Pulmonary/ Critical Care Flashcards

1
Q

What is necrotizing Enterocolitis

A

inflammation and necrosis of the intestines in view of Gas-producing bacteria

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2
Q

NEC is common in

A

premature babies ( < 29 weeks)
Low birth weight < 1.5kg
on enteral feeds, formula

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3
Q

Features of NEC on Abdoxray ?

A

Distended abdomen
Bilious vomit
Bloody stools
Pneumatosis intestinalis ( air in the wall of the intestines)
Pneumoperitoneum ( air in the wall of the abdomen).

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4
Q

What is cystic fibrosis ?

A

Autosomal recessive disease with cysts in pancreas and fibrosis.
Improper mucus secretion from the lungs

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5
Q

Function of CFTR channel in Sweat glands and other exocrine galnds ?

A

Sweat glands: reabsorb Cl-
Exocrine glands (pancreas, GI) secretes Cl-

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6
Q

CF has improper —– GENE

A

CFTR

Sweat galnds: excrete Cl-.. salty sweat
Exocrine glands: No cl- secretion, thick secretions, which clog the pancreatic duct that leads to pancreatic insufficiency ( unable to absorb fat soluble vitamins, Steattorhea: stool that floats on water)

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7
Q

Defective CFTR gene is due to

A

Deletion of 3 nucleotides and missing phenealanine

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8
Q

CF of CF ?

A

Coughing copious amounts of pus ( recurrent Sinopulmonary Infections)
Dry skin (loss of Water and salt) Pancreatic insufficiency -> pancreatitis -> Steatorrhea (unable to rebasorb the Fat) Type 1 DM ( in view of pancreatic failure)
Bilateral Nasal polyp in children
Clubbing
Female/ Male infertility
Gallstones (obstructive jaundice, because the bile ducts are clogged)
Clog the intestines –> meconium plug –> meconium ileus

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9
Q

MC organisms causing infection in CF

A

Before age of 20: Staph. aureus
After age of 20: Pseudomonas

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10
Q

How to diagnose CF ?

A

Administer Pilocarpine, which is a Parasympathomimetic

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11
Q

Allergic Brunchopulmonary Aspergilosis

A

seen in CF with siopulmonary infections not resolving with abx. Associated with eosinophilia and IgEs.

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12
Q

What is invasive pulmonary aspergilosis

A

fungal infection
MC in immunocompromised patients ( Neutropenia, Post-transplant)

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13
Q

CF of invasive Pulmonary aspergillosis

A

Fever
hemoptysis
Pleuritic chest Pain

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14
Q

Diagnostics of Invasive Pulmonary Aspergillosis ?

A

Positive cell wall markers ( Beta-d glucan and galactomann)
CT: nodule with ground glass opacitiies ( surrounding halo)

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15
Q

What kind of shoch does PE give ?

A

Obstructive shock

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16
Q

CF of obstructive shock ? (pre-pulmonary)

A

high Central venous P. ( preload of Righ. side of the heart)
Low or N Pulmonary Capillary wedge pressures
Low Cardiac Output
High SVR ( hypotension)

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17
Q

CF of Obstructive shock ( Post-Pulmonary)

Obstruction at the level of L. side of the heart

A

High PCWP
High CVP (everything is congested backwards from hear to the lungs)
low CO
High SVR

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18
Q

CF of Hypovolemic shock

A

low CVP
Low CPWP
low CO
high SVR

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19
Q

CF of Septic (distributive) shock

A

Vasodilation i.e
low SVR
Low CVP
low CPWP
high CO

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20
Q

early feature of Septic/ distributive shock ?

A

bounding peripheral pulses. Increased Cardiac index and stroke vokume increases pilse pressure (sbp-dbp) leading to bounding pulses.

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21
Q

How to differentiate between Gestational Asthma and Dyspnea of Pregnancy

A

Gestational asthma: more likely in a pt. with asthma previously. Worsens at night. Intermitent

Dyspnea of pregnancy: Persistant, and no diurnal variation.

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22
Q

Pathophysiology behind Dyspnea of pregnancy

A

increased progesterone that induces medullary respiratory center

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23
Q

What happens in the lungs when Medulllary respirator center is activated in dyspnea of pregnancy ?

