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Reserve Step I Cards > Pulm > Flashcards

Pulm Flashcards

1
Q

What path does fetal blood take from the placenta to the heart?

A

Umbilical vein - liver - ductus venosus - IVC - heart

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2
Q

T-test versus analysis of variance (ANOVA)

A

A t-test is used to compare the difference between the means of (2) groups. ANOVA compares bbetween the means of 2 or more groups.

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3
Q

Deletions or additions of a number of base pairs which are not a multiple of three, indicate that a ___________ mutation has occured.

A

Frameshift

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4
Q

What type of drug is ipratropium and what type of bronchoconstriction is affected by it?

A

It is an antimuscarinic agent

Only reverses vagally-mediated bronchoconstriction

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5
Q

What kind of drug are theophylline and aminophylline? What is their MOA?

A

They are Methylxanthines

They cause bronchial dilatation by decreasing phosphodiesterase enzyme activity, thereby increasing intracellular camp.

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6
Q

What are Hamartomas? How do they present? What are they composed of?

A

The most common benign lung tumor

Present as asymptomatic peripherally located “coin lesion” in patients 50-60 y/o

Composed of disorganized cartilage, fibrous and adipose tissue

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7
Q

What are the (2) key functions of type II pneumocytes?

A
  1. Regeneration of the alveolar lining
  2. Surfactant production
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8
Q

What is responsible for the green discolortion of pus or sputum during bacterial infections?

A

Myeloperoxidase (MPO) from neutrophil azurophilic granules. MPO is a heme-containing pigmented molecule.

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9
Q

Omalizumab MOA/ indication

A

Anti-IgE antibody

Add-on therapy for patients with severe allergic asthma

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10
Q

What are the (4) major causes of hypoxemia? Which has a normal A-a gradient?

A
  1. Alveolar hypotension (normal A-a gradient)
  2. V/Q mismatch
  3. Diffusion impairment
  4. Right-to-left shunting
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11
Q

Main potential AE of neonatal oxygen therapy?

A

Retinal damage

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12
Q

What are the structural differences between MHC Class I and Class II?

A

MHC Class I: Heavy chain and B2-microglobulin

MHC Class II: Alpha and beta polypeptide chains

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13
Q

Describe Type IV Hypersensitivity

How are antibodies involved?

What are the (4) T’s of this hypersensitivity?

A

Aka delayed (T-cell mediated) type

Sensitized T cells encounter antigen and then release cytokines (leading to macrophage activation)

No antibodies involved

4 T’s:

T cells

Transplant rejections

TB skin tests

Touching (contact dermatitis)

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14
Q

Interstitial lung disease has what effect on lung volumes? Lung elastic recoil?

How does this affect expiratory flow rates?

A

Decreased lung volumes

Increased lung elastic recoil

The increased recoil leads to radial traction (outward pulling) of airways, leading to increased corrected expiratory flow rates.

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15
Q

When amniocentesis is performed to check phospholipids, what are we really checking for?

A

Fetal lung maturity

Phospholipids (such as lecithin aka phosphatidylcholine) are a majory component of pulmonary surfactant

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16
Q

What is the negative predictive value and how do we calculate it?

A

NPV represents the probability of not having a disease given a negative test result. NPV = true negatives/total negative tests

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17
Q

Sensitivity vs Specificity

A

Sensitivity = true-positive rate

(the probability that a test detects disease when a disease is present)

Specificity= true-negative rate

(Probability that a test indicates no disease when disease is absent)

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18
Q

What type of epithelium makes up the true vocal cords?

A

Stratified squamous

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19
Q

What is hypocapnia and what does it imply for a patient?

A

A state of reduced CO2 in the blood. Always implies alveolar hyperventilation.

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20
Q

Describe the common presentation for sarcoidosis

A
  1. Hilar adenopathy
  2. Pulmonary infiltrates
  3. Non-caseating granuloma
  4. AA Woman
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21
Q

Describe the pathogenesis of Sarcoidosis

A

Granuloma formation as a manifestation of cell-mediated immunity driven by products of Th1 type CD4 helper T-cells, particularly IL-2 and IFN-y, which stimulate Th1 type cell proliferation and macrophage activation, respectively.

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22
Q

Th1 vs Th2

What do they secrete? What do they recruit/activate? How are they activated? How are they inhibited?

