Term
The body produces acid in 2 forms |
|
Definition
oVolatile carbonic acid, H2CO3: 20,000 mEq/day
oFixed, non-volatile organic acids (uric, lactic, etc): 30-80 mEq/day |
|
|
Term
|
Definition
|
|
Term
MECHANISMS of ACID-BASE REGULATION
oThe Buffer System |
|
Definition
oBicarbonate, hemoglobin,phosphate, protein etc.
oWorks within seconds (ECF) to hours (ICF): Most efficient |
|
|
Term
MECHANISMS of ACID-BASE REGULATION
|
|
Definition
oExcess H2CO3 is excreted as CO2
oWorks within minutes |
|
|
Term
MECHANISMS of ACID-BASE REGULATION
oThe Renal System
|
|
Definition
oExcretes bicarbonate and fixed acids
oRequires hours to days |
|
|
Term
| METABOLIC ACID-BASE IMBALANCES |
|
Definition
oInitially caused by gain or loss of H+ or HCO3-:
oMetabolic acidosis
oMetabolic alkalosis
oCompensation: pulmonary system |
|
|
Term
| RESPIRATORY ACID-BASE IMBALANCES |
|
Definition
oInitially caused by a rise or fall in PCO2:
oRespiratory acidosis
oRespiratory alkalosis
oCompensation: renal system |
|
|
Term
| Common causes of METABOLIC ACIDOSIS |
|
Definition
oIncrease in Acid
oIngestion, production, infusion of a fixed acid
oKetoacidosis (diabetes, malnutrition, etc.)
oDecreased renal excretion of H+
oDecrease in Base
oLoss of bicarbonate or other bases from ECF
oTrue metabolic acidosis:
oAccumulation of lactic acid
oRespiratory compensation: Kussmaul breathing |
|
|
Term
| Common causes of METABOLIC ALKALOSIS |
|
Definition
oIncrease in Base
oIngestion, infusion, or excessive renal absorption of bases (e.g. bicarbonate): ulcer treatment with antacids
oDecrease in Acid
oExcessive loss of fixed acids (vomiting, gastric suctioning, etc.)
oRespiratory compensation: hypoventilation |
|
|
Term
| Common causes of RESPIRATORY ACIDOSIS |
|
Definition
oImpaired Gas Exchange
oRestrictive or obstructive lung disease (COPD’s, pneumonia, asthma, ARDS, etc.)
oImpaired Neuromuscular Function
oInterference with neural transmission to respiratory muscles (Polio, M.D., etc)
oImpaired Respiratory Control (Brainstem)
oDepression of respiratory centers (trauma, drugs, etc.)
Renal compensation: increased excretion of fixed acids (and increased concentration of bicarbonate |
|
|
Term
| Common causes of RESPIRATORY ALKALOSIS |
|
Definition
oCommon causes (C&B, Box 25-4): any dysfunction leading to hyperventilation
oHyperventilation syndrome
oDrugs, hormones, toxic substances
oCNS disease or disorders
oFever
oMechanical overventilation
oAscent to high altitudes
oRenal compensation: decreased excretion of fixed acids |
|
|
Term
|
Definition
o50%of total body weight (females)
o60% of total body weight (males)
oFluid volume decreases with age |
|
|
Term
oIntracellular Compartment Fluid (ICF): |
|
Definition
oVolume: 2/3 of total body fluid volume
Composition: K+, Mg+, HPO4--, proteins |
|
|
Term
oExtracellular Compartment Fluid (ECF): |
|
Definition
oVolume: 1/3 of total body fluid volume
Composition: Na+, Cl-, HCO3-, Ca++
(low in K+, Mg+, HPO4--) |
|
|
Term
|
Definition
| moving of fluid into interstatial space and getting trapped |
|
|
Term
|
Definition
Interstatial(Extravascular)
and
intravascular |
|
|
Term
|
Definition
| The pressure exerted on a differential permeable membrane by a solution containing one or more solute that cannot penetrate the membrane, which is permeable only by the solvent surrounding it. |
|
|
Term
oHydrostatic & oncotic pressures |
|
Definition
The pressure exerted by plasma proteins on the capillary wall.
