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Patho Exam 2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Aspiration - restrictive or obstructive

A

restrictive

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2
Q

Atelectasis

A

restrictive

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3
Q

bronchiolitis

A

restrictive

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4
Q

pulmonary fibrosis

A

restrictive

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5
Q

inhalation disorders

A

restrictive

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6
Q

restrictive disorders

A

things that reduce lung compliance

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7
Q

pulmonary edema

A

restrictive

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8
Q

most common cause of pulmonary edema?

A

left-sided heart disease

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9
Q

other causes of pulmonary edema?

A

toxic injury to capillary endothelium, such as with ARDS or blockage of lymphatic vessels

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10
Q

s/s of pulmonary edema?

A

-dyspnea, orthopnea, hypoxemia, and increased work of breathing -inspiratory crackles -dullness to percussion over bases -s3 gallop and cardiomegaly -JVD -severe: pink frothy sputum, hypoventilation, and hypercapnia

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11
Q

3 causes of pulmonary edema?

A

-blockage of lymphatic vessels -injury to capillary endothelium (ARDS) -Valvular dysfunction, CAD, LVF

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12
Q

I think ARDS and pneumonia are obstructive or restrictive?

A

restrictive

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13
Q

Causes of ARDS

A

sepsis, COVID-19, severe trauma

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14
Q

ARDS characterized by:

A

-v/q mismatch with with shunting -dyspnea and hypoxemia even with oxygen supplementation -hyperventilation and respiratory alkalosis at first and then later hypercapnia and respiratory acidosis and worsening hypoxemia -organ dysfunction

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15
Q

treatment for pulmonary edema when caused by heart failure

A

-diuretics -vasodilators -drugs that improve the contraction of the heart muscle -goal is to improve cardiac output and volume status

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16
Q

Clinical manifestations of COPD

A

wheezing, increased work of breathing (accessory muscle use), decreased forced expiratory volume in one second (FEV1)

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17
Q

List of obstructive pulmonary diseases

A

COPD (emphysema and chronic bronchitis), asthma

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18
Q

COPD is innate or adaptive immune response? COPD is reversible or not? What WBCs is involved? Low what?

A

-Innate immunity -Not fully reversible -Innate immune response to toxins and irritants -NEUTROPHILS and CD8 (cytotoxic lymphocytes) -Low TH2

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19
Q

Asthma is innate or adaptive immune response? Is reversible or not? What WBCs is involved? Responsive to what tx?

A

-ADAPTIVE Type I hypersensitivity -Reversible -Hypersensitivity to allergens: involves both innate and adaptive -Eosinophilic inflammation involving TH2 (t helper) lymphocytes -Responsive to corticosteroid therapy

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20
Q

A1 antitrypsin deficiency can cause emphysema – AAT does what?

A

AAT is synthesized by the liver and is a serine protease inhibitor. It prevents breakdown of proteins by enzymes. AAT prevents elastase from digesting the alveolar septi of the lungs

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21
Q

Chronic bronchitis causes what? Think patho and s/s

A

Bronchial edema, hyper-secretion of mucus, bacterial colonization of airways s/s: -chronic, productive cough -purulent sputum -hemoptysis -mild dyspnea initially -cyanosis -peripheral edema (due to cor pulmonale) -crackles, wheeze

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22
Q

Complications from chronic bronchitis

A

-polycythemia vera d/t hypoxemia - increase in RBC -pulmonary HTN d/t reactive vasoconstriction from hypoxemia -Cor pulmonale from chronic pulmonary HTN

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23
Q

what is cor pulmonale?

A

Cor pulmonale is a condition that causes the right side of the heart to fail. Long-term high blood pressure in the arteries of the lung and right ventricle of the heart can lead to cor pulmonale

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24
Q

Systemic effects of COPD?

A

-renal and hormonal abnormalities -malnutrition -muscle wasting -osteoporosis -anemia

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25
Q

How do you definitively diagnose COPD?

A

-spirometry -FEV1/FVC < 70 post bronchodilator is diagnostic of obstructive airway disease (showing it is not reversible)

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26
Q

What does COPD do to FVC and FEV1

A

FVC will be normal or maybe slightly reduced, while FEV1 will be reduced…this is how FEV1/FVC is less than 70

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27
Q

FVC = what? What is normal FEV1/FVC?

A

TV+IRV+ERV 0.75-0.85

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28
Q

What are the most common obstructive pulmonary diseases?

A

-Asthma -Chronic bronchitis -Emphysema

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29
Q

COPD with air trapping

A

remember muscle contraction during expiration causes bronchial walls to collapse and trap air

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30
Q

With both COPD and Chronic Bronchitis

A

airway obstruction, air trapping, loss of surface area for gas exchange, frequent infections

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31
Q

Systemic effects of COPD

A

malnutrition, muscle wasting, osteoporosis, anemia

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32
Q

Dx criteria for chronic bronchitis

A

cough for 3 months out of the year for 2 consecutive years

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33
Q

Primary vs. secondary emphysema

A

primary would be the inherited deficiency of alpha 1 anti-trypsin, and secondary is mainly cigarette smoke but can be air pollution, or childhood respiratory infections

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34
Q

In emphysema what is broken down?

