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Flashcards in Exam 2 pt. 2 Deck (224):
1

general deficiency of BOTH PROTEIN AND CALORIES

Marasmus

*weight below 60th percentile

2

presents with:
-Prominent abdomen from edema due to low albumin**
-Sparing of subcutaneous fat and muscle
-Hair loss
-Pale, scaly skin
-Fatty liver
-Recurrent infections

Kwashiorkor

3

deficiency of PROTEIN ONLY

Kwashiorkor

4

presents with:
-Lack of edema since albumin normal or slightly reduced**
-Muscle breakdown/loss
-Subcutaneous fat loss
-Very thing extremities
-Old appearance
-Apathetic, withdrawn, and lethargic
-Vitamins and mineral deficiency
-Recurrent infections

Marasmus

5

deficiency of protein and calories that is second to CANCER

Cachexia

*Inadequate intake of proteins and calories in the diet

6

presents with:
- tumor necrosis factor, proteolysis-inducing factor secreted leads to increased catabolic activity

Cachexia

*Similar appearance to marasmus,

7

self-induced starvation, marked weight loss

anorexia

8

Binge eating followed by self-induced vomiting

bulimia

*Sometimes shows Russell’s sign on knuckles

9

presents with:
-Amenorrhea
-Decreased bone density
-Dry skin and hair
-Cold intolerance
-Bradycardia
-Electrolyte imbalance
-Unregulated potassium
-Cardiac arrthymias

anorexia and/or bulima

10

presents with:
-Night blindness
-Dry conjunctiva (xerosis), small grey plaques (Bitot’s Spots)
-Ulceration and necrosis of cornea (keratomalacia)
-Skin changes to dry with popular eruptions
-Immune dysfunction
-Increased risk for infection

Vit. A deficiency

11

presents with:
-Rarely occurs in elderly after excess ingestion
-Acute and chronic toxicity
-Bone pain, liver damage, weight loss

Hypervitaminosis A

12

presents with:
-Nervous and cardiovascular systems
-Beriberi disease forms
-alcohol abuse (Korsakoff’s Syndrome or Wernicke'ss Encephalopathy)
-edema

Vit. B1 (thiamine) deficiency

13

thiamine

Vit. B1

14

Beriberi Disease Forms

1. “Dry” – peripheral neuropathy
2. “Wet” – Cardiomyopathy
3. “Infantile” – Cardiac failure, cyanosis

15

korsakoff’s Syndrome

amnesia, psychosis

16

Wernicke’s encephalopathy

abnormal gait, aphasia, confusion

17

presents with:
-Seen in elderly and chronic alcoholics
-Scurvy**

Vitamin C Deficiency

18

signs of scurvy

1. Swollen, bleeding gums
2. Poor wound healing
3. Loss of teeth
4. Hyperkeratosis of hair follicles
5. Easy bruising
6. Petechia- minor skin hemorrhages

19

presents with:
Rickets
Osteomalacia

Vit. D Deficiency

20

adults characterized by bone thinning and muscle weakness

Osteomalacia

21

in children characterized by impaired bone development and growth (bowing of extremities)

Rickets

22

Essential for calcium and phosphate homeostasis and caused by inadequate sun, malabsorption, and hepatic/renal disease

vit. D deficiency

23

presents with:
-Dehydration
-Muscle weakness
-Constipation
-High levels of calcium → calcification of heart, vasculature and kidneys

Hypervitaminosis D

24

the most common form of Vit. E deficiency

Tocopheral

25

presents with:
-malabsorption: fat soluble vitamin
-Results in anemia, spinocerebellar ataxia: slowly progressive and irreversible disorder of gait

Vit. E deficiency

*vit. E acts as an antioxidant

26

presents with:
-increased bleeding
-Elevation of lipids
-Depressed thyroid hormones
-Blotchy skin

Hypervitaminosis E

*rare and excess acts like an anticoagulant

27

-Essential for synthesis of coagulation factors 10, 9, 7, 2
-Obtained from diet

vit. K

28

-Adults are rarely deficient (more common in newborns)
-Liver disease/chronic alcoholics
-Anticoagulant mediactions (secondary)
-Inflammatory bowel disease
-Malabsorption syndromes
-Cystic fibrosis

