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CardioPulmonary Vascular Disease > Pulmonary Vascular Diseases > Flashcards

Pulmonary Vascular Diseases Flashcards

1
Q

Right Heart Failure & pulmonary HTN are associated with what?

A

pulmonary emoblism

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2
Q

List the 3 components of
Virchow’s Triad?

A

Stasis, endothelial injury, hypercoagulability

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3
Q

saddle emboli occur at the bifurcation of what vessel?

A

Right & Left Pulmonary Artery

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4
Q

Normal pulmonary BP is clinically defined as ……… of systemic BP.

A

1/8th

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5
Q

Pulmonary HTN is clinically defined as ……….. of systemic BP.

A

1/4th

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6
Q

Mutation of what protein receptor causes primary pulmonary hypertension and what is the protein’s function?

A

BMPR2; in vascular smooth muscle, inhibits proliferation and promotes apoptosis

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7
Q

Pulmonary HTN is morphologically defined by what characteristics?

A

medial hypertrophy of pulmonary vessels & RVH, pulmonary fibrosis, loss of capillary beds

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8
Q

Grade 1 PHTN is characterized by what histological features?

A

medial hypertrophy without intimal changes

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9
Q

Grade 2 PHTN is characterized by what histological features?

A

Medial Hypertrophy with intimal cellular proliferation

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10
Q

Grade 3 PHTN is characterized by what histological features?

A

medial hypertrophy, intimal proliferation & intimal fibrosis

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11
Q

Grade 4 PHTN is characterized by what histological features?

A

progressive generalized vascular dilatation; occlusion by intimal fibrosis; fibroelastosis; plexiform lesions

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12
Q

Grade 5 PHTN is characterized by what histological features?

A

veinlike branches of hypertrophied muscular arteries; cavernous lesions; angiomatoid lesions

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13
Q

Grade 6 PHTN is characterized by what histological features?

A

necrotizing arteritis

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14
Q

Group 1 PHTN is associated with what medical conditions?

A

autoimmune diseases

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15
Q

Group 2 PHTN is associated with what medical conditions?

A

congenital or acquired heart disease

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16
Q

Group 3 PHTN is associated with what medical conditions?

A

Obstructive Sleep Apnea

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17
Q

Group 4 PHTN is associated with what medical conditions?

A

recurrent thromboemboli

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18
Q

Describe the pathogenesis of Goodpasture syndrome?

A

circulating autoantibodies against a3 chain of collagen IV

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19
Q

what are the pulmonary histological findings of GP syndrome?

A

red-brown consolidation; focal necrosis of alveolar walls assoc. w/ intra-alveolar hemorrhages; hemosiderin-laden macrophages; in later stages: thickening pulmonary fibrosis, type II pneumocyte & alveolar space hyperplasia

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20
Q

what are the renal histological findings of GP syndrome?

A

focal proliferative glomerulonephritis

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21
Q

What are the clinical hallmarks of idiopathic pulmonary hemosiderosis?

A

cough, hemoptysis, anemia

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22
Q

What are the histological hallmarks of idiopathic pulmonary hemosiderosis?

A

hemosiderin laden macrophages in alveolar spaces

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23
Q

what are the histological hallmarks of granulomatosis with polyangiitis?

A

necrotizing granulomas in URT; granulomatous vasculitis of small to medium sized vessels; focal crescentic glomerulitis

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24
Q

Fibromuscular Intimal Hyperplasia is driven by what biological response and what types of vessels does it affect?

A

inflammation or mechanical injury; muscular large arteries

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25
Q

Monckeberg medial sclerosis affects which vascular layer?

A

Tunica Media; “pipestem” appearance on x-ray

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26
Q

Hyaline arteriolosclerosis is defined as what and is associated with which clinical conditions?

A

proteins leaks into vessel wall; commonly seen with cases of essential HTN & DM

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27
Q

Hyperplastic arteriolosclerosis is defined as what and is associated with which clinical conditions?

A

thickening of vessel wall by hyperplasia of smooth muscle; commonly seen with malignant HTN and appears as an “onion-skinning” pattern under the microscope

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28
Q

arteriolosclerosis affects which type of vessels?

A

small arteries & arterioles

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29
Q

Atherosclerosis affects which type of vessels?

A

tunica intima

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30
Q

what is the definition of an Atheroma?

A

raised focal lesion within the intima; consists of cholesterol covered by a fibrous cap

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31
Q

List the 3 major components of atheromas?

A

cells: SM, macrophages, t-lymphocytes; ECM: collagen, elastic fibers, proteoglycans; Intracellular & extracellular lipid

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32
Q

Systemic inflammation is indicated by which biomarker?

A

C-reactive protein (CRP)

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33
Q

monocytes & t-lymphocytes bind to which receptor on dysfunctional endothelial cells?

A

VCAM-1

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34
Q

VSMC recruitment to the tunica intima is mediated by which factors?

A

PDGF & FGF

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35
Q

What components involved in the mediation of endothelial dysfunction can destabilize a plaque?

A

macrophages; high microvessel density; thin fibrous cap; presence of intraplaque hemorrhage; cap rupture; superimposed thrombus; large lipid core; increased levels of MMPs; SM hypoplasia

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36
Q

Describe the 6 stages of atherosclerosis progression?

A

I: isolated macrophage foam cells; II: intracellular lipid accumulation; III: II + extracellular lipid accumulation; IV: II + more severe III; V: lipid core & fibrotic layer, calcific; VI: hematoma, hemorrhage, thrombosis

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37
Q

Aneurysm arise from which vessel layer & what are the physiological consequences?

A

thickened tunica intima means less O2 diffusion to other layers of the vessel wall causing atrophy of media and adventitia layers

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38
Q

Define Angina pectoris.

A

uncomfortable chest sensation produced by myocardial ischemia

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39
Q

Define stable Angina.

A

transient angina precipitated by exercise and relieved by rest; oxygen demand exceeds available blood supply

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40
Q

Define unstable angina.

A

increased frequency and duration of episodes produced at rest; oxygen demand unchanged

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41
Q

Define Variant Angina.

A

chest discomfort at rest due to coronary artery spasm rather than increased myocardial oxygen demand

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42
Q

Tn-I & Tn-2 begin to rise after how much time after an MI and peaks when and remains elevated for how long?

A

2 - 4 hrs.; peaks at 24 hr.; remain elevated for 7-10 days after MI episode

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43
Q

CK-MB begin to rise after how much time after an MI, peaks when, & and returns to normal after how much time?

A

rises within 4-8 hrs.; peaks at 24 hr. & returns to normal by 72 hrs.

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44
Q

Why is CK-MB a more useful biomarker for determining re-infarctions than troponins?

A

B/C levels should return to normal after 72 hrs. from initial episode while troponins take several days to go back down to normal

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45
Q

What MI changes can be seen 0-30 min after initial episode?

A

nothing

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46
Q

what MI changes can be seen b/t 30 min-4 hrs. after initial MI episode?

A

wavy fibers

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47
Q

what MI changes can be seen b/t 4 & 12 hrs. after initial MI episode?

A

start of coagulative necrosis, edema, & hemorrhage; focal mottling

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48
Q

what MI changes can be seen b/t 12 & 24 hrs. after initial MI episode?

A

pyknosis, myocyte hypereosinophilia, neutrophil infiltrate; contraction band necrosis; dark mottling

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49
Q

what MI changes can be seen after 1-3 days following a MI episode?

A

loss of nuclei, interstitial infiltration of neutrophils, yellow-tan infarct center

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50
Q

what MI changes can be seen 3-7 days following an MI episode?

A

yellow-tan center; phagocytosis of dead cells by macrophages

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51
Q

what MI changes can be seen 7-10 days after an MI episode?

A

maximal yellow tan w/ depressed red-tan margins; early granulation tissue

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52
Q

what MI changes can be seen 10-14 days after MI episode?

A

red-grey infarct borders; mature granulation tissue w/ angiogenesis, formation of collagen

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53
Q

what MI changes can be seen 2-8 weeks following an MI episode?

A

grey-white infarction scar; increased collagen density, decreased cellularity & vascularity

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54
Q

what MI changes can be seen after 2 months following an MI episode?

A

scarring complete; all that remains is a dense collagen scar where the infarct occured

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55
Q

What are the physiological consequences of vascular ischemia?

A

decreased oxidative phosphorylation assoc. w/ decreased ATP production; decreased function of Na+ pump; subsequent influx of H20 & Na+ causing cells to swell

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56
Q

Describe the pathogenesis of contraction bands.

A

Form in cells where ATP is greatly diminished or absent; such is the case for ischemia induced MIs which causes hypercontraction of myocyte sarcomeres leading to a tetanic state; assoc. w/ reperfusion injury

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57
Q

Arrhythmias assoc. w/ SA & AV Nodes involve which coronary artery?

A

RCA

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58
Q

Arrhythmias assoc. w/ Bundle of his involve which artery?

A

LAD

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59
Q

What are the clinical symptoms & signs assoc. w/ pericarditis?

A

Symptoms: sharp pain aggravated by inspiration relieved by leaning forward or sitting up, Hypotension assoc. w/ pulsus paradoxus; Signs: friction rub on PE, Water bottle configuration of radiography, EKG findings: ST segment elevation & PR segment depression

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60
Q

What is the pathogenesis of Dressler’s syndrome?

A

autoantibodies directed against damaged pericardial antigens; autoimmune induced fibrinous pericarditis

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61
Q

What can cause myocardial rupture & how many days after an MI does it usually occur?

A

b/t 3-7 days after MI episode; myocardium weakened by coagulative necrosis, neutrophilic infiltrate, & lysis of myocardial connective tissue

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62
Q

Describe different pathogenesis that can lead to rupture of the ventricular free wall.

A

Cardiac Tamponade: compression of heart by a fluid-filled pericardium; Kussmaul sign: paradoxical rise in JVP on inspiration indicative of limited filling of the right ventricle

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63
Q

What is a false aneurysm?

A

when the epicardium & pericardium form an adherent wall

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64
Q

What is a true ventricular aneurysm?

A

narrowing of ventricular wall that budges outward into the pericardial space

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65
Q

What is the most common cause of a papillary muscle rupture?

A

occlusion of RCA leading to ischemia of posterior LV 1/3 septum where posterior leaflet of mitral valve attaches

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66
Q

what are the most common causes of rupture to the ventricular septum?

A

Lt. to rt. shut; JVD; pedal edema; right sided heart failure; assoc. w/ LAD coronary artery thrombosis

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67
Q

List the components of metabolic syndrome?

A

large waistline; high level of TGs; Low HDL; high LDL; HTN; glucose intolerance

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68
Q

what is the precursor for bile salts?

A

cholesterol

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69
Q

How is cholesterol eliminated from the body?

A

via feces

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70
Q

Lipids have poor solubility; what does the body due to increase solubility?

A

hydroxylation & carboxylation increase solubility of bile salts

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71
Q

What are the 2 main primary bile acids synthesized by the body and makes makes them primary bile acids?

A

cholic acid; chenodeoxycholic acid; primary b/c they are produced in the liver

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72
Q

What are the 2 main secondary bile acids synthesized by the body and what makes them secondary bile acids?

A

deoxycholic acid; lithocholic acid; secondary b/t they are produced from bacterial enzymes in the small intestine from primary bile acids

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73
Q

Why are secondary bile acids more likely to be excreted than primary?

A

they are less soluble due to loss of hydroxyl group and therefore harder to reabsorb

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74
Q

Describe the biological process of bile acid conjugation.

A

addition of an amino acid to the carbon 24 carboxylate: the two main ones are glycine and taurine

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75
Q

conjugated bile salts have a lower pKa than physiological pH; therefore what form will be more prevalent in the small intestine where the pH is 6?

A

higher percentage of ionized form

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76
Q

Where in the colon does bile acid reabsorption take place?

A

Ileum

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77
Q

Describe the pathogenesis of choleithiasis.

A

cholesterol gallstone disease due to imbalance of cholesterol, phospholipids, & bile salts

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78
Q

what is another name for Type I hyperlipoproteinemia?

A

Familial lipoprotein lipase deficiency

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79
Q

what is another name for Type IIa Hyperlipoproteinemia?

A

familial hypercholesterolemia

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80
Q

what is another name for Type IV Hyperlipoproteinemia?

A

familial hypertriacylglycerolemia

81
Q

What are some common risk factors for DVT?

A

Immobility; H/o of thromboembolic disease; use of estrogen; pregnancy; neoplasia; CHF; MI; obesity

82
Q

Why is smoking while taking oral contraception not advised?

A

use of estrogen already increases risk of PE & DVT 6x from baseline and smoking will only increase this factor

83
Q

Why is pregnancy considered a risk factor for thromboembolic disease?

A

uterine enlargement promotes venous stasis of LEs; thrombocytosis; increased platelet adhesiveness; release of thromboplastin at time of placental separation

84
Q

What types of neoplasia are assoc. w/ increased risk of TED?

A

lung; pancreas; breast; GI; GU

85
Q

Trousseau sign of malignancy indicates what and in what veins can this sign be seen?

A

indicates migratory thrombophlebitis in superficial veins

86
Q

what kinds of deficiencies can increase risk of TED?

A

Antitrhombin III; Protein C (extremely rare); protein S; plasminogen activators

87
Q

Why do mutations of Factor V Leiden increase risk of TED?

A

results in factor V being more resistant to cleavage by protein C

88
Q

What is the clinical presentation of PE?

A

dyspnea (most common); angina; anxiety; syncope; cough; hemoptysis (not commom)

89
Q

What are the typical PE findings assoc. w/ PE?

A

tachypnea; tachycardia; fever; focal crackles; rarely wheezing & cyanosis

90
Q

Pulmonary infarction is more commonly assoc. with what preexisting conditions?

A

LVF; mitral stenosis; COPD

91
Q

What is the gold standard for diagnosing DVT?

A

Venous ultrasonography; venography

92
Q

D-Dimer testing can only be used to rule out DVT if what is low and negative?

A

pretest probability of PE

93
Q

what is the gold standard for diagnosing PE?

A

pulmonary angiogram

94
Q

what is the drug of choice for prophylaxis of venous thromboembolism?

A

low molecular weight heparin

95
Q

RVF is commonly assoc. w/ what type of PE?

A

submassive PE with SBP > 90 mmHG

96
Q

What type of PE is assoc. w/ hemodynamic compromise & shock?

A

massive PE; SBP < 90 mmHg

97
Q

Stable Angina is assoc. w/ what % of vessel occulsion?

A

70%

98
Q

Stable Angina is associated w/ low V/Q ratio; how does this affect Oxygen supply and demand?

A

decreased O2 supply and increases O2 demand

99
Q

what are the 4 factors that when increased will also increase O2 demand?

A

HR; inotropy; preload; afterload

100
Q

What is Monday Disease?

A

seen in pts. that work in nitrate factories

101
Q

ACS encompasses

A

Unstable Angina; NSTEMI; STEMI

102
Q

unstable angina occurs when there is a ……% occlusion of coronary blood vessels.

A

90%

103
Q

Unstable angina is usually assoc. w/ what kind of MI?

A

NSTEMI

104
Q

STEMIs are assoc. w/ what % of artery occlusion?

A

100%

105
Q

Other than EKG findings, how else can unstable Angina w/ MI be distinguished from unstable angina with no MI?

A

NSTEMIs and STEMIs are going to indicate elevated plasma levels of Troponin & CK-MB

106
Q

what factors are used to calculate level of risk for recurrent CVD episodes?

A

History; EKG; Age; secondary risk factors; troponin

107
Q

Why should fibrinolysis be avoided for pts. w/ NSTEMIs?

A

This is basic fluid mechanics; fluids will naturally flow through routes of the least resistance; in the case of stenosis, the blood vessel is already narrowed so fluid is not going to want to naturally flow into the occluded artery in any case

108
Q

Why is fibrinolysis indicated for STEMIs and not NSTEMI?

A

the fluid mechanics do not change; so blood will still want to flow away from the occluded artery; however if the vessel was 100% occluded which is the case in STEMIs, then even a partial opening will at least stabilize the pt. temporarily until an angioplasty can be done

109
Q

what are absolute CIs for Fibrinolysis treatment of occluded arteries?

A

cerebral vascular lesion; ICH; intracranial neoplasm; ischemic stroke within last 3 months; pre-existing bleeding disorders; head trauma

110
Q

Ventricular arrhythmias induced by MI complications typically occur how long after the MI?

A

0-24 hrs.

111
Q

Pericarditis typically presents as an MI complication how long after the MI?

A

1-3 days

112
Q

Dressler syndrome can occur how many days after an MI?

A

2 weeks to several months

113
Q

what does the ASCVD risk calculator assess?

A

probability of a CVD event in a 10 yr. period

114
Q

what is the recommended daily sodium intake?

A

2300 mg/day

115
Q

what is the most common culprit of PAD?

A

atherosclerosis

116
Q

What is the typical clinical presentation for myalgia induced PAD?

A

claudication that is relieved by rest; impaired wound healing of the LEs

117
Q

What are the main symptoms of spinal stenosis induced claudication?

A

positional relief; paresthesia; radiculopathy

118
Q

If a pt. is complaining of claudication in their popliteal fossa, where is the vessel obstruction most likely located?

A

femoral artery

119
Q

what is the qualitative definition of ABI?

A

ratio of ankle pressure to systemic pressure

120
Q

how is ABI calculated?

A

measure brachial, dorsalis pedis, & posterior tibia BPs; then take the highest BP for the LE and divide by the brachial BP

121
Q

What is the clinical significance of the ABI?

A

The ABI gives you an indication of how severe the atherosclerosis is; the lower the ratio the more severe the PAD

122
Q

what would be the next step for a pt. w/ an ABI < 0.9?

A

Imaging w/ CTA or MRA; DSA is gold standard b/c it is the most sensitive but more invasive and very expensive

123
Q

What is commonly seen in pts. w/ an ABI < 0.4?

A

ischemic rest pain & tissue loss

124
Q

what does an ABI > 1.3 indicate?

A

pt. has calcified arteries rendering the ABI invalid for diagnosing PAD

125
Q

What are the main clinical signs of Acute limb ischemia?

A

LE palpitations; pallor; pain; paresthesis; paralysis; poikilothermia

126
Q

What are the main clinical signs for chronic Limb-threatening ischemia?

A

ABI < 0.4; rest pain; ulcers & gangrene in LEs

127
Q

What are the main differences b/t CAD & PAD?

A

CAD is assoc. w/ STEMI & NSTEMI; PAD is assoc/ w/ gangrene rest pain & claudication

128
Q

What is another term for Aortoiliac occlusive disease?

A

leriche syndrome

129
Q

what are the clinical signs of leriche syndrome?

A

claudication of buttock & thigh; decreased femoral pulses; Erectile dysfunction

130
Q

what is the most common culprit of a stroke?

A

carotid atheroembolus

131
Q

What is the clinical presentation for Transient Ischemic Attack?

A

focal cerebral deficits (depending on which artery in circle of Willis is occluded); episode lasts 2-15 min; unilateral motor, sensory loss and sometimes aphasia and dysarthria

132
Q

If a pt. presents with symptoms of transient monocular blindness what branch of the IC is most likely occluded?

A

ophthalmic division

133
Q

How is carotid stenosis screened?

A

duplex U/S

134
Q

What is May-Thurner Syndrome?

A

compression of common iliac vein by common iliac artery

135
Q

Why are pts. with a h/o DVT at increased risk for CVI & post-thrombotic syndrome?

A

DVT can damage the vessel walls which will promote coagulation & inflammation leading to endothelial damage

136
Q

where are venous and arterial ulcers in LEs most commonly located?

A

venous ulcers: 2-3 above medial malleolus and appear more fibrous; arterial ulcers: will appear more gangrenous & found in distal toes and on top of bony prominences

137
Q

what are primary causes of lymphedema?

A

milroy disease (LE edema in subQ and extensive ST hypertrophy); hypoplastic toenails; praecox (extensive ST swelling); isolated dorsal foot swelling

138
Q

what are common secondary causes of lymphedema?

A

infection (W. bancrofti); trauma; prior surgery; lymph node dissection; radiation; cancer

139
Q

What are the the clinical signs of Stage 1 lymphedema?

A

pitting that is relieved by elevation

140
Q

what are the clinical signs of State 2 lymphedema?

A

not fully relieved by elevation; pitting is variable

141
Q

what are clinical signs of State III lymphedema?

A

elephantiasis w/ severe fibrosis, warty overgrowths; fat deposition; no pitting

142
Q

Lymphangiosarcoma is most commonly found in what region of the body?

A

UEs

143
Q

Unlike atherosclerosis, which only affects the tunica intima, aneurysms affect all 3 vascular layers; describe the different types in your own words.

A

fusiform: the entire perimeter of the vessel is swollen; saccular: only a portion of the vessel perimeter is affected; eccentric: looks like a round bud coming off of the main vessel

144
Q

What is a pseudoaneurysm?

A

false aneurysm b/c only the tunica media & intima are affected; adventitia remains intact

145
Q

what are risk factors for aneurysm?

A

chronic use of tobacco products; HTN, AS, diseases of chronic inflammation

146
Q

how are aneurysms formed in the blood vessel?

A

form when there is a reduction of strength and elasticity of the tunica media

147
Q

what can cause the tunica media to loose its elasticity?

A

leiomyo hypoplasia; increased proteinase activity; destruction of ECM; chronic inflammation

148
Q

what is the most important risk factor for thoracic aortic aneurysms?

A

HTN!!!!!!!!!!!!

149
Q

What congenital diseases are accoc. w/ increased risk for TAA?

A

Marfan syndrome (defective fibrillin); EDS Type IV (defect of type III collagen); Loeys-Dietz (defective TGF-beta receptor); bicuspid aortic valve heart defect

150
Q

what infectious agents can cause TAA?

A

syphilis, S. Aureus

151
Q

what are other risk factors for TAA?

A

aortitis; chest trauma

152
Q

what is the most common place for traumatic aortic injury (TAI)

A

aortic isthmus just distal to the left subclavian artery

153
Q

why is TAI a pseudoaneurysm?

A

does not affect the tunica adventitia

154
Q

why is the aortic isthmus the most common location for TAI?

A

Isthmus is a latin term for a narrowing making this part of the aorta intrinsically weaker; this is also a transition zone for ascending and descending aorta; shear stress from the ligamentum arteriosum can also cause this region to be weaker

155
Q

what is the most common cause of death for pts. w/ marfan syndrome

A

aortic dissection/rupture

156
Q

what is the most common cause of death for Type IV EDS?

A

arterial rupture

157
Q

What are clinical distinctions that can be made b/t Marfan & Loeys-Dietz syndromes?

A

bifid uvula; hypertelorism; cervical spine deformity; these are all unique to LDS and typically not seen in pts. w/ marfan

158
Q

what is the physiological consequence of having a bicuspid Aortic valve instead of a tricuspid one?

A

decreased valve cross-sectional area; this will increase the aortic pressure and cause increased wall stress; result is overdilation of aorta and more susceptibility for developing a TAA

159
Q

syphilis affects what part of the aorta?

A

vasa vasorum

160
Q

obliterative endarteritis causes what biological response?

A

inflammation and tissue proliferation leading to occulsion

161
Q

TAA can be categorized into what 3 subtypes?

A

Ascending Thoracic Aorta; Aortic Arch & Descending Thoracic Aorta

162
Q

A TAA in the ATA can lead to what physiological consequences?

A

aortic regurgitation leading to HF

163
Q

what are clinical signs of a TAA in the coronary artery of the AA?

A

myocardial ischemia or infarction

164
Q

what are clinical signs of a TAA in the superior vena cave portion of the AA?

A

JVD, facial and UE edema

165
Q

what are clinical signs of a TAA in the pulmonary artery portion of the AA?

A

PE-like symptoms

166
Q

what are the clinical signs of a TAA in the airway portion of the AA?

A

dyspnea, cough, wheezing

167
Q

If the left recurrent laryngeal nerve is being affected by a TAA in the AA, what is the most common sign?

A

hoarseness

168
Q

what would be the main CC of a TAA in the DTA?

A

back pain

169
Q

What are signs of a TAA that can be seen on a CXR?

A

widened mediastinum; aortic knob hypertrophy; trachea deviation

170
Q

TAAs in the DAT are susceptible to thrombus formation; where do these thrombi typically emolize to?

A

disal regions of the body such as the renal arteries and arteries in the LEs

171
Q

Rupture of the TAA can lead to what physiological conseqneces?

A

acute pericardial tamponade

172
Q

What would be the physiological consequences if the TA were to rupture?

A

pleural effusion; hemorrhagic shock; respiratory failure

173
Q

what is the main culprit of abdominal aortic aneurysm?

A

AS!!!!!!!!!!!!!

174
Q

what is the most affected blood vessel by AS?

A

abdominal aorta

175
Q

why is the infrarenal aorta the most common site for AAAs?

A

lacks a vasa vasorum of its own and therefore relies on diffusion from the tunica intima of the Abdominal aorta for oxygen and nutrients

176
Q

what are the histological hallmarks for inflammatory AAAs?

A

dense, periaortic fibrosis of the tunica adventitia

177
Q

Mycotic AAAs are caused by what?

A

bacterial infections: S. Aureus, Salmonella (often assoc. w/ gastroenteritis), S. epidermidis (usually on occur if an AAA already exists)

178
Q

What is a clinical hallmark for AAA on PEs?

A

pulsatile abdominal masses

179
Q

What is the most common diagnostic tool for AAA?

A

Ultrasound

180
Q

Tearing of which two layers defines an aortic dissection?

A

tearing of the tunica intima & media from the aortic wall

181
Q

The new cavity that forms from the result of an aortic dissection is referred as what?

A

false lumen

182
Q

what is the definitive diagnosis for AD?

A

CTA

183
Q

What would be the signs of a clinical vignette for a pt. w/ aortic dissection?

A

sudden onset of severe chest pain described as “tearing” with radiation to the back

184
Q

Describe a DeBakey I AD in your own words?

A

dissection of the TAA that propagates to all portions of the TAA perimeter

185
Q

Describe a DeBakey II AD in your own words?

A

dissection of the TAA isolated to one region in the vessel

186
Q

describe a DeBakey III AD in your own words?

A

AD of the DTA or the AAA after leaving the left subclavin artery

187
Q

what are clinical signs of malperfusion syndrome related to an AD that spreads to the coronary arteries?

A

myocardial ischemia or MI

188
Q

what are clinical signs of malperfusion syndrome related to an AD that spread to the carotid arteries?

A

TIA, stroke, dysphasia, neurologic deficits

189
Q

what are clinical signs of malperfusion syndrome related to an AD that spread to the mesenteric arteries?

A

abdominal pain, mesenteric ischemia

190
Q

what are clinical signs of malperfusion syndrome related to an AD that spread to the renal arteries?

A

acute renal failure, oliguria or anuria

191
Q

JVP will be reduced when this happens?

A

hypovolemia

192
Q

the diaphragm is better for detecting what kind of sounds?

A

high-pitched; S1, S2, S4

193
Q

the bell is better for detecting what kind of sounds?

A

low-pitched; S3; mitral stenosis

194
Q

how can you discern if a murmur is assoc. w/ systole or distole?

A

murmur is also heard with auscultation of the carotids

195
Q

A cardiomyopathy of the aortic & pulmonary valves are most likely to be heard in which regions of the chest?

A

base of the heart B/L 2nd ICS

196
Q

cardiomyopathies of the AV valves can be heard where on the chest?

A

tricuspid valve: sternal aspect of the left apex; bicuspid (mitral): posterolateral of tricuspid area no further than the 5th ICS (left midclavicular line)

197
Q

What are clinical indications of a palpable PMI that is sustained or stuck out?

A

LVH

198
Q

What are clinical indications of a palpable PMI that is diffusely distributed?

A

CHF; dilated cardiomyopathy

199
Q

Cardiac sympathetic innervation is in what vertebral levels? And parasympathetics?

A

T1-T5 for sympathetic innervation; Parasympathetic: right vagus for SA node & left vagus for AV node

CardioPulmonary Vascular Disease (7 decks)

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