Patho Exam 2 Flashcards
largest organ of the body
skin
functions of the skin
temperature control/regulation barrier protection secretion/absorption vitamin D production immunological surveillance indicative of disease process, overall health
how to increase absorption rate @ skin?
put medication of skin, occlude (cover). will increase rate of absorption, effects.
approximately what percentage of PCP visits are related to skin conditions?
50%
why are skin disorders more likely with age?
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)
____% of Americans have a skin condition; ____% of older adults have some form of skin disorder
30%; 90%
epidermis
aka stratum germinativum
outermost layer of skin
few cells thick
stratum germnivatum
two layers: basal and squamous
contains column-shaped basal cells, move upward towards skin and flatten, die, shed
stratum granulosum
contains more keratinocytes moving upward toward surface
stratum lucidum
only on palms of hands, soles of feet
stratum coreum
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)
keratin
insoluble fibrous protein that forms barrier of skin
principle hardening protein of hair, nails
has the ability repel pathogens and prevent excessive fluid loss
three specialized cells @ epidermis
melanocytes (produce pigment) Langerhans cells (1st line immune defense) Merkel cells (mechanoreceptors, transmit stimuli, involved in f'n of touch)
largest portion of skin
dermis
dermis
largest portion of skin
provides strength, structure
includes connective tissue, blood capillaries, oil/sweat glands, nerve endings, hair follicles
hypodermis (subcutaneous tissue)
innermost layer of skin primarily adipose tissue thickness varies by person vital for body temp regulation provides cushioning between skin/muscle/bone
how does skin control/regulate temp?
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
80% of heat loss occurs via the…?
skin
how does the skin provide barrier protection to body?
- -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
how skin is involved in excretion
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
what waste products are excreted @skin?
water, heat, salt, carbon dioxide, ammonia, and urea
what is absorbed @ skin?
- -fat-soluble substances (Vit ADEK)
- -O2, CO2, organic solvents, CCl4, heavy metal salts, poison ivy/oak oils
- -fat soluble medications (skin permeable to them)
how is skin involved in the production of Vit D?
1st step in vit D synthesis is @ skin: 7-dehydrocholesterol converted to cholecalciferol (precursor to vit D)
–then, synthesis @ liver, kidney
what does vitamin D do?
- -regulates Ca2+ and P (phosphorous) metabolism
- -facilitates calcium absorption from the intestine
- -affects bone cell development
innate immune response @ skin
- -keratinocytes regulate immune response and secrete inflammatory mediators
- -Lagerhorn cells detect foreign antigens and present them to lymphocytes (adaptive immune response)
how does skin act as mirror for underlying disease processes, overall health?
changes in skin color, texture, temperature swelling, diaphoresis, etc. commonly indicate underlying disease processes
people who lack sufficient oxygen pay present as what color?
cyanotic (blue)
people with excess bilirubin may present as what color?
yellow, jaundiced (liver disease)
people with erythema pay present as what color?
extreme redness (capillary engorgement)
people presenting with pallor indicate?
extreme paleness (anemia or shock)
atrophy
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
bulla
large blister (greater than 0.5 cm in diameter) INFECTION, contact irritants, IMMUNE RESPONSE, and systemic health conditions may cause bullae
crust
dried yellowish and yellow-brown exudate on the skin…the result of drying of plasma or exudate on the skin.
erythema
- -reddened skin
- -area blanches with pressure
- -caused by hyperemia (increased blood flow) in superficial capillaries
- -occurs with any skin injury, infection, or inflammation.
excoriation
scratches that break the skin’s surface
fissure
crack in skin that breaks through keratin barrier
induration
hardening or thickening of skin
keloid
irregular, elevated scar tissue formed by excessive collagen growth during wound healing
Lichenification
hardening or thickening of the skin with markings; often develops from repeated trauma (i.e. scratching)
macule
defined, flat area of altered pigmentation
papule
raised, well-defined lesion smaller than 0.5 cm
plaque
raised, flat-topped lesion larger than 2cm in diameter
nodule
solid lump greater than 0.5 cm in diameter
purpura
purplish lesion caused by free red blood cells in the skin. Does NOT blanch on pressure and may be nodular.
