Cardiovascular imported Flashcards

1
Q

Drug given to close PDA

A

Indomethacin

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

increased LV diastolic pressure in patient with mitral stenosis indicates what other pathologic condition in this patient’s heart?

A

dysfunctional aortic valve

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

isolated Mitral stenosis causes changes in vascular pressure in what anatomical location

A

pulmonary artery pressure (pulmonary hypertension)

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

Effect of long standing pulmonary hypertension

A

results in reduced pulmonary compliance due to endothelial-mediated pulmonary vasoconstriction, reactive hypertrophy of arterial muscle layer, and partial obliteration of pulmonary capillary bed.

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

isolated mitral stenosis causes elevated pressure in what heart chamber

A

left atrium, which is then transmitted to pulmonary veins and capillaries (increase pulmonary wedge cap pressure)

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

Diastolic pressure in left ventricle in patient with severe mitral stenosis

A

usually normal or even decreased

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

absence of peripheral edema is best explained by which compensatory mechanism

A

tissue lymphatic drainage

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

chronic hypoxia in COPD leads to…

A

pulmonary vasoconstriction, increased pulmonary artery pressure, and right heart failure

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

Right heart failure causes what changes in systemic vascular pressure

A

increased CVP and excessive hydrostatic pressure, predisposing to peripheral edema

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

factors that favor development of peripheral edema (4)

A
  1. elevated capillary hydrostatic pressure2. decreased plasma oncotic pressure3. sodium and water retention 4. lymphatic obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

peripheral edema is accumulation of fluid in what compartment

A

interstitial space

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

holosystolic murmur best heard at apex of heart that radiates to axilla

A

MITRAL REGURGITATION; generated by regurgitant blood flow from LV back to LA during diastole; produces audible S3

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

Why is audible S3 heard in mitral regurgitation?

A

elevated pressure and blood volume in LA, increased the amount of blood reentering LV during DIASTOLE;

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

mechanism behind audible s3 gallop

A

generated by the sudden cessation of blood flow into LV during passive filling phase of diastole. LV is unable to accommodate excess blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when you see S3, think..

A

classically associated with heart failure

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

Absence of S3…

A

used to exclude severe chronic MR

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

S4

A

low-frequency diastolic sound that occurs during the atrial kick of ventricular diastole, reflects blood colliding with stiff ventricular wall

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

S4 pathology

A

indicated hypertrophic caridiomyopathy or concentric left ventricular hypertrophy (due to hypertension or aortic stenosis)

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

mid-systolic click

A

characteristic or mitral valve prolapse; occurs earlier in systole with physical maneuvers that decrease left ventricular volume

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

opening snap

A

early diastolic sound after S2 in patients with mitral or tricuspid stenosis; decrease interval between S2 and opening snap correlates with increase severity (more stenotic mitral valve)

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

hypertrophic cardiomyopathy inheritance

A

typically autosomal dominant; patients often have family history of HCM or unexplained sudden cardiac death

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

ECG findings of HCM

A
  1. overall increase in LV mass2. reduced LV cavity size –>impairing diastolic function3. asymmetric increase in LV wall thickness, predominantly affecting septum4. normal/increased LV ejection fraction5. left atrial enlargement (secondary to increased LV end-diastolic pressure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

coronary capillary situation in hypertrophic cardiomyopathy

A

poorly developed coronary capillary network; evidence of chronic ischemia in hypertrophied regions (ie fibrosis, scarring)

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

Difference between athlete’s heart (cardiac adaption) and pathologic hypertrophic cardiomyopathy

A

athlete’s heart does not have reduced LV cavity size and localized septal wall thickening

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

severe coronary artery disease associated cardiomyopathy

A

ischemic cardiomyopathy that typically manifests as dilated cardiomyopathy with enlarged LV cavity and thin LV walls with impaired systolic fxn

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

viruses (5) that can cause viral myocarditis

A

adenoviruscoxsackie bparvovirus B19HIVHHV-6viral myocarditis may sometimes lead to dilated cardiomyopathy with eccentric hypertrophy and impaired LV systolic function

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

meiotic nondisjunction

A

when chromosomes fail to separate, allowing one or more daughter cells to pass on extra copy of a chromosome. most common consequences of maternal nondisjunction=trisomies 21 (down syndrome), 18 (edwards syndrome), and 13 (patau syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

compensation of chronic aortic regurgitation to maintain cardiac output

A

increase LV stroke volume; due to increase in LV end-diastolic volume (volume overload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

type of hypertrophy that occurs in aortic regurgitation

A

eccentric hypertrophy due to volume overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

principle behind pharmacologic stress tests with coronary vasodilators

A

pharmacologic stress agents (ie, adenosine, dipyridamole) are used during myocardial perfusion imaging to simulate the generalized coronary arteriole dilation caused by exercise to assist in identifying areas of ischemic myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

coronary steal syndrome

A

redistribution of blood flow directed toward newly vasodilated areas of nonischemic myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Change in cardiac cycle regarding mitral regurgitation

A

increased LA atrial pressure (normal is approx. 10 mm Hg); results in early and large V wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

best time to hear mumur throughout cardiac cycle

A

when the difference in pressure between the two areas (ie LV and aorta) are at largest difference (when LV pressure is highest compared to aortic valve pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

holosystolic murmur found in…

A
  1. VSD2. tricuspid regurgitation3. mitral regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

holosystolic mumur best heard where (anatomic location)?

A

lower left sternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

bifid carotid pulse with brisk upstroke found in what pathology?

A

characteristic of hypertrophic cardiomyopathy, a condition with dynamic LV outflow tract obstruction during systole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

decreased femoral-to-brachial blood pressure ratio is found in …

A

coarctation of aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

fixed splitting of S2 found in

A

atrial septal defect, causes increased SpO2 in RA compared with vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

eisenmenger syndrome caused by

A

uncorrected left-to-right shunt (VSD, ASD, PDA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Down syndrome CV abnormalities

A

endocardial cushion defects (ostium primum atrial septal defects, regurgitant AV valves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DiGeorge syndrome CV abnormalities

A
  1. tetralogy of fallot2. interrupted aortic arch (complete form of coarctation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Friedreich ataxia CV abnormalities

A

hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Kartegener syndrome CV abnormalities

A

situs inversus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Marfan syndrome CV abnormalities

A
  1. cystic medial necrosis (eg aortic dissection and aneurysm)
  2. mitral valve prolapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Tuberous sclerosis CV abnormalities

A

valvular obstruction due to cardiac rhabdomyomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

turner syndrome CV abnormalities

A
  1. aortic coarctation2. bicuspid aortic valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

change in pulse pressure seen in aortic regurgitation

A

widened pulse pressure due to compensatory increase in SV + reduced diastolic pressure in AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

characteristic physical findings in Aortic Regurgitaton

A

head bobbing and ‘pistol-shot’ femoral pulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

aortic root dilation is one of the most common causes of ? in developing countries?

A

chronic aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Aortic arch derivatives

A

1st root: part of maxillary artery (branch of external carotid artery)
2nd root: stapedial artery and hyoid artery
3rd root: common carotid and proximal part of internal carotid
4th root: on left, aortic arch; on right, proximal part of subclavian artery
6th root: proximal part of pulmonary arteries and (on left only) ductus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

coarctation of aorta associations

A

bicuspid aortic valve, other heart defects, and Turner syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

bicuspid aortic valve sound/location

A

associated with aortic ejection sound; early systolic, high-frequency click heard over the right second interspace

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

rheumatic heart disease and affect on valve

A

affects mitral valve; early lesion=mitral valve regurgitation , late lesion=mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

TTN gene

A

encodes for sarcomere protein titin; most common cause of familial DCM –absence of titin proteins leads to myocardial dysfunction

fxn: connects Z-line to M-line

55
Q

arrhythmogenic right ventricular cardiomyopathy

A

characterized by fibrosis and scarring of right ventricular myocardium, which predisposes to ventricular arrhythmias and sudden cardiac death. the disease results from impaired desmosome function due to mutations in genes encoding desmosomal proteins (ie plakoglobin, desmoplakin)

56
Q

Hemosiderin-laden macrophages in lungs are usually result of …

A

chronic passive lung congestion in the setting of heart failure (ie left ventricular systolic dysfunction)

57
Q

most common etiologic agent in subacute bacterial endocarditis following dental work

A

Streptococcus viridans

58
Q

etiologic agent that causes bacteremia or endocarditis that is associated with colon cancer

A

Streptococcus gallolyticus (aka S. bovis)

59
Q

mechanism of increased serum creatine kinase

A

cells within heart, brain, or skeletal muscle are injured, the enzyme creatine kinase leaks across the damaged cell membrane and into circulation

60
Q

typical right-sided heart failure physical findings

A
  • distended jugular veins
  • pulsatile and tender hepatomegaly
  • abdominal distension with ascites
  • lower extremity edema
61
Q

Etiology of Acute pericarditis

A
  • viral or idiopathic (most common cause)
  • autoimmune disease
  • uremia
  • post MI: early–peri-infarction pericarditis, late–dressler syndrome
62
Q

acute pericarditis clinical feautures

A
  • pleuritic chest pain
  • pericardial friction rub
  • ECG: diffuse ST elevation (due to inflammation of ventricular myocardium)
  • pericardial effusion on ECG
63
Q

Pericarditis typically presents with…

A

substernal pleuritic chest pain that may radiate to bilateral scapulae posteriorly

64
Q

free wall rupture (MI)

A

typically occurs within first 5-14 days post MI due to weakening area of infarcted myocardium via: coagulative necrosis, neutrophil and macrophage infiltration, and enzymatic lysis of connective tissue

65
Q

common pathology that occurs due to free wall rupture (MI)

A

cardiac tamponade (presented with sudden onset of chest pain and profound shock and rapid progression to death)

66
Q

wide and fixed splitting seen in…

A

atrial septal defects with left to right shunting

67
Q

Decreased CO (CHF) and RAAS

A

RAAS system increases activity in CHF, leading to to mechanisms being activated via Angiotensin II:

  • potent vasoconstrictor
  • stimulation of aldosterone
68
Q

how to assess degree of mitral stenosis?

A

measure A2 to opening snap time interval. Shorter interval=more severe. the OS occurs due to abrupt tensing of the valve leaflets as the mitral valve reaches its maximum diameter during forceful opening. AS-OS interval becomes shorter as left atrial pressure increases.

69
Q

How much time is needed for myocardium to stop contracting?

A

loss of myocyte contractility occurs within 60 seconds after the onset of total ischemia. Ischemia lasting less than 30 min, restoration of blood flow leads to reversible contractile dysfunction. After 30 minutes of total ischemia, ischemic injury becomes irreversible.

70
Q

how is brain natriuretic peptide released/activated?

A

released from ventricular myocytes in response to increase tension (increased in ventricular wall stress).

ANP is released from atrial myocytes in response to increase blood volume and atrial pressure

fxn:
1. natriuretic peptides stimulate both venous and arterial VASODILATION to decrease cardiac preload and afterload and reduce strain on myocardium

  1. stimulate salt and water excretion by kidneys to facilitate diuresis
71
Q

when and where is left-sided S4 best heard?

A

cardiac apex with patient in left lateral decubitus position; will intensify during expiration due to increased blood flow from lungs to left atrium

72
Q

Pathology behind abnormal S4

A

reduced ventricular compliance; atrial kick

S4 is a diastolic dysfunction

73
Q

pathology behind abnormal S3

A

rapid ventricular filling; associated with increase filling pressures

74
Q

notable changes to pressure tracings that occur in Aortic regurgitation

A
  • loss of aortic dicrotic notch
  • steep diastolic decline of aortic pressure
  • high peaking left ventricular and aortic systolic pressure; combined with low aortic diastolic pressure leads to wide pulse pressure
75
Q

myocardial infarction leading to mitral regurgitation due to papillary muscle dysfunction

A

MI leading to ischemia of papillary muscle results in hypokinesis and outward displacement of papillary muscle, creating increased tension on attached chordae tendinae and preventing complete closure of corresponding mitral valve cusp.

76
Q

prolonged systemic hypertension leads to..

A

Concentric LV hypertrophy via addition of myocardial contractile fibers in parallel

77
Q

negative changes that occur with concentric hypertrophy

A

thickening of LV walls–>reduces LV compliance–>impaired diastolic filling and heart failure with preserved ejection fraction

78
Q

isolated diastolic heart failure diagnostic findings

A
  • increased LV end-diastolic pressure
  • normal LV end-diastolic volume
  • normal LV ejection fraction (preserved)
  • elevated LV filling pressures

diastolic dysfunction can be due to conditions that decrease LV compliance such as impaired myocardial relaxation or increased intrinsic ventricular wall stiffness

79
Q

jugular venous pulse ‘a wave’

A

generated by atrial contraction; ABSENT IN ATRIAL FIBRILLATION

80
Q

jugular venous pulse ‘c wave’

A

RV contraction (closed tricuspid valve bulging into atrium)

81
Q

jugular venous pulse ‘x wave’

A

relaxation of right atrium

82
Q

jugular venous pulse ‘y wave’

A

abrupt decrease in right atrial pressure during early diastole after tricuspid valve opens and RV begins to fill passively

83
Q

renin secretion occurs from what cells?

A

juxtaglomerular cells of kidney

84
Q

Process of RAAS

A

Renin secretion (juxtaglomerular cells of kidney)–> converts angiotensinogen (produced by liver) into angiotensin I in systemic circulation –> Angiotensin I converted to Angiotensin II by ACE in the small pulmonary vessels. Angiotensin II will reach kidney and release aldosterone.

85
Q

Prostaglandin E1 (2 fxns)

A
  • keep PDA open
  • causes afferent arteriolar vasodilation in kidneys

produced in multiple types of cells: endothelial, mast cells, and macrophages

86
Q

Ruptured Left ventricular free wall

A
  • due to MI
  • mechanical compliation that occurs within the first 5-14 days post MI
  • abrupt rupture leads to hemopericardium and cardiac tamponade
  • patients present with sudden onset of chest pain and profound hypotension and shock
87
Q

acute pericarditis physical findings

A
  • decreases when patient sits and leans forward
  • pericardial friction rub=most specific physical finding
  • may be caused by myocardial infarction, rheumatologic disease, uremia, or viral infection
88
Q

Kussmaul sign

A

paradoxical increase in jugular venous pressure on inspiration; occurs because of impaired right-sided diastolic filling in conditions such as constrictive pericarditis, restrictive cardiomyopathy, and tricuspid stenosis.

89
Q

what is precordial knock

A

brief, high frequency, precordial sound heard in early diastole (shortly after S2) in patients with constrictive pericarditis

90
Q

aortic stenosis causes what pathologic change in the myocardium of the heart (and in what location)?

A

hypertrophy of LV

91
Q

compartment of heart that contributes significantly in concentric hypertrophy?

A

LA

92
Q

Effect of atrial fibrillation in LA

A

decreased filling in LV; decreased emptying in LA; back up of fluid to pulmonary veins, leading to acute pulmonary edema

93
Q

what organism synthesizes dextrans from sucrose

A

Streptococcus sanguinis (viridans streptococci); dextrans bind to fibrin-platelet aggregates on damaged heart valves, causing subacute bacterial endocarditis

dextran is a extracellular polysaccharide

viridans streptococci adhere to affected valve in patients with pre-existing valvular lesions.

94
Q

what do Neutrophils bind to on endothelial cells during inflammatory response

A

endothelial surface glycoproteins mediate binding of immune cells to endothelium, facilitated by expression of cell adhesion molecules on surface of inflamed endothelium

95
Q

physical findings of constrictive pericarditis

A
  • slowly progressive dyspnea
  • chronic edema
  • ascities
  • *rapid y-descent during inspiration observed on jugular venous pressure tracing (not unique to constrictive pericarditis)
96
Q

aortic dissection key findings

A
  • sudden chest pain that radiates to the back

- double aortic lumen seen on CT of chest

97
Q

classic presentation of ischemic heart disease

A
causes pressure (substernal chest pain) that radiates to left shoulder 
calcifications in coronary arteries and aorta are usually seen on CT
98
Q

normal LV ejection fraction

A

55%

99
Q

diastolic heart failure is caused by

A

decreased ventricular compliance and is characterized by normal LV ejection fraction, normal LV end-diastolic volume, and elevated filling pressures

100
Q

S4 heart sound

A
  • ‘atrial kick’ working against still LV wall (hypertrophy)
  • considered abnormal regardless of age
  • often associated with restrictive cardiomyopathy and LV hypertrophy
101
Q

most common cause of dilated cardiomyopathy in young patients who develop heart failure

A

viral myocarditis

102
Q

buldging of interventricular septum into LV side is usually due to

A

venous blood increasing during inspiration in patient with cardiac tamponade

103
Q

systolic anterior motion of mitral valve found in

A

hypertrophic cardiomyopathy that causes dynamic outflow obstruction

104
Q

auscultation change in patient with elevated pulmonary artery pressure (pulmonary hypertension)

A

increased intensity of the pulmonic closure sound (P2)

105
Q

noturnal dyspnea usually caused by

A

impaired LV function

106
Q

patient with mitral regurgitation, how do you increase ratio of forward to regurgitant blood flow?

A

reduction in systemic vascular resistance

107
Q

final stage of MI healing process involves what collagen type

A

collagen type I

type I found mostly in interstitial connective tissues and bone

108
Q

cartilage and nucleus pulposus are composed of what types of collagen?

A

type II

109
Q

basement membrane is composed of what type of collagen

A

type IV

110
Q

granulation tissue is composed of what type of collagen

A

type III; granulation tissue lasts approximately 7 days and eventually replace by type I; forms reticular fibers in organs such as spleen, lymph node, and bone marrow

111
Q

primary collagen found in mature scars

A

type I

112
Q

familial hypercholesterolemia is what type of inheritance

A

autosomal dominant

113
Q

LDL receptor defect leads to..

A

high LDL levels; increases risk of premature atherosclerosis

*Homozygous familial hypercholesterolemia (a rarer and more severe form of the disease due to inheritance of 2 defective LDL receptor alleles) –often presents with coronary heart disease in [childhood/adolescence]

114
Q

pulsus paradoxus

A

exaggerated drop in systolic blood pressure (>10mmHg) during inspiration; usually seen in cardiac tamponade

115
Q

unlike S3 sound, S4 sound is always pathologic in ______ patients

A

younger

116
Q

classic characteristics of cardiac tamponade (3)

A
  • muffled heart sounds
  • jugular venous distension
  • hypotension
117
Q

breath sounds heard in tension pneumothorax

A

absent; hyperresonance to percussion on affected side

118
Q

aortic rupture causes ________ shock

A

hypovolemic

119
Q

cardiac tamponade leads to decreased ______ pressure during _______

A

systolic pulse pressure; inspiration

120
Q

_______ is beat-to-beat variation in pulse amplitude due to change in systolic blood pressure

A

pulsus alternans

121
Q

a dicrotic pulse is a pulse with 2 distinct peaks. when do these peaks occur

A

one during systole; one during diastole

122
Q

____________ pulse is a rapidly rising pulse with high amplitude due to rapid ejection of a large stroke volume against a decreased afterload.

A

hyperkinetic; occurs with aortic regurgitation and high-output conditions (ie thyrotoxicosis, arterio-venous fistula)

123
Q

______________ aka slow-rising low amplitude pulse

A

pulsus parvus et tardus; occurs during fixed LV outflow tract obstruction due to diminished stroke volume and prolonged ejection time

124
Q

Left ventricular gallops (S3/S4) will be best heard at cardiac apex in Left lateral decubitus position. At what point in the breathing cycle are they best heard?

A

End of expiration; lungs are decreased in volume and brings the heart closer to chest wall

125
Q

straining phase (phase 2) of valsalva maneuver increases/decreases venous return to heart?

A

decreases; just like standing does

126
Q

molecule that is important for excitation-contraction coupling in smooth muscle cells, which lack troponin, unlike cardiac and skeletal muscles

A

calmodulin

127
Q

calcium efflux from cardiac cells prior to relaxation due to

A

Na/Ca exchange pump

128
Q

intracellular calcium moved from cytosol into sarcoplasmic reticulum

A

SERCA pump; decreases calcium concentration within cytosol

129
Q

isolated systolic hypertension usually caused by..

A

age-related stiffness and decrease in compliance of the aorta and major peripheral arteries

130
Q

mechanism behind plaque rupture

A

activated macrophages infiltrate thin-cap fibroatheromas (characterized by large necrotic core covered by thin fibrous cap) and secrete metalloproteinases which break down ECM proteins (ie collagen), destabilizing the mechanical integrity of the plaque, leading to plaque rupture.

131
Q

what strengthens extracellular collagen fibers by mediating cross-link formation?

A

lysyl oxidase; cross-links between lysine and hydroxylysine residues (requires copper)

132
Q

mechanism behind decreased pulse on palpitation during inspiration in cardiac tamponade

A

due to impaired expansion into the pericardial space, the increased RV volume that occurs with inspiration leads to bowing of interventricular septum towards LV. This leads to decrease in LV end-diastolic volume and forward stroke volume, with a decrease in systolic pressure during inspiration

133
Q

most common site for aortic injury during blunt trauma?

A

aorta close to left subclavian artery (aka aortic isthmus) which is close to ligamentum arteriosum

134
Q

Name the 2 areas where baroreceptors are found what nerve innervates these areas

A

Carotid sinus: hering nerve (branch of glossopharyngeal nerve); afferent limb; travels to medullary center

Aortic body: parasympathetic fibers via vagus nerve travel down to aortic arch