Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
270 Cards in this Set
- Front
- Back
Erythrocytes
|
Red Blood Cells
Concave-->large surface-to-volume ratio, transport gases |
|
Erythropoietin
|
low blood O2 levels-->kidneys produce erythropoietin (hormone)-->signals bone marrow-->RBC production
|
|
Leukocytes
|
White blood cells: Granulocytes, Monocytes, Basophils
|
|
Granulocytes
|
Neutrophils, Eosinophils, Basophils
|
|
Lymphocytes
|
B & T Cells - Antibodies; immune production; raise w/viral infections
|
|
Neutrophils
|
Protect against bacteria, fungal infections - die within 1-2 days
|
|
Eocinophils
|
Parasites, allergies; fight inflamation
|
|
Basophils
|
Histamine-->vasodilatation-->increased capillary permeability-->release Heparin & bradykinin.
|
|
Agranulycytosis
|
no granuloycytes due to drug suppression of bone marrow
|
|
Thrombocytes
|
Platelets; fragments of cells
|
|
Anemia
|
Decrease in quantity or quality of RBC's leading to hypoxia
|
|
Causes of Anemia
|
blood loss, damage or destruction (lysis) of RBC's -
|
|
Signs/Symptoms of Anemia
|
Decreased hematocrit & HBF,
Pallor, tachacardia, Angina, CHF, Dyspnia, Headache, Dizziness, Tinnitus, A-N-C-D, hypoxia |
|
Tachacardia
|
Fast heart rate - more than 100
Normal is 60-100 |
|
Angina
|
Chest Pain
|
|
CHF
|
Congestive heart failure
|
|
Dyspnea
|
shortness of breath
|
|
Three indications of decreased BF to CNS
|
Headache, Dizziness, Tinnitus
|
|
A-N-C-D
|
Anorexia, Nausea, Constipation, Diarrhea
|
|
Hypoxia
|
Decreased oxygenation-->
Increases erythpoietin secretion-->bone pain in iliac crest or sternum |
|
ends in "cytic"
|
refers to cell size
|
|
ends in "chromic"
|
refers to hemoglobin content (also color)
|
|
microcytic
|
below 81; normal is 81-96; iron deficient = small RBC
|
|
macrocytic
|
too large; deficient in Vit B-12
|
|
hypo-chromic
|
pale; too little hemoglobin
|
|
hyper-chromic
|
too much hemoglobin
|
|
Slow chronic bleed
|
continuous period; ulcers - too much aspirin
|
|
megaloblasts
|
Abnormally large stem cells-->erythrocytes too large in thickness & volume
|
|
Newborn Anemia
|
megaloblastic; B-12 deficiency, deficiency in intrinsic factor
|
|
Intrinsic factor
|
protein produced by parietal cells of stomach, needed to absorb Vit B-12
|
|
Polycythemia
|
Increase in number of RBC's
|
|
Clinical manifestations of polycythemia
|
Headache, Dizziness, Weakness, Increased BP, Itching/Sweating
|
|
Primary polycythemia (vera)
|
Cause unknown; increase in platelets & bone marrow cells
Benign tumor of marrow-->increased # of stem cells-->RBC's & spleenomeglia |
|
spleenomeglia
|
enlarged spleen
|
|
Secondary polycythemia
|
chronic hypoxia-->overproduction of erythropoietin-->stimulates bone marrow-->development of thrombosis because of thick blood
|
|
S/S secondary polycythemia
|
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).
|
|
Who is at risk for Secondary polycythemia?
|
Persons in high altitudes, smokers, COPD patients, Congestive heart failure patients
|
|
COPD
|
two disease processes:
Chronic bronchitis and emphysema-->elevated HBG & HTC |
|
HbG
|
Glycated hemoglobin (HbG) concentration is a retrospective measure of mean blood glucose
|
|
HCT
|
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.
