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CardioResp > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What type of cells in respitory tract correlate with the following functions

Conduction, gas exchange, host defense, communication, olfaction

A
  • Conduction (the flowing of air) – pseudostratified, columnar, both of which can be ciliated
  • Exchange of gases – simple squamous epithelium
  • Host defense
    • Simple squamous, pseudostratified, columnar, stratified squamous +/- keratinization
  • Communication
  • Olfaction – cells with chemoreceptors
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2
Q

Function of squamous mucosa

A
  • On the left, stratified squamous with keratinization is in areas with mechanical trauma (i.e. the vocal cords where they slam together)
    • Stratified squamous (+/- keratin) are in areas of mechanical trauma – the mouth, the tonsils, the vocal cords, the first portion of the nose
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3
Q

Function of respirtory mucosa

A
  • On the right, the respiratory mucosa have goblet cells which secrete mucous and cilia to move the mucous + antigen/dust/particles out of the respiratory tract
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4
Q

Function of following olfactory cell types..

sustentacular nuclei, olfactry nuclei, Bowman glands

A

The sustentacular nuclei are for structure/barrier

The olfactory cell nuclei are olfactory neurons that turn over every month

Beneath the surface with chemoreceptors, Bowman’s Glands secrete a fluid that dissolves the chemicals that give scents

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5
Q

How many times do bronchi branch

A

23

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6
Q

Epithelial type 1 versus 2

A
  • Epithelial type I cells participate in gas exchange
  • Epithelial type II cells generate surfactant
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7
Q

Explain this pic

A
  • C is the capillary
  • A is the alveolar space
  • O2 crosses the plasma membrane of the cells lining the alveolus and the capillary (2 cells with thin plasma membranes) and a basement membrane to diffuse into blood
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8
Q

Identify

A

right: respiratory mucosa
left: stratified squamous

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9
Q

Triggers for PE

A
  • Trigger for thrombus formation: Virchow’s Triad
    • Endothelial damage
    • Hypercoagulability
    • Stasis
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10
Q

Signs of PE (5)

A
  • Signs
    • DVT – common thrombus that can travel to the lung
    • Elevated JVD – backup of fluid due to increased pulmonary resistance
      • In lung with clot, perfusion decreases
      • In lung without clot, perfusion increases because the blood has to go somewhere
    • Tachycardia – decreased SV leads to increased HR to maintain CO
    • Tachypnea – higher RR compensating for the increased PCO2
      • In lung with decreased perfusion, there is a increased V/Q ratio
      • The lung will have an area that is ventilated, but not perfused, leading to increased A-a gradient with O2 and increased PaCO2
    • Shock – decreased CO due to decreased volume return to left side of heart
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11
Q

Symptoms of PE (3)

A
  • Symptoms
    • Chest pain – infarction of lung
    • SOB – increased PCO2
    • Syncope – decreased CO
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12
Q

Complications of PE (3)

A
  • Complications
    • Mortality when untreated: 30%
    • Recurrent embolism due to thrombogenicity of first embolism
    • Recurrent PEs require lifetime treatment
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13
Q

Explina the rationale behind these PE diagnosistic tests

EKG, CT angiography, scintigrapghy, D-dimer

A
  • EKG shows inverted Tw, showing the possibility for ischemia + tachycardia
  • CT pulmonary angiography
    • Avoid in renal failure
  • Ventilation-perfusion scintigraphy
    • Ventilation scan: inhalation of radiotracer
    • Perfusion scan: injection of radiotracer albumin
      • Can see hypoxic pulmonary vasoconstriction in lung with PE
  • D-Dimer – fibrin degradation product
    • Highly sensitive (good at ruling diagnosis out) and low specificity (not good at ruling diagnosis in)
    • Because of low specificity, you need other diagnostic tests to confirm a PE diagnosis
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14
Q

Acute vs, Longterm tx of PE

A
  • Acutely: enoxaparin or unfractionated heparin
  • Long term: oral Xa inhibitors or warfarin
  • If unable to anticoagulated: IVC filter
  • When serious, give the clot buster! Give systemic thrombolytics: tPA
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15
Q

Varenicline

MOA, Use, AE

A

MOA:Nicotine receptor agonist

Use: Eases withdrawal symptoms and blocks pleasurable effects

AE:

  • Transient nausea
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16
Q

Bupropion

MOA, Use, AE

A

MOA:Inhibits dopamine reuptake (lasting feeling of pleasure)

Use: Smoking cessation aid

AE:

  • Tremors
  • Insomnia
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17
Q

Omalizumab

Class, MOA, Use, AE

A

Class:MAB

MOA:Binds to IgE

Use: allergic asthma

AE:

  • expensive
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18
Q

Ipratropium

Tiotropium

Class, MOA, Use, AE

A

Class:Anticholinergics

MOA:Block M3 receptors (Gq receptors)

