Exam 2 pt. 2 Flashcards
(224 cards)
1
Q
general deficiency of BOTH PROTEIN AND CALORIES
A
Marasmus
*weight below 60th percentile
2
Q
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
A
Kwashiorkor
3
Q
deficiency of PROTEIN ONLY
A
Kwashiorkor
4
Q
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- Apathetic, withdrawn, and lethargic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
A
Marasmus
5
Q
deficiency of protein and calories that is second to CANCER
A
Cachexia
*Inadequate intake of proteins and calories in the diet
6
Q
presents with:
- tumor necrosis factor, proteolysis-inducing factor secreted leads to increased catabolic activity
A
Cachexia
*Similar appearance to marasmus,
7
Q
self-induced starvation, marked weight loss
A
anorexia
8
Q
Binge eating followed by self-induced vomiting
A
bulimia
*Sometimes shows Russell’s sign on knuckles
9
Q
presents with:
- Amenorrhea
- Decreased bone density
- Dry skin and hair
- Cold intolerance
- Bradycardia
- Electrolyte imbalance
- Unregulated potassium
- Cardiac arrthymias
A
anorexia and/or bulima
10
Q
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
A
Vit. A deficiency
11
Q
presents with:
- Rarely occurs in elderly after excess ingestion
- Acute and chronic toxicity
- Bone pain, liver damage, weight loss
A
Hypervitaminosis A
12
Q
presents with:
- Nervous and cardiovascular systems
- Beriberi disease forms
- alcohol abuse (Korsakoff’s Syndrome or Wernicke’ss Encephalopathy)
- edema
A
Vit. B1 (thiamine) deficiency
13
Q
thiamine
A
Vit. B1
14
Q
Beriberi Disease Forms
A
- “Dry” – peripheral neuropathy
- “Wet” – Cardiomyopathy
- “Infantile” – Cardiac failure, cyanosis
15
Q
korsakoff’s Syndrome
A
amnesia, psychosis
16
Q
Wernicke’s encephalopathy
A
abnormal gait, aphasia, confusion
17
Q
presents with:
- Seen in elderly and chronic alcoholics
- Scurvy**
A
Vitamin C Deficiency
18
Q
signs of scurvy
A
- Swollen, bleeding gums
- Poor wound healing
- Loss of teeth
- Hyperkeratosis of hair follicles
- Easy bruising
- Petechia- minor skin hemorrhages
19
Q
presents with:
Rickets
Osteomalacia
A
Vit. D Deficiency
20
Q
adults characterized by bone thinning and muscle weakness
A
Osteomalacia
21
Q
in children characterized by impaired bone development and growth (bowing of extremities)
A
Rickets
22
Q
Essential for calcium and phosphate homeostasis and caused by inadequate sun, malabsorption, and hepatic/renal disease
A
vit. D deficiency
23
Q
presents with:
- Dehydration
- Muscle weakness
- Constipation
- High levels of calcium → calcification of heart, vasculature and kidneys
A
Hypervitaminosis D
24
Q
the most common form of Vit. E deficiency
A
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
