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[3] Step 1 USMLE > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

What type of sweat is found in [Cystic Fibrosis] pts (2)

A

Eccrine sweat with [High Concentrations of Cl]

and

[High Concentrations of Na+ (follows Cl)]

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2
Q

How do pts with ____ minimize their [Work of Breathing]

A: Obstructive Disorders

B: Restrictive Disorders

A

A: O**bstructive= [slOO**w + Deep] Breaths

B: Restrictive= [fast + shallow] Breaths

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3
Q

MOD of [Idiopathic Pulmonary Fibrosis]

A

Repeated Epithelial injury and resulting healing] –> [Elevated TGF-b–>inhibits Caveolin —>[Abnormal Epithelial Repair = Fibroblastic Proliferation (especially SubPleura)] –> Alveoli collapse and cystic space formation –> Honeycomb Fibrosis eventually

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4
Q

Clinical Presentation for [Idiopathic Pulmonary Fibrosis] (2)

A
  • [Velcro End inspiratory Crackles]
  • [Insidiously progressive DOE]
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5
Q

A: [INC Erythrocyte Sedimentation Rate] is a nonspecific marker for ________

B: Explain why ESR Increases?

A

A: Inflammation

B: [IL 1 / 6 / TNFa] stimulate Liver –> secrete [Acute-phase proteins (fibrinogen/CRP/[amyloid A & P])] to bind to microbes and fix compliment during infection.

**[Acute -phase proteins] ALSO bind to RBC –>RBC becomes more dense –> Falls at faster rate as [Rouleaux stacks] = [INC ESR]

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6
Q

Clinical SIGNS for Silicosis (2 CXR / 1 Histo)

A
  1. CXR: [Eggshell Calcification of Hilar Lymph nodes]
  2. CXR: Bilateral Nodular Apical densities
  3. Histology: [Birefringent silica particles] surrounded by fibrous= [Nodules w/whorled appearance]
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7
Q

A: Which 3 Carcinomas are associated with Asbestos? Which is most common?

B: When does Asbestos pathology onset?

A
  • Laryngeal
  • Bronchogenic (most common)
  • Mesothelioma

B: 25-40 years post exposure

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8
Q

[Cavity w/ Fluid Level] in the Lungs indicates what 3 possibilities?

A

CFL = A>N>B

[Cavity w/Fluid Level] = Abscess > [Necrotic Tumor] > [Bacterial endocarditis]

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9
Q

List the 4 Etiologies for Full Whiteout on CXR

A

“I PAID in Full” = Full White out=

[Pulm Edema (will be accompanied w/Cardiomegaly)] can —> Pleural Effusion - shown in image

[ARDS = (Adhesive Atelectasis)]

Influenza

[Diffuse Alveolar Dz]

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10
Q

Describe [Meconium iLeus]

A

[dehydrated meconium plug] causing [iLeus distal sbo] in [cystic fibrosis infants]

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11
Q

What’s Vitamin A role in Epithelial maintenance

A

Vitamin A maintains proper differentiation of specialized epithelium ([Conjunctiva columnar] / Respiratory / Pancreatic / Urinary] )

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12
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

When does Congestion onset?

A
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13
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

When does [Red Hepatization]​ onset?

A
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14
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

When does [Gray Hepatization]​ onset?

A
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15
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the MACROscopic Appearance of Congestion (2)

A
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16
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the MACROscopic Appearance of [Red Hepatization]​ (3)

A
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17
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the MACROscopic Appearance of [Gray Hepatization]​ (3)

A
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18
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the MACROscopic Appearance of Resolution**​

A

Normal Architecture

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19
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the microscopic appearance of Resolution**​

A
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20
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe microscopic appearance of [Gray Hepatization] (3)**​

A

Alveolar Exudate contains:

FN: Fibrin / Neutrophils

[Fragmented Erythrocytes after disintegration]

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21
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe microscopic appearance of [Red Hepatization] (3)**​

A

Alveolar Exudate contains:

EFN:Erythrocytes/ Fibrin / Neutrophils

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22
Q

There are 4 Stages for [Lobar PNA / Consolidation]

Congestion –> [Red Hepatization]–> [Gray Hepatization] –> Resolution

Describe the microscopic appearance of Congestion (2)**​

A
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23
Q

Which lung structure is affected most by [Chronic Rejection following lung transplant]? What sydrome does this cause?

A

A: Small Airways —> [Bronchiolitis Obliterans Syndrome]

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24
Q

A: Most common BENIGN lung tumor

B: Clinical Presentation

A

A: [Bronchial Hamartoma (made of lung tissue & cartilage)]

B: Asx peripherally located “coin lesion” in pts 50-60 y/o

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25
Q

Clinical Presentation of Asthma (3)

A

1) Intermittent Respiratory sx but with normal CXR
2) occasional sputum eosinophils
3) DEC FEV1 (Normal is > 80%)

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26
Q

What is the function of the [lamellar bodies in Type 2 GCC Pneumocytes]

A

A: They store and secrete PULMONARY SURFACTANT from [Type 2 GCC-Granular Club Clara] into fluid layer lining the alveoli.

Surfactant DEC surface tension and without it –> [alveolar adhesive atelectasis]

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27
Q

Name the 5 major associations with Eosinophils

A

Phil is in the NAACP

Neoplasia

Asthma

Allergic rxn

Chronic Adrenal Insufficiency

Parasites-invasive (Helminths)

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28
Q

Histological Features of Chronic Bronchitis (3)

A
  1. [Patchy Squamous Metaplasia of Bronchial Mucosa] —> Mucous gland Enlargement–> Reid Index > 50%
  2. Thickened Bronchial Walls
  3. Neutrophil infiltrate
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29
Q

Name the Conditions in which Diffusion Capacity is INCREASED (3)

A

A: [CHF vs. Polycythemia vs. Hemorrhage] –> INC DLCO

**all others DEC diffusion capacity**

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30
Q

A: Common manifestations of Sarcoidosis (10)

B: Which demographic is most commonly affected

A

CD4 TH1 mediated

A: LAR CUBED

[Liver with scattered noncaseating granulomas around portal triad] + [Lymphadenopathy-Bilateral Hilar]

ACE elevation & [Asteroid vs. Schumann bodies]

Restrictive cardiomyopathy (RAMILIES)

Calcemia INC (hyperCalcemia)

Uveitis

Bell’s Palsy (Facial CN7)

Erythema Nodosum (SubQ Fat lesions)

Diffuse Intersitial Fibrosis (INC FEV1/FVC ratio)

B: AA Females

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31
Q

Where does [SOLC-Small Oat Cell Lung Carcinoma] arise from and describe its pathogenesis?

