B3 Ibe CPR Flashcards
1
Q
medicines block Ca2+ channels in myocardial action potentials
A
Nitrendipine, nimodipine, nifedipine
bind DHPR
Class of calcium blocking so block muscle contracation
2
Q
t tubule in cardiac contraction
A
large ca stores (diameter 5x)
mucopolysacchardies bind calcium ions
3
Q
increasing dose of caclium channel blockers
A
decreases impulse conduction
decrease in contraction
4
Q
hyperkalemia
A
raise rest potential
promote K+ efflux
reduce conduction velocity
decrease rate of phase 0
5
Q
hypokalemia
A
lower rest potential
reduce K+ efflux (excess in cell)
take longer get back to resting potential (longer 3)
6
Q
acetylcholine effect phase 4 nodal contraction
A
decrease rate of diastolic depolarization
decrease HR
7
Q
catecholamine effect phase 4 nodal contraction
A
increase depolarization
increase HR
8
Q
sympathetic stimulation phase 4 nodal contract
A
increase chance funny channel open
increase HR
9
Q
refractoriness determinant of
A
susceptibility to arrythmias
facilitate reentry & arrythmia
10
Q
prevent tetany in cardiac
A
refeactory period
allow heart chamber time refill
11
Q
slow action potential locations
A
SA node
AV node
12
Q
fast action potential locations
A
atrial myocyte, ventricular myocyte, purkinje, bundle His
13
Q
positive dromotropic
A
increase in conduction velocity
increase Ca vis SNS
14
Q
negative dromotropic
A
decrease conduction velocity
decrease Ca, Increase K via PNS
15
Q
cause of heart block via conduction velocity
A
increase PNS
damage to AV node
16
Q
Stokes Adams syndrome
A
delaay in pickup heartbeat
5-20s lack blood to brain
delay in HR = syncope
17
Q
specialized excitatory/conductive tissue
A
nodal pacemakers
automaticity
own contraction
excitatorymsystem control HR
18
Q
distribution of blood in body determine by
A
output L ventricle
contractile state of arterioles
19
Q
where are greatest pressure drop
A
arterioles
20
Q
max resistance location
A
arterioles
21
Q
receptors in arterioles
A
alpha 1
beta 2
22
Q
receptors venules/veins
A
alpha 1
23
Q
vein resevoirs
A
spleen, liver, large ab veins, venous plexus
24
Q
cardiac factors affect cardiac out[put
A
heart rate
myocardial contractility
25
coupling factors affect cardiac output
afterload
preload
functional coupling between heart & blood vessels
26
flow of adult
5L
27
determine blood fllow
pressure difference ends of vesel
resistance of vessel
28
cause turublent blood flow
high velocity
sharp turns
rough surfaces
rapid narrow
causes murmurs
29
thrill
palpable murmur
30
S1
close AV valves
hear in mitral (L, 5th intercostal)
31
S2
close Semilunar
hear L sternal (2nd intercostal)
32
S3
abnormal, early diastole
rapid ventricular filling
apex
33
S4
abnormal
turbulent flow
ventricle non-compliance
apex
34
aortic stenosis murmur
crescendo-decrescendo
systolic ejection
LV greater pressure than aorta in systole
radiate to carotid
35
aortic stenosis can lead to what on exertion
Syncope
Angina
Dyspnea
36
Mitral/Tricupsid Regurgitation sound
holosystolic, high pitch
blowing
37
cause mitral regurge
ischemic heart disease
mitral valv prolapse
left ventricle ddilation
38
cause tricupsid regurge
right ventricle dilation
39
mitral valve prolapse sound
late systolic
crescendo with midsystolic click
40
cause of mitral valv prolapse
sudden tense chordae tendineae
41
ventricular septal defect sound
holosystolic
harsh sound
hear @ tricupsid (5th intercostal, midclavicular)
42
aortic regurge sound
high pitch blowing
early diastolic
decrecendo
hear @ aortic root dilate or L sternal border
43
symptom aortic regurge
hyperdynamic puls (bounding)
head bobbing
44
causes of aortic regurge
Bicupsid aortic valve
Endocarditis
Aortic root dilate
Rheumatic fever
45
aortic regurge progress to
left sided heart failure
46
mitral stenosis sound
mid to late diastolic
follows opening snap
47
mitral stenosis a sign of
rheumatic fever, pulmonary congestion, hypertension, left atrial dilaiton, atrial fibrillation
48
patent ductus arteriosus sound
continuous machine like
L infraclavicular
49
causes of patent ductus arteriosus
congenital rubella
premature birth
50
polycythemia effect on blood flow
decrease flow (increasing viscosity)
increase resistance
excess of RBC makes too difficult to mvoe
51
