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Skin/Musculoskeletal > SM: Week 2 > Flashcards

SM: Week 2 Flashcards

1
Q

What are some characteristics of fungi?

A
  • eukaryotic organisms
  • have cell wall for protection
  • ergosterol is dominant membrane sterol
  • require preformed organic compounds for growth (heterotrophic)
  • comes in three different forms: yeast, mold, dimorphic
  • forms spores which can be used to identify the source of fungi
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2
Q

What are some features of yeast?

A
  • single celled fungi

- reproduce through budding (blastoconidia) – if the bud remains it forms pseudohyphae

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3
Q

What are some features of mold?

A
  • multicellular
  • grows in forms called hyphae
  • many produce cross walls of hyphae called septae
  • nonseptate hyphae do not exist
  • masses called mycelia
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4
Q

What are some features of dimorphic fungi?

A
  • exist as yeast in the body, mold in the environment
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5
Q

What are some different fungal spores?

A
  • conidia (asexual spores of mold)
  • arthroconidia (formed from joints in hyphae then fragmentation)
  • blastoconidia (yeast cell buds)
  • haustoria (hyphae on parasitic fungi)

o Spores are used to identify the source of the infectious fungi

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6
Q

Polyenes: Amphortericin B and Nystatin

  • mechanism, spectrum, distribution, toxicity
A

Fungicidal
o Mechanism: binds ergosterol, creates holes in membrane which allows leakage of electrolytes
o Spectrum: broad, used for invasive systemic fungal infections (meningitis) in immunocompromised patients, active against yeast and mold
o Distribution: long tissue half-life, liposomal form can cross BBB, small fraction is excreted
o Toxicity: 80% nephrotoxicity!!!! toxic because binds cholesterol, nystatin is toxic systemically – topical use only

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7
Q

Azoles: Fluconazole, Itraconazole, Ketoconazole

  • mechanism, spectrum, distribution, toxicity, resistance
A

Fungistatic
o Mechanism: binds fungal P-450 enzyme (Erg11) – blocks production of ergosterol
o Spectrum: widely used, spectrum varies
o Distribution: orally available, efflux pump in brain
o Toxicity: drug-drug interactions, hepatotoxicity, nephrotoxicity, alters hormone synthesis (AVOID DURING PREGNANCY!)
o Resistance: altered cytochrome P-450

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8
Q

Allylamines: Terbinafine (Lamisil)

  • mechanism, spectrum, toxicity, resistance
A

Fungicidal
o Mechanism: inhibits squalene epoxidase –> toxic accumulation of squalene
o Spectrum: dermatophytes
o Toxicity: topical drug interactions with CYP2D6 substrates
o Resistance: rare human pathogens, mutant binding site, efflux transporters

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9
Q

Flucytosine (5-FU)

  • mechanism, spectrum, distribution, toxicity, resistance
A

Fungistatic
o Mechanism: antimetabolite, selectively taken up, converts to 5-FU in fungi; interferes with DNA/RNA synthesis
o Spectrum: narrow – yeast forms of candida albicans and cryptococcus
o Distribution: oral, penetrates CNS
o Toxicity: only partially selective for yeast, leads to bone marrow suppression
o Resistance: cotreat with amphotericin B to increase uptake and minimize resistance

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10
Q

Griseofulvin

  • mechanism, spectrum, distribution, toxicity, resistance
A

Fungistatic
o Mechanism: binds to microtubules and inhibits spindle formation –> multinucleate cells
o Spectrum: dermatophytes (greater uptake)
o Distribution: lipids increase oral absorption, concentrates in dead keratinized layer of skin
o Toxicity: teratogenic
o Resistance: change to beta-tubulin

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11
Q

Echinocandins: caspofungin

  • mechanism, spectrum, distribution, toxicity, resistance
A

Fungicidal (candida), Fungistatic (aspergillus)
o Mechanism: cell wall inhibitor – block synthesis of beta (1,3)-d-glucan (polysaccharide)
o Spectrum: candida albicans, systemic
o Distribution: IV, large molecular wt prohibits CNS penetration
o Toxicity: limited, fever, rash at site of injection
o Resistance: unknown (new drug)

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12
Q

There are two types of cutaneous fungal infections. What are these?

A
  • tinea versicolor (pityrosporium versicolor)

- dermatophytes

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13
Q

What are the diagnostics used in fungal skin infections?

A
  • collect skin, nail, or hair
  • 10% KOH, can add stain
  • view under microscope
  • Wood’s lamp (UV-A light), cause some fungi to fluoresce
  • PCR
  • culture (some use Sabouraud’s agar)
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14
Q

What is the causative agent of tinea versicolor and what are some characteristics of this fungus?

A

Malassezia furfur

  • is a yeast that is part of the normal flora
  • converts to mold in disease (dimorphic)
  • requires lipids, primarily found in sebaceous glands in young individuals (15-24 yo)
  • associated with seborrheic dermatitis, cradle cap
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15
Q

What are some diagnostic findings for tinea versicolor and what is the effective treatment of this fungus?

A
  • Diagnosis:
    o KOH
    o Wood’s lamp – yellow-green
    o culture requires olive oil
    o skin scrapping – “spaghetti and meatballs”
  • Treatment:
    o topical therapy = selenium sulfide or ketoconazole shampoo; reoccurrence is common
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16
Q

What is the pathogenesis, diagnosis, and treatment of dermatophytes?

A
  • Pathogenesis: monomorphic molds enter through breaks in the skin and secrete proteases and keratinases; grow best at 25C, unable to survive at 37C – remain in the skin
  • Diagnosis: KOH test, grow on Sabouraud’s agar
  • Treatment: topical griseofulvin, terbinafine, itraconazole

Note: dermatophytes require keratin to grow so restricted to hair, nails, and superficial skin

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17
Q

What are the three different causative agents of dermatophytes?

A
  • trichophyton rubrum (tinea pedis)
  • microsporum canis/fulvum (hair and skin)
  • epidermophyton floccosum
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18
Q

What fungus causes subcutaneous infections?

A

sporothrix schenckii (dimorphic) – “rose gardener’s disease”

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19
Q

What is the pathogenesis, diagnosis, and treatment of sporothrix schenckii?

A
  • Pathogenesis: fungi spread from initial lesion through lymphatics and form nodular lesions; can spread to bone and joints
  • Diagnosis: biopsy of lymph node, culture in Sabouraud agar containing antibiotics, grow at different temps to confirm dimorphism
  • Treatment: oral itraconazole for 3-6 months
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20
Q

What fungus causes an opportunistic infection?

A

candida albicans

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21
Q

What is the pathogenesis, diagnosis, and treatment of candida albicans?

A
  • Pathogenesis: seed in areas with less normal flora, chronic mucocutaneous candidiasis may suggest individual has T-cell dysfunction, may be a sign of diabetes (poor circulation)
  • Diagnosis: based on clinical appearance, can do skin scrapping
  • Treatment: keep skin dry, clotrimazole or other azole cream
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22
Q

Where are common sites to see candida albicans infections?

A
  • superficial infections – diaper dermatitis (skin folds and around anus)
  • corners of mouth (anagular cheilitis)
  • toenail or edge of nails (paronychia)
  • oropharyngeal (thrush)
  • vaginal and systemic infections (binds to mucosa)
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23
Q

Within the visceral nervous system, where are the cell bodies of afferent sensory neurons located?

A
  • cell bodies are located in the DRG (pseudounipolar)
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24
Q

Within the ANS, where are the cell bodies of the efferent motor neurons located?

A

Two neuron system:

  • preganglion - located within gray matter in brainstem or spinal cord (CNS)
  • postganglion - located in peripheral motor (autonomic) ganglia (PNS)

o can be either parasympathetic or sympathetic

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25
Q

Recount the steps from the sympathetic preganglionic neuron from its cell body to the sympathetic chain.

A
  • Preganglionic cell body found in the intermediolateral cell column (lateral horn) within the spinal cord (multipolar neurons)
  • axons go out the ventral root to the spinal nerve and continue to the ventral ramus and pass through the white communicating ramus to either synapse on:
    o paravertebral ganglia (sympathetic chain ganglia)
    o prevertebral ganglia, by passing through the sympathetic chain ganglia
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26
Q

What are the four options for a sympathetic preganglionic neuron to travel once its entered the sympathetic chain?

A
  • ascend within the chain
  • descend within the chain
  • synapse once enter chain (at same level as entered)
  • pass through chain to form the splanchnic nerves, then synapse on the prevertebral ganglia
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27
Q

What spinal cord segments give rise to sympathetic preganglionic neurons and where are the cell bodies of the neurons located?

A
  • T1- L2 (location of intermediolateral cell column, aka lateral horn)
  • this is the location of the preganglionic cell bodies
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28
Q

Where will the preganglionic sympathetic neurons terminate?

