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Anat/Phys > Final Comprehensive > Flashcards

Final Comprehensive Flashcards

1
Q

3 types of muscle, where and characteristics

A
  1. Skeletal Muscle- Attached to skeleton- voluntary- have strations-does not undergo mitosis during immaturity
  2. Cardiac Muscle- only in heart-involuntary-striated, no mitosis during maturity
  3. Smooth muscle- in walls of hollow visceral organs-involuntary-no striations- does undergo mitosis during maturity
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2
Q

4 functions of muscles

A
  1. provide movement
  2. maintain posture/ body position
  3. stabilize
  4. generate heat
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3
Q

myosin

A
  • responsible for actin based motility- thick filament
  • head has filamentous actin and uses ATP hydrolysis to generate force and to “walk” along the filament
  • contractions depend on myosin and actin
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4
Q

actin

A
  • thin filaments- protein
  • binding sites for myosin found on actin (inhibitor- tropomyosin)
  • make up myofilament with myosin
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5
Q

crossbridge

A

the globular heads of myosin link thick & thin filaments together, forming crossbridges
- these crossbridges act as motors to generate tension developed by a contracting muscle cell

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6
Q

tropomyosin

A

-rod-shaped protein(polypeptide) that helps stabilize actin and in relaxed muscles, blocks the binding site for myosin on actin

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7
Q

troponin

A

-initiated by AP, this is the protein Ca2+ binds to , to change the shape of tropomyosin, exposing binding site for myosin on the thin filaments(actin)

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8
Q

sarcoplasmic reticulum

A

-GOING TO REGULATE THE INTRACELLULAR LEVELS OF CALCIUM

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9
Q

T-tubules

A
  • at the A-band/ I-band junction, the sarcolemma protrudes into the cell, making an elongated tube (T-transverse)
  • they run between terminal cisternae of the SR forming triads
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10
Q

sliding filament model of contraction

A

-during contraction, your thin filaments slide past the thick ones, making actin and myosin filaments overlap more

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11
Q

acetylcholine ACh

A
  • neurotransmitter found in small membraneous sacs ( synaptic vesicles) that are located at axon terminal
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12
Q
  1. 6 seconds of exercise Short term
A
  • ATP stored in muscles is used first
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13
Q
  1. 10 seconds of exercise short term
A
  • ATP is formed form creatine phosphate and ADP
  • creatine phosphate is high energy molecule stored in muscle
  • creatine phosphate + ADP= (cat. creatine kinase) creatine + ATP
  • stored ATP + CP provides for 14-16 seconds of muscle contraction
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14
Q
  1. 30-40 seconds to end of short term exercise
A

-glycogen stored in muscles is broken down to glucose, which is oxidized to generate ATP

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15
Q

4.Hours of exercise-long term

A
  • ATP is generated by breakdown of several nutrient energy fuels by aerobic pathway
  • Glucose + oxygen = CO2 + water + ATP
  • aerobic provides lots of ATP but its slow and requires O2
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16
Q

slow oxidative fibers

A
  • slow to contract
  • aerobic respiration
  • resistant to fatigue
  • LOW POWER
  • endurance type: marathon, maintaining posture
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17
Q

fast glycolytic fibers

A
  • contract rapidly
  • anaerobic respiration
  • tire quickly
  • contract powerfully
  • good for short-term, intense or powerful movements, weight lifting , hitting baseball
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18
Q

fast oxidative fiber

A
  • contracts rapidly
  • aerobic respiration
  • moderate fatigue
  • moderate power
  • good for walking, sprinting
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19
Q

what is muscular dystrophy?

A
  • Duchenne muscular dystrophy-sex-linked recessive disease
  • diagnosed at early childhood and only live into 20s
    a. DMD is caused by lack of protein DYSTROPHIN, that links the cytoskeleton to the extracellular matrix and helps stabilize the sarcolemma
    b. the sarcolemma tears, allowing excess calcium to enter, damaging the fibers
  • eventually apoptosis occurs and muscle mass is lost
    c. there is no cure for DMD, but animal testing is underway for processes which will allow the body to produce dystrophin
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20
Q

hormone

A
  • “to excite”
  • chemical messengers released into blood, to send signals throughout the body
  • long distance chemical signals traveling thru blood or lymph
  • endocrine system
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21
Q

Endocrinology

A

study of hormones and endocrine system

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22
Q

target cells

A

tissue cells that are given hormone influences

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23
Q

cyclic AMP

A

Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3’-5’-cyclic adenosine monophosphate) is a second messenger important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.

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24
Q

steps of Cyclic AMP

A
  1. a hormone(1st messenger) binds to its receptor on the plasma membrane
  2. This binding causes the receptor to change its shape and activates G-protein by causing GTP to attach to it
  3. When GTP attaches to G Protein and activates it, active G protein attaches to the enzyme Adenylate Cyclase
  4. It catalyzes the formation of the second messenger cyclic AMP from ATP
  5. Cyclic AMP activates protein kinase A. A kinase is an enzyme that catalyzes phosphorylation of proteins. The phosphorylation activates some proteins, & inhibits others.
    6) The action of cAMP is short-lived becuase it is rapidly degraded by the intracellular enzyme phosphodiesterase.
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25
Q

upregulation

A

target cells form more receptors in response to rising blood levels of cells
ex. high estrogen levels cause cells to produce more progesterone receptors

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26
Q

downregulation

A

target cells become disensetised in high blood levels of hormones; they lose their receptors
ex. progesterone induces loss of estrogen receptors

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27
Q

permissiveness

A

one hormone can’t work completely without the other being present
ex. thyroid is necessary for reproductive development

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28
Q

synergism

A

each hormone will have the same effect alone but when together there is much larger effect
ex. glucagon and epinephrine together cause the release of glucose from the liver into the blood to by 150% of that of releases when each is working alone

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29
Q

antagonism

A

one hormone opposes the action of the other

ex. insulin which lowers blood glucose levels is antagonized by glucagon which raises glucose levels

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30
Q

tropic hormone

A

-4 of the 6 ant. pituitary hormones- TSH, ACTH, FSH and LH- are TROPINS or tropic hormones.
These hormones regulate the secretory action of other endocrine glands. All ant, pituitary hormones except GH affect their target cells via a cyclic AMP second-messenger system.

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31
Q

tropic vs. nontropic

A

Non-tropic hormones are hormones that directly stimulate target cells to induce effects. This differs from the tropic hormones, which act on another endocrine gland.
-ex. glucocorticoids, vasopressin, estrogen, testosterone, estrogen, oxytocin, epinephrine & norepinephrine

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32
Q

nervous vs. endocrine action

A

The nervous system controls rapid, precise
responses (ex. reflex)
• The endocrine system controls activities that
require long duration (ex. body growth)
– energetically more efficient
• These two systems interact and regulate each other

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33
Q

Endocrine glands

A
  • produce hormones
  • ductless glands
  • include: pineal gland, pituatary, thyroid, parathyroid, adrenal
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34
Q

Organs that perform both endocrine and other functions:

A
  • hypothalamus
  • thymus
  • pancreas
  • ovary(female)
  • testis(male)
  • placenta
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35
Q

2 major categories of hormones

A
  1. amino acid based

2. steroid based

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36
Q

Amino acid-based hormones

A

(made up of proteins, chains of amino acids)

1) water-soluble
2) attaches to EXTRAcellular receptors
3) can’t cross cell membrane

ex. antidiuretic hormone

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37
Q

steroid-based hormones

A

(made of lipids, with a cholesterol base):

1) lipid soluble
2) crosses cell membrane
3) attaches to INTRAcellular receptors

ex. estrogen and testosterone

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38
Q

5 ways hormones alter target cells:

A

1) induce secretion
2) stimulates protein synthesis within the cell( aldosterone in kidneys, more Na+K+ pumps)
3) induce mitosis ex. growth hormone
4) change membrane permeability/potential)
5) activate or inactivate enzymes ex. insulin

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39
Q

lipid soluble hormones(steroids & TH) work by

A

-direct gene activation since they can cross the cell membrane

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40
Q

Direct gene activation

A

-hormones move into the target cells by DIFFUSION and attach to an intracellular receptor.
The hormone/receptor complex moves into the nuclear chromatin and attaches to a specific region of the cell’s DNA, causing a gene to be turned “on”.
This means that the gene is being transcribed (mRNA being made), then translated on a RIBOSOME in cytoplasm.
Specific proteins are then synthesized from this info to promote metabolic activities, or synthesis of other proteins

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41
Q

All the amino acid based hormones except thyroxin use

A

Second messenger systems
- the hormone is the 1st messenger in these systems and when is attaches to the receptors on the membrane of the target cell , it causes the formation of an intracellular second messenger

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42
Q

Best studied 2nd messenger system

A

1) cyclic AMP system

2) PIP-Calcium

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43
Q

3 types of stimuli can trigger release of hormones

A
  1. humoral stimuli
  2. neural stimuli
  3. hormonal stimuli
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44
Q

humoral stimuli

A

changes of blood level & certain levels ions or nutrients will trigger hormone release
ex. parathyroid hormone is secreted in response to low Ca2+ levels, others are insulin & aldosterone

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45
Q

neural stimuli

A

nerve fibers stimulate hormone release

ex. Sympathetic nervous system stimulates the adrenal medulla to release norepinephrine and epinephrine during stress

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46
Q

hormonal stimuli

A
  • same hormones will cause the release of other hormones
    ex. release of most pituitary hormones is regulated by releasing and inhibiting hormones produced by the hypothalamus. The anterior pituitary hormones can control release of other hormones. Once the hormones of the target gland are high, they then inhibit production of anterior pituitary hormones.
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47
Q

Anterior pituitary hormones

A
  1. growth hormone GH
  2. thyroid-stimulating hormone TSH
  3. Adrenocorticotropic hormone ACTH
  4. Follicle-stimulating hormone FSH
  5. Luteinizing hormone-LH
  6. Prolactin PRL
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48
Q

Growth hormone GH

A
  • nontropic
  • anabolic hormone because it is a tissue building hormone
  • GH stimulates most body cells to increase in size & divide
  • Hypersecretion:children(gigantism), adults (acromegaly)
  • Hyposecretion: children(pituitary dwarfism), adults -no prob
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49
Q

Thyroid Stimulating hormone TSH

A
  • tropic
  • release caused by TRH from anterior pituitary but there is no TIH
  • rising blood levels of TH will inhibit TSH secretion
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50
Q

Adrenocorticotropic

A
  • tropic
  • AKA corticotropin
  • stimulates the ADRENAL CORTEX to release corticosteroid hormones(glucosteroid) to help resist stressors.
  • CRH from the hypothalamus triggers release and rising levels of gluco-corticoids inhibits release.
  • ACTH has a daily rhythm with levels peaking in the morning.
  • things like fever, low blood sugar and other stressors can change the normal ACTH rhythm by triggering CRH release
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51
Q

Gonadotropins- Follicle-stimulating hormone FSH, Luteinizing hormone LH

A
  • tropic & nontropic
  • act on gonads (testes & ovaries)
  • role for FSH is to trigger gamete formation(sperm or egg)
  • LH triggers secretion of reproductive hormones
  • these are absent until puberty , when GnRH from the anterior pituatary begins to stimulate their release
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52
Q

Prolactin PRL

A

-nontropic
- stimulates milk production
-both PRH and PIH regulate its secretion
-PIH is also neurotransmitter dopamine(inhibits prolactin).
-levels rise briefly before the menstrual period; this causes breast tenderness & swelling
Hyposecretion- not a prob except for nursing women
Hypersecretion- -abnormality of adenohypophyseal tumors, in women causes inappropriate lactation, lack of menstrual cycle and in men, impotence.

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53
Q

Posterior pituitary hormones

A
  1. oxytocin

2. Antidiuretic hormones ADH or vassopressin

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54
Q

Oxytocin

A
  • non-tropic
  • peptide mostly from neurons in paraventricular nucleus of hypothalamus
  • target organs: uterus, stimulates uterine contractions; initiates labor; breast; initiates milk ejection
  • in nonpregnant, nonlactating females and males oxytocin is involved in sexual arousal and orgasms, also promotes nurturing & affectionate behavior
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55
Q

Antidiuretic hormone ADH or vasopressin

A
  • non-tropic
  • peptide, mostly from neurons in supraoptic nucleus of hypothalamus
  • works against diuresis (urine production)
  • ADH targets the kidney tubules via cAMP, and causes them to reabsorb more water, leading to lower urine production
  • alcohol inhibits ADH secretion and leads to copious urination and next day hangover effects of dehydration
  • AKA vasopressin because it can cause vaso constriction when blood pressure is too low
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56
Q

Hyposecretion of ADH

A
  • Diabetes Insipidus(tasteless)- marked by large amounts of urine and intense thirst
  • this can be caused by a blow to the head that damages the hypothalamus or posterior pituitary
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57
Q

hypersecretion of ADH

A
  • syndrome of inappropriate ADH secretion (SIADH)
  • can be caused by meningitis, injury or surgery to the brain or cancer cells that are secreting ADH
  • symptoms include fluid retardation, headache, disorientation due to brain edema(brain swelling), weight gain, decrease solute concentration in the blood
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58
Q

thyroid gland hormones

A
  1. Thyroid hormone (TH) made up of : thyroxine (T4) and triiodothyroxine (T3) AND 2. CALCITONIN
    -T4 is the main hormone, and T3 is actually a conversion from T4
    -T4 has four bound iodine atoms and T3 has 3
    IPFL2R52
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59
Q