A

hyperventilation –> increase minute ventilation –> increase pa02 and decrease paco2.

The diaphragm position compresses over the basilar alveoli causing atelectasis, decrease residual functional capacity and residual volume

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24
Q

How does LAMA work ?

A

Blocking muscarinc receptors, preventing bronchoconstriction and reducing mucus secretion.

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25
Q

Lab findings of Empyema or complicated parapneumonic pleural effusion ?

A

Low in Glucose ( < 60)
Low PH
High in proteins because of increased permeability of vessels

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26
Q

Diff. between empyema and Complicated parapneumonic pleural effusion

A

Empyema presence of pus or +ve gram stain

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27
Q

Why is fluid glucose low in empyema ?

A

Because of the high metabolic activity of leukocyte/ bacteria

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28
Q

What is a DAH

A

bleeding into the alveoli

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29
Q

foul smelling pleural fluids are suggestive of ?

A

aneorobic oral organisms causing empyema

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30
Q

What is Acute Asthma Exacerbation Rx ?

A

SABA/ SAMA, Magnesium and Steroids.

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31
Q

Pathophysiology of ACEI causing cough

A

Inhibt ACE –> acc. of kinins and substance P that increases prostaglandins.

Also activates arachidonic acid pathway –> increased levels of thromboxane -> bronchoconstriction.

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32
Q

Modified Wells score for PE

A

+3: Other diagnosis is less likely
Signs of DVT
+1.5: previous PE
Tachy
Recent history of immob.

+1: hemoptysis, Malignancy

PE LIKELY >4
PE Unlikely <4

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33
Q

Management of PE, if PE is likely

A

if PE is likely ( Modified wells score >4) and patient has no Controindications. Start Anti-coagulants before Diagnostic test like CT angio.

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34
Q

CF of Consolidation on chest exam

A

Increased breath sounds and tactile fremitus
Dullness to percussion

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35
Q

What is the best step in understanding an undiagnosed Pleural Effusion ?

A

A thorcacocentesis ( investigate if the fluid is transudate or exudate)

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36
Q

When is LTOT indicated ?

A

COPD patients with spo2 < 88% on RA.
or < 89% in patients with corpulmonale, R. sided HF and Hematocrit > 55%

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37
Q

Patho. Diff between Lambert Eaton Syndrome and Myasthenia Gravis

A

Lamb: Abs. against volatged gated Calcium channels (pre-synaptic), Improves with movement

MG: Abs. against Ach receptors ( at Neuromuscular jt.)
Woresens with movement

Lambert Eaton has autonomic signs and symptoms.

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38
Q

CF of Myasthenia Gravis

A
  1. Ptosis and diplopia ( extraocular
    muscle weakness)
  2. Bulbar muscles ( difficulty chewing, swallowing and dysarthria)
  3. Proximal muscles: Difficulty standing from a chair, hair brushing and climbing stairs
  4. Resp failure.
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39
Q

Pathophysiology of MG 3 steps

A
  1. Abs. block Ach receptors –> no muscle activation and weakness
  2. Internalization of Ach R. and further weakness
  3. Complement activation and muscle lysis –>
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40
Q

MG is associated with ?
Lambert Eaton Syndrome ?

A

Thymoma
Small cell lung cancer

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41
Q

Rx of MG ?

A

Pyridostigmine ( Inhibits Ach esterese Inhibitor –> increase Ach in synaptic cleft which competes with Achr. Blockers and increase muscle strength).

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42
Q

Features of Amyotrophic lateral Sclerosis

A

Muscle weakness
( upper and lowe limbs and bulbar muscles) hence dysarthria
along with clumsiness, dropping things
Fasciculations.

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43
Q

Rx of ALS ?

A

Relouzole

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44
Q

Advantages Mechanical Ventilation

A
  1. Protection: preventing alveolar distention ( TV: 6mls/kg)
  2. Permissive hypercapnia (low Ph, high pco2)
  3. Oxygenation: aiming spo2 92-96% to aviod Oxygen toxicity ( Pao2: 60-90), Fio2 <60
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45
Q

In Mechanical ventilation paO2 is affected by ?

A

PEEP and Fio2

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46
Q

In Mechanical Ventilation PaCO2 is affected by ?

