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Renal-Pulm > Quiz 3 > Flashcards

Quiz 3 Flashcards

1
Q

The foregut is which embryologic layer and surrounded by what?

A
  • in the dorsal body wall

- endoderm surrounded by (splanchnic) mesoderm

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2
Q

Respiratory system development

  • derived from
  • endoderm forms?
  • mesoderm forms?
A
  • sprouts from foregut
  • endoderm -> inner epithelium and glandular epithelium
  • mesoderm -> conn tissue, smooth muscle and cartilage
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3
Q

Esophageal atresia

  • definition
  • associated with
  • can cause
  • sxs after birth
A

def -> blind-ending esophagus

assoc -> esophagotracheal fistula = esophagus connected to trachea

causes polyhydramnios -> too much amniotic fluid

Sxs

  • aspiration upon feeding
  • frothing at the mouth -> can’t swallow saliva
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4
Q

Pulmonary agenesis

A

lung buds fail to develop

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5
Q

Pulmonary hypoplasia

A

deficiency of later branching of lung bud

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6
Q

list 3 late events in lung development

A
  1. inc alveolar surface area
  2. activation of alveolar defense systems
  3. surfactant production
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7
Q

Neonatal respiratory distress syndrome is often seen in?

A

premature infants

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8
Q

Hereditary surfactant deficiency

  • gene for?
  • chronic or acute?
A

surfactant B protein gene

long term issue

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9
Q

Describe the movement of diaphragm during development

A

cranially -> inferiorly -> dorsally -> dividing intraembryonic coelom in thoracic duct and abdominal cavities

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10
Q

The gaps b/w pleural cavity and peritoneal cavity are called?
Are filled in by?

A
  • pericardioperitoneal canals

- filled in by pleuroperitoneal membranes

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11
Q

Embryological derivatives

  • central tendon
  • muscular diaphragm? (innervation)
  • outer diaphragm (innervation)
  • right and left crura
A

septum transversum -> central tendon

myoblasts -> migrate from septum transversum to pleuroperitoneal membrane -> muscular diaphragm
-phrenic nerve

body wall mesenchyme -> outer diaphragm

  • segmental
  • T7-T12 intercostal nerves

gut mesenchyme -> Right and left crura

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12
Q

visceral vs parietal pleura derivation

A

visceral -> outer layer of bronchial buds

parietal pleura -> inner layer of thoracic wall

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13
Q

what divides thoracic cavity into pericardial, right and left pleural cavities?

A

fusion of pleuropericardial folds w/ foregut

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14
Q

Congenital diaphragmatic hernia is due to

  • which side more common?
  • complications?
  • management?
A

failure of one of the pericardioperitoneal canals to close

USUALLY LEFT

pulmonary hypoplasia -> life threatening
can get pneumothorax in opposite lung

tx w/ surgery before week 16

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15
Q

Which cells give rise to small cell lung carcinoma

A

Kulchitsky cells -> neuroendocrine

  • secretory granules on basal aspect
  • derived from neural crest cells
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16
Q

Cystic fibrosis

  • inheritance
  • defective channel/gene
A

AR

defective ATP-gated Cl- channel

  • protein stuck in RER
  • CFTR gene

dec Cl- secretion -> inc Na+/H2O reabsorption into cells -> thick mucous

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17
Q

Oxymetazoline (Afrin)

  • MoA
  • indications
A
  • for nasal congestion

- stimulates alpha-1 receptors -> vasoconstriction -> reduced edema

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18
Q

Vocal vs vestibular fold histology

  • glands
  • epithelium
A

VESTIBULAR

  • has glands
  • respiratory epithelium

VOCAL

  • no glands!!!
  • stratified squamous non-keratinized epithelium
  • lacks blood vessels
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19
Q

Epiglottis histology

-epithelim

A

Anterior and posterior tip -> in contact with food
-stratified squamous epithelium

Posterior
-respiratory epithelium

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20
Q

CC16

  • what is it?
  • which cells produce it?
  • where are these cells found?
  • disease implications
A

CC16 -> clara cell secretory protein
-proteinaceous surfactant called surface-active agent

Made by clara cells which are most abundant in terminal bronchioles

CC16 levels in lung disease

  • decreased in bronchiolar lavage
  • increased in blood
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21
Q

What forms the air-blood barrier?

A

Type I pneumocyte, fused basal laminal, endothelial cell

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22
Q

Type II pneumocytes

  • morphology
  • produce (from which specific part)
A
  • cuboidal

- surfactant produced in lamellar bodies

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23
Q

Emphysema vs pneumonia on histology

A

Emphysema
-destruction of alveolar walls

Pneumonia
-exudate infiltrate w/ WBCs in alveoli and enlarged capillaries

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24
Q

Positive likelihood ratio

  • equation
  • significant value
A

PLR = Sn/(1-Sp) = true positive rate/false positive rate

> 10

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25
Q

Negative likelihood ratio

  • equation
  • significant value
A

NLR = false neg rate/TN rate = (1-Sn)/Sp

<0.1

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26
Q

Which lung capacity allows the lung to stay inflated?

A

FRC

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27
Q

Describe how FRC is affected in restricted vs obstructive lung diseases

A

RV changes

Obstructive -> inc RV

Restrictive -> dec RV

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28
Q

Minute ventilation vs alveolar vent

A

Subtract out dead space for alveolar vent

Va = (Vt - Vd) x RR

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29
Q

Given constant rate of CO2 production, what determines PACO2?

A

ALVEOLAR VENTILATION

PACO2 = (VCO2 x K)/VA

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30
Q

What is located in the pre-Botzinger complex

A

respiratory pacemaker neurons which generate the respiratory rhythm

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31
Q

Compare dorsal and ventral respiratory groups

A

Both in medullary respiratory center

  1. DRG
    - dorsomedial part of medulla
    - inspiratory neurons
  2. VRG
    - ventral part of medulla
    - inspiratory AND expiratory neurons
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32
Q

Location and fx of pneumotaxic center

A
  • located in upper pons
  • turns OFF inspiration
  • limits TV and regulates RR
  • normal breathing persists in its absence
  • has an inhibitory effect on the apneustic center
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33
Q

Apneustic center

-location and fx

A
  • lower pons
  • apneustic breathing -> prolonged inspiratory gasps followed by brief expiratory movements

concurrent removal of input from the vagus nerve and the pneumotaxic center causes this pattern of breathing -> POOR PROGNOSIS

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34
Q

Orthopnea vs. playpnea

A

orthopnea -> dyspnea lying down

platypnea -> dyspnea relieved when lying down 

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35
Q

Compare central vs peripheral chemoreceptors

A

CENTRAL

  • respond to H+ (from CO2 diffusing into CNS)
  • ventral surface of medulla

PERIPHERAL

  • carotid body
  • respond mainly to O2 (< 60mmHg)
  • somewhat to CO2 and H+
  • CN IX
  • type I cells are the sensors of pO2

note: do NOT respond to dec in O2 bound to Hb; only to changes in O2 TENSION
- anemia
- CO poisoning

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36
Q

Effect of chronic exposure to low pO2 on carotid body

A

HYPERTROPHY

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37
Q

List 3 effects of acute exposure to high altitude
-effect on the brain?

Acclimatization after several hours - weeks

A

ACUTE

hypoxemia -> hyperventilation

  • hypoxia
  • hypocapnia
  • respiratory alkalosis -> inhibits central chemoreceptors (low H+) -> cerebral vasoconstriction -> cerebral hypoperfusion -> CNS impairment

-one of the hallmarks of severe altitude sickness is loss of balance and coordination

Mechanism of cerebral vasoconstriction

  • direct effect of high pH -> constriction of blood vessels
  • low H+ -> more binding of Ca+ to albumin -> hypocalcemia -> cell membrane instability -> vasoconstriction + parasthesia)

ACCLIMATIZATION

  • renal comp of resp alk (w/in a day)
  • erythropoiesis (3-5 days)
  • reduction of bicarb in CSF
  • stabilization of CV parameters
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38
Q

Long term high altitude exposure on pulmonary blood flow

-consequences?