Thyroid Hormone TH

A
  • TROPIC
  • TH is the body’s major metabolic hormone that affects virtually every cell in the body
  • falling TH blood levels trigger release of TSH, and rising TH levels inhibit release of TSH
  • also, GHIH, dopamine, rising levels of glucocorticoids, and high blood concentration of iodine inhibit TSH release
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60
Q

Hyposecretion of TH

A
  • MYXEDEMA- hypothyroid syndrome; symptoms include: chills, constipation, thick dry skin, adema, you become lethargic and mentally slow
  • MYXEDEMA resulting from the LACK of IODINE- Goiter (enlarged thyroid)
  • in infants- CRETINISM- severe hypothyroidism, this leads to mental retardation, get sgort bodies with thick tongue and neck
  • if diagnosed early enough, it is preventable by hormone relacement therapy.
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61
Q

Hypersecretion of TH

A
  • autoimmune disorder-GRAVES DISEASE- abnormal antibodies produced against thyroid follicle cells, mimick TSH and that cuases release of TH
  • symptoms include: EXOPTHALMOS (symptoms of hyperthyroidism)-protrusion of eyeballs
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62
Q

Calcitonin

A
  • NON-TROPIC
  • produced by parafollicular cells of the thyroid, lowers blood CA2+ levels, antagonizing effects of parathyroid hormone
  • it acts on the skeleton, causing release of calcium from bone and inhibits bone resorption, and stimulates calcium uptake
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63
Q

parathyroid hormones

A
  • these 4 glands are located posterior of the thyroid

- the hormone secreted by the parathyroids is the PARATHYROID HORMONE PTH

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64
Q

parathyroid hormone PTH

A
  • NON-TROPIC
  • elevates blood calcium levels in 3 ways:
    1. increase CA2+ released by bone
    2. enhance resorption CA2+ by kidney
    3. Promote activation of Vitamin D by kidney -increase CA2+ absorption from food in intestine
  • vitamin D is ingested pr produced in its inactive form and must be transformed by the kidneys to vitamin D form.
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65
Q

hyperparathyroidism

A
  • caused by a parathyroid gland tumor
  • symptoms include: brittle bones (calcium is leeched out), depression of the CNS and formation of kidney stones due to excess calcium
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66
Q

hypoparathyroidism

A
  • caused by parathyroid gland trauma or removal

- symptoms include TETANY-loss of sensation, muscle twitches and convulsions

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67
Q

hormones secreted by adrenal glands

A

Steroid hormones-3 classes for each layer of adrenal gland- CORTICOSTEROIDS

  1. outer-zona glomerulosa- MINERALCORTICOIDS
  2. middle-zona fasciculata- GLUCOCORTICOIDS
  3. inner- zona reticularis- GONADOCOTICOIDS
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68
Q

mineralcorticoids

A
  • NON-TROPIC
  • help water and mineral balance
  • main is ALDOSTERONE- this hormone targets the distal parts of the kidney tubules, where it causes more K+ to be excreted in the urine, and more NA+ to be reabsorbed in the blood
  • the result is that blood levels of NA + increase and blood levels of K+ decrease
  • release is caused by low Na+ in the blood, low blood volume, low blood pressure, high blood K+
  • effects ~20 min
  • RENIN-enzyme that increases blood pressure
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69
Q

hypersecretion of aldosterone-mineralcorticoid

A

-ALDOSTERONISM, caused by adrenal tumors

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70
Q

glucocorticoids- CORTISOL

A
  • NON-TROPIC
  • cortisol is secreted in sig. amounts
  • ACTH( adrenocorticotropic hormone0 promotes cortisol release
  • secretion follows diurnal pattern, levels highest in the early morning
  • stress causes an increase in cortisol production, because cortisol promotes GLUCONEOGENESIS( formation of new glucose using fats & proteins)
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71
Q

hypersecretion of cortisol

A
  • CUSHING’S SYNDROME
  • cause is high doses of glucocorticoid drugs
  • other causes: an ACTH-releasing pituitary tumor or tumor of the lungs, kidneys , pancreas or adrenal glands
  • symptoms of Cushings syndrome: moonface, a buffalo hump, bruise easily, poor wound healing
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72
Q

hyposecretion of cortisol

A

-ADDISON’S DISEASE- discoloration, weight loss, low blood glucose & sodium, rise in K+

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73
Q

gonadocorticoids

A
  • NON-TROPIC
  • these are androgens, male sex hormones
  • their role contributes to the onset of puberty, sex drive in women
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74
Q

hypersecretion of androgens

A

-in females, production of a beard, male pattern body hair and enlarged clitoris

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75
Q

hormones secreted by adrenal medulla are..

A

1- epinephrine
2- norepinephrine
-these centers of the adrenal glands are part of the sympathetic nervous system

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76
Q

epinephrine

A

NON-TROPIC

  • released in larger amounts and is a better stimulator of metabolic activities, bronchiole dilation-and increased blood flow to the skeletal muscles
  • also used ad HEART STIMULANT and to dilate bronchioles during acute asthma attacks or anaphalaxys
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77
Q

norepinephrine

A
  • NON-TROPIC

- peripheral vaso-constriction and influences blood pressure

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78
Q

hyposecretion of both hormones of adrenal medulla

A

-no real effect, these hormones just intensify the activities of neurons

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79
Q

hypersecretion of adrenal medulla hormones

A

-caused by a tumor, causes uncontrolled sympathetic nervous system activity, hyperglycemia, increased metabolic rate, rapid heartbeat and palpitations, hypertension, intense nervousness and sweating-kicks body into overdrive

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80
Q

pineal gland hormone

A
  • pineal gland secretes melatonin
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81
Q

melatonin

A
  • TROPIC
  • peaks during night
  • powerful antioxidant and amine hormone derived from serotonin, causes drowsiness
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82
Q

pancreas hormone-producing cells

A
  • 1)Alpha cells- produce GLUCAGON

- 2)beta cells-produces INSULINGLUCAGON

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83
Q

glucagon-alpha cells

A

-NON-TROPIC
-hyperglycemic hormone (raises blood sugar) that targets the liver
Promotes following actions in liver:
1. breakdown of glycogen to glucose (glycogenolysis)
2. synthesis of glucose from lactic acid and noncarbohydrate molecules (gluconeogenesis)
3. release of glucose to the blood by liver cells, causing glucose levels to rise