A

Both are CD4+ Helper T-cells

Th1

  1. Secretes IFN-y
  2. Activates macrophages and cytotoxic T cells
  3. Activated by INF-y and IL-12
  4. Inhibited by IL-4 and IL-10 (from Th2)

Th2

  1. Secretes IL-4, 5, 10, and 13
  2. Recruits eosinophils for parasite defense and promotes IgE production by B cells
  3. Activated by IL-4
  4. Inhibited by IFN-y (from Th1 cells)
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23
Q

What is the most common CFTR mutation associated w/ CF?

A

F508 mutation. This causes impaired postranslational processing (improper folding and glycosylation) of the CFTR. As a result, the abnomormal protein is targeted for degradation.

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24
Q

What are the classic sputum findings for Extrinsic Allergic Asthma

A

Eosinophils and Charcot-Leyden crystals (crystalloid bodies containing eosinophil membrane proteins).

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25
Q

What key interleukin/cytokines are responsible for converting a helper T-cell into a Th1 cell? Th2 cell? Th17 cell?

A

Helper T to…

Th1 (via IL-12)

Th2 (via IL-4)

Th17 (via TGF-B and IL-6)

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26
Q

Describe the main roles for IL-1 through IL-6 when secreted by macrophages

A

Hot T-Bone stEAK

IL-1: fever (hot)

IL-2: stimulates T cells

IL-3: stimulates bone marrow

IL-4: stimulates IgE production

IL-5: stimulates IgA production

IL-6: stimulates aKute-phase protein production

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27
Q

Stimulation of the vagus nerve would have what effect on the lungs?

A

It would cause bronchoconstriction and increased bronchial mucus secretion via Ach binding to M3 receptors. This ultimately increases the work of breathing.

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28
Q

What is the MOA and Indication for both Cromolyn and Nedocromil? How effective are they compared to drugs with a similar indication?

A

They are mast cell stabilizing agents which inhibit mast cell degranulation independent of stimuli.

They are a second-line treatment for allergic rhinitis and bronchial asthma. Glucocorticoids are the first line prophylactic and are a superior drug.

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29
Q

What is a pancoast tumor? Where is the most likely location for a pancoast tumor to occur? What is the most common presentation?

A

Carcinoma in the apex of the lung. These usually arise in the superior sulcus (groove fromed by the subcalvian vessels)

Common presentation:

  1. Pt. w/ extensive smoking history
  2. Shoulder pain- most common symptom
  3. Horner syndrome
  4. Pain in distribution of C8-T2 roots (spinal cord compression)
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30
Q

Idiopathic Pulmonary Artery Hypertension

Pathogenesis/pathophys?

Presentation?

Treatment?

A

Pathogenesis: If familial form, result of inactivation of the pro-apoptotic BMPR2 gene. Results in increased endothelial and smooth muscle cell proliferation and vascular remodeling

Presentation: Dyspnea, excercise intolerance in women 20-40

Treatment: Lung transplant and bosentan (endothelin-receptor antagonist) in the meantime

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31
Q

What virus is the pictured biopsy associated with?

What is the normal type of patient who has this virus?

Describe the virus?

A

This biopsy is associated with cytomegalovirus (CMV).

This is particuarly common among patients who have recently had lung transplants or are generally immunocompromised.

It is an enveloped double-stranded DNA virus

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32
Q

Ghon Complex and TB reactivation (who is it in and what characterizes it?)

A

This complex characterizes the initial stages of M. tuberculosis infection. It consists of a lower lobe lung lesion (Ghon focus) and ipsilateral hilar adenopathy.

Reactivation of TB occurs most often in immunosuppressed patients and is characterized by apical cavitary lesions and hemoptysis.

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33
Q

X-linked agammaglobulinemia

Pathogenesis?

Diagnostics?

Presentation?

A
  • A mutation in Bruton tyrosine kinase gene causes failure of BM pre-B cells to mature.
  • These patients have:
  1. low B-cells in peripheral blood (CD19+, CD20+, CD21+)
  2. pan-hypogammaglobulinemia (low Ig’s)
  3. Increased risk of infection w/ encapsulated bugs and certain viruses and parasites
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34
Q

Mechanisms of bacterial transfer: Transformation vs Conjugation vs Transduction

A

Transformation: Direct uptake of naked DNA form the environment

Conjugation: One way transfer of chromosomal or plasmid DNA between bacteria via direct physical contact (one of them must have F factor which codes for a sex pilus).

