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1

first messengers

outside cell for homeo, hormones and NT.
- categorized by polarity, secretion, composition

2

polar first messenger

bind to mem, can be desensitized,
- ligand gated, g protein, NO synthase, tyrosine kinase AFTER mem receptor!

3

agonist

receptor binds with specificity
- does physio response

4

antagonist

ligand does NOT do response

5

desensitization

downregulation of receptors due to sustained response

6

receptor sequestration

whole receptor swallowed by endosome, signal gets pulled back + receptor returns
- done in high affinity binding

7

receptor down reg

receptor + ligand pulled into a lysosome + destroyed!
- done when 1st molec is ALWAYS present

8

receptor inactivation

separate signalling pathway gets activated, generates 2nd molec which blocks receptor directly

9

inactivation of signalling protein

separate signalling pathway gets activated, generates 2nd messenger protein, block's receptor's SECOND MESSENGER (indirect block)

10

production of inhibitory protein

1st molecule activates second which causes receptor A to downreg

- second messenger also does cell response but also -ve feedback

11

local mediators

short half life, auto and paracrine
- ex inflamation!
- mast cells release histamine

12

neurotransmitters

1st messenger delivered directly to a synaptic cleft by the terminus

13

hormones

long 1/2 life to travel in blood and long distance
- endocrine and neurendocrine
- different EMBRYO origins

14

COMP: AA derived

enzymatic changes in AA generate 1st messenger
- EX. TYROSINE

15

tyrosine

rate limiting: tyrosine hydroxylase
- hydrophilic manipulations
- tyrosine + o2 = L-dopa -co2+ dopamine + o2 = norepinephrine + methyl = epinephrine

- dopamine, norepi are NT
- epi is hormone

16

tyrosine and locations

basal ganglia does dopamine (2 enzyme genes)
sympathetic neuron does norpineprhine (3)
adrenal medulla does ephinephrine (4)

17

COMP: protein

mostly polar
- start of as gene, then trascribe and translated into precursur protein + modified in rough ER and golgi
ex. insulin, pro-opiocortin

18

Insulin

preproinsulin gets cut by ER and cross linked = proinsulin then golgi cuts off c peptide to give insulin and then secreted into blood (stored in golgi vescicles)
- c peptide is wasted!
- enzymes clip lys-arg and arg-arg

19

pro-opiocortin

cleaved in corticotrope cells of ANTERIOR PIT
- each is stress/pain related
pro-opiocortin split
1) corticotropin (ACTH) --> a MSH (sunburn!)
2) b lipotropin --> gamma lipotropin, b MSH, b endorphin

20

corticotropin (ACTH)

- stim release of cortisol from adrenal cortex

21

MSH

increases pigmentation in melanocytes

22

lipotropin/endorphin

endogenous opiates

23

prostegagens

prep uterine lining for preg + maintains

24

glucocorticoids

cortisol promote gluconeogenesis and degrades fats + proteins

25

mineralcorticoids

aldosterone act in nephron to increase Na absorption, K and H secretion

26

androgens/ estrogens

maintain repro development

27

vitamin D

increase calcium absorption in intestine

28

cholsteral hormones

prostegagens,glucocorticoids,mineralcorticoids, androgens/ estrogens,vitamin D
- NONPOLAR

29

cholesterol hormone pathway

LDL transport cholesterol --> released by lysosome to cytoplasmic cholesterol (split 2 ways)
1) kidney, skin, liver, UV modify into vit D
2) enzyme cholesterol desmolase (1st step in steroid hormone process) --> pregnolone --> progesterone
split 2 ways 1) gluco + mineral (enzyme 21- HYDROLASE) 2) androgens --> estrogen

30

androgen estrogen stuff

1) menopause ovaries stop converting estrogen to androgens so masculinization
2) if mutation with 21- hydrolase, then all progesterone gets turned to androgens (in embryo). male then precocius puberty, and female is hermaphrodism

31

neurotransmitter receptors when bind acetylcholine

called cholinergic (all membrane bound)
1) nicotinic: ligand - gated. ach binds and changes shape, channel opens
2) muscarinic: second messenger mediated. ach binds, turns second messenger on, which then opens channel

*ach changes the shape of protein and allows channel to open... thus Na+ that flows can be second messenger!

32

second messengers

intracell receptors that do biochem reactions like increasing speed of signals and increase control in feedback mechs
ex. ligand gates and G proteins

33

ligand gates

2nd messenger
- receptor itself may be an ion channel that opens upon ligand binding. changes membrane potential and transports calcium
- glutamate, GABA, IP3 receptor?

34

G s/I proteins

G proteins are GTPases that change shape when ligand binds. G protein exchanges GDP for GTP, alpha subunit releases and diffuses to peripheral enzyme such as adenylyl cyclase and phospholipase C
S is stim, I is inhibitory
** amplifies signal!

35

G protein adenylyl cyclase

ligand binds, receptor changes shape, alpha subunit gets GTP, converts ATP to cAMP by adenyly cyclase and then returns to receptor
(keeps going until ligand UNbinds)
cAMP then activates protein kinase A which does cell responses

activated by: epi, glucagon, ACTH, TSH, calcitonin

36

getting rid of cAMP

- regulate this path: ADH, Oxytocin, catecholamines, GF

use cAMP phosphodiesterase even after cAMP production is off, cAMP molecules remain floating around

37

vibrio cholera

causes cholera (diarrhea)
- vibrio toxin binds to receptor and stops alpha subunit ability to hydrolyze GTP to GDP and adenylyl cyclase is always on! increases cAMP which opens ion channels and water leaves

38

phospholipase C pathway

1st mess binds, receptor changes shape, alpha subunit breaks loose, activates phospholipase C (only with GTP!), which then breaks bown between DAG and PIP2 giving DAG and IP3 (sugar). ip3 then binds to smooth ER receptor releasing calcium. calcium then
1) binds to calmodulin to decrease cAMP (inactication of signalling protein!)
2) binds with DAG to kinase C (adds p to serine or thyroxine)

39

smooth er

stores calcium

40

phospholipase C

special phospholipid on INTRACELL

41

NO pathway

1st messenger binds to receptor on endothelium of blood and activates NO synthase
- this turns l-arganine and NADPH to Nitrix oxide (nonpolar)
- NO diffuses through to smooth muscle and activates NO guanylate cyclase protein to make cGMP = smooth muscle relaxation

42

smooth muscle relaxation

vasodilation means more blood flow

43

tyrosine kinase

can be direct or indirect
- both ways, kinase cause phosphate binding to a tyrosine AA

44

direct tyrosine kinase

ex. insulin ligand
- kinase has tyrosine AA IN it, and the ligand adds a p directly, which changes shape
- directly adds a phosphate to another enzyme?

45

indirect tyrosine kinase

a and b are separate portions of the receptor, and the ligand binds them together to make the whole receptor, this then pulls in kinases that phosphorylate such as JAK and STAT
- ex growth factor, cytokine

46

kinase A, and tyrosine kinase both...

phosphorylate tyrosine

kinase C does NOT (serine or thyronine)

47

bb development

embryo starts as cells, hollows out then forms a tube. this is ENDODERM. tube then has finger-like projections called diverticula which form stuff

48

adenohypophysis formation

oral ectoderm has diverticulum called rathke's pouch, which grows UP. when infundibulum meets the pouch, pouch breaks down. part of puch continues to form anterior lobe of pituitary!

- originates in endoderm so ADENO

49

neurohypophysis

inside hypothal there is infundibulum, which grows down and forms median eminence (controls pit gland, neural tissue). this then grows posterior lobe
- neuro origin!

