A&P Exam 4 Flashcards

1
Q

Pituitary Gland Gross Anatomy

A
  • = pea on stalk (infundibulum)
  • 2 Lobes (anterior and posterior)
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2
Q

Anterior Pituitary Lobe

A

Adenohypophysis
Makes / release 6 hormones

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3
Q

Posterior Pituitary Lobe

A

-Made of Neurohypothesis infundibulum
-Makes 2 hormones

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4
Q

Posterior Pituitary Hormone Acquisition and release steps

A
  1. Gets hormone from hypothalamus
  2. Cell bodies in nucleus synthesize hormones
  3. Transported down axon (hypothalamic-hypophyseal tract)
  4. When N. fires → H releases into posterior capillaries releasing hormone
    5.Releases 2 Hormones= Oxytocin and Antidiuretic Hormone
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5
Q

Oxytocin

A

Produced :
-by hypothalamic paraventricular nuclei & released from posterior pituitary
Releases:
Positive feedback for uterus and cervix

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6
Q

Antidiuretic Hormone

A

Produced:
-Hypothalamic supraoptic nuclei, released post pituitary
Target:
-Renal CD (principal cells)
Effect:
-Reabsorbs H2O= less urine and increase blood volume
Release:
-Increases blood osmolality
-Drop in blood volume

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7
Q

What does too much antidiuretic hormone do?

A

Syndrome of Inappropriate ADH Secretion (SIADH):
-Retain Water
-Edema
-increased blood pressure
-Concentrated urine
-Increase in blood osmolality

Negative Feedback Loop:
-Stimulates hypothalamus to make ADH which is released by posterior pituitary
-Causes renal collecting ducts to reabsorb H2O
-Drops blood Osmolality

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8
Q

What does too little antidiuretic hormone do?

A

Diabetes Insipidus:
-Large amt of dilute urine, Thirst, and dehydration
Alcohol:
-Inhibits inhibits it

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9
Q

Posterior Pituitary Hormone Acquisition and Release

A

Hypothalamus controls it via hypophyseal portal system (blood vessels):
-Neurons release inhibiting and releasing hormones
-Picked up by primary capillary plexus to hypophyseal portal veins to secondary
capillary plexus to pituitary cells

*Sometimes called master endocrine gland

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10
Q

Growth Hormone

A

Target:
-Almost all cells
Effect:
-Mobilizes fat as fuel
-Increases size of cells (hypertrophy)
-Spares glucose increasing plasma glucose levels
-Stimulates protein synthesis
-Induce mitosis (long bone growth/ increase muscle mass)
Regulation:
-GHRH →increase Gh
-GHIH→decreases GH
-Highest at night

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11
Q

Too little Growth Hormone

A

Child→ pituitary dwarfism
4ft , but proportional
Tx= Growth hormone

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12
Q

Too Much Growth Hormone in Children

A

Gigantism:
-Typically from tumor
Example=
Robert Wadlow
Born 1919
4ft toddler
Died at 22
8ft 11in.
439 lbs.

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13
Q

Too Much Growth Hormone in Adults

A

-Overgrowth of membranous bone on Skull, face, hands
-Diabetes mellitus

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14
Q

Thyroid Stimulating Hormone

A

Target:
-Thyroid Gland
-Tropic hormone
Effects:
-Stimulates synthesis and release of Thyroid hormones
-Stimulates development of thyroid gland
Regulation:
-Increases by low thyroid levels and TRH
-Decreases by high Thyroid Hormone
Too Much:
-Hyperthyroidism
Too Little:
-Hypothyroidism

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15
Q

Adrenocorticotropic Hormone

A

Target:
-Adrenal cortex
Effects:
-Stimulation secretion of corticosteroid hormones
Regulation:
-Increased by stress, fever, drop in glucose levels (tend to be higher in morning)
-Decreases by high levels of corticosteroid hormone
Stops hypothalamus and anterior pituitary gland
Too Much:
-Cushing’s Disease
Too Little:
Rare

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16
Q

Gonadotropin Types

A

Follicle Stimulating Hormone and luteinizing Hormone

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17
Q

Gonadotropins

A

Target:
-Gonads
Effect:
-Regulate gonadal function
In Women=Oogenesis(egg production) &
Estrogen and progesterone production
Male=Spermatogenesis & Testes make testosterone
Regulation:
-Gonadal Releasing Hormone increases it
-Estrogen, progesterone, testosterone shuts it off
Too Much:
-Decrease libido
Too little:
-Fail to mature sexually
-Infertility
-amenorrhea

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18
Q

Prolactin

A

Target:
-Breast
Effects:
-Stimulate milk production
Regulation:
-Prolactin Inhibiting Hormone= dopamine
-Prolactin Releasing Hormone= suckling and estrogen
Too Much:
-Galactorrhea
Too Little:
-Lactation failure

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19
Q

Melanocyte Stimulating Hormone

A

Target:
-Melanocytes
Effect:
-Increases melanin production
-Sot significant in humans

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20
Q

6 Hormones released by anterior pituitary gland

A

1.Growth Hormone
2.Thyroid Stimulating Hormone
3. Adrenocortropic Hormone
4.Prolactin
5.Follicle Stimulating Hormone(gonadotropin)
6.Lutenizing Hormone

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21
Q

Hormone Produced by middle pituitary gland

A

Melanocyte Stimulating Hormone

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22
Q

Hormones produced by thyroid gland

A

1.Thyroid Hormone
2.Calcitonin

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23
Q

Thyroid Anatomy

A
  1. 2 lobes and isthmus
  2. Largest purely endocrine gland
  3. Has good blood supply
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24
Q

What does the Thyroid gland arise from in embryology?

