SLE)

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type 3 reaction - complexes form against collagen & cellular DNA deposit in multiple sites

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Rheumatoid Arthritis

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Type 3 reaction

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Type 4 reactions

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T-cell mediated reactions - cytotoxic or lymphokine producing T cells activated by antigen-->cell destruction; delayed reaction 24-72 hrs

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Autoimmune Thyroiditis (Hashimoto's disease)

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Type 4 reaction
T-Cells produced against thyroid

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Tissue / graft /tumor reaction

Back 113

Type 4 reaction
Due to specific interaction of T-cellls with antigen

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Delayed allergic reactions

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Type 4 reaction
poison ivy, TB test, multiple sclerosis

Front 115

Allergic Contact Dermatitis

Back 115

Type 4 reaction
Poison ivy, poison oak, dyes

Front 116

Latex allergy

Back 116

delayed 48-96 hours; triggered by latex protein s/s: urticaria, rhino-conjunctivitis, asthma, vesicles

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urticaria

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hives

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Immuno and Inflamatory deficiencies

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Caused by impaired function of any or all WBC's; congenital or acquired; may follow illness, infection, prolonged stress - BODY UNABLE TO RESPOND

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congenital deficiency

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Genetic defect may involve one or all T and B cells; severe causes death in early childhood - DiGeorge Syndrome

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DiGeorge Syndrome

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Impaired thymus, t-lymphocytes Recurrent infection, heart defects, facial features: low set ears, eyes slant downward, underdeveloped chin. Part of Chromosome 22 missing

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Acquired immunodeficiency

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Effects T, B or both cells-->dysfunction o f humoral immune system. Causes: infection, malnutrition, chronic disease, pregnancy; systemic diseases, immunosuppressed radiation, chemo, surgery, anesthesia

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Conditions of elderly related acquired immunodeficiency

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low function of thymus, decreased BF, diabetes, poor nutrition,

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Systemic diseases related acquired immunodeficiency

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diabetes, renal failure, cirrhosis of the liver

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Humoral immune response

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Secreted antibodies (humors=body fluids) by T, B lymphocytes bind to antigens on surface of microbes

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Consequences of immunodeficiency

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unable to fight frequent, unusual infections
B and T-cell deficiency, HIV destroys helper T cells-->can not turn on B-cells

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T-cell deficiency

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viral and yeast infections

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B-cell deficiency

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bacteria

Front 128

Allergy

Back 128

Environmental antigen-->over-stimulation of inflammatory reactions-->multiple IgE antibodies

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Allergen encountered

Back 129

mast cell degranulation
release of histamine
S/S depends on where allergen is encountered

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Causes of allergy

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unclear; genetic predisposition may involve: excessive IgE binding, limited T-suppressor cells, excessive t-helper cells, overexposure to antigens: Infants/children exposet to cigarette smoke-->asthma-->resp allergies

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Allergy - clinical manifestations

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localized swelling, itiching, redness of skin vesicles, hives. GI - cramps, diarrhea. RESP - itchy eyes, runny nose, swelling, congestion/breathing problems

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Allergy complications

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anaphylactic shock - bee stings, may result in death

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allergy diagnosis

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skin tests; serum analysis - raised basophil and eosinophil count

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SLE

Back 134

systemic lupus erythematosus
failure to distinguish self form no-self; chronic autoimmune disease, Type 3. coagulation cascade

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Causes of SLE

Back 135

unknown; genetic tendency for autoimmune disease - low T-suppressor cells, faulty HKA antigen, stress from pregnancy, UV radiation

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S/S, clinical manifestations of SLE

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polyarthralgia, arthritis, fever (from chronic inflammation), butterfly rash, fingertip lesions, sclerosis of fingers, mouth sores, anemia, bleeding, scaling lesions, eye/feet edema

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HLA

Back 137

human leukocyte antigen system

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Polyarthralgia

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joint pain

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Complications of SLE

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renal failure, pericarditis, pleuritis, bronchitis, vasculitis (peripheral & cerebral, CNS - stroke; seizure, personality changes - psychosis (may be related to drugs or disease)

