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Patho 2 > Lecture 5 - Cardiac Disorders > Flashcards

Lecture 5 - Cardiac Disorders Flashcards

(62 cards)

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1
Q

Overview of heart disease

A

Any condition hat effects the structure of function of the heart

Influenced by genes and environment

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2
Q

Ischemic heart disease (IHD)

A

General term for diseases where hypoxia leads to damage of the myocardium

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3
Q

IDH is also called (2)

A

CAD and coronary heart disease

It is almost always due to Coronary artery atherosclerosis

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4
Q

IHD can lead to: (5)

A

Angina
MI
Chronic IHD wiht HF
Cardiac dysrhymias
Sudden death oh no

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5
Q

IDH etiology

A

Chronic IHD results form progressive narrowing of coronary arteries

Myocytes adapt fo hypoxia, so effects are not felt until 70% blocked

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6
Q

Body’s compensatory mechanism for IHD

A

Generation of bypasses in the circulator system to get around blockages

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7
Q

Risk factors of IHD (modifiable)

A

High LDL
HTN
Smoking etc
Diabetes
Fat
Weak n slow
Eat like shit
Hypercoagulabilty

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8
Q

IHD pathogenesis in three steps

A
  1. Narrowing of coronary arteries
  2. Myocardial ischemia
  3. Myocardial damage
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9
Q

Angina

A

Chest pain due to intermittent ischemia in myocardium

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10
Q

Angina mechanism of action

A

Injured cells (hypoxia injury) release chemical that activate nociceptors.

Leads to referred pain due to spinal innervation (abdomen, shoulder, neck, jaw etc)

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11
Q

3 patterns of angina

A

Stable
Vasospastic
Unstable

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12
Q

Stable angina

A

Most common

Has stenotic artherosclerotic coronary vessels that dilate poorly

Manifests when cardiac workload is increased

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13
Q

Stable angina management
(Pharm + no pharm)

A

Rest
Beta blockers
Vasodilators
Antiplatet drugs
Statins
Ace inhibitors

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14
Q

Vasospastic angina other names

A

Prinzmetal or variant angina

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15
Q

Vasospastic angina is most common in:

A

Folks under 50

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16
Q

Vasospastic angina is characterized by (2)

A

Unpredictable attacks of pain

Vasospastic of a coronary artery
(Muscle hyper reactivity, ANS imbalance)

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17
Q

Management of Vasospastic angina

A

CCBs
Nitro
Address risk factors for CV diseases

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18
Q

All three types of angina in one point each

A

Stable
- predictable, demand driven

Unstable
- unpredictable, supply driven

Vasospastic
- random as fuck, spasm of muscle in coronary artery

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19
Q

Unstable angina other name

A

Crescendo angina

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20
Q

Unstable angina is characterized by:

A

Chest pain that is longer, worse, more frequent

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21
Q

When dose unstable angina occur

A

When a stenotic coronary artery is further blocked (embolism, ruptured plaque)

Severe obstuction

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22
Q

In unstable angina, what is suspected/confimred?

A

Actute myocardial ischemia/infarction

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23
Q

Unstable angina vs MI
(In terms of clots)

A

Angina
- clot dissolves before myocardial tissue dies
- can progress to MI

MI
- occlusion is complete and there is tissue death

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24
Q

MI

A

Necrosis of cardiac muscle tissue due to prolonged ischemia

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25
MI is often due to:
Change in an atherosclerotic plaque leading to thrombosis and coagulation This will occlude coronary artery lumens
26
How long before permanent damage occurs in an MI
20-30 mins
27
How does an MI spread ( what part of teh heart is affected first)
Blood flow form epicardium to endocardium This means that the farthest point (endo) will die first
28
Factors affecting the severity of an MI (lots)
Location Rate of obstuction Size of area obstructed Duration Metabolic need of the area at risk Development of Vasospastic HR Cardiac rhythm Blood O2
29
The bigger the _______, the worse the MI will be
Supply and demand mismatch
30
How long before myocardium is cyanotic
Seconds
31
What happens once permanent damage occurs in teh myocardium (cellularly)
Sarcolemma breaks down Releases ions, myoglobin, TROPONIN
32
When is necrosis morphologically detectable
6 hours
33
Infarct type of necrosis
Coagulation
34
What happens to teh dead myocardial tissue
Contracts and turns in scar tissue
35
MI clinical manifestations
25% mild/asymptomatic 2/3 of pts with angina that becomes worse
36
Diagnosis of MI
Electrocardiography is used to see electrical activity of the heart to determine the type of MI
37
STEMI
ST segment elevation MI
38
NSTEMI
Non ST segment elevation MI
39
STEMI treatment
Immediate reperfusion therapy due to total occlusion 25-40% of MIs
40
NSTEMI treatment
Antiplatlet therapy and anticoagulaiton drugs Reperfusion thereapy needed, but not priority over STEMI ( not full occlusion0
41
Serum biomarkers: MI
Cardiac troponin I and T is preferred - elevated within a few hours and remains elevated for 2 weeks Others: creatine kinase, myoglobin, CKMB
42
Most important part of MI diagnosis and why
ECG determination of STEMI or NSTEMI Determines treatment needs
43
Treatment of ACS goal
Decrease myocardial O2 demand and increase o2 supply
44
Acute pharm approaches for ACS
Pain relief - morphine O2 admin Anitplatelet therapy Anticoagulants (heparin) Nitrates Beta blockers
45
Procedural approaches for ACS
PCI CABG
46
Secondary prevention of ACS
Lifestyle modifications and meds (Statins, BBs, anti thrombotic drugs)
47
Reperfusion therapy
PCI, CABG, fibrinolysis Priority goes to STEMI
48
Reperfusion injury
Production of ROS Leads to Ca overload which causes exaggerated contractions and mitochondrial dysfunction Activates inflammatory response
49
MI prognosis
Variable, depends on severity, duration, location, age Most deaths form MI occur before someone gets to teh hospital
50
MI prognosis stats
12% hav uncomplicated recovery Mortality 30% in first year + 3-4% every year after
51
MI complication (big list, individual cards coming)
Arrhythmias Cardiogenic shock Myocardial rupture Pericarditis Ventricular aneurysm Papillary muscle dysfunction Mural thrombus Congestive HF
52
MI complications: arrhythmias
Dead cells block conduction pathway for signals VFIB is most serious
53
MI complications: cardiogenic shock
Large infarction of ventricular wall = blood cannot be ejected enough to maintain needs Pump no work Mort rate 70 percentos
54
MI complications: myocardial rupture
Damaged tissue (dead) much weaker than regular Shortly after MI, dead tissue is present while heart is still contracting, can lead to ventricular or septum rip Usually happens 1-4 days after before scar tissue forms
55
MI complications: pericarditis
Underlying inflammation irritates pericardium
56
MI complications: ventricular aneurysm
Thin scar tissue of ventricular wall bulges with contraction
57
MI complications: papillary muscle dysfunction
Rupture of papillary muscle = cardiac valve regurgitation
58
MI complications: mural thombus
Abnormal contractility (causing stasis) and damage to endocardium can cause thrombus Can embolize oh no
59
MI complications: congestive HF
Heart cannot provide sufficient CO to meet Body needs
60
Sudden cardiac arrest
Unexpected death from cardiac caused within an hour of symptom onset Ischemia produced VFIB
61
Chronic ischemic cardiomyopathy
Progressive HF due to ischemic myocardial damage Most people with this have history of angina or MI or bypass surgery
62
What is chronic ischemic cardiomyopathy caused by
Slow progressive atrophy and death of cardiomyocytes from ischemia Dead cells are spread throughout the heart rather than a localized spot like an MI Poor prognosis

Patho 2 (4 decks)

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