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Pathology > blood vessels and heart dx > Flashcards

blood vessels and heart dx Flashcards

1
Q

Cardiovascular System parts

A

*Blood vessels
*Heart
*(Blood)

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2
Q

examples of each?

Mechanisms of Vascular Disease

A
  • Narrowing of lumen
    –Athersclerosis
  • Obstruction of lumen
    –Thrombus
    –Embolus
  • Weakening of wall
    –Dilation
    –Rupture
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3
Q

Three patterns of arteriosclerosis

A

–Atherosclerosis (Atheromas)
–Arteriolosclerosis
–Medial Calcific Sclerosis

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4
Q
  • Constitutional risk factors (non-modifiable) of atherosclerosis
A

– Age
– Gender
– Family history
– Genetic abnormalities

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5
Q
  • Major risk factors (modifiable) of atherscelrosis
A

– Hyperlipidemia
– Hypertension
– Cigarette smoking
– Diabetes mellitus

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6
Q

serum lipids of atherosclerosis WNL levels

A
  • Total Cholesterol (< 200 mg/dl)
  • Low Density Lipoprotein (< 100 mg/dl)
  • High Density Lipoprotein (> 40 mg/dl)
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7
Q
  • Low Density Lipoprotein
A

– “Bad cholesterol”
– Delivers cholesterol to peripheral tissues

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8
Q

HDL

A

“Good cholesterol”
– Mobilizes cholesterol from atheromas and transports it to the liver for excretion

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9
Q
  • Additional risk factors of atherosclerosis
    – weight?
    – Physical activity?
    – Personality type?
    – drinking?
    – which fatty acids?
    – which Lipoprotein?
    – homocystine?
    – inflammatory state?
A

– Obesity
– Physical activity
– Personality type
– Alcohol
– Trans fatty acids
– Lipoprotein a
– Hyperhomocystinemia
– Systemic inflammatory state (C-reactive protein CRP)

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10
Q

Atherosclerosis defined

A
  • Atheromatous plaques project into and obstruct the lumen and weaken the media
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11
Q

Pathogenesis of Atherosclerosis

A
  • A chronic inflammatory response of the arterial wall initiated by injury to the endothelium
  • Atheromatous plaques located in intima obstruct vessel lumen and weaken vascular wall
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12
Q

Pathogenic Events of Atherosclerosis in order

A
  • Endothelial Injury
  • Accumulation of lipoproteins
  • Monocyte adhesion to the endothelium
  • Platelet adhesion
  • Factor release from activated platelets, macrophages, endothelial cells
  • Smooth muscle cell proliferation and ECM production
  • Lipid accumulation
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13
Q

histological Progression of Atherosclerosis

A
  • Fatty streak
  • Atheroma (plaque) –covered by fibrous cap
  • Complicated plaque –ulcerated
  • Eventually clinical events occur and
    symptoms produced
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14
Q

Fatty Streak

A
  • Earliest lesion of atherosclerosis
  • Lipid filled foam cells within the intima
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15
Q

Atheroma

A
  • Plaque like lesion that begins in the intima
    and impinges on lumen
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16
Q

complicated plaque

A

Ulceration exposes thrombogenic material

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17
Q

progression of dx and clinical results possible

atherosclerosis preclinical and clinical stages

A
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18
Q

Complications of Atheromas
1. Ischemia?
2. Disruption of plaque?
3. Thrombosis?
4. Emboli?
5. Hemorrhage?
6. Aneurysms?

A
  1. Ischemic injury - compromised blood flow to distal organs
  2. Disruption –exposes thrombogenic substances
  3. Thrombosis - clotting on surface of ulcerated plaque causes
    further narrowing
  4. Embolization –thrombus or plaque material may embolize
    (thromboembolus)
  5. Hemorrhage –a hematoma may expand or rupture plaque
  6. Aneurysm - weak wall may dilate and rupture
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19
Q

Major Clinical Consequences of
Atherosclerosis
* Myocardial?
* Cerebral?
* Aorta?
* Peripheral vasculature?

A
  • Myocardial infarct -heart attack
  • Cerebral infarct - stroke
  • Aortic aneurysm -rupture
  • Peripheral vascular disease -gangrene of legs
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20
Q

Atherosclerosis can be seen where with dental xrays?