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Tests for SLE

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antinuclear antibodies present 95% of the time may occur on those without the disease
anti-DNA antibodies, protein in urine

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Treatment for SLE

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ASA, NSAIDS, corticosteroides, antimalarial drugs

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monocytes & macrophages

Back 142

circulate in blood-->enter injured tissue; monocytes mature into macrophages

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macrophages

Back 143

large, digest large amounts of debris/bacteria; phagocytize lysed RBC & WBC

Front 144

Reticuloendothelial cell system

Back 144

monocyte-macrophage cell system - colonize skin tissue, lymph nodes, lungs ; remain there for years

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Lymphocytes

Back 145

primary immune cells: B & T cells; specific; memory; derived from cells in lymphoid tissue of spleen, bone marrow, lymph glands, thymus and tonsils

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B lymphocytes

Back 146

comprise humoral immune system; circulate in blood; mature in bone marrow, become active when exposed to specific microorganism or protein

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Actions of B-lymphocytes

Back 147

Eliminated bacterial invaders
neutralize bacterial toxins
prevent viral infection
immediate allergic responses

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T cells

Back 148

cellular immune system; programmed during maturity via thymus gland. Activation-->destroys substance that activated it.

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NK

Back 149

Natural killer cells
large glandular lymphocytes
NEITHER B or T cells
spontaneous-->react to antigen-->lyze targets-->kill virus infected cells, tumor cells & IgG coated cells

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Platelets

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cytoplasmic fragments of special WBC's from bone marrow (not cells)
go to inflamed area-->release serotonin-->increased BF, increased cap perm-->initiate clotting-->isolates/contains infection & prevents blood loss

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Immune response

Back 151

begins when B or T cells bind to foreign cell; hundreds of thousands produced during fetal development-->bid to specific protein: bacterium, mycoplasma, virus coat, pollens, dusts, food. Every cell on/on a person has surface proteins that recognize foreign B/T cells from another person

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Antigen

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Protein that binds with B or T cell; immunogenic antigen causes B or T cell activation-->multiply or differentiate-->immune response

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5 T-cell subtypes

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Cytotoxic T cells
Delayed Hypersensitivity cells
Helper T cells
Suppressor T cells
Memory Cells

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Cytotoxic T cells

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Killer cells - CD8
Destroy antigen via release chemicals-->punch hole in cell

Front 155

Delayed Hypersensitivity cells

Back 155

stimulate inflammatory cells; eg: macrophages-->release lymphokines

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Helper T cells

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T4 cells CD 4 - master switch for immune system
Secrete chemicals-->stimulate other t-cells-->stimulate humoral immune response; essential for B-cell destruction of micro-organism

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Suppressor T cells

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stop cell mediated and humoral immune responses. When T cells function poorly, immune reactions become uncontrolled and direct against self antigens. Age=decrease in number and function

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Memory cells

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host responds immediately to next presentation of antigen

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Leukopenia

Back 159

Decreased number of WBC's - all or one

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Causes of leukopenia

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Radiation/chemo, anaphylactic shock, autoimmune disease, SLE, spenomegaly, infections, stress, leukemia, thyroid, cushings

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Leukocytosis

Back 161

Increased WBC's - all or one

Front 162

causes of leukocytosis

Back 162

stressors, disease, anesthesia, excersise pregnancy

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Left shift

Back 163

more bands than segs

Front 164

Right shift

Back 164

more segs than bands

Front 165

Thrombocytopenia

Back 165

Decrease in circulating platelets-->bleeding; hemorrhage

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Thrombocytopenia - causes

Back 166

4 major causes - decrease in platelet production, decrease in life-span of platelets, blood pooling in the spleen, dilution of the bloodstream. Primary - Autoimmune disease
Secondary - various drugs, viral infect, bacterial infect, DIC

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DIC

Back 167

Disseminated intravascular coagulopathy - capillary circulatory blood starts to clot and uses up clotting factors-->hemorrhage

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Thrombocytyosis

Back 168

too much clotting

Front 169

Thrombocytosis - causes

Back 169

Primary -leukemia, polycythemia vera, bone marrow disease
Secondary (short lived) - infection, excersise, stress, ovulation