Transduction: Transfer via bacteriophage

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35
Q

Name the key characteristics of which distinguish Slicosis from other forms of pneumoconiosis (2)

How can silicosis impair immune function?

A
  1. Eggshell calcification at the hilar nodes
  2. Birefringent silica particles surround by fibrous tissue on histology

Silicosis impairs the macrophages, by disrupting them with internalized silica particles

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36
Q

Klebsiella

Encapsulated or not?

Lactose-fermenting or not?

Usual presentation/ patients affected/characteristics?

A
  1. Encapsulated
  2. Lactose fermenting (grows pink on MacConkey agar)
  3. It causes pneumonia in subjects with impaired host defenses, especially alcoholics
  4. Characterized by tissue necrosis, early abscess formation and currant jelly sputum
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37
Q

What is the relationship between CO2 and cerebral perfusion?

A

CO2 is a potent cerebral vasodilator and therefore a drop in CO2 (due to hyperventilation and subsequent hypocapnia for example), causes a linear decrease in cerebral perfusion.

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38
Q

At the FRC, the airway pressure is? alveolar pressure is? Intrapleural pressure is?

A

Airway pressure = 0

Alveolar pressure = 0

Intrapleural pressure = Negative, with a value of -5cm H2O (prevents pneumothorax)

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39
Q

Mesothelioma

What is it?

Risk factor(s)?

Presentation?

Dx factors? (3)

A
  • Rare malignant neoplasm of mesothelial cells.
  • Primary risk factor is consistent Asbestos exposure
  • Symptoms include: dyspnea and chest pain
  • Dx tests will show:
  1. Hemorrhagic pleural effusion
  2. Pleural thickening on radiographic study
  3. Long slender microvilli and abundunt tonofilaments on histo.
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40
Q

You see a large cell with multiple nuclei in the shape of a horshoe. What is it called and what disease process is it associated with?

A

Langhans Giant Cells. Formed from macrophages which are activated in response to pulmonary TB.

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41
Q

Name the potential sequelae of Obstructive Sleep Apnea (3)

A

Systemic and Pulmonary HTN, and right heart failure

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42
Q

Sarcoidosis

Pathophys?

Presentation?

Dx?

Treatment?

A
  1. Path:Immune mediated, widespread noncaseating granulomas
  2. Pres: Black women w/ possible erythema nodusum, arthralgia, elevated ACE levels, etc.
  3. Dx: Bilateral hilar adenopathy on CXR
  4. Tx: Steroids
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43
Q

What are the (4) stages associated with Lobar Pneumonia? Describe the exudate.

A
  1. Congestion (first 24 hours): Vascular dilation; exudate contains bacteria
  2. Red hepatization (days 2-3): erythrocytes, PMNs and fibrin in exudate
  3. Gray hepatization (days 4-6): RBCs disintegrate. Exudate contains PMNs and fibrin
  4. Resolution: Enzymatic digestion of exudate
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44
Q

Chronic Granulomatous Disease

  1. Pathogenesis?
  2. Clinical Manifestations?
  3. Dx?
A
  1. Pathogenesis: Inactivating mutation affecting NADPH oxidase. Impaired respiratory burst inhibits phagocytic intracellular killing
  2. Clinical Manifestation: Recurrent infections in child w/ catalase (+) bacteria/fungi (commonly in lungs, skin, LNs and liver). Diffuse granuloma formation
  3. Diagnosis: DHR flow cytometry (prefered); Nitroblue tetrazolium (NBT) testing
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45
Q

Describe the pathogenesis of centriacinar emphysema

A
  1. Oxidative injury to the respiratory bronchioles by smoking
  2. Macrophage activation
  3. Inflammatory recruitment of neutrophils
  4. Release of proteases by neutrophils and macrophages
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46
Q

What is the common clinical presentation for a pneumothorax?

What is often the cause of spontaneous pneumothorax?

