Hypersensitivities, Autoimmune & Immunocompromised Disorders

Hypersensitivities, Autoimmune and Immunocompromised Disordersv    HypersensitivityØ     Classified I-IV by:§       Source of antigen: Environmental, acquired, etc§       Time sequence:       Immediate vs. delayed§       Basic immunologic mechanism causing the injury·       Histamine release, etc.Ø     Causes§       Foods:        Chocolate, eggs, wheat, milk, nuts, seafood (iodine), strawberries§       Medications:                        Antibiotics (Major Offender)§       Dyes in diagnostic tests:       Iodine/Barium §       Animals/pets§       Venoms                              Bees, hornets, wasps, spiders§       Inhalants:                            Allergies, Pollens, dust, cigarette smoke, pollutants    §       Serums: from animals:         Horse serum used in antitoxins§       Contactants:                       Tape, cosmetics§       Intrinsic:                             Bacteria: (G-) shockv    Types of Hypersensitivity ReactionsØ     Type I- IgE mediated§       Exposure to antigen §       Bind with Mast cells—severe inflammation§       Histamine release— permeability  §       Autonomic nervous system—Controls BP & constriction  §       Genetic predisposition—atopic §       Life threatening—anaphylaxis only§       Desensitization—allergy shotsØ     Type II- Tissue Specific§       Involves tissues and organs§       Antigen reacts with antibody on cell wall§       Antigen-antibody complexes form§       Destruction by:·       Activation of complement cascade resulting in cytolysis·       Enhanced phagocytosis·       Cytoxic T-cell interaction: b/c it thinks it will fight·       Malfunction of cell: if it doesn’t die§       Transfusion Reaction—within 15 minutes. ·       Symptoms:¨     Chills, N/V, Fever, Low back pain from kidneys!       ¨     Hypotension, Tachycardia    ¨     Shock, Anxiety                    ¨     Hyperkalemia         Ø     Type III§       2ndary to antigen-antibody complexes§       Complexes deposited in tissues/blood vessels/joints tissue damage §       Local or systemic§       Immediate or delayed§       Common sites: kidneys, skin, joints§       Examples: SLE, RAØ     Type IV- T-Cell mediated!§       Delayed Hypersensitivity: Start S&S in 24 hrs, but can be months/years.§       T-cells – toxin killing mechanism·       Attack and destroy cells/multiply ·       Recruit phagocytic cellsØ     Example: tissue graft rejection, tuberculin reaction, allergic reactions—delayed and topical. Ex: Poison Ivy.  Usually localized. v    Autoimmune DisordersØ     SystemicØ     Tissue specificØ     Genetic susceptibilityØ     Environmental factors Ø     Systemic Lupus Erythematosus (SLE)§       Chronic§       Inflammatory§       Deposition of immune complexes: Type III Hypersensitivity §       Etiology·       Genetic: Women age 18-40, Blacks, and twins ·       Environmental·       Autoantibodies: against own tissues ·       Anti-nuclear antibodies (ANA)·       Anti-DNA antibodies·       Affect blood cells§       Clinical manifestations·       Facial rash—butterfly rash.  ·       Renal problems—inflammation damages kidneys ·       Arthritis·       Presence of ANA·       Hematological disorders: WBC/RBC & platelets.§       Diagnosis·       History: Occupation, exposures as child·       PE·       Serum analysis: Anti-DNA antibody most specific §       Treatment:  All treat symptoms b/c no cure!·       NSAIDS—                                Pain & inflammation ·       Antimalarial medication—         Plaquenil ·       Corticosteroids—                     Anti-inflammatory ·       Immunosuppresive Medsv    Host-Verses-Graft RejectionØ     Pathophysiology§       HLA antigens§       Type IV reaction                 T-cells!§       Hyperacute rejection—      Immediate §       Acute rejection—               daysmonths.  Antibodies against HLA antigen§       Chronic rejection—            monthsyears. Weak Type 4 reactionv    Graft-Versus-Host Disease:   Graft is rejecting YOU!