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A&P 2 lecture > unit 1 test > Flashcards

unit 1 test Flashcards

1
Q

what are the endocrine glands and organs?

A
  • pituitary
  • hypothalamus
  • thyroid
  • parathyroid
  • adrenal
  • pineal
  • pancreas
  • ovary
  • testis
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2
Q

anterior pituitary

A
  • produces and secretes own hormones

- regulated by hypothalamus and neg. feedback

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3
Q

posterior pituitary

A

stores and secretes hormones produced by hypothalamus, sent from anterior pituitary

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4
Q

what does the thymus do and why didn’t we see one on our adult models?

A

the thymus makes WBC called t-cells to help fight diseases and infections. They are mostly made before birth and will last until puberty

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5
Q

define hormone

A

long-distance chemical signals that interact with target cell receptors.

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6
Q

what does corticotropin-releasing hormone (CRH) stimulate

A

adrenocorticotropic hormone (ACTH)

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7
Q

what does thyrotropin-releasing hormone (TRH) stimulate?

A

thyroid stimulating hormone (TSH)

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8
Q

what does Gonadotropin-releasing hormone (GnRH) stimulate

A
  • follicle-stimulating hormone (FSH)

- Luteinizing hormone (LH)

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9
Q

Growth hormone (GH)

A
  • anterior pituitary
  • to bone, muscle and organs
  • promotes amino acid and protein synthesis
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10
Q

thyroid stimulating hormone (TSH)

A
  • anterior pituitary
  • thyroid gland
  • produce T3 and T4
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11
Q

Adrenocorticotropic hormone (ACTH)

A
  • anterior pituitary
  • adrenal cortex
  • secrete glucocorticoids
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12
Q

follicle stimulating hormone (FSH)

A
  • anterior pituitary
  • ovaries and testes
  • growth of ovarian follicle and sperm
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13
Q

Luteinizing hormone (LH)

A
  • anterior pituitary
  • ovaries and testes
  • ovulation and testosterone
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14
Q

prolactin (PRL)

A
  • anterior pituitary
  • breasts
  • milk production
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15
Q

anti-diuretic hormone (ADH)

A
  • posterior pituitary
  • kidneys
  • water retention
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16
Q

oxytocin

A
  • posterior pituitary

- breasts and uterus

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17
Q

hypophyseal-hypothalamic portal system

A

connect brain to anterior pituitary to release and inhibit hormones

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18
Q

hypersecretion of GH causes?

A

gigantism

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19
Q

hyposecretion of GH causes?

A

pituitary dwarfism

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20
Q

hypothyroidism

A
  • weight gain
  • iodine deficiency
  • cant produce t3 and t4 but thyroid tells it to so thyroid gets bigger
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21
Q

Hyperthyroidism

A
  • weight loss
  • autoimmune
  • too much thyroid
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22
Q

hyper secretion- Cushings disease

A

depresses cartilage bone formation and immune system

back of neck

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23
Q

hyposecretion- Addisons disease

A

deficits of mineralocorticoids, weight loss, dehydration

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24
Q

what are the cardinal signs of diabetes?

A
  • polyuria; urine
  • polydipsia; thirst
  • polyphagia; hunger
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25
Q

diabetes mellitus

A
  • frequent urination
  • type 1; cant produce insulin
  • type 2; cant keep up, too much
  • gestational; insufficient insulin
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26
Q

diabetes insipidus

A
  • water imbalance within the body
  • ADH deficiency due to damage to hypothalamus or posterior pituitary
  • head trauma
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27
Q

water soluble hormones

A
  • need receptors

- second messengers; cAMP and PIP2 calcium

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28
Q

lipid soluble hormones

A

directly bind in the cell and activate genes

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29
Q

steps for cAMP

A
  1. bind to receptor
  2. activate a G protein
  3. G protein activates adenylate cyclase
  4. adenylate cyclase converts ATP to cAMP
  5. cAMP activates protein kinases
  6. phosphorylated proteins are activated or inactivated
  7. cAMP degenerates phosphodiesterase
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30
Q

steps for PIP2 calcium

A
  1. protein G activates phospholipase C
  2. phospholipase splits PIP2 into diacylglycerol (DAG) or inositol triphosphate (IP3)
  3. calcium ions act as another messenger
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31
Q

lipid soluble steps?

A
  1. receptor hormone complex enters nucleus and binds to DNA

2. initiates DNA transcription

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32
Q

what are the 4 second messengers?

A
  1. cAMP
  2. PIP2 calcium
  3. DAG
  4. iP3
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33
Q

how does a hormone know which cells to act on?

A

target cells- tissues with receptors for a specific hormone

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34
Q

what changes can be caused by a hormonal stimulus?

A

cellular changes by binding to receptors in target cells

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35
Q

what are the formed elements of blood?

A
  • erythrocytes (RBC)
  • leukocytes (WBC)
  • platelets (thrombocytes)
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36
Q

what is the blood pH?

A

7.35-7.45

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37
Q

what is the average blood volume?

A

5 L

  • male: 5-6
  • female: 4-5
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38
Q

define hematocrit and how can you increase/decrease it?

A
  • precent of blood volume that is RBC

- you can increase or decrease by EPO

39
Q

neutrophils

A
  • 3 or more round things

- kill/inhibit the growth of bacteria

40
Q

eosinophils

A
  • red staining
  • eyes or ear mufs
  • allerges and parasitic worms
41
Q

basophils

A
  • purple
  • lots of grains
  • histamine and heparin
42
Q

lymphocytes

A
  • big nucleus covering most of the cell
  • b and t cells
  • immunity
43
Q

monocytes

A
  • kidney shaped

- macrophages

44
Q

granulocytes

A
  • larger and shorter lived
  • cytoplasmic granules
    1. neutrophils
    2. eosinophils
    3. basophils
45
Q

Agranulocytes

A
  • lack granules
    1. lymphocytes
    2. monocytes
46
Q

wha is EPO?

