Systemic Pathology 400 (CV pathologies) Flashcards
CV system, anatomy
..
Heart Layers
fibrous pericardium
parietal layer of serous pericardium
visceral layer of serous pericardium (epicardium)
Myocardium,
Endocardium
Heart Valves
Atrioventricular Valves,
Semilunar Valves
The Cardiac Cycle and movement of blood through the heart
..
Movement of Blood throughout the blood vessels (systemic and pulmonary)
..
HYPERTENSION
Persistent elevation of
diastolic blood pressure (higher than 90mm Hg),
systolic blood pressure (higher than 140mm Hg),
or both
Hypertension Classification
Hypertension can be classified according to
type,
cause,
severity,
risk
Primary Hypertension
(aka Essential):
idiopathic, 95%
Secondary Hypertension
identifiable cause, 5%
E.g. of “identifiable cause”
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.
why corticosteroids high BP
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.
Hypertension risk factors
Genetics
Smoking
Obesity
High cholesterol
Ethnicity
Diet
Inadequate sleep
Hypertension pathogenesis
Blood Pressure is related to blood flow and total peripheral vascular resistance
BP
BP = CO x TPR
TPR
= blood viscosity
= diameter of BV (arterioles)
= total length of BV (arterioles)
CO
CO = HR * SV
Pathogenesis of hypertension involves
Increased cardiac output (CO)
Increased peripheral vascular resistance (TPR)
Increased cardiac output (CO)
aka increased HEART RATE
and increased STROKE VOLUME
Increased peripheral vascular resistance (TPR)
aka increase blood viscosity
decreased BV diameter
increased total BV length (esp arterioles which contribute most)
hypertension other contirbuting factors
Abnormal sodium transport
Sympathetic nervous system stimulation
Renin-angiotensin-aldosterone system
Vasodilator deficiency
Pathological Changes (to vasculature and organs)
(Early HTN)
None
Pathological Changes (to vasculature and organs)
(Late HTN)
End-organ damage
CV system, brain, kidneys
Acceleration of the development of atherosclerosis
(Death related to the above)
End-organ damage
“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]”
end organ
“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.”
Hypertension
Clinical Manifestation (mid stage)
Asymptomatic in some
Headache
Vertigo
Flushed face
Blurred vision
Nocturia
Frequency
Nose bleeds
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.”
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.”
hyeprtension medication
Diuretics,
adrenergic blockers (BETA BLOCKERS)
vasodilators,
ACE inhibitors,
calcium antagonists
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.”
Hypertension
Managing modifiable risk factors
Quit smoking
Weight reduction
Regular cardiovascular exercise
Supplements
Diet
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
Etiology
1) Idiopathic
2) Environmental
—> Drugs
—> Viruses
—> Alcohol
—> Maternal Disease
E.g.
Diabetes, Obesity, Lupus
3) Genetic
—> Chromosomal defects (10%)
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.
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
does septal defect necessarily have to occur on its own?
Can occur in isolation or in conjunction with other heart defects
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.
Clinical Manifestations of VSD (Ventricular septal defect)
Asymptomatic
Heart murmur
Cyanosis
Treatment (VSD)
Self-limiting
otherwise:
Surgery
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
most common cause of neonatal cardiac cyanosis
tetralogy of fallot
what percentage of congenital heart defects is TOF
10%
TETRALOGY OF FALLOT:
Stenosis of the pulmonary artery or valve
&
Ventricular septal defect
+
Overriding of the aorta
=
Hypertrophy of right ventricle
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
Tetralogy of Fallot: Clinical Manifestations
Cyanosis
Heart murmur
Failure to thrive
Failure to thrive
(especially in young children or animals) failure to grow or to gain or maintain weight.
TOF Diagnosis
Prenatal screening
Clinical manifestation
Tetralogy of Fallot: Treatment
Surgery (treat ventricular septal defect/shunt + stenosed pulmonary valve)
Prognosis (TOF)
Good (with treatment?)
RHEUMATIC FEVER
Rheumatic fever is a systemic, immunologically mediated disease, related to infection by group A streptococcal bacteria (GAS)
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
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
Rheumatic fever
Etiology and Pathogenesis
…
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
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
what type of hypersensitivity is rheumatic fever
(Type II hypersensitivity)
(cytotoxic Ab mediated)
hypersensitivity types
anaphylactic type (1)
cytotoxic Ab mediated (2)
immune complex mediated (3)
delayed cell-mediated (4)
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
rheumatic fever clincial manifestations
Sydenhams Chorea (or St. Vitus’ dance)
SOB (dyspnea)
Nocturnal cough
Subcutaneous nodules
Erythema marginatum (5%)
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) (?)
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.”
Rheumatic Fever
Clinical Manifestation
Pharyngitis
Acute migratory polyarthritis
Carditis
Fever, malaise, weakness, weight loss, anorexia
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.