A
  1. Sudden unilateral chest pain
  2. Hyperresonance
  3. Absent breath sounds
  4. Often seen in tall, thin males around age 20

Can be the spontaneous result of the rupture of an apical subpleural bleb

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47
Q

Describe the process of granuloma formation for TB

A
  1. Macrophages eat m. tuberculosis
  2. Macrophages present to T cells and also secrete IL-12
  3. T-cells differentiate to Th1
  4. Th1 produces IFN-y which activates macrophages
  5. Activated macrophages produce TNF-a, increasing recruitment, allowing for walling off of infection
48
Q

Mycobacterium Avium Complex

  1. What is it?
  2. Risk factors?
  3. Normal presentation?
  4. How do you differentiate MAC from disseminated TB?
A
  1. An infection caused by nontuberculous mycobacteria M avium and M intracellulare.
  2. Risk factor: CD4 count
  3. Presents w/ nonspecific symptoms- fever, weight loss, and diarrhea in HIV patient
  4. Differs from TB due to hepatosplenomegally, anemia, and elevated alk phosp/ LDH
49
Q

In what conditions do we see Cheyne-Stokes breathing? (2)

A
  1. CHF
  2. Neurologic disease
50
Q

Fat Embolism

  1. Presentation?
  2. Staining?
A
  1. Severe resp. distress + diffuse neurological impairment + upperbody petechial rash, following long bone injury
  2. Fat emboli turns block from stain w/ osmium tetroxide
51
Q

What is the most frequent cause of lung abscess and what type of conditions increase their risk.

Name (1) key example of this cause.

Tx (2)?

A

Anaerobic bacteria normally found in the oral cavity are the most common cause. Risk factors include anything that increases aspiration risk (seizure, alcholism, drug abuse, stroke, dementia, etc.)

Ex: Actinomycosis

Tx: Penicillin or Clindamycin (if hypersensitive to Penicillin)

52
Q

Superior Vena Cava Syndrome

  1. Pathogenesis?
  2. Presentation?
A
  1. Path: Compression of SVC leading to impaired venous return
  2. Presentation: Dyspnea, facial swelling, and dilated collateral veins in upper trunk
53
Q

Legionella pneumophila

  1. Description of bug
  2. Symptoms
  3. Dx info
  4. Pathogenesis
  5. Tx
A
  1. Facultative intracellular gram-negative bacillus
  2. Symptoms- high fever, elevated transaminases, cough, confusion, and diarrhea,
  3. Dx- Hyponatremia and sputum gram stain showing many neutrophils but few to no organisms
  4. Passed from contaminated water
  5. Respiratory fluroquinolones or newer macrolides
54
Q

What type of gating does the CFTR channel have?

A

ATP-gated

55
Q

What effect does left ventricular HF have on lung compliance?

A

Leads to fluid accumulation in the lung interstium resulting in decreased lung compliance.

56
Q

Pulmonary Embolism

  1. Presentation
  2. Lab data (blood gases?acidosis or alkalosis?
  3. Other diagnostic tests
A
  1. Acute-onset dyspnea, calf-swelling (indicative of DVT), obesity, Hx of prolonged immobility
  2. Hypoxemia and respiratory alkalosis
  3. CT pulm angiography is image testing of choice
57
Q

Type I Hypersensitivity

Explain the mechanism. What mediates these reactions?

A

Mediated by the interaction of allergen w/ preexisting IgE bound to basophils and mast cells. Cross-linking occurs allowing for degranulation and immediate allergy signs.

58
Q

What are lamellar bodies?

A

They are organelles which contain parallel stacks of membrane lamellae and are a component of type II pneumocytes. They function to store and release pulmonary surfactant.

59
Q

What illnesses can result in cold agglutinins (3)

A
  1. Mycoplasma pneumoniae
  2. EBV infection
  3. Hematologic malignancy
60
Q

What (3) types of drugs disrupt the peptidoglycan cell wall of gram-positive/ gram-negative organisms?

A
  1. Penicillans
  2. Cephalosporins
  3. Vancomycin
61
Q

Selective IgA Deficiency

  1. Pathology
  2. Presentation
  3. What are these patients at risk for?
A
  1. Pathology: Failure of B-cells to switch from IgM to IgA production. Very common
  2. Presentation: Usually asymptomatic but can have recurrent sinopulmonary and GI tract infections
  3. Risk: Many of these patients form IgG antibodies directed against IgA so risk anaphylaxis during transfusion
62
Q

What is the relationship between Cystic Fibrosis, ADEK, and squamous metaplasia?

