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Unit 2: LGS > Week 1 > Flashcards

Week 1 Flashcards

1
Q

3 layers of skin

A

Epidermis, Dermis, Subcutaneous Tissue

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2
Q

Skin Types

A

Glaborous and Hairy

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3
Q

Glaborous Skin -where found? -receptors?

A

-without hair -Ventral surface of fingers, palm of hand, pads of toes, sole of foot, ear lobes, external genetalia -dense collection of somatosensory receptors; Meissener corpuscles, Merkels discs, ruffini nerve endings, pacinian corpuscles, free nerve endings

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4
Q

Hairy Skin -where found -receptors?

A

-hair protruding from hair folllicles; density varies -where glaborous skin does not occur -hair follicles have free nerve endings around base, sense movement -meissner corpuscles sparse/absent; merkels cells less dense; pacinian corpuscles in subcutaneous layer

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5
Q

3 types of receptors

A

Mechanoreceptors (touch, pressure, vibration, hair movement); Thermoreceptors (skin temp); Nociceptors (pain)

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6
Q

Mechano receptors -function -types (5)

A

-respond to an object that comes in contact with skin and causes deformation (touch, pressure, vibration, hair movement) -Ex: meissner corpuscle, merkel disk, ruffini endings, pacinian corpuscle, hair follicle

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7
Q

Thermoreceptor -function -kinds (2) -nerves

A

-identifies changes in skin temperature -warmth: small unmyelinated nerve fibers increase action potential with increasing skin temp between 30C and 45C ; cold:small myelinated and unmyelinated fibers increase action potential with decreasing temperature between 43C and 25C -free nerve endings in both epidermis and dermis

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8
Q

Nociceptors -function -types (4) -nerves

A

-response to changes in the immediate environment of the nerve endings that are due to stimuli that are about to cause/causing tissue damage/inflammatory responses -chemical: secretions associated with inflammation; thermal: extremes of temperature (above 45C and lower than 20C); mechanical: extreme pressure; polymodal: responds to 2 of the 3 above -free nerve endings in dermis and epidermis

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9
Q

Nerve pathway for mechano receptors

A

-sensory information received, travel to spinal cord and up dorsal column -primary synapse at medulla, where signal crosses over and continues to travel up though medial lemniscus -secondary synapse at thalamus -tertiary synapse at post central gyrus in the primary somatosensory cortex

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10
Q

Nerve pathway for thermoreceptor/nociceptors

A

-primary synapse at dorsal horn where it crosses over -travels up ventrolateral spinothalamic tract -second synapse at VPL of thalamus -third synapse at post central gyrus (somatosensory cortex)

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11
Q

If injury occurs in right dorsal column T5-T7 what is affected?

A

-dorsal column contains mechanoreceptor tract (fine touch), since it is tract, sensation of fine touch will be decreased on right side from T5 down.

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12
Q

If injury occurs to left dorsal root ganglion at T10 what is affected?

A

-all senses are affected fine touch, curde touch, pain, and temp -the decrease in sensation will only be felt on the right side in the T10 zone (dermatome), because injury occurs in ganglion instead of tract

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13
Q

If injury occurs to right side of medulla oblongata damaging the ventrolateral tract what is affected?

A

-Decrease in crude touch, temp, pain perception to left side (contralateral) of the body which will include hand and foot

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14
Q

Sweat glands -function -structure

A

-secrete sweat to control body temp -2 parts; coiled cell (contains sympathetic nerve innervation and iso-osmotic fluid), duct cell (impermeable to water, but allows for reabsorption of Na and Cl in interstitum creating hypo-osmotic fluid)

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15
Q

What controls sweat gland?

A

-Sympathetic innervation (SPECIAL) because it only responds to ACH instead of Epi and is a muscarinic receptor instead of adrenergic

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16
Q

What type of fluid does a sweat gland release? Why?

