Wk 1: Respiratory and Hematology Flashcards
upper versus lower resp. tract
larynx and up is upper, trachea down is lower respiratory tract
allergic rhinitis
what is it?
Sx?
what is it triggered by?
-inflammatory disorder
-occurs in upper (more common) lower airways (asthma), and eyes
-Sx: sneezing, rhinorrhea, pruritus, nasal congestion, water/itchy eyes
-triggered by allergens (IgE antibodies)
dust, dust mites, mold
histamine
what do they do?
causes a majority of Sx associated with allergic reactions
where are histamines stored?
mast cells and basophils
when activated, histamines cause what?
hives, itchy skin
dilation of blood vessels causing erythema and hypotension
bronchoconstriction: SOB
effects sleep/wake cycle
increases secretion of acid in stomach
different kinds of URI’s
viral
self limiting
rhinitis
sinusitis
laryngitis
laryngotracheobronchitis
acute bronchitis
influenza
bacterial versus viral URI symptoms
bacterial: white spots in throat, tonsils swollen, throat is red, tongue is “furry”
viral: reddened throat, tonsils red/slight swollen, NO white patches. Abx wont work
rhinitis
how is it spread?
Sx ?
-common cold
-spread by droplets
-Sx: low grade fever, HA, fatigue, nasal congestion, rhinorrhea, cough
sinusitis
what is it?
Sx?
Trx?
may be secondary infection
-can be bacterial
-anything inside the nose can increase risk
-Sx: pain above/below eyes, cloudy green or yellow discharge, throat irritation
-hard to Trx with Abx (7+ days)
-use decongestants
Rhinovirus
how long can it live outside the body?
how is it spread?
-usually causes common cold
-fall/spring/summer
-can live 3 hours outside of body, on objects
-spread: droplet or contaminated objects
what are the components of the pharynx?
palate
tonsils
uvula
how to test for pharyngitis ?
cultures and rapid stress test
-can be viral or bacterial
main Sx with pharyngitis
difficulty swallowing
laryngitis
what is it?
Sx?
inflammation of larynx (vocal cords)
-Sx: difficulty speaking, scratchy voice
croup (laryngotracheobronchitis)
what is it?
Sx?
-common in kids
-inflammation of larynx involving trachea and bronchioles
-Sx: bark like cough, stridor, expiratory wheezing
Acute bronchitis
inflammation of the bronchial tree
-Sx: increased cough and sputum production (clear to yellow)
-usually viral
influenza
types
profilaxis
Sx
-usually viral
-types A, B, C (can mutate)
-vaccine once a year
-Sx: rapid onset of F, chills, BA
-secondary PNA can be deadly
normal sputum production
color
function
mucus is secreted by the respiratory tract
-white/ clear color
-traps particles that enter the bronchioles
-cilla help move mucus and captured particles out of the body
epiglottitis
what is it?
Sx?
-inflammation of epiglottis
-can be very dangerous
-Sx: inspiratory stridor, retractions, rapid onset of F, drooling, difficulty swallowing, pain,
different between croup and epiglottitis ?
the barking cough is present with croup, but not with epiglottitis
steeple sign
XR finding that indicates epiglottal swelling
drugs to treat URI’s
antihistamines
sympathomimetics
antitussives
expectorants
what does it mean when an airway is obstructive?
narrowed airways causing worsened expiration
-air then trapped in lungs with increased worked of breathing, a V/Q mismatch and hypoxemia
how do we measure the rate at which the lungs are emptying?
forced expiratory volume in one second (FEV1)
what is a V/Q mismatch
the blood and air within the lungs does not match up
air trapping within the lungs, caused by obstructive airways causes what?
hypoventilation and hypercapnia
air trapping occurs when?
when the person is not able to fully exhale, so air is stuck in the alveoli so we don’t get gas exchange. we get CO2 buildup within the blood
-lungs hyper-inflate when air is trapped in alveoli
air trapping causes chronically ____ CO2 levels and ___ O2 levels
- high
- low
asthma
Definition?
