Systemic Pathology 400 (CV pathologies) Flashcards

1
Q

CV system, anatomy

A

..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Heart Layers

A

fibrous pericardium

parietal layer of serous pericardium

visceral layer of serous pericardium (epicardium)

Myocardium,

Endocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Heart Valves

A

Atrioventricular Valves,

Semilunar Valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The Cardiac Cycle and movement of blood through the heart

A

..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Movement of Blood throughout the blood vessels (systemic and pulmonary)

A

..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HYPERTENSION

A

Persistent elevation of

diastolic blood pressure (higher than 90mm Hg),

systolic blood pressure (higher than 140mm Hg),

or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypertension Classification

A

Hypertension can be classified according to

type,
cause,
severity,
risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary Hypertension

A

(aka Essential):

idiopathic, 95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Secondary Hypertension

A

identifiable cause, 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

E.g. of “identifiable cause”

A

E.g.
Renal disease,

vascular disease,

endocrine disorders,

adrenal disorders,

hyperthyroidism,

coarctation of the aorta,

excessive alcohol intake,

use of oral contraceptives,

sleep apnea,

corticosteroids,

cocaine,

pregnancy, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

why corticosteroids high BP

A

Because cortisone is involved in regulating the body’s balance of water, sodium, and other electrolytes, using these drugs can promote fluid retention and sometimes cause or worsen high blood pressure. Self-care tips: Watch for swelling of your ankles, and report this to your doctor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypertension risk factors

A

Genetics

Smoking

Obesity

High cholesterol

Ethnicity

Diet

Inadequate sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypertension pathogenesis

A

Blood Pressure is related to blood flow and total peripheral vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

BP

A

BP = CO x TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

TPR

A

= blood viscosity

= diameter of BV (arterioles)

= total length of BV (arterioles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CO

A

CO = HR * SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathogenesis of hypertension involves

A

Increased cardiac output (CO)

Increased peripheral vascular resistance (TPR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Increased cardiac output (CO)

A

aka increased HEART RATE

and increased STROKE VOLUME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Increased peripheral vascular resistance (TPR)

A

aka increase blood viscosity

decreased BV diameter

increased total BV length (esp arterioles which contribute most)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hypertension other contirbuting factors

A

Abnormal sodium transport

Sympathetic nervous system stimulation

Renin-angiotensin-aldosterone system

Vasodilator deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathological Changes (to vasculature and organs)

(Early HTN)

A

None

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pathological Changes (to vasculature and organs)

(Late HTN)

A

End-organ damage

CV system, brain, kidneys

Acceleration of the development of atherosclerosis

(Death related to the above)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

End-organ damage

A

“End organ damage is severe impairment of major body organs due to systemic disease.”

“Commonly this is referred to in diabetes, high blood pressure, or states of low blood pressure or low blood volume.[1] This can present as a heart attack or heart failure, pulmonary edema, neurologic deficits including a stroke, or acute kidney failure.[2]”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

end organ

A

“The ultimately affected organ in a chain of events, such as a disease process (pathophysiology) or a drug’s mechanism of action (sometimes called a target organ in this sense)”