anemia effect blood flow
increase flow (decreasing viscosity)
decrease resistance
52
vascular conductance
measure of blood flow through vessel for given pressure change
53
54
series vs parrallel arrangement
series are within same organ
parrrallel are across multiple organs (independent flow regulation)
55
what holds most/least volume blood
least - arteries
most - veins
56
MAP drives
blood to organs and capillaries
57
R atrial pressure
5
58
R ventricle pressure
25/5
59
pulmonary trunk pressure
25/10
60
L atrial pressure
<12
61
L ventricle pressure
130/10
62
aortic pressure
130/90
63
veins more distensible than arteries
8x
64
aged arteries
least amount of capitance & compliance
65
why aged arteries decrease compliance
walls stiffer, less compliant
arterial pressure increse
66
veins & cardaic output
constricted = lots bl.ood move to heart
increase output
67
factors affect opulse pressure
stroke volume (direct correlation)
arterial compliance (inverse correlation)
68
arteriosclerosis pulse pressure
stiffer, less compliant
increase pulse pressure
69
aortic stenosis pulse pressure
SV descreased
all pressures decreased
70
PDA pulse pressure
low diastolic, high systolic
high piulse
71
aortic regurge pilse pressure
backward flow
high pulse pressure
72
factors increase R atrial pressure
increase blood volume
increased venous tone
dialte arterioles
decrease cardiac function
73
P wave represent
atrial depolarization
74
PR interval represent
initial depolarization of atria to initial depolarization of ventricles
75
QRS represent
ventricles depolarize
76
T wave represent
repolarization ventricles
77
QT interval represent
first ventricular depolarization to last ventricular repolarization
78
PR interval length
0.12-0.2s
79
QRS interval length
0.06-0.11s
80
QT interval length
0.36-0.44s
81
repolarizations towards & away from reference electrode are .... deflections in EKG
towards: negative
away: positive
82
inferior leads of heart
II, III, aVF
83
lateral leads
I, aVL, V5, V6
84
right side lead
aVR, V1
85
anterior leads
V2, V3, V4
86
aVR electrode locations & vector
+ R arm
- L arm
- L leg
-150 degree
87
aVL electrode location & vector
+L arm
- R arm
- L leg
-30 degree
88
aVF electrode location ^ vector
+L leg
- R arm
- L arm
90 degree
89
first vs second half p wave
first: R atrial depolarization
second: L atrial depolarixation
90
normal leads to see variant of Q wave
III & aVR may have deeper Q
91
hyperkalemia change EKG
peak T
wide PR
widen QRS
none/flat P
92
hypokalemia change EKG
long QT
flat T wave
93
wolf parkinson white ekg
delta wave with wide QRS
supraventricular tachicardia
94
abnormla impulses of wolff parkinsosn white syndrom
extra connection of impulse from ventricle back to atria
lead to tachy
95
atrial fibrillation ekg
no P wave
weird R-R
96
risk factors of atrial fibrillatoin
Hypertension
coronary artery disease
holiday heart - excessive alcohol
97
atrial flutter EKG
sawtooth pattern
back-back atrial depolarization
98
ventricular fibrillation EKG
irratic
she crazy
99
EKG first degree block
long PR, >0.2
100
EKG 2 degree TI block
R-R varies (regularly irregular)
PR lengthen until beat drop
101
EKG 2 degree TII block
drop beat but no change PR interval
preogreess to 3 degree
102
third degree block
disassoc ventricle & atria
no rhythm to PQRS
103
one cause of third degree block
Lym3 disease
104
Einthoven Law
potential of anyh limb = sum pf pther two
105
what does heart axis represent
average direction of ventricular depolarization during ventricle contraction
106
L axis deviation
Positive in lead I
Negative lead II
107
R axis deviation
Negative lead I
Positive lead II
108
causes L axis deviation
laying down, expiration, fat
hypertrophy of Left ventricle (hypertension, aortic stenosis, aortic regurge)
109
Is right axis deviation ever normal
yes in newbornscau
110
causes R axis deviation
R ventricular hypertrophy ( pulmonary hypertension, pulmonary valve stenosis, IV septal defect, situs invertus)
111
L ventricular hypertrophy EKG
R wave of aVL >11mm
R wave V5-6 >35mm
S wave if V1 >35 mm
112
pathologic Q wave indicate what
prior mI
absence of electricity
scar is electrically dead
113
Qwave pathological if :
>1mm wide
>2mm deeo
>25% depth QRS
114
EKG sinus arrythmia