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Lymphadenopathy

Back 170

swollen lymph glands AKA lymphoid hyperplasia

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Lymphadenopathy - causes

Back 171

proliferation of B & T cells due to infection; regional (localized) or generalized: AIDS

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Lab tests - clotting

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PTT, PT, INR
Bleeding time

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PTT test

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Partial thromboplastin time

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PT test

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Pro times - clotting time

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INR test

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International normalized ratio - keep clotting time longer than normal.
Normal is below 2.0
eg: atrofibulation (chronic) blood clots in atrium & ventricles - give anticoagulants - coumadin;Deep vein thrombosis - keep blood clotting between 2.0 - 3.0;
Mechanical valve - keep blood thinner

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DVT

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Deep vein thrombosis

Front 177

Aplastic anemia

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AKA megablastic - Normalcytic, normalchromic
only RBC's - bone marrow failure, infections

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Normalcytic

Back 178

Normal size

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Normalchromic

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Normal color

Front 180

Aplastic anemia - causes

Back 180

bone marrow disorders, cancer, autoimmune disease, radiation, chemotherapy, renal failure, lack of erythropoietin, B12/folate deficency, toxins, drugs - chloramphenicol

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Aplastic anemia - S/S

Back 181

classic hypoxia symptoms,
decreased hair & skin quality
bleeding, brusing, recurrent infections, poor healing of sores

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Hemolytic Anemia

Back 182

RBC's formed but broken down-->decrease in RBC's but remaining are NORMALCYTIC/NORALCHROMIC; bone marrow can not keep up
Increase in erythropoietin

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Causes of hemolytic anemia

Back 183

Hereditary - genetic predisposition
Acquired - autoimmune response, blood transfusions, infection, systemic disease, drugs, toxins, physical trauma, Sickle cell anemia, malaria, Hemolytic disease of newborn (Rh factor)

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Hemolytic Anemia S/S

Back 184

Classic hypoxia PLUS
fatigue, dypsnia, jaundice - biliruben released-->deposited in skin/eyes

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Sickle cell Anemia

Back 185

Needs 2 copies on gene, one from each parent; defective hemoglobin "S"
Crescent shape not flexible-->trapped in capillaries-->obstruct BF, ischemia (anerobic metabolism)-->infarction; bone and spleen tissue have highest death

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Sickle cell trait

Back 186

Inherited - only 40% hem "S"; ONE defective gene - person is essentially normal

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Sickle cell S/S

Back 187

Intense pain w/vascular occlusion, frequent bacterial infections. splenomeglia

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Sickle cell complications

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Liver dammage, spleen, heart, kidney, retinal (microcirculation), stroke, septicemia (sepsis-->release of histamine)-->death

Front 189

Thalassemias

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Cooley's or Mediterranean anemia - most sever anemia; O2 depletion evidences w/in 1st 6 mos of life; untreated=death w/in a few years.
2 defective genes-->problematic; hetrozygotes=normal

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Thalassemias - S/S

Back 190

Growth retardation, spleenomegla, heptomeglia, bone marrow expansion; Blacks, Asians, Mediterranean

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Malaria

Back 191

Parasitic infection of RBC; Protozan from saliva of mosquito (vector); acute to chronic

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Malaria - patho

Back 192

parasite-->fragile RBC-->hemolysis-->jaundice; liver infected 1st-->RBC's
As RBC's break, parasite is released
Cycle every 72 hrs --> temp spike

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Malaria S/S

Back 193

Chills, fever, headache, heptomeglia, spleenomeglia, jaundice

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Malaria complications

Back 194

hypoglycemia (low blood sugar), respiratory distress, shock, coma

Front 195

Hemolytic disease of the newborn

Back 195

Immune mediated destruction of incompatible blood cells, usually RBC but sometimes WBC (not as severe)

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monocytes

Back 196

remove debris/bacteria/virus via macrophage; CHRONIC INFECTIONS

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Sickle cell crisis

Back 197

RBC's sickle at a rapid rate

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Hypoxia S/S

Back 198

Rapid Breathing, Cyanosis, Poor Coordination, Lethargy,
Executing Poor Judgment, Air Hunger, Dizziness, Headache
Mental and Muscle Fatigue
Nausea, Hot and Cold Flashes
Tingling, Visual Impairment,
Euphoria

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Thrombocytopenia - S/S

Back 199

Petechiae, bleeding bruising, oral blood blisters, fatigue, weakness, pupura

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Petechiae

Back 200

little hemorrhages in the tissue-->flat/red/purple dots-->chest/arms/neck

Front 201

Von Willebrand Disease

Back 201

Inherited; von Willebrand factor-->decreased factor VIII-->Factor X not triggered in cascade-->Defect in platelet functions.

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Von Willebrand disease - S/S

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Hemophilia - missing of clot factors-->bleeding

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Hemophilia A

Back 203

Decrease in factor VIII-->does not trigger Factor X-->prevents fibrinogen-->fibrin

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Hemophilia B

Back 204

Decreased factor IX-->does not trigger Factor X-->prevents fibrinogen-->fibrin

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Hemophilia C

Back 205

Factor XI does not coagulate -Mild - different from B & A because it does not lead to bleeding in the joints

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DIC causes

Back 206

Precipitated by an initial disease response: trauma, infections, pregnance, burns, emboli, carcinomas, heat stroke, snakebites, shock, cardiac arrest, necrotic situations, blood transfusion reactions, transplant rejection, liver necrosis, cirrhosis, fat emboli

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DIC S/S

Back 207

Dysrhythmias - clots in artieries, cynotic, absent/unequal pulses, Hypoxia, respiratory distress, aphasia (clot in brain)

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Polycemia vera S/S

Back 208

Headache, dizziness, sensory deficits, chest pain, hypertension, thromboses, splenomeglay, ruddy appearances, dusky lips, clubbing of fingers

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AIDS

Back 209

Viral disease that causes collapse of the immune system; Allergy at one end, AIDS at the other

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HIV

Back 210

Retrovirus, single strand RNA-->enters cell host-->enzymatic actions-->replicate-->mutate-->killing immune system over a period of time
HIV1-US; HIV2-Africa

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How HIV infects cell-->cellular death

Back 211

Infects cells that carry CD4 (surface protein used as a marker) and binds to CD4-->infects T-helper cells, macrophages, blood cells, immune cells of skin, mucous membrane cells

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HIV - where do infected cells accumulate?

Back 212

Lymph nodes, spleen, bone marrow; any cells that pass through can pick up virus

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Which cell does HIV infect first?

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Macrophages; does not kill them but lives there for years-->decades (asymptomatic)

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HIV replication & activation

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Infected T4-helper cells activated-->HIV is reproduced-->destroys cell membrane-->T4-helper cell dies-->infects other cells-->cell mediated immune system is decreased

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T4 Cells

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"master switch"; B cells and macrophages are dependent on them

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HIV course of infection

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Macrophages (initially can remain dormant)->T-cells infected-->T-cell count decreases 200-300 in 2-10 yrs;
(normal is 1000)

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AIDS diagnosis

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T-cell count below 200-->immune system severely compromised/immune suppressed

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AIDS - increase risk for..

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Cancer, dementia, opportunistic infections; defenseless against: bacteria, fungus, protozoans, parasites. As each infection occurs, T-cell count keeps getting lower

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First HIV symptoms

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Fungal infections, shingles, Low T-cell count; eventually severe infections

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HIV contraction

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10-20 % of population that are exposed never get disease (gene coding/resistance)
Presence of virus = contagion
Body fluids - blood, semen, vaginal fluid, breast milk

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Fluids w/HIV present in low concentration

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Urine, GI, Tears, sweat, saliva

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At risk for HIV

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Persons involved in: Blood transfusions, contaminated needles, exposure to semen or vaginal fluids, anal sex, Gay men;
presence of venereal disease increases risk

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HIV infection dependent on:

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Immune system, nutritional status, general health, amount of virus.

