Exam 1 Flashcards
1
Q
Where do parasympathetic preganglionic neurons originate from
A
CNs 3,7,9 (dissectible) and 10 and S2, 3 and 4
2
Q
where do sympathetic preganglionic neurons originate from
A
spinal cord segments T1 to L2/3
3
Q
rami communicantes - part of what autonomic substystem, what kinds and functions
A
sympathetic
white = myelinated (carries preganglionic to sympathetic chain ganglion)
gray = unmyelinated (carries postganglionic to target organ)
4
Q
BVs get what kind of innervation and have what kind of receptors
A
sympathetic
beta 2 in skeletal muscle responds to epi (vasodilation)
alpha 1 in rest of body responds to epi/NE (vasoconstriction)
5
Q
Resistance in series equation
A
R = R1 + R2 + R3 + …
6
Q
Resistance in parallel equation
A
1/R = 1/R1 + 1/R2 + 1/R3 + …
7
Q
velocity equation (with regards to BVs)
A
V = Q/A (Q = flow rate, A = cross-sectional area)
8
Q
what percentage of blood is in veins
A
2/3
9
Q
large arteries have high ____
A
pressure
10
Q
arterioles have high _____
A
resistance
11
Q
veins have high ____
A
volume
12
Q
compliance equation
A
change in volume/change in pressure
slope of pressure to volume is compliance - stress point = end of compliance of vessel
13
Q
over 24 hours, how much plasma leaks from capillaries?
A
1 gallon
14
Q
Ohm’s law
A
Q (flow) = change in pressure/ resistance
resistance = pressure/flow
15
Q
Poiseuille’s law
A
Q = (pi x deltaP x radius^4) / (8 x L x viscosity)
think of straws
16
Q
changing radius by 15% does what to flow
A
changes flow by 50%
17
Q
is critical closing pressure higher or lower in dilated vessels (as compared to constricted ones)
A
lower in dilated (already stretched)
18
Q
anemia and gas exchange
A
anemia, lower hematocrit, lower viscosity, faster flow, not enough time for diffusion in capillaries – increased Re because increased velocity
19
Q
reynolds ratio
A
determines if you’ll get turbulence (over 1,000 when branching, over 2,000 otherwise)
Re = (diamater x density x velocity) / (viscosity)
20
Q
when you decrease diameter 2 fold, what do you do to velocity and reynold’s number
A
increase velocity 4 fold, increase Re 2 fold
21
Q
transmural pressure
A
pressure inside - outside vessel wall
22
Q
LaPlace’s equation
A
wall stress = (transmural pressure x radius) / (wall thickness)
23
Q
tension equation with respect to vessels
A
tension = wall stress x wall thickness = pressure x radius
24
Q
active congestion
A
hyperemia with inflammation - arterial active congestion - tissue becomes redder, fills with oxygenated blood, inflammation, increased blood flow
25
passive congestion
venous, when you blocked the venous return to heart, increased blood volume in vascular spaces and increased hydrostatic pressure in capillaries. deoxygenated blood, becomes hypoxic
26
acute pulmonary congestion
lots of blood, result of MI, lots of RBCs, diestended capillaries, congestion and edema
27
chronic heart failure and lung pathology
increased pressure in capillaries which rupture into alveoli, macrophages take up RBVs and contain hemosiderin (heart failure cells)
28
liver congestion
seen with right heart failure because of blood flow from portal vein to liver. hepatocyts around central vein are last to be perfused and become degenerated
29
splenic congestion
due to backup from portal vein from liver leading to splenomegaly
30
signs of inflammatory edema
redness, warmth, swelling, protein rich exudate
31
non-inflammatory edema causes
increased capillary hydrostatic pressure, decreased plasma oncotic pressure, obstruction, hypervolemic state
32
how much of sudden blood volume loss will send you into shock
40%
33
muscarinic receptors - structure, coupling, response
G-protein coupled, respond to Ach, slow response via second messenger cascade (cAMP, phospholipase C
34
M2 and M4
contracts GI SM by inhibiting AC and decreasing cAMP through Ga(i)
slows heart rate in SA node by opening I channels via hyperpolarization through K+ channels
35
M1, M3 and M5
cause ciliary muscle contraction via stimulation of phospholipase C and increasing Ca2+
36
nicotinic Ach receptors
Nn - neuronal - permeable to Na+, K+ and Ca2+
| Nm - skeletal muscle - only alpha1
37
muscarinic agonists (2) and uses
- carbachol (eye drops only - nicotinic at high doses)
- bethanechol
overcoming postoperative paralytic ileus, urinary retention and glaucoma
NOT metabolized by acetylcholinesterase
38
muscarinic antagonists (2) and uses
atropine (crosses BBB, preanesthetic for intubation)
| ipratropium (NO BBB crossing, used for COPD bronchodilation)
39
nicotinic agonists (3) and uses
trimethaphan (use for acute dissecting aortic aneurysm to rapidly control BP)
vecuronium (skeletal muscle blocker - use in surgery, reversed by neostigmine)
succinylcholine (use for rapid sequence induction endotracheal intubation, causes fasciculations, metabolized by cholinesterase - no neostigmine)
40
indirect nicotinic agonists (5) and uses
edrophonium (diagnose myasthenia gravis)
neostigmine (treat myasthenia travis, give with atropine to reduce muscarinic receptor activation)
physostigmine (used for miotic glaucoma, crosses BBB, otherwise same as neostigmine)
donepezil (treatment for alzheimers)
sarin (nerve gas, irreversible anticholinesterase)
41
botulinum toxin mechanism
binds presynaptic membrane receptor, endocytoses, cleaves SNAP-25, which is required for release, and thus blocks Ach release from cholinergic nerve
42
catecholamines list (5)
```
epinephrine
norepinephrine
isoproterenol
dopamine
dobutamine
```
43
alpha agonists
phenylephrine and ephedrine (Also beta agonist)
44
beta 2 agonists
terbutaline
| albuterol
45
heart has what kind of adrenergic recetpors
```
BETA 1 (be my number 1)
causes increased rate
```
46
BVs have what kind of receptors
all have alpha 1 for constriction, skeletal muscles have beta2 for dilation
47
what drug would you use for bronchial asthma
terbutaline (beta 2 agonist)
48
what drug would you use for cardiogenic shock
dopamine (catecholamine)
49
what drug would you use for heart failure
dobutamine (Catecholamine)
50
what drug would you use for rhinitis
phenylephrine (alpha agonist)
51
what drug would you use for hypertension
guanethidine (inverse agonist - looks like NE, gets stored in vessicles as NE gets eaten by MAO)
52
what drug would you use for angine pectoris
propranolol (Beta blocker)
53
what drug would you use for supraventricular arrhythmias
propranolol (Beta blocker)
54
feedback for NE
- alpha 2 on presynaptic provides negative feedback
- heteroreceptor PGE2 if released from another neuron will neg feedback NE release
- angiotensin receptor gives boost to NE release
55
beta 1 receptors are coupled to...
Gs - stimulates AC, increases cAMP
56
alpha 2 receptors are coupled to...
Gi - inhibitory, decreases cAMP
57
alpha 1 receptors are coupled to...
Gq, causes Ca2+ increase and PKC
58
guanethidine
used for BP
| looks like NE, gets stored in vessicle, MAO eats up NE, lowers bp because guanethidine doesn't react with receptors
59
reserpine
used for BP, no transporter needed, binds to NE transporter that brings NE into vessicle, resulting in empty vessicles and no NE release
60
MAOI
inhibits MAO, gives NE more of a chance to get stored, dumps out more NE, only trying to elevate in the brain, but also raises BP
61
amphetamine
utilizes NE transporter, looks like NE, displaces NE, gets dumped outside, can result in hypertensive crisis (facilitated exchange diffusion)
62
tyramine
get it from diet (wine, cheese, fava beans), digested by MAO, displaces NE by getting into transporter, can get hypertensive crisis if on MAOI
63
cocaine
raises dopamine levels, but not specific for dopamine and also causes hypertensive crisis by raising NE levels by blocking NE transporter
64
imipramine
does same thing as cocaine, it's a tricyclic antidepressant
65
atomoxetine
ADD med. like cocaine
66
phenylephrine
for rhinitis, agonist, works directly at alpha receptor, causes downregulation
67
isoproterenol
beta agonist, downregulates receptor
68
propranolol
beta blocker, antagoinst, upregulates receptors
69
phentolamine
alpha blocker, antagonist, upregulates receptors
70
NE likes to bind to...
the 1's - alpha 1 and beta 1
71
ISO likes to bind to...
