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Platelet and Bleeding Disorders > Week 7 > Flashcards

Week 7 Flashcards

1
Q

environmental history

A 
Activities
community
household
hobbies 
occupation
oral behaviors
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2
Q

Why are fetus/children most vulnerable?

A 
toxins cross placenta
rapid state of growht/development
different absorption, metabolism
unique habits/eat and drink, breathe faster
longer life span
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3
Q

Restrictive lung disease

A

reduction in TLC on PFTS from Lung disease that result in decreased compliance (decreased volumes) and extra pulmonary restriction limiting ability to generate negative pleural pressure

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4
Q

Restriction due to lung disease

A

Lower compliant lungs (at any given pressure, lung volume will be less)
less compliant chest wall (any given pressure, lung volume less)
weakness (lower maximal inspiratory pressure-going to have a lower TLC)

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5
Q

Restrictive lung disease PFTS CW

A

lower TLC, lower RV, normal/low DLCO (lungs are fine)

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6
Q

Restrictive lung disease lung parenchyma

A

lower TLC, lower RV, super low DLCO

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7
Q

Restrictive lung disease muscle weakness

A

lower TLC, higher RV (hard to blow air out), normal DLCO

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8
Q

Extrapulmonary causes of restrictive lung disease

A

Chest wall (obesity), pleural disease, neuromuscular weakness

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9
Q

Pulmonary causes of restrictive lung disease

A

Pulmonary edema, cardiogenic edema, pneumonia, lung injury/inflammation, ILD

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10
Q

Pneumonia

A

infection in pulmonary parenchyma–initiates inflammatory response

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11
Q

Pneumonia histology

A
  1. alveolar lumens filled with neutrophils and macrophages
  2. congested capillaries
  3. thickened alveolar walls
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12
Q

Pneumonia causes

A

lower compliance lung from loss of aerated lung (exudate), atelectatic units, flood alveolar units (less participation in ventilation

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13
Q

Lung inflammation causes

A
  1. autoimmune (lupus, scleroderma, rheumatoid arthritis)
  2. injury (aspiration, noxious inhalation, trauma)
  3. meds (methotrexate, blemycin, nitrofurantoin, amiodarone)
  4. hypersensitivity pneumonitis
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14
Q

Lung inflammation results in

A
  1. widened alveolar septa
  2. increased elastic recoil forces (compliance decreases)
  3. increased work of breathing
  4. loss of alveolar/capillary units (obliterate capillary)
  5. hypoxemia
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15
Q

Cardiogenic pulmonary edema pathophysiology (Restrictive lung disease)

A

Rising capillary hydrostatic forces cause:

  1. increase in interestitial edema
  2. overwhelm lymphatic drainage
  3. development of alveolar edema

**fluid is transudative (low protein, low cells)

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16
Q

Cardiogenic pulmonary edema results in

A
  1. decreased compliance (interstitial water, flood alveolar units-no ventilation similar to pneumonia)
  2. hypoxemia
  3. activation of alveolar stretch receptors (J)-respond to increased interstitial fluid and stimulate ventilation (RR)
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17
Q

ARDS (pulmonary edema due to damage to alveolar capillary membrane)

A

low pressure pulmonary edema-acute respiratory failure

  1. injury and disruption of membrane
  2. alveolar flooding with protein rich exudate
  3. severe hypoxemia
  4. reduced lung compliance
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18
Q

Berlin definition ARDS

A

acute: within one week of known clinical insult
bilateral pulmonary infiltrates on CXR/CT
non cardiac reasons
hypoxemia P:F <300

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19
Q

P:F ratio

A

ratio of PaO2 to FiO2, lower means worse oxygenation

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20
Q

ARDS pathophysiology (acute)

A

initial injury to capillary endothelium/and or alveolar epithelium–leak alveolar capillary units and elaboration of protein rich cell rich exudates into alveolar space. Results in intense inflammatory reaction and deactivation of surfactant

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21
Q

ARDS and Diffuse alveolar damage DAD

A
  1. alveolar septal thickening (edema and inflammation)
  2. hyaline membranes (proteinacious deposits in alveolar spaces, results from fibrin rich exudative fluid and necrotic epithelial cells )
  3. Type II cell hyperplasia to attempt repair
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22
Q

Hypoxemia in ARDS

A

low PaO2
higher PAO2–leads to large Aa gradient
slight respiratory alkalosis (low PCO2, high pH) due to stimulation of ventilation from J receptors

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23
Q

Acute hypoxemia respiratory failure AHRF in ARDS

A 
airspace flooding (edema, pus, blood in alveoli)
intrapulmonary shunt physiology-refractory to oxygen supplementation
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24
Q

ARDS causes

A
  1. decreased lung compliance from flood and collapsed alveolar units 9surfactant dysfunction)
  2. interstitial edema/inflammation
  3. difficulty inflating/ventilating, loss of ventilated alveoli leads to over dissension and barotrauma
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25
Q

ARDS pathophysiology chronic

A
  1. fibroproliferative phase: fibroblast proliferation and collagen deposition (scarring), Type II epithelial cell proliferation for repair, iniate resorption of exudate

Survivors: full reepitheliazation, endothelial restoration, resolution of scar formation (over months)

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26
Q

ARDS management

A

supportive care
lung protective ventilator strategy (low tidal volumes, permissive hypercapnia, limit alveolar distending pressure <30 cm H20, non toxic FiO2

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27
Q

Interstitial lung disease

A

disorders predominately affecting the interstitial space of the lung
primarily affects the lung parenchyma (alveolar/capillary units) with inflammation, fibrosis, architectural distortion

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28
Q

Common pathophysiology of ILDs

A
  1. accumulation of inflammation and connective tissue in alveolar interstitial spaces of lung which causes

increased elastic recoil (low TLC, FRC ,RV)
destruction of alveolar/capillary gas surfaces (low DLCO and high Aa gradient)
thickening of alveolar capillary interface (diffusion limitation and exercise induced hypoxemia

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29
Q

Clinical findings in ILDs

A 
dyspnea on exertion
fatigue
non productive paroxysmal cough
abnormal breath sounds (inspiratory crackles)
abnormal CXR CT (interstitial opacities)
hypoxemia
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30
Q

ILDs Idiopathic pulmonary fibrosis

A

most common form of idiopathic interstitial pneumonia

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31
Q

Idiopathic pulmonary fibrosis pathophysiology

A
  1. induction of lung injury
  2. tissue injury and response (inflammation)
  3. abnormal wound healing
  4. parenchymal fibrosis and architectural distortion
    leads to decreased SA, VQ mismatch, hypoxemia, and breathlessness
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32
Q

Clubbing

A

seen in IPF, asbestosis, lung cancer, CF, less common in COPD

due to growth factors such as VEGf, PDGF

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33
Q

IPF diagnosis

A

usually 50+ age

  1. exclude other causes (drug, environment, collage vascular disease)
  2. exam shows inspiratory crackles and clubbed digits
  3. UIP radiographic patern
  4. PFTs show restriction, reduction in DLCO
  5. surgical biopsy shows UIP
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34
Q

Usual Interstitial Pneumonia

A

irregular reticular lines (diffuse)
sub pleural, posterior, lower lobe predominance
sub pleural honeycombing
interlobular septa thickened by scarring
some normal areas of lung (heterogeneity)
loss of normal lung architecture/distortion

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35
Q

Acute exacerbation of IPF

A

acute SOB, new radiographic infiltrate, worsening gas exchange and no evidence of other causes (infection, HF, thromboembolism pneumothorax)

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36
Q

Disease course is variable in IPF

A

some people have faster progression than others, some have more exacerbations etc

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37
Q

IPF management

A

pirfenidone and nintedanib (inhibit fibrogenic pathways)
pulmonary rehab
supplemental O2
lung transplant for eligible patients

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38
Q

Pneumoconioses

A

accumulation of dust in lungs and the tissue reactions to its presence

results in nodular fibrosis and diffuse fibrosis

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39
Q

Abestos exposure

A

plumbing, sheet metal, shipbuilding, dockworkers, remodeling/demolition, mining, soils

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40
Q

Abestos related thoracic disease

A

Pleural disease: pleural plaques, benign asbestos pleural effusion, rounded atelectasis

malignant mesothelioma
bronchogenic carcinoma (asbestosis and smoking)
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41
Q

Abestosis pathophysiolgy

A

fibers are persistent and active-can lead to oxygen free radicals which injury tissue and slowly leads to fibrosis

long latency >20 years

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42
Q

Abestosis diagnosis

A 
reliable history (exposure and latency)
evidence of interstitial lung fibrosis (crackles, clubbing,  certified B reader for CT/CXR)
absence of other causes
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43
Q

Abestosis Chest CT

A

peripheral and basilar intersititial fibrosis and honeycombing (like UIP)

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44
Q

ferruginous bodies

A

asbestos coated fiber with iron, engulfed by macrophage, but they are rare, not required for dx

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45
Q

Benigng abestos pleural effusion BAPE

A

one of the first things to occur-short latency, not a precursor for mesothelioma. often bloody and eosinophilic, typically resolves

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46
Q

hyaline pleura plaques

A

most common CXR abnormality
usually asymptomatic
discrete areas of fibrosis/thickening of parietal pleura

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47
Q

rounded atelectasis secondary to pleural adhesions

A

usually asymptomatic comet tail sign on chest CT

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48
Q

Malignant mesothelioma

A

rare tumor from pleural or parietal mesothelium forming a mass or rind with associated effusion, not related to tobacco use. poor prognosis (6-18 mo)

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49
Q

Primary lung cancer

A

abestosis and smoking-need to quit smoking

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50
Q

Silicosis

A

inhaled and poorly cleared from UPPER lung zones

chronic-upper lung nodules and mediastinal lymph nodes (egg shell calcifications)

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51
Q

Acute silicosis

A

short term high intensity exposure with latency of weeks to months
dyspnea, cough fatigue, alveolar filling with exude

52
Q

Chronic silicosis

A

chronic exposure >5 years, latency >20 years, upper lobe nodules and egg shell calcifications of mediastinal lymph nodes

results in upper lobe fibrosis, restriction on PFT, dyspnea on exertion, progressive massive fibrosis

complicated by mycobacterial infections (TB), cor pulmonale, malignancy

53
Q

Progressive massive fibrosis

A

found in chronic silicosis–basically obliterate the upper portion of the lung

54
Q

Silicosis histology

A 
pigment laden macrophages
cholesterol clefts
carbon deposits
pink collage
emphysema (associated with silicosis not sure why)
55
Q

Silicosis tx

A

no proven therapies

avoid exposure and stop smoking

56
Q

Hypersensitivity pneumonitis

A

lung disease from recurrent exposure to ORGANIC particles, smaller than 5 microns–disease in very tiny bronchioles (bronchiolcentric)

57
Q

HP antigens

A

farmer’s lung (moldy why), hot tub, pigeon breeders, humidifier lung, spelunkers, cheese washers, industrial spray painters

58
Q

Acute HP

A

rare presentation, associated with large exposure, mediated by immune complex deposition, fevers, chills, muscle aches, cough ,dyspnea, occasionally fine crackles

typically resolves on own

59
Q

Chronic HP

A

chronic repetitive small exposures, dyspnea on exertion

cough, crackles (velcro) inspiratory squeaks early during inspiratory cycle

possible fibrosis on chest CT
poor prognosis

60
Q

HP and PFTs

A

mixed obstructive/restrictive pattern
high RV
low FVC and FEV1
low FEV1/FVC

most common is isolated restrictio

61
Q

Chronic HP on imagin

A

upper lobe predominant
diffuse bilateral reticule nodular pattern
ground glass opacities
areas of air trapping

62
Q

HP with fibrosis imaging

A

honeycombing may be mid central (IN UIP IT IS LOWER AND PERIPHERAL)

63
Q

HP pathology

A

poorly formed loose granulomas centered around small airways, multinucleated giant cells, diffuse mixed interstitial inflammation

