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patho 2 > cardio > Flashcards

cardio Flashcards

1
Q

Mi characterized by

A

O2 demand exceeds O2 supply

supply of coronary blood cannot meet the demand of the myocardium and leads to ischemia

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2
Q

decreased supply can be caused by

A 
narrowing of coronaries due to atherosclerosis
coronary artery vasospasm
hypoxia
anemia
aortic insufficiency
aortic stenosis
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3
Q

increased demand

A

sever hypertension

tachycardia

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4
Q

MI risk factors

A

age >75, male, hypercholestremia, DM, HTN, smoking, family hx, obesity, PVD, menopause, high-estrogen BC, sedentary life style, psychosocial characteristic

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5
Q

atherosclerotic plaque leads to

A

unstable plaque with ulceration or rupture and thrombosis—ACS—sustained ischemia—MI—Myocardial inflame with necrosis—myocardial remodeling

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6
Q

Acute coronary syndrome

A

atherosclerotic processes–stable plaque formation or unstable plaque–rupture or thrombus
thrombus–transient ischemia–unstable angina
vessel obstruction sustained–MI with inflame and necrosis

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7
Q

Mycocardial remodeling

A

a process mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative stress, and inflammatory cytokines, which causes myocyte hypertrophy, scaring, loss of contractile function

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8
Q

myoctye hibernation

A

persistently ischemic undergoes metabolic adaption to prolong myocyte survival

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9
Q

atherosclerotic plaque

A

has lipid-rich core and thin fibrous cap

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10
Q

cause rupture of plaque

A

shear force
inflam
apoptosis
macophage-derived degradation enzyme

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11
Q

after plaque ruptures what happens to lesions

A

thrombus formation over lesion, and vasoconstriction of vessel and increased inflam with cytokine release
platelet activation and adherence
production of thrombin and vasoconstrictors

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12
Q

unstable angina or MI ultimately from

A

acute decrease in coronary blood flow

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13
Q

vulnerable plaque is a what and characteristics

A

rupture prone atherosclerotic plaque
t-cells recruited to shoulder (where wall most vulnerable)
marcophages cluster around Tcell
thin fibrous cap
newly formed intrawall capillaries
lymphocyte and mast cell infiltration
**vulnerability more of a concern than size

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14
Q

plaques, whats more significant

disrupted plaque characteristics

A

*instability more significant than size
*become disrupted from hemodynamic trauma
*mechanical stress is max at fissure at the junction of fibrous cap and plaque free vessel wall
eccentric-not uniformed
large soft necrotic core
covered by thin necrotic core
rich in macrophages and T cells
Metalloproteinases-degreade collagen cap

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15
Q

role of stress in acute cardiac events

A

from central and ANS activation: can effect the demand side

pain, anesthesia stress

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16
Q

physiologic response to stress

A

increased catecholamines, HR, BP
all lead to increase ECG instability, demand
leads to VF/VT–sudden cardiac death
*increased demand can also lead to ischemia–MI
also decreased plasma volume and increased coronary constriction leads to
decreased supply–ischemia and plaque rupture–MI
and increased platelet activity leads to coronary thrombosis —MI

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17
Q

Stable angina

A

CP caused by myocardial ischemia
luminal narrowing and hardening of arterial walls
-vessel can’t dilated in response to increased demand
no change in precipitating factors for @ least 60 days
*relieved by rest, decreased demand, vasodilator ex: nitro

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18
Q

ask pt CP

A

frequency of pain, how do the tx, duration of pain, has it changed

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19
Q

unstable angina

A 
caused by less than normal activity
last for prolonged period
occurring more frequently 
signals impeding MI
*Crescendo, pain starts slow and grow
*increased frequency, duration, 
*acute plaque changes
*usually partial thrombosis
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20
Q

Prinzmetal Angina

A

At rest
cononary spasm
in plaque area or normal area
sometimes associated with other vasospastic disease ex: Raynauds

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21
Q

Infarction

A

Necrosis caused by ischemia with in 20-30 min of ischemia
begins in subendocardial regions
reaches full size in 3-6hrs
size depends on proximity of lesion, collateral circulation

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22
Q

Infarction complications 10

A

papillary muscle dysfunction-valvular disease
external rupture of infarct–day 4-7 most common–tamponade–death
mural thrombi-stable, Risk for stroke
acute pericarditis: most common day 2-3
ventricular aneurysm-fibrous outputting of ventricle-anteroapical region–most common
arrhythmias
LVF +/- pulm edema
cardiogenic shock–rare
rupture of wall, septum, papillary muscle
thromobembolism

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23
Q

site of MI and vessel involvement RCA LCA LAD LCX

A

RCA: posterior inferior
LCA: anterolateral
LAD: anteroseptal
LCX: (circumflex) Lateral

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24
Q

vascular hypertension

A

sustained systolic 140mmhg diastolic 90

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25
Q

HTN is the most important risk factor in….5

A

CAD, CVA, cardiac hypertrophy, renal failure, aortic dissection

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26
Q

types of HTN

A

systolic and diastolic:
essential HTN
2ndary–renal, endocrine, cardiovascular, neurologic

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27
Q

regulation of normal BP

A

BP= COxPVR
CO factors: cardiac factors, blood volume, HR, SV
PVR factors: neural factors, humoral factors, constrictors, dilators, blood viscosity

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28
Q

patho of essential (primary) HTN risk factors

A

genetic-polygenic and heterogeneous (look different per pt), polymorphism @ several gene loci
environmental–stress, obesity, smoking, salt consumption, sedentary life-style

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29
Q

Heavy salt consumption

A

increased BP with age directly correlate with increase levels of Na intake
consume little Na-no HTN but increased Na intake and develop HTN
large Na load over short period of time–develop increased SVR
most pt with HTN have increased Na in vascular tissue and blood cells
Na restriction decrease BP, diurtics-antiHTN by promoting Na excretion

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30
Q

HTN theory 2

A

1 renal retention of excess Na
existence genetic factors
decrease Na excretion
increase fluid volume/CO
vasoconstriction occurs (autoregulation): increase BP
cyclical
2. vasoconstriction and vascular hypertrophy
increase in vascular resistance caused by
1. factors that induce functional vasoconstriction–neurogenic, release of vacocontrictor agents, genetic defect in transport of Na and Ca
2. stimuli that induce structural change in vessel walls
3. both

31
Q

Pathogenesis of 2ndary HTN

A 
oral contraceptives (unknown, most likely Na retention) 
renal parenchymal disease (disturbances in filtration, reabsorption of Na)
renin-secreting tumors (causes increase in angiotensin and aldosterone)
primary aldosteronism (aldosterone promotes Na retention) 
cushings syndrome (Glucocorticoids facilitate sodium and water retention)
pheochromocytoma (Excess catecholamines raise vascular tone)
32
Q

HTN tx drug

A

diuretic where first line, others now

33
Q

HTN tx non-drug

A

lifestyle change: wt reduction, smoking cessation, increase physical activity
Na restriction diets
ETOH
relaxation techniques

34
Q

HTN crisis definition, tx

A

sudden increased in DIASTOLIC above 130
due to: activation of renin-angiotensin-aldosterone system
Tx: prompt, controlled decreased in BP with NTP (0.5-10mcg/kg/min IV)
monitoring UOP and intraarterial BP
*decrease DBP carefully to 100-110 over several min-hr

35
Q

LV hypertrophy

A 
increase in size to LV
decrease volume (blood)
decreased compliance
contractility normal
leads to Lheart failure
36
Q

stenosis

A

high pressure
valve orifice is constricted and narrowed
*impeding forward flow
**avoid:
-increased HR bc decreases CO and limits diastolic filling
-decreased SVR bc poor CPP and coronary perfusion

37
Q

regurgitation

A

High Volume
cusps fail to shut completely, allows blood to flow when suppose to be closed
Avoid these bc:
*slow HR allows for more time and worsening regurg
*increased SVR increases the regard fraction

38
Q

Mitral stenosis

A

fusion of mitral value leaflets at commissure during healing process of acute rheumatic fever
when mitral value area is <1cm need 25mmhg of pressure to maintain adequate CO
LA enlargement predispose to afib
Stasis of blood in distended atria predispose pt for thrombi– pts often on chronic anticoagulants
**avoid increased HR and decreased SVR

39
Q

mitral stenosis symptoms

A

DOE when increase in CO, Pulm Edema
Severe MS lead to CHF
Think left heart

40
Q

Aortic stenosis

A

Isolate non-rheumatic- results from progressive calcification and stenosis of congenitally abnormal bicuspid valve (mitral)
Rheumatic fever-aortic stenosis almost always occurs in association with mitral stenosis
hemodynamically: associated with a transvalvular pressure gradient >50mmhg
-aortic valve orifice area <1cm2 (normal 2.5 to 3.5)
*leads to L heart failure
(LV hypertrophy, pulm edema, syncope)
**avoid increased HR and decreased SVR

41
Q

Aortic stenosis s/s

A

triad: angina (often in absence of ischemic heart disease)
DOE
syncope
“SAD”

42
Q

Mitral regurgitation

A

usually due to rheumatic fever and almost alway associated with mitral stenosis
LA volume overload by retrograde flow of LV SV
responsible for V wave on the PAWP: size correlates with magnitude of regurgitant flow
(LA hypertrophy, Lheart failure, pulm edema)
**Want small increased HR and decreased SVR

43
Q

Aortic regurgitation

A

acute: infective endocarditis, trauma, dissection of a thoracic aneurysm (big problem, hasn’t had time to compensate)
Chronic: prior rheumatic fever, persistent systemic HTN
hemodynamic problem: regurg part of ejected SV from aorta back to LV, decrease forward L ventricular SV
(LV hypertrophy, pulm edema, syncope)

44
Q

Endocarditis definition, risk, patho

A

infection and inflamm of endocardium
*bacterial: streptococci, staph, and entero
Risk factors: prosthetic valve, turbulent blood flow, endocardial damage
Patho: bacteria enters blood screen from IV drugs use, dental procedures, trauma
-vegetative lesion occurs on heart valves and surrounding structure
inaccessible to host defenses bc embedded in protective fibrin clots

45
Q

Endocarditis s/s

A

fever, night sweats, malaise, weight loss, murmur, petechia, osler nodes (on fingers and toes) jane way lesions (palms, soles)

46
Q

Non-bacterial endocarditis

A

thrombotic vegetation
bland thrombus with virtually no inflamm in value cusp or thrombotic deposit
thrombus is only loosely attached to cusp

47
Q

Inflam myocarditis early and late s/s

A

dilated cardiomyopathy
early s/s: fatigue, dyspnea, palpitations **vague s/s-difficult to diagnosis
progress to: CHF, pulses alternans (SBP differs with each beat), tachycardia, pulm edema
*complete recovery with abx: IV and home on PO

48
Q

Non-inflam cardiaomypathy

A

manifest as CHF
due to: toxicity (ex ETOH), idiopathic, degenerative, infiltrative, post MI
characterized by: increased filling pressure, failure of contractile strength- beyond Franks curve, increased arterial impedance (resistance) and decreased SV

49
Q

dilated cardiomyopathy

A

diminished systolic performance of heart

impaired systolic function–leads to increased intracardiac volume, ventricular dilation

50
Q

decreased contractility

A

causes ventricles dilate to compensate–increased cardiac work–increased O2 consumption–decreased CO–increased SNS outflow to increased HR and SVE

51
Q

clinical picture of CHF associated with dilated cardiomyopathy
forward failure

A
  • *forward failure: fatigue, hypotension, oliguria(CO to kidneys decreased)–caused by decreased CO and decreased organ perfusion
  • decreased renal perfusion– activation of renin-angiotension-aldosterone system: increased volume through Na and H20 retention
52
Q

clinical picture of CHF associated with dilated cardiomyopathy
backward failure

A

increase filling pressure required by heart

2ndary mitral regard caused by dilation of ventricle

53
Q

Left sided failure

A

orthopena,
pulm edema,
paroxysmal nocturnal dyspnea (episode of SOB during sleep)

54
Q

Right sided failure

A

Hepatomegaly
JVD
peripheral edema

55
Q

Hypertrophic Cardiomyopathy other names

A

idiopathic hypertrophic subaortic stenosis (IHSS)
asymmetric septal hypertrophy
hypertrophic obstructive cardiomyopathy
muscular subaortic stenosis

56
Q

Hypertrophic Cardiomyopathy: clinical features

A

autosomal dominant trait- main defect is contractile elements of heart–then increased density of Ca channels
pt often asymptomatic
increased HR worst thing for these pt
s/s: dyspenia, angina, syncope, ventricular dysrhythmias
become symptomatic in 2-3decade of life
most frequent finding in autopsy in young previously health adults with sudden cardiac death

57
Q

Hypertrophic Cardiomyopathy patho

A

asymmetric myocardial hypertrophy
diastolic dysfunction
enlargement of inter ventricular septum–usually top portion right below aortic valve
rapid LV ejection–80% during early systole
Often sub aortic pressure gradient
imbalance in myocardial O2 requirements

58
Q

Hypertrophic Cardiomyopathy dynamic obstruction is worsened by

A

decreased preload, after load
increased contractility
* these produce a decrease in ventricular volume thus increase proximity of anterior MV leaflets to IVS

59
Q

Hypertrophic Cardiomyopathy: factors that impair contractility do what to systolic function

A

improve it

the factors are: volume loading, vasoconstriction, myocardial depression

60
Q

Hypertrophic Cardiomyopathy have what valve problem and what kinda of compliance

A

MR- vasodilators worsen MR while vasoconstrictors decreased obstruction and MR
Poor diastolic compliance: atrial contribution maybe as high as 70%

61
Q

Hypertrophic Cardiomyopathy medical mgmt and surgical and ECHO finding

A

Beta-blockers–blunt SNS mediated increase in sub aortic stenosis, decreased tacky
Ca channel blockers–improves diastolic relaxation
surgical: myomectomy–cut out part of heart, don’t survive long
Echo: thickening IVS-base to apex
poor septal motion
anterior displacement of mitral valve

62
Q

Left to Right shunts

A

Atrial septal defects (ADS)
Ventricular septal defects (VSD)
Patent ductus arteriosus (PDA)
sometimes lead to tardive cyanosis (late) but does not cause cyanosis from onset

63
Q

Atrial septal defects

A

most commonly diagnosed in adulthood
forms btwn 4-6 weeks of embryonic life
due to foamen oval not closing properly/completely
s/s: eventually leads to pulm HTN
can use R to L shunt with enough pressure–cause cyanosis and CHF
can also be associates with Mitral insufficiency

64
Q

Ventricular septal defects

A 
Most common heart defect at birth
vent-septum develops btwn 4-8 weeks 
may close in childhood spont
can cause sever L to R shunt: with pulm HTN and CHF as well as infective endocarditis 
surg needed for large VSD
65
Q

Patent ductus arteriosus

A

btwn PA and aorta–allowing bypass of unO2 lungs in utero
constricts and closes at birth due to: increased O2 levels, decreased pulm resistance, decreased PGE2
high pressure L to R shunt
Pulm HTN cyanosis and CHF with bigger lesion: infective endocarditis can occur

66
Q

R to L shunts

A

cyanotic at birth
poorly O2 blood form R side of heart goes directly into arterial circulation via L heart
*tetralogy of Fallot
*transposition of great vessels

67
Q

Tetralogy of Fallot

A

Most common cause of Cyanotic congenital heart disease
caused by abnormal division of trunks arteriosus into a pulm trunk and aortic root
4 components:
VSD
Dextraposed (shifted to R)aortic root that overrides VSD
RV outflow obstruction
RV hypertorphy

68
Q

TET s/s

A

R to L shunt
decreased blood flow to lungs as well as increased blood flow to aorta
extent of shunting really depends on degree of outflow obstruction

69
Q

TET manifestation

A 
can be avoided by surg
due to chronic cyanosis:
erythrocytosis
increased blood viscosity: increased hemtocrit
Digital clubbig: poor O2 to periphery
Infective endocarditis
Systemic emboli
Brain abscesses
70
Q

Transposition of Great Vessels

A

Aorta rises from R ventricle
PA rises from L ventricle
must be associated with ASD, VSD, or PDA–to survive
**cyanosis

71
Q

Coarctation of the aorta (COA)

A

abnormal narrowing of aorta
more common in males
preductal or postductal
**most common postductal

72
Q

Preductal COA

A 
infrantile
weak femoral pulses
cyanosis of lower exterminates 
CHF
surgical correction needed to survive
73
Q

Postductal

A

older children/young adults
collateral have developed
decreased perfusion to kidneys: decreased SV, activates RAS
high pressure in upper extremity and low pressure in lower extremities
intermittent claudication can also arise

patho 2 (2 decks)

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