1
Q
pulmonary and systemic circulations are arranged how
A
in series
2
Q
organ circulations are arranged how
A
in parrallel
3
Q
arteries have high or low pressure and velocity
A
high pressure and high velocity
4
Q
do veins have high or low pressure
A
low
5
Q
how is blood flow determined through capillaries
A
precapillary sphincters regulated by local factors
timing and flow of blood controlled by smooth muscle in arterioles contracting/relaxing
6
Q
metaarterioles do what
A
shunt blood from arterioles to venules
7
Q
most of the blood in the body is where
A
systemic circulation
most in veins (they are a reservoire)
8
Q
how is blood distribution to organs regulated
A
altering resistance
9
Q
what factors alter the resistance of vessels
A
local metabolic factors
autonomic nervous system
10
Q
cardiac output
A
colume of blood pumped by heart per unit time
stroke volume x heart rate
11
Q
what determines flow through the cardiovascular system
A
pressure (higher gradient higher flow)
resistance (lower resistance higher flow)
pressure gradient/resistance
12
Q
resistance poiseuilles law
A
R=8Ln/pir^4
L is length (negligible in vessels)
n is viscosity
r is radius
13
Q
factors determining pressure
A
gravity (hydrostatic pressure difference between upper body and lower body)
compliance (change in volume/change in pressure)
viscosity (hematocrit)
inertia (pulsatile flow causes pressure changes when velocity changes)
14
Q
blood usually has what kind of flow
A
laminar
flow at steady rate
less viscous blood has faster flow in the middle
15
Q
what is turbulent flow
A
when blood encounters an obstruction causing eddy currents which increases resistance
16
Q
tendency for turbulent flow is measured how
A
reynolds number
v x 2r x p / n
v is velocity
r is radius
p is density
n is viscosity
> 2000 = turbulent
<2000 = laminar
17
Q
layers of endocardium
A
endothelium
connective tissue
subendothelium (inner layer, smooth muscle, outer layer, blood vessels)
18
Q
layers of epicardium
A
blood vessles/nerves
subepicardium
mesothelium
19
Q
annulus fibrosus
A
all 4 rings of cardiac skeleton
support and electrical barrier
mitral ring
tricuspid ring
aortic root
pulmonary root
20
Q
valves are made of what
A
folds of endocardium
chordae tendinae attach to them
21
Q
where is the SA node located
A
right atrium near opening of SVC
22
Q
what connects the SA and AV nodes
A
myocardium
23
Q
where is the AV node located
A
in teh septal wall
in subendocardial layer
24
Q
what are the characteristics of purkinje cells
A
2x width of cardiac cells
foamy cytoplasm
no t tubules
reduced myofilaments
25
what happens to the number of vessels at each level of branching
they increase
26
what happens to the radius of individual vessels as you branch
it decreases
27
what happens to aggregate cross sectional area of vessels as you branch
it increases
28
what happens to mean linear velocity in individual vessels as you branch
it decreases (fastest in aorta, slowest in capillaires)
29
what happens to flow in indiviual vessels as you branch
it decreases (highest in aorta and lowest in capillaries)
30
what is relative blood volume
the fraction of total blood in all vessels at a given time
31
how can you classify relative colume
systemic (85%) and pumonary (10%)
high pressure (15%) and low pressure (80%)
systemic (85%) and other (15%)
always 5% in heart chambers
32
circulation time is usually what
about 1 minute
can change with volume and flow
33
high pressure circuit includes what
left ventricles to the systemic arterioles
34
low pressure circuit includes what
systemic capillaries to left atrium
35
pulmonary artery systolic pressure/diastolic pressure/capillary pressure
25
8
7-10
36
what is the major site of control of vascular resistance
terminal arteries and arterioles
37
distensibility
ability to be stretched
veins most
38
compliance
quantity of blood stored in relation to pressure