inconsistent R-R
115
EKG sinus arrest
<3s duration of dropped beat
116
EKG PAC
no T wave
irregular R-R
abnormal P wave
117
EKG PAC bigeminy
every other beat is PAC
118
EKG atrial tachy
P waveinvert
119
Junctional EKG
regular R-R
40-60bpm
abnormal P wave
120
Left bundle branch b lock EKG
V1 shows W looking QRS
V6 shows M looking QRS
WiLLiaM
121
R bundle branch block EKG
V1 hsow M looking QRS
V6 show W looking QRS
MoRRoW
122
PVC EKG
QRS with no P
same shape if unifocal
123
ventricular pacemaker EKG
spike make wide QRS
124
atrial pacemaker
spike where P wace should be
125
AV pacemaker EKG
first spike with p wave
second spike make wide QRS
126
AC interference EKG
electronic device or pacemaker near patiuent
127
muscle tremor EKG
lots of random spike
128
wandering baseline
undulates
somethign between electrode & machine
129
mitral stenosis P changes
pulmonary capillary wedge pressure is greater than end diastolic presure
130
prelead
stretch of myocardium
EDV
131
afterload
systemic vascular resistance
ESV
132
increase preload causes
increase cardiac output
increase force of contraction
increase vlood volume
133
when does frank starling graph line curve to plateau
high level of EDV
ventricle reach limit and can't maintain venous return amount of blodd
134
what happen to systole on frank starling law graph as volume reaches maximum
systole decreases as actin/myosin no longer close to each other
135
phases of pressure volume loop
1- filling ventricles (EDV)
2 - isovolumetric contract ventricles
3 - eject of ventricle
4 - isovolumetric relax of ventricle (ESV)
136
increase preload cuases
greater EDV
greater SV
137
increase afterload cuases
decrease SV
increase ESV
138
increased contractility causes
increase SV
ESV decrease
139
4 factor that inacrease contractility
positive ionotropi agents - B1 receptors
increased calcium entry - more AP & more trnsion created
increased troponin C affinity fro Ca
force increases when stretch more (frnak starling)
Cardiac glycosides
140
S4 heart sound
turbulence from ventricle non-compliance
vibrate ventricular wall in atrial contraction
141
S1 noise
AV valve closes, start systole
142
why does ventricular volume decrease during rapid ejev=ction
SV ejected in this phase & ready for atrial fill
143
Pressure changes during reduced ejection
ventriclar pressure fall slightly
aortic pressure decreases
atrial pressures rise (venous return increased)
144
splitting of S2
inspiration delays close pulmonary valve
both aortic & pulmonary valve close here
145
what is peak L atrial pressure named in isovol relax
V wave
increase volume against closed tricupsid
146
when is S3 sound normal
kids and pregnant peoiple
147
wide splitting of S2 occur when
pulmponic stenosis, R bundle block
delayed pulmonic as delay R ventricle empty
148
fixed splitting S2 occure\ when d
delayed pulmonic closure
independent of respiration
149
change in pressure-volume loop aortic stenosis
incerase afterload
increase ESV
150
change in pressure-volume loop aortic regurge
increase preload
increase EDV
151
change in pressure-volume loop mitral stenosis
decrease EDV & ESV
152
change in pressure-volume loop mitral regurge
decrease ESV
increase EDV
153
4 reasons venour return oncrease SV in exercise
veins contstrict
skeletal miuscle pump
thoracic pump
sympathetic stimulation
154
SV declione in prolong exercise
high bT
redistribute blood flow to skin
excess fluid loss
decrease plasma volume
dehydrate
155
formula cardaic output
CP = SV * HR
156
fick formula cardiac output
CO = (O2 consumed)/(arterial O2 - venous O2)
157
CO maintain in exercise
early: increase HR & SV
later: increase HR
diastolic shorten with increase HR
158
factors directly affect CO
metabolism
exercise
age
body size
159
caffeine affect CO
stimulatory afffect
increase HR by increase depolarization
160
ion concentration affect CO
increase SAA nodal cell or contracility
161
abnormla body temp affect CO
decrease temp = decrease metabolism
lower HR & force contract
162
resistance to venous return determinants
2/3 by venous resistance
1/3 byu arterial resistance
163
effect increase blood volume on mean vasc fxn curve
increase mean systemic fill pressure (venous return shift R)
cardiac output & atrial pressure increase