Rheumatic Heart Disease
Endocarditis
Myocarditis
Pericarditis
OR…
Pancarditis (everything)
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
Myocarditis
(during rheumatic heart disease – during rheumatic fever)
common; can result in arrhythmia, cardiac conduction problems
Pericarditis
(during rheumatic heart disease – during rheumatic fever)
rare; only in severe cases
is endocarditis during rheumatic fever considered to be bacterial endocarditis?
Yes (?)
Rheumatic Fever Dx
Jones criteria, throat culture, ECHO
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?
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.”
rheumatic fever treatment ?
Antibiotics*
Anti-inflammatories
Corticosteroids
CNS depressants
Surgery (?)
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.
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%)
ENDOCARDITIS
Infection (typically staphylococci or streptococci) of the endocardium, including the heart valves
which valve is most commonly affected in endocarditis?
Damage occurs most commonly to the mitral valve
what percentage endocarditis affects right side of heart?
Only ~10-20% affect the right side of the heart
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)
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.”
which age is endocarditis most common?
Can occur at any age, most common in 60+
which gender is more affected by endocarditis?
2:1 men to women
endocarditis risk factors
Damaged valves
Prosthetic heart valves
IV drug users
Immunocompromised
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
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
NIDUS define
(Medicine)
a place in which bacteria have multiplied or may multiply; a focus of infection.
nidus etymology
‘place in which an insect deposits its eggs’
“nest”
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
VERRUCOUS
verrucous define:
of, pertaining to, marked by, or like a wart or warts
“from Latin verruca “a wart; a hillock,””
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.
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 (?)
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
endocarditis
Clinical Manifestation
Variable
Endocarditis can develop insidiously and asymptomatically for months, or symptoms can develop immediately
SSx when symptomatic (endocarditis)
Heart murmurs
Heart failure
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
Endocarditis Tx
Antibiotics
Valve replacement surgery
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
which side of heart has better prognosis for endocarditis?
Right side has better prognosis than left side
MYOCARDITIS
Relatively uncommon acute or chronic inflammatory condition of muscular walls of the heart
AKA Acquired inflammatory cardiomyopathy
Myocarditis etiology
Viral or bacterial infection
Chest radiation
Ischemic heart disease
Drugs
Sarcoidosis
SLE
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.”
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
Myocarditis clinical manifestations
Mild, continuous chest pain
Soreness (epigastric, sternal)
Palpitations
Fatigue
Dyspnea
Heart failure
Arrhythmias
Dilated (congestive) cardiomyopathy
Sudden death
Dilated (congestive) cardiomyopathy
Dilated cardiomyopathy is a type of heart muscle disease that causes the heart chambers (ventricles) to thin and stretch, growing larger.
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.
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
myocarditis Px
Depends on extent of damage
Pericarditis
Inflammation of the pericardium
Etiology pericarditis
Most often VIRAL infections,
but can be BACTERIAL
or FUNGAL as well
Drugs
Autoimmune conditions
Infarct
pericarditis complications may include
Complications may include heart failure
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
pericarditis, complications
Myocarditis
Cardiac tamponade (Excess pericardial fluid)
Heart failure
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.”
Pericarditis Dx
History, manifestation, auscultation, x-ray, ECG, blood tests, CT, MRI, ECHO
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.
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.
pericarditis Tx
Treatment – variable, treat the underlying condition, prevention of future complications
pericarditis Px
variable (?)
CARDIOMYOPATHY
A group of conditions affecting heart muscle so that contraction and relaxations of myocardial muscle fibers are impaired
cardiomyopathy classifications
Primary – Genetic, mixed, acquired; confined to the heart muscle
Secondary – systemic conditions that affect the heart and other tissues
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
which condition increased risk for developing dilated cardiomyopathy?
myocarditis
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
which heart condition is most commonly caused by inherited chromosomal abnormality?
HYPERTROPHIC CARDIOMYOPATHY
Appears to be related to inherited chromosomal abnormality (autosomal dominant)
Restrictive cardiomyopathy (STIFF HEART MUSCLES (fibrosis))
Occurs as a result of myocardial fibrosis (amyloidosis*, sarcoidosis, drugs, etc)
Exercise intolerance, fatigue, SOB, edema, ascites
cardiomyopathy, clinical manifestations
General signs and symptoms for cardiomyopathies are the similar to heart failure
Dyspnea
Orthopnea
Tachycardia
Palpitations
Peripheral edema
Distended jugular vein
orthopnea
Orthopnea is shortness of breath when lying down that’s relieved by standing or sitting up
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.”
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 (?)
Cardiomyopathy Dx
ECHO, chest x-rays, blood analysis, genetic testing (ESP HYPERTROPHIC CARDIOMYOPATHY?), ECG
cardiomyopathy, tx
Determined by underlying cause
Px variable