50

how is the anterior lobe connected to median eminence control?

using the hypothalamic pituitary portal system.
- median eminence has neurosecretory cells (neuroendocrine) which secrete hormone into cap bed 1, which then travel to cap bed 2 and bind to cells in anterior pit (endocrine) and then they release hormone

51

pituitary gland anatomy

located in small bony cavity formed by sphenoid bone of skull (wings of bone cradle the cranium and has fossa extending). grove of sphenoid is called sella turcica

- confined space means that any tumor can increase pressure and cause gland to be crushed!
- also shearing forces in concussion can rip out pituitary stalk!

52

posterior pituitary

NUCLEI IN HYPOTHAL: paraventricular nucleus secretes oxytocin and supraoptic nuc secretes ADH/Vasopressin release

STORED IN PP TO RELEASE in BLOOD

53

ADH and osmolarity

iso-osmotic is 270-300 mOsm (normonatremia)
- maintains this pressure

54

hyponatremia

low solute and high water outside cell, water moves inside the cell
hypotonic

55

hypernatremia

high solute and low water outside cell, cell then shrinks!

56

osmotic pressure

pressure in semi-permeable membrane that stops water moving from high to low

57

in hyposmotic, ADH

cell swells, ADH level drops, less water is reabsorbed (less water in blood), more volume of dilute urine

58

in hyperosmotic, ADH

cell shrinks, increase ADH levels, high water reabsorption (high water in blood), low vol of concentrated urine

59

hormones released

hypothal releases "releasing hormone" in cap bed 1, then anterior pit releases "-trope" to release another hormone

60

GH process

Hypothal: GHRH anterior pit cells: somatotropes release: GH affects: liver

61

ACTH

Hypothal: corticotrope releasing hormone anterior pit cells: corticotrope release: ACTH affects: adrenal cortex to release gluco, mineralocorticoids and androgens

62

TSH

Hypothal: thyrotropin RH anterior pit cells: thyrotropes release: TSH affects: thyroid

63

FSH/ LH

Hypothal: gonadotropin RH anterior pit cells: somatotropes release: FSH/ LH affects: ovary and testes to make estrogen/proges or testos

64

prolactin

Hypothal: prolactin INHIBITORY or RH anterior pit cells: lactotropes release: prolactin affects: breast

*can inhibit too

65

somatostatin

released from hypothal and stops GH, TSH, and prolactin

66

two ways to stop GH

1) somatostatin from median eminence or 2) somatomedin from liver!

67

GH affects

Increase protein synth by metabolising gluc and fats for energy, also cause liver to release somatomedin (causes long bone growth!)

68

bone

made of collagen (protein with three strands enforced with hydroxyapatite so high tensile strength).

69

bone making process

chondrocytes lay down collagen models, osteoblasts replace with bone. these get trapped in bone so called osteocytes.
- can be a single trebeculae or osteon (concentric rings)

70

osteon

blood vessel lies in middle of layer called haversian canal. osteocytes get nutrients from canals since they sit in hollow cavity with fluid called lacunae. connected by cannaliculi

71

somatomedin

long bone growth

72

Gh and metabolism

- increases AA uptake, stops catabolism, increase transcription translation etc by making energy available! want to be hyperglycemic. stop storage of glucose so PREVENT skeletal muscle uptake and adipose tissue taking it. skeletal muscle doesnt' LET GO OF GLUC!
- increases gluconeogenesis by making ketone bodies (2 acetyl's). body uses ketone body not gluc (for brain)

73

45 % of anterior pit cells are somatotropes!

gives us energy for breakfast (hyperglycemia)

74

acromeglia

gives MORE gh then hyperglycemia, pancreas will release insulin and burn out the beta cells. this is diabetes melitus (type 1)
- if its after puberty, growth hormone will cause regular bone growth (not long bone!) so feet/face etc grow

adenoma in pituitary (

75

thyroid gland

filled with follicles with colloid fluid thyroglobulin
- cells have apical membrane (inside) and basal lateral membrane (outside)
- parafollicular c cells surround the follicles

76

T3 and T4 release

hypothal: thyrotropic releasing hormone
anterior pit: thyrotrope cells release TSH
thyroid gland then makes 7% t3 and 93% t4

** t3 and t4 can also block both anterior pit and hypothal!

77

t3 vs t4

t 3 is active, t4 takes time to lose iodine. we have three months supply. more released in cold weather to increase metabolism. there is a delay of t4 release so april t3 is actually t4 from march.

