Final Flashcards

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1
Q

What is an MHC2 Molecule?

A

Major histocompatibiltiy complex class 2, with APC MHC II binds to the antigen and presents/attacks after APC cells have presented to CD-8 Cells.

Basically the protein bound on the antigen presented by the APC that marks this antigen as bad - everyone come over! Alarm bell.

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2
Q

Which antibodies cross the placenta?

A

IgG because of size

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3
Q

When does the baby’s immune system kick in?

A

Born with passive immunity, but active immunity (own significant production of IgG) not until 6 mo, and full antibody response doesn’t activate for years.

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4
Q

Difference between innate and adaptive immunity with examples.

A

Innate - general physical and biochemical barriers that respond generally
adaptive - cellular and humoral components that respond to specific foreign substances. These two systems work together. Example of innate - skin. Example of adaptive - immunity to a disease.

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5
Q

Stages of implantation (blastocyst, zona pellucida)

A

Apposition (interaction b/w blastocyst and epithelium),

Adhesion (increase in interaction),

Invasion (penetration)

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6
Q

4 main functions of the placenta

A

Endocrine, Immuno, and Metabolic, Transport (gases, nutrients, and wastes)

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7
Q

Indications for Rh immunoglobulin (winro, Rhogam)

A

28 weeks of gestation

72 hours of birth if infant Rh +.

Would be given earlier to Rh - person in abortion, pregnancy loss, bleeding, amniocetis (?)or significant injury.

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8
Q

Common antigens to cause incompatibility (ABO, RH)

A

Allomunization is a response to NON SELF

● Rh D antigens are more common to cause incompatibility because they are highly immunogenic. Also are well developed at birth. Plasma does not normally have any anti-D antibodies. (Rh - parent, Rh + bb)

Indirect Coombs test and tests maternal blood for existence of anti-D antibodies in Rh(neg) birther. Having anti-D antibodies in plasma is a sign that isoimmunization (alloimmunization is synonymous) has occurred and is dangerous if baby is Rh(pos).

● ABO incompatibility can occur in first pregnancy, occurs when mother is Type O and baby is Type A, B, or AB
● ABO antibodies cause less damage because the proteins are not expressed as profusely and are not well developed at birth.
■ Larger antigens, usually IgM, so can’t cross the placenta
■ A/B antigens also appear on somatic cells and in body fluids, so the antibodies get “bound up” on other cells, other than RBCs.
■ Fewer A/B antigens on fetal RBCs, A/B antigens are weak

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9
Q

When concerned about RH isoimmunization (characteristics of baby and birther)

A

● Rh isoimmunisation occurs if a D-neg person is exposed to D-pos RBCs, which triggers an immune response and the D-neg person starts making anti-Rh antibodies
● Does not normally happen in first pregnancy, but at birth of first child fetal blood mixes with maternal blood causing pregnant person to develop antibodies, but then when next Rhpos baby is present, there are anti Rh+ IgG antibodies, which cross the placenta and attack the developing fetus

● If the RdD(neg) birther becomes isoimmunized and passes IgG anti-D antibodies across the placenta to the Rh(pos) fetus, the newborn baby can develop Hemolytic Disease of the Newborn. The anti-D antibodies bind the RBC cells in the newborn, the resulting lack of RBCs can result in anemia and the break down of the excessive RBCs can lead to hyperbilirubinemia (pathological jaundice). The presence of maternal anti-D antibodies in the newborn is tested with the direct Coombs test.

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10
Q

Which test determines amount of fetal maternal haemorrhage (KHB test or Rosette?) (qualitative vs quantitative)

A

● Rosette = qualitative = IF there was mixing
● KB test = quantitative = HOW MUCH mixing occurred

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11
Q

2 steps of determining ABO blood grouping? “Sometimes its genes, sometimes its genes and environment; think about those things.”

