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Semester 4 > Systemic Pathology 400 (CV pathologies) > Flashcards

Systemic Pathology 400 (CV pathologies) Flashcards

1
Q

CV system, anatomy

A

..

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2
Q

Heart Layers

A

fibrous pericardium

parietal layer of serous pericardium

visceral layer of serous pericardium (epicardium)

Myocardium,

Endocardium

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3
Q

Heart Valves

A

Atrioventricular Valves,

Semilunar Valves

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4
Q

The Cardiac Cycle and movement of blood through the heart

A

..

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5
Q

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

A

..

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6
Q

HYPERTENSION

A

Persistent elevation of

diastolic blood pressure (higher than 90mm Hg),

systolic blood pressure (higher than 140mm Hg),

or both

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7
Q

Hypertension Classification

A

Hypertension can be classified according to

type,
cause,
severity,
risk

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8
Q

Primary Hypertension

A

(aka Essential):

idiopathic, 95%

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9
Q

Secondary Hypertension

A

identifiable cause, 5%

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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.

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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.

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12
Q

Hypertension risk factors

A

Genetics

Smoking

Obesity

High cholesterol

Ethnicity

Diet

Inadequate sleep

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13
Q

Hypertension pathogenesis

A

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

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14
Q

BP

A

BP = CO x TPR

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15
Q

TPR

A

= blood viscosity

= diameter of BV (arterioles)

= total length of BV (arterioles)

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16
Q

CO

A

CO = HR * SV

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17
Q

Pathogenesis of hypertension involves

A

Increased cardiac output (CO)

Increased peripheral vascular resistance (TPR)

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18
Q

Increased cardiac output (CO)

A

aka increased HEART RATE

and increased STROKE VOLUME

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19
Q

Increased peripheral vascular resistance (TPR)

A

aka increase blood viscosity

decreased BV diameter

increased total BV length (esp arterioles which contribute most)

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20
Q

hypertension other contirbuting factors

A

Abnormal sodium transport

Sympathetic nervous system stimulation

Renin-angiotensin-aldosterone system

Vasodilator deficiency

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21
Q

Pathological Changes (to vasculature and organs)

(Early HTN)

A

None

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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)

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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]”

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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.”

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25
Q

Hypertension

Clinical Manifestation (mid stage)

A

Asymptomatic in some

Headache

Vertigo

Flushed face

Blurred vision

Nocturia

Frequency

Nose bleeds

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26
Q

vertigo

A

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.”

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27
Q

why nocturia, high BP

A

“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.”

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28
Q

hyeprtension medication

A

Diuretics,

adrenergic blockers (BETA BLOCKERS)

vasodilators,

ACE inhibitors,

calcium antagonists

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29
Q

ACE inhibitor define

also –> beta-blockers (?)

also –> Calcium channel blockers

A

“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.”

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30
Q

Hypertension

Managing modifiable risk factors

A

Quit smoking

Weight reduction

Regular cardiovascular exercise

Supplements

Diet

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31
Q

CONGENITAL HEART DEFECT

A

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

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32
Q

Etiology

A

1) Idiopathic

2) Environmental
—> Drugs
—> Viruses
—> Alcohol
—> Maternal Disease
E.g.
Diabetes, Obesity, Lupus

3) Genetic
—> Chromosomal defects (10%)

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33
Q

Congenital Heart Defect

Clinical Manifestation

A

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.

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34
Q

Congenital Heart Defect

E.g.
SEPTAL DEFECTS

A

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

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35
Q

does septal defect necessarily have to occur on its own?

A

Can occur in isolation or in conjunction with other heart defects

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36
Q

Pathogenesis of Ventricular Septal Defect

A

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.

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37
Q

Clinical Manifestations of VSD (Ventricular septal defect)

A

Asymptomatic

Heart murmur

Cyanosis

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38
Q

Treatment (VSD)

A

Self-limiting

otherwise:
Surgery

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39
Q

TETRALOGY OF FALLOT

A

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

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40
Q

most common cause of neonatal cardiac cyanosis

A

tetralogy of fallot

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41
Q

what percentage of congenital heart defects is TOF

A

10%

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42
Q

TETRALOGY OF FALLOT:

A

Stenosis of the pulmonary artery or valve

&
Ventricular septal defect
+
Overriding of the aorta

=
Hypertrophy of right ventricle

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43
Q

Tetralogy of Fallot: Pathogenesis

A

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

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44
Q

Tetralogy of Fallot: Clinical Manifestations

A

Cyanosis

Heart murmur

Failure to thrive

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45
Q

Failure to thrive

A

(especially in young children or animals) failure to grow or to gain or maintain weight.

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46
Q

TOF Diagnosis

A

Prenatal screening

Clinical manifestation

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47
Q

Tetralogy of Fallot: Treatment

A

Surgery (treat ventricular septal defect/shunt + stenosed pulmonary valve)

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48
Q

Prognosis (TOF)

A

Good (with treatment?)

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49
Q

RHEUMATIC FEVER

A

Rheumatic fever is a systemic, immunologically mediated disease, related to infection by group A streptococcal bacteria (GAS)

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50
Q

GAS

A

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

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51
Q

is rheumatic fever common in developed countries?

A

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

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52
Q

Rheumatic fever

Etiology and Pathogenesis

A

…

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53
Q

how long after streptococcal infection does rheumatic fever develop?

A

Usually develops ~2 weeks after an acute episode of strep throat (streptococcal infection)

Exact mechanism unclear

54
Q

pathogenesis?

A

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
Q

what type of hypersensitivity is rheumatic fever

A

(Type II hypersensitivity)

(cytotoxic Ab mediated)

56
Q

hypersensitivity types

A

anaphylactic type (1)

cytotoxic Ab mediated (2)

immune complex mediated (3)

delayed cell-mediated (4)

57
Q

how often does rheumatic heart disease take place during rheumatic fever?

A

Rheumatic heart disease (scarring and deformity of heart valves) occurs in 50% of cases

58
Q

rheumatic fever clincial manifestations

A

Sydenhams Chorea (or St. Vitus’ dance)

SOB (dyspnea)

Nocturnal cough

Subcutaneous nodules

Erythema marginatum (5%)

59
Q

erythema marginatum

A

“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
Q

Sydenhams Chorea (or St. Vitus’ dance)

A

“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
Q

Rheumatic Fever

Clinical Manifestation

A

Pharyngitis

Acute migratory polyarthritis

Carditis

Fever, malaise, weakness, weight loss, anorexia

62
Q

migratory (poly)arthritis

A

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
Q

Rheumatic Heart Disease

A

Endocarditis

Myocarditis

Pericarditis

OR…
Pancarditis (everything)

64
Q

Endocarditis

(during rheumatic heart disease – during rheumatic fever)

A

most common; inflammation of the endocardium, including the valves which can result in permanent damage and valvular defects

65
Q

Myocarditis

(during rheumatic heart disease – during rheumatic fever)

A

common; can result in arrhythmia, cardiac conduction problems

66
Q

Pericarditis

(during rheumatic heart disease – during rheumatic fever)

A

rare; only in severe cases

67
Q

is endocarditis during rheumatic fever considered to be bacterial endocarditis?

A

Yes (?)

68
Q

Rheumatic Fever Dx

A

Jones criteria, throat culture, ECHO

69
Q

Jones Criteria

A

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
Q

echo (?)

A

“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
Q

rheumatic fever treatment ?

A

Antibiotics*

Anti-inflammatories

Corticosteroids

CNS depressants

Surgery (?)

72
Q

why would surgery be required for rheumatic fever?

A

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
Q

RF Prognosis

A

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
Q

ENDOCARDITIS

A

Infection (typically staphylococci or streptococci) of the endocardium, including the heart valves

75
Q

which valve is most commonly affected in endocarditis?

A

Damage occurs most commonly to the mitral valve

76
Q

what percentage endocarditis affects right side of heart?

A

Only ~10-20% affect the right side of the heart

77
Q

which group is most at risk for right-side endocarditis?

A

IV drug users will have a much higher incidence of right-sided endocarditis (30-70% of cases)

78
Q

IV drug users and right side endocarditis?

A

“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
Q

which age is endocarditis most common?

A

Can occur at any age, most common in 60+

80
Q

which gender is more affected by endocarditis?

A

2:1 men to women

81
Q

endocarditis risk factors

A

Damaged valves

Prosthetic heart valves

IV drug users

Immunocompromised

82
Q

why are damaged valves and prosthetic valves risk factors for endocarditis?

A

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
Q

endocarditis pathogeneiss

A

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
Q

NIDUS define

A

(Medicine)
a place in which bacteria have multiplied or may multiply; a focus of infection.

85
Q

nidus etymology

A

‘place in which an insect deposits its eggs’

“nest”

86
Q

endocarditis pathogenesis (continued)

A

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
Q

VERRUCOUS

A

verrucous define:
of, pertaining to, marked by, or like a wart or warts

“from Latin verruca “a wart; a hillock,””

88
Q

VERRUCOUS ENDOCARDITIS

A

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
Q

Libman-Sacks endocarditis

A

“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
Q

what can happen to vegetations on valves in verrucous endocarditis?

A

Infected valvular vegetations may break off and give rise to septic emboli that usually affect the kidneys, brain, extremities

91
Q

endocarditis

Clinical Manifestation

A

Variable

Endocarditis can develop insidiously and asymptomatically for months, or symptoms can develop immediately

92
Q

SSx when symptomatic (endocarditis)

A

Heart murmurs

Heart failure

93
Q

acute bacterial endocarditis

A

Acute bacterial endocarditis – may present as an acute febrile illness of sudden onset

Subacute bacterial endocarditis – mild temperature elevations that wax and wane

94
Q

Endocarditis Tx

A

Antibiotics

Valve replacement surgery

95
Q

Endocarditis Px

A

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
Q

which side of heart has better prognosis for endocarditis?

A

Right side has better prognosis than left side

97
Q

MYOCARDITIS

A

Relatively uncommon acute or chronic inflammatory condition of muscular walls of the heart

AKA Acquired inflammatory cardiomyopathy

98
Q

Myocarditis etiology

A

Viral or bacterial infection

Chest radiation

Ischemic heart disease

Drugs

Sarcoidosis

SLE

99
Q

sarcoidosis

A

“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
Q

Myocarditis pathogenesis

A

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
Q

Myocarditis clinical manifestations

A

Mild, continuous chest pain

Soreness (epigastric, sternal)

Palpitations

Fatigue

Dyspnea

Heart failure

Arrhythmias

Dilated (congestive) cardiomyopathy

Sudden death

102
Q

Dilated (congestive) cardiomyopathy

A

Dilated cardiomyopathy is a type of heart muscle disease that causes the heart chambers (ventricles) to thin and stretch, growing larger.

103
Q

dilated cardiomyopathy and myocarditis

A

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
Q

Myocarditis Tx

A

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
Q

myocarditis Px

A

Depends on extent of damage

106
Q

Pericarditis

A

Inflammation of the pericardium

107
Q

Etiology pericarditis

A

Most often VIRAL infections,

but can be BACTERIAL

or FUNGAL as well

Drugs

Autoimmune conditions

Infarct

108
Q

pericarditis complications may include

A

Complications may include heart failure

109
Q

pericarditis SSx

A

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
Q

pericarditis, complications

A

Myocarditis

Cardiac tamponade (Excess pericardial fluid)

Heart failure

111
Q

Cardiac tamponade

A

“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
Q

Pericarditis Dx

A

History, manifestation, auscultation, x-ray, ECG, blood tests, CT, MRI, ECHO

113
Q

echo scan define

A

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
Q

ecg vs echo

A

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
Q

pericarditis Tx

A

Treatment – variable, treat the underlying condition, prevention of future complications

116
Q

pericarditis Px

A

variable (?)

117
Q

CARDIOMYOPATHY

A

A group of conditions affecting heart muscle so that contraction and relaxations of myocardial muscle fibers are impaired

118
Q

cardiomyopathy classifications

A

Primary – Genetic, mixed, acquired; confined to the heart muscle

Secondary – systemic conditions that affect the heart and other tissues

119
Q

Dilated cardiomyopathy

A

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
Q

which condition increased risk for developing dilated cardiomyopathy?

A

myocarditis

121
Q

Hypertrophic cardiomyopathy

A

Appears to be related to inherited chromosomal abnormality (autosomal dominant)

Frequently asymptomatic

Most common cause of sudden cardiac death in young competitive athletes

122
Q

which heart condition is most commonly caused by inherited chromosomal abnormality?

A

HYPERTROPHIC CARDIOMYOPATHY

Appears to be related to inherited chromosomal abnormality (autosomal dominant)

123
Q

Restrictive cardiomyopathy (STIFF HEART MUSCLES (fibrosis))

A

Occurs as a result of myocardial fibrosis (amyloidosis*, sarcoidosis, drugs, etc)

Exercise intolerance, fatigue, SOB, edema, ascites

124
Q

cardiomyopathy, clinical manifestations

A

General signs and symptoms for cardiomyopathies are the similar to heart failure

Dyspnea
Orthopnea
Tachycardia
Palpitations
Peripheral edema
Distended jugular vein

125
Q

orthopnea

A

Orthopnea is shortness of breath when lying down that’s relieved by standing or sitting up

126
Q

why does orthopnea occur?

Shouldn’t it be easier when lying down since blood doesn’t pump against gravity (?)

A

“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
Q

Cardiomyopathy, why distended jugular vein?

A

“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
Q

Cardiomyopathy Dx

A

ECHO, chest x-rays, blood analysis, genetic testing (ESP HYPERTROPHIC CARDIOMYOPATHY?), ECG

129
Q

cardiomyopathy, tx

A

Determined by underlying cause

Px variable

130
Q
A

Semester 4 (30 decks)

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