A

endoderm

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25
Q

Histology of Thyroid Gland

A
  1. Has spherical follicles full of colloid
  2. Surrounded by cuboidal follicular cells
  3. Colloid filled follicles are filled with thyroglobuline and iodine (stores enough thyroid hormone to 2-3 months)
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26
Q

What is thyroid hormone made of?

A

-Amino acid + Iodine
-Lipid soluble (needs a carrier)

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27
Q

Thyroid Hormone Target

A

all cells

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28
Q

4 Effects of Thyroid Hormone

A

1.Stimulates synthesis of enzymes that oxidize glucose
-Increases metabolic rate
2.Regulates growth and development
-Nervous system
-Skeleton
-Reproductive organs
3.Maintains BP by increasing the number of adrenergic receptors
4.Has intracellular receptor
Causes mRNA transcription

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29
Q

How is thyroid hormone regulated?

A
  1. Thyroid stimulating hormone releases stored TH and synthesis of New TH
  2. TSH increases by low levels of thyroid hormone, chronic cold exposure, and
    Pregnanacy
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30
Q

How is thyroid hormone synthesized?

A

1.Follicle cells make thyroglobulin and Iodine and pump it into follicle
2.Iodine attaches to tyrosine on thyroglobulin
3.Follicle cells endocytose thyroglobulin and releases T3 and T4 into blood
4.TH transported by thyroid binding globulin (TBG)(Cells convert T4→T3)

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31
Q

monoiodotyrosine (MIT)

A

1st iodine onto tyrosine

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32
Q

diodotyrosine (DIT)

A

2nd iodine onto tyrosine

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33
Q

triiodotyrosine (T3)

A

1.most active
2.Thyroid hormone
3.3rd iodine onto tyrosine

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34
Q

thyroxine (T4)

A

1.made most
2.Thyroid hormone
3.4th iodine onto tyrosine

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35
Q

Hypothyroidism Symptoms

A

-Feel cold, weight gain, decrease metabolic rate, constipated, brain fog, dry eyes

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36
Q

Hypothyroidism In Adults Called

A

full blown →myxedema

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37
Q

Hypothyroidism In Kids

A

cretinism →jaundice, poor feeding

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38
Q

Hypothyroidism causes

A

1.Not enough iodine (can cause goiter)
2.Defective pituitary and thyroid gland
3.Decrease TSH
autoimmune= hashimoto’s
(OVERALL NOT ENOUGH THYROID HORMONE)

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39
Q

Tx Hypothyroidism

A

give thyroid hormone

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40
Q

Hyperthyroidism Symptoms

A

increase metabolic rate= increase heat, sweaty, lose weight, nervous

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41
Q

Hyperthyroidism Tx

A

Surgery to remove
Take radioactive iodine

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42
Q

Hyperthyroidism Causes

A
  1. Too much TSH
  2. Autoimmune= Grave’s Disease
    -IgG antibody works against TSH Receptors–>Caucasus goiter and bulging eyes (exophthalmos)
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43
Q

Calcitonin

A

-Polypeptide
-Produced by: Parafollicular cells of the thyroid gland
-Target: Bones
Effect:
1. Stimulates uptake of calcium in bone and drop calcium levels in the blood
2. Stimulate Osteoclast activity=Increases bone density
Release: High calcium= store calcitonin

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44
Q

How many parathyroid glands are there?

A

4

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45
Q

Parathyroid Hormone

A

Target: Bones and kidney
Effect:
1.Stimulates osteoclasts(digest bone and releases calcium into blood)
2.Kidney=Reabsorb calcium from the filtrate
3.Activate vitamin D = calcitriol (causes increase calcium absorption from the gut)
Release: Decrease in blood calcium= release

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46
Q

Hypoparathyroidism

A
  • too little parathyroid hormone
    -Can cause hypocalcemia
    -Occurs when gland is removed
    -Excites neurons=Twitches, tetany, and seizures
    ( b/c increase resting membrane potential= easy to
    depolarize)
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47
Q

Hyperparathyroidism

A

-Too much parathyroid hormone
-Can cause hypercalcemia
-Caused by:
1.Increase parathyroid hormone from gland or is ectopic
2.Lack of vit min D
3.Renal failure
Causes:
1.Leaches calcium from bones
2.Leads to fractures
3. Depresses neurons
4. Decrease reflexes
5.Weakness
(b/c membrane is hyperpolarized= harder to depolarize)
Causes Kidney Stones

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48
Q

Lipid Soluble Hormones (steroids)

A

Made from cholesterol
Made by gonads and adrenal
Can go through the pa=lasma membrane
Made to order
Long-half life in blood (days)
Need to be metabolized by the liver

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49
Q

Amino acid Based aka proteinaceous Hormones

A

Can’t cross plasma membrane
Can be stored in gland
Most hormones
Aka proteinaceous
Bits od peptide or protein
Modified amino acids→ thyroid, epinephrine, or norepinephrine
Short hald life in blood (mins)–> removed by the kidneys

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50
Q

How do proteinaceous hormones act?