Ø     Pathophysiology§       Immunocompromised transplantation—common w/ bone marrow transplant§       GVHD development·       Functional cellular immune component—from T-cells·       Foreign antigens·       Immunocompromised recipient§       Acute§       Chronicv    ImmunodeficienciesØ     Congenital=inherited & often opportunistic §       Abnormalities in cell maturation§       Hypogammaglobulinemia— antibodies in blood §       Severe combined immunodeficiencies (SCIDs)·       Cell mediated T-cells & antibody (plasma B-cells)§       Adenosine deaminase deficiency (ADA)·       Lacks enzyme so toxins buildup.  Causes lymphocytes to not mature properly §       Purine nucleoside phosphorylase deficiency (PNP)Ø     DeGeorge Syndrome§       T-Cell deficiency§       Defect on chromosome 22§       Clinical manifestations·       Facial disorders·       Low set and angulated ears·       Hypocalcemia·       Chronic infections§       Treatment·       Thymus transplant·       Bone marrow transplantØ     Selective Immunoglobulin A Deficiency§       Affects mature B cells·       Genetic·       Environmental§       Symptoms·       Asymptomatic·       URI’s·       Allergic manifestations§       Treatment·       NoneØ     Acquired§       Nutritional§       Iatrogenic§       Trauma§       Stressv    AIDSØ     HIV§       Retrovirus§       RNA§       Reverse transcriptase§       Double stranded DNA§       New genetic make-up§       Viremia§       Low HIV levels – 10 to 12 years (poss)·       Replicating at fast rate§       HIV looking for CD4 receptors·       Lymphocytes·       Monocytes/macrophages·       Astrocytes·       Oligodendrocytes §       T cells have more CD4 receptors·       Unfortunate: T- cells play a key role in the immune system’s ability to recognize and defend itself against pathogens·       Normal CD-4 level is 800 – 1200 cells/microliter·       Normal life span = 100 days; HIV = 2 days·       Destroys 1 billion CD4 T cells every day·       Healthy immune system = CD4 T at 500 cells/microliter·       CD4 T= 200-499 – immune problems·       CD4 T= < 200 – opportunistic infectionsØ     Transmission of HIV§       Blood§       Semen and Vaginal fluid§       Breast milk§       Saliva§       Tears§       Sweat§       InsectsØ     Variables for Transmission§       Duration & frequency of contact§       Volume of fluid§       Virulence & concentration of the organism§       Host immune statusØ     Primary Infection Phase§       High viral load§       Dramatic drop in CD4 cell counts§       Flu-like symptoms§       Window period§       Antibodies develop (usually can be detected in 4-12 weeks) Ø     Latency Phase: Initial§       Asymptomatic phase§       Vague symptoms§       CD4 T count > 500 cells/microliter§       High risk à even though no symptoms, can still transmit HIV to othersØ     Latency Phase: Intermediate§       Asymptomatic but virus is replicating§       May have recurrent infections of sinuses/respiratory tract, ^ fatigue§       CD4 T counts continue to fall – between 200-500§       Damage to lymphatic structures à loose ability to  contain destructive HIVØ     Latency Phase: Late§       Continued decrease of CD-4 Cells§       Occurrence of opportunistic infections·       Oropharyngeal candidal infection·       Shingles·       P. carinii pneumonia·       Oral/genital herpes·       Kaposi Sarcoma·       Oral hairy leukoplakiaØ     Overt AIDS Phase§       Diagnosis of AIDS (Acquired Immunodeficiency Syndrome)§       Immune system becomes severely compromised§       CDC Diagnostic criteria for AIDS= HIV positive§       At least one of: ·       CD4+ below 200/ul.·       Opportunistic infection·       Development of opportunistic cancer·       Wasting syndrome occurs (loss of 10% ideal body mass)·       Dementia Ø     Diagnosis§       HIV antibody test (ELISA)§       Western Blot Assay§       PCR§       OraSure test§       Ora Quick Rapid HIV-1 Antibody TestØ     Treatment§       NO CURE§       Anti-Retroviral medication= HAART§       Drugs§       Antibiotics§       Antifungals§       Vaccines§       Influenza§       Pneumonia 

Add comment February 24, 2008

HIV and Immune System Pharmacology

HIV and Immune System Pharmacologyv    MOAØ     Nucleoside Reverse Transcriptinase Inhibitors (NRTI’s) §       Mimics neucleocides needed to convert RNADNA & Inhibits enzyme Ø     NonNucleoside Reverse Transcriptinase Inhibitors (NNRTI’s)§       Binds near active site to inactivates reverse transcriptase enzymeØ     Protease Inhibitors (PI’s)§       Inhibit protease enzyme needed from DNA at tail end of process.  §       Prevents new RNA virus from splitting Ø     Fusion Inhibitors§       Targets 1st step w/ fusion & initial entry w/ cell§       Tie up CD4 receptor site so virus can’t latch on§       Last-ditch effort v    Therapy recommendationsØ     Single-Drug: IneffectiveØ     HAART: Highly Active Antiretrovial Therapy§       Combinations of RT’s and PI’s into nice cocktailv    IndicationsØ     Active HIVv    ContraindicationsØ     Severe allergy: weigh pros/consØ     Intolerable toxicity:  N/V, diarrhea, rash, pancreatitis, liver/kidney toxicity, bone marrow depression, hepatitis patients v    Side Effects/Adverse EffectsØ     Same and nonretroviral: nausea, vomiting, diarheaØ     Tolerate: Strict drug schedule.Ø     Myalgias/ joint painv    Drug interactionsØ     MULTIPLE!!  Look up!v    Specific AgentsØ     NRTI’s: §       Zidovudine (AZT, Retrovir): ·       Newborns with HIV mom  ·       Post-exposure prophylaxis§       Lamivudine (Epivir): ·       Rapid PO absorption. ·       Bactrim level to toxicicity.  §       Tenovir (Viread): ·       effecacy of PI’s Ø     NNRTI’s: Great PO & heavily metabolized by cytochrome P450 system §       Delavirdine (Rescriptor): ·       Nasty rash §       Efavirenz (Sustiva): ·       Psychiatric problems §       Nevirapine (Viramune):·       Stevens-Johnson Syndrome·       No women with CD4 count 200- hepatotoxicity risk Ø     Protease Inhibitors (PI’s): ∆ fat distribution, cholesterol & blood sugars§       Amprenavir (Agenerase):           Take w/ fatty meal§       Nelfinavir (Viracept):       Take w/ fatty meal§       Indinavir (Crixivan):        Kidney stones. Combo w/ 2 retrovirals. §       Lopinavir/ritonavir (Kaletra):      Ritonavir metabolism of lopinavir  Ø     Fusion Inhibitors: §       Enfuvirtide (Fuzeon):       Limited usage—last efforts v    Immunosuppressant AgentsØ     MOA:§       Varies§       Suppress certain T lymphocyte cells w/ cellular immunity Ø     Indications§       Organ rejection prevention§       SLE-lupus§       RA§       Psoriasis§       IBS§       Crones Disease Ø     Contraindications§       Allergy§       Relative·       Renal/hepatic failure·       Pregnancy & teratogens Ø     Side Effects/Adverse Effects§       Susceptibility to infection§       Hepatotoxcitity!Ø     Interactions§       Cyclosporine has many·       Cardiovascular meds:                      cyclosporine level ·       Cytochrome P-450 system ·       Nephrotoxic agents·       HIV agents ·       Anti-infectives:                    cyclosporine levelsØ     Specific Agents§       Cyclosporine (Neoral)·       Post-transplant ·       RA & psoriasis §       Azathioprine (Imuran)·       B & T cell production ·       Severe RA & kidney transplant§       Basiliximab (Simulect)·       Interleukin 2 antagonist w/ complement cascade·       Perioperative care w/ kidney transplants§       Sirolimus (Rapamune)·       T-cell function·       Combo w/ steriods/Cyclosporin for kidney transplants§       Mycophnolate mofetil (CellCept)·       B & T cells·       Renal/Heart transplants·       Combo w/ steroids/Cyclosporin§       Tacrolimus (Prograf)·       Inhibits T-cell activation·       Liver/Kidney transplants… Nephrotoxicity w/ Cyclosporin Ø     Special Considerations§       Contact with others §       Pregnancy§       Leukocyte count- 3,000 dangerous§       RBC counts§       Children§       Co-morbidities v    Immunizing AgentsØ     Toxoids§       Inactivated bacterial toxins§       Usually enough to stimulate antibody response§       Immunity may not be lifelong b/c toxoid inactivatedØ     Vaccines§       Usually lifelong§       Not as strong as live vaccine, may require boosters§       Live vaccines usually attenuated (weakened) of bacteria/virus which sets off immune system.  Can have lifelong immunity. Ø     Immunoglobulin Therapy§       Passive immunity where we give you antibodies to help pt fight.  v    MOA: Ø     Immune responseØ     Active: Vaccines and toxoidsØ     Passive: Immunoglobulins: need quick antibodiesv    IndicationsØ     ImmunityØ     Temporary protectionv    ContraindicationsØ     Allergies§       Toxin§       Synthetic components: Many ppl allergic to synthetic components and not toxoid itself. Ex: egg product/horsesØ     Febrile illness§       Important for kids b/c many immunizations when children.  Immune system already busy.  Kids that are febrile PRIOR to getting med.Ø     Immunocompromised state§       Don’t give any LIVE vaccine to thesev    Side EffectsØ     Fever AFTER immunization§       Soreness at injection site§       Expect to go away after few daysv    Adverse EffectsØ     Serum Sickness: Caused by equine vaccines/toxins that causes laryngeal swelling/tongue and facial edema, and rash v    Special PopulationsØ     Preterm infants- (if child born 2 weeks premature and is 4 wks old, really only 2 weeks old.)  Immunize based on REAL birthday. Ø     Pregnancy:  Never give live vaccines. After 1st trimester if necessary.Ø     Limited Immunodeficient: Not immunocompromized but immunodificient. ARE able to receive vaccines. Ø     Active disease: Want to give toxoids (=killed bacteria)/killed vaccines /immunoglobulins.  v    Specific Agents (active)Ø     Haemophilus influenzae (Hib)§       Only vaccinate for kids under 5§       Cause meningitis, epiglotitis Ø     Hepatitis B (Recombivax)§       What we get.  Get boosters.  Ø     Influenza (FluShield)§       Live immunizationØ     Measles, mumps, rubella (MMR II)§       Viral illnesses.  Have boosters§       Not recommended/contraindicated w/ pregnant womemØ     Diptheria, tetanus, and pertussis (DTaP)§       Both Toxoids.  Pertussis is inactivated, but back in gear.  Ø     Pneumococcal (Pneumovax)§       Fights pneumococcal pnemonia, but other pneumococcal.  Don’t call “pnemonia vaccine” b/c fights other stuff.  Given to those over age 65 and few kids. 23 strains.Ø     Polio (IPV)§       Completely inactivated b/c very dangerousØ     Varicella (Varivax)§       Live; childhood immunization.  Pts older than 13 and never been exposed to chickenpox or vaccinated, may give this.  Ø     Meningococcal (Menomune)§       Ppl in dorms.Ø     Rabies (Imovax)§       Kills quickly.  If body can’t fight, die in 3 days.§       Only get it if you’ve had risk for exposure.  Ø     HPV (Gardasil)§       Very common. STD ONLY!!  Protect with strains that lead to cervical cancer. Men always asymtomatic.  Given w/ ages 9-26.  v    Passive: (many times combo w/ active)Ø     Hepatitis B immune globulin (H-BIG2)Ø     Immune globulin (Gammagard)§       Just IgG that’s powerful with fighting infection.Ø     Rabies immune globulin (RIG)Ø     Tetanus immune globulin (Hyper-Tet)Ø     Varicella zoster immune globulin (VZIG) 

Add comment February 24, 2008

Role of the Nurse

  • Role of the Nurse:
    • Provider of care- direct care or delegated care supervision. (LVN, Tech
      • eg. initial teaching is required by the RN to do. Admin. meds, and blood is also for RN to do.
    • Communicator- (includes education)
    • Consumer of research and information-(utilizing the current evidence-based information to deliver care)
    • Manager- other nurses, ourselves, eg. case manager-plan of care-pt. family, social work, pt/ot, pharmacists.
  • Nursing Process: ADPIE
    • Assessment
    • Analysis (Diagnosis)
    • Planning
    • Implementation
    • Evaluation: Did the intervention work? yes-outcome met; partially met-need to reassess; no-outcome not met.
  • Evidence-Based Practice –research; conscientious use of the best evidence (i.e. findings from research, quality improvement, and practice management initiatives, and patient assessment) in combo with clinical decision making.
  • Roles: Safe and effective care; safety and infection control; health promotion and maintenance; psychosocial integrity; maintaining physiological integrity; pharmacological therapy; spiritual care.

Add comment February 23, 2008

Human Needs

  • Holistic-physiological, psychological, social, spiritual
  • Nursing- the dx and treatment of human resources to actual and potential health problems.
  • Health-each human exists on a health-illness continuum that may move from high level of wellness to severe illness and death.
  • Role of the Nurse-Assist individuals, families, and communities to attain the highest level of health possible–through assisting them to meet their various health related needs.
    • Levels of prevention:
      • Primary Prevention:
        CONCERNED WITH THE PREVENTION OR DELAY OF THE ACTUAL OCCURRENCE OF A SPECIFIC ILLNESS OR DISAESE.
        Example: maintenance of diet, body weight; safe sex; cessation of smoking; limiting alcohol intakeSecondary Prevention:
        PROMOTE EARLY DETECTION (case finding and screening) AND EARLY TREATMENT OF DISEASE
        Example: breast self-exam; TB screening; newborn screening; genetic counselingTertiary Prevention:
        DIRECTED TOWARD PREVENTION OF COMPLICATION AND REHABILITATION AFTER THE DISEASE
        Goal: support adaptation to risk; optimal reconstitution; ad Establishment of wellness.
    • Theories of illness causation derive from the underlying cognitive orientation of a cultural group, and therapeutic practice usually follows the same cultural logic.
    • Wellnes- is a balance; dynamic state (always changing)
    • Illness- a state of homeostatic imbalance in which needs are not specifically met.
    • Maslow’s Hierarchy of Needs-
    • Maslow’s Hierarchy of Needs
    • Acute/Chronic Illness-6 months or longer

Add comment February 23, 2008

Nutrition, Health & Pregnancy

nutrition.jpg

  • Body Mass & Health Mesurements
    • BMI does not distinguish fat from lean muscle
    • Waist to Hip ratio: Max-0.8 (Cardiovascular health)
    • FBS (fasting blood sugar) , TG’s (Triglycerides), HDL
  • Weight Charts
    • Set to correspond with the lowest mortality rates
    • Not factored for lifestyle
    • Optimum BMI: 19.8-24.5 (2 fold risk); 21-27 
  • Mortality & Weight
    • Positive correlation between weight and mortality. Controlled for smoking. (one goes up/other goes up)
    • Mortality rates up to 35% or higher with BMI greater than 25.
  • Chronic Disease & BMI
    • Type 2-diabetes
    • Hypertension
    • Chronic Heart Disease
    • Cholelithisais
    • Postmenopausal breast cancer–all breast cancer
    • Cancer
  • Even a gain of 11-22 lbs. can result in an increased RR-Relative Risk of 1.5 to 3 for Chronic Heart Disease, Diabetes, & Hypertension
    • Relative Risk:
      • 1.0 = no increase risk; standard
      • 1.5 = 50% risk over population
      • 2.0 = 100% risk over population
  • MyPyramid.gov My Pyramid
  • Pre-Pregnancy BMI & (Weight gain recommendations)
    • less than 19.8 = underweight (28-40lbs)
    • 19.8-24.9 = normal weight (25-35lbs)
    • 25.0-29.9 = overweight (15-25lbs)
    • equal to/above 30 = obese (less than/equal to 15lbs)
      • Twins range= 35-45lbs
      • Higher end of range for young/black/S.Asian women
  • High risk for poor weight gain groups
    • Smokers
    • Substance users
    • Very young adolesants
    • Poor
    • Busy professional women
    • Multiple gestation
  • Pregnancy Risk Related to Overweight
    • hypertension
    • diabetes
    • Cesarean
    • Macrosomia (too big)
    • Shoulder Dystocia (baby shoulder caught)
    • NTD (neural tube defect)
    • Late intrauterine death
    • Infection
  • Distribution of weight in pregnancy:
    • 7.5-8.5lbs = fetus
    • 7.5lbs = fat & protein
    • 4.0lbs = blood
    • 2.7lbs = tissue fluids
    • 2.0lbs = uterus
    • 1.8lbs = amniotic fluid
    • 1.5lbs = placenta & umbilical cord
    • 1.0lbs = breasts
    • TOTAL = 28-29lbs
  • Weight gain & birth weight
    • when weight gain is within IOM (Institute of Medicine) recommendations incidence of SGA or LBW is reduced.
  • Calorie Requirements:
    • After 20 weeks, ADD 300 CALORIES, and 25 GRAMS of PROTEIN to the woman’s non-preg calorie and protein requirements.
  • Risk associated with LBW
    • Mortality
    • Mental retardation
    • Cerebral palsy
    • Learning disabilities
    • Neurologic defects
    • Vision/Hearing impairments
    • Stunted growth and development
  • Brain growth
    • malnutrition during hyperplasia leads to a decrease in the number of brain cells that is irreversible.
    • BW of 3000 grams is critical
  • Alcohol: No known safe level. Avoid all alcohol including beer and wine
  • Caffine & Pregnancy: Half-Life prolonged in the fetus; fine, but do not overdue it; 300mg-400mg/day = SAFE amount of coffee and soft drinks
  • Pregnancy Requirements:
    • 300Kcal/day
    • 25-60grams protein/day
    • Iron 30mg/day beginning at 12th week
    • Folate 400mcg/day
    • Calcium 1200mg/day (dairy, spinich, supplements)
  • Sources of IRON:
    • not enough can cause–anemia
    • Liver, meats, whole grain or enriched breads and cereals, deep green leafy vegetables, legumes, dried fruits
    • take on an empty stomach
    • may cause stools to be black/green
  • Sources of CALCIUM:
    • Milk & Yogurt –rich in Ca+
    • Milk, cheese, yogurt, sardines or other fish eaten with bones left in, deep green leafy vegetables except spinach or Swiss chard, calcium-set tofu, baked beans, tortillas
    • Daily Recommendations During Pregnancy dailyrecommendationsduringpreg.jpg
  • Nutrition & Prenatal Care
    • 24hr recall
    • Cultural sensitivity
    • Consistancy weighing
    • Set weight goal at initial visit
    • Additional time with high risk groups
  • Morning Sickness:
    • Dry crackers/starches
    • Upright after meals
    • Eat slowly
    • Small frequent meals
    • Ginger

Add comment February 12, 2008

Diagnosis of Pregnancy

Signs & Symptoms of Pregnancy:

**Objective 1: Identify the presumptive, probable and positive signs of pregnancy 

  • Presumptive Signs:[Pregnant woman notices] Maternal physiological changes that a woman may experience.
    • Abrupt cessation of menses
    • Nausea and vomiting
    • Tingling, tenseness, nodularity, and enlargement of breasts and nipples
    • Increased frequency of urination
    • Fatigue
    • Color changes of breast:  darkening of nipples; primary and secondary areolar changes
    • Appearance of Montgomery’s tubercles (glands, breast-around nipple)
    • Continued elevation of BBT in the absence of infection
    • Expression of colostrom from nipples (3rd trimester)
    • Excessive salivation
    • Quickening (first feel the baby move)
    • Skin pigmentation and conditions, e.g. chloasma, breast and abdominal striae, linea nigra, vascular spiders, palmar erythema
  • Probable Signs: [RN Notices] Maternal physiological and anatomical changes detected upon examination (other than presumptive signs)
    • Chadwick’s sign
    • Enlargement of abdomen
    • Change in the shape of the uterus
    • Ballotment (pateller test)
    • Palpation of fetal outline
    • Fetal movement palpated (probable or positive)
    • Piskacek’s sign
    • Hegar’s sign
    • Goodell’s sign
    • Palpation of Braxton Hicks contractions
    • Positive pregnancy test
  • Positive Signs: Directly attributed to the fetus as documented by the examiner
    • *ONLY* Fetal heart tones
    • Ultrasound confirmation

 **Objective 2: Differentiate between quantitative and qualitative pregnancy tests

  • Ask ahead of time: “How would you feel about being pregnant right now?”
  • Pregnancy Tests
  • Detect HCG(corpus luteum) in blood or urine; Recognition of hCG (or a subunit) by an antibody to the hCG molecule usually the $-subunit of hCG 
    • Qualitative:  positive or negative
      • Urine: morning sample is the best; but any will do
    • Quantitative:  provides an amount for hCG
      • Blood test: will give an amount (hCG can be detected in the serum 8-9 days after fertilization; and somewhat later in the maternal urine) –3 days after pregnancy
    • Clinical tests: sensitive at the time of missed menses

**Objective 3: Describe how to determine last menstrual period and estimated date of delivery

  • Dating: LMP – 3months + 7 days 
  • Nagele’s Rule: first day of LMP, minus three months, plus one week and one year.  This equal 280 days from LMP.  No research supports 280 days as the length of pregnancy.
  • Example: Dec.1st (so,) Dec.1st-3months=Sept.1st + 7days=Sept.8th
  • Research has shown that the pregnancy mean is closer to 283-284 days from LMP or 269-270 days from ovulation
  • Always determine if LMP was a normal period for the woman. Spotting at the time of implantation is not uncommon.  This scanty bleeding may be interpreted as a period unless a through menstrual history is obtained.  Remember, LMP refers to the first day of her last NORMAL period.  If a woman is a poor historian and has difficulty determining her LMP, it may be useful to use holidays or other events to help her focus her memory.
  • Gestational Wheel: At the beginning of the wheel is the 1st day of menses; outside of wheel calendar year. middle wheel months; also, 280 marker (40weeks) ex. Sept.10-June 17
  • Gestational Wheel

DATING METHODS Level 1 – most reliable

  • 1.  LMP which is normal, regular, & certain (1-2 wk range of accuracy)
  • 2.  Basal body temperature with coital record, showing ovulation & sustained temperature elevation. (2-5 days range of accuracy)
  • 3. Ultrasound between 7 & 10 weeks of menstrual age, using crown-rump length to calculate gestational age. (accurate to within  3-5 days)
  • 4. Serum hCG levels <10,000 on two separate occasions one week apart, rising appropriately. . (accurate to within  3-5 days)
  • 5. Urine pregnancy testing, which may initially be negative, but becomes positive as soon as detectable levels of hCG are present in maternal urine. This timing will vary according to the type of urine test used.
  • 6. Two ultrasounds <26 weeks gestational age, which estimate dates of delivery within 2.6 weeks of each other.  Use the EDD based upon the earlier ultrasound, unless obtained between 10 & 13.     

Add comment February 12, 2008

Antepartal Care: Teratology

  • Teratogens (birth defects) any agent or non-genetic factor that produces permanent abnormal embryonic physical development of physiology.
  • Historical Events:
    • 1941: Rubella (blindness, Congenital Heart defects)
    • 1950’s: Methylmercury (neurotoxicity)
    • 1960’s: Thalidomide (phocomelia)
    • 1970’s: Alcohol (fetal alcohol syndrome)
  • Principles of Teratology:
    • All or none phenomenon (from conception to implantation)-prenatal death
    • Dose dependency
    • Critical periods for certain effects
    • Duration of exposure
    • Host suseptibility
    • Drug interactions
      • BEST: Single drug; lowest dose
  • Critical periods during human development:
  • Embryonic 3-8weeks; Gestational age 5-10weeks
  • Critical Periods for Human Development
  • Effect of teratogen by (gestational) week exposure:
    • 1-6 weeks: CNS
    • 2-7 weeks: Heart
    • 3-8 weeks: Extremities
    • 3-8 weeks: Eyes
    • 5-8 weeks: Palate
    • 6-10 weeks: External Genitalia
  • Thalidomide:
    • Introduced in 1956 as a seditive & anti-nausea agent
    • Withdrawn in 1961
    • Discovered to be human teratogen causing absence of limbs or limb malformations in newborns
    • 5000-7000 infants effected
    • Resulted in new drug testing rules
  • Pre-Embryonic Stage:
    • Time of fertilization & up to implantation
    • First 2 weeks of gestation
    • Exposure to teratogens in this period may lead to improper implantation & spontaneous abortion, Also called “All or None”.
  • Critical Period- Embryonic Period:
    • From day 14-18 to day 54-60 post-conception (this is the critical period)
    • Period of most extensive organ differentiation (the heart-first 38days; arms/legs-first 49days; teeth-first 56days, etc.)
    • Exposure to teratogens during this period can cause structural and functionatl birth defects.
  • Fetal Period:
    • From day 56 of gestation to delivery
    • Differentiation of the palate, external genitalia, and ear are examples for this period. Structural defects as well as fetal growth retardation can occur.
  • Known or strongly suspected Teratogens (Drugs & Chemicals)
    • Alcohol
    • Androgens (testosterone)
    • ACE Inhibitors (hypertensive medications)
    • Antithyroid medications
    • Coumadin
    • Carbamezepine, Phenytoin, Valproic Acid (cleft palate)
    • Folic Acid Antagonist (Hyper/Hypobilrubemia
    • Cocaine
    • Lead, Mercury+
    • Lithium (Bipolar meds. -cardiac defects)
    • NSAID’s
    • Tetracycline (discolor teeth/effect bone growth)
    • Thalidomide
    • NO Sulfa-drugs
  • Known or Strongly Suspected Teratogens (INFECTIONS)
    • CMV-cytomet.virus
    • Rubella
    • Syphilis (Treat w/ PCN-not for babies/PCN desensitizes preg.women) baby bleeds to death
    • Toxoplasmosis
    • Varicella
  • SSRI’s and Birth Defects (To treat depression)
    • Paxil, after 20th.wk, 1st trimester
      • Persistant Pulmonary Hypertension; taken after 20th wk; respiratory problems; 6 times greater risk
      • RR of atrial and ventricular septal defects w/ 1st trimester use; fetal echocardiography to screen in women exposed
    • Prozac, third trimester use
      • preterm delivery, respiratory difficulty, admission to NICU, jitteriness
    • JAMA, May 2008: SSRI’s-late in preg-3times greater risk-respiratory prob. in newborns (including Effexor)
    • FDA Category D
  • FDA Categories:
    • A: Controlled studies in humans/ but not shown an increased risk for BD’s
    • B: Animal studies show negative for BD’s/no adequate human studies OR animal/human studies not available
    • C: Animal Studies show risk/ lack in human data
    • D: Human data-show risk (benefit may outweigh)
    • X: Animal/Human data positive
  • Smoking in Pregnancy
    • Associated with reduced birth weight (IUGR & LBW), pematurity, stillborn, placental abruption
  • Fetal Alcohol Syndrome (FAS)
    • First described in 1970s
    • Facial abnml, growth retardation, CNS effects, reduced intelligence
    • Facial effects: microcephaly, flat face, thin lips, missing groove above lip, short nose
    • Effects 4-12 thousand infants per year
    • Fetal Alcohol effects: (FAE) milder form but still CNS involvement

Add comment February 12, 2008


Categories

  • Blogroll

  • Feeds