chronic inflammation of bronchial AIRWAYS
-bronchial hyper-responsiveness, causing constriction of airways
-chronic Dz with acute exacerbations
-obstruction is reversible
RF for asthma
allergies
familial link
levels of allergy exposure
urban residency
exposure to air pollution
tobacco exposure
recurrent resp. tract infections
GERD
asthma pathophysiology
-exposure to antigen (trigger)
-airway inflammation
-mucus release, constricted airway muscles, swelling
-causing narrow breathing passage
-Sx: wheeze, cough, SOB, increased WOB, chest tight
-lots of immune cells in process
common asthma triggers
exercise
second hand smoke
climate
dust/ mites
pet dander
pollen/airborne allergens
early asthmatic response
vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucus secretion
late asthmatic response
4-8 hours after early response d/t WBC’s causing another release of inflammatory mediators causing same symptoms
**important teaching point for Pt
airway remodeling (chronic asthma)
untreated inflammation d/t asthma that can lead to longterm airway damage that is IRREVERSIBLE
what are the two main body responses/ symptoms of asthma?
bronchoconstriction
inflammation
what is used to diagnose asthma?
PFT’s (looking for decreased expiratory flow rate)
Sx of asthma
wheezing
SOB
cough
chest tightness
severe: accessory muscles, decreased/ absent breath sounds, inability to speak, diaphoresis, can leave to respiratory failure
asthma management
avoid irritants
use PFM
low dose corticosteroids
short acting beta agonist inhaler
antiinflammatory meds for severe
immunotherapy
status asthmaticus
unrelenting
silent chest
pCO2>70
life theatening emergency
chronic bronchitis
definition
hyper-secretion of mucus and chronic productive cough (can be purulent if resp. infection)
lasting 3 months out of the year for two years
-as Dz progresses: more cough, SOB, dyspnea
two major types of bronchitis
- simple (acute) bronchitis: inflammation of bronchi and bronchioles
-bacterial or viral
-NO airflow obstruction
-supportive care, lasts 3-4 weeks - chronic bronchitis
-90% d/t smoking
-THEY DO HAVE an airflow obstruction (form of COPD)
-can have acute exacerbations
-lead to premature morbidity and mortality
how to diagnose chronic bronchitis
H/o Sx
PE
CXR
PFT
(decreased expiratory volume )
usually by the time the patient is seen, it is irreversible
chronic bronchitis causes an increases size and number of ____ cells and mucus glands
goblet
(causes thick tenacious mucus to be produced that cannot be cleared b/c of impaired cilia
late clinical manifestations of chronic bronchitis
pulmonary HTN
right sided HF (cor pulmonale)
chronic bronchitis treatment
prevention
irreversible
Dz process can be halted (not cured) if pt stops smoking
bronchodilators
expectorants
Abx occasionally
CPT
steroids with acute exacerbations or late in Dz
home O2
what is emphysema?
abnormal, permanent enlargement of gas exchange airways, accompanied by destruction of alveolar walls
-obstruction is secondary to change in lung tissue
-d/t inflammation and destructive changes in lung tissues
-loss of elastic recoil in alveoli
-abnormal permanent enlargement of air spaces distal to terminal bronchioles
-destruction of alveolar walls and capillary beds
-lung hyperventilation
emphysema RF
smoking
air pollution
childhood respiratory infections
genetic emphysema (<2%)
emphysema clinical manifestations
DOE, increasing SOB, eventually SOB at rest, prolonged expiratory phase, wheezing, malnourished, barrel chest, decreased muscle mass, pursed lip breathing, decreased breath sounds throughout
how to diagnose emphysema
PFT (FEV1 decreased)
CXR (hyperinflation)
ABG (respiratory acidosis, low pH)
AAT
barrel chest
emphysema treatment
smoking cessation
bronchodilators and anti-inflammatory agents
supplemental O2
breathing retraining
relaxation techniques
Abx for acute infections
what are most bronchodilators given through inhalation?
decreases the chances of systemic side effects
MDI vs. DPI inhalers
DPI is breath activated, easier to use, dry powder, good for children
what is the first line of treatment for an acute asthma attach
albuterol
albuterol can be used as prevention for what?
EIA
exercise induced asthma
long acting Beta 2 agonist salmeterol is used for what?
as a maintenance drug
BID
indications for salmeterol use
worsening COPD
moderate to severe asthma
**always give wth an inhaled corticosteroid
not intended for monotherapy
leukotrienes cause what? (this is why we block the with LTRA medications )
cause inflammation, bronchoconstriction, ad mucus production
*leukotrienes are released by mast cells
if you are an asthma patient, what is the best way to take inhaled corticosteroids?
take on a regular schedule, NOT PRN
-take bronchodilator first for higher absorption rate of steroids
inhaled glucocorticoids and bronchodilators are often combined to treat what?
asthma
**NEVER for acute attacks
what are the long term medications (the classes) you can use as PREVENTORS for asthma
anticholinergics
xanthine derivative
inhaled corticosteroids
leukotriene modifers
mast cell stabilizers
LABA
what are the medications (classes) of quick relief, or rescue, meds for asthma ?