A

Water soluble
Do not need a carrier
Bind to plasma membrane receptors= G protein coupled receptors which
activate 2nd messenger (cAMP)–>trigger a preprogrammed response in cell

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51
Q

How do fat soluble hormones act?

A

Need a carrier in blood
Bind to intracellular receptor
Directly activate genes

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52
Q

3 stimuli that control the release of hormones

A

1.Humoral
2.Hormonal
3.Neural

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53
Q

Humoral Stimulation

A

Ions= K and Ca
Nutrients= Glucose, amino acides

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54
Q

Neural Stimulation

A

SNS→ adrenal medulla→epi and norepinephrine

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55
Q

Hormonal Stimulation

A

Tropic hormones cause hormone release
Glands may respond to mmore than 1 hormone

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56
Q

Describe the different ways a hormone will interact with its target cell

A
  1. Cells need a receptor for the hormones to be able to respond to it
    Hormones bind and turns on preprogrammed response
  2. Response also depends on:
    -Blood leveol hormone
    -# of receptors on target cells
    -Affinity of receptors for hormone
    3.Target cell can change # of receptors
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57
Q

How hormones interact with the same target cell

A

Permissiveness
Synergism
Antagonism

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58
Q

Permissiveness

A

A Must be there for B to have effect

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59
Q

Synergism

A

A same effect
B has same effect
A+B increases effects

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60
Q

Antagonism

A

A opposes the effects of B

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61
Q

Right shift in Curve=

A

-Increase saturation of oxygen
-Weakens Hb and O2 bond which decreases affinity (bohr Effect)

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62
Q

Bohr Effect

A

Lower pH & increase Co2= more O2 release

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63
Q

External respiration

A

-co2 in blood→air
-deoxyhemoglobin(O2=40and CO2=45 and gets swapped) encounters
-pulmonary gas exchange and becomes oxyhemoglobin (O2=100 and CO2=40)
-driven by pressure

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64
Q

Internal respiration

A

-gas exchange that occurs with tissues
-blood has O2=100 and CO2=40 and tissue has O2-40 and CO2=45
-O2 enters and Co2 leaves tissue

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65
Q

What Decreases Hemoglobin saturation?

A

Greater temp
Lower pH
Greater Co2

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66
Q

What increases Hb saturation?

A

-Less temp
-Lower pH
-Lower CO2
-Metabolically active tissue

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67
Q

What happens during quiet inspiration?

A

Inspiration → enlarge thoracic cavity
Decreases pressure (less than atmospheric) → air moves in
Muscle:
Flattens diarphragm= increase height of the thoracic cavity
External intercoatals= lift ribs and sternum= greater diameter by a few m
Decreases pressure by 1mmHg=500ml

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68
Q

What happens in deep inspiration?

A

Mucles:
Accessory muscles →scalenes, …→ scalenes erect spine

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69
Q

Expiration

A

Muscles engaged in inspiration relax= causes passive recoil
Decreases thoracic cavity volume→ decreases volume→ increase pressure by 1mmHg

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70
Q

Forced Expiration

A

Oblique and transverse abs
Force abdominal organs against the diaphragm
Internal Intercostals
Depress rib cage further
Both of these decrease thoracic volume which increases pulmonary pressure

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71
Q

Adrenal Gland Anatomy

A

-Above kidneys
-Cushioned by fat and fibrous capsule
-2 glands:
1.Medulla
2.Cortex

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72
Q

Medulla (ectoderm) of the Adrenal Gland Anatomy

A

-knot of nervous tissue
-Part of SNS

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73
Q

Cortex (mesoderm) of the Adrenal Gland Anatomy

A

-True gland makes> 30 corticosteroids from cholesterol
-Lipid Soluble Hormones
-Made to order/not stored
-Need carrier in blood
-Use intracellular receptors/modify gene expression

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74
Q

Adrenal Gland Layers out to in (histology)

A

1.Zona Glomerulosa
2.Zona Fasciculata
3.Zona Reticularis

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75
Q

Zona Glomerulosa details

A

Mineralocorticoids
Determines mineral and water balance

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76
Q

Zona Fasciculata Details

A

Glucocorticoids
metabolism

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77
Q

Zona Reticularis (details)

A

Gonadocorticoids
Sex hormones

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78
Q

Mineralocorticoids

A

-95% are aldosterone
-produced= zona glomerulosa of adrenal cortex
-Target=kidney (distal convoluted tubule and collecting duct)
-Effect:
-Effect BP and B volume
-Stimulate production of sodium potassium pumps in the distal convoluted tubule
-reabsorption of sodium in exchange for K
-H2O follows Na

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79
Q

Too Much Mineralocorticoids

A

-aka Aldosronism
-Caused by adrenal tumor= retain water
-Edema
-Hypertension (BP increase)
-Low potassium

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80
Q

Too Little Mineralocorticoids

A

-aka Addison’s Disease
-Decrease BP and increase K

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81
Q

How are Mineralocorticoids Regulated

A

-RAAS
-has 4 paths

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82
Q

RAAS Path 1

A
  1. Drop in BP and volume (AKA SNS)
  2. Causes granular cells to release renin
  3. Converts angiotensinogen to angiotensin 1
  4. Angiotensin 1 becomes 2 by the angiotensin converting enzyme (ACE) in the lungs
  5. Angiotensinogen 2
    Causes:
    -Thirst
    -ADH release
    -Vasoconstriction
    -Aldosterone release:
    1.Increase the amount of potassium in the urine
    2.Decrease the amount of sodium and water in urine
    3.Increases blood volume
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83
Q

RAAS Path 2

A

Increase plasma potassium= increase aldosterone

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84
Q

RAAS Path 3

A

Increase in ACTH = increase BP and B vol

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85
Q

RAAS Path 4

A

ANP:
1.Stretch of heart increases ANP
2. Increased ANP blocks release of renin and aldosterone
3. Causes lose of water and salt and increase urine and decreas

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86
Q

Glucocorticoids Production, Target, and Effects

A

-Essential to life
Produced:
-Zona fasciculata of adrenal cortex
Target:
-Most cells
Effect:
-Maintains blood glucose levels
Glucogenesis
-Breakdown fats to glycerol and fatty acids for fuel
-Breaks down proteins to amino acids for fuel repair
-Resist stressors and depress inflammatory
-In excess = decrease inflammation and immune response
Maintains BP w/ SNS

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87
Q

Glucocorticoids Regulation

A

-Increase Stress
-Higher in the morning
-Stress is positively stimulating hypothalamus
-Hypothalamus with CRH stimulates anterior pituitary gland which causes the release of ACTH stimulating the adrenal cortex
-Adrenal cortex releases cortisol suppressing stress, hypothalamus, and anterio

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88
Q

Too Little Glucocorticoids

A
  • aka Addison’s Disease
    -Decrease ACTH
    -Autoimmune disorder
    -Destroys glands decrease production of glucocorticoids and mineralocorticoid
    -Symptoms:
    Decrease weight
    Drop in sodium
    Decrease glucose
    Increase potassium
    Decrease BP leading to dehydration and eventually death
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89
Q

Too Much Glucocorticoids

A

-aka Cushing’s syndrome
-Caused by to much ACTH Secretion
-Caused by tumor or adrenal damage
Symptoms:
Increase glucose= steroid diabetes
Loss of muscle mass and bone density=weakness, prone to fracture
Retain water and salt= increase BP and edema
Redistributes fat= moon face, buffalo hump
Increase in the number if infections

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90
Q

Gonadocorticoids

A

-Weak androgen
-Produced by zona reticularis and adrenal cortex
-Target= many cells
-Effect:
-Tissue converts to testosterone or estrogen
-Axillary and pubic hair growth
Too Much:
-Masculinization
-female= beard, male hair patterns
-Male= beard, sex drive
Too Little:
-unknown

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91
Q

Catecholamines

A

….

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92
Q

Adrenal Medulla

A

-Short term stress response= fight or flight
-Modified ganglionic sympathetic neurons
-hormones= catecholamines
-80% Epinephrine & 20% Norepinephrine

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92
Q

Adrenal Medulla Too Much and Too Little

A
  1. Too Little= no problem
  2. Too Much
    -Tumor=pheochromocytoma
    -Symptoms:
    Uncontrolled sympathetic activity
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92
Q

Targets and Effects of the Adrenal Medulla

A

-Mimics SNS
1. Heart:
-Increased HR, Force, & BP
-Beta 1
2. Blood Vessels
-Constrict & Increase BP
-alpha1
3. Lungs
-Dilate bronchioles
- Beta 2
4. Liver
-Increase Blood glucose
-Beta 2

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93
Q

Pineal Gland

A

-Root of 3rd ventricle of diencephalon
-Melatonin effect= regulates sleep and wake cycle

94
Q

Pancreas Anatomy

A

-Mixed gland
1. exocrine= acinar cells (digestive enzymes), dects (bicarbonat eand water)
2. Endocrine (pancreatic Islets)
Cells sense glucose levels in the blood
3. Alpha cells make glucagon and increase blood glucose
4. Beta cells make insulin to drop blood glucose
-arises from gut endoderm

95
Q

Glucose Metabolism in Pancrease

A

-Burns glucose to make ATP
-Can convert glucose to fat and amino acids or glycogen (glycogenesis)
-Can make glucose from glycogen, lactose, or amino acids= glucogenesis

96
Q

glycogenolysis

A

Glycogen → glucose

97
Q

glycogenesis

A

Glucose→glycogen

98
Q

gluconeogenesis

A

Pyruvic acid→glucose

99
Q

glycolysis

A

-Glucose→pyruvic acid
-Pyruvic acid makes lactic acid and acetylCoa and water
-These release water, CO2, heat ATp, and Ketones

100
Q

Lipogenesis

A

Glycerol +3 fatty acids –>Tryglicerides

101
Q

Lipolysis

A

-Triglycerides → Glycerol + 3 Fatty Acids
-Fatty acids can become acetyl COa and O2 via beta oxidation

102
Q

Protein can become what

A

amino acids and vice versa

103
Q

Amino acids become what

A

NH3 and Keto acids and vice versa

104
Q

Keto acids can become what

A

glucose and vice versa

105
Q

Glucagon Production, Target, and Effect

A
  1. Produced: by alpha cells of pancreatic Islets
  2. Target (hepatocytes
  3. Effect:
    1 molecule release 1000,000,000 glucose molecules form liver
    Increase blood glucose by:
    Breaking down glycogen to glucose (glycogenolysis)
    Making glucose from non carbs= gluconeogenesis
106
Q

glucagon release

A

-Decrease blood glucose, Increse SNS, and Increase amino acids
-Increases glucagon
-Increase blood glucose, growth hormone, and insulin
Decrease glucagon

106
Q

Insulin Production, Target, effects

A
  1. Produced by Beta cells of pancreatic islets
  2. Target=Many body cells
  3. Effects
    A. Decrease Blood glucose by
    Enhancing membrane transport of glucose into muscles and fat cells
    (liver , kidney, and brain cells don’t need insulin to get glucose)
    -Inhibits glycogenolysis→ stimulates glycogenesis
    -Inhibits gluconeogenesis→stimulates lipogenesis
    -Inhibits protein breakdown→stimulates protein synthesis
    B. Increase oxidation of glucose by glycolysis= ATP
107
Q

Too Low Glucagon

A

low blood glucose

107
Q

Too Much Glucagon

A

high blood glucose

108
Q

How is Insulin Released

A

-Increase Blood glucose and PSNS= increase insulin
-Decrease blood glucose, SNS, growth hormone & Increase glucagon= decrease
insulin

109
Q

Too Low Insulin

A

Diabetes Mellitus
- is low and BG high, but cells can’t use BG
1. Causes
A. SNS stimulation
-Increase glucagon–>Increase glugogenesis, Lypolysis, and glycogenolysis
B. Breaks down fat
-Too much fat in blood= heart disease
-ketones= acid/ decrease pH= ketoacidosis
C. BV’s damaged
-By osmotic effects of glucose in -blood→hands and feet

110
Q

Symptoms of Diabetes Mellilitus

A

-Excessive hunger=polyphagia
-Pee a Lot=Polyuria
-Glucose in urine is osmotic, so it pulls water into urine
function as a diretic →dehydration→polydipsia
(always thirsty so drink a lot)

111
Q

Too Much Insulin

A

-decreases Blood Glucose

112
Q

Gonads Release What?

A

-Release estrogen, progesterone, and testosterone

113
Q

Placenta Releases What?

A

-Human gonadotropic hormone, progesterone, and estrogen

114
Q

Adipose Tissue Releases What?

A

-Leptin
-Caused from increase fat
-Decreases appetite

115
Q

What do the GI Tract Enteroendocrine Cells Release?

A

Gastrin, secretin, Cholecystokinin

116
Q

What does the skin help release?

A

Sun + cholesterol= cholecalciferol activated by kidney to calcitriol

117
Q

What do Kidneys release?

A

Erythropoietin, renin

118
Q

What does the thymus release?

A

Hormones for T cell development, thymopoietin, and thymosin

119
Q

What are the 4 roles of the reproductive system?

A

1.Form Gametes: ova and sperm
2.Bring male and female gametes together= intercourse
3.Combine Gamet DNA= fertilization of zygote
4.Support New Life=gestation of embryo to fetus; parturition of baby

120
Q

Sister chromatids

A

=identical part of the chromosome

121
Q

Centromere

A

the points where two chromatids touch

122
Q

Somatic Cells

A

Diploid: 2n = 23 pairs of homologous chromosomes
One from mom, one from dad
Carry genes for same traits
22 autosomes and 1 pair of sex chromosomes

123
Q

Gametes:

A

Haploid: n = 23 chromosomes

124
Q

Primary Reproductive organs

A

Gonads=Testis and Ovaries

125
Q

Primary Reproductive organ Functions

A

-Produce gamets via Meiosis
-Make sex hormones
Female=estrogen and progesterone, males: testosterone
-Cause growth and development of reproductive organs and other organs/accesory reproductive organs

126
Q

Accessory reproductive organs

A

-ducts, glands, external genitalia
estes

127
Q

Main Male Glands

A

-Seminal Vesicle
-prostate
-Bulbourethral Gland

128
Q

Seminal Vesicle

A

-60% of the semen
Yellow, viscous, alkaline, fructose

129
Q

Prostate

A

-30% of the Semen
-Milky, acidic fluid

130
Q

Bulbourethral Gland

A

-Thin clear mucous that lubricates penis with ejaculation

131
Q

Penis Parts

A

-Root
-Body
-Glans

132
Q

Scrotum Muscles

A

-has septum
-cremaster muscle
-Dartos muscle

133
Q

Cremaster muscle

A

→ covers spermatic cord and testes
-Temperature control
-Pulls toward body when cold

134
Q

Dartos Muscle

A

-Attaches to the fascia of scrotum skin
-Adjusts temperature
-Wrinkles

135
Q

Testes

A

-Make testosterone
-Make sperm and fluid in seminiferous tubules
-Parts:
1.Ductus Epididymis
2.Ductus Deference
3.Spermatic Chord

136
Q

Ducts Epididymis

A

Sperm matures and is stored

137
Q

Ductus Deference

A

Uses peristalsis→ moves sperm out through ejaculatory duct and urethra (prostatic→ membranous→spongy)

138
Q

Spermatic Chord

A

Inguinal canal → ductus deference→ Testicular artery→pampiniform plexus→vein
For temp regulation of

139
Q

Diploid

A

22 pairs of autosomes
1 pair sec chromosomes
xx=female
xy=male

140
Q

Gene

A

DNA that codes for one protein

141
Q

Locus

A

Location of gene on chromosomes

142
Q

Alleles

A

Different forms of the same gene

143
Q

Homozygous Dominant or recessive

A

BB,bb

144
Q

Heterozygous

A

Bb

145
Q

Dominant

A

suppressive allele

146
Q

Types of Traits that are dominant

A

Widows peaks
Dwarfism
Dimples
Freckles
astigmatism

147
Q

Recessive

A

Repressed Allele

148
Q

Types of Traits That are Recessive

A

Normal vision
Albinism
Cystic fibrosis

149
Q

Genotype

A

gene= Bb, BB

150
Q

Phenotype

A

Physical expression of genes

151
Q

Independent assortment

A

2^n=2^23=8.5millin variations of genetic material
Variation in tetrad genetic information
Crossing over=Chromosomes exchange gene segments
-Random Fertilization
-Results=72 trillion different zygote, possible

152
Q

Pattern of Inheritance

A

-Dominant-Recessive Inheritance
-Dominants will mask recessive

153
Q

Codominance

A

-Both alleles are expressed
-ABO blood type=AB blood(both dominant), O recessive

154
Q

Sex Linked

A

-X linked
-X has 25000+ genes essential to life
-Females= one x is inactive
-Barr Body
-Y has 78 genes, only 5 % are not sex related
-Traits are x linked
-Always expressed in males
-Passes mother to son

155
Q

Ovary

A

-Follicles house oocytes
-Ligaments that attach to it
-Ovarian Ligaments= suspensory and mesovarium
-Covered by tunica albuginea
-Egg rips out of ovary (ouchy)

156
Q

Cortex of Ovary

A

Games

157
Q

Medulla of Ovary

A

-BVs and Nerves

158
Q

Uterine Tube

A

-Goes from Ovary to infundibulum, ampulla, isthmus
-Smooth muscle supported by mesosalpinx

159
Q

Uterus

A

Egg enters
Supported by cardinal, uterosacral, and round ligament
Broad Ligament:
-Mesouarium
-Mesosalpinx
-Mesometrium

160
Q

Parts of Uterus from top to bottom

A

Fundus, body, cervix

161
Q

Wall 3 layers out to in

A

-Perimetrium
-Myometrium (Smooth muscle)(Contracts in labor)
-Endometrium (Lines cavity)

162
Q

2 layers of Endometrium

A
  1. Functional layer (Changes cyclically)(Is shed)
  2. Basal Layer(Stays during period)(Forms new functional layer)
163
Q

Cervix

A

-below uteris
-secretes mucosa
-Top-internal Oz
-bottom= external oz

164
Q

Vagina

A

-Thin walled tube below cervix
-Receives penis during sex and is a passage way for the baby to come out

165
Q

Wall of Vagina in to out

A

-Mucosal
-Smooth Muscle=Musculans
-Adventitia

166
Q

Vulva

A

-Mons pubis= fatty area covered with pubic hair
-Labia majora and labia minora
-Skin folds that protect vestibule

167
Q

Vestibule

A

-Urethral opening= pee only
-Vaginal Opening
-Vestibular Glands
-Lubricate
Clitoris
Richly innervated, swells when stimulated
More nerve endings than penis

168
Q

Clitoris

A

-Richly innervated, swells when stimulated
-More nerve endings than penis

169
Q

5th week

A

Mesoderm–>gonadal ridges
Gonads→ cortex and medulla
Cortex→ ovary
Medullar→ testes

170
Q

6th weeks

A

Mesonephric duct forms
Paramesonephric duct forms

171
Q

7th Week

A

-XY makes testosterone (⅔ of level of teens)
-Paramesonephric duct→degenerates
-Seminephric tubules join -mesonephric duct→ ductus deferens, epididymis

172
Q

8th week

A

-XX
-Mesonephric duct degenrates
-Paramesonephric duct→uterine tubes, uterus, and vagina
1. Genital tubercle
-Clitoris in female
-Penis in males
2.Genital groove
-Vestibule in females
3.Urethral folds
-Labia minora females
-Fuse into vental penis= males
4.Labial scrotal swelling
-Labia majora in females
-Scrotum in males

173
Q

7th month

A

-Gonads are tethered to labial-scrotal swelling by gubernaculum stop growing and becomes fibrous
-As body grows→ gonads are pulled into pelvis
-Takes BVs and nerves with them
-Males=Testes will descend through the inguinal canal into the scrotum
-Takes some of the parietal peritoneum with it and forms tunica vaginalis
-Females=Ovaries descend→ stopped by broad ligament
-Gubernaculum divides in to ovarian ligament and round ligament

174
Q

Describe Steps of Male Sexual Response

A

1.Erection
2.Ejaculation
3.Resolution
4.Final Neural Transmitter Response

175
Q

Erection

A

-From Tactile stimulation or erotic sights, sounds, or smells causes erection
-Goes from CNS→PSNS
PSNS Reflex
-How:
Nitrous Oxide is Released →dilates arterioles→ engorges corpora cavernosa
Expansion of the corpora cavernosa compresses venous drainage
The bulbo urethral gland →lubricates penis

176
Q

Ejaculation

A

=Propulsion of semen
-SNS spinal reflex to erection
How:
1.Bladder constricts
2.No urine goes out and no semen goes into bladder
3.Reproductive ducts and accessory glands contract
4.Semen in urethra and initiates spinal reflex→bulbospongiosus contracts and propels semen (500cm/sec aka 11mph=orgasim (intense pleasure)

177
Q

Resolution

A

-Skeletal muscles relax
-SNS constrict arterioles feeding penis= flaccid
-refractory period=unable to achieve another orgasm (can be minutes to hours

178
Q

Final Neural Transmitter Response

A

-Dopamine levels increase during sex
-Rewards certain behaviors
-Promotes Bonding b/w male and female
-Causes synapses in the brain to remodel so easier to have sex= good in marriage

179
Q

Spermatogenesis

A

-Make the male gamete (sperm)
-Make 90 million sperm per day
-Body cells= 46 diploid
-haploid=23

180
Q

Cells Involved in Spermatogenesis

A
  1. Basal Lamina
  2. Myoid Cells
  3. Interstitial endocrine Cells
  4. Sustenocytes
181
Q

What Occurs in basal Lamina of Sperm Production?

A

-spermatogonium=sperm stem cell
Reproducing via mitosis:
1. Daughter “A” stays
2. Daughter “B” is primary spermatocyte Undergoes meiosis 1
3.Causes independent assortment
Crossing over= chiasmata
4.Forms secondary spermatocytes
5.Secondary Spermatocytes undergo Meiosis 2
6. Result = spermatids
Early spermatids can’t swim, so they are infertile

182
Q

Myoid cells

A

Move sperm and fluid
3-5 layers

183
Q

Interstitial Endocrine cells

A

Above myoid cells
Make testosterone

184
Q

Sustenocyte (sertoli)

A

-produce / secrete testicular fluid
-Regulate spermatogenesis
-Phagocytize faulty sperm and excess cytoplasm
-Forms blood testis barrier=tight junctions
-Protects sperm from male immune system
b/c sperm produced at puberty)

185
Q

Sperm Components

A

1.head
2.Mid piece
3.Tail

186
Q

Sperm Tail

A

Flagellum
4mm/min

187
Q

Sperm Mid-piece

A

Metabolic area
Has mitochondria
Burns fructose

188
Q

Sperm Head

A

Has nucleus
Has acrosome
Lysosome that contains proteases that penetrate the egg

189
Q

Hormone Effects of male Puberty

A

-Decrease sensitivity of hypothalamus to the se hormones
-This increases gondal hormones and testosterone
-Causes spermatogenesis and follicle stimulating hormone

190
Q

Anabolic effects of Puberty

A

Reproductive organs grow 8-14yrs old
Hair in axilla, groin, face, body
Deeper voice=larynx enlarges
Skin thickens= more acne prone
Bone growth and density
Estrogen closes epiphyseal plate @ 19-21
Increase in muscle mass
Increase in basal metabolic rate
Shapes brain= arousal, sex drive

190
Q

Describe how male sex hormones are released

A

Hypothalamus
1. Releases Gonadal Releasing Hormone Via Portal blood
2. Anterior Pituitary release FSH and LH
3. Gonads release estrogen, progesterone, Testosterone affecting Target cells
4.Estrogen, Progesterone, and Testosterone inhibit previous responses

191
Q

What are hormones like before puberty in males

A

-Sex hormone is low
-Gonadal Releasing Hormone is Suppressed

192
Q

Oogenesis and follicle development before birth

A

-oogonia= stem cells go through mitosis

193
Q

Oogenesis and follicle development at birth

A

Primary oocytes–>Start meiosis and Stop at prophase 1
2 million at birth, release 500
With age, not stable

194
Q

Puberty # of oocytes

A

-400,000 oocytes left

195
Q

Cycle oogenesis and follicle development

A

-Secondary Oocytes + 1st polar body
-Arrests in metaphase 2
-Ovulation
-Sperm Penetrates
-Completes Meiosis 2

196
Q

Main Stages of follicle development

A

1.Primordial Follicle
2.Primary Follicle
3.Secondary Follicle
4.Vesicular Follicle
5.Vesicular Follicle

197
Q

Primordial Follicle

A

-Meiosis 1= suspended in prophase
-Has layer of simple squamous granular cells
-primary oocyte in the center

198
Q

Primary Follicle

A

Stimulated by local chemicals to develop–>Granulosa Cells → cuboidal and multiply
-Layer around oocyte is formed= Zona Pellucida (glycoprotein membrane) that enables fertilization

199
Q

Secondary Follicle

A

-Stratified layer of granulosa cells
-Make progesterone
-Convert androgen into progesterone
-Outhecal cells make andogens

200
Q

Vesicular Follicles (Tertiary)

A

-Stimulated by FSH
-Fluid filled antrum
-2.5 cm bulge off of ovary
-Corona Radiata=Granular cells around oocyte persist
-Cumulus Ouphorus=Connects egg to wall

201
Q

Ovulation is when you make what?

A

secondary oocyte

202
Q

What occurs if oocyte is not fertilized in Ovulation

A

-Lost during menstrual cycle
-Corpus luteum= space after oocyte rips out
-Degenerates in 10 days
-b/cms scarred corpus albicans

203
Q

What occurs if oocyte is fertilized in ovulation?

A

-Complete meiosis 2
-Corpus luteum persists until placenta grows and develops to take over hormone duties
-Implants at day 20 HCG= human chorionic gonadotropin
-Corpus lutenum of pregnant= grows 3x before placenta takes over

204
Q

Phases of Ovarian Cycle

A

1.Follicular Phase
2.Ovulation Phase
3.Luteal Phase

205
Q

Follicular Phase (Days 1-14)

A

-Vesicular follicles make estrogen
-One follicle stimulated each cycle to ovulate (most FSH sensitive)
-LH surge→meiosis1→ inflammation, weakens ovary

206
Q

Ovulation

A
207
Q

Luteal Phase

A

-corpusluteum forms
-progesterone is high=makes andometrium more excepting of blastocyte
-However homone released by corpus luteum suppresses FSH and LH, so it slowly dies

208
Q

Uterine Phases

A

1.Menstrual Phase
2.Proliferative Phase
3.secretory phase

209
Q

Menstrual Phase

A

-days1-4
-Drop in progesterone → targets arteries (spasms= pain and blood gushes out)
-Lose 20-80 ml

210
Q

Proliferative Phase

A

-days 5-14
-Increase in estrogen= stops bleeding
-Functional layer regenerates

211
Q

Secretory Phase

A

Day 15-28
Progesterone prepares the breasts and endometrium for implantation

212
Q

What happens to ovaries in childhood before puberty

A

-ovaries grow because of the small amount of estrogen

213
Q

What happens in female puberty?

A

-ages 8-13
-Hypothalamus decreases in sensitivity
(Women need fat and leptin to go into puberty)
Gonadal relaeasing Hormone increases→ increases in FSH and LH→ increases estrogen

214
Q

What does the increase luteinizing hormone do in puberty?

A

increase in progesterone preps breasts for lactation and uteri

215
Q

What does Estrogen stimulation do in female puberty?

A

Oogenesis and follicle growth
Development of uterus, tubes, and vagina
Breast development
Growth spurt (testosterone from theca)
Increase bone length and mass
Closes epiphyseal plate
Contributes to wider pelvic
Extra fat is given to breasts and thighs

216
Q

Details about adult ovulation

A
217
Q

Arousal in female sexual response

A

-PSNS
-By touch, psychological stimuli
-Structures engorge with blood: clitoris, vaginal mucosa, labia, breasts
-Secretion from vestibular glands and vaginal wall= lubrication for penis

218
Q

Orgasms in female sex response

A

-SNS response
-Increase in muscle tension, heart rate, and blood pressure
-Rhythmic contractions of the uterus and pelvic floor muscles
-Refractory Period= None

219
Q

Mechanical Methods of Birth Control

A

1.Abstinence=0%, avoid STI’s
2.Withdrawal=30%, cost lots of control
3.Douching= worthless=>40% failure rate
4.Unprotected=85%

220
Q

Main Mechanisms of Birth Control

A
  1. Preventing development and release of oocyte
  2. Prevent Union of sperm and secondary oocyte
  3. Alter likelihood of implantation and growth
221
Q

Combination pill

A

Pill, ring, or patch
Prevent development and release of oocyt
Suppress ovulation
Inhibits hypothalamus’ gonadal releasing hormone
Thickens cervical mucus
FR= 0.3-8%

222
Q

Progesterone Only (mini pill, shot, implant)

A

Suppress luteinizing hormone
Thin endometrium of uterus
FR=0.5%

223
Q

IUD

A

Prevents fertilization, but person will still ovulate
FR=0.1-2%

224
Q

Mirena Implant

A

Progesterone only
Irregular or absent menses

225
Q

Paragard

A

Copper
Toxic to sperm and egg
Nonhormonal
Thins endometrial lining
Thickens cervical mucus
Inhibits sperm function, transport, and fertilization
Tubal Ligation
Prevent egg and sperm from uniting
Failure rate= 0.5%

226
Q

Spermicides

A

Cream, gell, foam, film, ect.
5-25% failure rate
Prevent egg and sperm from coming together

227
Q

Vasectomy

A

O.01%
Prevent egg and sperm from meeting

228
Q

Condoms

A

Prevent against sexual transmitted infection
2-15% for males
20% for females

229
Q

Diaphragm

A

20%
Prevent union of egg and sperm

230
Q

Cervical Cap

A

20-40% failure
Prevent union of egg and sperm