Cardiovascular Patho Part 1 Flashcards
Hyperlipidemia
Hyperlipidemia is a major risk factor for the development of _______
(3) types of lipids found in the body
Because _______ and ______ are insoluble in plasma they are encapsulated by special fat-carrying proteins called _________
(5) Types of lipoproteins (classified by density)
Atherosclerosis
- Triglycerides
- Phospholipids
- Cholesterol
Triglycerides, Cholesterol, Lipoproteins
- Chylomicrons
- Very-low density lipoproteins (VLDL)
- Intermediate-density lipoproteins (IDL)
- Low-density lipoproteins (LDL)
- High-density lipoproteins (HDL)
Lipoproteins
Lipoproteins are named based on their ______ content measured by density.
Density determined by centrifugation: highest density is pushed down
- Chylomicrons and VLDL mostly made up of and delivers ______
- LDL: mostly made up and delivers ______
- HDL: mostly ______
- Primary role:
protein
- triglycerides
- cholesterol
- protein
- regulate amount of LDL in circulation
Structure of a Lipoprotein
- (1): Make up outer layer and have hydrophobic water soluble heads and fat soluble tails -> therefore heads face ____ and fatty acid tails face the ____
- Inside (2)
- (1): Acts as identifying markers for lipoproteins so each diff type of lipoprotein (HDL, LDL, etc) has diff ones - allows cell to _____ which one it is and determine its m_____ fate
- Phospholipids, plasma, lipoprotien core
- Cholesterol, Triglycerides
- Apoproteins, recognzie, metabolic
Sources of Lipids and Lipoprotein Synthesis
- Consumed cholesterol and triglycerides converted to _______ (made up of mostly triglycerides) by intestinal ______ cells -> then absorbed by intestines and goes a few places
- Stored in (2) (consumed for energy)
- (1): dissamebles these chylomicrons and produces ____ and _____ and release into circulation
- VLDLS along with the rest of the chylomicrons already in circulation get converted into ____ then _____
-
chylomicrons, epithelial
- adipose tissue, skeletal muscle
- liver, HDL and VLDL
- IDL and LDL
Uses of LDL (Notes)
- Maintains plasma _____ ______
- Taken up by ______ glands to produce _____ hormones
- Liver takes up 70% of LDLs and uses it to produce ______
- (1): All of htese cells take up LDL using their own LDL receptors
- membrane structure
- endocrine, steroid
- bile
- Receptor Mediated Uptake
Ways LDL is removed from the Body (Notes)
- (1) Pathway
- (1): 2nd method LDL is removed through circulation by binding to HDL and come back to the liver
- (1) Pathway: the pathway that makes LDL damaging to the body, how?
- Receptor Dependent Pathway
- Reverse Cholesterol Transport
-
Scavenger Pathway
- “bad guy cholesterol” -> excess LDL beyond what is needed for receptor pathway and HDLs “good guys”
- they interact with reactive O2 species and damage lining of blood vessels-> macrophages then come in as part of inflammatory response to consume and remove them
- So since HDL regulates LDL and removes them this is why we want HDL to be high and LDL low
Common Strategies to Reduce Excess LDL (Notes)
(3)
-
Oat bran solution (cheerios)
- increases water soluble fiber: binds with bile in GI tract and forces you to excrete it, less return of bile to liver increases demand so pulls more cholesterol from bloodstream -> lowers circulating LDLs
-
Bile Acid Sequestrants
- medication that also binds to bile and increases excretion will also reduce circulating LDLs (modest effect)
-
Statins: HMG-Co-A Reductase inhibitors
- prevents hmg coa reductase enzyme in liver necessary for synthesis of cholesterol -> reduces ability of liver to produce cholesterol -> so it will take more from bloodstream to meet its needs (greatest effect bc blocks liver synthesis)
Hyperlipidemia
Hyperlipidemia or dyslipidemia is the presence of _____ levels of certain lipoproteins in the _____ (chylomicrons, LDLs, VLDLs, IDLs)
Two forms of hypercholesterolemia
Primary Hypercholesterolemia:
- Defective synthesis of _____, lack of LDL ______, d_____ receptors
Secondary Hypercholesterolemia:
- Examples
However, no matter if primary or secondary?
elevated, blood
: Elevated levels of cholesterol that develops independent of other health problems or lifestyle behaviors, often genetic
- apoproteins, lack of LDL receptors, defective receptors so are not recognized and taken up by cells in our body like liver
:Associated with lifestyle and behavior
- obesity, high caloric intake, DM etc
Both have greater risk of atherosclerosis
Disorders of Blood Vessels and Circulation
Disturbance of Blood Vessels and Circulation
- Vessel ____: ex atherosclerosis, vasculitis
- Acute vessel ______ due to thrombus or embolus or vasospasm: ex-Raynauds
- Abnormal vessel ______: ex aneurysms
- ______ of vessels by outside forces: ex tumors, edema, firm surfaces
Interrupted blood flow causes impaired delivery of ___ and _____ to tissues (when arteries are affected)
And impaired clearance of blood from capillaries, impaired removal of ____ from tissues, and impaired return of blood to the _____ (when veins are affected)
- Walls
- Obstruction
- Dilation
- Compression
O2, nutrients
waste, blood return to heart
Disorders of Blood Vessels and Circulation (Notes)
Both vessel wall problems will ____ size of vessel and limit flow
- Embolus:
- Vasospasm:
- ______: defined by how it manifests and many causes behind this syndrome (ie. RA)
- effects blood flow mostly to ____- and ____ and very ____ dependent
- Changes in color:
- _____: most commonly with crushing injuries -> compartment syndrome, edema presses up against the fascia and compromises blood flow
narrow
- usually blood clot that detaches from where it initially forms but not always a blood clot
- Acute extreme constrictions of wall of the vessel
- Raynauds
- fingers, toes, temperature
- Blanched/pale from constriction of arterial flow or blue/purple from constriction of venous outflow -> pain when blood returns -> first become red then normal if stays warm enough
- Ed
- Edema
Atherosclerosis
A disease of _____-_____ arteries involving the accumulation of ______, ____ ____ cells, and _____ within the ______ of arterial vessel walls
- Most common cause of _____ problems
- Does not effect small arteries and veins bc medium and large size arteries have higher ______* -> persistent lvl of _____ on these endothelial walls makes it more likely for injuries -> inflammation -> plaque formation
- Intima:
medium to large, lipids, smooth muscle cells, collagen, INTIMA
- circulation
- pressure -> stress
- inside layer that faces blood flow, made up of endothelial cells and a little bit of connective tissue just under endothelium
Atherosclerosis (Notes)
- Accumulation just under the epithelium of the intima which is a tiny space -> lumen ______
- In essence, Atherosclerosis is a chronic _____ disease
- So what causes inflammation?
-
(1): early development of scar tissue caused by chronic injury to endothelium lining of vessels
- Sources of injury: _______ #1 risk factor, H__, H_____ from DM, S_____
- narrows
- inflammatory
- chronic injury -> fibrosis
-
Atherosclerotic plaque
- Hypercholesterolemia, HTN, Hyperglycemia, Smoking
Common Sites of Severe Atheroslcerosis in Order of Frequency
- Abdominal ____- and _____ Arteries
- Proximal ______ Arteries
- Th_____, F______, and P_____ Arteries
- Internal ______ Arteries
- V_____, B______, and middle C____ Arteries AKA the?
- Abdominal Aorta, Iliac
- Coronary
- Thoracic aorta, Femoral, Popliteal
- Carotid
- Vertebral, Basilar, Cerebral - CIRCLE OF WILLIS: set of arteries found in the base of the brain
Fatty Streaks
- Caused by the deposition of lipid engorged ______ (____ cells) within the intima of the walls of medium to large arteries
- Found in children by age __, increases in number until age __. Streaks then either ______ or remain _____
lipid engorged macrophages (Foam Cells)
1-20, regress or remain static
Fatty Streaks (Notes)
- Fatty Streaks: _______ healing stage in vessels (analagous to cabs) from injury
- Endothelium releases ______ -> neutrophils -> monocyte -> _______ spew out reactive O2 species -> _______ LDLs in the area and macrophages eat them up and move underneath endothelial to accumultae dt increased ______ forming fatty streaks -> allows ______ -> fatty streak _______
- intermediate, acute injury
- cytokines -> macrophages -> oxidize LDLs and eat them -> permeability -> healing -> dissapears
Physical Features of an Atherosclerotic Plaque
Right pic:
Is Atherosclerosis reversible?
Arteriosclerosis inside blood vessel that is mostly fibrotic tissue
Yes
Pathogenesis of Atherosclerotic Plaque 1
_____ to endothelial wall
Endothelial cells release _____ and trigger monocytes to become macrophages to come to the area
Injury
Cytokines
Pathogenesis of an Atherosclerotic Plaque II
Macrophage ______ and starts releasing _ _ _ that oxidizes ___
Endothelium becomes more _____ -> plasma carrying LDL rushes in and macrophages eat them up
Macrophages continue to eat LDL until bloated (_____)
adheres, ROS, LDL
permeable
engorged
Pathogenesis of an Atherosclerotic Plaque III
(1) Lipid engorged macrophages: now beneath endothelium and still releasing ___ species and drawing ____ macrophages to area
Macrophages are inflammatory mediators but is also the cell that triggers ______
But these macrophages are ____ getting healing cues, more cues for continued _____ -> HOT MESS - the few that are trying to heal release __ and ____ that gets wrapped up in the mess
Foam Cells -> O2 -> more macrophages
Healing
NOT, just continued inflammation, GF, collagen
Pathogenesis of an Atherosclerotic Plaque IV
- Plaque is formed
- Foam cells start to ___ bc can’t get out -> ______ tissue
- Overproduction of (2)
- More ______ to area
- Beginning of Atherosclerosis: hardening and _______ of vessel wall bc down the line, plaques get large and necrotic tissue starts to ______ -> hard calcium deposits push against vessel wall depriving cells of blood flow
- _______ of artery wall can occur if injury is taken away and not too far into fibrosis stage
- Plaque is formed
- die -> necrotic
- collagen, smooth muscle
- macrophages
- fibrosis, calcify
- Healing
Atherosclerotic Plaque Fissure and Rupture
-
(1): small plaque that narrows vessel a bit, not enough to cause symptoms
- ex) little plaque in the top right hand corner
- Biggest danger: plaque ______
- (1): weakest point of plaque where rupturing always happens
- Exposed ______ triggers _____ formation
- Symptoms asctd with rupture: sudden onset of ____, ____ if in carotids, _____ if in cerebral artery
-
Close ____, Unstable _____, __\_: If clot stays small and doesn’t completely occlude vessel
- Dangerous possibilities: clot continues to grow and completely occludes vessel or detaches and forms embolus -> A______ -> TISSUE _____ (__, _____)
-
Silent plaque
- rupturing
- Shoulder
- Collagen, clot
- pain, AMS, balance
- Call, Angina, TIA
- ANOXI -> DEATH (MI, STROKE)
Factors that Influence the Likelihood of Plaque Rupture
-
______ on the cap
- Stress is related to wall _____
-
T = ___ x ____
- If R1 > R2 and P is the same then T1 __ T2
-
Overall _____ of the plaque (related to ______)
- Plaques are more likely to rupture if they contain relatively more (1) and relatively less (2)
- ie: lipid to protein ratio is _____
-
Stress
- Tension
-
P (intraluminal pressure) x R (radius)
- T1 > T2 if radius is bigger
-
Weakness (composition)
- Macrophages (Foam Cells), less collagen and smooth muscle
- High
Emboli
An Embolus, usually a ____ ____, is actually ___ abnormal _____ found in circulation that can _____ from one area to another.
Can include (7)
- Originating in venous tree =
- Originating in arterial tree =
blood clot, any substance, travels
- Pieces of tissue
- Air bubbles
- Amniotic fluid
- Fat (long bone fracture causes fat in marrow to immobilize into blood stream)
- Bacteria
- Tumor cells
- Foreign substances
- Pulmonary Embolism
- Brain, kidneys, arms/legs causing ischemia or infarction
Deep Vein Thrombosis (DVT)
DVT Manifestations
(3)
Unilateral Swelling
Redness
Pain (dull ache)
Arterial Occlusive Disease
=
Don’t memorize just understand that the manifestations are associated with ____ of _____ tissue of whereever the occlusion
- Plaque in vestibular system =
- Mesenteric artery =
- Lower limb =
Atherosclerotic plaques in diff places of arterial tree
ischemia of downstream tissue
- balance problems
- bowel ischemia
- intermittent claudication
Aneurysm
-
True Aneurysm =
- Tend to see ____ more than _____
- _____ symptoms unless rupture
- Example (1)
-
False Aneurysm =
- Frequently happens where (2)
- Takes time to ____
- Major Complications (2): of _____ meds for MI/stroke
- Arterial Dissection =
- Dilation of one or both sides of entire vessel wall
- fusiform > saccular
- Minimal
- AAA just a pulsatile mass, however if ruptures very fatal and presents like MI
- Part of vessel wall ruptures and blood forms hematoma, kept from rupturing and bleeding out from connective tissue
- Brain, Mesenteric arteries in GI tract
- heal
- Intracerebral hemorrhage, GI bleed, Fibrinolytic meds
- Tear in the intima forces blood through intima forming a false lumen and causing tearing away of intima from wall of artery
Aneurysms associated with Atherosclerosis occur most commonly in the?
Abdominal Aorta Aneurysm (AAA)
AAA
Clinical Features and Consequences of AAA
- Rupture into the _______ cavity with massive, potentially fatal _____
- _______ of a branch vessel resulting in _____ injury of downstream tissue ie) iliac (leg), renal (kidney), mesenteric (GI), vertebral (spinal cord)
- ______ from atheroma or mural thrombus
- I_______ on an adjacent structure ie compression of ureter or erosion of vertebrae
- Presentation as an abdominal _____ (often palpably ______) that simulates a tumor
Risk Factors (3)
Risk of rupture is directly related to ______
- Generally, aneurysms > ___ cm managed aggresively usually by ____ bypass involving prosthetic _____
- peritoneal/retroperitoneal, hemorrhage
- Obstruction, ischemic
- Embolism
- Impingement
- mass, pulsating
HTN, Atherosclerosis, collagen disorders (marfan syndrome)
Size
- >5cm, surgery, prosthetic grafts
What type of Aneurysm is Most Commonly Associated with Hypertension?
Thoracic Aortic Aneurysm
Aortic Dissection
