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Path Part Deaux > MT notes cardiovascular > Flashcards

MT notes cardiovascular Flashcards

1
Q

RHEUMATIC FEVER

A

⋅ Characterized by damage to the heart valves

– considered cardiovascular pathology rather than joint pathology

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2
Q

Rheumatic fever causes

A

-β-hemolytic Streptococcus group A (aka pyogenes)

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3
Q

β-hemolytic Streptococcus group A (strep pyogenes) causes what?

A

-glomerulonephritis
-rheumatic fever
- MOLECULAR MIMICRY
-

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4
Q

Lacunar Tonsillitis ⋅

A

– pockets form in tonsils where bacteria and pus collect; can be removed by gargling

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5
Q

Follicular Tonsillitis ⋅

A

– inflammation of follicles of lymphoid tissue, pus cannot be removed

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6
Q

Retrotonsillar Abscess

A

– formation of pus behind tonsils causing bulging of pharyngeal walls, if not treated enters
layers of mediastinum
– Must be surgically removed and pus evacuated – May be due to any tonsillitis
– Drinking cold water after excersing….BAD IDEA

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7
Q

Manifestations of Rheumatic Fever

A
  • migratory arthritis
  • molecular mimicry (due to beta group A strep pyogenes)
  • erythema annulare (marginatum) circular skin rash
  • subcutaneous nodules on knuckles
  • syndenhams chorea
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8
Q

Syndenham’s Chorea

A 
⋅ Age <15 y/o 
⋅ Only in women 
⋅ Mild vasculitis of cerebral vessels 
⋅ Usually recover completely 
⋅ Striatum neurons 
⋅ Curable
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9
Q

Huntingdon’s Disease

A 
⋅ Age over 30-35
⋅ More common in males
⋅ Genetic
⋅ Incurable, inevitably results in profound
dementia and death within 10-15 years 
⋅ Destruction of striatal nuerons
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10
Q

rheumatic myocarditis

A

-occurs 100% of the time with myocardium

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11
Q

pericardium involvement in rheumatic fever

A
  • 10-15% of cases
  • fibrinous inflamation
    - bread and butter pericarditis
  • heard as bruits
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12
Q

Rheumatic endocarditis

A

-involves heart valves (since valves are made of endocardium)
-80% of cases this occurs
-irreversible
-MC valve is the mitral
-2:aortic, 3tricuspid, 4th pulmonary
-vegetation
-

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13
Q

what is vegetation

A

-fibrin deposits on the margin of the cusps

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14
Q

what does vegetation cause

A

stricture of healed cusps resulting in valvular insufficiency or valvular regurgitation
-leads to adhesions of the cusps (stenosis)

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15
Q

adhesions due to valvular insufficiency lead to

A

stenosis of atrioventricular and mitral stenosis

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16
Q

Mitral stenosis

A

-narrowing of the mitral valve, usually develops with valvular insufficiency.
-Enlargement of left atrium occurs as a response to mitral stenosis. Leads to the compression of
bronchi, recurrent laryngeal artery (leading to hoarseness of voice).
-pulmonary edema
-hypertrophy of left atrium compresses bronchi and displaces esophagus
-RIGHT VENTRICLE HYPERTROPHY
-LEFT ATRIUM WILL FAIL
-ball thrombus

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17
Q

aortic stenosis

A
  • left ventricular hypertrophy
  • left heart deviation
  • calcific stenosis
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18
Q

aortic insufficiency

A

-low diastolic pressure may be ZERO

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19
Q

aortic insufficiency causes

A
  • Bacterial endocarditis (MC)
  • rheumatic fever
  • tertiary Syphilis
  • ankylosing spondylitis
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20
Q

Bacterial Endocarditis

A

– most common cause of aortic stenosis and insufficiency
-Infectious disease of the heart valves – most commonly affecting the aortic valve followed by the mitral valve
⋅ Common, dangerous. 2 types:
-acute
-subacute

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21
Q

Rheumatic Fever

A

– most commonly affects mitral valve, followed by aortic valve, tricuspid valve
● NEVER Pulmonary!!!!!!

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22
Q

TERTIARY SYPHILIS

A
  • 80% characterized by cardiovascular pathology
  • de musset’s sign
  • pulse pressure is visualized
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23
Q

Ankylosing Spondylitis

A

– systemic disease affecting the spine, also a cause of aortic insufficiency

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24
Q

BEAM

A

Bacterial
Endocarditis
Aortic
Mitral

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25
Q

rheuMATic fever

A

most commonly affects:
Mitral
Aortic
Tricuspid

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26
Q

Acute Bacterial Endocarditis

A

⋅ Sudden onset with high mortality rate

⋅ Most commonly caused by Staphylococcus aureus

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27
Q

Subacute Bacterial Endocarditis

A
  • α-hemolytic strep viridans/mitis
  • bacteremia
  • chronic causes amyloids
  • Aortic valves are most commonly involved
  • aortic or mitral insufficiency
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28
Q

Subacute Bacterial Endocarditis areas of chronic infection

A
  • teeth
  • genital organs
  • skin
  • lungs
  • gallbladder
  • amyloidosis
  • aortic valves (MC)
29
Q

Subacute Bacterial Endocarditis valvular involvement

A

-aortic MC mitral #2
-results in aortic or mitral insufficiency
– Release of enzymes lead to destruction of valves, erosion and perforation of cusps
– 2nd Mitral Valve: conus of the valves may slip, forming an embolism
– Very often results in the development of stroke

30
Q

Complications of Subacute Bacterial Endocarditis:

A

⋅ Congenital Heart Disease: Ductus Arteriosus

  • Ischemic-Hemorrhagic stroke
  • clubbing of fingernails
31
Q

clubbing of fingernails aka’s

A
  • drumstick syndrome
  • hypertrophic pulmonary osteoarthropathy
  • malignant cause is called “Paraneoplastic syndrome)
32
Q

ARTERIOSCLEROSIS

A 
⋅ Arteriosclerosis is a generic term reflecting arterial wall thickening and loss of elasticity
⋅ 3 types:
1)arteriolosclerosis
2)monckeberg medial sclerosis
3)atherosclerosis
33
Q

ATHEROSCLEROSIS (ATHERA= MUSH, PORRIDGE)

A

⋅ Normal tissue is replaced by atheroma (atherosclerotic plugs/plaque), forming in the arteries
– Progression of atherosclerosis increases risk of stroke
-affecting small arteries and arterioles, may cause downstream ischemic injury
▪ Hyaline Arteriolosclerosis
▪ Hyperplastic Arteriolosclerosis

34
Q

MOCKENBERG’S MEDIAL CALCIFIC SCLEROSIS

A

⋅ Ring-like calcification in the tunica media layer of medium to small arteries of obscure course, occurring in people
over 50
– Walls of arteries are completely filled with calcium, appears radiopaque on film
⋅ This does not lead to narrowing of the vascular lumen
⋅ Arteries commonly affected include: radial, ulnar, tibial, femoral, and the small arteries to the genitals
*Usually extremities

35
Q

Hyaline Arteriolosclerosis

A

⋅ Associated with extracellular hyaline deposition in arteriole walls
– People with hypertension or diabetes mellitus are most vulnerable.
– Extracellular deposition of protein leads to dramatic narrowing of the lumen and thickening of the vessels
which may lead to ischemia

36
Q

Hyperplastic Arteriolosclerosis

A

⋅ Associated with thickening of the basement membrane of arterioles (no deposition of protein)
– Duplication of basement membrane and smooth muscle cells lead “Onion skinning” (fibrinoid necrosis of the kidneys.)
⋅ Occurs with malignant hypertension, with a minimum 120 diastolic pressure ⋅

37
Q

Hyperplastic Arteriolosclerosis

Complications:

A

– Thickening of vascular wall and narrowing of lumen is the most serious problem, resulting in loss of blood
supply to tissues, especially the kidneys – necrotizing arteriolitis

38
Q

Hyaline Arteriolosclerosis Complications:

A

● Kidney is the most vulnerable tissue, resulting in the development of benign nephrosclerosis,
death of the glomeruli and development of glomerulonephritis.
– Walls become brittle, increasing the risk of arterial stroke

39
Q

ISCHEMIC HEART DISEASE (AKA Coronary Heart Disease, Coronary Artery Disease)

A

⋅ Refers to a group of closely related syndromes caused by imbalance between the myocardial oxygen demand and
the blood supply.
⋅ A group of disorders characterized by a lack of blood flow and oxygen to the heart
⋅ Critical stenosis: clinical manifestations usually occur after the lumen of the coronary artery is 75% occluded.

40
Q

ISCHEMIC HEART DISEASE (AKA Coronary Heart Disease, Coronary Artery Disease)
Risk factors:

A

– Atheroma complications can directly lead to MI development
– arteriothrombosis is the most common
cause of MI, predisposed by disease and progression of atherosclerosis
-Atherosclerosis: narrowing of lumen and occlusion of blood vessels
– Smoking: coronary artery is very sensitive to nicotine; risks increase with hypercholesterolemia and hypertension

41
Q

ISCHEMIC HEART DISEASE (AKA Coronary Heart Disease, Coronary Artery Disease)
pathogenesis

A
  • calcification, cracking, ulceration, necrosis, emboli form from plaques
  • platelette aggregation (forms thrombus)
  • Coronary artery thrombosis – Coronary artery vasospasm (aka prinzemetal’s angina)
42
Q

Coronary artery vasospasm aka

A

– prinzemetal’s angina

  • vasoconstriction of SMOOTH muscle layer of blood vessels near an atheroma
  • may be due to /\ of catecholamine in blood
43
Q

Types of Ischemic Heart Disease (4 Major Diseases):

A

1) angina pectoris
2) acute MI
3) Chronic IHD with CHF
4) sudden cardiac death

44
Q

Angina Pectoris

A

– Intermittent chest pain caused by transient, reversible myocardial ischemia

  • no pinpoint spot
  • manifests as Frogs Chest (squeezing heart)
  • Radiation of pain into left arm traveling along ulnar side, left shoulder, scapula, entire left portion of chest
45
Q

PRINZMETAL’S (VARIANT) ANGINA (NOT A GOOD DEVELOPMENT OF HEART DISEASE)

A

⋅ Occurs at rest, caused by coronary artery spasm
– Usually occurs on or near existing atherosclerotic plaque, though a completely normal vessel can be
affected
– Can occur in anyone, patient does not always have coronary artery occlusion
⋅ Responds to vasodilators such as nitroglycerin and calcium channel blockers

46
Q

UNSTABLE ANGINA (AKA CRESCENDO ANGINA, PREINFARCTION ANGINA)

A

⋅ Stable may become unstable
⋅increasingly frequent pain at rest
–severe pain in the heart may wake patient in their sleep “nocturnal
angina”
– pain closer together, more severe
⋅ Ass w/plaque disruption, thrombosis, and/or
vasospasm
–occlusion of coronary artery, due to narrowing of lumen
⋅ MI> caused by complete vascular occlusion.

47
Q

CHRONIC ISCHEMIC HEART DISEASE (AKA ISCHEMIC CARDIOMYOPATHY)

A

– heart cannot pump correctly
⋅ Type of IHD which develops in patients with prolonged ischemia of the heart that has not reached critical point
⋅ Myofibrils undergo degeneration due to ischemia and decrease in metabolism (lack o2 = atrophy = more scar tissue)
⋅ Connective tissue replaces damaged tissue, leading to myocardiosclerosis and decrease of functioning tissue

48
Q

SUDDEN CARDIAC DEATH

A

⋅ Death occurs within 24 hours of the onset of cardiac pain (symptoms). May be the 1st & last manifestation of IHD.
⋅ 300,000 annual deaths, 50% have ischemic heart disease (coronary artery problem, coronary atherosclerosis,
developmental abnormalities, coronary artery embolism, vasculitis, dissection, etc.)
– Myocardial diseases – cardiomyopathies, myocardiditis, right ventricular dysplasia
– Valvular diseases – mitral valve prolapse
⋅ Causes include vasospasm and arrhythmia. Arrhythmia is the number one cause.

49
Q

CONGESTIVE HEART FAILURE

A

⋅ Multisystem derangement that occurs when the heart is no longer able to eject blood delivered to it by the venous
system – heart fails to pump blood

50
Q

CONGESTIVE HEART FAILURE ADAPTIVE RESPONSES

A
  • Activity of the sympathetic nervous system
  • hypertrophy of heart muscle
  • dilation of heart chambers
51
Q

CHF Activity of the sympathetic nervous system

⋅

A

⋅ Sympathetic division is responsible for
⋅ Increasing heart contractility = positive inotropic effect
⋅ Increase of heart rate = positive chronotropic effect
⋅ Hypertrophy- increased size (thickness) due to workload
⋅ Together, these two effects (inotropic and chronotropic) compensate for weakness of heart muscle

52
Q

Inotropic effect:

A

increase heart contraction

53
Q

chronotropic effect:

A

increase heart rate

54
Q

Hypertrophy of heart muscle in CHF

A

⋅ Hypertension or stenosis (usually aortic) lead to increased loads of blood to heart muscle
⋅ Increased resistance causes myofibrils to increase in diameter (width) but not length

55
Q

Concentric Hypertrophy in CHF

A

muscle enlargement with no change in size of heart chambers
– Usually in response to increased load to the heart and increased resistance to blood flow (e.g., aortic
stenosis, where normal flow of blood is prevented) – Normal ratio between L and R ventricular wall is 2:1 – this ratio is increased in hypertrophy, resulting in left
deviation

56
Q

Eccentric Hypertrophy

A

– increase in heart muscle thickness with increase of heart chamber size
– Fluid creates hydrostatic pressure, causing distention to the area
– Eventually hypertrophy becomes ineffective and cardiac failure results

57
Q

Dilation of heart chambers

A

⋅ Due to valvular problems, increased load and increased blood in the chambers.
⋅ Eccentric hypertrophy results, with elongated hypertrophied fibers
– Eventually results in dilation, based on Frank-Starling law (elongation of heart myofibril results in increased
heart contractility)
– Most common adaptive response
⋅ If the dilated ventricle is able to maintain cardiac output at a level that meets the needs of the body, the patient is
said to be in compensated heart failure
⋅ If further dilation no longer results in increased contractility, but instead leads to a progressive decrease in
myocardial contractility and a decline of cardiac out, the patient is said to be in decompensated heart failure.

58
Q

LEFT-SIDED CONGESTIVE HEART FAILURE

A

Causes: resulting in weakness of left ventricle, left atrium, or both, manifested by lung edema
⋅ systemic hypertension,
⋅ mitral/aortic valve disease
– stenosis or insufficiency depending on the degree of involvement,
⋅ ischemic heart disease – including myocardial infarction, affects function of heart muscle, and
⋅ primary diseases of the myocardium
– myocardiopathies (idiopathic), myocarditis

59
Q

MitraL stenosis

left sided issues

A
  • excess blood in L atrium
  • eccentric hypertorphy
  • hypertrophic dilation
  • pulmonary edema
60
Q

Brown induration of the lungs (pulmonary hemosiderosis)

A

– lungs will be heavy and filled with brown fluid

– Lung edema is always a result of left heart failure

61
Q

The most common causes of left-sided heart failure:

A
  • systemic hypertension
  • Mitral or aortic valve disease
  • Ischemic heart disease
  • Primary diseases of myocardium
62
Q

Right sided heart failure

A

-blood backs up into the R Ventricle causing hypertrophy of the R Ventricle and increased hydrostatic
pressure
– Blood backs up into the R Atrium, then Vena Cava, and increases hydrostatic pressure here as well
– Congestion of the venous system develops in the liver
● Increase intrahepatic pressure compresses hepatocytes and leads to atrophy and nutmeg-like
appearance of the liver
-pitting or pedal edema

63
Q

pitting edema in other cavities

A

● Abdominal cavity – ascites
● Pleural cavity – pleural effusion
● Pericardial cavity – pericardial effusion

64
Q

RIGHT-SIDED CONGESTIVE HEART FAILURE

A
  • L Ventricular failure
  • Cor Pulmonale
    ⋅ Cor Pulmonale due to primary lung disease such as emphysema or interstitial lung disorders
65
Q

RIGHT-SIDED CONGESTIVE HEART FAILURE organs effected

A

-Liver (MC) nutmeg liver

66
Q

anasarca

A

total swelling of the body (everything swollen, including cavities) in all soft tissues and cavities

67
Q

Most common causes of right ventricular heart failure

A
  • Left ventricular failure

- Cor pulmonale- enlargement of right heart.

68
Q

the most common manifestation of LEFT ventricular failure is

A
  • dyspnea (breathlessness)

- tachycardia

69
Q

Clinical manifestations of congestive heart failure

A

-Dyspnea
-▪ Muscle fatigue
▪ Enlarged heart
▪ Tachycardia
▪ Fine rales in lung bases (rales are rattle sounds)
▪ High pitched systolic murmur
▪ Atrial fibrillation- lacks specific
▪ Enlargement of heart ▪ Distended neck veins (congestion is vena cava superior)
▪ Enlarged and sometimes tender liver ▪ Edema of the feet and lower legs
▪ Accumulation of fluid in the body cavities
▪ Cyanosis
▪ Muscle fatigue (not adequate supply of oxygen)
▪ Elevated venous pressure
▪ Dilation of the right ventricle
▪ Mitral valve disease
▪ Prolonged circulation time

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