A

TV and Respiratory rate

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47
Q

Diff between Emphysema and Chronic Bronchitis

A

Emphysema related to distal bronchioles
Chronic bronchitis related to proximal bronchioles

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48
Q

What type of emphysema is caused by COPD, Alpha 1 anti-trypsin ?

A

COPD: Centrilobular emphysema of upper lobes
Alpha-1 anti: Panacinar of lower lobes

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49
Q

Causes of Emphysema ?

A

Cigarette smoking
alpha 1 anti-trypsin defic.

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50
Q

Causes of Neonatal Resp. Distress ?

A

Premature lungs, low surfactant. like having premature neonates or Fetus of Mother with hyperglycemia.

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51
Q

Pathophysiology of mother hyperglycemia on Lung maturation

A

Hyperglycemia in mother–> hyperglycemia in fetus –> hyperinsulinism–> inhibits cortisol and thus formation of phospholipids important for surfactant.

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52
Q

Features of NRDS on Xray ?

A

Diffuse reticuloglandular pattern and air bronchograms

the collpased alevoli leads to air in the bronchioles.

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53
Q

Rx of NRDS ?

A

antenal steroids, ideally 24 hours before birth.

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54
Q

CF of Foreign Body Aspiration

A

Presents with wheeze unresponsive to albuterol, prolonged expiration and hyperresonance; Unilateral
Sudden onset cough and dyspnea
CXR: mediastinal shift to the unaffected side and hyperinflation of the affected side.

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55
Q

CF of Diaphragmatic rupture ?

A

Post- MVA
Avulsion or rupture of L. diaphragm most common.
CXR: bowels inside the lungs, might cause stramgulation.
and Mediastinal shift away from the affected side

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56
Q

What is Transient Tachypnea of newborn

A

a condition where there is delayed resoprtion of fluids in the lungs

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57
Q

Features of Transient Tachypnea of newborns ?

A

Fluid in the interlobar fissure

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58
Q

What are the features of a Solitary Pulmonary Nodule

A

< 3cm
no LN involved
Round opacity
Surrounded by Pulmonary Parenchyma

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59
Q

What increases the probability of malignancy in a SPN ?

A

hx of smoking
large size
female
Older age
irregular borders
location (upper lobes)
Family/ personal hx of lung Cancer.

60
Q

Management of SPN < 0.6 cm, and > 0.8 cm with high probability of malignancy ?

A

<0.6 cm no surveillance needed
> 0.8 + high malig –> Bx or excision.

61
Q

Lung Cancer Screening

A

Age: 50-80
> 20 pack year Smoking
Currently smoking or quit smoking within 15years

62
Q

Granulomatosis with polyangitis pathophysiology ?

A

Small to medium vessels vaculitis, due to Abs against proteinase 3 on surface of Neutrophils.
c-ANCA positive, PR3-ANCA positive

63
Q

Clinical features of Granulomatosis with polyangitis ?

A

ENT: chronic Rhinosinusitis
Upper and Lower Resp Tract infections and hemoptysis
Glomerulonephritis ( nephritic syndrome): Pauci immune and cresnteric appearancce ( proliferatio. of epithelial layer of bowmans capsule).

64
Q

What is Acute bronchitis

A

Cough lasting > 5 days
post upper viral infection
yellowish sputum occasionally blood tinged
Normal vitals

O/e: Wheeze that clears with cough.

65
Q

MC organism of Bronchiolitis ?

A

RSV

Palivizumab used in patients wth high risk of Bronchiolitis

66
Q

Paradoxical breathing movement of the chest indicates ?

A

Phrenic nerve injury

67
Q

Apnea of Prematurity

A

periods of > 20 seconds of no respiratory effort. asc with bradycardia and Hypoxia.
Related to immuature respiratory centers

68
Q

Rx of Apnea of prematurity ?

A

Caffeine which stimulates resp. drive until centers mature ( 34-37 weeks)
CPAP.

69
Q

causative organism of Croup

A

-ve sense, RNA Parainfluenza virus

70
Q

CF of Croup

A

Barking cough especially at night
Hoarsness of voice ( dysphonia)
Inspiratory stridor
Subglottic edema and obstruction (steeple sign on Xray)

MC 3months and 3 years

71
Q

Pathophysiology of Croup ?

A

Edema of proximal trache

hence treating with racemic epinephrine

72
Q

Rx of Croup ?

A

Oxygen
Steroids
Nebulized epinephrine ( constriction of subglottic vessels, decrease hydrostatic pressure and as such decrease edema).

73
Q

What is Acute epiglotitis ?

A

is a cellulitis of the supraglottic tissue due to H. infleunza B.

Also step pneumonea, staph aureus and Non-typeable H. infl.

74
Q

CF of Acute epiglotitis ?

A

Muffled voice
Insp. Stridor
Drooling (dysphagia)
Fever (bacterial infection)
Tripod sign
Intercostal muscle retrations

CXR: thumb sign

75
Q

Types of Lung Cancer ? and locations

A

Adenocarcinoma (peripheral)
Small cell Lung cancer (central)
Sqaumous cell lung cancer ( central)
Large cell lung cancer (peripheral)

76
Q

Which Lung Ca. is asc with hypercalcemia, high PTHrP low PTH ?

A

Sqamous cell lung cancer

77
Q

Which Lung Cancer is asc with SIADH, cushing Syndrome and Lambert Eaton Syndrome ?

A

Small cell Lung Can

78
Q

Which Lung cancer causes SVC, hoarness and cough ?

A

Large Cell lung Cancer

79
Q

Bronchial Carcinoid Ca. is MC in ?

A

Children/ young adults

80
Q

CF of Seretonin syndrome

A

Diarrhea, flushing and hypotension

81
Q

Type of Pancoast Tumors ?

A

MC sqamous cell

82
Q

Location of Pancoast tumors ?

A

Apec of the lungs

83
Q

CF of Pancoast Tumors ?

A

Shoulder pain and Upper limb weakness ( pressing on brachial plexus)
Horner syndrome ( pressing over the sympathetic chain, miosis, ptosis and anhidrosis)

84
Q

How to prevent Post-op Atelectasis ?

A
  1. Deep breathing excercises
  2. Proper pain control
85
Q

What are the causes of Post-op Atelectasis ?

A

Poor pain control (like abdominal pain, that results in poor cheste xpansion and alveolar collapse)

Mucus plug ( causing obstruction of airways and alveolar collapse)

86
Q

Atelectasis due to bronchial mucus plug on CXR

A

Huge opacification
Mediastinal shift towards the side of Atelectasis

(o/e: decreased breath sounds and dullness to percussion).

87
Q

Pulmonary Artery HTN is common in ?

A

Limited Cutaneous Systemic sclerosis

R ventricular heave ( over the L. parasternum).

88
Q

When does a Fat Emboli Syndrome occur ?

A

24-72 hours after a ortho surgery or Fracture

89
Q

Pathophysiology of GPS ?

A

anti-GBM abs ( against alpha3 chain of type IV collagen)

90
Q

Management of Anaphylaxis ?

A
  1. IM Epinephrine ( can be repeated every 3-5 mins)
  2. IV fluids
  3. Albuterol for bronchoconstriction
  4. Steroids/ Anti histamines
  5. Glucagon to reverse Beta-blockers
91
Q

CF of antiglomelural BM disease ?

A

Renal: hematuria, RBC cast with dysmoprhic RBCs
Pulmonary: hemoptysis, cough and dyspnea.

92
Q

In case of Venous air embolism, in what position should the patient be placed and why ?

A

left lateral Decubitus. It prevents causing obstruction of RV outlet. Keep air emobli on the lateral wall of RV and with administration of oxygen allows for dissolving of air embolus with blood.

93
Q

MC of CAP ?

A

Strep Pneumoniae

94
Q

What is Cor pulmonale ?

A

Right sided HF due to Lung or Pulmonary vasculature causes (like COPD, PE, Bronchiectasis).

95
Q

Rx of CAP based on severity

A

CURB-65
>3: admission to Medical ward… Betalactam+ macrolide or fluoroquinolone ( Avoided in elderly)
Inpt +ICU: Betalactam and macrolide or beta lactam + fluro

Outpt.

96
Q

CF of Cor Pulmonale

A

Dyspnea
Cough
Syncope, chest pain on exertion
pitting edema
Possible Ascites

and features of underlying etiology

97
Q

What is CURB-65 criteria

A

Used to decide management of patients with CAP
>65 y.o
Confusion
Urea high >20
RR >30
Bp < 90 sbp or <60 dbp

98
Q

Signs of Cor Pulmonale

A

Distended Jv
Parasternal heave
Loud second heart sound often split (pulmonary part)
Clubbing
Hepatomegaly

99
Q

Obstructive Pulmonary disease classification based on DLCO

A

Decreased DLCO: emphysema
Normal DLCO: Chronic bronchitis
Increased DLCO: Asthma

100
Q

CF of Sarcoidosis

A
  1. Granuloma
  2. Uveitis anterior
  3. Erythema nodosum
  4. Arthritis
  5. Lupus pernio ( involvement of cheeks and nose)
  6. ILF
  7. Negative TB
  8. gammaglobulenemia
    And of course Hypercalcemia signs and symptoms ( due to elevated alpha 1 hydroxylase that increase 1,25 dihydroxyvitamin D)

Guerling mnemonic

101
Q

CXR findings of
1. chronic bronchitis
2. bronchiectasis
3. emphysema

A
  1. thickened bronchiovascular markings
  2. dilated airways
  3. obliteration of alveolar septa and hyperlucency of lungs
102
Q

What type of Granuloma is seen in Sarcoidosis ?

A

Non-caseating granuloma

103
Q

Adrenal Insufficiency

A

Hyoicorticolism ( drops in BP)
Hypoadrenalism ( hyponatremia and Hyperkalemia) exacerbated by release of ADH.

104
Q

Lofgren Syndrome

A

Triad of:
Migratory polyarthritis (usually ankles and bilateral)
Erythema nodosum
Bilateral Hilar lymphadenopathy
and fever

105
Q

If a Patient is having an Asthma attack and he still is maintaining normal PH and CO2 levels what does that indicate

A

the the patient is unable to keep a good ventilation despite the increased work of breathing due to muscle fatigue

106
Q

SE of vasopressors

A

peripheral limbs (digital) ischemia
Mesenteric Ischemia

Acting on both alpha and beta receptors

107
Q

SCD effect on the lungs

A

due to intravascular hemolysis –> endothelial injury and pulmonary vessels hyperplasia and remodeling and increased Pulmonary vascular resistance which causes decreased RV outflow and signs of R. sided HF ( hepatomegaly, distended JV and Peripheral edema).

108
Q

What is Occupational Asthma ?

A

Asthma related to work place.
Asthma symptoms improve when away from work

109
Q

Diagnosing Occupational Asthma ?

A

serial PEFR at home and work place
Skin prick test or Allergy specific serum IgE

110
Q

Pathophysiology of Clubbing ?

A

Megakaryocyte escapes fragmantation in the lungs, deposits in distal Connective tissue and release FGF and VEGF leads to connective tissue hypertrophy and capillary permeability and vascularity

111
Q

Indication for Thoracotomy ?

A

Bloody output >1.5l
> 200mls/hr over 2 hours

112
Q

Complications of drowning ?

A

Aspirated fluid washes out surfactant and leads to hypoxemia and possible RDS.

Must be watched for 8 hours before discharge

113
Q

What does a cavitary lUNG infiltrate with air fluid level indicate ?

A

Lung Abscess

114
Q

ABx used to treat lung abscess of aneorobes g+

A

Ampicillin-Sulbactam

115
Q

How does Sleeping position affect perfusion of lung ?

A

the side that is lower will receive more perfusion with the help of the Gravity

116
Q

How does sleeping position affect lungs in case of Pneumonia

A

Patient sleeping on the side where pneumonia is present, means this side is more perfused ( but less ventilated in view of pneumonia) and as a result results in V/Q Mismatch

117
Q

What is the MC mycosis in the US ?and how is it transmitted ?

A

Histoplasma Capsulatum. Transmitted from birds/ bats.

presented as granulmona with narrow based budding yeast

MC in cave = capsule

118
Q

What is the indication of asbestos exposure on cxr

A

Pleural plaques
Linear opacities at lung bases

Dumbbells like ferriginous in alveolar sputum

119
Q

What are the complications post Lung Transplant ?

A

Bronchiolitis obliterans/ Organnizing pneumonia

120
Q

Pathophysiology of Chronic Bronchitis

A

Chronic inflammation with lymphocytes of submucosa which will eventually lead to fibromyxoid tissue in the airway lumen leading to obliteration.