“An end organ is the last organ affected in a chain of events, for instance a disease process. Examples are the liver, brain, kidney or heart.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Hypertension Clinical Manifestation (mid stage)
Asymptomatic in some Headache Vertigo Flushed face Blurred vision Nocturia Frequency Nose bleeds
26
vertigo
Vertigo is a condition in which a person has the sensation that they are moving, or that objects around them are moving, when they are not. Often it feels like a spinning or swaying movement. WHY DOES HIGH BP CAUSE VERTIGO? ---> "Increased blood pressure damages blood vessels, including those in the ear. The inner ear helps maintain balance, and when hypertension affects the blood vessels, it can lead to episodes of dizziness. Furthermore, hypertension is a known risk factor for stroke, which can disrupt the brain's control of balance."
27
why nocturia, high BP
"From Guyton's natriuretic curve, we can infer that salt-sensitive hypertensive patients who consume too much salt do not excrete salt during the daytime and are forced to excrete salt at night, resulting in increased urine production and nocturia."
28
hyeprtension medication
Diuretics, adrenergic blockers (BETA BLOCKERS) vasodilators, ACE inhibitors, calcium antagonists
29
ACE inhibitor define also --> beta-blockers (?) also --> Calcium channel blockers
"Angiotensin-converting enzyme (ACE) inhibitors are medicines that help relax the veins and arteries to lower blood pressure." "ACE inhibitors prevent an enzyme in the body from making angiotensin 2, a substance that narrows blood vessels." **** Note also BETA-BLOCKERS: "Beta-adrenergic receptors (β-ARs) are G protein-coupled receptors that mediate physiological responses to adrenaline and noradrenaline." ++++ Calcium? "Calcium channel blockers are medicines used to lower blood pressure. They stop calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open."
30
Hypertension Managing modifiable risk factors
Quit smoking Weight reduction Regular cardiovascular exercise Supplements Diet
31
CONGENITAL HEART DEFECT
Any defect involving the heart and/or large vessels that is present at birth Develop in utero during the 1st trimester Incidence: 8/1000 newborns Prevalence: 1 million adults
32
Etiology
1) Idiopathic 2) Environmental ---> Drugs ---> Viruses ---> Alcohol ---> Maternal Disease E.g. Diabetes, Obesity, Lupus 3) Genetic ---> Chromosomal defects (10%)
33
Congenital Heart Defect Clinical Manifestation
Quality & quantity of defects: ---> Variable depending on the severity of the defect and single versus multiple defects Can be asymptomatic, apparent at birth, life-threatening, non-compatible with life, etc.
34
Congenital Heart Defect E.g. SEPTAL DEFECTS
The most common form of congenital heart disease (up to 40%) Defect in the septum between the left and right side of the heart ---> Can be atrial (atrial septal defect) – due to defects in the foramen ovale ---> Can be ventricular (ventricular septal defect) – more common, but can be more serious
35
does septal defect necessarily have to occur on its own?
Can occur in isolation or in conjunction with other heart defects
36
Pathogenesis of Ventricular Septal Defect
Pressure within the left heart chamber exceeds the pressure within the right heart chamber Arterial blood flows from left to right side of heart (left-to-right shunt) ---> This backflow overburdens the right side of the heart which then must work harder, leading to right ventricular hypertrophy ---> The increased flow of blood through the pulmonary arteries leads to pulmonary HTN ---> These changes lead to increased pressure in the right side of the heart, causing blood to flow to the left side of the heart (right-to-left shunt) The blood that flows to the left side of the heart is deoxygenated leading to cyanosis.
37
Clinical Manifestations of VSD (Ventricular septal defect)
Asymptomatic Heart murmur Cyanosis
38
Treatment (VSD)
Self-limiting otherwise: Surgery
39
TETRALOGY OF FALLOT
A complex congenital defect of the heart and the major vessels The most common cause of neonatal cardiac cyanosis Accounts for 10% of all congenital heart defects
40
most common cause of neonatal cardiac cyanosis
tetralogy of fallot
41
what percentage of congenital heart defects is TOF
10%
42
TETRALOGY OF FALLOT:
Stenosis of the pulmonary artery or valve & Ventricular septal defect + Overriding of the aorta = Hypertrophy of right ventricle
43
Tetralogy of Fallot: Pathogenesis
Narrowed pulmonary artery/valve limits amount of blood that can enter lungs Right ventricle attempts to compensate by pumping harder Venous blood in right ventricle shunted through septal defect into aorta and LV Aorta overrides septum leading to deoxygenated blood into systemic circulation
44
Tetralogy of Fallot: Clinical Manifestations
Cyanosis Heart murmur Failure to thrive
45
Failure to thrive
(especially in young children or animals) failure to grow or to gain or maintain weight.
46
TOF Diagnosis
Prenatal screening Clinical manifestation
47
Tetralogy of Fallot: Treatment
Surgery (treat ventricular septal defect/shunt + stenosed pulmonary valve)
48
Prognosis (TOF)
Good (with treatment?)
49
RHEUMATIC FEVER
Rheumatic fever is a systemic, immunologically mediated disease, related to infection by group A streptococcal bacteria (GAS)
50
GAS
Group A streptococcal (GAS) infections occur when bacteria enter your body and causes an illness. Most illnesses are mild and affect the skin and throat. aka Streptococcus pyogenes
51
is rheumatic fever common in developed countries?
The overall incidence of rheumatic fever is decreasing due to the use of antibiotics and more efficient treatment of the bacterial infections that precede rheumatic fever
52
Rheumatic fever Etiology and Pathogenesis
...
53
how long after streptococcal infection does rheumatic fever develop?
Usually develops ~2 weeks after an acute episode of strep throat (streptococcal infection) Exact mechanism unclear
54
pathogenesis?
Antibodies produced by the immune system in response to streptococcal antigens attack self-antigens of the heart, brain, kidneys, muscles, and joints Creates immune response w/ inflammation and scarring of tissues note: somewhat similar to post-lyme / chronic lyme disease (?) ---> where even after treatment, Ab's attack self antigens even in absence of the bacteria
55
what type of hypersensitivity is rheumatic fever
(Type II hypersensitivity) (cytotoxic Ab mediated)
56
hypersensitivity types
anaphylactic type (1) cytotoxic Ab mediated (2) immune complex mediated (3) delayed cell-mediated (4)
57
how often does rheumatic heart disease take place during rheumatic fever?
Rheumatic heart disease (scarring and deformity of heart valves) occurs in 50% of cases
58
rheumatic fever clincial manifestations
Sydenhams Chorea (or St. Vitus’ dance) SOB (dyspnea) Nocturnal cough Subcutaneous nodules Erythema marginatum (5%)
59
erythema marginatum
"Erythema marginatum is an acquired skin condition which primarily affects the arms, trunk, and legs. It is a type of erythema characterised by bright pink or red circular lesions which have sharply-defined borders and faint central clearing." "Erythema marginatum is reactive inflammatory erythema seen most commonly in association with acute rheumatic fever" "Although a rare cutaneous manifestation, it is of utmost diagnostic value for acute rheumatic fever as well as other rare disorders." "It is an early feature of acute rheumatic fever though not pathognomonic of it" ---> (CAN TAKE PLACE W/ A FEW OTHER CONDITIONS AS WELL) (?)
60
Sydenhams Chorea (or St. Vitus’ dance)
"a form of chorea chiefly affecting children, associated with rheumatic fever." "a neurological disorder characterized by spasmodic involuntary movements of the limbs or facial muscles." "Most children will completely heal from SC. Very few will have symptoms that last for a long time. Symptoms usually last for three to six weeks, but sometimes they can last for months." "Sydenham chorea is caused by a hypersensitivity humoral response triggered by an infection with group A β-hemolytic Streptococcus." "The subsequent immune inflammatory response attacks and destroys cells of the basal ganglia."
61
Rheumatic Fever Clinical Manifestation
Pharyngitis Acute migratory polyarthritis Carditis Fever, malaise, weakness, weight loss, anorexia
62
migratory (poly)arthritis
Migratory arthritis is a pattern of joint pain that begins in one or more joints, resolves, and then reappears in other joints. It is usually caused by an underlying condition such as rheumatic fever, lupus, inflammatory bowel disease, or Lyme disease.
63
Rheumatic Heart Disease
Endocarditis Myocarditis Pericarditis OR... Pancarditis (everything)
64
Endocarditis (during rheumatic heart disease -- during rheumatic fever)
most common; inflammation of the endocardium, including the valves which can result in permanent damage and valvular defects
65
Myocarditis (during rheumatic heart disease -- during rheumatic fever)
common; can result in arrhythmia, cardiac conduction problems
66
Pericarditis (during rheumatic heart disease -- during rheumatic fever)
rare; only in severe cases
67
is endocarditis during rheumatic fever considered to be bacterial endocarditis?
Yes (?)
68
Rheumatic Fever Dx
Jones criteria, throat culture, ECHO
69
Jones Criteria
Jones Criteria for Diagnosis of Rheumatic Fever Diagnose acute rheumatic fever Questions 1. Evidence of Antecedent Strep Infection? 2. Polyarthritis? 3. Chorea? 4. Erythema Marginatum? 5. Subcutaneous Nodules? 6. Carditis? 7. Arthralgia? 8. Previous rheumatic fever or rheumatic heart disease? 9. Elevated Acute Phase Reactant? (ESR or CRP) 10. Prolonged PR interval? 11. Fever?
70
echo (?)
"An echocardiogram (echo) is a test that diagnoses and manages heart disease. An echo uses ultrasound to create pictures of your heart's valves and chambers."
71
rheumatic fever treatment ?
Antibiotics* Anti-inflammatories Corticosteroids CNS depressants Surgery (?)
72
why would surgery be required for rheumatic fever?
Treatment depends in large part on how much damage has been done to the heart valves. In severe cases, treatment may include surgery to replace or fix a badly damaged valve. The best treatment is to prevent rheumatic fever. Antibiotics can often treat strep infections and keep rheumatic fever from occurring.
