Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Z - M2 Cardiology > M2 Cardiology Key Facts - Week 1 > Flashcards

M2 Cardiology Key Facts - Week 1 Flashcards

1
Q

Impact of Gs of Cardiac Myocytes (3)

A

All via PKA

1) Increase Phospholamban = Increases SERCA = Increase Ca in the SR for Release
2) Increase L-Type Ca Channels - More Ca coming In
3) Uncouples Troponin I/C to induce relaxation and prep for next contraction

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

Heart Sounds - Increase S1 - Causes (3)

A

1) Short PR (Rapid Atrial Contraction)
2) Mild Mitral Stenosis
3) High CO (Short Diastole)

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

Heart Sounds - Decreased S1 - Causes (4)

A

1) Long PR (1st Degree AV Block)
2) Mitral Regurg.
3) Significant Mitral Stenosis
4) Stiff Left Ventricle (LVH Hypertrophy)

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

Heart Sounds - Physiological P2 Splitting - When + Causes (1)

A

Description - Increased Delay of P2 (E.g. A2 then P2 both heard) on inspiration
Increased Venous Return from Cause - Inspiration delays RV systole (more blood to pump) + Pulmonic Closure

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

Heart Sounds - Widened P2 Splitting - Description + Causes (2)

A

Description - Increased P2 Delay on Inspiration

Causes - Delayed Right Depolarization/Emptying - RBBB + Pulmonic Stenosis

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

Heart Sounds - Fixed P2 Splitting - Description + Causes (1)

A

Description - Split on Expiration and Inspiration match

Causes - ASD = R/L Pressures balanced by ASD flow no matter venous return

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

Heart Sounds - Paradoxical P2 Splitting - Description + Causes (2)

A

Description - P2 Heard First on Expiration and S2 Together on Inspiration
Cause - Delayed Left Depolarization/Emptying - LBBB + Advanced Aortic Stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Heart Sounds - Early Systolic Click - Description + Causes (3)

A

Description - Ejection Click right after S1 due to audible opening of the Semilunar
Causes - Aortic/Pulmonic Stenosis + Dilated Aortic Root

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Heart Sounds - Mid Systolic Click - Description + Causes (1)

A

Description - Click in mid-systole
Squatting (Increase Venous Return) - Makes the Murmur Occur Later
+ Decreases the Murmur - Valsava Increase Murmur

Causes - Mitral Valve Prolapse

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

Heart Sounds - Opening Snap - Description + Causes (2)

A

Description - Diastolic Murmur heard after P2 regardless of inspiration/expiration
Causes - Mitral/Tricuspid Stenosis

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

Heart Sounds - S3 - Description + Causes (2)

A

Description - Heard Right after P2 - Lub Dub Dub

Causes - Normal in children - significant heart failure in adults

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

Heart Sounds - S4 - Description + Causes (2)

A

Description - Late Diastole sound right before new S1 - Tub Lub Dub
Cause - Atrium contracting into a stiff LV - E.g. Hypertrophy

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

5 Major Clicks/Snaps/Extra Sounds + Diseases

A

1) Early Systolic/Ejection - Aortic/Pulmonic Stenosis + Aoritc Root Dilation
2) Mid-Systolic - Mitral Prolapse
3) Opening Snap (Diastolic) - Mitral/Tricuspid Stenosis
4) S3 - Early Systole - CHF
5) S4 - Late Systole - LVH

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

Mitral Stenosis Murmur Notes (Extra from Lecture 2) - 4

A

1) Hockey Stick Look
2) LA Dilation causes Afib
3) Opening Snap (Diastole) with increased S1 (Atrial Contraction at the end of diastole pushes hard on the stenosis)
4) Short Snap Interval = More Severe Stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
Define Phase of Each Wave JVD/RA Wave
Initial Upslope 
Initial Downslope
Notch on Initial Downslope
Second Upslope
Second Downslope
A

