6. Endocrine - Hormones Flashcards

1
Q

Hormone vs autacoid and NT

A
Hormones - chem messenger
ductless gland
release circ
travel distant targ cell
act spec protei rec

Autacoid
chem messenger - act target cell close site release
local hormone/ paracrine
Histamine / PG

NT
chem messenger - rel neurones act adjacent cell usually neurones
periph - adjace effect muscle or gland
action rapid - broef durn
NA/ACH
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2
Q

MOA hormones

A

Present in blood stream low conc -targ cell need spec/sensitive - recog and resspon

Spec -receptor
all recept are protein nature

Combo - hormone and receptor - signal = specfic response

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3
Q

Classif hormones

A

Receptor locn

signal mediates action

Group 1
Lipophilic - receptor intracellu

Steroid - gluc minereal sex

Calctriol - not steroid derived prescuorse
thyroid
retonic acid

Group 2
hydrophilic horm - Rec in membrane

IIa- cAmp as second mssgr
ADH, Beta adreg, tsh

IIB
CGmp
ANP

IIc
Calciu,/pdei - 2nd
Musc recp oxytocin gastrin

IID- second messgr not est
GH Insulin prolactin

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4
Q

Could you outline major diff grp 1 & Grp 2

A

Grp1 steroid & thyorid - all lipphilic - carried bound tport prot
long t1/2
rec = intrace;; second mssgr - act hormone rec complex - bind spec part DNA - alter prodctuion mRNA

Grp 2
Hydrophillic - not bound protein blood and short t1.2
Typically not pro bound blood
short half lices
receptor - loc cell membrane - activation w/ receptor - sep second messenger

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5
Q

Second messenger?

Third mssgr

A

Chem mssgr -

Formed result spec hormone recptor combination

Acts intrcell - affect metab processes

Second msgr - intermid carry signal horm to site action

Kinase casdes - act cell second messgr - metabolic alterations in cell

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6
Q

Insulin

A

51aa hormone
B cell islet langehans panc

major anabolic hormone

carb lip pro metab

Two peptide chain disuplh bridge
Rem cpept precursor proinsulin

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7
Q

Actions Insulin carbohydrate metabolism

A

Lower pl gluc - gluc enter cells

Insulin combine spec membrane bound recprot - diff effect diff cells - two types response act rec
Increased act spec gluc tport membrane
act TK on B subunit rec

Cells effect
Mesucle adipose - incrase facil diff gluc into cyto = carrier prote

hepato
Increase entry gluc - conseq change intracell metabolism
cell

activity membrane carrier - not increased insulin - norm permeable
Intracell metabo
increase glucokinase - trap clu in cell
increased glycogenis - inc act gluc sythn - inhib glycogen phosporylase
increase oxidation glucose -
inhib gluc 6 phos -> glycolyis / conversion to starch/glyocgen

All main fav diffusion gradeint gluc hepatocyt e- keep gluc conc low

No diffrect effect inulin gluc entry most other cell
indir chjange occur in blood glucose level - msucel and adipose 80% body - effect inslin improtant over all metabolism

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8
Q

Does insulin act AVw/ CAMP

A

No

Insul - cell membran rece - autophos TK intrcell part B sub
affect activtyy intracell enxyme - meidate activated intracell pro kinase - protein cascde - probable third messenger

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9
Q

Effect insulin on lipid protein metabolism

A

Lipid
Increase entry glucose into adipose cell - increase syn fatty acids in cells - insulin receptor

increased activity lipoprot lipas e- blood increased bdown tg in chlyomicron to fa - enter adipose

Act hormonse sensitive lipase adipose inhib
intracell bdown fat adipose inhibited

Protein metab
Increased activity - glyolyic path - hepatocytes - decrease gluconeo from AA
metob protein aa into energy decreased - protein sparing effect insulin
Increase entry AA muscle and adipose