Betas
72
E at low levels binds to...
betas
73
E at high levels binds to...
alpha 1 and betas
74
dopa at low levels binds to...
DA and beta1
75
dopa at high levels binds to...
everything
76
dobutamine at low levels binds to
beta 1 contractility
77
dobutamine at high levels binds to...
alpha 1 and beta 2
78
alpha stimulators do what and examples (2)
used for decongestion of mucous membranes, raise BP, dilate pupils, eye drops
phenylephrine and ephedrine
79
beta stimulators do what and examples (2)
stabilize mast cells, open airways (beta2), relax pregnant uterus
albuterol and terbutaline (selective beta2)
80
caffeine
resembles sympathetic receptors stimulation - accumulation of cAMP, keeps cAMP high, wakes you up (theophylline dilates bronchi)
81
where do you see lines of Zahn
large arterial and mural thrombi (white layers = platelets, dark lines = RBCs)
82
channels in SA node
I (f), Ca2+, TEA K
83
ventricular channels
voltage gated Na+, voltage gated Ca 2+, TEA K and K1
84
a type baroreceptors
react to both mean pressure increases AND rapid pressure changes
85
c type baroreceptors
react (slower) to mean pressure increases
86
trigeminal cardiac reflex
decreases HR by increasing para to heart and symp to BVs - preserve cardiac demand by slowing heart rate but constricting everywhere
87
cushing reflex
ischemia in brain - increase BP by withdrawing para, increasing symp
88
tracheal epithelium
PCC with goblet cells, brush cells with microvilli, APUD cells with basal granules, mixed serous and mucus glands
89
bronchial epithelium
same as trachael, but PCC are not as tall
90
bronchiole epithelium
have club cells (that secrete surface active materials and club cell secretory proteins that increase in blood and decrease in lavage during COPD) no cartilage, NO goblet cells, thin layer of SM
91
terminal bronchiole epithelium
less ciliated, more club, no alveoli yet
92
respiratory bronchiole epithelium
some alveoli - gas exchange can happen, ciliated cells are fewer and shorter
93
alveoli epithelium
squamous type 1 (95%) - thin, flattened, for gas exchange
cuboidal, septal type 2 cells, for synthesis and secretion of surfactant (5%)
tight junctions in between them
94
how much space is in between air space and blood?
0.1 micrometer
95
surfactant - compostiion
phospholipid protein with carbohydrate component,
made from type 2 cells combining amino acids, choline, glucose and fatty acids
96
type 2 cellular comonents
lots of SER, RER and gogli
| contain multilamellar bodies - vessicles with surfactant in them that look like plasma membrane inside them
97
atelectasis
collapse of alveoli
98
what are the rudiments that form lungs
```
respiratory diverticulum (foregut, endoderm)
splanchnic mesoderm
```
interact via reciprocal induction
99
what does splanchnic mesoderm become?
lamina propria, mural cartilate, SM, CT, BV and lymph
100
what does bone marrow make in the resp develpment
phagocytes
101
what does NCC make in resp development
APUD cells, but they may be endodermal
102
histogenesis stages of lung development
1. pseudoglandular period (5-16 weeks)
2. canalicular period (16-26 weeks)
3. terminal sac period (26-term)
4. alveolar period (32-childhood)
103
what happens in pseudoglandular period
between 5-16 weeks. terminal bronchioles, no respiratory bronchioles, no blood cell development, not viable at this age
104
what happens in canalicular period
16-26 weeks
some respiratory bronchioles, some alveolar ducts, have type 1 and type 2, possibility of gas exchange, but BVs are too far away - can't survive well
105
what happens in terminal sac period
26-term
have type 2 and alveolar sacs
BVs are close, so babies can breathe, but might have RDS early on
106
what happens in alveolar period
32-childhood
| BVs intimately related, many type 2
107
RDS - when does it happen
most common death in premature babies - severe prior to 28 weeks (Before type2 development and surfactant production)
AKA Hyaline Membrane Disease
108
presentation of babies with RDS
- cyanotic (blue)
- low pO2, high pCO2
- tachycardic
- grunting, difficulty breathing
- clavicular depression
- dense lungs on CXR
- transudate layer on alveoli because of high blood flow but no surfactant - HYALINE membrane
109
what to do to prevent premature labor
bed rest and glucocordicoids
110
why test amniotic fluids in women who might give birth prematurely
can measure surfactant production by looking at lecitin and comparing it with sphingomyelin which remains at baseline - get a ratio of L/S - higher is better
111
what to give baby who was born prematurely
right level of O2 (not too much, causes blindness), artificial surfactant in aerosol
once air gets in, type 2 will differentiate (first couple days are dicey, gets better with time)
112
accessory muscles for inspiration
sternocliedomastoid
external intercostals
scalenes
113
accessory muscles for expiration
abdominal
| internal intercostals
114
lung compliance equation
compliance = change in lung volume/ change in interpleural pressure
115
do stiff lungs have higher or lower compliance than normal
stiff lungs have reduced compliance because they take more pressure to fill a certain volume
116
hysteresis
difference seen in graphing lung inflation and deflation with air - not seen when lung is filled iwth saline - takes more pressure to inflate lung and keep it there, than it does to deflate it
117
at the beginning of inspiration - before any air enters - what is alveolar pressure and interplural pressure
alveolar pressure is atomospheric pressure, or zero, and interpleural is negative (example -5)
118
what is the transpulmonary pressure at rest
+5 --> alveolar minus pleural (0- -5 = +5)
119
what is transpulmonary pressure at the beginning of inspiration
+7.5 --> at first, alveolar dips with pleural, and creates drive for air to enter
120
what is alveolar pressure at the end of inspiration
0 again - because air has reached the alveoli
121
what happens to alveolar pressure at beginning of expiration
becomes positive, and pleural pressure becomes more postive (still negative). so pressure in alveoli is higher than in the mouth, so air moves out to equalize
122
diaphragm contraction does what to transpulmonary pressure
increases
123
diaphragm relaxation on expiration does what to transpulmonary pressure
decreases
124
what are the two factors that contribute to compliance factors of the lung
1. tissue forces (elastic properties of CT) - area above the expiratory curve
2. surface forces - area between expiratory and inspiratory curves
125
surfactant and surface tension
alters surface tension depending of volume of surface
126
pressure required to keep a sphere open
P = 2x surface T/ radius
127
surface tension in a small balloon is _____ than a large baloon
higher
128
functional residual capacity
point at which pressure from chest wall is the opposite but equal to lung pressure
129
relationship between elastic recoil and compliance
stiff rubberband has high elastance - high recoil, but low compliance
130
how many branch points before you see alveoli
16-18
131
flow equation
V = delta P/R
132
poiussel's law solving for R
R = 8 L viscosity / pi r^4
133
is resistance higher in central airways than smaller airways? or lower?
higher, because surface area is larger in smaller - resistance in parallel instead of series
134
at which level is resistance the highest?
at 4th generation of airways in conducting zone
135
what does vital capacity mean
ventilatory reserve - what we can call upon for max ventilation of the lung
136
the lower the lung volume the ______ the airway resistance, why?
higher because radius of alveoli enlarges
137
people who have narrowing of airway, such as in asthma or COPD, is it harder to get air into lungs or out of lungs?
harder to get air out because airways are narrowing even more upon expiration, so you see increase in residual volume - air trapping, that can't be pushed out at lower lung volumes
138
what controls airway smooth muscle tone
beta 2 adrenergic - dilation (helped by bronchodilator drugs)
vagus nerve cholinergic - background constriction tone
(can use anticholinergic to dilate airways)
139
equation of motion, solving for pressure
P = (volume / compliance) + (flow x resistance)
140
work of breathing equation
W = P x V
141
what is ventilation, where does it occur
bulk movement of flow of air through conducting airways. slows as it goes further down, and at terminal bronchioles, no longer bulk flow (pressure equalizes), but diffusion for gas exchange
142
what is the average tidal volume
500mL
143
what is normal breathing frequency
12-15 breaths per minute
144
what is dead space ventilation?