The pressure pushing from interior of the vessel out |
|
|
Term
Determinants of Body Fluid Distribution
& Concentration |
|
Definition
oOsmosis & osmotic pressure
oHydrostatic & oncotic pressures
oOsmotic = oncotic = colloid osmotic = plasma protein pressures
oFiltration
oFluid concentration:
oOsmolarity, tonicity |
|
|
Term
|
Definition
|
|
Term
|
Definition
opposes hydrostatic pressure
and filtration |
|
|
Term
HYDROSTATIC PRESSURE: SAME
ONCOTIC PRESSURE:SAME |
|
Definition
|
|
Term
HYDROSTATIC PRESSURE: INCREASE
ONCOTIC PRESSURE: SAME |
|
Definition
OUTCOME: EDEMA
EXAMPLE: PURE PORTAL HTN |
|
|
Term
HYDROSTATIC PRESSURE: SAME
ONCOTIC PRESSURE: DECREASES |
|
Definition
OUTCOME: EDEMA
EXAMPLE: LIVER FAILURE |
|
|
Term
HYDROSTATIC PRESSURE: INCREASE
ONCOTIC PRESSURE: DECREASE |
|
Definition
OUTCOME: SEVERE EDEMA
EXAMPLE: LIVER FAILURE W/
PORTAL HTN |
|
|
Term
|
Definition
oVolume imbalances
oConcentration imbalances |
|
|
Term
|
Definition
oPotassium
oCalcium
oMagnesium
oPhosphate |
|
|
Term
|
Definition
(= saline imbalances):
imbalances of extracellular fluid volume, or amount |
|
|
Term
|
Definition
| imbalances (= “water imbalances”): imbalances of body fluid concentration, NOT amount |
|
|
Term
|
Definition
oConcept: removal of Na+ containing isotonic fluid (saline)
from the body.
oEtiology:
oGI excretion of excess saline
oRenal excretion of saline
oOther loss of saline
oClinical findings: wt loss, postural hypotension, dizziness, oliguria |
|
|
Term
|
Definition
oConcept: excessive volume of saline.
oEtiology:
oExcessive IV saline infusion
oRenal retention of Na+ and water
oClinical findings: wt gain, edema, circulatory overload (distended neck veins, rales, dyspnea) |
|
|
Term
CONCENTRATION IMBALANCES:
Hyponatremia |
|
Definition
oEtiology:
oGain of relatively more water than salt
oLoss of relatively more salt than water
oClinical findings: (neuronal swelling): CNS dysfunction (malaise, N&V, headache, confusion, lethargy, seizures, coma), death |
|
|
Term
CONCENTRATION IMBALANCES:
Hypernatremia |
|
Definition
oEtiology:
oGain of relatively more salt than water
oLoss of relatively more water than salt
oClinical findings: (neuronal shrinkage): CNS dysfunction similar to those of
hyponatremia, death in severe cases. |
|
|
Term
|
Definition
oBy Histology
oExtracellular edema
oIntracellular edema
oBy Morphology
oPitting edema
oNon-pitting edema |
|
|
Term
oEtiology and Pathogenesis |
|
Definition
oIncreased capillary pressure
oVasodilation
oDecreased colloid osmotic pressure
oLymphatic obstruction lymphedema
oSodium/Body water excess |
|
|
Term
ELECTROLYTE IMBALANCES:
Hypokalemia |
|
Definition
oEtiology:
oDecreased K+ intake
oK+ redistribution from ECF into cells
oIncreased K+ loss (normal & abnormal routes)
oClinical findings: (abnormal conduction): cardiovascular (EKG changes, A&V premature beats, V fib); neuromuscular (weakness); neuropsychiatric (confusion)
|
|
|
Term
ELECTROLYTE IMBALANCES:
Hyperkalemia |
|
Definition
oEtiology:
oIncreased K+ intake
oShift of K+ out of cells (into ECF)
oDecreased excretion of K+
oClinical findings: (abnormal conduction): cardiovascular ( arrhythmias, death by asystole or V fib); neuromuscular (weakness, paresthesia, agitation) |
|
|
Term
ELECTROLYTE IMBALANCES:
