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BOARDS! > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Sarcoidosis

  1. CXR
  2. Bloodwork
  3. Liver biopsy
  4. Sequelae
A

chest xray: enlarged hilar lymph nodes

bloodwork: elevated serum ACE level

liver biopsy: scattered granulomas which affect the portal triads to a greater degree than the lobular parenchyma

can cause: arthralgias and skin changes

can also cause skin lesions:

subcutaneous nodules (erythema nodosum), erythematous plaques, or macules that are slightly rddened and scaling

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2
Q

What is fat embolism syndrome?

A

>>pulm insufficiency, diffuse neuro impairement, thrombocytopenia, and anemia

>>fat globules dislodge from BM enter the marrow vascular sinusoids and occlue pulm nicrovessels imparing gas exchange

>>microvascular occlusion in the cerebral white matter, brain stem, and SC causes the neuro manifestation

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3
Q

CF

  1. CP
  2. Cause/Genetics
  3. Sequelae
A

>>CP: recurrent sinopulmonary infections pancreatic insufficiency, and GI malabsorption

>>cause: mutation affecting CFTR (cystic fibrosis transmembrane conductance regulator), a chloride channel that is activated by cAMP-mediated phosphorylation and subsequently gated by ATP

>>most common CFTR gene mut: found in approx 70% of cases, is a 3-bp deletion that removes a phenylalanine at AA position 508 (deltaF508).

>>>>this causes impaired post-translational processing (improper folding and glycosylation) of CFTR which is detected by the ER

>>>abnml protein is targeted for proteasomal degradation, preventing it from reaching the cell surface

>>most common cause of meconium ileus (inspissated green mass suggestive of distal ileum obstruction by dehydrated meconium)

deaths: cardiorespiratory complications-pneumonia (persistent, tx-resistant, infectious), bronchiectasis, bronchitic obstructive pulmonary diease, and cor pulmonale

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4
Q

Why do silicosis pts have increased susceptibility to pulmonary TB?

A

increased susceptibility to pulmonary TB due to disruption of macrophage phagolysosomes by internalized silica particles, macrophage killing of intracellular mycobacteria may be impaired

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5
Q

What is Kartagener syndrome?

>AR. form of primary ciliary dyskinesia, due to mutations that impair the structure or function of cilia, a form of primary ciliary dyskinesia (PCD) due to failure of dynein arms to develop normally

>>triad: situs inversus, chronic sinusitis, bronchiectasis

A
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6
Q

What are the 4 main clinical manifestations of asbestos exposure?

A
  1. pleural plaques-hallmark of asbestos exposure that typically affects the parietal pleura along the lower lungs and diaphragm.

>>plaques are composed of: discrete circumscrbied areas of dense collagen that frequently bacome calcified

>>pleural disease usually develops within 15yrs following intial exposure and is asymptomatic unless there is a significant colapse of adjacent lung parenchyma

  1. Asbestosis-characterized by progressive, diffuse PULMONARY FIBROSIS and the presence of asbestos bodies

>>clinical manifestation: 15-20yrs after intial exposure; get dyspnea, and reduced lung volumes (restrictive lung disease)

  1. bronchiogenic carcinoma-most common malignancy associated with asbestos exposre.

>>smoking and asbestos exposure have a synergistic effect on the development of lung carcinoma. a. in NONsmoking pts, increase risk by 6x

b. in smoking pts, 60x
4. malignant mesothelioma-rare malignancy of the pleura, asbestos=only known environmental RF.

>>less common than bronchogenic carcinoma in asbestos-exposed patients, but mesothelioma is more specific for heavy asbestos exposure

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7
Q

A. What is the function of the medullary respiratory center?

B. What are the three types of chemoreceptors?

A

MRC: controls the depth and rate of respiration based on input from central and peripheral chemoreceptors and airway mechanocreceptors

  1. Central chemoreceptors: located in medula, stimulated by decreases in pH of surrounding CSF. BBB is impermeable to H+, so blood pH has little effect on them. On the other hand, CO2 readily diffuses through the BBB and forms H+ in the CSF. Therefore, increased PaCO2 is the major stimulator of ctl chemoreceptors, leading to an increase in respiration.

In pts with COPD, response to PaCO2 is blunted and hypoxmia becomes important contributor to respiratory drive.

  1. peripheral chemoreceptors found in the carotid and aortic bodies are the primary sites for sensing arterial PaO2 and are stimulated by hypoxemia; can be suppressed with oxygen administration
  2. Pulmonary stretch receptors include myelinated and UNmyelinated C fibers in the lung and airways. these receptors regulate the duration of inspiration depending on the degree of lung distension (Hering-Breuer reflex) and act predominantly to protect the lung from hyperinflation.
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8
Q

ARDS

A
  • major RF: acute necrotizing pancreatitis
  • path: diffuse injury to alveolocapillary membranes results in interstitial and intraalveolar edema, acute inflamm, and alveolar hylaine membranes
  • hyaline membranes: from alveolocapillary membrane leakage, consists of fibrin exudate and plasma protein rich edema fluid mixe with cytoplasmic and lipid remnants of necrotic epithelial cells
  • acute stage: lungs are heavy, red, boggy
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9
Q

What is the Bohr effect?