|
|
BANDS
|
immature neutrophils
|
|
SEGS
|
mature neutrophils
|
|
left shift
|
more bands=more "baby" white cells-->body is trying to fight off very active actue infection
|
|
right shift
|
more segs than bands = chronic infection
|
|
Immune system
|
responds to microroganisms; memory of encounter remains; subsequent encounter = quicker response
|
|
Inflamatory system
|
after injury or infection; benificial. Delivers WBC & platelet to tissue-->limit damage -->promote healing
|
|
WBC functions
|
protects-->infection, cancer; assist in healing
|
|
WBC types
|
Neutophils, basophils, eosinophils
|
|
Neutophils
|
1st to arrive-->begins phagocytosis in cells & debris
|
|
Eosinophils
|
appears at allergic response sites, protective, ends inflamatory reaction. Defends against parasitic reactions
|
|
Basophils
|
releases histamine, bradykinin, seratonin. vasodilation; secrets heparin, allergic responses-->simular to mast cells
|
|
B - cell response to antigen
|
B-cell binds-->matures-->becomes either plasma or memory cell
|
|
plasma cell
|
produces antibodies against antigens, detects in 6 months, 10 mil copies/hour, after primary exposure: 2 weeks to a year. Next exposure: immediate
|
|
Antibodies=immunoglobins
5 specific |
IgG, IgM, IgA, IgE, IgD
|
|
IgG
|
IgG - most common (80%),crosses placenta-->transfers immunity
|
|
IgG protections and deficeincies
|
protects: bacteria, virus, toxins
deficiencies :URI, OM, sinusitis, pneumonia |
|
IgM
|
largest antibody, produced first, higher concentration during 1st exposure; 1st MADE in newborn
|
|
IgA
|
secretions: saliva, breastmilk, vaginal mucus, GI, lung, semen
|
|
IgM prevention
|
local (not systemic), prevents attachement of virus, bacteria to epithelial cell
|
|
IgA defiencies
|
URI, GI infection, allergies, asthma, autoimmune, malignancies; self corrected by age 14
|
|
IgE
|
resposible for allergic reactions, stimulated during parasitic infection, combats inflammation. allergy binding of antigen-->histamine and other mediators. Activates mast cells and eosinophils.
|
|
IgD
|
function not clear, low concentration in plasma, elevated in cronic infections, serves as an antigen receptor-->initiating B cell differentiation
|
|
memory cells
|
B cells-->memory cells--> always circulates, new exposure to antigen-->immed. activation-->rapid immune response
|
|
Direct immunoglobin destruction of a microorganism
|
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
|
|
Indirect immunoglobin destruction of a micro-organism
|
Fc portion activated-->imflammatory reaction, complement and macrophage activity and phagocytosis
|
|
histocompatibility(HLA)
|
unique, fingerprint, inherited, same in twins, poor match=graft rejection.
|
|
RBC antigens
|
mismatch bet. mother and fetus, RBC lysis and anemia; Rh- mom Rh+, Rhogam
|
|
Immune reactions against mismatch blood
|
s/s inflammation, blood clotting (renal thrombosis), death; O=universal donor. AB=universal recipient
|
|
Innate immunity
|
species immunity, present at birth, physical barriers include-->skin, cough, mucus membranes.
|
|
passive immunity
|
short-term, IgG, transfered through placenta, IgA transferred through breast milk,
|
|
active immunity
|
aquired, cellular and humoral response, after exposure to micro-organsim or toxin(disease or immunization), memory in B and T cells.
