Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Final > Flashcards

Final Flashcards

1
Q

nasopharynx

A

the upper part of the throat that connects the nasal passages to the larynx and trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

oropharynx

A

the middle part of the throat located behind the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

laryngopharynx

A

the lower part of the throat that connects the pharynx to the esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cricoid cartilage

A

the only complete ring of cartilage around the trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hyoid bone

A

horseshoe shaped bone in the front of your neck

supports the tongue and plays a key role in speaking and swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

carina

A

a ridge of cartilage at the bottom of the trachea that separates the opening of the right and left primary bronchi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

spirometry: pulmonary function test (PFT)

A

tests pulmonary volumes and airflow times

measures the volumes of your lungs

airflow times = how fast you can breathe in and out a set volume

measures tidal volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

tidal volume

A

how much air you can breathe in and out of your lungs during each breath

about 500mL going in and out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

arterial blood gas

A

checks oxygen, CO2, bicarbonate buffer, and serum pH

increased CO2 in the blood makes the pH decrease -> more acidic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

oximeters

A

measurement of hemoglobin O2 saturation

pulse oximeter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

exercise tolerance testing

A

aka the stress test

can be used on pts with chronic pulmonary disease

pts walk of the treadmill

want to get to 80% Mac HR
calculated by 220-age = max HR

pt hooked up to an EKG and check BP

complete imaging of the heart and lungs at rest and after the stress test -> ultrasound, chest x-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

radiography

A

helpful in evaluating tumours and infections

chest x-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

bronchoscopy

A

perform biopsies of the lungs or
check site of lesion or bleeding

uses a bronchoscope with a camera on the end and enters through the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

C+S tests for respiratory diagnostic test

A

sputum testing for presence of pathogens

determine antimicrobial sensitivity of pathogen -> whether is is viral, bacteria, or fungal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

general manifestations of respiratory disease

A
  • sneezing
  • coughing
  • sputum
  • change in breathing patterns and characteristics
  • dyspnea (SOB)
  • cyanosis
  • pleural pain
  • friction rub
  • clubbed fingers/toes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

sneezing

A

(neural reflex from the medulla oblongata):
- reflex response to irritation in upper respiratory tract
- removes irritants from nasal passages
- is associated with inflammation or foreign material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

coughing

A

neural reflex from the medulla oblongata)
- due to inhaled irritants in the oropharynx
- inflammation or foreign material in lower respiratory tract
- dry, unproductive cough = fatiguing
- wet, productive cough = beneficial
- expectorant med or humidifier also helps remove secretions if thick/sticky -> creates more secretions and waters them down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

sputum

A

yellowish-green/cloudy/thick
- often an indication of bacterial infection

rusty or dark coloured
- usually sign of pneumococcal pneumonia
- bit of blood in sputum, some capillary damage in the lungs from infection

large amount of purulent sputum with foul odour
- associated with bacterial infections
- frequent infection may cause bronchiectasis

thick mucus
- asthma or cystic fibrosis
- blood tinged sputum may result from chronic cough -> ruptures capillaries
- may also be a sign of tumour or TB

hemoptysis
- bright red frothy sputum
- associated with pulmonary edema
- fluid in the alveoli getting coughed up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pneumonia

A

an umbrella term for any infection in the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

bronchiectasis

A

scarring, widening of the bronchioles

makes it easier for the airways to collapse

due to chronic damage

lots of mucus and inflammation, will plug the alveoli

less air gets into the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

eupnea

A

normal breathing rate

10-18 breaths per min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

kussmaul respiration

A

“air hunger”

deep rapid respiration -> typical for acidosis, or following strenuous exercise

ok during exercise, bad if at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

medulla oblongata

A

breathing centre in the brain

increase in CO2 signals the medulla oblongata to stimulate the diaphragm to breath faster and deeper to get rid of the CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

laboured breathing

A

prolonged inspiration or expiration

often associated with obstruction in the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

wheezing

A

whistling sounds

indicate obstruction in the small airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

stridor

A

high-pitched crowing noise

indicated an upper airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

apnea

A

cessation of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

hyperpnea

A

increased depth of respiration with normal to increased rate and regular rhythm

faster than eupnea

hyperventilating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cheyne-stokes respiration

