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Nur 326 Pathopharm I > Wk 1: Respiratory and Hematology > Flashcards

Wk 1: Respiratory and Hematology Flashcards

1
Q

upper versus lower resp. tract

A

larynx and up is upper, trachea down is lower respiratory tract

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2
Q

allergic rhinitis
what is it?
Sx?
what is it triggered by?

A

-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

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3
Q

histamine
what do they do?

A

causes a majority of Sx associated with allergic reactions

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4
Q

where are histamines stored?

A

mast cells and basophils

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5
Q

when activated, histamines cause what?

A

hives, itchy skin
dilation of blood vessels causing erythema and hypotension
bronchoconstriction: SOB
effects sleep/wake cycle
increases secretion of acid in stomach

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6
Q

different kinds of URI’s

A

viral
self limiting
rhinitis
sinusitis
laryngitis
laryngotracheobronchitis
acute bronchitis
influenza

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7
Q

bacterial versus viral URI symptoms

A

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

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8
Q

rhinitis
how is it spread?
Sx ?

A

-common cold
-spread by droplets
-Sx: low grade fever, HA, fatigue, nasal congestion, rhinorrhea, cough

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9
Q

sinusitis

what is it?
Sx?
Trx?

A

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

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10
Q

Rhinovirus

how long can it live outside the body?
how is it spread?

A

-usually causes common cold
-fall/spring/summer
-can live 3 hours outside of body, on objects
-spread: droplet or contaminated objects

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11
Q

what are the components of the pharynx?

A

palate
tonsils
uvula

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12
Q

how to test for pharyngitis ?

A

cultures and rapid stress test

-can be viral or bacterial

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13
Q

main Sx with pharyngitis

A

difficulty swallowing

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14
Q

laryngitis

what is it?
Sx?

A

inflammation of larynx (vocal cords)
-Sx: difficulty speaking, scratchy voice

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15
Q

croup (laryngotracheobronchitis)

what is it?
Sx?

A

-common in kids
-inflammation of larynx involving trachea and bronchioles
-Sx: bark like cough, stridor, expiratory wheezing

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16
Q

Acute bronchitis

A

inflammation of the bronchial tree
-Sx: increased cough and sputum production (clear to yellow)
-usually viral

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17
Q

influenza

types
profilaxis
Sx

A

-usually viral
-types A, B, C (can mutate)
-vaccine once a year
-Sx: rapid onset of F, chills, BA
-secondary PNA can be deadly

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18
Q

normal sputum production

color
function

A

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

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19
Q

epiglottitis

what is it?
Sx?

A

-inflammation of epiglottis
-can be very dangerous
-Sx: inspiratory stridor, retractions, rapid onset of F, drooling, difficulty swallowing, pain,

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20
Q

different between croup and epiglottitis ?

A

the barking cough is present with croup, but not with epiglottitis

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21
Q

steeple sign

A

XR finding that indicates epiglottal swelling

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22
Q

drugs to treat URI’s

A

antihistamines
sympathomimetics
antitussives
expectorants

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23
Q

what does it mean when an airway is obstructive?

A

narrowed airways causing worsened expiration
-air then trapped in lungs with increased worked of breathing, a V/Q mismatch and hypoxemia

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24
Q

how do we measure the rate at which the lungs are emptying?

A

forced expiratory volume in one second (FEV1)

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25
Q

what is a V/Q mismatch

A

the blood and air within the lungs does not match up

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26
Q

air trapping within the lungs, caused by obstructive airways causes what?

A

hypoventilation and hypercapnia

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27
Q

air trapping occurs when?

A

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

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28
Q

air trapping causes chronically ____ CO2 levels and ___ O2 levels

A
  1. high
  2. low
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29
Q

asthma

Definition?

A

chronic inflammation of bronchial AIRWAYS
-bronchial hyper-responsiveness, causing constriction of airways
-chronic Dz with acute exacerbations
-obstruction is reversible

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30
Q

RF for asthma

A

allergies
familial link
levels of allergy exposure
urban residency
exposure to air pollution
tobacco exposure
recurrent resp. tract infections
GERD

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31
Q

asthma pathophysiology

A

-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

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32
Q

common asthma triggers

A

exercise
second hand smoke
climate
dust/ mites
pet dander
pollen/airborne allergens

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33
Q

early asthmatic response

A

vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucus secretion

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34
Q

late asthmatic response

A

4-8 hours after early response d/t WBC’s causing another release of inflammatory mediators causing same symptoms
**important teaching point for Pt

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35
Q

airway remodeling (chronic asthma)

A

untreated inflammation d/t asthma that can lead to longterm airway damage that is IRREVERSIBLE

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36
Q

what are the two main body responses/ symptoms of asthma?

A

bronchoconstriction
inflammation

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37
Q

what is used to diagnose asthma?

A

PFT’s (looking for decreased expiratory flow rate)

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38
Q

Sx of asthma

A

wheezing
SOB
cough
chest tightness

severe: accessory muscles, decreased/ absent breath sounds, inability to speak, diaphoresis, can leave to respiratory failure

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39
Q

asthma management

A

avoid irritants
use PFM
low dose corticosteroids
short acting beta agonist inhaler
antiinflammatory meds for severe
immunotherapy

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40
Q

status asthmaticus

A

unrelenting
silent chest
pCO2>70
life theatening emergency

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41
Q

chronic bronchitis
definition

A

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

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42
Q

two major types of bronchitis

A
  1. simple (acute) bronchitis: inflammation of bronchi and bronchioles
    -bacterial or viral
    -NO airflow obstruction
    -supportive care, lasts 3-4 weeks
  2. 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
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43
Q

how to diagnose chronic bronchitis

A

H/o Sx
PE
CXR
PFT
(decreased expiratory volume )
usually by the time the patient is seen, it is irreversible

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44
Q

chronic bronchitis causes an increases size and number of ____ cells and mucus glands

A

goblet

(causes thick tenacious mucus to be produced that cannot be cleared b/c of impaired cilia

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45
Q

late clinical manifestations of chronic bronchitis

A

pulmonary HTN
right sided HF (cor pulmonale)

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46
Q

chronic bronchitis treatment

A

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

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47
Q

what is emphysema?

A

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

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48
Q

emphysema RF

A

smoking
air pollution
childhood respiratory infections
genetic emphysema (<2%)

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49
Q

emphysema clinical manifestations

A

DOE, increasing SOB, eventually SOB at rest, prolonged expiratory phase, wheezing, malnourished, barrel chest, decreased muscle mass, pursed lip breathing, decreased breath sounds throughout

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50
Q

how to diagnose emphysema

A

PFT (FEV1 decreased)
CXR (hyperinflation)
ABG (respiratory acidosis, low pH)
AAT
barrel chest

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51
Q

emphysema treatment

A

smoking cessation
bronchodilators and anti-inflammatory agents
supplemental O2
breathing retraining
relaxation techniques
Abx for acute infections

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52
Q

what are most bronchodilators given through inhalation?

A

decreases the chances of systemic side effects

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53
Q

MDI vs. DPI inhalers

A

DPI is breath activated, easier to use, dry powder, good for children

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54
Q

what is the first line of treatment for an acute asthma attach

A

albuterol

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55
Q

albuterol can be used as prevention for what?

A

EIA
exercise induced asthma

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56
Q

long acting Beta 2 agonist salmeterol is used for what?

A

as a maintenance drug
BID

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57
Q

indications for salmeterol use

A

worsening COPD
moderate to severe asthma
**always give wth an inhaled corticosteroid
not intended for monotherapy

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58
Q

leukotrienes cause what? (this is why we block the with LTRA medications )

A

cause inflammation, bronchoconstriction, ad mucus production

*leukotrienes are released by mast cells

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59
Q

if you are an asthma patient, what is the best way to take inhaled corticosteroids?

A

take on a regular schedule, NOT PRN
-take bronchodilator first for higher absorption rate of steroids

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60
Q

inhaled glucocorticoids and bronchodilators are often combined to treat what?

A

asthma

**NEVER for acute attacks

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61
Q

what are the long term medications (the classes) you can use as PREVENTORS for asthma

A

anticholinergics
xanthine derivative
inhaled corticosteroids
leukotriene modifers
mast cell stabilizers
LABA

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62
Q

what are the medications (classes) of quick relief, or rescue, meds for asthma ?

A

SABA
albuterol/proventil

63
Q

pneumonia

definition?
what does it do to the lungs?
how is it transmitted?

A

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

64
Q

RF for PNA

A

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

65
Q

CAP versus HAP versus VAP versus HCAP

A
  1. Community acquired PNA:
    -most common reason for hospitalization
    -easier to treat
  2. Hospital acquired PNA:
    • developed within 48 hours after admission
      -worse outcomes
    • usually associated with ICU care
  3. ventilator associated PNA:
    -associated with endotracheal intubation
    • VAP bundle to prevent
  4. Healthcare associated PNA:
    -technically still apart of community acquired PNA
66
Q

what is the most common route for PNA to occur?

A

aspiration of oropharyngeal secretions

67
Q

how do exudative fluids and inflammatory cells get into the alveoli, creating PNA?

A

this is d/t the failure of the mucociliary defense mechanism

-mucociliary clearance mechanism is ineffective in smokers

68
Q

clinical manifestation of PNA

A

-starts as URI
-fever, chills, productive or dry cough, malaise, pleural pain, dyspnea, hemoptysis

severe PNA: tachypnea, severe respiratory distress or failure

69
Q

bacterial PNA presents with what kind of cough?

A

productive / purulent cough with sputum that may be green or rusty looking

70
Q

what kind of cough is present with viral PNA?

A

nonproductive/scanty cough

**often cause of CAP

71
Q

respiratory distress versus respiratory failure

A
  1. distress: compensating by increasing work of breathing
    sx: tachypnea, nasal flaring, stridor, AMS, tachycardia, pale
  2. 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
72
Q

how we get a clinical diagnosis of PNA

A

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)

73
Q

bacterial PNA

A

typically from HAP
-can be gram + (staphylococcus the most common with HAP, streptococcus most common with CAP)
-gram (-) make you sicker, harder to treat

74
Q

aspiration PNA

A

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

75
Q

who is at risk for aspiration PNA?

A

NG tube, ALOC, decreased gag reflex, decreased gastric emptying

76
Q

what is the most common cause of viral PNA?

A

influenza

77
Q

treatment for viral PNA?

A

supportive
NO Abx (unless secondary infection is seen)

78
Q

what are some atypical PNA?

A
  1. pneumocystis carni PNA
    -related to immune suppression
    • it is a yeast like fungus
  2. mycoplasma PNA
    • “walking PNA”
    • mild PNA. cough, HA, earache
    • properties of bacterial and viral
  3. legionella PNA
    • gram negative
    • spread via water systems (air conditioners, mists on
      produce, hot tubs) HAVE to report to health dept.
  4. aspergillus PNA
    • fungal PNA
      -walls of old buildings, reconstructions, graine, dead
      leaevs
      -affects lung tissues
79
Q

treatment for bacterial PNA

A

ABx

80
Q

other measure that can be done to treat PNA?

A

ventilation / oxygenation
adequate hydration
good pulmonary hygiene
nebulizer treatment

81
Q

what is tuberculosis ?

A

any infection caused by bacteria mycobacterium
-characterized by granulomas in the lungs (nodules)
-aerobic bacillus rod shaped and needs lots of O2 to grow

82
Q

how is TB transmitted?

A

-very contagious and slow growing
-transmitted via humans, cattle, or birds

83
Q

infectious TB

A

if a persons immune system become impaired then the bacteria can reactivate and spread through the body, even if it was latent TB

84
Q

in active TB symptoms develop gradually or quickly?

A

gradually

85
Q

symptoms of active TB

gradual Sx along with advanced Sx

A

fatigue, weight loss, lethargy, anorexia, low grade fever, productive cough, night sweats, anxiety

later in the dz you develop: dyspnea, CP, hemoptysis

86
Q

Sx of extrapulmonary TB

A

neurologic deficits, meningitis Sx, bone pain, urinary problems

87
Q

two categories of antitubercular drugs

A
  1. first line: primary care
  2. second line: more complicated case that are resistant to first line
88
Q

drug resistant TB

A

problem nationally and globally
-issue with HIV/AIDS community, also with underprivileged communties
-usually brought to US from other countries

89
Q

how to treat drug resistant TB

A

second line TB drugs

90
Q

go over normal A&P of blood cells

A

check week one modules

91
Q

hemoglobin function

A

molecule within red blood cells that reversibly binds to oxygen and transports it.

92
Q

what is an important component in producing hemoglobin?

A

iron

93
Q

what else can bind to hemoglobin, other than oxygen

A
  1. carbon monoxide
    -higher affinity for carbon monoxide than O2
    -Trx with 100% O2
  2. glucose
94
Q

what can cause anemia?

A

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)

95
Q

hematocrit

A

level of RBC contained within a sample of blood

-expressed in percentages

96
Q

what are two large factors when thinking about the reasoning for disease of RBC’s?

A
  1. quantity (# of RBCs)
  2. quality (low iron, irregular cell shape )

both result in a reduced oxygen carrying capacity

97
Q

absolute anemia

A

you do not have enough red blood cells

98
Q

relative anemia

A

d/t dilution

-increase in plasma, so it appears we have lower RBC’s but we dont.
-happens with pregnancy, athletes, fluid overload

99
Q

polycythemia

A

too many RBC’s

100
Q

Sx of anemia

A

pale
pale mucus membranes
fatigue quickly
hypotensive (severe)
increased HR
increased RR
fainting
CP
impaired cognition*
insomnia*
SOB
dizzy

101
Q

clinical manifestations of anemia:
1. mild
2. mild-moderate
3. moderate-severe

A
  1. asymptomatic
  2. fatigue, Wk, tachy, dyspnea
  3. tachy, high RR, hypotension, pale, faintness, cardiovascular Sx
102
Q

with anemia, oxygen going to muscle is decreased, causing what symptom?

A

weakness

103
Q

with anemia, energy production is decreased, causing which symptom?

A

fatigue?

104
Q

with anemia cardiac output is increased, causing which symptoms? (2)

A

tachycardia
palpitations

105
Q

with anemia the secretion of erythropoitin increases, causing which symptom?

A

bone pain

106
Q

with anemia the cardia muscle experiences hypoxia, this can cause which condition? can cause which symptom?

A

heart failure
chest pain

107
Q

with anemia the patients overall oxygenation levels decrease, causing hypoxia, this causes which two respiratory symptoms?

A

dyspnea
increased RR

108
Q

anemia occurs when there is not enough healthy RBC’s or _____

A

hemoglobin

109
Q

what are three reasons that you would have anemia due to a decreased number of circulating erythrocytes ?

A

decreased production
increased destruction
loss

110
Q

what are two reasons that a patient could have anemia due to decreased Hgb content within the blood?

A

loss of iron
loss of key nutrients (Vitamin B12, folate)

111
Q

anemia d/t abnormal hemoglobin

two examples

A

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)

112
Q

T/F: with sickle cell, the cells clump together easier, causing blockages. this can cause pain or ischemia distal to where it occurs

A

true

-common in liver, spleen, heart, kidneys, retina

113
Q

when someone has an iron deficiency anemia does the MCV get low or high?

A

low

microcytic anemia

114
Q

when someone has a vitamin B12 or folate deficiency does the MCV get smaller or larger?

A

larger

macrocytic anemia

115
Q

a high reticulocyte count can indicate what?

A

blood loss or decreased production of RBC’s

-lots of immature RBC’s trying to catch up with the loss of blood

116
Q

what is the most common type of anemia ?

A

iron deficiency

117
Q

what are some different causes for iron deficient anemia?

A

decreased intake of iron
decreased absorption
increased demand
excessive loss (GIB, menstration)

118
Q

where is iron stored?

A

liver

119
Q

when erythrocytes reach their end of life cycle, what happens to iron?

A

it is reused

120
Q

clinical manifestations of iron deficient anemia

A
  1. epithelial atrophy
    brittle hair and nails
    koilonychia (indented nails)
  2. GI issues
    smooth tongue
    mouth sores
    dysphagia
  3. PICA (craving of non-food), pagophagia (craving ice)
    4.normal S/Sx of anemia (wk, fatigue, etc..)
121
Q

vitamin B12 and folic acid deficiency leads to altered ____ synthesis

A

DNA

122
Q

vitamin B12 deficiency can also cause _____ which will then lead to neurological disorders

A

demyelination

123
Q

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?

A

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

124
Q

folate deficiency can be due to what?

A

alcoholism
diet
cirrhosis
*increased need when pregnant
-folate deficiency is NOT as issue with absorption

125
Q

vitamin B 12 needs to be combined with what to be absorbed in the terminal ileum?

A

intrinsic factor (IF)

126
Q

what are some conditions that reduce intrinsic factor or inhibit the absorption of vitamin B12? (3)

A

gastric bypass
gastrectomy
bowel resection

127
Q

what are some neurological S/Sx of anemia ?

A

depression, paranoia, confusion, anger/irritability, anxiety, balance issue, gait issues, memory loss

128
Q

anemia of CKD is d/t what?

A

impaired erythropoeitin production causing a decreased number of circulating erythrocytes
-has nml S/Sx of anemia

129
Q

what is aplastic anemia ?

A

primary condition of bone marrow stem cells
-congenital or acquired (idiopathic)

130
Q

what kind of problems will a patient with aplastic anemia have? (other than anemia)

A

-decreased RBCs, WBC’s, platelets
-risk for infection
-risk for bleeding

131
Q

where do RBC’s come from?

A

stem cells

132
Q

what are some causes of aplastic anemia ?

A
  1. idiopathic
  2. high dose exposure to toxic agents (chemicals/rad)
  3. autoimmune mechanisms (infection)
133
Q

what leads to an increased destruction of RBC’s?

A

Abnormal hemoglobin
Thalassemia
Acquired hemolytic anemia

134
Q

what is acquired hemolytic anemia?

common causes?

A

premature destruction of RBC’s caused by an EXTERNAL agent

causes: autoimmune attack, blood incompatibilities, drug reactions

135
Q

what are some clinical manifestations you will look for in a patient with hemolytic anemia ?

A

low Hbg
high reticulocyte count
mild jaundice
hemoglobinuria
decreased haptoglobin

136
Q

blood loss anemia can present as ____ or _____ (2)

A

gross bleeding (obvious)
occult blood (hidden)

137
Q

what is a major consideration with blood loss anemia

A

the rate of it
-rapid=unable to compensate, complications
-slow loss= all about time, time to compensate

138
Q

50 % of blood loss leads to?

A

shock and death

139
Q

40 % blood loss leads to?

A

high HR, low BP when supine, air hungry, cold, clammy

140
Q

30% blood loss leads to?

A

flat neck veins, high HR, low BP when sitting/standing

141
Q

20% blood loss leads to?

A

increased HR

142
Q

with chronic blood loss you need to watch organ functions, which ones ?

A

brain
lungs
heart
kidneys

143
Q

heme iron (dietary)

A

40% of iron in meat
-well absorbed

144
Q

non-heme iron (dietary)

A

60% of iron in animal tissues
-all iron in plants
-less well absorbed

145
Q

what is the issue with having too many RBC’s?

A

increased blood viscosity which causes things such as HTN

146
Q

what is relative polycythemia?

A

an isolated DECREASE in PLASMA volume which elevates the Hgb, Hct and RBC count

-Sx depends in

147
Q

what can be the cause of relative polycythemia?

A

severe dehydration
“smokers polycythemia”

148
Q

what is primary polycythemia (polycythemia vera) ?

A

->60 y/o
-over production of blood cells, neoplastic Dz
-risk of clotting

149
Q

polycythemia vera pathogenesis

A

-malignant Dz
-single stem cell mutates into a cell that overproduces al blood cells

150
Q

clinical manifestations of polycythemia vera

A

-many complaints (HA, fatigue, weight loss, dyspnea)
-HTN
-clotting issues
-ruddy color

151
Q

secondary polycythemia

A

adaptive, or compensatory, response to tissue hypoxia
-happens to provide more oxygen carriers by increasing RBC production

152
Q

what kind of patients develop secondary polycythemia ?

A

COPD

153
Q

what are the risk factors for polycythemia ?

A

chronic hypoxia
high altitudes
smoking, longterm
genetics
CO exposure, longterm

154
Q

pathogenesis of secondary polycythemia

A

hypoxemia stimulates erythropoietin, increases RBC production

Nur 326 Pathopharm I (2 decks)

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