Initial Upslope - A Wave - Backflow from Atrial Contraction
Initial Downslope - X Wave - Decline after a wave + atrial relaxation
Notch on Initial Downslope - C Wave - Tricuspid closure deflection
Second Upslope - V Wave - Atrial Filling with closed Tricuspid
Second Downslope - Y Wave - Tricuspid opens and blood flows into RV

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

Major Changes in JVD/RA Waves + Causes (4)

A

Increased A Wave - Strong Atrial Contraction - RVH or Tricuspid Stenosis
Increased P Wave - Abnormally large amount of venous return in diastole = Tricuspid Regurgitation
Blunt Y Wave - Decreased Filling = Cardiac Tamponade
Exaggeration of the Y Wave - Constrictive Pericarditis

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

Murmur Pitch Meaning (Lecture 2) - High vs. Low

A

High - Tight Opening + High Pressure Difference

Low - Loose Opening + Low Pressure Difference

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

Maneuvers to Increase Murmurs (5) + Impacted Murmur

A

1) Valsalva + 2) Standing - Decreased Venous Return + High Thoracic Pressure - Increase Left Flow Murmurs
3) Inspiration - Increased Venous Return + Low Thoracic Pressure - Increase Right Flow Murmurs
4) Squatting - Increase Venous Return - Increase LV Volume - Increase Aortic Stenosis + Delay Mitral Valve Prolapse
5) Clenching Fist - Increase Resistance/Afterload - Increases BP - Increases Backflow Murmurs (AR/MR/VSD)

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

Hypertrophic Cardiomyopathy Murmur vs. Aortic Stenosis Murmur - Maneuvers

A

Both Systolic Outflow Murmurs (Crescendo + Decrescendo)
AS - Increased with Squatting (Increased LV Volume) - Valsalva/Standing Decreases
HCM - Increased with Valsalva + Standing (Decreased Venous Return) = less filling + more resistance to forward flow - Squatting Decreases

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

Key Cardiac Imaging Planes (2)

A

Vertical Long Axis - Verticle Cross-Section from Mitral to Apex - Shows Half LA/LV
Short Axis - Horizontal Sections of LV/RV - Most important axis because it gives you volumes

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

Imaging Uses - CXR - 1

A

CHF - See Enlarged Mediastinum + Lung Edema + Loss of Bronchi

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

Imaging Uses - Normal Echo - 2

A

Valves (Long Axis) + LV Fucntion

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

Imaging Uses - Transesophageal Echo - 3

A

Right behind LA - Uses for Endocarditis + ASD + Thrombus in LA before cardioversion

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

Imaging Uses - Contrast MRI - 1

A

MI - Area + Size of Infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Imaging Uses - Nuclear Imaging/PET - 2

A

CAD + Myocardial Blood Flow (MBF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Imaging Uses - Electron Beam CT Angiography - 1

A

Coronary Artery Calcifaction - Only way to see soft plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Baroreceptor Reflex - Pathway + Response to Low BP

A

Receptors in Aortic Arch (CNX) + Carotids (CNIX) - High BP = High Baroreceptor Signal = Increased Vagal + Decreased Symp. Tone
Low BP = Less Baroreceptor Firing + Less Parasymp stimulation + less symp. blocking

28
Q

Systolic HTN - Mechanism + Age Group

A

Elderly HTN - Increased large vessel stiffening with age - increases with life

29
Q

Diastolic HTN - Mechanism + Age Group + Risk Factors

A

Young HTN - Increased Systemic vascular resistance - More dangerous + genetic + progressive

30
Q

Indications of Secondary HTN (3) + Key HTN Risk Drug

A

1) Resistant (to 3 or more HTN Meds)
2) Diagnosis before age 30 w/o FH or obesity
3) Rapid Changes/Onset
NSAIDs - Can cause HTN!!

31
Q

Major Cause of Secondary HTN (Pathoma)

A

Renal Artery Stenosis - Hypoperfusion of the Glomerulus - Thinks you have low blood volume - activates RAAS to increase

32
Q

Major Use of Wedge Pressure (From Right Swann-Ganz Cath)

A

Estimates LA Pressure - Also during Diastole LA/LV Pressure Approx. Equal - Allows for estimate of LV diastolic pressure and preload

33
Q

Continuous Elevated Pulm. Artery Pressure - Normal Pressure + Associated Diseases (3)

A

Normal = 2-10 mmHg = Wedge + LA too

Diseases - Left HF + Parenchymal Long Disease (COPD) or Pulm. Vascular Disease (HTN/PE)

34
Q

Reduced Pulm. Artery Pulse Pressure - Associated Diseases (3)

A

Right Heart Ischemia/Failure + PE + Tamponade

35
Q

Left Cath. Findings in Pathology (3)

A

Abnormally High LA-LV Pressure Gradient in Diastole = Mitral Stenosis
Low Systolic Pressure Gradient between Aorta/LV = Aortic Stenosis
Large Systolic v wave on LA JVP = Regurgitation

36
Q

Modifiable Atherosclerosis Risk Factors (5)

A

1) Dyslipidemia
2) Tobacco Smoking
3) HTN
4) Diabetes
5) Sedentary

37
Q

Non-modifiable Atherosclerosis Risk Factors (3)

A

1) Advanced Age
2) Family History
3) Male (Estrogen protects until menopause)

38
Q

Markers of Increased Atherosclerosis Risk (2)

A

Elevated CRP - C-Reactive Protein - Inflammation Marker

Elevated Homocysteine - Increased by low levers of B12, B6. and Folate

39
Q

Normal Endothelium Features (5)

A

1) Impermiable to Large Molecules
2) Resists Leukocyte Adhesion
3) Promotes Vasodilation (NO/Prostacyclin)
4) Anti-Inflammation
5) Anti-thrombotic (heparin sulfate + thrombomodulin)

40
Q

Atherosclerosis Progression (7 Stages)

A

1) Endothelial Injury
2) LPL Entry/Modification
3) Inflammation via cytokine release
4) Leukocyte adhesion via VCAMs
5) Foam Cell Formation when macrophages take up LPL with scavenger receptors
6) Foam Cell PDGF (Platelet derived growth factor) pulls smooth muscle into the intima
7) Smooth muscle cells use collagen type I to promote extracellular remodeling

41
Q

Factors Impacting Fibrous Cap Formation in Atherosclerosis (3)

A

Promote Cap = PDGF + TGF-Beta

Inhibit Cap = IFN-Gamma from Lymphocytes

42
Q

4 Major Manifestations of Atherosclerosis

A

1) Stroke (Thrombotic + Embolic)
2) CAD - Angina/Ischemia/MI
3) Aneurysms (AAA - Weakening of vessel walls)
4) Renal Artery Disease = Emboli Occlusion + Renal Artery Stenosis

43
Q

Primary vs. Secondary Hemostatsis

A

Primary - Platelet Aggregation mediated by vWF - Not strong enough, needs clotting cascade to secure it
Secondary - Clotting cascade to form a thrombus + secure the original clot with cross-linked fibrogen

44
Q

Von Wilabran Factor (vWF) - Functions (2)

A

1) Release Factor VIII to increase Factors IX and X to increase secondary hemostasis
2) Responds exposed collagen in the sub-endothelial matrix - recruits platelets for primary hemostatsis

45
Q

Vascular Injury - 3 Effects Mediating Hemostatsis

A

1) Vasoconstriction
2) Collagen Exposure (recruits vWF) + Primary Hemostatsis
3) Tissue Factor Exposed (Binds Factor VII and activates Secondary Hemostatsis)

46
Q

Primary Hemostatsis - 4 Steps

A

1) vWF Binds the newly exposed collagen
2) vWF Links with a platelet via the platelet’s GP Ib receptor - Activates the Platelet
3) Activated platelet links to other platelets via its GP IIb and IIIa receptors - Fibrin Link
4) Platelet aradonich acid is activated via COX1 to release TXA2 and recruit more platelets

47
Q

Secondary Hemostasis - Common Pathway

A

Meeting point of Intrinsic/Extrinsic Pathways - Xa activates Va which activates IIa (Thrombin) which triggers fibrin cross linking

Factor XIII Performs the Cross-Linking (Activated by Factor IIa)

48
Q

Secondary Hemostatsis - Extrinsic Pathway

A

TF Exposed on injured endothelium - Binds Factor VII - Activates Factor X + Common Pathway + IX (Intrinsic Pathway)

49
Q

Secondary Hemostatsis - Intrinsic Patthway

A

XII - XI - IX Cascade - Activates More Factor X - Rapid acceleration of the clotting

50
Q

Tissue Factor Pathway Inhibitor - Mechanism + Types

A

Mechanism - Activated By Factor Xa - Goes back and turns of TF-VII Complex
Alpha - Circulating Anti-Coagulation
Beta - On endothelium - keep thrombus from spreading

51
Q

Thrombomodulin Pathway - 2 Effects

A

On endothelium - Turned on by IIa which it then inactivates

Activates Protein C

52
Q

Protein C Pathway

A

Protein C (Protein S Co-Factor) - Inhibit Factor Va/VIIIa

53
Q

Antithrombin III - Location + Activity

A

Circulating from Endothelium + Liver

Inhibits Factors II and X - Action enhanced by heparin sulfate

54
Q

Coagulation Testing - PT vs PTT (4 Possibilities)

A

PT - Extrinsic Pathway (PeT) - Long = TF, VII, V, X, II
PTT - Intrinsic Pathway (PeTiTe) - Long = XII, XI, IX, X, V, II
Both Long = Common = X, V, II
Both Normal = Outside the Box = VIII, Platelet Function, Fibrinogen, Fibrinolysis

55
Q

Major Clotting Disorders (4)

A

Factor 5 Lieden Mutation
Hemophilia A
Hemophilia B
ADAMTS-13

56
Q

Factor 5 Lieden Mutation

A

Mutation in Factor V - Activated Protein C (APC) Deficiency - Can’t cleave V to turn off

57
Q

Hemophilia A

A

Bleeding Disorder - Factor VIII Deficiency - IIa cannot activate more VII and IX to rapidly expand the clot

58
Q

Hemophilia B

A

Bleeding Disorder - Factor IX Deficiency - Loss of the Intrinsic Pathway to rapidly expand the clot - Less serious than Factor VIII (Still have Facto VII expansion)

59
Q

ADAMTS-13

A

Responsible for the breakdown of vWF and platelet aggregation - to much = bleeding disorder

60
Q

Vitamin K Dependent Clotting Factors (6)

A

Factors II, VII, IX, X + Proteins C/S

61
Q

Fibrinolysis

A

Plasminogin - Activates to plasmin via tPA - breaks down the fibrin crosslinking
Balanced by Plasminogen Activator Inhibitor (inhibts tPA)

62
Q

D-Dimer

A

Detects PE via looking for small pieces of broken down fibrin from fibrinolysis - indicates clot

63
Q

Acquired Factor VIII Deficiency - Pathology + Diagnostic Findings

A

Pathology - Bleeding Disorder - Auto-Immune disorder targets Factor VIII
Findings - Long PTT (Indicates problem with XII, XI, IX, or VIII) + Normal PT (no problems with common pathway) + Does not respond to platelets (should do fine with new factors being replaced but does not because autoimmune still knocks out the new Factor VIII)

64
Q

DVT without Provocation (2 Causes)

A

Cancer + Pregnancy

65
Q

Protein S Level Changes - Cause + Pathology

A

Cause = Pregnancy
Protein S is normally half bound to C4b - In pregnancy more C4b takes up more Protein S - Reduces the ability of Protein C to inhibit clots - hypercoagulation state

66
Q

Lethal Fetal Hypercoagulation Disorders (2)

A

Homozygous Protein C Deficiency + Anti-Thrombin III Deficiency

Z - M2 Cardiology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions