Ch. 18 (TEST #3) Flashcards
What are the three layers of the artery?
Tunica intima - endothelial layer (smooth surface decreases resistance and friction)
Tunica media- smooth muscle layer (constricts and dilates)
tunica externa - collagen and elastic fibers (protects and anchors, also is infiltrated with nerves to communicate with media)
What are some functions of the vascular endothelium?
Its a semi-permeable membrane - food and O2 to the tissues and waste and CO2 into vessel (on the capillary level)
Creates compounds that cause vasodilation or vasoconstriction
Creates growth factors that stimulate smooth muscle growth (important in vessel healing) IF STIMULATED AT WRONG TIMES MUSCLE CAN OVERGROW AND LEAD TO TURBULENT FLOW
Forms a smooth lining that resists clot formation
creates compounds to promote clot formation in injured areas
metabolizes hormones
regulates immune and inflammatory reactions
THINK ABOUT THESE WHEN ASKED ABOUT SOME ENDOTHELIAL DYSFUNCTIONS
What are some functions of the vascular smooth muscle cells?
Vasoconstriction and vasodilation
Synthesizes components of extracellular matrix (collagen and elastin)
Regulated by angiotensin II, catecholamines, and growth promoters
Which vessel layer can expand to accomodate pressure changes (mainly arterial)?
Tunica media (smooth muscle layer)
What are some disorders of the arterial circulation?
Hyperlipidemia => atherosclerosis
- is a progressive disorder
- affects any artery in the body
Vasculitis
- caused by direct injury, infection, immune reaction
- affects not only arteries, but veins and capillaries
aneurysms
- caused by a weakness in the arterial wall
- affects arteries only
What do we have to look out for with arterial circulation disorders (think abou arteries role)?
Hypoxia (disorders in flow could prevent cells from getting nutrients)
cells dont get nutrients and O2 => hypoxia => eventually leads to cell injury => can lead to necrotic cell death => spilling of cellular components => further increase inflammatory processes
What is hyperlipidemia?
High amount of lipids in the blood
What happens to the high amount of lipids with hyperlipidemia?
They will accumulate in the vascular endothelium => plaque formation => blocks flow through artery or causes turbulent flow
What are lipoproteins and how are they related to density?
These are proteins that carry lipids
more protein = higher density
less protein = lower density
Are lipids soluble in plasma?
NO, thats why they have to be transported by proteins
Are lipids good or bad?
They are good (we need them to repair lipid bi-layer or make new bi-layer during cell reproduction also schwann cells for myelin sheath in nerves) in a certain quantity
What are the different densities of lipoproteins from most dense to least dense?
HDL
LDL
VLDL
Chylomicrons
What makes HDLs heart healthy
They mainly help carry lipids out of the body (take them from peripheral tissues back to the liver for excretion)
Why are LDL considered bad?
These are the bodies main carriers of lipids.
What are triglycerides?
these are what we get from our diet directly (fats broken down into them), basically are a precursor to cholesterol (these are 80%-90% of what chylomicrons are)
So if someone hasnt fasted for a cholesterol test, what will be falsely elevated?
triglycerides (not cholesterols though it may a little, it takes a little more to make cholesterol)
What are the two ways we get lipids?
Through our diet (small intestine)
Through our liver making them (
SO EVEN WITH A LOW FAT DIET OUR LIVER CAN STILL MAKE CHOLESTEROL
What does our small intestine do with the fats we get in our diet (exogenous pathway)?
gets packaged into chylomicrons and absorbed into our blood vessels and carried by proteins
Then it can be deposited into our adipose and skeletal muscle tissues OR taken straight to the liver
Whatever is left is packaged as IDLs and eventually LDLs and are sent to the liver.
What is the livers role in lipid transportation (endogenous pathway)?
The liver takes in the LDLs that are left over from the exogenous pathway as well as left overs from the liver endogenous secretions of VLDL that werent absorbed by tissue (which are now LDLs) through its LDL receptors.
Once taken in by the LDL receptors the receptor pathway can break it down into Bile acid and cholesterol and excrete it by the GI system, or it can be converted into HDL and reversely transported back through the body picking up cholesterol form peripheral tissues (also can inhibit cellular absorption of LDL) and sent back to the liver to be excreted as bile acid and cholesterol by the GI system.
The liver can also make VLDLs that are sent back into the bloodstream to distribute more energy (adipose or skeletal muscle) which will then be processed again by the receptor pathway of the liver once they are converted to LDLs.
What happens when we have an issue with our liver or its receptors, what is an alternative pathway we can take?
An alternative, not so good pathway is known as the scavenger pathway, if we have to use this pathway we usually will already be having deposits in our vessels
So dietary lipids are absorbed as what?
chylomicrons
What takes up triglycerides from chylomicrons?
Fat (adipose) and muscle tissue
What happens with the left over chylomicrons after absorbtion?
The reminants are IDLs which convert to LDLs and are sent to the liver (where they will then be released from the liver as either HDLs or VLDLs
Why would we send the chylomicrons to the fat and muscle tissue to be absorbed?
THEY ARE A GREAT SOURCE OF ENERGY
they either get used by the muscle cells for energy or get stored in the fat tissue for use later
So if we eat a lot of fat but dont use our muscles very often then a lot of it will be stored in the fat tissue
What are endogenous triglycerides?
triglycerides that are made by the liver
So after our liver releases VLDLs into the blood stream and the triglycerides are distrubuted for energy, what form are they sent back to the liver in?
LDLs
What are our main carriers of cholesterol?
LDLs
So cholesterol can be affected by how many LDL receptors our liver has, or how well they function?
YES YES YES
we need our receptors to take in the LDLs for removal
What percentage of all LDLs are removed by the receptor pathway?
60%
How does the nonreceptor dependent pathway work?
This is where the LDLs are taken up by phagocytic monocytes (macrophages) and other scavenger cells (this is how foam cells are made)
Why would the nonreceptor pathway be activated?
If the receptor pathway is broken or there is too much LDL for the receptor pathway to handle itself.
Where are HDLs made mostly?
In the liver
What makea HDLs so good again?
They go out and pick up more cholesterol and bring it back to the liver to be excreted through our GI tract. They can take up cholesterol that has gone through either pathway (meaning that it can take up cholesterol from foam cells)
What is one of the only ways to increase HDLs?
exercise (specifically cardio active)
What are the normal cholesterol lab values we want to see?
total: 60
What is the difference between hypercholesterolemia and hyperlipidemia?
Hypercholesterolemia - high cholesterol in blood
hyperlipidemia - based on blood-lipid studies
IT DEPENDS ON THE LIPID PROFILE… WE COULD HAVE TWO PEOPLE OVER 200 BUT ONE PERSON HAS HIGH HDL THAT WILL PROTECT THEM EVEN IF THEY HAVE HIGH LDL, SO THEIR TOTAL WOULD SHOW HYPERCHOLESTEROLEMIA BUT THEY COULD STILL BE PROTECTED… BUT THEY WOULD BE IN TROUBLE IF THEY HAD A LOWER HDL IN COMPARISON TO LDL..
So the risk for atherosclerosis is dependent on the RATIO of HDL and LDL, not necessarily the independent numbers?
YES YES YES
What would we see in early diabetes in regards to triglyceride levels?
they would be elevated
What are the causes of hyperlipidemia/ hypercholesterolemia?
too much intake (diet)
too much made by the liver
not enough removed by the liver
- not enough receptors
- broken receptors
- not able to handle the workload
diseases (liver disease)
medications
What is another place where we could see deposits of cholesterol (plaques)?
The skin (hands, eyelids, arms, legs)
SIMILAR TO PLAQUE IN ARTERIES
Describe what is happening with atherosclerosis.
lipids get into the vascular endothelium => WBCs try to clear the lipids away => foam cells => WBCs and endothelium release growth factors to promote plaque formation => plaque that blocks arteries
What are some non-modifiable risks of atherosclerosis?
increasing age
male gender
genetic disorders of lipid metabolism
family hx
What are some potentially modifiable risks for atherosclerosis?
smoking
obesity
HTN
diabetes (might not prevent but can control)
hyperlipidemia
What are some non-traditional risks for atherosclerosis?
elevated c-reactive protein
hyperchromocysteinia
increased lipoprotein (a) levels
With hypertension and atherosclerosis, how do they connect in one big circle?
atherosclerosis hardens the arteries/ so does HTN
atherosclerosis hardens the walls of arteries, which increases blood pressure, blood pressure damages the arteries, which increases risk for atherosclerosis
Why does atherosclerosis develop?
scavenger cells are having to take in the fatty deposits on the arterial lining, they do this by:
attempting to destroy by oxidizing the fats => the oxidized fats injure the endothelium => clots begin to form and the endothelium (as well as platelets that have adhered and been aggregated to form clot) release growth factors => Smooth muscle grows over the fatty core (which is where the foam cells are trying to oxidize and eat the fats) => once this core is closed off the HDLs can no longer get to them
Describe the the innermost layer of vessel out.
When a plaque has formed there we will have our endothelial lining of our vessel (tunica intima)
then the smooth muscle layer that has formed over the core
Then fatty (necrotic) core which contains the foam cells
then comes the tunica media
Go more in depth about the steps of the formation of an athersclerotic plaque.
- The LDL enters the intima through its intact endothelium
- The intimal LDL is oxidized by monocytes that are checking the endothelial lining in the bloodstream by releasing free radicals
- These oxidized LDLs cause adhesion and transmigration of monocytes and T cells across the endothelium (also since they are oxidized they are now toxic to the endothelium and cause damage)
- Monocytes differentiate into macrophages and begin to consume the LDL in large amounts, transforming into foam cells
- The foam cells secrete growth factors (cytokines) that encourage atherosclerosis
If a plaque doesnt have a very strong cap, what can happen?
If the fibrous plaque has a cap that isnt very strong it may rupture and damage endothelium which could lead to a clot formation on top of an atherosclerotic plaque, which limits blood flow even more, or can break off (this is called a complicated athersclerotic lesion)
What is the first thing you will see before an atherosclerotic lesion?
Fatty streaks (can be seen between 10-14 years old and increase in number till 20, then they either stay static or regress, BUT they can become a fibrous plaque)
This is the beginning stages of LDL oxidation and foam cell formation
THESE DO NOT HAVE ANY CAPS, HAVE TO TURN TO FIBROUS PLAQUE BEFORE CAUSING SYMPTOMS OR BECOMING COMPLICATED ATHERSCLEROTIC LESION
With the poor diets of kids now, when have we started seeing fatty streaks in kids?
2-4 years old
Describe a fibrous atheromatous plaque.
This is the basic lesion of athersclerosis
There has been an accumulation of intracellular and extracellular lipids as well as proliferation of vascular smooth muscle cells and the formation of scar tissue (cap is made of this)
THIS IS WHEN THE CAP FORMS, YOU WANT A STRONG CAP TO PREVENT A COMPLICATED LESION, BUT EVEN THE CAP CAN GET TOO BIG AND OCCLUDE A VESSEL TOTALLY
describe a complicated atheromatous lesion.
This is characterized by hemorrhage, ulceration, and scar tissue deposits
What is the most important complication of atherosclerosis?
Thrombosis (formation of a clot)
`Does a vessel with a plaque lose it ability to dilate and constrict efficiently?
YES YES YES
CAN CAUSE ISSUES WITH BLOOD PRESSURE
What are the differences between stable and unstable plaques?
Stable: thick fibrous caps
partially blocked vessels
Dont tend to form clots or emboli
NORMALLY HAS ENOUGH BLOOD FLOW, UNLESS UNDER VERY HIGH DEMAND
Unstable plaques: have thin fibrous caps
can rupture and cause a clot to form
may completely block artery
clot may break free and become an embolus
Do the clinical manifestations of atherosclerosis depend on the the vessel involved?
YES YES YES
What are some things that atherosclerosis can cause?
Narrowing of the vessel and ischemia
vessel obstruction caused by plaque hemorrhage or rupture
thrombosis and formation of emboli resulting from endothelial injury
aneurysm formation caused by weakening of the vessel wall
What is atherosclerosis of the coronary arteries called?
CAD (coronary artery disease)
If someone has atherosclerosis of the carotids or arteries in the brain what are they at risk for?
stroke
What do we call atherosclerosis of the peripheral vessels?
PVD (peripheral vascular disease)
What is vasculitis?
inflammatory injury of the blood vessels
What causes vasculitis?
Direct injury
infectious agents
immune processes
secondary to systemic disease
PATIENT HAS CIRCULATING ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES
What are the clinical manifestations of vasculitis?
fever
myalgia
arthalgia
malaise
So we have small, medium, and large vessel vasculitis. What distinguishes these?
Small: type III immune complex hypersensitivities
Medium: necrotizing damage (kawasakis disease, beurgers disease)
Large: giant cell arterides = temperol arteritis
– cause acute and chronic inflammation of artery
What is the plural word for vasculitis?
vasculitides
What is raynauds disease and phenomenon (a type of peripheral arterial disease)?
The small arteries and arterioles of the fingers (MOST COMMON), and toes (LESS COMMON) vasoSPASM = ischemia
THE ETIOLOGY IS UNKNOWN
Cold (doesnt go away once out of cold, cold is just a trigger) or stress can be a trigger
Vasospasm leads to skin color change and change in sensation caused by ischemia => hyperemia shown by intense redness, throbbing, paresthesia => return of normal color
SKIN WILL TURN FROM BLUE AT FIRST THEN TO WHITE
What is another name for beurgers disease?
throboangititis obliterans
What demographic does beurgers disease like to affect?
young men 25-40 yeas old who smoke heavily
What is beugers disease?
vasculitis of medium sized arteries, usually foot and lower leg causing distal arterial ischemia
inflammatory
HIGH RISK FOR CLOTS
What is the predominant symptom of beurgers?
PAIN (CAN PRESENT WITH ACTIVITY) called intermittent claudication
(may also have decreased pulse, cooler skin distal to affected area, may have cyanosis)
What is peripheral arterial disease?
This is the athersclerosis of the peripheral arteries
PRESENTS INTERMITTENT CLAUDICATION
What is an interesting treatment for intermittent claudication that she talks about?
People use whatever the affected part of the body is until they have the pain and then stop, they do this repeatedly to eventually form collateral circulation through angiogenesis.
What is an aneurysm?
These are local dilations or outpouchings of a vessel wall or cardiac chamber.
What is the different between a true aneurysm and a false aneurysm?
True: bound by a complete vessel wall
- fusiform
- circumferential
false: dissection or tear in inner wall
- - saccular (appears as a sac)
What are the risks with an aneurysm?
Rupture and hemorrhage
clot formation
What is a berry aneuysm and where are they most common?
These are commonly found in the brain (cerebral area) and they usually occur where vessel biforcate
Describe a fusiform aneurysm?
This is an aneurysm that affects the whole circumference of the vessel.
INTERNAL LUMEN BECOMES LARGER
Can aneurysms at branching point affect those peripheral arteries blood flow?
YES YES YES
What is a dissection?
blood gets into the inner wall and starts filling space.
THE INTERNAL LUMEN IS UNAFFECTED IN THIS CASE
