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CardioResp > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Some underlying principles or respiratroy diseases in children

A

Pediatric patients are at higher risk for respiratory disorders due to anatomical risk factors

Oxygen consumption in infants is double that in adults, giving rise to an increased RR

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2
Q

biphasic response in children

A

Biphasic response – periodic cycles of hyperventilation due to hypoxia, but this hyperventilation is not sustainable in infants due to respiratory fatigue (see below)

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3
Q

why are lungs immature in children

A

Lung capacities and flows continue to increase until late adolescence

Therefore, pediatric patients don’t have the full capabilities of a normal adult lung

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4
Q

3 ways FRC is actively maintained in infants

A
  • Sustained inspiratory muscles throughout the respiratory cycle maintains FRC
  • Narrowing of the glottis during expiration – traps air in lungs
  • Inspiration starting in mid-expiration
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5
Q

Upper airway differences in children (4)

what are the consequnces of these differences

A

​TELT

  • Bigger (relative) base of Tongue – has the ability to block upper airway
    • Displacing the tongue by placing towel under back opens up airway
  • Epiglottis – larger and floppier
    • Advantage: makes a better seal from the airway for sucking
    • Disadvantage: increased risk for aspiration during increased RR
  • Location of Larynx – located higher in the neck (at C2-C3) than in adults (C4-C5)
  • Trachea – smaller and less rigid
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6
Q

Lower airway differences in children (2)

what is the consequences of this difference

A
  • Lower airway – increased resistance from increased narrowing
    • Narrowing due to underdeveloped bronchioles
    • Reduced collateral connections between bronchioles in infants → reduced collateral ventilation of alveoli → increase in risk for atelectasis (collapsed lung)
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7
Q

Chest wall differences in childern

what are the consequences

A
  • Chest wall compliance is 3x than the lung compliance
    • In infants, the chest wall is made up of cartilage, not bone; therefore, it has less elastic force to expand chest wall – increased work of breathing
      • Decreased elasticity results in decreased ability to change tidal volume
    • To increase minute ventilation, infants must increase RR because they cannot increase tidal volume
    • As we age, ossification of the sternum leads to chest wall compliance = lung compliance, decreasing the work needed for expiration
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8
Q

what are the consequences of rib structure differences in children

A
  • Lack of angulation of ribs and square shape of thorax in infants → does not allow for ribs to help diaphragm in breathing process → paradoxical inward rib movement during inspiration → increased work to maintain this breathing motion
    • This is fixed by adulthood
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9
Q

whats the difference in the diaghram of ped patients what does this result in

A
  • Diaphragm differences
  • Lack of type 1 muscle fibers – tires easily
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10
Q

Signs of respiratory fatigue in pediatrics pts

A
  • Head bobbing
  • Grunting – noise made at the end of inspiration to increase pressure and keep air in
  • Tripod stance – bent over posture to recruit as many muscles to get as much air in as possible
  • Nasal flaring
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11
Q

“Talk about children sleeping.”

A
  • Infants sleep more and spend more time in REM
    • REM decreases your ability to breathe
      • Decrease in minute ventilation
      • RR decreases
      • FRC decreases because muscles relax and only muscle working is diaphragm
      • Upper airway resistance doubles – the tongue relaxes
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12
Q

Congenital diaphragmatic hernia

descritpion, diagnosis, complications

A
  • Description: abnormal development of pleuroparitoneal canal → herniation of bowels into thorax → decreased development of lung and pulmonary vasculature
    • Major concern is lung hypoplasia
  • Diagnosis: prenatally via US
  • Complications: pulmonary HTN, respiratory distress, decreased breath sounds on affected side
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13
Q

Congenital cystic adenomatoid malformation (CCAM)

descritpion, diagnosis, complications

A
  • Description: lesion caused by localized arrest in the development of fetal bronchial tree and limited to a single lobe
  • Diagnosis: bowel-looking structures on CXR
  • Complications: malignancy, pneumothorax, infection, hemoptysis, respiratory distress
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14
Q

que es esto

A

Congenital cystic adenomatoid malformation (CCAM)