164
increase TPR on vasc fxn curve
decrease CO, decrease venous return
165
normal interpleural presure & how changes
-4mmHG
if increased require more R atrial pressure
166
risk factors & features of hypertension
increased age, diabetes, inactivity, high sodium, excess alcohol, smoking, black
90% cases related increased CO or increased TPR
167
hypertensive urgency
180/120, no organ damage
168
hypertensve emeregncy
180/120 with end organ damage
stroke, hemorrhage, MI, aortic dissection etc
169
determinants of BP
cardiac output
total peripheral resistance
170
short term regualtion BP
baroreceptors (seconds)
chemoreceptors
CNS
171
intermediate regulation BP
RAAS (minutes)lon
172
long term regulation BP
kidney Na/H2O (hours to dyas)
173
stimulation baroreceptors effect
from increased BP causing stretch
cardioinhibitory stimulated
vasodilation occur
decrease CO & restore BP
174
carotid sinus & barorecepturs
has afferent limb - glossopharyngeal N
efferent - vagus N
decrease in BP as vasodilate
175
conditions predispuise carotid sinus syndromw
atherosclerosis
more senstive
light touhc = bradycardia
176
RAS
decrease BP
baroreceptors secrete renin
angiotensinogen become angiotensin I
ACE in lung makes it angiotensin II
make aldoserone
icnreases Na and H2O reabsorb
increase plasma volume = increase out put = increase BP
177
exercise & BP
up to 85% total outpt to muscles if strenuouus
only modest increase mean BP due to vasodilate in active muscles
178
what does SNS not innervate
capillaries, precapillary sphincters
179
PNS on heart
responsible for control HR
not affect contractibility
180
vasoconstrictor effect
kidney, gut, spleen, skin
181
vasomotor center components
vasodilator
vasoconstrictor
sensry
182
functions VMC
partial state of contraction via sympathetic tone
Lateral - heart activitt by increase HR/contract
medial - signal via vagus ot decrease HR
183
VMC & arterial presssure
increase by constricting arterioles/large vessels
increasing CO/HR
184
where are baroreceptors located
carotid sinus
walls of aortic arch
185
carotid sinus baroreceptor respond to
pressure 60-180 mmHGd
186
most senstive baroreceptor @
100mmHg
187
what happen baroreceptor as pressure increase
impulses increases - lead to inhibition of constrictor, activate vagal
188
orthostatic hypotension
impaired baroreceptor reflex
when go from laying to standing, should increase SNS to compensate
189
vasovagal syncope
from cardioinhibitory & vasodepressor response
increased PNS
190
carotid/aortic chemoreceptors respond when
lack of oxygen
excess CO2
excess H+
pressure below 80mmHg
191
Response to blood loss
decrease blood volume = decrease CO & arterial pressure
carootid sinus sense decrease and increase SNS
if present with ischemia, chemoreceptors inobvlved
if arteriolar vasoconstriction senseed they decrease capillary pressure & favor absorbtion
adrenal medulla release Epi/NEpi
RAAS activated and angtiotensin II vasoconstricts, aldosterone increase NaCL reabsorb
192
Cushing reaciton
specuial CNS ischemic response
inccrease pressure of CSF cut blood to brain
193
Bainbridge reflex
prevent damming of blood
atrial stretch = increase HR
194
Valsalva maneuver
monitor change BP/HR with brief strain
done regularly
195
hypotension & baroreceptor
increase BP, vasoconstrict
important for big hemorrhage
196
ANP
from atrial myocyte
respond to increase blodd volume
vasodilate afferent, constrict efferent and aldosterone escape
197
Brain NP
ventricular myocyte
help diagnose hearfailure
increase Na absorbtion
198
What isAV shunt & where located
connect arteriole to veing, bypass capillary
if dilate & relax, arteriole send blood to venule
nose, lip, penis
199
contunuous non fenestrated capillary location
muscle, skin, fat, nerve tissue
200
fenestrated capillary line
intestines, kidneys, endocrine
201
sinusoidal capillary location/fxn
vascular channel mve lots blood
bone marrow, liver, spleen
202
why is it imoprtant that endothelium lines capillaries
derived relaxing factor that is sensative to NO
M3 receptors activate synthesis of NO
allow vasodilation
203
how much of blood is reabsorbed on venous side of cpaillary
85%
204
solid structures in interstitium
collagen fibers
proteoglycan filaments
205
lymph affect by hyrostatic pressure
increase interstitial fluid hyrostatic pressure creates increas lymph flow
206
Peripheral Artery disease
impaired arteriolar autoregultaion
can't adjust to metabolic needs
ischemia and pain as can't dilate in response
207
ultrafiltration & its determinmants
process blodd plasma filters across capillary to make interstitial fluid
capillary hydrostatic pressure
interstitial fluid pressure
plasma colloid osmotic pressure
interstitial fluid colloid osmotic pressure
208
captillary hydrostatic pressure fxn
pull fluid out from capillary
209
interstitial fluid pressure fxn
push fluid into capillary
210
plasma colloid osmotic pressure fxn
pull fluid back into capillary
211
interstitial fluid colloid osmotic pressure fxn
pull fluid out of capillary
212
how to increase capilary pressure
decrease arteriole resistance
increase venous pressure
213
what is another namoe for plasma colloid osmotic pressure
plasma protein
214
diseases that lead to decreased plasma colloid osmotic presure & effect
cirrhosis, nephrosis, dilutional
decreases means interstitial fluid colloid osmotic is unapposed and can pull fluid to cause edema
215
factors determine plasma colloid osmotic pressure
75% from albumin
25% globulins
216
capillaru factors decrease filtration
creates decrease interstitial fluid
decease capillary pressure (constrict arteriole)
decrease osmotic tissue pressure (more lymph, less edema)
increase osmptoc colloid pressure (dehydration)
217
capillary factors increase filtration
interstitial fluid form
increase capillary pressure (dilate arterioles)
increase osmotic tissue pressure (block lymph)
decrease osmotic colloid pressure (liver fail)
218
4 causes of edema
increase capillary hydrostatic pressure
loss plasma protein
increased capillaru permeability
blockage of lymph return
219
what can increase capillary hydrostatic pressure
hypertension, heart failure
220
causes loss plasma proteins
nephrosis, burns, wounds, liver disease
particularly albumin loss
221
cause of lymph block
infection or cancer
local edema
222
cause of increased capillary permeability
allergic rxn/burn
localized but can spread
223
thirst mechanism
osmoreceptors in hypothalamus
224
antidieuretic hormone fxn
reabsorb water into blood from kidney
prevent water lloss
225
aldosterone fxn
resorption of sodium ions & water
226
Atrial natriuretic peptide fxn
increase glomerular filtration rate
inhibit ADH
Inhibit renin secreation
227
hyperemia
increased amount blood in vessls of organ or tissue
228
active hyperemia
increased metabolic = increased metabolites
causes increased dilation & flow
229
reactive hyperemia
after an occlusion occurs
during ischemia metabolites build up
excess blood flow required to wash away after
230
blood flow determinant & equation
pressure difference & resistance
Q = (P1-P2)/(R)
231
vasodilators for blood flow control
adenosine
CO2
lactic acid
ADP compounds
histamine
K+
H+
232
precapillary sphincters & tissue demand
numper of sphincter open at any time is about same as requirerment for nutirtion of tissu
meet metabolic ozygen needsmetab
233
metabolic autoregulation theory
as arterial P decreases, oxygen decreases
cause vasodilator release
234
myogenic autoregulation theory
as arterial P decrease, artieroles will dilate
in response to wall tension
235
kidney blood flow control
feedback of tubules & arterioles
236
brain blood flow conrol
CO2 & H+ concentration
237
Laplace law & hypertension
wall thickens as adaption to minimize wall tension
minimize oxygen demand as a result
238
long term local blood flow regulation occur by
change size and number of vascular vessels
239
when does angiogenesis occur
factors release from
ischemic tissue
rapid growing tissue
tisue with high metabolic rattes
240
humoral blood flow regulation - vasoconstrictors
NEpi & Epi
Angiotension II
Vasopressin
Endothelin
241
humoral blood flow regulation - vasodilators
Bradykinin
serotonin
histamine
prostoglandins
NO
adenosine
242
acute response heart fail
increase SNS
243
chronic response heart failure
sympathetic contract kidney arterioles
decrease filtration & urine
Na/H2o retention
increase volume, decrease resistance
BNP excerete extra Na = strong heart fail indicator
244