A

SOLC needs AAAA

Arises from [primitive neuroendocrine Kulchitsky cells] of bronchial epithelium–> [small blue central tumor] –> [Lambert Eaton Myasthenic Syndrome] &Paraneoplastic syndromes (AAAA)] = POOR PGN

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32
Q

Virulent mycobacteria will grow as ____ cords on enriched media because of ______ factor.

B: How does this factor establish virulence for Virulent mycobacteria? (3)

A

Virulent mycobacteria will grow as Serpentine Cords on enriched media because of Cord Factor

B: Cord Factor allows virulence by:

1) Neutrophil inhibition
2) Mitochondrial Destruction
3) Inducing release of [Tumor Necrosis Factor]

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33
Q

Centriacinar Emphysema MOD and location

A

Large Cystic Spaces in [Upper Lobe-Respiratory Bronchioles] are formed by [neutrophil/macrophage] release of elastase (type of proteinase)

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34
Q

What lab manifestations would you expect to see in X-linked agammaglobulinemia (2)

A

[Mutated Tyrosine Kinase] –> DEC [CD19 and CD20 B- cells]

+

[Pan-hypOgammaglobulinemia] –> DEC Ab

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35
Q

How does Elastin recoil back to original position in the lung upon release of tension

A

[Extracellular Lysyl Hydroxylase] crosslinks DesmoSine with [4 different Lysines] on [4 different elastin chains]

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36
Q

A: Describe Chronic Granulomatous Dz

B: Lab test for CGD

A

“Cats Give [Neutrophils w/out NADPH] Dz”

A: CGD-Chronic Granulomatous Dz=

X-linked Dz DEC [NADPH Respiratory Burst in neutrophils] –> susceptibility to [Catalase + organisms]

B: Will NOT turn Blue with [Nitroblue Tetrazolium]

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37
Q

Where in the respiratory tree do you find [Pseudostratified Columnar Mucus Secreting Epithelium] (4)

A
  • Pseudo*stratified
    1. Nose and Nasopharynx

2 Paranasal Sinuses

  1. Larynx (laryngeal vestibule)
  2. Tracheobronchial Tree
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38
Q

OmaLizumab

MOA

A

Anti-IGE Antibody

BLOCKS A in image

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39
Q

H1 Blockers

Indication (2)

A
  1. Allergy Sx
  2. Chronic Urticaria
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40
Q

Describe the following Hemolysis patterns:

[Beta vs. alpha vs. gamma Hemolysis]

A

BAG

Beta Hemolysis = COMPLETE Hemolysis

alpha Hemolysis = inComplete Hemolysis

gamma Hemolysis= NO Hemolysis

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41
Q

Kartagener Syndrome

Clinical Presentation (4)

A

1º Ciliary Dyskinesia

SIBS:

1) [Situs Inversus Dextrocardia] (cilia is required during embryogensis)
2) Infertility
3) Bronchiectasis
4) Sinusitis-chronic

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42
Q

What does the Cell Wall of bacteria do for them?

A

Allows [GRAM staining Bacteria] to survive osmotic stress (hypOtonic vs. Hypertonic solutions)

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43
Q

Cystic Fibrosis MOD

A

Mutation in CFTR gene product –> [Defective postTranslational folding and glycosylation] –> Degradation of CFTR prior to reaching surface

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44
Q

Clinical Presentation of Haemophilus Influenzae (4)

A

HaEMOPhilus

Epiglottis-cherry red

Meningitis –> Septicemia

Oitits Media

PNA

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45
Q

List the Obstructive causes of Bronchiectasis (2)

A

A:

1) Tumor
2) Foreign Body

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46
Q

List the Infectious causes of Bronchiectasis (2)

A

1) TB
2) [Aspergillus Fumigatus in ABPA]-Allergic BronchoPulmonary Aspergillosis] –> will be associated with [recurrent transient pulm infiltrates]

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47
Q

List the Congenital causes of Bronchiectasis (3)

A

1) Immunodeficient Syndromes
2) cystic fibrosis
3) Kartagener (1° Ciliary Dyskinesia)

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48
Q

List the Random causes of Bronchiectasis (3)

A

1) Rheumatoid Arthritis
2) Lupus
3) Graft

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49
Q

Describe Cold Agglutinin formation

A

[Clumped Agglutination] of RBCs by specific antibodies at LOW temperatures

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50
Q

[Large Spherules filled with small round endospores] is pathomneumonic for what pathogen?