SABA
albuterol/proventil
pneumonia
definition?
what does it do to the lungs?
how is it transmitted?
ANY kind of infection in the lower respiratory system
-can be fungal, viral, protozoa, or parasitic
-causes inflammation within the lung tissues, alveoli air spaces become filled with purulent inflammatory cells called fibrin (reducing gas exchange)
-transmitted: inhaling infectious droplets
droplet precautions
RF for PNA
age extremes (children <5, adults >80)
compromised immunity
underlying lung Dz (COPD, pulm HTN)
alcoholism (aspiration risk)
ALOC (aspiration risk)
impaired swallowing (aspiration risk)
nursing home resident
hospitalization / immobilized / intubated
influenza
*usually starts with some kind of URI that travels down
CAP versus HAP versus VAP versus HCAP
- Community acquired PNA:
-most common reason for hospitalization
-easier to treat - Hospital acquired PNA:
- developed within 48 hours after admission
-worse outcomes - usually associated with ICU care
- developed within 48 hours after admission
- ventilator associated PNA:
-associated with endotracheal intubation- VAP bundle to prevent
- Healthcare associated PNA:
-technically still apart of community acquired PNA
what is the most common route for PNA to occur?
aspiration of oropharyngeal secretions
how do exudative fluids and inflammatory cells get into the alveoli, creating PNA?
this is d/t the failure of the mucociliary defense mechanism
-mucociliary clearance mechanism is ineffective in smokers
clinical manifestation of PNA
-starts as URI
-fever, chills, productive or dry cough, malaise, pleural pain, dyspnea, hemoptysis
severe PNA: tachypnea, severe respiratory distress or failure
bacterial PNA presents with what kind of cough?
productive / purulent cough with sputum that may be green or rusty looking
what kind of cough is present with viral PNA?
nonproductive/scanty cough
**often cause of CAP
respiratory distress versus respiratory failure
- distress: compensating by increasing work of breathing
sx: tachypnea, nasal flaring, stridor, AMS, tachycardia, pale - failure: cannot compensate for inadequate oxygenation anymore, resp. arrest will most likely follow soon
sx: RR > 60, retractions, grunting, mottling, head bobbing, severe air hunger, bradycardia, hypotension
how we get a clinical diagnosis of PNA
S/Sx: cough, fever, chills, wet breath sounds (rhonchi), pleuritic chest pain, dyspnea, DOE,
pulmonary consolidations: dullness to percussion, inspiratory crackles, increased tactile fremitus(palpable vibrations when a person speaks), egophony (prolonged “ah” heard over auscultation when the patient says “E” )
diagnostic testing: CXR (infiltrates), CBC (is it bacterial?), + sputum for C&S (gold standard)
bacterial PNA
typically from HAP
-can be gram + (staphylococcus the most common with HAP, streptococcus most common with CAP)
-gram (-) make you sicker, harder to treat
aspiration PNA
material from GI tract causing PNA
-severity of the inflammatory response depends of the pH of the aspirate
*more acidic, more of an inflammatory response
who is at risk for aspiration PNA?
NG tube, ALOC, decreased gag reflex, decreased gastric emptying
what is the most common cause of viral PNA?
influenza
treatment for viral PNA?
supportive
NO Abx (unless secondary infection is seen)
what are some atypical PNA?
- pneumocystis carni PNA
-related to immune suppression- it is a yeast like fungus
- mycoplasma PNA
- “walking PNA”
- mild PNA. cough, HA, earache
- properties of bacterial and viral
- legionella PNA
- gram negative
- spread via water systems (air conditioners, mists on
produce, hot tubs) HAVE to report to health dept.
- aspergillus PNA
- fungal PNA
-walls of old buildings, reconstructions, graine, dead
leaevs
-affects lung tissues
- fungal PNA
treatment for bacterial PNA
ABx
other measure that can be done to treat PNA?
ventilation / oxygenation
adequate hydration
good pulmonary hygiene
nebulizer treatment
what is tuberculosis ?
any infection caused by bacteria mycobacterium
-characterized by granulomas in the lungs (nodules)
-aerobic bacillus rod shaped and needs lots of O2 to grow
how is TB transmitted?
