Brainscape's Knowledge GenomeTM

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


See full index

UWorld > Pulm > Flashcards

Pulm Flashcards

1
Q

What is the gram stain of strep pneumo?

A

Gram + lancet shaped diplococci

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

What is the most common cause of lobar pneumonia?

A

Strep pneumo

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

Why is pO2 in the left atrium and ventricle lower than the pulmonary capillaries?

A

Oxy blood from the pulmonary veins mixes with deoxy blood from the bronchial arteries/thebesian veins in the LA.

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

Where does aspiration pneumonia normally develop?

A

“Swallow a bite, goes down the right”

Right main bronchus is larger, shorter, and straighter.

Due to gravity, people who are supine aspirate to the posterior parts of the upper lobes and superior parts of the lower lobes.

Patients who are upright aspirate into the basilar segments of lower lobes.

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

What nerve is impaired by foreign bodies lodged in the piriform recess?

A

Internal laryngeal nerve, branch of the superior laryngeal (CN X)

This damages the cough reflex

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

What do dyspnea, facial swelling, and dilated collateral veins in the upper trunk indicate?

A

SVC syndrome–tumor compressing the SVC. Most common are lung cancer, then non-Hodgkin’s lymphoma.

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

What is indicated by shoulder pain and Horner’s syndrome?

A

Pancoast tumor of the superior sulcus, arising at the apex of the lungs.

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

How do patients with pulmonary fibrosis minimize the work of breathing?

A

High respiratory rate, low tidal volume (fast, shallow breaths)

This is due to increased elastic resistance

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

How do patients with COPD and asthma minimize the work of breathing?

A

Low respiratory rate/high tidal volume (slow, deep breaths)

This is due to increased airflow resistance

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

What is the difference between minute ventilation and alveolar ventilation?

A

Alveolar ventilation does not include dead space.

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

What is the formula for minute ventilation?

A

Minute ventilation =

tidal volume x breaths/min

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

What is the formula for alveolar ventilation?

A

Alv ventilation =

(tidal vol - dead space vol) x breaths/min

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

Biopsy of a lung lesions shows a large spherule with small, round endospores. What is the cause?

A

Coccidioides.

  • Dimorphic fungus that exists in the environment as mold hyphae
  • Desert of US and Mexico
  • Silver stain shows thick walled spherule packed with endospores
  • Sabouraud’s agar also used
  • Lung disease in immucompetent people and disseminated disease in immunocompromised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the non-selective beta blockers?

A

Nadolol
Timolol
Propanolol

Not Target Pros

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

What are B1 selective beta blockers?

A

Atenolol
Acebutolol
Metoprolol*
Esmolol

AAME (“Aim”) for one target.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do macrophages activate native helper T cells in TB infection?

A

Through IL-12, they induce differentiation into the TH1 subtype

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

How do TH1 cells activate macrophages to improve their ability to ingest TB?

A

Through IFN-gamma

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

What substance produced by macrophages allows them to recruit more monocytes and macrophages?

A

TNF-alpha

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

What is seen in pulmonary actinomyces?

A

Filamentous branching pattern

Sulfur granules

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

What is a risk factor for actinomyces infection?

A

Any mucosal disruption

  • Poor dentition
  • Alcoholics at greater risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for actinomyces?

A

Pencillin

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

What stimulates granuloma formation in TB?

A

CD4+ lymphocytes stimulate macrophages to wall off the bacteria

CD8 does not have a strong role

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

What is the most common lab abnormality seen with Legionella pneumonia?

A

Hyponatremia

  • May be related to inappropriate ADH secretion
  • May be related to renal tubuloiterstitial disease, imparing Na reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What variables determine the total O2 content of blood?

A
  1. Hg concentration
  2. O2 saturation of the Hg (SaO2)
  3. Partial pressure of dissolved O2 (PaO2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the cause of:

  • PaO2: normal
  • SaO2: decreased
  • O2 content: decreased
A

CO poisoning.

Normal amount of O2 dissolved in the blood, but not bound to Hg.

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

What is the cause of:

  • PaO2: normal
  • SaO2:normal
  • O2 content: decreased
A

Anemia (low Hg)

Normal amount of O2 dissolved and the Hg present is saturated, but there is not enough Hg present!

