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Anatomy III > Pregnancy and neonatal diseases > Flashcards

Pregnancy and neonatal diseases Flashcards

1
Q

Patho: Babies are born with limbs and internal organs deformities due to a medication used during pregnancy

A

Thalidomide Babies

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2
Q

Homeo: the embryo needs the celebron proteins but the X bind to it and affects all the development of the future baby

A

Thalidomide Babies

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3
Q

Outcomes: Medication norms and testing changes, they need to pass before being approved

A

Thalidomide Babies

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4
Q

S&S:

  • Phocomelia (limb atrophy)
  • Absence of the auricles with deafness
  • Defects of the muscles of the eyes and of the face
  • Absence or hypoplasia of arms, preferentially affecting the radius and the thumb
  • Thumbs with three joints
  • Defects of the femur and of the tibia
  • Malformations of the heart, the bowel, the uterus, and the gallbladder
A

Thalidomide Babies

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5
Q

Body.S: Damage to the limbs, ears, eyes, genitalia, internal organs (kidney, heart, GI tract), any tissue

A

Thalidomide Babies

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6
Q

Treatments: (no treatment)

  • Prosthesis
  • Pain management with medications such as analgesics
A

Thalidomide Babies

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7
Q

Patho: Hormones hPL and hPGH created by placenta cause insulin resistance = glucose to build up in the blood instead of being absorbed by the cells. Complications may lead to macrosomia and hypoglycemia in the baby.

A

Gestational Diabetes Mellitus

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8
Q

Homeo: Insulin and glucagon work together to maintain the regulation of the blood glucose level. When blood sugar is too high, the pancreas secretes more insulin and when the blood sugar drops, the pancreas secretes glucagon to raise the blood sugar back.

A

Gestational Diabetes Mellitus

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9
Q

Outcomes: Pre-eclampsia, HTN

A

Gestational Diabetes Mellitus

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10
Q

Body.S: Cardiovascular, nervous, musculoskeletal, digestive, urinary, reproductive, immune system

A

Gestational Diabetes Mellitus

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11
Q

S&S:

  • Glucose in urine, unusual thirst, frequent urination
  • Fatigue, nausea, blurred vision
  • Frequent vaginal, bladder and skin infections
A

Gestational Diabetes Mellitus

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12
Q

Diagnostic:

  • Blood tests
  • Glucose challenge test (glucose screening test)
  • Oral glucose tolerance test
A

Gestational Diabetes Mellitus

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13
Q

Treatment:

  • Diet of foods high in fiber and low in fat and calories (vegetables, whole grains, fruits, refined carbohydrates)
  • Exercise
  • Monitoring blood glucose levels
  • Medications (insulin injections, glyburide, metformin)
A

Gestational Diabetes Mellitus

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14
Q

Patho:

  1. Holes in the heart means less oxygen carried to child’s body. Ventricular septal defect (hole between right and left ventricles), Atrial septal defect (hole between atriums), Atrioventricular canal defect (hole in center of heart).
  2. Obstructed blood flow, heart works extra hard to pump blood through narrow vessels = heart gets bigger and thicker muscles of heart
  3. Abnormal blood vessel formation, transposition of the great arteries (pulmonary arteries and aorta wrong side), coarctation of the aorta (gets narrow), total anomalous pulmonary venous connection (bv of lungs attached wrong area of heart)
  4. Heart valves abnormalities, do not open and close correctly, blood can’t flow smoothly. Ebstein’s abnormally (tricuspid valve malformed), pulmonary atresia (pulmonary valve is missing)
  5. Underdeveloped heart, hypoplastic left heart syndrome (heart not develop enough to effectively pump enough blood to body)
  6. Combination of defects, some born with many. Tetralogy of fallot: defects (4) , hole in the wall between ventricles, narrowed passage between right ventricle and pulmonary artery, a shift in the connection of the aorta to the heart and thickened muscle in the right ventricle.
A

Congenital Heart Defects

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15
Q

Homeo:
Circulation pattern impaired. Congenital heart defects range in severity from simple problems, such as “holes” between chambers to the heart, to very severe malformations, such as the complete absence of one or more chambers or valves. Then, such problems may or may not have disruptive effect on a person’s circulatory system
X = increase risk of pulmonary hypertension, arrythmias and heart failure

A

Congenital Heart Defects

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16
Q

Body S: Heart

A

Congenital Heart Defects

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17
Q

S&S:
Serious sings that become evident soon after birth or during first month of life: heart murmur, pounding hearts, weak pulse, gray or blur color skin/lips/fingernails, sleepiness while feeding or being very sleepy, swollen belly or legs or puffiness around eyes, trouble breathing or fast breathing.
Less serious signs, may not be diagnosed until later in childhood: easily becoming SOB during exercise or activity, easily tiring during exercise or activity, fainting or swelling during exercise.