A

**● Step 1: ABO Typing **
■ Mixing of blood and antibodies against type A & B blood (in separate vials/tests) to determine which combos agglutinate
**● Step 2: Back Typing **
● Serum is mixed with blood that is known to be type A (contains anti-B antibodies) or type B (contains anti-A antibodies) to determine antibody presence

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12
Q

Causes for low platelets

A

● Hemodilution= the overall plasma volume is increased, but the platelet count stays the same, so total number of platelets per volume of blood will be lower
Also medical conditions related to bone marrow – blood cancers. Also autoimmune diseases
● Gestational thrombocytopenia
● Immune thrombocytopenia
● Thrombotic macroangipopathy
● Autoimmune disease
● Drugs
● Preeclampsia
● HELLP syndrome

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13
Q

Hemodilution in pregnancy - components of the blood

A

● Overall blood volume increases (30-40%) o
● Plasma volume increases 40-60%
● Hypervolemia
● Net lower RBC/platelet volume (RBC’s increase but not as much as plasma and volume)

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14
Q

Iron deficiency anemia - what is LOW (be specific, eg. mean corpuscular volume) LOOK AT CHART

A

Iron deficiency anemia =
LOW: RBCs, hemoglobin, MCV, MCH, MCHC, & ferritin

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15
Q

What is a sex linked disorder

A

a genetic mutation on the X chromosome.

These are also inherited in a dominant or recessive pattern.

There are also disorders associated with the Y chromosome, but these are inherited less frequently. (ex. colour blindness)

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16
Q

Define aneuploidy

A

The addition of deletion of an entire chromosome in a normal set of 23 pairs resulting in an abnormal number of chromosomes in a haploid set (something other than 2 pairs of each chromosome) (ex. downs syndrome)

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17
Q

Recessive and dominant expression (What if allele is recessive? What state would cause that allele to be expressed?)

A

effects of an allele are overridden by the effects of a different allele
● o Male is hemizygous for X chromosome b/c he only has one copy of X
● o If there is a recessive allele on X chromosome, male will show recessive trait (no dominant allele to override it)

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18
Q

How do bacteria reproduce (process)?

A

Bacteria reproduce vis binary fission, which is very fast asexual reproduction that produces a daughter cell that is an exact replica of the mother cell CLONE

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19
Q

What is the main culprit for yeast infections?

A

● Candida albicans (anaerobic and facultative bacteria)

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20
Q

Which STI infections occur together

A

● Chlamydia and Gonorrhea
● Trich increases HIV transmission

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21
Q

Where do you take pap sample from? (specific cells)

A

■ columnar epithelial cells (endocervix = within the neck; q-tips stuffed in a TP roll!)
■ mature squamous epithelial cells (ectocervix = around the os; chocolate button roof tiles on tower cake)

Get these at the transformation zone where there columnar epithelial are changing into squamous epithelial - and where most cell mutations of the cervix occur.

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22
Q

What is the predominant good bacteria in vagina?

A

Lactobacillus

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23
Q

Symptoms of YEAST INFECTION?

A

● discharge is thick, white, and curd-like; OR it can be thin and watery; OR adherent to vaginal walls, can also develop in baby’s mouth.

vaginal itching
burning, irritation (vaginitis)
dyspareunia (pain after or during peneterative sex), increased vaginal discharge: thick, white, curd like, can also be watery and sticky to vaginal walls
vulva can be red and swollen

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24
Q

Is screening for vaginitis part of routine T1 screening?

A

No only for those with symptoms

or those with PPROM, low birth weight, miscarriage, stillbirth, endometritis, premature delivery @ tested 12-16 weeks

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25
Q

What is gram staining?

A

● Gram staining is to classify bacteria on their ability to soak up dye, which is due to glycoproteins in the cell wall.
gram positive = soaks up dye
gram negative = does not soak up dye

Helps us determine what particular strain of antibiotic to give.

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26
Q

What does screening for BV look like?

A

Only offer BV screening for those who have symptoms or other Hx listed. Swab vagina and look for 3/4 of Amsel’s criterea.

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27
Q

What technique/magnification do you use to identify bacteria under microscope?