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84
Q

Insulin- beta cells

A
  • NON-TROPIC
  • hypoglycemic hormone (lowers blood suger)
  • Does this in 3 main ways:
    1. by enhancing membrane transfer of glucose into body cells especially fat and muscle cells( but not the liver, kidney and brain
    2. by inhibiting the breakdown of glycogen to glucose
    3. by inhibiting the conversion of amino acids or fats to glucose
  • elevated blood glucose levels or rising plasma levels of amino acids & fatty acids stimulate insulin release
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85
Q

hypersecretion of insulin

A

-hyperinsulinism; hypoglycemia, tremors, disorientation, convulsions

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86
Q

hyposecretion or hypoactivity of insulin

A
  • Diabetes mellitus
  • become nauseated -hyperglycemia
  • this triggers “fight or flight” response that casues glycogenolysis( sugar breakdown), lipolysis(breakdown of fat) and gluconeogenesis making glucose levels even higher
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87
Q

signs of diabetes mellitus

A

1-polyurea-high urine leads to dehydration
2- polydipsia- excessive thirst
3- polyphagia- excessive hunger and food consumption ( because although glucose is produced it cannot be used)

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88
Q

Hemoglobin

A

-protein makes RBC’s red, this binds easily & reversibly with oxygen

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89
Q

erythropoietin EPO

A
  • direct hormonal stimulus for creating RBC production
  • EPO is produced by the kidneys & liver; so when kidney cells become low on O2 (hypoxic), the signaling molecule HYPOXIA-INDUCIBLE FACTOR. HIF is no longer broken down.
  • accumulation of HIF speeds up the production/release of erythropoietin
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90
Q

anemia

A

-RBC disorders where blood has abnormal low capacity to carry O2 , you can get pale, short of breath (lungs try to compensate for lack of O2)

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91
Q

Antigens

A
  • (agglutinigins)
  • blood type differentiation -ABO blood types based off this
  • Glycoproteins on cell surface ; cell-cell recognition, cause destruction of cells that don’t have appropriate antigen present
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92
Q

antibodies

A
  • agglutinins
  • exist in the plasma
  • attack antigens not present in persons own blood cells
  • ex. blood type A will produce Antigens, Anti-B antibodies
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93
Q

Functions of blood

A
  1. Distribution
  2. Regulation
  3. Protection
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94
Q

Distribution of blood

A
  1. Deliver oxygen & nutrients to all body cells
    2 . Takes waste (CO2 & metabolic wastes) from cells to areas if elimination (eg. Lungs, kidneys)
  2. Transports hormones from endocrine organs to target areas.
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95
Q

regulation

A
  1. maintains body temp; absorbs and distributes heat throughout the body and to skin surface to encourage heat loss.
  2. helps maintain normal pH; proteins and other solutes in the blood act as buffers to serious changes in pH that could be detrimental and blood holds a reserve of bicarbonate atoms
  3. helps maintain adequate fluid volume for circulatory system; Salts and blood proteins act to prevent excessive blood loss from bloodstream into tissues
96
Q

protection

A
  1. preventing blood loss; platelets and plasma initiate clotting
  2. preventing infection; antibodies, complement proteins and WBC defend the body against bacteria and viruses.
97
Q

function and range # of RBC

A
  • 4-6 million/ul

- transporting respiratory gases

98
Q

wbc function

A

-4800-10800 WBC/ul
only true cell
-defense against bacteria, viruses, parasites, toxins and tumor cells

99
Q

plateletes

A

-150k-400k platelets/ ul

seal small tears in blood vessels; instrumental in blood clotting

100
Q

why is iron important for the hemoglobin structure?

A

Hemoglobin is made up of protein globin bound to red heme pigment

  • each heme group bears an atom of iron set like a jewel in its center
  • the hemoglobin molecule can transport 4 molecules of oxygen because iron atom can combine reversibly with one molecule of oxygen
101
Q

hematopoieses, what is it and where it occurs

A

HEMATOPOIESIS- blood cell formation; occurs in red bone marrow .

102
Q

drop in O2 that triggers EPO release results from:

A
  1. lower number of RBC due to hemorrage (bleeding out) or excessive RBC destruction
  2. Don’t have enough hemoglobin per RBC
    - iron deficiency
  3. low oxygen-at high altitude of during pneumonia
103
Q

erythrocyte disorders-Anemias

A

blood has abnormally low capacity to carry O2 , you get pale , short of breath (lungs try to compensate for lack of O2)

104
Q

Common causes for anemia

A
  1. insufficient # of RBCs
  2. Low hemoglobin
  3. Abnormal hemoglobin
105
Q

hemorrhagic anemia

A
  • blood loss-rapid(ex. stab wound)

- or gradual overtime (bleeding ulcer)-loss of more blood overtime

106
Q

hemolytic anemia

A
  • RBC lyse prematurely, takes on too much water, or mismatched blood transfusion, hemoglobin abnormality, or certain bacterial or parasitic infections that cause cells to break down
107
Q

aplastic anemia

A
  • destruction of red bone marrow

- by chemicals, rediation, viruses, side effect of chemo(bone marrow cancer)

108
Q

iron deficiency anemia

A
  • not enough iron in diet, loose all your blood

- RBCs produced called MICROCYTES are small and pale

109
Q

pernicious anemia

A
  • vitamin B12 deficiency , could be mutation of factor to breakdown B12 , can’t process
  • developing RBCs grow but don’t divide, resulting in large pale cells called MACROCYTES
110
Q

thalassemias

A
  • you have a missing or faulty globin chain

- you would need blood transfusions

111
Q

sickle-cell anemia

A
  • alteration of a single amino acid in a beta chain of the globin molecule causes beta chains to link under low O2 condtiions and the RBCs become crescent shaped
  • Results: rupture easily & don’t deliver oxygen very well
  • 2 allele disease - partial sickle - can’t get malaria -become carrier
  • fetal hemoglobin won’t sickle and other treatments are stem cell transplants and gene therapy
112
Q

leukocytosis

A

WBC count that is over 11,000 cells per microliter, indicates you have infection

113
Q

3 steps of hemostasis

A
  1. vascular spasm- damaged vessels constrict to prevent blood loss
  2. Platelet Plug formation- platelets aggregate to form a temporary seal
  3. Coagulation-Blood clotting reinforces platelet plug with fibrin threads
114
Q

3 phases of clotting

A

Phase 1- Clotting may be started by either a fast acting intrinsic pathway (initiated by blood factors) or a slow acting extrinsic factors(initiated by tissue factors); both which lead to formation of prothrombin activator
Phase 2- Prothromin activator catalyzes transformation of prothrombin (plasma protein) to the active enzyme Thrombin
Phase 3- Thrombin catalyzes transformation of soluble clotting factor FIBRINOGEN into FIBRIN, this glues platelets together and traps elements

115
Q

hemophilia

A

hereditary bleeding disorder, minor trauma can cause long term bleeding

116
Q

transfusion reactions

A

-mismatched blood is infusion and the donors red blood cells will be attacked by the recipients plasma agglutinins

117
Q

blood typing

A
  • crossmatching tests are done to test for agglutination of donor RBCs by recipient’s serum
118
Q

pacemaker potentials

A

spontaneously changing membrane potentials that will initiate action potentials that will then spread throughout the heart to trigger contraction

