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ISBM > Exam #4 > Flashcards

Exam #4 Flashcards

1
Q

N+ K+ ATPase - necessary conditions for actions

A

Na+ inside cell
K+ outside cell
ATP

Note: insulin and thyroid hormone increase expression

3 Na+ out and 2 K+ in - electrogenic pumping mechanism

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2
Q

Na+-dependent co transport - secondary active transport

A

uses integral membrane protein

has specificity and is saturable

require conc. gradient of one substance (Na+) to drive mov’t of 2nd substance

Note: Na K+ ATPase critical for maintaining conc. gradient of Na+

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3
Q

voltate-gated ion channels

A

sensitive to distribution of electrical charge across the membrane; depolarization causes them to open (Na+ first then K+)

  • Action potential occurs through these channels when threshold potential of Em is reached
  • Ca+2 channels at axon terminals are voltage-dependent
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4
Q

ligand-gated ion channels

A

have a binding spot for a specific ligand (chemical) to bind which alters 3-D conformation and increases the conductance for a specific substance across the membrane

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5
Q

features of channel proteins

A
  • span membrane
  • glycosylated: alter microenvironment
  • have aqueous porins through which ions move (aquaporins)
  • no active processes occur (no ATP hydroxylation) - gate opens and ions flow through (drivers are strictly electrical and chemical)
  • possess gating mechanisms that are sensitive to membrane potential (voltage-gated)
  • selective for specific ions (somewhat)
  • localized to specific area of membrane
  • very fast!
  • electro-chemical driving force determines direction of ion movement
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6
Q

ionic equilibrium

A

ions move across permeable membrane until there is a equal concentration of ions and electrical neutrality

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7
Q

electron motive force (EMF)

A

voltage that exists b/t side 1 and 2 of a membrane; occurs with establishment of a transmembrane potential

  • equal and opposite to the chemical fore (concentration gradient)
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8
Q

diffusional potential

A

potential for ions to diffuse though permeable channels based on conc. gradient and electrical charges across membrane

NOTE: determines resting membrane potential

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9
Q

electro-chemcial equilibrium

A

point at which conc. gradient is equal to electrochemical gradient but opposite in direction

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10
Q

Nernst potential (E ion)

A

statement of electrochemical equilibrium

For a single ion, point at which the voltage or electrical gradient is equal and opposite the concentration (chemical) gradient

All ions that are uniquely distributed across a membrane and can cross the membrane (permeable), have a Nernst potential

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11
Q

principle of electrical neutrality (PEN) - change balance

A

total positive charges in a single solution much equal total negative charges in that solution (this much occur on each side of membrane)

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12
Q

osmotic balance across membranes

A

to avoid movement of water, osmolarity of substances on either side of the membrane must be equal

Note: valence does not effect osmolarity

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13
Q

Gibbs Donnan equilibrium (Donnan Rule)

A

For permeant ions at equilibrium when a non-permeant ion is present on one side

Suggests that the presence of an impairment substance will alter the distribution of charged particles capable of crossing the membrane

Product of concentrations of permeable ions on inside = product of concentrations of permeable ions on outside

([K+]i * [Cl-]i = [K+]o * [Cl-]o)

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14
Q

polarization

A

cell membranes are polarized; more negative the potential, greater the degree of polarization

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15
Q

hyperpolarizing the cell

A

becoming more negative - less likely an AP will occur

  • increase in magnitude of potential
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16
Q

depolarizing the cell

A

becoming more positive; creating less of a potential

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17
Q

resting membrane potential

A

potential the exists across a membrane in the absence of any stimulus; determined by permeability (“leakage”) factors
- K is more permeable (Na and Cl too)

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18
Q

GHK equation

A

equation used to estimate the membrane potential (Em)

  • any ion that can cross the membrane will effect Em
  • uses relative permeability and the Nernst (equilibrium) potentials for all ions
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19
Q

neuronal resting membrane potential

A

-70mV (with respect tot ECF at 0mV)

Dependent on Na and K movement

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20
Q

skeletal and cardiac muscle cell membrane potential

A

-90mV with respect tot ECF at 0mV)

skeletal muscles have greater permeability of Cl-

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21
Q

threshold potential

A

depolarization in membrane potential (stimulus) necessary to result in an “upsweep of action potential” - rush of Na+ into cell

results in an explosive change in membrane’s conductance to Na+

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22
Q

Molecules that alter AP - block Na+ or K+ channels

A

alkaloids: TTX and STX - block Na+ channels from the outside
- work in conc. dependent manner
- found in puffer fish and dinoflagellates

Procaine: block Na+ channels in use-dependent manner (from inside cell)
- found in local anesthetics (no Na+ mov’t so signal is not transferred to CNS = no pain)

TEA (tetra ethyl ammonium): block movement of K+
- work in conc. dependent manner

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23
Q

myelin

A

insulating material around plasma membrane of axons; layers of sphingomyelin (electrical insulator that decreases ion flow through membrane)

  • increased conduction velocity of an AP
  • made by schwann cells (in periphery) and oligndendricytes (in CNS)
  • no Na+ channels present under myelin
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24
Q

Nodes of Ranvier

A

breaks in myelin on axon; axonal membrane exposed to ECF; high conc of Na+ channels; huge ability for inward current (APs) in these locations

25
Q

saltatory conduction

A

describes the behavior of a myelinated nerve fiber

  • no ions are able to escape from beneath the myelinated portion of the nerve fiber
  • APs occur only at the nodes - nerve impulse jumps along the fiber

Important:

  • increases velocity of AP transmission (5-50 fold)
  • conserves energy of axon (less ion shift and less energy needed to re-establish baseline concentrations)
  • depolarization can happen more quickly
26
Q

gap junctions

A

Small region between cells; contain protein pores that small the plasma membrane of both cells and create continuity between the cytoplasms of the cells
- offer reduced resistance, increasing current flow

27
Q

electrosecretory coupling

A

nerve AP-> electrosecretory coupling -> NT release -> receptor interaction -> electrophysiologic change

Combination of voltage (electrical) - dependent changes leading to secretion of NT, resulting in changes to post-synaptic cell due to ligand (chemical) binding

28
Q

quantal theory of NT release

A

spontaneous and unstimulated movement of Ca++ across patent channels in pre-synaptic membrane leads to fusion of vesicles with pre-synaptic membrane and release of NT

this quantal release results in slight depolarizations of the post-synaptic membrane resulting in MEPPs

29
Q

excitatory NTs

A

acetylcholine, asparate, and glutamate

always elect an EPSP (and MEPP) through depolarization of post-synaptic membrane

30
Q

inhibitory NTs

A

glycine, GABA, valium (benzodiazepenes)

hyperpolarize post-synaptic membrane and decrease likelihood of AP (drives membrane potential further from threshold)

activate Cl- channels which open and Cl- moves in due to chemical gradient (Cl- highly concentrated in ECF)

31
Q

hypothalamic hypophyseal portal vessels

A

vessels between hypothalamus and pituitary gland (capillary bed, portal views, capillary bed); cause resistance series - slow blood flow, concentrating hormone

32
Q

mediators of GH release

A

hormonal: regulation of somatotrophs of AP
neurologic: neural control of GH release
metabolic: independent, metabolic factors (hypoglycemia)

33
Q

specific influences of GH release

A

stimulate: factors related to nutrition state and stress
- starvation/fasting
- hypoglycemia
- high AA
- decreased FA
- excitement or trauma

Inhibitors:
- somatostatin

34
Q

GH main actions - direct effects

A

reduce sensitivity of cells to glucose uptake
-drive lipolysis, drive cell proliferation (cell size and #) - anabolic actions

adipose: dec. glucose uptake, inc. lipolysis
muscle: inc. AA uptake and protein synthesis; dec. glucose uptake (reduce sensitivity to insulin)

Liver: inc. gluconeogenesis; inc. somatomedin release

35
Q

why is GH diabetogenic

A

GH induces insulin resistance which counteracts insulin’s normal actions (uptake and utilization of glucose)