progressive change in CO curve after MI show
heart never recovers to intital cpacity
245
moderate cardiac damage fluid retention
lower CO & flow to kidneys
moderate retention
246
sever cardiac damge fluid retention
excessive retention weakens heart more
0 urine outpit
247
decompensated heart failure
CO can't sustain renal fxn
fluid retention
elevate mean fill pressure
elevate right atrial pressure
248
L heart fail
forward
R side continues normal
pulmonary congestion
249
acute pulmonary edema
with chronic heat fail, increase load on already weak hearttre
250
treat acute pulmonary edema
fast dieuretics
oxygen
cardiotonic drug
251
arterio-venous fistula
blood bypass resistance = low TPR
CO must increase to maintain BO
chronic elevation leads to excess venous return & heart fail
252
Beriberi
b1 deficent for peripheral tissues
extreme vasodilate in peripheral with low TPR
high CO
seen in alcoholics
253
what predominates coronary blood flow
metabolic effects (vasodilation)
even if SNS active
254
Circle of Willis
arterial blood continuous to tissues
255
most to least oxygen in fetus
umbilical
atrium
internal ilian ratery
inferior vena cava
256
autoregulation lungs factor
hypoxia cause vasoconstrict
257
autoregulation heart factor
vasodilatory metabolites
NO, CO2, low O2
258
brain autoregualtion factors
casodilatory metaboiltes
CO2, H+
259
kidney autoregulation factors
myogenic, tubuloglomerular feedback
260
skeletal muscle autoregulation factors
vasodilatory metabolites in exercise
sympathetic tone @ rest
261
vasodilatory metabolites in exercise
CHALK
CO2, H+, Adenosine, Lactate, K+
262
skin autoregulation factors
sympathetic vasoconstriction
263
key events hemostasis
vessel spasm (constrict)
form plug (gp1b)
blood coagulation (intrinsic vs extrinsic)
clot retraction (polymerize fibrin)
clot lysis (plasmin)
264
ligand for platelet adhesion
Von Willebrand facotr
bind to gp1b/1a
265
platelet alpha granules
vWF, factor V, fibrinogen, growth factors
266
platelet dense granules
ATP, ADP serotonin, Ca
267
coagulation factors
vWF, fibrinogen, Factor V/XI/XII
268
adhesion factpors
gp1b/1a, gpIIb/111a
269
what does vWF bind
Gp1b/1a activates more plateletes & bridges form
270
fibrinogen bind
GpIIb/IIIa
platelet plug
271
prothrombin dependent on
vitamin K
for clotting
272
fibrinogen depend on
synthesis in liver
intravascular for clotting
273
extrinsic clot patheay
Ca with factor VII makes VIIa
more Ca, VIIa & factor X form activated X
with factor V activates prothrombin activator
Prothrombin + platelet phospholipid + prothomabin + Ca makes thrombin
Thrombin can then make more factor 5 to continue
274
Intrinisc clot pathway
XII to XI to IX with CA
VIII with thrombin & Ca activates factor X\Calcium ads to & activate prothrombin
makes thrombin
275
thrombin-thrombomodulin
activate protein C (also need protein S)
inactivates factors V & VIII
276
regulation of fibrinolysis
plasminogen activator inhibitor 1 & 2
prevent breakdown and leave as clots
277
vitamin K defieency
lack bile production/delivery cause fat malabsorption
inactivates VII, IX, X & Protein C+S
278
Factor II (Prothrombin) deficiency
excessiive bleed/hemorrhange
dyspro(...) = abnormal structure
Hypo(...) = inadequaate productionhem
279
hemophilia A
deficeny of factor 8
85% all hemophilias
family history of
lab will show prolong PTT
280
hemophilia B
deficiency factor 9
281
hemophilia C
defciency facto 11
282
Disseminated Intravascular Coagulation (DIC)
decrease in all cloting factors
increase fibrin degradfing factor
bleed out
283
bleed tiem
1-6 minutes
platelet fxn
284
clotting time
6-10min
285
Prothrombin Time
extrtinsic pathway assess
12s
286
Partial Thromboplastin Time
assess intrinsic
factor 8
287
bernard soulier syndrome
d=defect in adhesion with decrease GpIb
288
glanzmann thrombasthenia
defect in aggregation
decrease GpIIb/IIIa
no platelet clump
289
immune thrombocytopenia
destruction platelet in splee
anti-gpIIb/IIIa antibodies
290
Von Willebrand disease
decreas vWF
decrease factor 8
increases PTT
291
factor V Leiden
mutant factor 5
resistant to degradation by protein C
lead to thrombosis, DVT
292
protein C or S deficency
decrease ability to inactivate factors V & VIII
Protein C cancels & Protein S stops coagulation