A

periodic breathing with periods of apnea

alternates regularly with a series of respiratory cycles -> gradually increases, then decreases in rate and depth

no breathing .. fast/shallow… bit slower/deeper… fast/shallow… no breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ataxic breathing

A

periods of apnea alternating irregularly with a series of shallow breath of equal depth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

apneusis

A

long gasping inspiratory phase followed by a short, inadequate expiratory phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

rales

A

light bubbly or crackling sounds with serous secretions in the alveoli

sign of damage or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

rhonchi

A

deeper or harsher sounds from thicker mucous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

atelectasis

A

collapsed lung or portion of the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

dyspnea

A

feeling short of breath

may be due to increased CO2 or hypoxemia

exercise

if severe it is indicative of respiratory distress
- flaring nostrils
-use of accessory respiratory muscles
- retraction of muscles between or above ribs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

orthopnea

A

occurs when you are lying down

secretions may pool in the lungs, making it more difficult to breath

due to pulmonary congestion

sit pt up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

paroxysmal nocturnal dyspnea

A
  • sudden acute type of dyspnea
  • common in pts with left side congestive failure
  • requires supplemental O2
  • occurs typically at night
  • sections pool but won’t drain fast enough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

pleural pain

A

results from inflammation of infection of parietal pleura

membrane that sounds the lung

increased pain during inspiration or coughing

rubbing between the visceral and parietal pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

friction rub

A

soft sound produced as rough inflamed scarred pleural rub and move against each other

usually paired up with pleural effusion -> build up of fluid between the pleural layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

clubbed fingers and toes

A

result from chronic hypoxia associated with respiratory and cardiovascular disease

painless, firm, fibrotic enlargement at the end of toes and fingers

looks like grapes at the end of toes and fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

hypercapnia

A

increased CO2 in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

changes in ABGs

A

could be due to deficit in

RBC
anemia
inadequate perfusion
hemoglobin
CO poison
inadequate cardiac output
blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

aging on the respiratory system

A
  • elastic tissues deteriorate, decrease lung elasticity and lowers vital capacity (air that can get into and out of the lungs)
  • arthritic changes -> restricted chest movements, reduced respiratory minute volume (how much air can get into and out of the lungs in one minute)
  • emphysema (destruction of alveoli and bronchioles) –> can affect individuals over 50, depends on exposure to respiratory irritants, and loss of alveolar septa which is the gas exchange surface area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

basic therapies for respiratory disorders

A
  • don’t expose yourself to inhaled irritants -> cigarette smoke
  • ensure good ventilation
  • up to date on vaccinations, prevent infections and reduce injury to respiratory system
  • humidify air -> break down mucus
  • moderate exercise
  • deep breathing and coughing/ chest physiotherapy
  • supplemental oxygen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

drugs therapies for respiratory disorders

A
  • decongestants -> vasoconstriction of nasal mucosa
  • expectorants -> thins respiratory secretions for easier removal
  • antitussives -> reduces cough reflex
  • antihistamines -> block histamine receptors to reduce allergic response
  • analgesics
  • antimicrobials
  • bronchodilators -> stimulate beta-2 receptors
  • glucocorticoids -> anti-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

surgical interventions for respiratory disorders

A
  • thoracentesis -> removal of excess fluid from pleural cavity, prevent atelectasis (collapsed lung)
  • tracheotomy - incision into the trachea below the larynx
  • surgery -> remove lung tumor, abscess, or damaged tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

pericardium

A

not expandable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

steps to ARDS

A
  1. direct lung cell damage and indirect causes (septic shock)
  2. results in excessive release of chemical mediators
    -> increases permeability or alveolar capillary membranes
    -> increases fluid and protein in interstitial areas and alveoli
    -> fibrous membranes form from protein rich fluid in the alveoli and platelet aggregation , blocks gas diffusion, causes stiffness and decreased compliance
    ->micro thrombi (mini clots) develop in the pulmonary circulation
    -> damage surfactant producing cells

may end of with necrosis and fibrosis -> stiff lung, less compliant, and makes it hard to breathe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ARDS death rate