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15
Q

Pulmonary Sequestration

description, complications

A
  • Description: sequestered lung lobe that is not connected to airway or proper pulmonary vasculature
    • Connected to the aorta (in similar fashion to renal arteries)
    • Result from abnormal tracheobronchial bud
  • Complications: mainly asymptomatic, but can cause respiratory distress or recurrent infections
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16
Q

types of pulmonary sequesteration

A

Intralobar – lower lobes

Extralobar – posteromedial left lower chest

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17
Q

Bronchogenic Cyst

A

Description – cystic structure near tracheal bifurcation

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18
Q

ఇది ఏమిటి

A

Pulmonary Sequestration

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19
Q

zer da hau

A

Bronchogenic Cyst

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20
Q

Croup

description, diagnosis, complication, treatment

A
  • Description: edema of subglottic tissues due to a viral infection (typically parainfluenza virus types I or II)
  • Diagnosis: Most common cause of inspiratory stridor and barking seal-like cough
  • Complications: “steeple” sign due to inflammation
  • Treatment: humid and cool air
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21
Q

Epiglottitis

Description, diagnosis, etiology, treatment

A
  • Description: airway obstruction with progressive edema of supraglottic structures
  • Diagnosis: manifests with pain, fever, and stridor
  • Etiology: bacterial (H. influenza)
  • Treatment: abx
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22
Q

Bronchiolitis

description, natural history, diagnosis, treatment

A
  • Description: acute inflammatory response in airways dominated by netrophilia
  • Etiology: RSV
  • Natural history: Initial upper respiratory symptoms with coryza, fever and cough, which precede abrupt lower respiratory symptoms (dyspnea and tachypnea)
  • Diagnosis: widespread bilateral crackles; CXR shows overinflation and regional atelectasis
  • Complications: otitis media, apneas, asthma
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23
Q

Obstructive sleep apnea (OSA)

descrpition, patho, symptoms

A
  • Description: disturbed sleep due to abnormal breathing
  • Pathophysiology: anatomic structures in the upper respiratory tract including the tonsils block airflow during sleep
  • Signs/symptoms: snoring, paradoxical inward rib cage motion during sleep, apnea, night sweats
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24
Q

Obstructive sleep apnea (OSA)

complication, diagnosis, risk factors

A
  • Complications: failure to thrive and other systemic organ-based problems (i.e. neuro, cardio, etc.)
  • Diagnosis: nocturnal polysomnography (measures brain activity in conjunction with airflow)
  • Risk Factors: certain congenital syndromes (down syndrome), sickle cell disease, obesity
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25
Q

HAP/VAP risk factors

A
  • Risk Factors for HAP/VAP
    • Hospitalized > 2 days in the last three months
    • Resides in nursing home/long-term care facility
    • Hemodialysis
    • Abx use in the last 3 months
    • 48 hrs post intubation (VAP)
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26
Q

HAP/VAP - micro

A

MSSA,MRSA,Pseudomonas aerginosa, klebsiella

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27
Q

HAP/VAP - treatmen

A
  • Ensure coverage of Gram + (+/- MRSA)
  • Ensure coverage of Gram – (+/- Pseudomonas)
  • Atypicals are covered by fluoroquinolones
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28
Q

MRSA

natural history, risk factors, tx

A
  • Natural history
    • Recent influenza, superinfection (gets better, then worse)
  • Risk factors
    • Prior IV use
    • Hospitalizations
  • Treatment
    • Vancomycin OR linezolid (po)
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29
Q

MSSA - tx

A
  • Treatment
    • Piperacillin-tazobactam or cefepime or levofloxacin
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30
Q

Pseudomonas Aeruginosa

clinical stuff, tx

A
  • Green sputum
  • Patients with cystic fibrosis or bronchiectasis (abnormal dilation of bronchi)
  • Multi-drug resistance
    • Treatment:
      • Beta Lactamase + Fluoroquinolone
        • Piperacillin-tazobactam + ciprofloxacin
        • Cefepime + levofloxacin
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31
Q

co to je

A

Peudomonas Aeruginosa -

Patients with cystic fibrosis or bronchiectasis (abnormal dilation of bronchi)

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32
Q

Klebsiella pneumoniae

clinical stuff, complications, risk factors

A
  • Currant jelly sputum (red)
  • Risk Factors
    • Poor dentition (bad teeth), alcoholics, diabetics, COPD patients
  • Can cause necrotizing PNA
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33
Q

CAP - risk factors

A

Sick contacts (daycare, public areas)

