Cardiac Manifestations of Systemic Dz Flashcards

1
Q

How can systemic dz affect the heart?

A

By increased demands on heart, can cause arrhythmias, & enable coronary artery dz (leads to ischemic heart dz). It can also distort cardiac structure (pericardium, myocardium, and endocardium (valves)).

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2
Q

Diabetes is an independent risk factor for which diseases?

A

CAD, PAD, CV heart dz and MI

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3
Q

What is the MC cause of death in DM T1 & T2?

A

CAD

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4
Q

Why is the prognosis of CAD worst for DM pts?

A

Because they have a larger infarct size, greater CAD burden, and greater post-infarct complications (CHF, death)

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5
Q

Why do DM pts have a greater risk for MI?

A

D/t CAD burden

Need to have a high level of suspicion of an MI in DM pts

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6
Q

What are the post-infarct complications d/t greater CAD burden?

A

HF
Shock
Death

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7
Q

Why dose DM result in an atypical ischemic presentation?

A

d/t autonomic dysfunction.

Neuropathy leads purkinje fibers, AV node do not work as well

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8
Q

What are the symptoms of a Silent Heart Attack (DM presentation of MI)?

A
Nausea
Dyspnea
Pulm edema
Arrhythmias
Heart block
Syncope
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9
Q

Why does CAD happen (in relation to DM pts)?

A

Increased insulin resistance –> elevated Pai-1 –> elevated coagulation & thrombosis formation & platelet dysfunction

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10
Q

Why does cardiomyopathy happen (in relation to DM pts)?

A

increased intraventricular collagen/fibrosis/inflammation –> decreased mechanical compliance during diastole –> decreased myocardial relaxation –> diastolic HF seen in early failure

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11
Q

What is the treatment approach to DM?

A
Maintain A1c - 7%
tx dyslipidemia w Statin
tx HTN w ACEi/ARB, subsequently add HCTZ, BB, CCB
BP goal <130/80
tx CAD - revasularization (PCI or CABG)
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12
Q

What are the 3 populations seen with Thiamine deficiency?

A

HF pts
Alcoholics
Anorexia nervosa

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13
Q

Why are many HF pts thiamine deficient?

A

D/t diuretic induced renal excretion & decreased PO intake

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14
Q

Why is thiamine deficiency common in alcoholics?

A

Malnutrition
Malabsorption
imparied cellular B1 utilization & decreased tissue oxygenation

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15
Q

What is the clinical presentation of thiamine deficiency?

A

tachycardia, high out-put HF (increased CO w/o meeting metabolic needs), wide pulse pressure, S3, apical systolic murmur

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16
Q

What syndrome is the MC complication of alcohol related thiamine (B1 deficiency)

A

Wernike-Korsakoff syndrome

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17
Q

What are the symptoms of Wernike-Korsakoff syndrome?

A

Encephalopathy, oculomotor, ataxia then anterograde-retrograde amnesia

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18
Q

What are the 3 cofactors in metabolism of homocysteine?

A

B6, B12, folate

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19
Q

What can you eat to get folate?

A

leafy green vegetables

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20
Q

What is B6 and how can you get it?

A

It is a co-factor in >100 enzymes involved in AA metabolism, it is present in all food groups

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21
Q

What are the causes of B12 deficiency and when do clinical signs appear?

A

D/t chronic gastric atrophy, auto-antibody formation to gastric intrinsic factor, gastrectomy.
Clinical signs will be seen after a year or more

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22
Q

What is elevated homocysteine an independent risk factor for?

A

Atherosclerotic vascular disease

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23
Q

What process does homocysteine trigger?

A

formation of atheromas (atherogenic) –> creates endothelial oxidative stress –> prothrombotic

24
Q

What is the replacement tx for folate?

A

1-5mg/d x 3 mo until levels normalize

25
Q

What is the replacement tx for B12?

A

1000mg/d x 3 mo until levels normalize

26
Q

What is the replacement tx fo B6?

A

according to age & sex until levels normalize

27
Q

Approx what % of US adults are overweight?

A

> 68%

28
Q

What is obesity associated with?

A

elevated glucose intolerance, DM, HTN, atherosclerosis, CAD, decreased adiponectin and HF

29
Q

What are the cardiac manifestations of obesity?

A

pts have greater central & total body volume, heart is over burdened in attempts to address excess adipose tissue

30
Q

In obesity, greater blood volume leads to…?

A

Increased CO, increased R & L ventricular filling pressure in attempt to support blood demand of excess adiposity

31
Q

In obesity, what does chronic blood volume overload lead too?

A
HTN
RVH, LVH and dilation
Poor exercise resistance d/t overworked cardiopulmonary system even at rest
Poor cardiac reserves = HF
pulm congestion
32
Q

What is the treatment approach to obesity? What does this lead too?

A

Weight reduction

Decreased blood volume, CO, HTN, hypertrophy

33
Q

What is the role of thyroid hormone in metabolic activity?

A

It is an essential determinant of metabolic activity:
O2 consumption
Increase/decrease cardiac workload, exerts effect on cardiac activity: inotropic, chronotropic, dromotropic

34
Q

What is the clinical presentation of hyperthyroidism?

A

Sinus tachycardia, palpitations, afib, HTN, fatigue

35
Q

What are the clinical signs of hyperthyroidism?

A

Hyperdynamic precordium, widened pulse pressure, Loud S1 (MT), Pleuropericardial friction rub

36
Q

What is the treatment of hyperthyroidism?

A

Methimazole/PTU

37
Q

What is the clinical presentation of hypothyroidism?

A

Myofibrillar edema, intersitial fibrosis –> decreased CO –> decreased SV, PP HR

38
Q

What are the clinical signs of hypothyroidism?

A

Pericardial effusion (slowly develops), distant heart sounds, weak arterial pulses, hypercholesterolemia, hypertriglycerides

39
Q

What will be seen on ECG for hypothyroidism?

A

Low voltage, sinus bradycardia, & prolonged QT interval

40
Q

What will be seen on CXR for hypothyroidism?

A

Water bottle sign (effusion), cardiomegaly

41
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (watch for onset of angina & MI)

42
Q

What is Rheumatoid Arthritis (RA)?

A
chronic, systemic, inflammatory condition that affects:
joints
muscles
vessels
ligaments
tendons
hematologic
neurologic
pulmonary
cardiac 
can all be attacked too
43
Q

What are cardiac manifestations of RA?

A
CVD = MCC of death d/t higher rate of carotid atherosclerosis and CAD
Pericarditis = MC finding
pericardial effusion - echo
Mitral/aortic valvular vegetations
CHF (2x rate > non RA)
44
Q

What are the diagnostic labs associated w RA?

A

Rheumatoid factor, anti-CCP antibody, elevated ESR/CRP

45
Q

What are the treatments for RA?

A
NSAIDs
DMARDs (methotrexate)
glucocorticoids 
anti-TNF
immuno-modulators (abatacept)
pericardiocentesis (if tamponad)
pericardiodectomy (if constrictive)
46
Q

What is Systemic Lupus Erythematosus (SLE)?

A

inflammatory, autoimmune dz w systemic damage of organs mediated by auto-antibodies & immune complexes
Affects skin, renal, cardiac, joints, hematologic, neurologic

47
Q

What are the cardiac manifestations of SLE?

A

can affect all layers of the heart
MC complication - pericarditis (rare tamponade or constrictive)
Myocarditis (assoc w HF in HTN pts)
fibrinous endocarditis (valvular abnl, leads to mitral or aortic regurg)
Accelerated atherosclerosis

48
Q

What causes accelerated atherosclerosis in SLE pts? What does this put the pt at greater risk for?

A
D/t endothelial damage from:
-autoimmune attack
-chronic inflammation
-oxidative damage to arteries
Chronic glucocorticoid use

Higher risk for MI

49
Q

What are the treatments for cardiac dz in relation to SLE?

A

Lifestyle modifications (smoking cessation, diet/exercise)
Statins
Hydroxychloroquine vs glucocorticoids when possible
Control HTN/CHF

50
Q

What causes rheumatic heart dz (RHD)?

A

Acute Rheumatic Fever (ARF) - caused by GABHS - upper airway infection (strep throat)
Seen in 60% of untreated or recurrent infections

51
Q

What are the clinical symptoms of RHD?

A

fever, malaise, arthralgias, scarlet fever rash with strawberry tongue and chest pain (pericarditis)

52
Q

What are the possible heart diseases that can result from RHD?

A

mitral/aortic valve dz = hallmark of rheumatic carditis

Pancarditis, endocarditis, arrhythmias

53
Q

How can you dx RHD?

A

Throat swab, rapid strep test, ASO titer, ADB titer

54
Q

What is the pathophys of ARF?

A

caused by GABHS - triggers autoimmune reaction and damages cardiac structures.
endocarditis & valve damage w vegetation deposit (mitral regurg and dilation from back flow)
myocardium (recruit of Ascoff cells and myocarditis)
pericardium (serofibrinous pericarditis)

55
Q

What are the treatments for RHD?

A

Acute inflammatory process can subside w/o tx but leaves behind damaged tissue

Valve repair/replacement
ASA/NSAIDs (little effect on RHD related carditis)
control HTN
Tx HF (loop diuretics, ACEI, BB, high dose, short course glucocorticoids for AHF)

56
Q

What is the prevention for RHD?

A

Treat GABHS
long term strategy to prevent recurring episodes = PCN for 5-10yrs
allergy = erythromycin