Use: Bronchodilation

AE:

  • Dry mouth (opposite of SLUD)
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19
Q

Theophylline, caffeine

Class, MOA, Use, AE

A

Class:Methylxanthines

MOA:

  • Inhibits PDE3, activating PKA and causing vasodilation
  • Inhibits PDE4, inhibiting inflammatory processes
  • Enhance catecholamine secretion to work on beta-2

Use: Used if other drugs do not work, Nocturnal asthma

AE:

  • Stimulant
  • Diuretic affects
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20
Q

Albuterol (short-acting)

Salmeterol (long-acting)

Class, MOA, Use, AE

A

Class:Beta-2 agonists

MOA:Beta-2 agonist

Use: Bronchodilation

AE:

  • Tachycardia
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21
Q

Montelukast

Class, MOA, Use, AE

A

Class:Leukotriene modifiers

MOA:Acts on leukotriene receptors C4, D4, E4, decreasing LT effect on Gq receptors

Use: Decreases bronchoconstriction

AE:

  • Well Tolerated
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22
Q

Cromyln

Class, MOA, Use, AE

A

Class:Mast cell inhibitor

MOA:Stabilize plasma membrane of mast cells and basophils and eosinophils to prevent degranulation and release of histamine and leukotrienes

Use: Prevents degranulation and release of histamine and leukotrienes

AE:

  • Well Tolerated
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23
Q

Fluticasone

Budesonide

Class, MOA, Use, AE

A

Class:Glucocorticoid

MOA:Acts as a nuclear transcription factor to antagonize mucous production and inflammatory mediators

Use: Prophylaxis, Upregulation of beta receptor

AE:

  • Thrush (can avoid with water)
  • Change in vocal chords (can avoid with water)
  • Decrease in bone density
  • Abruptly stopping drug is bad because cortisol inhibits HPA
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24
Q

What is the pharyngeal pouch made of…

A

The pharyngeal pouch is made up of cells from the neural crest, endoderm, mesoderm, and ectoderm

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25
Q

What strucutres come form the endoderm, splanchnic mesoderm, somatic mesoderm

A
  • The endoderm forms the pulmonary epithelium and glands of the larynx, trachea, and bronchi
  • The splanchnic mesoderm forms the cartilage, connective tissue, visceral pleura, and smooth muscle
  • The somatic mesoderm forms the parietal pleura (which is why you can feel pain)
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26
Q

Lung Development

What happens in week 6,7,16,24,32

A
  • Week 6: secondary bronchial buds form, which represent future lung lobes

Week 7: tertiary bronchial buds form, which represent future bronchopulmonary segments

Week 16: terminal bronchioles form

Week 24: vasculature and first primitive alveoli form

Week 32: mature alveoli develop

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27
Q

Lung Development

What happens in week 4 and 5

A
  • Week 4: the laryngotracheal diverticulum from the endoderm and mesoderm forms the respiratory diverticulum (lung bud)
    • Endoderm is internal epithelium
      • Initial proliferation of internal epithelium occludes larynx, but at week 10, apoptosis leads to larynx recanalization
    • Mesoderm is connective tissue and smooth muscle
  • Week 5: Respiratory diverticulum branches into left and right bronchial buds
    • This process creates the carina (septum) in the laryngotracheal tube resulting in the formation of the trachea (which is everything superior to the bronchial buds)
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28
Q

Describe the Pseudoglandular stage

A
  • Pseudoglandular stage – 5 to 17 weeks
    • The developing lung at this point resembles a branched, compound gland
    • At this point, there are no alveoli, so respiration is not possible
      • Also only modest vascularization
    • Conductive structures (aka bronchi) are the only ones developed
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29
Q

Describe the Canalicular Stage

A
  • Canalicular Stage – 16 to 26 weeks
    • Terminal bronchioles mature
    • Alveolar ducts begin to form… prognosis of premature babies is poor at this stage
    • Highly vascularized
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30
Q

Describe the Terminal Saccular Stage

A
  • Terminal Saccular Stage – 24 weeks to birth
    • Increase in the number of primordial alveoli
    • Surfactant production increases
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31
Q

Describe the alveolar stage

A
  • Alveolar Stage – 32 weeks to 8 years old
    • Alveolaocapillary membrane forms and proper gas exchange can occur
32
Q

Laryngeal atresia

A
  • Laryngeal atresia – failure of recanalization –> obstruction of the upper airway
33
Q

Laryngeal web

A
  • Laryngeal web – partial occlusion due to mucous membrane covering the vocal cords
    • Results in a hoarse cry
34
Q

Tracheo-esophageal fistulas (TEF)

A
  • Tracheo-esophageal fistulas (TEF) – incomplete division of the respiratory diverticulum in week 4
    • Results in an abnormal connection between the esophagus and trachea, allowing food to enter the lungs (depending on the type of TEF)
35
Q