119
Q

autorythmic cells

A

make up the intrinsic conduction system and do not maintain a stable resting potential (*unlike skeletal muscle fiber and other contractile heart cells)
- unstable resting potential continuously depolarizes, drifting slowly towards threshold

120
Q

systole

A

-contractions of the heart that force blood from the chambers of the heart

121
Q

diastole

A

-relaxation where the heart is filling with blood

122
Q

cardiac output (CO)

A
  • amount of blood pumped by each ventricle in one minute

- ~ 5.25 L/min - how fast its moving

123
Q

stroke volume

A

-volume of blood pumped out by one ventricle with each beat

124
Q

Cardiac intrinsic system and locations

A
  1. Right atrium- SA node(pacemaker)-75bpm, sinus rhthym
  2. Right atrium- Atrioventricular AV node-impulse delayed 0.1s
  3. Atrialventricular septum- Atrioventricular AV bundle of His
  4. Interventricular septum- Right & Left Bundle Branches
  5. Ventricular walls- Purkinje fibers
125
Q

what causes “lub dup” heart sounds?

A

closing of the heart valves

126
Q

What is normal heart rate for fetus, women, men?

A

Fetus- fastest (140-160 beats/min)
Women- (72-80 beats/min)
Men- (64-72 beats/min)

127
Q

Blood flow

A
  • volume of blood going through a vessel, organ or system within measurable time period (ml/min)
  • thru entire system fairly constant at rest=CO
  • varies thru organs
128
Q

Blood pressure(BP)

A
  • force per unit area exerted on vessel wall by blood within
  • expressed as a millimeters of mercury (mm Hg). So BP of 120 mmHg= pressure exerted by column of mercury 120 mm high
  • BP= your systemic arterial BP, found in large arteries near the heart
  • blood moves from higher pressure to lower pressure
129
Q

Resistance

A
  • opposition to flow, amount of friction blood is encountering on the vessel walls
  • more resistance is encountered in the peripheral (systemic) circulation so the common term is PERIPHERAL RESISTANCE
  • sources of resistance : viscosity (1-3)
130
Q

Systolic pressure

A
  • highest pressure, when your ventricles are contracting and blood is being pushed into aorta
  • in healthy adults avg. systolic is 120mmHg
  • Blood moves forward because pressure is higher at aorta than vessels away from the heart
131
Q

diastolic pressure

A
  • when heart is relaxing; semilunars closed, aortic pressure at its lowest point
  • in healthy adults average diastolic pressure is 70~80mmHg. The elastic walls of the aorta recoil and maintain enough pressure to keep blood flowing forward
132
Q

pulse pressure

A

-difference between systolic and diastolic pressure; felt as a throbbing pulsation during systole as the elastic arteries expand due to blood being forced into them

133
Q

mean arterial pressure (MAP)

A
  • pressure that propels blood to the tissues

- MAP= diastolic pressure + pulse pressure/3

134
Q

Baroreceptors

A
  • located in the coratid sinuses to supply the brain and in the aortic arch and walls of the larger arteries in the neck & thorax to supply the systemic circuit
  • excitement of vasomotor center would cause vasoconstriction
135
Q

what 3 sources of resistance and which is most important?

A

1) Blood viscosity
2) Total blood vessel length
3) Blood vessel diameter-*most important

136
Q

What 2 factors control arterial blood pressure?

A

1) COMPLIANCE OR DISTENSIBILITY- amount the elastic arteries near the heart can stretch
2) The volume the blood being forced into them at any time.

137
Q

How do arteriol, capillary and venous pressure differ?

A
  • ARTERIOL-(SYSTOLE)-120mmHg (DIASTOLE)-70~80mmHg
  • CAPILLARY-(initial)-35mmHg-(initial)- 15mmHg
  • VENOUS- 15 mmHg
138
Q

What factors maintain BP? How are these related?

A
  • BP is maintained by CO, peripheral resistance, blood volume
  • F=(change in P/R)
  • CO=(change in P/R)
  • (change P)= CO X R
139
Q

How Chemoreceptors modify vasomotor activity?

A
  • when CO2 level rise, or pH falls, or O2 content of blood drops sharply, chemoreceptors in the aortic arch and large arteries of the neck transmit impulses to cardiacceleratory center, increase CO and to the vasomotor center, which causes reflex vasoconstriction, this increases BP leading to faster return of blood to the heart and lungs
140
Q

How do the higher brain centers modify vasomotor activity?

A
  • BP is regulated through the medulla, but the hypothalamus and cerebral cortex can modify BP by relaying through the medulla
    ex. fight or flight mediated by the hypothalamus
141
Q

how do baroreceptors help maintain homeostasis, if BP is too hi

A
  1. Stimulus: BP rising, goes beyond normal
    - baroreceptors in coratid sinuses and aortic arch stimulated
    - stimulate cardio-inhibitory
    - inhibit cardio-acceleratory
    - impulses to heart decline: lower HR, lower CO
    - inhibit vasomotor center - vasodilation
    - lower resistance, return BP to homeostatic range ( decrease BP)
142
Q

Too low?

A

Stimulus: declining BP , below normal

  • impulses from baroreceptors: stimulate cardio-acceleratory
  • inhibit cardio-inhibitory
  • Baroreceptors then inhibited
  • stimulate vasomotor center-vasoconstriction
  • increase heart rate and force, CO increase, R increased=return to normal BP
143
Q

What are the 4 hormones that affect blood volume and pressure and in what direction?

A
  1. Epinephrine and norepinephrine-cause vasoconstriction, increase BP
  2. Angiotensin II- increase BP
  3. Atrial natriuretic peptide-decrease BP and blood volume by vasodilation and causing the kidneys to excrete more
  4. Antidiuretic hormone ADH- usually stimulates kidneys to conserve water, but can help if BP drops really low by also causing vasoconstriction
144
Q

Direct renal mechanism

A

-increased blood volume and increased BP signals the kidneys to release water (lowering blood volume and BP);whereas decreased blood volume and decreased BP signals the kidneys to retain water (increasing blood volume and raising BP).

145
Q

Indirect renal mechanism

A
  • when BP drops, the kidneys release the hormone RENIN which causes the production of ANGIOTENSIN II, which will increase BP in 3 ways:
    1. vasoconstriction
    2. Stimulates the pituitary release
    3. Stimulates secretion of Aldosterone
146
Q

how do substances move in and out of capillaries?

A

1) diffusion ex. gases
2) pass through intercellular capillary clefts ex. amino acids & sugars
3) fenestrations (opening in wall)
4) Pinocytotic (cellular drinking) vesicles

147
Q

What are the measures for hydrostatic and colloid osmotic pressure? Where is each highest?

A
  1. Hydrostatic pressure: “pushes”-35mmHg; dominates at the arteriole end of the capillary bed so fluids flow out of capillaries
  2. Colloid osmotic pressure: “sucks”-24mmHg; dominates at the venule end of capillary bed so fluids flow into capillaries
148
Q

lacteals

A

-lymphatic capillaries in the digestive system which play a role in absorbing digested fats from the intestine and produce chyle to be carried to the blood stream

149
Q

lymphangitis

A

inflamed lymphatic vessels , congestion of related blood vessels and swollen tender areas

150
Q

lymphedema

A

-edema of the lymphatics occur because of blockage of a tumor or removed part of lymphatics(cancer)

151
Q

buboes

A
  • swollen lymph nodes that are full of large # of infected bacteria, symptom of Bubonic plague
152
Q

tonsillar crypts

A

-in tonsils:invaginations of overlying epithelium to trap bacteria and particulate matter which then work their way into lymphoid tissue and most destroyed

153
Q

elephantiasis

A

where your lymphatics in lower limbs accumulate with parasitic worms

154
Q

Hodgkin’s disease

A
  • malignancy of lymphoid tissue, causing swollen but non-painful lymph nodes
  • fatigue, fever & sweating
  • B cells are malignantly transformed into giant Reed-sternberg cells
  • treated with chemo and radiation therapy
155
Q

lymphoma

A

any tumor of the lymphoid tissue

156
Q

What are 3 functions of lymph

A
  1. returns extra fluid to blood stream
  2. returns leaked proteins to the blood
  3. carry absorbed fats from intestine to blood
157
Q

T cells

A

directly attack and destroy infected cells

158
Q

b cells

A

produce plasma cells that then secrete antibodies

159
Q

lymphoid macrophages

A
  • phagocytize foreign substances and help activate T cells
160
Q

What are 2 functions of lymph nodes

A
  1. Filter lymph- using macrophages to destroy microorganisms and other debris
  2. help activate the immune system- strategically located sites where lymphocytes encounter antigens and are activated to mount attack against them
161
Q

spleen function

A
  • largest lymphoid organ
    1) cleanse blood by extracting RBCs + has phagocytes that remove debris and foreign matter
    2) stores and releases the breakdown products of hemoglobin ex. Iron
    3) stores platelets
    4) acts as hematopoietic site in the fetus
162
Q

thymus function

A
  • most active during youth
  • where T cells precursors will mature
  • no B cells, no follicles
  • does not directly fight antigens
163
Q

tonsils

A
  • the simplest lymphoid organ
  • trap pathogens from food and air
  • contain tonsillar crypts
164
Q

peyer’s patches

A
  • aggregated patches in distal portion of sm. intestine

- destroy bacteria before it can breach the intestinal wall and generate memory cells for long term memory

165
Q

macrophage

A
  • derived from monocytes (WBCs) that leave the bloodstream and enter the tissues
166
Q

phagosome

A
  • forms when phagocyte adheres to a pathogen or debris , engulfs it using pseudopods
167
Q

opsonization

A
  • to make tasty

- complement proteins or antibodies will coat (bind) foreign particles, makes it easier for macrophages to phagocytize

168
Q

respiratory burst

A

-helper T cells release chemicals that stimulate macrophages to release chemicals like hydrogen peroxide and bleach to kill invaders

169
Q

natural killer cells

A

-“police” blood & lymph to find cancer cells and virus-infected body cells
-they recognize the lack of self surface receptors(glycoproteins) and surface sugars of the target cells and kill target cells directly by causing apoptosis
+ secrete chemicals to enhance imflammatory response

170
Q

toll-like receptors

A
  • surface membrane receptors on macrophages that recognize specific classes of attacking microbes
  • trigger release of cytokines that promote inflammation and attract WBCs
171
Q

mast cells

A

release histamine

-aids in inflammatory process

172
Q

interferons IFNs

A
  • help protect uninfected cells from viral infection by synthesize proteins proteins that interfere with viral replication
  • reduce inflammation
  • activate macrophages
  • mobilize natural killer cells
173
Q

complement

A

-a group pf 20 plasma proteins that are normally inactive in the blood, but when activated release chemicals that will modify inflammation and induce bacterial cell lysis

174
Q

membrane attack complex MAC

A
  • complement protein that is inserted into a cell membrane, response to C3b molecules activating it
  • insertion of MAC makes a hole in the membrane, and lets water in causing the cell to lyse
175
Q

pyrogens

A

-secreted by leukocytes and macrophages, the body responds to foreign substances by increasing body temperature

176
Q

antigens

A

substances that can mobilize the adaptive immune response and provoke it
-proteins found on foreign substances

177
Q

immunogenicity

A
  • the ability to stimulate proliferation to specific lymphocytes and antibodies
178
Q

reactivity

A

the ability to react with activated lymphocytes and antibodies
-complete antigens include foreign proteins, polysaccharides, lipids, pollen grains, microorganisms

179
Q

active immunity

A

when B cells encounter antigens and produce antibodies

Acquired 2 ways: 1. naturally acquired 2. artificially acquired

180
Q

passive immunity

A
  • antibodies taken from a serum that (animal or human) is immune
  • only lasts as long as antibodies do
181
Q

What are the immune systems 3 lines of defense?

A
  1. 1st line of defense- external body coverings:skin & mucosa- try to protect and keep everything out
  2. 2nd line-antimicrobial proteins, phagocytes
  3. 3rd line- adaptive (specific) defense system-attack particular foreign substances
    ex. B-cells & T-cells
182
Q

examples pf physical and chemical barriers to microorganisms

A
  1. secretions in the skin, sweat, vaginal secretion that are acidic, helping to prevent bacterial growth
  2. The stomach mucosa secretes concentrated HCL , and other digestive enzymes that kill microorganisms
  3. Saliva and lacrimal fluid of the eye contain lysozyme(enzyme) that destroys bacteria
  4. The digestive and respiratory tracts, sticky mucous traps organisms
183
Q

What are benefits of inflammation?

A
  1. prevent spread of damaging agents to other tissues
  2. Dispose of cell debris and pathogens
  3. Set the stage for repair
184
Q

What are 4 cardinal signs of inflammation, and what causes them?

A

redness, heat, swelling and pain

  • chemicals involved in inflammation cause arterioles to dilate in an injured area, leading to hyperemia (increased blood flow to area) which accounts for REDNESS & HEAT
  • these chemicals also cause exudate to seep from blood into tissues: leading to SWELLING
  • swelling presses on nerve endings, and this along with release of bacterial toxins and the sensitizing effects of prostaglandins and kinins causes PAIN
185
Q

function of B cells

A
  • self-reactive B cellss are either elminated by apoptosis or undergo receptor editing to try to change the self-reacting antigen receptor
  • if self-reacting B cells leave the bone marrow, they are inactivated
186
Q

function T cells

A

-must be able to bind to MHC molecules (these present antigens to T cells for recognition) and not react to self-antigens

187
Q

Antigen presenting cells APCs

A
  • engulf antigens and present fragments of them to be recognized to T cells
  • APCs: dendritic cells, macrophages, b-lymphocytes
188
Q

How & where T cells are “educated” to determine immunocompetence and self-tolerance?

