blood vessels and heart dx Flashcards
(112 cards)
1
Q
Cardiovascular System parts
A
*Blood vessels
*Heart
*(Blood)
2
Q
examples of each?
Mechanisms of Vascular Disease
A
- Narrowing of lumen
–Athersclerosis - Obstruction of lumen
–Thrombus
–Embolus - Weakening of wall
–Dilation
–Rupture
3
Q
Three patterns of arteriosclerosis
A
–Atherosclerosis (Atheromas)
–Arteriolosclerosis
–Medial Calcific Sclerosis
4
Q
- Constitutional risk factors (non-modifiable) of atherosclerosis
A
– Age
– Gender
– Family history
– Genetic abnormalities
5
Q
- Major risk factors (modifiable) of atherscelrosis
A
– Hyperlipidemia
– Hypertension
– Cigarette smoking
– Diabetes mellitus
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)
7
Q
- Low Density Lipoprotein
A
– “Bad cholesterol”
– Delivers cholesterol to peripheral tissues
8
Q
HDL
A
“Good cholesterol”
– Mobilizes cholesterol from atheromas and transports it to the liver for excretion
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)
10
Q
Atherosclerosis defined
A
- Atheromatous plaques project into and obstruct the lumen and weaken the media
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
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
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
14
Q
Fatty Streak
A
- Earliest lesion of atherosclerosis
- Lipid filled foam cells within the intima
15
Q
Atheroma
A
- Plaque like lesion that begins in the intima
and impinges on lumen
16
Q
complicated plaque
A
Ulceration exposes thrombogenic material
17
Q
progression of dx and clinical results possible
atherosclerosis preclinical and clinical stages
A
18
Q
Complications of Atheromas
1. Ischemia?
2. Disruption of plaque?
3. Thrombosis?
4. Emboli?
5. Hemorrhage?
6. Aneurysms?
A
- Ischemic injury - compromised blood flow to distal organs
- Disruption –exposes thrombogenic substances
- Thrombosis - clotting on surface of ulcerated plaque causes
further narrowing - Embolization –thrombus or plaque material may embolize
(thromboembolus) - Hemorrhage –a hematoma may expand or rupture plaque
- Aneurysm - weak wall may dilate and rupture
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
20
Q
Atherosclerosis can be seen where with dental xrays?
A
carotid aa
21
Q
Arteriolosclerosis
can result from?
A
- Hypertension
- Small blood vessel disease
22
Q
- Hyaline Arteriolosclerosis
A
–Diabetic microangiopathy
23
Q
- Hyperplastic Arteriolosclerosis is due to?
A
–Malignant hypertension
24
Q
Medial Calcific Sclerosis
A
- Calcification of media
- Does not encroach on vessel lumen- not clinically sig
25
Abdominal Aortic Aneurysm
Atherosclerotic Aneurysm that arises below renal aa and above aoritc bifurcation
potential to rupture
26
# due to?
Syphilitic Aneurysm
* Syphilitic aortitis of ascending aorta may occur in tertiary syphilis
* Due to obliterative endarteritis of the vasa vasorum leading to loss of elasticity
27
Congenital “Berry” (Saccular) Aneurysm:
Subarachnoid Hemorrhage at circle of willis
28
Arterial Dissection
* An intimal tear allows dissection of blood into media - may rupture leading to massive hemorrhage
29
aa dissection risk factors
hypertension
connective tissue abnormality (Marfan Syndrome)
30
what can occur with aa dissection at the heart?
cardiac tamponade leading to compression of ventricles and atria with fluid in pericardia
31
Temporal (Giant Cell) Arteritis
* Most common form of? demo?
* histo?
* symptoms?
* Branches of what aa? signs of each?
* Treatment?
* 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
32
Polyarteritis Nodosa
* Necrotizing arteritis involving multiple organs –lungs spared
33
Polyarteritis Nodosa assc. with what virus?
HepB
34
# classic demo? signs?
Polyarteritis Nodosa presentation
* Classical presentation –young adults
– Hypertension –renal artery involvement
– Abdominal pain with melena –mesenteric artery involvement
– Neurologic disturbances
– Skin lesions
35
what is a varix
dialated vv
36
Esophageal Varices
* Cirrhosis of liver causes portal hypertension
* Rupture producing massive upper GI bleed
37
# etiology?
Vasculitis
* Inflammation of the blood vessel wall
* Etiology unknown –most cases are not infectious
38
# sys and local
vasculitis clinical features
– Systemic - non-specific symptoms of inflammation –fever, fatigue, weight loss, myalgias
– Local - symptoms of organ ischemia due to luminal narrowing or thrombosis
39
Classifications of Vasculitis
* Large vessel vasculitis –aorta and major branches
* Medium vessel vasculitis –muscular arteries that supply organs
* Small vessel vasculitis –arterioles, capillaries, venules
40
# target organs
Wegener Granulomatosis
* Necrotizing granulomatous vasculitis
* Target organs: nasopharynx, lungs, kidneys
41
Wegener Granulomatosis Classic presentation
middle-aged male with:
– Nasopharyngeal ulceration, sinusitis
– Hemoptysis –lung involvement
– Hematuria –renal involvement –glomerulonephritis
* “Strawberry” gingiva
42
Wegener Granulomatosis lab finding
* c-ANCA –anti-neutrophil cytoplasmic antibody
43
forms of hypertension
* Primary hypertension (essential hypertension) –no identifiable etiology
* Secondary hypertension –identifiable etiology
44
* Risk factors for hypertension
– Age
– Smoking
– Male gender
– Race - AA > C
– Obesity
– Family history
– Sodium intake
– Ethanol use
– Psychological stress
45
* Optimal blood pressure
* Normal blood pressure
* Stage I Hypertension
* Optimal blood pressure: <120 and <80
* Normal blood pressure <130 and <85
* Stage I Hypertension 140-159 or 90-99
46
End Organ Damage and
Complications of Hypertension at Cardiovascular system
– Accelerated process?
– oxygen demand?
– remodeling?
– Heart in general?
– Increased risk for?
– Accelerated coronary atherosclerosis
– Increased myocardial oxygen demand
– Ventricular remodeling
– Heart failure
– Increased risk for arrhythmias
47
# including aorta
End Organ Damage and
Complications of Hypertension at peripheral vasculature
– Atherosclerosis
– Aortic dissection
– Abdominal aortic aneurysm
– Peripheral vascular disease
48
End Organ Damage and
Complications of Hypertension at renal
– Hypertensive nephrosclerosis
– End-stage renal disease
49
End Organ Damage and
Complications of Hypertension at CNS
– Hemorrhagic CVA (stroke)
– Thromboembolic CVA (stroke)
50
End Organ Damage and
Complications of Hypertension visually
– Retinal infarction
– Hypertensive retinopathy
– Blindness
51
# common path? defined? preceeded by?
“Congestive” Heart Failure
* 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
# dysfunctional phases? how these occur?
What Causes Heart Failure?
* Systolic dysfunction - deterioration of contractile function
– Ischemic heart disease
* Diastolic dysfunction - inability to relax, expand and fill
–due to Left ventricular hypertrophy
53
# compensates for?
Cardiac Hypertrophy
* Compensatory mechanism to
–Pressure overload
–Volume overload
54
Pressure-Overloaded Hypertrophy
* Seen in?
* Concentrically increased wall thickness
* Seen in hypertension, aortic stenosis
55
Volume-Overloaded Hypertrophy seen as?
* Dilation of chambers
* Valvular incompetence
56
which is pressure overload and which is V overload hypertrophy?
L: pressure
R: V
57
Classification of Heart Failure/ signs?
* Left-sided heart failure - pulmonary edema
* Right-sided heart failure - peripheral edema
58
Left-Sided Heart Failure caused by:
– Ischemic heart disease
– Hypertension
– Valvular disease - aortic and mitral valves
59
Left-Sided Heart Failure clinical effects result from?
– Decreased peripheral blood pressure and flow
– Backup of blood in pulmonary circulation
60
findings of LSHF
* Pulmonary congestion
* Pulmonary edema
HF cells in lung
61
symptoms LSHF
* Dyspnea
* Orthopnea
* Paroxysmal nocturnal dyspnea
62
Right-Sided Heart Failure Caused by:
– Left sided heart failure MAINLY
– Chronic severe pulmonary hypertension
63
Right-Sided Heart Failure clinical efects result from?
– Hepatic and splenic enlargement
– Peripheral edema
– Pleural effusion
– Ascites
64
Findings in Right-Sided Heart Failure
* Cor Pulmonale
* Pure right-sided heart failure
* Right ventricular hypertrophy and dilation
* Pulmonary hypertension
65
# where?
RSHF and congestions
* Congestion in systemic and portal venous circulations
* Congestive hepatomegaly - chronic passive congestion - “nutmeg” liver
* Congestive splenomegaly
66
RSHF and pleural space?
pleaural effusion possible (build up in pul ciruit)
67
RSHF edema
peripherla-pitting
68
most common cause RSHF
LSHF
69
Ascites May be associated with dx of what organs?
cardiac, hepatic and renal disease
70
Ischemic Heart Disease (IHD) can be due to?
* Result of coronary artery atherosclerosis
* Imbalance between myocardial oxygen supply and demand
* Angina pectoris
* Myocardial infarction
71
Risk of Developing Detectable
Ischemic Heart Disease based on what factors involving athersclerosis?
* Number, distribution and structure of
atheromatous plaques
* Degree of narrowing
72
Angina Pectoris
* 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
Stable Angina
* Due to?
* what produces ischemia?
* Relieved by?
* 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
Unstable Angina
* Due to?
* Frequently occurs when?
* Medical emergency?
* Due to a complicated plaque –a variable stenosis
* Frequently occurs at rest
* Medical emergency -may evolve into MI
75
Variant Angina –Prinzmetal Angina
* Coronary arterial spasm secondary to
vascular hyper-reactivity
* Occurs at rest
* May be unassociated with ASCAD
* Cocaine users -> vasospasm
76
Pathogenesis of Transmural Acute Myocardial Infarction with existing coronary atherosclerosis
* Coronary atherosclerosis
* Complicated plaque
* Platelet adhesion and activation
* Thrombus formation
* Vessel occlusion
* Myocardial infarction (cellular necrosis)
77
Myocardial Infarction necrosis pattern
coagulative
78
Serum Cardiac Markers for MI
* Cardiac-specific Troponin (T or I), sensitive and specific
* Creatine phosphokinase (MB fraction) –CPK-MB, can be used to monitor recurrence
79
Post-MI Complications
* 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
Valvular Heart Disease forms
* Stenosis - doesn’t open completely (impedes forward flow)
* Insufficiency/incompetence - doesn’t close completely (allows reverse flow)
81
results of abnormal flow in valvular dx
murmurs
82
Major Valvular Lesions
* Aortic stenosis
* Aortic insufficiency
* Mitral stenosis – from rheumatic heart disease
* Mitral insufficiency - myxomatous
degeneration (mitral valve prolapse)
83
can valve be replaced
yes mechanical valve prothesis
84
Acute Rheumatic Fever
* complication of?
* Antibodies cross reaction?
* Inflammation leads to?
* Hypersensitivity Reaction?
* 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
Acute Rheumatic Fever pericardium
Fibrinous Pericarditis
86
Rheumatic Heart Disease effects?
* Pericardium?
* Myocardium?
* Valves?
* Pericardium - fibrinous pericarditis
* Myocardium - myocarditis
* Valves
– Mitral vegetations
– Thickened leaflets
– Fused commissures
87
Infective Endocarditis cause/course?
* Most frequently bacterial
– Strep viridans
– Staph aureus –IV drug abusers
* Virulence of organism determines course
88
Infective Endocarditis causes the formation of?
* Thrombus formation on damaged endothelium (vegetations)
* Bacteremia results in microbial colonization of vegetations
* Septic emboli
89
Infective Endocarditis most commonly effects what part of the heart?
* Left side of heart affected most commonly
(aortic valve)
90
infective endocardidits occur on the right side when?
IV drug abuse
91
infective endocarditits mortality due to?
HF
92
Cardiac Conditions Requiring Antibiotic
Prophylaxis for Infective Endocarditis
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
Congenital Heart Disease
what is affected?
when this occurs/why?
sus to?
* Abnormalities of the heart and great vessels
* Faulty embryogenesis - weeks 3 to 8
* Susceptibility to infective endocarditis –antimicrobial prophylaxis
94
Etiology of Congenital Heart Disease
* Most have no identifiable cause - multifactorial environmental, genetic and maternal factors
95
# drugs/infections?
enviornmental factors of congential heart dx
– Infectious - fetal rubella or cytomegalovirus infection
– Drugs –accutane, lithium, anti-seizure medications, cocaine, alcoh
96
genetic disorders related to congenital heart dx
trisomy 21 and turner syndrome
97
Categories of Congenital Heart
Disease*
* Malformations causing Left-to-Right Shunts
* Malformations causing Right-to-Left Shunts
* Malformations causing Obstructions
98
Right-to-Left Shunts effect on pul blood flow, result?
* Pulmonary blood flow is decreased, allowing poorly-oxygenated blood to enter the systemic circulation
* Cyanotic Congenital Heart Disease
99
R to L shunts associated with what odd emboli?
May be associated with paradoxical
embolism –a septal defect allows venous emboli to bypass the lungs and enter systemic arterial circulation
100
fingers with R to L shunts
Cyanosis and Clubbing of Fingers
101
Tetralogy of Fallot
* Right-to-Left Shunt
* Most common form of cyanotic congential heart disease
102
Tetralogy of Fallot pts have what defects at the heart
1. Ventricular septal defect (VSD)
2. Sub-pulmonary stenosis
3. Right ventricular hypertrophy
4. Aorta overrides VSD
103
most common form of congnetial heart dx
VSD
104
most common form of cyanotic congnetial heart dx
tetraology of fallot
105
Transposition of the Great Arteries
* Separate systemic and pulmonary circulations is incompatible with post-natal life and requires shunt for survival
106
Transposition of the Great Arteries possible shunts
* Stable shunt
– Ventricular Septal Defect
* Unstable shunts- will regress, must be re-established
– Patent Foramen Ovale
– Patent Ductus Arteriosus
107
ventricles with transposition of the great vessels
RV- hypertrophy, acts as systemic ventricle
LV- atrophy, acts as pul ventricle
108
Left-to-Right Shunts effects on pul blood flow, result?
* Pulmonary blood flow increased
–Pulmonary hypertension
109
potential forms of L to R shunts
* Ventricular Septal Defect
* Atrial Septal Defect
* Atrial-Ventricular Septal Defect
* Patent Ductus Arteriosus
110
# can this be a shunt? progression?
Patent Ductus Arteriosus
* 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
# frequent indicative finding?
Coarctation of the Aorta
* Obstructive defect located in the area of the ductus that may be asymptomatic until adulthood
* Rib notching due to collateral circulation
112
Coarctation of the Aorta, bp's related to the coarctation
* Hypertension proximal to coarctation
* Hypotension distal to coarctation