Vitamin K Deficiency

29

presents with:
-Anemia
-Bruising
-Bleeding of gums/nose/heavy menstrual periods

Platelets: normal
PT: elevated
PTT: elevated

Vitamin K Deficiency

30

why is Vit. K deficiency more common in newborns

-Placental transfer of Vitamin K is low
-Get insufficient amounts in breast milk

31

what is the precursor for niacin

Tryptophan

32

another name for niacin

Vit. B3

33

Vitamin B3 (Niacin) Deficiency is most common where

Developing countries
Chronic alcoholics

34

presents with:
Pellagra (rough skin) Disease
-Dermatitis
-Diarrhea
-Dementia

Vitamin B3 (Niacin) Deficiency

35

Pellagra disease

rough skin: dermatitis, diarrhea, dementia

36

results in:
-Alcoholism/liver disease
-Celiac disease (intestinal malabsorption)
-Increased demand (pregnancy, cancer)
-Medications (methotrexate)
-Megaloblastic Anemia

Folate deficiency

37

presents with:
-Pernicious anemia* (lack of intrinsic factor)/ Megaloblastic Anemia
-Malabsorption
-Bacterial overgrowth in bowel
-Parasitic infection with fish tapeworm

B12 deficiency

38

what nutritional deficiencies lead to anemia

Vit. E deficiency
Vit. K deficiency
Excess lead
Folate and B12 Deficiency

39

-Low number of RBCs
-SMALLER than normal RBCs
-Low hemoglobin content in RBCs (hypochromic)

Microcytic anemia

40

-Decreased number of RBCs
-LARGER than normal RBCs
-Variation in size of RBCs
-Abnormal WBCs (hypersegmented nuclei)

Megaloblastic anemia/macrocytic

41

what causes macrocytic anemia

folate and B12 Deficiency

42

what vitamins are essential for DNA synthesis

folate and B12

43

presents with:
macrocytic anemia
palpitations
neural tube defects in fetus

folate Deficiency

44

presents with:
macrocytic anemia
spinal cord sclerosis
peripheral neuropathy
ataxia

B12 Deficiency

45

what trace elements cause disorders when in EXCESS

aluminum
copper
lead

46

what trace elements cause disorders when deficient

Zinc
Iodine
Selenium

47

what causes:
Chronic dialysis patients
Encephalopathy
Skeletal abnormalities

excess aluminum

48

excess copper can cause

wilsons disease

49

presents with:
-Copper accumulates in tissues
-Cirrhosis
-Neurological damage
-Kayser-Fleischer ring

wilson's disease due to excess copper

50

what causes:
-Peripheral nerve damage
-Renal damage
-Anemia

excess lead

51

what causes:
-Alopecia
-Diarrhea
-Impaired wound healing
-Dermatitis
-Inherited - Acrodermatitis enteropathica

too little Zinc

52

what causes:
Hypothyroidism/Goiter

too little iodine

*common in developing countries

53

what causes:
-Cardiac failure
-Hepatic necrosis

too little selenium

54

what factors contribute to obesity

genetics
nutrition
environment
psychological

55

associations of obestity

-Type 2 Diabetes
-Dyslipidemias
-Cardiovascular disease
-Hypertension
-Cancer

56

what BMIs are considered overweight and obese

overweight : 25-30 kg/m2
Obese: >30kg/m2

57

mean, medium, and mode are about equal

Gaussian/normal/bell-shaped

58

mean, medium, and mode are not equal

Skewed/nonparametric

59

population you’re looking at; what’s considered normal, usually middle 95%

reference Range/Interval

60

accuracy of instrument

reportable range

61

most tests have upper and lower limits of accuracy; determine cut-off points for reporting only

linearity

want 1:1

62

MEAN +/- 2 SD = central 95% for normal distributions

Normal 1 for reference range

63

PERCENTILEs, median instead of mean for skewed distributions

Normal 2 for reference range

64

therapeutic rangee vs toxic range

normal 4 for reference range

65

risk factor (i.e. myocardial infarction

normal 3 for reference range

66

how is a reference range determined

1. Mean +/- 2 SD
2. Percentiles (use median instead of mean for skewed distributions)
3. risk factors
4. therapeutic range vs toxic range
*come from healthy ppl (can depend on age/gender/race

67

how close to target value

accuracy

68

how much variability in result

precision

69

ability to detect disease when present, TP/diseased

sensitivity

70

ability to rule out disease when absent, TN/nondiseased

specificity

71

likelihood of accurately predicting diseased state with positive results

PPV

72

likelihood of accurately predicting nondiseased state with negative results

negatve PV

73

draw the +/- PV table

first column: disease+: TP, FN
second column: nondisease: FP, TN

Row1: + test
Row 2: - test

74

A more precise test has a _______ CV

LOWER

75

Sensitivity rules___ , specificity rules ___

out

in

76

Sensitivity optimized by a____ cut-off point

low

77

Specificity optimized by a____ cut-off point

high

78

how do you establish cutoff

Receiver operator curves (ROCs)
*usually want to achieve highest sensitivity with lowest false positives (1-specificity) for optimum test