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34
Q

CAP - micro

A

strep pneimoniae, haemophilus influenzae, moraxella catarrhalis, legionella, clamydia, influenza A, RSV, adenovirus, rhinovirus, H1N1

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35
Q

CAP - outpatient tx

A
  • Reasoning: cover both typical and atypical PNA
  • Drugs: macrolides (i.e. azithromycin), doxycycline, fluoroquinolone (i.e levofloxacin)
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36
Q

CAP - inpatient tx

A
  • Drugs:
    • Choice A: fluoroquinolone (i.e. levofloxacin)
    • Choice B: cephalosporin (i.e. ceftriaxone) + macrolides (i.e. azithromycin)
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37
Q

Strep pneumoniae

A
  • Most common cause of CAP (95%)
  • Yellow/green sputum
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38
Q

Haemophilus influenzae

A

Elderly patients at risk

Otitis, sinusitis, meningitis (-itis very common)

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39
Q

Legionella PNA

A

Damp environments, construction sites

Non-pulmonary sx (GI, CNS, renal)

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40
Q

Aspiration PNA - risk factors

A
  • Neuromuscular disease/stroke patients
  • Dysfunctional swallowing mechanism
  • Alcoholics
  • Epileptics
  • Post-intubation/surgery
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41
Q

aspiration PNA - micro

A

Gram – (most commonly found in stomach)

Anaerobes (oral flora)

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42
Q

aspiration PNA - CHR

A

Bilateral lobe infiltrates or right middle lobe infiltrate (direct shot from trachea)

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43
Q

typical PNA

general characterisitic, CXR, micro

A
  • General Characteristics
    • Abrupt onset
    • Productive cough w/ sputum
    • Pleuritic CP
    • Unilateral crackles
    • Egophony
  • CXR
    • Focalized, dense consolidation
    • Usually unilateral
    • Pathology language: Lobular PNA
  • Microorganisms
    • Strep pneumoniae, s. pyogenes, h. influenzae
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44
Q

atypical PNA

general characterisitic, CXR, micro

A
  • General characteristics
    • Progressive onset
    • Fever w/o chills
    • Dry cough
    • Headache, malaise, myalgia
    • Bilateral crackles
    • Usually w/o egophony
  • CXR
    • Diffuse, patchy
    • Usually bilateral
    • Pathology language: Interstitial PNA and bronchopneumonia
  • Microorganisms
    • viral
    • fungal
    • mycobacteria
    • mycoplasma
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45
Q

how to diagnosis viruses

A

Respiratory virus panel – nasal swab

Rapid antigen test – detects influenza A

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46
Q

Respiratory Synctial Virus (RSV)

A
  • Peak incidence in winter
  • Affects all ages
  • Causes bronchiolitis and wheezing in kids
  • Contagious via contact
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47
Q

Influenza A

symptoms, complications, tx

A
  • Transmitted via airborne droplets (large particles)
  • Symptoms
    • Fever, headache, malaise, myalgias
    • Nonproductive cough, sore throat
  • Complications
    • Superinfection (gets better and then worse)
      • Suspected if new fever and worsening cough
  • Treatment
    • For severe viral PNA, treat abx that cover MRSA
    • Oseltamivir (Tamiflu)
    • Vaccinations decrease the risk of death, not illness (give to anyone 6 mo or more)
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48
Q

Adenovirus

description, transmision, complications

A
  • Description: DNA virus that causes common febrile illness in children, immunosuppressed patients
  • Transmitted by aerosol and survives a long period of time
  • Complications
    • Pharyngitis, conjunctivitis, laryngeotracheitis, bronchitis
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49
Q

Cytomegalovirus

description, symptoms, prognosis, tx

A
  • Description: common in HIV/immunosuppressed/transplant patients
  • Symptoms: fever, dyspnea
  • Prognosis: Poor for long term survival
  • Treatment: ganciclovir
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50
Q

Herpes simplex virus (HSV)

description, tx

A
  • Description: causes vesicular lesions that can spread to trachea
  • Can be asymptomatic, but life-threatening if immunocompromised
  • Treatment: Acyclovir
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51
Q

Varicella Pneumonia

description, tx

A

Description: may accompanies chicken pox, which can lead to PNA

Emergency if immunocompromised patient

Treatment: Acyclovir

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52
Q

Mycoplasma

diagnosis, tx

A
  • Extrapulmonary manifestations (hemolysis and joint symptoms)
    • Diagnosis:
      • Hemolytic anemia (cold agglutinin)
      • WBC is normal
      • Ground-glass CXR
    • Treatment:
      • Macrolide abx (Azithromycin)
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53
Q

Lung Abscesses

A

Description: pus-filled cavity often caused by aspiration

Associated with high fevers and bacteremia

CXR: sacs filled with fluid (pus and necrotic tissue)

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54
Q

Empyema

A

Description: pus in pleural space

Diagnosis: thoracentesis

Treatment: Chest tube

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55
Q

Qu’est-ce que c’est

A

typical PNA

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56
Q

wat is dit

A

atypical PNA

57
Q

这是什么

Zhè shì shénme

A

Mycoplasma

58
Q

Aspergillus (mold)

clinical features and types

A

Ubiquitous in the environment especially in moist areas; inhaled spores

  • Allergic Bronchopulmonary Aspergillosis (ABPA) – hypersensitivity responses with high levels of IgE and eosinophilia
  • Aspergilloma – develops in old cavities (esp. those with structural lung disease)

Invasive Aspergillus – angio-invasive disease with galactomannan antigen

59
Q

Non-tuberculosis mycobacteria (NTM)

clinical features plus stages

A
  • Ubiquitous in the environment
  • Common presentation – frail old lady with small little coughs (Lady Wyndemere Syndrome)
60
Q

TB

clinical features plus stages

A
  • Spread through droplets in close proximity (aka 6 ft)
  • Primary – initial infection in lower or middle lobe and lymph node (Ghon complex)
  • Latent – infected but contained with granulomas
  • Reactivation – organism previously latent become activated due to compromised immune system from age or sickness (upper lobes)
61
Q

Coccidioidomycosis

clinical features

A
  • Exposure in Southwest USA (soil, inhalation of spores)
  • Skin manifestations - erythema multiforme
  • Fibrocavitary PNA in lungs
62
Q

Blastomycosis

clinical features

A
  • Exposure in Central and Southeast USA (soil, inhalation of spores)
  • Has typical PNA presentation
63
Q

Histoplasmosis

clinical features

A
  • Exposure in Ohio and Mississippi River Valley (soil, inhalation of spores)
  • Acute/Primary – caseating granulomas with nodular calcifications (in spleen)
  • Chronic – occurs in preexisting structural disease causing cavitary lesions in the upper lobe
  • Disseminated – pulmonary and systemic manifestations
64
Q

Mucormycosis (mold)

clinical features

A
  • Spore inhalation from the environment

Causes sinopulmonary disease –tissue necrosis and nasal eschars

Angioinvasive

65
Q

Cryptococcus (budding yeast)

clinical features

A
  • Spore inhalation from soil/bird droppings

Complications include PNA, meningitis

66
Q

candida

clinical features

A

Lives in respiratory tract

Causes disease when in the blood stream

67
Q

Aspergillus (mold)

dx, tx (by type)

A

dx:

Hyphae with 45 degree angles

ABPA – high levels of IgE

Aspergilloma – CT shows air crescent around ball in lung

Invasive Aspergillus – CT shows ground glass (fuzzy) appearance

tx:

ABPA – steroids

Voriconazole

Amphotericin B (severe)

68
Q

Non-tuberculosis mycobacteria (NTM)

dx, tx

A

dx:

Acid fast stain

Tree in bud on CT chest

tx:

Antibiotics (macrolide)

69
Q

TB

dx, tx

A

dx:

CXR – cavitations

PPD – size of redness after 72 hours post prick

IGRA – blood test

Acid fast staining

tx:

4 drug cocktail

  • Rifampin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
70
Q

Coccidioidomycosis

dx, tx

A

dx:

Tissue culture/biopsies – showing round endospore

tx:

Fluconazole

Amphotericin B (severe)

71
Q

Blastomycosis

dx, tx

A

dx:

Broad budding yeast

tx:

Itraconazole

Amphotericin B (severe)

72
Q

Histoplasmosis

dx, tx

A

dx:

Serum and histo antigen test

tx:

Acute – none

Chronic – itraconazole

Disseminated - amphotericin B (severe)

73
Q

Mucormycosis (mold)

dx, tx

A

dx:

Tissues show hyphae with 90 degree angles

tx:

Surgical debridement

Amphotericin B (severe)

74
Q

Cryptococcus (budding yeast)

dx, tx

A

dx:

Bilateral pulmonary infiltrates with pleural nodules

tx:

Fluconazole

Amphotericin B (severe)

75
Q

Candidia (yeast)

dx, tx

A

dx:

Blood culture/skin biopsy show Pseudohyphae with 45 degree angles

tx:

Fluconazole

Amphotericin B (severe)

76
Q

què és això

A

Coccidioidomycosis

77
Q

ما هذا

ma hdha

A

Blastomycosis

78
Q

he aha kēia

A

Cryptococcus (budding yeast)

79
Q

For mesothelioma, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Caused by asbestos exposure
    • Gross: grey/white pleural nodules
    • Complications: pleural effusions
      Morphological:
    • Epithelioid – eosinophilic cytoplasm??
    • Sacromatoid – spindle looking cells
80
Q

What are paraneoplastic syndromes?

A
  • Paraneoplastic syndromes are rare disorders that are triggered by an altered immune system response to a neoplasm.
  • They are defined as clinical syndromes involving non-metastatic systemic effects that accompany malignant disease.
81
Q

Name 1 pleural tumor of the lung.

A
  • Mesothelioma
82
Q

Name 4 neuroendocrine tumors of the lung.

A
  • Small cell carcinoma
  • Large cell carcinoma
  • Carcinoid tumor
  • Hamartoma
83
Q

For carcinoid tumors, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Gross: polyp like mass
    • Two types
      • Typical – less severe
      • Atypical – more severe with necrosis
        Morphological:
    • Nests or cords of cells
    • Moderate cytoplasm with fine nuclei
84
Q

For large cell carcinoma, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Peripheral location
      Morphological:
    • Organoid nests (think of it as a single big cell)
    • Sheets of poorly differentiated large cells
85
Q

For small cell carcinoma, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Central Location
    • Associated with paraneoplastic syndrome
    • Commonly metastasizes
      Morphological:
    • Sheets of poorly differentiated small cells with granulated nuclei
    • Very little cytoplasm
86
Q

For squamous cell carcinoma, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Can get luminal occlusion and atelectasis
    • Gross: white-grey mass
      Morphological:
    • Sheets of neoplastic cells
    • Keratin pearls or intracellular bridge
87
Q

For adenocarcinoma in-situ (bronchioalveolar carcinoma), list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Pre-invasive lesion – lepidic growth pattern (alveolar structures are respected but cell are bigger)
  • Morphological:
    • Columnar cells that grow along preexisting bronchioles and alveoli
88
Q

For adenocarcinoma, list:

  • Clinical features
  • Morphological features
A

Adenocarcinoma

  • Clinical:
    • Most common in nonsmokers
    • Peripheral Location
  • Morphological:
    • Cells do not respect normal architecture and build glandular structures (gland)
89
Q

What are the nromal hemodynamics of the pulmonary vascular system?

  • What occurs in pulmonary arteries with an increase in CO?
  • What are the three properites of pulmonary circulation?
A
  • An increase in CO does only slightly changes the mean pulmonary artery pressure due to its ability to increase capacitance and recruitability
  • Properties of the pulmonary circulation
    • Low resistance
    • High capacitance
    • High recruitability
90
Q

What is pulmonary hypertension defined as numerically?

A
  • mPAP > 25 mmHg
91
Q

What are the three underlying causes of pulmonary hypertension and give examples of each?

A
  • Underlying causes of PH
    • Post-capillary
      • LVHF
      • Mitral stenosis
    • Capillary
      • ARDS
    • Pulmonary arteries
      • PAH – coming from disease in the arteries themselves
        • PAH is not a disease – it is the hemodynamic consequences/complications of a specific disease
92
Q

What is pulmonary arterial hypertension defined as numerically?

A
  • mPAP > 25 mmHg
  • PCWP < 15 mmHg
  • PVR > 3 units
93
Q

What is the general etiology of pulmonary arterial hypertension?

A
  • Disease causes imbalance of normal endogenous vasocontrol systems or increased PVR
94
Q

What three hormones cause vasoconstriction excess?

A
  • Endothelin II – over-expressed in pulmonary arteries of PAH patients
    • Vasoconstriction
  • Nitric Oxide – under-expressed in pulmonary arteries of PAH patients
    • vasodilation
  • Prostacyclin (PGI2) – under-expressed in pulmonary arteries of PAH patient
    • vasodilation
95
Q

What is the general pathway for nitric oxide?