A

Congenital Heart Defects

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18
Q

Treatments:

  • Surgeries to repair heart or bv
  • Some don’t need surgery, only cardiac catheterization
  • Medications; ACE inhibitors, beta blockers, diuretics, digoxin for symptoms
  • Routine checkups with cardiologist
  • Many are not cured
A

Congenital Heart Defects

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19
Q

Diagnostic Test

  • Medical and family hx
  • Physical exam
  • Echocardiogram
  • Electrocardiogram
  • Chest x ray
  • Pulse oximetry
A

Congenital Heart Defects

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20
Q

Patho: Affects a child due to exposure of alcohol (wine, beer, etc.)during mother’s pregnancy, defects irreversible. Alcohol goes through umbilical by crossing placenta and reaches the fetus = higher blood alcohol concentrations in fetus circulation = interferes with delivery of oxygen and optimal nutrition to the developing fetus

A

Fetal Alcohol Syndrome

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21
Q

Homeo: No liver to process alcohol, so development of tissues, organs and cause permanent brain damage

A

Fetal Alcohol Syndrome

22
Q

Body S.: Nervous and Musculoskeletal

A

Fetal Alcohol Syndrome

23
Q

S&S:

  • small head, low nasal bridge, short nose, small eye opening, thin upper lip, underdeveloped jaw, smooth philtrum, flat midface, epicanthal folds
  • trouble w/ attention and processing info, reasoning and problem solving
  • problems with communication, vision and hearing
  • intellectual disability, learning disorders, delayed development
A

Fetal Alcohol Syndrome

24
Q

D. Tests: no lab tests that can prove X, to diagnose Dr look:

  • unusual facial features, small head size
  • lower than average height, weight
  • problems with attention, hyperactivity and poor coordination
A

Fetal Alcohol Syndrome

25
Q

Treatments: (Can’t be cured, early diagnosis and treatment improve child development and outlook)

  • Children do better: diagnosed before age 6, in a loving, nurturing, stable home, not exposed to violence and get special education and social services.
  • Antidepressants (moods, sleep irritability, aggression, problems in school)
  • Stimulants to treat behavioral issues (hyperactivity, trouble concentrating, poor impulse control)
A

Fetal Alcohol Syndrome

26
Q

Patho: fever lasts for more than 24hrs within first 10days after woman has had baby, fever due to an infection, most often of the placental site within the uterus, if infection involves bloodstream, it’s a puerperal sepsis.
Organisms like Streptococcus pyogenes staphylococci and the anaerobic streptococci, may be present after a long and injurious birth and unskilled instrumental deliver.

A

Puerperal Fever

27
Q

Homeo: Body temp increase >38.0 Celsius, blood stream may be invaded causing problems like septicemia, can also invade the lymphatic system causing problems like sepsis, cellulitis, and pelvic or generalized peritonitis.

A

Puerperal Fever

28
Q

Body.S: female reproductive tract, common in uterus, cardiovascular, genitourinary and lymphatic system

A

Puerperal Fever

29
Q

S&S:

  • Fever greater than 38.0, chills, low abdominal pain, possibly bad smelling vaginal discharge
  • Usually occurs after the first 24hrs and within the first 10 days following delivery
A

Puerperal Fever

30
Q

Diagnostic:

  • Postpartum infection diagnosed by Dr by physical exam
  • Urine or blood sample is set for routine analysis and culture
  • Endometritis suspected, endometrial brush sample collected for aerobic and anaerobic culture and molecular detection of bacterial etiologic agents
A

Puerperal Fever

31
Q

Treatments:

  • Commonly with oral antibiotics
  • Dr may prescribe clindamycin (Cleocin) or gentamicin (Gentasol)
  • Antibiotics tailored to type of bacteria the Dr suspects
  • Due to risks following a Caesarean section, recommended all women receive a preventive dose of antibiotics dose of antibiotics such as ampicillin around the time of surgery
A

Puerperal Fever

32
Q

Patho:
PRE- X(high BP, occurs after 20 weeks of pregnancy, second half, in women with original normal BP).
X (more severe, rare but severe, when high BP results in seizures).

A

Preeclampsia/eclampsia

33
Q

Homeo: During placental development, cytotrophoblasts invade maternal spiral arteries that supply blood to endometrium of the uterus with turns them into high caliber vessels, they are now able of supplying adequate placental perfusion for the fetus to grow. During invasion of cytotrophoblasts, they differentiate from epithelial (outer) to endothelial (interior), its vascular mimicry. In preX, cytotrophoblasts do not do this, the spiral arteries become shallow and remain small calibre vessels.

A

Preeclampsia/eclampsia

34
Q

Body.S:
Mother: kidneys, lungs, liver, heart, neurological system.
Fetus: risk of placental abruption, poor fetus growth, reduced amount of amniotic fluid

A

Preeclampsia/eclampsia

35
Q

S&S: Changes in vision, nausea and vomiting, persistent or severe headaches, abdominal pain, swelling on hands and face, sudden weight gain

A

Preeclampsia/eclampsia

36
Q

D.tests: If mother has:

  • Elevated resting BP on 2 separate recordings (above 140/90)
  • Excess protein in urine ( = or + 0.3g of protein in 24 hr urine collection OR 3+ protein on a urine dipstick)
A

Preeclampsia/eclampsia

37
Q

Treatments: (delivery of child is best treatment)

  • Medication to manage HTN (B-blockers, a-methyldopa, calcium channel blockers)
  • Magnesium sulfate can be used during labor, delivery and postpartum to prevent seizures
A

Preeclampsia/eclampsia

38
Q

Patho: Sporadic autosomal dominant syndrome, a hereditary genetic defect. There is a genetic deletion of 50 amino acids during coding for Lamin A from the LMNA gene, this causes telomere dysfunction and DNA damage and impairs DNA repair. Damage in the DNA causes upregulation of protein P53 which induces cellular senescence (biological aging) and apoptosis.

A

Progeria (Hutchinson Gilford Progeria Syndrome)

39
Q

Types:
HGPS: Mutation on gene LMNA, sporadic autosomal dominant trait, onset is in early childhood (1 to 2 years old)
Werner syndrome: Mutation on gene WRN, a recessive trait, onset is following puberty.

A

Progeria (Hutchinson Gilford Progeria Syndrome)

40
Q

Outcomes: Treatment are generally successful in managing complications and maintaining QOL. Most die 15 y.o due to HF, heart attack, stroke. Some live longer than 20 years depending on the type.

A

Progeria (Hutchinson Gilford Progeria Syndrome)

41
Q

S&S:

  • Baldness, alopecia, pinched nose, bulging eye, delayed tooth formation
  • short stature, high pitched voice, stiffness in joints
  • loss of body fat, progressive cardiovascular diseases and arteriosclerosis, stroke
A

Progeria (Hutchinson Gilford Progeria Syndrome)

42
Q

Diagnostics:

  • Based on physical symptoms mainly
  • X ray
  • Genetic test (blood test) is used for early detection of the disease
A

Progeria (Hutchinson Gilford Progeria Syndrome)

43
Q

Treatments: (incurable)

  • physical therapy (joint stiffness)
  • anticoagulant therapy (vascular blockage)
  • nitroglycerin (angina)
  • Zokinvy (Lonafarnib) PO (increases lifespan by an average of 1.6 years, prevents buildup of X, prevents cellular senescence)
  • Pravastin (lowers cholesterol and slows the progress of atherosclerosis)
A

Progeria (Hutchinson Gilford Progeria Syndrome)

44
Q

Patho: Group B Streptococcus (GBS) is a kind of gram positive bacteria and mainly lives in the GI tract, vagina, and urethra. Infection of GBS during pregnancy untreated can cause septicemia, pneumonia, meningitis to neonates. Onset of neonatal GBS results from aspiration of amniotic fluid or birth canal transmission during childbirth (more likely). Early onset is within the first week of life and late onset within the first week to 3 mo. of life.

A

Strep B Infection in Pregnancy

45
Q

Homeo: GBS causes beta-hemolysis or complete hemolysis. GBS is covered by a layer rich in sialic acid, immune cells in newborn confuse GBS for self-cells, allowing them to survive in the body. They have pili which allow them to attach to hostel cells. They posses C5a-ase enzyme that inactivates C5a, it hinders the accumulation of neutrophils at the site of infection.

A

Strep B Infection in Pregnancy (GBS)

46
Q

Body.S: reproductive, cardiovascular, urinary, neurological, immune, digestive, respiratory

A

Strep B Infection in Pregnancy (GBS)

47
Q

S&S:
Mother: often unnoticed, UTI, sepsis, infection of placenta and amniotic fluid, preterm birth
Newborn: EARY ONSET (sepsis, pneumonia, meningitis, fever, feeding problems, drowsiness)
Newborn: LATE ONSET (fever, feeding problems, drowsiness, more likely to have meningitis which can lead to cerebral palsy, hearing loos and death)

A

Strep B Infection in Pregnancy (GBS)

48
Q

Stats:

  • Early-onset X has dropped 80% in babies between the early 1990s and 2010,when the widespread onset of late-pregnancy testing and the use of antibiotics in X-positive women during labor.
  • X colonization has an incidence of 10-30% in pregnancy
  • Without preventative measures, early onset X infection occurs in 1% to 2% of neonates born to mothers with X colonization
  • Preterm infants with early-onset X infection have a case fatality rate between20% to 30% compared to 2% to 3% in term infants
A

Strep B Infection in Pregnancy (GBS)

49
Q

Diagnostic:

  • Obstetrics perform a rectovaginal culture of X in all pt. between 35-37 wk. gestation (also detected by urine)
  • Antibiotic susceptibility testing performed on all X culture to guide antibiotic prophylaxis in penicillin allergic pt.
A

Strep B Infection in Pregnancy (GBS)

50
Q

Treatments:

  • Prevention is best, principles defense against early onset X is the administration of antibiotic prophylaxis to mothers during labour and delivery (greater then 4 hrs before delivery).
  • IV penicillin G for intrapartum antibiotic prophylaxis
  • Ampicillin can be used as an alternative is penicillin G in unavailable
  • Vancomycin can be used in case of allergies to penicillin
A

Strep B Infection in Pregnancy (GBS)

Anatomy III (4 decks)

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