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Early Clinical manifestations of HIV

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1st - 4th week after exposure: flu-like symptoms (stimulating immune system), low grade fever, chills;
Symptoms correspond w/antibody production, symptoms go away but virus survives in macrophages and infected cells

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Later clinical manifestations of HIV

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2-10 yrs: opportunistic infections, onset of AIDS. Vaginal and oral yeast infections: Candida, Thrush, chicken pox, shingles, herpes, cytomeglia virus infections, PID - pelvic inflammatory disease

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External factors that effect T-4 level

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Stress, drugs, smoking, alcohol use

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Clinical manifestations/infections associated w/AIDS

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Pneumocystic carinii, pneumonia, respiratory infection, multiple drug resistand TB (spreads to bone and brain) Brain-->headache, motor defectsm seziures, personality changes, dementia, blindness, coma (related to TB), CNS symptoms (brain inflammation), diarrhea (protozoa/bacterial infections, wasting, ulcers, bedsores, various cancers

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Cancers related to AIDS

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Kaposi carcoma - cancer of vascular system: red lesions on skin, lymphocytic leukemia, multiple myloma (bone cancer), colon cancer,

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Diagnostic tests for HIV

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Wait until 6 months after exposure to detect antibodies;
Alesia test - detects antibodies - if positive then Western blot test used to confirm

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Transfusion reaction

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Immune mediated destruction of incompatible blood cells. Most often RBC but sometimes WBC.
Incompatibility between donor and host antigens

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Transfusion reaction - clinical manifestations

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Immediate & life threatening;
Heat in arm, flank pain (kidney), RBC's lyse & block renal tubules-->kidney damage, drop in BP, shock, increased heart-rate, dyspenia; stop blood, don't pull IV line

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Transfusion reaction - complications

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renal failure, anyphatic shock

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Post-hemorrhagic anemia

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Normalcytic, normalchromic
sudden blood loss-->drop in BP-->decrease in tissure profussion-->anerobic-->lactic acid-->stim of SNS:
Shock-->epi & norepi-->rise in BP (due to vasoconstriction;
Kidney profusion ↓kidneys secrete renin→changed to angiotensin 1 & 2 (vasoconstrictor)→stim of aldosterone, tissue profussion↓Brain is most sensitive restlessness, LOC; resp↑ tachypnea

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Post hemorrhagic anemia S/S

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↑HR↑RR ↓BP ↓LOC - fatal if loss exceeds 40-50%

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Post hemorrhagic anemia - treatment

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restore blood volume via IV - Saline, Dextran, Albumin, Plasma, whole blood

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Pernicious Anemia

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Lack of Vit B→not enough HCL, ↓intrinsic factor→malabsorption;

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Causes of pernicious anemia

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Malabsorption diseases, vegetarian, genetic predisposition, age, Drugs, radiation

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Pernicious anemia - S/S

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Weakness (↓RBC), sore tongue (papillae), numbness (extremities), poor coordination, pallor (hypoxia), jaundice of sclera

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Treatment of Pernicious anemia

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V-12 injections

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Folate deficiency

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Macrocytic, normalchromic;
Essential for DNA/RNA synthesis/DNA proofreading enzymes - normally seen in young women & malnourished; absorbed in small intestine (intrinsic factor not needed)

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Folate deficiency - S/S

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Signs of anemia plus malnourishment, glossitis (large, red tongue), diarrhea, anorexia

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Folate deficiency - complications

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If pregnant→neural tube defects

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Iron deficiency anemia

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microcytic, hypochromic - most common among women -
Slow, chronic bleeding. Children-growth demands & ↓ iron

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Iron deficiency anemia S/S

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all signs of anemia & fatigue. Women seek help when hemoglobin is < 8 (normal 12-16)
Pale palms, conjuctiva, earlobes

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Iron deficiency anemia quick check

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pull fingers back, creases should turn red; pull down lower eye lid should be pink, not pale.
Men - could be chronic ulcer or blood in urine

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Sideroblastic Anemia

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Immature RBC's→iron in mitochrondria rather than hemoglobin→abnormal hemoglobin→hypoxia.
Kidneys secrete erythropoietin→RBC production→more immature RBC production→congestion of bone marrow→increased anemia