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

What is the cause of:

  • PaO2: normal
  • SaO2: normal
  • O2 content: increased
A

Polycythemia (high Hg)

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

Why is EPO increased in COPD?

A

Hypoxia is sufficient to stimulate EPO production in cortical cells of kidney

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

What is the best antibiotic for treating lung abscess?

A

Clindamycin

- Covers anaerobic oral flora AND aerobic bacteria

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

What drug prevents bronchoconstriction produced by acetylcholine?

A

Ipratroprium

  • Blocks action of Ach at muscarinic receptors
  • Less effective than a b2 agonist in treating asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What differentiates MAC infection from TB?

A

Anemia
Hepatosplenomegaly
Elevated alk phos and LDH
Grows well at high temperatures, optimum growth at 41C

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

What is used for MAC prophylaxis?

A

Azithromycin

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

What kind of metabolic derangement does heroin OD cause?

A

ACUTE respiratory acidosis

  • Suppresses resp centers
  • Causes hypoventilation
  • CO2 retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does MI impact the lungs?

A

Causes LV failure, fluid accumulates in the lung interstitium, results in decreased compliance

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

What is the most common diagnosis for a “coin lesion” with “popcorn calcifications”?

A

Hamartoma

  • Excessive growth of a tissue type native to the organ of involvement
  • Most common in lungs
  • Often contains hyaline cartilage, fat, smooth muscle cells, and clefts lined by respiratory epithelium
  • Benign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the most common benign lung tumor?

A

Hamartoma, aka pulmonary chondroma

- Disorganized cartilage, fibrous, and adipose tissue

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

What is the respiratory defense mechanism for particles 10-15 microns in size?

A

Trapping in the URT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the respiratory defense mechanism for particles 2.5-10 microns in size?

A

Enter the trachea and bronchi, cleared by mucociliary transport

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

What is the respiratory defense mechanism for particles less than 2 microns in size?

A

These are the smallest particles. They reach the terminal bronchioli and alveoli, and are phagocytosed by macrophages

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

How to pneumoconioses arise?

A

Alveolar macros take up dust particles and release cytokines

Cytokines produce injury and inflamm of alveolar cells

Growth factors in PDGF and IGF are released, stimulating fibroblasts to proliferate and produce collagen

Inflammation and fibrosis result

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

What is the normal tracheal PO2 and alveolar PO2?

What is responsible for the difference?

A

Air enters at 150mmHg in the trachea, and then equilibrates in the alveoli to about 104 (balance between tracheal 150 and venous 40)

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

Is O2 equilibration diffusion or perfusion limited?

A

Perfusion
- Means the rate of alveolar capillary perfusion determines the speed at which alveolar air equilibrates with venous blood gases

  • If perfusion is poor, equilibration may not occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the mechanism of Rifampin resistance?

A

Rifampin blocks DNA-dep RNA-poly, inhibiting transcription.

Riframpin resistance = modification of rifampin binding site on the DNA-dep RNA-poly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What do erythema nodosum + arthralgias + hilar lymphadenopathy + elevated ACE levels suggest?

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is liver involvement of sarcoidosis?

A

Non-caseating granulomas

Seen in 75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the possible presentations of sarcoidosis?

A 
Erythema nodosum
Arthralgias
Hilar lymphadenopathy
Elevated aCE
Non-caseating granulomas of liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What does the triad of

  • Acute onset neuro abnormality
  • Hypoxemia
  • Petechial rash

in the background of long bone/pelvic fracture indicate?

A

Fat embolism syndrome

- Traumatic event dislodges fat from bone marrow, and is lodged in pulmonary microvessels

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

What are EM findings in mesothelioma?

A

Many long, slender microvilli
Abundant tonofilaments

Gross: pleural thickening + effusions

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

What is the FVC expected in COPD?

A

Normal or decreased

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

What is the expected FEV1 in COPD?

A

Decreased–the whole problem is an issue getting air out

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

What is the FEV1/FVC expected in COPD?

A

Decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the total lung capacity expected in COPD?

A

Chronic bronchitis-normal

Emphysema-increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the expected FRC in COPD?

A

Increased!

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

What is the expected pulmonary compliance in COPD?

A

Chronic bronchitis-normal

Emphysema-increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the bronchodilator response expected in COPD?

A

Chronic bronchitis-partial response

Emphysema-none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the expected DLCO in COPD?

