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BIO 176 LAB + LEC > Endocrine Organs Part 2 > Flashcards

Endocrine Organs Part 2 Flashcards

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1
Q

how is the HYPOTHALAMUS and PITUITARY GLAND CONNECTED?

where is the PITUITARY GLAND found/basic anatomy?

A

connected through a stalk known as the “INFUNDIBULUM”

HYPOTHALAMUS
secretion of RELEASING & INHIBITING HORMONES onto the ANTERIOR PITUITARY
- this regulates HORMONE SECRETION

PITUITARY GLAND (HYPOPHYSIS)
- has TWO MAJOR LOBES
- lies within the SELLA TURCICA of the SPHENOID BONE

POSTERIOR PITUITARY (NEUROHYPOPHYSIS)
- composed of NEURAL TISSUE
- secretes TWO HORMONES

ANTERIOR PITUITARY (ADENOHYPOPHYSIS)
- composed of GLANDULAR TISSUE
- secretes SEVEN HORMONES

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2
Q

how does the HYPOTHALAMUS release HORMONES from the ANTERIOR PITUITARY GLAND?

A

ANTERIOR LOBE (ADENOHYPOPHYSIS)
*made up of GRANDULAR TISSUE

use of the PITUITARY PORTAL SYSTEM or HYPOPHYSEAL PORTAL SYSTEM

  • secretion of inhibitory and releasing hormones–while it is then secreted into the blood and reach its target cells
  • portal system is made up of TWO CAPILLARY PLEXUSES that are connected by PORTAL VEINS
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3
Q

how does the HYPOTHALAMUS release HORMONES from the POSTERIOR PITUITARY GLAND?

A

POSTERIOR LOBE (NEUROHYPOPHYSIS)
**made up of NEURAL TISSUE

use of the HYPOTHALAMIC HYPOPHEASEAL TRACT + system of NEUROSECRETORY CELLS

  • secretion of OXYTOCIN (UTERUS) + ADH (KIDNEYS)
  • hormones travel down AXONS OF HYPOTHALAMIC NEURONS–causation of HORMONAL RELEASE from AXON TERMINALS
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4
Q

which HYPOTHALAMIC NEURONS produce OXYTOCIN & ADH?

A

OXYTOCIN
- produced by PARAVENTRICULAR NEURONS

ADH
- produced by SUPRAOPTIC NEURONS

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5
Q

what are the FUNCTIONS of OXYTOCIN and ADH?

A

both are composed of NINE AMINO ACIDS
(just differ in two)

OXYTOCIN
UTERUS:
stimulation of UTERINE CONTRACTIONS
BREAST
stimulation of MILK EJECTION/PRODUCTION

ADH (VASOPRESSIN)
KIDNEYS
stimulation of KIDNEY TUBULE CELLS to REABSORB WATER
- specific OSMORECEPTORS activate NEUROSECRETORY CELLS to RELEASE ADH

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6
Q

what STIMULATES the RELEASE OF ADH + what are its TARGET TISSUES?

A

STIMULATIONS:
- HIGH BLOOD OSMOTIC PRESSURE
INHIBITIONS:
- LOW BLOOD OSMOTIC PRESSURE

specific OSMORECEPTORS activate NEUROSECRETORY CELLS to RELEASE/INHIBIT ADH

TARGET TISSUES
KIDNEYS:
- RETAINING OF WATER– decreases urine
SUDORIFEROUS GLANDS:
- RETAINING OF WATER–decreases water loss
ARTERIOLES:
- CONSTRICT–increases BLOOD PRESSURE

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7
Q

what is DIABETES INSPIDIUS?

A

HYPOSECRETION OF ADH:

the LACK OF ADH due to DAMAGE within the **HYPOTHALAMUS or POSTERIOR PITUITARY
- can be NEPHROGENIC (INSENSITIVITY/RESISTANCE TO ADH) or CENTRAL (FAILURE TO MAKE)

must stay WELL HYDRATED

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8
Q

what is the SYNDROME OF INAPPROPRIATE ADH SECRETION (SIADH)?

A

HYPERSECRETION OF ADH

the RETENTION OF FLUID–creation of increased HEADACHES + DISORIENTATION
- the EXCESSIVE FREE WATER–DILUTIONAL HYPONATERUMIA
must have FLUID RESTRICTION–blood sodium level monitoring

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9
Q

what are the ANTERIOR PITUTIARY HORMONES’ specific CLASSIFICATIONS?