64
Q

HP dx

A
  1. known exposure to inciting antigen (history, serologic IgG)
  2. compatible clinical findings (crackles, cough, SOB, wheeze, fatigue, fever and CXR/CT findings)
  3. bronchoalveolar lavage with lympocytosis
  4. positive inhalation challenge (improve with removal or worsen with re exposure)
  5. histopathology (surgical lung biopsy for granulomas and mononuclear cell infiltrate)

1,2,3 or 1,2,4 or 2,3,5

65
Q

HP tx

A

avoid exposure, corticosteroids for acute events
steroid sparing agents (mycophenolate, mofetil, azathioprine, rituximab for progressive disease
lung transplant evaluation

66
Q

Sympathetic activity

A

fight or flight, increase sweating, piloerector, send blood to muscles, pupils dilate, increase HR

67
Q

parasympathetic activity

A

rest and digest, increase salivation, increase gut acitivy, pupil constriction, decrease HR

68
Q

Sympathetic origins and path

A

T1-L2 cell bodies, short presynaptic to sympathetic chain ganglia, post ganglionic to organs and skin (glands) releasing AcH or NE.

divergence allows for faster whole body reaction

69
Q

Parasympathetic origins and path

A

brainstem and S2-S4, long pre synaptic, synapse in terminal ganglia (no divergence), organs only and Ach only

70
Q

Sympathetic preganglionic cell bodies

A

lateral horn of gray matter in T1-L2

71
Q

Sympathetic chain

A

or sympathetic trunk-runs length of ENTIRE vertebral column, contain post ganglionic cell bodies

72
Q

Communicating rami (white)

A

On ramp, have myelin, slightly more lateral, lead In to the sympathetic chain, located only on T1-L2, preganglionic only

73
Q

Communicating rami (gray)

A

off ramp, no myelin, slightly more medial, lead OUT of sympathetic chain, post ganglionic fibers only, located in ALL spinal nerves

74
Q

Splanchnic nerves

A

go to organs, exit anteriorly from sympathetic chain

75
Q

Collateral ganglia

A

house post ganglionic cell bodies that are only going to innervate organs (not skin) located on anterior surface of aorta

76
Q

autonomic plexuses

A

found in thorax and abdomen, follow blood vessels to destinations

77
Q

Sympathetic innervation

A 
T1-T3 head and salivary glands
T4-T6 heart, lungs, esophagus
T7-9 stomach liver, gall bladder, pancreas
T10-11 appendix, colon
T12-L2 rectum, bladder, uterus
78
Q

Sympathetic pathway to skin and limbs

A

Cell bodies in lateral horn–>through ventral root–>through spinal nerve–>through white rami–>synapse in sympathetic chain–>post ganglionic leaves gray ramps–>exits via dorsal or ventral rami

T1-L2

79
Q

Sympathetic pathway to thoracic organs

A

cell bodies in lateral horn–>through ventral root–>spinal nerve–>white rami–>sympathetic chain (NO SYNAPSE)–>on to the splanchnic nerve where it synapses–>post ganglionic through cardiopulmonary plexus

T1-T6

80
Q

Sympathetic pathway to abdominal organs

A

Cell bodies in lateral horn–>exit via ventral root–> through spinal nerve–>white rami–>chain ganglion (NO SYN)–>thoracic splanchnic–>synapse in collateral ganglion–>travel via autonomic plexus to abdomen

T5-T12

81
Q

Sympathetic pathway to adrenal medulla

A

cell bodies in lateral horn–>ventral root–>spinal nerve–>white rami–>ganglia–>thoracic splanchnic–>collateral ganglion–>chromatin cells (second neuron)

T8-L1

82
Q

Parasympathetic nerves

A

CN III tears snot saliva
CN VII
CN IX
CN X vagus

83
Q

Vagus nerve

A

left recurrent laryngeal, cardiopulmonary plexus (in between carina and left atrium), esophageal plexus, vagal trunks (left vagus-anterior and right vagus-posterior), autonomic plexuses to other organs

84
Q

Pelvic splanchnics

A

hind gut and pelvic organs, lateral horn of S2-S4, exitvcia ventral rami (more in HFT)

85
Q

autonomic dysreflexia

A

noxious stimuli like full bladder or bed sore causes a stress response (sympathetic)–sends up spinal cord but doesn’t get to brain due to injury. However, autonomic reflexes will cause vasoconstriction in bottom half (increase BP). high BP sensed in aorta and carotid-top half sends signal to brain to decrease HR and BP.

emrgency

86
Q

ANS myelin

A

little to none

no myelin on post synaptic cells

87
Q

Fetal circulation

A

very high pulmonary vascular resistance (low oxygen tension, low vasodilation, high vasoconstrictor) because we don’t need blood going to lungs

foramen ovale and ductus arterioles shunt blood

88
Q

Post natal circulation

A

reduction in PVR (alveolar oxygenation)

unless you have persistent pulmonary HTN of news born-PVR fails to drop

89
Q

Normal pulmonary presures

A

RA: 0-7
RV 15-25 sys or 3-12 dia
PA 15-25 sys or 8-15 dia or 10-20 mean
PAOP 8-12

90
Q

Pulmonary vascular resistance

A

PVR: mPAP-LAP/CO (x80 if doing dynes)
PVR decreases with rising CO because of recruitment and distention of capillaries

mPAP will rise with rising CO (mPAP=PVRxCO + LAP)

91
Q

as SV increases, what is effect on RV and LV

A

RV has dramatic increase in pulmonary pressure because it can’t handle the increased after load. LV is better adapted

92
Q

Hypoxic pulmonary vasoconstriction

A

ALVEOLAR (not arterial) hypoxia controls vasoconstriction

93
Q

mechanism of Hypoxic pulmonary vasoconstriction

A

small pulmonary arteries sense hypoxia and this inhibits K channels on smooth muscle cell leading to depolarization–>VCa channels let in Ca which increases myosin light chain phosphorylation and smooth muscle contraction.
inhibits perfusion to hypoxic areas and redirects to better ventilated areas

94
Q

Pulmonary vasoconstrictors

A

Hypoxia, acidosis, hypoventilation, hypercarbia

so decreased pH is going to result in greater pulmonary vasoconstriction at same PO2

95
Q

Pulmonary vasodilators

A

alkalosis, hyperventilation, oxygen, NO

96
Q

humoral mediators of pulmonary pressure (vasoconstrictor)

A

endothelin 1, thromboxane A2, serotonin, angiotensin II

97
Q

humoral mediators of pulmonary pressure (vasodilators)

A

prostaglandin I2, E2
oxygen
vasoactive intestinal peptide

98
Q

Pulmonary hypertension

A

Mean PAP>25 mmHg at rest
usually high mortality from R heart failure
dyspnea, syncope, chest pain, edema

99
Q

Causes of Pulmonary HTN

A
  1. Idiopathic Pulmonary arterial HTN
  2. left heart disease
  3. lung disease and chronic hypoxia
  4. chronic thromboembolic disease
100
Q

Idiopathic pulmonary arterial hypertension

A

intimal, medial, adventitial thickening of muscular pulmonary arteries
pulmonary artreiits
concentric onion skinning
plexiform lesions

101
Q

Pulmonary HTN due to left heart disease

A

systolic heart failure, diastolic heart failure, valvular disease, congenital anomalies of left ventricular outflow tract.

less common: restrictive pericarditis, infiltrative cardiomyopathy (sarcoid, amyloid)

left atrial enlargement/dilation results in passive venous congestion of Pulmonary veins–can lead to distension and vascular remodeling

102
Q

PHTN mechanism in left heart disease

A

passive increase in mPAP (loss of LA compliance, diastolic dysfunction, etc) leads to endothelia dysfunction, decrease NO and increase ET, vasoconstriction, decreased BNP vasodilation (further increase mPAP) which leads to vascular remodeling which may cause RV failure and death

103
Q

PH in left heart disease differentiation from PAH

A

MOST COMMON CAUSE of PHTN

differentiate via elevated left atrial pressure (PCWP)

104
Q

Tx of PHTN LH dz

A

treat the left heart disease (Stent, ace inhibitors, HF drugs, diuretics)

