Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

need to knows > Cards (F.A.) > Flashcards

Cards (F.A.) Flashcards

(81 cards)

Start Studying
1
Q

what is the embryological derivative of the Ligamentum Teres? (Round ligament(

A

Umbilical Vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is the Ligamentum Teres found

A

Falciform ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the embryological derivative of the MediaN ligament and the MediaL ligament

A

MediaN- Allantois/urachus

MediaL- Umbilical A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

an RCA infarction will present in which EKG leads?

A

II, III, avF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

a LCX infarction will present in which EKG leads?

A

I, V5, V6, avL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

an LCA infarction will present in which EKG leads

A

V1,V2 - interventricular septum

V3, V4- anterior LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the (2) equations to determine Cardiac Output?

A 
CO= HR * SV 
CO = rate of O2 consumption/ (arterial O2 - venous O2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are (2) equations to calculate MAP

A 
MAP= 2/3 DBP + 1/3 SBP 
MAP = CO * TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to calculate Pulse Pressure

A

SBP- DBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how to calculate Stroke Volume?

A

SV= EDV- ESV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what 3 factors affect SV

A

contractility, afterload, preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do you calculate wall tension

A

wall tension = pressure * radius

hence, tension increases with increasing radius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do you calculate wall stress

A

Pressure * radius / 2* wall thickness

wall tension/ 2* wall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Driving Pressure in a vessel=

A 
P= Q * R
Pressure= Flow rate * Resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how are size of the vessel and flow through the vessel related

A

Q= (P1-P2/ nL) * r^4

so in radius is cut in half (1/2), flow decreases by (1/16)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is an S3 sound related to

A

dilated ventricle or increased filling pressure (like bc of MR)
think- SYSTOLIC dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is an S4 sound related to

A

stiff ventricle

think - DIASTOLIC dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

JVP tracing: a wave (1)

absent in??

A

R. atrial contraction

absent in Afib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

JVP tracing: c wave (2)

A

R. ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

JVP tracing: x descent (3)

A

ventricular ejection, caused by downward motion of Tricuspid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

JVP tracing: v wave (4)

A

“villing” -increase in atrial pressure due to diastolic filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

JVP tracing: y descent (5)

absent in??

A

RA emptYing into RV

absent in constrictive pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

normal splitting
what is it?
why does it happen?

A

a normal split in S2, with P2 coming after A2 during inspiration
- increased VR in inspriration causes delayed Pulmonic valve closing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Wide splitting
what is it?
why does it happen?

A

an abnormal split in S2- with P2 coming MUCH after A2 in inspiration due to conditions that delay P2 closure
- RBBB or pulmonic stenosis which is exaggerated by the increased VR in inspiration causes wide split