Hypocalcemia |
|
Definition
oEtiology:
oDecreased Ca++ intake or absorption
oDecreased physiologic availability of Ca++
oIncreased Ca++ excretion (normal routes)
oClinical findings: (abnormal conduction): increased neuromuscular irritability, (+) Trousseau and Chvostek, paresthesias, muscle twitching & cramping, tetany, seizures, laryngospasm, etc. |
|
|
Term
| ELECTROLYTE IMBALANCES: Hypercalcemia |
|
Definition
oEtiology:
oIncreased Ca++ intake or absorption
oShift of Ca++ from bone into ECF
oDecreased Ca++ excretion
oClinical findings: (abnormal conduction): anorexia, N&V, constipation, fatigue, muscle weakness, decreased reflexes, headache, confusion, lethargy, personality changes, cardiac arrhythmias, etc. |
|
|
Term
ELECTROLYTE IMBALANCES:
Hypomagnesemia |
|
Definition
oEtiology:
oDecreased Mg++ intake or absorption
oDecreased physiologic availability of Mg++
oIncreased Mg++ loss through normal routes
oMg++ loss through abnormal routes
oClinical findings: (increased neuromuscular activity): increased neuromuscular excitability (insomnia, increased reflexes, muscle cramping/twitching, (+) Chvostek/Trousseau, dysphagia, tetany); cardiovascular (arrhythmias) |
|
|
Term
ELECTROLYTE IMBALANCES:
Hypermagnesemia |
|
Definition
oEtiology:
oIncreased Mg++ intake or absorption
oDecreased Mg++ excretion
oClinical findings: (decreased neuromuscular activity): decreased reflexes, lethargy, hypo-tension, flushing and diaphoresis, drowsiness, flaccid paralysis, respiratory depression, cardiac arrhythmias (including bradycardia) and arrest |
|
|
Term
ELECTROLYTE IMBALANCES:
Hypophosphatemia |
|
Definition
oEtiology:
oDecreased PO4 intake or absorption
oShift of PO4 from ECF into cells
oIncreased PO4 excretion through normal renal route
oLoss of PO4 through abnormal routes
oClinical findings: (decreased energy source): anorexia, malaise, paresthesias, hemolysis, decreased reflexes, muscle aches and weakness, confusion, stupor, seizures, coma, repiratory failure, impaired cardiac function (including cardiomyopathies)
|
|
|
Term
ELECTROLYTE IMBALANCES:
Hyperphosphatemia |
|
Definition
oEtiology:
oIncreased PO4 intake or absorption
oShift of PO4 from cells into ECF
oDecreased PO4 excretion
oClinical findings: (hypocalcemia): deposition of CaPO4 crystals in soft tissues (joints > arthritis; kidneys > obstruction; heart > arrhythmias; lungs > fibrosis; eyes > “uremic red eye”) |
|
|
Term
| Definition of inflammation |
|
Definition
| A series of dynamic processes by which tissues respond to injury. |
|
|
Term
CLASSICAL SIGNS TISSUE EVENTS LEWIS’ TRIPLE RESPONSE
Calor/ rubor
Tumor
Dolor
Functio Laesa |
|
Definition
CLASSICAL SIGNS TISSUE EVENTS LEWIS’ TRIPLE RESPONSE
Calor/ rubor Hyperemia flush/flare
Tumor Exudtion wheal
Dolor Emigration of Leucocyte
Functio Laesa |
|
|
Term
ACUTE INFLAMMATION
I. HYPEREMIA |
|
Definition
TISSUE INJURY-->
CELL DAMAGE-->
RELEASE OF
CHEMICAL
MEDIATORS-->
(e.g.: Histamine)
VASCULAR DILATION-->HYPEREMIA
and
VASCULAR DAMAGE-->leakage |
|
|
Term
EFFECTS OF HISTAMINE:
VASODILATION / PERMEABILITY |
|
Definition
LEAKAGE OF:
1. FLUID
2. PROTEIN
3. MORE FLUID |
|
|
Term
ACUTE INFLAMMATION
II. EXUDATION |
|
Definition
Hyperamia + Vascular damage--->
PROTEIN LOSS FROM CAPILLARIES-->