A

Coccidioides Immitis

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51
Q

Describe the Histo and identify the organism

A

[Small Ovoid bodies within a macrophage] = Histoplasma Capsulatum

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52
Q

Name the most common Asthma drugs (5)

A

“OIL Alleviates Asthma”

1) [Leukotriene (C4 / D4 / E4) Blockers]
2) [AcH Blockers]
3) OmaLizumab- Anti**-IgE Ab
4) Albuterol-short acting
5) [Inhaled Corticosteroids-Chronic Asthma 1st line tx**]

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53
Q

Based on the image:

Is the pathology Obstructive vs. Restrictive vs. Tracheal Stenosis

A

Obstructive - Emphysema (intraAlveolar wall destruction)

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54
Q

Obstructive Sleep Apnea

Sx (3)

A

1) [Pulm AND Systemic HTN]
2) [R HF –> Arrhythmia –> Sudden Death]
3) HA
* Sx come from Nocturnal hypoxia*

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55
Q

List the 4 major things that recruit neutrophils to inflammation sites

A

“Recruit Neu people using 8 Lil Hot Caligirls”

  1. IL8
  2. Leukotriene B4
  3. 5-HETE (Leukotriene precursor)
  4. [C5a complement]
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56
Q

Describe Fat Embolism Syndrome

A

Occurs when a pt sustains Severe [Long bone (femur) vs. Pelvic Fractures]–> Occlusion of microvessels by fat globules

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57
Q

List the Connective Tissue causes of Pulmonary HTN (2)

A

[Scleroderma vs. Lupus]

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58
Q

List the Genetic cause of Pulmonary HTN

A

AKA Primary Pulm HTN = Double Hit mechanism involving mutation of BMPR2. Affects [Females 20-40].

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59
Q

List the Drug cause of Pulmonary HTN (5)

A

CARFAx

[Cocaine/Amphetamine/Rapeseed/FenFlurimina/Aminorex]

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60
Q

A: What bacterial organisms are the most Frequent cause of Lung Abscess? (4)

B: Where are these bacteria normally found?

A

A: “FP went to BP so he could go to LA” –> [CFL - Cavity w/Fluid Level on CT

Fusobacterium

Prevotella

Bacteroides

Peptostreptococcus

B: [Oral Flora AnAerobes]

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61
Q

Describe [Primary Tuberculosis] manifestation

A

Ghon Complex (ipsilateral Hilar Nodes + Ghon focus in lower lung) can –> Healing vs. Lung Dz vs. Bacteremia vs. Dissemination

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62
Q

Describe Mesothelioma

A

Rare neoplasm arising from pleura or peritoneum, strongly associated with Asbestos

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63
Q

A: Describe [Lung SQC]

B: Radiographic manifestation

A

A: p53 mutation –> Bronchi neoplasm

B: Hilar mass

DO NOT GIVE Bevacizumab

[Image C = Hilar Mass] ; [Image D = Keratin pearls + intercell bridging]

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64
Q

What is the Major stimulator of respiration normally?

A

PaCO2 (INC in PaCO2 –> INC ventilation rate)

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65
Q

Define Minute Ventilation and give formula

A

Total volume of new air entering respiratory pathways per minute: [MV= (tidal volume-(L)) x (# breaths in 1 min)]

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66
Q

Describe the PaO2 / SaO2 / Oxygen Content levels for:

CO Poisoning

A
  • TOTAL O2 Content= [(O2 binding capacity x %Saturation])+ (% of free floating O2)= [Amount of Blood HgB]
  • [PaO2 = Free Floating O2]
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67
Q

A: Between [Pulmonary Capillaries] and [L Atrium and Vt], which has lower pO2

B: Explain why

A

A: [L Atrium and Vt] has lower pO2! because …

B: [Pulmonary Veins] that feed [L Atrium and Vt] ALSO receive DeOxygenated blood from [Bronchial a. & Thebesian Veins]

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68
Q

Why does [Lung Ventilation/Perfusion Ratio] DECREASE as you travel from Lung Apex –> Base?

A

[Perfusion INC as you go from Lung Apex–>Base] BUT [Ventilation slightly INC from Lung Apex –> Base]

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69
Q

List the O2 & CO2 changes that occur in [Mixed Venous Blood] during Exercise

A

1) DEC O2 in Mixed Venous Blood
2) INC CO2 in Mixed Venous Blood –> DEC pH

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70
Q

A: O2 Equilibration between [alveolar and pulmonary capillaries] in normal pts is ________ limited (Diffusion vs. Perfusion)

B: What conditions causes the other limitation? (2)

A

A: Perfusion-limited

B: Diffusion limited

1) Physiological: Exercise
2) Fibrosis

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71
Q

A: Name the 4 causes of hypOxemia (low PaO2)

B: Which cause is different and how?

A

A:

  1. alveolar hypOventilation (Will have Normal Alveolar-Arterial gradient)
  2. [Ventilation-Perfusion mismatch] (V/Q is normally HIGH in apices due to gravity pulling blood to bases but this is Normal!!)
  3. Diffusion impairment
  4. [R Heart –> L Heart shunting]
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72
Q

Primary Reason [RBC of venous blood] have HIGH Cl content

A

Venous blood pulls CO2 out of tissue and (via Carbonic Anhydrase) converts –> HCO3. This HCO3 LEAVES the RBC back into the acidic tissue BUT Cl comes into RBC as exchange. –> HIGH Cl content in [RBC of venous blood]

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73
Q

[Pulmonary Function Test] of Interstitial Lung Dz will show what (2)

A
  1. DEC [Total Lung Capacity]
  2. [INC Lung Elastic inward recoil] –> [INC outward radial traction on airways] –> [MARKED INC EXPIRATORY FLOW RATES]
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74
Q

Methacholine

A: Pharmacologic MOA

B: Clinical MOA

A

A: [Muscarinic Cholinergic Agonist]

B: Induces [Bronchoconstriction and Bronchial secretions] –> Used to demonstrate dz in asthmatics

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75
Q

Classic Clinical Presentation of Pulmonary Embolism (4)

A
  1. [Tachypnea (from Hypoxemia) & Dyspnea]
  2. Tachycardia
  3. Cough
  4. [Pleuritic Chest Pain]
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76
Q

Name the ONE thing that stays EQUAL between Systemic and Pulmonary circulations at all times (even during exercise)!

A

RATE of Blood Flow / minute

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77
Q

Where does [Ciliated Epithelium] line the Pulmonary Airways?