121
Q

Pathophysiology of Kartageners syndrome

A

defective dynein which leads to dysfunctional Cilia

122
Q

CF of karatgeners Syndrome

A

Dextrocardia (Situs Inversus)
Sinopulmonary infections
Bronchiectasis
Infertility
Conductive hearing loss

123
Q

What is Mesothelioma

A

is a malignancy that encases the lungs
After exposure 25-40 years of asbestosis
Leads to hemorrhagic pleural effusion

124
Q

Asbestos exposure is high in

A

shipyard workers
plumbers
mining
people who work in insulation
tile worker

125
Q

OSA

A

Patient hypoxic at night, develops hypercapnia that resolves when patient wakes up

126
Q

OSA+ OHS (obesity hypoventilation syndrome)

A

hypoxia continues even during the day which leads to respiratory acidosis, kidneys will compensate for that by retaining HCO3- and decreasing cl- reabsorption.

low chloride.

127
Q

Why do patients with OHS develop PHTN

A

in view of chronic hypoxic vasoconstriction

128
Q

Step by step management of massive hemoptysis ?

A
  1. Patent airway (intubation)
  2. Bronchoscopy
  3. If it fails pulmonary angiography
  4. if the upper 2 fail, urgent thoracotomy
129
Q

How does high flow oxygen affect patients with COPD ?

A
  1. High flow oxygen decreases the vasoconstriction (previously induced by hypoxemia) at the alveoli and thus increase v/q mismatch
  2. decreases respiratory drive ( the body will sense. more oxygen, so will decreade ventilation rate and thus co2 will accumulate)
  3. Increased oxyhemoglobin will reduce uptake of co2 from the tissues.

thus leading to confusion

Block 4, Q 9

130
Q

How does hypoxic-ischemic brain injury affects the brain

A

hypoxia causes cell death and necrosis –> cerebral edema –>increased ICP –> Cushing triad ( bradycardia, htn and abnormal breathing).

131
Q

What are the major risk factors for Ventilator-associated pneumonia ?

A
  1. Acid supression
  2. Subglottic secretions pooling
  3. Supine position
  4. Xs. sedation
  5. Xs. patient movement while intubated
132
Q

CF of theophylline toxicity

A

Insomonia/ headaches
arrythmias
Vomiting

133
Q

Who is Brunchopulmonary dysplasia diagnosed in ?

A

newbors who require ventilation > 28 days

134
Q

What are the pathologic findings of Brunchopulmonary dysplasia ?

A

Decreased number and septation of alveoli

Common in Mechanically ventilated neonates in view of RDS.

135
Q

Management of COPD exacerbation

A
  1. Oxygen
  2. Bronchodilators inh ( SABA and SAMA)
  3. Systemic steroids
  4. ABX if > cardinal signs
  5. NIPPV
  6. Intubation if NIPV fail
  7. Oseltamivir if Influenza posi.
136
Q

What is the Antidote to Benzodiazepene ?

A

Flumazenil

137
Q

Risk of Lung Ca. with exposed to Asbestose w/o smoking is increased by ?

138
Q

Risk of Lung Ca. w asbestos and smoking is increased by

139
Q

CF of interstitial Lung disease ?

A

progressive dyspnea
dry cough
bibasilar fine crackles
Finger nail clubbing

140
Q

Asbestose exposure increases the risk of ?

A

Bronchogenic carcinoma with smoking ( cavitary lesion on xray and weight loss)

Mesothelioma (hemorrhagic Pleural effusion)

141
Q

Thymus on CXR ?

A

Common in children < 3 years
Sail sign
Regresses at puberty

142
Q

What are the best predictors of Post-op Pulmonary Morbidity

A

pre-op FEV1 and DLCO

143
Q

Definition of ARDS

A
  1. Abnormal X-ray
  2. Resp. failure less than 1 week of a known trigger
  3. Decreased PaO2/ fIo2
  4. Exclusion of cardiogeneic pulmonary edema
144
Q

Pathophysiology behind ARDS

A

Acute onset inflammation, leads to increased vascular permeability.
Neutrophils leave BV and attack alveoli, leading to edema ( intra aleveolar and interstitial). leading to hypoxia and hypercapnia