Systemic Pathology 400 (CV pathologies) Flashcards
CV system, anatomy
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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)
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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
…