A

Shifting to the right of the oxyhemoglobin curve (INCREASED: H+, 2,3DPG, and temperature)

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10
Q

What happends to HbS aggregates in the deoxy state?

A
  • polymers form fibrous strands that decrease RBC membrane flexibility and promote sickling
  • sickling at low pH, high 2,3-BPG
  • inflexible erythrocytes lead to microvascular occlusion and microinfarcts
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11
Q

Pulmonary embolism

A
  • risk groups: hospitalized and post-op patients
  • CP: tachypnea, tachycardia, cough, pleuritic CP
  • pt develops hypoxemia because of V/Q mismatch
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12
Q

Cyanide poisoning

A
  • CP: rapidly developping cutaneous flushing, tachypnea, HA, tachycardia, N/V, confusion, weakness, respiratory distress, cardiac dysfunction
  • Lab: severe lactic acidosis and lessened differece between arterial and venous O2
  • tx: NITRITES**(oxidizing agent, causes methemoglobinemia), sodium thiosulfate
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13
Q

ALL; T-cell

A
  • CP:
    • mediastinal mass that can compress great vessels=SVC syndrome
    • can compress esophagus=dysphagia
    • can compress trachea=dyspnea and stridor
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14
Q
A

*

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15
Q

What is true of the pulmonary system at all times?

A

rate of blood flow through the pulmonary circulation must equal the rate of blood flow through the systemic circulation (at ALL times)

-arterial pressures and oxygen contents will be different

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16
Q

Equilibrium of O2 in a nml indiv at rest is…

A
  • perfusion-limited!
  • DIFFUSION limited in disease states:
    • emphysema
    • pulmonary fibrosis
    • and in states of very high pulmonary blood flow (exercise)
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17
Q

What are som RF for ARDS?

What is the process?

A
  • some RF: pulm infection and sepsis
  1. cytokines stim pulm epithelium
  2. inflamm response mediated by neutrophils
  3. capillary damage
  4. leakage of protein and fluid into the alveolar space
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18
Q

Pleura

A
  • visceral pleura: covers all lung surfaces and does NOT carry pain fibers
  • parietal pleura: outer boundary of pleural space
    • costal pleura
    • pleura innervated by phrenic nerve (C3-C5) at base of neck and over the shoulder:
      • mediastinal pleura
      • diaphragmatic pleura
    • cervical pleura
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19
Q

Steroids for asthma tx

A
  • inhaled for chronic asthma
  • systemic for acute exacerbations
  • inhibits inflamm mediator formation
  • decreases leukocyte extravasation
  • stimulates apoptosis of inflamm cells
  • decrease mucus production by goblet cells
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20
Q

brachiocephalic vein obstruction

A
  • s/s similar to SVC syndrome BUT on one side of thebody
  • BCV drains ipsilateral jugular and subclavian veins
  • bilat form SVC
  • CP: face and arm swelling and engorgement of subq vein on ipsi neck
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21
Q

persistent bronchial asthma

A
  • chronic AW inflamm and edema leads to bronchial wall thickening and remodeling
  • AW HYPERresponsiveness and increased bronchoconstriction
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22
Q

Pulmonary HTN

A
  • specific morphologic findings in branches of the puolmonary artery:
    • increased arteriolar smooth muscle thickness (medial hypertrophy)
    • intimal fibrosis
    • significant luminal narrowing
  • in severe HTN, lesions can progress to form interlacing tufts of small vascular chanels=plexiform lesions
    • can occur in pulm HTN due to underlying lung, vascular, or cardiac dz and in idiopathic or familial pulm arterial HTN (PAH)
      • PAH CP: dyspnea and exercise intolerance in women, 20-40yo
      • familal form: inactivating mutations involving the pro-apoptotic BMPR2 gene
        • resulting increas in endothelial and smooth mu cell proliferation leads to vascular remodeling, elevated pulm vascular resistance, and progressive pulm HTN
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23
Q

Where do you place a chest tube for drainage of pleural effusion?

