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Nursing-Sem 1 > Patho Exam 2 > Flashcards

Patho Exam 2 Flashcards

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1
Q

largest organ of the body

A

skin

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2
Q

functions of the skin

A 
temperature control/regulation
barrier protection
secretion/absorption
vitamin D production
immunological surveillance
indicative of disease process, overall health
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3
Q

how to increase absorption rate @ skin?

A

put medication of skin, occlude (cover). will increase rate of absorption, effects.

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4
Q

approximately what percentage of PCP visits are related to skin conditions?

A

50%

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5
Q

why are skin disorders more likely with age?

A

amount of elastin/collagen decreases (can’t heal as well), skin thins and gets weaker, immune system decreases so cannot fight off conditions as well (skin cancer) or mount inflammatory response as well, cumulative effects of environmental exposure (sun, chemicals, topical agents over time)

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6
Q

____% of Americans have a skin condition; ____% of older adults have some form of skin disorder

A

30%; 90%

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7
Q

epidermis

A

aka stratum germinativum
outermost layer of skin
few cells thick

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8
Q

stratum germnivatum

A

two layers: basal and squamous

contains column-shaped basal cells, move upward towards skin and flatten, die, shed

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9
Q

stratum granulosum

A

contains more keratinocytes moving upward toward surface

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10
Q

stratum lucidum

A

only on palms of hands, soles of feet

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11
Q

stratum coreum

A

outermost layer of epidermis
made of dead, flat, keratinocytes that shed every 2 weeks
whole layer shed every 3-4 weeks
dead cells contain large amt of keratin (insoluble fibrous protein that form barrier of skin)

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12
Q

keratin

A

insoluble fibrous protein that forms barrier of skin
principle hardening protein of hair, nails
has the ability repel pathogens and prevent excessive fluid loss

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13
Q

three specialized cells @ epidermis

A 
melanocytes (produce pigment)
Langerhans cells (1st line immune defense)
Merkel cells (mechanoreceptors, transmit stimuli, involved in f'n of touch)
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14
Q

largest portion of skin

A

dermis

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15
Q

dermis

A

largest portion of skin
provides strength, structure
includes connective tissue, blood capillaries, oil/sweat glands, nerve endings, hair follicles

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16
Q

hypodermis (subcutaneous tissue)

A 
innermost layer of skin
primarily adipose tissue
thickness varies by person
vital for body temp regulation
provides cushioning between skin/muscle/bone
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17
Q

how does skin control/regulate temp?

A

skin has temp sensors, send info to hypothalamus
brain sends signals to skin’s sweat glands and blood vessels
Cooling: glands excrete sweat to cool down body (evaporation)
Heating: erector muscles contract, raise hair on skin to trap air, provide insulation, and keep body warm

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18
Q

80% of heat loss occurs via the…?

A

skin

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19
Q

how does the skin provide barrier protection to body?

A
  • -natural barrier, keratinized cells
  • -skin has bacteria, thick lipid film (sweat, sebaceous secretions) that repels virulent bacteria/ prevents infection
  • -surface film, thick surface layer (stratum corneum) prevent antigens from entering body & keep it waterproof
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20
Q

how skin is involved in excretion

A

By influencing the composition and volume of sweat, the skin influences total fluid volume and quantity of excreted waste products
minor compared to renal, respiratory excretion

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21
Q

what waste products are excreted @skin?

A

water, heat, salt, carbon dioxide, ammonia, and urea

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22
Q

what is absorbed @ skin?

A
  • -fat-soluble substances (Vit ADEK)
  • -O2, CO2, organic solvents, CCl4, heavy metal salts, poison ivy/oak oils
  • -fat soluble medications (skin permeable to them)
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23
Q

how is skin involved in the production of Vit D?

A

1st step in vit D synthesis is @ skin: 7-dehydrocholesterol converted to cholecalciferol (precursor to vit D)
–then, synthesis @ liver, kidney

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24
Q

what does vitamin D do?

A
  • -regulates Ca2+ and P (phosphorous) metabolism
  • -facilitates calcium absorption from the intestine
  • -affects bone cell development
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25
Q

innate immune response @ skin

A
  • -keratinocytes regulate immune response and secrete inflammatory mediators
  • -Lagerhorn cells detect foreign antigens and present them to lymphocytes (adaptive immune response)
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26
Q

how does skin act as mirror for underlying disease processes, overall health?

A

changes in skin color, texture, temperature swelling, diaphoresis, etc. commonly indicate underlying disease processes

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27
Q

people who lack sufficient oxygen pay present as what color?

A

cyanotic (blue)

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28
Q

people with excess bilirubin may present as what color?

A

yellow, jaundiced (liver disease)

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29
Q

people with erythema pay present as what color?

A

extreme redness (capillary engorgement)

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30
Q

people presenting with pallor indicate?

A

extreme paleness (anemia or shock)

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31
Q

atrophy

A

thinning and loss of skin layers; characterized by the reduction of its volume, as well as the qualitative changes in the tissue, especially elastic fibers

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32
Q

bulla

A

large blister (greater than 0.5 cm in diameter) INFECTION, contact irritants, IMMUNE RESPONSE, and systemic health conditions may cause bullae

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33
Q

crust

A

dried yellowish and yellow-brown exudate on the skin…the result of drying of plasma or exudate on the skin.

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34
Q

erythema

A
  • -reddened skin
  • -area blanches with pressure
  • -caused by hyperemia (increased blood flow) in superficial capillaries
  • -occurs with any skin injury, infection, or inflammation.
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35
Q

excoriation

A

scratches that break the skin’s surface

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36
Q

fissure

A

crack in skin that breaks through keratin barrier

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37
Q

induration

A

hardening or thickening of skin

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38
Q

keloid

A

irregular, elevated scar tissue formed by excessive collagen growth during wound healing

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39
Q

Lichenification

A

hardening or thickening of the skin with markings; often develops from repeated trauma (i.e. scratching)

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40
Q

macule

A

defined, flat area of altered pigmentation

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41
Q

papule

A

raised, well-defined lesion smaller than 0.5 cm

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42
Q

plaque

A

raised, flat-topped lesion larger than 2cm in diameter

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43
Q

nodule

A

solid lump greater than 0.5 cm in diameter

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44
Q

purpura

A

purplish lesion caused by free red blood cells in the skin. Does NOT blanch on pressure and may be nodular.