A

PEPTIDE HORMONES
GROWTH HORMONE–only one that DOES NOT use cAMP SECOND MESSENGER SYS
ONLY TWO are NOT TROPIC HORMONES

TROPIC (TROPINS) HORMONES:
- REGULATES SECRETION OF OTHER HORMONES

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10
Q

what are the ANTERIOR PITUITARY HORMONES?

what are the HYPOTHALAMIC RELEASING HORMONES (for STIMULATION OF SECRETION)?

what are the HYPOTHALAMIC INHIBITING HORMONES (for SUPRESSION of SECRETION)?

A
  1. HUMAN GROTH HORMONE (hGH) aka SOMATOTROPIN
    - has GROWTH HORMONE RELEASING HORMONE (GHRH) aka SOMATOCRININ
    - has GROWTH HORMONE INHIBITING HORMONE (GHIH)
  2. THYROID STIMULATING HORMONE (TSH) aka THYROTROPIN
    - has THYROTROPIN-RELEASING HORMONE (TRH)
    - has GROWTH HORMONE INHIBITING HORMONE (GHIH)
  3. FOLLICLE-STIMULATING HORMONE (FSH)
    - has GONADOTROPIN-RELEASING HORMONE (GnRH)
  4. LUTENIZING HORMONE (LH)
    - has GONADOTROPIN-RELEASING HORMONE (GnRH)
  5. PROLACTIN (PRL)
    - has PROLACTIN-RELEASING HORMONE (PRH)
    - has PROLACTIN-INHIBITING HORMONE (PIH) aka DOPAMINE
  6. ADRENOCORTICOTROPIC HORMONE (ACTH) aka CORTICOTROPIN
    - has CORTICOTROPIN-RELEASING HORMONE (CRH)
  7. MELANOCYTE-STIMULATING HORMONE (MSH)
    - has CORTICOTROPIN-RELEASING HORMONE (CRH)
    - has DOPAMINE (inhibiting)
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11
Q

what are the FUNCTIONS of GROWTH HORMONE (GH)?

A

GROWTH HORMONE/SOMATOTROPIN:
- produced by SOMATROTROPIC CELLS

FUNCTIONS
- has DIRECT ACTIONS on METABOLISM
- has INDIRECT ACTIONS on GROWTH PROMOTING FACTORS
- helps INCREASE SKELETAL AND EXTRASKELETAL FORMATIONS
(such as CARTILAGE FORMATION and SKELETAL GROWTH)
- helps INCREASE FAT AND CARB METABOLISM)
(such as FAT BREAKDOWN and BLOOD GLUCOSE/ANTI-INSULIN EFFECTS)

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12
Q

what happens if we have HOMEOSTATIC IMBALANCES of the GROWTH HORMONE?

A

HYPERSECRETION OF GH:
- children: GIGANTISM
- adults: ACROMEGALY

HYPOSECRETION OF GH
- children: PITUITARY DWARFISM

example: even HYPOGLYCEMIA and HYPERGLYCEMIA play a role
- hGH SPEEDS UP BREAKDOWN OF GLYCOGEN INTO GLUCOSE

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13
Q

what is the REGULATION of THYROID HORMONE SECRETION? what is its PATHWAY?

A

THYROID STIMULATING HORMONE
- also known as THYROTROPIN
- produced by THYROTROPIC CELLS
- functions as the DEVELOPMENT and SECRETORY ACTIVITY of the THYROID

PATHWAY
- hypothalamus (TRH)
- anterior pituitary (TSH)
- thyroid gland (thyroid hormones)
- target cells

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14
Q

what is the REGULATION of ADRENOCORTICOTROPIC HORMONE (ACTH)?

A
  • also known as CORTICOTROPIN
  • produced and secreted by CORTICOTROPIC CELLS
    (precursor–opiomelanocortin)

REGULATION:
- triggered by CORTICOTROPIN-RELEASING HORMONE (CRH)
- ACTH stimulates the ADRENAL CORTEX to RELEASE CORTICOSTEROIDS

FUNCTION:
- release of our STRESS RESPONSE–CORTISOL

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15
Q

what is the REGULATION of the GONADOTROPINS (FSH + LH)?