A

Inc pulm resistance -> inc pulm artery pressure -> RVH

-inc in pulmonary resistance due to hypoxia induced vasoconstriction

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39
Q

High altitude pulmonary edema through to be due to

A

high altitude pulm HTN + idiopathic non-inflammatory inc in permeability of vascular endothelium

-genetic predisposition

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40
Q

Describe the mech by which HIFs work

  • degradation
  • maintenance
A

HIFs are constantly being produced but immediately broken down under normal pO2

  1. Under normal O2 levels
    - O2 dependent degradation domain (ODDD) is hydroxylated at the proline (using proline hydroxylase)
    - ODDD + VHL polyubiquinate HIFs -> targeted for degradation by proteasomes

-backup mech to block HIF action -> asparagine hydroxylation (using FIH) -> prevent HIF from interacting at its domain

Hypoxemia

  • none of the above occur and HIFs can act at their target sites to reverse hypoxic conditions
  • PHD and FIH activity will be LOW
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41
Q

Diving physiology

  • Pressure inc by 1 atm for how many feet deep
  • what effects does this have on gasses and breathing?
  • nitrogen
A 
1 atm (760 mmHg) pressure inc for every 33 ft
-makes sure to add this to sea level atm = 1 atm

Effects

  • partial pressure of each gas inc
  • density and viscosity inc as well
  • inc pressure -> diminished volume of lungs -> inc resistance of airways -> harder to breathe

Nitrogen

  1. dissolves mainly in fat tissue -> compression sickness upon rapid ascent
  2. narcosis -> at depth of > 100 ft
    - CNS problems -> euphoria, memory loss, irrational behavior
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42
Q

Heliox

A
  • 21% O2 and 78% He
  • causes more laminar flow -> reduced resistance -> easier to breath
  • does not dissolve in tissue as much as N2

CNS
-HPNS -> tremor, nausea, vomiting, dizziness

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43
Q

Elastic recoil properties of lung are due to?

A

elastin and collagen in lung tissue

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44
Q

Compare accessory muscles for inspiration vs expiration

A

Inspiration

  • external intercostals
  • SCM
  • scalenes

Expiration

  • abdominal
  • internal intercostal
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45
Q

Transmural pressure in the lung defined as

A

Difference b/w intralveolar and intrapleural pressures

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46
Q

Define compliance

  • measures
  • inversely related to
  • is the slope of the
  • compare compliance at apex vs base
  • compare compliance in emphysema vs fibrosis and how this related to functional residual capacity
A

C = V/P

  • P is the TRANSMURAL PRESSURE
  • measures the distensibility of the lungs and chest wall
  • inversely related to elastance (elastic tissue)
  • slope of pressure-volume curve
  • apex this is why ventilation is better at the base (slinky analogy)
  • Emphysema -> INC compliance -> collapsing tendency of lung is less than expanding tendency of chest wall at FRC -> compensatory inc in FRC to balance forces -> barrel chest
  • Fibrosis -> DEC compliance -> collapsing tendency of lung is greater than expanding tendency of chest wall at FRC -> compensatory DECREASE in FRC to balance forces
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47
Q

Lymphangioleiomyomatosis (LAM)

  • population
  • associated with?
  • can cause?
  • tx?
A
  • rare
  • women of childbearing age
  • sporadic or w/ tuberosclerosis complex
  • 50% w/ LAM -> pneumothorax
  • multiple lung cysts
  • tx -> lung transplant
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48
Q

Birt-Hogg Dube syndrome

  • mutation
  • inheritance
  • causes what?
A
  • mutation in folliculin gene (FLCN)
  • autosomal dominant
  • folliculomas on cheeks, chest and back
  • lung cysts and spontaneous pneumothorax
  • kidney tumors
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49
Q

Why do COPD patients expire through pursed lips?

A

COPD -> loss of elastic fibers -> decreased elastic recoil of lung -> intraalveolar pressure can become lower than intrapleural pressure -> negative transmural pressure -> lung collapse

-pursing the lips -> slow expiration -> inc airway pressure to counteract negative transmural pressure -> less resistance to expiration

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50
Q

Compare compliance of lung during expiration vs inspiration

what explains this phenomenon

A

Remember C=V/P

For a given pressure, lung volume is greater during expiration

  • concept of hysteresis
  • due to presence of surface forces at the air-liquid interface in the alveolus
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51
Q

Law of LaPlace states that?

A

P = 2T/R

p = collapsing pressure of alveolus (or pressure required to keep it open)

t = surface tension

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52
Q

Surfactant production

  • which cells
  • when
  • most important component
  • which ratio is checked for adequate surfactant production
  • effect on compliance
  • effect on transudation of fluid into alveoli
A
  • type II cells
  • 24-35 gestational week
  • dipalmitoyl phosphatidylcholine (DPCC) -> amphipathic -> hydrophobic components repel each other
  • lecithin:sphingomyelin > 2:1
  • INCREASES compliance
  • PREVENTS transudation of fluid into the alveoli
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53
Q

Tx for neonatal respiratory distress syndrome?

effect on V/Q?

A
  • artificial surfactant
  • air enriched in O2
  • maternal steroids before birth

-DECREASED V/Q

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54
Q

Where in the respiratory tract is laminar air flow MOST likely to occur? why?

A

TERMINAL BRONCHIOLES

  • low flow of air
  • large cross sectional area (parallel arrangement -> dec resistance)
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55
Q

The major site of airway resistance is at the?

A

MEDIUM-SIZED SEGMENTAL BRONCHI

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56
Q

ANS effect on bronchial smooth muscle

A

Sympathetic b2 adrenergic agonists -> bronchodilation

PNS -> acetylcholine -> bronchoconstriction

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57
Q

Lung volume and airway resistance relationship

-apply this to asthma

A

Inverse relationship

asthma -> airway constriction -> compensatory inc lung volume (similar to emphysema) -> helps keep airways open

58
Q

Diffusion vs perfusion limited

  • separate by gases
  • compare maintenance of gradient of partial pressure
A

Diffusion limited

  • CO -> immediately binds to Hb and very little is dissolved in blood
  • O2 (only in fibrosis and emphysema)
  • CO2 (disease states)
  • gas does NOT equilibrate by the time blood reaches end of capillary -> gradient is maintained

Perfusion limited

  • N2O = ideal example
  • O2 (normal health) -> equilibrates at about 1/3 length of capillary
  • CO2 -> also equilibrates at 1/3 length
  • gradient NOT maintained and equilibrium is reached
  • diffusion can be increased by increasing blood flow (perfusion)
59
Q

Compare O2 and CO2 in terms of solubility and diffusion

-implications with regards to pathology?

A

CO2 24x more soluble in water and diffuses 20x faster

  • pressure difference also smaller for CO2
  • CO2 also undergoes chemical modification

implication -> Pathological conditions will have much bigger impact on O2 than CO2 diffusion

60
Q

Which lung volume is most representative of alveolar air after diffusion is complete?

A

ERV - end of forced expiration

61
Q

List 3 categories of conditions that dec diffusing capacity of lung

A
  1. Thickening of barrier
    - edema
    - fibrosis
    - sarcoidosis
    - scleroderma
  2. Dec surface area
    - emphysema
    - tumor
    - low CO
    - low pulm capillary blood volume
  3. Dec uptake of O2 by blood
    - anemia
    - low pulm blood flow
62
Q

Diffusion equation

A

Vgas = (Area/thickness) x Dk(P1 - P2)

Area dec in emphysema
thickness inc in fibrosis

Dk(P1 - P2) -> difference in partial pressures

63
Q

Effect of exercise on diffusing capacity

A

INCREASES IT -> opening of dormant pulmonary capillaries

better V/Q match

64
Q

Diffusing capacity of CO, O2 and CO2 under normal conditions

A

CO - 25 ml/min/mm Hg

O2 - 21 ml/min/mm Hg

CO2 - 420 ml/min/mm Hg (20x higher diffusing capacity than O2)

65
Q

Primary cause of pulmonary edema

A

INCREASED CAPILLARY HYDROSTATIC PRESSURE

-fluid can get in interstitium or alveoli

66
Q

Normal O2 binding capacity (show calculation)

A

20.1 ml O2/100 ml blood

15g Hb/100ml) x (1.34 ml O2/g Hb

67
Q

How much O2 is dissolved in the blood (show calculation)?

A
  1. 3 ml O2/100 ml
  2. 003 ml O2/100 ml blood/1 mmHg

100 mmHg = pO2 of arterial blood

68
Q

Define P50 for Hb

A

P50 = pO2 at which Hb is 50% saturated

25mmHg under normal conditions

69
Q

Factors affecting oxygen-Hb dissociation curve

A

Increasing all the following cause a right shift (dec affinity) -> p50 is INCREASED

C - CO2
A - acid (H+)
D - 2,3-DPG (inc production at high altitude)
-binds to beta chain in Hb dec affinity for O2
-HbF lacks binding site for 2,3-DPG (no beta chain)
E - exercise
T - temperature

70
Q

Describe the haldane effect

A

deoxy form of Hb is better H+ acceptor than oxy Hb

in lungs -> oxygenation of Hb -> dissociation of H+ from Hb -> CO2 released for expiration

71
Q

3 ways in which CO2 is transported

A
  1. HCO3 - (90%)
  2. Carbamino-Hb (5%)
    - bound to N terminus of GLOBIN (not heme)
  3. dissolved CO2 (5%)
72
Q

What 2 effects does CO have on O2 binding to Hb

A
  1. Dec O2 binding capacity of Hb (dec % O2 sat of Hb)

2. Shifts dissociation curve to the left

73
Q

Hyperbaric O2 works by increasing which aspect of O2 content?

A

Dissolved O2

74
Q

Equation for pulmonary vascular resistance

A

[P(pulm artery) - P(left atrium)]/Cardiac output

Left atrial pressure = PWP

75
Q

Natural shunting is due to

A

-venous blood from bronchial and cardiac veins delivering blood to left heart

Around 2%

76
Q

Ruler to assess readiness, confidence and importance of behavior change

A

1-2: Pre-contemplation
3-4: Contemplation
5-6: Preparation
>7: Action - IMPORTANT

77
Q

READS skill of MI

-useful for?

A 
R: Roll with Resistance 
E: Express Empathy
A: Avoid Argumentation 
D: Develop Dissonance 
S: Support self-efficacy

Useful to navigate AMBIVALENCE

78
Q

OARS skill of MI

A

O: Open-ended questions
A: Affirmations -> “I’m glad you’re here today”
R: Reflective Listening
S: Summarizations

79
Q

List 5 types of reflective statements

A

 Content: direct restatement of what the person said

 Meaning: Making a guess about the meaning behind the statement

 Feeling: Making a guess about the feeling behind the statement

 Amplification: Overstates what the person says

 Double sided reflection: Captures both sides- dissonance

80
Q

SMART goals

A 
 Specific
 Measurable
 Achievable
 Related directly to the goal 
 Time Specific
81
Q

How can you tell an interstitial lung disease from a neuromuscular disease?

A

ILD

  • low TLD (restrictive)
  • low DLCO

NM disease

  • low TLC
  • NORMAL DLCO
82
Q

Isolated DLCO w/ no other PFT abnormality may signal

A

pulmonary vascular disease (e.g. pulmonary HTN)

83
Q

Describe the flow-volume loops for the following

  • normal
  • mild to moderate obstruction
  • mild restriction
A

NORMAL
-straight even slope

OBSTRUCTION
-concave scooping

RESTRICTION

  • high peak
  • steep slope
84
Q

Downside of lung dilution technique and plethysmography

A

Lung dilution

  • underestimates FRC inpatients with severe airway disease (ventilation distribution is poor)
  • N2 uNderestimates lung volume

Plethysmography
-measures all intrathoracic gas regardless of whether it is communicated w/ airways

85
Q

List 5 things that decrease DLCO

A
  1. Loss of surface area
  2. Dec blood vol
  3. inc diffusion distance
  4. dec Hb
86
Q

Ballpark values for assessing severity of lung defects

A 
High: 120%+
Normal: 80 - 120
Mild: 65 - 80
Moderate: 50 - 65
Severe: <50
87
Q

FEV1/FVC ratio to use when LLN not give?

when it is give?

A

0.7

> 75% LLN

88
Q

What’s the cutoff for a good bronchodilator response?

A

12% and 200ml inc in either FEV1 or FVC

89
Q

Low FVC w/ normal FEV1/FVC indicates? must confirm with?

A

Restrictive disease

confirm with lung volume

90
Q

Define pseudorestriction

A

Dec FEV1 and FVC due to increase in RV

  • can confirm this by checking TLC
  • seen in obstructive pathologies
91
Q

Flattening of both inspiratory and expiratory limbs of FVL indicates?

A

fixed upper airways obstruction

e.g. tracheal stenosis due to long term tracheostomy tube

92
Q

Criteria for giving Oxygen

A

O2 sat 88% or below

OR

PaO2 on ABG of 55 or lower

93
Q

With normal CXR, 90% of cough is 1 of the following:

-list 3

A

Asthma
GERD
Allergic rhinitis (hay fever)

94
Q

Most common cause of hemoptysis

A

acute bronchitis

-often streaked sputum

95
Q

Ideal position of an endotracheal tube tip

  • relative to carina?
  • if carina not visualized?
A

in the trachea 5cm +/- 2 cm above the carina

If carina not seen -> T3 or T4 vertebral body

Carina at T5, T6, or T7 level in > 90% of patients

96
Q

What shape should the aortic pulmonic window be?