A

Chronic bronchitis-normal

Emphysema-decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does a PV loop with reduced expiratory flow rate, and increased total volume indicate?

A

COPD

- chronic bronchitis and/or emphysematous destruction of interalveolar walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What values of:

  • pH
  • PaO2
  • PaCO2
  • HCO3

are expected after 5 days at high altitude?

A

Breathe a lot to get rid of CO2, so:

  • Alkalosis
  • Low PaO2 (~60, bc thin air)
  • Low paCO2 (~20)
  • Low HCO3 (compensate for alkalosis by excreting HCO3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why don’t you use Isoniazid monotherapy for active TB?

A

Fast resistance muts

  • Decrease in bacterial expression of catalse-peroxidase enzyme required for INH activation
  • Modification of protein target binding site for INH

Can use INH only in PPD+ and CXR- indivs (no evidence of clinical disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does streptomycin work?

A

Inhibits INITIATION of protein synthesis by binding to the 30s ribosomal subunit and distorting it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

In a child, what is the differential for rhonchi, wheezing secondary to airway obstruction?

A

Asthma or bronchiolitis caused by RSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the rx for RSV bronchiolitis?

A

Ribavarin

  • Nucleoside analog that inhibits the synthesis of gunanine nucleotides
  • Active against RSV and HCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What would happen if the lamellar bodies produced by type II pneumocytes were destroyed?

A

No surfactant (which is released in these lamellar bodies)

Patchy atelectasis would result, i.e. NARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is responsible for stimulating ventilatory drive in individuals with chronic COPD?

A

These patients are desensitized to CO2, so O2 plays a significant role.

  • Peripheral chemoreceptors in the carotid and aortic bodies are stimulated by hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What does oral thrush, interstitial pneumonia, and severe lymphopenia in the first year of life indicate?

A

Vertical HIV transmission

Treat with Zidovudine (ZDZ/AZT)
- NRTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the 4 main cause of hypoxemia (low PaO2)?

A
  1. Diffusion impairment (high A-a)
  2. V/Q Mismatch (high A-a)
  3. R-L shunt (high A-a)
  4. Hypoventilation (normal A-a)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

When does impaired gas diffusion occur?

A

Diseases that cause thickening of alveolar capillary membranes
- Alveolar hyaline membrane dsieases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

When does V/Q mismatch occur?

A

Pneumonia
Obstruction: COPD, asthma
PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the main pulmonary effect of increased Vagus stimulation?

A

Bronchoconstriction

  • Mediated by Ach released from post-ganglionic parasymps
  • Act on M3 receptors
  • M3 also causes increase secretions

Bronchoconstriction + mucous = increased work of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How do muscarinic Ach antagonists work?

A

Tiotropium
Ipratropium

Block M3 receptor, lessening bronchoconstriction + secretions

Useful in asthma and COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What cells and interleukins are involved in allergic asthma?

A

Allergen activated TH2 cells release IL-5

IL-5 recruits eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are sputum findings in allergic asthma?

A

Charcot-Leyden crystals (crystalloid bodies containing eosinophil membrane protein)

Eos (granule containing cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the most common site of colonization of MRSA?

A

Nasopharynx–nares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is a common complication of aspiration pneumonia?

A

Lung abscess caused by bacteria of the gingivodental suclus

  • Fever, malaise, weigth loss, clubbing, leukocyosis
  • Cough with copious foul-smelling sputum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the mechanism of chronic rejection in lung transplant?

A

Attack of the small airways–bronchioles

Causes Bronchiolitis Obliterans

  • Inflammation and fibrosis of bronchiolar walls, leading to narrowing and obstruction of affected bronchioli
  • Dyspnea, non-productive cough, wheezing
76
Q

What is the difference between chronic rejection in lung transplant and other organs, like renal transplant?

A

Lung: attack on small airways
- Bronchiolitis Obliterans

Renal: vascular obliteration

77
Q

What ratio indicates fetal lung maturity?

A

Lecithin (phosphatidylcholine): sphingomyelin

  • Lecithin increases sharply after 30 wks
  • Sphingomyelin stays the same
78
Q

What is the same in the pulmonary and systemic circulations?

  • Arterial oxygen content
  • Arterial pressures
  • Blood flow/min
A

Blood flow! Must be the same because they are part of a continuous circuit.