A

carotid aa

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21
Q

Arteriolosclerosis
can result from?

A
  • Hypertension
  • Small blood vessel disease
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22
Q
  • Hyaline Arteriolosclerosis
A

–Diabetic microangiopathy

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23
Q
  • Hyperplastic Arteriolosclerosis is due to?
A

–Malignant hypertension

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24
Q

Medial Calcific Sclerosis

A
  • Calcification of media
  • Does not encroach on vessel lumen- not clinically sig
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25
Q

Abdominal Aortic Aneurysm

A

Atherosclerotic Aneurysm that arises below renal aa and above aoritc bifurcation
potential to rupture

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26
Q

due to?

Syphilitic Aneurysm

A
  • Syphilitic aortitis of ascending aorta may occur in tertiary syphilis
  • Due to obliterative endarteritis of the vasa vasorum leading to loss of elasticity
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27
Q

Congenital “Berry” (Saccular) Aneurysm:

A

Subarachnoid Hemorrhage at circle of willis

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28
Q

Arterial Dissection

A
  • An intimal tear allows dissection of blood into media - may rupture leading to massive hemorrhage
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29
Q

aa dissection risk factors

A

hypertension
connective tissue abnormality (Marfan Syndrome)

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30
Q

what can occur with aa dissection at the heart?

A

cardiac tamponade leading to compression of ventricles and atria with fluid in pericardia

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31
Q

Temporal (Giant Cell) Arteritis
* Most common form of? demo?
* histo?
* symptoms?
* Branches of what aa? signs of each?
* Treatment?

A
  • Most common form of vasculitis in older adults (females over 50y)
  • Granulomatous vasculitis
  • Flu-like symptoms with muscle and joint pain. ESR elevated
  • Branches of carotid artery
    – Headache (temporal artery)
    – Visual disturbances (ophthalmic artery) –risk of blindness
    – Jaw claudication –pain in masticatory muscles while chewing
  • Treatment with corticosteroids
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32
Q

Polyarteritis Nodosa

A
  • Necrotizing arteritis involving multiple organs –lungs spared
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33
Q

Polyarteritis Nodosa assc. with what virus?

A

HepB

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34
Q

classic demo? signs?

Polyarteritis Nodosa presentation

A
  • Classical presentation –young adults
    – Hypertension –renal artery involvement
    – Abdominal pain with melena –mesenteric artery involvement
    – Neurologic disturbances
    – Skin lesions
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35
Q

what is a varix

A

dialated vv

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36
Q

Esophageal Varices

A
  • Cirrhosis of liver causes portal hypertension
  • Rupture producing massive upper GI bleed
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37
Q

etiology?

Vasculitis

A
  • Inflammation of the blood vessel wall
  • Etiology unknown –most cases are not infectious
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38
Q

sys and local

vasculitis clinical features

A

– Systemic - non-specific symptoms of inflammation –fever, fatigue, weight loss, myalgias
– Local - symptoms of organ ischemia due to luminal narrowing or thrombosis

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39
Q

Classifications of Vasculitis

A
  • Large vessel vasculitis –aorta and major branches
  • Medium vessel vasculitis –muscular arteries that supply organs
  • Small vessel vasculitis –arterioles, capillaries, venules
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40
Q

target organs

Wegener Granulomatosis

A
  • Necrotizing granulomatous vasculitis
  • Target organs: nasopharynx, lungs, kidneys
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41
Q

Wegener Granulomatosis Classic presentation

A

middle-aged male with:
– Nasopharyngeal ulceration, sinusitis
– Hemoptysis –lung involvement
– Hematuria –renal involvement –glomerulonephritis
* “Strawberry” gingiva

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42
Q

Wegener Granulomatosis lab finding

A
  • c-ANCA –anti-neutrophil cytoplasmic antibody
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43
Q

forms of hypertension

A
  • Primary hypertension (essential hypertension) –no identifiable etiology
  • Secondary hypertension –identifiable etiology
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44
Q
  • Risk factors for hypertension
A

– Age
– Smoking
– Male gender
– Race - AA > C
– Obesity
– Family history
– Sodium intake
– Ethanol use
– Psychological stress

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45
Q
  • Optimal blood pressure
  • Normal blood pressure
  • Stage I Hypertension
A
  • Optimal blood pressure: <120 and <80
  • Normal blood pressure <130 and <85
  • Stage I Hypertension 140-159 or 90-99
46
Q

End Organ Damage and
Complications of Hypertension at Cardiovascular system
– Accelerated process?
– oxygen demand?
– remodeling?
– Heart in general?
– Increased risk for?

A

– Accelerated coronary atherosclerosis
– Increased myocardial oxygen demand
– Ventricular remodeling
– Heart failure
– Increased risk for arrhythmias

47
Q

including aorta

End Organ Damage and
Complications of Hypertension at peripheral vasculature

A

– Atherosclerosis
– Aortic dissection
– Abdominal aortic aneurysm
– Peripheral vascular disease

48
Q

End Organ Damage and
Complications of Hypertension at renal

A

– Hypertensive nephrosclerosis
– End-stage renal disease

49
Q

End Organ Damage and
Complications of Hypertension at CNS

A

– Hemorrhagic CVA (stroke)
– Thromboembolic CVA (stroke)

50
Q

End Organ Damage and
Complications of Hypertension visually

A

– Retinal infarction
– Hypertensive retinopathy
– Blindness

51
Q

common path? defined? preceeded by?

“Congestive” Heart Failure

A
  • The final common pathway of many forms of heart disease
  • Inability of the heart to pump a sufficient amount of blood through the body
  • Onset preceded by compensatory
    mechanisms (cardiac hypertrophy
52
Q

dysfunctional phases? how these occur?

What Causes Heart Failure?

A
  • Systolic dysfunction - deterioration of contractile function
    – Ischemic heart disease
  • Diastolic dysfunction - inability to relax, expand and fill
    –due to Left ventricular hypertrophy
53
Q

compensates for?

Cardiac Hypertrophy

A
  • Compensatory mechanism to
    –Pressure overload
    –Volume overload
54
Q

Pressure-Overloaded Hypertrophy
* Seen in?

A
  • Concentrically increased wall thickness
  • Seen in hypertension, aortic stenosis
55
Q

Volume-Overloaded Hypertrophy seen as?

A
  • Dilation of chambers
  • Valvular incompetence
56
Q

which is pressure overload and which is V overload hypertrophy?

A

L: pressure
R: V

57
Q

Classification of Heart Failure/ signs?

A
  • Left-sided heart failure - pulmonary edema
  • Right-sided heart failure - peripheral edema
58
Q

Left-Sided Heart Failure caused by:

A

– Ischemic heart disease
– Hypertension
– Valvular disease - aortic and mitral valves

59
Q

Left-Sided Heart Failure clinical effects result from?

A

– Decreased peripheral blood pressure and flow
– Backup of blood in pulmonary circulation

60
Q

findings of LSHF

A
  • Pulmonary congestion
  • Pulmonary edema
    HF cells in lung
61
Q

symptoms LSHF

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
62
Q

Right-Sided Heart Failure Caused by:

A

– Left sided heart failure MAINLY
– Chronic severe pulmonary hypertension

63
Q

Right-Sided Heart Failure clinical efects result from?

A

– Hepatic and splenic enlargement
– Peripheral edema
– Pleural effusion
– Ascites

64
Q

Findings in Right-Sided Heart Failure

A
  • Cor Pulmonale
  • Pure right-sided heart failure
  • Right ventricular hypertrophy and dilation
  • Pulmonary hypertension
65
Q

where?

RSHF and congestions

A
  • Congestion in systemic and portal venous circulations
  • Congestive hepatomegaly - chronic passive congestion - “nutmeg” liver
  • Congestive splenomegaly
66
Q

RSHF and pleural space?

A

pleaural effusion possible (build up in pul ciruit)

67
Q

RSHF edema

A

peripherla-pitting

68
Q

most common cause RSHF

A

LSHF

69
Q

Ascites May be associated with dx of what organs?

A

cardiac, hepatic and renal disease

70
Q

Ischemic Heart Disease (IHD) can be due to?

A
  • Result of coronary artery atherosclerosis
  • Imbalance between myocardial oxygen supply and demand
  • Angina pectoris
  • Myocardial infarction
71
Q

Risk of Developing Detectable
Ischemic Heart Disease based on what factors involving athersclerosis?

A
  • Number, distribution and structure of
    atheromatous plaques
  • Degree of narrowing
72
Q

Angina Pectoris

A
  • Transient myocardial ischemia
  • Paroxysmal, recurrent precordial chest discomfort, constricting, squeezing, choking, knife-like
  • May radiate to: arm, mandible
  • Does not produce myocardial necrosis (infarction)
73
Q

Stable Angina
* Due to?
* what produces ischemia?
* Relieved by?

A
  • Due to a fixed stenosis –an atherosclerotic plaque reduces coronary perfusion to critical
    level
  • Increased demand produces ischemia
  • Relieved by rest or by nitroglycerin
74
Q

Unstable Angina
* Due to?
* Frequently occurs when?
* Medical emergency?

A
  • Due to a complicated plaque –a variable stenosis
  • Frequently occurs at rest
  • Medical emergency -may evolve into MI
75
Q

Variant Angina –Prinzmetal Angina

A
  • Coronary arterial spasm secondary to
    vascular hyper-reactivity
  • Occurs at rest
  • May be unassociated with ASCAD
  • Cocaine users -> vasospasm
76
Q

Pathogenesis of Transmural Acute Myocardial Infarction with existing coronary atherosclerosis

A
  • Coronary atherosclerosis
  • Complicated plaque
  • Platelet adhesion and activation
  • Thrombus formation
  • Vessel occlusion
  • Myocardial infarction (cellular necrosis)
77
Q

Myocardial Infarction necrosis pattern

A

coagulative

78
Q

Serum Cardiac Markers for MI

A
  • Cardiac-specific Troponin (T or I), sensitive and specific
  • Creatine phosphokinase (MB fraction) –CPK-MB, can be used to monitor recurrence
79
Q

Post-MI Complications

A
  • Contractile dysfunction
  • Arrhythmias
  • Myocardial rupture
  • Pericarditis
  • Right ventricular infarction
  • Infarct extension (new)
  • Infarct extension (dilatation)
  • Mural thrombus
  • Ventricular aneurysm
  • Papillary muscle dysfunction
  • Progressive late heart failure
80
Q

Valvular Heart Disease forms

A
  • Stenosis - doesn’t open completely (impedes forward flow)
  • Insufficiency/incompetence - doesn’t close completely (allows reverse flow)
81
Q

results of abnormal flow in valvular dx

A

murmurs

82
Q

Major Valvular Lesions

A
  • Aortic stenosis
  • Aortic insufficiency
  • Mitral stenosis – from rheumatic heart disease
  • Mitral insufficiency - myxomatous
    degeneration (mitral valve prolapse)
83
Q

can valve be replaced

A

yes mechanical valve prothesis

84
Q

Acute Rheumatic Fever
* complication of?
* Antibodies cross reaction?
* Inflammation leads to?
* Hypersensitivity Reaction?

A
  • Acute rheumatic fever is a complication of Group A streptococcal pharyngitis
  • Antibodies cross react with cardiac antigens
  • Inflammation leads to fibrotic valvular
    disease
  • Type II Hypersensitivity Reaction
85
Q

Acute Rheumatic Fever pericardium

A

Fibrinous Pericarditis

86
Q

Rheumatic Heart Disease effects?
* Pericardium?
* Myocardium?
* Valves?

A
  • Pericardium - fibrinous pericarditis
  • Myocardium - myocarditis
  • Valves
    – Mitral vegetations
    – Thickened leaflets
    – Fused commissures
87
Q

Infective Endocarditis cause/course?

A
  • Most frequently bacterial
    – Strep viridans
    – Staph aureus –IV drug abusers
  • Virulence of organism determines course
88
Q

Infective Endocarditis causes the formation of?

A
  • Thrombus formation on damaged endothelium (vegetations)
  • Bacteremia results in microbial colonization of vegetations
  • Septic emboli
89
Q

Infective Endocarditis most commonly effects what part of the heart?

A
  • Left side of heart affected most commonly
    (aortic valve)
90
Q

infective endocardidits occur on the right side when?

A

IV drug abuse

91
Q

infective endocarditits mortality due to?

A

HF

92
Q

Cardiac Conditions Requiring Antibiotic
Prophylaxis for Infective Endocarditis

A
  1. Prosthetic cardiac valves, including transcatheter-implanted prostheses and
    homografts.
  2. Prosthetic material used for heart valve repair, such as annuloplasty rings, chords or clips.
  3. Previous IE.
  4. Unrepaired cyanotic congenital heart defect (birth defects with oxygen levels
    lower than normal) or repaired congenital heart defect, with residual shunts or valvular regurgitation at the site adjacent to the site of a prosthetic patch or prosthetic device.
  5. Cardiac transplant with valve regurgitation due to a structurally abnormal valve.
93
Q

Congenital Heart Disease
what is affected?
when this occurs/why?
sus to?

A
  • Abnormalities of the heart and great vessels
  • Faulty embryogenesis - weeks 3 to 8
  • Susceptibility to infective endocarditis –antimicrobial prophylaxis
94
Q

Etiology of Congenital Heart Disease

A
  • Most have no identifiable cause - multifactorial environmental, genetic and maternal factors
95
Q

drugs/infections?

enviornmental factors of congential heart dx

A

– Infectious - fetal rubella or cytomegalovirus infection
– Drugs –accutane, lithium, anti-seizure medications, cocaine, alcoh

96
Q

genetic disorders related to congenital heart dx

A

trisomy 21 and turner syndrome

97
Q

Categories of Congenital Heart
Disease*

A
  • Malformations causing Left-to-Right Shunts
  • Malformations causing Right-to-Left Shunts
  • Malformations causing Obstructions
98
Q

Right-to-Left Shunts effect on pul blood flow, result?

A
  • Pulmonary blood flow is decreased, allowing poorly-oxygenated blood to enter the systemic circulation
  • Cyanotic Congenital Heart Disease
99
Q

R to L shunts associated with what odd emboli?

A

May be associated with paradoxical
embolism –a septal defect allows venous emboli to bypass the lungs and enter systemic arterial circulation

100
Q

fingers with R to L shunts

A

Cyanosis and Clubbing of Fingers

101
Q

Tetralogy of Fallot

A
  • Right-to-Left Shunt
  • Most common form of cyanotic congential heart disease
102
Q

Tetralogy of Fallot pts have what defects at the heart

A
  1. Ventricular septal defect (VSD)
  2. Sub-pulmonary stenosis
  3. Right ventricular hypertrophy
  4. Aorta overrides VSD
103
Q

most common form of congnetial heart dx

A

VSD

104
Q

most common form of cyanotic congnetial heart dx

A

tetraology of fallot

105
Q

Transposition of the Great Arteries

A
  • Separate systemic and pulmonary circulations is incompatible with post-natal life and requires shunt for survival
106
Q

Transposition of the Great Arteries possible shunts

A
  • Stable shunt
    – Ventricular Septal Defect
  • Unstable shunts- will regress, must be re-established
    – Patent Foramen Ovale
    – Patent Ductus Arteriosus
107
Q

ventricles with transposition of the great vessels

A

RV- hypertrophy, acts as systemic ventricle
LV- atrophy, acts as pul ventricle

108
Q

Left-to-Right Shunts effects on pul blood flow, result?

A
  • Pulmonary blood flow increased
    –Pulmonary hypertension
109
Q

potential forms of L to R shunts

A
  • Ventricular Septal Defect
  • Atrial Septal Defect
  • Atrial-Ventricular Septal Defect
  • Patent Ductus Arteriosus
110
Q

can this be a shunt? progression?

Patent Ductus Arteriosus

A
  • The ductus arteriosus is a normal fetal blood vessel that allows blood to bypass the lungs
  • PDA is a left-to-right shunt from the aorta to the pulmonary artery
  • When pulmonary hypertension develops, shunt reverses and cyanosis develops**
111
Q

frequent indicative finding?

Coarctation of the Aorta

A
  • Obstructive defect located in the area of the ductus that may be asymptomatic until adulthood
  • Rib notching due to collateral circulation
112
Q

Coarctation of the Aorta, bp’s related to the coarctation

A
  • Hypertension proximal to coarctation
  • Hypotension distal to coarctation

Pathology (19 decks)

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