Net result - increased store fat and ptoein
anabolic action insulin

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10
Q

Does insulin cross bbb or placenta

A

No -

No direct effect on neuronal glucose uptake
powerful indir effect change in plasma gluc

brain norm gluc almost excluse as substrae - adeq gluc reequired fucntion
brains RQ .99 - total use carb

Maternal insulin increase during preg - almost double by 3rd trimester
Overcome insulin resitsance d/t place hormone esp hum placetn lactogen. oetriol, progest

Ensure adeq mat pro synth

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11
Q

Regulation of blood glucose

A

4-7 ref range
fal 3-3.5 fasting

neo lower
2.2 min

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12
Q

Outline factors involved in control blood gluc

Glucostat fxn liver?

A

Blood gluc - main narrow - despite vary intrake

Body mech - prevent hyperhlyc - fater meal

Input glucose into blood
Gut- small bowel
episdoic vary

Liver - gluc fall - releases gluc into blood
hormonal reg

Output
muslce and adipose - take up
uptake dep need
Urine 
gluc high - lost in urine

Gucodtat liver - buffer increase and decrease

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13
Q

How factor min flux in blood gluc after meal fasting

carb meal

A

Blod gluc rise - absorebed
senosre b cell det increase and relase insulin
Liver - insulin entry - by enz effect
muscle and adipose - two thrid taken up liver
major store - glycogen - some oxidose to Co2 - some util in FA synth

Muslce and adpose - increase entry - convereted stor carbn glycogen muscle cell gyler fat cell
glyerol util synth TG

Blood gluc return normal

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14
Q

Fasting

A

Gluc level fall -

Insulin
sens panc det dcerease - insulin falls

Result reer effect hep enzy - glycogenlysis, gluconeogen increase G6Phos
more gluc release liver

Glucagon
Acell - sense decrease+ gluc sec increase

Gluc bind - rec hepatocyte - rises cAMP

Spec enz activated – glycogenolysis + gluconeo
requires cortisol

Resul synergistic falling inmsulin rising gluca - increase rel gluc liver into blood

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15
Q

Why is sugar control so important

A

Main reason gypoglc - only energy sub in CN -retina

Uptake depend adeq blood gluc level - not affect insulin

Hypergly:
osmotic effect - dehydrate
lost urine - wawste
osmotic diures loss fluid and electo

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16
Q

Glucose stores

A

Glyocgen live rand muscle
branched polymer - con a1,4 a1,6 link

Glycogen broken down - rel cell blood main pl guc

Glyco - muscle broken gluc reside - meatb muscle - gluc not relase muscel
No g6 phosp in muslce

Sto glucose - glycogen osmotic effect smaller than glucose molecule

Max total size glyco store 100 liver 400g muslce
500 gr - 2000kclas energy 24h supply

Gluc store circ small
blood gluc 1g/L
5g gluc whole circ

Total gluc ecf - 10g
Equv 40kclas
proveides site - cells recieve supply

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17
Q

Other insulin glucagon - what hormones effect gluc level

A

Corticosteroid
Permsisve glucagon exert effect liver - increase gluconeo
Hypo - increase secretion
inhib utilatsion gluc - favour fat util body cell
Increase blood blucose level -
diabetes occurs excess cortico

Catechol - adren
Increase blood gluc - hpeatic glycogen output liver
lrise

GH 
sec increase hypogly
inhib gluc uptake musl cell
inc rel gluc liver
rise

Thyrpod
Increase GIt abs gluc
may decr - hep glycogen-increase blood gluc level

Oestro - insulin restiance mil

Progest - insulin resitance

HPL - insulin resitsance
increase

Soatostatin

inhib relase insulin glucagon indir effect bgl

18
Q

Plasma glucose levels in baby after birth

A

Pl gluc fall min 2.8 by 6h birth

Main foetal supply mother
transpalcetan
birth source suddenyl lost
low or no carb intake

Hep glyco - maj source inital period birth
falling insulin increased glucagon
symp stim contrib increased glycogen - main gluc

