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Physiology > Cell Physiology > Flashcards

Cell Physiology Flashcards

1
Q

Homeostasis

A

Maintenance of nearly constant conditions in the human body

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2
Q

Negative feedback

A

promoting stability. ex: blood pressure - adjusting for what we do during exercise. Body
will maintain BP not at normal level, but at level needed for exercise.

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3
Q

Feed forward

A

anticipates change. ex: brain functions, anticipates it before anything actually happens. ex: salivation when seeing food

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4
Q

Positive feedback

A

promotes change in one direction, instability

ex: childbirth, uterine contractions

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5
Q

Negative feedback: arterial pressure

A

decrease in arterial pressure (trauma, exercise), leading to an increase in sympathetic activity (releases hormones), which leads to an increase in BP and vasoconstriction, which then returns loop to decreased arterial pressure.

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6
Q

Positive feedback: nerve signals

A

cell depolarization (from AP), leads to an increase of cell Na permeability, leading to an influx of Na, which then decreases the cell membrane potential, and returns cell to increased state of Na permeability.

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7
Q

3 PT implications of homeostasis:

A
  1. inflammation
  2. atrophy (need protein synthesis to build muscles back up again!)
  3. diabetes
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8
Q

Important components of a cell

A

nucleus, smooth and rough ER, golgi apparatus, mitchondria, ribosomes, and cell membrane

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9
Q

mitochondria is important for:

A

energy

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10
Q

ribosomes on rough ER are important for:

A

protein synthesis

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11
Q

Cell membrane: 4 important components

A
  1. lipid bilayer: allows some things to pass through - protection
  2. integral protein: transmembrane protein, spans width of membrane, think ion channel
  3. peripheral protein: attached to IP, will help recognize a hormone or synthesis
  4. carbohydrates: attach to PP
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12
Q

Smooth and Rough ER

A

Smooth: no ribosomes, site of lipid synthesis
Rough: ribosomes, site of protein synthesis, needed for protein folding and transport.

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13
Q

Why do we need proteins?

A

for energy, muscle building, body and cell functions, growth and repair

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14
Q

Why do we need lipids?

A

fat, absorption

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15
Q

Golgi apparatus function

A

receives transport vesicles from smooth ER, processes them, and concentrates, sorts and packages them for secretion.

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16
Q

Vesicles going to golgi apparatus undergo:

A

endocytosis

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17
Q

Lysosomes function

A

digestion, breaks down bad things body doesn’t want or things that are too big.

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18
Q

PT implications: faulty lysosomes

A

Tay-sachs disease: don’t release needed enzymes, thus overproducing other byproducts from protein and lipid synthesis. This will interrupt the neurons, changing the resting membrane potential, which will in turn prevent the action potential from being stimulated. This could result in muscle disruption, mental retardation, not properly developed musculoskeletal system.
autosomal-recessive disorder - from birth
different kind could onset as an adolescent
different kind could onset in adulthood, but longer lifespan expected

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19
Q

Peroxisomes

A

counterpart to lysosomes, oxidize substances that may otherwise be poisonous (alcohol)

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20
Q

Mitochondria

A

extracts energy from nutrients through oxidative phosphorylation. Takes place in enzymes.

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21
Q

ATP Production: Step 1

A

Breakdown of things so they can actually be used. carbs - glucose, proteins - AAs, fats - fatty acids.

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22
Q

ATP Production: Step 2

A

Glucose, AAs, and FAs are processed into AcetylCoA, which is need for Krebs cycle

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23
Q

ATP Production: Step 3

A

aerobic metabolism: AcetylCoA reacts with O2 to produce ATP

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24
Q

How many molecules of ATP can be produced from a single broken down glucose?

A

38 molecules.

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25
Q

What are 3 things ATP used for in the cells?

A
  1. membrane transport
  2. synthesis of chemical compounds
  3. mechanical work
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26
Q

Cytoskeleton function and types of filaments:

A

function: to maintain the structure of the cell
1. actin filament
2. microtubule
3. intermediate filament

27
Q

PT implications: ALS

A

neurofilaments are disrupted, neuron gets disorganized, and thus the necessary membrane potential, action potential cannot occur, and the person will have muscle disruption, loss of control of muscles, and eventually, death of motor neurons.

28
Q

Transcription

A

starts with DNA and transcribes to RNA. Use DNA to tell us what RNA to make, like matching pairs. Takes place in the nucleus.

29
Q

Translation

A

starts with RNA and translates it to protein. This is used for cell structure, enzymes and function. Takes place in the cytosol.

30
Q

Transfer RNA

A

transfer RNA - tRNA. Use tRNA to help to detect the sequence on the RNA that needs to translate. Takes place on the ribosome.

31
Q

transcription inhibitors

A

proteins that prevent transcription from happening there

32
Q

Negative regulation

A

Repressor operators bind to repressor proteins, interfering with the ability of RNA polymerase to bind to the promoter. Results in no transcription.

33
Q

Positive regulation

A

Activator operators bind to activator proteins, which facilitates RNA polymerase binding to the promoter. Results in enhanced transcription.

34
Q

Life cycle of the cell: interphase

A

> 95% of time in interphase. Contains:
G1: period of cell growth before DNA is duplicated
S: period where DNA is duplicated
G2: period after DNA duplication, prepares cell for division.

35
Q

What 3 things determine cell growth?

A
  1. growth factors
  2. contact inhibition
  3. cellular secretions (negative feedback)
36
Q

Examples of rapid vs. slow cell growth

A

rapid: bone marrow, skin, intestinal epithelia
slow: neurons, striated muscle, smooth muscle

37
Q

Cell differentiation

A

changes in physical and function properties of cells as they proliferate. They become more specific! Results from selective repression/expression of specific genes.

38
Q

PT implications: Cancer

A

dysregulation of cell growth, caused by mutations or abnormal expression of specific genes that control cell growth/mitosis.

  1. proto-oncogenes: normal
  2. oncogenes: abnormal
  3. antioncogenes: supress the abnormal
39
Q

Cancer arises from:

A

DNA mutations and uncontrolled proliferation of those genes

40
Q

Cell membrane: lipid bilayer

A

barrier to water and water-soluble substances, but other things can get through!

41
Q

PT implications: membranes

A

phospholipid membrane is disrupted, leading to fatty plaques and tangles at the neurons, causing disruption of nerve signals at the brain.

42
Q

PT implications: absence of dystrophin

A

dystrophin helps to stabilize actin and myosin within the membrane and initiate movement, so if it is disrupted, then the muscles will have trouble moving, going thru the sliding filament theory, leading to atrophy.

43
Q

Membrane proteins

A

provide specificity and function to membrane.

  1. ion channels: specific to the ion
  2. carrier proteins: specific to size of protein
44
Q

Diffusion

A

high to low concentration gradient, no mediator or energy required.
ex: water (osmosis)

45
Q

Active Transport

A

low to high gradient, involves a carrier and requires energy

46
Q

Facilitated Diffusion

A

does not require energy, but needs a carrier for it to go through. These carrier proteins undergo conformational changes to prevent just anything from passing through the membrane.

47
Q

3 Factors that effect net rate:

A
  1. concentration difference: the greater the concentration difference, the greater the net rate, or the faster it will go in
  2. pressure: higher pressure, more energy to cause net movement from high to low pressure
  3. size
48
Q

Osmosis

A

net diffusion of water down the concentration gradient, from pure water to water/salt solution

49
Q

2 types Active Transport

A
  1. primary AT: molecules pumped against a concentration gradient, needs energy
  2. secondary AT: transport driven by energy stored in the concentration gradient of another molecule
50
Q

Primary active transport: Na/K Pump

A

Na out, K in: in order to do this: breakdown of ATP into ADP, caused by the enzyme ATPase on carrier protein
we want to maintain charge and difference

51
Q

Primary active transport: Other examples

A

Ca2+ ATPase control: Ca conc. in muscle cells binds to troponin (need it for muscles contractions!!) Ca is pumped in when we need muscle contraction. This maintains a low cytosolic Ca concentration.
H+ ATPase: use HCl to control acidity in stomach and blood PH.

52
Q

Secondary active transport

A

moving Na within primary active transport generates energy to move glucose thru secondary active transport

53
Q

Resting membrane potential

A

cells are charged because we have ions and different concentrations. Membrane potential is this charge difference.
In nerve cells, its generally -90mV.
Na and K are not equally balanced. They have different attractions, and thus we have this.
In skeletal muscle, -70mV.

54
Q

Action potential (AP)

A

rapid depolarization of membrane potential that propagates along an excitable membrane.

55
Q

Four properties of APs

A
  1. all or nothing event
  2. initiated by depolarization (can be induced in nerve or muscle)
  3. have constant amplitude
  4. have constant conduction velocity (keeps us from being choppy)
56
Q

Three Functions of APs

A
  1. info delivery to CNS
  2. info encoding by frequency
  3. rapid transmission over distance
57
Q

AP Membrane Permeability

  1. during upstroke:
  2. during downstroke
  3. during hyperpolarization
A
  1. Na permeability increases (open Na channels)
  2. Na permeability decrease (Na channels close), and K permeability increases (K channels open)
  3. not always seen, increased K conductance (delayed K channels closing)
58
Q

Ion channels

A

gates that span the membrane, have inactivated states, respond to changes in the membrane potential

59
Q

Refractory periods

A

safety mechanism: it doesn’t let you initiate another action potential for a few milliseconds
allows yourself to completely reset to that -90mV resting membrane potential

60
Q

Propagation

A

spread of depolarization to local and surrounding membranes, opening more Na channels

61
Q

Myelination

A

Jumping from node to node increases how quickly the action potential can happen, and conserve energy (jump over non-myelinated parts). Sphingomyelin decreases membrane capacitance and ion flow 5,000 fold

62
Q

Saltatory conduction

A

increased velocity and energy conservation as APs only occur at nodes of Ranvier

63
Q

PT implication: MS

A

MS is an immune mediated inflammatory demyelinating disease of the CNS that interrupts the jumping from node to node, stopping it and stopping the action potential

Physiology (4 decks)

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