pustule
papule filled with pus
scale
fragment of dry skin
scar
permanent replacement of normal skin with connective tissue
telangiectasia
fine, irregular red lines produced by dilatation of the capillaries
ulcer
loss of epidermal and dermal tissue
vesicle (blister)
blister smaller than 0.5 cm in diameter
wheals/ urticaria
transient pink, itchy, elevated papules that evolve into irregular red maculo-papular patches //hives
phases of wound healing (list)
inflammatory, fibroblastic, maturation
inflammatory phase of wound healing (describe)
begins at time of injury
lasts 3-5 days
characterized by local edema, pain, redness, warmth
fibroblastic phase of wound healing (describe)
begins the 4th day after injury
lasts 2-4 weeks
characterized by formation of scar and granulation (wound bed) tissues
maturation phase of wound healing (describe)
begins as early as 3 weeks after injury
may last 1 year
scar tissue becomes thinner, more firm, and inelastic on palpation
different levels of intention (list, describe)
- -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.
granulation tissue is indicative of what intention of healing?
second
types of exudate
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
skin cancer
malignant lesion @ skin, may or may not metastasize
risk factors for skin cancer
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
basal cell cancer
arises from basal cells in epidermis
metastasis rare
underlying tissue damage can progress to organ tissues
treat with removal
squamous cell carcinoma
tumor of epidermal keratinocytes
can infiltrate surrounding tissues
can metastasize to lymph nodes
treatable, but often caught late
melanoma
- -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
ABCDEs of melanoma
A: asymmetry B: borders irregular C: different colors or color change D: diameter > 0.5 cm E: evolution (changes over time)
level I melanoma
cancer cells extend to epidermis
level II melanoma
cancer cells extend to papillary dermis
level III melanoma
involves layers down to papillary-reticular dermal interface
level IV melanoma
involves layers down to the reticular dermis
level V melanoma
involves layers down to subcutaneous tissue
three C’s to use when assessing nails
color, consistency, configuration
alopecia
loss of hair from any cause
i.e. male pattern baldness (androgenic alopecia–loss of androgen and shrinking of hair follicle)
what to look for in hair assessment
color, texture, distribution, loss, other changes (unusual patterns, etc.)
hirstuism
in women, increased hair distribution on face, chest, shoulders due to post-menopausal levels of estrogen (decreased)
diagnostic evaluations of skin
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)
primary functions of the cardiovascular and circulatory systems
- -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
only artery that carries deoxygenated blood
pulmonary artery
only vein that carries oxygenated blood
pulmonary vein
circulation of blood
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
left side of heart pumps blood to…
systemic circulation
right side of heart pumps blood to…
the lungs
high pressure side of heart
left (systemic circulation, needs to transport longer distance) @ 90-100 mmHg
low pressure side of heart
right (pulmonary circulation, shorter distance, slower flow) @ 12 mmHg
valves act reciprocally in order to…
keep blood flowing in same direction
do arteries or veins have valves?
veins, to keep blood from back flowing (have to push blood upwards and work against gravity)
endocardium
innermost layer of heart
endothelial tissue with small vessels and bundles of smooth muscle
myocardium
- -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
what is the difference between sarcomeres @ cardiac muscle versus skeletal muscle?
sarcomeres are shorter, more compact @ myocardium than @ skeletal muscle
what does syncytium describe (in reference to myocardium)
all cells behave as a single unit and not as individuals
what regulates calcium mediated contractions?
troponin and tropomysin
epicardium
- -outermost layer of heart and visceral layer of pericardium
- -made of squamous cells overlying connective tissue
pericardium
- -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)
pericardial space, fluid
space between pericardium layers, contains serous fluid for lubrication, allows heart to move easily during contractions
cardiac or pericardial tampenade
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
atrioventricular (AV) valves
tricuspid and mitral–between atria and ventricles
semilunar valves
pulmonic and aortic values
chordae tenodonae and valve opening/closing
papillary muscles relax to pull chordae tendonae and open valves and contract to relax chordae tenodonae and close valves
cardiac cycle (1 heartbeat)
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
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)
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.
describe what happens @ coronary vessels during systole and diastole
@ systole: blood is ejected into aorta
@diastole: blood flows back into CAs.
does blood get O2 during systole or diastole?
diastole
widow-maker
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.
what is a main contributor to coronary artery disease?
hypertension!
RCA
right coronary artery
supplies blood, O2 to right atrium, most of right ventricle and inferior left ventricle
LCA
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
coronary veins
lie superficial to arteries
most empty into the largest, Coronary Sinus, which opens directly into right atrium
anterior cardiac veins empty into right atrium
conduction system @ heart
SA node (pacemaker, 60-100bpm) AV node (backup, 40-60bpm) Bundle of His / AV bundle Purkinje fibers (quaternary backup, like 20bpm)
what makes the heart beat?
depolarization and depolarization of heart muscles. impulse travel.
p wave represents
atrial depolarization (contraction)
QRS complex represents
ventricular depolarization (contraction) and atrial re-polarization
T wave represents
ventricular repolarization
ECG visualizes…
electrical activity/impulses @ heart
PR interval represents
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.
steps for reading ECG
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)
if don’t have a P wave, you know what?
impulse not originating @ SA node
“fat” QRS waves mean what?
took a long time for the ventricles to depolarize (muscle damage “roadblock”)
impulse may be coming from ventricles
peak T waves are present with what?
hyperkalemia
cardiac output
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)
Starling’s law
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.
preload
volume coming into ventricles (end diastolic pressure)
afterload
resistance left ventricle must overcome to circulate blood
preload is increased with…?
hypervolemia, regurgitation @ cardiac valves
after load is increased with…?
hypotension, vasocontriction
inc. afterload = inc. cardiac workload
components of cardiac performance
cardiac output, myocardial contractility, cardiac output, ejection fraction
myocardial contractility
depends on stroke volume and preload
affected by inotropic agents, O2 and CO2 levels
ejection fraction
% of ventricular volume ejected with each systole
what determines stroke volume?
preload, after load, and contractility
formula for cardiac output
stroke volume X HR
BP = ______ x ______
cardiac output X peripheral resistance
difference between arteries and veins
veins have valves to prevent back flow
layers of vessels
lumen
tunica intima
tunica media
tunica externa aka adventitia
adventitia is what?
outermost layer of vessels
lumen is what?
innermost layer of vessels
lumen aka “emptiness” b/c inside space of a tubular structure
varicose veins
a vein in which blood has pooled
distended, tortuous, palpable
what causes varicose veins
trauma or gradual venous distension
risk factors for varicose veins
age, female, family hx, obesity, pregnancy, DVT, prior leg injury, standing on feet for long periods
having varicose veins increases your risk for…?
DVT
chronic venous insufficiency
inadequate venous returns over longer period of time due to varicose veins or valvular incompetence
may lead to venous stasis ulcers (ankles)
signs of venous insufficiency
edema @ lower legs, ankles, feet
varicose veins
skin changes & color
skin ulceration @ ankles
thrombus formation @ veins
obstructs venous flow and increases venous pressure
Factors that influence: triad of virchow, cancer, surgery, trauma, immobility, heart failure
triad of virchow
factors leading to formation of thrombus @ veins
includes: venous stasis, venous endothelial damage, and hypercoagulable states
biggest risk factor for developing a clot?
immobility
thrombus vs. embolism
thrombus = stationary clot embolism = broken off clot that is moving through circulation
hypertension
high BP–consistent elevation of arterial BP
“silent killer”
140/90
primary and secondary types
primary HTN
essential, idiopathic HTN
genetic, environmental factors
92-95% with HTN have this kind
risk factors: high Na2+, inflammation, obesity, insulin resistance
secondary HTN
caused by systemic disease processes that raise peripheral vascular resistance or cardiac output
biggest cause of secondary HTN? other causes?