Glyocgen depleted newborn - mob tg - ffa rise - alternative energy source
incrased level catechol - import causing change fat metab - catechol effective rasing FFA than raising glucose

Introduction provide gluc - stabil plasma days aftrer birth

19
Q

Net atp prod

A
Glcolysis
cytopalsm
1gluc -> 2 pyruvate - 2 atp +2nadh
pyruvate oxidse to acetyl CoA 2NADH/pyruvate
then enter krebs - citric acid cycle

Krebs
Mitochonddia - 2atp 8nadh 2fadh2

ETP mitochon 32 atp

20
Q

Synth thyroid hormones

Where in the bowel is dietary iodide absorbed

A

Diet iodine con to idodie abosrbed upper SB
typical west diet contrain more than min amt idoide reqd

Idodide in BS taken thryroid or excreted in urine

21
Q

Synthesis throyid hormones

A

T4 T3 syhtn gland

1 Uptake Iodewdi in folluc cell
active tpor
tport against elec grad and conc grad
carrier subj competitive inhib other anion 0 similar size to idodie
anion r/f iodide uptake inhib

Iodide iodine diffuse folluc lumen - reacts tyr to prod MIT
cat thy perox

Thyrosine AA reside - held peptide link - thyroglobulin - reaction cell coloid interface

Further Iodination MIT - prod DIT

TWO DIT oxida couple throytix - remin aa backobne thryoglob
MIT and DIT - reside T2 reside

22
Q

How are hormone secreted

A

Stored colloid part thyroglob - secrretion
glob undergo endocyto into cyto of follic cell
Join lyossymes and thryoglob digested release free thryorix t2 mit dit

t3 + t4 secreted but t4 higher
both high protein bound carrier prote and blumin

mIT AND DIT brokken down and iodied recycle

23
Q

How is secretion cotrlled

A

Hypothol prod TRH
reach ant pit - hpyohseal prot circ - release TSH fyhrotrope ant pit

TSH bind GPCR in membrane follicular cell
AC Activate - result increase Iodide uptake increased synthesis - relase thyroid hormones

Free T3 + T4 provide neg feedback - inhib release TRH hypothal - inhib TSH rel ant pit

24
Q

Pituitary

A

Post - ADH and Oxytocin

Struc sim nonapept

Struct ant pit
pars tubertalise intermidus distalis

Ant develop thakes pouch

Ant most pars dstalis - all trophic
Proteins
GH
Prolaction

Glycoprote -
FSH
LH
TSH

Polypept
ACTH
MSH

25
Q

Which cells prod hormones

A

acidophil - HG Prlaction

Basopl glycoprote and polypept

26
Q

Control calcium

Ref range

what {ca icf]

[Ca in bag blood]

A

2.2-2.55

free Ca ++ 50%
Ca bound alb 45%
Ca complexes 5-10%

Low 100nm grad free ca - 10000
ecf 1mM ICF 100nM

0 calcium bound citrate - mech ensure not clot

27
Q

Type coagulip caused hypocal

A

None ca- low enough affect coag not compat life

Hypocalc massive tfusion depress contractily

28
Q

Mech maintain ca blood level stable

A

ECF [Ca] fairly tight hormnaol control - predom PTH, calcitonin, 1 25 dihtdo - caltriol

calcitrol act vit d
Plasma [ca] control sign

PTH
release pth gland response hypoCa
act bone kidney - indirect gut calcitriol - rise plasma Ca

Calcitriol
Formed kidney act bone and gut
intest abosrp ca increased
osteclast act increased
Actions rise plasma ca 

Calcitonin
parafollic thyroid cell
effective lower Ca - phys role not est

29
Q

Renal actions PTH

A

Reabs Ca dist tube
Decrease reab Phos prox tube
Increase Calcitriol - prox tub cell

Net reslts - plus act PTH on bone - increa ca mobil and act calcitriol bowel = net increased plasma [Ca]

30
Q

How do hormones interact w/ cells

A

Hormones attach spec recportop on or in cells

Most recport in cell memnbrae some locate nucleus or cytoplasm

Brin biolog change - occupatin ligand alter effector mech

1 Intermed couplin gmech to effector
receptor connect effector mech thru intermed coupling mech gpor - result second messenger ion channel

2 Ligan gated Ion channel
Ligan bind direct ion chanell and affect open / closing
gaba receprot cl chanell
nic rec Na

3 Bind intracell rec affter tcipt mRNA
bind intracell rec affect cpsepc mrna bind DNA

Receptor both ligand bind and enzymatic fxn
Rec - enzym activty which act conform change ligand bind
tk act gf Gcycl anp

31
Q

What are gpro

A

Cell embrane assoc pro - import signal tduction

Hetertrimer 3 sub unit a b y

diff gene subunit cominbed - diff gpor
a - def effect usual interact effector mech

bind gdp and gtp
nuceoltide - guanosine analoge adp and atp resepct

inactive state GDP bound grpo
gdp dissoc + gtp bind = grpo act

32
Q

Diff gpro

A

Gs - stim effect ac act

Gi inhib AC inhib

Gt involve photorecp eye

Gq inbolbe Plc reg

33
Q

How gpro involved signal transduction mech

A

Coupling between activation spec receptor cell membrane and activation effector mech - affect intracell process

Activation of effector - AC Plc - production second messenger

Ion channel - affect directly or by second messnger (Ca IP3)

signal carried accross membrane by process

Signall mech provides amplication signal

Amplification signal:
Intric gtpase activity of activated gpo important sev reasons

1 Rate hyrdol gtp slow
- assists sustain signal allow greater amplication

2 Slef reg gpro - terminate own activty certain time

3 Directionalaity - reaction propagates 1 direct

34
Q

What are fts of receptors couple gpro

A

Signif struct sim gpcr - superfamily

all consits single polypept chain - 7 transmembrane a helical segment
specific ligand binds in pocket between transmembrane signal

35
Q

How does GPro signal transduction signal work

Seq event

A

Modules work sequence - cary excell signal - across cell embrane and activate specific second messenger in cell

Ligand bind spec gpcr - membrane

confomrational change - result spec assoc gpro activate

a subunit gpro - release gdp and binds gtp
gpro sep gtpa + gtpby

gtpa - interact effector protein (enz/íchan)

results activation or inhib of enzyme - or open / close channel

GTP hydro to GDP - gtpase act a subunit
and gdp aby inactive form and gpro - reconsitiude

Ex - nind norad to beta
act SA
Act GS
AC act
Camp prod
Gs act hydro gtp ->gdp
36
Q

Name sone non gpro horomones / nt

A

ACH- nic rec

GABA at gaba

Steroid + thyroid - bind intracell rec

Insulin + insulin rec

ANP + guanylate cyclate act

37
Q

Metabolic rate

A

Rate energy production body

all energy apperas heat - form w/ highest entropy

Thermal equil - all heat must be lost

38
Q

WHAT is the BMR

A

Metabolic rate - standard cond
rest
room temp
12h after meal

result repot as % above or below age adjust standard value

39
Q

How is it determind

A

Calorimetry

direct
- Total amt heat energy prod body ody
subject -atwater benedict chamber
met rate - amt heat energyt in 1 hr

Indirrect
est - measure o2 consump as its proportional
o2 consumo 250ml min - 15l hr
mult 4.8 72.3 kcal hr
divide by body surf area - standrd result
typical 70kg - 40kcals m2

40
Q

How is o2 consumption measured

A

Subjects breath oxy from wet spiurometer
exp co2 absorbed

circ close and co2 abs
rate decrease equal to oxy cosnump
cona be connected rotating ddrum - circu vvol v time

slope proportioal o2 consump

41
Q

why is oxygen consumption to bmr

A

Vast maj energy derived aerobic metab

prod atp via ox phos mito obligatory a/w fixed o2 consump
final rx etpc

cyto ox
- irrev
2H 1/2 O2 => H20