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Primary sideroblastic anemia

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genetic defect on X chromosome seen primarily in males

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Secondary sideroblastic anemia

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Chemo, lead poisoning

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Clinical manifestations of sideroblastic anemia

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Regular S/S of anemia.
accumulation of iron→hepatomeglia & spleenomeglia

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Mononucleosis

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Acute infection of B lymphyocytes - self limiting - Incorporates into DNA of B cells; children normally build up resistance

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Mononucleosis - causes

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children who did not have exposure when they were young; lack of sleep, poor diet

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Mononucleosis S/S

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sore throat, fever, swollen lymph tissue, spleen, tonsils, lymph notes

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Mononucleosis - complications/testing/treatment

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Hepatisis, meninthtis, encephalitis, Gullain-barre syndrome, EBV.
monospot test shows antibodies to EBV
No aspirin; self-limiting

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Gullian-barre syndrome

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neural disease - paralyzation of body starting w/feet

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Leukemia

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Cancer of one type blood cell in bone marrow - proliferates to the exclusion of others

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Leukemia - risk factors

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Genetic or damaged
Abnormal chromosomes
radiation
chemotherapy
other disease prcesses: hodgkins, multiple myuloma, polycythemia vera, siderblastic anemia

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Leukemia - classifications

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Acute or chronic
And
Myeloid or lymphoid

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Leukemia acute characteristics

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rapid onset, fatigue, pallor, bleeding, fever, frequent infections, bleeding/bruising, anorexia, lymphadopothy, liver and spleen enlargement, headache, vomiting, papilledima (swelling of optic nerve), facial palsy, viaual & auditory disturbances, meningeal irritation

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Leukemia - chronic characteristics

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well differentiated, gradual onset myeloblastic or lymphocytic

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Leukemia - chronic course of disease

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Incidence increases after 40 yrs
Chronic phase - 4 yrs
Short accelerated phase 6-12 mos
Terminal blas crisis phase - 3 mos

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Leukemia chronic - initial symptoms

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splenomegaly, extreme fatigue, weight loss, night sweats, low grade fever

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Leukemia - chronic treatment, etc.

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Myeloid or lymphoid
Treat - chemo, bone marrow transplant, non-myyloablative transplant, monoclonal antibodies

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Hodgkin's disease

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Cancer of lymphoid tissures - liver & spleen
common in young male adults
4 classifications based on cell type and if nodular

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Hodgkin's disease - staging

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1 & 2 more easily curable
3 & 4 more difficult
Clonal disorder - one abnormal cell likely B or T
Neoplastic cells are Reed-Stemberg cells - dispersed w/normal lymph tissue

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Hodgkin's disease - S/S & cause

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Painless enlargement of lymph notes - usually in neck & under arms
evening fevers, night sweats, weight loss (advanced stages)
Cause - unknown possibly from reduced T-cell immunity, herpes virus or genetic

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Non-hodgkin's lymphoma

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Cancers of lymph node, spleen, occasionally bone marrow
No Reed-Stemberg cells
Profused t/o lymphatic tissue
Seen in older adults

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Non-hodgkins lymphoma - causes & S/S

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Possible cause - B-cell deficiency;
aggressive - fatal or slow growing
Painless enlargement of lymph notes, spleenomeglia, GI, fever, fatigue, weight loss, back/neck pain w/hyperflexia - irritated menenges

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Multiple myloma

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Bone cancer - clonal disorder
B-lymphocyte cells→proliferation of B and plasma→circulate t/o body→deposit in bone tissue→bone breakdown and inflamation

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Multiple myloma - antibodies produced

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IgA, IgG - by plasma cells
Bence-Jones proteins (antibodies)- monoclonal fragments found in urine

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Multiple myloma - cause, S/S, complications

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Cause - unknown
S/S - bone pain/fracture→high calcium→neurological problems, Recurrent infections due to B-cell function, fatigue
Complications - Bence-Jones proteins deposit in renal tubules→Renal failure