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Patho > Q2 - Cardiac > Flashcards

Q2 - Cardiac Flashcards

1
Q

What is the most common primary dx in the US?

A

HTN

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2
Q

Which type of HTN is strongly associated with cardiovascular and cerebral vascular events?

A

Isolated systolic HTN

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3
Q

If you have aortic stenosis, which ventricle is impacted and what happens to it?

A

L ventricle
L ventricle hypertrophy and dilation

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4
Q

If you have mitral valve regurg? What areas of the heart are affected and what happens?

A

Mitral valve btwn LA and LV. Back flow to the LA during LV systole.
LA hypertrophy/dilation -> arrhythmias -> LV dilation and hypertrophy -> decreased CO ->pulmonary HTN.

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5
Q

What is affected with mitral stenosis and what happens?

A

Narrowing/stiffening of mitral valve.
LA hypertrophy and dilation.
Incomplete emptying of LA.
Pulmonary HTN
Eventually RV failure if not treated
Dysrhythmias.

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6
Q

Elevated BP
Stage1
Stage 2

A

120-129 AND <80
130-139 OR 80-89
>140 OR >90

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7
Q

What are some less known risk factors for HTN?

A

OSA
High Na, low K
Glucose intolerance
Obesity

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8
Q

HTN can be caused by 2 main things:

A

Increase in CO (either HR or SV)
OR
Increase in PVR (blood viscosity or vasoconstriction)

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9
Q

Cascade of events with Increase in SNS activity

A
  1. Increased HR and vasoconstriction (PVR)
  2. increased insulin resistance -> endothelial dysfunction ->narrowing of vessels and vasa spasm
  3. Vascular remodeling -> narrowing and vasospasm
  4. Procoagulant effects -> narrowing of vessels.
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10
Q

Over activity of the RAAS means (2)

A

More Na and H2O retention
Increased vascular resistance.

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11
Q

What effect do natriuretic peptides have?

A

Opposite of RAAS - increased dieresis, enhanced renal blood flow and increased GFR, inhibition of SNS, vasodilation and aldosterone inhibition.

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12
Q

Endothelial injury and dysfunction in primary HTN is further affected by

A

Increased production of vasoconstrictors
Decreased NO production.

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13
Q

Irreversible damage - less likely to have negative sequellae because it’s already damaged.

A
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14
Q

What are the classes/types of aneurysm?

A

True - involves all 3 layers of the wall with weakening.
- Fusiformcircumfrencial
- fusiform saccular
- dissecting, saccular
False (pseudo) - extravascular hematoma.

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15
Q

What law is involved with the patho of aneurysms?

A

Pousielle’s Law = Tension = transmural pressure x radius

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16
Q

Most common locations for occurrences of aneurysms

A

Thoracic or abdominal aorta.

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17
Q

3 main pathological features of aneurysm

A

Extracellular matrix remodeling
Loss of vascular smooth muscle cells
Accumulation of inflammatory cells

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18
Q

Aneurysms most commonly occur in_______

A

Thoracic and abdominal aorta.

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19
Q

Causes of aneurysm:

A

HTN/atherosclerosis
Infections (syphilis)
Collagen disorders (marfans’)
Trauma.

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20
Q

When does a ventricle wall aneurysm happen?

A

Post MI. Causes a bulging and a reservoir that collects blood, reducing SV and therefore CO.

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21
Q

A Type A aneurysm disection________
A Type B disection______

A

A - immediate surgical intervention.
B - medical management may be possible.

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22
Q

Progression of atherosclerosis:
(Draw this out!)

A
  1. HTN, smoking, DM, age cause injury to the endothelial cells that line the artery wall.
  2. Since these injured endothelial cells can’t produce the normal amount of antithrombotic cytokines, LDLs penetrate and are trapped.
  3. Oxidized LDLs and inflammation cause endothelial cells to express adhesion molecules that bind to inflammatory immune cells
  4. Lipid-laden macrophages or FOAM CELLS accumulate and make a FATTY STREAK
  5. Enzymes, inflammatory cytokines and growth factors are release which cause smooth muscle cells to migrate over the fatty streak and form a FIBROUS PLAQUE.
23
Q

What is special about a COMPLICATED atherosclerotic plaque? Why is it dangerous?

A

A plaque that has ruptured - activated inflammation, apoptosis of plaque cells and bleeding.

Causes rapid thrombus formation that can turn into an embolus.

24
Q

Peripheral artery disease is atherosclerotic disease of the _______

A

Peripheral arteries that perfuse the limbs

25
Q

PAD _______ the risk of developing CVD.

A

Doubles.

26
Q

Intermittent claudication can be a sign of __________ and is most often mistaken for________

A

Gradual PAD onset.
Routine/expected age related health changes.

27
Q

_______use to Dx PAD.

A

ABI.

28
Q

CAD has the highest incidence among _________

A

Native Hawaiians and other Pacific Islanders.

29
Q

1 cause of death in both men and women

A

CAD and associated MIs.

30
Q

Myocardial cells become ischemic w/in ______ of occlusion
Irreversible cell death happens after _______

A

10 seconds.
20minutes.

31
Q

In stable angina, pain is relieved by

A

Rest and nitrates.

32
Q

? What is the difference between variant angina and unstable angina?

A

Prinzmentals or variant angina may not have EKG changes since they are usuallly <10-20min . Normal bio markers.

Unstable angina shows transient EKG changes (ST depression or T-wave inversion) that are associated with transient, reversible ischemia lasting 10-20minutes that goes away once the pain subsides. Normal bio markers.

33
Q

If your patient has new onset angina, occurring at rest with increasing severity or frequency, what type of angina do they have?

A

Unstable

34
Q

Difference between unstable angina and MI?

A

Elevated bio markers (Troponin)

35
Q

Non-ST elevation MI (also called __________) involves _______
STEMI (also called __________) involves _________

A

Subendocardial infarction - involves only mycardium directly beneath the endocardium.
Transmural infarction - infarct extends from endo-epicardium (all layers)

36
Q

When myocardial cells loose O2, they start __________ which requires less ______ but only supplies _________ of the energy needed. This causes elevation in _________ and ________ and eventually ________ and _________

A

Anaerobic metabolism
ATP
65-70%
H ions and lactic cid
Electrolyte imbalances
Oxygen deprivation.

37
Q

Explain the negative feedback loop in MI

A

Ischemic cells release Catecholamines with exacerbate SNS response, Ang II, vasoconstriction and increased cardiac workload -> potentiating the effects of ischemia.

38
Q

LV involvement in MI leads to _________
RV involvement leads to ________

A

Pulmonary congestion. (L-L)
increased systemic venous pressure (R-?)

39
Q

Wwhat is the classic symptoms of acute pericarditis?

A

Retro sternal chest pain worsens with lying down and respiratory movement.

40
Q

T/F: there must be a large fluid accumulation in the pericardial sac in order to get symptoms.

A

False. Even a small amount of fluid (if it develops RAPIDLY) can cause s/s of tamponade.

41
Q

Difference between dilated cardiomyopathy and hypertrophic cardiomyopathy.

A

Dilated - impaired SYSTOLIC function with NORMAL WALL THICKNESS caused by ischemic heart disease, valvular disease, renal failure, alcohols or drug tox, infection. Intracardiac volume increased -> dilation of the ventricle and HFrEF.
Hypertrophic - genetic or due to increased resistance. THICKENING of LV WALL.

42
Q

What type of cardiomyopathy is most commonly seen with HTN and valvular stenosis.
Ischemic heart disease or infection?

A

Hypertrophic. (Something that the heart has to work hard against)
Dilated (something that weakens the heart itself)

43
Q

Narrowing of the aortic SL valve, increased LV pressure, LV hypertrophy are all signs of
A. Mitral stenosis
B. Aortic stenosis
C. Mitral regurg
D. HF

A

B- Aortic Stenosis
A - autoimmune, scarring and fibrous changes to valve leaflets and incomplete emptying of the LA causes elevated atrial pressure. Pulmonary HTN and RV failure
C - backflow of blood from LV to LA during systole = atrial dilation and AFIB.

44
Q

differences between aortic regurg and mitral regurg and mitral stenosis and mitral valve prolapse.

A

Aortic regurg = DIASTOLIC Decreschendo murmur. improper closure of valve leaflets during DIASTOLE. Ejected blood flows back into the LV during diastole so that LV receives blood from aorta AND LA during diastole. LVEDV increases. LV dilates/hypertrophies to accommodate. Systolic HTN. Wide PP. Ends in HF
Mitral Regurg = Backflow of blood from LV into LA during systole. Atrial dilation and AFIB. LA enlarges. increased LA volume means LV has to stretch to maintain CO = hypertrophied LV. LV impairment results in pulmonary HTN-> R heart failure.
Mitral Stenosis = autoimmune, scarring and fibrous changes to valve leaflets and incomplete emptying of the LA causes elevated atrial pressure. Pulmonary HTN and RV failure
Mitral Prolapse= issues with mitral valve complex support. Cusps billow up into the LA during systole and may allow backflow of blood into the LA. Often asymptomatic w/ excellent prognosis.

45
Q

Mitral stenosis and mitral regurg have both of the same s/s and pathology, however 1 is autoimmune/inflammatory (stenosis) while the other is caused by mitral prolapse, rheumatic heart disease, MI or Marfan’s (regurg)

A

Mitral regurg can happen in Mitral stenosis. Mitral stenosis can be the CAUSE of mitral regurg

46
Q

L-sided HF - systolic = HFrEF
-diastolic = HFpEF

A
47
Q

How can frank-starling law explain L-sided HF?

A

With Lsided HF, there is an increase in LVEDV, which may initially improve CO UP TO A POINT and then after that, SV plateaus or decreases

48
Q

When the body senses decreased CO, what happens? How does this exacerbate HF?

A

HF with decreased CO activates SNS to try to increase CO. This causes fluid retention (worsening preload, afterload)
Vasoconstriction has a further deleterious effect.

49
Q

If someone has pulmonary congestion despite normal SV and CO, they may have _______

A

Left diastolic HF (HFpEF)

50
Q

A patient has JVD, hepatosplenomegaly and peripheral edema. What side of their heart is failing?

A

R side.

51
Q

What is the most common cause of R sided HF?

A

Left sided. HF

52
Q

R HF in the absence of L HF could be caused by

A

Pulmonary HTN from diffuse hypoxic pulmonary disease (cor Pulmonale)
COPD
CF

53
Q

What are some pathologies of cardiac high-output failure?

A

Anemia - heart is still pumping a normal CO but not enough O2 carrying capacity
Sepsis - CO adequate, but metabolic rate too high and vasodilation/leaking fluid.
Hyperthyroidism - CO can’t keep up with increased metabolic demand
Thiamine deficiency (beriberi) - can be both high or low.

Patho (18 decks)

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