A
  • T cells are educated in thymus
  • T cells must be able to bind to MHC molecules (these present antigens to Tcells for recognition) and not react with self-antigens
  • Positive Selection: Chooses T-cells capable of binding to MHC molecules, all others are eliminated
  • Negative Selection- After Positive selection, T cells are tested to be sure that they do not recognize and bind too tightly on Self-MHC, if they do , they are eliminated by apoptosis
  • only 2% survive
189
Q

Where are B cells “educated” and how?

A
  • B cells-self reactive B cells are either eliminated by apoptosis or undergo receptor-editing to try to change the self-reacting antigen receptor
  • if self-reacting B cells leave the bone marrow, they are inactivated
190
Q

differences between primary and secondary immune response

A

Primary: occurs first time someone contacts an antigen-lag if 3-6 days to allow B cells to proliferate-antibodies peak in ~10days then decline
Secondary: 2nd time exposure-2-3 days , quick, high levels of antibodies are produced which bind more tightly to invading antigens
-faster, last longer & more effective

191
Q

What are 2 ways of acquiring active immunity?

A

active immunity- when B cells encounter antigens and produce antibodies

  1. naturally acquired-get bacterial or viral infection
  2. artificially acquired-get these through vaccines
192
Q

Antibodies cannot directly destroy antigens, but what 4 ways they inactivate them and/or tag them for destruction?

A

PLAN

1) NEUTRALIZATION-antibodies will block specific sites on viruses or bacterial endotoxins/prevents them from binding to tissues
2) AGGLUTINATION-Antigen-Antibody complexes bind to each other and cause clumping of foreign cells.
3) PRECIPITATION-Where soluble antigens that are linked to antibodies settle out of solution. Makes it easier for phagocytes to capture.
4) Complement fixation and activation- chief defense against bacteria or mismatched RBCs; when several antibodies bind close together on the same cell, complement can fix to the cell surface and cause lysis

193
Q

How does HIV work?

A
  • Human immunodeficiency virus
  • destroys helper T cells, depressing cell-mediated immunity
  • HIV targets cells displaying CD4 proteins into which the virus can insert itself and begin directing the cell to produce copies of viral RNA and proteins to infect other cells
194
Q

What are the 6 stages of digestion?

IPMCAD

A

1) INGESTION- taking in food
2) PROPULSION-moving food thru the alimentary canal via swallowing & peristalsis (alternating contraction & relaxation of smooth muscles in gut wall)
3) MECHANICAL DIGESTION- preparing food for chemical digestion by chewing, mixing with saliva, churning in the stomach and segmentation(constriction of sm. intestine, that will mix food w/ digestive substances
4) CHEMICAL DIGESTION- enzymes breaking food down into its basic chemical components
5) ABSORPTION-diegsted products (vitamins, minerals, water) will go thru the walls to blood & lymph
6) DEFECATION- Elimination of leftovers, indigestible substances.

195
Q

Where is intrinsic factor produced and what does it do?

A

The only stomach function essential to life is: secretion of intrinsic factor that is req. for intestinal absorption of vitamin B12, needed to produce more erythrocytes.

196
Q

What is gastrin ?

A

GASTRIN- hormone that stimulates secretion of enzymes and HCL to regulates gastric juice secretion

197
Q

what are the 3 types of stimuli that influence gastric activity and how do they work?

A

1) CEPHALIC-(reflex) triggered by the aroma, taste, sight or the thought of food we like to eat or want to eat-olfactory receptors/taste buds - goes down to stomach gland
2) Gastric -3-4hrs and produces 2/3 of gastric juice
3) Intestinal -2 phases
a. excitatory- partially ingested food in sm. intestine trigger release of gastrin , keeps gastric glands secreting
b. inhibitory-chyme triggers enterogastric reflex triggered, prevents food from entering intestine

198
Q

pancreas

A
  • produces enzymes to breakdown food

- these enzymes are in pancreatic juice released for use int the sm. intestine

199
Q

sm. intestine

A
  • partially digested material travels through the sm. intestine for 3-6 hrs and absorption of most of the water and all of the nutrients occur here
  • slow process allows for digestion and absorption
200
Q

L. intestine

A
  • contains 10 million types of bacteria (synthesize our B-complex vitamins and Vitamin K
  • main purpose: simply force fecal material to the anus -Haustral contractions
201
Q

liver

A
  • the liver produces bile ( stored in gall bladder) which is used to help breakdown fats
202
Q

stomach

A
  • temporarily stores food and where chemical breakdown of proteins occurs to form chyme
  • intrinsic factor req. to absorb Vit B12
203
Q

carbohydrates

A
  • digested in mouth and sm. intestine

- salivary amylase, pancreatic amylase

204
Q

proteins

A
  • stomach and sm. intestine

- pepsin, carboxypeptidase

205
Q

lipids

A
  • sm. intestine

- lipases

206
Q

nucleic acids

A
  • sm. intestine

- pancreatic nucleases

207
Q

what is gluten-sensitive enterotherapy (celiac disease)?

A

A genetic condition caused by a reaction to gluten food found in many grains
- breakdown products of gluten interact with molecules of the immune system in the GI tract, activating Tcells which attack the intestinal lining

208
Q

tidal volume TV

A

what goes in and out of lungs in a single normal breath

~500mL

209
Q

Bohr effect

A

acidosis and increasing Pco2 weaken the Hb-O2 bond, so O2 is dropped where it is needed most

210
Q

hypoxia

A

inadequate O2 delivery to the tissues

211
Q

Haldane Effect

A

the lower the Po2 and the lower the extent of Hb saturation with O2, the more CO2 that can be carried in the blood

212
Q

What is Boyle’s Law and how does it relate to our ability to breathe?