A

Hypo-osmotic, because the ductal part of the sweat gland in impermeable to water, trapping it in the duct but allowing for ions to transfer back into the interstitium, reducing the amount of solute in the water being released from gland.

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17
Q

Importance of hypo-osmotic secretion

A

In patients that have been sweating a lot, you will commonly see that their plasma is hyperosmotic because the solute from the sweat is being re-absorbed with the body while the water is being released through the gland creating a high solute concentration in the body

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18
Q

What part of nervous system controls blood flow in the skin?

A

sympathetic nervous system; can dilate or contract

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19
Q

Decrease in sympathetic stimulation causes

A

reduced NE resulting in Vaso-dilation

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20
Q

Increase in sympathetic stimulation causes

A

increased NE resulting in Vaso-constriction

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21
Q

What causes vasodilation?

A

elevation in core temp (caused by hot environment, exercise, etc); allowing for increase of blood at skin surface, allows for release of heat to environment

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22
Q

How is personhood affected by illness?

A

When a person is ill their life style will be affected; ex. pain experienced from shingles could cause decrease in ability to do work

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23
Q

What is normal set point temperature for the body?

A

98.6F or 37C

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24
Q

What determines core body temp?

A

-Heat gained -Heat lost to environment

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25
Q

How is heat gained?

A

-Metabolism and muscle shivering

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26
Q

How is heat lost to environment

A

-convection/conduction: related to skin temp and temp of air -radiation: related to skin temp and temp of objects around skin -evaporation:

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27
Q

How does core temperature change?

A

There is disturbance in balance between heat lost and heat gained

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28
Q

How does body regulate system to minimize changes in core temperature?

A

-has to offset disruption in balance before a big change is noticed by the body -ex: increase in heat lost; need to increase heat gained through shivering

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29
Q

Mechanisms used to regulate change in core body temp

A

-vasodilation/ constriction -muscle shivering -sweat

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30
Q

What controls mechanisms used to regulate change in core temp?

A

Preoptic anterior hypothalamus

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31
Q

What does the pre-optic anterior hypothalamus compare core body temp to?

A

set point temperature

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32
Q

Can set point differ? Why?

A

Yes, during times of illness the body will increase the set point temperature to induce a fever and to aid in fighting off infection

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33
Q

How is fever induced?

A

Cytokines; IL-1, TNF alpha, IL-6

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34
Q

How does pre-optic anterior hypothalamus know what core temperature is in the body?

A

Tc Sensors-thermo receptors

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35
Q

Influence of hot environment on Tc? Why?

A

Reduction in loss of heat to environment, because environment is hotter than you are

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36
Q

Thermoregulatory response to exposure to heat? -causes -end result

A

-sweating, vasodilation -caused by decrease in sympathetic innervation with NE causing vasodilation and ACH causing sweating

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37
Q

Role of skin temperature with heat

A

-signals behavioral response–go into AC or shade -lowers threshold for sweat response–makes it easier to sweat by lowering amount of heat needed to trigger sweat response

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38
Q

Influence of cold environment on Tc? Why?

A

Increase in heat lost to environment because the environment is colder than you are

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39
Q

Thermoregulatory responses to cold environment -caused by? -end goal?

A

-shivering and vasoconstriction -sympathetics? -decrease amount of heat lost to environment while simultaneously increasing the amount of heat generated by body

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40
Q

Role of skin temperature with cold?

A

Decrease in skin temperature raises threshold for activating shivering

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41
Q

Influence of exercise on Tc? Why?

A

Increase in Tc because increase in metabolism

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42
Q

Thermoregulatory responses to exercises? -Causes? -End goal?

A

-Vasodilation and sweating -Increase in sympathetics -Increase amount of heat lost to environment

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43
Q

Tc in response to dehydration

A

Core temp will rise with dehydration because ECF will become hyperosmotic. This means there is not enough water to release sweat and decrease in fluid from ECF will cause vasoconstriction to help with blood pressure.

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44
Q

What does an increase in set point do to core temp?