A
  • through the skin and subcutaneous fat into the 4th or 5th intercostal space in the anterior axillary or midaxillary line
  • tube traverses through the serratus anterior muscle, intercostal muscles, and parietal pleura
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24
Q

Cystic Fibrosis

A
  • CP: white child with recent pulm infections and malabsorption
  • AR D/O of exocrine secretion
  • non-functional CFTR (CF transmembrane conductance regulator)
    • responsible for transporting chloride ions across mucosal epithelial cell membranes
    • with mut, transport of chloride and water from the cells is suppressed=secretion of viscous mucus
    • stasis and accumulation of these viscous secretions in tissues
  • Clinical findings:
    • increased viscosity of bronchial secretions=impaired mucociliary clearance of bacteria
      • repeated pulm infecions, **Pseudomonas aeruginosa
      • mucus plugging of bronchi causes dilatation and bronchiectasis
    • viscous pancreatic secretions are not transported to intestinal lumen, accumulate in pancreatic ducts
      • pancreatic insufficiency causes s/s of malabsorption (steatorrhea and poor weight gain)
      • fibrosis of pancreatic tissue
    • decreased secretion of water by the intestinal epithelium may cause intestinal obstruction
      • neonates with CF may develop meconium ileus
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25
Q

local spread of a lung tumor

A
  • horner syndrome (ipisi miosis, ptosis, anhydrosis) in assoc with tumors of lung apex (Pancoast tumor), disrupts oculosympathetic nerve pathway
    • lung ca in this location can also invade rami of brachial plexus (C5-T1) and cause shoulder pain
  • centrally located tumor or mediastinal spread: SVC syndrome (commonly assoc with small cell lung carcinoma)
    • CP: HA, facial and upper ectremit edema, dilated veins of the upper torso
  • involvement of recurrent laryngeal nerve: hoarseness
  • dysphagia if tumor compressed esophagus
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26
Q

pulmonary vascular resistance (PVR)

A
  • alveolar resistance is INC at HIGH lung volumes
  • extra-alveolar resistance is INC at LOW lung volumes
  • total PVR takes shape of a U curve
  • pt at which PVR is lowest is near the FRC
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27
Q

CF/mutations

A
  • mc cause: 3-bp deletion in the CF transmembrane conductance regulator (CFTR) gene at AA 508 (deltaF508)
  • mut impairs post-translational processing of CFTR=shunting of CFTR toward the proteasome with complete absence of the protein the apical membrane of affected epithelial cells
  • elevated sweat chlorie concentrations are found in most pts with CF
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28
Q

Inflammation and Abscess

A
  • tissue damage and resultant abscess formation is primarily caused by lysosomal enzyme release from neutrophils and macrophages
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29
Q

Eosinophilic granules

A
  • contain major basic proteins
  • MBP=cationic protein that causes damage to parasites (+helminths)
    • also contribs to bronchial epithelial damage sustined by pts with atopic (extrinsic allergic) asthma
  • ocassionally MBP will cause lysis of epithelial cells=host tissue damage
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30
Q

Mass cell degranulation

A
  • mast cells have a cell surface receptor to bind the Fc aspect of the IgE antibody
  • when the mast.cell.bound IgE recognize Ag, mast cells degranulate and release histamine and products of arachnoid acid oxidation
  • series of events occurs during anaphylactic rxns
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31
Q

What is responsible for the rubber like proerties of elastin

A
  • extensive cross-linking between elastin monomers which is facilitate by lysyl oxidase
  • pts with A1AT deficiency can develop early-onset, LOWER lober-predominant emphysema d/t xs alveolar elastin degradation
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32
Q

Supine pt aspiration

A
  • d/t gravity, sup pts aspirate into:
    • (UP) posterior segments of the upper lobes
    • (LS) superior segments of the lower lobes
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33
Q

Upright (or semi-recumbent) pts aspiration

A
  • into basilar segments of the lower lobes
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34
Q

Is aspirated material more likely to travel down the left or right main bronchus

A

RIGHT main bronchus, because it is wider and more vertical

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35
Q

Sarcoidosis immunology

A
  • CD4+ T-helper cells are predom type oflymphocyte in sarcoid granulomas
  • intra-alveolar and interstitial accumulation of CD4+ T cells in sarcoidosis often results in high CD4+/CD8+ T-cell ratios (>2:1) in bronchoalveolar lavage fluid
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36
Q

which markers identify the B cell lineage

A
  • CD19,20,22
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37
Q

Sarcoidosis epidemiology

A

young black adults

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38
Q

Sarcoidosis clinical

A
  • constitutional symptoms
  • cough, dyspnea, CP
  • extra-pulmonary findings:
    • skin lesions anterior/posterior uveitis
    • Lofgren syndrome
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39
Q

Sarcoidosis imaging

A
  • bilat hilar adenopathy
  • pulm reticular infiltrates
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40
Q

Sarcoidosis Lab

A
  • hypercalcemia/hypercalciuria
  • elevated serum ACE level
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41
Q

Sarcoidosis pathology

A
  • bx w/ NONCASEATING GRANULOMAS that stain negative for fungi and acid-fast bacilli
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42
Q

ABPA (allergic bronchopulmonary aspergillosis)

A
  • Hx:
    • asthma (A)
    • CF
  • chest imaging
    • recurrent fleeting infiltrates
    • bronchiectasis (B) (on CT)
  • diagnosis:
    • eosinophilia
    • positive skin test (P) & Ig for Aspergillus (A)
    • elevated IgE
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43
Q

Lung Volumes (LITER)

A

<lung></lung>

  • IRV
  • TV
  • ERV
  • RV
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44
Q

What are the characteristics of persistent bronchial asthma

A
  • chronic AW inflamm
  • edema
  • leading to bronchial wall thickening and remodeling
  • airflow can be further compromised by airway hyper-responsiveness and INC broncho-constriction–occurs d/r an acute asthma exacerbation
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45
Q

Corticosteroids

A
  • have the strongest and most predictable effects on the inflamm component of asthma
  • inhaled corticosteroid form the cornerstone of chronic therapy for pts with persistent asthma and can reduce the number and severity of acute astham exacerbations
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46
Q

What are the two categorizations for etiologies of hypoxemia

A
  • nml alveolar to arterial gradient
  • elevated alveolar to arterial gradient
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47
Q

nml alveolar to arterial gradient (2 main causes)

A
  • hypoventilation (opiod use)
    • obesity
    • hypo-ventilatio syndrome
    • neuromuscular d/o
  • low inspired fraction of oxygen
    • high altitude
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48
Q

elevated alveolar to arterial gradient (3)

A
  • R-to-L shunt
    • cardiac septal defects
    • pulm edema
  • V/Q mismatch
    • PE
    • chronic obstructive lung dz
  • Impaired diffusions (diffusion limitation)
    • interstitial lung dz
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49
Q

What are the three groups of oxygen deprivation

A
  • hypoxemia (DEC Pao2-arterial)
  • hypoxi-A (DEC O2 delivery to tissue)
  • ischemia (loss of blood flow)
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50
Q

What are the two types of ischemia (loss of blood flow)

A
  • impeded arterial flow
  • DEC venous drainage
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51
Q

What is one of the important causes of hypoxemia with a nml alveolar to arterial oxygen gradient

A
  • obesity hypO-ventilation syndrome; characterized by:
    • chronic fatigue
    • dyspnea
    • difficulty concentrating
    • evidence of hypO-ventilate (partial pressure of CO2 [PaCO2]>45 mmHg while awake)
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52
Q

negative predictive value (NPV)

A
  • represents probability of not having a dz given a NEGATIVE test result
  • unlike Sn and Sp, NPV varies based upon dz prevalence and is inversely proportional to the prevalence of a dz
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53
Q

Reid Index

A
  • ratio of the thickness of the mucous gland layer in the bronchial wall sub-mucosa TOOOO the thickness of the bronchial wall between the respiratory epithelium and bronchial cartilage
  • normally 0.4
  • as chronic bronchitis progresses both the total bronchial wall thickness and reid index increase
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54
Q

idiopathic pulmonary artery HTN (IPAH) treatment

A
  • BOSENTAN
  • endothelin-receptor ANT-agonist
  • MOA: blocks effects of endothelin (potent vsoconstrictor that also stimulates endothelial proliferation
  • Ci: DEC pulmonary arterial pressure and lessens the progression of vascular and RVH
55
Q

IPAH Path

A
  • muscularization of small arteries
  • medial hypertrophy and intimal hyperplasia
  • intimal fibrosis (onion skinning)
  • formation of capillary tufts (plexiform lesion)
56
Q

PAH CP

A
  • dyspnea and exercise intolerance
  • women 20-40
  • familial form: inactivating mutations of pro-apoptotic BMPR2 gene
57
Q

Acid-fastness

A
  • acid fast stain identifies organisms that have mycolic acid present in their cell walls
    • ex: Mycobacterium and some Mocardia
  • Acid fast stainig is carried out by:
    • applying an aniline dye (carbolfuchsin) to a smear–penetrates bacterial cell wall, binds mycolic acids
    • decolorizing with HCL and alcohol to reveal whether the organisms present are “acid fast”
  • nocardia is more weakly acid fast
58
Q

Mucociliary clearance

A
  • responsible for removing vast majority of inhaled particles that lodge within the bronchial tree
  • ciliated.mucosal.epithelium
    • lines pulm airways from trachea to proximal portions of respiratory bronchioles
    • mucus secreted onto this epithelial surface acts to trap particles suspended in the inspired air
    • particles and mucus are constantly swept uUPWARD from the bronchiles toward the pharynx by cilia that collectively beat in the direction of the pharynx
    • once mucus reaches the pharynx it is swallowed or expectorated
59
Q

goblet cells

A
  • mucus-secreting cells interspersed throughout the respiratory mucosa from the trachea down to the larger bronchioles
  • not found within the terminal bronchioles
  • nondigestible material must be transported by macrophages to the pulmonary lymphatics or to ther terminal bronchioles (for clearance by the mucociliary system)
60
Q

Type 1 and 2 pneumocytes

A
  • line the alveolar ducts an alveoli
  • 1: thin cells stretch across the alveolar wall that mediate GAS EXCHANGE
  • 2: produce surfactant, divide and differentiate into 1 to replace damaged cells
61
Q

dimorphic fungal species

A
  • different morphologic characteristics in different environments
  • DIMORPHIC
    • mold (with hyphae) in ambient temps (25-30)
    • yeasts (single cells) at body temp (37)
  • FIVE species of thermally dimorphic fungi (butterfly):
    • sporothrix schenckii
    • coccidioides immitis
    • histoplasma capsulatum
    • blastomyces dermatitidis
    • paracoccidioides brasiliensis
62
Q

sporothrix schenckii (epi and CP)

A
  • epid
    • assoc with gardening
    • often transmitted via thorn prick
  • CP:
    • pustules
    • ulcers
    • subQ nodules along lymphatics
63
Q

sporothrix schenckii (lab diagnosis)

A
  • culture (25C0
    • branching hyphae
  • biopsy:
    • round or cigar-shaped budding yeasts
64
Q

coccidiodes immitis (epi and CP)

A
  • epid:
    • SW states (desert area–Ex: south and central Cali, Arizona, new Mexico, western Texas)+northern Mexico
    • mold form is present in soil
  • CP:
    • pulm form:
      • flu-like illness
      • cough
      • erythema nodosum
    • disseminated form:
      • affects skin, bones, lungs
65
Q

coccidiodes immitis (lab diagnosis)

A
  • culture (25)-forms hyphae
  • bx: 37 forms THICK-WALLED SPHERULES filled with endospores
66
Q

Histoplasma capsulatum (Epi and CP)

A
  • epi:
    • ohio and mississippi river valleys
    • soil, bird and at dropping (chicken coops, caves)
  • CP:
    • pulm: similar to TB (lung granulomas with calcifications)
    • disseminated: lungs, spleen, liver
67
Q

Histoplasma capsulatum (Lab diagnosis)

A
  • culture (25): branching hyphae
  • bx: oval yeast cells WITHIN MACROPHAGES
68
Q

Blastomyces dermatitidis (Epi and CP)

A
  • Ohio and Mississippi river valleys-Great lakes region, soil
  • pulm pneumonia (in immunocompromised host), disseminated is common and severe (mc in skin and bones)
69
Q

Blastomyces dermatitidis (Lab diag)

A
  • 25 culture-branching hyphae
  • bx: large round yeasts with DOUBLY REFRACTILE WALL and SINGLE BROAD-BASED BUD
70
Q

Paracoccidiodes brasiliensis (Epi and CP)

A
  • ctl and south america
  • mucoQ:chronic mucoQ or Q ulcers…can progress to LN and lungs
71
Q

Paracoccidiodes brasiliensis (Lab diagnosis)

A
  • 25 cultures: multipe blastoconidia
  • bx: cells covered in budding blastoconidia
72
Q

Chronic Bronchitis (blue bloaters) Morphology

A
  • thickened bronchial wall
  • neutrophilic AND lymphocytic infiltration
  • mucous gland enlargement with INC number of goblet cells (INC mucus production)
  • patchy squamous metaplasia of the bronchial mucosa
  • CIGARETTE SMOKING=leading cause
73
Q

hypoxemia and polycythemia

A
  • COPD can cause hypoxia sufficient to stimulate INC erythropoietin production by the cortical cells of the kidney
74
Q

what are the three main causes of COPD

A
  • chronic bronchitis
  • bronchial asthma
  • emphysema
75
Q

how do chronic bronchitis and emphysema cause hypoxia

A
  • many smokers have bother chronic bronchitis and centrilobular emphysema
  • CB causes hypoxia by DEC diameter of conducting airways=prevent adequate airflow
  • emphysema causes hypoxia by dilating the aleolar spaces so that there is insufficient contact between the airspaces and deoxy blood in the alveolar capillaries
76
Q

What happens to oxygenated blood from the placenta?

A

it is delivered to the fetus via the umbilical vein…therefore the umbilical vein has the HIGHEST OXYGEN CONTENT in the fetal circulation

77
Q

What is the remnant of the umbilical vein in the adult

A

ligamentum teres

78
Q

where is blood from the umbilical vein first delivered

A
  • to the LIVER where it bypasses the hepatic circulation via the ductus venosus and enters the IVC (pretty high oxygen content)
79
Q

where does blood go from the IVC

A
  • blood is delivered to the heart and one of two things can hapen:
    • pumped into the pulmonary circulation
    • cross directly from the right heart to the left heart via the foramen ovale
80
Q

what happens to a fraction of the blood pumped into the pulmonary circulation

A
  • it may bypass the lungs via the ductus arteriosus and pass directly into the descending aorta
  • from the aorta, blood circulates to all of the fetal tissue
81
Q

how is deoxygenated blood delivered fro the fetus back to the placenta

A

by the paired umbilical arteries

82
Q

ductus arteriosus

A
  • shunts blood from the pulmonary artery into the descending aorta
  • blood is mixed with completely deoxygenated blood from the systemic circulation
83
Q

Response to exercise

A
  • during aerobic exercise:
    • INC oxidative mtabolism of glucose and FA in skeletal mu
    • INC skeletal mu O2 consumption and CO2 production INC the PCO2 of mixed venous blood
    • homeostatic mechs maintain arterial blood gas levels and arterial pH near the resting values
  • O2 consumption is balanced by INC CO/skeletal mu perfusion
  • CO2 production is balanced by ventilation
84
Q

Mycoplasma and AB

A
  • all organisms in the Mycoplasma genus (inc ureaplasma) lack peptidoglycan cell walls=resistant to agents that attack the peptidoglycan cell wall such as:
    • peniciliins
    • cephalosporins
    • carbapenems
    • vancomycin
  • mycoplasma infections can be treated with anti-ribosomal agents (tetracycline, macrolides)
85
Q

Th1 rundown

A
  • type of immunity: cell mediated
  • function: activate macrophages and cytotoxic T-cells
  • substances secreted: IL2, IFN-gamma, lymphotoxin beta
  • result:cytotoxicity, delayed hypersensitivity
86
Q

Th2 rundown

A
  • type of immunity: humoral (ab-mediated)
  • function: activated B-cells, promote class-switching
  • substances secreted: IL4,5,10,13
  • result: secretion of antibodies
87
Q

pulmonary vascular bed

A
  • unique-tissue hypoxia results in a vasoconstrictive response
  • hypoxic vasoCONSTRICTION occurs in the small muscular pulmonary arteries to divert blood flow AWAY from the underventilated regions of the lung toward better-ventilated areas
88
Q

which components of the pulmonary function test are INC in emphysema

A
  • TLC
  • FRC
  • pulmonary compliance
89
Q

What is the primary virulence factor of S. pneumo (without which it cannot cause dz)

A

polysaccharide capsule that inhibits phagocytosis

90
Q

IPF (idiopathic pulmonary fibrosis)

A
  • progressive exertional dyspnea +dry cough
  • PFT: restrictive profile
  • also: interstitial fibrosis with cystic air space enlargement
  • pathologic findings: usual interstitial pneumonia and show patchy involvement with dense fibrosis
    • +”honeycomb” changes
    • +fibroblastic foci in subpleural and paraseptal spaces
91
Q

Nocardiosis micro

A
  • gram positive rod (beaded or branching)
  • partially acid fast
  • aerobic
92
Q

Nocardiosis epi

A
  • endemic in soil
  • dz from spore inhalation or traumatic inoculation into skin
  • immunocompromised or elderly pts
93
Q

Nocardiosis Clinical features+Tx

A
  • pneumonia-similar to TB
    • often misdiagnosed as TB!!!
  • CNS involvement-brain abscess
  • cutaneous involvement
  • tx: Treimethoprim-Sulfamethoxazole
    • or surgical drainage of abscesses
94
Q

Pertussis

A
  • CP: paroxysmal cough lasting >2wks associated with post-tussive emesis or inspiratory whoop after a severe coughing episode
95
Q

What are the three phases of pertussis

A
  • catarrhal stage
    • similar to many routine URTI
  • paroxysmal stage
    • marked by severe coughing spells with the classic whoop or post-tussive emesis
  • convalescent stage-cough improves
96
Q

Cord Factor

A
  • virulent mycobacteria will grow as “serpentine” cords on enriched media secondary to the presence of cord factor (a mycoside)
  • cord factor established virulence through:
    • neutrophil inhibition
    • mitochondrial destruction
    • induced release of tumor necrosis factor
97
Q

airway resistance

A
  • regional airway resistance within the first 10 generations of bronchi contributes to most of the total airway resistance of lower respiratory tract
  • resistance is maximal in the 2nd-5th generation airways (inc segmental bronchi)
  • airways <2mm in diameter (bronchioles) contribute <20% of the total airway frictional resistance
98
Q

thorax anatomy

A
  • thoracentesis:
    • above the 8th rib in the midclavicular line
    • the 10th rib along the midax line
    • 12th rib along posterior scapular or paravertebral line
  • r/o penetrating abdo structures, subcostal neurovascular bundle on inferior margin
99
Q

relative polycythemia

A
  • erythrocytosis=HCt>52 men >48 women
  • measurement of RBC mass to distinguish absolute from relative erythrocytosis
  • nml RBC mass indicates plasma volume contraction as the cause of polycythemia
100
Q

CF Pathophys

A
  • where? respiratory and gastric glands
  • impaired functioning of the CFTR transmembrane protein reduces luminal chloride secretion and INC sodium and NET water absorption
    • results in DEHYDRATED mucus and a more negative transepithelial potential difference
  • in sweat glands: abnml CFTR function causes reduced luminal salt absorption=production of hypertonic sweat with high chloride content
  • pts with CF have INC ENaC activity along the nasal mucosa
101
Q

inactivated (killed or component) viral vaccines VS. live-attenuated viral vaccines

A
  • inactivated: predominantly generate a humoral immune response
    • induce neutralizing Ab vs. the hemagglutinin Ag (influenza vaccine)
    • upon subsequent exposure to influenza virus through natural infection, Ab inhibit binding of hemagglutinin to sialylated receptors on the host cell membrane
      • prevents the virus from entering cells via endocytosis
  • live-attenuated: generate a STRONG cell-mediated immune response IN ADDITION to providing humoral immunity
102
Q

What is the mc lab abnormality seen with Legionella pneumonia?

A

hypO-natremia

103
Q

what is the mc overall c/o CAP?

A
  • Strep pneumo!! (grampositive diplococci on Gram stain)
  • lobar consolidation is classic
104
Q

What are the four stages of lobar penumonia

A
  1. congestion (first 24 hrs)
  2. red hepatization (days 2-3)
  3. gray hepatization (days 4-6)
  4. resolution
105
Q

stage 1 of lobar pneumonia: congestion (first 24 hrs)

A
  • macro: affected lobe is red, heavy, boggy
  • micro:
    • vascular dilatation
    • alveolar exudate contains mostly bacteria
106
Q

stage 2 of lobar pneumonia: red hepatization (days 2-3)

A
  • macro: red, firm lobe (liver-like consistency)
  • micro: alveolar exudate contains erythrocytes, neutrophils, and fibrin
107
Q

stage 3 of lobar pneumonia: gray hepatization (days 4-6)

A
  • macro: gray-brown firm lobe
  • micro:
    • RBCs disintegrate
    • alveolar exudate contains neutrophils and fibrin
108
Q

stage 4 of lobar pneumonia (resolution)

A
  • macro: restoration of nml architecture
  • micro: enzymatic digestion of the exudate
109
Q

How do you identify colonized women who require INTRAPARTUM AB

A
  • universal prenatal screening for group B strep colonization by vaginal-rectal culture at 35-37 wks gestation is recommended to id colonized women
  • most frequently with penicillin or ampicillin to prevent neonatal GBS sepsis, penumonia and meningitis
110
Q

Aspergilloma

A
  • Aspergillus fumigatus causes a wide spectrum of dz
  • opportunistic infxn in immunosuppressed and neutropenic pts (invasive pulm aspergillosis)
  • aspergillosis can be colonizing (aspergilloma) when it forms a fungus ball within a preexisting lung cavity
  • can also cause a lung hypersensitivity rxn in allergic bronchopulmnoary aspergillosis in indivs with asthma
111
Q

special pulm infections and abscesses seen in alcoholics

A
  • more likely than genpop to develop pulm infections and abscesses involving combinations of anaerobic oral flora:
    • bacteroides
    • prevotella
    • fusobacterium
    • peptostreptococcus
    • +aerobic bacteria
  • CLINDAMYCIN covers most of these organisms, so is the AB of choice for treating lung abscesses
112
Q

Candida as nml commensal

A
  • Candida albicans is a nml inhabitant of the GI tract (including oral cavity) in up to 40% of the pop
  • common contaminant of sputum cultures
  • its presence in sputum does NOT indicate dz
113
Q

OSA and hypoglossal nerve

A
  • neuromuscular weakness of the oropharynx is involved in the pathophys of obstructive sleep apnea
  • elctrical stim of the hypoglossal nerve INC the diameter of the oropharyngeal AW and DEC the frequency of apneic events
114
Q

Nommage/Destruction of dust particles of different sizes

A
  • 10-15: trapped in URT
  • 2.5-10: enter trachea and bronchi, cleared by mucociliary transport
  • <2 (finest particles): reach terminal bronchioli and alveoli
    • phagocytized by macrophages
    • alveolar macrophages take up dust particles, become activated, rleease cytokines
      • some cytokines induce injury and inflamm of alveolar cells
      • PDGF and IGF stim fibroblasts to proliferate and produce collagen
      • inflamm with subsequent fibrosis results
      • mech for pneumoconiosis (interstitial lung fibrosis secondary to inhalation of inorganic dust)
115
Q

What is the intrapleural pressure at the FRC

A
  • -5 cm H2O
  • at FRC balance of CW wanting to expand and lung wanting to collapse
116
Q

septic pulm emboli

A
  • pulm emboli typically appear as mutiple wedge-shaped hemorrhagic lesions in the periphery of the lung (venous thromboembolism to pulm vasculature can also lead to this, but need RF: prolonged immobility and hypercoaguable state)
  • IVDU are at risk for developing septic pulm emboli as a complication of tricuspid valve endocarditis
117
Q

Cromolyn

A
  • and nedocromil
  • are mast cell-stabilizing agents
  • MOA: inhibit mast cell degranulation independent of the triggering stimulus
  • less effective than inhaled glucocorticoid
  • CI: second line for the tx of allergi rhintis and bronchial astham
118
Q

What is the mc presentation of cryptococcus neoformans infection

A
  • meningoencephalitis-diagnose by India ink staining of CSF
  • occurs in immunosuppressed pt
  • cryptococcal pneumo is diag by mucicarmine staining of lung tissue and bronchoalveolar washings
119
Q

Varenicline

A
  • partial agonist of nicotinic ACH receptors
  • CI: help pts with cessation of tobacco use by reducing withdrawal cravings and attenuating the rewarding effects of nicotine
120
Q

Proteinase/ANTI-proteinase balance

A
  • Proteinases:
    • elastase-neutral protease in macrophage lysosomes and azurophilic (primary) granules of neutrophils
      • can destroy terminal lung parenchyma (emphysema) when secreted in excess or if DEFICIENT ANTI acitivty
    • cathepsin G
    • matrix metalloproteinases
  • ANTI:
    • A1AT
    • A2 macro-globulin
    • TIMPs
121
Q

OSA sequelae

A
  • systemic HTN
  • pulm HTN and RHF
122
Q

chloride shift

A
  • CA activity within erythroytes forms bicarb from CO2 and water
  • many of the bicarb ions diffuse out of the RBC into the plasma
  • to maintain electrical neutrality chloride ions diffuse into the RBC to take their place
  • principal cause of high RBC choride content in venous blood
123
Q

X-linked agammaglobulinemia

A
  • low or absent circulating CD19+ and CD20+ B cells and pan-hypo-gamma-globulinemia
  • affects pts hv INC susceptibility to:
    • pyogenic bacteria
    • enteroviruses
    • Giardia lamblia
    • —d/t absence of opsonizing and neutralizing Ab—
124
Q

Granuloma formation

A
  • helps in dz containment
  • occurs maily throughinteraction among:
    • macrophages
    • multinucleated giant cells
    • CD4 T-lymphocytes
  • extensive macrophage activation can result in collat tissue damage–>caseous necrosis with formation of cavitary lung lesions
125
Q

advantages of polysaccharide vaccine

A

DEC incidence of replacement strains d/t lack of mucosal immunity

126
Q

Advantages of conjugate vaccine

A
  • INC efficacy in the elderly and kids <2yo
  • INC mucosal immunity reduces colonization (herd protection)
  • INC immunogenic memory
127
Q

DTH (delayed-type hypersensitvity rxns)

A
  • Examples:
    • contact dermatitis
    • granulomatous inflamm
    • tuberculin skin testCandida extract skin rxn
  • cells that mediate DTH rxns are TH1-lymphocytes that release IFN-g to cause recruitment and stim of macrophages
  • DTH rxns take days to reach their peak activity
  • (other HSR cause clinical effects within minutes of Ag exposure)
128
Q

asbestos-related pleural dz

A
  • pleural thickening
  • calcification of the posterolateral midlung zones and diaphragm
    • calcified lesions are one of the hallmarks of asbestos exposure
    • usually affect the PARIETAL pleura (espec b/w 6th and 9th ribs)
    • benign pleural effusions can also occur
  • many pts are asymptomatic despite visible dz on imaging and commonly: 20-30 y latency between asbestos exposure and onset of symptoms
129
Q

Asthma diagnosis

A
  • airway challenge testing with Methacholine=high sensitive but nospecifc
  • can detect the degree of bronchial HYPER-reactivity in pts suspected of having asthma
  • NEG methacholine challnege test can help rule out the diag
130
Q

Squamous metaplasia

A
  • reversible, adaptive response to chronic irritation (such as smoking)
  • nml columnar epithelium is replaced by sq epithelium (more resistant to irritation, but has reduced mucociliary clearance)
131
Q

chronic granulomatous disease

A
  • Xlinked d/o
  • PP: deficiency of NADPH oxidase-enzyme responsible for formation of reactive oxygen species in phagosomes
  • neutrophils affected by this d/o are unable to kill catalase-producing prganism=recurrent bacterial and fungal infections that frequently involve the lungs, skin, LN
132
Q

predisposing conditions for aspiration pneumonia

A
  • altered consciousness impairing cough reflex/glottic closure
    • dementia
    • drug intoxication
  • dysphagia d/t neurologic deficits:
    • stroke
    • neurodegenerative disease
  • upper GI tract d/o: GERD
  • mechanical compromise of aspiration defenses
    • nasogastric and endotracheal tubes
  • protracted vomiting
  • large-volume tube feedings in recumbent position
133
Q

what are the dominant organisms in the oral cavity

A
  • peptostreptooooo-coccus
  • Bacteroides
  • Prevotella
  • Fusobacterium

BOARDS! (14 decks)

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