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Fixed Splitting what is it? why does it happen?
- an abnormal split in S2- with P2 coming after A2 in inspiration and expiration - ASD, causes Right heart volume overload all the time, so always causing delayed pulmonic valve closure
26
paradoxical splitting what is it why does it happen
- an abnormal split in S2- with A2 coming before P2 usually. But on inspiration, the split is actually reduced bc P2 closure is delayed - caused by delays in aortic valve closure-LBBB and aortic stenosis
27
AS- describe the murmur
crescendo- decrescendo systolic ejection murmur, with presence of possible ejection click
28
MR/TR- describe the murmur
holosystolic, high pitched, blowing murmur
29
MVP - desrcibe the murmur
late crescendo murmur with midsystolic click
30
VSD- describe the murmur
holosystolic, harsh sounding murmur
31
AR - describe the murmur
early diastolic decrescendo murmur, blowing, high pitched
32
MS - describe the murmur
diastolic, OS followed by diastolic delayed rumble
33
PDA- describe the murmur
constant and machine like
34
pulsus parvus et tardis is associated with which murmur
AS
35
inspiration makes which murmurs louder? | why?
all right heart murmurs | - bc increased VR to RH
36
handgrip makes which murmurs louder? | why?
- MR, AR, and VSD | - because increase in afterload
37
handgrip softens or delays which murmurs
- AS, and click of MVP as well as HOCM | - it increases afterload, which increases LV vol
38
valsalva/standing up does what to HOCM murmur?
it increases HOCM murmur because it decreases preload
39
valsalva does what to MVP click
it makes MVP click earlier bc it decreases preload making LV vol smaler
40
what does rapid squatting do? whats the murmur it makes better?
it increases preload and afterload. | makes HOCM better, because it increases preload, it also makes MVP happen later for same reason
41
Romano Ward Syndrome
congenital QT prolongation AD pure cardiac phenotype
42
Jervell and Lange-Lielsen
congenital QT prolongation AR accompanied by sensineural deafness
43
Brugada syndrome
AD in asian males pseudo RBBB and St elevations in V1-V3 risk of V tach and SCD
44
1st degree AV block
prolonged PR (>200 msec) benign
45
2nd degree AV block, type I (Mobitz I)
regularly irregular progressive PR lengthening until dropped beat asymptomatic
46
2nd degree AV block, type II ( Mobitz II)
randomly dropped beats, theres no change or progressive PR interval length preceding it may become type 3 heart block, may need pacing
47
3rd degree AV block
atria and ventricles beat separately
48
capillary fluid exchange formula
Flow out of capillary = ( hydrostatic capillary P - oncotic capillar pressure) - (hydrostatic interstitial P- oncotic interstitial P)
49
hyperplastic arteriosclerosis seen in
extreme hypertension
50
hyaline arteriosclerosis seen in
diabetes, maybe low levels of hypertension
51
list most common sites of atherosclerosis
abdominal aorta > CORONARY As > popliteal A > carotid As
52
claudication symptoms caused by
atherosclerosis
53
what is AAA associated with, how about Thoracic Aortic Aneurysm?
AAA- atherosclerosis | TAA- cystic medial degeneration
54
unstable angina vs NSTEMI vs STEMI
UA- no cardiac biomarker elevation NSTEMI- cardiac biomaker elevation but ST DEPRESSION due to SUBendocardial infarct STEMI- cardiac biomarker elevation but ST ELEVATION due to TRANSmural infarct
55
MI: first 4 hours
no change
56
MI: 4-12 hours
wavy fibers w/ edema, hemorrhage, and start of coag necrosis
57
MI: 12-24 hr
cytopia and neutrophils begin to appear
58
MI: 1-3 days
extensive coagulative necrosis | acute inflammation with neurtophil abundance
59
MI: 3- 14 days
``` granulation tissue (collagen III) macrophages ```
60
MI: 2 wks- months
scar tissue complete (collagen I)
61
an infarct in PDA will show changes in which EKG leads?
V7-V9 has elevations ( note depression in V1-V3)
62
MI complication: within the first few days
``` arrhythmia (death before 24 hr) postinfarction pericarditis (1-3 days) - note this is not autoimmune, and it only overlies area of necrosis ```
63
MI complication: before first week
Papilary Muscle Rupture - usually posteromedial papillary and will cause MR Interventricular septal rupture - causes VSD, is macrophage mediated
64
MI complication: within first two weeks
ventricular pseudoaneurysm - contained free wall rupture | free wall rupture- causes cardiac tamponade
65
Mi complication: several weeks following
true ventricular aneurysm- outward bulge w contraction and assn with fibrosis Dressler Syndrome- autoimmune fibrinous pericarditis
66
Kussmaul Sign
increase JVP on inspiration sign of constrictive pericarditis, restrictive cardiomyopathy, or ventricular tumor you would expect JVP to decrease on inspiration bc drop in transthoracic pressure, but an increase suggests that the drop in transthoracic pressure is not transmitted to heart
67
vasculitides with focal granulomatous inflammation
Large Vessel- GCA and Takayasu
68
vasculitides affecting Medium size vessels
Polyarteritis Nodosa, Thromboangiitis Obliterans (Buerger) and Kawasaki
69
PAN key features?
segmental transmural inflammation with fibrinoid necrosis spares pulmonary As Hep B assn renal microaneurysms form
70
Kawasaki key features?
``` risk of: coronary artery aneurysms CRASH& BURN C- conjunctival injection R- rash A- adenopathy S- strawberry tongue H- hand and foot changes BURN- fever ```
71
Thromboangiitis Obliterans (Buerger) key features?
young male HEAVY smoker - gangrene and Raynaud's "segmental thrombosing vasculitis"
72
What are the small vessel vasculitides?
- Wegener's - Churg- Strauss - Henoch Schonlein - Microscopic Polyangitis
73
Wegener's (Granulomatosis with Polyangitis) Vasculitis
granulomas in lung+ glomerulonephritis + "focal necotizing vasculitis" c-ANCA (aka pr3 ANCA)
74
Churg Strauss (Eosinophilic Granulomatosis with polyangitiis)
asthma + peripheral neuropathy (foot drop) p-ANCA (MPO ANCA)
75
Henlock Schonlein Vasculitis
triad: GI disturbance + Arthralgia + palpable purpura on legs and butt IgA complex deposition
76
Osler-Weber- Rendu syndrome
AD disorder of blood vessels. Telengiectasias (blanching), recurrent nosebleeds/ GI bleeds/ hematuria, AVMs
77
Leukocytoclastic Vasculitis
a drug response (penicillin) nonblanching palpable purpura sm vessel vasculitis
78
which vasculitis are p-ANCA (MPO ANCA) positive?
microscopic polyangitis | churg strauss
79
Ranolazine
used in refractory angina | inhibits late phase sodium current without affecting contractility or HR
80
Ivabradine
selective inhibition of funny Na+ current which slows phase 4 depol in nodes WITHOUT ionotropy used for stable angina for pts who cant take B blockers ae: visual brightness, htt, bradycardia
81
How to calculate Flow Rate?
Q= CSA * velocity of flow

need to knows (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions