Term test 2- Reproduction & Immunology Flashcards

1
Q

which two hormones from the anterior pituitary, are necessary for breast milk?

A

PRL and GH

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2
Q

Describe the breast structure.

A

15-20 lobes divided by adipose tissue then subdivided into lobes containing alveoli that secrete milk.

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3
Q

Why is milk production during pregnancy prevented?

A

this is due to the high levels of estrogen during pregnancy. High levels of estrogen, increase secretion of PIH through positive feedback.

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4
Q

what are the two hormones needed for milk to be secreted from the breast, and where are they found?

A

prolactin from the Anterior pituitary, and oxytocin from the posterior pituitary.

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5
Q

what role does prolactin play in breast milk?

A

it stimulates production

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6
Q

what role does oxytocin play in breast milk?

A

it releases the milk.

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7
Q

what are some stimuli for the release of breast milk?

A

1) a child’s cry 2) suckling

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8
Q

why does oxytocin play such an important role, and why is it present in both male and females?

A

It is a key element in the trust factor developed by humans. it is a neuropeptide that place a key role in social attachment and affilation in non-human mammals. It causes substantial increase in trust among humans.

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9
Q

what determines gender?

A

A particular gene on the Y chromosome induces the emrbyonic gonads to become testes. females lack a Y chromosome, and the absence of this gene causes the development of ovaries.

A gene known as SRY *(sex-determining Region of the Y) is though to be important for male determination

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10
Q

What is special about the SRY?

A

it is a conserved gene, meaning it has no evolved much over the years, and development of multiple species.

it is the ultimate maleness gene, and action after 6 weeks of conceptions, it triggers fromation of the testies (from primordial gonads). These testes produce testosterone, and without the SRY gene, a fetus would develop into females. regarless of the Y chromosome’s presence.

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11
Q

in the fetus, sec differentiation beging with the developement of the gonad from a bipotential primordium. Explain the female development.

A

1) abscence fo the SRY protein-gonadal tissue develops into ovaries
2) no testosterone, so no mullerian inhibition factor (MIF) is made from sertoli cells, so wolffaian duct degenerates, and the mullerian duct presences is maintained
3) absence of MIF allows the mullerian duct to become the fallopian tube, uterus and vagina.

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12
Q

in the fetus, sec differentiation beging with the developement of the gonad from a bipotential primordium. Explain the male development.

A

1) presence of SRY protein- gonadal tissue develops into testes
2) presence of testosterone, so MIF is made from sertoli cells which causes the wolffian duct to be maintained, while the mullerian duct degenerates.
3) testosterone allows Wolffian duct to become seminal vesicle, vas deferens, and epididymis.

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13
Q

Which parent determines if you are a girl or boy?

A

this is up to the father, since mothers have two X’s, their haploids will only contain X chromosomes, but since males are XY, their haploids will produce 22 single chromasomes, and one sex chromosome being either X or Y, from the original diploid cell.

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14
Q

there is another factor that controls maleness in humans, what is it? (the person is SRY possitve, XY possitive, and still developed a completely female phenotype)

A

the insulin receptor family played a roll here. To have male anatomy there must be the presence of these 3 receptors:

1) Insulin receptor (INSR)
2) insuline-like growth factor 1 receptor (IGF1R)
3) insuline receptor-related recepetor (INSSR)

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15
Q

hermaphrodites is an intersex condition where individuals have what?

A

borth ovary and testies tissue, can be 46XX with SRY mosaicism

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16
Q

what is/ who are pseudohermaphrodites?

A

congenital condition where a person has external genitalia of one gender and internal sex organs of the other gender.

it is an endocrine disorder.

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17
Q

what are the conditions to be a female pseudohermaphrodite, vs. a male?

A

Males can have the defective enzyme 5 alpha-reductase, functional testosterone, and inadequate levels of DHT. these males have poorly developed genitalia, and were caused by inapproriate exposure to androgens during easly gestation.

Most common female case is congenital adrenal hyperplasia. (excessive secretion of androgens from the adrenal cortex).

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18
Q

Whats the difference between female puberty and male puberty?

A

Females will experience puberty before boys, and will experience their growth spurt before puberty (menarche)

boys on the other hand will go through puberty while they experience their growth spurt. The testes will develop, then the penis, then the pubic hair, as they follow a chart flow.

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19
Q

explain the metamorphosis of the child into the adult.

A

1) puberty= activation of the HPG axis resulting in gonad maturation
2) adolescence= maturation of adult social and cognitive behaviors
3) coupling of both through interactions between the nervous system and gonadal steroid hromones

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20
Q

if children are GnRH deficient, what can we do to help them mature sexually? and why do we use this method?

A

you need to treat with GnRH pulses simular to those that occur normally, the pulsaic method triggers puberty. if you treat with steady infusions of GnRH through drug-delivery pumps there is no proper development.

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21
Q

what are some variations that can affect puberty?

A

1) genetic variations in timing of onset of puberty
2) environmental factors
3) nutrition (eating disorders)
4) chronic illness (IBD, TB)
5) theoretical concern over synthetic hormones, other environmental chemicals
6) precocious puberty (very early onset)

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22
Q

why is Genghis Khan so influential?

A

You can track his lineage in mongolia history, due to men carrying a Y chromosome characteristic. he was a huge war lord in mongolia!

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23
Q

what cells are located at the outermost region of the seminiferous tubules, right against the basement membrane?

A

the stem cells caleld spermatogonia

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24
Q

as spermatogonia develop they move where?

A

towards the lumen of the seminiferous tubules

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25
Q

describe spermatogenesis in 4 steps

A
  1. spermatogonium stem cell gives rise to one daughter cell
  2. it ramins at the basement membrane as a stem cell
  3. a second daughter cell (primary spermatocyte) moves toward the tubule lumen.
  4. the daughter cell undergoes 2 meiotic divisions to form 4 spermatides.
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26
Q

how many stem cells migrate to the embryonic testes? what happens there? how many sperm go through with ejaculation?

A

1000-2000 stem cells migrte to the embryonic testes. they produce sperm trhoughout the adult life the meiosis step is crucial. the median ejaculation contains ~255 million sperm.

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27
Q

what is a main concern with the immunity system and the developing sperm?

A

The body recognizes the developing sperm as forgien material, and will attempt to attach the sperm to kill it.

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28
Q

what are 2 methods the body uses to defend sperm agains the immunology system? and how do they do it?

A

sertoli cells help seminiferous tubules as an immunologically previledged site by

1) blood-testies barrier (tight junctions, and basement membrane)
2) production of FAS ligand- this bind to the FAS receptor on T-cells triggering apoptosis of the T-cells and preventing immune attack on developing sperm.

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29
Q

how long will sperm survive once is has been ejaculated? what are the survival aids to spermatoza?

A

sperm 80 hrs.

1) cervical mucus helph in maintaining metabolic requirements of spermatozoa
2) when migrating in the genital tract, they are rapidly separate from the seminal plasma and resuspended un the female genital fluid.
3) spermatozoa undergo “capacitation” during their passage through the reproductuve tract

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30
Q

name methods the female system uses to cut down on sperm count

A

1) most spermatozoa are eliminated at the selective barriers: cervix, an uterotubal junction
2) majority of sperm are removed by phagocytosis
3) damaged or immotile spermatozoa are carried back to the cervix by ciliated cells

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31
Q

what is capacitation?

A

the process of physicological changes occuring in mammalian spermatozoa during passage trhough the female reproductive tract that enables them to penetrate the egg membrane. it is defined as the alteration of the glycoprotein surface of spermatozoa under the influence of secretion of the tissues of the female reproductive tract

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32
Q

explain fertilization

A

series of processes beginning with the spermatozoa penetrating the corona rasiata and ending with the intermingling of maternal and paternal chromosomes after the spermatozzon entered the egg.

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33
Q

what is in-vitro fertilization?

A

its artificial fertilization (done in a test tube first and planted back into the mother)

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34
Q

give an example of how some failures can lead to succes?

A

the creation of sildenafil was ment to help for agina, it was a terrible drug, and had a side effect of giving men bonners. So they decided with a little tweeks they can solve erictile dysfunction, thus Viagra was born.

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35
Q

what are the steps to erection formation?

A

the artery dilates, and the corpus-cavernosm compresses. This allows the viens to contract and less blood to flow out. This results in an increased intracavernosal pressure which creates the errection.

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36
Q

what are the roles of nitric oxide in erection of the penis?

A

NO acts on VSMC which activates the GTP, producing cGMP. cGMP caues Ca2+ channels in VSMC to close (due to the cytoplasmuc [Ca 2+] decrease. finally as a resul the VSMC relaxes, causing vasodilation of penis and engorgement of the erectile tissue.

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37
Q

what does viagra do? (how does it promote erections?

A

viagra inhibits the phosphodiesterase that catalyzes the breakdown of cGMP. this increases the availability of cGMP and promotes the erection.

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38
Q

whats a major problem with shift work, and what can viagra do to help?

A

viagra helps with the problem of jet leg, now the problem with shift work is that it alterates the sleeping pattern really bad and inc reases the levels of stress making it a probable carinogen (this elevates risk of heart disease and cancer). Viagra is looking to be used for people with shift work and allow them to aid in the jetleg/sleep pattern they get stuck in. IT basically elevates cGMP levels to temporarily speed up the internal body clock in the brain

39
Q

when can fertilization occur? why?

A

fertilization can occur if intercourse takes place within a 3-day period piror to the day of ovulation, however the secondary oocyte following ovulation disintergrates 12-24 hours after ovulation if its doesn’t go into its division cycles. therefore fertilization can not occur lter then 1-day post ovulation.

40
Q

how long can sperm survive in the female reproductive tract

A

it can survive up to 3 days

41
Q

how much sperm does a man ejaculate, and whats their characteristics’?

A

2-6 ml/ejaculate, 40-120 million spermatozoa are mixed with mildly alkaline fluids from the seminal vesicles (60%) and the prostate (30%). The pH must be 7 and 8.3

42
Q

where does fertlization usually happen?

A

in fallopian tubes

43
Q

explain how sperm reaches the egg

A

it penetrates the outer layer granulosa cells (corona radiata), it penetrate protective glycoprotein coat; zona pellucide. the first sperm that binds to the receptor fuses with the egg, (it then blocks to polyspermy)

te sperm head engulfed by the egg (DNA inside).

44
Q

explain the 3 types fo twins

A

dizygotic twins (fraternal twins, heterologous twins): develop from the two seperate oocytes fertilized at the same time.

monozygotic (identical) twins: two individuals developed from on fertilized oocyte; they have identical genomes

conjoined twins: monozygotic twins whose bodies are joined to a varying extent.

45
Q

implantation of the blastocyst

A

produces enzymes to implant into uterine wall on the 6th day after fertilization. ~75% of lost pregnancies are due to failure of implanatation.

46
Q

name some examples of ectopic pragnancy

A

its an implantation in a different site than the posterior wall of uterine cavity

examples are tubal pragancy: infundibular (17%), ampular (54%), isthmis (25%), intramural (2%)

ovarian pregnancies (0.5%)

placenta previa (made it to the uterus but to low) (0.3%)

47
Q

what hormone is detected during a pregnancy test?

A

the human chorionic gonadotropin (HCG) is secreted by the blastocyst and not the mother during time of pregnancy. the [^] from the 1st to 3rd month of pregnancy.

48
Q

how are hormones measured?

A
  1. immunoassay: tagged Ab specific to hormone hCG(detects in blood and urine)
49
Q

what keeps the pregnancy going before the placenta is formed?

A

HCG (blastocyst) maintains corpus luteum

50
Q

why is the corpus luteum needed to synthesize progesteron.

A

early pregnancy causes corpus luteum synthesize

  1. progesterone to keep the endometrium intact
  2. progesterone, estrogen, inhibin: feedback suppression to pituitary
51
Q

what does the placenta do for the fetus?