A

Boyle’s Law: Relationship between pressure and volume : P1V1=P2V2

  • pulmonary ventilation- breathing in and out, depends on volume changes in the thoracic cavity
  • volume changes lead to pressure changes, and pressure changes lead to the flow of gases to equalize pressure
213
Q

Steps of Inspiration

A

1) inspiratory muscles (intercostals) contract, lifting the rib cage and pushing the sternum outward; the diaphragm also gets pushed downward
2) Together, these actions cause an increase of thoracic volume of 500mL
3) Lungs are stretched and the intrapulmonary volume increases
4) This causes intrapulmonary pressure to decrease by ~ 1mmHg, making it lower than atmospheric pressure
5) This change in intrapulmonary pressure causes air to flow down its pressure gradient to enter the lungs until the intrapulmonary is 0 (equal to the atmospheric pressure)

214
Q

Steps of Expiration

A

1) Inspiratory muscles relax causing the rib cage to descend and the diaphragm to rise
2) This leads to a decrease in thoracic volume
3) Elastic lungs recoil passively, causing intrapulmonary volume to decrease as well
4) this causes an increase in intrapulmonary pressure of 1mmHg
5) This change in Pip allows air to leave the lungs flowing down its pressure gradient until intrapulmonary pressure is 0.
* During inspiration Pip actually declines to about 6mmHg relative to Patm; and it increases during expiration back up to 4mmHg relative to Patm (its normal pressure).

215
Q

What is the importance of surfactant in the lungs?

A

Surfactant, a detergent-like, complex of lipids & proteins, decreases the cohesiveness of water in the lung fluid, decreasing surface tension and allowing the alveoli to overcome it when they expand during inspiration

216
Q

What are the approx. partial pressures of O2 and CO2 in deoxygenated blood and in the alveoli?

A

O2: Alveoli (104mmHg) Deoxygenated blood (40mmHg)
CO2: Alveoli (40mmHg) Deoxygenated blood (45mmHg)

217
Q

ventilation-perfusion coupling: mismatch where low ventilation (little gas) and/or high perfusion of alveoli (lots of blood flow)

A

1) If there is a mismatch where low ventilation(little gas) and/or high perfusion of alveoli (lots of blood flow) cause local Pco2 to be high and local Po2 to be low
-Pulmonary arterioles serving those alveoli constrict and local bronchioles dilate
RESULT: Arteriolar constriction decrease blood flow (perfusion) and bronchiolar dilation allows more air flow/(increase in CO2 leaving the lungs).
-both ventilation and perfusion are now matched and excess CO2 that has built up can leave

218
Q

ventilation-perfusion coupling: mismatch where high ventilation (much gas) and/or low perfusion of alveoli (low blood flow)

A

2) If there is a mismatch where high ventilation (much gas) and/or low perfusion of alveoli (low blood flow) lead to a build up of Po2 and low Pco2
-pulmonary arterioles will dilate and bronchioles will constrict
RESULT: Arteriolar dilation increases blood flow (perfusion) and bronchiolar constriction decreases the CO2 leaving the lungs
- both ventilation & perfusion are now matched and CO2 levels are increased

219
Q

What is the main transport mechanism for O2 and why?

A

98.5% of O2 is transported bound to hemoglobin and only 1.5 % dissolved in plasma because oxygen is poorly soluble in water

220
Q

Does hemoglobin release all of its O2 with each circuit through the body?

A
  • normally only 20-25% of O2 is unloaded in one systemic circuit, so if O2 drops to very low levels in the tissues, such as vigorous exercise, more O2 can be unloaded to compensate
221
Q

What are the ways that CO2 is transported in the body and in what percentages?

A

CO2 is transported from tissues to the lungs 3 ways:
1) Dissolved in plasma (7-10%)
2) Bound to hemoglobin (just over 20%); it is bound and carried in the RBCs as carbaminohemoglobin. CO2 + HbHbCO2
3) Bicarbonate in plasma (70%)
CO2 +H2O H2CO3 H+ + HCO3-

222
Q

How does carbonic acid/bicarbonate buffer system work to maintain pH in the blood?

A

If H+ concentration becomes too high in the the blood, excess H+ is removed by combining with HCO3- (a weak base) to form H2CO3 (a weak acid)
-If H+ becomes to low, H2CO3 dissociates releasing H+

223
Q

prostaglandins function

A
  • decrease the viscosity of mucus in the cervix and stimulate reverse peristalsis in the uterus to facilitate sperm movement in the female reproductive tract
224
Q

relaxin

A

In males, relaxin enhances motility of sperm in semen

225
Q

What is corpus luteum?

A
  • The remaining granulose cells increase in size and long with the internal thecal cells, form the corpus luteum.
  • the corpus luteum produces progesterone and some estrogen
226
Q

function of acrosome on the sperm

A
  • the acrosome, located on the tip of the head contains hydrolytic enzymes that enable sperm to penetrate and enter the egg
227
Q

what chemical is released into the penile tissue during erection and function?

A

NO(Nitric Oxide)- it relaxes the smooth muscles in the blood vessel walls; let’s them dilate and fill w/ blood.

228
Q

what function does expansion of the CORPORA CAVERNOSA and CORPUS SPONGIOSUM perform during erection?

A

1) CORPORA CAVERNOSA- compresses drainage veins -keeps blood there
2) CORPUS SPONGIOSUM- expands to keep the urethra open for ejaculation

229
Q

pathway of sperm thru the male reproductive tract

A

-formed in seminiferous tubules(site of meisosis) - straight tubule (tubule rectus)-rete testis- efferent ductule-epididymis-ductus deferens-urethra-exterior

230
Q

Process sperm undergoes before being capable of fertilizing an egg, 3 major events

A

Spermatid in spermiogenesis:

1) elongation
2) shedding excess cytoplasm
3) forming a tail

231
Q

What 2 hormones stimulate spermatogenesis indirectly, and how do they work?

A

1- FSH- stimulates spermatogenesis indirectly by causing sustentacular cells to release androgen-binding proteins, which allows spermatogenic cells to bind and concentrate testosterone (stimulates spermatogenesis directly)
2- LH- stimulates the interstitial cells to make testosterone.

232
Q

What does testosterone stimulate at puberty?

A

spermatogenesis, as well as anabolic effects on the body

233
Q

During___________, a primary diploid spermatocyte gives rise to 4 haploid spermatids. Where does the process take plac?

A
  • Meiosis

- takes place in seminiferous tubules of the testes

234
Q

What are the 2 phases of ovarian cycle?

A
  1. The Follicular Phase (follicle growth from days 1-14) and the…
    2) Luteal Phase (corpus luteum activity from days 14-28)
235
Q

3 phases of the uterine cycle

A

1) Menstrual Phase -days 1-5- uterine lining is shed. Ovarian hormones at the at their lowest layers
2) Proliferative Phase- days 6-14- the endometrium (inner lining of the uterus) is rebuilding as blood estrogen levels rise. SPIRAL ARTERIES increase in #. In the ovary. ovulation, which only takes 5 min, occurs at the end of this phase. Cervical mucus thins to aid sperm in entering uterus
3) Secretory Phase-days 15-28- this phase is the most constant, timewise. Uterine lining continues to build up, and cervical mucus thickens again, to form a cervical plug that blocks entry to the uterus in case an embryo is implanting. If fertilization did not occur, the corpus luteum degenerates ~day 25, LH levels fall, spiral arteries kink and go into spasms, and menstruation begins.

Anat/Phys (15 decks)

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