A

CONCAVE

97
Q

Compare pulmonary artery to main bronchus on right and left side

A

LEFT
-PA arches up over the left main bronchus

RIGHT
-PA course in front of and below the right main bronchus

98
Q

List 3 signs of air space consolidation

A
  1. Air space opacity is poorly marginated except where is abuts the pleura (e.g. fissure)
  2. Air Bronchograms: A pattern of air-filled (low-attenuation) bronchi on a background of opaque (soft tissue attenuation) airless lung
    - normally can’t separate out bronchi from aerated lung farther out from hila b/c bronchi are too thin
  3. It obscures adjacent vessels
99
Q

Silhouette sign is useful for?

A

localizing disease w/in chest

which lobe?

100
Q

Blunting of costophrenic angle is classic sign of?

A

pleural effusion

101
Q

Which views of CXR is MOST sensitive for picking up a pleural effusion?

A

LATERAL DECUBITUS VIEW
-only 10 ml of fluid needed for blunting of CP angles

LATERAL VIEW is next best

FRONTAL VIEW is the worst

102
Q

Which type of pleural fluid can appear like a tumor (pseudotumor)
-how to tell apart?

A

Loculated interlobar pleural fluid

-lenticular tapering shape is clue that it’s not a tumah

103
Q

Presence of deep sulcus in supine patient indicates?

A

pneumothorax

104
Q

Tension pneumothorax

  • trachea
  • diaphragm
A

trachea shifts to opposite side

diaphragm pushed down

105
Q

3 most common origins of pulmonary thromboembolism

A
  1. deep veins of legs > 95%
  2. pelvic veins
  3. upper extremities w/ IV access <10%
106
Q

Virchow’s triad

A
  1. hypercoagulability
  2. Endothelial damage
  3. venous stasis
107
Q

Most common sign and sx of pulmonary thromboembolism

A

Sx - dyspnea

Sign - tachypnea

108
Q
  1. When should thrombolysis be used to tx pulmonary thromboembolism?
  2. When should IVC filter be used?
A
  1. only for hemodynamically unstable patients
    - massive/life threatening PE
    - huge risk of severe bleeding
  2. IVC filter only when anticoag is contraindicated or failed
109
Q

Chronic PE

  • risk of development following acute PE?
  • optimal management?
  • end result if not tx?
  • marker for poor prognosis?
  • gold standard for dx? other imaging?
A

1% - clot doesn’t dissolve
-fibrin not being deposited properly

surgery!!!
-medications don’t work

pulmonary HTN and right ventricular failure
-vascular changes in small peripheral resistance vessels throughout the lung

mPAP greater than or to 30mmHg -> poor prognosis
-5 year survival only 10% with mPAP >50mmHg

V/Q scan = gold standard

  • multiple segmental defects
  • pulmonary angiogram also need to be done
110
Q

Basic morphology for Wegener’s

Classic triad

A

Morphology

  • vasculitis -> lymphocytes
  • parenchymal necrosis
  • granulomatous inflammation -> large macrophages and lymphocytes surround necrotic area

Classic triad

  • lungs (lower respiratory tract)
  • upper respiratory tract
  • kidney (glomerulonephritis)
111
Q

Tx for Wegener’s?

A

Cyclophosphamide/azithoprine or corticosteroids

112
Q

What’s done to make a diagnosis of alveolar hemorrhage

A

Sequential bronchoalveolar lavage

-increasingly bloody lavage is diagnostic

113
Q

Idiopathic pulmonary hemosiderosis

  • population
  • associated with
  • bx will show
A

–Primarily a pediatric disease (>80%)

–Associated with celiac disease and elevated IgA in 50% of patients

–Biopsy with bland hemorrhage; no immune complexes

114
Q

Initial tx for Goodpasture syndrome, vasculitis, capillaritis and connective tissue disease

A

pulses w/ high dose steroids

-can use plasma exchange afterwards for goodpasture’s

115
Q

Dx for pulmonary HTN requires mPAP of

A

Greater than or equal to 25

116
Q

How is PH dxed?

A

Right heart cath showing elevated pulmonary pressures

117
Q

What histological characteristic is present in all of the following:

IPAH
HPAH
unrepaired congential heart disease
drug and HIV associated PH

A

PLEXOGENIC PULMONARY ARTERIOPATHY

  • looks like a glomerulus
  • vessel trying to recanalize itself
•  Intraluminal
capillary networks
•  Dilated vessels
•  Thrombosis
•  Recanalization
118
Q

Heritable PAH mutation

A

70% have BMPR2 mutation - TFG-beta receptor family

119
Q

List 2 major classes of associated PAH

A
  1. Conn tissue diseases
    - scleroderma -> MUST SCREEN
    - RA
    - SLE
  2. Congenital systemic pulmonary shunts
    - sheer stress due to left to right shunt
    - eventually reversed to right to left shunt
120
Q

WHO classification for pulmonary HTN

A

I - PAH

II - left heart disease

III - lung disease and/or hypoxia

IV - chronic thromboembolic pulmonary HTN

V - unclear multifactorial mechanisms

121
Q

Tx for PH includes (list 4)

A
  • oral anticoagulant tx
  • diuretics
  • oxygen -> Keep sat >90%
  • inotropic agents (digoxin)
122
Q

3 endogenous pathways that can be altered for vasodilator tx in patients w/ NEGATIVE vasoreactivity trials

A
  1. Endothelin
    - powerful vasoconstrictor
    - can block it
  2. NO - vasodilator
    - give extra
    - block breakdown of cGMP (viagra = PDE inhibitor)
    - turn on adenylate cyclase
  3. Prostacyclin
    - inc
123
Q

Which class of drugs are associated with PAH?

A

STIMULANTS (meth, cocaine, fat burners etc.)

124
Q

What’s another term for hypoxic respiratory?

What’s another term for hypercarbic resp failure?

A
  1. Oxygenation failure

2. Ventilatory failure

125
Q

Equation for oxygen delivery

A

DO2 = CO x oxygen content

= CO x 1.34Hb x O2sat + (PaO2 x 0.003)

126
Q

What causes elevated DLCO

A

alveolar hemorrhage

127
Q

ARDS presentation and imaging

A

RAPID ONSET
-dyspnea and tachypnea

SEVERE HYPOXEMIA
-refractory to O2 tx

DIFFUSE PULMONARY INFILTRATES
-seen on CXR

HIGH MORTALITY

128
Q

Which cells undergo hyperplasia in the proliferative/organization phase of diffuse alveolar damage?

A

TII pneumocytes

129
Q

Cryptogenic organizing pneumonia is responsive to?

-how does it present?

A

STEROIDS

-acute onset of cough, dyspnea, fever and malaise

130
Q

Describe histology of organizing pneumonia

-acute or subacute?

A

fibroblastic plugs w/in bronchioles, alveolar ducts and alveoli

patch distribution

SUBACUTE

131
Q

minute ventilation (VA) is proporiton to?

A

VCO2/PaCO2

132
Q

List 5 causes of hypoxic resp failure

A

VDASH

V/Q mismatch
Diffusion limitation
Altitude/low PbO2
Shunt
Hypoventilation
133
Q

List 4 causes of hypercapnic resp failure

A

asthma
COPD
Neuromuscular disease
Narcotic/drug overdose

134
Q

Most useful method for measuring adherence in clinical setting?

A

Patient questionnaires; self-report

135
Q

Most efficacious interventions for promoting adherence have what to components?

A

Behavioral AND Educational

136
Q

Calculation for serum osmolality

A

2Na(mEq/L) + urea(mg/dL)/2.8 + glucose(mg/dL)/18

137
Q

Vaptan

  • mech
  • indication
A
  • interferes with action at the vasopressin receptors
  • used in the treatment of hyponatremia, especially in patients with congestive heart failure, liver cirrhosis or SIADH

CAUSE AQUARESIS

138
Q

Normal total body Na and K

A

Na - 1960mEq (14L)

K - 3820mEq (28L)

Total = 5880mEq

139
Q

luke compensation mech

A

met acid
met alk
resp acid
resp alk

10->12
10->6
10->4
10->4

140
Q

Milk-alkali syndrome is due to?

A

Too much vit D and Ca supplementation

Renal-Pulm (9 decks)

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