79
Q

What are the 5 catalase + infections that occur predominantly in CGD?

A 
Burkholderia 
Aspergillus
Nocardia
Serratia
Staph aureus

NADPH “BANSS” infection, except in CGD

80
Q

What effect does the CFTR mutation have in respiratory and gastric glands?

A

Normally, the CFTR channel increases salt and water content be secreting Cl-, and inhibits the ENaC that absorbs Na

Less CFTR = more Na absorbed > dehydrated, viscid mucus

81
Q

What effect does the CFTR mutation have in sweat glands?

A

Normally, the channel reduces salt content of sweat, activating ENaC to increase Na absorption

Mutation = too much NaCl

82
Q

If steroids do not work in asthma, what is a moAb therapy that could work?

A

Omalizumab targets IgE

  • Useful in asthma because Ig-E may be excessively high in asthmatics
  • Inhibits IgE binding to mast cells

OmaNOasthma

83
Q

Where is aspergillus likely to colonize?

A

Old lung cavities, from TB, emphysema, or sarcoidosis

Aspergillus can be

  • Colonizing (aspergilloma)
  • Invasive (aspergillosis)
  • Allergic (ABPA)
84
Q

When is PVR in the lungs highest?

A

At max inspiration AND max expiration

Increased lung volume causes alveolar expansion and stretching of the blood vessels.

INSPIRATION increases length and REDUCES DIAMETER, increasing alveolar vessel resistance

Decreased lung vol causes extra-alv arteries and veins to become narrowed due to decreased radial traction from adjacent tissues and compression by positive intrathoracic pressure

EXPIRATION causes increase in extra-alveolar resistance

85
Q

When is PVR it he lungs lowest?

A

At FRC, right between max inspiration (top of IC) and expiration (bottom of VC)

86
Q

What immune cells respond/react in sarcoidosis, and are found in the granulomas?

A

CD4+

Look for CD4:CD8 ratio > 2:1 in bronchoalveolar lavage to make diagnosis

87
Q

What do TH2 CD4 cells secrete?

A

IL-13, IL-4 > B cell class switching to IgE

IL-5 > activates eos, promotes IgA

Part of humoral adaptive immunity

88
Q

What do TH1 CD4 cells secrete?

A

IFN-gamma, IL-2 > activate macrophages, stimulate CD8 killer T cells

Part of cell-mediated adaptive immunity and type IV delayed hypersensitivity

89
Q

How does PE cause hypoxemia?

A

V/Q mismatch

  • Occludes pulmonary circulation, raises pulmonary resistance, raises RV afterload
  • Less blood to lungs
90
Q

What are the affects of theophylline OD?

A

Methylxanthines cause mild cortical arousal and insomnia, like caffeine.

Tox = abdominal pain, vomiting, seizures (main cause of death)

Can also get tachyarrhythmias

Rx: gastric lavage, charcoal, cathartics, beta blockers for heart, benzos/barbs for seizure

91
Q

Biopsy of lung shows columnar mucin-secreting cells lining alveolar spaces without invading the stroma or vessels.

What is this? Is it malignant or bening?

A

Adenocarcinoma in situ

  • Most common type of lung cancer in the US
  • Arises from alveolar epithelium
  • Located at lung periphery
  • Growth along intact septa
  • Well-diff, dysplastic, column cells
  • +/- mucin

MALIGNANT
- Can easily become invasive

92
Q

What is indicated by an increased ESR?

A

Non-specific inflammation

93
Q

What cytokines cause increase in ESR?

A

IL-1, IL-6, and TNF-a are released from neutrophils and macros

Stimulate hepatic production of acute phase reactants

Acute phase reactants bind to microbes and fix complement

Fibronogen, an acute phase reactant, causes erythrocytes to form stacks (rouleaux) that sediment more slowly

94
Q

What do IL-1, IL-6, and TNF-a do?

A

They are released from neutros and macros and stimulate acute phase reactants in inflammation

95
Q

What cellular process occurs in the nucleolus?

A

Nucleolus is round, dense, basophilic body in the nucleus

Site of rRNA transcription
-Conducted by RNA pol I

96
Q

Lack of which vitamin in CF can cause squamous metaplasia of epithelia to a keratinizing epithelium?