A

● Wet mount/wet prep done with 2 samples:

first in saline at 10x to get an overview 

then in KOH solution magnified at **40x to identify cells etc **
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28
Q

???What vaginal infection can be diagnosed just using microscope?

A

Yeast I think

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29
Q

Whats it called when UTI gets to kidneys?

A

● Infection of urethra: urethritis
● Infection of bladder: cystitis
Infection of kidneys: pyelonephritis

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30
Q

What bacteria is main culprit in UTIs? Why are preg ppl more prone?

A

E. Coli (have pili which is why they can climb up the urinary system).

Urinary stasis; things move around more slowly; progesterone contributes to dilation of urinary tract, pressure on urethra from uturus

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31
Q

Bacteria vaginosis 4 amcel’s criteria - how is it diagnosed?

A

● Amsel’s criteria is a way of diagnosing BV, where 3/4 symptoms must be present for diagnosis (however 50% of people are asymptomatic with BV)
1) Vaginal Discharge
2) Clue Cells - 40x microscope, vaginal cells w/bacteria cells stuck to them
3) pH higher than 4.5 (more neutral)
4) Positive whiff test - fishy smell when discharge and KOH are combined

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32
Q

Informed Choice Discussion benefits and harms of genetic screening

A

Estimates risk of down syndrome, trisomy 18, Open neural tube defect

benefits
know the likelihood you are carrying a child with T21
Time to prepare to end the pregnancy
Time to prepare to have a child with T21
reassurance

harms
Anxiety while waiting for results
False alarm
Difficult decisions
False reassurance (2/4500)

NOT DOING TEST

benefits

Avoid anxiety and unecessary extra testing
Stay true to personal values
Avoid difficult decisions

Harms

Not knowing your risk of carrying a fetus w T21
Anxiety from not knowing
Social pressure to do the test.

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33
Q

What are the different screenings available? Who is reccomended what? What amalytes are involved in provincial screening?

A

SIPS (2 blood samples 10-11 weeks and 15-16 weeks) offered to all

IPS = SIPS + nuchal transperency

IPS and SIPS are screening for liklihood of T21, T18, or NTD

Amniocentesis - diagntostic

IPS offered to twins and 35 yo and older and IVF/ICSI

IPS and SIPS are the sam except for NT

QUAD is the second SIPS test late into care

If a client does NIPT, they aren’t eligible for provincial screening.

Late into care - Usually 17, 18 weeks get results still screening, offered amnio to confirm.

FUNDED NIPT: Positive screen IPS, SIPS, QUAD; documented history of fetus/child w previous trisomies; client who has increased risk of downs baby w results from SIPS/IPS/QUAD

FTS (first trimester screening) blood test and ultrasound 11 weeks - through fertility centre - precude them from provincial screening?

NIPT - non-invasive prenatal screening test - neither neural tube defect (don’t do provincial screening, offfered nuchal transulsency at 2nd trimester ultrasound).

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34
Q

Nuchal translucency US - what is it and who is eligible?

A

Ultrasound done at 11-13+6 weeks. Measures pocket of fluid at back of fetal neck to assess for genetic abnormalites.

Eligible

1) Clients 35 years or older at EDD
2) Twins
3) Clients pregnant following IVF or ICSI
4) People who have opted into NIPT

Done at 2nd trimester detailed ultrasound if have had NIPT

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35
Q

How accurate is the NIPT?

A

Approaching 100 percent for DOWNS(trisomy 21), 97 % for trisomy 18, 93 % Trisomy 13

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36
Q

When is the cost covered for NIPT?

A

Positive screen IPS, SIPS, QUAD; documented history of fetus/child w previous trisomies; client who has increased risk of downs baby w results from SIPS/IPS/QUAD

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37
Q

SIPS IPS Quad - what is it measuring? What analytes or hormones? The elevation of what analytes shows indication for what? what are the analytes or hormones that are actually being measured? When might you expect certain analytes to be elevated?