A

Will make body think you’re cold so there will be a rise in core temperature.

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45
Q

Thermoregulatory response to cytokines -phases-causes

A

-chill phase: will raise set temperature, make body shiver and vasoconstrict; due to influx of cytokines -deferverscent phase: will lover set temp back to normal, cause you to sweat and vasodilate; due to decrease in cytokines

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46
Q

Other causes for increased set temp

A

-Menstrual cycle: causes increase after ovulation -Diurnal rhythms: set temp lowers during sleep and elevates when awake

47
Q

What are the protective barriers of the skin?

A

-Physical: squamous (will shed) -Chemical/biochemical: pH (acidic), sweat, temp (too cool for most bacteria) -Immune barrier: langer haans cells (dendritic cell in skin) and microbiome (normal flora)

48
Q

What kind of sample would you take when a patient has crust (scab)

A

Skin scrape

49
Q

What does tinea mean?

A

Fungal infection

50
Q

What does … mean? -corporis -pedis -cruris -capitis -unguium

A

-entire body except for feet,groin,face, scalp, beard -foot -groin -scalp -nail

51
Q

Most common species of fungi in the US?

A

-candida albicans -histoplasma (bird/bat droppings) -blastomyocytes (soil) -coccidioides (soil)

52
Q

Forms of fungi

A

spores and hyphae

53
Q

Spores

A

-form when fungi is not proliferating due to environment not being adequate -grows at 25C, would need nutrient in order to grow

54
Q

Hyphae

A

-form when fungi is proliferating -grows at 37C

55
Q

Amphotericin B

A

-attacks synthesis of ergosterol which will disrupt cell wall fungi -toxic -IV -Last resort

56
Q

Flucytosine

A

-metbolite 5UTP will prevent RNA being made into DNA which will stop cell cycle and proliferation

57
Q

Azole

A

-14-ethyl-steromethodase prevents production of ergosterol -all Azole have same MOA

58
Q

Miconazole and Clotirmazole

A

-only topical; for athletes foot

59
Q

Ketoconazole

A

-not typically used because it is toxic

60
Q

Itraconazole

A

-metabolized in liver, needs to be taken with food

61
Q

Fluconazole

A

-metabolized in kidneys, readily available

62
Q

Griseofulvin

A

-inhibits microtubules -used when fungi has invaded hair follicle

63
Q

How to get rid of spores?

A

autoclaving will kill most

64
Q

Terbinafine

A

-inhibiting squalene monooxygenase, thus blocking the biosynthesis of ergosterol

65
Q

Questions needed to be asked for acne?

A

-diet -hygiene -shaving -personal and family hx of acne -activity -OTC products used

66
Q

Causes of acne

A

-stress -hygiene -diet -hormone

67
Q

How do hormones cause acne?

A

increase in androgen causes follicular epidermal hyperproliferation causing overgrowth of keratin causing increase in sebum causing blockage of pores. Increased sebum causes continued growth of keratin causing increase in inflammation causing ruptured comodome which releases the sebum and causes increase in proliferation of p.acne

68
Q

Why use prescription based selsun blue?

A

To reduce inflammation

69
Q

Alternative treatments for acne

A

-low sugar diet (high sugar causes increase in insulin growth factor) -low milk diet (skim) -salycilic acid: breaks down keratin

70
Q

Retinoids

A

-class of medications that are chemically derived from vitamin A and regulate numerous transcription factors including RAR and RXR located within the nucleus of various cells. Nuclear receptors increase the production of procollagen and function to block the release of inflammatory mediators. Act as comedolytic agents and work by unclogging blocked pores. -They work synergistically with topical antibiotics to allow them to enter the pore and eradicate the underlying bacteria causing the acne breakout.

71
Q

Retinol

A

MOA

72
Q

Adapalene

A

-binds to specific retinoic acid nuclear receptors (gamma and beta) and retinoid X receptors normalizing the differentiation of follicular epithelial cells resulting in decreased microcomedone formation.

73
Q

Tazarotene

A
  • Tazarotene undergoes esterase hydrolysis to form its active metabolite, tazarotenic acid. Tazarotenic acid binds to all three members of the retinoic acid receptor (RAR) family.
  • When treating acne tazarotene may be taken in conjunction with an oral antibiotic.
  • Use at night
74
Q

Benzozyl Peroxide

A

-decomposes to release oxygen after topical application. This oxygen acts as a bactericidal agent towards Proprionibacterium acnes, the bacteria present in acne vulgaris. Benzoyl peroxide also increases the turnover rate of epithelial cells, thereby peeling the skin and promoting the resolution of comedones. -cannot be taken with dapsone

75
Q

Dapsone

A

-acts against bacteria and protozoa by inhibiting the synthesis of dihydrofolic acid through competition with para-amino-benzoate for the active site of dihydropteroate synthetase. The anti-inflammatory action of the drug is unrelated to its antibacterial action and is still not fully understood.

76
Q

Erythromycin

A

-penetrates the bacterial cell membrane and reversibly binding to the 50 S subunit of bacterial ribosomes or near the “P” or donor site so that binding of tRNA (transfer RNA) to the donor site is blocked. -exact mechanism by which erythmromycin reduces lesions of acne vulgaris is not fully known: however, the effect appears to be due in part to the antibacterial activity of the drug.

77
Q

Clindamycin

A

-inhibits protein synthesis of bacteria by binding to the 50S ribosomal subunits of the bacteria. Specifically, it binds primarily to the 23s RNA subunit. Topical clindamycin reduces free fatty acid concentrations on the skin and suppresses the growth of Propionibacterium acnes

78
Q

Atopic dermatitis -other names -cause -how irritation is caused

A

-eczema, the itch that rashes -related to a gene variation that affects the skin’s ability to retain moisture which causes a breach in protection - irritation is caused by release of cytokines from keratinocytes that are damaged

79
Q

Cytokines released by keratinocytes

A

-IL6: pro-inflammation -IL-1: pro-inflammation -TGF-beta: anti-inflammation

80
Q

What happens with inflammation caused by cytokines released by keratinocytes?

A

-inflammation causes for patient to feel itchy which leads them to scratch which further damages the skin and causes increased injury

81
Q

Treatment for atopic dermatitis

A

-skin hydration (take warm 10 min baths to hydrate skin, then use moisturizer to lock in hydration–use oil based) -identifying allergen (allergy testing) -avoiding allergen and substances that could cause irritation (use fragrance free, dye free, sensitive skin products)

82
Q

Alternative treatment for atopic dermatitis

A

-coal tar: anti-itch, anti-inflammation -lactic acid: add moisture -phototherapy: sunlight -probiotics: lactus bacilluc -chinese herbs: anti-itch -oral omega 3: add moisture -peanuts: introduce early

83
Q

Intracellular vs Extracellular amounts of Na

A

I: 10-14 mEq/L E: 135-145 mEq/L

84
Q

Intracellular vs Extracellular amounts of K

A

I: 140-150 mEq/L E: 3.5-5 mEq/L

85
Q

Intracellular vs Extracellular amounts of Cl

A

I: 3-4 mEq/L E: 98-106 mEq/L

86
Q

Intracellular vs Extracellular amounts of Ca

A

I: less than 1 mEq/L E: 8.5-10.5 mg/dL

87
Q

Intracellular vs Extracellular amounts of HCO3

A

I: 7-10 mEq/L E: 24-31 mEq/L

88
Q

Which way will Na and K move during activation of Na ion channel?

A

Na: into cell K: will not move

89
Q

Which way will Na and K move during activation of Na/K ion pump?

A

Na: 3 out of cell K: 2 into cell

90
Q

Which way will Na and K move during activation of K ion channel?

A

Na: won’t move K: out of cell

91
Q

If a cell is permeable only to Na, will its charge change?

A

Yes, it will become positive

92
Q

When does voltage stop changing?

A

When chemical force equals electrical force bc these are the only two forces acting on the molecule, so once they are in balance there will be nothing to push/pull the molecule from one side of the membrane to the other

93
Q

How do electrical and chemical force equilibrate?

A

The charge of Na intracellularly will become too much and will begin to push Na out of the cell (Na/K pump) which will equal the amount of Na trying to be pushed in by the chemical gradient, therefore there will be the same number of Na coming in as being pushed out

94
Q

What generates resting potential?

A

-The reversal potential. -Since the cell has K leak channels the resting potential is established when those leak channels are balanced out by the same amount of K coming in as leaving

95
Q

Reversal potential

A

Amount of K wanting to leave (due to flowing down concentration gradient) equals the amount of K wanting to be pulled back in (due to negative charge of cell being attracted to positive charge of K)

96
Q

Alternative names for reversal potential

A

Nernst potential or Equilibrium potential

97
Q

How to calculate reversal potential (Eion)

A

=60/z *log ([ion]out/[ion]in -where z = charge of ion -ex. z of K = 1, and z of Ca=2

98
Q

What is Eion?

A

reversal potential if the cell membrane was only permeable to a specific ion

99
Q

How is cell membrane potential calculated?

A

by adding the Eion of all the ions the cell is permeable to

100
Q

How does hypokalemia affect cell behavior?

A

-refers to low potassium on outside of cell -would cause more intracellular potassium to move out of cell, making resting membrane potential more negative, making it harder to get to threshold for action potential to propagate

101
Q

How does hyperkalemia affect cell behavior?

A

-refers to high potassium on outside of cell -would cause less potassium to leak out of cell making resting membrane potential more positive, allowing for threshold to be reached faster

102
Q

Where is the voltage headed on the rising phase of the action potential? -in relation to ion concentration

A

Equilibrium potential of sodium ion

103
Q

Where is the voltage headed on the descending phase of the action potential? -in relation to ion concentration

A

Equilibrium potential of potassium ion

104
Q

What are problems of body solved by evolution of movement?

A

coordination–t tubules, multipolar neurons, and gap junctions

105
Q

how are movements accomplished using neurons and muscles?

A

neurotransmitters release Ach onto muscle receptors which triggers influx of Ca into muscle cell allowing for contraction of muscles

106
Q

what part of brain triggers upper motor neuron?

A

pre-central gyrus, motor cortex

107
Q

How is signal carried from brain to muscle?

A

lateral corticospinal tract, from precentral gyrus to muscle innervation

108
Q

How is signaling done quickly?

A

Movement of ions, which is much faster than other modes of communication, specifically ligand gated channels

109
Q

How is force generated at level of single muscle cell?

A

Mechanics of angle between head and tail of myosin allow for force

110
Q

How is force generated at level of whole muscle

A

contractility?

111
Q

How can skeletal muscle generate smooth range of force?

A

Having many small motor units allows for fine control while having few big motor units allows for gross control of muscle

112
Q

How is contraction coordinated among many sarcomeres?

A

T-tubules

113
Q

How is contraction coordinated between many muscle fibers?

A

gap junctions

114
Q

Explain what happens at each point on graph

A

Point A –> B: Voltage-gated Na+ channels are open. Never fully reaches Na+ voltage because it is still slightly permeable to K+ leak channels

Point B –> C: Na+ channels close and Voltage-gated K+ channels open.

Point C –> D: K+ channels remain open causing cell to hyperpolarize, does not quite reach Ek+ because some of Na+ channels still open

Point D –> E: K+ channels close, cell begins to re-establish resting membrane potential by pumping K back into cell while pumping Na out via K/Na atpase pump

Point E –> F: cell reaches resting membrane potential as amount of K released through leakage channels is in equilibrium with amount of K being pumped in via K/Na atpase pump

Unit 2: LGS (5 decks)

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