This leads to increased blood glucose and compensatory inc. in insulin secretion

Excess GH secretion can lead to metabolic problems similar to those in DM Type 2

36
Q

ACTH impacts all aspects of steroid hormone synthesis

A

Immediate: binds to Gs, phosphorylation via PKA, inc. CEH, free cholesterol into pregnenolone (enzyme - desmolase/P-450 scc)

Subsequent: increases expression of genes that code for enzymes key in biosynthesis
- also, inc. in LDL receptors (50% CE)

Long-term: regulates size and # of cells in adrenal cortex (ILGF-2)

37
Q

biosynthesis of steroid hormones - key enzymes

A

desmolase (P-450 scc): removes side chain from cholesterol, leaving pregnenolone

hydroxylases: key in production of aldosterone and cortisol

DHEA: key intermediate on path to androgens

Aromatase: produce estrogen from testosterone / androstenedione

38
Q

cortisol’s main actions

A

Stimulates gluconeogenesis
o Increases enzymes needed to covert AA into glucose in the liver cells
o Increases blood glucose levels (excess cortisol = hyperglycemic state)

Mobilizes FAs from storage depos in adipose tissue to inc. blood fatty acids

Mobilization of AA from protein (proteolytic activity in muscle tissue)

Increases the BUN because deamination leads to more urea cycle activity

Promotes glycogen synthesis in liver

anti-insulin activity

anti-inflammatory effects at high levels

39
Q

stimulators of aldosterone release

A

Circulating levels of Angiotensin II – key regulator!

Plasma (ECF) Na concentration

Plasma (ECF) K concentration

ACTH

Drop in EC fluid volume (i.e. drop in pressure)

40
Q

main actions of aldosterone

A

Drive increase in absorption of Na+ in ECF / Plasma
• Na+ will bring along H2O into ECF and, thus, BP increases

Drive decrease in K+ in ECF / Plasma and, thus, inc secretion of K+ in urine

Within the cells of the kidney (and other places in GI tract), aldosterone enters from ECF (since hydrophobic), promotes activities of mRNA to create proteins
• Inc expression of NaK ATPase pump across basolateral cell membrane
• Inc expression of Na and K channel proteins on apical membrane
• Stimulates production of ATP

NOTE: aldosterone alters Na+ and K+ levels in DCT

41
Q

actions of glucagon and epinephrin

A

similar, but epi’s actions are border (glucagon only on adipose and liver)

  • increase gluconeogenesis (AA transaminate; FAs used for energy; can result in inc. ketones)
  • inc .in plasma AA biggest stimulator of glucagon
  • both sore with hypoglycemia
42
Q

what is measured to monitor thyroid hormone replacement therapy

A

TSH

43
Q

effects of thyroid hormone

A

Note: every cell (except RBC) responsive to TH

Sets stage of basal metabolic activity:

  • inc Na/K ATPase
  • mitochondrial actions (ramps up # and machinery)
  • see inc. O2 consumption, sweating, CO2 levels, BUN levels

Dictate expression of key receptors for NE, epic, cortisol, GH, and glucagon

Inc. rate and force of myocardial contraction

Key in developing fetus

44
Q

actions of TSH

A

peptide hormone that promotes TH release from thyroid gland by promoting iodide pump, AA uptake, and metabolically ramping up cell

  • leads to inc. thyroglobulin production, coupling reactions, engulfing colloid, and release of T3 and T4
45
Q

medications for hyperthyroid (inhibit TH)

A

inhibit peroxidase activity
diminish iodide oxidation and couplong rxs
lower production of T3 and T4

46
Q

prolactin stimulators (i.e. dopamine antagonists)

A

pregnancy, estrogen, nursing / mechanical stimulation, stress, sleep

47
Q

how does suckling induce milk creation

A

afferent stimulus to CNS, blocks TIDA neurons limiting dopamine production, prolactin releasing factor has effect, prolactin bind to mammary gland receptors and stimulated production of enzymes that make milk constituents (JAK) - milk in alveoli

48
Q

how does suckling or hearing / seeing a baby stimulate milk let down

A

oxytocin is a neurocrine; suckling increases afferent to CNS, depolarized supraoptic nucleus, increases oxytocin release, triggers myoepithelial contraction, delivers milk

  • visual and auditory stimuli also send message to PP to release oxytocin (neural input)
49
Q

physiological roles of free Ca++

A

membrane potential and stabalization (Ca++ outside)
cellular excitability
muscle contraction
regulation of enzyme activity (Ca+ so low intracellular)
exocytosis (seen with insulting release and fusion of vesicles with axon terminal)
cellular adhesion

50
Q

what do you see with hypercalcemia

A

stones, bones (degradation), and groans

51
Q

albumin acts as a buffer (controls acid/base balance) in free Ca++ levels

A

acidemic, most H bound to albumin, high free Ca++

alkalemic, most Ca++ bound to albumin, low free Ca++

52
Q

parathyroid hormone (PTH) - short term regulator of free Ca++ and PO4

A

released from chief cells; regulates free Ca++ (and phosphate)
- secreted when free Ca++ levels are low

causes liberation of hydroxyapatite ((Ca++)10(PO4)6(OH)2) from bone (Ca++ reabsorbed but PO4 is not - inhibits TRP)

NOTE: hydroxyproline (OH-proline) in urine is marker for bone demineralization (degradation)

53
Q

Ca++ reabsorption from nephron to ECF - two routes

A

Paracellular route: passive movement through tight junctions due to electrochemical gradient for Ca++ (in ascending loop of Henle)

Transcellular route: active movement regulated by PTH; inc. in Ca++ channels on apical membrane; inc. in CaATPase and Ca++/NA+ antiport exchange mechanisms on basal lateral membrane (in DCT)

54
Q

vitamin D3 - long term regulator of Ca++ and PO4

A

PTH promotes active form of vitamin D (1,25 hydroxy vitamin D3)

  • active vit D3 promotes Ca++ and PO4 absorption from GI tract and renal tubules by promoting expression of calcium (and PO4) channels through transcription and translation
  • slower to come about; long term regulator

Vit D also modifies expression of different proteins that influence absorption of dietary available Ca++

55
Q

vitamin D3 - synthesis

A 
steroid hormone (made from cholesterol)
we make it De Novo and get from diet

Skin: UV light breaks cholesterol ring and created pre-vitamin D3,
Liver: subject to hydroxylation to form 25 hydroxy it D3
Kidney: PTH converts to active form (1,25 hydroxy D3) - called calcitriol

56
Q

calcitonin

A

third hormone involved in Ca++ and PO4 homeostasis

released from parafollicular cells of thyroid gland

opposite effects of PTH (promoted bone mineralization in response to high Ca++)

57
Q

how to distinguish between excess Vit D and PTH

A

serum levels of circulating free phosphate:

  • excès vit D: high
  • excess PTH: low
58
Q

prostaglandins (thromboxanes) and leukotrienes

A 
paracrine substances (local effects)
made from essential fatty acid (linoleic acid)
linoleate--> arachidonic acid (enzyme PL-A2)

Note: inc. in intra-cellular Ca++ stimulates PL-A2 to liberate arachidonic acid from phospholipid membrane

Two pathways:

  • COX - prostaglandins and thromboxines
  • 5-lipoxygenase - leukotrienes (WBCs)
59
Q

substances that inhibit prostaglandins, thromboxane, and leukotrienes

A

cortisol stimulated production of family of proteins (lipocortins) that block phospholipase-A2 (anti-inflammatory actions of cortisol)

NSAIDS: inhibit COX-1 and COX-1; low does aspirin (NSAID) given to dec. clotting (TXA2) - irreversible inhibitor of COX
- tylenol is a competitive inhibitor of COX

Leukotrienes cause bronchial smooth muscle contraction; block LTs for asthmatics

ISBM (7 decks)

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