A

FOLLICLE-STIMULATING HORMONE (FSH) + LUTEINIZING HORMONE (LH)
- secreted by GONADOTROPIC CELLS of the anterior pituitary
- stimulated by GONADOTROPIN-RELEASING HORMONE (GnRH)

FUNCTIONS:
- FSH:
stimulates PRODUCTION OF GAMETES–EGG AND SPERM
- LH
stimulates and PROMOTION OF GONADAL HORMONES

GONADAL HORMONES:
- FEMALES
aids in maturation of FOLLICLES of the EGG–OVULATION–release of ESTROGEN and PROGESTERONE
- MALES
aids in the stimulation of the PRODUCTION of TESTOSTERONE

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16
Q

what is the REGULATION of PROLACTIN (PRL)?

A
  • secreted by PROLACTIN CELLS of the anterior pituitary

REGULATION:
- controlled by PIH also known as DOPAMINE
- prevents release UNTIL NEEDED

FUNCTION:
stimulation of MILK PRODUCTION IN FEMALES

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17
Q

what are some HOMEOSTATIC IMBALANCES of PROLACTIN?

A

HYPOSECRETION OF PRL
- much more COMMON–no serious issue, except if wanting to nurse baby

HYPERSECRETION of PRL
- HYPERPROLACTINEMIA
seen in ANTERIOR PITUITARY TUMORS
- shows signs of INAPPROPRIATE LACTATION and INFERTILITY IN FEMALES

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18
Q

describe the THYROID GLAND

A

THYROID GLAND:
- a butterfly-shaped gland located INFERIOR to the LAYRNX and is ANTERIOR to the TRACHEA
- our body’s MAIN METABOLIC HORMONE–controlling of ANABOLIC & CATABOLIC REACTIONS

ANATOMY:

  • has RIGHT AND LEFT LATERAL LOBES connected by an ISTHMUS
  • can sometimes have a **PYRAMIDAL LOBE (projection from ISTHMUS)
  • has COLLOID FILLED CELLS–contains THYROGLOBULIN + IODINE (precursors)
  • has PARAFOLLICULAR CELLS–which secrete CALCITONIN (regulation of blood calcium levels)
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19
Q

what are the THYROID HORMONES?

A

THYROXINE (T4) and TRIIODOTHYRONINE (T3)

produced from FOLLICULAR CELLS
stimulated by TSH

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20
Q

what are the EFFECTS OF the THYROID HOROME?

A
  • maintains BLOOD PRESSURE
  • INCREASE of BASAL METABOLIC RATE
  • creation of HEAT PRODUCTION–CALORGENIC EFFECT
  • regulation of TISSUE GROWTH + DEVELOPMENT
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21
Q

what are some HOMEOSTATIC IMBALANCES of TH?

A

HYPOSECRETION (adults) of TH
- MYXEDEMA–GOITER–due to the lack of IODINE
- seen with a LOW METABOLIC RATE, EDEMA, ETC..

HYPOSECRETION (infants) of TH
- CRETINISM–due to the lack of THYROXINE from birth or lack of the thyroid gland
- use of the HEEL-STICK method to CHECK

HYPERSECRETION of TH
- GRAVE’S DISEASE
specific type of autoimmune disease–body begins to make ABNORMAL ANTIBODIES against THYROID FOLLICULAR CELLS
- antibodies MIMICK TSH–more TH made
- symptoms of elevated metabolism, weight loss, and EXOPHTHALMOS–protruding eyes

(TREATMENT)
removal of THYROID or RADIOACTIVE IODINE

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22
Q

how is the THYROID HORMONE SYNTHESIZED?

A

TRANSPORTATION
- T3 and T4 moved by THYROXINE-BINDING GLOBULINS (TBGS)

23
Q

describe CALCITONIN

A

produced by the PARAFOLLICULAR CELLS
- a specific ANTAGONIST to the PARATHYROID HORMONE (PTH)

FUNCTION:
- INHIBITS OSTEOCLAST ACTIVITY and release of Ca from bone matrix
- STIMULATION of Ca UPTAKE + INCORP. into BONE MATRIX

24
Q

describe the PARATHYROID GLANDS

A

LOCATION:
- seen in the POSTERIOR ASPECT of the THYROID
- small FOUR to EIGHT YELLOW-BROWN GLANDS

CELLS:
- has OXYPHIL CELLS
- has PARATHYROID CELLS–secretion of the PARATHYROID HORMONE

FUNCTION:
- the MOST IMPORTANT HORMONE for CALCIUM HOMEOSTASIS
- secreted in response to LOW BLOOD CALCIUM LEVELS (HYPOCALCEMIA
- INHIBITED by RISING LEVELS of CALCIUM

25
Q

what are the TWO TYPES of CELLS within the PARATHYROID GLANDS?