most in veins
39
volume pressure curve
steeper curve = less compliant (arteries)
40
laplaces law
wall tension increases as radius increases
T=change in P x r
high wall tension needed to withstand high pressure
41
what causes the dicrotic notch
slight increase in pressure when aortic valve closes
42
what two factors affect pulse pressure
stroke volume
compliance of arterial tree
43
what happens to pressure pulses as you migrate down the arterial tree
they decrease bc distensibility allows for continuous flow with little pulsation in smaller vessels
44
what happens in venoconstriction
greatly increase venous return in the case of losing blood or massive drop in pressure
45
what is central venous pressure
the pressure in the thoracic vena cava right next to the right atrium
46
right atrial pressure is regulated by what
ability to pump blood out of r atrium
ability of blood to flow from veins into r atrium
47
factors that increase venous return
increase blood volume
increase venous tone
dilation of arterioles
48
as r atrial pressure increases what happen to venous return
it decreases
49
what is mean systemic filling pressure/circulatory filling pressure
the pressure in all the circulatory system if there is no flow
determined by blood volume and vascular compliance
blood volume or venoconstriction changes this point
50
what happens to venous return if r atrial pressure decreases
it increases
51
what happens to the venous return curve in arteriolar vasoconstriction
it shifts down (counterclockwise) without changing mean systemic filling pressure
52
what happens to the venous return curve in arteriolar vasodilation
it shifts up (clockwise) without changing mean sstemic filling pressure
53
what do lymphatics do
route for fluid from interstitial space to blood
carry proteins and large matter from tissue space
return excess fluid to blood
major route for absorption of nutrients in GI tract
54
where does lymph come from for the right lymphatic duct
right head/neck/arm
55
where does lymph come from for the thoracic duct
left head/neck/arm and entire lower body
56
in lymph capillaries endothelial cells are attached by what
anchoring filaments
57
what are lymph valves formed by
endothelial cells
58
what factors determine lymph flow
interstitial fluid pressure
lymphatic pump
59
what is a major reason for edema
loss of negative interstitial pressure
60
causes of extracellular edema
abnormal leakage of fluid
failure of lymphatics to return fluid (lymphedema)
61
starling equation
K x (Pc + piif) - (Pif + pip)
if positive then flow is outward
62
63
increase in capillary filtration does what to lymph
increase activity
64
what is washdown of interstitial fluid
increased fluid filtration
increases interstitial fluid hydrostatic pressure
increases lymph flow
decreases protein concentration in interstitial fluid
65
what is interstitial edema
increased salt and water in extracellular space
66
hydrostatic forces cause edema how
when standing and not moving legs lymph doesnt move in lower limbs
slight increase in hydrostatic pressure of pulmonary capillaries leads to pulmonary edema (often caused by blood backing up from l side heart failure)
67
nephrotic syndrome does what
leads to decrease of protein in blood so decreases the ability of capillaries to retain fluid
68
pregnancy does what to fluid
too much plasma volume and not enough protein so edema happens in extremities
69
what happens in dehydration
increase plasma protein concentration which increases capillary colloid osmotic pressure and pulls fluid from the interstitial space
70
how does inflammation cause edema
release of vasodilators increases filtration of fluid to interstitial space
71
how does cerebral edema occur
breakdown of tight endothelial barrier of cerebral vessels
72
layers of vessels
tunica intima
-endothelium
-subendothelium
-internal elastic membrane