movement of air that never reaches repiratory airways - in anatomic dead space. first air that you expire thus has a high amount of O2 because it doesn't participate in gas exchange
145
how large is the anatomical dead space
150mL
146
how much gas in in alveoli
3000mL - takes a couple minutes for all O2 in reservoir to be depleted - allows you to hold breath without dying
147
effective alveolar ventilation equation
ventilation = frequency x alveolar inspiration
= 15 breaths/min x 350mL --- just over 5,000mL of effective alveolar ventilation each minute, which about mirrors cardiac output of 5,000mL flowing through the lung ---- ventilation is matched to perfusion
148
how to estimate someone's anatomical dead space
= lead body weight in pounds
149
tidal volume equation
VT = VD (anatomical dead space volume) + VA (alveolar volume)
150
minute ventilation equation
amount through the mouth each minute
VT x frequency = (VD x frequency) + (VA x frequency)
AKA
V(.)expired = V (.)D x V(.)A
151
what is physiological dead space, how to estimate
includes anatomical dead space plus alveoli that aren't able to exchange gas (blocked by clot etc.)
can use CO2 in the blood to calculate physiological dead space:
VD = VT x (ParterialCO2 - PexpiredCO2) / ParterialCO2
REMEMBER - when measuring Pexpired, you can't use first 150-200mL, you have to measure the alveolar expired air
152
Bohr's equation, and normal value
measures physiological dead space
VD/VT = (ParterialCO2 - PexpiredCO2) / ParterialCO2
normal range: 0.2-0.35
higher is indicative of physiological dead space increase
153
stress
something that disrupts homeostasis, pressure to adapt
154
acute stress
fight/flight/freeze - automatic and autonomic survival response that can have pathogenic processes, especially if repeated
155
chronic stress
endocrine involvement - can get long term medical effects. what causes it? subordinate status, lacking control, (discriminatory status for poverty)
156
traumatic stress
threat to survival for self or close others, threat to things that give life meaning, mix of autonomic and neuroendocrine response
157
what happens in the cortical and limbic areas with regards to stress
cortex ascribe meaning to things, and can suppress or exaggerate the emotional (limbic) stress response
158
limbic structures and stress
amygdala - tiny cluster of cells, connects to hippocampus (where working memory forms) which connects to prefrontal cortical tissues. triggers hypothalmus reflexively
hypothalmus - secretes secretoryhormones that go to pituitary which secretes stimulating hormones to end organs, cortisol feeds back and shut it down
159
chronic stress and atherosclerosis
increased floating metabolites like glucose and cholesterol - clogs up arteries
160
systemic coritsol responses (4)
increases IL-6
increases white cell count
prevents storage and mobilizes nutrients
terminate adrenergic response
161
chronic cortisol effects and disease
autoimmunity, cancer, infections, metabolism disorders (obesity, diabetes)
162
physiologic changes with traumatic stress
amygdala gets big enough to image, hippocampus shrinks, can be reversed
163
U curve
certain amount of stress is necessary for development, overwhelming stress can impede development
164
cognitive distortion
making generalized comments personal, catastrophizing events, negative prediction, underestimation of ability to cope
165
3 levels of psychological defenses
1- primative (denial of reality)
2- immature (displacement)
3- mature (realistic)
166
is denial always bad?
no, patients with denial in ICU had better outcomes - only in certain contexts
167
stress and development
early stress can make permament changes genetically and physiologically (cns and endocrine)
can increase sucseptibility to disease later on
168
stress in the elderly
more memory but less reserve
more resilient but have more stressors (loss, pain, etc.)
frailty with existing disease
allostatic load - stress that leads to wear and tear
169
homeostenosis
reserve that helps maintain homeostasis in youth declines over time
170
what determines rate of homeostenosis
```
genetics (telomer length)
environment
food
oxidative stress
aging
```
171
frailty and homeostenosis
frailty is point in homeostenosis decline at which someone becomes more at risk for illness and rapid decline
172
seratonin
modulator of NE and E and dopa in brain
173
common antidepressants
zoloft, prozac, paxil - used as antianxiety
174
functional residual capacity (FRC)
= expiratory reserve + residual volume (That can't be expired)
175
inspiratory capacity
= tidal volume + inspiratory reserve
176
vital capacity
= expiratory reserve + inspiratory capacity
177
gas dilution method
indirectly measures residual volume by finding FRC: measures the total volume by measuring change in nitrogen (using 100% O2) or amount of helium (C1 x V1 = C2 (V1 +V2))
178
body plethsmography
indirectly measures residual volume by measuring FRC -
measure changes in pressure in a box in which the patient is sitting and panting -- THIS IS more sensitive than gas dilution (Better for people with airways disease)
179
normal reserve volume percentage
25-35%
180
total lung capacity percentage in restrictive conditions (less compliance)
reduced below 80% normal lung capacity
181
flow thermister
can measure volume compartments, which shows you about compliance
182
forced vital capacity maneuver, why is it useful
volume vs time curve - measure volumes, the same as slow vital capacity maneuver, except for people with airways diseases, the added pressure of forced exhalation will cause collapse and decreased volume being exhaled as it would be in slow
183
what percentage of vital capacity will a normal person expire in 1 second doing forced vital capacity
at least 70%
184
what is midflow and what is its significance
FEF - forced expiratory flow -midflow = FEF slope measured between first quarter and 3rd quarter of forced expiration
if there's a normal ratio, but low midflow, and then give bronchodilator and the midflow increases - indicative of small airways diseases and air trapping (asthma will correct, COPD will not)
185
volume time graph for obstructive disorders
decreased vital capacity, and proportionatly lower FEV1 - around 40%
186
volume time graph for restrictive (low compliance) disorders
deceased vital capacity, proportionaly higher FEV1 - around 90%
187
flow-volume loop
measures both inspiration (Can detect upper airways issues like tracheal tumor) and expiration.
shows that max flow is right at beginning of expiration when lung is near max inflation (resistance it as its lowest and driving pressure is highest - forced maneuver)
188
why does the flow-volume loop graph taper out linearly
there is limiting flow at low lung volumes - called equal pressure point. When you have increased intrapleural pressure (with forced expiration), when that pressure is equal to the pressure within the lungs, the airway narrows, and it does so at the same point regardless of the initial intrapleural pressure - as long as it's positive with forced expiration.
189
what does flow-volume loop graph look like with obstructive disease
concavity in the taper - higher than normal resistance, airways collapse quickly (emphysema)
190
what does flow-volume loop graph look like with restrictive disease
compliance issue - like insterstitial lung disease - you see very rapid fluctuation of flow - relatively small peak and quick decline (tall steep mountain)
191
what qualifies as reversibility (asthma)
12% improvement of FEV1 and FVC and at least 200mL absolute change in these parameters
192
what is allowed deviation for normal lung volume fluctiation
20% on either direction - between 80% and 120% is okay.
193
examples of obstructive ventilitory diseases
asthma, COPD, chronic bronchitis, bronchiectasis, cystic fibrosis, emphysema
194
examples of restrictive ventilatory diseases
interstitial lung disease, chest wall disease, pleural disease, space occupying intrathoracic lesion, extra-thoracic conditions (obesity, pregnancy etc.)
195
what value is significant if obesity is the cause of the restriction?