A
  • CHIEF CELLS or PRINICPAL CELLS –makes PTH
  • OXYPHIL CELLS–function not clear; makes EXCESS PTH in PARATHYROID CANCER
26
Q

how does the PARATHYROID and THYROID GLAND WORK TOGETHER?

A

HIGH LEVELS OF CALCIUM
- stimulation of THYROID GLAND to release CALCITONIN–calcium goes DOWN (parafollicular cells)

LOW LEVELS OF CALCIUM*
- stimulation of PARATHYROID GLAND to release PARATHYROID HORMONE–calcium goes UP (chief cells)

27
Q

describe the ANATOMY of the ADRENAL GLANDS

A

ADRENAL GLANDS:
or also known as SUPRARENAL GLANDS–located on TOP OF EACH KIDNEY

made up of the ADRENAL CORTEX and the ADRENAL MEDULLA

ADRENAL CORTEX
- made up of THREE LAYERS OF GLANDULAR TISSUE

ADRENAL MEDULLA
- made up of NERVOUS TISSUE that is part of the SYMPATHETIC NERVOUS SYSTEM

28
Q

what are the HOMEOSTATIC IMBALANCES of PTH?

A

HYPERPARATHYROIDISM
- due to TUMOR
- an ELEVATION of CALCIUM–begins to depress the nervous system and the formation of KIDNEY STONES
- bones also begin to SOFTEN and DEFORM

HYPOPARATHYROIDISM
- due to GLAND TRAUMA or DIETARY DEFICIENCY
- results in TETANY, RESPIRATORY PARALYSIS, and DEATH

29
Q

describe each LAYER of the ADRENAL CORTEX and the ADRENAL MEDULLA

A

ADRENAL CORTEX

ZONA GLOMERULOSA
- secretion of the MINERALOCORTICOIDS such as ALDOSTERONE

ZONA FASCICULATA
- secretion of the GLUCOCORTICOIDS such as CORTISOL

ZONA RETICULARIS
- secretion of the ANDROGENS aka GONADOCORTICOIDS

ADRENAL MEDULLA
- has the CHROMFFAIN CELLS–secretion of EPINEPHRINE & NOREPINEPHRINE

30
Q

what is the function of MINERALCORTICOIDS? what is the function of ALDOSTERONE?

A

MINERALCORTICOIDS
- important in function for REGULATING ELECTROLYTE CONCENTRATIONS (NA and K) within the ECF
(Sodium is important since it AFFECTS ECF VOLUME)–very important regulator
(potassium important for RESTING MEMBRANE POTENTIAL in cells)

ALDOSTERONE:
- the MOST POTENT MINERALOCORTICOID
- important in STIMULATION OF Na REABSORPTION within the KIDNEYS
- this INCREASES BLOOD VOLUME and BP
- DECREASES POTASSIUM LEVELS

31
Q

describe the mechanism control of ALDOSTERONE RELEASE

A

RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM:
1. decreased blood pressure - stimulation of special cells within our kidneys
2. special cells release RENIN into the blood
3. RENIN cleaves off plasma protein - ANGIOTENSIN - triggers enzyme cascade - conversion to ANGIOTENSIN II

ANGIOTENSIN II:
a POTENT STIMULATOR of ALDOSTERONE RELEASE (through the VASOCONTRICTION of ARTERIOLES)

32
Q

what are the HOMEOSTATIC IMBALANCES of ALDOSTERONE?

A

ALDOSTERONE
- HYPERSECRETION–due to ADRENAL TUMORS
- have an EXCESSIVE AMOUNT OF SODIUM– leads to HYPERTENSION and EDEMAS
- have an EXCRETION of K–leads to ABNORMAL FUNCTION OF NEURONS and MUSCLE

33
Q

what is the function of GLUCOCORTICOIDS?
what is the function of CORTISOL?

A

GLUCOCORTICOID FUNCTION:
- aids in PROTEIN BREAKDOWN
- **GLUCOSE FORMATION
- STRESS RESISTANCE
- INFLAMMATION
- IMMUNE RESPONSE

CORTISOL (HYDROCORTISONE)
- the MOST PRODUCED
- causes INCREASE within BLOOD GLUCOSE LEVELS, FATTY ACIDS AND AMINO ACIDS–supresses the secretion of CRH and ACTH
- important for GLUCONEOGENESIS
- regulated by NEGATIVE FEEDBACK

34
Q

what happens if we have EXCESSIVE LEVELS of GLUCOCORTICOIDS?

A
  • continued DISRUPTION OF NORMAL CARDIOVAS., NEURAL and GI FUNCTIONS
  • DEPRESSED IMMUNE SYSTEM
  • INHIBITION OF INFLAMMATION
  • DEPRESSES CARTILAGE and BONE FORMATION
35
Q

what are the HOMEOSTATIC IMBALANCES of GLUCOCORTICOIDS?

A

HYPERSECRETION
- CUSHING’S DISEASE
continued DISRUPTION OF NORMAL CARDIOVAS., NEURAL and GI FUNCTIONS
- DEPRESSED IMMUNE SYSTEM
- INHIBITION OF INFLAMMATION
- DEPRESSES CARTILAGE and BONE FORMATION
- can have TWO TYPES: either EXOGENOUS (too much glucocorticoid) and ENDOGENOUS (tumor)
- SIGNS:
- moon face
- hyperglycemia
- thin skin

HYPOSECRETION
- ADDISON’s DISEASE
- a DECREASE in glucocorticoids etc…
- DECREASE in GLUCOSE and SODIUM LEVELS
SIGNS:
- bronzed appearance
- severe dehydration
- weight loss

36
Q

what is the function of GONADOCORTICOIDS?
what is the function of DHEA?

A

DEHYDROEPIANDROSTERONE (DHEA):
- the MAJOR ANDROGEN secreted by the ADRENAL CORTEX

MALES:
- use of the hormone TESTOSTERONE–no virtual effect on DHEA

FEMALES:
- has a MAJOR ROLE of DHEA–promotion of LIBIDO and conversion into ESTROGENS

37
Q

what HOMEOSTATIC IMBALANCES effects GONADOCORTICOIDS?

A

ADRENOGENITAL SYNDROME (MASCULINIZATION):
- seen in FEMALES and PREPUBERTAL MALES

FEMALES
- more breads and MASCULINE PATTERN of BODY
- CLITORIS resembles small penis

BOYS
- greater MATURATION of REPRODUCTIVE ORGANS
- early set on SECONDARY SEX CHARACTERISTICS

38
Q

what is the function of the ADRENAL MEDULLA?

A

MEDULLARY CHROMAFFIN CELLS
- the synthesis of EPINEPHRINE (80%) and NOREPINEPHRINE (20%)

EPINEPHRINE:
- important for METABOLIC ACTIVITIES–such as BRONCHIAL DILATION, BLOOD FLOW

NOREPINEPHRINE
- important for PERIPHERAL VASOCONSTRICTION–increases BP

both secrete in response to STRESS
- this INCREASES our HEART RATE and BLOOD GLUCOSE
- greater VASOCONSTRICTION–blood is diverted to BRAIN, HEART and SKELETAL MUSCLES

39
Q

what are the HOMEOSTATIC IMBALANCES OF the ADRENAL MEDULLA?

A

HYPERSECRETION
- HYPERGLYCEMIA
- HYPERTENSION
- RAPID HR and PALPATIONS
- can be due to PHEOCHROMOCYTOMA–TUMOR OF MEDULLARY CHROMAFFIN CELLS

HYPOSECRETION
- dont worry about it

40
Q

describe the PINEAL GLAND

A

PINEAL GLAND
- small gland that hangs from the ROOF OF the THIRD VENTRICLE
has PINEALOCYTES–these secrete MELATONIN–derived from SEROTONIN

41
Q

the function of MELATONIN?

A
  • timing of SEXUAL MATURATION + PUBERTY
  • DAY/NIGHT CYCLES
  • important for PHYSIOLOGICAL PROCESSES that SHOW RHYTHMIC VARIATIONS (body temp, sleep, appetite)
42
Q

what are the PANCREATIC ISLETS?

A

specific TRIANGULAR GLAND that is found PARTIALLY BEHIND the STOMACH
- contains ENDOCRINE CELLS
- has ACINAR CELLS, ALPHA, AND BETA CELLS

ACINAR CELLS
(EXOCRINE)
- produces ENZYME RICH JUICE for DIGESTION

ALPHA CELLS
- produces GLUCAGON (hyperglycemic)

BETA CELLS
- produces INSULIN (hypoglycemic)

also has SOMATOSTAIN (inhibits secretion) and PANCREATIC POLYPEPTIDE (stimulates secretion)

REMEMBER PANCREAS IS BOTH ENDOCRINE AND EXOCRINE

43
Q

how does INSULIN and GLUCAGON WORK TOGETHER?

A

GLUCAGON:
- extreme POTENT HYPERGLYCEMIC AGENT
- triggered by LOW BLOOD SUGAR LEVELS, RISING AMINO ACID LVLS, SNS
- targets the LIVER–stimulation of GLYCOGEN BREAKDOWN

INSULIN
- secreted when BLOOD GLUCOSE LEVELS ARE HIGH
- STIMULATES GLYCOGEN FORMATION

44
Q

how does GLUCAGON increase blood levels?

A

affects the processes of GLYCOGENOLYSIS and GLUCONEOGENESIS

GLYCOGENOLYSIS:
- the breakdown of glycogen to glucose

GLUCONEOGENESIS:
- the synthesis of glucose from lactic acid and noncarbohydrates

  • this in turn makes the RELEASE OF GLUCOSE into the BLOOD
45
Q

what is DIABETES MELLITUS?

A

have TWO TYPES:
TYPE ONE
- due to HYPOSECRETION

TYPE TWO
- due to HYPOACTIVITY

can have dangerous effects due to BLOOD GLUCOSE LEVELS STAYING HIGH
- can cause NAUSEA and even activate FIGHT OR FLIGHT RESPONSES
- can have GLYCOSURIA–glucose spilled into urine
- can have LIPIDEMIA and cause KETOACIDOSIS (also leading to HYPERNEA) and even death

46
Q

what is HYPERINSULINISM?

A

EXCESSIVE INSULIN secretion
- can cause HYPOGLYCEMIA–low blood glucose
- anxiety, nervousness, disorientation etc..

47
Q

describe the OVARIES and TESTES

A

GONADS (OVARIES and TESTES)
- produces the GAMETES (OOCYTES AND SPERM)

OVARIES
- creation of TWO ESTROGENS; ESTRADIOL and ESTRONE
- also PROGESTERONE, RELAXIN, AND INHIBIN

TESTES
- creation of TESTOSTERONE

48
Q

what does PLACENTA SECRETE?

A

estrogens, progesterone, and HUMAN CHORIONIC GONADOTROPIN (hCG)
– allows for the secretion within FIRST TRIMESTER of PREGNANCY
- thickens uterus lining

49
Q

what 3 hormones are secreted by ADIPOSE TISSUE?

A
  • LEPTIN:
    • appetite control; stimulation of increased energy expenditure
  • RESISTIN:
    • insulin antagonist
  • ADIPONECTIN:
    • enhances sensitivity to insulin
50
Q

what hormones are secreted by the KIDNEYS?

A
  • ERYTHROPOIETIN:
    • signals production of red blood cells
  • RENIN:
    • initiates the renin-angiotensin-aldosterone mechanism
51
Q

function of ATRIAL NATRIURETIC PEPTIDE?

A

decreases blood Na concentration—blood volume and blood pressure drop

52
Q

what hormone is secreted by the SKELETON (OSTEOBLASTS)?

A
  • OSTEOCALCIN:
    • controls pancreas to SECRETE MORE INSULIN—restriction of fat storage and improves glucose handling
    • activated by INSULIN
53
Q

what hormone is secreted by the SKIN?

A
  • CHOLECALCIFEROL:
    • precursor of vitamin D
  • CALCITRIOL:
    • active form of vitamin D
      • helps absorb calcium from the intestines
54
Q

what hormones are secreted by the THYMUS?

A
  • THYMUS:
    • large in infants and children; shrinks as we age
    • has THYMULIN, THYMOPOIETINS, & THYMOSINS
      • develops T lymphocytes in immune response
      • acts as PARACRINE—has hormones that effect on itself

BIO 176 LAB + LEC (20 decks)

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