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Pathology 205 > cardiac > Flashcards

cardiac Flashcards

1
Q

HEART STATISTICS

A 
72 beats per min
103,680 per day
728,252 per wk
3,155,760 per month
37,869,120 per year
2,900,000,000 per lifetime
7,568 litres/day
53,162 l/wk
230,370 l/mo
2764445 l/yr
211,700,000 l/lifetime
1,331,552 barrels/ lifetime
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2
Q

trace a drop of blood through the heart

A

superior vena cava- right atrium- through tricuspid valve- right ventricle- pulmonary semi lunar valva- pulmonary arterie- lung- pulmonary vein - left atrium- mitral valve (bicuspid)- left ventricle- aortic valve- to the body

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3
Q

coronary arteries

A

supllies blood to the heart

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4
Q

Systole

A

when the heart contacts with ejection of blood

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5
Q

what is the most common deseases in western world

A

cardiovascular disease (atherosclorosis, then hypertensive heart desease)

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6
Q

Ischemic vascular disease

A

Atherosclerosis
coronary heart disease
Main Regions and Pathology Resulting from Atherosclerosis
Systemic Inflammatory Disease affecting Arteries
brain, aorta, peripheral vascular (gangrene- diabetic)

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7
Q

Atherosclerosis, CAD (specific to the heart starts with ischemia then injury then necrosis)& IHD- start off with ischemic episode- leads to heart failure

A

Coronary arteries supply blood and nutrients to the heart muscle
Coronaries fill during diastole
Atherosclerosis of the coronary arteries = Coronary Artery Disease (CAD)
CAD = Ischemic Heart Disease
Ischemic Heart Disease can lead to Heart Failure

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8
Q

Pathogenesis of Atherosclerosis

A

Endothelial injury: is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA

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9
Q

Pathogenesis of Atherosclerosis!!!!!!!

A

hallmark is Endothelial injury!!!!!! (hypertension, diabetes, obesity): is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA

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10
Q

first layer in the lumen is the subendothelial matrix then the smooth muscles

A

athelrosclorosis affects the endothelial injury- circulating LDL gets into the endothelial injury
monocytes adhere on the lumena nd enter the endothelium and act on the cytochines - become macrophages and engulf the LDL and are now stcuk - gets into foam cells - become fatty steak and then become palque and can be ruptured - miocardial infarction

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11
Q

can recover from ischemia if not too long

A

if too long- necrosis- no coming back

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12
Q

angina pectororis

A

chest pain

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13
Q

Types of Ischemia

A

(1) Tolerable ischemia, which has a low degree of reduced blood flow
(2) Critical ischemia, which reflects a modestly severe flow reduction
(3) Lethal ischemia, which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction

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14
Q

Tolerable ischemia

A

which has a low degree of reduced blood flow

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15
Q

Critical ischemia

A

which reflects a modestly severe flow reduction

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16
Q

Lethal ischemia,

A

which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction

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17
Q

atherosclorosis start in the

A

first decade of life and continuously grows - usually gets too big at aroud the fourth decade

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18
Q

risk factor!!! modifiable and non modifiable

A 
Non-modifiable
Increasing Age
Male gender
Heredity (genetic predisposition)
Potentially modifiable
Hyperlipidemia
Hypertension
Physical inactivity
Smoking
Obesity 
Stress 
Diabetes mellitus
19
Q

Symptoms of Coronary Stenosis!!!

know the desease (pathology)- the symptoms-

A 
Angina pectoris
Asymptomaticv(
Arrhythmia (cardiac rhythm abnormalities)
Sudden death
Myocardial infarction
Congestive heart failure
20
Q

Angina Pectoris

2 types- stable and unstable

A

Transient discomfort in the chest or adjacent area caused by myocardial ischemia brought on by exertion: no myocardial necrosis.

Two types: 
Stable
Unstable
Pain of ischemia
 Precipitated by exercise
 Relieved by rest, nitroglycerine (vasodilator)
21
Q

Complications of CAD

A

Myocardial Infarction (MI)
Sclerosis: hardening due to collagen deposits surrounding the atheroma
Thrombosis: surface of atheroma may ulcerate  and sometimes sudden death without previous warning symptoms
Aneurysms: a weakened wall may dilate and rupture (ruptured aneurysm- bleed out) (weakening of wall of the blood vessle- blood can stagnant )

22
Q

Myocardial infarct (MI)

A

Heart Attack
Blockage of a vessel causes tissue to become ischemic ( lack of oxygen to tissue bed)
The ischemia causes tissue necrosis (infarction: death)
Dead tissue: subjected to normal body processes of removal and repair with formation of scar tissue.
Diagnosis may be clinical: cardiac biomarkers, ECG,
Cardiac catheterization, post mortem

23
Q

MI Clinical symptoms

A

Choking or pressure like pain most commonly in left chest extending up neck, down left arm.
However, can be anywhere above umbilicus to teeth in lower jaw down either arm to wrist & between shoulder blades.
May become unconscious
Sweating, pallor
Symptoms of shock – weak or imperceptable pulse

24
Q

The most common cause of death from Acute MI is !!!!

A

an Arrhythmia: Ventricular Fibrillation

- first rythm is v tact

25
Q

Complications of MI

A 
Sudden death 25% of cases
Arrhythmia (v-fib arrest)
Heart failure
Cardiogenic shock
Multisystem organ failure
Weakening of the arterial wall-
Aneurysm (localized dilatation)
Valvular regurgitation
26
Q

Myocardial infarction

A 
Death of myocardial cells due to obstruction of blood flow
80% result from a thrombus obstructed a narrowed artery
Gross
Necrosis (pale yellow)
Microscopic
Necrotic myocardial cells
Hemorrhage 
Inflammation
27
Q

left anterior descending artery obstruction!!!!

know them all

A

lad lesion artery obstruction- artery of sudden death, anterior infraction, 50% of cases

28
Q

How do you diagnose AMI

A

Patients present to ER or family doc with a variety of histories, time of onset etc
In some MIs, there is no associated pain
Can happen in the relatively young ie mid 30s
Can happen in patients without obvious risk factors

29
Q

Diagnosis of myocardial infarction

A

Risk factors, history, clinical presentation
12 lead ECG – by changes in electrical patterns of the heart (look at st segment- if it elevated then we know the heart has been comprimised)

Biomarkers- by release of compounds by the ischemic or necrotic heart tissue -(certain protein released into the circulation- can be mesures (high troponin levels))

In most provinces, in the very old, sudden death will be assumed to be myocardial infarction, without autopsy evidence

30
Q

Biomarkers of Myocardial Infarction

A

During an acute coronary event, a coronary artery becomes completely occluded. This deprives cardiac muscle of bloodflow (ischemia) and oxygen (hypoxia) causing death of the muscle and destruction of the cell (necrosis)
Products of this ischemic and necrotic process find their way into the bloodstream where they can be measured . These are called biomarkers and can be diagnostic for myo-cardial infarction and necrosis.

31
Q

Cardiac Markers

A

Troponin
Part of the contractile apparatus of muscle
Different in heart and skeletal muscle

32
Q

Myoglobin- used to be used but could be released from muscles from exercising)

A

Mol wt 16,000 daltons
Found in all muscle
Non-specific marker
Released earlier than other larger markers ie in the 1st several hours after an infarct

33
Q

Creatine Kinase (CK)

A 
Present as a dimer with mol wt of 86,000 daltons
Skeletal muscle has MM dimer
Heart has MM and MB dimers
Brain has BB dimer
MB!!!! useful for MI diagnosis
34
Q

know slide #2!!! be aware of these times

A

myoglobin is released early (less than 5 hours), ck mb is release is slower and peaks at 12 hours, but now troponin had a peak aroun 8 hours and is long lasting- even at 35 hours

35
Q

Complications of myocardial infarction

A 
Mural thrombus
Ventricular aneurysm
Myocardial rupture (death)
Cardiac tamponade
   (pericardial effusion)
36
Q

Course of Action

A 
Labs, 12 lead ECG
If symptomatic and labs and or ECG are conclusive 
Cardiac catheterization (Angiogram)
(1) no lesions
(2) lesions < 50%
(3) lesions > amenable to PCI
(4) multiple lesion in multiple vessels
37
Q

Percutaneous Coronary Intervention (PCI)

A

PCI refers to a invasive procedure in which a high grade coronary stenosis is dilated with a balloon tipped catheter system and/ or supported by metal prosthetic stents (scaffolds) to increase lumen diameter, restore blood flow and prevent myocardial ischemia.

38
Q

Treatment

A

Medical – Clot busting drugs (tPA, urokinase, streptokinase)
Medical – Percutaneous Coronary Intervention
Surgical – CABG –Coronary artery bypass graft

Secondary prevention (
Means prevention of another event after the first one has already occurred
diet, exercise, anticoagulant drugs (aspirin) etc, cholesterol lowering drugs(statins) antihypertensive drugs (ACE Inhibitors), beta blockers
Primary prevention - diet, exercise, anticoagulant drugs (aspirin) etc, cholesterol lowering drugs(statins

39
Q

Congestive Heart Failure

A

Pump failure -> failure to pump out all blood that enters heart
Congestion=Back pressure to all organs behind failed chamber

Left heart failure -> pulmonary congestion & edema

Right heart failure -> peripheral congestion & edema in the periphery (legs (large jugular veins)

Pulmonary Edema results from LHF
Alveolar sacs fill with fluid  Dyspnoea (shortness of breath)
 On exertion
 Nocturnal
 Constant
40
Q

cabg

A

grafts anatomosed to the heart

41
Q

Rheumatic Fever& Rheumatic Heart Disease (RHD)

A

Systemic immunologic disease related to streptococcal infections
Occurs two weeks after “strep throat”
Antibodies to Streptococcus cross-react with cardiac antigens
Cell mediated immune reaction
Supressor/cytotoxic T lymphocytes and macrophages damage tissue
Pathology of Rheumatic Fever
Pancarditis (Endocarditis, Myocarditis, Pericarditis)

vegetative growths develops on left side (aortic valves..)- leads to endocarditis

42
Q

Endocarditis

A

Inflammation of valves on the left side of the heart (valvulitis and ulcer formation)

deposition of inflammatory cells, fibrin and platelets: (VEGETATIONS)
Healing by fibrous scarring causes valve deformation
Contracture leads to valve stenosis or valve insufficiency
aortic valve stenosis- stiff

43
Q

Valve Disease

A 
Valve Insufficiency (regurgitation)
Mitral valve regurgitation reflux of blood from ventricle to atrium during systole
Aortic regurgitation causes back flow of blood into the left ventricle during diastole
The ventricles become dilated or hypertrophic- allows back flow of blood= coingestion instead of the ventricle being able to fill with new blood. - mitral regurgitation= the left atrium

Valve Stenosis
Mitral stenosis causes a stagnation of blood into the LA
Result in LA, pulmonary and right ventricular hypertension
Aortic Stenosis causes a stagnation of blood into the left ventricle
Results in LV hypertrophy and can lead to LA and pulmonary hypertension

Pathology 205 (23 decks)

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