ERV will be more reduced than others
196
diffusion of the lung test measures what
if alveolar membrane is intact or compromised (anemia can also affect these values)
197
what pO2 do you want to keep your patients above
60 - above pO2 of 60, the curve flattens out (correlates to a pulseox (hem saturation) of 90%)
198
what is the pO2 at 100% hem saturation
120
199
what is pO2 at 50% hem sat
27
200
altitude and symptoms related to hypoxia at 90% O2 sat
corresponds to altitude of 10,000ft
decreased night vision, high altitude pulmonary edema
201
altitude and symptoms related to hypoxia at 80-89% O2 sat
10,000-15,000 ft
drowsiness, poor judgement, impaired coordination and efficiency
202
altitude and symptoms related to hypoxia at 70-79% O2 sat
15,000-20,000 ft
impaired handwriting, speech, vision, memory, judgement, intellect, pain sensation
203
altitude and symptoms related to hypoxia at below 69% O2 sat
over 20,000 ft
circulatory failure, CNS failure, convulsions, cardiovascular collapse and death
204
what is pO2 change as you go from arterial side after lungs, to venous side normally (AKA after unloading in tissues)
40 (corresponds to 75% hem sat - loss of one O2 molecule into tissue)
205
left shift and O2 affinity (what are the surrounding environmental factors - pH, pCO2, temp, 2,3 DPG)
left shift = higher affinity (good in lung)
higher pH, decreased temp, less pCO2, less 2,3 DPG
206
right shift and O2 affinity (what are the surrounding environmental factors - pH, pCO2, temp, 2,3 DPG)
right shift = lower affinity (good in tissue)
decreased pH, increased temp, increased pCO2, increased 2,3 DPG
207
2,3 DPG changes slowly or fast?
slowly - has to do with altitude
208
what else moves the curve to the left (pathological)
carbon monoxide and
| methemoglobin
209
does fetal hemoglobin have higher or lower affinity - right or left shift?
left shift = higher affinity
210
acute respiratory distress syndrome - what do you see on CXR and labs
white stuff in lungs, lungs aren't efficient - right shift
pO2 is 40 (should be 90-100) in arteries is 48, pCO2 (should be around 40) pH is low
211
what should you do for this patient with ARDS immediately
give him bicarb to bring back his pH to 7.40 (is 7.20 now)
212
difference between ARDS and climbing mount everest
pO2 was 28 on top of mount everest, but pH was 7.70 (difference between ARDS is here pH is higher, left shift)
213
oxygen carrying capacity (bound to hemoglobin)
how many mL of O2 per gram of hemoglobin --- 1.39 mL
214
what is O2 solubility coefficient (dissolved in plasma)
0.0031
215
arterial O2 content equation
= (1.39[Hb] x SarterialO2) + (0.0031 x ParterialO2)
216
venous O2 content equation
= (1.39[Hb] x SvenouslO2) + (0.0031 x PvenousO2)
217
systemic oxygen delivery equation
= arterial O2 content x cardiac output x 10
218
Fick's principle for tissue O2 consumption
= cardiac output x (arterial O2 content - venous O2 content)
219
does it matter where you measure arterial O2 content?
no
220
does it matter where you measure venous O2 content?
yes - different organs require different amounts of O2, or during exercise etc.
so we measure mixed venous blood in pulmonary artery
221
what are usual values for PO2 and PCO2 in arteries
```
pO2 = 100
PCO2 = 40
```
222
what are normal values for pO2 and pCO2 in mixed venous blood
```
pO2 = 40
pCO2 = 45
```
223
extraction ratio
= O2 consumption/ O2 delivery
at rest around 20%
may rise to about 80% during exercise
224
what determines how much O2 gets exchanged in capillaries?
PO2 in cappilaries
225
what is the effect of anemia on the oxygen dissociation curve
no effect
226
what curve does anemia effect?
oxygen CONTENT curve
227
how are the anemia content curve and CO content curve similar
both start at half arterial O2 content and both have high or normal pO2
228
how are the anemia and CO content curves different
difference in how they fall - CO ends up with much lower mixed venous pO2 - CO doesn't have enough pressure to get O2 from capillary into tissue, but anemia does (not as efficient, but possible)
229
what cell does not produce CO2
RBC - no TCA cycle
230
what are the two sources of CO2?
aerobic metabolism (glucose, TCA, oxygen transport etc)
anaerobic metabolism (lactate and bicarb)
231
mechanisms of CO2 transport
1. dissolved in plasma (5%)
2. bicarbonate buffer system (85%)
- fast process in RBC (chloride shift), slow in plasma
3. bound to Hb as carbamino-Hb (10%)
232
CO2 content curve (not used clinically)
extra CO2 is released in the lungs - causes the curve to drop more than expected
233
greater the ventilation the ____ the pCO2
lower
234
an acute change of PCO2 by 10mm Hg results in reciprocal change in blood pH of _____
0.08 units
235
what's the ideal atmospheric oxygen partial pressure
160 mmHg (at sea level)
236
what's the partial pressure of water vapor in the air
47 mmHg
237
what's the real atmospheric oxygen partial pressure in DC
150 mmHg
=O2% x (Patm - Pwater)
=0.21 x (760 - 47)
238
alveolar air equation
alveolar PO2 = %O2 x (Patm - Pwater) - ParterialCO2/0.8
in DC,
= 150 - (ParterialCO2/0.8)
= 150 - (40/0.8)
= 100 mmHg
239
diffusion capacity for O2 (From alveoli to BV) equation
DLO2 = rate of O2 uptake / (PalveolarO2 - ParterialO2)
240
alveolar arterial oxygen gradient equation
alveolarPO2 - arterialPO2
241
what's an abnormal value for alveolar arterial oxygen gradient
1/2 patient's age
if larger, it's abnormal
if gradient is more than 30 it's abnormal
242
what is the ideal ratio of alveolar air ventilation to lung blood perfusion
1:1
243
what does "shunted" mean in terms ventilation/perfusion ratio
V = 0, so V/Q = 0 (will be the same as venous blood)
244
what is normal ventilation/perfusion rate
1 (because alveolar ventilaion is around 5,000, and so is cardiac output)
245
what is ventilation/perfusion rate in trachae
happens in physiological dead space. infitinty, because as much as V increases, there is no Q
246
3 zones of the lung
```
zone 1 (doens't exist in normal lung - very top, no blood flow, V/Q >>1)
zone 2 (flow depends on pressure difference between artery and arteriole, V/Q >1)
zone 3 (bottom of lung, flow depends on the difference between the artery and the vein, V/Q
```
247
most blood goes to areas of the lung with what V/Q ration
1:1
248
in what disease do you see shunting
ARDS (everything else is considered V/Q mismatch)
249
in people with lots of shunting, when you increase FiO2, what happens to the PO2
only increases a little bit
250
which has more shunting, pneumonia in lower lung, or upper lung
lower lung, because have more blood flow - more perfusion, but no ventilation because there's fluid in the way
251
how far does blood have to traverse through the alveolar capillary to exchange most of O2 and CO2
1/3
252
what pathologies do you see for asthma on histology
1. airway inflammation (eosinophils, mast cells)
2. goblet cell metaplasia
3. mucous gland hyperplasia (increase sterile, eosinophilic "allergic" mucus)
4. airway muscular hypertrophy
253
hypoxemia vs hypoxia
hypoxemia is low O2 in blood, hypoxia is low oxygenation in alveolar spaces
254
how to quantitate SM hyperresponsiveness
methylcholine challenge - increase doses, repeat spirometry, high enough methylcholine will cause SM contraction. so for asthmatics, the reaction will be super early (greater than 20% fall) because already primed
255
atopic asthma presentation/characteristics
- childhood onset
- family history
- preceded by allergic rhinitis, urticaria or eczema
- triggered by environmental antigens
- positive prick skin tests
256
intrinsic asthma presentation/characteristics
- mechanism less clear (maybe viral or air pollutants)
- more severe hyperresponsiveness and sustained
- no family history, allergic prick skin tests, normal IgE
257
respiratory viruses leading to hyperreactivity and inflammation - characteristcs of presentation
RSV and rhinovirus
- last 4 weeks
- neutrophilic response
- increased IL8, GM-CSF, RANTES
- potentiates eosinophilic airway inflammation
258
confounding conditions to asthma
sleep apnea, GERD, sinusitis, ABPA (allergic bronchopulmonary aspergillosis)
259
why are symptoms worse at night
more constricting tone at night because of circulating bronchodilators (adrenergics) are low
260
4 key symptom expressions of asthma
- daytime asthma symptoms
- how frequently you wake up at night because of symptoms
- frequency of use of short acting beta agonist
- if it's limiting daily activity
261
how long should an albuterol inhaler last?
1 year
262
what clinical findings present with pneumonia (4)
- fever
- tachypnea
- tachycardia
- consolidation on chest exam
263
what would you give for pneumonia?
oral azithromycin
264
besides CXR, what would you do for pneumo in hospitalized patients
- blood culture
- sputum gram stain and culture
- urine antigen test for pneumococcus and legionella
265
what bacterial pathogens commonly cause community acquierd pneumo (6)
- strep pneumo
- h flu
- mycoplasma pneumo
- chlamidophila pneumo
- legionella
- stauph aureas
266
what bacterial pathogens would you see in COPD patient causing pneumonia (2)
- moraxella
| - gram negative rods
267
what viruses cause penumonia
- influenza
- adenovirus
- RSV
- parainfluenza
- MERS/SARS
268
prognosis for community acquired pneumonia
```
C - confusion
U - BUN>19 mg/dL
R - RR >30/min
B - BP <90/60
65 - over 65y/o
```
score >1 = hospitalized
269
for someone who has comorbitidies or use of antibiotics in past 3 months, what do you give for pneumonia
beta lactam + macrolide (amox/clavulanate)
or respiratory quinolone
or ceftriaxone, cefotaxime or cefuroxime
270
how long do you treat community acquired pneumonia for?
7-10 days
271
reasons for lack of response to CAP treatment
resistance
wrong drug/wrong dx
comorbidities
spread to empyema or lung abcess
272
causes of acute bronchitis
viral (influenza, parainfluenza, RSV, corona, rhino, adenovirus)
nonviral (mycoplasma pneumo, chlamydophila pneumo, bordatella)
273
what can cause pharyngitis (in adult) - 5
```
group A strep
adenovirus
EBV
CMV
neisseria gonorrhoeae
diptheria
```
274
tx for antrhax
cipro and clinda
| PLUS mAb
275
what are the central rhythm generators
pons and medulla
276
what can supercede central rhythm generators
cortical influence (like in exercise, or conscious influence)
277
periperhal chemoreceptors sense mainly ____ central sense _____
O2, CO2
278
GROUPS in the medulla
dorsal and ventral respiratory group
279
dorsal group is responsible for____ and what are the outputs
inspiration
| output 12-15/min (RR) for 1-2 sec each and then ceases - to diphragm and external intercostals
280
ventral group is reponsible for ____ and what are the outputs
expiration
| output is normally silent, active during stress and heavy exercise - to abdominal and internal intercostal muscles
281
dorsal is also commonly referred to as
pacesetting center
282
apneusic center is caused by a cut at what level in brainstem/medulla/pons and is responsible for what
cut at level 2 in mid pons and vagus cut too
apneustic breathing - deep inspiration until stretch receptor -
without check by pneumotaxic center
283
what suppresses rhythmic activity in medulla
1. drugs (alchohol, benzons)
2. increased intracranial pressure
3. acute poliomyelitis
284
where are central chemoreceptors located
in retrotrapezoid nucleus (RTN) in ventral medulla
285
arterial pCO2 control over medullary respiratory center (2 varieties)
normal increase (45 mmHg) causes activation of medullary respiratory center
high increase (when pCO2 > 70-80 mmHg) in inhibits
286
relationship between O2 levels on pCO2 and ventilation curve
when hypoxic, the slope is steeper and left shifted - lowering threshold and more sensitive response
287
other factors that left-shift CO2 response curve (2)
acidosis and exercise - although those are only threshold changes, not stronger response as in hypoxia - just a left shift, no change in slope
288
factors that right-shift CO2 response curve (4)
sleep
morphine
COPD
anesthesia
289
peripheral chemoreceptors
carotid and aortic
| O2 content feedback goes through glossopharyngeal nerve (CN9) to brain
290
what are thresholds for O2 and ventilation increase
around 60mmHg
| at around 30mmHg, lower response threshold
291
effect of PCO2 on O2 ventilation curve
at increased CO2, there's a right shift - now sensative to smaller drop in O2 (instead of 60, now you start hyperventillating at 70 if you have a PCO2 of 45 instead of 40)
292
do peripheral chemoreceptors respond to partial pressure or total content of O2
Partial pressure - so they don't respond to CO poisoning or anemia - because partial pressure is the same
293
Hering-Breuer reflex
AKA inflation reflex
generated by stretch receptors in walls of bronchi and visceral pleura
protects against hyperinflation (more significant for newborns)
294
Juxtapulmonary-capillary receptrors respond to what and cause what
between alveolar wall and capilarry - C-fibers,
respond to alveolar inflammation, congestion and edema, seratonin/bradykinin or PE
activation causes rapid shallow breathing
295
peripheral proprioceptors
joints/muscles/tendons -- response to sudden pain causes apnea (also sudden cold)
-- response to prolonged pain causes hyperventilation
296
phase 1 of exercise
rapid increase - thinking about excercise - anticipation, caused by cortical input
297
what receptors does nicotine bind to
alpha4beta2
| alpha7
298
what controls addiction and craving
addiction -- activation of the MIDBRAIN REWARD PATHWAY causes increased release of DA in NUCLEUS ACCUMBENS -
craving - many centers
299
midbrain reward pathway
GLU (with presynaptic ALPHA7 receptors) input to DA neurons (with ALPHA4BETA2 receptors) in ventral tegmental area which synapses in nucleus accumbens (with ALPHA4BETA2 prsynaptic) releases DA (more release with nicotine). nucleus accumbens has pathways to prefrontal cortex - pleasure reward sensations
300
varenicline (mechanism, use, adverse)
AKA Chantix
binds to alpha4beta2 as a PARTIAL AGONIST so even at its best it's not as strong an activator as nicotine BUT it blocks nicotine's access to these receptors
success rates are the best
start 1 week prior to quit attempt
not as much craving.
but get suicidal ideation, depression, contraindicated in pregnancy and lactation
301
5 A's approach to quitting
```
ask
advise
assess
assist
arrange follow-up
```
302
beta 2 agonists
short acting = albuterol
| long acting = salmeterol
303
muscarinic agonists
short acting = ipratropium bromide
| long acting = tiotroprium
304
ideal size for particles for inhalation
2-5 micrometers
305
inhaled corticosteroids have what affect on asthma
suppress the inflammatory process - DO NOT CURE disease. don't raise the level because you can have systemic affects, add a beta2 agonist
306
mechanism of action for cotricosteroids
1) transrepression of NFkB
2) decrease production of prostaglandin/leukotriene products by inhibiting phospholipaseA2 and COX2 synthesis
3) inhibit monocyte proliferationa nd antigen presentation
4) decrease synthesis of pro-inflammaotry cytokines (IL-1, -6, TNFalpha)
307
adverse systemic effects of corticosteroids
- bone resoprtion
- skin thinning
- growth retardation
308
systemic gucocorticoids for asthma
- prednisone - short term use for asthma exacerbations not controlled by other methods
- prednisolone IV for status asthmaticus in ER
REDUCE INFLAMMATION, DO NOT BRONCHODILATE
309
3 classes of bronchodilators
- beta agonists
- muscarinic antagonists
- theophylline
310
theophyline mechanism
inhibits PDE which is the enzyme which degrades cAMP
311
what does cAMP do to airway smooth muscle
relaxes airway smooth muscle
312
what action do beta2 adrenergic agonists have? (3)
1) raise cAMP levels - relaxing SM
2) inhibit release of mast cell mediators - inhibiting leakage and improving mucociliary transport
3) increase glucocorticoid receptor nuclear transport
313
can you take LABA alone for asthma?
NO! needs to be used with corticosteroid (sometimes used alone for copd)
314
what are the SABA and LABA protptyles
albuterol and salmeterol
315
how long to SABA and LABAs last?
SABA works within 3-5 minutes and lasts 3-6 hours
LABA lasts over 12 hours
316
mechanism of action for Beta2 agonists
bind to Beta adrenergic receptor (G protein) coupled to AC, which increases cAMP causing smooth muscle relaxation
317
systemic adverse effects of beta agonists
tremors, hyperkalemia, tachycardia
318
if SABA is used more than 2 times a week, is this controlled?
no
319
muscarinic antagonist action (1)
1) decrease bronchial muscle tone and mucus secretion by blocking Ach receptor
320
do you use muscarinic agoinists in asmtha?
not usually, unless they're intolerant of beta2 agnosits
- use SAMA Ipratropium or LAMA triotropium for maintenance
321
do you use muscarinic agonists in copd
yes, blocking tone is effective
322
adverse effects of muscarinic agonists
1) dry mouth
| 2) caution in older men with prostatic hyperplasia - urinary retention (systemic effect)
323
methyxantine prototype
theophylline
324
is theophylline inhaled?
no it's oral
325
use of theophylline in COPD
can increase diaphragm muscle contractility
326
adverse effects of theophylline
oral, so narrow therapeutic window
- cardiovascular effects (Vasodilation, tachycardia, arrhythmias)
- CNS stim (nervousness, anxiety, tremor)
- GI (nausea, vomiting)
327
leukotriene pathway inhibitor prototype
montelukast
328
leukotriene inhibitor action
1) inhibit bronchoconstriction - effective for aspirin-sensitive asthmatics
329
do leukotriene inhibitors help COPD
no
330
mechanism of action for montelukast
inhibit the binding of leukotrienes to target receptors
331
adverese effects
not so much for montelukast
332
anti IgE prototype
Omalizumab
333
mechanism of action for IgE inhibitor
binds to Fc receptor of IgE (block allergen binding site)
334
adverse effects of IgE inhibitors
- $$$
- maybe anaphylaxis
- only helpful in allergic asthma
335
COPD treatments
LAMA or LABA for maintenance, inhaled corticosteroids when FEV is really low (below 50)
336
amygdala controls
fight and flight - amygdala and below control resp.
337
acidemia and alkalemia values
arterial pH <7.35 = acidemia
arterial pH >7.45 = alkalemia
acidosis in the process that will cause decrease in pH
338
primary buffers in body (4)
bicarbonates
proteins (lactate, pyruvate)
phosphates
hemoglobin
339
henderson equation
{H+} = 24 x (PaCO2/HCO3)
340
when pH changes by 0.5, how much does [H+] change
by 5 in the opposite direction
341
PaCO2 alterations are caused by _____ disturbances
bicarbonate concentration alterations are caused by _____ disturbances
and how does pH change
PaCO2 -- respiratory disturbances (pH changes in opposite direction)
bicarb concentrations -- metabolic disturbances (pH changes in same direction)
342
causes of acute respiratory acidosis (4)
- airway obstruction
- respiratory center depression
- neuromuscular disorder
- pulmonary disorder
343
how much does pH change with pCO2 in acute processes
with a rise of 10 pCO2, your pH decreases by 0.08
344
in chronic respiratory acidosis, how does HCO3- change with changing PaCO2
HCO3- increases 3.5 for each increase of 10 PaCO2
345
in chronic respiratory acidosis, how does pH change with PaCO2
pH decreases by 0.03 with each increase of 10 PaCO2
346
in acute respiratory alkalosis, how does HCO3- change with PaCO2
HCO3- decreases 2 for each decrease of 10 PaCO2
347
causes of respiratory alkalosis
- hypoxemic respiratory drive
- mechanical overventilation
- respiratory center stimulation
- fever/infection
- pregnancy
- pain
348
when can you have a normal pH with abnormal blood gas situation
chronic respratory alkalosis (like pregnancy)
349
in chronic respiratory alkalosis, how does HCO3- change with PaCO2
HCO3- decreases 5 with each decrease of 10 PaCO2
350
what causes acute metabolic acidosis (5)
```
ketoacidosis
lactic acidosis
starvation
toxins
GI issues
```
351
winter's formula
for metabolic acidosis expected respiratory compensation
expected pCO2 = [1.5 x (HCO3)] + 8 +/- 2
352
formula for expected respiratory compensation for metabolic alkalosis
(not as common)
increase in PaCO2 = 0.6 - (0.7 x delta[HCO3])
353
3 signs that there is a complex disorder
1. normal pH (except in respiratory alkalosis)
2. PaCO2 and HCO3 deviate in opposite directions
3. pH changes in opposite direction for KNOWN primary disorder
354
is CF AR or AD?
AR - most common AR disease (35,000 in US every year)
355
what is the main mutatioin in cf?
CFTR gene, deltaF508 on long arm of chromosome 7 (7q31)
356
different classes of CF mutations
class 1 - no protein at all, class4 - functioning but not fully
357
how to diagnose CF (3)
chloride test - testing concentration of sodium or chloride in sweat (>60mmol/L)
newborn screening - immunoreactive trysinogen on Guthrie Card
genetic confirmation
358
how does CF effect exocrine gland function
nasal, sweat, sinusitis, bonchitis, pancreatitis, diabetes, intestinal blockage, reduced fertility portal hypertension etc.
359
daily treatment routine for CF
1. neubluizers: (albuterol, hypertonic saline, pulmozyme, tobramycin)
2. percussive physiotherapy to dislodge mucus
3. pills 3x day for pancreatic enzymes, vitamins (ADKE), and antibiotics
4. oxygen and feeding tube at night
360
new treatments for CF
- Ivacoftor
| - Ivacoftor/Luvacoftor
361
genetic risk factor for COPD
alpha1-antitrypsin deficiency
362
characteristics of COPD inflammation
- neutrophilic
- macrophages
- oxidative stress
- IL-8 and CD8 and TNFa
- protease/antiprotease imbalance
- loss of elastic recoil
363
definition of chronic bronchitis
cough productive of sputum most days during at least 3 consecutive months for more than 2 successive years
leads to hypoxemia - more obstruction in small airways, small V/Q ratio -- leads to right heart failure (blue and bloated)
364
parameters for qualifying COPD (ABCD rating scale)
1) FEV1
2) how short of breath are you
3) how often are exacerbations
365
treatment for acute COPD exacerbation
- SABA and SAMA
- systemic oral glucocorticoids (prednisone 40 mg per day for 5 days)
- oxygen admistration if SpO2 <88 (with venturi principle face mask)
366
emphysema characteristics
- breakdown of surface area - distal (alveolar sacs) decreased O2 exchange, sensed as dyspnea
- NO scarring, more like atrophy
367
types of emphysema
- central lobular - associated with smoking
- panacinar with alpha1-antitrypsin deficiency (can save lives)
- paraseptal - very distal, associated with pneumothorax
368
clinical emphysema picture
- no/little sputum (more dyspnea over cough)
- fewer exacerbations or infections
- loss of elastic recoil
- low DLCO
369
Chronic bronchitis characteristics
- persistent cough with sputum
- inflmmatory leads to change in architecture
- acute exacerbations
- more proximal
- cor pulmonale (right ventricular failure)
370
Reid index
mucus glands/entire mucosal length
normal is 0.4
371
BODE index
```
systemic disease factor
B - body mass
O - obstruction of flow
D - dyspnea
E - exercise capacity
```
372
bronchiectasis
abnormally dilated airways
cycle of obstruction inflammation damage mucus secretions obstruction etc.
leads to mucus plugs and abscesses - hemoptysis
373
bronchogenic cancers
```
non small cell lung cancers (85%)
- adenocarcinoma
- scc
- large cell ca
small cell lung cancers (15%)
```
374
common caracinogens in tobacco
- tobacco specific N-nitrosamine
- Polycyclic aromatic hydrocarbons
induces modulation of oncogenes (Ras, onc) and tumor suppressor genes (p53)
375
genetic risk factors for developing lung cancers
mutations in RB and p53 or EGFR (nonsmokers) KRAS (smokers)
376
size of environmental pollutants that cause problems
less than 2.5 micro meters
377
how to identify early lung cancer
CT
378
which lung cancer has most metastesis
small cell (95%) (see weight loss, skeletal pain, CNS complaints)
379
paraneoplastic syndrome
1) hypercalcemia (ectopic PTH) primarily with squamous cell carcinoma - stones bones abdominal groans and psych
2) hypernatremia (SIADH) - small cell
3) clubbing - non small cell lung cancers
380
when do you get false positive pET scans
in inflammatory processes related to infections or recent surgeries
381
when do you get false negative PET scans
small lesions or hyperglycemia
382
ceptral vs peripheral lung cancers
central - squamous and small (can use sputum or bronchoscopy)
periperhal - adeno and large (can use CT biopsy)
383
EGFR mutations seen in
adenocarcinoma, young, women, non smoking asian
384
Stage 1a
only in lung, less than 3cm
385
stage 1b
only in lung, gibber than 3cm, not bigger than 4
sx as first line
386
stage 2a
only in lung, less than 5cm
sx with chemo as first line
387
stage 2b
partial collapse, involve visceral pleural
sx with chemo as first line
388
stage 3
lymph, airways, trachea etc
sx with chemo as first line if resectable, if not, chemo
389
stage 4
metastesis outside thorax
chemo first line, look for mutations
390
who can tolerate a pneumonectomy
FEV greater than 2
391
who can tolerate lobectomy
FEV greater than 1.5
392
recent MI and thoracic surgery
contraindicated
393
small lung cancer treatment
mostly advanced, surgery not an option
limited disease = one hemithorax, treat with chemo and radiotherapy
extensive disease (and malignant pleural effusion) = outside hemithorax, treat with chemo alone
394
solitary pulmonary nodule characteristics and evaluation
single opacity up to 3cm surrounded by normal lung (more than 3 is lung mass)
majority are not cancer, have to look at probability (history, growth over 2 years, pattern of calcification (stippling or eccentric - bad), margin regularity)
395
neuroendocrine lung tumors
carcinoid, atypical carcinoid
small (same as scc) and large NE carcinoma
cause paraneoplastic syndromes
396
anatomical vs phyiological staging
TNM - is the tumor ressectible
| physiological - is the patient operable
397
lepidic
growth along the alveolar surface of the lung - excellent survival
adenocarcinoma in situ (make serous or mucin) AKA minimally invasive adenocarcinoma (MIA)
398
diagnostic features of squamous cell carcinoma (3)
- squamous pattern with intercellular bridges (on EM)
- squamous keratin pearls
- cytologic keratin production
399
small cell carcinoma histological criteria (2)
- neuroendocrine markers - dense core neurosecretory granules
- mitoses and tumor necrosis
400
large cell carcinoma histological criteria
- no distinctive differentiation - diagnosis by exclusion
401
diagnostic features of adenocarcinoma (2)
- glandular (Acinar, papillary, solid)
| - mucin production and vacuoles
402
neuroendocrine carcinoma - typical carcinoid characteristics
well differentiated- good prognosis, low grade, NO mitoses NO necrosis NO LN mets
403
diffuse mesothelioma characteristics
- thick collagen
- tubularpapulary pattern
looks like adenocarcinoma BUT:
- keratin positive
- CEA negative
- calretinin positive
- mucin negative
404
immunotherapy in lung malignancies
block PD-1/PD-L1 to upregulate immune response to tumor cells
405
penumococcal vaccine
first give conjugate and then follow with polysaccharide (for those over 50)
406
pleural fluid characteristics in empyema
low pH
low glucose
pus in pleural space
thick rind
staph aureas, legionella, strep pneumo, anaerobe
407
mycosplasma pneumonia dx and treatment
no culture - clinical dx
| treat with macrolides (azithro)
408
legionella pneumonia, characteristics, dx, tx
```
cavitation
fevers
GI symptoms and headache
temp-pulse dissociation
hyponatremia
```
dx with urinary antigen, sputum on charcoal
tx fluoroquin
409
klebsiella pneumonia, characteristics, tx
necrotizing pneumonia
associated with alcoholism
bulging fissure - really mucoid
tx - pennicilin with beta lactamase inhibitor
410
H. flu
have to use beta lactamase inhibitor
411
MRSA, characteristics, tx
follows viral infection, hematogenous dissemination with peripheral nodules, cavitation
tx with linezolid
412
strep pyogenes pneumo characteristics
rapidly progressive, associated with preceding viral illness, can cause empyemas
413
invasive pulmonary aspergillosis, characteristics, dx, tx
long term steroid treatment or advanced immunosuppression
nodular infiltrates with halp sign, requires biopsy
usually fatal if no neutrophil recovery
tx. voriconazole
414
PCP, characteristics, dx, tx
diffuse pneumonia, ground glass appearance
T cell autoimmunity, chronic steroid, chemo
sick for weeks
dx - silver save sputum or lavage
tx - oral bactrim
415
pulmonary tuberculosis in children vs adults
children - primary
adults - apical infiltrates with cavitation without adenopathy, with monocytosis
416
primary localized TB
granulomatous, Ghon lesion, drain into hilar LN with caseous necrosis
417
primary disseminated TB
immunocompromised individuals with caviation and miliary pattern
418
secondary TB
reactivation who develop immunodeficiency
419
lung abcesses mostly caused by
staph aureus or klebsiella
| destruction and pus with outer organization of fibroblasts
420
what do you look for in neutropenic patients
gram pos neg and fungus
421
what do you look for in B abnormalities
encapsulated
422
what do you look for in T abnormalities
pcp cmv and fungal (histo, cocciodio, crytpto)
423
aspergillus presentations (3)
- aspergilloma (non-invasive)
- mycetoma (round/oval mass -
occupying cystic cavity)
hypersensitivity
424
coccidio
spherules
SW united states
no budding
purulent AND granulomatous response (to spherules and endospores)
425
crypto
budding
immunocompromized
patients with birds
426
histo
```
middle america
localized primary pneumonia
disseminated with HIV
dimorphic
budding yeast
```
427
what kind of inclusions does CMV have?
nuclear AND cytoplasmic
428
lipid pneumonia
sterile
seen with obstruction
macrophages
429
do you see wheezing with diffuse parenchymal lung disease?