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45
Q

pustule

A

papule filled with pus

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46
Q

scale

A

fragment of dry skin

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47
Q

scar

A

permanent replacement of normal skin with connective tissue

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48
Q

telangiectasia

A

fine, irregular red lines produced by dilatation of the capillaries

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49
Q

ulcer

A

loss of epidermal and dermal tissue

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50
Q

vesicle (blister)

A

blister smaller than 0.5 cm in diameter

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51
Q

wheals/ urticaria

A 
transient pink, itchy, elevated papules that evolve into irregular red maculo-papular patches
//hives
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52
Q

phases of wound healing (list)

A

inflammatory, fibroblastic, maturation

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53
Q

inflammatory phase of wound healing (describe)

A

begins at time of injury
lasts 3-5 days
characterized by local edema, pain, redness, warmth

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54
Q

fibroblastic phase of wound healing (describe)

A

begins the 4th day after injury
lasts 2-4 weeks
characterized by formation of scar and granulation (wound bed) tissues

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55
Q

maturation phase of wound healing (describe)

A

begins as early as 3 weeks after injury
may last 1 year
scar tissue becomes thinner, more firm, and inelastic on palpation

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56
Q

different levels of intention (list, describe)

A
  • -first/primary: approximated edges
  • -second/ary: wounds with tissue loss, require gradual filling in of the dead space with connective tissue
  • -third/tertiary: delayed primary closure, wound left open for irregation, removing debris/exudate, then closed by 1st intention.
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57
Q

granulation tissue is indicative of what intention of healing?

A

second

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58
Q

types of exudate

A

serous: clear-straw color; normal healing
sero-sanguineous: pink-clear; normal healing
sanguineous: red from blood; trauma
hemorrhaging: frank blood; emergency
purulent: yellow, gray, green; infection

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59
Q

skin cancer

A

malignant lesion @ skin, may or may not metastasize

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60
Q

risk factors for skin cancer

A 
overexposure to sun
chronic skin damage (repeated injury)
genetic predisposition
ionizing radiation
light skinned race
age older than 60 years
outdoor occupation
exposure to chemical carcinogens
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61
Q

basal cell cancer

A

arises from basal cells in epidermis
metastasis rare
underlying tissue damage can progress to organ tissues
treat with removal

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62
Q

squamous cell carcinoma

A

tumor of epidermal keratinocytes
can infiltrate surrounding tissues
can metastasize to lymph nodes
treatable, but often caught late

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63
Q

melanoma

A
  • -may occur anywhere on body, esp w/ birthmarks, new moles present
  • -highly metastatic to brain, bone, lungs, liver
  • -survival depends on early dx and tx
  • -Assess using ABCDEs
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64
Q

ABCDEs of melanoma

A 
A: asymmetry
B: borders irregular
C: different colors or color change
D: diameter > 0.5 cm
E: evolution (changes over time)
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65
Q

level I melanoma

A

cancer cells extend to epidermis

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66
Q

level II melanoma

A

cancer cells extend to papillary dermis

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67
Q

level III melanoma

A

involves layers down to papillary-reticular dermal interface

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68
Q

level IV melanoma

A

involves layers down to the reticular dermis

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69
Q

level V melanoma

A

involves layers down to subcutaneous tissue

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70
Q

three C’s to use when assessing nails

A

color, consistency, configuration

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71
Q

alopecia

A

loss of hair from any cause

i.e. male pattern baldness (androgenic alopecia–loss of androgen and shrinking of hair follicle)

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72
Q

what to look for in hair assessment

A

color, texture, distribution, loss, other changes (unusual patterns, etc.)

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73
Q

hirstuism

A

in women, increased hair distribution on face, chest, shoulders due to post-menopausal levels of estrogen (decreased)

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74
Q

diagnostic evaluations of skin

A

biopsy, immuno-florecense, patch testing (contact dermatitis, allergens, nickel jewelry), skin scrapings (fungal) , Tzanck’s smear (herpes zoster), woods light (fungal), clinical photographs (monitor changes over time)

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75
Q

primary functions of the cardiovascular and circulatory systems

A
  • -transport O2, CO2, nutrients, electrolytes, hormones to all body tissues
  • -transport of waste products for elimination
  • -precise delivery to meet O2, nutritional demands of tissues
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76
Q

only artery that carries deoxygenated blood

A

pulmonary artery

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77
Q

only vein that carries oxygenated blood

A

pulmonary vein

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78
Q

circulation of blood

A

deoxygenated blood from systemic circulation to vena cavas > right artia > through tricuspid > right ventricle > through pulmonic > to lungs (pulm artery) > pulm capillaries pick up O2, deposit CO2> oxygenated blood to heart (pulm veins) > left atria > through bicuspid/mitral > left ventricle > through aortic valve to systemic circulation

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79
Q

left side of heart pumps blood to…

A

systemic circulation

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80
Q

right side of heart pumps blood to…

A

the lungs

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81
Q

high pressure side of heart

A

left (systemic circulation, needs to transport longer distance) @ 90-100 mmHg

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82
Q

low pressure side of heart

A

right (pulmonary circulation, shorter distance, slower flow) @ 12 mmHg

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83
Q

valves act reciprocally in order to…

A

keep blood flowing in same direction

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84
Q

do arteries or veins have valves?

A

veins, to keep blood from back flowing (have to push blood upwards and work against gravity)

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85
Q

endocardium

A

innermost layer of heart

endothelial tissue with small vessels and bundles of smooth muscle

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86
Q

myocardium

A
  • -muscle layer of heart
  • -sarcomeres (contractile units) more compact than @ skeletal muscle
  • -contains large amount of mitochondria (larger energy requirements)
  • -arranged in interconnecting latticework
  • -behave as single unit not individual cells (syncytium)
  • -tropomysin and troponin regulate calcium medicated contractions
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87
Q

what is the difference between sarcomeres @ cardiac muscle versus skeletal muscle?