renal disease
others: brain tumors, drugs
why is HTN called the “silent killer”
involves so many complications if not controlled, such as kidney failure, blood vessel damage (atherosclerosis), stroke, vision loss, heart attack, and bone loss
BP normal BP prehypertensive BP stage 1 HTN BP stage 2 HTN BP HTN crisis
normal: >120/ > 80
prehypertensive: 120-139/ 80-89
stage 1 HTN: 140-159 / 90-99
stage 2 HTN: 160+/ 100+
crisis: 180+ / 110+
malignant HTN
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
orthostatic hypotension
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
aneurysm
Local dilation or outpouching of a vessel wall or cardiac chamber
can cause aortic dissection (tears longitudinally) or rupture
area most susceptible to aneurysm
aorta, esp abdominal
factors contributing to development of aneurysm
hypertension, atherosclerosis
embolism
Bolus of matter that is circulating in the bloodstream (like dislodged clot, air bubble, amniotic fluid, fat deposit, bacteria, cancer cells, foreign substance)
thromboembolus
small piece of blood clot that breaks off and travels through circulation. can lodge elsewhere and cause serious complications (pulmonary, brain)
atherosclerosis
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
progression of atherosclerosis
endothelial inflammation cell proliferation macrophages migrate, adhere LDL oxidation, form foam cells fatty streak fibrous plaque complicated plaque
risk factors for atherosclerosis
diabetes, smoking, hyperlipidemia, dyslipidemia, HTN
peripheral artery disease
atherosclerotic disease of arteries that perfuse the limbs
common sites for PAD
iliac artery, femoral artery, popliteal artery, tibial arteries
coronary artery disease
any vascular disorder that narrows/occludes the coronary arteries leading to myocardial ischemia–local, temporary ischemia
most common cause: atherosclerosis
risk factors for CAD (modifiable and non modifiable)
modifiable: dyslipidemia, HTN, smoking, diabetes, obesity, sedentary lifestyle, fast food
nonmodifiable: older age, family hx, being male, post menopausal women
ECG sign of CAD
inverted T waves
acute coronary syndromes include..
unstable angina, myocardial infarction
unstable angina
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
myocardial infarction
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)
structural changes @ heart seen with MI
myocardial stunning
“hibernating” myocardium
myocardial remodeling
labs for measuring MI
troponin I level (only found @ myocardium)
normal < 0.4
CPK-MB: <5 normal (slower to show signs than troponin I)
manifestations of MI
sudden, severe chest pain–may radiate
nausea, vomiting
sweating
SOB
complications associated w/ MI
Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability
ECG sign of MI
elevated ST segment (more elevated = more damage)
disorders of the pericardium include..?
heart wall disorders including acute pericarditis, pericardial effusion (tamponade), and constrictive pericarditis
constrictive pericarditis
results from scarring & consequent loss of elasticity of pericardial sac
pericardial effusion
aka pericardial tamponade
fluid builds up in pericardial sac and puts pressure on heart
cardiomyopathies include…?
disorders of the myocardium
congestive, hypertrophic, and restrictive
valvular disorders
disorders of the endocardium valvular stenosis (aortic, mitral) valvular regurgitation (aortic, mitral, tricuspid) mitral valve prolapse
stenosed valve vs. regurgitant valve
stenosed: doesn’t open all the way
regurgitant: doesn’t close all the way
infective endocarditis
inflammation of the endocardium
caused by : pathogens (bacteria, virus, fungi, rickettsiae, parasites)
pathogenesis: endocardium damaged > blood-borne pathogen adheres > pathogen proliferates (vegetations)
manifestations of infective endocarditis
fever new, change in cardiac murmur petechial lesions (skin, conjunctiva) Osler nodes (painful lesions, fingers, toes) Janeway lesions (non-painful hemorrhagic lesions @ palms, soles)
heart failure
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
Left heart failure
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
Systolic heart failure
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
Diastolic heart failure
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
symptoms of left sided heart failure
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
right sided heart failure
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
symptoms of right sided heart failure
fatigue, inc. peripheral venous pressure, ascites, enlarged liver/spleen, JVD, anorexia and GI distress, swelling hands and fingers, dependent edema
primary function of respiratory system
provide O2 for metabolism @ tissues
remove CO2, waste from metabolism
secondary functions of respiratory system
facilitate sense of smell produce speech maintain acid-base balance maintain body water levels (hydration) maintain body temp (heat balance)
upper respiratory system
trachea and up
nose, sinuses, pharynx, larynx, epiglottis
lower respiratory system
trachea and down
trachea, mainstem bronchi, bronchioles, alveoli, alveolar ducts, lungs,
function of the nose
humidifies, warms, and filters inspired air
function of sinuses
air-filled cavities within hollow bones that surround nasal passages and provide resonance during speech
pharynx
passageway for respiratory, digestive tracts located behind oral and nasal cavities
divided into naso-, oro-, and laryngopharynx
if cannot breathe through nose, air goes…
straight to lungs. allergens not filtered, air not warmed or humidified nearly as much
larynx
located behind pharynx at the root of the tongue
contains vocal chords (2 pairs with opening between the two called the glottis)
glottis
between 2 pairs of vocal chords
fundamental role in coughing, which is the most fundamental defense mechanism of the lungs
most fundamental defense mechanism of lungs
coughing (glottis)
epiglottis
leaf-shaped elastic flap over larynx that prevents food, liquids from entering the tracheobronchial tree.