A
  • CF can lead to pancreatic insufficency, fat malabsorption, and an ADEK deficiency.
  • Vitamin A maintains orderly differentiation of specialized epithelia.
  • Avitaminosis A can cause squamous metaplasia of such epithelia to keratinizing epithelium
63
Q

Describe the Chloride Shift

A
  • Carbonic Anhydrase activity w/in erythrocytes forms bicarb from CO2/water
  • Many of the bicarb ions diffuse from the RBC to the plasma
  • To maintain electroneutrality, chloride ions diffuse into the RBC
64
Q

Asbestos exposure

  1. Potential clinical manifestations? (3)
  2. What two cancer types can Asbestos lead to? Which is most common?
A
  1. Pleural plaques which affect the parietal pleura alongthe lower lungs/diaphragm; progressive/ diffuse pulmonary fibrosis; presence of asbestos bodies.
  2. Bronchogenic carcinoma (most common and can occur w/o asbestos) and malignant mesothelioma (rare but more specific to heavy asbestos exposure)
65
Q

Histoplasma Capsulatum

  1. What is it/where is it found?
  2. How is it transmitted?
  3. Pathology?
  4. Presentation?
  5. Dx?
A
  1. A mold found in soils of Mississippi and the Ohio River Valley
  2. It is transmitted by the respiratory route when bird/rat droppings containing fungal spores are inhaled
  3. Pathology: In the lungs, the fungus is ingested by macrophages and a granuloma forms, similar to TB
  4. Presentation: Asymptomatic if immunocompetent. May develop acute pulmonary disease, or develop chronic pulmonary histoplasmosis (looks like TB). May see lymphadenopathy and hepatosplenomegally
  5. Dx.: small oval bodies w/in macrophages
    6.
66
Q

Tension Pneumothorax

  1. Pathology?
  2. Clinical presentation?
  3. Dx?
  4. Tx?
A
  1. Pathology: As an increasing volume of air accumulates w/in the pleural space, the lungs and mediastinum shift to the opposite side and this pressure drops systemic venous return to the heart, leading to decreased cardiac output
  2. Presentation: Tachycardia, hypotension, tachypnea, hypoxemia
  3. Dx: Hx, mediastinal shift on CXR, absent breath sounds and hyperresonance to percussion on affected side
  4. Tx: Emergency needle thoracostomy or chest tube
67
Q

Chronic Granulomatous Disease

  1. Pathogenesis?
  2. Key organisms involved?
  3. Presentation?
A
  1. Pathogenesis: A genetic defect in the NADPH oxidase complex decreases the formation of reactive oxygen species which have a direct microbicidal activity and also activate granule proteases.
  2. Key Organisms: Catalase-postive bugs which destroy their own hydrogen peroxide (specifically: S. aureus, Burkholderia cepacia, Serratia marcescens, Nocardia, and Aspergillus)
  3. Presentation: Child with recurrent bacterial and fungal infections
68
Q

CREST Syndrome

  1. What is this disease a subset of?
  2. Pathology?
  3. What are the sx?
  4. Potential consequences
  5. Dx
A
  1. Limited scleroderma
  2. Increased proliferation and accumulation of monoclonal T-cells in affected tissues. Leads to increased TGF-B release and thus increased production of collagen and ECM
  3. Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia
  4. Can have sclerosis of rejal, pulm, CV, and GI systems (due to small vessel deposits)
  5. Antibodies (anti-centromere)
69
Q

Theophylline

  1. Indication
  2. MOA
  3. Metabolization
  4. AE
A
  1. Used as an alternate therapy for asthma and COPD
  2. Adenosine receptor antagonist and phosphodiesterase inhibitor that causes bronchodilation by increasing cAMP levels and has mild anti-inflammatory effects
  3. Metabolized predominantly by hepatic cytochrome oxidase
  4. AE: Theophylline toxicity
70
Q

Pertussis (Whooping cough)

  1. Who gets it?
  2. Describe the (3) phases
  3. What causes it?
A
  1. Was mostly in kids prior to vaccinations. Now usually adolescents/adults w/o a booster
  2. (phases)
    • Catarrhal stage- similar to many routine URI’s
    • Paroxysmal stage- severe coughing spells w/ classic whoop (post-tussive emesis)
    • Convalescent stage- during which cough improves
  3. Caused by gram-negative Bordetella pertussis.
71
Q

Risks of secondhand smoke exposure (7)

A
  1. SIDS
  2. Low birth weight
  3. Dental caries
  4. Middle ear disease
  5. Asthma
  6. LRTI
  7. Decreased GFR
72
Q

Nocardiosis (Nocarda asteroides infection)

  1. Key micro characteristics
  2. Epidemiology (where is it, how does it get to people and who does it affect?)
  3. Clinical features (3)
  4. Tx
A
  1. Gram positive rod (beading/branching); acid-fast; Aerobic
  2. Endemic in soil; get disease from spore inhalation/ trauma inoculation; immunocomprimised/elderly
  3. Pneumonia (similar to TB); CNS (abscess); Cutaneous involvement
  4. Tx: Bactrim and surgical drainage of abscess
73
Q

Tissue damage and resultant abscess formation is primarily caused by…

A

Lyosomal enzyme release from neutrophils

74
Q

Kartagener Syndrome

  1. Pathology
  2. Presentation (3)
A
  1. Form of primary ciliary dyskinesia, that is autosomal recessive in nature
  2. Presentation
    • Recurrent respiratory infections (e.g., sinusitis, bronchiectasis)
    • Situs inversus (reverse organ positioning)
    • Infertility
75
Q

Blastomyces dermatitidis

  1. Endemic to where?
  2. Characterisitics?
  3. Presentation?
A
  1. Endemic to southeastern US (east of mississippi river)
  2. Characteristics: Dimorphic fungus which is a large yeast (in the human body) with a single, broad-based bud.
  3. Infxn follows inhalation and may present as a lung infection (with GRANULOMA) or cause flu-like illness/pneumonia in the immunocompetent. Can present as systemic disease in immunocomprimised patients.
76
Q

Adenocarcinoma In-situ

  1. Pathology
  2. Microscopy
  3. Presentation
  4. Imaging
A
  1. Arises from alveolar epithelium at the periphery of lung
  2. Microscopy shows well-differentiated, dysplastic columnar cells w/ or w/o mucin
  3. Similar to other lung cancers (SOB, cough, hemoptysis)
  4. Discrete mass or pneumonia-like consolidation on imaging
77
Q

What is the difference in the response generated by inactivated vs live-attenuated viral vaccines?

A

Inactivated: Generate a humoral response, inducing neutralizing antibodies which keep virus from entering the cell membrane

Live-attenuated: Generate a strong cell-mediated response, in addition to a humoral response

78
Q

Describe Aspergillus fumigatus colonization

  1. What is it?
  2. How does it look on imaging?
  3. Sx
A
  1. Aspergillus develops in old lung cavities (from TB, emphysema, sarcoidosis, etc) and it forms a fungus ball w/o tissue invasion
  2. Appears on CXR as radioopaque structure which shifts when Pt changes postion
  3. Can cause hemoptysis (otherwise asymptomatic)
79
Q

Aspergillus fumigatus

  1. Describe its structure
  2. How do people get it?
  3. Describe associated disease processes
A
  1. Mold that froms septate hyphae that branch at 45-degree angles
  2. Spores are inhaled and particularly impact those in immunocompromised states
  3. Wide spectrum of diseases:
    • Invasive pulmonary aspergillosis (for the immunosuppressed/ neutropenic)
    • Aspergillus colonization in preexisting lung cavities
    • Allergic bronchopulmonary aspergillosis (lung hypersensitivity reaction) for patients w/ asthma
80
Q

Name the (4) key neutrophil chemotactic agents during inflammation

A
  1. Leukotriene B4
  2. 5-HETE (leukotriene precursor)
  3. C5a (complement component)
  4. IL-8
81
Q

H. flu

  1. What does it require in order to grow?
  2. What does its pathogenicity depend on?
  3. Which strain is most invasive?
  4. How does it present in unvaccinated individuals?
A
  1. Requires both X factor (hematin) and V factor (NAD+) to grow
  2. Pathogenicity depends on the presence of a capsule
  3. Type B strain = most invasive and virulent
  4. Type B causes- severe epiglottitis, meningitis, and bacteremia; Non-type B causes noninvasive sinusitis, bronchitis, otitis media and conjunctivitis
82
Q

Transudate vs exudate

A

Transudate- plasma only. Due to hemodynamic changes

Exudate- plasma + ions. Due to structural damage

83
Q

Coccidioides immitis

  1. Describe the (2) forms
  2. Where is it endemic to?
  3. How is it transmitted?
  4. How does it present (5)
A
  1. Mold in the cold, endospore in the heat
  2. Southwest US, northern Mexico, regions of Central and South America
  3. Transmitted via spore inhalation which form endospores that rupture and disseminate
  4. Presentation:
    • acute pneumonia (most common)
    • chronic pneumonia
    • pulmonary nodules and cavities
    • extrapulmonary nonmeningeal disease
    • meningitis
84
Q
  1. What do Central Chemoreceptors sense?
  2. What do Peripheral Chemoreceptors sense?
  3. What do Pulmonary Stretch Receptors sense?
A
  1. Central: Increased PaCO2
  2. Peripheral (carotid and aortic bodies): PaO2 – stimulated by hypoxemia
  3. Pulm Stretch: Regulates duration of inspiration based on degree of lung distension
85
Q

Meconium Ileus

What is it and what disease is it associated w/?

