Cardiac Manifestations of Systemic Dz Flashcards

(56 cards)

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
What is the replacement tx for B12?
1000mg/d x 3 mo until levels normalize
26
What is the replacement tx fo B6?
according to age & sex until levels normalize
27
Approx what % of US adults are overweight?
>68%
28
What is obesity associated with?
elevated glucose intolerance, DM, HTN, atherosclerosis, CAD, decreased adiponectin and HF
29
What are the cardiac manifestations of obesity?
pts have greater central & total body volume, heart is over burdened in attempts to address excess adipose tissue
30
In obesity, greater blood volume leads to...?
Increased CO, increased R & L ventricular filling pressure in attempt to support blood demand of excess adiposity
31
In obesity, what does chronic blood volume overload lead too?
``` HTN RVH, LVH and dilation Poor exercise resistance d/t overworked cardiopulmonary system even at rest Poor cardiac reserves = HF pulm congestion ```
32
What is the treatment approach to obesity? What does this lead too?
Weight reduction | Decreased blood volume, CO, HTN, hypertrophy
33
What is the role of thyroid hormone in metabolic activity?
It is an essential determinant of metabolic activity: O2 consumption Increase/decrease cardiac workload, exerts effect on cardiac activity: inotropic, chronotropic, dromotropic
34
What is the clinical presentation of hyperthyroidism?
Sinus tachycardia, palpitations, afib, HTN, fatigue
35
What are the clinical signs of hyperthyroidism?
Hyperdynamic precordium, widened pulse pressure, Loud S1 (MT), Pleuropericardial friction rub
36
What is the treatment of hyperthyroidism?
Methimazole/PTU
37
What is the clinical presentation of hypothyroidism?
Myofibrillar edema, intersitial fibrosis --> decreased CO --> decreased SV, PP HR
38
What are the clinical signs of hypothyroidism?
Pericardial effusion (slowly develops), distant heart sounds, weak arterial pulses, hypercholesterolemia, hypertriglycerides
39
What will be seen on ECG for hypothyroidism?
Low voltage, sinus bradycardia, & prolonged QT interval
40
What will be seen on CXR for hypothyroidism?
Water bottle sign (effusion), cardiomegaly
41
What is the treatment for hypothyroidism?
Levothyroxine (watch for onset of angina & MI)
42
What is Rheumatoid Arthritis (RA)?
``` chronic, systemic, inflammatory condition that affects: joints muscles vessels ligaments tendons hematologic neurologic pulmonary cardiac can all be attacked too ```
43
What are cardiac manifestations of RA?
``` 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
What are the diagnostic labs associated w RA?
Rheumatoid factor, anti-CCP antibody, elevated ESR/CRP
45
What are the treatments for RA?
``` NSAIDs DMARDs (methotrexate) glucocorticoids anti-TNF immuno-modulators (abatacept) pericardiocentesis (if tamponad) pericardiodectomy (if constrictive) ```
46
What is Systemic Lupus Erythematosus (SLE)?
inflammatory, autoimmune dz w systemic damage of organs mediated by auto-antibodies & immune complexes Affects skin, renal, cardiac, joints, hematologic, neurologic
47
What are the cardiac manifestations of SLE?
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
What causes accelerated atherosclerosis in SLE pts? What does this put the pt at greater risk for?
``` D/t endothelial damage from: -autoimmune attack -chronic inflammation -oxidative damage to arteries Chronic glucocorticoid use ``` Higher risk for MI
49
What are the treatments for cardiac dz in relation to SLE?
Lifestyle modifications (smoking cessation, diet/exercise) Statins Hydroxychloroquine vs glucocorticoids when possible Control HTN/CHF
50
What causes rheumatic heart dz (RHD)?
Acute Rheumatic Fever (ARF) - caused by GABHS - upper airway infection (strep throat) Seen in 60% of untreated or recurrent infections
51
What are the clinical symptoms of RHD?
fever, malaise, arthralgias, scarlet fever rash with strawberry tongue and chest pain (pericarditis)
52
What are the possible heart diseases that can result from RHD?
mitral/aortic valve dz = hallmark of rheumatic carditis | Pancarditis, endocarditis, arrhythmias
53
How can you dx RHD?
Throat swab, rapid strep test, ASO titer, ADB titer
54
What is the pathophys of ARF?
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
What are the treatments for RHD?
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
What is the prevention for RHD?
Treat GABHS long term strategy to prevent recurring episodes = PCN for 5-10yrs allergy = erythromycin