78

TSH in blood does what

in blood it goes thru thyroid gland by binding to receptor on basal lateral membrane then 1) make thyroglobulin and move iodone or 2) make/break t3 and t4

79

make thyroglobulin

DNA/RNA/Protein then sticking out of protein is AA tyrosine

80

make t3 and t4

TSH increases activity of iodine receptors, which use atp to bring iodine from basal lateral mem. go thru apical membrane and is now charged. to uncharge this, a peroxidase oxidizes. then iodine is added to thyroglobulin tyrosine.

2 iodines + tyrosine = diiodotyrosine
1 iodine + tyrosine = monoiodotyrosine

these will then get conjugated in colloid.
2 DIT = t4 --> thyroxine
DIT + MIT = T3

then into blood by endocytosis

81

breakdown of t3 and t4?

done to maintain homeostasis.

82

what t3 does

turns on genes generate atp using gluconeogenesis and glycogeneolysis
- increase protein catabolism, increase FA in blood
- use that ATP in cell with sodium potassium pump
- causes increase in mito number, increase SA of christae, increase in ETC
- increase number of na/k pumps to move ATP

** only 10% of atp is used to move! rest is heat thus INCREASE in body temp!

3 na out 2k in

83

non-metabolic effects of T3/t4

proper dev of CNA, bone growth

84

hypothyroidism

accumulation of glycoproteins, decrease HR, lethargy, goiter

85

hyperthyroidism

goiter and more t3/t4 stuff increase

86

c cells

when increase calcium, release calcitonin and put ca back in bone. kidney deals with calcium in tissue. stops osteoclasts

87

PTH effects

parathyroid glands in thyroid release PTH. starts rapid phase: bind to osteocyte and blast receptors. bone cells will stop picking up ca which accumulates in blood. if this doesn't work in min/ hours then start slow phase. osteoclasts release citric and lactic acid to dissolve bone.

88

vitamin d

hormone released when low calcium. cause calcium to be absorbed in intestine

89

membrane potentials and calcium

hypercalcemia: increases the membrane potential (harder to generate AP)
hypocalcemia: decreases membrane potential (easier to generate AP). if too low, then muscles always contracted and can cause suffocation!!

90

hyperglycemia:

caused naturally by GH and cortisol!!

91

adrenal cortex formation

endocrine tissue pinching off and neutral tissue growing in.

all stress lads

Medulla is neural and the cortex is endocrine

92

adrenal cortex layers

Glomerulosa Minera
Fasciculata Gluco
Reticularis Steroids

93

cortisol pathway

hypothal: corticotropic releasing hormone anterior pit: corticotrope cells release ACTH stim adrenal cortex to release cortisol

* ACTH primes glomerulosa and reticula to be able to release cortisol when signal comes
* Cortisol is also a primer for GH!

94

Gh can't work without

primer cortisol

95

cortisol immunosuppression theories

1) immune requires lots of energy and cortisol diverts it away to muscles
2) immune cells leave bloodstream and go back to "Stations" cells not down but just protecting sites. die pretty quick tho

ex. finals getting sick after

96

adrenal insufficiency

low cortisol and low aldosterone. this means no feedback on ACTH and so increase ACTH. pro-opiocortin = high MSH! hyperpigmentation

addisons)

97

adrenal hyperplasia

increase number of cells (no tumor) so high cortisol and aldosterone
- cortisol causes fat redistribution on face and back, hyperglycemia, muscle wasting from protein breakdown
- aldosterone increases sodium in blood and so high water and high BP
** hypernatremia!

(cushings)