A

Small bowel obstruction due to abnormally dehydrated meconium in a patient w/ cystic fibrosis

86
Q

How does sepsis lead to ARDS? Describe step by step.

A

During sepsis, cytokines circulate in response to infection, activate pulmonary epithelium and provoke an inflammatory response mediated by neutrophils. This leads to capillary damage and the leakage of protein/fluid into the alveolar space.

87
Q

What pathology does this histological image indicate?

A

Coccidioides immitis

88
Q

What is the usual clinical presentation for Hyper-IgM syndrome? (2)

A
  1. Lymphoid hyperplasia
  2. Recurrent sinopulmonary infections
89
Q

What is the clearence mechanism for inhaled particles which are…

  1. 10-15 um?
  2. 2.5-10 um?
  3. less than 2um?
A
90
Q

What type of RNA can be infective, what type cannot, and why?

A
  1. Purified single-stranded positive-sense RNA can be infectious
  2. Single-stranded negative sense or double stranded RNA cannot be infectious

For a purified RNA molecule to induce viral protein synthesis in a host cell, it must be able to act DIRECTLY AS mRNA USING HOST INTRACELLULAR MACHINERY for translation.

91
Q

Chronic transplant rejection

  1. Pathology/ histopathology
  2. Presentation
  3. Dx
A
  1. Lymphocytix inflammation + epithelial destruction in small airways. Exudate and granulation tissue later found ultimately leading to fibrosis. Leads to obstructive lung disease bronchiolitis obliterans.
  2. Dyspnea + dry cough
  3. Dx: Spirometry shows airflow limitation w/ a drop in FEV1 and FEV1/FVC
92
Q
  1. Who should be vaccinated against Strep Pneumo?
  2. What are the (2) main vaccines?
A
  1. Elderly/ young children are most at risk
  2. Both affect the outer polysaccharide covering:
    • Pneumococcal polysacharide vaccine
    • Pneumococcal conjugate vaccine
93
Q

Pulmonary Fibrosis

  1. Microscopic view
  2. Clinical presentation
  3. Dx
  4. What disease can help cause it?
A
  1. Microscopic: Progresive fibrosis an lead to cystically-dilated bronchioles that later coalesce to from “honeycomb” appearance
  2. Presents with gradual-onset dyspnea, first w/ exertion and then eventually even at rest
  3. Physical exam can show end-inspiratory crackles and PFTs show restriction (decreased FEV1 and FVC w/ normal ratio)
94
Q

Cryptococcus neoformans

  1. How do they look?
  2. Who do they affect/ how is it passed?
  3. Most common disease processes caused
  4. Dx
A
  1. Budding yeasts w/ thick capsules
  2. Passed via pigeons/soil and affect only immunocompromised
  3. Meningoencephalitis is the most common disesase caused
  4. India Ink/ Mucarmine
95
Q

What is ARDS?

  1. Pathology?
  2. Presentation?
  3. Histo?
  4. What main diseases/issues can lead to ARDS?
A

Acute Respiratory Distress Syndrome

  1. Characterized by diffuse injury to the pulmonary microvascular endothelium and alveolar epithelium, resulting in increased pulmonary capillary permability and a leaky alveolocapillary membrane
  2. Presents as progressive hypoxemia refractory to O2 therapy and diffuse interstitial edema w/o cardiogenic cause.
  3. Hyaline membranes on histo
  4. Pancreatitis
96
Q

At what point in the respiratory cycle is the total pulmonary vascular resistance at its lowest?

A

The functional residual capacity (the trough of the tidal volume)

97
Q

Small Cell (Oat Cell) Carcinoma

  1. Where does it often spread?
  2. Histology (what do they stain (+) for?)
  3. How do they look on histo?
  4. What do they synthesize?
  5. Tx/prognosis
A
  1. Often spreads to lungs
  2. These tumors stain for neuroendocrine markers (like NCAM, enolase, or chromogranin).
  3. On histo they are round or oval cells with scant cytoplasm and abundant mitoses
  4. Synthesize hormones and hormone-like substances
  5. Chemo/radiation sensitive/ poor prognosis
98
Q

Hyperacute rejection vs acute rejection vs chronic rejection

(particularly in the lung)

Time-frame? What part of the lung is affected?