A

Vitamin A

ADEK are poorly absorbed in CF
(pancreatic insufficiency)

Vitamin A maintains differentiation of specialized epithelia

97
Q

What are apical subpleural blebs a precursor to?

A

Spont pneumothorax

98
Q

At what level should thoracocentesis be performed?

A

Above the 7th rib in the midclavicular line
Above the 9th rib along the midaxillary line
Above the 11th rib at the posterior scapular line

Insertion below may penetrate ab organs
Insertion on the inferior rib margin injures NAV

99
Q

In what disease in Cheyne-Stokes respiration seen?

A

CHF

100
Q

What is the definitive treatment for idiopathic pulmonary arterial HTN?

A

Lung transplant

101
Q

What is the intermediate treatment for idiopathic pulmonary arterial HTN?

A

Bostentan

  • Endothelin R antagonist
  • Endothelin is a vasoconstrictor that also stimulates endothelial proliferation
102
Q

What is the airway pressure at FRC?

A

Zero

103
Q

What is the intrapleural pressure at FRC?

A

About -5

104
Q

How does H flu achieve pathogenicity?

A

Capsule

105
Q

What are polyenes?

A

Class of anti-fungals that include amphotericin B and nystatin

106
Q

How do amphotericin B and nystatin kill fungi?

A

Bind to ergosterol in the fungal MEMBRANE

107
Q

What is the treatment for chronic preventative treatment of bronchial asthma?

A

INHALED corticosteroids, like fluticasone

High dose systemic steroids are used for initial management of acute asthma exacerbations

108
Q

How does cell structure progress distally down the respiratory tract?

A

Pseudostratified ciliated columnar > ciliated simple cuboidal (at the terminal bronchioles)

Goblet cells, mucous glnads, serous glands, and cartilage end at the smallest bronchi

Epithelial cilia persist to the end of the respiratory bronchioles (important to have cilia beyond mucin-secreting cells to clear obstruction)

109
Q

How do you differentiate absolute vs. relative erythrocytosis?

A

RBC mass

  • If normal > relative
  • Relative = dehydration or diuresis
  • If increased > absolute
  • Absolute = PV or secondary
110
Q

How do you differentiate primary vs. secondary (Absolute) erythrocytosis?

A
  • Polycythemia Vera: all 3 cell lines increase
  • Secondary erythrocytosis: only RBCs increase
  • 2: hypoxia or EPO tumors (differentiate with O2 sat
111
Q

From where does small cell carcinoma arise, and where is it located?

A

Basal layer of cells

  • Round or oval cells with scant cytoplasm and large hyperchromatic nuclei
  • Smaller than lymphos

Centrally located in the lung

112
Q

What does small cell carcinoma stain for with immunohistochemistry?

A

Neuroendocrine markers

  • Enolase
  • Chromogranin
  • Synaptophysin
113
Q

What kind of channel is the CFTR?

A

Transmembrane ATP-gated chloride channel

114
Q

Where does the antifungal Caspofungin (Echinocandin) act?

A

Cell WALL

115
Q

Where does the antifungal Flucytosine act?

A

DNA & RNA synth

116
Q

Where do the antifungal Azoles act?

A

Cell Membrane

- Inhibit synth of ergosterol

117
Q

Where do the antifungals Amphotericin B and Nystatin (Polyene) act?

A

Cell membrane

- Bind erogsterol

118
Q

What are the most frequent bacterial causes of lung abscess?

A

Anaerobes found in the oral cavity

  • Peptostreptococcus
  • Prevotella
  • Bacterioides
  • Fusobacterium
119
Q

What are risk factors for lug abscess?

A

Anything that causes oropharyngeal aspiration

  • Loss of consciousness
  • Dysphagia

Alcoholism, drug OD, seizure, prolonged anesthesia, severe neuro disease like stroke, dementia

120
Q

In what stage of TB infection is a Ghon complex found?

A

Primary infection

  • Lower lobe lesion (Ghon focus) and ipsilateral hilar adenopathy
  • It does not remain, but is resolved!
121
Q

What stimulates neutrophil migration to a site of inflammation?

A

Leukotriene B4

122
Q

What infections do CGD patients get?

A

Recurrent infection with catalase + bacteria and fungi:

  • Pneumonia
  • Skin and organ abscesses
  • Suppurative adenitis
  • Osteomyelitis
123
Q

What are the tests to assess neutrophil superoxide production?