A

placental a2-adrenoreceptors control vascular development at the interface between mother and embryo. the placenta performs the functions of the digestive, respiratory and renal systems for the parasitic fetus.

it exchange of nutrients/waste, O2/CO2, chemical agents

52
Q

explain what hCG, Estrogen, Progesterone, PTHrP and CRH does?

A

hCG maintains corpus luteum

estrogen: uterine muomerium, breast ducts
prgesterone: supresses uterine contractions, cervical plug, and milk glands,

PTHrP mobilizes mothers bone calcium

CRH fetal lung maturation, “placental clock”

53
Q

there are 4 kinds of conttaceptions. Name them and give an example.

A

block sperm transport (sterilization)

gamete supression (birthcontrol pills, testosterone)

block implantation (IUD, plan B)

pregnancy termination (RU 486)

54
Q

explain how bith (parturition) occurs via hormonal control (ie possitive feedback)

A
  1. Fetal adrenal gland secretes DHEAS and cortisol upon stimulation by CRH and ACTH
  2. Cortisol stimulates the placenta to secrete CRH, producing a possitive feedback loop
  3. DHEAS is converted by the placenta into estriol, which together with prostaglandins and oxytonin, stimulate the myometrium of the mothers uterus to undergo changes leading to labour.
55
Q

describe the theory of basis of modern medicine until the 17th century

A

the humours of the body and the elements of the physical world thus shared a common qualitative nature, and the microcosm and the macrososm were related to each other.

their idea “opposites cure opposites”, cold remedy cures a hot illness

and illness was seen as an internal disorder of the body, not the result of a specific agent like a bacteria.

56
Q

what are the red flags of Quackery?

A

testimonials

helps your body

celeberity doctor

ancient wisdom

57
Q

name some stats on the years accomplisments from 1200-1800

A

1200-1550: notions of pulmonary circulation

1600- valves in veins, bloods circulated by the heart

1658- first descroption of RBS

1661- the capillary system

1665- 1st recorded bood transfusing dog:dog

1667 1st human blood transbusion (lamb:boy)

1674: RBCs size

1700-1800 transfusions still failing

58
Q

who descovered the first bacteria, and how?

A

in 1683, Leeuwenhoek took plaque of his family memebers teeth and studied it under a miscrosope. He discovered bacteria, although he didnt know what it was, he knew they were moving and alive.

59
Q

name some stats of some accomplishments from 1800-today?

A

1800-1900 properties of the blood emerge, and leads to successful transplants

1917 optimize citrate-glucose solutions; prevent coagulaiton

1959: x ray crystallography reveals Hb structure, protein in RBS that carries oxygen

1965- slowlyt thaw frozen plasma: it precipitates factor V111 with great clotting power. (100x stronger then raw)

1971: hep B ag discovered, and infected donors
1981: first cases of AIDS hemophiliacs develop aids a blood borne component?
1983: aids virus identifies

60
Q

how were blood tranfusion evolving?

A

blood transfusions had to be done instantaneously beside eachother, then they learned to store blood in glass bottles, and now they store blood in plastic bags

61
Q

what are the 3 specific functions of the circulatory system?

A

transportation

regulation

protection

62
Q

describe transportation in the circulatory system

A

all substances are essential for cellular metabolisn, and are transported by the circulatory system:

respiratory (RBC)

Nurtitive (digestive)

excretory (waste)

63
Q

describe the regulation and protection in the circulatory system:

A

regulation (Hormonal and temperature)

Protection (from injury and pathogens)

64
Q

name the 7 cells found in the formed elements portion of blood

A

neurophils, eosinophils, basophils, lymphocytes, monocytes, platelets, erythrocytes

65
Q

what is erythropoiesis and how is it done?

A

its the production of RBC

uncommitted stem cells go through a series of stages in the bone marrow. one the nucleus is expressed leading to the formation of the reticulocyte, the cell is released into circulation where it becomes a mature RBC.

once the nucleus is expelled, the reticulocyte moves into circulation and becomes the RBC.

66
Q

what is leukopoiesis and how is it done?

A

the formation of white blood cells.

uncommitted stem cells in the bone marrow also give rise to the progenitor cells for the remaining blood cells and platelets.

platelets: develop to the magakaryocyte stage in the bone marrow, and are released as platelets in the circulation

neutrophils, monoctes, and basophils: progenitor cells give rise to these cells which are found in circulation

Lymphocytes: are derived from their own lineage of lymphocyte stem cells in the bone marrow, which give rise to lymphocytes in the circulation.

67
Q

what is hematopoiesis?

A

the basic formation of blood cells, hematopoietic stem cells originate in the embryo and migrate to different tissues:

the liver: major hematopoietic organ of the FETUS!

bone marrow: major hematopoietic organ after birth.

68
Q

what is a hematocrit?

A

a test that messures the % total volume of packed red blood cells (females is 35-46%, and male 41-53)

hemoglobin levels measured (female 12-16g/100ml, male 13.5-17.5g/100ml)

red blood cell count 4.5-5.9 million/mm3

white blood cell count: 4500-11000

69
Q

describe hemoglobins properties

A

each RBC has ~280 million hb- which gives it its red blood color.

Hb: 4 globin proteins, each which a heme group binding Fe

Heme Fe combines with oxygen (lungs), releases oxygen in tissues.

70
Q

what shape is a RBC?

A

its bioconcave disc shape.

71
Q

describe the plasma component of blodo.

A

its a straw colored liquid containing 92% water, 1% dissoved solutes and trace eleemnts, and 7% organic molecules

the organic molecules break down into: proteins, amino acids, glucose, lipids and nutrogenous waste

albumins account for most of the plasma protein

72
Q

what do the following 3 blood proteins do for the blood?

Albumins, globulins and fibrinogen?

A

albumins: provide the osmotic pressure needed to draw water from the surrounding tissue fluid into capillaries
globulins: alpha and beta transport lipids and fat soluble vitamins. Gamma globulins are antibodies
fibrinogen: is important for glot formation.

73
Q

what is a symbiotic mircrobe? commensal microbe? and parasitic microbe?

A

symbiotic: they and we benefit
commensal: only one parter benefits, the other is neutral
parasitic: one partner benefits at the expense of the other

74
Q

whats the microbe to human cell ratio?

A

10:1

75
Q

why are RBCs concave?

A

the cytoskeleton of RBCs create its unique shape. They are flexible and well in hypotonic medium and chrink in hypertonic medium, they have no nucleus.

76
Q

how much oxygen can RBS carry?

A

Erythrocutes and Hb function to aid in oxygen delivery to tissues. most O2 in blood is in RBCs bounbd to Hb.

So each RBC can carry over a billion molecules of O2,

(280 million Hb molecules/RBC x4 hemes)

77
Q

what is the total arterial O2 carrying capacity in blood?

A

200 ml O2/L blood.

78
Q

Describe the O2 saturation ration in blood at a given location?

A

blood entering tissues contains 200 ml O2/Lblood (97%)

blood leaving tirrues contains 155 ml O2/L blood (75%)

therefore 45 ml of O2 of blood is unloaded to the tissues. (22% of the oxygen )

79
Q

some physiologic factos affect Hb- O2 binding,give some examples.

A

decreased pH: decreased Hb affinity for O2

(happens with body acitvity where muscle fibers produce lctiv acid and release H+)

increased temperature: decreased Hb affinity for O2.

(weakens the bond between oxygen and hemoglobin, allowing more to be unleased into the tissues)

80
Q

explain shifts on the curves to:

decreased pH/increased pH

increased temerature/decreased temperature

A

decreased pH the Hb-O2 dissociation curve shifts right

increased pH the Hb-O2 dissociation curve shifts left

increased temperature: decreases the Hb affinity for O2 and shifts right

decreased temperature: increases the Hb affinity for O2 and shifts left

81
Q

Red blood cells dont have a nucleus and mitrochondria, and thus dont respire aerobically. explain how RBC get their energy.

A

they get it through anaerobic metabolism of glucose. At a certain point in the glycotic pathway a “side reaction” occurs in the RBS that results in the production of 2,3-DPG (2,3-disphosphoglyceric acid). the enzyme that produces 2,3_DPG is inhibited by oxyhemoglobin. therefore when its [decreased] the production of [2,3-DPG] ^. its higher levels causes an increased in oxygen unloading and shifts the curve right.

82
Q

explain the death of the RBC

A

it takes 7 days to develop and die usually after 120 days.

there is no mitochondria, and no nucleus, making it become fragil quicly.

After it dies bilirubin is produced by the RBC leftovers produced by the spleen. the liver enzymes bind bilirubin and excres into bile.

83
Q

what is Jaundice, and what are the physiologic characteristics of healthy newborns and premies?

A

its associated with high blood concentration of bilirubin.

in healthy newborns, there is a rapid fall in blood Hb which occurs at birth

in premies, it inadequate amounts of liver enzymes needed to bind bilirubin so it can be excreted in the bile (toxic)

84
Q

what are some symptoms and what can cause it?

A

if blood bilirubin levels rise: hyper-bilirubin-enemia, skin and whites of eyes turn yellow.

it can be caused by damage to liver (through blood virus or alcohol damage).

85
Q

explain thalaseemia (alpha and beta) and where is it common?

A

its the excessive destruction of RBCs leading to stillborn, anemia, growth abnormalities, iron overload leading to heart failure in young adults. The alpha thalaseemia is the decreased synthesis of a-Hb chains, and beta thalaseemia is where the synthesis of b-chains is impaired.

86
Q

explain sickle cell anemia, what is its cause?

A

its an inherited recessive disease where 2 copies of gene producing Hb S instead of normal Hb A.

single amino acid substitue in the beta globin chain (it causes the hemoglobin to dump the O2)

when the hemoglobin is deoxygenated, hemoglobin S polymerizes into long fibers, creating the sickle cells, promoting hemolysis.

87
Q

how is sicle cell anemia formed/developed?

A

the genetic code alters the Hb and gives up O2, but it cant re-uptake so it ends up crystallizing, and the RBC defroms into a sickle shape.

88
Q

what is the basis for blood typing?

A

agglutination (clumping) of RBCs occurs when A-type RBCs are mixed with anti-A-type abs.

Agglulation (clumping) of RBCs occurs when B-type RBCs are mized with anti-B-type Abs.

89
Q

there are 3 types of antigens on RBCs what are they and what do they symbolize

A
  1. Antigen A, and they produce anti-B
  2. Antigen B, and they produce anti-A
  3. Rh is a factor that indicates if the blood is possitive or negative. (if its present its possitive(
90
Q

whats a probelm with Rh factors and pregnacy? how can it be treated

A

nothing happens at the beginning of the preganacy, but its at birth where the mother will be come sensitized to the antigen, and the next pregancy can cause the mothers new made antibodies to kill the new babys’ RBC.

its treated by giving mom-Iv at -Rh Ab after birth of Rh+ baby. destroys fetal cells in circulation before they elicit immune response (should be given within 72 hours, and only effects mother who are - and babies who are +)

91
Q

how does blood clot?

A

Extrinsic pathway of clot formation is initiated by tissue factor (or tissue thromboplastin, or factor III), a membrane glycoprotein found inside the walls of blood vessels and the cells of surrounding tissue.
When the blood vessel is injured, tissue factor becomes exposed to factor VII and others in the blood and makes a complex, then act as an enzyme to activate factor X.
This pathway then generates thrombin, which can generate fibrin. Fibrin is where we want to get to for clotting!

92
Q

what is clot dissolution, and how does it happen?

A

its the deformation of a clot and it happens when plasminogen converted to plasmin, an enxyme that digests fibrin promoting dissolution of clots. it then cleaves the fibrin. this plamibnogen is converted via kallikerin, tissue plaminogen activator (TPA).

93
Q

what is a good STEMI (heart attack) treatment, and why?

A

fibrinolytics, they achieve reperfusion. They act by converting plaminogen to plasmin, which in turn cleaves fibrin, thereby cuasing clot dissolution and restoration of blood flow to ischemic tissues.