A

SIPS 2 blood tests
QUAD 2nd blood test only

Amalytes:
1 test PAPP- A (low, trisomy, INVASION) LOW

2nd test
AFP(made in yolk sack - peak at 10-13 then decline, low DOWNS), LOW
uE3 (low trisomy), LOW
HcG (increase T21, decrease T18, normal NTD), UP T21, DOWN T18, NORMAL NTD
Inhibin A (CL, high Downs) HIGH

38
Q

Definitions of positive predictive value, sensitivity, specificity, false negative and positive, etc

A

**Sensitivity **refers to how often the probability of a true positive with the test (low sens = high false posi)

specificity refers to the probability of a true negative of the test. (low spec - high false negi)

A positive predictive value is the ratio of patients truly diagnosed as positive to all those who had positive test results.

39
Q

Follow up tests: CVS and Amnio, what GA are they performed at? Accuracy?

A

**CVS **- less than 13 weeks gestation
**Amnio **- greater than 15 weeks gestation

Offered with positive screen or NIPT.

Nucleic Acid amplifying

both diagnostic 100%

40
Q

Times of ultrasounds?

A

**First trimester ultrasound **assessed fetal viability, pregnancy dating, chorionicity and amnionicty for twins, ectopic / molar pregnancy and pelvic masses. (7-12 weeks)

**NT ultrasound **is looking for a pocket of fluid at the back of the fetal neck that is indicative of T21, and is done between 11-13+6 wks, approaches 100% accuracy for T21 screen.

Second trimester (18-20 wks) is detailed, assesses fetal anatomy and growth, and looks at where placenta is, higher detection rate for neural tube efects, and ability to test for soft markers NT will be done here for folks with NIPT.

41
Q

Varicella exposure, history, gestational varicella risk (chicken pox)

A

● Expect ‘REACTIVE’ measuring immunoglobulins from past exposure or vaccine
● Theoretical risk of varicella vaccine during pregnancy, although no evidence
● If active chicken pox during pregnancy, OB can decide whether transfer of care is necessary, otherwise = shared care
● Worse for babe in the middle of the pregnancy (2nd tri)
● Worse for pregnant person in 3rd trimester

42
Q

Recommendation for syphilis screening, followup tests necessitated, what does positive result mean?

A

To screen in the 1st trimester and offer all first appointments syph screening.

First a TPA test which looks for antibodies. If the initial TPA test is positive or equivocal, an RPR test will be performed.

If the RPR test is positive, a confirmatory RPR titer will be performed.

If the RPR is negative, a confirmatory TPA by EIA test will be performed.

43
Q

What infectious diseases are within our scope to screen for?

A

Sexually transmitted diseases (chlamidya, gonorrhea, trichomonas, HPV, HIV, HSV, etc), immunity to rubella and varicella

44
Q

How would genital herpes influence care?

A

HSV screening based on client hx, not routine prenatal care
● 3rd trimester viral suppression therapy for recurrent outbreaks (so that an active outbreak does not occur during delivery)
● We about a hx of genital herpes, not which virus type caused them (cold sores are fine)
● Risk of transmission at birth = 50%
● Offer viral medication @36 weeks to decrease odds of passing it on to baby because infant mortality rates are quite high - transmission can also occur post-nasally
● Offer testing on presentation of symptoms

45
Q

What defines a virus vs. bacteria? (reliance upon host, size, reproduction, etc.)

A

Viruses small, rely on host cell for reproduction, DNA/DNA in capsid

46
Q

When does thyroid glad appear in fetus?

A

● First gland to appear,
● Starts secreting hormones at **18-20 **weeks

47
Q

Feedback loop of Thyroid - what stimulates release of what from what?

A

Thyroid - controls metabolsim

Hypothalamus makes TRH (thyroid releasing hormone) stimulates anterior pituaitary TSH (thyroid stimulating hormone) stimulates Thyroid to make T3 and T4 (uses iodine to produce which stimulates TSH.

If TSH too high - hypothyroidism - Thyroid is low

IF TSH too low - hyperthyoidism - thyroid is high

48
Q

What pregnancy hormone messes up thyroid function?

A

HcG - acts like TSH (t4 increases in first semester) TSH decreases and T4 leveles increase

49
Q

Implications of Gestational Diabetes later in life

A

Increased risk of GD in future preg, and increased risk of Diabetes in life.

50
Q

Who we offer TSH testing to?

A

1st trimester TSH testing is recommended in those with risk factors for thyroid disease

Older than 30
2 prior preg
history of preg loss
BMI greater than 40
HIstory of current symptoms of thyroid disease
Family history thy disease
etc

Results –> TSH in the first trimester should be slightly below the typical, non pregnant reference range and gradually return to normal in the 2nd and 3rd trimesters. TSH increases w pregancy

If TSH outside of ranges fT4 should be ordered.

51
Q

When assessing thyroid function, what are we measuring?

A

If anterior pituitary gland produces normal amounts of TSH, and if thyroid can respond to TSH and produce T3 and T4

52
Q

Which lab values that constitute Gestational diabetes: what values are elevated and how many?

A

If glucose challenge is high - reccomended to do glucose tolerance (diagnostic if above** 11.1**). If glucose tolerance is high then diagnostic for diabetes (if 1 value is met or exceeded)

53
Q

Physiology of gestational diabetes, why and how does it occur in body?

A

It is a disease of insulin resistance; because of the hormonal changes in pregnancy there is altered cell receptivity to insulin.

Glucose levels may be lower in early pregnancy, however hPL increases as gestational increases which can lead to a higher resistance to insulin and thus higher glucose levels.

When the pancreas is unable to increase insulin to compensate for the increased resistance, that is gestational diabetes.

Diabetes is Abnormal glucose tolerance and gestational diabetes is Abnormal glucose tolerance in pregnancy

54
Q

Other than hormone, what else puts someone at risk of gestational diabetes?

A

risk factors: age > 35 yrs, member of high risk population (basically just not white), pre-pregnant BMI >30kg/m2 or BMI > 25, previous history of GDM or glucose intolerance, pre-diabetes, family history of diabetes in 1st degree relative, macrosomia, history of PCOS.

55
Q

Glucose challenge test vs. glucose tolerance test - how do they differ? What is the process?

A

Options: (bw 24 - 28 weeks gestation) - earlier if high risk factors

1) Do nothing - relate to family history, normal BMI, normal weigh gain, risk factors

2) Straight to glucose tolerance test DIAGNOSTIC - over night 10 hour fast, fasting blood glucose, drink 57 g glucose Blood tested twice at 1 hour , then 2 hours.

1 step diagnostic if elevated

3) Glucose challenge test (screening test), Breakfast w protien and go to lab 2 hours later. 15 g glucose, blood 1 hour later - screening but if negative no further testing. (diagnostic if levels really hight)

Other tests: Order 2nd set of CBC and bloodtype, antibody screen to make second documented blood type.

56
Q

Common clinical indication of hypothyroidism (slowing down)

A

Tired, weight gain

57
Q

Why do we recommend antibiotic prophylaxis to GBS positive?

A

○ A percentage of babies that are colonized by GBS at birth develop infections that can be catastrophic, leading to meningitis, pneumonia and death.

Providing prophylactic antibiotics at PROM or at onset of labour reduces the likelihood of the newborn developing Early Onset GBS Disease (EOBGSD).

58
Q

How to collect GBS swab?

A

The client or the healthcare provider swabs for GBS with a vagino-rectal swab between 35-37 weeks. It is then sent to the lab to cultured.

A positive GBS result means that the client is colonized (not infected) hence prophalatyic antibiotics

59
Q

GBS Risk of transmission - percentage of babies exposed and affected, percentage of babies asymptomatic/sick

A

○ **10-30% **of pregnant people are colonized with GBS, when untreated 50% of babies acquire it at birth
OGBSD develops in 1% to 2% of these infants
6-9% with may die

60
Q

IF water breaks and GBS positive, what is community standard? (indication for…)

A

Community standard: provide Intravenous prophalaxsis for GBS at onset of labour or when membranes rupture. every 4 hours until birth.