|
|
primary humoral immunity
|
B lymphocytes-->plasma cells-->antibodies, when antigen introduced lag period before dectection of anitbodies
|
|
secondary humoral immunity
|
B lymphocytes-->plasma cells-->antibodies, rise in antibodies is rapid, higher level due to memory cells
|
|
cell mediated immunity
|
production against virus, cancer cells, T cell action, and macrophages,
|
|
Complement system
|
primary mediator, enables body to produce inflammation and localize infection
|
|
immune status of fetus and newborn
|
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
|
|
inflammatory response=vascular
|
injury/infection-->immediate, dialation=raised BF, raised BP, raised plasma -->interstitual place=swelling, release of histamine
|
|
inflammatory response=cellular
|
begins after rasided BF--> WBCs and platletes--> capallaries-->phagocytosis of dead cells-->clotting
|
|
release of histamine and bradykinin
|
raised capallary permablilty=endothelial cells surrounding capalliries pull apart, vasodiliation, bronchiolar constriction to smooth muscles and causes itching
|
|
mast cell
|
inflammation due to rupture cell releases histamine
|
|
prostaglandins
|
raises BF and capallary permeabilty, stimulates pain receptors. synthesis blocked by non-steroidal anti-inflammatory drugs including ASA-->too much= renal damage
|
|
leukotrienes
|
raises vascular permeability
|
|
inflammatory exudates
|
serous=plasma, fibrinous=fibrogen/thick mesh like, membranous=necrotic cells in fibrinopurulent exudate
|
|
bradykinin
|
pain, acts like histomine and prostoglandins
|
|
cytokines
|
regulates immune response aka immunotransmitters, released by WBCs, act as hormones-->stimulation of other immune cells-->increase/activate during infection/inflammation
|
|
interleukin-1
|
cytokine that mediates inflammation, 2nd signal in CD-4 activiation; tumor necrosis factor
|
|
interleukin-2
|
cytokine needed for proliferation and function of T helper, Cytotoxic T, B, and NK cells
|
|
interferrons
|
cytokine; proteins released by cells that are infected by virus, protects other cells-->interfer with viral replication-->activate immune system
|
|
Tumor necrosis factor
|
cytokine; induces fever, sleep. responsible for tissue wasting during cronic inflammation.
|
|
Local characteristics of inflamation - 5 signs
|
Redness - raised BF
Heat - raised BF Swelling - raised cap. perm. Pain - stretching of nerves due to swelling Altered function - because of pain/swelling |
|
Fever - Systemic characteristics
|
elevation of set point-->hypothalamus-->shivering-->raised BMR (interluekin 1 released by neutrophils, macrophages & injured cells)
|
|
Interleukin-1
Systemic characteristics |
prostaglandin-->hypothalamus-->fever. ASA & NSAIDS-->inhibit prostaglandins-->block fever
|
|
Leukocytosis
|
raised WBC's. Prolonged infection-->immature neutrophils (myloid cells)-->left shift; righ shift when infection lowers and mature cells released
|
|
Chronic inflamation
|
Longer than 2 weeks following acute, unresolved infection; wound. Infections walled off (TB, leprosy)-->granuloma
|
|
Factors affection inflamation and healing
|
poor circulation - diabetes
persistent infection bone depression (lower WBC) immuno-depressed patients steroids nutritional deficiencies |
|
Type 1 hypersensitivity
|
allergic - IgE antigen-->histamine-->vasodilation-->swelling-->bronchial constriction
|
|
Type 1 hypersensitivity symptoms
|
specific to tissue:
nose-->congestion, hay fever, allergies hives. GI-->darrhea, vomiting |
|
type 1 hypersensitivity - severe anaphlactic reaction
|
exposure to antigen-->rapid IgE-->histamine-->vasodilation-->lower BP-->tissue perfusion-->closure of respiratory.
Itching, abdominal cramps, flushing, GI upset. |
|
Type 2 hypersensitivity
|
Cytotoxic Autoimmune reactions
IgG or IgM-->edema-->lysis-->phagocytosis |
|
Autoimmune Hemolytic anemia
|
Type 2 hypersensitivity
against thyroid |
|
Autoimmune hemolytic anemia
|
Type 2 hypersensitivity against RBC's
Transfusions against donor cells |
|
Autoimmune thrombcytopenic purpura
|
Type 2 hypersensitivity against platelets = bleeding
|
|
Good pasteur's syndrome
|
type 2 hypersensitivity against renal/lung tissue; associated w/flu, smoking.