A

From [Trachea –> [Proximal part of Respiratory bronchioles]]

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78
Q

Define [Secondary Bacterial Pneumonia]. What Bacteria cause it? (3)

A

PNA that develops right AFTER Influenza infection

[Strep Pneumo] > [Staph Aureus] > [H. Influenzae]

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79
Q

Delayed Hypersensitivity

List the 4 Examples

A

1- Granulomatous Inflammation

2- Tuberculin Skin Test

3- [Candida Extract Skin Test]

4- Contact Dermatitis

Image shows Non-Caseating Granulomas

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80
Q

Identify

A

Langerhan Giant Cells

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81
Q

List MOA for Polysaccharide Vaccines

A

Polysaccharide binds to [B-cell receptor] and that B-cell produces a [Moderate level of intermediate-affinity IgM abs]

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82
Q

List MOA for Conjugate Vaccines

A

[Polysaccharide WITH PROTEIN CONJUGATE (orange triangles)] binds to [B-cell receptor] and that B-cell activates T-cells as well –> produces a [High level of High-affinity IgG abs] with memory cell formation

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83
Q

[Croup Laryngotracheitis]

Clinical Presentation (3)

A

A:

1) [Brassy Barking cough]
2) Dyspnea
3) [Recent hx of URI]

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84
Q

Name the Causes of ARDS (10)

A

ARDS

A= Aspiration vs. [Acute Pancreatitis] vs. [Air Fluid Embolus (amniotic)]

R= Radiation

D= Drugs vs. DIC vs. Drowning

S= Sepsis vs. Smoking vs. Shock

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85
Q

Nystatin MOA and [Route of Admin]

A

A: Binds to [Fungal cell membrane Ergosterol] and forms pores.

B: [Oral Swish and Swallow Agent] - since it is not absorbed by GI tract

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86
Q

List 2 examples of [Respiratory AcH Blockers] and their MOA

A

“OIL Alleviates Asthma”

[Ipratropium vs. TiOtropium(lOnger acting)] Reverses VAGUS-nerve mediated Bronchoconstriction

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87
Q

Name the components of Surfactant (4)

A
  1. [Lecithin DPPC- DiPalmitoyl PhosphatidylCholine]
  2. [Sphingomyelin]
  3. Phosphatidylglycerol
  4. [Protein A1B1C1D]
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88
Q

Anatomically, During Thorancentesis how would you access:

A: [Lungs & Visceral Pleura] (3)

B: Which visceral structures are you attempting to Avoid by using these positions?? (2)

A

image

B:

  1. Abdominal Structures
  2. [Subcostal Neurovascular bundle]
    * Paravertebral = [POST Scapular]*
89
Q

[Cromolyn and Nedocromil] MOA

A

[Mast Cell Stabilizing agents] –> Inhibit Mast cell degranulation indepedent of stimuli.

BLOCKS D in image

90
Q

Zileuton MOA

A

“OIL Alleviates Asthma”

MOA: [Lipooxygenase pathway Inhibitor] –> DEC Leukotriene formation (BLOCKS B and C in image)

91
Q

Why is the Piriform Recess clinically significant?

A

Foreign Bodies (Chicken vs. Fish bones) can become lodged in Piriform Recess and possibly –> [Internal Laryngeal n. Damage] which sits above vocal cords but underneath Piriform Recess

92
Q

There are 4 Major Opportunistic infections in HIV pts

Describe: Pneumocystis Jirovecii

A: Risk Factors (2)

B: Px

A
93
Q

There are 4 Major Opportunistic infections in HIV pts

Describe: Toxoplasma Gondii

A: Risk Factors (2)

B: Px

A
94
Q

There are 4 Major Opportunistic infections in HIV pts

Describe: [MAC -Mycobacterium Avium Complex]

A: Risk Factor

B: Px

A
95
Q

There are 4 Major Opportunistic infections in HIV pts

Describe: Histoplasma Capsulatum

A: Risk Factors (2)

B: Px

A

Histoplasma is in [oHio & Miss. River Valleys]

96
Q

Pleuritic Chest Pain of the [Diaphragmatic & Mediastinal Parietal Pleura] area is carried by which nerve?

A

[Phrenic n.–>C3-C5 nerve roots of the shoulder/neck] (carries motor innervation to diaphragm + pain fibers for diaphragmatic & mediastinal pleura]

97
Q

Varenicline MOA (2)

A

[Partial Nicotinic ACh Receptor Agonist] –>

*DEC [nicotine withdrawal cravings]

*DEC reward response from nicotine

98
Q

Pancoast Tumor Clinical Presentation (5)

A
  1. UE pain (Brachial plexus compression)
  2. UE weakness (Brachial plexus compression)
  3. Ipsilateral Ptosis (cervical sympathetic ganglion involvement)
  4. Ipsilateral Miosis (cervical sympathetic ganglion involvement)
  5. Pt Presents with smoking hx
99
Q

Pathophysiology of CF

A

(Cl) is supposed to be ReAbsorbed before leaving as outside sweat, but [CFTR ATP-gated Chloride channels] are dysfunctional

100
Q

How do you diagnose CF

A

[High Concentrations of Cl] in the sweat

101
Q

Genetic cause of cystic fibrosis

A

[auto recessive]- Phenylalanine deletion on Chromo 7 of CFTR gene

102
Q

Common Characterstic Findings of [Idiopathic Pulmonary Fibrosis] (4)

A
  1. Cobblestone Pleura
  2. [White Rubbery Surface]
  3. [Cystic Spaces lined by Type 2 Pneumocytes or Bronchial epithelium]
  4. [Honeycomb Fibrosis] from heavy cyst formation
103
Q

Tx for [Idiopathic Pulmonary Fibrosis] (3)

A

[Lung Transplant] / [PirFenidone] / [NinTedanib]

104
Q

B: Describe Silicosis Epidemiology

C: What are these pts more susceptible to and why?

A

B: Most prevalent [Chronic World Occupational Dz]

C: INC TB Susceptibility 2° to [Impaired Macrophage Phagolysosome formation and Cell-mediated immunity]

105
Q

Silicosis MOD

A

Macrophages are unable to phagocytize due to impairment by [internalized silica particles]

106
Q

Explain why [Cavity w/ Fluid Level] lesions forms in the Lungs

A

CFL = A>N>B

Macrophages and Neutrophils release Lysosomal content in the process of addressing the problem—> Lung Damage (such as Abscess)

107
Q

What carcinoma is [Avitaminosis A (Vitamin A deficiency)] associated with?

A

Squamous Metaplasia which converts regular epithelium –> [Keratinizing Epithelium]

108
Q

Clinical Presentation of [Chronic Rejection following lung transplant] (3)

A
  • [Dyspnea & Wheezing] –> [Obstructive Spirometry (FEV1 )]
  • Lymphocytic inflammation
  • Fibrosis –> [Bronchiolitis Obliterans Syndrome]
109
Q

When does [Acute Lung Rejection] onset?

A

Within the first 6 months (and is usually asx with mononuclear cell infiltrates)

110
Q

Hamartomas are ______ of tissue in their ___ location. Histology is made up of ____ (3)

A

Hamartomas are [Benign Disorganized tissue overgrowths] in their native location; made of FAD

  1. Disorganized Cartilage
  2. Fibrous tissue
  3. Adipose
111
Q

What’s the Most common type of Asthma

A

Exrinsic Allergic Asthma (provoked by inhaled allergens like animal dander)

112
Q

Asthma Etx

A

Excess TH2 cells (recruited by hypersensitive APC to inhaled allergens) secrete IL4 –>activates [B-lymphocyte class switching for IgE Ab]–> IgE binds to Mast cells which will then secrete IL5 –> Recruits Eosinophils–>which release mediators like Leukotrienes.

113
Q

How is Asthma Diagnosed via Testing?

A

[DEC in (FEV1 > 20%) after Methacholine challenge] = ASTHMA

114
Q

Explain how the product made by [lamellar bodies in Type 2 GCC Pneumocytes] protects us

A

SURFACTANT prevents alveoli (especially small alveoli) from collapsing during expiration since Laplace’s Law states radius of sphere w/constant surface tension is inversely correlated to [collapse distending tension]

Surfactant DEC surface tension and without it –> [alveolar adhesive atelectasis]

115
Q

Name the major protein of Eosinophils, how it protects us and how it hurts us

A

Phil is in the NAACP

Eosinophils secrete [Major Basic Protein] which kills [Helminth Parasites] but ALSO causes bronchial damage in pts with [Atopic Extrinsic Asthma]

116
Q

Most common cause of Chronic Bronchitis

A

Cigarettes!

117
Q

What is the normal Diffusion Capacity and how is it measured?

A

Normal DLCO = 25.

Formula = [COinhaled - COEXhaled should = 25]

118
Q

Which T-cells would you likely find in a bronchoalveolar lavage of Sarcoidosis pts?

A

LAR CUBED

[CD4 TH1 Helper T] (found in sarcoid non-caseating granulomas. Interferon-gamma secreted by TH1)

119
Q

What is SOLC caused by? (2)

A

SOLC needs AAAA

1) Smoking
2) [Inactivation of p53 and RB]

120
Q

What labs are used to diagnose SOLC? (3)

A

SOLC needs AAAA

Positive Immunohistochemical stains (also seen in Bronchial Carcinoid):

“Need to C SOLC”

*[Neuron-specific enolase]

*Chromogranin

*Synaptophysin

121
Q

SOLC Histology (2)

A
  • [round/oval/small blue cells with High Mitosis]
  • scant cytoplasm
122
Q

Which demographics are associated with Centriacinar Emphysema (2)

A

1) Male Smokers
2) Coal Pneumoconiosis

123
Q

What pathogens are X-linked agammaglobulinemia pts at risk for? (3)

A

1) Pyogenic bacteria
2) Enteroviruses
3) Giardia Lamblia

124
Q

What 5 Amino Acids make up Elastin

A

[Glycine + Alanine + Valine] and [Proline + Lysine]

125
Q

C: Organisms most associated with Chronic Granulomatous Dz (6)

D: tx

A

“Cats Give Neutrophils w/out NADPH Dz”

C:

  • Burkhodleria Cepacia
  • Staph aureus (can produce Factor 5-NAD+ and 10-leiden)
  • E.Coli
  • Aspergillus
  • Serratia
  • Nocardia

D: IFN-gamma

126
Q

Where do you find [Stratified Squamous Epithelium] (4)

A

Stratified “Strat up the TOLE!”

  1. Oropharynx
  2. Laryngopharynx
  3. ANT Epiglottis and [upper half POST epiglottis]
  4. [True Vocal Cords]
127
Q

OmaLizumab

Indication

A

[Severe Uncontrolled Asthma]

BLOCKS A in image

128
Q

Pts that recover from [Meconium iLeus] are more likely to die from ____ (4)

A
  • [PNA].
  • Bronchiectasis.
  • [Bronchitic Obstructive Pulm dz]
  • [Cor Pulmonale]
129
Q

Kartagener Syndrome

MOD

A

1º Ciliary Dyskinesia

Mutation in [Cilia structure/function]–> [Absence/shortening of Dynein Arms]

130
Q

Kartagener Syndrome

Mode of Inheritance

A

1º Ciliary Dyskinesia

Auto Recessive w/variable penetrance

131
Q

What can Kartagener Syndrome be confused with?

A

1º Ciliary Dyskinesia

Cystic Fibrosis (won’t be accompanied with [Situs Inversus Dextrocardia**]

132
Q

Which Abx target the Cell Wall (3)? What’s their MOA?

A

[D-alanine D-alanine analogs] prevents [Peptidoglycan cell wall] cross-linking

  • Penicillin
  • Cephalosporin
  • Vancomycin
133
Q

What happens to the bacteria once their Cell Wall is destroyed?

A

Bacteria will disintegrate once they’re in an osmotically stressed environment

134
Q

Which bacteria are resistant to the Cell Wall Abx and why?

A

Mycoplasma genus (including Ureaplasma) since they LACK [Peptidoglycan Cell Walls] - have to use [macrolides vs. tetracycline]

135
Q

How do you calculate [Cystic Fibrosis probability of acquisition] if given Carrier Frequency of each parent?

A

Multiply [Each Carrier Frequency (1 from each parent)] x 0.25

136
Q

[Haemophilus Influenzae] Tx (5)

A

HaEMOPhilus

[FAT MC]

[Fluroquinolone vs. Ampicillin vs. Tetracycline vs. Macrolide(NOT ERYTHRO) vs. Ceftriaxone]

137
Q

Explain The Vaccine for Haemophilus Influenzae

A

HaEMOPhilus

Type B Vaccine contains [capsular polysaccharide (PRP)] conjugated to Diphtheria toxoid

138
Q

What is Bronchiectasis

A

[Chronic Necrotizing Inflammation of Bronchi & Bronchioles]—> [Permanent Dilatation of Bronchi & Bronchioles] —> [Daily Copious Mucus production]

139
Q

Which pathogenic processes cause Cold Agglutinin formation (3)

A

1) Mycoplasma Pneumoniae
2) Epstein Barr Virus
3) Hematologic Malignancy

140
Q

Clinical Presentation of [Histoplasma Capsulatum] (4)

A

Pts usually from a Cave visit

1) Disseminated Mycosis in Immunocompromised
2) Painful oral ulcers
3) LAD
4) Hepatosplenomegaly

141
Q

[Obstructive Sleep Apnea] Clinical Presentation (4)

A
  • Daytime Sleepiness from fragmented sleep
  • Snoring (nocturnal upper airway obstruction)
  • Obese pt
  • Pulsus Paradoxus (Pulsus for CAPOT)
142
Q

Which Cranial Nerve can be electrically stimulated to improve [Obstructive Sleep Apnea] and why?

A

[Hypoglossal CN12] stimulation –>[DEC Neuromuscular weakness of oropharyngeal airway]–> [INC diameter of [oropharyngeal airway]

143
Q

A: [Fat Embolism Syndrome] Clinical manifestations (3)

B: When does onset?

A

A:

  • Neurologic abnormalitites (confusion)
  • hypOxemia
  • Petechial Rash

B: 1-3 days post injury usually (but can develop up to 2 weeks post injury)

144
Q

Histology for Fat Embolism Syndrome

A

Fat Emboli stain BLACK with [Osmium Tetroxide stain]

145
Q

how does Pulmonary HTN manifest? (3)

A
  • Loud S2 (pulmonary component)
  • Cor Pulmonale (R HF signs)
  • [Pulm Arterial pressure > 20/10]
146
Q

Describe the Histology for Pulmonary HTN (4)

A

[small artery muscularization] –> [Medial Hypertrophy]–> [Onion Skin Intimal Fibrosis] –> [Plexiform lesion Capillary Tufts]

147
Q

A: Which conditions INC risk of developing Lung Abscess from Bacteria that normally cause Lung Abscess? (3)

B: Tx for this group of bacteria

A

“FP went to BP so he could go to LA” –> [Air Fluid level Abscess] on CT

A: Conditions that INC Aspiration:

  • Seizures
  • Alcoholism!!!
  • [Stroke vs. Dementia]

B: Clindamycin

148
Q

Describe [Secondary Tuberculosis] manifestation

A

[Fibrocaseous cavitary lesion of upper lobe] (indicates REINFECTION/Reactivation of previous TB in lungs)-Immunocompromised are at INC risk

149
Q

If TB infection is well-controlled and does not manifest sympatically in a pt, what is the immune mechanism that enables this?

A

1 °TB infection may be controlled via [CD4 TH1 lymphocytes] & [macrophages] which work together to form a Caseous Granuloma –>allows macrophages to kill TB organisms from the inside –> NO Sx

150
Q

Mesothelioma Radiographic manifestation (2)

A

[Pleural Thickening & Pleural Effusions]

151
Q

Mesothelioma Histology (3)

A
  • PSoMMoma bodies
  • Tumor cells with numerous [long slender microvilli]
  • Abundant Tonofilaments
152
Q

[Lung SQC] Histology (3)

A
  1. Keratin Pearls
  2. Intercellular bridges (desmosomes holding tumor cells together)
  3. Bright Orange on PAP Stain

DO NOT GIVE Bevacizumab

[Image C = Hilar Mass] ; [Image D = Keratin pearls + intercell bridging]

153
Q

Which rx is contraindicated in [Lung SQC]

A

Bevacizumab!

154
Q

Major stimulator of respiration in COPD pts? Why is oxygenation a problem for these pts?

A

[low O2] becomes the gauge for ventilation in COPD pts since PaCO2 in COPD pts is always high

Giving O2 to COPD pts –> DEC Ventilation rate since COPD body bases ventilation on low O2

155
Q

Where are the receptors that detect arterial O2? (2)

A

Peripheral Chemorceptors (Aortic Arch & Carotid Bodies)

156
Q

Define Alveolar Ventilation and give formula

A

Volume of new air reaching gas exchange areas per min: [AV= [(tidal volume(L)) - (dead space volume)] x (breaths/min)]

157
Q

What parameter measures the difference between Minute and Alveolar Ventilation

A

Dead space Volume

158
Q

Describe the PaO2 / SaO2 / Oxygen Content levels for:

Cyanide Poisoning

A
  • TOTAL O2 Content= [(O2 binding capacity x %Saturation]) + (% of free floating O2)= [Amount of Blood HgB]
  • [PaO2 = Free Floating O2]
159
Q

Describe the PaO2 / SaO2 / Oxygen Content levels for:

Anemia

A
  • TOTAL O2 Content= [(O2 binding capacity x %Saturation]) + (% of free floating O2)= [Amount of Blood HgB]
  • [PaO2 = Free Floating O2]
160
Q

Describe the PaO2 / SaO2 / Oxygen Content levels for:

Polycythemia

A
  • TOTAL O2 Content= [(O2 binding capacity x %Saturation]) + (% of free floating O2)= [Amount of Blood HgB]
  • [PaO2 = Free Floating O2]
161
Q

Describe the PaO2 / SaO2 / Oxygen Content levels for:

High Altitude

A
  • TOTAL O2 Content= [(O2 binding capacity x %Saturation]) + (% of free floating O2)= [Amount of Blood HgB]
  • [PaO2 = Free Floating O2]
162
Q

Which Bronchial airway segment contributes the MAXIMUM airway resistance?

A

2nd to 5th airway generations (including segmental bronchi)

163
Q

Which Bronchial airway segment contributes MOST of the [Total Airway Resistance]

A

[First 10 generations of bronchi (Regional airway resistance)]

164
Q

What happens to Lung Compliance during Emphysema? Pulmonary Fibrosis?

A

Refer to image

165
Q

How does Heroin OD cause Respiratory Acidosis

A

hypOventilation

166
Q

Which vessel system does not have a large change during Exericse?

A

Arterial Blood (Homeostatic mechanisms maintain arterial blood gas levels near normal pH)

167
Q

Define Functional Residual Capacity (3)

B: Where is it located on the [airway pressure/volume curve]

A

Resting state in which..

*[airway pressure in lung = 0]

*[intrapleural pressure in lung = -5]

* [(PVR-Pulm Vascular Resistance) is at its lowest!]

B2: CENTER of [airway pressure/volume curve]

168
Q

What is the pO2 for…

  • Inspired Air
  • Trachea
  • Alveoli (p<strong>A</strong>O2)
  • [Final arterial] (paO2)
A

pO2 for..

  • Inspired Air = 160 mm Hg
  • Tracheal = 150 mm Hg (DEC from 160 is due to addition of water vapor partial pressure)
  • Alveoli (p<strong>A</strong>O2)= 104 mm Hg (Normal Final alveolar AND arterial PaCO2= 40 mm Hg)
  • [Final-arterial (paO2)] = Should be 100 mm Hg
169
Q

List the 2 ways CO2 is transported in RBC

A
  • 15% RBC CO2 is carried by HgB as carbamate
  • Remainder of RBC CO2 is bicarbonate ion
170
Q

Clinical Presentation of Erythrocytosis (2)

A

Erythrocytosis (absolute vs. [relative from HF vs. blood loss]) =

[Men with Hematocrit > 52%] and [Women with Hematocrit >48%]

Erythrocytosis is AKA Polycythemia

171
Q

What type of Erythrocytosis is Hypoxic Erythrocytosis and when does it onset

A

Absolute Erythrocytosis that only onsets when ([SaO2 which is same as [PaO2

Erythrocytosis is AKA Polycythemia

172
Q

Methacholine

Diagnostic parameter

A

: [DEC in (FEV1 > 20%) after Methacholine challenge] = ASTHMA

173
Q

Name the common Asthma environmental triggers (3)

A
  • Cold air
  • Exercise
  • Histamie
174
Q

Does PE cause Respiratory Acidosis or Alkalosis? WHY? How does this affect the Brain (2)

A

Respiratory ALKALOSIS.

HypOxemia –> [Tachypnea/Hyperventilation from resp. drive], and since PaCO2 is more dependent on Lung Ventilation change –> Respiratory ALKALOSIS –> [Cerebral vasoconstriction] & [DEC Cerebral blood flow]

175
Q

Why do PE pts get hypOxemia?

A

Pulmonary Embolism–> [Ventilation/Perfusion mismatch] –> HypOxemia (normal Arterial PaO2 = 75-100)

176
Q

Where does [Goblet / Glands / Cartilage] line the Pulmonary Airways?

A

From [Trachea –> Bronchi] (does NOT include Bronchioles and lower)

177
Q

A: Demographic for [Secondary Bacterial Pneumonia]

B: Clinical Presentation (2)

A

A: [Age > 65]

B: [Pt > 65] presenting with respiratory sx

plus

[reports of similarly ill household children (who could have spread influenza)]

178
Q

[Delayed Hypersensitivity] MOA

A

[TH1 Lymphocytes] secrete Interferon-gamma –> [macrophage recruitment & stimulation] and IL2 –> [TH1 Lymphocyte proliferation]

Image shows Non-Caseating Granulomas

179
Q

How long before [Delayed Hypersensitivity] reaches PEAK activity?

A

Days (other hypersensitivity rxns only take minutes)

Image shows Non-Caseating Granulomas

180
Q

Describe Histology of Multinucleated Giant Cells in Delayed Hypersensitivity

A

Central collection of tightly clustered [epithelioid macrophages] surrounded by a rim of [mononuclear cells]

Image shows Non-Caseating Granulomas

181
Q

Describe the Histology. How is this formed?

A

Langhan Giant Cells

Multiple nuclei peripherally organized in a horseshoe shape. Formed by macrophages, which are activated by [CD4 TH1 lymphocytes]

182
Q

What conditions is this associated with?

A

Langhan Giant Cells

Granulomatous conditions (including TB)

183
Q

Advantages to Polysaccharide Vaccines

A

DEC incidence of replacement strains due to lack of mucosal immunity

184
Q

Advantages for Conjugate Vaccines (3)

A
  1. INC Effect in Elderly and [Children
  2. INC Mucosal immunity –> DEC colonization –> Herd Immunity
  3. INC Immunogenic memory
185
Q

[Croup Laryngotracheitis]

Demographic

A

Kids

186
Q

[Croup Laryngotracheitis]

Causative Pathogen (2)

A

[Parainfluenza ParamyxoVirus] vs. [Coronavirus]

187
Q

ARDS —> DEC _____ —> _____ Atelectasis

A

ARDS –> [DEC Surfactant all across lungs] –> ADHESIVE ATELECTASIS (FULL WHITE OUT ON CXR)

188
Q

Is ARDS Obstructive or Restrictive?

