Heart Disease Flashcards

1
Q

Acute Coronary Syndrome

A

Onset of chest pain w/o exertion b/c of clotting and plaque rupture

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2
Q

Stable Angina

A

Chest pain during exertion
Coronary Artery Stenosis
NO PLAQUE RUPTURE

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3
Q

ACS Diagnosing

A

STEMI - after using ECG - can determine if ST elevation
- no need for blood test

Unstable Angina - don’t get tissue death - should be - no blood test

NSTEMI - have a lab test

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4
Q

1st biomarker and best one now

A

AST -non specific though: muscle, heart and liver

Troponin

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5
Q

1979 MI Defition

A

2 of 3 Crit:
Symptoms need to be suggestive (but this is subjective)
-STI change
-Unequivocal serial enzyme changes-but enzyme levels may be still normal

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6
Q

2018 MI Definition

A

Objective Evidence - from imaging or ECG + injury to heart + symptoms + troponin rise or fall

Now need biochemical evidence of damage to heart

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7
Q

MI types

A

Type I - thrombosis and plaque rupture -NSTEMI
T2 - injury to heart but no evidence of clot - supply - called supply-demand
T3-troponin measurements but pass away early
T4- PCI - complications
T5 - MI after cardiac surgery

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8
Q

Cardiac Troponin

A

11 mg/tissue
cTnTIC complex
T and I specific to cardiac
-Can get some segregation from CTnTIC into CTNI-C and CTnT

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9
Q

Impact of WHO diff definitions

A

Negative for both def- almost 100% survival rate
Positive for both - almost 75% survival rate
Positive for both =almost 50% survival rate

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10
Q

More sensitive troponin testing

A

Decreased amount of time needed to detect MI

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11
Q

High-sensitivity cardiac troponin testing

A

Perhaps after one hour

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12
Q

High Sensitivity Assays Lab Measurements

A

3 diff concentrations of QC at least one per day

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13
Q

High Sensitivity Assays Use

A

Could measure once
Quicker results
Might even be able to get risk stratification

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14
Q

Clinical Utility of High Sensitivity Assay

A

5 ng - 99% NPV

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15
Q

Heart Failure

A

Fatigue, shortness of breath, exercise intolerance + fluid retention

Chronic

  • unable to supply oxygen-enriched blood to tissues to meet metabolic demands
  • impairment of filling due to disorders of myocardium, endocardium, pericardium etc
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16
Q

Risk Factor for HF and Types

A

Heart Disease = due to tissue death, Type 1 MI, hypertension, diabetes + metabolic syndrome

17
Q

HFref

A

Left Ventricular Ejection Fraction lower than 40%

Scan and see less

Has been treated more b/c has been around more

18
Q

HFpef

A

Preserved EF

19
Q

What does less blood flow lead to in heart failure

A

RAA activation

  • Vasoconstriction
  • Na and H20 Retention
  • Hypertension

In response, heart stretching leads to vasodilation and naturesis

  • due to BNP/ANP release
  • ANP released from atrium but B from ventricle
20
Q

What does shape change of heart result in for heart failure

A

You get cardiac enlargement and remodelling

Spherical shape is dilated and not energetically efficient

21
Q

BNP releaase

A

Also releases BNP and NT-proBNP

  • NT-pro is inactive -longer half life
  • Gets released in 1:1 ratio
  • Marker for BNP production
  • Higher classes = more BNP release
22
Q

BNP production

A

Pre-proBNP processed to pro

  • Pro cleaved by furin or corin to from NT-pro and BNP
  • Active BNP will bind to 2 main NP receptors
  • Results natiuresis and vasodilation
23
Q

BNP and proteases

A

Proteases can cleave BNP like NEP
Patients with NEP inhibitors do better and increase NP levels
proBNP can be glycosylated so proBNP also elevated in heart disease patients

24
Q

HFpef vs HFref BNP levels

A

lower BNP/NP relative to those w/ HFref

25
Q

Heart Failure Diagnosis

A

Initial tests like ECG - can measure NP

- NP levels based on clinical measurements

26
Q

Can BNP and NT-proBNP used to diagnose equally

A

no bc different peptides and different assays but both can be used to identify HF

27
Q

Diff mechanisms and location of the infarct can affect

A

which markers increased + severity of increase

28
Q

Vasospasm

A

From cocaine
Type 2 no plaque or rupture - so no inflammatory response
-CRP - C Reactive Protein - Acute Response w/ Infection CRUP normal
-Troponin and NP normal

29
Q

Rupture at Apex

A

BNP normal

CRP and Troponin Elevated

30
Q

Rupture at LAD -

A

occlusion at left anterior descending artery

-all markers increased

31
Q

Heart behaviour - acute presentation

A
Plaque Instability -30 Days Before
-Rupture
Pain 
Ichemia - 0 to 6 hours 
Necrosis - 6 to 24 hours 
Remodelling after 24 hours to 7 days- heart doesnt work well
32
Q

Inflammation w/ acute HF presentation

A

High inflammation corresponds with ischemia

33
Q

Cardiac Troponin w/ Acute presentation

A

High troponin w/ necrosis and lowers w/ remodelling

34
Q

BNP/NT-proBNP

A

Gets higher w/ remodelling