A

Hyperacute: Occurs in minutess. Preformed antibodies lead to graft blood vessel spasm and diffuse intravascular coagulation (white graft rejection)

Acute: 1-2 weeks. Due to recipients rection to the HLA of the graft. Causes vascular damage and bronchial infiltration. Perihilar and lower lobeopacities on CXR.

Chronic: months to years after transplant. Inflmmation of the small bronchioles leading to narrowing and obstruction

99
Q

What substances are capable of inactivating enveloped viruses?

A

Organic solvents (ex. Ether)

[Non-enveloped viruses are generally resistant to the action of ether]

100
Q

Viral Laryngotracheitis

  1. Also known as?
  2. Presentation?
  3. Most common virus responsible?
A
  1. Croup
  2. Brassy, barking cough; Dyspnea; Recent history of upper respiratory infection (URI)
  3. Parainfluenza virus is the most common cause
101
Q

If a pneumonia patient has a CD4+ count greater than 400cells/uL, what bug do you expect to be the cause?

A

>400?: strep pneumo

pneumo jiroveci (PCP)

102
Q

What type of Bacteria are capable of surviving boiling?

A

Spore forming

103
Q

Walking pneumonia

  1. What bug causes it?
  2. Dx?
  3. What type of medium is required for this bug to grow?
  4. Sx?
A
  1. Mycoplasma pneumoniae
  2. CXR looks much worse than the clinical appearance of the patient indicates
  3. Cholesterol medium
  4. Nagging unproductive cough, low-grade fever, and malaise
104
Q
  1. A subset of patients stricken by influenze got on to develop secondary…
  2. What types of patients are these?
  3. What are the most common causes for this secondary disease state?
A
  1. …Bacterial pneumonia
  2. Elderly
  3. S. Pneumo, S. Aureus, H. Flu
105
Q
  1. Acid-fast stans ID organisms that have ______ ______ (2) in their cell walls.
  2. How do acid fast stains specifically work?
A
  1. Mycolic Acid (like mycobacterium and some Nocardia species)
  2. Aniline dye is applied to a smear and then is decolorized w/ acid alcohol
106
Q

What types of drugs are not effective against organisms of the mycoplasma species? What type are? Why?

A

All of these organisms lack peptidoglycan cell walls and are therefore resistant to agents that attack this wall, uch as penicllins, cephalosporins, carbapenems, and vanco.

Must treat with anti-ribosomal agents (tetracycline and macrolides)

107
Q

Candida Albicans

  1. What does it give rise to when heated?
  2. Where is it found normally in humans?
A
  1. Gives rise to true hyphae when incubated at 37 degrees C
  2. Normally found in the GI tract (including the oral cavity) and thus is a common contaminant of sputum cultures
108
Q

Allergic bronchopulmonary aspergillosis (ABPA)

  1. History commonly associated (2)?
  2. Chest imaging?
  3. Dx?
A
  1. Asthma and CF
  2. Recurrent infiltrates and Bronchiectasis
  3. Eosinophilia; Positive skin test and Ig for Aspergillus; Elevated IgE
109
Q

What specific component of the H. Flu capsule is the vaccine set against?

A

Polyribosyl-ribitol-phosphate (PRP)

110
Q

Name the A’s of small cell (oat cell) carcinoma

A
  1. May produce ACTH
  2. SIADH
  3. Antibodies against presynaptic Ca2+ channels (Lambert-Eaton)
  4. Amplification of myc oncogenes
111
Q
A
112
Q

Acute Arsenic Posioning

  1. Presentation
  2. Source
  3. Antidote
A
  1. Garlic odor breath + diarrhea + N/V
  2. Insecticides
  3. Cure = Dimercaprol
113
Q

What does the candidal antigen test assess?

A

The activity of T cell-mediated immunity via recruitment of macrophages, and CD4+ and CD8+ T lymphocytes

114
Q

What (3) parts of the body does the iliohypogastric nerve innervate?

A

Sensation to the suprapubic and gluteal regions

Motor function to the anterolateral abdominal wall muscles

115
Q

What is the site of lowest osmolarity in the nephron?

A

DCT

116
Q

Where do the ureters sit in respect to the common, external, and internal iliac?

A

Anterior (right on top of them)

Reserve Step I Cards (10 decks)

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