79

____ is value most affected by prevalence or incidence of disease

PPV

80

ability of diagnostic test to identify true disease without missing anyone by leaving disease undiagnosed

sensitivity

81

if screening test is negative, you have ruled out possibility of disease since you’re setting cut off so low to catch as many people as possible with disease at expense of calling some people diseased when they’re truly not

sensitivity

82

screening tests tend to have a high ____

Confirmatory tests tend to have a high ___-

sensitivity

specificity

83

ability of diagnostic test to be negative “correctly” in absence of disease; high specificity test has few false positives and is effective in ruling conditions in

specificity

84

After screening test calls someone diseased (which could very well be false), highly specific test will then confirm result of screening test or rule disease in (remember set cutoff so high that positive result is very likely to be from diseased patient)

specificity

85

Further value is away from “normal,” more likely it’s:

clinically significant

86

are normal lab values always good?

NO
*As part of typical disease processes certain tests are expected to be abnormal, Failure to change can indicate inability of body to respond appropriately

87

two sets of date may have similar means but be otherwise very dissimilar

variance

88

standard deviation/mean x 100%; relative standard deviation

coefficient of Variation (CV)

89

list ways that sample quality can be compromised

1. collection (Patient ID, labels, tube/container- anticoagulant/preservative, sample type – blood/urine), phlebotomy technique (needles size, stasis, contamination)
2. processing (time and temp)
3. hemolysis (shaking, small needle, heat, cold, absorbs light)

90

Some analytes found in higher concentraitno in RBCs than in serum
*large increases

K, LDH, AST

91

Some analytes found in higher concentraitno in RBCs than in serum
*modeate increases

ALT, coag test, folate iron, lithium (if on therapy)

92

Some analytes found in higher concentraitno in RBCs than in serum
*small increases

Mg, phosphate, Ca bilirubin

93

Some analytes found in higher concentraitno in RBCs than in serum
*moderate decrease

haptoglobin

94

Difference between patient’s present laboratory result and previous result which exceeds predefined limit

delta check

*reported by laboratory

95

Delta checks are investigated by the lab internally to rule out:

1) mislabeling
2) clerical error or
3) possible analytical error

96

hormones associated w/ pregnancy

1. estrogens
2. progesterone
3. hCG (human chorionic gonadotropin)
4. human placental lactogen (hPL)
5. Inhibin

97

what hormones does the placenta produce

hCG
hPL (human placental lactogen)

98

when is hCG detectable

early as 1 day after implantation (8-9 days after fertilization)

*doubles every 2-3 days with

99

what function does hCG have

-Prevents regression of corpus luteum via interaction with LH receptors
-Promotes secretion of progesterone and prevents menstruation

100

pathologic conditions associated with hCG

ectopic pregnancy
*causes it to rise abnormally

101

also promotes fetal growth, exerts glucose-sparing effect on maternal metabolism

hPL
*Like GH (growth hormone) spares glucose and protein and shifts to fat metabolism

102

stimulates E2 and Pr to promote breast maturation for lactation

hPL

103

pathological conditions due to hPL

contributes to gestational diabetes

104

what spikes first in pregnancy and what spikes last

1st- hCG (then drops about week 26)
last- estsrogen

105

ectopic pregnancy effects 1 in out many pregnancies

1:150

106

most ectopic pregnancies occur wher

90% in fallopian tube and also in ovary, cervix, abdomen

*35-50% w/ prior PID

107

how do you diagnose ectopic pregancy

1. Clinical symptoms (pain, spotting)
2. β-hCG (rises abnormally)
3. ultrasound
4. endometrial curetting

*Serum hCG test → positive → ultrasound → identify IUP → if not, is hCG in discriminatory zone?