A

sarcomeres are shorter, more compact @ myocardium than @ skeletal muscle

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88
Q

what does syncytium describe (in reference to myocardium)

A

all cells behave as a single unit and not as individuals

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89
Q

what regulates calcium mediated contractions?

A

troponin and tropomysin

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90
Q

epicardium

A
  • -outermost layer of heart and visceral layer of pericardium
  • -made of squamous cells overlying connective tissue
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91
Q

pericardium

A
  • -fibrous sac surrounding heart, great vessels
  • -two portions: fibrous and serous pericardium
  • -fibrous: tough outer layer, fits loosely around heart
  • -serous: thin, smooth inner portion with visceral (innermost layer, adheres to surface of heart) and parietal layers (lines inside of fibrous layer)
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92
Q

pericardial space, fluid

A

space between pericardium layers, contains serous fluid for lubrication, allows heart to move easily during contractions

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93
Q

cardiac or pericardial tampenade

A

too much fluid in pericardial sac, fibrous layer doesn’t expand so it just puts pressure on the heart. can cause cariogenic shock, SOB, weakness

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94
Q

atrioventricular (AV) valves

A

tricuspid and mitral–between atria and ventricles

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95
Q

semilunar valves

A

pulmonic and aortic values

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96
Q

chordae tenodonae and valve opening/closing

A

papillary muscles relax to pull chordae tendonae and open valves and contract to relax chordae tenodonae and close valves

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97
Q

cardiac cycle (1 heartbeat)

A

atrial systole > beginning of ventricular systole (S1 heart sound, closing of AV valves) > period of rising pressure > beginning of ventricular diastole (S2 heart sound, SL valves closing) > period of falling pressure

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98
Q

atrial systole (contraction) makes a _____% difference in the blood volume moved by the heart (compared to just opening and letting gravity move blood into ventricles)

A

30% more blood moved with atrial contraction. if don’t have contraction, have Afib. less blood moving, less efficient, can cause heart failure, stroke, etc.

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99
Q

describe what happens @ coronary vessels during systole and diastole

A

@ systole: blood is ejected into aorta

@diastole: blood flows back into CAs.

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100
Q

does blood get O2 during systole or diastole?

A

diastole

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101
Q

widow-maker

A

clot at the left coronary artery (feeds majority of left ventricle, if cut off O2, rapid death of left side of heart, stop systemic circulation, death). Often people with clot a LCA don’t show symptoms and then suddenly drop dead.

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102
Q

what is a main contributor to coronary artery disease?

A

hypertension!

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103
Q

RCA

A

right coronary artery

supplies blood, O2 to right atrium, most of right ventricle and inferior left ventricle

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104
Q

LCA

A

left coronary artery
supplies blood, O2 to left atrium, most of left ventricle, most of inter ventricular septum, and collateral circulation
splits into anterior descending (LAD) and circumflex arteries

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105
Q

coronary veins

A

lie superficial to arteries
most empty into the largest, Coronary Sinus, which opens directly into right atrium
anterior cardiac veins empty into right atrium

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106
Q

conduction system @ heart

A 
SA node (pacemaker, 60-100bpm)
AV node (backup, 40-60bpm)
Bundle of His / AV bundle
Purkinje fibers (quaternary backup, like 20bpm)
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107
Q

what makes the heart beat?

A

depolarization and depolarization of heart muscles. impulse travel.

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108
Q

p wave represents

A

atrial depolarization (contraction)

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109
Q

QRS complex represents

A

ventricular depolarization (contraction) and atrial re-polarization

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110
Q

T wave represents

A

ventricular repolarization

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111
Q

ECG visualizes…

A

electrical activity/impulses @ heart

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112
Q

PR interval represents

A

the amount of time taken from beginning of impulse @ SA node (P) to ventricular depolarization (R). Important because it can tell you if there is conduction interference (muscle damage) between SA and AV nodes.

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113
Q

steps for reading ECG

A

1) look for P wave.
2) does every P have have QRS complex?
3) determine PR interval (3-5 small squares).
4) R to R intervals consistent? (reg or irreg)
5) det ventricular rate (#R waves in 6 sec times 10)
6) determine duration of QRS complex (<3 small squares)

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114
Q

if don’t have a P wave, you know what?

A

impulse not originating @ SA node

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115
Q

“fat” QRS waves mean what?

A

took a long time for the ventricles to depolarize (muscle damage “roadblock”)
impulse may be coming from ventricles

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116
Q

peak T waves are present with what?

A

hyperkalemia

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117
Q

cardiac output

A

Volume of blood flowing through either the systemic or pulmonary circuit in liters per minute
determined by preload and after load
preload: Left ventricular end-diastolic volume
afterload: Resistance to ejection of blood from left ventricle (load muscle must move after starts to contract–determined by system vascular resistance in aorta)

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118
Q

Starling’s law

A

can stretch cardiac muscles to certain point (to get more contraction), but at some point, that stretching becomes detrimental, can’t push out as well.

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119
Q

preload

A

volume coming into ventricles (end diastolic pressure)

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120
Q

afterload

A

resistance left ventricle must overcome to circulate blood

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121
Q

preload is increased with…?

A

hypervolemia, regurgitation @ cardiac valves

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122
Q

after load is increased with…?

A

hypotension, vasocontriction

inc. afterload = inc. cardiac workload

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123
Q

components of cardiac performance

A

cardiac output, myocardial contractility, cardiac output, ejection fraction

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124
Q

myocardial contractility

A

depends on stroke volume and preload

affected by inotropic agents, O2 and CO2 levels

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125
Q

ejection fraction

A

% of ventricular volume ejected with each systole

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126
Q

what determines stroke volume?

A

preload, after load, and contractility

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127
Q

formula for cardiac output

A

stroke volume X HR

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128
Q

BP = ______ x ______

A

cardiac output X peripheral resistance

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129
Q

difference between arteries and veins

A

veins have valves to prevent back flow

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130
Q

layers of vessels

A

lumen
tunica intima
tunica media
tunica externa aka adventitia

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131
Q

adventitia is what?

A

outermost layer of vessels

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132
Q

lumen is what?

A

innermost layer of vessels

lumen aka “emptiness” b/c inside space of a tubular structure

133
Q

varicose veins

A

a vein in which blood has pooled

distended, tortuous, palpable

134
Q

what causes varicose veins

A

trauma or gradual venous distension

135
Q

risk factors for varicose veins

A

age, female, family hx, obesity, pregnancy, DVT, prior leg injury, standing on feet for long periods

136
Q

having varicose veins increases your risk for…?

A

DVT

137
Q

chronic venous insufficiency

A

inadequate venous returns over longer period of time due to varicose veins or valvular incompetence
may lead to venous stasis ulcers (ankles)

138
Q

signs of venous insufficiency

A

edema @ lower legs, ankles, feet
varicose veins
skin changes & color
skin ulceration @ ankles

139
Q

thrombus formation @ veins

A

obstructs venous flow and increases venous pressure

Factors that influence: triad of virchow, cancer, surgery, trauma, immobility, heart failure

140
Q

triad of virchow

A

factors leading to formation of thrombus @ veins

includes: venous stasis, venous endothelial damage, and hypercoagulable states

141
Q

biggest risk factor for developing a clot?

A

immobility

142
Q

thrombus vs. embolism

A 
thrombus = stationary clot
embolism = broken off clot that is moving through circulation
143
Q

hypertension

A

high BP–consistent elevation of arterial BP
“silent killer”
140/90
primary and secondary types

144
Q

primary HTN

A

essential, idiopathic HTN
genetic, environmental factors
92-95% with HTN have this kind
risk factors: high Na2+, inflammation, obesity, insulin resistance

145
Q

secondary HTN

A

caused by systemic disease processes that raise peripheral vascular resistance or cardiac output

146
Q

biggest cause of secondary HTN? other causes?

A

renal disease

others: brain tumors, drugs

147
Q

why is HTN called the “silent killer”

A

involves so many complications if not controlled, such as kidney failure, blood vessel damage (atherosclerosis), stroke, vision loss, heart attack, and bone loss

148
Q 
BP normal
BP prehypertensive
BP stage 1 HTN
BP stage 2 HTN
BP HTN crisis
A

normal: >120/ > 80
prehypertensive: 120-139/ 80-89
stage 1 HTN: 140-159 / 90-99
stage 2 HTN: 160+/ 100+
crisis: 180+ / 110+

149
Q

malignant HTN

A

rapidly progressive
diastolic usually >140 mmHg
life-threatening organ damage (esp @ kidney, brain, eyes–retinal hemorrhages)
constant high pressure causes vascular stretching > inflammation > epithelial damage > inc. permeability
tx: administer vasodilators

150
Q

orthostatic hypotension

A

BP drops by 20mmHg systolic or 10mmHg diastolic when go from lying to sitting and sitting to standing

lack normal BP to compensate for gravitation changes in circulation

151
Q

aneurysm

A

Local dilation or outpouching of a vessel wall or cardiac chamber

can cause aortic dissection (tears longitudinally) or rupture

152
Q

area most susceptible to aneurysm

A

aorta, esp abdominal

153
Q

factors contributing to development of aneurysm

A

hypertension, atherosclerosis

154
Q

embolism

A

Bolus of matter that is circulating in the bloodstream (like dislodged clot, air bubble, amniotic fluid, fat deposit, bacteria, cancer cells, foreign substance)

155
Q

thromboembolus

A

small piece of blood clot that breaks off and travels through circulation. can lodge elsewhere and cause serious complications (pulmonary, brain)

156
Q

atherosclerosis

A

thickening, hardening of the arteries caused by the accumulation of lipid laden macrophages @ arterial wall

characterized by: plaque development
results in: inadequate perfusion, ischemia, necrosis

157
Q

progression of atherosclerosis

A 
endothelial inflammation
cell proliferation
macrophages migrate, adhere
LDL oxidation, form foam cells
fatty streak
fibrous plaque
complicated plaque
158
Q

risk factors for atherosclerosis

A

diabetes, smoking, hyperlipidemia, dyslipidemia, HTN

159
Q

peripheral artery disease

A

atherosclerotic disease of arteries that perfuse the limbs

160
Q

common sites for PAD

A

iliac artery, femoral artery, popliteal artery, tibial arteries

161
Q

coronary artery disease

A

any vascular disorder that narrows/occludes the coronary arteries leading to myocardial ischemia–local, temporary ischemia

most common cause: atherosclerosis

162
Q

risk factors for CAD (modifiable and non modifiable)

A

modifiable: dyslipidemia, HTN, smoking, diabetes, obesity, sedentary lifestyle, fast food
nonmodifiable: older age, family hx, being male, post menopausal women

163
Q

ECG sign of CAD

A

inverted T waves

164
Q

acute coronary syndromes include..

A

unstable angina, myocardial infarction

165
Q

unstable angina

A

chest pain due to lack of blood flow @ heart
can be indicative of heart attack
usually caused by atherosclerosis
vague to dx, tx because not many markers

166
Q

myocardial infarction

A

aka heart attack
Sudden and extended obstruction of the myocardial blood supply
ischemia and then cell injury/death/tissue necrosis
STEMI (ST elevation) or NSTEMI (no ST elevation)

167
Q

structural changes @ heart seen with MI

A

myocardial stunning
“hibernating” myocardium
myocardial remodeling

168
Q

labs for measuring MI

A

troponin I level (only found @ myocardium)
normal < 0.4

CPK-MB: <5 normal (slower to show signs than troponin I)

169
Q

manifestations of MI

A

sudden, severe chest pain–may radiate
nausea, vomiting
sweating
SOB

170
Q

complications associated w/ MI

A

Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability

171
Q

ECG sign of MI

A

elevated ST segment (more elevated = more damage)

172
Q

disorders of the pericardium include..?

A

heart wall disorders including acute pericarditis, pericardial effusion (tamponade), and constrictive pericarditis

173
Q

constrictive pericarditis

A

results from scarring & consequent loss of elasticity of pericardial sac

174
Q

pericardial effusion

A

aka pericardial tamponade

fluid builds up in pericardial sac and puts pressure on heart

175
Q

cardiomyopathies include…?