closes over glottis to block off during swallowing.
what has led to the reduction in # of cases of epiglottitis we see now?
vaccinations, specifically HIB vaccine.
trachea
located in front of the esophagus
branches into the left and right mainstream bronchi @ the carnia
carnia
location where trachea branches into left and right mainstream bronchi
mainstem bronchi
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
bronchioles
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
acinus/acinii
term used to indicate structures distal to the terminal bronchiole
alveolar ducts
branch off from the respiratory bronchioles and contain sacs with clusters of alveoli that are the site for gas exchange
type II alveolar cells
produce surfactant (phospholipid protein) that lubricates lungs, reduces surface tension so that alveoli don’t collapse
lungs (location)
in pleural cavity in the thorax
extend from above clavicles to diaphragm
right lung (3 lobes) larger than left (2 lobes)
why is the left lung narrower than the right?
to accommodate for the heart
what innervates the respiratory structures?
phrenic, vagus, and thoracic nerves
parietal pleura
lines inside of the thoracic cavity, including upper surface of diaphragm
visceral pleura
covers pulmonary surfaces
between visceral and parietal pleura
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
pulmonary circulation system
deoxygenated blood from heart > oxygenated blood back to heart
accessory muscles for respiration include…?
1) scalene muscle to elevate 1st two ribs
2) sternocleidomastoid muscles to raise sternum
3) trapezius and pectoralis muscle to fix shoulders
process of respiration
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.
effective gas exchange depends on…?
respiration, ventilation (gas exchange), and perfusion (blood delivering O2 to tissues)
ventilation
gas exchange @ alveoli (to capillaries, circulation)
perfusion
gas exchange @ tissues (from capillaries to cell tissues)
O2 transport, CO2 transport process
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
respiration vs. ventilation
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)
air resistance is determined by…
radius of airway, lung volume, airflow velocity
obstruction!
causes of increased air resistance
- -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)
compliance
the elasticity and expandability of lungs and thoracic structures
increased compliance occurs when…?
lungs become over distended, like with emphysema
decreased compliance occurs when…?
lungs, thorax are still (i.e. obesity, pneumothorax, hemothorax, fibrosis, pleural effusion, ARDS)
requires greater energy to achieve normal levels of ventilation
tidal volume
Volume of air inhaled and exhaled with each breath
inspiratory reserve volume
Maximum volume of air that can be inhaled after a normal inhalation
expiratory reserve volume
Maximum volume of air that can be exhaled forcibly after normal exhalation
residual volume
Volume of air remaining in the lungs after maximal exhalation
(cannot be measured, only calculated)
vital capacity
Maximum volume of air exhaled from point of maximum inspiration
inspiratory capacity
Maximum volume of air inhaled after normal expiration
functional residual capacity
Volume of air remaining in the lungs after normal expiration
total lung capacity
Volume of air in the lungs after maximum inspiration
when is the best time of day to obtain sputum samples?
early in the morning before pt has had anything to eat or drink
pulmonary function tests
Used to aid in the diagnosis of chronic respiratory disease
Measure FVC, FEV1, FEV1/FVC ratio, FEF25-75
pulmonary diffusion
O2 and CO2 are exchanged from areas of high concentration to areas of low concentration @ the air-blood interface
pulmonary perfusion
actual blood flow through the pulmonary vasculature
blood pumped into lungs by pulmonary artery
influenced by: alveolar pressure, pulmonary artery pressure, gravity
ventilation/perfusion balance
measured by the V/Q ratio
alveolar ventilation/ cardiac output
V = ventilation (air > alveoli)
Q = perfusion (blood > alveoli)
alterations in ventilation occur with…?
(plenty of blood but not air)
airway blockages, local changes in lung compliance, gravity
alterations in perfusion occur with…?
(plenty of air but not blood)
pulmonary embolism, alveolar pressure, gravity
primary ways to change the V/Q ratio
change ventilation or change perfusion
V/Q under normal conditions
(4 L/min) // (5 L/min)
link between V/Q ration and ABG?
the ratio 4/5 (0.8) gives us our normal level for blood gasses
V/Q imbalance occurs as a result of…?
inadequate ventilation, inadequate perfusion, or both
V/Q scan
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)
bronchodilator challenge
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)
Methacholine/histamine/mannitol challenge
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
prednisone challenge
same as bronchodilator challenge, but use steroids instead of albuterol
GI issue that causes many of the same symptoms as asthma
GERD (gastroesophageal reflux disease)
affects of chronic acid reflux
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.
O2-hemoglobin dissociation curve
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.
What causes O2-hemoglobin curve to shift to right (decrease in affinity of hemoglobin for O2)?
inc in temp
inc in PCO2
dec in pH
OXYhemoglobin dissociation curve
shows relationship between PaO2 and SaO2.
% saturation affected by:
CO2, H+ concentration (pH), temperature, 2,3-diphosphoglycerate
dyspnea
sensation of shortness of breath
common with cardiac and pulmonary diseases
what are some causes of sudden onset dyspnea?
PE
ACS (acute coronary syndrome)
Pneumothorax
aspiration
acute episodes of dyspnea are called _____ and associated with _____
bronchospasms; asthma
chronic dyspnea is associated with…?
COPD
orthopnea
SOB when lying flat
orthopnea is a common indication of…?
heart failure
nocturnal dyspnea is associated with…?
why
heart failure; asthma
serum cortisol (protects against inflammation) levels drop at night
cough
involuntary response to mechanical or chemical stimulation of the bronchial tree
can occur as a result of airway blockage
chronic coughs are generally due to…?
infection, inflammation, GERD, bronchospasm, heart failure, COPD, asthma
expectoration
coughing up sputum
color indication w/ sputum: clear, thin profuse, yellow/green, thick rusty, pink tinged hemoptysis grey-tinged
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
hemoptysis
production of sputum that contains blood
important! differentiate between blood @ sputum (bright red) vs GI bleed in vomit (dark, coffee-colored)
atelectasis
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
common cause and process of atelectasis?
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
what can you do to help pt. if worried about atelectasis?
breathing exercises inspiration spirometry (hourly, ideally) have them sit, stand, walk make them do breaths when you assess lung sounds talk, laugh
alveolar fibrosis
thickening of alveolar wall
emphysema
alveolar-capillary destruction
interstitial edema
swelling, increased fluid @ interstitial space between capillary, alveoli
pneumonia
alveolar consolidation (fill with fluid)
pulmonary edema
inc. fluid at lungs. frothy secretions.
URIs
upper respiratory infections commonly caused (50%) by rhinoviruses
incubation period for URIs, process
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
Do mucopurulent secretions indicate bacterial superinfection @ respiratory system?
no! normal with viral infections.
rhinitis
Inflammation of the mucous membranes of the nose
allergic vs nonallergic rhinitis
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
rhinosinusitis (acute, chronic)
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
why are sinusitis issues hard to treat?
hard to get meds to them
warm dark cavities
not much blood flow to deliver meds
pharyngitis
painful inflammation of the pharynx
(strep throat)
usually viral infections
chronic pharyngitis
persistent inflammation of pharynx
causes: occupational environment, overuse voice, chronic cough, habitual alcohol/tobacco use
chronic post-nasal drip feel, irritation @ throat
tonsillitis
is inflammation of the tonsillar tissue (lymph tissue) and is managed with either antibiotics or supportive therapy depending upon the cause of inflammation
adenoiditis
inflammation of adenoids (lymphatic tissue near the center of the posterior wall of the nasopharynx)
peritonsillar abscess
Acutely ill patient
May drool because of inability to swallow
Often seen in the ED setting because of rapid onset and severe pain
laryngitis
inflammation of the larynx caused by voice abuse, environmental exposure to irritants, vocal chord infection, GERD
symptoms of laryngitis
hoarseness, severe cough, dry & sore throat
Obstructive sleep apnea
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
risk factors for sleep apnea
male, increasing age, obesity, large neck (>16-17 in), use of alcohol/CNS depressants
acute bronchitis
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
pneumonia
inflammation of lung parenchyma by bacteria, mycobacteria, fungi, viruses.
can be community acquired, hospital acquired, healthcare associated, or ventilator acquired types.
most common cause of death from infectious disease in the US?
pneumonia
most common pathogen with community acquired pneumonia
S. pneumoniae
type of pneumonia that appears in interstitial space rather than alveoli
mycoplasma pneumoniae (droplet transmission)
virus that causes most pneumonia in elderly or co-morbid populations
H. influenzae
viruses responsible for causing most community pneumonia also responsible for most cases of…?
acute bronchitis
common pathogens that cause hospital/health care acquired pneumonia
legionella, s. aureus, G- baccili
MDR pneumonia seen usually in what setting?
hospital or healthcare acquired
clinical presentation of pneumonia
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)
complications with pneumonia
pleuritis, pleural effusion, empyema, lung abscess, bacteremia
pneumonia spreads to brain heart liver ...what are these called?
meningitis
endocarditis
peritonitis
risk factors for pneumonia
more mucus production (COPD, smoking), immunosuppression, smoking, immobility, depressed cough reflex, aspiration, supine position, alcohol intoxication, anesthesia, older, RT w/ dirty equipment
tuberculosis
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
clinical manifestations of active TB
insidious (gradual onset w/o symptoms) low grade fever cough night sweats fatigue weight loss may present for weeks, months
diagnostic tests for TB
tuberculin skin test sputum smears sputum cultures chest X ray bronchoscopy
lung abscess
necrosis of parenchyma caused by microbial infection (generally aspirated)
>2 cm on xray
pleural effusion
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
empyema
Accumulation of thick, purulent fluid within the pleural space where infection is located
usually complication of pneumonia, abscess
ARF (acute respiratory failure)
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
causes of impaired airway function with acute respiratory failure
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)
early vs late signs of ARF
early: restlessness, fatige, headache, SOB, “air hunger”, inc HR, inc BP
late: confusion, lethargy, inc HR, inc RR, central cyanosis, sweating, respiratory arrest
how to correct ARF?
Treat the underlying cause!!
ARDS
acute respiratory distress syndrome
spectrum of diseases
key component: inflammation
critically ill: intercostal retractions, crackles
how to differentiate between ARDS and cariogenic pulmonary edema?
BNP (brain natriuretic peptide) labs
key component of ARDS
inflammation!
damage to alveolar epithelium and capillary endothelium
fluid @ alveoli
ABGs with ARDS
dec PO2, inc SOB
s/s ARDS
inc RR SOB retractions hypoxia inc HR dec pulmonary compliance
COPD
chronic obstructive pulmonary disease
umbrella term for emphysema, chronic bronchitis
1 contributing factor for COPD?
smoking; paralyzes cilia. induces goblet cells to make mucus, but can’t move it, so cough (smokers cough)
symptoms of COPD
cough, wheeze, SOB, chest tightness, smothering sensation, recurrent/chronic bronchitis, activity intolerance
chronic bronchitis
large airways = overgrowth, enlargement of mucus producing glands
small airways = inc. mucus and inflammation producing cells, inc. smooth muscle
some responsiveness to therapy
emphysema
Dec. alveolar-capillary gas exchange
Loss of elastic recoil
Damage @ alveolar ducts and bronchioles
Low responsiveness to therapy
Bronchiectasis
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.
asthma
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
______ may be the only symptom present in some pts with asthma
cough
cough without _______ is often not asthma
wheeze
asthma triggers
70% allergens resp infections cold/ humid weather exercise stress GERD pregnancy medications (BB, NSAIDS) environment/ occupational irritants
CF
cystic fibrosis
Autosomal recessive disorder that affects epithelial cells of the respiratory, gastrointestinal, and reproductive tracts and leads to abnormal exocrine gland secretions.
