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M & R🪸🟣 > MR > Flashcards

MR Flashcards

1
Q

What are the roles of the Na+/K+-ATPase in cellular
physiology?

A

1-It has role in activating exchanger
2_preventing accumulation of na + and so water then cell swelling and death
3_if the na accumulate the na_ca exchanger will be reversed and a lot of ca will accumulate and cell toxicity and cell death

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2
Q

Electro neutral exchanger

A

Na independent exchanger (cl- _Hco3 exchanger )
Which’s function mail]nly to prevent alkalosis

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3
Q

In which part of kidney bicarbonate is reabsorbed and how ?

A

First by activation of na k ATPase in the wall between blood vessel and cell na will go to blood while k increase inside the cells
So in the lumen we have a salt (NaHco3) will be disconnected to Hco3 combine with H+ to form H2CO3 and in order to enter the cell it has to be converted to H2O and CO2 by CARBONIC ANHYDRASE

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4
Q

Mechanism of Na+ reabsorption by kidney

A

60% reabsorbed in proximal tubule by Na-H exchanger
30% reabsorbed in thick ascending loop of Henle by Na-k-2cl cotransporter
7% absorbed in distal convoluted tubule by Na-cl exchanger
3% reabsorbed in collecting ducts when aldosterone activate serum and glucorticoid regulated kinase genom that activate ENAC

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5
Q

A mechanism of increasing and decreasing of Na in cell

A

Increasing :by aldosterone
Increasing :by inhibiting Na k ATPase by QUABAIN GLYCOSIDE
decreaseing :by AMILORIDE (antihypertensive ) and ANT ,inhibit EnaCs and increase Na loss through urine

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6
Q

What is electrical potential and it’s unit

A

If the opposite sign charges ions come together they have the potential to do work this potential called electrical potential
Measured by MILLIVOLTS (typically between -20 to -90 mV)

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7
Q

Selective permeability of membrane mainly controlled by

A

Ion channels
Which characterizes by
SELECTIVITY ,GATING ,dowen electrochemical Gradient ,not always opened

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8
Q

Resting membrane potential ranges in nerve ,smooth, cardiac,skeletal muscle

A

➢ Nerve Cells have resting potentials in the range -50 to -75 mV
➢ Smooth Muscle Cells have resting potentials of around -50 mV
➢ Cardiac and Skeletal muscle cells have the largest resting potentials of -80 to -90mV

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9
Q

What is equilibrium potential

A

➢ The Equilibrium Potential for an ion is the membrane potential at which there is no net movement of the ion across the membrane. (Conc. Gradient = Elec. Gradient)
➢ The Nernst Equation can be used to calculate the Equilibrium Potential.
*Membrane is IMPERMEABLE to ANIONS

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10
Q

Main determinat of RMP

A

is leakage channel
Na+/ka+ has minor roel even though it’s essential indirect contribution

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11
Q

Where does channels (the tissue)primary found?

A

Although these classes of ion channels are found primarily in the cells of NERVES & MUSCULAR tissue, they also can be found in the cells of epithelial and connective tissues.

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12
Q

Neurotramission types

A

ELCTROCHEMICAL NT
Electrical (fast ) transmission:by physical gab junctions such as in cardiac muscle
Chemical (synaptic )transmission (it could be fast ,slow ,+,-)
Fast :ion channels (ionotropic ) mS
Slow :G protein (metabotropic receptor) seconds to hour

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13
Q

Examples of excitatory and inhibitory NT

A

+ :acetylcholine receptor agonists cause depolarization ,GLUTAMATE
-:GABA &GLYCINE open channels that cause negative equilibrium such as cl-,k+ that cause hyperpolarization

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14
Q

Excitable tissues in the body

A

Nerves and muscles (cardiac and skeleton )

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15
Q

What is AP(spike )

A

Action Potential is the change in voltage across membrane, it depends
on ionic gradients and relative
Permeability to certain ions.

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16
Q

Name three Drugs that affect AP

A

1-PROCAINE :local anesthetic,block Na channels
2-tetrodotoxin : block voltage gated Na channels (Japanese poison ☠️)
3-AMINOPYRIDINE :blocks voltage gated K channels (broader AP)

17
Q

Classification of voltage gated Ca+2 channels

A

They were initially divided into two classes
• High Voltage activated (HVA) : L, N, P/Q & R-
types channels
• low-voltage-activated(LVA) Ca+2 channels: T- type channels. (tiny, transient)
• R-type is occasionally classified as ( IVA ) channels

18
Q

Myasthenia graves

A

is a neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors (neostigmine)or immunosuppressants and in selected cases with thymectomy.

19
Q

Regulation of Ca+ homeostasis

A

1- vit D
2- parathyroid H(increase)
3-calcitonin (decrease)
By acting on bone ,kidney,intestine

20
Q

Setting up and maintaining Ca2+ Gradient depend on

A
  1. Relative impermeability of the pl. membrane
  2. The ability to expel Ca2+ across the plasma membrane by: a) PMCa2+ ATPase ( primary active ) , high affinity +low capacity
    b) Na+ Ca2+ exchanger ( secondary active), low affinity +high capacity
  3. Ca2+ buffering mechanisms
  4. Intracellular Ca2+ stores:
    a) rapidly releasable b) non-rapidly releasable
21
Q

Basal ca2+ conc and global ca+ conc

A

} Basal [Ca2+]i is around 100nM =0.1μM
} The global [Ca2+ ]i can reach around 1μM to regulate aspects of cellular activity

22
Q

What is Ca 2+ micro domains

A

Are subcellular region of high Ca 2+,near the plasma membrane or internal stores

23
Q

Mechanism of increasing Ca 2+ intra cellular

A
  1. Ca2+ influx across the plasma membrane
    a) Voltage-operated Ca2+ channels (VOCC)
    b) Receptor-operated ion channels (ionotropic receptors)
  2. Ca2+ release from ‘rapidly-releasable’ stores:
    a) G-protein-coupled receptors (GPCRs)
    b) Ca2+ induced Ca2+ release (CICR)
  3. Non-rapidly releasable stores (mitochondria)
24
Q

To return to Ca basal requires
Termination of the signal ,ca removal and store refilling
How the stores are refilled

A

1-recycling cytosolic Ca
2-capacitation Caentery

25
Q

Ligand classification

A

o -Agonist: activation of a receptor (heroin, morphine)
o -Antagonist: without activation of receptor (naltrexone, naloxone)
o -Partial agonists: stimulate the receptor, unable to produce maximum cell response (buprenorphine)

26
Q

Examples about acceptors

A

1-dehydrofolate reductase :inhibited by binding of methotrexate
2- voltage gated Na + channels :modulated by local anesthetic (anticonvulsant) and neurotoxicity molecules (lead ,ethanol,nitric oxide)

27
Q

ROLE OF RECEPTORS IN CELLULAR PHYSIOLOGY

A

o Signaling by hormones and local chemical mediators
o Neurotransmission
o Cellular delivery (low density lipoprotein, transferrin)
o Control of gene expression (steroids, thyroid hormones),
o Release of intracellular calcium stores (Inositol 1,4,5-trisphosphate receptors)
o Immune responses

28
Q

Phagocytosis

A

Occur in PHAGOCYTES & NEUTROPHILS
extend pseudopods and internalized particles by MEMBRANE ZIPPING MECHANISIM

29
Q

Pinocytosis

A

Refer as cell drinking ,which is invagination of plsama membrane to form lipid vesicle

30
Q

Receptor Mediated Endocytosis (RME)

A

Characterized by SPECIFICITY

31
Q

Physiological function of H1 &H2 receptors

A

H1:increase vascular permeability cause symptoms of allergy (in smooth muscle)
H2:stimulate acid secretion (in stomach)

32
Q

Diseases associated with GCPR

A

Retinitis pigmentosa 👁️:mutation in rhodopsin
Nephrogenic diabetes insipidus :mutation in V2 vasopressin receptor
Precocious puberty in male : mutation in luteinizing hormone receptor

33
Q

Cholera toxin and pertussus toxins effect on G protein

A

They contain ADP-RIBOSYL TRANFERASE that modify G proteins
CHOLERA :Eliminates function of GTPase activity in Gs alpha cause IRREVERSIBLE ACTIVATION
PERTUSSUS:interferes with GDP/GTP exchange in Gi-alpha cause IRRVERSIBLE INACTIVATION

34
Q

Gq examples
Gi examples
Gs examples

A

Gq

-M1,3,5
-H1

-alpha2
-D2
-M2

-beta
-D1
-H2

35
Q

Modulation of NT release

A

NT mostly regulated by PREYNAPTIC GPCR

NOTE:there are Gbeta-gamma i ,can inhibit VOCC which can reduce NT release

36
Q

What is drug resistance

A

Loss of drug effectiveness for anti microbial and anti tumor drugs

37
Q

What is rebound phenomenon
What does REFRACTORINESS mean

A

symptoms that were either absent or controlled while taking a medication, but appear when that same medication is discontinued, or reduced in dosage.they can reoccur worse than before

REFRACTORINESS :loss of therapeutic efficacy

38
Q

What is the main cause of idiosyncratic reactions?

A

Genetic abnormalities

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