A

90% untreated

50% treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

effect of the inflammatory response in the lungs

A

neutrophils will begin to produce toxic products within the alveoli such as:
- leukotrienes
- oxidants
- platelet activating factors (PAF)
- proteases -> will degrade the protein and lead to the formation of a hyaline membrane creates an added membrane to gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

S+S of ARDS

A
  • rapid onset
  • severe dyspnea, rales, productive cough, cyanosis, hypoxemia
  • rapid, shallow, respirations -> decreased tidal volume and vital capacity
  • increased HR
  • restlessness, anxiety -> leads to lethargy, confusion, altered LOC
  • combo of respiratory and metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

tx of ARDS

A
  • tx underlying cause
  • supply supplemental oxygen
  • if person survives, their may be an accumulation of fluid and it could develop into pneumonia -> treat it!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

blood gas level in respiratory failure

A

PaO2 <50mmHg
PaCO2 >50mmHg

will lead to respiratory arrest then cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

shock

A

not enough blood flow to tissues

55
Q

infant respiratory distress syndrome IRDS

A

common in premature babies -> 7 to 8 months

inadequate surfactant production -> leads to atelectasis

will follow same steps as ARDS

56
Q

obstructive lung diseases

A
  • cystic fibrosis
  • lung cancer
  • aspiration
  • obstructive sleep apnea
  • COPD -> emphysema, chronic bronchitis, chronic asthma
57
Q

cystic fibrosis

A

inherited genetic disorder

autosomal recessive -> have to inherit the mutated allele from both parents
- the CFTR gene, located on chromosome 7, controls chloride ion transport

if there’s a problem in the bodies salt channels, the mucus is not as watery -> thicker and sticky

tenacious mucus from the exocrine glands

primary effacers in lungs and pancreas

58
Q

cystic fibrosis effect on lungs

A
  • mucus obstructs airflow in bronchioles and small bronchi
  • cause permanent damage to bronchial walls
  • bacterial infections are common in stagnant mucus -> can cause repetitive pneumonia
59
Q

cystic fibrosis on the digestive tract

A
  • meconium ileus in newborns (may be the first sign that a baby has CF) -> blocked excretion of meconium (newborns first stool)
  • blockage of pancreatic ducts -> blocks digestive enzyme secretion , enzymes start breaking down the pancreas -> may cause type 1 diabetes
  • obstruction of bile- ducts c-> blocks fat digestion and fat soluble vitamin absorption (DEAK) -> back uo can cause liver damage
  • salivary glands may be mildly affected
  • reproductive tract:
  • obstruction of the vas deferens
  • obstruction of the cervix
  • both can lead to sterility
  • sweat glands (another first sign that a maybe might have CF) -> sweat with high sodium chloride content, excessive loss of electrolytes during exercise
60
Q

S+S of cystic fibrosis

A
  • meconium ileus (newborns first stool that is abnormally thick and sticky, blocks the small intestine) -> may occur at birth
  • salty skin -> may lead to a sweat test
  • signs of malabsorption -> steatorrhea (fatty stool), abdominal distention, constipation
  • chronic cough and frequent respiratory infections
  • failure to meet growth milestones
  • can lead to car pulmonale -> due to pulmonary fibrosis and vasoconstriction, heart has to work harder to push blood into the lungs
61
Q

diagnosis of cystic fibrosis

A
  • gentic testion
  • sweat testing
  • stool test
  • radiographs
  • pulmonary function tests
  • ABGs
62
Q

tx of cystic fibrosis

A
  • chest physiotherapy
  • well balanced diet
  • regular, moderate, aerobic exercise

average lifespan = 37 yrs
-> due to respiratory failure or cor pulmonale

63
Q

lung cancer

A

90% of cases is related to smoking

women are more susceptible

cigarette smoke predisposes to malignant neoplasm because smoking causes metaplasia and dysplasia in the epithelium

detected late usually

early sings:
- productive cough
- facial or arm edema
- headahce
- dysphagia

effects:
- obstruction of airflow
- inflammation and bleeding
- tumor may cause pleural membrane erosion
- paraneoplastic syndrome -> when tumour cells secrete hormones or hormone like substances

64
Q

systemic signs of lung cancer

A
  • weight loss
  • anemia
  • fatigue
65
Q

signs of paraneoplasric syndrome

A
  • indicated by signs of an endocrine disorder
  • related to the specific hormone secreted
66
Q

diagnosis of lung cancer

A
  • imaging -> xray, CT scans, MRI, PET
  • chest radiographs
  • bronchoscopy
  • biopsy
67
Q

tx of lung cancer

A
  • surgical resection
  • radiation
  • chemo
  • photodynamic therapy (laser to destroy cells)
68
Q

asthma

A

chronic inflammatory disease

bronchial obstruction -> severe but reversible periods

in people with hypersensitive or hyper responsive airways

frequent attacks can cause permanent lung damage

may occur as a child or adult

69
Q

extrinsic asthma

A

typical onset in children

acute episode triggered by type 1 hypersensitivity reactions (type 1 gives rise to allergies)
- stimuli include an inhaled antigen

-Ige antibodies stick onto mast cells and basophils

  • allergic reaction cause bronchoconstriction and mucus secretion

allergic reaction is presented as asthma

70
Q

intrinsic asthma

A

onset occurs in adulthood

hyper responsive tissue in airway initiates acute attack

stimuli include
- respiratory infection
- stress
- cold
- inhalation of irritants
- exercise
- drugs

71
Q

extrinsic asthma steps and effects

A
  1. first 10 to 20 mins
    - activated mast cells release histamine -> inflammation of mucosa with edema, brochoconstriction, secretion of mucus, partial or complete obstruction of airflow
  2. 4-8 hours
    - leukocytosis (proliferation and migration of basophils, neutrophils, and eosinophils), due to the activated macrophages secreting chemokines which attract more WBC
    - eosinophils releases leukotrienes prolonging inflammation, bronchonstriction, and epithelial damage
  3. if attack continues…
    - partial obstruction due to air trapping, air trapped in the alveoli
    - hyperinflation of the lungs -> less force is available to move air out and forces expiration often collapses the bronchial wall
  4. total obstruction
    - mucus plug completely blocks air flow, leads too atelectasis
    - hypoxemia triggers vasoconstriction of pulmonary partiers, which increases workload for the right side of the hear leading to right sided HF
    - more attacks = more damage = lead to COPD
72
Q

mechanisms of intrinsic asthma

A

not sure -> chronic T cell activation to internal antigen?
or ANS imbalance?

both types of asthma can lead to damage to epithelial cells, blood vessel proliferation and permanent remodelling

73
Q

S+S of asthma

A
  • non productive cough (due to thickened mucus)
  • SOB
  • tight in chest
  • wheezing
  • tachpnea
  • hypoxia
  • laboured breathing
  • tachycardia
    -pulsus paradoxus ( BP differs on inspiration and expiration, large decrease in systolic BP during inspiration >10mmHg)

people can outgrow asthma

74
Q

risk factors of asthma

A
  • family history -> allergies, possibly genetic
  • viral upper respiratory tract infections
  • sedentary, obesity, pollutants
  • rural kids are less at risk
75
Q

ABGs in asthma attacks

A
  1. respiratory alkalosis
    - initially due to hyperventilation
  2. respiratory acidosis
    - due to air trapping, less oxygenated blood and CO2 builds up
  3. severe respiratory distress (decreased respiratory effort with weak cough)
    - hypoventilation leads to hypoxemia and respiratory acidosis, and loss of cell function
  4. respiratory failure
    - PaO2 < 50mmHg
    - indicated by decreasing responsiveness, cyanosis
76
Q

status asthmaticus

A
  • persistent severe attack of asthma
  • doesn’t respond to inhalers
  • medical emergency
  • may be fatal due to severe hypoxia and acidosis -> lead to cardiac arrhythmia/CNS depression

to prevent:
- use peak flow meter
- take meds as prescribed

77
Q

diagnosis of asthma

A
  • spirometry lung tests -> reduced forced expiratory volume

general
- skin test for allergic reactions
- avoidance of triggers
- good ventilation

78
Q

glucocorticoids in asthma

A

blocks chemotaxis of neutrophils and eosinophils

79
Q

prevention and treatment for chronic asthma

A

must take before an attack occurs

  • leukotriene receptor antagonists
  • cromolyn sodium -> reduce WBC activity
  • smooth muscle relaxants
80
Q

cor pulmonale

A

right sided CHF due to pulmonary hypertension caused by lung damage

81
Q

emphysema

A

destruction of alveolar walls
leads to large, permanently inflated alveolar air spaces

progressive difficulty with expiration

increased air trapping, overinflation of lungs, barrel chest

classified on specific location:

centriacinar = enlarged spaces in the central region of the alveoli

panacinar(global) = all of the alveoli sac is affect

82
Q

contributing factors to emphysema

A
  • genetic deficiency - only 1%, the rest is due to smoking
    -> lack of alpha 1- anti trypsin, is needed to decrease elastase activity -> degrades elastic fibres in alveoli
  • cigarette smoke
  • increases number of neutrophils which release proteases -> also decreases alpha 1 - anti trypsin -> more elastase -> more elastic fibre breakdown
  • pathogenic bacteria
    -> also relates proteases
83
Q

elastase

A

released from neutrophils and macrophages as they protect the lungs

breaks down elastic fibres that hold the alveoli open -> increased air trapping

from cigarette smoke or infections

84
Q

ventilation-perfusion ratio

A

if there’s little oxygenated blood in the alveoli, the pulmonary arteriole constricts -> in COPD this can lead to pulmonary HTN

if there’s oxygenated blood in the alveoli, the pulmonary arteriole dilates

85
Q

S+S of emphysema

A
  • slow onset
  • dyspnea (difficulty breathing)
  • hyperventilation
  • barrel chest
  • sitting foward
  • weight loss
  • clubbed finger
86
Q

tx of emphysema

A
  • avoidance
  • immunization
  • pulmonary rehab
  • bronchodilators
  • breathing techniques
  • surgical interventions
87
Q

chronic bronchitis

A

inflammation, obstruction, from repeated infections

chronic productive cough lasting for 3 months or longer per year in 2 subsequent years

hx of smoking or living in urban area can cause inflammation

leads to hypertrophy or hyperplasia of mucus glands, increased number of goblet cells

can cause pulmonary HTN

88
Q

pink puffer

A

= emphysema

89
Q

blue bloaters

A

= chronic bronchitis

  • cyanosis
  • SOB
  • excess body fluid, ascites or edema
90
Q

S+S of chronic bronchitis

A
  • constant productive cough
  • tachypnea, SOB
  • frequent thick and purulent secretion
  • bronchiectasis -> abnormal large bronchioles
91
Q

polycythemia

A

abnormally high level of RBC

when someone is hypoxemic, the kidney make more erythropoietin and increases the number of RBCs

92
Q

tx of chronic bronchitis

A
  • cessation of smoking
  • tx of infection
  • vaccination
  • expectorants
  • bronchodilators
  • chest therapy
  • supplemental O2
  • nutritional supplements
93
Q

pulmonary embolus

A
  • clot or mass that obstructs pulmonary artery or branch
  • depends on material, size, location

small emboli may occlude a small area of lung, still be able to live

large emboli may cause sudden death

90% of pulmonary emboli come from DVT

94
Q

S+S of pulmonary emboli

A

small emboli:
- transient chest pain, cough, dyspnea

large emboli:
- increased chest pain. with coughing or deep breathing, tachypnea, dyspnea develop suddenly
- vasoconstriction reflex, less blood return to heart, decreased cardiac output
- cough with hemoptysis (blood)
- fever
- hypoxia

massive emboli:
- severe crushing chest pain
- low BP
- rapid weak pulse
- loss of consciousness

95
Q

risk factors of PE

A
  • immobility -> DVT
  • trauma
  • surgery to legs
  • CHF
  • cancer
  • long airline flights
  • dehydration
96
Q

atelectasis

A

non aeration or collapse of a lung

alveoli become airless

process interferes with blood flow through the lungs

gas exchange is impaired

97
Q

obstructive atelectasis

A

total obstruction of airway

blocking bronchioles

collapse of alveoli

98
Q

compression atelectasis

A

mass/tumor puts pressure on a part of lung causing pressure within the pleural cavity

increased air/fluid/mass leads to loss of adhesions between pleural membranes

99
Q

pleural effusion

A

presence of excessive fluid in the pleural cavity

effect depends on the amount of fluid

prevents the expansion of the lung

100
Q

contraction atelectasis

A

fibrotic tissue in lungs or pleural

contracts, restricts expansion, leads to collapse

101
Q

postoperative atelectasis

A

24-72 hours post surgery

due to pain or abdominal distention (shallow breaths), anesthetics, increased secretions

encourage mobility and deep breathing

102
Q

transudate effusions

A

watery effusions due to hypertension

due to HTN

103
Q

exudative effusion

A

response to inflammation

protein and WBC leak into pleural cavity

104
Q

hemothorax

A

blood in the pleural cavity

105
Q

empyema

A

purulent fluid in pleural cavity

106
Q

pneumothorax

A

air in the pleural cavity

107
Q

closed pneumothorax

A

rib cage intact

simple/spontaneous pneumothorax:
- tear on lung surface

Secondary pneumothorax:
- leakage coming from alveoli -> emphysema bleb
- from a associated respiratory disease

108
Q

open pneumothorax

A

puncture wound

sucking wound

large opening in chest wall

may be some movement of the trachea and mediastinum

109
Q

tension pneumothorax

A

flap closing over the hole, creates more pressure

will effect the healthy lung as well

traps air in lungs

110
Q

hypothalamus

A

produces ADH and oxytocin directly

111
Q

anterior pituitary gland

A

produces:
ACTH
TSH
GH
PRL
FSH
LH
MSH

112
Q

posterior pituitary lobe

A

releases oxytocin and ADH

113
Q
A
114
Q

lubb

A

closing of the AV valves

turbulence of the blood that makes the sound

115
Q

dubb

A

closure of the semilunar valves

turbulence of the blood that makes the sound

116
Q

pulse deficit

A

difference in rate between the apical and radial pulse

the pulse is not reaching the periphery due to decreased stroke volume -> resulting from poor filling or poor ejection

117
Q

conduction of the heart

A
  1. SA node (contracts the atria) -> pacemaker of the heart, will use the cardiomyocytes to conduct to the AV node
  2. AV node (contracts the ventricles) -> located in the floor of the right atrium
    - can become the pacemaker if the SA node stops working
  3. AV bundle (bundle of His)
  4. purkinje fibres -> terminal fibres
118
Q

p wave

A

depolarization of atria

119
Q

QRS

A

depolarization of ventricles

120
Q

T wave

A

repolarization of ventricles

121
Q

cardiac control centre

A

medulla oblongata

controls rate and force of contraction in response to baroreceptors and chemoreceptors

creates either a SNS or PNS stimulation

SNS = increased HR (speed up the depolarization rate on the SA node) -> will dump epinephrine on the SA node (beta 1 receptors)
PNS = decreased HR -> dumps Ach on the SA node -> will depolarize slower by opening K+ channels = hyper polarize

122
Q

baroreceptors

A

one in the aortic arch and the carotid artery

detects changes in BP

123
Q

chemoreceptors

A

detect changes in blood pH, pCO2, pO2

located in the brain ventricles, aorta, and carotid arteries

124
Q

cardiac output

A

CO or Q

blood ejected by a ventricle in one min

CO = SV x HR

average = 4900-5000 mL

125
Q

stroke volume

A

volume of blood pumped out of a ventricle per contraction

126
Q

preload

A

amount of blood delivered to the heart by venous return

127
Q

afterload

A

force required to eject blood from ventricle, determined by peripheral resistance in arteries

left ventricle -> aorta

128
Q

starlings law

A

increasing the amount of fluid going into the heart (ventricle fill volume) results in a corresponding increase in the SV

129
Q

respiratory pump

A

during inspiration, pressure in thoracic cavity drops which increases pressure in vein in thorax

sucks blood up like a straw

130
Q

anastomosis

A

connected between beaches of two arteries

lots occurs in the apex

131
Q

collateral circulation

A

if an artery in the heart is blocked, it will release cytokines that will stimulate near by arteries to grow to provide circulation to that area of the heart

132
Q

right coronary artery

A

conduction disturbances

nourishes the SA and AV node

133
Q
A

Pathophysiology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions