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ABSN > 406 patho - wk 1 > Flashcards

406 patho - wk 1 Flashcards

1
Q

myocarditis

A

an inflammatory disease of the myocardium that be mild to lethal and can cause degeneration & necrosis of cardiac myocytes
conduction disruption is common

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2
Q

what is the most common cause of myocarditis

A

viruses
coxsackie A & B

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3
Q

treatment of myocarditis

A

-anti inflammatories
-anti virals
-heart transplant (severe)

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4
Q

pericarditis

A

when the pericardium undergoes inflammation, fluid accumulates in the pericardial space -> the fluid is called pericardial effusion and it surrounds the heart
edema of pericardial space

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5
Q

when fluid around the heart accumulates to 200ml or greater and the heart becomes compressed, this is called

A

a cardiac tamponade

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6
Q

cardiac tamponade

A

the heart chamber are restricted by the surrounding pericardial fluid so they cannot stretch or fill with blood

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7
Q

a cardiac tamponade is a

A

medical emergency -> the fluid needs to be drained very quickly
pericardiocentesis

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8
Q

signs of acute pericarditis

A

-sharp chest pain that worsens w/ a deep breath
-fever
-dyspnea
-pericardial friction rub (scratching sound)
-ECG finds of ST elevations
-hyoptension/JVD/muffled heart sounds/confused/dizzy d/t tamponade
-pulsus paradoxus

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9
Q

pulsus paradoxus

A

a decrease in systolic blood pressure of 10 mmHg or more w/ inspiration (seen best w/ an ART line)
systolic should increase slightly w/ inspiration

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10
Q

treatment for pericarditis

A

-nsaids
-asa
-corticosteroids
-colchicine

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11
Q

aneurysms usually occur w/ what

A

high blood pressure -> the pressure weakens the arterial walls which causes bulges in the arterial wall (aka the aneurysm itself)

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12
Q

aneurysm facts

A

-cause turbulent blood flow
-susceptible to rupture
-bruits may be heard over them
-most common areas are aorta & cerebral arteries

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13
Q

risk factors for aneurysm

A

atherosclerosis, hypertension, diseases of blood vessels, trauma, tobacco use, >65yrs

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14
Q

aortic aneurysm

A

-abdominal aortic aneurysm (triple A)
-thoracic
-dissecting aortic aneurysm

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15
Q

cerebral aneurysm

A

anywhere in the brain

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16
Q

saccular aneurysm

A

-balloon shaped
-involves only one part of circumference
-wide neck

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17
Q

Berry aneurysm

A

subtype of saccular
-small neck
-located at bifurcation (commonly circle of willis)

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18
Q

how to dx a berry aneurysm

A

-angiography
-hx & clinical manifestations

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19
Q

treatment of a berry aneurysms

A

-medical control of HTN & vasospasm
-surgical: drain, clipping, or coiling

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20
Q

where is the circle of willis located

A

base of brain
so vessels off of it supply majority of blood to the brain

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21
Q

fusiform aneurysm

A

-entire circumference of vessel
-gradual/progressive dilation
-potentially extensive involvement or can only be monitored
related to diffuse of anterior sclerotic changes

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22
Q

false (pseudo) aneurysm

A

-localized dissection or tear in inner artery wall
-type of hematoma
-complication of vascular interventional procedures
-can be self limiting
leakage in between vascular graft and natural artery

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23
Q

abdominal aortic aneurysm (AAA)

A

-auscultation of a bruit over the abdominal aorta suggests presence
-if a pulsatile mass is evident in the abdomen during inspection or light palpation -> deep palpation should not be performed until the possibility a AAA is ruled out
-if ruptured, pt can bleed out very quickly

24
Q

dissection aneurysm

A

layers of the wall of the artery are separated & blood enters the region
can be a medical emergency

25
Q

aortic dissection clinical manifestations

A

-sudden severe, tearing pain
-elevated BP (early)
-later stages: BP unobtainable, syncope, hemiplegia, paralysis of lower extremities
-cardiovascular collapse -> shock -> death
emergency, minutes count

26
Q

aneurysm can be “” where dissections will have “”

A

asymptomatic ; severe sudden pain

27
Q

aortic dissection dx

A

CT scan or MRA (angiogram)

28
Q

emergency pharmacotherapy for aortic dissection

A

beta blockers
nitrates

29
Q

aneurysms are

A

dilation or out pouching of a vessel wall
true aneurysm involve all 3 layers of the arterial wall

30
Q

acute coronary syndrome (ACS)

A

umbrella term for situations where the blood supply to the heart muscle is suddenly blocked or compromised -> blockage can be sudden and complete or come & go (either way, tissue is dying)
medical emergency

31
Q

what 3 conditions do we think about w/ ACS

A

1) unstable angina -> most blood is able to get through
2) a non ST segment elevation MI (non stemi) -> reduced blood flow
3) a ST elevate segment elevated MI (stemi) -> blood flow is completely blocked

32
Q

unstable angina

A

new or unchanging chest pain caused by ischemia

33
Q

what do we do to differentiate between is causing the ACS

A

ECG

34
Q

variant / vasospastic angina

A

prinzemtal angina
-causes: coronary artery spasm d/t endothelial dysfunction
-may or may not have CAD
-sx occur usually at rest & at night
-possible elevated ST segment

35
Q

treatment for variant / vasospastic angina

A

nitrate

36
Q

unstable plaque characteristics that lead to ACS

A

-large lipid core
-active inflammation
-smooth muscle cells proliferate into intima (middle lining of blood vessel)

37
Q

unstable angina

A

1) chest pain occurring for the first time (myocardial ischemia)
2) chest pain more severe than usual w/ chronic angina (new regions of the heart myocardial ischemia)
emergency situation

38
Q

what is our main concern w/ unstable angina

A

plaque rupture & the thrombus formation bc size of clot & blockage determines how much blood gets through

39
Q

if a clot ruptures w/ unstable angina but no infraction occurs, what could be the reason

A

1) occlusion is partial
2) thrombus dissolved
cardiac enzymes will not be elevated

40
Q

what factors contribute to increasing SNS activity

A

-psychological stress
-exercise
-circadian rhythms

41
Q

theory of plaque rupture (look more in depth, basic overview)

A

increased SNS activity -> plaque rupture -> thrombus formation

42
Q

difference between ACS and stable angina + pt teaching

A

-severity & duration (stable should last 5 min & be gone within 15, ACS is longer than 15)
-ACS pt get no relief from nitrates, stable will
-stable “my chest is tight”, ACS “an elephant is sitting on my chest”
-ACS will have more diaphoresis, SOA, n/v, feeling of impending doom

43
Q

ACS signs in men

A

-discomfort or tingling in arms, back, neck, shoulder or jaw
-chest pain
-SOB

44
Q

ACS signs in women

A

-sudden dizziness
-heartburn like feeling
-cold sweat
-unuasal tiredness
-N/v

45
Q

S/s of an MI

A

diaphoresis, dyspnea, extreme anxiety, levine’s sign (fist to chest), pallor, retrosternal crushing chest pain that radiate to should, arm, jaw or back
-weak pulses

46
Q

what is an acute myocardial infarction

A

ruptured plaque + thrombus w/ an infarction d/t prolonged blow flow disruption or total blood flow disruption
will see ECG changes & an increase in cardiac enzymes

47
Q

is acute MI damage reversible

A

no -> it is prolonged ischemia w/o recovery & the myocardial cells suffer irreversible ischemic necrosis

48
Q

ischemia defined

A

“when the oxygen supplied does not meet the heart’s metabolic demands”

49
Q

infarction defined

A

“actual irreversible tissue death”

50
Q

can myocardial cells make ATP

A

no -> cells need a continuous supple of oxygen to make ATP so if oxygen levels go down so does the cells main source of energy

51
Q

what is the relationship between acute ischemia & ATP

A

when you have acute ischemia, ATP goes down instantly followed by decreased ability to contract

52
Q

irreversible injury w/ MI occurs within

A

30 mins - 4 hrs then tissue necrosis begins

53
Q

when is necrotic tissue cleared after an MI

A

in 1-2 weeks then the myocardium is very weak and susceptible to rupture
by 6 weeks, completely replaced by scar tissue

54
Q

three zones of damage w/ an MI

A

1) infarction = necrosis
2) injury = some recovery possible
3) ischemia = full recovery possible
to avoid infarction, increase oxygen & decrease demand on the heart

55
Q

what does the extent of damage depend on w/ an MI

A

-location or level of occlusion in the coronary artery
-length of time that the coronary artery has been occluded
-heart’s availability of collateral circulation

56
Q

STEMi: ST seg, QRS, T wave, Troponin, size, outcomes

A

ST seg: elevated
QRS: pathologic (wide), develops over hours
T wave: peaked then inverted
Troponin: elevated
size: larger
outcomes: poor

57
Q

NSTERMI: ST seg, QRS, T wave, Troponin, size, outcomes

A

ST seg: depression or normal
QRS: normal
T wave: inverted
Troponin: elevated
size: smaller
outcomes: better

ABSN (145 decks)

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