Uworld Pulm I Flashcards

1
Q
As the tissue oxygen content increases, the vascular resistance decreases. What organ would this happen in?
A. brain
B. heart
C. kidneys
D. lungs
E. small intestine
A

D. lungs
pulmonary vasculature, where vascular resistance decreases in well-aerated alveoli compared to underventilated alveoli => hypoxic vasoconstriction => blood flow diverted away from underventilated regions of the lung, toward better ventilated areas where gas exchange occurs more efficiently => decreasing physiological shunting.

reverse relationship applies systemically, ensuring hypoxic tissues receive increased blood flow

mechanism for hypoxic pulm vasocon => increase in pulm artery smooth muscle cytosolic Ca2+ secondary to hypoxia induced modulation of K+ channels and/or decreased production of reactive oxygen species

A. cerebral circulation, hypoxia => arteriolar dilation where partial pressure of oxygen subendocardial blood flow mediated by local tissue PO2, adenosine, prostacyclin, nitric oxide; decreased tissue PO2 => vasodilation of arterioles in myocardium

C. increase symp tone => vasoconstriction of renal vasculature, hypoxia does not have this effect

E. intestinal blood flow increases in response to digestive chyme passing over intestinal mucosa. fasting state => symp tone large role, decrease in splanchnic blood flow occurs with exercise or significant hypovolemia

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2
Q

64 yo, worsening SOB, speak in short sentences only, desaturates with minimal exertion. respiratory failure, intubated. dies several days later in ICU. history: HTN, dyslipidemia, 1pack a day smoked for 40 years, 25 years as a nickel miner. autopsy => thickened bronchial walls, neutrophilic infiltrates, mucus gland enlargement, patchy squamous metaplasia of bronchial mucosa. What was the greatest contributor to biopsy findings?

A. allergic
B. behavioral
C. genetic
D. infectious
E. neoplastic
F. occupational
A

B. behavioral
respiratory failure, hypoxia, thickened bronchial walls with neutrophilic infiltrates and mucous gland enlargement => CHRONIC BRONCHITIS
-chronic productive cough with airflow limitation
-tobacco smoking
-pollutants, grain, cotton, silica dusts
Biopsy:
-thickened bronchial walls
-neutrophilic and lymphocytic infiltrates
-mucus gland enlargement with increased # goblet cells (increasing mucus production)
-patchy squamous metaplasia of bronchial mucosa

A. allergic asthma => pathologic remodeling of bronchial wall

  • thickening of bronchial epithelium, basement membrane, bronchial smooth muscle
  • edema
  • inflammatory infiltrates of eosinophils and mast cells
  • submucosal mucous gland enlargement
  • cig smoking more commonly causes chronic bronchitis than asthma

C. no known genetic factors predispose to chronic bronchitis

D. repeated bronchial/bronchiolar bacterial and viral infections => chronic bronchitis, less significantly than cig smoking. infection => mucous plugging, mural inflammation
cig smoking predisposes to infection by impairing ciliary clearance and directly damaging resp epithelium

E, F. Nickel is carcinogen, occupational exposure => nasal and lung cancer; neoplastic transformation does NOT contribute to development of chronic bronchitis. TOBACCO SMOKING MOST IMPORTANT RISK FACTOR FOR CHRONIC BRONCHITIS

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3
Q

56 yo male smoker complains of chronic cough. hospitalized several times in past for respiratory infections requiring parenteral antibiotics. smoked 30 years. O2 sat 90% at rest, 84% with moderate exertion. What additional finding most likely in this patient?

A. increased expiratory flow rates
B. decreased functional residual capacity
C. decreased right ventricular afterload
D. increased left ventricular compliance
E. increased EPO prod
A

E. increased EPO
COPD secondary to longstanding cig smoking
COPD caused by bronchial asthma, chronic bronchitis, emphysema
smokerscan have both chronic bronchitis and centrilobular emphysema.
chronic bronchitis => hypoxia decreasing diameter of conducting airways, prevent adequate airflow
emphysema => hypoxia dilating alveolar air sacs so insufficient contact between airspaces and doex blodo in alveolar capillaries

smoking independently => hypoxia increasing concentration of carboxyhemoglobin

hypoxia- sensed by cells in renal cortex => release EPO => erythrocyte production

A. peak expiratory flow rates decreased in obstructive lung disease; COPD, FEV1 decreased while FVC much less decreased => decreased FEV1/FVC

B. COPD, FRC increased; decreased in restrictive lung diseases

C. Right ventricular afterload increased in COPD due to chronic pulm HTN => increased jugular venous pressure and right heart failure (cor pulmonale)

D. left ventricular compliance increased in patients with dilated cardiomyopathy, not directly affected in COPD

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4
Q

63 yo hospitalized b/c dyspnea on exertion, generalized fatigue. hospitalized 3 times in past year for heat failure exacerbations. essential HTN for 20 years, MI age 58, hypercholesterolemia. 36 pack year smoking history, 10 year history of alcohol abuse. tachycardia, distended neck veins, bilateral crackles on lung auscultation, S3, pedal edema. appropriate therapy initiated. 3rd day of hospitalization, hematocrit increases to 50%, up from 44% on admission. ABG PaO2 70mmHg. 51Cr-tagged rbc infusion => normal rbc mass. Which of the following is the most likely cause of this patient’s polycythemia?

A. polycythemia vera
B. hypoxic erythrocytosis
C. renal disease
D. occult neoplasia
E. relative erythrocytosis
A

E. relative erythrocytosis

polycythemia (erythrocytosis) hematocrit >52% (men) or >48% (women)- result of true increase in RBC mass (absolute) or decrease in plasma volume (relative)

Absolute => polcythemia vera (all 3 cell lines increase)
=> secondary- only rbc increases, normal wbc and platelets
=> secondary- hypoxia, EPO producing tumors

Relative => dehydration, excessive diuresis

  1. absolute v relative erythrocytosis- need direct measurement of rbc mass; hemoglobin, hematocrit not helpful in distinguishing; increase = absolute; normal = relative
  2. Primary v secondary erythrocytosis-
    primary- low EPO- myeloproliferative disorders- polycythemia vera
    secondary- increased EPO due to chronic hypoxia from high altitudes, smoking, COPD, abnormal secretion by neoplastic/diseased tissue
  3. hypoxic v other caues of secondary eythrocytosis- SaO2 (arterial oxygen sat)- important to exclude hypoxemia; SaO2 secondary polycythemia; SaO2 (%), PaO2 (mmHg)

A. polycythemia vera myeloproliferative disorder- marked erythrocytosis, modest increases in granulocytes and platelets.low EPO characteristic, increased RBC mass

B. hypoxia; SaO2 EPO prod abnormal => increased rbc mass, increased EPO; chronic renal disease => decreased EPO typically

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5
Q

7mo old boy irritability, white patches in his mouth. PMH sig 3 episodes otitis media, 2 ep bronchiolitis required hospitalization; history of chronic loose stools. small for his age and ill-appearing. head and neck exam show white patches consistent with oral candidiasis, otherwise normal. auscultation of lungs => expiratory wheezing. cardiac exam normal. labs:

sodium: 140
K+ 3.8
Cl- 98
bicarb 24
Ca2+ 9.6

serum protein electrophoresis => very low gamma globulin level

chest x-ray reveals absent thymic shadow what is the most likely diagnosis?

A. common variable immunodeficiency
B. DiGeorge
C. SCID
D. Wiskott-Aldrich
E. X-linked agammaglobulinemia
A

C. SCID

Ataxia-telangiectasia: ataxia, telangiectasias, sinopulmonary infections

Chediak-Higashi- oculocutaneous albinism, pyogenic infections, progressive neurologic dysfunction

Chronic granulomatous disease- severe bacterial and fungal infections, granuloma formation

DiGeorge- congenital heart disease, dysmorphic facies, hypocalcemia

SCID- severe bacterial n viral infections in infancy, chronic diarrhea, mucocutaneous candidiasis

