Unit 1

CHAPTER 5

congenital defects: abnormalities present at birth; caused by genetic, environmental, or intrauterine factors

single-gene disorders

• autosomal dominant: 50% chance of transmission, delayed onset, variable gene expression

  • ex: NF, von Willebrand disease, Marfan syndrome (connective tissue disorder)

• autosomal recessive: 25% chance of transmission, later onset, impairs function of an enzyme

  • ex: PKU, cystic fibrosis, sickle cell disease, Tay-Sachs disease

• x-linked recessive: females = carriers, males = affected

  • ex: hemophilia A, fragile X, Duchenne dystrophy

inherited multifactorial disorders

caused by genes + environmental factors

• ex: cleft lip/palate, club foot

chromosomal disorders

alterations in chromosome duplication, number, or structure

• ex: trisomy 21 (Down syndrome), monosomy X (Turner syndrome), polysomy X (Klinefelter syndrome)

deletion: a part of a chromosome or a sequence of DNA is left out during DNA replication

translocation: a chromosome segment changes position

nondisjunction: unequal separation during meiosis (→ aneu/poly-ploidy)

mosaicism: possession of more than one genetic line

dysgenesis: abnormal organ development during embryonic growth & development

NTD

caused by folic acid deficiency

anencephaly: absence of brain

myelomeningocele: sac-like protrusion of the brain’s meninges & spinal cord due to incomplete closure of the spine & its canal

meningocele: sac-like protrusion of spinal fluid, involves little to no nerve damage

CHAPTER 33

rupture of membranes

• PROM: occurred prior to onset of labor

• SROM: spontaneous, occurred on its own during labor

• AROM: artificial, done by provider

• PPROM: occurred prior to full-term gestation

cervical changes

• ripening: softening of the cervix

• effacement: 0-100%

• dilation: 0-10 cm

true vs false labor

cervical changes, contractions are relieved with movement or fluids, contractions are irregular, contractions are regular and gain intensity

4 P’s

1. passageway: 4 pelvic types (gynecoid, anthropoid, android, platypelloid)

2. passenger (fetus): fetal head (fontanels), attitude (position of head & extremities), and lie (longitudinal, oblique, or transverse)

3. position: cephalic presentation (vertex***, military, brow, face), breech presentation (frank, footling, complete), or transverse/shoulder presentation

   • engagement: 0 (ischial spines)

   • station: -5 → +5

   • occiput (O) = vertex (head)

   • mentum (M) = face

   • sacrum (S) = breech

   • acromion process (A) = shoulder

ideal: LOA or ROA

4. powers: primary forces (uterine muscle contractions) and secondary forces (abdominal muscle pushing)

   • increment: building up

   • acme: peak

   • decrement: letting up

   • frequency = how often?

   • duration = how long?

   • intensity = how strong?

stages of labor

1st:

• latent: cervix 0-6 cm, lasts 8-20 hrs. (primip) // 5-14 hrs. (multip), mild-moderate & regular contractions Q 10-30 → 5-7 minutes lasting 30-40 seconds

• active: cervix 6-8 cm, lasts 1-4 hrs., strong contractions Q 2-5 minutes lasting 40-60 seconds

• transition: cervix 8-10 cm, strong contractions Q 1.5-2 minutes lasting 60-90 seconds

  • increased rectal pressure, urge to bear down, increased amount of bloody show

2nd: begins with complete dilation and ends with birth

- duration: 3-4 hrs. (primip) // <15 minutes (multip)

- contractions: Q 1.5-2 minutes lasting 60-90 seconds, strong

3rd: begins with birth of infant and ends with delivery of placenta

4th: 1-4 hours after birth

physiological readjustment of mother’s body begins: ~500 mL average blood loss, BP drops, moderate tachy, thirsty/hungry, shaking chill, hypotonic bladder, uterus contracted & midline, fundus midline between symphysis pubis & umbilicus, cervix remains open immediately after birth

postpartum hemorrhage (PPH)

blood loss > 1000 mL + sxs of hypovolemia

causes: retained placental tissue, placenta previa, birth trauma, prolonged labor, precipitous (too fast) labor, overdistension of the uterus (multiparity, macrosomia, polyhydramnios)

manifestations: passing multiple/large blood clots (>nickel-golf ball size), may be minimal visible blood loss, may not be evident (by vital signs) until 1800-2100 mL of blood loss!!!

4 T’s

• tone

  • uterine atony: loss/lack of muscle tone leading to relaxation of the uterus LEADING CAUSE OF EARLY PPH

• tissue

• trauma

• thrombin

lacerations

1. skin

2. perineal

3. anal sphincter

4. anterior rectal wall

other

• chorioamnionitis: inflammation of fetal membranes (usually d/t infection)

  • fever, tachycardia, sore/painful uterus, foul smelling amniotic fluid

neonates

adaptations

respiratory

1. lung expansion must occur

2. pulmonary circulation must increase

cardiovascular

foramen ovale: in utero, blood with higher oxygen content is diverted to the heart/brain and there are limited amounts of blood to the lungs

ductus arteriosus: in utero, shunts blood directly to inferior vena cava

ductus venosus: in utero, connects pulmonary artery to descending aorta

immune

IgG crosses placenta (primarily during 3rd semester) to allow for a few weeks-months of protection

poor hypothalamic response to pyrogens

limited inflammatory response because immune system not fully activated

alterations

preterm (<37 weeks)

• respiratory distress d/t low surfactant

• lanugo

• microsomia

post term (>42 weeks)

• aging placenta

• meconium aspiration

• macrosomia

• dry/cracked/peeling skin

• long nails

• meconium-stained skin/hair/nails

• caput succedaneum (serum filled)

• cephalhematoma (blood filled)

birth trauma

• fractures (skull, clavicle, humerus, femur)

• PNS injuries

• CNS injuries (subdural hemorrhage/hematoma, etc.)

CHAPTER 8

intracellular fluid (ICF) stores 2/3 of body fluids

extracellular fluid (ECF) stores 1/3 of body fluids

electrolytes

• sodium (135-145): highest outside the cell, extra/intracellular shifts are controlled by Na+/K+-ATPase pump, THINK BRAIN

  • baroreceptors (“pressure sensors”): regulate circulating volume

  • atrial natriuretic peptide (ANP): released in response to atrial stretch & overfilling, increases sodium excretion by kidneys

  • renin-angiotensin-aldosterone system (RAAS): stimulated by changes in arterial pressure, GFR, & sodium

  • thirst: controlled in hypothalamus, regulates water intake, osmoreceptors respond to changes in ECF osmolality by swelling (→ - thirst) or shrinking (→ + thirst)

  • anti-diuretic hormone (ADH): regulates water output, responds to changes in ECF osmolality and volume

  • hyponatremia: → cellular swelling

  • hypernatremia: → cellular dehydration, thirst, increased ADH

• potassium (3.5-5.0): highest inside the cell, extra/intracellular shifts are controlled by Na+/K+-ATPase pump, THINK HEART

functions: regulates resting membrane potential, opening of sodium channels that control current flow during action potential, etc.

• calcium (9-11): exists in 3 forms (protein bound, complex, ionized)

• phosphate (2.5-4.5):

functions: major role in bone formation

• magnesium (1.8-3.0):

functions: all reactions that require ATP, energy metabolism, smooth muscle relaxant, neuroprotective agent, potassium channel activity

fluid exchange

forces:

1. filtration/hydrostatic (blood pressure) = pushing

2. oncotic/osmotic/colloidal = pulling

location:

1. intravascular/blood/capillary

2. tissue/interstitial

• edema: accumulation of fluid in interstitial space (between cells)

  1. increased capillary filtration pressure (increased arterial/venous pressure & capillary distension)

  2. decreased capillary colloidal osmotic pressure (inadequate production/abnormal loss of plasma proteins)

  3. increased capillary permeability (enlarged/damaged capillary pores)

  4. obstructed lymph flow

• third-space fluid accumulation: accumulation of (non-functional) fluid in transcellular space (in a compartment)

fluid volume deficit (FVD)

• isotonic FVD: reflect decrease in ECF volume

  • sx: thirst, signs of h20 conservation, impaired temp regulation

fluid volume excess (FVE)

• isotonic FVE: increase in interstitial and vascular fluids