tunica media
-smooth muscle
-elastic and collagen fibers
tunica adventitia
-external elastic layer
-connective tissue
73
large elastic arteries
up to 60 elastic spiraling fenestrated laminae
thin adventitia
74
medium arteries
intima thin with prominent internal elastic membrane
media 25-40 layers thick
adventitia thicker and has external elastic membrane
75
arterioles
media 1-6 layers
76
capillaries
4-10 microns
continuous - tight junctions
fenestrated - have 60-80 nm fenestrations
sinusoid - large diameter fenestrations
77
venules
intima - no subendothelium
media - 0-2 layers
78
small/medium veins
large lumen
intima - medium has internal elastic membrane
media - 1-3 layers
adventitia - thick with some smooth muscle
79
large veins
intima - subendothelium thicker
media - little smooth muscle
adventitia - thick bundles of muscle
80
lymph vessles
possess all 3 layers but generally thinner than veins
adventitia - thickest
thoracic duct - media w 2 layers and adventitia poorly defined
81
flow and velocity in veins
slow velocity but high flow
82
flow and velocity in arteries
fast velocity but slow flow
83
how to calculate flow with velocity and cross sectional area
flow = v x A
84
what has the most influence on flow
radius
85
resistance in parrallel
more resisters decreases resistance
86
resistance in series
more resisters increases resistance
87
flow in relation to volume and time
flow = volume/time
88
cardiac output
hr x sv
89
total peripheral resistance (systemic vascular resistance) is what
resistance of the entire systemic circulation
90
cardiac output using MAP and TPR
CO = MAP/TPR so
MAP = CO x TPR
91
total pulmonary vascular resistance
TPVR = pressure gradient/CO
92
mean arterial pressure
MAP = diastolic BP + 1/3PP
93
what lipids must be transported by lipoproteins
triglycerides
phospholipids
cholesterol and cholesterol esters
94
what lipids are transported by albumin
free fatty acids
95
what do chylomicrons do
transport dietary fat from intestines to liver
96
what do VLDLs do
transport endogenous fat from the liver
97
what fo LDLs do
deliver cholesterol to liver and tissues
98
what do HDLs do
transport cholesterol from membranes in tissue to IDLs (which go back to the liver)
99
lipoproteins from least dense to most dense
chylomicrons
VLDLs
IDLs
LDLs
HDLs
100
what is the lipoprotein core made of
nonpolar lipids (TGs and cholesterol esters)
101
what is the surface of lipoproteins made of
amphiphatic molecules (apolipoproteins)
102
ApoA1
HDLs then chylomicrons
activates LCAT
103
ApoB48
chylomicrons
assembly/secretion of chylomicrons from small intestine
104
ApoB100
VLVL, IDL, LDL
VLDL assembly/secretion
ligand for LDL receptor
105
ApoC2
chylomicrons, VLDL, IDL, HDL (all but LDL)
cofactor of lipoprotein lipase
gotten from HDL
106
ApoE
chylomicron remnants, IDL, HDL
ligand for LDL receptor
given to others by HDL in blood
107
what does lipoprotein lipase do
hydrolyze TGs of chylomicron
insulin stimulates its synthesis
activated by ApoC2
108
how are chylomicron remnants taken up by the liver
ApoE
109
transport via VLDL
VLDL created in liver w ApoB100
ApoC2 activates lipoprotein lipase to digest TGs turning into IDL
OR
VLDL remnant taken up by LDL receptor via ApoE
110
what happens to the IDL
hepatic triglyceride lipase digests TGs turning into LDL
111
what happens to LDL
taken up by liver via ApoB
OR
sent to gonads/adrenal tissues for steroid synthesis
OR
taken up by macrophages
112
LDL endocytosis
LDL receptor endocytosis into clathrin coated pits
becomes endosome
endosome fuses w lysosome
lipids hydrolyzed
113
what happens to cholesterol to be stored as cholesterol ester
in tissues synthesized by ACAT in cytosol of cells
in blood synthesized by LCAT in serum
114
high cholesterol does what to LDL receptor levels
decreases them
115
high cholesterol levels does what to HMG CoA reductase
decreases activity
116
high cholesterol does what to storage of cholesterol by ACAT
increases
117
how does reveerse cholesterol transport work
HDL removes cholesterol from membranes
LCAT converts to cholesterol ester (ApoA1)
CETP transfers CE for TG in IDLs and VLDLs
118
tangiers disease
accumulate cholesterol because defective transport of cholesterol out of cell by AC1 transporter protein
119
ApoA1 Milano mutation
hypertriglyceridemia with no atherosclerosis
better at reverse cholesterol transport
120
what is the primary clinical outcome of atherosclerosis
peripheral artery disease
121
primary sites of PAD
abdominal aorta and iliac arteries
femoral and politeal arteries
more distal vessels
122
causes of PAD
atherosclerosis
vascular inflammation/buergers
thrombosis/embolism
vasculitis
123
insidious development of PAD
causes local thrombus
124
acute development of PAD
emboli occludes vessel
125
risk factors of embolic PAD
atrial fibrillation
myocardial infarction
valvular disease
126
buergers disease
young smokers
digit ischemia
127
chronic limb threatening ischemia
chronic ischemic pain at rest, ulcers, gangrene
128
acute limbischemia
hypoperfusion with pain, pallor, nonpalpable pulses, paresthesias, paralysis
129
ischemic rest pain
severe vascular compromise in extremity perfusion
provoked by elevating lower extremity
can improve with walking or gravity
130
PAD on physical exam
diminished pulses
bruits
muscle atrophy
cool extremities
ulcers
palor
dystrophic nails
shiny skin and hair loss
131
how to test for PAD
ankle brachial index
1-1.4 normal
0.91-0.99 borderline
<0.9 abnormal
>1.4 noncompressible vessels
132
further testing when ABI >0.9 but still suspect PAD
post exercise ABI
133
further testing when ABI >1.4
toe brachial index or imaging
134
further testing if CTLI suspected
TBI, transcutaneous oxygen pressure, skin perfusion pressure
135
when to test in asymptomatic patients
abnormal or absent pedal pulses
over 70
50-69 with smoking history or diabetes
136
when to test symptomatic patients
CLTI is diagnostic for PAD
if have claudication or atypical leg symptoms do ABI
137
PAD treatment
supervised exercise therapy
cilostazol
lipid lowering therapy
antiplatelet therapy
antihypertensive therapy
stop smoking
foot care
revascularization
138
complications of PAD
tissue loss
infection
amputation
increased risk CVD events
osteomyelitis
139
phases of cholesterol synthesis
acetyl coA to mevalonate (HMG CoA reductase)
mevalonate to squalene
squalene to lanosterol
lanosterol to cholesterol
140
isoprene units of cholesterol synthesis are used where
steroid hormones/bile salts
ubiquonone (coenzyme Q)
dolichol
these are precursors to cholesterol
141
stages of atherogenesis
endothelial dysfunction
smooth muscle proliferation
architectural disruption of plaque
142
endothelial dysfunction
internilization and oxidation of LDLs (malonaldehyde or glucose do this)
monocytes recruited from cytokines
monocytes form into macrophages which ingest cholesterol and become foam cells
143
smooth muscle proliferation
smooth muscle cells move from media into intima
forms bulk of plaque
144
architectural disruption of plaque
stress caused by plaque fissuring or intramural hemorrhage triggers clotting and luminal occlusion
145
ROS that attack lipid membranes can be protected against by what
antioxidant vitamins
A, C, E
146
what are the fatty yellow nodules called that indicate excess lipid levels
xanthomas
147
friedwald equation
LDL = total chol - HDL chol - (TG/5)
148
risk factors of atherogenesis
homocysteinemia
lipoprotein a
elevated CRP/IL6
infections
149
VLDL carries mostly what
TGs
150
LDL carries what
cholesterol
greatest contributor to atherosclerosis
151
HDL does what
reverse cholesterol transport
GOOD
152
what is first line in lowering LDL
statins
153
side effects of statins
muscle and liver issues
154
initial labs to conduct
fasting lipid panel
baseline LFTs
baseline CK
155
monitor labs how often
4-12 weeks after initiation or change
every 3-12 months once stable
156
goal levels
total cholesterol <200
LDL <100
TG < 150
HDL >40-50
157
statins MOA
HMG CoA reductase competitive inhibitor
reduces cholesterol synth
upregulates LDL receptors
increase clearing of LDL
158
which statin has high risk for myopathy
simvastatin
159
statin drug interactions
glucocorticoids
fibrates
niacin
160
low intesity statins
So - simvastatin
Low - lovastatin
Poor - pravastatin
Fella - fluvastatin
161
hihg intensity statins
right - rosuvastatin
attack - atorvastatin
162
ezetimibe
cholesterol absorption inhibitor
impairs absorption at brush border by NPC1L1 transporter
most common nonstatin used to decrease LDL
163
PCSK9 inhibitors
alirocumab, evolocumab
PCSK9 usually binds and degrades LDL receptor
inhibition prevents LDL receptors degradation
SC injections
164
ACL inhibitor
bempedoic acid
inhibits ATP citrate lyase which is upstream of HMG CoA reductase
upregulates LDL receptor
165
bile acid sequestrants
cholestyramine, colestipol, colesevelam
bind bile acid so it is excreted in feces stimulating further conversion of cholesterol into bile acid
decrease hepatic LDL and up regulate LDL receptors
166
fibric acid derivatives
fenofibrate, gemfibrozil
agonist of PPARalpha which induces transcription of lipoprotein lipase
increases elimination of TG particles and increases HDL
can increase LFTs
167
niain
inhibit release fatty acids from adipose and increase lipoprotein lipase
lowers TG and increases HDL
can cause flushing
168
omega 3 fatty acids
icosapent ethyl
lower TGs
suppress lipogenic gene expression and increase LPL
169
75 or less with ASCVD
high statin
170
over 75 with ASVD
moderate or high statin
171
primary severe hypercholesterolemia
high statin
172
diabetes
40-75 moderate statin
over 75 analyze risk benefit
20-39 depends
173
10 year ASCVD risk
<5 low
5-7.4 borderline
7.5-19.9 intermediate
>20 high risk
174
hypertriglyceridemia
lower TG
omerga 3 fatty acids
fibrates
175
what are intercalated disks
gap junctions allowing rapid diffusion of ions
176
how do cardiac muscle cells act
as syncytium
177
cardiac contraction force is dependent on what
concentration of Ca
178
catecholamines do what
increase production of cAMP which potentiates voltage gated Ca channels
179
preload does what for contraction
leads to optimal actin mysoin overlap to increase force
180
neural regulation of blood flow
sympathetic innervation of vascular smooth muscle
181
metabolic mechanisms to regulate blood flow
oxygen supply matched to metabolic activity
uses vasodilators (CO2, H, K, lactate, adenosine)
182
myogenic mechanisms to regulate blood flow
autoregulation in response to increased stretching
183
endothelial mechanism to regulate blood flow
endothelial cells produce substances to control vascular smooth muscle
184
coronary flow is tightly coupled to what
oxygen demand
185
most common cause of deminished coronary flow
atherosclerosis
186
reactive hyperemia
increase in organ blood flow following brief period of ischemia
187
cerebral circulation controlled by
sensory stimuli from CO2, O2, pH
detect CO2 indirectly through H
188
skeletal muscle controlled mainly by what
neural control and local metabolic factors
189
sympathetic innervation of skeletal muscle
alpha 1 - vasoconstriction
beta 2 - vasodilation
190
main control of splanchnic circulation
sympathetic vasoconstrictor nerves
191
fetal ductus venosus
bypasses liver (umbilical vein to vena cava)
192
fetal foramen ovale
shunt blood from r atrium to L atrium
closes after birth bc high pressure in left atrium
193
fetal ductus arteriosis
shunt blood from pulmonary artery to aorta
closes 1-8 days after birth bc pulmonary vasodilation and increased aorta pressure
194
cutaneous circulation controlled mainly by what
sympathetic stimulation
195
vasodilator agents
adenosine
bradykinin
histamine
nitric oxide
196
vasoconstrictor agents
norepinephrine
epinephrine
angiotensin II
vasopressin (AVP, ADH)
endothelin (damaged tissue)
197
vascular control by ions
calcium - constrict
potassium - dilate
magnesium - dilate
CO2 - dilate
198
major catecholamine (sympathetic) receptor in heart
beta 1
increase HR, electric conduction, contractility
199
baroreceptor reflex
stretch in carotid body
pressure drops = decrease firing = increase sympathetics
pressure raises = increase firing = increase parasympathetics
200
carotid and aortic chemoreceptors
sensitive to low ozygen, high carbon dioxide, increased H
low oxygen = low flow = increase sympathetics
201
bainbridge reflex
increase in right atrial pressure causes increase in HR and contraction strength
202
depolarization
step 0
fast in ventricles and atrium (Na)
slow in SA/AV node (Ca)
203
first depolarization
step 1
closure of Na channels and K starts coming in
204
plateau
step 2
open Ca channels and open K channels
205
final repolarization
step 3
close Ca open K
206
inward rectifier
step 4
gradient restored by opening of voltage gated K channels and activation of ATPase ion pumps
207
what is the current for pacemaker cells
If, funny current
depolarization deactivated funny current
Na and K channels open
208
regulating pacemaker activity
parasympathetic - acetylcholine decreases funny current
sympathetic - catecholamines increase funny current
209
ventricular diastole
open AV valves
atrial contraction w P wave
210
ventricular systole
increase in pressure closes AV valves
pressure increases until opens semilunar valves and decrease volume and pressure until empty
211
isovolumetric contraction
no change in volume
increase in pressure until semilunar valves open
212
isometric relaxation
semilunar valves close
pressure decreases
213
S1
AV valves close
214
S2
semilunar valves close
215
S3
in diastole when blood flowing from atria into ventricles
216
S4
atrial contraction
217
split S2
aortic valve closes just before pulmonary
218
increasing preload does what to stroke volume
increases is
219
afterload depends on what
peripheral resistance to flow
increased pressure increases afterload
increased afterload reduces SV
decreased SV deacreses CO
220
increased contractility does what
decreases end systolic volume
increases stroke volume
221
how to calculate ejection fraction
EF = SV/EDV
222
filtration in the kidneys is done where
bowmans capsule
223
what happens in the tubule of the kidney
reabsorption - remove solutes and water from tubule back into blood
secretion - transport substances into the tubule
224
what is excretion
exit of substances from body
225
each segment of tubule has different jobs to do, what are the major players
proximal tubule - water/salt reabsorption (carbonic anhydrase inhibitor)
loop of henle - major reentry back into blood for sodium and chloride (loop diuretics)
juxtaglomerular apparatus
-macula densa salt sensor (signal renin angiotensis)
-juxtaglomerular cells pressure sensors
distal convoluted tubule - reabsorb salt with little water (thiazide diuretics)
cortical collecting duct - k sparing diuretics
226
vasopressin
secreted because increased osmolality
decreases urine formation
increases blood volume
227
RAAS system
renin secreted because decrease in arterial pressure and converts angiotensinogen to angiotensin I
angiotensin I converted to angiotensin II by angiotensin convertine enzyme
angiotensin II causes salt and water retention
angiontensin causes aldosterone release
aldosterone increases salt and water reabsorption
228
chronic hypertension
impaired renal fluid excretion
229
primary hypertension
CO increased
SNS increased
angiotensin and aldosterone increased
renal pressure mechanism impaired
230
thiazide effects
hypokalemia, hyponatremia, hypomagnesemia
hypercalcemia, hyperuricemia, hyperglycemia
231
loops effects
hypokalemia, hyponatremia, hypomagnesemia, hypocalcemia
hyperuricemia, hyperglycemia
232
potassium sparing diuretics effects
hyperkalemia, gynecomastia
233
carbonic anhydrase inhibitor MOA
proximal tubule
inhibit NaHCO3 reabsorption
-acidosis
-for glaucoma, mountain sickness, alkalosis
234
loop diuretics MOA
TAL of loop of henle
block Na K Cl symport
-alkalosis
-for edema/congestive heart failure
235
thiazide diuretics MOA
early distal tubule
block Na Cl symport
-alkalosis
-for HtN
236
potassium sparing diuretics MOA
LDT and CCT
block Na channels
block aldosterone receptors
-acidosis
-for hypokalemia and hyperaldosteronism
237
osmotic diuretics MOA
TDL of henle loop and proxiimal tubule
increase osmolarity of tubular fluid
-for cerebral edema/intraocular pressure
238
hyperkalemia does what to the heart
makes it less reactive
239
hypercalcemia does what to the heart
makes it more reactive
240
how to calculate flow using oxygen consumption
oxygen consumption / (ateriovenous oxygen difference)
241
how does gated radionuclide imaging assess cardiac volumes
estimate ejection fraction
242
how does angiography assess cardiac volumes
calculate absolute volumes
243
inhalation does what to HR and pressure
decreases them
244
emotional stress does what
activate SNS
release epinephrine from adrenal medulla
decrease splanchnic blood flow
constrict veins
245
vasovagal syncope
massive parasympathetic stimulation
loss of all sympathetic tone
246
hemorrhage compensatory response
fluid moves from interstitium to vasculature
increase plasma proteins
sympathetic stimulation
247
aortic dissection
intima tear
hypertensive men (Marfans or Ehler Danlos)
often have cystic medial necrosis
248
aneurysms
vessel dilation/outpouching
true = all 3 layers
false = hole covered w hematoma
often bc atherosclerosis, trauma, congenital defects
249
abdominal aortic aneurysm
men over 50
atherosclerosis
below renal arteries above bifurcation
250
thoracic aortic aneurysm
males over 50
genetic factors or cystic medial necrosis, bicuspid aortic valve, syphilis
251
what do people with vasculitis often have
elevated ESR and CRP
constitutional symptoms
252
leukocytoclastic vasculitis
inflammed small vessels
hypersensitivity allergic rxn
can be confined to skin or affect organs
253
raynaud phenomenon
pallor and cyanosis of digits bc cold
254
giant cell arteritis
over 50 usually female
arteries of head
granulomatous w giant cells
can have polymyalgia rheumatica (pain)
tx - steroids
255
Takayasu arteritis
asian women
granulomatous w giant cells
aortic arch at branch points
weakened upper extremities pulses
tx - steroids
256
polyarteritis nodosa
young adults
usually hepatitis positive
necrotizing in many organs but not lungs
can cause stroke
tx - steroids
257
buerger disease
men under 40 who smoke
digit ischemia
tx - stop smoking
258
granulomatosis with polyangiitis
wegner
40s
small vessels in lungs, upper respiratory, kidneys
c ANCA
tx - immunosuppressive drugs, TNF antagonists, steroids
259
microscopic polyangiitis
necrotizing of small vessels
children and adults
precipitated by drugs, infections, immune disorders
most have pulmonary renal syndrome
p ANCA
tx - immunosuppressive drugs, TNF antagonists, steroids
260
eosinophilic granulomatosis w polyangiitis
churg strauss syndrome
small vessel of skin, lungs, heart, spleen, kidneys, GI, respiratory
eosinophilia typically present
p ANCA
tx - steroids, cyclophosphamide
261
lateral leads
I, AVL, V5, V6
circumflex artery
262
inferior leads
II, III, AVF
right coronary artery
263
anterior leads
V1, V2, V3, V4
left anterior descending artery
264
normal P-R interval
.12-.2 s
>.2 first degree block
<.12 preexcitation
265
PR segment
depression in pericarditis
depression or elevation in atrial ischemia
266
ST segment
elevation or depression in myocardial ischemia/infarction
STEMI = st segment elevation myocardial infarction
NSTEMI = non ST segment elevation myocardial infarction/myocardial ischemia
267
prolonged QT
>440 men or >460 women
>500 increase risk torsades de pointes
bc hypokalemia, hypomagnesemia, hypocalcemia, hypothermia
268
QRS interval
normally 70-110 ms
269
sinus bradycardia
QRS narrow
rate less than 60
P before every QRS
270
sinus tachycardia
QRS narrow
rate over 100
P before every QRS
271
mildly irregular rhythm
one P before every QRS
one P wave morphology
272
sinus arrhythmia
heart rate varies by more than 10%
273
sinus arrest
SA node stops and there is a pause and there is no P wave before it picks back up
274
wandering pacemaker
at least 3 P wave morphologies
rate less than 100
275
multifocal atrial tachycardia
at least 3 P wave morphologies
rate over 100
276
atrial fibrillation
no P waves seen
ventricular rhythm is irregularly irregular
277
ventricular fibrillation
no identifiable P, QRS, or T
rate 150-500
coarse then fine
amplitude decreases wtih duration
278
premature atrial contraction
normal PR interval
narrow QRS
occur earlier than you would expect
pause after PAC
279
premature junctional contraction
no P wave
narrow QRS
followed by pause
280
premature ventricular contraction
broad QRS
no P wave
followed by pause
281
wolff parkinson white
preexcitatory syndrome
accessory pathway - bundle of kent
short PR
delta wave
long QRS
282
atrial flutter
rate of 300 in atria
re entry loop
saw tooth baseline
283
paroxysmal supraventricular tachycardia
no P waves
rate over 100
regular rhythm
carotid massage can help
284
ventricular tachycardia
wide QRS
rate over 100
can attempt cardioversion
monomorphic = uniform
polymorphic = irregular
3 or more PVCs in a row
285
torsades de pointes
twisting of the points
prolonged QT interval
QRS spirals around baseline like twisted ribbon
286
first degree block
one P to every QRS
prolonged PR interval
287
second degree block mobitz type 1
PR interval progressively lengthens
nonconducted P wave occurs and the following beat has a shortened PR
288
second degree block mobitz type 2
normal and constant PR interval but has dropped beats (P waves followed by non conducted beats)
289
third degree block
P-P and R-R intervals regular and consistent
290
right bundle branch block
RSR' in leads V1 and V2
deep/wide slurred S waves in I, aVL, V5, V6
291
left bundle branch block
RSR' in V5 and V6
deep S waves in V1 and V2
292
normal axis
up I
up AVF
293
left axis deviation
up I
down AVF
294
right axis deviation
down I
up AVF
295
extreme right axis deviation
down I
down AVF
296
atrial enlargement
diphasic p wave in V1
297
right ventricle hypertrophy
R waves larger in V1 than V6
298
left ventricular hypertrophy
R waves bigger in V6 then V1
299
ischemia
inverted T waves
always abnormal if inverted T waves in V2-V6
300
injury
ST segment elevation
need in at least 2 contiguous leads
301
pathologic q waves
indicate infarction or necrosis
at least 1 mm wide and 1/3 amplitude of QRS
302
ST depression
ischemia
subendocardial infarct maybe
can be reciprocal change STEMI
303
anterior infarction
Q wave in V1, V2, V3, V4
304
lateral infarction
Q waves in I, AVL, V5, V6
305
inferior infarction
Q waves in II, III, AVF
306
posterior infarction
large R and ST depression in V1 and V2
307
acute pericarditis
diffuse ST elevation (usually not AVR or V1)
PR depression (usually not AVR or V1)
ACOM
flashcards
Decks in class (23)
# Cards
-
Exam Block 2158
-
Molecular Medicine Block 3359
-
anatomy block 3105
-
anatomy block 4215
-
molecular medicine block 4174
-
Anatomy Block 5222
-
Molecular Medicine Exam Block 5299
-
Neuro Block 1123
-
Neuro Block 2102
-
Neuro Block 3198
-
MSK Exam 1206
-
MSK Exam 2344
-
Heme Lymph Exam 1324
-
Heme Lymph Exam 2491
-
Derm Exam 1295
-
Derm Exam 2140
-
Cardio Block 1307
-
Cardio Block 2261
-
cardio block 3272
-
Respiratory Exam 1299
-
Respiratory Exam 2208
-
Respiratory Exam 3190
-
Renal Exam 1216
