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Spring '20/ L. A&P > osmosis etc. > Flashcards

osmosis etc. Flashcards

1
Q

osmolarity

A

Is the concentration of osmotically active particles in a solution
osmolarity=GxC
g-number of particles in a solution
c-concentration

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2
Q

Osmosis

A

Flow of water across a semipermeable membrane from a solution of low solute concentration (where the water conc. is high) to a solution of high solute concentration (where the water conc. is low)

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3
Q

osmotic pressure

A

increases when the solute concentration increases.

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4
Q

oncotic pressure

A

Colloid osmotic pressure, (Oncotic pressure) is the osmotic pressure created by plasma proteins [=28mmHg]

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5
Q

hypotonic 200

A

.45 saline

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6
Q

hypertonic 360

A

3% saline

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7
Q

isotonic 280

A

0.9 saline

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8
Q

hypernatremia

A

increased water loss
excessive sweating
central or nephrogenic diabetes insipidus

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9
Q

hyponatremia

A

large water ingestion

siadh

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10
Q

ion channel ungated

A

determined by size, shape, distribution of charge etc.

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11
Q

Voltage-gated channels

A

are opened or closed by changes in membrane potential.

e.g. the activation gate of the Na+ channel in nerve is opened by depolarization; when open the nerve membrane is permeable to Na+ (e.g. during the upstroke of AP). Inactivation gate of Na+ channel in nerve is closed by depolarization; when closed, the nerve membrane is impermeable to Na+ (e.g. during the repolarization phase of AP)

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12
Q

Ligand-gated channels

A

are opened or closed by hormones, second messenger, or neurotransmitter

e.g. Nicotinic receptor for Acetylcholine at motor end plate is an ion channel that opens when Ach binds to it. When open, it is permeable to Na+ and K+ ,causing the motor end plate to depolarize.
Chloride channel are ligand-gated. These channels open when GABA binds to its receptor. When open , it allows inward movement of chloride ions in the cells (simple diffusion)
Other examples : Glutamate and 5-HT (Serotonin) receptors

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13
Q

Receptor binding GABA

A

Binding of GABA causes the chloride channels to open

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14
Q

Receptor binding GABA and benzodiazepine

A

Binding of GABA is enhanced by benzodiazepine, resulting in a greater entry of chloride ion which HYPERPOLARIZES (makes the cell less responsive) the cell making it more difficult to depolarize and therefore, reduces neural excitability

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15
Q

Receptor Empty (no agonist)

A

Empty receptor is inactive ,and the coupled chloride channels is closed

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16
Q

agonist

A

drug has an affinity for a receptor and stimulates it

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17
Q

antagonist

A

drug has an affinity for a receptor but displays little or no intrinsic activity

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18
Q

competitive antagonist blocker

A

competes with agonist for receptor sites, occupies the receptor site- NO ACTIVITY

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19
Q

non competitive antagonist

A

binds to the site other than receptor site and changes the shape of receptor-NO ACTIVITY

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20
Q

resting membrane potential

A

Membrane electrical potential difference (membrane potential) is generated by diffusion of K+ ions through ‘leaky’ K+ channels
resting membrane potential -70 to -90mv

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21
Q

resting membrane potential

A

-90 At rest, K+ slowly leaks out from cell  Resting membrane potential (-90 mV)

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22
Q

depolarization

A

Makes the cell membrane potential less negative due to movement of positively charged sodium ions (Na+) into the cell increasing excitability

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23
Q

repolarization

A

Change after depolarization, that returns the membrane potential back to resting potential. Repolarization results from the movement of positively charged potassium ions (K+) out of the cells.

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24
Q

hyperpolarization

A

Makes the membrane potential more negative due to movement of negatively charged chloride ions (Cl-) into the cell.
DECREASE excitability

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25
Q

inward current

A

is the flow of positive charge into the cell. inward current depolarizes the membrane potential

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26
Q

outward current

A

is the flow of positive charge out of the cell. outward current hyper polarizes the membrane potential.

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27
Q

action potential

A

Is a property of excitable cells (nerve & muscle) that consists of a rapid depolarization, or upstroke, followed by repolarization of the membrane potential. Action potential have stereotypical size and shape, are propagating and are all-or-none

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28
Q

threshold

A

Is the membrane potential at which the action potential is inevitable. At threshold potential, net inward current becomes larger that net outward current. The resulting depolarization becomes self-sustaining and gives rise to upstroke of action potential. If net inward current is less than net outward current, no action potential will occur (i.e. all- or- none response)

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29
Q

during the upstroke of an action potential

A

Na permeability increases
Due to opening of Na+ channels
Inward movement of Na+

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30
Q

During the downstroke of an action potential

A 
Na permeability decreases 
due to inactivation of Na+ channels
K permeability increases 
due to opening of K+ channels
Outward movement of K+
31
Q

After hyperpolarization of membrane following an action potential:

A

There is increased K+ conductance

due to delayed closure of K+ channels

32
Q

Resting membrane potential

A

is the measured potential difference across the cell membrane in mV (-70 to - 90mV)
At rest , the nerve membrane is far more permeable to K+ than to Na+
Leaky K+ channels are responsible for resting membrane potential.
The Na+/K+ pump maintains resting membrane potential ( 3Na+ out and 2K+ in)

33
Q

Action Potential “Nerve Impulse”

A

is a property of excitable cells (nerve, muscles) that consist of a rapid depolarization (interior becomes less negative) or upstroke , followed by repolarization of membrane potential.

34
Q

Lidocaine (depolarization)

A

Inward Na+ movement

Lidocaine block these voltage sensitive Na+ channels and abolish action potential

35
Q

Downstroke of the Action potential (repolarization)

A 
Outward K+ movement
Inward current (flow of Na+ into the cell) depolarizes the membrane potential , while outward flow of  K+  hyperpolarize the membrane potential. Both ions flow by simple diffusion.
36
Q

Properties of AP

A 
Constant  size and shape
Propagation/ spread ( 60 m/sec )
Myelinated vs. non-myelinated fibers
All-or-none Law (no percentage)
Threshold is the membrane potential at which the AP is inevitable
37
Q

Refractory periods

Absolute refractory period

A

is a period during which another action potential cannot be elicited, no matter how large the stimulus.
Due to closure of inactivation gates of Na+

38
Q

refractory periods

Relative refractory period

A

is a period during which an action potential can be elicited only if a larger than usual stimulus is provided

39
Q

refractory period

A

Refractory period protects the cell from over-excitation. It allows a recovery period between the action potentials.

40
Q

local anesthetics mechanism of action

procaine, cocaine, lidocaine, bupivacaine

A

Local anesthetics are weak bases present in un-ionized form (LA) and ionized form (LAH+)
Un-ionized form (LA) penetrates the cell membrane.
The pH is slightly acidic inside the cells  more ionized form (LAH+) produces.
Ionized form (LAH+) blocks the Na+ channels (from inside)
Inhibit conduction of pain impulses from periphery to CNS (afferent fibers)
Uses: minor surgical procedures, spinal anesthesia

41
Q

local anesthetics

A

slow the rate of depolarization of the nerve action potential such that the threshold potential is not reached. As a result, an action potential cannot be propagated in the presence of local anesthetic and conduction blockade results.

42
Q

Inhaled Anesthetics

A

Isoflurane, Desflurane, Sevoflurane
Enhance the effect of GABA
Increase entry of Cl-
Hyperpolarization of cell (makes the cell less responsive) - more difficult to depolarize and therefore, decreased neural excitability

43
Q

hypokalemia

A

Hypokalemia increase the diffusion gradient leads to hyperpolarization leading to muscle weakness

44
Q

hyperkalemia

A

decrease the diffusion gradient leading to depolarization. AP does not occur because inactivation gates of Na+ channels are closed by depolarization. Without AP , there is no contraction leading to muscle weakness.

45
Q

K+ rich cardioplegic

A

(heart paralysis) solution causes rapid membrane depolarization. But No repolarization can occur due to high extracellular K+ . Na+ channels are locked in the inactive state. The heart muscle is essentially in a permanent absolute refractory period. “pharmacological arrest”.

46
Q

succinylcholine

A

causes continuous depolarization leading to resistance to depolarization leading to flaccid paralysis

47
Q

what do local anesthetics block?

A

Local anesthetics interrupt nerve conduction by blocking Na+ channels.

48
Q

Inotropic receptors

A

ligand gated channels

49
Q

cAMP Mechanism

A

hormone (first messenger) binds to a receptor on cell membrane. activates g protein (middle man) g (stimulatory) protein stimulates adenylate cyclase, g (inhibitory) inhibits the adenylate cyclase. activated adenylate cyclase converts atp to cAMP (second messenger). ( increased camp inhibits adenylate cyclase and decreases camp levels). camp activates protein kinase-a which phosphorylates proteins and creates cellular action.
(ie calcium)

50
Q

caffeine and amionphollin

A

phosphodiesterase of camp and increasing cAMP level.

51
Q

IP3 (inositol triphosphate) Mechanism

A

Hormone binds to a receptor on the cell membrane which activates a g protein (middle man) to activate phospholipase C which liberates diacylglycerol (DAG) and IP3 (inositol triphosphate) from membrane lipids. ip3 makes calcium release from endoplasmic reticulum. calcium plus dag activate protein kinase c which phosphorylates proteins and causes specific physiological actions.

52
Q

what action does IP3 cause

A

action of acetylcholine on muscarinic receptor

53
Q

atropine and ipratroprium MOA

A

block the acetylcholine on the muscarinic receptor. causing bronchodilation

54
Q

dobutamine

A

In cardiac muscle, beta agonist such as dobutamine acts through cAMP. increase cAMP results activation of protein kinases that enhances the entry of Ca++ into the myocardial cell increase force of contraction

55
Q

milrinone-

A

phosphodiesterase inhibitors prevent hydrolysis of cAMP and prolong the action of protein kinase. (increasing the amount of calcium into the cell)

56
Q

steroid hormone

A

diffuse across cell membrane and binds to a cytosolic receptor and then nuclear receptor. (this causes a change in the receptor which exposes a DNA-binding domain) transcription is initiated and new mRNA is formed. mRNA is translated in the cytoplasm and produces specific proteins that have physiological actions.

57
Q

nitric oxide

A

diffuses across the cell membrane and works on cGMP causing bronchodilator.

58
Q

terbutaline

A

beta2 receptor activates g protein which activates adenylyl cyclase. atp forms cAMP. activates protein kinase and causes BRONCHODILATION.

59
Q

Thick filament

A

contains myosin

60
Q

thin filament

A 
Contain actin, tropomyosin and troponin
Tropomyosin covers the active site
Troponin is a complex of 3 proteins
Troponin T ( binds with tropomyosin)
Troponin I (binds with actin)
Troponin C ( binds with calcium)
61
Q

T tubules

A

Are continuous with the cell membrane

Invaginate the cells at the Z lines and carry AP into the cell interior

62
Q

Sarcoplasmic reticulum (SR)

A

Are small diameter tubules in close proximity to the contractile elements
Are the site of storage and release of Ca++ for excitation-contraction coupling

63
Q

Steps in excitation-contraction coupling“Conduction to contraction

A

action potential spreads from the cell membrane into the t tubules- L-type calcium (diphydrophyridine receptors) calcium enters the cell. causing a calcium spark/releast from the ryanodine receptors from the sarcoplasmic reticulum. intracellular calcium increases!

64
Q

dantrolene

A

decrease calcium release from ryanodine receptors on sr.

65
Q

calcium channel blockers

A

block L-type calcium channels dihydropyridine receptors.

66
Q

how does actin and myosin binding work with calcium

A

Ca++ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of the actin and myosin binding.
Actin and myosin bind, the thick and thin filaments slide past each other and the muscle contract. (power stroke). The magnitude of the tension that develops is proportional to the intracellular [Ca++]

67
Q

Norepinephrine

A

acts on 1 receptors on heart and causes  cAMP that in turn  Ca++ influx through L-type Ca++ channels  increase force of contraction. (Acetylcholine does the opposite)

68
Q

Camp

A 
Beta 1
Beta 2
Alpha receptors 2
Gluconate
Hcg 
Calcitonin
Tsh
Pth
Lh
Fsh
Adh v2
ACTH
69
Q

Ip3

A 
Alpha 1 receptors
Adh v1
Trh
Gnrh
Ghrh
Oxytocin
Cholinergic Muscarinic receptors
Angiotensin ii
70
Q

Steroid hormone

A 
Vitamin d
Thyroid hormone
Glucosteriods
Esterogen
Progesterone
Aldosterone
Testerone
71
Q

Tyrosine kinase

A

Insulin

IGF-1

72
Q

CGMP

A

Nitric oxide

Anp

73
Q

Nicotine receptors and ach

A

Allow sodium in and potassium out permeability and cause the motor end plate to depolarize

74
Q

Troponin c

A

Calcium

Spring '20/ L. A&P (21 decks)

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