A

Nitroblue tetrazolium
- Normal = reduce yellow to blue

Dihydrorhodamine flow cytometry
- Fluorescent green = NADPH oxidase activity is normal

124
Q

What type of cell is impaired in CGD?

A

Neutrophils!

- Lack NADPH oxidase

125
Q

What are the markers of small cell carcinoma?

A

Neuroendocrine markers:

  • Enolase
  • Chromogranin
  • Synpatophysin

+/- Neurofilaments

126
Q

How does cerebral resistance change with increased CO2?

A

Decreased resistance to allow for increased blood flow

  • Avoid hypoxia
  • Also increases ICP
127
Q

What are the liver sequelae of a1 anti-trypsin deficiency?

A

Liver damage from stored enzyme can cause cirrhosis or HCC

128
Q

What is seen on liver histology in a1 anti-trypsin deficiency?

A

Pink granules on PAS (unsecreted enzyme)

129
Q

How does increased CO2 (as seen in COPD) affect cerebral ICP?

A

Vasodilation (decreased resistance) to increase perfusion

This increases ICP.

130
Q

The nose, paranasal sinuses, nasopharynx, most of the larynx, and tracheobronchial tree contain what kind of epithelium?

A

Pseudostratified columnar–mucous secreting

131
Q

The oropharynx, laryngopharnynx, anterior epiglottis, upper 1/2 posterior epiglottis, and vocal folds (true vocal folds) contain what kind of epithelium?

A

Stratified squamous

132
Q

What cells release elastase?

A

Macrophages & neutrophils

133
Q

What inhibits elastase?

A

a1 anti-trypsin

134
Q

What disease is caused by increased balance of elastase?

A

Emphysema

135
Q

Where in the bronchial tract does the mucociliary escalator end?

A

Continues up to terminal bronchials

136
Q

What are the sputum findings in ALLERGIC asthma?

A

Charcot Leyden crystals & eosinophils

137
Q

How are eosinophils activated in allergic asthma?

A

By IL-5 released by Th2 cells

HOT T BONE stEAK

138
Q

What is the MOA of Ipratopium?

A

Antimuscarinic

Reverses vagally-mediated bronchoconstriction

139
Q

What is the clincal use of Ipratopium?

A

Antimuscarinic that enhances the bronchodilatory effects of B2 agonists

140
Q

What do the following symptoms indicate?

  • Chronic nasal discharge
  • Atrophic nasal mucosa
  • Thinning of nasal septum
  • Headache
A

Cocaine abuse

  • Vasoconstrictor
  • Intranasal use
141
Q

What are the possible long term nasal consequences of cocaine abuse?

A

Septum perforation
Oropharyngeal ulcers
Osteolytic sinusitis

142
Q

What is the pathogenesis of dyspnea in LH failure?

A

LV failure (post- MI) >
Fluid in lung interstitium >
Decreased lung COMPLIANCE >
Dyspnea

143
Q

What is the result of the F508 mutation on the channel protein implicated in Cystic Fibrosis?

A

POST TRANSLATIONAL PROCESSING is altered

- Mut. impairs FOLDING and GLYCOSYLATION

144
Q

What are the 2 less common mutations that can cause Cystic Fibrosis?

A

Premature termination
Defective ATP binding

Post translational processing impairment, as a result of F508, is the most common

145
Q

How do patients with obstructive lung disease (COPD, asthma) minimize the work of breathing?

A

Slow, deep breathing

Because they have increased airways resistance

146
Q

How do patients with restrictive lung disease (fibrosis) minimize the work of breathing?

A

Fast, shallow breathing

147
Q

From what type of bond does elastin derive its elastic properties?

A

Covalent bonds between LYSINE residues

- Called desmosine cross-linking

148
Q

What enzyme is responsible for cross-linking elastin?

A

Lysyl hydroxylase

149
Q

What molecule is hydroxylated, is linked by disulfide bridges, and forms triple helixes?

A

Collagen

NOT Elastin

150
Q

What is the superior extension of the lung apices?

A

Above the clavicle and first rib, through superior thoracic aperture

151
Q

What types of globin show a hyperbolic O2 binding curve?

A

Myoglobin and individual subunits of hemoglobin (unbound a, b chains)

152
Q

Where does deoxygenated bronchial blood drain?

A

Directly into the LA

153
Q

What is the differential for hypoxemia + normal A-a gradient?

A

Hypoventilation (of any cause)

154
Q

What are the lung effects of acute heart failure?

A

Transudate of plasma into lung interstitium + alveoli >

Acute pulmonary edema + pulmonary venous congestion

155
Q

What are the lung effects of chronic heart failure?

A

Hemosiderin laden macrophages = “heart failure cells”

156
Q

What is the pulmonary defense against particles 10-15 microns?

A

Trapped in the upper respiratory tract

157
Q

What is the pulmonary defense against particles 2.5-10 microns?

A

Mucociliary escalator

158
Q

What is the pulmonary defense against particles

A

Phagocytosed by macrophages in terminal bronchioles

159
Q

What metabolic (Acid/base) derangement is seen heroin OD?

A

Respiratory acidosis

  • Heroin suppresses respiratory centers > hypoventilation
  • Low pH, high CO2, normal HCO3 (no time to compensate)
160
Q

At what point is Pulmonary Vascular Resistance lowest?

A

Functional Residual Capacity (FRC)

  • Balance between muscles pulling out at higher lung vol and lack of radial traction at lower lung vol
161
Q

How does silicosis impact TB?

A

Increased susceptibility

Silica damages macrophage phagolysosomes
Macro killing of TB is impaired

162
Q

On what type of lung cancer is surgery NOT performed?

A

Small cell carcinoma

  • Bc it’s a very invasive cancer
163
Q

What does air-fluid level on CT indicate?

A

Inflammation and abscess

164
Q

What is the process of inflammation and abscess formation in the lung?

A

Lysosomal enzymes are released from macros and neutros, causing pus > abscess

165
Q

What lung disease is indicated with meconium ileus at birth?

A

Cystic Fibrosis

166
Q

What is the problem with the respiratory mucosa in CF?

A

It’s dehydrated!

167
Q

What’s the pathogenesis of dehydrated respiratory mucosa in CF?

A

Less Cl- secreted, so less Na secreted, so less H20 secreted

168
Q

What is the change in conductance of the CFTR channel in the lungs in CF?

A

Decreased Cl- out

169
Q

What is the change in conductance of the CFTR channel in sweat glands in CF?

A

Increased Cl- out

170
Q

What leukotrienes are involved in bronchospasm?

A

LTC4, D4, E4

171
Q

What leukotriene is NOT involved in bronchospasm?

A

LTB4

- It is chemotactic

172
Q

Why do you see granulomas in the lungs of IV drug users?

A

Foreign substances in the drugs, like talc

173
Q

What is a cough suppressant with minimal analgesia and some abuse potential?

A

Dextromethorphan

174
Q

What is the MOA of Bosentan?

A

Endothelin receptor blocker

175
Q

What is the indication for Bosentan?

A

Pulmonary Arterial Hypertension

176
Q

List the steps in fetal circulation.

A
  1. Umbilical vein
  2. Ductus venosus (bypass hepatic artery)
  3. IVC
  4. Heart
    - Pulmonary Veins, Ductus arteriosus, Descending aorta
    OR
    - PFO, L heart, Body
  5. Umbilical arteries
  6. Placenta
177
Q

What does the umbilical vein of fetal circulation become?

A

Lig. teres hepatis

TV MArt

178
Q

What do the umbilical arteries of fetal circulation become?

A

Medial umbilical ligaments

TV MArt

179
Q

Where is thoracocentesis performed?

A

9th rib, midscapular/clavicular line

ABOVE rib to avoid NAV

180
Q

What is the MOA of Cromolyn Sodium

A

Mast cell stabilizer

181
Q

What is the indication for Cromolyn Sodium?

A

Asthma, immediate + long term

182
Q

What nerve is likely severed in a jaw break?

A

Inferior alveolar nerve = dental nerve

- Branch of Mandibular, V3

183
Q

What controls respiration in COPD?

A

PaO2, though PaCO2 controls respiratory drive in healthy people, it is blunted in COPD

184
Q

What is the treatment for inflammatory asthma?

A

Corticosteroids, like Fluticasone

not Albuterol!

185
Q

What lung volumes increase with COPD?

A

Residual volume and TLC

UWorld (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions