Cardiovascular Disorders Flashcards
What are the three most basic components of Cardiovascular system?
Vessels, Blood, Heart
Lymphatic system includes
Lymphatic tissue, vessel and nodes
What is Hyperlipidemia?
What is a Lipoprotein (+ Types)
•Abnormally elevated fats/lipids in blood (cholesterol, phospholipids, and triglycerides)
o Lipids in blood do not move on their own, require carriers (i.e. Apoproteins) - carry lipids/fats
o lipid +apoprotein= lipoprotein
o Lipoprotein vary density
Produced by Liver-
LDL = trouble! since mostly cholesterol
HDL (good) equal parts lipid and protein. Returns cholesterol from peripheral tissue
VLDL (Fig 22-2) + (Fig 22-3) provide lipid transport to skeletal and adipose tissue
Produced in intestinal epithelial cells-
Chylomicrons- largest carry triglycerides
What is Atherosclerosis?
Word Breakdown
A disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls.
Athero- soft and pasty
Osis- generally formation of something, and a deposition of something)
Sclerosis- scaring/hardening
What is plaque?
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. (Generally just means a lesion) Forms progressively, hardens arteries and often leading to a narrowing of the vessel.
What is Atheroma?
An atheroma is an accumulation of degenerative material in the tunica intima (inner layer) of artery walls. The material consists of (mostly) macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
Basically a fibro fatty lesion that forms in the intima of larger arteries
3 lesions associated with the progression of Atherosclerosis?
(see pages 470-471)
1) Fatty streak- deposit of lipids + macrophages, neutrophils, etc
o Macrophages ingest lipids (becoming foam cells) release free radicals/growth factors which encourages further growth
2) Fibrous Atheromatous plaque- cells, platelets, lipids, defence cells, WITH the addition of smooth muscle cells
3) Complicated lesion- Earlier stages were inside the wall, final stage we see changes in the lumen. After bleeding into the plaque a thrombus forms in the vessel
Pathogenesis of Atherosclerosis?
pg 470
- Insidious origin with subtle endothelial injury -> inflm
- Monocytes & other cells associated w/ inflame bind to endothelium (w/ adhesion molecules)
- Monocytes enter intima -> become macropahges -> release free radicals (from oxidizing fat) causing further inflm/injury & engulf lipids (becoming foam cells)
- Foam cells release growth factors and smooth muscle cells proliferate
- Later stages bleeding into plaque
- Atheroma forms
Common sites for atherosclerosis in order of frequency
Abdominal aorta and iliac arteries
proximal coronary arteries
Thoracic aorta, femoral and popliteal arteries
Internal carotid artery
Vertebral, basilar and middle cerebral arteries
Why use C reactive protein in diagnosing atherosclerosis?
CRP is a serum marker for inflm. If there is no specific injury or trauma yet CRP lab value remains high, vessel wall damage/inflm is a common cause of value
What are foam cells?
Foam cells are fat-laden macrophages formed when the body sends them to the location of a fatty deposit on the blood vessel walls.
What compensatory mechanism manages BP
At rest?
On exertion?
BP= CO x PR
• At rest PR changes to maintain BP (CO stable)
• Exertion CO changes
4 major control systems of Bp?
review Fig 23-2
- Arterial baroreceptors (strategically located receptors to detects changes in pressure)
- Renin-angiotensin system
- Vascular Autoregulation
- Regulation of fluid volume
What is the Renin-Angiotensin system?
It’s a paragraph answer that needs to be summarized, so just describe it in general terms
The renin-angiotensin-aldosterone system (RAAS) is a signaling pathway responsible for regulating the body’s blood pressure.
Stimulated by low blood pressure or certain nerve impulses (e.g. in stressful situations), the kidneys release an enzyme called renin. This triggers a signal transduction pathway: renin splits the protein angiotensinogen, producing angiotensin I. This is converted by another enzyme, the angiotensin-converting enzyme (ACE), into angiotensin II.
Angiotensin II not only causes blood vessels to narrow (vasoconstriction), it also simultaneously stimulates the secretion of the water-retaining hormone vasopressin (also called AVP) in the pituitary gland (hypophysis) as well as the release of adrenaline, noradrenaline and aldosterone in the adrenal gland.
Whereas adrenaline and noradrenaline enhance vasoconstriction, aldosterone influences the filtration function of the kidneys. The kidneys retain more sodium and water in the body and excrete more potassium. The vasopressin from the pituitary gland prevents the excretion of water without affecting the electrolytes sodium and potassium.
In this way, the overall volume of blood in the body is increased: more blood is pumped through constricted arteries, which increases the pressure exerted on the artery walls – the blood pressure.
What is the difference between primary and secondary HTN?
1* HTN (140/90)
• essential or idiopathic
• about 90% of cases
• Et: multifactorial (kidney implicated)
2* HTN (>140/90) identifiable Et (eg renal disease) about 10% of cases
What is Systolic HTN?
Systolic HTN
• Systolic p* >140, diastolic p* reduced elasticity -> increased systolic pressure but not diastolic pressure
What is malignant HTN
o Diastolic >120
Not referring to cancer, just a serious issue
Can pregnancy cause HTN
Yes, Gestational HTN
What is White Coat HTN
Refers to Bp measuring higher then usual when individual is in a clinical setting
What is the only Mnft of HTN
High BP, everything else is a complication related to HTN
What are the complications associated with HTN?
o Fatigue,
o palpitations (sensation of a forceful irregular heartbeat)
o AM headaches (Bp has circadian rhythm, highest in the AM)
o Blurred visions (damage from aneurism in retina capillaries)
o Dizziness
• *** Those of progressive organ damage (heart, kidney, eyes, vessels)
Tx for Stage 1 and (maybe) Stage 2 HTN
Tx often includes only mngmt, not tx of underlying cause
• Life style modification- diet, exercise, body weight
Tx for Stage 2 to Stage 3 HTN (Pharmaceutical)
1rst and 2nd line of defence?
• 1st line- diuretics
• 2nd line : if req add 1 or more of
o Ca channel blockers (prevents Ca from crossing cell membrane, inhibits cardiac muscle contraction, reduces Bp)
o Angiotensin ll receptor blocker (Angiotension loop) blocking receptor
o ACE (Ace inhibitor) Prevents formation
What is Peripheral Vascular Disease (PVD)?
Two sub categories?
A common circulatory problem in which narrowed arteries reduce blood flow to your limbs. Your extremities — usually your legs — don’t receive enough blood flow to keep up with demand. This causes symptoms, most notably leg pain when walking (intermittent claudication)
Separated into Acute Arterial Occlusion (thrombus) and Artherosclerotic Arterial Occlusion (gradual dev and intermittent)
PVD- Atherosclerotic occlusive disease
Who is at risk? Common Mnfts?
Anyone with chronic vascular damage (Elderly and Diabetics)
Intermittent claudication (ischemic pain while walking)
o impedes perfusion -> ischemia -> tissue damage
o venous or lymphatic stasis – fluid and waste accumulation in legs
PVD- What happens when body tries to compensate?
Likely outcome w/o tx?
- Body attempts compensation w/ vasodilation (Quick response, but vessel already damaged, already dialated) anaerobic metb & collateralization occur
- W/O effective tx -> ulceration & gangrene -> amputation
What is an Aneurysm and where is it likely to occur?
Risk Factors?
- Localized dilation of artery (bulge)
- Permanent (not reversible)
- Increases near corners or bifurcation of vessels
- d/t degeneration/damage change in vessel wall
Risk factors
• HTN, atherosclerosis, congenital defects
Three types of Aneurysms?
(Fig 22-10)
- Saccular- One sided- forms a pouch or sac
- Fusiform- Both sides or around the vessel completely
- Dissecting- Blood flows between two layers of blood wall
Specific common sites of an aneurysm?
- Abdominal and thoracic aorta, femoral iliac and popliteal
* Vessels which lack external support, bends and bifurcation