A

proteases break down elastin = loss of elastic recoil of bronchial walls

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35
Q

bullae vs bleb

A

bullae - air spaces within lung parenchyma bleb - air spaces adjacent to pleurae ‘Blebs’ are blister-like air pockets that form on the surface of the lung. Bulla (or Bullae for pleural) is the term used for air-filled cavities within the lung tissue. Bullae and blebs are not effective in air exchange and can lead to pneumothorax

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36
Q

In which type of COPD does hypoventilation and hypercapnia occur later in the disease and why is this?

A

Emphysema d/t compensatory dyspnea and increased rate of breathing (is my guess) -you see hypoventilation and hypercapnia earlier with chronic bronchitis

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37
Q

In which type of COPD do you see dyspnea sooner?

A

Emphysema - initially dyspnea on exertion that progresses to dyspnea at rest

38
Q

Normal AP chest diameter ratio vs Abnormal in COPD w/barrel chest

A

Normal: 5:7 Abnormal: 1:1

39
Q

Emphysema clinical manifestations

A

-tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips -to increase lung capacity: leans forward with arms extended and braced on knees

40
Q

Prolonged expiration

A

Occurs with both chronic bronchitis and emphysema

41
Q

Tx of COPD based on what? What are the mainstays of tx?

A

Symptoms not on grade -Beta agonists and antimuscarinics

42
Q

Beta 2 agonists action?

A

stimulate the beta 2 receptors on bronchial smooth muscles causing them to relax and dilate

43
Q

Antimuscarinic drug action?

A

anticholinergic block the muscarinic and nicotinic receptors on the bronchial smooth muscle leading to bronchodilation

44
Q

Remember chronic hypoxemia and acidosis causes…

A

vasoconstriction leading to pulmonary HTN and cor pulmonale

45
Q

S/s of cor pulmonale

A

peripheral edema, ascites, JVD, anascara (widespread swelling)

46
Q

With asthma the obstruction is _______

A

reversible

47
Q

Esophageal reflux can contribute to

A

development of asthma

48
Q

In asthma what immune cells are responsible

A

IgE on mast cells – IgE binds antigen and causes degranulation of mast cells (bradykinins, histamine, PGs, etc.) Also antigens picked up by dendritic cells presented to TH2 cause more antibody production

49
Q

Remember that asthma is a _______ lung disease

A

obstructive

50
Q

Pathophysiology of asthma

A

-smooth muscle constriction -degranulation of mast cells -mucus accumulation + plugs -hyperinflation of alveoli d/t air getting trapped

51
Q

Early asthma response

A

IgE binds to mast cell and causes degranulation of contents (histamine, PGs, bradykinins, etc.) -This induces bronchospasm, edema from increased capillary permeability, and airway mucus secretion from goblet cells -Increase in IgE production

52
Q

Late asthmatic response

A

-begins 4-8 hrs after early response -inflammatory cells: neutrophils, eosinophils, and lymphocytes -leukotrienes cause prolonged smooth muscle contraction -eosinophil mediators lead to airway scarring Results: -damage to ciliated epithelial cells -synthesis of toxic NO, oxidative injury and chronic inflammation -Untreated chronic inflammation can lead to irreversible airway damage = airway remodeling

53
Q

Clinical effects of late asthmatic response

A

Initially hyperventilation in response to hypoxemia leads to decreased PaCO2 and respiratory alkalosis Later as obstruction progresses, hyperinflation causes CO2 retention and respiratory acidosis Hyperinflation occurs distal to obstruction

54
Q

Likely not asthma - these are isolated and likely NOT asthma

A

-isolated cough -chronic sputum production -SOB associated w/dizziness and paresthesia - panic attack -chest pain -exercise induced dyspnea with noisy INSPIRATION

55
Q

reduced FEV1/FVC with?

A

asthma and COPD However, FEV1/FVC is improved in patients with asthma after bronchodilator (reversible)

56
Q

Can you treat this patient in the office? Acute asthma attack -able to talk in phrases -PEF > 50% predicted or best -Not using accessory muscles -pulse rate 100-120 -O2 sat 90-95% on RA

A

Yes, you can tx this pt in the office

57
Q

What is PEF

A

Peak expiratory flow - maximal rate that a person can exhale during a short maximal expiratory effort

58
Q

Can you treat this asthma patient in the office? -able to talk in only words -agitated -respiratory rate > 30 -use of accessory muscles -Pulse >120 -O2 sat < 90 on RA -PEF <50%

A

NO CALL 911

59
Q

How do you tx acute asthma attack in the office? When would you use epi?

A

-b-2 agonist -O2 if needed sats 93-95% -Epinephrine ONLY if anaphylaxis and angioedema -Oral corticosteroids -ABX are NOT indicated -Education on peak flow meters

60
Q

Asthma action plan - green, yellow, red

A

green = good yellow= may need to change med red = emergency room

61
Q

All asthma should be treated with what?

A

inhaled corticosteroid - because asthma is an inflammatory disease we need to have even pts with mild asthma on inhaled corticosteroids along w/beta adrenergic on PRN basis -Do not use inhaled bronchodilator alone or LABA alone in asthma (ok in COPD)

62
Q

Clinical manifestations of asthma

A

-expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea -pulsus paradoxus (decrease systolic BP with inhalation) -REMEMBER NONPRODUCTIVE COUGHING

63
Q

Know how to interpret ABGs

A

…

64
Q

Remember with asthma hyperventilation initially causes…and then hypoventilation causes…

A

Respiratory alkalosis w/hyperventilation and then respiratory acidosis

65
Q

what causes cystic fibrosis?

A

Abnormal expression of CFTCR gene (cystic fibrosis transmembrane conductance regulator (CFTCR) protein This affects chloride secretion and Na+ reabsorption.

66
Q

What organs does CF affect?

A

respiratory, pancreas, reproductive (vas deferens in men)

67
Q

Pancreatic effects of CF

A

90% pancreatic insufficiency -abnormal ion transport of Cl and Na -thick secretions cause plugging of smaller pancreatic ducts causing autodigestion or atrophy of acinar cells

68
Q

Function of acinar cells

A

The pancreatic acinar cell is the functional unit of the exocrine pancreas. It synthesizes, stores, and secretes digestive enzymes. Under normal physiological conditions, digestive enzymes are activated only once they have reached the duodenum.

69
Q

Lung effects of CF -increased number of what? -End stage causes? -Defective _____ secretion and excess ______ absorption -Chronic inflammation caused by?

A

-mucus plugging -chronic inflammation w/airway remodeling -chronic infections -PUL HTN and COR PULMONALE - end stage -increased number of goblet cells -defective chloride secretion and excess Na absorption -neutrophils - produce oxidants and proteases that damage structural proteins and causes airway remodeling and development of bronchiectasis

70
Q

airway remodeling w/CF can cause?

A
  • bronchiectasis d/t damage of structural proteins of lungs - lungs are unable to maintain structure
  • parenchymal involvement leads to peribronchial fibrosis

-airway obstruction and weakening of the alveoli can lead to formation of bullae and pneumothorax

-hemoptysis from erosion of bronchial arteries

71
Q

With CF which parts of immunity are destroyed?

Which immune modulator causes more problems?

What immune cell plays a role in long-term damage?

A
  • IgG and complement (which are needed to destroy pathogens) - this causes reduction in phagocytosis of pathogens
  • This occurs d/t production of IL-8 - IL-8 also causes proliferation of neutrophil elastase (protease) this causes degradation of structural proteins = bronchiectasis that progresses to respiratory failure
72
Q

Clinical manifestations of CF

A

-wheeze, cough, sputum production (remember dry cough is with asthma)

73
Q

Two tests for CF? Test for abnormality in CFTCR (CF transmembrane conductance regulator)

A

Sweat test > 60mEq/L

OR

Immunoreactive trypsinogen (IRT) blood test

74
Q

Tx for CF?

Nutrition tx? And what to monitor?

A
  • oscillation vest, PEP device, aerosol therapy (hypertonic saline, bronchodilators), abx, targeted therapy w/oral CFTR modulators, lung transplant for end stage
  • Nutrition: monitor growth parameters, control fat malabsorption, maintain adequate protein and caloric intake (HIGH CALORIE SNACKS)
  • Diet is HIGH in CALORIES and FAT
  • Must take exogeenous pancreatic enzymes with meals and snacks in order to absorb nutrients and control malabsorption
75
Q

Remember that pulmonary embolism can be caused by?

A
  • tissue fragments, air, foreign body
  • remember most common cause is thrombotic - embolization of clot from a DVT
76
Q

Virchow’s Triad - from PE slides

what is it?

A

-condition that promotes blood clotting

Triad:

  • venous stasis (immobility, heart failure)
  • hypercoagulation (inherited disorders, malignancy, hormonal)
  • endothelial injury (trauma, caustic IV infusions)
77
Q

Pahtophysiology of PE

What is the V/Q like?

A
  • inflammatory mediators are released + angiotensin II and catecholamines (think epinephrine)
  • this causes widespread vasoconstriction and further impedes blood flow to the lung
  • increased pulmonary artery pressures can cause right heart failure
  • increased v/q
  • decreased surfactant worsens hypoxemia
  • if severe enough, can lead to infarction of lung tissue, dysrthymias, decreased CO, shock, and death
78
Q

What happens to PE clot if no infarction? If infaction what happens?