Terminal complement deficiency- recurrent neisseria infection

Wiskott-Aldrich - recurrent infections worsen with age, easy bleeding, eczema

SCID- impaired T and B cell development and function => compromised cell and humoral immunity => severe viral and bacterial infections
-mucocutaneous candidiasis, persistent diarrhea, failure to thrive; labs: low or absent CD3+ T cells, hypogammaglobulinemia; thymic hypoplasia/aplasia

A. common variable- hypogammaglobulinemia; recurrent infections in adults and children; cell mediated immunity not as impaired as in SCID, thymic aplasia unlikely

B. DiGeorge- craniofacial abnormalities, conotruncal cardiac anomalies, hypoplastic thymus, hypocalcemia from PTH hypoplasia; this is a form of SCID, the absence of other characteristic findings makes this less likely than SCID

D. Wiskott-Aldrich- abnormal cytoskeletal functioning => impairmed T and B cells. recurrent viral, bacterial, fungal infections worsen with age, bleeding due to thrombocytopenia, eczema

E. X-linked/Bruton’s agammaglobulinemia insufficient production of mature B cells => predisposes to recurrent infections with encapsulated pyogenic bacteria => strep pneumoniae, H. influenzae type B; quantity and functioning of T cells not affected, so absent thymic shadow unlikley

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6
Q

Relationship between smoking status and forced expiratory flow between 25% and 75% of vital capacity (FEF25-75%) in 4 groups. Group A- 200 nonsmokers; B- light smokers; C- 8-22cigs; D- heavy smokers; measure in all participants. What is the most appropriate stat method to compare in all 4 groups?

A. analysis of variance
B. chi square test
C. meta-analysis
D. multiple linear regression
E. pearson correlation coefficient
F. two sample t-test
A

A. analysis of variance

null: all samples drawn from the same population
alternate: samples drawn from dif populations (u1 not equal to u2 not equal to u3)
- if there is a large apparent difference between means of samples => reject null

ANOVA- sig dif between means of 2+ independent groups. ANOVA compares means between groups relatve to variability within groups, signficantly different

B. chi square- association btwn 2 categorical variables

C. meta-analysis- pooling of data from several studies; analysis having gretaer stat power than individual studies

D. multiple linear regressions- linear relationship between dep var and2+ indep vars

E. Pearson correlation coeficient- measure of strength and direction of linear relationship between 2 variables

F. 2 sample t test when 2 group means compared

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7
Q

19 yo woman MVA, med history celiac disease, 3 episodes pneumonia; BP 80/45, pulse 130. pallor, splenic laceration. blood transfusion with O-neg packed rbcs. tranfusion => facial swelling, generalized hives, SOB. diagnosis?

A. ABO incompatibility
B. C1 inhib deficiency
C. leukocyte adhesion deficiency
D. selective IgA deficiency
E. SCID
A
D. selective IgA def
clinical features: usually asymptomatic
recurrent sinopulmonary, GI infections
autoimmune disease
anaphylaxis during transfusions

diagnosis: low or absent serum IgA levels
normal IgG and IgM

history of recurrent pneumonia, celiac, anaphylactic rxn during blood transfusion => selective IgA def = most common primary immunodeficiency.

IgE antibodies against IgA

A. acute hemolytic reactions occur when patient’s preexisting IgM or IgG antibod cross reacts with antigens in transfused blood - A, B, Rh, Kell; fever and chills to severe hemolysis, circulatory collapse. anaphylaxis IgE mediated, does not reult from ABO incompatibility

B. C1 inhibitor def => hereditary angioedema, triggered by transfusions. would not have urticaria or wheezing

C. Leukocyte adhesion deficiency => poor leukocyte adherence and transmigration through vasculature. recurrent skin and mucosalinfections, not increased risk for anaphylaxis during transfusions

E. SCID => failure of T cell development, severe defect in cell mediated and humoral immunity. severe bacterial, viral, fungal infections beginning in infancy

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8
Q

Students develop fever, cough and malaise from cave exploration trip to Central US. Pulmonary infiltrates and hilar adenopathy CXR. lung tissue specimens would show:

A. multinucleated spherules
B. ovoid cells within macrophages
C. budding yeast with thick capsule
D. pseudohyphae and blastoconidia
E. septate hyphae with dichotomous branching
A

B. ovoid cells within macrophages
histoplasma capsulatum dimorphic fungus- mold in soil; bird and bat droppings, endemic to Mississippi and Ohio river basins. history of exploring caves (vats), or cleaning bird cages/coops

H. capsulatum respiratory route when bird or bat droppings contain fungal spores. fungus ingested by macrophages in lungs, light microscopy as OVAL BODIES- immune reaction to histoplasma similar to M. tuberculosis- granuloma formation. targets histiocytes and reticuloendothelial systemi => lympadenopathy and hepatosplenomegaly

majority of immunocompetent hosts asymtomatic, some may develop cute pulm disease- cough, fever, pleuritic chest pain and pulm infiltrates. individual with underlying lung disease develop chronic pulm histopasmosis- similar to tuberculosis (cough, malaise, weight loss, cavitations in upper lung lobes) disseminated disease in immunocompromised individuals

A. spherules- endospores with Coccidioides immitis; can cause pulm disease in immunocompetent individuals. endemic to southwestern US, not associated with cave exploration

C. Cryptococcus neoformans- budding yeast with thick capsule- soil containing pigeon droppings. fungus tends to cause disease (meningoencephalitis and pulm disease0 in immunocompromised

D. Candida- yeasts form pseudohyphae; blastoconidia spores that grow as buds on fungal hyphae. not associated with pulm infiltrates or lymphadenopathy

E. aspergillus fumigatus- pulm disease in immunocompromised patients. tissue sections as septate hyphae with V shaped branching

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9
Q

63 yo man admitted to hospital from suffering cerebral infarction. swallow study => oropharyngeal dysphagia. episode of vomiting while lying on back, subsequently develops pneumonia. while lung regions most likely affected?

A. anterior segment of the left upper lobe
B. basilar segments of right lower lobe
C. lingular segments of left lung
D. middle lobe segments of right lung
E. posterior segment of right upper lobe
A

E. posterior segment of right upper lobe
gravity => aspiration pneumonia develops most dependent portiosn of lung. aspirate while lying supine => posterior segments of upper lobes, superior segmentsof lower obes. right main bronchus more prone to aspiration than left because largerdiamter, shorte,r mroe vertically oriented than left main bronchus- swallow a bite, goes down the riht

aspirate in upright/semi-recumbent positions- aspirate into basilar segments of lower lobes

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10
Q

56 yo 2 episodes low volume hemoptysis. streaks of blood in sputum. chronic cough over last several years, mostly in morning. several recent respiratory infections. smoked pack of cigs for last 40 years. CXR => hyperinflated lungs, no infiltrates or masses. foci of bronchial mucosa- stratified squamous epithelium. pathogenesis is similar to what?

A. Barrett esophagus
B. Cervical Cancer
C. Hypertrophic cardiomyopathy
D. Interstitial cystitis
E. Minimal change disease
A

A. Barrett Esophagus

normal bronchi lined by pseudostratfied ciliated columnar cells propel inhaled particles toward oropharynx for removal by swallowing or expectoration. interspersed goblet cells produce mucus trap inhaled debris. mucociliary clearance.

smoking => squamous metaplasia => lack of cilia and goblet cells => prevents efective mucociliary clearance and increases risk of respiratory infections

persistent irritant exposure => dysplasia/squamous cell carcinoma

metaplasia- Barrett Esophagus- esophageal squamous epithelium replaced by intestinal columnar epithelium in response to chronic acid exposure, increased risk of malignancy

B. squamous cell carcinoma of cervix- oncogenic strainsof HPV- integrate into host cell genome => viral genes inactivate host tumor suppressor protein. squamous metaplasia of cervix normal response to vaginal acidity, not associated with malignancy

C. HCM- aut dom defect of beta myosin heavy chains = disordered myocardial fibers, left ventricular outflow obstruction, arrhythmia, increased risk for sudden death

D. Interstitial cystitis- urinary frequency, urgency, pelvic pain. gross findings- erythema, ulceration of bladder mucosa; histopath shows inflammatory infiltrates and fibrosis

E. Minimal change disease- effacement of processes of glomerular podocytes, visible only on EM, underlying cell type is not altered

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