A

Restrictive

189
Q

ARDS MOD

A

RAPID onset (24-72 hrs post [Endo & Epithelial lung tissue injury]) –> [Life threatening Arterial hypoxemia]–> Cyanosis–> Multisystem organ failure

190
Q

Nystatin Indication

A

[Oropharyngeal Candidiasis in immunocompotent pts]

191
Q

List 2 examples of Methylxanthines and their MOA

A

[Theophylline vs. Aminophylline] [Phosphodiesterase AND Adenosine Receptor] Inhibitor –> INC cAMP –> BronchoDilation

192
Q

SE for Methylxanthines (4)

A

Methylxanthine (Theo vs. Amino) SE:

Never Carry Tapes & CD’s

[Narrow theraputic window / Convulsions / Tachycardia / Circulatory Collapse]

193
Q

Which Events (Drugs vs. Conditions) are Contraindicated with Methylxanthines (5)

A

[Cimetidine / Cipro / Macrolides / Verapamil / [Infection + Fever]

194
Q

What happens to Surfactant components at…

  • 30 week gestation
  • 36 week gestation
  • in Mature Lungs
A
  • 30 week gestation = [Lecithin DPPC] INC
  • 36 week gestation = [Phosphatidylglycerol] INC
  • Mature Lungs = ([Lecithin DPPC] : Sphingomyelin Ratio > 2:1 ) = Surfactant is adequate in the neonate and NRDS is unlikely
195
Q

Anatomically, During Thorancentesis how would you access:

A: Parietal Pleura (3)

B: Which visceral structures are you attempting to Avoid by using these positions?? (2)

A

image

B:

  1. Abdominal Structures
  2. [Subcostal Neurovascular bundle]
    * Paravertebral = [POST Scapular]*
196
Q

Are [Cromolyn and Nedocromil] More or Less effective than Inhaled Corticosteroids

A

Less Effective

BLOCKS D in image

197
Q

[Cromolyn and Nedocromil] Indication (2)

A

[Allergic Rhinitis and Bronchial Asthma] 2nd line tx

BLOCKS D in image

198
Q

Zileuton Cx

A

Hepatic Dz!

199
Q

[Montelukast / Zafirlukast]

-MOA

A

[Montelukast / Zafirlukast]

-MOA: [Leukotriene D4 Receptor Blockers] = [Chronic Asthma Px] (BLOCKS D in image)

200
Q

What nerve is associated with the Piriform Recess and what Reflex is it responsible for?

A

[Internal Laryngeal n.] ; [Cough Reflex: Afferent Limb]

201
Q

There are 4 Major Opportunistic infections in HIV pts

[MAC -Mycobacterium Avium Complex]

Which 2 organisms make up this Complex

A

[Acid Fast M. Avium]

[Acid Fast M. Intracellulare]

202
Q

There are 4 Major Opportunistic infections in HIV pts

[MAC -Mycobacterium Avium Complex]

What are 2 Distinguishing characteristics of this Complex

A
  • Grows at 41°C
  • Hepatosplenomegaly
203
Q

Pleuritic Chest Pain of the _____ is carried by which nerve?

[Remainder of Parietal Pleura] area

A

Intercostal n. (usually more localized)

204
Q

Varenicline Indication

A

Smoking Cessation

205
Q

[Idiopathic Pulmonary Fibrosis] Demographic

A

[Male 40-70 y/o]

206
Q

SOLC Clinical manifestation (4)

A

SOLC needs AAAA

[Eaten Lambert & Paraneoplastic syndromes (AAAA)] = POOR PGN

ACTH secretion

SIADH

[Ab against pre-synaptic Ca+ channel = Eaten Lambert]

Amplification of [myc oncogene]

207
Q

[Lung SQC] Demographic (2)

A

Males vs. Smokers

DO NOT GIVE Bevacizumab

[Image C = Hilar Mass] ; [Image D = Keratin pearls + intercell bridging]

208
Q

How does [Carbon Monoxide] affect Methemoglobin?

A

IT DOESN’T

209
Q

How does [Carbon Monoxide] affect [PaO2 Free Floating O2]?

A

IT DOESN’T

210
Q

What type of Hypersensitivity is [Hypersensitivity Pneumonitis]

A

Type 3 & 4

211
Q

[Hypersensitivity Pneumonitis] Demographic (2)

A

[Pigeon exposure] & Farmers

212
Q

What compounds are most implicated in Lung CA (3)

A
  1. [Polycyclic Aromatic Hydrocarbon]- smoker
  2. Arsenic - smoker
  3. Radon - basements/uranium miners
213
Q

Describe Bronchial Hamartoma

A

[Benign Calcified Coinlesion tumor made of lung tissue & cartilage] in lung

Coinlesions can also be Lung CA/Histoplasma/TB

214
Q

Which Lung CA can secrete PTHrP as apart of its paraneoplastic syndrome

A

Squamous cell carcinoma

215
Q

[Multiple Cannon-ball nodules] on Lung CXR typically indicates what?

A

Colon/Breast Metastasis TO the Lung

216
Q

Where does Carcinoid Tumor of Lung arise from? Central or Peripheral? Classic imaging?

A

[primitive neuroendocrine cells = chromogranin +]; EITHER OR; [polyp like bronchial mass when centrally located]

217
Q

Which chemoreceptors (central vs. peripheral) are responsible for sensing arterial O2

A

PERIPHERAL (carotid sinus vs. aortic body)

218
Q

Bohr Haldane effect

A

Acidosis (like INC Co2) [DEC HgB O2 affinity] so O2 can be dropped off @ tissue

219
Q

A: What is Cheyne-Stokes Breathing?

B: What is this breathing associated with? - 3

A

A: Cyclic breathing in which apnea is followed by [INC and then DEC tidal volumes] all the way up until the next apneic period

B:

  1. [Advanced CHF]
  2. [Comatose BL Cortical metabolic encephalopathy]
  3. Elderly during sleep

[3] Step 1 USMLE (8 decks)

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