A
  • embolus will be dissolved by fibrinolytic system
  • affected area shrinks and scars
79
Q

Clinical Manifestations of PE

A
  • pleuritic chest pain (sharp pain w/deep breathing)
  • tachypnea, dyspnea, tachycardia, unexplained anxiety
  • occasionally: syncope or hemoptosis
  • large emboli: pleural friction rub, pleural effusion, fever, and leukocytosis
  • Pleural friction rub is heard on inspiration and expiration and sounds like a low-pitch harsh/grating noise.
80
Q

Dx of PE?

A
  • cxr normal initially
  • ABGs: show hypoxemia and respiratory alkalosis d/t hyperventilation
  • Serum D-Dimer - measures products of thrombus degradation by fibrinolytic system): if normal, PE unlikely
  • ECG: strain on right side of the heart
  • Sprial CT arteriography: highly specific
81
Q

Tx PE

A
  • prevention: early ambulation, pneumatic calf compression, prophylactic anticoagulation
  • oxygen, hemodynamic stabilization
  • anticoagulation
  • fibrinolytic agent depending on how large the clot is
  • emergent embolectomy
82
Q

Explain the process of thyroid secretion from hypothalamus to thyroid gland

A

TRH from hypothalamus goes to ant pit and ant pit secretes TSH and THS travels to thyroid and thyroid releases T3 and T4

83
Q
A
84
Q

explain how the adrenal gland secretes cortisol what are the steps?

A

Corticotrophin releasing hormone (CRH) released by hypothalamus –> anterior pituitary releases adrenocorticotrophic hormone (ACTH) –> adrenal gland secretes cortisol

85
Q

What is Cushing’s syndrome? What is the most common cause?

A
  • anything that causes excess secretion of cortisol
  • exogenous (drugs – most common cause); endogenous – pituitary microadeonma, adrenal adenoma, etc.
86
Q

Effects of cortisol?

A
  • inhibits the immune system
  • inhibits bone formation
  • raises blood glucose

-increases metabolism

-increases alertness

Cortisol plays a key role in the stress response

87
Q

Clinical features of Cushing’s Disease

A
  • prone to infections
  • osteoporosis
  • hyperglycemia and could cause TypeII DM
  • increased metabolism
  • increased alertness

Clinical picture: central obesity w/abdominal striae, round face, thin arms, proximal muscle weakness, fatigue, SOB, moon face, thin skin, fat deposits on back

88
Q

Pneumonic for clinical picture of Cushing’s

A

Mneumonic: Cushing AEO

C- central obesity, Comedones (acne)

U – unusual bruising

S – striae (purple)

H – hypercortisolism, HTN, hirsutism

I – iatrogenic steroid

N – Na and fluid retention

G – glucose intolerance, Gynaecomastia

A – amenorrhea, appearance (plethoric)

E – emotional changes (psychosis, depression)

O – osteoporosis, mOOn facies

89
Q

Diagnosis of Cushing’s

A

Serum cortisol estimation

Loss of circadian rhythm

Dexamethasone suppression test – most common test and most common question

Failure of suppression = adrenal hyperplasia, adrenal adenoma

Suppression positive = pituitary adenoma

90
Q

Dexamethasone Suppression Test - what does it test for and how does it work? What is a positive result in low dose test? What does the high dose test confirm?

A
  • Tests for Cushings
  • Give dexamethasone at 10pm and next morning around 9amm you measure cortisol and ACTH levels
  • There are two stages to the test:

1- Low dose test: 1mg dexamethasone. Use this to make sure the patient has a normal response and a normal adrenal axis OR to confirm that they actually have Cushing’s syndrome. IN NORMAL situation - 1mg of dexamethasone (that acts like cortisol) will act on hypothalamus to suppress CRH and on anterior pituitary to reduce ACTH production. So a NORMAL response would be a reduction in cortisol. This is a negative result. A POSITIVE RESULT would be that cortisol remained high or w/i normal range and this indicates presence of Cushing’s syndrome.

2- High dose 8mg dexamethasone test is to confirm the cause of excessive cortisol production

91
Q

High dose dexamethasone suppression test results

A
  • Low CRH, low ACTH, low cortisol = pituitary adeonma (Cushing’s disease) - big dose of dexamethasone is enought o suppress the ant pituitary adenoma
  • Low CRH, low ACTH, high cortisol = Adrenal gland tumor
  • HIGH cortisol, HIGH ACTH = Lung cacner or some other neoplasm produces ectopic ACTH. Reduces CRH from hypo, reduces ACTH from ant pituitary but still high ACTH from tumor

Patho Exam 2 (4 decks)

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