decrease PLASMA ONCOTIC PRESSURE-->
FLUID LEAKAGE-->
EXUDATION
(FLUID SHIFT) -->
EDEMA
|
|
|
Term
oCLASSIFICATION of exudates |
|
Definition
oBy Type
oNon-Cellular
oSerous
oFibrinous
oCellular
oPurulent
oSuppurative
oMixed |
|
|
Term
ACUTE INFLAMMATION
III. EMIGRATION OF LEUKOCYTES |
|
Definition
FLUID EXUDATION-->
INCREASE BLOOD VISCOSITY-->
SLUGGISH BLOOD FLOW-->
LEUKOCYTE MARGINATION & PAVEMENTING-->
EMIGRATION OF LEUKOCYTES( CHEMOTACTIC FACTORS) |
|
|
Term
WHEN BLOOD FLOW UNDER NORMAL CONDITIONS HAS |
|
Definition
PLASMATIC ZONE
AXIAL FLOW |
|
|
Term
HEMOCONCENTRATION BLOOD FLOW HAS |
|
Definition
LOSS OF PLASMATIC
ZONE AND AXIAL FLOW
MARGINATION AND
PAVEMENTING
DIAPEDESIS
EMIGRATION OF
LEUKOCYTES |
|
|
Term
| SELECTED EXAMPLES OF INFLAMMATORY DISEASES |
|
Definition
oCoronary artery disease
oARDS
oAsthma
oPneumonia
oGlomerulonephritis
oPyelonephritis
oInflammatory diseases of the colon
oLiver cirrhosis |
|
|
Term
| ACUTE INFLAMMATION: CONSEQUENCES |
|
Definition
oResolution: restoration of function
oSuppuration:
oAbscesses, Fistulas, Calcification
oRepair: tissue of origin
oOrganization: scar, granulomas
Chronicity: chronic inflammation |
|
|
Term
|
Definition
oHealing by First Intention (primary union):
oPlanned surgical incision
oHealing by Second Intention (secondary union):
oTissue loss: trauma, necrosis
oWound contraction |
|
|
Term
|
Definition
| Periodic, reversible episodes of bronchial spasms which impair ventilation. Associated with edema of the mucosa and mucus production. |
|
|
Term
| Primary manifestation of Asthma |
|
Definition
| severe dyspnea. Lungs are voluminous, without emphysema. |
|
|
Term
|
Definition
oAtopic asthma (=Extrinsic, or Allergic)
oNon-atopic asthma (=Intrinsic, or Idiopathic)
oExercise-induced asthma (EIA)
oMixed asthma |
|
|
Term
| ATOPIC ASTHMA: Characteristics |
|
Definition
oMostly infants and children
oUsually associated with other allergies
oAttacks often diminish in later years
oSeldom associated with chronic bronchitis and emphysema
oAttacks triggered by specific allergens. |
|
|
Term
| NON-ATOPIC ASTHMA: Characteristics |
|
Definition
oUsually adults
oNo clear evidence of allergy
oAttacks tend to increase in severity
oOften associated with nasal polyps, chronic bronchitis, and emphysema
oAttacks triggered by various non-specific stimuli |
|
|
Term
oExercise-induced asthma (EIA) characteristics |
|
Definition
oChildren, usually of school age
oAttacks develop after increased activity
oSubjects healthy and asymptomatic before attack |
|
|
Term
| MIXED ASTHMA characteristics |
|
Definition
oAdults, usually with past history of atopic or non-atopic asthma
oAccounts for the majority of cases |
|
|
Term
| ATOPIC ASTHMA: Pathogenesis |
|
Definition
sensitization
Immune reaction with
IgE formation
IgE / mast cell coupling
Reexposure to allergen
Release of chemical mediators:
Histamine, Bradykinin, Leukotrienes
Bronchial spasms
Respiratory distress |
|
|
Term
| NON-ATOPIC ASTHMA: Pathogenesis |
|
Definition
Genetically controlled defect in
synthesis / metabolism of c-AMP
Decrease available c-AMP
Blockage of beta-adrenergic
receptors in the bronchi
Decrease
beta-adrenergic
stimulation
Unopposed constriction of
peribronchial smooth muscles
Bronchial spasms
Respiratory distress |
|
|
Term
| ASTHMA: Morphological changes |
|
Definition
oPeribronchial smooth muscle layer è hypertrophied
oBasement membrane è thickened
oBronchial mucosa è edematous with inflammatory inflitrates (exudates)
oLumen è reduced diameter, with mucus plugs |
|
|
Term
| ASTHMA: Consequences of morphological changes |
|
Definition
oImpaired ventilation
oImpaired expiratory function
oProgressive pulmonary hyperinflation |
|
|
Term
| ASTHMA: Disease progression, early stages |
|
Definition
Progressive airway obstruction
Prolonged expiration:
dyspnea, wheezing
Increased volumes of air trapped.
Increased residual volume
Decreased IRV and vital capacity.
Patient breathing with decreased air volumes,
and uses more energy.
Fatigue, loss of tussive force |
|
|
Term
| ASTHMA: Disease progression, later/advanced stages |
|
Definition
Expiratory difficulty worsens
Patient must increase muscular efforts to expel air.
Transpulmonic pressure.
Progressive respiratory
impairment.
Decreased alveolar ventilation.
V/Q mismatch
Progressive gas exchange
impairment
CYANOSIS |
|
|
Term
| ASTHMA: Clinical features |
|
Definition
oDuration of attacks
oIntervals between attacks
oSeverity of attacks
oComplication: status asthmaticus
oCauses of death |
|
|
Term
| ASTHMA: Treatment considerations |
|
Definition
oPreventive measures:
oAvoid known irritants
oAvoid breathing cool air
oAvoid strenuous exercise
oTreatment approaches:
oLong-term bronchodilators
oAntiinflammatory agents
oShort-term bronchodilators |
|
|
Term
|
Definition
oAny agent capable of eliciting an immune response
oEndogenous antigens (=self, or natural antigens)
oExogenous antigens (non-self) |
|
|
Term
| CELLS OF THE IMMUNE SYSTEM |
|
Definition
oLymphocytes:
oT-cells
oB-cells
oMacrophages
oNull cells |
|
|
Term
|
Definition
oCytolytic T-Cells: cause lysis
oRegulatory T-Cells: secrete lymphokines:
oHelper T-Cells
oSuppressor T-Cells
oPrimed T-Cells: memory cells |
|
|
Term
|
Definition
oPlasma Cells: secrete antibodies
(or immunoglobulins)
o Primed B-Cells: memory cells |
|
|
Term
IMMUNOGLOBULINS
(Antibodies) |
|
Definition
oIgD - undetermined function
oIgE (Reagin) - histamine release
oIgA - shock surfaces; breast milk
oIgM (Macroglobulin) - ABO antibodies
oIgG - transplacental passage |
|
|
Term
| ANTIBODY - ANTIGEN INTERACTION |
|
Definition
oAntigen-specific reactions:
oPrecipitation: soluble antigens
oAgglutination: particulate antigens
oAntitoxic reaction: toxins
oNon-specific reaction:
oComplement system activation |
|
|
Term
COMPLEMENT SYSTEM Functions of C3 - C5:
|
|
Definition
1. Chemotaxis
2. Opsonization
3. Histamine release
4. Platelet “effects”
C9- Membrane Attack Function |
|
|
Term
|
Definition
oElements: T-Cells
End-Point: Target destroyed by Cytolytic action
(Cell-to-Cell Killing |
|
|
Term
|
Definition
oElements: B-Cells
oEnd-Point: Target inactivated by Antibody action
(Immune Reaction) |
|
|
Term
| HYPERSENSITIVITY STATES: Classification |
|
Definition
oTYPE I: Immediate Hypersensitivity
(atopy, anaphylaxis)
oTYPE II: Cytotoxic Hypersensitivity
oTYPE III: Immune Complex Disease
oTYPE IV: Delayed/Cell-Mediated Response |
|
|
Term
| HYPERSENSITIVITY STATES: Type I Hypersensitivity |
|
Definition
oPrerequisite: IgE/mast cell coupling.
oResult: histamine release
oAntigen administration:
oLocal è local/regional response
oE.g., hay fever, rhinitis, asthma
oSystemic è systemic response
E.g., anaphylactic shock |
|
|
Term
| HYPERSENSITIVITY STATES: Type II Hypersensitivity |
|
Definition
oPrerequisite: complement activation
oResult: cell destruction by C9
oExample: immune-mediated hemolytic anemia |
|
|
Term
| HYPERSENSITIVITY STATES: Type III Hypersensitivity |
|
Definition
oPrerequisite: complement activation
oResult: vasculitis by C3-C5 fractions
oAntigen administration:
oLocal è local/regional response (Arthus reaction)
oE.g., localized vasculitis, farmer’s lung
oSystemic è systemic response
oE.g., serum sickness |
|
|
Term
| HYPERSENSITIVITY STATES: Type IV Hypersensitivity |
|
Definition
oPrerequisite: sensitized lymphocytes and activated macrophages
oResult: tissue destruction by macrophages: “reaction to a reaction”
oExamples: graft rejection, contact dermatitis |
|
|
Term
| AUTOIMMUNE DISEASE: Definition |
|
Definition
Immune System’s Inability to Distinguish
“Self” from “Non-Self |
|
|
Term
| AUTOIMMUNE DISEASE: Pathogenesis |
|
Definition
oDevelopment of immune tolerance: prenatal and early postnatal life
oLoss of immune tolerance:
anytime during postnatal life
oTriggers: usually unknown
oCharacteristic: usually associated with other autoimmune diseases |
|
|
Term
HIV DISEASE
Historical Considerations |
|
Definition
oFirst cases reported in the US: 1981
oVirus identification: 1983
Antibody tests: 1985/1987 |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Steps in Viral Replication |
|
Definition
oRecognition of appropriate receptors
oAttachment (fusion) to target cell
oInternalization of viral core
oReverse transcription (RNA è DNA)
oDNA replication
oIntegration
oActivation and viral replication |
|
|
Term
COMPETENT
IMMUNE
SYSTEM T4 COUNT |
|
Definition
|
|
Term
SUPRESSED"
IMMUNE
SYSTEM T4 COUNT |
|
Definition
|
|
Term
AIDS-INDICATOR
VALUES T4 COUNT |
|
Definition
|
|
Term
|
Definition
oRT-PCR (quantitative polymerase chain reaction)
obDNA (branched-chain DNA)
oNASBA (nucleic acid sequence- based amplification)
|
|
|
Term
|
Definition
|
|
Term
|
Definition
oELISA: screening test
o WESTERN BLOT: confirmatory test |
|
|
Term
|
Definition
oPolymerase chain reaction (PCR)
o Viral cultures |
|
|
Term
|
Definition
o2 ELISAs and 1 WB:
99.964% accuracy |
|
|
Term
Clinical Category A
By disease process:
|
|
Definition
oAcute Retroviral Syndrome (ARS)
oNegative antibody test
Acute, self-limiting, "flu-like" symptomatology /
r
oAsymptomatic Infection
oPositive antibody test
No HIV-associated disease processas
oPersistent Generalized Lymphadenopathy (PGL)
oPositive antibody test
oWell defined lymphadenopathy |
|
|
Term
By disease process:
Clinical Category B |
|
Definition
oUsually a positive antibody test
Presence of various (non-A, non-C) disease processes, including (but not limited to)
oVulvovaginal candidiasis, persistent, frequent, refractory
oCervical dysplasia or cervical carcinoma in situ
oHerpes zoster (multi-dermatome)
oPeripheral neuropathy
oConstitutional symptoms (fever, diarrhea) |
|
|
Term
| Clinical Category C (AIDS) |
|
Definition
oUsually a positive antibody test
oPresence of AIDS-defining conditions:
oOPPORTUNISTIC INFECTIONS
oMALIGNANCIES
oNEUROLOGIC DISEASE
oHIV WASTING SYNDROME
|
|
|
Term
| Classes of Antiretrovirals |
|
Definition
oMost commonly used (U.S.):
oReverse Transcriptase Inhibitors
oSynthetic Nucleoside Analogues
oNon-Nucleoside Analogues
oProtease Inhibitors
oOther modalities:
oIntegrase inhibitors
oFusion inhibitors |
|
|
Term
|
Definition
| Indinavir + lamivudine (3TC) + zidovudine (AZT) |
|
|
Term
|
Definition
oREPLACEMENT APPROACH:
oBone marrow transplant
oLymphocyte transfer
oImmunoglobulin infusion
oBIOLOGIC RESPONSE MODIFIERS:
oInterleukin-2
oInterferons
oOther cytokines |
|
|
Term
| Modes of HIV Transmission |
|
Definition
oSEXUAL ACTIVITY
oBLOOD-TO-BLOOD CONTACT
oVERTICAL TRANSMISSION |
|
|
Term
HIV Transmission:
Blood-to-Blood Contact |
|
Definition
oInjecting drug users (IDUs) who share needles
oRecipients of contaminated blood productS
oHealthcare workers with occupational exposure
|
|
|
Term
HIV Transmission:
Vertical Transmission |
|
Definition
Transplacental transmission
oIntrapartum transmission
oEvidence
oTwin study
oVaginal vs. Cesarean delivery
Prevention implications: ACTG 076
oTransmission through breast milk
|
|
|
Term
| Body Fluids to which Universal Precautions Apply |
|
Definition
oBLOOD
oSEMEN
oVAGINAL SECRETIONS
oAMNIOTIC FLUID
oPLEURAL FLUID
oPERITONEAL FLUID
oPERICARDIAL FLUID
oCEREBROSPINAL FLUID
oSYNOVIAL FLUID |
|
|
Term
| Body Fluids to which Universal Precautions need not Apply * |
|
Definition
oSALIVA
oBREAST MILK (?)
oFECES
oURINE
oNASAL SECRETIONS
oSPUTUM
oSWEAT
oTEARS
oVOMITUS
(*) UNLESS THEY CONTAIN VISIBLE BLOOD |
|
|
Term
HOSPITAL-BASED MEASURES
FOR HIV CONTROL |
|
Definition
oHeat sterilization (autoclaving)
Various antiseptic product |
|
|
Term
| HOUSEHOLD AVAILABLE PRODUCTS FOR HIV CONTROL |
|
Definition
oClorox bleach (undiluted)
oHydrogen peroxide (undiluted)
oAlcohol (various types)
Thorough use of soap and water
|
|
|
Term
|
Definition
oIron deficiency
oThalassemias
oAnemia of chronic disease |
|
|
Term
|
Definition
oAplastic anemia
oAcute and chronic blood loss
oAnemia of chronic disease |
|
|
Term
|
Definition
oLiver disease
oB12 and folate deficiency anemias |
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Term
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Definition
oLiver disease
oB12 and folate deficiency anemias |
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Term
oFunctional Classification of Anemia |
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Definition
oAnemias of blood loss
oAcute blood loss: acute hemorrhage
oChronic blood loss: chronic hemorrhage
oHemolytic anemias
oIntrinsic (intracorpuscular) abnormalities
oExtrinsic (extracorpuscular) abnormalities
oImpaired RBC production
oStem cell disturbances
oNutritional or functional defects |
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