A

process of formation of RBC’s that takes about 15 days

47
Q

what stimulates the production of EPO?

A

lack of O2

48
Q

where is EPO produced?

A

kidney

49
Q

what are the steps to make a RBC?

A
  1. hematopoietic stem cell transforms to myeloidn stem cell
  2. myeloid transforms to proerythroblast
  3. proerythroblast divides, into basophilic erythroblasts
  4. basophilic synthesizes ribosomes which stain blue
  5. polychromatic erythroblasts synthesize red hemoglobin showing pink and blue
  6. orthochromatic erythroblasts make concave shape, nucleus degrades
  7. reticulocytes have small ribosomes
  8. mature erythrocyte
50
Q

what is a reticulocyte and why is it important?

A

they are immature RBC

they help determine the umber of RBC before it leaves

51
Q

hemorrhagic anemia

A

rapid blood loss

52
Q

chronic hemorrhagic anemia

A

slight but persistent blood loss

53
Q

iron deficiency anemia

A

low iron intake, cant synthesize hemoglobin

54
Q

pernicious anemia

A

intrinsic factor

55
Q

renal anemia

A

lack of EPO

56
Q

aplastic anemia

A

destruction or inhibition of red bone marrow

57
Q

sickle cell anemia

A

genetic, causes sickling

58
Q

what is a benefit of sickle cell anemia

A

prevention of malaria

59
Q

describe the steps of hemostasis

A
  1. vascular spasm; smooth muscle contracts
  2. platelet plug formation; stick to collagen fibers and release chemicals to make platelets sticky to plug the exposed tissue
  3. coagulation; blood clotting, replaces platelet plug with fibrin threads
60
Q

describe the steps of coagulation

A
  1. prothrombin activation; intrinsic or extrinsic pathways to get to 10 (X)
  2. transformation to thrombin; transformation of prothrombin to activate thrombin
  3. fibrin mesh; converts fibrinogen to fibrin along with Ca2 activates XIII to cross linked fibrin mesh
61
Q

what is fibrinogen/fibrin?

A
  • a soluble protein from which fibrin is produced by thrombin
  • formed from fibrinogen during clotting of blood, makes mesh to stop the blood flow
62
Q

blood typing

A
  • A: a antigen, cant take B
  • B: b antigen, cant take A
  • AB: ab antigen, can take anything
  • O: no antigen, cant take a or b

Rh pos: Rh antigen, can take anything
Rh neg: no antigen, can only take when seen

63
Q

antigens

A

on cell surface to help immune system recognize the cells, what it can receive

64
Q

antibodies

A

response to foreign cells, what it cant get

65
Q

universal donor

A

O-

66
Q

universal recipient

A

AB+

67
Q

erythroblastosis fetalis

A

antibodies cross placenta causing hemolysis of fetal RBC’s, when Rh- mother has Rh+ baby

68
Q

structural characteristics of RBC that make it good for gas transport

A
  1. size and shape
  2. hemoglobin makes p 97% of cell
  3. no mitochondria
69
Q

functions of blood

A
  • transport
  • regulation
  • protection
70
Q

what may cause a bleeding disorder?

A

anemia, leukemia

71
Q

what the the three layers of the heart wall?

A
  1. epicardium- visceral
  2. myocardium- muscle
  3. endocardium- SS epi.
72
Q

what are the two different layers of the pericardium?

A
  1. fibrous pericardium; protect

2. serous pericardium; parietal and visceral layer

73
Q

what causes auscultations (heart sounds)?

A

closing of the valves

74
Q

describe the 4 phases of contraction

A
  1. ventricular filling
  2. ventricular systole
  3. isovolumetric relaxation
  4. isovolumetric contraction
75
Q

what systole and diastole?

A

systole- contraction

diastole- relaxiation

76
Q

p wave

A

SA- partial depolarization

77
Q

QRS wave

A

ventricular depolarization

78
Q

T wave

A

ventricular repolarization

79
Q

similarities between skeletal and cardiac muscle

A
  • depolarizing action potential
  • release Ca2+
  • excitation contraction with Ca2+
80
Q

differences between skeletal and cardiac muscle

A
  • pacemaker; automatic
  • all together
  • extracellular
  • tetanic disent occur
  • aerobic respiration
81
Q

what is the importance of Ca2+ in contraction and action potential?

A

prolonged depolarization

82
Q

describe the absolute refractory period in the heart

A

the time where no matter how intense the stimulus is, you can not get another action potential

83
Q

pericarditis

A

inflammation of pericardium, friction rubbing together

84
Q

cardiac tamponade

A

excess fluid leaking into the pericardial space, compress heart

85
Q

angina pectoris

A

thoracic pain by deficiency in blood to myocardium, weak cells

86
Q

myocardial infraction

A

heart attack, coronary blocked

87
Q

what is the fossa ovalis?

A

depressed structure of right atrium for fetal circulation, we don’t use when older

88
Q

right atrium

A
  • deoxygenated blood from vena cava from body

- release from pulmonary. artery to lungs

89
Q

left atrium

A
  • receives oxygenated blood from pulmonary. veins from lungs

- leaves the aorta into the body

90
Q

what is functional synctium

A

gap junctions allowing ions to pass

91
Q

what is preload?

A

stretching of the muscle cells before contraction, ventricular filling

92
Q

what is afterload?

A

load against which the heart has to contract to eject the blood

93
Q

how to calculate EDV, ESV and SV

A

SV = EDV - ESV

94
Q

how to calculate cardiac output (CO)

A

CO = SV x HR

A&P 2 lecture (12 decks)

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