A
  • NO stimulates cGMP production → dephosphorylation of myosin light chain → vasodilation
96
Q

What is the general pathway for prostacyclin?

A
  • Increases cAMP → activates PKA → PKA phosphorylates MLCK, inactivating it → vasodilation
97
Q

What else can cause pulmonary arterial hypertension (other than overconstriction or underdilation)?

  • Name 4 examples that can cause this.
A
  • Vasoconstruction – structural remodeling
    • BMPR2 is major gene that can be inherited
    • Scleroderma
    • Congenital heart disease
    • HIV
98
Q

What are the signs and symptoms associated with PAH?

A
  • Symptoms: dyspnea, fatigue, syncope, chest pain
  • Signs: accentuated P2, JVD, hepatomegaly, ascites, peripheral edema
    • Wheezes and rales are usually absent
99
Q

What is the general outline for prostacyclin, nitric oxide, and endothelin?

A
100
Q

tf dis shit?

A

Mesothelioma

101
Q

My man is messed up. What cancer fucked him up?

A

Mesothelioma

102
Q

Oooh this one is good. Name the murderer (the disease)?

A

Carcinoid tumor

103
Q

Oh, my fam is dead. Easy. What killed him?

A

Large Cell Carcinoma

104
Q

This guy was so small. Damn, what cancer?

A

Small Cell Carcinoma

105
Q

This one looks like it hurts. What cancer?

A

Squamous Cell Carcinoma

Intracellular bridges and shit

106
Q

tf dis shit?

A

Squamous Cell Carcinoma

Keratin pearls (damn they got extract these pearls and sell them)…squamous cell cancer can make you bank!!!

107
Q

Lol wut wrong with this brotha?

A

Adenocarcinoma In-situ (Bronchioloalveolar carcinoma)

108
Q

What cancer this dude got?

A

Adenocarcinoma

Bottom right: glandular structure

109
Q

What are non-specific treatments for PAH (3)?

A
  • Non-specific
    • Diuretics to control volume level
    • Oxygen to prevent hypoxemia
    • Nifedipine to reduce hypertension
110
Q

What are specific treatments for PAH (3) and know their MOAs? Recognize examples lmao

A
  • Prostacyclin analogs
    • MOA: direct vasodilators of pulmonary and systemic arterial vascular beds; by decreasing TPR, you increase CO and SV
    • Eporostenol, treprostanil, iloprost, and selexipag
  • Endothelin receptor antagonists
    • MOA: blocks endothelin receptor on smooth muscle cells
    • Bosentan**, Ambris_entan, Macitentan_**
  • PDE-5 inhibitors
    • MOA: inhibit conversion of cGMP (activates vasodilation pathway) to GMP
    • Sildenafil** (Viagra), tadal_afil_** OR a NO receptor agonist like Riociguat
111
Q

$22.36 if you can get this on your first try

A

Chronic passive congestion (right): hemosiderin-laded macrophages in alveoli, interstitial fibrosis

112
Q

$10 if you can get this on your first try

A

Pulmonary edema: lungs are heavy and contain increased fluid, particularly at the bases

113
Q

What are three things that can cause an embolism?

A

Embolism: can be caused by sepsis, fat, bone marrow

114
Q

Tf wrong with this brotha?

A

Pulmonary hypertension: Thick media layer due to hypertrophy of smooth muscle cells

115
Q

What is goodpasture syndrome (lol dw, i don’t know either)? What is the etiology?

A

No, nothing to do with cows. Good try though

  • Goodpasture Syndrome: necrotizing hemorrhage interstitial pneumonitis and glomerulonephritis
    • Etiology: antibodies to glomerular basement membrane antigen
116
Q

What is granulomatosis with polyangitis? What is the etiology?