|
|
hemoptysis
|
coughing up blood
|
|
Type 3 reactions
|
Immune complex - occurs when antibody-antigen precipitate out of BV-->activates mast cells
|
|
Serum Sickness
|
Type 3 reaction - eg: IV drug use-->injection of foreign material-->antibodies form-->inflammation
|
|
Vasculitis
|
Type 3 reaction --> inflammation of vascular bed; seen in SLE (systemic lupis) - Acute glomerulonephritis
|
|
Glomerulonephritis
|
Type 3 reaction - Antigen-antibody complex-->deposits in vascular bed, joints, kidneys, in response to infection (usually strep)
|
|
Systemic Lupus Erythematosus (SLE)
|
type 3 reaction - complexes form against collagen & cellular DNA deposit in multiple sites
|
|
Rheumatoid Arthritis
|
Type 3 reaction
|
|
Type 4 reactions
|
T-cell mediated reactions - cytotoxic or lymphokine producing T cells activated by antigen-->cell destruction; delayed reaction 24-72 hrs
|
|
Autoimmune Thyroiditis (Hashimoto's disease)
|
Type 4 reaction
T-Cells produced against thyroid |
|
Tissue / graft /tumor reaction
|
Type 4 reaction
Due to specific interaction of T-cellls with antigen |
|
Delayed allergic reactions
|
Type 4 reaction
poison ivy, TB test, multiple sclerosis |
|
Allergic Contact Dermatitis
|
Type 4 reaction
Poison ivy, poison oak, dyes |
|
Latex allergy
|
delayed 48-96 hours; triggered by latex protein s/s: urticaria, rhino-conjunctivitis, asthma, vesicles
|
|
urticaria
|
hives
|
|
Immuno and Inflamatory deficiencies
|
Caused by impaired function of any or all WBC's; congenital or acquired; may follow illness, infection, prolonged stress - BODY UNABLE TO RESPOND
|
|
congenital deficiency
|
Genetic defect may involve one or all T and B cells; severe causes death in early childhood - DiGeorge Syndrome
|
|
DiGeorge Syndrome
|
Impaired thymus, t-lymphocytes Recurrent infection, heart defects, facial features: low set ears, eyes slant downward, underdeveloped chin. Part of Chromosome 22 missing
|
|
Acquired immunodeficiency
|
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
|
|
Conditions of elderly related acquired immunodeficiency
|
low function of thymus, decreased BF, diabetes, poor nutrition,
|
|
Systemic diseases related acquired immunodeficiency
|
diabetes, renal failure, cirrhosis of the liver
|
|
Humoral immune response
|
Secreted antibodies (humors=body fluids) by T, B lymphocytes bind to antigens on surface of microbes
|
|
Consequences of immunodeficiency
|
unable to fight frequent, unusual infections
B and T-cell deficiency, HIV destroys helper T cells-->can not turn on B-cells |
|
T-cell deficiency
|
viral and yeast infections
|
|
B-cell deficiency
|
bacteria
|
|
Allergy
|
Environmental antigen-->over-stimulation of inflammatory reactions-->multiple IgE antibodies
|
|
Allergen encountered
|
mast cell degranulation
release of histamine S/S depends on where allergen is encountered |
|
Causes of allergy
|
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
|
|
Allergy - clinical manifestations
|
localized swelling, itiching, redness of skin vesicles, hives. GI - cramps, diarrhea. RESP - itchy eyes, runny nose, swelling, congestion/breathing problems
|
|
Allergy complications
|
anaphylactic shock - bee stings, may result in death
|
|
allergy diagnosis
|
skin tests; serum analysis - raised basophil and eosinophil count
|
|
SLE
|
systemic lupus erythematosus
failure to distinguish self form no-self; chronic autoimmune disease, Type 3. coagulation cascade |
|
Causes of SLE
|
unknown; genetic tendency for autoimmune disease - low T-suppressor cells, faulty HKA antigen, stress from pregnancy, UV radiation
|
|
S/S, clinical manifestations of SLE
|
polyarthralgia, arthritis, fever (from chronic inflammation), butterfly rash, fingertip lesions, sclerosis of fingers, mouth sores, anemia, bleeding, scaling lesions, eye/feet edema
|
|
HLA
|
human leukocyte antigen system
|
|
Polyarthralgia
|
joint pain
|
|
Complications of SLE
|
renal failure, pericarditis, pleuritis, bronchitis, vasculitis (peripheral & cerebral, CNS - stroke; seizure, personality changes - psychosis (may be related to drugs or disease)
|
|
Tests for SLE
|
antinuclear antibodies present 95% of the time may occur on those without the disease
anti-DNA antibodies, protein in urine |
|
Treatment for SLE
|
ASA, NSAIDS, corticosteroides, antimalarial drugs
|
|
monocytes & macrophages
|
circulate in blood-->enter injured tissue; monocytes mature into macrophages
|
|
macrophages
|
large, digest large amounts of debris/bacteria; phagocytize lysed RBC & WBC
|
|
Reticuloendothelial cell system
|
monocyte-macrophage cell system - colonize skin tissue, lymph nodes, lungs ; remain there for years
|
|
Lymphocytes
|
primary immune cells: B & T cells; specific; memory; derived from cells in lymphoid tissue of spleen, bone marrow, lymph glands, thymus and tonsils
|
|
B lymphocytes
|
comprise humoral immune system; circulate in blood; mature in bone marrow, become active when exposed to specific microorganism or protein
|
|
Actions of B-lymphocytes
|
Eliminated bacterial invaders
neutralize bacterial toxins prevent viral infection immediate allergic responses |
|
T cells
|
cellular immune system; programmed during maturity via thymus gland. Activation-->destroys substance that activated it.
|
|
NK
|
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 |
|
Platelets
|
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 |
|
Immune response
|
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
|
|
Antigen
|
Protein that binds with B or T cell; immunogenic antigen causes B or T cell activation-->multiply or differentiate-->immune response
|
|
5 T-cell subtypes
|
Cytotoxic T cells
Delayed Hypersensitivity cells Helper T cells Suppressor T cells Memory Cells |
|
Cytotoxic T cells
|
Killer cells - CD8
Destroy antigen via release chemicals-->punch hole in cell |
|
Delayed Hypersensitivity cells
|
stimulate inflammatory cells; eg: macrophages-->release lymphokines
|
|
Helper T cells
|
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 |
|
Suppressor T cells
|
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
|
|
Memory cells
|
host responds immediately to next presentation of antigen
|
|
Leukopenia
|
Decreased number of WBC's - all or one
|
|
Causes of leukopenia
|
Radiation/chemo, anaphylactic shock, autoimmune disease, SLE, spenomegaly, infections, stress, leukemia, thyroid, cushings
|
|
Leukocytosis
|
Increased WBC's - all or one
|
|
causes of leukocytosis
|
stressors, disease, anesthesia, excersise pregnancy
|
|
Left shift
|
more bands than segs
|
|
Right shift
|
more segs than bands
|
|
Thrombocytopenia
|
Decrease in circulating platelets-->bleeding; hemorrhage
|
|
Thrombocytopenia - causes
|
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 |
|
DIC
|
Disseminated intravascular coagulopathy - capillary circulatory blood starts to clot and uses up clotting factors-->hemorrhage
|
|
Thrombocytyosis
|
too much clotting
|
|
Thrombocytosis - causes
|
Primary -leukemia, polycythemia vera, bone marrow disease
Secondary (short lived) - infection, excersise, stress, ovulation |
|
Lymphadenopathy
|
swollen lymph glands AKA lymphoid hyperplasia
|
|
Lymphadenopathy - causes
|
proliferation of B & T cells due to infection; regional (localized) or generalized: AIDS
|
|
Lab tests - clotting
|
PTT, PT, INR
Bleeding time |
|
PTT test
|
Partial thromboplastin time
|
|
PT test
|
Pro times - clotting time
|
|
INR test
|
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 |
|
DVT
|
Deep vein thrombosis
|
|
Aplastic anemia
|
AKA megablastic - Normalcytic, normalchromic
only RBC's - bone marrow failure, infections |
|
Normalcytic
|
Normal size
|
|
Normalchromic
|
Normal color
|
|
Aplastic anemia - causes
|
bone marrow disorders, cancer, autoimmune disease, radiation, chemotherapy, renal failure, lack of erythropoietin, B12/folate deficency, toxins, drugs - chloramphenicol
|
|
Aplastic anemia - S/S
|
classic hypoxia symptoms,
decreased hair & skin quality bleeding, brusing, recurrent infections, poor healing of sores |
|
Hemolytic Anemia
|
RBC's formed but broken down-->decrease in RBC's but remaining are NORMALCYTIC/NORALCHROMIC; bone marrow can not keep up
Increase in erythropoietin |
|
Causes of hemolytic anemia
|
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) |
|
Hemolytic Anemia S/S
|
Classic hypoxia PLUS
fatigue, dypsnia, jaundice - biliruben released-->deposited in skin/eyes |
|
Sickle cell Anemia
|
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 |
|
Sickle cell trait
|
Inherited - only 40% hem "S"; ONE defective gene - person is essentially normal
|
|
Sickle cell S/S
|
Intense pain w/vascular occlusion, frequent bacterial infections. splenomeglia
|
|
Sickle cell complications
|
Liver dammage, spleen, heart, kidney, retinal (microcirculation), stroke, septicemia (sepsis-->release of histamine)-->death
|
|
Thalassemias
|
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 |
|
Thalassemias - S/S
|
Growth retardation, spleenomegla, heptomeglia, bone marrow expansion; Blacks, Asians, Mediterranean
|
|
Malaria
|
Parasitic infection of RBC; Protozan from saliva of mosquito (vector); acute to chronic
|
|
Malaria - patho
|
parasite-->fragile RBC-->hemolysis-->jaundice; liver infected 1st-->RBC's
As RBC's break, parasite is released Cycle every 72 hrs --> temp spike |
|
Malaria S/S
|
Chills, fever, headache, heptomeglia, spleenomeglia, jaundice
|
|
Malaria complications
|
hypoglycemia (low blood sugar), respiratory distress, shock, coma
|
|
Hemolytic disease of the newborn
|
Immune mediated destruction of incompatible blood cells, usually RBC but sometimes WBC (not as severe)
|
|
monocytes
|
remove debris/bacteria/virus via macrophage; CHRONIC INFECTIONS
|
|
Sickle cell crisis
|
RBC's sickle at a rapid rate
|
|
Hypoxia S/S
|
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 |
|
Thrombocytopenia - S/S
|
Petechiae, bleeding bruising, oral blood blisters, fatigue, weakness, pupura
|
|
Petechiae
|
little hemorrhages in the tissue-->flat/red/purple dots-->chest/arms/neck
|
|
Von Willebrand Disease
|
Inherited; von Willebrand factor-->decreased factor VIII-->Factor X not triggered in cascade-->Defect in platelet functions.
|
|
Von Willebrand disease - S/S
|
Hemophilia - missing of clot factors-->bleeding
|
|
Hemophilia A
|
Decrease in factor VIII-->does not trigger Factor X-->prevents fibrinogen-->fibrin
|
|
Hemophilia B
|
Decreased factor IX-->does not trigger Factor X-->prevents fibrinogen-->fibrin
|
|
Hemophilia C
|
Factor XI does not coagulate -Mild - different from B & A because it does not lead to bleeding in the joints
|
|
DIC causes
|
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
|
|
DIC S/S
|
Dysrhythmias - clots in artieries, cynotic, absent/unequal pulses, Hypoxia, respiratory distress, aphasia (clot in brain)
|
|
Polycemia vera S/S
|
Headache, dizziness, sensory deficits, chest pain, hypertension, thromboses, splenomeglay, ruddy appearances, dusky lips, clubbing of fingers
|
|
AIDS
|
Viral disease that causes collapse of the immune system; Allergy at one end, AIDS at the other
|
|
HIV
|
Retrovirus, single strand RNA-->enters cell host-->enzymatic actions-->replicate-->mutate-->killing immune system over a period of time
HIV1-US; HIV2-Africa |
|
How HIV infects cell-->cellular death
|
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
|
|
HIV - where do infected cells accumulate?
|
Lymph nodes, spleen, bone marrow; any cells that pass through can pick up virus
|
|
Which cell does HIV infect first?
|
Macrophages; does not kill them but lives there for years-->decades (asymptomatic)
|
|
HIV replication & activation
|
Infected T4-helper cells activated-->HIV is reproduced-->destroys cell membrane-->T4-helper cell dies-->infects other cells-->cell mediated immune system is decreased
|
|
T4 Cells
|
"master switch"; B cells and macrophages are dependent on them
|
|
HIV course of infection
|
Macrophages (initially can remain dormant)->T-cells infected-->T-cell count decreases 200-300 in 2-10 yrs;
(normal is 1000) |
|
AIDS diagnosis
|
T-cell count below 200-->immune system severely compromised/immune suppressed
|
|
AIDS - increase risk for..
|
Cancer, dementia, opportunistic infections; defenseless against: bacteria, fungus, protozoans, parasites. As each infection occurs, T-cell count keeps getting lower
|
|
First HIV symptoms
|
Fungal infections, shingles, Low T-cell count; eventually severe infections
|
|
HIV contraction
|
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 |
|
Fluids w/HIV present in low concentration
|
Urine, GI, Tears, sweat, saliva
|
|
At risk for HIV
|
Persons involved in: Blood transfusions, contaminated needles, exposure to semen or vaginal fluids, anal sex, Gay men;
presence of venereal disease increases risk |
|
HIV infection dependent on:
|
Immune system, nutritional status, general health, amount of virus.
|
|
Early Clinical manifestations of HIV
|
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 |
|
Later clinical manifestations of HIV
|
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
|
|
External factors that effect T-4 level
|
Stress, drugs, smoking, alcohol use
|
|
Clinical manifestations/infections associated w/AIDS
|
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
|
|
Cancers related to AIDS
|
Kaposi carcoma - cancer of vascular system: red lesions on skin, lymphocytic leukemia, multiple myloma (bone cancer), colon cancer,
|
|
Diagnostic tests for HIV
|
Wait until 6 months after exposure to detect antibodies;
Alesia test - detects antibodies - if positive then Western blot test used to confirm |
|
Transfusion reaction
|
Immune mediated destruction of incompatible blood cells. Most often RBC but sometimes WBC.
Incompatibility between donor and host antigens |
|
Transfusion reaction - clinical manifestations
|
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 |
|
Transfusion reaction - complications
|
renal failure, anyphatic shock
|
|
Post-hemorrhagic anemia
|
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 |
|
Post hemorrhagic anemia S/S
|
↑HR↑RR ↓BP ↓LOC - fatal if loss exceeds 40-50%
|
|
Post hemorrhagic anemia - treatment
|
restore blood volume via IV - Saline, Dextran, Albumin, Plasma, whole blood
|
|
Pernicious Anemia
|
Lack of Vit B→not enough HCL, ↓intrinsic factor→malabsorption;
|
|
Causes of pernicious anemia
|
Malabsorption diseases, vegetarian, genetic predisposition, age, Drugs, radiation
|
|
Pernicious anemia - S/S
|
Weakness (↓RBC), sore tongue (papillae), numbness (extremities), poor coordination, pallor (hypoxia), jaundice of sclera
|
|
Treatment of Pernicious anemia
|
V-12 injections
|
|
Folate deficiency
|
Macrocytic, normalchromic;
Essential for DNA/RNA synthesis/DNA proofreading enzymes - normally seen in young women & malnourished; absorbed in small intestine (intrinsic factor not needed) |
|
Folate deficiency - S/S
|
Signs of anemia plus malnourishment, glossitis (large, red tongue), diarrhea, anorexia
|
|
Folate deficiency - complications
|
If pregnant→neural tube defects
|
|
Iron deficiency anemia
|
microcytic, hypochromic - most common among women -
Slow, chronic bleeding. Children-growth demands & ↓ iron |
|
Iron deficiency anemia S/S
|
all signs of anemia & fatigue. Women seek help when hemoglobin is < 8 (normal 12-16)
Pale palms, conjuctiva, earlobes |
|
Iron deficiency anemia quick check
|
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 |
|
Sideroblastic Anemia
|
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 |
|
Primary sideroblastic anemia
|
genetic defect on X chromosome seen primarily in males
|
|
Secondary sideroblastic anemia
|
Chemo, lead poisoning
|
|
Clinical manifestations of sideroblastic anemia
|
Regular S/S of anemia.
accumulation of iron→hepatomeglia & spleenomeglia |
|
Mononucleosis
|
Acute infection of B lymphyocytes - self limiting - Incorporates into DNA of B cells; children normally build up resistance
|
|
Mononucleosis - causes
|
children who did not have exposure when they were young; lack of sleep, poor diet
|
|
Mononucleosis S/S
|
sore throat, fever, swollen lymph tissue, spleen, tonsils, lymph notes
|
|
Mononucleosis - complications/testing/treatment
|
Hepatisis, meninthtis, encephalitis, Gullain-barre syndrome, EBV.
monospot test shows antibodies to EBV No aspirin; self-limiting |
|
Gullian-barre syndrome
|
neural disease - paralyzation of body starting w/feet
|
|
Leukemia
|
Cancer of one type blood cell in bone marrow - proliferates to the exclusion of others
|
|
Leukemia - risk factors
|
Genetic or damaged
Abnormal chromosomes radiation chemotherapy other disease prcesses: hodgkins, multiple myuloma, polycythemia vera, siderblastic anemia |
|
Leukemia - classifications
|
Acute or chronic
And Myeloid or lymphoid |
|
Leukemia acute characteristics
|
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
|
|
Leukemia - chronic characteristics
|
well differentiated, gradual onset myeloblastic or lymphocytic
|
|
Leukemia - chronic course of disease
|
Incidence increases after 40 yrs
Chronic phase - 4 yrs Short accelerated phase 6-12 mos Terminal blas crisis phase - 3 mos |
|
Leukemia chronic - initial symptoms
|
splenomegaly, extreme fatigue, weight loss, night sweats, low grade fever
|
|
Leukemia - chronic treatment, etc.
|
Myeloid or lymphoid
Treat - chemo, bone marrow transplant, non-myyloablative transplant, monoclonal antibodies |
|
Hodgkin's disease
|
Cancer of lymphoid tissures - liver & spleen
common in young male adults 4 classifications based on cell type and if nodular |
|
Hodgkin's disease - staging
|
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 |
|
Hodgkin's disease - S/S & cause
|
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 |
|
Non-hodgkin's lymphoma
|
Cancers of lymph node, spleen, occasionally bone marrow
No Reed-Stemberg cells Profused t/o lymphatic tissue Seen in older adults |
|
Non-hodgkins lymphoma - causes & S/S
|
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 |
|
Multiple myloma
|
Bone cancer - clonal disorder
B-lymphocyte cells→proliferation of B and plasma→circulate t/o body→deposit in bone tissue→bone breakdown and inflamation |
|
Multiple myloma - antibodies produced
|
IgA, IgG - by plasma cells
Bence-Jones proteins (antibodies)- monoclonal fragments found in urine |
|
Multiple myloma - cause, S/S, complications
|
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 |