Tracheal bronchus

A

Tracheal bronchus – extra branches off of the trachea

36
Q

Respiratory Distress Syndrome (RDS)

A

Respiratory Distress Syndrome (RDS) – inadequate surfactant function, causing lungs to collapse and inadequate ventilation of some alveolar sacs

37
Q

obstructive lung diseases

symptoms (4)

A

Dyspnea (at rest)

Wheezing

Cough

Episodic

38
Q

obstructive lung diseases

Pathophysiology

A
  • Obstruction of air flow → air trapping in lungs→ FRC, TLC, and RV increases → barrel chest
  • Pulmonary Function Tests: large decrease in FEV1, smaller decrease in FVC→ hallmark decrease in FEV1/FVC ratio
39
Q

obstructive lung diseases

signs (3)

A

Diminished air flow

Wheezes/rhonchi

Chest hyperinflation

40
Q

asthma

triggers, patho. epidemiology, pathphysiology

A
  • Triggers: viral URIs, allergens, stress, exercise
  • Pathology: smooth muscle hypertrophy and hyperplasia due to eosinophilia
  • Epidemiology: 5 to 20% of population depending on age
  • Pathophysiology:
    • Reversible bronchoconstriction due to hyperresponsiveness
    • FEV1 decreases: bronchoconstriction leads to decreased flow of air during expiration
41
Q

chronic bronchitis COPD

presentation, epidemiology, patho

A
  • Presentation: “blue bloater” – hypoxemia due to right to left shunt of blood, cough with sputum
  • Epidemiology of COPD as a whole: 6-8% and is the only major cause of death that is increasing in prevalence
  • Pathology: hypertrophy and hyperplasia of mucus-secreting glands due to neutrophilia
42
Q

emphysema COPD

types

A

Centrialobular – associated with smoking

Panlobular – associated with alpha-1 antitrypsin deficiency

43
Q

emphysema COPD

presentation, patho, pathogensis, epidemiology

A
  • Presentation: “pink puffer” – pink complexion and pursed lips
  • Pathology: enlargement of air spaces due to collapse of alveoli
    • Loss of elastic fibers leads to decreased lung recoil à barrel chest
  • Pathogenesis: inflammation of the lungs normally leads to release of proteases by neutrophils and macrophages à protease damage causes destruction of alveolar air sacs
    • Smoking: excessive inflammation and protease mediated damage
    • Alpha-1 antitrypsin: neutralizes proteases
  • Epidemiology of COPD as a whole: 6-8% and is the only major cause of death that is increasing in prevalence
44
Q

Broncheictasis

CF vs. non-CF

A
  • Cystic Fibrosis Pathogenesis: impaired ciliary movement → mucus plug→ bronchodilation → mucus buildup → infection → chronic necrotizing infection → permanent dilation of bronchioles → loss of airway tone → air trapping
  • Non-CF Pathogenesis: immunodeficiency → infection → chronic necrotizing infection → increased cytokine production → increased mucus production → obstruction of airway → permanent dilation of bronchioles → loss of airway tone → air trapping
45
Q

Bronchiolitis

pathogensis, etiology

A

Pathogenesis: inflammatory disorder of small bronchioles

Etiology: often viral but can be idiopathic

46
Q

restrictive lung diseases

descritpion and PFT results

A
  • Restricted lung expansion (increased elastic recoil) causes decrease in forced vital capacity and total lung capacity
  • Pulmonary Functional Tests: proportional decrease in both FEV1 and FVC leads to relatively stable FEV1/FVC ratio
47
Q

restrictive lung diseases

pathogensis, symptoms, signs, lab findings

A
  • Pathophysiology
    • Antigen is picked up by the macrophages in the alveolar sacs à recruitment of fibroblasts à laying down of collagen à fibrosis
  • Symptoms
    • Short, shallow breaths
    • Dry cough
    • Flu-like illness may precede disease
  • Signs
    • Tachypneic
    • Cyanosis à clubbing
    • Chest CT: honeycomb appearance of lungs
48
Q

IDK WHAT TO DO ABOUT THIS PIC BUT HERE IT IS

MEMORIZE IT I GUESS

A
49
Q

Pneumoconiosis - Coal

Clinical Description, Pathological features

A

CD: Silicosis – Coal Workers’ Pneumoconiosis – inhalation of coal particles

PF:Anthracosis – small collections of dust-laden macrophages near respiratory bronchioles

50
Q

Pneumoconiosis - Silicosis

Clinical Description, Pathological features

A

CD: Silicosis – decades exposure to sand in mining industry with increased incidence of TB

PF:Dense pink fibrosis surrounded by histiocytes that have polarizable birefringent crystals