A

disorders of the myocardium

congestive, hypertrophic, and restrictive

176
Q

valvular disorders

A 
disorders of the endocardium
valvular stenosis (aortic, mitral)
valvular regurgitation (aortic, mitral, tricuspid)
mitral valve prolapse
177
Q

stenosed valve vs. regurgitant valve

A

stenosed: doesn’t open all the way
regurgitant: doesn’t close all the way

178
Q

infective endocarditis

A

inflammation of the endocardium
caused by : pathogens (bacteria, virus, fungi, rickettsiae, parasites)
pathogenesis: endocardium damaged > blood-borne pathogen adheres > pathogen proliferates (vegetations)

179
Q

manifestations of infective endocarditis

A 
fever
new, change in cardiac murmur
petechial lesions (skin, conjunctiva)
Osler nodes (painful lesions, fingers, toes)
Janeway lesions (non-painful hemorrhagic lesions @ palms, soles)
180
Q

heart failure

A

When the myocardium can’t pump effectively enough to meet the body’s metabolic needs

can be: systolic or diastolic, left or right sided, acute or chronic

181
Q

Left heart failure

A

aka CHF. can be systolic or diastolic, left or right.

Increased workload & end-diastolic volume enlarge the ventricle. Ventricles have stretched tissues vs functional tissue allowing pulmonary congestion

182
Q

Systolic heart failure

A

Reduced Ejection Fraction (HFrEF)
Left ventricle can’t pump enough blood out to systemic circulation during systole & ejection fraction falls (EF < 40% )
Blood backs up into pulmonary circulation pulmonary congestion

183
Q

Diastolic heart failure

A

Preserved Ejection Fraction (HFpEF)
Left ventricle can’t relax & fill properly during diastole & stroke volume falls
Resistance to filling of one or both ventricles (the ventricle is stiff/noncompliant) (EF > 50%)
Leads to signs of pulmonary congestion. Most pts don’t c/o symptoms at rest only on exertion

184
Q

symptoms of left sided heart failure

A

SOB, orthopnea, frothy sputum w/ cough, fatigue, dec. urine output, edema

Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension & a S3 gallop

185
Q

right sided heart failure

A

most commonly caused by a diffuse hypoxic pulmonary disease

Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

186
Q

symptoms of right sided heart failure

A

fatigue, inc. peripheral venous pressure, ascites, enlarged liver/spleen, JVD, anorexia and GI distress, swelling hands and fingers, dependent edema

187
Q

primary function of respiratory system

A

provide O2 for metabolism @ tissues

remove CO2, waste from metabolism

188
Q

secondary functions of respiratory system

A 
facilitate sense of smell
produce speech
maintain acid-base balance
maintain body water levels (hydration)
maintain body temp (heat balance)
189
Q

upper respiratory system

A

trachea and up

nose, sinuses, pharynx, larynx, epiglottis

190
Q

lower respiratory system

A

trachea and down

trachea, mainstem bronchi, bronchioles, alveoli, alveolar ducts, lungs,

191
Q

function of the nose

A

humidifies, warms, and filters inspired air

192
Q

function of sinuses

A

air-filled cavities within hollow bones that surround nasal passages and provide resonance during speech

193
Q

pharynx

A

passageway for respiratory, digestive tracts located behind oral and nasal cavities

divided into naso-, oro-, and laryngopharynx

194
Q

if cannot breathe through nose, air goes…

A

straight to lungs. allergens not filtered, air not warmed or humidified nearly as much

195
Q

larynx

A

located behind pharynx at the root of the tongue

contains vocal chords (2 pairs with opening between the two called the glottis)

196
Q

glottis

A

between 2 pairs of vocal chords

fundamental role in coughing, which is the most fundamental defense mechanism of the lungs

197
Q

most fundamental defense mechanism of lungs

A

coughing (glottis)

198
Q

epiglottis

A

leaf-shaped elastic flap over larynx that prevents food, liquids from entering the tracheobronchial tree.
closes over glottis to block off during swallowing.

199
Q

what has led to the reduction in # of cases of epiglottitis we see now?

A

vaccinations, specifically HIB vaccine.

200
Q

trachea

A

located in front of the esophagus

branches into the left and right mainstream bronchi @ the carnia

201
Q

carnia

A

location where trachea branches into left and right mainstream bronchi

202
Q

mainstem bronchi

A

starts @ carnia
right is slightly wider, shorter, more vertical
divide into secondary, lobar bronchi that enter each lobe in lungs
ciliated to propel mucus upward for expelling, swallowing

203
Q

bronchioles

A

branch out from secondary/lobar bronchi and subdivide into small terminal and respiratory bronchioles

no cartilage
depend on elastic recoil of lungs for potency
not ciliated
do not participate in gas exchange

204
Q

acinus/acinii

A

term used to indicate structures distal to the terminal bronchiole

205
Q

alveolar ducts

A

branch off from the respiratory bronchioles and contain sacs with clusters of alveoli that are the site for gas exchange

206
Q

type II alveolar cells

A

produce surfactant (phospholipid protein) that lubricates lungs, reduces surface tension so that alveoli don’t collapse

207
Q

lungs (location)

A

in pleural cavity in the thorax
extend from above clavicles to diaphragm
right lung (3 lobes) larger than left (2 lobes)

208
Q

why is the left lung narrower than the right?

A

to accommodate for the heart

209
Q

what innervates the respiratory structures?

A

phrenic, vagus, and thoracic nerves

210
Q

parietal pleura

A

lines inside of the thoracic cavity, including upper surface of diaphragm

211
Q

visceral pleura

A

covers pulmonary surfaces

212
Q

between visceral and parietal pleura

A

A thin fluid layer (produced by the cells lining the pleura) lubricates the visceral pleura and the parietal pleura so they can glide smoothly, painlessly during respiration

213
Q

pulmonary circulation system

A

deoxygenated blood from heart > oxygenated blood back to heart

214
Q

accessory muscles for respiration include…?

A

1) scalene muscle to elevate 1st two ribs
2) sternocleidomastoid muscles to raise sternum
3) trapezius and pectoralis muscle to fix shoulders

215
Q

process of respiration

A

diaphragm contracts (descends into abdominal cavity), creating negative pressure, which draws air from location of greater pressure (atmosphere) into lungs with lower pressure. @ lungs, air passes through terminal bronchioles into alveoli. gas exchange occurs. diaphragm, IC muscles relax and lungs recoil creating positive pressure, so air (plus waste) moves from alveoli > lungs > atmosphere.

216
Q

effective gas exchange depends on…?

A

respiration, ventilation (gas exchange), and perfusion (blood delivering O2 to tissues)

217
Q

ventilation

A

gas exchange @ alveoli (to capillaries, circulation)

218
Q

perfusion

A

gas exchange @ tissues (from capillaries to cell tissues)

219
Q

O2 transport, CO2 transport process

A

O2 carries to tissues in circulation to capillaries > enters tissues via diffusion through thin walls of capillaries > enters interstitial fluid and diffuses into cell tissues > O2 used by mitochondria > CO2 diffuses from cell tissues into interstitial space, then into capillaries and eventually alveoli > CO2 expelled with small amounts of water into atmosphere upon expiration

220
Q

respiration vs. ventilation

A

respiration: gas exchange bt atmospheric air and blood/cells of body (gas exchange)
ventilation: physical movement of thoracic cage and diaphragm to inc/dec capacity of chest and allow for air movement in/out of lungs (mechanics of air movement)

221
Q

air resistance is determined by…

A

radius of airway, lung volume, airflow velocity

obstruction!

222
Q

causes of increased air resistance

A
  • -contraction of bronchial smooth muscle (asthma)
  • -thickening bronchial mucosa (chronic bronchitis)
  • -obstruction of airway by foreign body/mucus/tumor
  • -loss of lung elasticity (emphysema, COPD)
223
Q

compliance

A

the elasticity and expandability of lungs and thoracic structures

224
Q

increased compliance occurs when…?

A

lungs become over distended, like with emphysema

225
Q

decreased compliance occurs when…?

A

lungs, thorax are still (i.e. obesity, pneumothorax, hemothorax, fibrosis, pleural effusion, ARDS)

requires greater energy to achieve normal levels of ventilation

226
Q

tidal volume

A

Volume of air inhaled and exhaled with each breath

227
Q

inspiratory reserve volume

A

Maximum volume of air that can be inhaled after a normal inhalation

228
Q

expiratory reserve volume

A

Maximum volume of air that can be exhaled forcibly after normal exhalation

229
Q

residual volume

A

Volume of air remaining in the lungs after maximal exhalation
(cannot be measured, only calculated)

230
Q

vital capacity

A

Maximum volume of air exhaled from point of maximum inspiration

231
Q

inspiratory capacity

A

Maximum volume of air inhaled after normal expiration

232
Q

functional residual capacity

A

Volume of air remaining in the lungs after normal expiration

233
Q

total lung capacity

A

Volume of air in the lungs after maximum inspiration

234
Q

when is the best time of day to obtain sputum samples?

A

early in the morning before pt has had anything to eat or drink

235
Q

pulmonary function tests

A

Used to aid in the diagnosis of chronic respiratory disease

Measure FVC, FEV1, FEV1/FVC ratio, FEF25-75

236
Q

pulmonary diffusion

A

O2 and CO2 are exchanged from areas of high concentration to areas of low concentration @ the air-blood interface

237
Q

pulmonary perfusion

A

actual blood flow through the pulmonary vasculature
blood pumped into lungs by pulmonary artery

influenced by: alveolar pressure, pulmonary artery pressure, gravity

238
Q

ventilation/perfusion balance

A

measured by the V/Q ratio
alveolar ventilation/ cardiac output
V = ventilation (air > alveoli)
Q = perfusion (blood > alveoli)

239
Q

alterations in ventilation occur with…?

A

(plenty of blood but not air)

airway blockages, local changes in lung compliance, gravity

240
Q

alterations in perfusion occur with…?

A

(plenty of air but not blood)

pulmonary embolism, alveolar pressure, gravity

241
Q

primary ways to change the V/Q ratio

A

change ventilation or change perfusion

242
Q

V/Q under normal conditions

A

(4 L/min) // (5 L/min)

243
Q

link between V/Q ration and ABG?

A

the ratio 4/5 (0.8) gives us our normal level for blood gasses

244
Q

V/Q imbalance occurs as a result of…?

A

inadequate ventilation, inadequate perfusion, or both

245
Q

V/Q scan

A

use dye to show how much air is moving in lungs. black = good.

helpful to dx obstructions, PE (but takes too long–45min– to be best test for PE)

246
Q

bronchodilator challenge

A

Do PFT. Give albuterol (bronchodilator). Wait 15 min. Repeat PFT. 12+% improvement is diagnostic for asthma (means bronchioles were constricted before, then got better with med). If doesn’t change, know to look at other dx (COPD, restrictive airway disease, pulmonary fibrosis)

247
Q

Methacholine/histamine/mannitol challenge

A

Do PFT. Gradually give mannitol/ methacholine/ histamie to “induce” asthma symptoms in those who may be prone to exacerbations. Used mostly in military to determine if fit for service in certain areas

248
Q

prednisone challenge

A

same as bronchodilator challenge, but use steroids instead of albuterol

249
Q

GI issue that causes many of the same symptoms as asthma

A

GERD (gastroesophageal reflux disease)

250
Q

affects of chronic acid reflux

A

when you have acid @ esophagus, lungs constrict to prevent anything from getting in them. induces cough. with chronic acid reflux, lungs constantly constriction, person coughing with reflux, feel like they can’t breathe. PPI may or may not help.

251
Q

O2-hemoglobin dissociation curve

A

When pressure of O2 is higher, hemoglobin binds to O2 better. As it drops, O2 sat drops quickly (trying to get more O2 to tissues).
When you hit just below 80, it start to dump all of the oxygen. So, as patients start to desaturate, can go downhill rapidly.

252
Q

What causes O2-hemoglobin curve to shift to right (decrease in affinity of hemoglobin for O2)?

A

inc in temp
inc in PCO2
dec in pH

253
Q

OXYhemoglobin dissociation curve

A

shows relationship between PaO2 and SaO2.
% saturation affected by:
CO2, H+ concentration (pH), temperature, 2,3-diphosphoglycerate

254
Q

dyspnea

A

sensation of shortness of breath

common with cardiac and pulmonary diseases

255
Q

what are some causes of sudden onset dyspnea?

A

PE
ACS (acute coronary syndrome)
Pneumothorax
aspiration

256
Q

acute episodes of dyspnea are called _____ and associated with _____

A

bronchospasms; asthma

257
Q

chronic dyspnea is associated with…?

A

COPD

258
Q

orthopnea

A

SOB when lying flat

259
Q

orthopnea is a common indication of…?

A

heart failure

260
Q

nocturnal dyspnea is associated with…?

why

A

heart failure; asthma

serum cortisol (protects against inflammation) levels drop at night

261
Q

cough

A

involuntary response to mechanical or chemical stimulation of the bronchial tree

can occur as a result of airway blockage

262
Q

chronic coughs are generally due to…?

A

infection, inflammation, GERD, bronchospasm, heart failure, COPD, asthma

263
Q

expectoration

A

coughing up sputum

264
Q 
color indication w/ sputum:
clear, thin
profuse, yellow/green, thick
rusty, pink tinged
hemoptysis
grey-tinged
A

clear, thin: normal
yellow/green/thick: infection
rusty, pink tinged: minor bleeding from cough
hemoptysis: large acts blood (TB, cancer, blood thinner)
grey-tinged: tobacco smoke

265
Q

hemoptysis

A

production of sputum that contains blood

important! differentiate between blood @ sputum (bright red) vs GI bleed in vomit (dark, coffee-colored)

266
Q

atelectasis

A

alveolar collapse
Complete or partial collapse of a lung or lobe of a lung — develops when the tiny air sacs (alveoli) within the lung become deflated

267
Q

common cause and process of atelectasis?

A

patients not taking deep enough breaths (bed bound, infection, pain, surgery, etc)

process: ventilation-perfusion mismatch. not getting enough air deep in lungs and they collapse. don’t have cilia, so if collapse, bronchioles become petri dishes for infection

268
Q

what can you do to help pt. if worried about atelectasis?

A 
breathing exercises
inspiration spirometry (hourly, ideally)
have them sit, stand, walk
make them do breaths when you assess lung sounds
talk, laugh
269
Q

alveolar fibrosis

A

thickening of alveolar wall

270
Q

emphysema

A

alveolar-capillary destruction

271
Q

interstitial edema

A

swelling, increased fluid @ interstitial space between capillary, alveoli

272
Q

pneumonia

A

alveolar consolidation (fill with fluid)

273
Q

pulmonary edema

A

inc. fluid at lungs. frothy secretions.

274
Q

URIs

A 
upper respiratory infections
commonly caused (50%) by rhinoviruses
275
Q

incubation period for URIs, process

A

24-72 hours incubation
scratchy, sore throat
sneezing, rhinorrhea, nasal obstruction, malaise
temp usually normal with rhinovirus, coronavirus
nasal secretions start watery, thicken
cough mild, lasts 2 weeks
most symptoms resolve in 10 days

276
Q

Do mucopurulent secretions indicate bacterial superinfection @ respiratory system?

A

no! normal with viral infections.

277
Q

rhinitis

A

Inflammation of the mucous membranes of the nose

278
Q

allergic vs nonallergic rhinitis

A

allergic: true IgE hypersensitivity to allergen (pollen, dust, mold)

non-allergic: body interprets inhaled irritants (smoke, odors, fumes) as a cold, dry air, so reacts with runny nose,, congestion

279
Q

rhinosinusitis (acute, chronic)

A

Inflammation of paranasal sinuses and nasal cavity

acute: pts really sick, can lead to complications if untreated (osteomyelitis, cysts, meningitis, brain abscess)
chronic: more subtle symptoms

280
Q

why are sinusitis issues hard to treat?

A

hard to get meds to them
warm dark cavities
not much blood flow to deliver meds

281
Q

pharyngitis

A

painful inflammation of the pharynx
(strep throat)
usually viral infections

282
Q

chronic pharyngitis

A

persistent inflammation of pharynx
causes: occupational environment, overuse voice, chronic cough, habitual alcohol/tobacco use
chronic post-nasal drip feel, irritation @ throat

283
Q

tonsillitis

A

is inflammation of the tonsillar tissue (lymph tissue) and is managed with either antibiotics or supportive therapy depending upon the cause of inflammation

284
Q

adenoiditis

A

inflammation of adenoids (lymphatic tissue near the center of the posterior wall of the nasopharynx)

285
Q

peritonsillar abscess

A

Acutely ill patient
May drool because of inability to swallow
Often seen in the ED setting because of rapid onset and severe pain

286
Q

laryngitis

A

inflammation of the larynx caused by voice abuse, environmental exposure to irritants, vocal chord infection, GERD

287
Q

symptoms of laryngitis

A

hoarseness, severe cough, dry & sore throat

288
Q

Obstructive sleep apnea

A

Intermittent absence of airflow through the nose and mouth during sleep. potentially life threatening. leading cause of daytime sleepiness. Inc. risk for heart disease, HTN

Dx w/ STOP: snoring, tired, observed apnea, blood pressure

Tx: CPAP, removal of tonsils

289
Q

risk factors for sleep apnea

A

male, increasing age, obesity, large neck (>16-17 in), use of alcohol/CNS depressants

290
Q

acute bronchitis

A

inflammation @ bronchi

causes: URI (pneumonia, influenza, aspergillus), toxic gas, chemical inhalation, impaired immune system, smoking
symptoms: cough, fever/chills, night sweats, headache, tired, SOB, wheezing, productive cough

291
Q

pneumonia

A

inflammation of lung parenchyma by bacteria, mycobacteria, fungi, viruses.
can be community acquired, hospital acquired, healthcare associated, or ventilator acquired types.

292
Q

most common cause of death from infectious disease in the US?

A

pneumonia

293
Q

most common pathogen with community acquired pneumonia

A

S. pneumoniae

294
Q

type of pneumonia that appears in interstitial space rather than alveoli

A

mycoplasma pneumoniae (droplet transmission)

295
Q

virus that causes most pneumonia in elderly or co-morbid populations

A

H. influenzae

296
Q

viruses responsible for causing most community pneumonia also responsible for most cases of…?

A

acute bronchitis

297
Q

common pathogens that cause hospital/health care acquired pneumonia

A

legionella, s. aureus, G- baccili

298
Q

MDR pneumonia seen usually in what setting?

A

hospital or healthcare acquired

299
Q

clinical presentation of pneumonia

A

rapid onset, fever, productive cough (rust colored from capillary breakdown or purulent), CRACKLES or fine RALES @ affected area, pleuritic pain w/ cough, pleuritic friction rub, SOB, cyanosis, inc. tactile fremitus, dullness w/ percussion, egophony (E becomes A when speaking)

300
Q

complications with pneumonia

A

pleuritis, pleural effusion, empyema, lung abscess, bacteremia

301
Q 
pneumonia spreads to 
brain
heart
liver
...what are these called?
A

meningitis
endocarditis
peritonitis

302
Q

risk factors for pneumonia

A

more mucus production (COPD, smoking), immunosuppression, smoking, immobility, depressed cough reflex, aspiration, supine position, alcohol intoxication, anesthesia, older, RT w/ dirty equipment

303
Q

tuberculosis

A

infection of M. tuberculosis @ lung parenchyma.
huge PH problem
associated with poverty, overcrowding, malnutrition, poor housing, lack healthcare
est. 1/3 worlds population
likes to live @ top of lungs
can be active or latent

304
Q

clinical manifestations of active TB

A 
insidious (gradual onset w/o symptoms)
low grade fever 
cough
night sweats
fatigue
weight loss
may present for weeks, months
305
Q

diagnostic tests for TB

A 
tuberculin skin test
sputum smears
sputum cultures
chest X ray
bronchoscopy
306
Q

lung abscess

A

necrosis of parenchyma caused by microbial infection (generally aspirated)
>2 cm on xray

307
Q

pleural effusion

A

collection of fluid in the pleural space that “squishes” lung
usually secondary to other diseases (heart failure, TB, pneumonia, etc.)
if large, can cause dyspnea

tx with chest tube or needle @ pleural space (NOT LUNG) to get fluid out

308
Q

empyema

A

Accumulation of thick, purulent fluid within the pleural space where infection is located

usually complication of pneumonia, abscess

309
Q

ARF (acute respiratory failure)

A

Sudden and life-threatening deterioration of gas exchange function of the lung

Lungs are not able to oxygenate the blood and remove carbon dioxide adequately to meet the body’s needs even at rest.

Consequence of severe respiratory dysfunction NOT A DISEASE

310
Q

causes of impaired airway function with acute respiratory failure

A

airway obstruction (spasm, obstruction), respiratory disease (asthma, emphysema, chronic bronchitis), neurologic (spinal cord injury, overdose, stroke), chest wall trauma (flail chest, pneumothorax), alveolar disorders (pneumonia, COPD), pulmonary edema (CHF, ARDS, drowning)

311
Q

early vs late signs of ARF

A

early: restlessness, fatige, headache, SOB, “air hunger”, inc HR, inc BP
late: confusion, lethargy, inc HR, inc RR, central cyanosis, sweating, respiratory arrest

312
Q

how to correct ARF?

A

Treat the underlying cause!!

313
Q

ARDS

A

acute respiratory distress syndrome
spectrum of diseases
key component: inflammation
critically ill: intercostal retractions, crackles

314
Q

how to differentiate between ARDS and cariogenic pulmonary edema?

A

BNP (brain natriuretic peptide) labs

315
Q

key component of ARDS

A

inflammation!
damage to alveolar epithelium and capillary endothelium
fluid @ alveoli

316
Q

ABGs with ARDS

A

dec PO2, inc SOB

317
Q

s/s ARDS

A 
inc RR
SOB
retractions
hypoxia
inc HR
dec pulmonary compliance
318
Q

COPD

A

chronic obstructive pulmonary disease

umbrella term for emphysema, chronic bronchitis

319
Q

1 contributing factor for COPD?

A

smoking; paralyzes cilia. induces goblet cells to make mucus, but can’t move it, so cough (smokers cough)

320
Q

symptoms of COPD

A

cough, wheeze, SOB, chest tightness, smothering sensation, recurrent/chronic bronchitis, activity intolerance

321
Q

chronic bronchitis

A

large airways = overgrowth, enlargement of mucus producing glands
small airways = inc. mucus and inflammation producing cells, inc. smooth muscle
some responsiveness to therapy

322
Q

emphysema

A

Dec. alveolar-capillary gas exchange
Loss of elastic recoil
Damage @ alveolar ducts and bronchioles
Low responsiveness to therapy

323
Q

Bronchiectasis

A

Chronic, irreversible dilation of the bronchi and bronchioles that results from destruction of muscles and elastic connective tissue.

caused by: obstruction, injury, long-term pulm infections, congenital disorders, genetics (CF), immune dysfunction

A lot of really thick mucus. Scarred airways. Irreversible. Cant treat. Manage symptoms but that’s it.

324
Q

asthma

A

A chronic inflammatory disease of the airways with the following clinical features

  • -episodic or chronic obstruction
  • -bronchial hyper-responsiveness to triggers
  • -partial reversibility of obstruction
  • -exclude alternative dx
325
Q

______ may be the only symptom present in some pts with asthma

A

cough

326
Q

cough without _______ is often not asthma

A

wheeze

327
Q

asthma triggers

A 
70% allergens
resp infections
cold/ humid weather
exercise
stress
GERD
pregnancy
medications (BB, NSAIDS)
environment/ occupational irritants
328
Q

CF

A

cystic fibrosis

Autosomal recessive disorder that affects epithelial cells of the respiratory, gastrointestinal, and reproductive tracts and leads to abnormal exocrine gland secretions.

Nursing-Sem 1 (13 decks)

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