73
RF Prognosis
Initial episodes of RF can last weeks to months 20% of cases will reoccur within 5 years (possible genetic/autoimmune component?) May cause long term heart damage Mortality is low (1-2%)
74
ENDOCARDITIS
Infection (typically staphylococci or streptococci) of the endocardium, including the heart valves
75
which valve is most commonly affected in endocarditis?
Damage occurs most commonly to the mitral valve
76
what percentage endocarditis affects right side of heart?
Only ~10-20% affect the right side of the heart
77
which group is most at risk for right-side endocarditis?
IV drug users will have a much higher incidence of right-sided endocarditis (30-70% of cases)
78
IV drug users and right side endocarditis?
"Further, it has been postulated that intravenous drugs can result in pulmonary hypertension leading to increased turbulent blood flow across the valve resulting in endothelial damage to the right-sided heart valves."
79
which age is endocarditis most common?
Can occur at any age, most common in 60+
80
which gender is more affected by endocarditis?
2:1 men to women
81
endocarditis risk factors
Damaged valves Prosthetic heart valves IV drug users Immunocompromised
82
why are damaged valves and prosthetic valves risk factors for endocarditis?
endocardium of damaged valves is compromised -- leading to increased likelihood of bacteria adhering to surface ---> Recall endocardium has an extremely smooth surface that is designed to eliminate friction what about prosthetic valves? same reason? increased friction
83
endocarditis pathogeneiss
Abnormality of endocardium and microorganisms in blood stream increase susceptibility Infection causes inflammation and destruction of the cardiac endothelium and connective tissues Microorganisms adhere to the surface of the endocardium and release lytic enzymes that further erode valves and create defects and deformities Defect of surface endocardium is covered with fibrin and platelet thrombi Serve as a NIDUS to attract more thrombogenic material
84
NIDUS define
(Medicine) a place in which bacteria have multiplied or may multiply; a focus of infection.
85
nidus etymology
'place in which an insect deposits its eggs' "nest"
86
endocarditis pathogenesis (continued)
Small bumps (vegetations) on valves grow rapidly into large wartlike structures - VERRUCOUS ENDOCARDITIS Inflammation destroys portions of the valves causing deformities and/or ulcerations Valves may rupture and cause regurgitation Infected valvular vegetations may break off and give rise to septic emboli that usually affect the kidneys, brain, extremities
87
VERRUCOUS
verrucous define: of, pertaining to, marked by, or like a wart or warts "from Latin verruca "a wart; a hillock,""
88
VERRUCOUS ENDOCARDITIS
The meaning of VERRUCOUS ENDOCARDITIS is endocarditis marked by the formation or presence of warty nodules of fibrin on the lips of the heart valves.
89
Libman-Sacks endocarditis
"Libman-Sacks endocarditis, also known as murantic or verrucous endocarditis, is a form of nonbacterial thrombotic endocarditis (NBTE)" different from the bacterial verrucous endocarditis we are discussing (?)
90
what can happen to vegetations on valves in verrucous endocarditis?
Infected valvular vegetations may break off and give rise to septic emboli that usually affect the kidneys, brain, extremities
91
endocarditis Clinical Manifestation
Variable Endocarditis can develop insidiously and asymptomatically for months, or symptoms can develop immediately
92
SSx when symptomatic (endocarditis)
Heart murmurs Heart failure
93
acute bacterial endocarditis
Acute bacterial endocarditis – may present as an acute febrile illness of sudden onset Subacute bacterial endocarditis – mild temperature elevations that wax and wane
94
Endocarditis Tx
Antibiotics Valve replacement surgery
95
Endocarditis Px
Fatal if untreated Poor prognosis in older people, drug-resistant organisms, and/or delayed treatment Poor for people with aortic or multiple valve involvement Right side has better prognosis than left side 25% mortality rate overall
96
which side of heart has better prognosis for endocarditis?
Right side has better prognosis than left side
97
MYOCARDITIS
Relatively uncommon acute or chronic inflammatory condition of muscular walls of the heart AKA Acquired inflammatory cardiomyopathy
98
Myocarditis etiology
Viral or bacterial infection Chest radiation Ischemic heart disease Drugs Sarcoidosis SLE
99
sarcoidosis
"a chronic disease of unknown cause characterized by the enlargement of lymph nodes in many parts of the body and the widespread appearance of granulomas derived from the reticuloendothelial system." "Sarcoidosis is a disease involving abnormal collections of inflammatory cells that form lumps known as granulomata." "The disease usually begins in the lungs, skin, or lymph nodes. Less commonly affected are the eyes, liver, heart, and brain, though any organ can be affected."
100
Myocarditis pathogenesis