A
  • Granulomatosis with Polyangitis
    • An autoimmune disease of lungs, upper respiratory tract, and kidneys
    • Associated with ANCA
117
Q
A

Lipoid Pneumonia

When aspiration allows for mineral oil or some other fat into the lung, results in these fat deposits seen in the histological slide

118
Q
A

Lobular Pneumonia

  • Consolidation of the whole lobe
  • Histology shows red hepatization (PMN and RBC in alveoli)
119
Q
A

Bronchopneumonia

Diffuse, patchy consolidations

120
Q
A

Lung Abscess

Degenerated neutrophils and necrotic debris

121
Q
A

Respiratory Syncytial Virus

Multi nucleated giant cell

122
Q
A

Influenza A

Diffuse alveolar damage – hyaline membrane

123
Q
A

Adenovirus

Smudge cells

124
Q
A

Herpes Simplex Virus

Intranuclear inclusion surrounded by halo

125
Q
A

Cytomegalovirus

Cellular and nuclear enlargements

126
Q
A

TB

Caseating granuloma

127
Q
A

Pneumocystis Jiroveci

  • Common in AIDS patients
  • Foamy eosinophilic material in alveolar spaces with honeycomb appearance
128
Q

Function of pericardium (5)

***SOME NIGGA FORGOT TO DO DEM FLASHCARDS FOOL***

A
  • Lubricating
  • Protection from infection
  • Prevention from over-distention
  • Contributes to ventricular stiffness in diastole which helps to enhance mechanical coupling of the ventricles
  • Releases prostaglandins in response to distension that can modulate efferent sympathetic response and may also impact coronary tone
129
Q

a differential diagnosis for a patient presenting with pericardial disease (4)

A
  • Acute coronary syndrome – positive for atherosclerotic lesions
  • Pulmonary embolism – positive D-dimer, V/Q mismatch
  • Myocarditis – elevated troponins with a viral etiology
  • Pericardial effusion – lack of pain and accumulation of fluid in pericardial space
130
Q

Etiology of pericardial disease

A

idiopathic, malignancy, uremia, drugs, hypothyroidism

131
Q

explain diagnostic modalities in pericardial disease

History, EKG, echo, Chest CT, inflammatory markers

A
  • History – 4-5 day pain in any age group
  • EKG – diffuse ST elevations, PR depressions
  • Echocardiography – excess pericardial space
  • Chest CT – excess pericardial space
  • Inflammatory markers – elevated CRP and ESR
132
Q

Distinguish between pericarditis and pericardial effusion

A
  • Pericarditis – inflammation that is painful in acute stage
    • May not be accompanied by effusion
  • Pericardial effusion – accumulation of fluid in the pericardial space without pain
    • Implies pericarditis
133
Q

Acute pericarditis

presentation, diagnosis, complications, tx

A
  • Presentation – postural (comfortable leaning forward) and pleuritic (sharp) chest pain
  • Diagnosis: pericardial rub (friction of pericardium rubbing against heart); diffuse ST elevation on EKG; leukocytosis; elevated ESR and CRP
  • Complications: myocarditis
  • Treatment: NSAID (aspirin/ibuprofen) or colchicine
134
Q

Pericardial tamponade

presentation, diagnosis, complications, tx

A
  • Presentation: triggered by pericardial effusion; tachycardic, tachypneic, hypotensive
  • Diagnosis: diminished pulses, pulsus paradoxus (>10 mmHg drop in BP during inspiration); JVD
  • Complications: death
  • Treatment: pericardiocentesis
135
Q

Constrictive pericarditis

presentation, diagnosis, complications, tx

A
  • Presentation: subtle and chronic decline to dyspnea, fatigue, edema (may be confused with HF)
  • Diagnosis: JVD, Kussmaul’s sign (paradoxical JVD during inspiration)
    • Ventricular interdependence
  • Complications: impaired RV filling due to “wool blanket”
  • Treatment: diuretics and pericardial stripping
136
Q

Normal caridac physiology during breathing cycle

aka

What happend during inspirations and expirations

A
  • Normal
    • BP differs slightly (<10 mmHg) during the breathing cycle
    • Inspiration: decrease in intrathoracic pressure allows increase in venous return
    • Expiration: increase in intrathoracic pressure leads to decrease in venous return
137
Q

explain cardiac physiology with cardiac tamponade

A
  • BP differs greatly (>10 mmHg) during the breathing cycle because compression by the fluid in the pericardial space does not allow for RV to expand outward, so the interventricular septum bends into the LV, therefore blocking the LVOT and decreasing LV volume → decrease in CO
138
Q

explian cardiac physiology with constrictive percariditis

A

Wool sheath over heart causes ventricular interdependence because neither the LV or RV can expand, causing the interventricular septum to fluctuate between the two ventricles

CardioResp (14 decks)

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