108

presents with:
-Adnexal/abdominal pain
-Amenorrhea or spotting
-Rupture= EMERGENCY
-Severe abdominal pain, shock (fainting, sweating)

ectopic pregnancy

109

Umbrella term with discrete diagnoses depending on which tissue type proliferates; abnormal proliferation of placental-type tissue

gestational trophoblastic disease (GTD)

110

diandric
diploid (46, XX)

complete mole

*2 copies from Dad

111

diandric triploid
(69, XXY)

partial mole

112

___% complete moles develop persistent GTD

___ % develop choriocarcinoma

20%

1-2%

113

example of GTDs

1. complete hydatidiform mole
2. partial hydatidiform mole
3. complete vs partial mole
4. choriocarinoma

114

how is a complete mole formed

-85% one sperm fertilizes anucleate egg and divides

-15% two sperm fertilize anucleate egg

(2 copies from dad only)

115

complete moles affect 1 in how many pregnancies in the US

1: 1500

116

risk factors for Complete hydatidiform mole

Extremes (both young and old) of childbearing years
*history of previous molar pregnancy

117

presents with:
elevated β-hCG, uterine size >> dates, hyperemesis gravidarum, vaginal bleeding, early pre-eclampsia, hyperthyroidism
“Grape-like” vesicles

Complete hydatidiform mole

118

histology:
-Hydropic (watery/edematous) villi-Scalloped shape
-Absent fetal development
-Circumferential trophoblast proliferation

complete hydatidiform mole

119

fetal development is driven by whos DNA

moms DNA

120

Circumferential trophoblast proliferation is driven by whos DNA

dads DNA

121

partially dad: 2 sets of dad, one of mom

Partial hydatidiform mole

122

histology:
-Admixture of hydropic and fibrotic villi
-“Lacy” trophoblast hyperplasia
-Villous inclusions

Partial hydatidiform mole

123

Association with fetal syndactyly (fusion of digits, especially ¾)

Partial hydatidiform mole

124

US results:
"Snowstorm” appearance, cystically dilated spaces without fetal parts

Complete hydatidiform mole (CHM)

125

US results:
Large cystic spaces, +/- fetal tissue, subtle

Partial hydatidiform mole (PHM)

126

Complete molar pregnancy puts women at higher risk for ___

choriocarcinoma

127

choriocarcinoma affects 1 in how many pregnancies

25,000-40,000

128

presents with:
-Vaginal bleeding, High serum β-hCG
-Single/multiple hemorrhagic well-circumscribed nodules

choriocarcinoma

129

how do you diagnose choriocarcinoma

-Biphasic pattern with hemorrhage and necrosis
- histologically
-detect recurrence with serum β-hCG

130

histology:
-Marked nuclear atypia and mitoses
-No chorionic villi present

choriocarcinoma

131

what causes post-partum hemorrhage

1. uterine atony (80%)
2. subinvolution of placental bed vessels
3. abnormal placental adherence
4. DIC (disseminated intravascular coagulation

132

-Lack effective myometrial contractions
Complicates 1 in 20 births

uterine atony

133

risk factors of uterine atony

overdistention
uterine fatigue
infection
retained placental tissue

134

-massive activation of clotting cascade results in widespread thrombosis
-Secondary depletion of platelets & coagulation factors leads to bleeding, ischemia, & shock

DIC

135

risk factors of DIC

1. Pregnancy is inflammatory/prothrombotic state
2. Amniotic fluid embolus (anaphylactoid, complement)
3. Fetal demise (retained >4 weeks, TF release)
4. Placental abruption (TF release)
5. Pre-eclampsia, eclampsia, HELLP (Hemolysis, Elevated Liver Enzymes, Low Platelets) (damaged endothelium)
6. Massive hemorrhage

136

why are there changes in laboratory values that occur in a normal pregnancy

1. things get diluted
2. things the fetus is actively taking
3. changes in metabolsim vis hPL
4. acute phase rxn

137

-Failure of decidual formation
-Trophoblast invade abnormally more deeply

abnormal placental adherence

138

Predisposing factors: prior C-section, endometrial ablation, multiple DandC’s

abnormal placental adherence

139

what are things that get diulted out during pregnancy

↓ electrolytes, hemoglobin, creatinine

140

what are things that the fetus is actively taking which changes lab values

(↓ glucose, calcium, iron)

141

what are changes in metabolism that are asscoiated w/ pregnancy

(↑ triglycerides, cholesterol)

142

what are changes in lab values that are a result of acute phase rxn (pregnacny as an inflammatory state)

↓ albumin, natural anticoagulants

↑ fibrinogen, coagulation factors, platelet activity

143

-Bacteria from cervico-vaginal flora
-Related to PTL/PROM*

acending chorioamnionitis

*PTL = Pre-term labor; PROM = Premature rupture of membranes

144

what causes fetal inflammatory response in ascending chorioamnioitis

maternal neutrophils in membranes

145

Histopathology:
chronic villitis, intervillositis, lymphoplasmacytic deciduitis

trans-placental (hematogenous) chorioamnionitis

146

trans-placental (hematogenous) chorioamnionitis is related to what?

Premature labor
hydrops
IUGR
IUFD
*TORCH

147

fetal inflammatory response

-Umbilical cord vasculitis
-Chorionic plate vasculitis

148

detachment of placenta from decidual seat

abruptio placentae

149

presents with:
total/acute with abdominal pain; most are partial & painless

abruptio placentae

150

if rapid and close to delivery, may find no histological evidence (“best clinical diagnosis”)

abruptio placentae

151

clot forms, then compresses underlying villous tissue
-Hemosiderin appears after 4-5 days

abruptio placentae

152

presents with:
fibrin clot with rim of villous infarction
-May see evidence of bleeding during pregnancy

chronic abruption (placenta)

153

Failure of decidual formation

abnormal placental adherence

154

pathophysiology:
Trophoblast invade abnormally more deeply

abnormal placental adherence

155

predisposing factors of abnormal placental adherence

prior C-section, endometrial ablation, multiple D and Cs

156

chorionic villi ADHERE directly to myometrium

placenta Accreta:

157

villi INVADE myometrium

Placenta INcreta

158

villi PERMEATE to serosa

Placenta PERcreta

159

abnormal location of placenta

Placenta Previa

*placenta covers internal cervical os

160

Placenta Previa increase your risk for:

abruption, postpartum hemorrhage, C-section

*absolute risk for c-section

161

Fetal vessels overlying cervical os (not protected by stroma)

vasa previa

*absoulte indication for c-section

162

Velamentous (membranous) insertion of cord

vasa previa

*not protected by Wharton's jelly

163

Unidirectional arterio-venous connections
-Donor twin is dehydrated & anemic, while recipient twin is plethoric

twin-twin transfusion syndrome

164

pathological association of short umbilical cord (

decreased fetal movement and neurodevelopmental problems

165

pathological association of long umbilical cord (>75cm)

-Associated with knots and fetal entanglement
*May correspond to later hyperactivity

166

presents with:
-increased blood pressure, proteinuria, +/- edema
-headache, visual disturbance, rapid weight gain

pre-eclampsia
aka toxemia of pregnancy

167

what percent of women are affected by pre-eclampsia and when

5-10%

usually 3rd trimester but 20 weeks GA--- 6 weeks postpartum

168

pathophysiology:
Defective implantation: Inappropriate re-modeling of spiral arterioles- Form of maternal malperfusion of placenta

pre-eclampsia

169

pathophysiology:
Abnormal Placentation: Cytotrophoblast fail to adopt an invasive endothelial phenotype--> Invasion of the spiral arteries is shallow
-->Small caliber, high resistance vessels

pre-eclampsia

170

fetal effects to the baby from pre-eclampsia

Placental hypoperfusion and ischemia → decreased oxygen to the baby

171

histology:
-Decidual vasculopathy: deposition of dense pink fibrinoid around vessels→ high resistnace system
-Tenney-Parker Change: widely spaced villi (white space) small terminal villi, big syncytial knot
-Infarcts and abruption: obliterated parenchyma (cessation mom’s blood flow)= infarct

pre-eclampsia

172

what is the cure of pre-eclampsia

delivery

173

causes of spontaneous abortion according to trimester

1st trimester- chromosomal
2nd trimester- structural defects, placental, infectious
3rd trimester- placental, structural defects

174

fasting glucose, random glucose, and HbA1c values for diabetes

Fasting glucose greater or equal to 126 mg/dL
Random glucose greater or equal to 200 mg/dL
Hemoglobin A1C greater or equal to 6.5%

175

fasting plasma glucose value for gestational diabetes


Fasting plasma glucose ≥92 mg/dL ,

176

etiology of symmetric IUGR

genetic

177

etiology of asymmetric IUGR

relative macrocephaly, placental or maternal etiology, often oligohydramnios

178

oligohydramnios

not enough amniotic fluid

179

Failure of normal embryogenesis

neural tube defect

*occurs in 1st month of pregnancy before women realize they are pregnant

180

what prevents neural tube defects

folic acid

181

fetal albumin which does many of same functions (maintain oncotic pressure, bind/transport substances)
-Initially produced in yolk sac then in larger quantities by fetal liver

alpha fetoprotein

182

what is suspected to happen to AFP with NTD

leak directly into amniotic fluid

183

high levels of AFP correlate w/ what

spina bifida and anencephaly

184

failure of spinal fusion

spina bifida

185

what is the difference between closed and open spina bifida

Closed = cord isn’t directly exposed (may have few symptoms)

open= exposed (meninges and/or cord) (symptoms are varialbe but not necessarily fatal)

186

meninges protrude through defect

meningocele

187

meninges and cord protrude

Myelomeningocele

188

braina nd skull malformation

anecephaly

*ultimately fatal

189

muscular abdominal wall defect allows peritoneal membrane and organs to protrude

Omphalocele

*usually w/ genetic syndromes

190

examples of ventral wall defects

1. omphalocele
2. gastroschisis

191

total abdominal wall defect allows portion of abdominal organs to protrude

Gastroschisis

*NOT usually w/ other genetic anomalies

192

Vental wall defects are associated with what

high maternal serum AFP (MoM)

193

most common neoplasm of newborn

Sacrococcygeal

194

45, XO

Monosomy X (turner syndrome)

195

presents with:
short stature, neck anomalies (webbing, cystic hydroma), gonadal hypoplasia/infertility
amenorrhea

Monosomy X (turner syndrome)

196

Most common genetic abnormality leading to fetal loss in 1st trimester

Monosomy X (turner syndrome)

197

47, XX (or Y) +21

trisomy 21 (downs syndrome)

198

presents with:
SGA, round/flat face with slanting palpebral fissures, transverse palmar crease (“simian” crease), gap between 1st and 2nd toes (“thong” toe)

trisomy 21 (downs syndrome)

199

presents with:
heart and GI anomalies; pancreatic, bone marrow fibrosis (predisposition to leukemias

trisomy 21 (downs syndrome)

200

47, XX (or Y), + 18

Trisomy 18 (edward syndrome)

201

presents with:
SGA, hand and face deformities, “rocker-bottom” feet
Omphalocele

Trisomy 18 (edward syndrome)

202

presents with:
heart anomalies, renal fusion (“horseshoe”)

Trisomy 18 (edward syndrome)

203

47, XX (or Y), +13

trisomy 13 (Patau syndrome)

204

presents with:
SGA, polydactyly and facial defects, cutis aplasia, “rocker-bottom” feet

trisomy 13 (Patau syndrome)

205

presents with:
heart, brain, kidney defects; pancreato-splenic fusion

trisomy 13 (Patau syndrome)

206

what does the triple test test for

AFP
hCG
Unconjugated estriol (uE3)

207

down syndrome cutoff for AFP, hCG, and Unconjugated estriol in the triple test

AFP (2.0 MoM)
Unconjugated estriol (,0.5 MoM)

208

what condition?
MSAFP- increased
uE3- normal
hCG- normal

neural tube defect

209

what condition?
MSAFP- low
uE3- low
hCG- increased

Trisomy 21

210

what condition?
MSAFP- low
uE3- low
hCG- low

trisomy 18

211

what condition?
MSAFP- low
uE3- low
hCG- very high

Molar pregnancy

212

what condition?
MSAFP- increased
uE3- normal
hCG- increased

Multiple gestations

213

what condition?
MSAFP- increased
uE3- low
hCG- low

fetal death (still birth)

214

what does the quad screen test?

AFP
uE3
β hCG
inhibin A

215

secreted by placenta and suppresses FSH, levels correlate with hCG

inhibin A

216

what is the best screening test for women who present for prenatal care in 2nd trimester?

Quad screen

217

Quad screen has a PPV of ____ with all ages for Down Syndrome

1:50

80% sensitivity

218

combined tests for down syndrome

-u/s for fetal nuchal translucency
-B-hCG increased
-PAPP-A increased (pregnancy associated plasma protein-A)

219

Produced by embryo and placenta

PAPP-A

220

Thought to help prevent recognition of fetus by maternal immune system (binds cytokines) and stimulate angiogenesis

PAPP-A

221

low levels of PAPP-A are associated with what?

down syndrome
IUGR
premature delivery
pre-eclampsia

222

how do you confirm DS or neural tube defect?

chorionic villus sampling
*test tissue for DNA

1% risk of SAB

223

measure of average RBC volume that’s reported as part of standard CBC

mean corpuscular volume (MCV)

224

levels of MCV of microcytic, normocytic, and macrocytic anemia

Microcytic - 100 fL