WHO? posi GBS screen 35-37 weeks, client prev infected w GBS, any doc GBS in current preg.

61
Q

What is ferning?

A

Fern like pattern emerges under micoscope when it is amniotic fluid (high sodium and protein)

62
Q

What is best method to determine membrane rupture?

A

Nitrazine has a high false posi and negi, so good only if waters obvs broke

Ferning is better for diagnosing.

63
Q

What could be the cause of a false positive for membrane rupture tests?

A

Cervical mucous and semen

64
Q

Respiratory acidosis - levels of CO2, base, etc (high/low)

A

Ph pCO2 HCO3- Base Deficit
Resp A Low High Normal Normal
Metab A Low Normal Low High
**Mixed A ** Low High Low High

**Resp A **normal
**Metabloic Acidosis **likley low APGAR - resuscitation
**Mixed **- agresive resus at birth

65
Q

What can we assess based on baby’s cord blood?

A

Samples artery and vein.

Info of met acidosis, not the duration

If umb artery cord gas pH less than 7 or higher than 12 then intrapartim hypoxic acidemia - triggers chart review

66
Q

What does CCHD screen for? (particular heart defect)

A

○** Critical Congenital Heart Disease** = structural heart defects associated with hypoxia (lack of O2 in the blood)
■ Identifies cyanosis (otherwise clinically undetectable) in first 24-36 hrs of life

67
Q

Why and how to do CCHD screening?

A

○ **Pulse Oximetry Screening **– attach pulse oximeter to right hand & either foot
■ babes over 34 wks GA
■ @ 24-36 hrs
○ Because cyanosis is otherwise undetectable – prevent serious morbidity or death

68
Q

What can adversely affect the blood spot newborn screen?

A

○ If collected at < 13 hrs of age, it will have to be repeated

Cut not sterilized, if foot placed directly on paper, and if foot squeezed.

If done before 24 hours doesn’t screen for everything.

69
Q

Vitamin K deficiency bleeding - 3 types and evidence for and against oral vs. injected versions

A

Oral
Oral version is comparable to treathing Early and Classic Vitamin K Deficieny bleeding

Not as good for preventing Late Vit K deficiency bleeding so Canadian Pediatric Association recommends injectable version.

Parents responsibilty (check-in, remind them)

3 doses of 2mg (6 hours, 2-4 weeks, 6-8 weeks)

**Injectable **

Administered within 6 hours post-birth

Protects against all 3 types of vit K deficiency bleeding

Care providers responsibility

1 dose (1mg)

3 types of bleeding: 24 hours - early vit k deficiency bleeding, after 24 hours and first week - classic vit k deficiency (oral and injection help this type of bleeding the same amount), first week of life to 6 mo of life - late onset vit k bleeding

70
Q

Positive newborn screen, when to perform sweat test?

A

○ Cystic fibrosis screening - babies with CF have elevated salt in their sweat

71
Q

Which babies are at risk for late onset Vitamin K deficiency bleeding - how are they fed?

A

○ Exclusively fed breast milk (breast/chest fed and/or pumped milk) because most formals are enhanced w Vit K

72
Q

Based on newborn screen - define and provide examples of metabolic disorder and endocrine disorder

A

Metabolic

Maple syrup urine disease - means the body cannot process certain amino acids (the “building blocks” of protein), causing a harmful build-up of substances in the blood and urine.

Endocrine

Congential Hypthyroidsim - occurs when the thyroid gland fails to develop or function properly

73
Q

What about babies’ physiology more at risk of jaundice? (think liver and bilirubin cycle)

A

○ Jaundice is caused by backup of byproducts of RBC turnover, leading to excess bilirubin
○ In newborns and preemies this is due to:
■ less mature liver function
■ Faster rate RBC turnover (generates more waste more quickly)
■ not eating much yet, which also means…
■ less excretion of waste than adults
■ less protein in their blood than adults
■ (which is why we would encourage parents to feed them often, to help move things through!)