51
Q

Pneumoconiosis - asbestos

Clinical Description, Pathological features

A

CD: Asbestos – silicate mineral with heaviest exposures in industries

PF:Lung adenocarcinoma, malignant mesothelioma, pleural plaques (fibrocalcific formation on parietal pleura), and asbestosis (long-thin crystal-like finding)

52
Q

Hypersensitivity pneumonitis

Clinical Description, Pathological features

A

CD: Type III or Type IV hypersentitivity reaction that produces granulomas

PF:Chronic inflammation of the bronchioles, granulomas, and fibrosis

53
Q

Interstitial pneumonia/follicular bronchiolitis from Collagen Vascular Disease

Clinical Description, Pathological features

A

CD: Common in Rheumatoid Arthritis, SLE, and Sjogren’s Syndrome

PF:

Interstitium is thick but architecture is respected and there is not a lot of fibrosis

  • Interstitial pneumonia (top) – many lymphocytes have invaded the interstitium but it is more cellular without fibrous tissue
  • Follicular bronchiolitis (bottom) – chronic inflammation with dark lymphoid aggregates
54
Q

Sarcoidosis

Clinical Description, Pathological features

A

CD: Systemic non-necrotizing granulomatous disease with bilateral hilar and mediastinal lymphadenopathy

PF:

Multinucleated giant cell due to fused histiocytes forming small nodules in interstitium

  • Schaumann body – Ca2+ and protein deposit in the giant cell
  • Asteriod body – cytoskeletal proteins in the giant cell
55
Q

Usual Interstitial Pneumonia (UIP)

Clinical Description, Pathological features

A

CD:

  • Diagnosis if there is no other explanation
  • Chronic symptoms upon presentation

PF:

  • Area of many inflammatory cells
  • Fibroblast foci with significant proliferation and collagen deposition
56
Q
A

Usual Interstitial Pneumonia (UIP)

57
Q
A

Sarcoidosis

58
Q
A

Interstitial pneumonia

59
Q
A

Follicular bronchiolitis

60
Q
A

Hypersesntivity pneumonitis

61
Q
A

Asbestos

62
Q
A

Silicosis

63
Q
A

Coal Workers’ Pneumoconiosis

64
Q

Spiromentry versus complete PFTs

A
  • Spirometry and complete PFTs provide information on lung volumes and capacities
    • PFTS give FRC, RV, TLC, and DLCO, which spirometry cannot
    • Spirometry can only “suggest” restrictive disease, which PFTs can confirm
  • Useful for diagnosis and disease monitoring
65
Q

Explain this pic

A
  • Extrathoracic airway obstruction
    • Flow becomes obstructed during inspiration because atmospheric pressure is greater than tracheal pressure
  • Variable intrathoracic airway obstruction
    • Flow becomes more obstructed during expiration because the difference between the intrapleural pressure and the alveolar pressure is less than normal
66
Q

process, focus and exampls of

asphyxiation, COPD, asthma, granulomatous lung disease, pneumoconiosis

A
67
Q

Anterior Mediastinal Diseases:

A
  • The Four Ts + Other:
    • Thymoma
    • Thyroid – goiters
    • Teratoma
    • Terrible Lymphoma
    • Congenital Diaphragmatic Hernia
68
Q

Middle Mediastinal Disease:

A
  • Cardiac/Great Vessels
  • Superior Vena Cava Syndrome
69
Q

Superior Vena Cava Syndrome

A

Patterns of Differentiation in Etiological Causes

Tumor – will cause dilated veins of chest

Trauma – will cause demarcated cyanosis of upper body

70
Q

Posterior Mediastinum Diseases:

A
  • Neurogenic tumors
  • Spine tumors
  • Descending aortic aneurysm/dissection
  • Bochdalek or hiatal hernias
  • Esophageal tumors
71
Q

Pneumomediastinum

some characteristics and ways to treat

A
  • You may or may not feel air under the skin around the neck region or chest on physical exam (“subcutaneous emphysema”)
    • Ability to palpate gas under the skin
    • Think crepitus around neck
  • You need to find the origin of the hole so as to control the leak; the differential includes anything along the aero-digestive track (esophagus, trachea, etc.)
    • Trauma of upper airway
    • Perforation of the stomach
    • Rupture of the esophagus
    • Rupture of the trachea
72
Q

Pancoast tumore

description and complications

A
  • Tumor near the apex of the lung that compresses the brachial plexus
  • Result is Horner’s Syndrome:
    • Anhidrosis – lack of facial sweating
    • Miosis – constricted pupil
    • Ptosis – dropping of eyelid
73
Q
A

Pneumomediastinum

74
Q
A

pancoast tumor

75
Q
A

small vessel vasculitis

excess of neutriphils in interstitial space

76
Q
A

fibrinous pleuritis

(right side) look at the extra fiberous layer - not normal

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