Involves active, healing, and healed stages that are characterized by inflammatory cell infiltrates leading to interstitial edema, focal necrosis, and fibrosis Ventricular arrhythmias may develop as a result
101
Myocarditis clinical manifestations
Mild, continuous chest pain Soreness (epigastric, sternal) Palpitations Fatigue Dyspnea Heart failure Arrhythmias Dilated (congestive) cardiomyopathy Sudden death
102
Dilated (congestive) cardiomyopathy
Dilated cardiomyopathy is a type of heart muscle disease that causes the heart chambers (ventricles) to thin and stretch, growing larger.
103
dilated cardiomyopathy and myocarditis
Dilated cardiomyopathy is a chronic form of heart disease involving dilatation, especially of the left ventricle and often leading to congestive heart failure. It may be a sequela of myocarditis. The disease has a high case fatality rate.
104
Myocarditis Tx
Treatment of the underlying condition usually resolves myocarditis E.g. Antibiotics for bacterial infections Cardiac medications to improve CO and reduce arrhythmias Corticosteroids for patients with lupus carditis
105
myocarditis Px
Depends on extent of damage
106
Pericarditis
Inflammation of the pericardium
107
Etiology pericarditis
Most often VIRAL infections, but can be BACTERIAL or FUNGAL as well Drugs Autoimmune conditions Infarct
108
pericarditis complications may include
Complications may include heart failure
109
pericarditis SSx
Chest pain Fever Dyspnea Can mimic, but is discernable from, MI ---> RECALL FROM LAST TERM'S NOTES, ACUTE PERICARDITIS CAN MIMIC Sx of MI
110
pericarditis, complications
Myocarditis Cardiac tamponade (Excess pericardial fluid) Heart failure
111
Cardiac tamponade
"compression of the heart by an accumulation of fluid in the pericardial sac." "Cardiac tamponade, also known as pericardial tamponade, is a compression of the heart due to pericardial effusion."
112
Pericarditis Dx
History, manifestation, auscultation, x-ray, ECG, blood tests, CT, MRI, ECHO
113
echo scan define
An echocardiogram, or “echo”, is a scan used to look at the heart and nearby blood vessels. It's a type of ultrasound scan, which means a small probe is used to send out high-frequency sound waves that create echoes when they bounce off different parts of the body.
114
ecg vs echo
Using electrodes, an ECG detects abnormalities in the electrical impulses of the heart, whereas an echocardiogram uses ultrasound to check for anomalies in the heart's structure.
115
pericarditis Tx
Treatment – variable, treat the underlying condition, prevention of future complications
116
pericarditis Px
variable (?)
117
CARDIOMYOPATHY
A group of conditions affecting heart muscle so that contraction and relaxations of myocardial muscle fibers are impaired
118
cardiomyopathy classifications
Primary – Genetic, mixed, acquired; confined to the heart muscle Secondary – systemic conditions that affect the heart and other tissues
119
Dilated cardiomyopathy
Occurs most commonly in black men, ages 40-60 Idiopathic (50%) or secondary to disease Risk factors include obesity, alcohol, hypertension, smoking, infections, pregnancy, genetics Characterized by fatigue, weakness, chest pain
120
which condition increased risk for developing dilated cardiomyopathy?
myocarditis
121
Hypertrophic cardiomyopathy
Appears to be related to inherited chromosomal abnormality (autosomal dominant) Frequently asymptomatic Most common cause of sudden cardiac death in young competitive athletes
122
which heart condition is most commonly caused by inherited chromosomal abnormality?
HYPERTROPHIC CARDIOMYOPATHY Appears to be related to inherited chromosomal abnormality (autosomal dominant)
123
Restrictive cardiomyopathy (STIFF HEART MUSCLES (fibrosis))
Occurs as a result of myocardial fibrosis (amyloidosis*, sarcoidosis, drugs, etc) Exercise intolerance, fatigue, SOB, edema, ascites
124
cardiomyopathy, clinical manifestations
General signs and symptoms for cardiomyopathies are the similar to heart failure Dyspnea Orthopnea Tachycardia Palpitations Peripheral edema Distended jugular vein
125
orthopnea
Orthopnea is shortness of breath when lying down that's relieved by standing or sitting up
126
why does orthopnea occur? Shouldn't it be easier when lying down since blood doesn't pump against gravity (?)
"When you lie flat, your blood redistributes from your legs to your lungs. This puts extra pressure on your lungs, making breathing difficult. If your heart is healthy, it pumps this extra blood out. But, if your heart is weak, it isn't strong enough to do this."
127
Cardiomyopathy, why distended jugular vein?
"Jugular vein distention happens when there's any kind of backup of blood in the superior vena cava or in your heart itself. Much like heavy traffic on a freeway can lead to backups and traffic jams, slowed blood flow in the heart or superior vena cava can cause blood to back up into the jugular veins." I.e. weak heart muscle? ---> fibrosis? (restrictive) ---> distended? ---> hypertrophic (?)
128
Cardiomyopathy Dx
ECHO, chest x-rays, blood analysis, genetic testing (ESP HYPERTROPHIC CARDIOMYOPATHY?), ECG
129
cardiomyopathy, tx
Determined by underlying cause Px variable
130