74
Q

What are the main cells of innate immunity?

A

All leukocytes (WBCs) and phagocytes. Neutrophils (most abundant, 1st players), Macrophages (leave capillaries CYTOKINES APC), Dendritic cells (Antigen presenting cell), NKCs (destroy infected host cell)

75
Q

What are the main cells of adaptive immunity?

A

B cells, T cells (Helper T and cytotixic T)

76
Q

Features of adaptive immunity?

A

(1) Specific - respond to distinct pathogens
(2) Diversity - wide variety of antigens (lock and keys)
(3) Memory - repeated exposure will make for a stronger response (doesn’t happen with innate/non-specific)
(4) Self limitation - Helper t, eventually non-reactive
(5) Non reactive to self - helper t cells
(6) Specializing - optimizing specific antigens

So So So Much Nice Dick

77
Q

Types of adaptive immunity?

A

Humoral - outside of cell in fluid - B-cells

Cell-mediated - in cells - T cells (Helper T and Cytotoxic T) (made in bone cells mature in Thymus)

78
Q

Describe the process of humoral immunity?

A

B-cells bind to pathogen and presents it. T cells are triggered and activate B cells once they bind. Once activated memory B cells are cloned, and plasma B cells - antibody factories. T cells release cytokines (alarm bells)

79
Q

Describe the process of cell-mediated immunity?

A

T cells duplicate into memory cell and effector cell (spit out cytokines), cytotoxic t cell bind and kill with perforins, granules, granzymes - but don’t kill themselves in the process.

80
Q

What are APCs?

A

Antigen Presenting Cells - Dendritic (I), Machrophage (I), and B-Cells (adaptive) connect with another protein and presents

81
Q

Examples of non-specific immunity?

A

1st line of immunity! Physical and biochemical: skin, mucosal, pH, acid mantle, saliva, bone marrow, lymph, temperature, proteins, enzymes, digestive enzymes

82
Q

Endocrine function of the placenta?

A

placental lactogen (increases glucose levels in parent - creates the differential and attracts glucose), progesterone, hCG, and estrogen… but many others as well, like serotonin.

These hormones maintain the pregnancy and guide metabolic functions in both the birther and the fetus

83
Q

Immuno function of the placenta?

A

Prevention of rejection from mother

Limited barrier to infection

Transfer of maternal antibodies IgG

84
Q

Metabolic functions of the placenta?

A

Placenta synthesizes glycogen, fatty acids, cholesterol, enzymes, and ammonia/lactate.

Insulinase - increases the barrier of insulin transfer between mother and fetus, making fetus independent of maternal insulin levels

11B HSD - increases barrier of maternal glucocoritids (cortisone - makes it inactive)

85
Q

Which alleles are recessive and co-dominant in ABO?

A

● ABO phenotypes are controlled by 3 alleles of the ABO gene
■ O - recessive
■ A/B - co-dominant

86
Q

What are the different ABO blood types?

A

A (has A antigen, anti B antibody), B (has B antigen, anti A antibody), AB (has a and b antigen, no antibodies), and O (neither B nor A antigen, both anti-B and anti-A antibodies)

87
Q

Phenotype vs Genotype?

A

ex A = phenotype (expression) , AO or AA (2 alleles) = genotype

88
Q

Primary stage syphilis ?

A

● 100% risk of congenital / fetal implications
Run 2 confirmation tests:
■ 1. Non-treponemal test – rapid plasma reagin (RPR); test for biomarkers
■ 2. Treponemal test – TP agglutination; test for antibodies from infection

89
Q

Best way to test for GA?

A

1st trimester ultrasound pregnancy dating is ideally 7-12 weeks.

90
Q

Hypoxemia vs hypoxia?

A

KNYPOXEMIA (decreased oxygen in blood) AND HYPOXIA (decreased oxygen in the tissues from Hypoxemia)