-very contagious and slow growing
-transmitted via humans, cattle, or birds
infectious TB
if a persons immune system become impaired then the bacteria can reactivate and spread through the body, even if it was latent TB
in active TB symptoms develop gradually or quickly?
gradually
symptoms of active TB
gradual Sx along with advanced Sx
fatigue, weight loss, lethargy, anorexia, low grade fever, productive cough, night sweats, anxiety
later in the dz you develop: dyspnea, CP, hemoptysis
Sx of extrapulmonary TB
neurologic deficits, meningitis Sx, bone pain, urinary problems
two categories of antitubercular drugs
- first line: primary care
- second line: more complicated case that are resistant to first line
drug resistant TB
problem nationally and globally
-issue with HIV/AIDS community, also with underprivileged communties
-usually brought to US from other countries
how to treat drug resistant TB
second line TB drugs
go over normal A&P of blood cells
check week one modules
hemoglobin function
molecule within red blood cells that reversibly binds to oxygen and transports it.
what is an important component in producing hemoglobin?
iron
what else can bind to hemoglobin, other than oxygen
- carbon monoxide
-higher affinity for carbon monoxide than O2
-Trx with 100% O2 - glucose
what can cause anemia?
blood loss
nutritional deficiency
defective hemoglobin
bone marrow disorders (where RBC are produced)
some chronic Dz (kidney Dz)
neoplasia
inflammation (prevents body from using iron stores)
iron deficiency *
maturational disorders (cells cant carry effectively)
hemolytic anemias (autoimmune dz)
hematocrit
level of RBC contained within a sample of blood
-expressed in percentages
what are two large factors when thinking about the reasoning for disease of RBC’s?
- quantity (# of RBCs)
- quality (low iron, irregular cell shape )
both result in a reduced oxygen carrying capacity
absolute anemia
you do not have enough red blood cells
relative anemia
d/t dilution
-increase in plasma, so it appears we have lower RBC’s but we dont.
-happens with pregnancy, athletes, fluid overload
polycythemia
too many RBC’s
Sx of anemia
pale
pale mucus membranes
fatigue quickly
hypotensive (severe)
increased HR
increased RR
fainting
CP
impaired cognition*
insomnia*
SOB
dizzy
clinical manifestations of anemia:
1. mild
2. mild-moderate
3. moderate-severe
- asymptomatic
- fatigue, Wk, tachy, dyspnea
- tachy, high RR, hypotension, pale, faintness, cardiovascular Sx
with anemia, oxygen going to muscle is decreased, causing what symptom?
weakness
with anemia, energy production is decreased, causing which symptom?
fatigue?
with anemia cardiac output is increased, causing which symptoms? (2)
tachycardia
palpitations
with anemia the secretion of erythropoitin increases, causing which symptom?
bone pain
with anemia the cardia muscle experiences hypoxia, this can cause which condition? can cause which symptom?
heart failure
chest pain
with anemia the patients overall oxygenation levels decrease, causing hypoxia, this causes which two respiratory symptoms?
dyspnea
increased RR
anemia occurs when there is not enough healthy RBC’s or _____
hemoglobin
what are three reasons that you would have anemia due to a decreased number of circulating erythrocytes ?
decreased production
increased destruction
loss
what are two reasons that a patient could have anemia due to decreased Hgb content within the blood?
loss of iron
loss of key nutrients (Vitamin B12, folate)
anemia d/t abnormal hemoglobin
two examples
count of hemoglobin might be normal, but the shapes are abnormal. causes difficulty binding to O2
-shorter lifespan
Ex. Sickle cell Dz or thalassemia (genetic disorder)
T/F: with sickle cell, the cells clump together easier, causing blockages. this can cause pain or ischemia distal to where it occurs
true
-common in liver, spleen, heart, kidneys, retina
when someone has an iron deficiency anemia does the MCV get low or high?
low
microcytic anemia
when someone has a vitamin B12 or folate deficiency does the MCV get smaller or larger?
larger
macrocytic anemia
a high reticulocyte count can indicate what?
blood loss or decreased production of RBC’s
-lots of immature RBC’s trying to catch up with the loss of blood
what is the most common type of anemia ?
iron deficiency
what are some different causes for iron deficient anemia?
decreased intake of iron
decreased absorption
increased demand
excessive loss (GIB, menstration)
where is iron stored?
liver
when erythrocytes reach their end of life cycle, what happens to iron?
it is reused
clinical manifestations of iron deficient anemia
- epithelial atrophy
brittle hair and nails
koilonychia (indented nails) - GI issues
smooth tongue
mouth sores
dysphagia - PICA (craving of non-food), pagophagia (craving ice)
4.normal S/Sx of anemia (wk, fatigue, etc..)
vitamin B12 and folic acid deficiency leads to altered ____ synthesis
DNA
vitamin B12 deficiency can also cause _____ which will then lead to neurological disorders
demyelination
you have a patient that is dealing with anemia that seems to be due to folic acid deficiency and you correct the anemia by giving them folic acid. the patient is now experiencing neurological symptoms, even though their anemia has been fixed. why is this?
you can fix their anemia by bypassing the B12 and just giving folic acid, but this still leaves the patient with a B12 deficiency. B12 deficiency will lead to neurological issues if not corrected
folate deficiency can be due to what?
alcoholism
diet
cirrhosis
*increased need when pregnant
-folate deficiency is NOT as issue with absorption
vitamin B 12 needs to be combined with what to be absorbed in the terminal ileum?
intrinsic factor (IF)
what are some conditions that reduce intrinsic factor or inhibit the absorption of vitamin B12? (3)
gastric bypass
gastrectomy
bowel resection
what are some neurological S/Sx of anemia ?
depression, paranoia, confusion, anger/irritability, anxiety, balance issue, gait issues, memory loss
anemia of CKD is d/t what?
impaired erythropoeitin production causing a decreased number of circulating erythrocytes
-has nml S/Sx of anemia
what is aplastic anemia ?
primary condition of bone marrow stem cells
-congenital or acquired (idiopathic)
what kind of problems will a patient with aplastic anemia have? (other than anemia)
-decreased RBCs, WBC’s, platelets
-risk for infection
-risk for bleeding
where do RBC’s come from?
stem cells
what are some causes of aplastic anemia ?
- idiopathic
- high dose exposure to toxic agents (chemicals/rad)
- autoimmune mechanisms (infection)
what leads to an increased destruction of RBC’s?
Abnormal hemoglobin
Thalassemia
Acquired hemolytic anemia
what is acquired hemolytic anemia?
common causes?
premature destruction of RBC’s caused by an EXTERNAL agent
causes: autoimmune attack, blood incompatibilities, drug reactions
what are some clinical manifestations you will look for in a patient with hemolytic anemia ?
low Hbg
high reticulocyte count
mild jaundice
hemoglobinuria
decreased haptoglobin
blood loss anemia can present as ____ or _____ (2)
gross bleeding (obvious)
occult blood (hidden)
what is a major consideration with blood loss anemia
the rate of it
-rapid=unable to compensate, complications
-slow loss= all about time, time to compensate
50 % of blood loss leads to?
shock and death
40 % blood loss leads to?
high HR, low BP when supine, air hungry, cold, clammy
30% blood loss leads to?
flat neck veins, high HR, low BP when sitting/standing
20% blood loss leads to?
increased HR
with chronic blood loss you need to watch organ functions, which ones ?
brain
lungs
heart
kidneys
heme iron (dietary)
40% of iron in meat
-well absorbed
non-heme iron (dietary)
60% of iron in animal tissues
-all iron in plants
-less well absorbed
what is the issue with having too many RBC’s?
increased blood viscosity which causes things such as HTN
what is relative polycythemia?
an isolated DECREASE in PLASMA volume which elevates the Hgb, Hct and RBC count
-Sx depends in
what can be the cause of relative polycythemia?
severe dehydration
“smokers polycythemia”
what is primary polycythemia (polycythemia vera) ?
->60 y/o
-over production of blood cells, neoplastic Dz
-risk of clotting
polycythemia vera pathogenesis
-malignant Dz
-single stem cell mutates into a cell that overproduces al blood cells
clinical manifestations of polycythemia vera
-many complaints (HA, fatigue, weight loss, dyspnea)
-HTN
-clotting issues
-ruddy color
secondary polycythemia
adaptive, or compensatory, response to tissue hypoxia
-happens to provide more oxygen carriers by increasing RBC production
what kind of patients develop secondary polycythemia ?
COPD
what are the risk factors for polycythemia ?
chronic hypoxia
high altitudes
smoking, longterm
genetics
CO exposure, longterm
pathogenesis of secondary polycythemia
hypoxemia stimulates erythropoietin, increases RBC production
