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MIDW 103 Applied Science > Midterm > Flashcards

Midterm Flashcards

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1
Q

What are the four major placental hormones?

A

Progesterone, Estrogen, hPL (human placental lagtogen), HcG (human chorionic gonadotropin)

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2
Q

What are the four major placental hormones?

A

Progesterone, Estrogen, hPL (human placental lagtogen), HcG (human chorionic gonadotropin)

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3
Q

What does progesterone do?

A

Maintains early fetus and starts labour. serves as the source of steroid production in fetus later on.

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4
Q

What does estrogen do?

A

helps uterus grow, maintains uterine lining, regulates other key hormones, and helps with growth of fetus’ organs.

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5
Q

What does hPL do?

A

promotes fetal growth by altering maternal metabolism.

Insulin antagonist (increases maternal blood sugar)

hPL downplays insulin in the fetal blood (decreases storage of glucose) - that bb needs the sugar!
And increases insulin the maternal blood (increases sugar)

Creating a gradient where the sugar flows to bb - placental lactogen!

Produced by synsitiotrophoblast

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6
Q

What does hCg do?

A

Maintains corpus luteum/decidua, the maintained corpus luteum keeps progesterone being emitted

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7
Q

What are the functions of the placenta?

A

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

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8
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

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9
Q

Immuno function of the placenta?

A

Prevention of rejection from mother

Limited barrier to infection

Transfer of maternal antibodies IgG

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10
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)

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11
Q

Describe Villi?

A

Stem villus, intermediate villi, anchoring villi, terminating villi

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12
Q

What are intervillous spaces?

A

 Spaces that pool with maternal blood; this is the source of transport and nutrients for the fetus, and umbilical arteries and veins attach to the capillary beds that perform their exchange in the intervillous spaces.

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13
Q

Features of syncitiotrophoblasts?

A

The syncytiotrophoblast is the outer thick layer of the trophoblast that lacks cell boundaries and grows into the decidua. Secrete HpL and HcG pushed further into endomentrium by cytorophoblasts and filled with capillaries

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14
Q

Where does the blastocyst hatch from?

A

Zona pellucida (1st step in implantation)

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15
Q

Stages of implantation?

A

Apposition (interaction b/w blastocyst and epithelium), Adhesion (increase in interaction), Invasion (penetration)

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16
Q

Blood flow to fetus?

A

2 arteries away from fetus (deoxygenated) 1 vein toward the fetus (oxygenated)

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17
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)

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18
Q

Describe NKCs

A

Cytotoxic cells Small granules in cytoplasm, attack cells displaying foreign MHC antigen, destroys with perforins and granules

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19
Q

What are the cells in Adaptive Immunity?

A

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

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20
Q

What are some 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

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21
Q

What are the 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

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22
Q

What are the 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)

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23
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)

24
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.

25
Q

What are APCs?

A

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

26
Q

What are MHC II complexes

A

Majot histocompatibiltiy complex class 2, with APC MHC II binds to the antigen and presents/attracks after APC cells have presented.

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

27
Q

Antibodies?

A

IgG (THROUGH PLACENTA), IgA, IgM(in placenta bad - maybe infection?), IgD, IgE

28
Q

Changes in pregnancy

A

Immunity is not ‘suppressed’. Rather

(Cytotoxic T cells DOWN) Cytotoxic adaptive immune responses are diminished, bypassed, or even abolished, while

(B cells + Helper T cells UP) regulatory adaptive immunity is enhanced

  • Pregnancy is NOT an immunocompromised state (this is an update to previous thoughts)
  • There is a decrease in cytotoxic cell activity (part of adaptive immunity)
  • Innate immunity is essentially unchanged

Because we still want the pregnant person to be able to fight pathogens but not to the extent that the success of the pregnancy is threatened

29
Q

When is ABO determination, antibody screen, and Rh status tested for?

A

With all pregnant people at initial visit and at 26-28 weeks.

30
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)

31
Q

Which alleles are recessive and co-dominant?

A

A & B allele are co-dominant, and O allele is recessive

32
Q

Phenotype vs Genotype?

A

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

33
Q

What do platelets do? And how do they act in pregnancy?

A

Platlets form the clotting plug and fibrin makes it stronger. Pregnancy is a hypercoaguble state - clotting factors increase, fibronolysis decreases, Reduced PPH risk, but increases chance of thromboloblys (stoke / heart attack)

34
Q

How do we determine ABO group?

A

Lab mixes up blood, does it agglutinate, if so it is the opposite blood. So AB would agglutinate with no type of blood, B would agglutinate with AB or A, A would agg with AB or B, and O would agglutinate with AB, A, and B

35
Q

What is alloimmunization?

A

It means we have formed antibodies to the D antigen. It is only in response to sensitization and is a STRONG immune response compared to the AB antibody response. (distinct from autonantibodies that arise from reacting to NON-SELF)

36
Q

Tell about ABO incompatibility?

A

Way more common and almost never an issue because antibodies are weak. Outcome may be jaundiced at birth.

37
Q

What is the Indirect Coombs and when is it done?

A

Done on pregnant person at intake, 26-28 weeks, and pp if parent Rh - and bb Rh +. If positive shows alloimunnization has occurred.

38
Q

What is the Direct Coombs test and when is it done?

A

Done on baby pp if mother is Rh - and bb is Rh +. If posi HEMOLYTIC DISEASE OF THE NEWBORN

39
Q

What is Rossette test and when is it done?

A

PP done on parent who is Rh - with Rh + bb. Qualitative test to show presence of fetal blood.

40
Q

What is Kelinhaure-Betke test and when is it done?

A

PP on parent, if Rosette positive quantitative test to show how much fetal blood is present.

41
Q

What are the symptoms of hemolytic disease of the newborn?

A

Increased BAD jaundice, severer anemia, congestive heart failure, death

42
Q

What is jaundice? And why are bb’s usually jaundiced?

A

Buildup of bilirubin in skin, product of RBC breakdown. In newborn there is increased RBCs, with decreased lifespan, and increased buildup of billirubin. It’s a bigger job!

43
Q

When to give prophalaxysis?

A

Rhogam, Winro 28 weeks gestation for Rh - and pp if baby is Rh +

44
Q

What values to RM’s care most about in CBC?

A

WBC, RBC, Hemoglobin (MOST IMPORTANT), Hemocrit, Platelet count info

45
Q

Blood components?

A

Plasma MOST ABUNDUNT- 55 %, buffy coat WBC - 2%, and RBC MOST DENSE 45% (include hemoglobin and hemocrit (proprortion of RBCs in body) - thin* = anemia)

46
Q

Hematological changes of pregancy?

A

PLASMA INCREASES (40-60%)

RBC increases slightly, but ratio of blood to RBC decreases

BLOOD VOLUME INCREASES (30 - 40%)

47
Q

What is hypervolemia?

A

The increase in plasma and blood volume is more than the increase in RBCs. Therefore blood becomes diluted,

48
Q

What are RBCs traits and what to RBCs do?

A

Carry oxygen around the blood VIA hemoglobin and CO2, Disk shaped, no mitochondria or nucleas

49
Q

What are the iron requirements in pregnancy?

A

Normally 12-18 mg, pregnancy 1000 mg

50
Q

What level is considered anemic in pregnancy re: hemoglobin?

A

Below 120, and ferratin lower than 12 confirms this iron deficient anemia in pregnancy

51
Q

What are the different possible abnormal lab values and what do they mean?

A

ALL LOW HEMOGLOBIN

Iron deficiency anemia - All values are LOW

Vit B 12 and folate deficiency (MEGABLASTIC ANEMIA) - Hemoglobin LOW, RBC and ferratin HIGH, MCV and MHC high, MCHC normal

Thallasemia - Heboglobin LOW RBCs NORMAL, Ferratin High, MCV, MHC, MCHC all low

52
Q

What is transcription?

A

RNA is synthesized from information from DNA. DNA unwinds

53
Q

What is translation?

A

Amino acids are polymerized into polypeptide chains (PROTEIN SYNTHESIS) occurring at Ribosomes

54
Q

DNA vs GENES?

A

All cells in body have same DNA, gene expression is what gets turned on in DNA or doesn’t, and gene regulation is the process which decides what genes are expressed and what ones aren’t GENOME all your genes

55
Q

What is a chromosome?

A

One long stretch of DNA (humans have 23 pairs)

56
Q

Genetics vs epigenetics?

A

Genetics study of genes (doesn’t change), epigenetics - study of changes in gene function (change in histone tails what gets expressed)

57
Q

Genes vs alleles?

A

Genes a region of the chromosome that codes for a protein. Allele - on version of a given gene

MIDW 103 Applied Science (2 decks)

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