phys exam 2

3 types of hormone

• peptides and proteins

• steroids

• amines

polypeptide hormone pathway in endocrine cells

• ribosome synthesize peptide as preprohormones

• rough ER cleave preprohormones to prohormones

• prohormones is transferred to golgi apparatus → packaged into vesicles and hormones → stored in cytosol → can then be secreted out of the cell

steroids are synthesized from

cholesterol

where are most steroid hormones synthesized in

adrenal cortex

amines are derived from

amino acid tyrosine

• all amines hormone (catecholamine and thyroid hormones) have base of tyrosine

most important amine hormone

• catecholamine - Epi, NE, and dopamine

• thyroid hormones

where are Epi and NE produced

adrenal medulla

where is dopamine produced

hypothalamus

what hormone travel unbound in plasma

peptides and catecholamines

what hormones travel bound in plasma

steroids and thyroid hormones (bc they are lipidphilic)

2 important steroid hormones

• aldosterone

• cortisol

3 primary inputs control hormone secretion

• ions and nutrients

• neurotransmitters

• hormones

hypocalcemia

• caused by

• lead to

• symptom

low ECF Ca2+ level

• caused by increase in pH (more Ca bind to plasma protein so not in free form)

• make cell more excitable

• tetany of skeletal muscle - fatal, seizures, cardiac arrhythmias

what maintains ECF Ca2+ homeostasis

parathyroid hormone (PTH)

what does PTH act on to increase ECF Ca2+ level

• kidney

• GI

• bone

when is aldosterone secreted

• increased ECF K+ conc

• drop in blood volume → increase number of Na+/K+ pumps → cause more reabsorption of Na+ (and therefore water) and secretion of K+

when is ADH secreted

• high osmolarity

• low blood volume

where is ADH secreted

hypothalamus - released from posterior pituitary gland

hypophysiotropic hormone

• releasing factor

• hormone from hypothalamus → bind to anterior pituitary cell receptor → hormone secretion

effects of increased plasma cortisol

• Cushing’s syndrome

• postabsorptive state - protein catabolism

• gluconeogenesis → increase in blood glucose

• vasoconstriction - hypertension

• inhibit immune system

thyroid hormones action

• increase metabolic rate

• make sympathetic ns effect stronger

• growth

two types of cholinergic receptors

• nicotinic - somatic (NMJ) or ANS (postganglionic, both sympathetic and parasympathetic)

• muscarinic - just PARASYMPATHETIC

adrenergic receptors

• binds NE and Epi

• sympathetic only

preganglionic and postganglionic neurons in sympathetic vs parasympathetic

sympathetic:

• short preganglionic

• long postganglionic

parasympathetic:

• long preganglionic

• short postganglionic

lambert-eaton syndrome

destroy Ca2+ channels on motor neurons → decrease in ACh release

what does botox do

block release of ACh

what do acetylcholinesterase drugs do

impair acetylcholinesterase → prolong action of ACh

what does curare do

blocks ACh receptor

myasthenia gravis

destroy ACh receptors

functional unit of muscle

sarcomere

muscle structure order

• sarcomeres connected together end to end → myofibril

• myofibrils packed in parallel → muscle fiber (single muscle cell)

• muscle fibers packed in parallel → fascicles

• muscle fascicles packed in parallel → muscle

what’s the contractile element in muscle

myofibril

what does titin do

• linkage from Z to M disc

• acts as molecular spring

H zone

myosin only

A band

the entire length of myosin (some part has actin some doesn’t)

t-tubule function

• Provide a means of transmitting an action potential in the muscle plasma membrane to the central portions of the fiber

• t-tubule is continuous with membrane

terminal cisternae is a part of

SR → store Ca2+

where is the t-tuble and terminal cisternae triad located

where A band and I band meets

explain how action potential lead to cross-bridge formation in skeletal muscle

• action potential propagate into T tubule

• activates DHP receptor

• DHP receptor induce conformational change and pulls open Ryanodine receptor in SR → release Ca2+

• Ca2+ bind to troponin, move tropomyosin off myosin binding site

• cross bridge formation

what on sarcomere shortens and what stay the same during contraction

A band stays the same

H, I, and Z shortens

cardiac output equation

stroke volume x HR

what’s intercalated disc

where cardiac muscles join end to end (where myofibrils attach)

what is within intercalated disc

• desmosome

• gap junction

what does gap junctions in intercalated disc do

allow heart muscle to function as syncytium

• simultaneously contract both atria, then both ventricles

pacemaker action potential

• K+ channels closing from previous action potential

• F-type Na+ channels open, Na+ flows in

• T-type Ca2+ channels open, Ca2+ flows in

• THRESHOLD

• depolarizing phase cause L-type Ca2+ channels to open (dramatic increase)

• K+ channels open to repolarize

how does sympathetic and parasympathetic input influence HR in terms of ion permeability

• sympathetic increase F-type Na+ permeability → reach threshold faster and increase HR (mediated by NE)

• parasympathetic decrease Na+ influx and increase K+ permeability → mediated by ACh

explain ventricular action potential

• high K+ permeability at rest

• rapid depolarization due to voltage gated Na+ channels

• LONG PLATEAU → high Ca2+ permeability due to voltage gated L-type Ca2+ channels

• repolarization - K+ permeability increase

pacemaker action potential vs ventricular action potential

• pacemaker generate electrical rhythm while ventricular cause contraction

• before ap - pacemaker has slow depolarization, while ventricular stays flat until stimulated

• AP upstroke for pacemaker is caused by L-type Ca2+ channel, while for ventricular is Na+ influx

• no plateau for pacemaker, L-type Ca2+ cause plateau in ventricular

• 
  

contraction in cardiac muscle vs skeletal muscle

• cardiac muscle contraction depends on EXTRACELLULAR (L-type) Ca2+ channel and SR

• in skeletal muscle, Ca2+ comes from SR only

how can stroke volume be influenced

• length tension

• contractility

• afterload

frank starling law

length tension can increase cardiac muscle force

• unlike skeletal muscle, “normal” resting cardiac muscle fibers length is NOT optimal

• increase PRELOAD stretches muscle fibers → improve myosin/actin overlap → stronger contraction → increase stroke volume

• 
  

how does contractility increase stroke volume

• sympathetic (NE/Epi) bind to beta 1 receptor

• G protein activate adenylyl cyclase

• adenylyl cyclase turns ATP into cAMP

• cAMP activates protein kinase

• protein kinase open L-type Ca2+ channels on cell membrane and the Ryanodine receptors on SR Ca2+ comes in

• more Ca2+ exposed more myosin binding sites on actin

• stronger contractility

• increase stroke volume

what is afterload

the pressure the ventricles must overcome to force open aortic and pulmonary valves

how does the change in afterload affect stroke volume

increase afterload decrease stroke volume

what’s in smooth muscle cells instead of Z discs

dense bodies - thin filaments anchored to these on cell membrane

cross bridge formation in smooth muscle

• NE bind to alpha 1 receptor on cell membrane

• G protein activates phospholipase C

• phospholipase C converts PIP2 into IP3

• IP3 acts as a ligand on SR Ca2+ channels, Ca2+ released from SR

• Ca2+ bind to calmodulin

• Ca2+-calmodulin activates myosin light chain kinase

• myosin light chain kinase use ATP to phosphorylate myosin head and allows binding - cross bridge cycling

• smooth muscle contraction

what happens for blood flow autoregulation when metabolic activity of organ increase

• decreased O2 and increased metabolite

• arteriole dilation

• increase blood flow to organ to carry waste out

what happens for blood flow autoregulation when arterial pressure is low in organ

• blood flow to organ decrease

• decreased O2 and increased metabolites, also decreased vessel-wall stretch in organ

• arteriole dilation in organ

• restoration of blood flow toward normal in organ