105
Q

PHTN due to lung disease/chronic hypoxemia

A

destroy lung parenchyma-lose vascular bed, stiffening of large pulmonary arteries, chronic hypoxia leads to medial hypertrophy and muscularizatin of small Pulmonary arteries, chronic inflammation leads to vascular remodeling

106
Q

PHTN and lung disease/hypoxemia

A

second most common cause of PHTN

typically only if you have severe disease (ILD IPF, COPD/emphysema, sleep disordered breathing

107
Q

Tx of PHTN from lung disease

A

treat underlying disease, avoid vasoconstrictors (hypoxia)

avoid vasodilators bc you will vasodilate areas that don’t ventilate well–messing with appropriate pulmonary hypoxic vasoconstriction

108
Q

Chronic thromboembolic disease

A

loss of vascular surface area due to clot, more common if recurrent PE, microvascular remodeling similar to PAH
1 in 4 have no prior history of PE
requires lifelong anticoagulation
evaluate for surgical emoblectomy

109
Q

Clinical presentation of PH

A

early-nonspecific dyspnea (60%), fatigue, chest pain, syncope
late-Right HF
nospecific labs-elevated BNP
CXR: enlarged PAs and RA/RV dilated
PFTs reduced DLCO but other will be normal

110
Q

If it is purely HTN due to right heart failure, you will not have

A

crackles

111
Q

Dx of PHTN

A

echo: primary screening test: look for PASP>35mmHg, LA/RA dilatation, tricuspid regard, RV hypertrophy, dysfunction

evaluate for cause:

  1. LFT, ANA, HIV
  2. ECHO (LHD)
  3. PFTs, overnight
  4. VQ scan

Right heart Cath is confirmatory!

112
Q

Dx of Idiopathic pulmonary arterial hypertension

A

diagnosis of exclusion
more common in females, 30-50
elevated blood pressure in pulmonary arteries can reach systemic values

113
Q

Tx of PAH

A

target the endothelin, NO, and prostacyclin pathways vasodilators and inhibition of pro proliferative response of pulmonary vasculature

114
Q

Why does RH fail in PHTN?

A

low pressure system, thin muscular wall, not as adaptable to higher strain

115
Q

Cor pulmonale

A

RV failure that develops from chronic pulmonary hypertension from pulmonary disorders
(primary pulmonary vascular problem or primary pulmonary airway/alveolar/parenchymal problem)

does not include RV failure secondary to LV failure
evidence of altered structure (hypertrophy or dilation) and impaird RV function

116
Q

Cor Pulmonale most common caues

A

COPD, pulmonary fibrosis

117
Q

Cor Pulmonale symptoms

A

progressive dyspnea, syncope, chest pain

118
Q

Cor pulmonale exam findings

A

elevated JVP, loud S2, holosystolic murmer at left lower sternal border, hepatomegaly, ascites, lower extremity edema

common cause of hospitaliztion/death

119
Q

Respiratory acidosis acute vs chronic

A

in acute: rise in PCO2 leads to small increase in HCO3, so pH decrease
in chronic: rise in PCO2 leads to large increase in HCO3, so pH normal

120
Q

Respiratory alkalosis acute vs chronic

A

in acute: fall in PCO2 leads to small decrease in HCO3, so pH is elevated
in chronic: fall in PCO2 leads to large increase in HCO#, so pH is normal

**chronic alkalosis is very uncommon

121
Q

Mild asthma attack values

A

low PaO2, low PaCO2, normal HCO3 and high pH

122
Q

Moderate asthma attack values

A

more decrease in PaO2, decrease in PaCO2, normal HCO3 and high pH

123
Q

Severe asthma attack value

A

very decreased PaO2, normal or elevated PaCO2, normal HCO3, normal or low pH

124
Q

very severe asthma attack values

A

very very low PaO2, high PaCO2, high HCO3, very low pH

125
Q

Early COPD values

A

decreased PaO2, normal or low PaCO2, Normal HCO3, normal or high pH

126
Q

Late COPD values

A

lower PaO2, high PaCO2, high HCO3, normal or low pH

127
Q

COPD exacerbation values

A

very very low PaO2, very very high PaCO2, higher HCO3, lower pH

Platelet and Bleeding Disorders (4 decks)

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