no
430
diffuse parenchymal lung disease of konwn causes:
- drugs (chemo, biologics)
- inhaled particles (inorganic - pneumocomyoses, small organic particles, paraquat)
- associated with collagen vascular disease
431
DPLD of unknown etiology (5)
- most common is idiopathic pulmonary fibrosis (IPF), idiopathic interstitial pneumonia
- non-specific interstitial pneumonia
- cryptogenic organizing pneumonia (airway filling)
- DIP and RBILD (tobacco related)
- sarcoidosis
432
neutrophilic DPLD
IPF, inorganic
433
lymphocytic DPLD
sarcoid, hypersensitivity pneumo (lower ratio of CD4 compared to sarcoid)
434
presence of adenopathy with intersitital ilfiltrates (2)
sarcoidosis, silicosis
435
presence of pleural effusions and interstitial infiltrates (3)
collagen vascular disease, drug hyperesnsitivity, asbestos
436
IPF clinical presentation
```
50-70y/o
progressive dyspnea
nonproductive cough
mid/late crackles
clubbing
heterogeneous histology
requires lung transplantation
```
437
NSIP
```
temporally uniform histology
no fibroblasts
some have connective tissue underlying
younger (40-50)
no association with cigarette
no clubbing
ground glass opacity with fine reticulation
```
438
RB-ILD
related to cig smoking
pigmented macrophages in first and second resp bronchioles
obstruction and reduction in DLCO
439
DIP
smoking
mean age 42
good response to corticosteroids
440
sarcoidosis
- young and middle-aged adults
- presents with BILATERAL symmetrical hilar (inside pleura) and mediastinal lymphadenopathy, ocular, skin lesions, infiltration
- liver, spleen, salivary glands, heart, muscle, CNS involvement
- non caseating granulomas orchestrated by CD4
441
hypersensitivity pneumonias
- immune mediated - IgG antibodies and lymphocytes
- combined type 3/4: immune complex (type 3) and type 4 (cell medatied)
- fungi in farmer's lung
- chronic exposure leads to progressive lung disease
- INTERSTITIAL, not intra-alveolar
- bronchiolitis with granulomas
442
pneumoconiosis
inorganic
occupational history (sandblasting, coal, asbestos)
silicosis
443
fine silicosis
asymptomatic
| fine pinpoint CXR
444
complicated
dyspnea, sputum
can lead to Right Heart Failures
masses at apeces - no pleural involvement
mycobacterial disease
445
asbestos related diseases
pleural plaques
parenchymal fibrosis
pleural effusions
malignancies
446
marker of interstitial lung disease
fibrotic foci
447
Hamman-Rich syndrome
RAPIDLY progression
diffuse isterstitial infiltrates
fibrosing alveolitis
pulmonary fibrosis
448
usual interstitial pneumonia
chronic, insidious 2-5 years, poor survival
confined to lung
fibroblasts
60+
idiopathic
DIFFERENT IN TIME AND SPACE (heterogenous) - old and new in same area, different stages of lesions (some quicker than other)
449
nonspecific interstitial pneumonia
similar, but homogenous rather than patchy, uniform rick lymphoplasmacytic infiltrate termporally
steroid responsive
idopathic
450
RBILD/DIP
```
ground glass (alveolar filling)
macrophages
hemosiderin
intra-alveolar
give steroids
```
451
beryliosis
```
type 4 pneumoconiosis
hypersensitivie
see in urine
can do lymphocyte stimulation test
non-caseous necrosis
```
452
where do you see fibrosis and macrophages in pneumoconiosis
in bifurcations
453
differences between visceral and parietal pleura
visceral = thick, mesothelial cells and dense CT, supplied by bronchial arteirs and pulmonary veins
parietal = thin, mesothelial and loose CT, supplied by systemic capillaries and intercostal nerves, has lymphatic lacunae that remove large particles (proteins and RBCs)
454
low thick is pleural space
20 microns
455
pleural fluid comp
protein ratio less than 0.5
no neutrophils or eos
mostly macros (75%), lympho (23%)
alkaline
456
symptoms with pleural effusions
dyspnea, chest pain, chest pressure, tachycardia, tachypnea, sometimes asymptomatic
457
what does white pleural fluid suggest
chylothorax
458
what does yellow/green pleural fluid suggest
rheumatoid arthritis
459
what does black pleural fluid suggest
old blod or aspergillosus nigra
460
light's criteria
PF/serum protein ratio >0.5
PF/serum LDH ratio >0.6
PF LDH >2/3 normal value LDH
IF ONE of the above is true it's an exudate
461
most common cause of exudative effusion and types
para pneumonic effusion (3 types):
- uncomplicated (from pneumonia, inflammation, tap is alkaline and no bacteria)
- complicated (more acidodic, bacteria)
- empyema (pus, low ph <7.2, low glucose <60, positive smear, need chest tube or sx. phases are exudative to fibroproliferative to organization phases - more fibrinous)
462
common causes of malignant effusion
- breast
- lung
- lymphoma
para-malignant (non malignant effusion with known malignancy) due to lymphatic obstruction
463
PE causing pleural effusion
always exudative, serosanginous, see PE on CT scan
464
TB causing pleural effusion
due to hypersensitivity to tuberculous protein
primary TB
fluid culture, smear, PCR, ADA>40 is likely
465
chylothorax
milky white exudate
due to trauma
needs to be drained
466
masses in anterior mediastinum
- thymoma
- teratoma
- lymphoma
- thyroid masses
467
masses in meddle mediastinum
- vascular masses
- enlarged lymph nodes
- pleural or pericardial cysts
468
masses in posterior mediastinum
- neurogenic tumors
| - meningocele
469
acute mediastinitis
fever and chest pain
due to esophageal perforation due to mediastinal surgery
need surgery
470
chronic mediastinis
TB, histoplasmosis cause
| symptoms related to compression of other ograns
471
pneumomediastinum
gas in mediastinal space, causes substernal chest pain
472
pulmonary edema - transudate and exudative causes
henodynamic (Starlings) forces caused by CHF, LV dysfunction cause transudate
alveolar injury causes exudate
473
ARDS - what do you see in exudate
- intra alveolar exudative effusion
- rule out cardiogenic pulmonary edema
- increased permeability of plasma proteins and inflammatory cells into alveolus
- see HYALINE FIBRINOUS MEMBRANE and CELLULAR (fibrinous) EXUDATE
474
ARDS - characteristcs
arterial hypoxemia refractory to oxygen therapy due to shunting - perfusion mismatch marked V/Q, stiff lung
475
ARDS - caused by
sepsis, shock, inhaled toxic injuries, trauma, drowning, burn injuries etc.
cause acute respiratory insufficiency
476
ARDS phases
- hyaline membrane within a few days, refractive hypoxemia with shunt
- exudative phase, now see angioblasts and fibroblasts (week)
- organizing (fibrosing) phase - interstitial fibrosis (few weeks)
- resolution or progression to pulmonary fibrosis
477
clinical features of ARDS
```
low PaO22/FiO2 -- (200-300)
pulmonary arterial wedge pressure <18
no L heart failure
arterial hypoxemia
rapid onset tachypnea and dyspnea
stiffness
shunt and dead space
```
478
what do you do for acute cardiogenic pulmonary edema therapy
```
LMNOP
Lasix
Morphine
Nitroglycerine
Oxygen
Positive pressure ventilation (pushes fluid back so that lymph can drain)
```
479
what do you hear iwth cardiogenic pulmonary edema and cause is fixable
wheeze, crackle cough
480
what do you hear with acute lung injury (ards)
cough crackle death
481
ARDS - 3 definite findings
- rapid onset
- bilateral infiltrates
- PaO2/FiO2 ratio under 300 on oxygenation (refractory to treatment), bilateral infiltrates, wedge pressure under 18 (this is not the heart causing this)
482
common direct insults causing ARDS
- aspiration pneumonitis (vomiting and aspirating)
| - pneumonia
483
common indirect insults causing ARDS
- sepsis
- shock
- trauma
484
treatment for ARDS
- low tidal volume ventilation
| ARMA
485
stridor
stridor is large airways (larynx and trachea)
| high pitched inspiratory sound
486
are crackles musical?
no. they are discontinuous. fine or coars, and at the end of inspiration
487
pleural friction rub description
continuous inspiratory AND expiratory rhythmic sounds
488
Hamman's sign
mediatsinal cruch with pneumomediastinum
489
ronchi
low pitched wheezes
| sound more like snoring, not musical
490
wheezing
small airways - hear over peripheral lung fields
bernoulli's principle - increased velocity, low pressure, airway walls collapse and vibrate
491
what causes stridor
infections:
croup, RSV, flu, pertussis, tracheitis, epiglottitis, retropharyngeal abcess
inhalation, aspiration, burns, or foreign bodies
492
what causes wheezing
```
asthma
acute bronchitis with bronchiolitis
COPD
CHF
PE
obstruction
vocal cord dysfunction
```
493
inspiratory stridor caused by internal or external problem
external
494
expiratory stridor caused by
internal (foreign bodies, compression by intrathroacic things- LNs)
495
bronchiolitis
inflammation in bronchioles, expiratory wheezing, viral cause (RSV)
496
bronchiectasis
purulent chronic sputum, destruction of bronchi, chronic inflammation, caused by TB or MAI, or CF
wheezes, sqeaks and focal crackles
cycle of nastyiness causing scarring and damage
497
PE is how common cause of death in in-patient
3rd and most common preventable cause of in-patient death
498
Virchow's triad
- stasis
- hypercoagulability
- vascular injury
499
most common cause of acquired thrombophilia
antiphospholipid antibody syndrome
500
Wells criteria for PE
- previous PE, tachycardia, SX, hemoptysis, cancer, DVT (1 or less, not suspicious)
501
D-Dimer
measures cross-linked fibrin derivatives - elevated in presence of acute thrombosis (activation of coag and fibrinolysis at same time)
also high in pregnancy, trauma etc.
502
best imaging for PE
Chest CT
503
westermark
no vascularity
504
hapton's hump
transudate/exudate on pleura for pulmonary infarction
505
McConnell's sign
echocardigram
| if you see free wall RV not doing much, while th eapex is moving a lot, then you see pE
506
when do you do IVC filter
if low risk PE
507
what is IVC filter
placed in inferior vena cava, take it out later. if you can't do anticoag treatment