A
  1. paravertebral ganglia (sympathetic chain)

2. prevertebral ganglia (celiac, superior/inferior mesenteric ganglia)

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29
Q

How do the postganglionic sympathetic neurons reach their destinations: spinal nerves, heart/lungs, head, other thoracic structures?

A
  • Spinal nerves/other visceral organs: gray communicating rami
  • Heart/lungs: cardiopulmonary nerves (cell bodies within the middle/inferior cervical paravertebral ganglia/upper 5 thoracic paravertebral ganglia)
  • Head: cephalic arterial rami, aka periarterial sympathetic plexus
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30
Q

How is the adrenal medulla innervated with sympathetic innervation?

A
  • preganglionic nerve via splanchnic nerves
  • the cells of the adrenal medulla act as cell bodies of the postganglionic neurons
    o release norepinephrine into the vascular system
    o causes system-wide sympathetic response as opposed to sympathetic innervation of specific cells
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31
Q

What cranial and spinal nerves are involved in the parasympathetic nervous system?

A

Cranial: CN III, VII, IX, and X
Sacral: S2,3,4

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32
Q

What are the preganglionic and postganglionic neurotransmitters/receptors and cell body locations for the sympathetic division of the ANS?

A

-Pre: cell body found in intermediolateral cell column (lateral horn)
o Neuro/receptor: ACh (nicotinic receptors)
- Post: cell body found in paravertebral or prevertebral ganglia
o Neuro/receptor: NE, E, sometimes ACh
• NE (a1, a2, B1, receptors)
• E (B2 receptors)

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33
Q

What are the excitatory and inhibitory receptors between a1, a2, B1, and B2 receptors?

A
  • excitatory = a1, B1

* inihibitory = a2, B2

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34
Q

What are the preganglionic and postganglionic neurotransmitters/receptors and cell body locations for the parasympathetic division of the ANS?

A
  • Pre: cell bodies found in the brainstem or sacral spinal cord
    o Cranial: CN III, VII, IX, and X
    o Sacral: S2,3,4
    • Neuro/receptor: ACh (nicotinic)
  • Post: cell bodies found in CN III, VII, IX
    o Neuro/receptor: ACh (muscarinic)
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35
Q

Compare and contrast the visceral and somatic sensory fibers in regards to cell body location and function of the fibers.

A

Cell bodies located in DRG (pseuodunipolar)

  • Visceral: peripheral process located by organ it is sensing (GI tract, smooth muscle, gland)
  • Somatic: peripheral process located in skeletal muscle, skin
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36
Q

What are some different types of skin ulcers?

A
  • pressure
  • venous
  • arterial
  • neurotrophic
  • special: pyoderma gangrenosum, cancer
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37
Q

What are the different stages of pressure ulcers?

A
  • Stage I: non-blanchable erythema.
  • Stage II: like an unroofed blister, dermis exposed.
  • Stage III: exposed subdermal tissues, note undermined edges.
  • Stage IV: exposed tendon or bone.
  • Unstageable: any wound with unobservable base due to eschar, exudate
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38
Q

How are pressure ulcers treated?

A
  • manage tissue loads (zero tolerance for pressure on wound)
  • manage bacterial colonization/infection (cleanse and debride wound, antibiotic?)
  • nutritional support (increase protein intake)
  • local wound care (cleanse, debride, avoid antiseptics – kill fibroblasts)
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39
Q

Wound care corresponds to the stage of the ulcer. What is the appropriate care for stage I ulcers?

A

o I: cleanse with non-drying soap and water, don’t apply dressings

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40
Q

Wound care corresponds to the stage of the ulcer. What is the appropriate care for stage II ulcers?

A

o II: cleanse with saline, dress with polyurethane film, hydrocolloid wafer
- Goal = provide environment conducive to granulation of tissue; keep surrounding skin dry

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41
Q

Wound care corresponds to the stage of the ulcer. What is the appropriate care for stage III ulcers?

A

o III: debridement if eschar or slough present; cleanse with saline; dress with hydrocolloid, alginate, or hydrogel
- Goal = debride necrotic tissue and protect granulation tissue

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42
Q

Wound care corresponds to the stage of the ulcer. What is the appropriate care for stage IV ulcers?

A

o IV: same as stage III

  • Odor can be a problem: apply metronidazole gel, activated charcoal
  • Osteomyelitis is main issue for non-healing
  • Operative repair could be considered; skin grafts used sometimes
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43
Q

What are some causes of pressure ulcers?

A
  • Occult fracture (hip, vertebral)
  • Stroke
  • Metabolic problem: hyponatremia, hyperosmolar, uremia
  • Medications: sedative, anticholinergic, steroid
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44
Q

Where are venous ulcers commonly found and why? What do venous ulcers look like?

A

They are typically seen in the medial malleolus due to the distribution of the saphenous vein.

The skin appears dark brown due to hemosiderin deposits, is edematous (tender to palpation), and will not diurese (drain).

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45
Q

What are the two venous systems in the leg?

A
  • Deep system (high pressure) – clots arising here are known as deep venous thrombosis (DVT), pose a risk for pulmonary embolism (PE)
  • Superficial system (low pressure) – protected from high pressure system due to valves in deep veins and perforators
    • Connected by perforator veins
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46
Q

What are some risk factors for venous ulcers?

A
  • Overload: CHF, obesity
  • Obstruction: clot, tumor
  • Pump malfunction: inactivity, neurological disease/injury
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47
Q

How are venous ulcers treated?

A
  • same debridement and cleansing regimens as pressure ulcers
  • control of edema is essential:
    o restore venous return by external pressure (30-40 mmHg in the ankle)
    • “TED” socks (provide ~18 mmHg)
    • Unna boot
    • commpression hose/pumps
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48
Q

What is the appearance and location of arterial ulcers?

A
  • Appearance: circumscribed, “punched out” ulcers, often multiple
  • Location: in well perfused areas: lateral malleolus, tibial, feet/toes
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49
Q

What are some features of arterial ulcers?

A
  • Claudication is a major sign – reduced blood flow to leg, results as cramping pain; decreased pain upon sitting/rest
    o may precede leg ulcer by months/years
  • Ulcerations at end-branch arteries most likely due to arterial ischema
    o Look for these signs: hair loss, absent pulses, Hx of hypertension, cigarette smoking, diabetes, or vascular disease (MI, abdominal aortic aneurysm)
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50
Q

What test is used to determine if the wound is an arterial ulcer? Describe what the findings out be.

A

Ankle-brachial Index (ABI):

  • normal = 1.0 or above
  • ABI below 0.8 causes claudication
  • ABI below 0.4 causes rest pain

o How to measure: the dorsalis pedis systolic BP divided by systolic pressure at brachial artery

o Note: ABI can also predict arteriosclerosis in pts and causes an increased risk of arteriosclerosis in coronary and cerebral arteries, thus pts often succumb to MI or strokes rather than complications of leg ischemia

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51
Q

What is the causation, location, and treatment of Buerger’s disease (thrombangiitis obliterans)?

A
  • often seen in young smokers
  • found in the hands and feet; associated with thrombophlebitis
  • Tx: STOP SMOKING!!!!!
    o fail to stop –> 43% result in amputation
    o stop smoking –> 6% result in amputation
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52
Q

What are some differentiating features of Buerger’s disease compared to atherosclerotic arterial ulcers?

A

In Buerger’s disease:

  • both have venous and arterial involvement
  • more diffuse involvement of upper and lower extremities
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53
Q

What is the test used for atherosclerotic occlusions?

A

Allen test:
- occlude both the radial and ulnar arteries after making a fist
- open hand and release pressure in ulnar artery (look for the return of pink)
o positive test = persistent pallor

54
Q

What are some treatments for arterial ulcers?

A
  • DON’T use external compression!!!
  • Smoking cessation – essential!!!
  • Revascularization
  • Skin graft
  • Amputation
  • Require same local care as pressure and venous ulcers to promote fibroblast growth and granulation tissue
55
Q

What is the appearance and location of neurotrophic ulcers?

A
  • appearance: prominent callus formation, charcot foot (collapse of ankle and foot due to neuropathy; foot assumes “rocker bottom”)
  • location: lateral plantar mid-foot or toes
56
Q

What is the cause of neurotrophic ulcers?

A
  • caused by peripheral neuropathy, usually diabetic
  • Screening for neuropathy:
    o monofilament test of touch sensation
    o self-surveillance for calluses, blisters, and other early signs of skin breakdown
57
Q

What is the treatment of neurotrophic ulcers?

A
  • Same cleansing, debridement, and dressing principles as pressure ulcers
  • Protection: footwear, total contact cast
  • Recombinant platelet-derived growth factor (PDGF) – becaplermin
  • Good diabetic management (hyperglycemia inhibits macrophage and fibroblast function)
  • Beware of infection (osteomyelitis)
58
Q

BCCs can ulcerate. Describe the appearance of these lesions.

A
  • Lesion usually starts as a small, smooth nodule which ulcerates as it grows – pearly nodularity around periphery with visible telangiectatic vessels overlying
  • Appears with “heaped up” or rolled edges
59
Q

SCC can also ulcerate. How does this happen?

A
  • May arise in a chronic ulceration such as venous ulcers perhaps as a malignant transformation due to persistent inflammation
  • May metastasize, check regional lymph nodes
  • If in doubt, biopsy
60
Q

What is the appearance, associated diseases, and treatment of pyoderma gangrenosum?

A
  • appearance: margins are serpiginous and elevated, edges have blue/purple hue with scalloped border, pustule/blisters precede with surround erythema
  • Associated diseases: Crohn’s disease, ulcerative colitis, RA, or leukemia
  • Tx: related to underlying disease, often involves corticosteroids
61
Q

What are the ABCs of burns?

A

Airway
Breathing
Circulation

62
Q

What are some things to keep in mind for the airway and breathing parts of the ABCs?

A

o With burns to the face it is important to intubate since inflammation will close the airway and reduce breathing/respiration rate
- Reasons to intubate: SOB/DIB, decreased O2 sat., inhaled smoke, carbonaceous sputum, facial burn, TBSA of trunk >30%
• If have facial burns, make sure the patient sees an ophthalmologist for an eye examination w/i 8 hours

63
Q

How is TBSA assessed?

A
  • Palm = ~1%
  • Rule of 9s
  • TBSA of 2⁰, 3⁰, or 4⁰ burns in respiratory airway + 25%
  • TBSA + age = ~mortality
64
Q

How is circulation addressed from the ABCs?

A

o Establish circulation by putting in IVs into UNburned skin

65
Q

What is the parkland formula used for and why is it useful?

A
  • used to determine how much fluid resuscitation to be started
  • 4 cc/ wt of pt in kg / TBSA affected
    • Give ½ of that volume in the first 8 hours
    • Give the other ½ in the next 16 hours
    • If have inhalation injury – add 25% more
66
Q

What are the benefits of IVF supplementation? What is added?

A
  • ascorbic acid is added (vitamin C)
  • studies have shown that ascorbic acid decreases the overall burn injury; thought to do so since Vit C is an antioxidant that scavenges free radicals found in organ damage associated with burn injuries
67
Q

Why are IV resuscitation necessary?

A

• Hyperemia increases blood flow and pushes the IVF from the Zone Of Stasis into the Zone Of Hyperemia, thereby decreasing Zone Of Coagulation (lessens the amount of burn)

68
Q

What is the best measurement of resuscitation?

A

URINE OUTPUT!!!

  • Peds: 1cc/kg/hour; neonate = 0.5cc/kg/hour
  • Adult: 0.5 cc/kg/hour
69
Q

What are some features of 1st degree burns?

A
  • occurs in the epidermis
  • ex.sunburn
  • characterized by erythema and edema
70
Q

What are some features of 2nd degree burns?

A
  • burns goes into dermis
  • Characterized by blisters:
    o clear – pop them; have high [inflammatory mediators] that lead to greater damage
    o hemorrhagic – leave them alone, protect deeper structures
71
Q

What are some features of 3rd degree burns?

A
  • burn goes down to the subcutaneous layer
  • painless since the burn goes deep enough to burn nerves
  • the skin needs to be grafted
72
Q

What are some features of 4th degree burns?

A
  • penetrates to bone, muscle, organ(s)

- severe and life-threatening

73
Q

What are some treatments for burns?

A
  • Silvadene
  • Mafenide acetate (Sulfamylon)
  • Silver Nitrate
  • Escharotomy
  • Skin grafts (typically use skin from thigh)
74
Q

What is a possible complication with silvadene use?

A
  • possibly causes neutropenia, if interrupt treatment then the neutrophil count can normalize
75
Q

What is the possible complication with use of Mafenide acetate (Sulfamylon) and some of its features?

A
  • drug-drug interaction with carbonic anhydrase inhibitors (causes metabolic acidosis)
  • penetrates eschar and is painful
  • accentuates post-burn hyperventilation
76
Q

What are the adverse effects of using SIlver Nitrate?

A
  • leaches Na+, K+, Ca2+, Cl- (causes hyponatremia, hypocaltremia, etc.)
  • not used much anymore
77
Q

What are things to keep in mind for electrical injuries and what are some treatment strategies?

A
  • there is always an in and out injury – think about what organs were affected in between…
  • amps are key –> squared in the heat eq.
  • Tx: ABCs, EKG, IVF to keep UO > 100 cc/hr –> give TONS of fluid!!!!!
78
Q

How are frostbites staged, what happens molecularly in this condition, and what are some treatment strategies?

A
  • staged the same way as burns (4th degree is gangrenous)
  • formation of ice crystals disrupts cellular membranes and physiology (causes microvascular occlusions)
  • Tx:
    o remove offending agent
    o DON’T heat, rub, debride, or amputate wound (slow warming), rapid warm parts? (~104 F, or 40 C)
    o NSAIDS
    o silvadene dressings
    o complete pressure relief
79
Q

Phosphorus is an elemental chemical. In what compounds is this chemical found in and what is it’s treatment?

A
  • used in munitions, fertilizers, insecticides, poisons
  • ignites on contact with air
  • Tx: irrigate and cover with wet dressings; copper sulfate (CuSO4) causes cupric phosphide particles, must be incised and drained (I&D) in the OR
80
Q

Acids in general cause what type of wounds, what should be avoided during treatment, and how does one treat this type of wound?

A
  • coagulation necrosis
  • Do NOT try to neurtalize – creates an exothermic rxn
  • H2O irrigation for hours until pain and burning are relieved
81
Q

Hydrofluoric acid is an acid that causes what types of tissue damage and how is it treated?

A
  • can progress to alkali-like liquefaction necrosis
  • Tx: 5% CaGluconate & (Mg2+) – topical, subcutaneous, and intra-arterial, treat until pain subsides and stays away; may need hemodialysis (HD)
82
Q

Alkali burns are caused by what agents, result in what type of tissue damage, and what is their treatment?

A
  • found in lye (easy-off), cement, plaster of paris (casts)
  • liquefaction necrosis
  • penetrates deeper, lasts longer, saponification – irrigate with H2O even longer
  • do NOT neutralize
  • Tx: Silvadene, irrogate with H2O
83
Q

What types of cells are found in the CNS and the PNS specifically?

A
  • CNS: astrocytes, oligodendrocytes, microglia, ependymal cells
  • PNS: Schwann cells, satellite cells
84
Q

What are the components of white matter?

A
  • Aggregation of axons
  • Includes nerves in the PNS and tracts, columns, and fasciculi of axons in the CNS
  • “white” is due to the large numbers of myelin-covered axons
85
Q

What are the components of gray matter?

A
  • Aggregation of nerve cell bodies and neuropil
  • Includes ganglia in the PNS and nuclei, layers in the CNS
  • “gray” due to the limited amounts of myelin
86
Q

What are the different components of a ‘generalized’ neuron?

A
  • plasma membrane
  • nerve cell body: nucleus, RER, golgi, neurofibrils, microtubules, actin filaments, inclusions, mitochondria
  • dendrites
  • sensory receptors
87
Q

What are the differences between encapsulated and unencapsulated sensory receptors?

A
  • Encapsulated:
    • composed of specialized CT or are terminal filaments of peripheral processes of sensory neurons, i.e. Meissner’s and Pacinian corpuscles
  • Unencapsulated:
    • receptors that respond to touch, pain, temp, pressure, etc.
    • i.e. free nerve endings, Merkel’s disks, hair follicle plexus
88
Q

What are the different types of synapses

A
  • axo-dendritic (shaft or spine)
  • axo-somatic
  • axo-axonal
  • serial (axo-axo-dendritic)
  • dendodendritic
89
Q

What are the components of a chemical synapse?

A
  • pre-synaptic structure (usually axon terminals)
  • synaptic cleft
  • post-synaptic structure (dendrites, cell body, axon terminal or target effector)
  • synaptic vesicles found within
90
Q

Explain synaptic vesicle recycling and renewal.

A

o Vesicle recycling and renewal means that vesicles created by the golgi are returned to the golgi once they release their neurotransmitter(s)
• Cycling is done by using dynein and kinesin motor proteins that use the microtubules present in the axon of the neuron

o Synaptic vesicles can either carry neurotransmitters down the axon or the vesicles can be empty and acquire small-molecules in the terminal

91
Q

What is the rate, state of the vesicle, and type of transport performed in slow axonal transport?

A
  • rate = 0.5 -3 mm/day
  • soluble macromolecules and small molecules are NOT packaged in vesicles
  • only have ORTHOGRADE transport (from cell body to axon terminal)
92
Q

What is the rate, transport materials, and type of transport involved in fast axonal transport?

A 
- rate:
     • orthograde = 400 mm/day
     •  retrograde = 200-300 mm/day
- transport materials:
     • orthograde: use synaptic vesicles made by golgi and carry neurotransmitters (ACh) or associated proteins (ACh-ase)
     • retrograde: the used synaptic vesicles return to the golgi, this is how viruses and toxins travel into the nervous system
- transportation involves microtubules:
     • orthograde: uses kinesin (ATPase)
     • retrograde: uses dynein (ATPase)
93
Q

What is the structure and function of astrocytes?

A

o Structure:
- fibrous (found in white matter), protoplasmic (found in gray matter)
- nuclei stain lighter and are larger than oligodendrocytes
- “end-feet” are pervasive and form perivascular feet on blood vessels, form external and internal glial limiting membranes when the “end-feet” terminate on the surface of pia mater and basal surface of ependymal cells, respectively.
o Functions (probable):
- structural support
- uptake extra K from extracellular space following neuronal activity
- phagocytosis and scar formation after injury
- isolation of nerve terminals and fibers
- regulation of substance entry into interneuronal spaces

94
Q

What is the structure and function of oligodendrocytes?

A

o Structure:
- have fewer processes than astrocytes
- nuclei are small, dense staining, and round compared to astrocyte nuclei
o Function:
- myelinate CNS
- provide putritive/maintenance functions to neurons

95
Q

What is the structure and function of microglial cells?

A

o Structure:
- cell body with many dendrites
o Function:
- derived from monocytes and thus have phagocytic activity

96
Q

What is the structure and function of ependymal cells?

A

o Structure:
- simple cuboidal or columnar epithelium, ciliated
o Function:
- cilia beat and move CSF in the ventricles
- formation of the choroidal epithelium which forms the choroid plexus (makes CSF by filtering plasma proteins from capillaries)

97
Q

What is the endoneurium coat of a peripheral nerve?

A

Endoneurium is a delicate collagent connective tissue surrounding the individual axons of nerve fibers; contacts the basement membrane of Schwann cells

98
Q

What is the perinerium coat of peripheral nerves?

A

Perineurium envelopes the fascicles of multiple nerve fibers, layer between the endo- and epineurium

99
Q

What is the epinerium coat of peripheral nerves?

A

Epineurium is a tough, dense layer of collagen that surround many fascicles.

100
Q

What is a myelinated axon?

A
  • “A” and “B” fibers
  • a nerve fiber that has either a glial cell or part of a glial cell that surrounds the axon; this allows for greater signal conduction velocity
101
Q

What is an unmyelinated axon?

A
  • “C” fibers
  • a nerve fiber that does not have a myelin covering it axon, results in slower signal conduction velocity
  • ex. Bundle of Remak (Schwann cells that engulf nerve fibers)
102
Q

How are axons myelinated in the CNS?

A
  • Oligodendrocytes myelinate the axons of CNS nerve fibers.
  • Oligodendrocytes have multiple “arms” that wrap around multiple axons to form the myelin sheath.
  • One oligodendrocyte can wrap around 10-40 different neurons.
103
Q

How are axons myelinated in the PNS?

A
  • Schwann cells wrap around a portion of the axon in a jelly-roll pattern
  • One cell is used to compose an internode on an axon
104
Q

What is a Node of Ranvier?

A

A Node of Ranvier is a periodic interruption of the myelin sheath on an axon

105
Q

What is a mesaxon?

A

A mesaxon is a region where the Schwann cell cytoplasm meets itself in the jelly-roll
- forms an internal and external mesaxon

106
Q

What is an internode?

A

An internode is a portion of the axon that is myelinated between adjacent Nodes of Ranvier

107
Q

What is an incisure of Schmidt-Lantermann?

A

These are faults in the smooth wrapping myelin sheath.

108
Q

Where are sensory ganglia of the body located and what type of neurons compose these ganglia?

A
  • DRG of all spinal nerves, CN III, VII, VIII, IX, and X

- pseudounipolar

109
Q

What type of cell surrounds the cell bodies within the sensory ganglia?

A 
Satellite cells (have neural crest origin, may be Schwann cells)
- play a role in ganglia metabolism
110
Q

What are the different types of autonomic (motor) ganglia?

A

sympathetic and parasympathetic

111
Q

What is the morphology of sympathetic ganglia?

A
  • they tend to be discrete structures with a CT capsule

i. e. paravertebral and prevertebral ganglia

112
Q

What is the morphology of parasympathetic ganglia?

A
  • they are very small, encapsulated structures located in the head, have isolated cell groups in the thorax, abdomen, and pelvic viscera
113
Q

What type of neuron is present in autonomic ganglia and where are the nuclei normally positioned?

A
  • multipolar

- nuclei are usually eccentrically placed, often binucleate

114
Q

Preganglionic axons are _______________ B fibers, and postganglionic axons are _____________ C fibers.

A

myelinated; unmyelinated

115
Q

What are some features and characteristics of satellite cells?

A
  • Very small cells that cover each ganglion neuron
  • Originate from neural crest cells
  • May be types of Schwann cells – form a continuous layer with Schwann cell sheath of peripheral nerves and share a continuous basement membrane
  • May play a role in ganglion neuron metabolism
  • Only cell nuclei appear in light microscopy
116
Q

What is orthograde (Wallerian) degeneration and what is the process?

A
  • Orthograde degeneration involves degeneration of portion of the axon separated from the cell body.
  • Process:
    • axon, axon terminal and myelin disintegrate
    • Schwann cell sheath and CT layers remain in PNS
    o No counterpart to this in CNS
    • Phagocytosis of debris completed by astrocytes and microglia in CNS, Schwann cells and macrophages in PNS
117
Q

What is retrograde degeneration and what is the process of degeneration?

A
  • retrograde degeneration involves changes in cell body and/or portion of the axon still attached to the cell body
  • Process:
    o degeneration of axon and myelin sheath near cell body
    o Chromatolysis, or death of cell without chromatolysis, or no “apparent” change
  • extent and severity of degeneration varies due to type of nerve cell, site of lesion, nature of injury, and age of individual
118
Q

What is chromatolysis?

A

Chromatolysis = cell body and nucleus swell, nucleus becomes eccentric, RER disintefrates and move to the periphery of cell body

119
Q

Regeneration is only successful in the ______ and does not occur in the _______ because _______________ are abortive and do not form a guiding tube.

A

PNS

CNS, oligodendrocytes

120
Q

The process of regeneration begins before degeneration is complete. What is the process of regeneration?

A
  • Multiple sprouts emerge from central stump of axon
  • One or more sprouts must enter and travel through the surviving tube of Schwann cells
  • One sprout survives and innervates a target receptor or effector
  • Remyelination occurs after successful reinnervation
  • Rate of regeneration is usually 1.5 mm/day
121
Q

What are some things to keep in mind about regeneration?

A
  • success of reinnervation depends on the type of injury
  • sensory fibers will innervate any sensory receptor
  • motor fibers will innervate any muscle
  • regenerated axons usually have a decreased conduction velocity
122
Q

What is plasticity?

A

Plasticity involves recovery of nervous innervation following an injury in the CNS.

  • cannot be explained by regeneration
  • possibly explained by collateral sprouting and establishment of new connections or unmasking of previously less significant connections
123
Q

Breast cancer is the most common cancer among women today, and is the ________ leading cause of deaths in women today.

A

second

124
Q

The USPSTF recommends _____________ mammogram screenings for women ____ to ____ years of age.

A

biennial (every two years); every two years

125
Q

Women below the age of 50 and above the age of 75 should talk with their physicians about whether obtaining a ______________ is important.

A

mammography

126
Q

The USPSTF recommends _________ teaching breast self-exam (BSE).

A

AGAINST

127
Q

The AAFP says that it’s important to recognize that the recommendations set forth by the USPSTF do not bring an end to screening in women ages _____ to _____, but promote ____________ ______ by having physicians speak with women about their medical history and whether mammography is right for them.

A

40 to 49; individualized care

128
Q

The ACS recommends that women age _____ and _______ should have a mammogram ______ _______ and should continue to do so for as long as they are in good health.

A

40 and older; every year

129
Q

Clinical breast exams performed every ______ years for women age ____ to _____, annually for women 40 and older.

A

three; 20-39

130
Q

What are the seven P’s for female/male breast assessments?

A
  • Position
  • Perimeter
  • Palpation
  • Pattern
  • Pressure
  • Patient education
  • Plan of action
131
Q

What is the general overview of a breast assessment?

A
  • Observe the patients breast tissue for dimpling, retraction signs, abnormal contours, etc.
  • Position arms relaxed at side, above head, and hands on hips
  • Palpate the entire perimeter of the breast using the three different pressure technique in either a vertical strip, pie or radial spoke, or circular pattern.
  • Patient education
  • Plan of action

Skin/Musculoskeletal (5 decks)

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