CVD Histology & Pathophysiology Flashcards
Basic organizaion of the cardiovascular system
- walk through by area
- deoxygenated blood from the IVC and SVC enter the right atrium of the heart
- right atrium: contains the SA node (problem here = arrythmias)
- pass through the tricuspid valve into the right ventricle
- right ventricle is the MOST ANTERIOR
- pass through the pulmonary semilunar valves into the pulmonary artery into lungs
- return from the lungs oxygenated through the pulmonary veins to the left atrium
- left atrium is most posterior structure point for thrombi formation
- pass through the mitral valve to the left ventricle
- pump (with great force) from the left ventricle to the aorta through the aotric semilunar valves
- travel trhough arteries to capilarrie beds when exchange occurs
interventricular septum seperates the ventricles
valvular dysfunction
- stenosis v regurgitation
- Mitral valve stenosis
- mitral valve prolapse & regurg
- aortic valve stenosis
- aortic regurg
stenosis: constriction or narrowing of the valves
-this impedes the forward flow of blood
Regurgitaions: incompletely closing of the leaflets
- allows flow backwards
mitral and aortic are where things are going wrong
Mitral Valve Stenosis
- increases pressure within the left atrium, pulmonary vasculature and the right side of the heart
- number 1 cause of this is rheumatic heart disease!!
Mitral Valve Prolapse
- the leaflets dont close properly & there is backward flow back into the left atrium
- Marfans & genetics
Aotric Valve Stenosis
- cannot pump blood through the aortia from left ventricle
- cause is degenerative calcifical due to age (70+)
- if from younger than 70 —> congenital disease
- turners syndrome
- SAD: syncope, angina, dyspnea on exertion
Aortic Regurgitation
- backward flow
- MI, endocartitis, trauma can cause this
- chronic: a calcification of the valve, root dilation
Heart Layers of cells
Pericaridum: the outer protective layer made of…
1. fiberous layer
2. parietal pericardium
3. pericardial cavity (fluid for dec. friction)
4. visceral pericaridum
5. myocardium (muscle layer)
6. endocardium (innermost lining of the heart)
Problems of the pericardium
- acute pericarditis
- constrictive pericarditis
- pericardial effusion and tamponade
problmes of the myocardium
-dialated caridomyopathy
-hypertrophic cardiomyopathy
acute pericarditits
- inflammation of the pericardium for less than 2 weeks
- usually a viral infection (cancer, uremia, sepsi too)
- pts. compains of chest pain which gets better when leaning forward & they are changes on the EKG
- treat underlying issue and NSAIDS
Constrictive Pericarditis
- calcifications and scarring between the layers – lost elasticity so cannot fill during diastole
- due to chronic inflammation
- surgical removal of the pericardium
Pericardial effusion & tamponade
- effusion: excess fluid in the space
- tamponade: the fluid now is impacting heart function
- due to infection, HF, trauma
- cardiomeg. on exam & necessary pericardialcentesis
Dialated cardiomyopathy (dialted – systolic cant pump)
- dilation of all chambers –> systolic contraction unable to happen (flabby and regurg.)
- genetic (MD)
- viral, drugs
- leads to HF
restricitive: the heart is thickening –> something is deposting into it and it cant expand and take in blood (sarcoidosis, hemochormatosis)
Hypertropic Cardiomyopathy (genetic – cant fill and flow)
- abnormal thickening of the muscle, specifcally the left ventricle and the septum –> diastolic dysfunction with relaxation (blocks outflow)
- genetic autosomial interitance
- thick young athletes with sudden cardiac death
- the electric cant pass through too much tangled cells
layers and cells of the Arteries v the Veins
- endothelium: what it does
- layers in ateries
- layers in veins
Artery =more smooth muscle
- tunica externa
- external elastic lamina
- Tunica media
- internal elastic lamina
- basement membrane
- tunica Interna (intima) = endothelial cells
endothelium= the continuous sheet of cells lining all teh vascular in the inside
- aids in regualtion of blood flow
- helps with cell growht
- maintains a permiable barrier
- expression of pro or anti thromboic molecules
inner most = lumen
Veins
- Tunica Externa
- Tunica Media
- basement membrane
- tunica interna
- veins have valves!! to prevent backflow!!
types of capillaries & what they allow to pass
continuous
fenestrated
sinusoid (discontinuous)
Continuous: in the skin, brain and skeletal muscle
- no breaks in the capillary walls –> only water, ions and very small molecules can pass
Fenestrated: in the kidneys, intestines and pancreas
-for fluid and larger molecules to pass
Sinusoid (discontinuous): large gaps between cells –> an incomplete basement membrane
- in the bone marrow, lymph nodes, liver and spleen
- areas where whole cells need to pass through to travel
neovascularization v. angiogenesis
mediated by
neovascularization: the formation of NEW blood vessels
angiogenesis: creating blood vessels from pre-existing vessels
- formation of collateral circulation due to poorly perfused tissue (heart, leg, etc.)
- angiogenesis: think of blood supply for a new metastisis
- both neo and angio. are mediated by VEGF: vascular endothelial growth factor
- —> VEGF increased in hypoxic conditions & can be secreted from healthy and cancerous cells
what is atherosclerosis
risk factors?
a disease of the arteries –> due to fatty plaque deposition in the lumen on the tunica intima
- results in narrowing
- can rupture & travel as a thrombi
- can weaken the underlying wall easy for an aneurysm to occur
Risk factors: modifiable and non-modifiable
- genetics, age& male
- smoking, hyperlipidemia, hypertension, obesity, DM
pathogenesis of atherosclerosis
- role of LDL
- there is injury to the endothelial cells in the tunica intima (injury from increased LDL, smoking, inc. homocysteine, immune molecules, stress with HTN)
- the inflammatory cells response to this injury & accumulate at site (pro-throm. phase)
- lipid (LDL) comes and accumulates
- the LDL gets oxidized —> recruits macrophages which try to eat it away
- the macrophages + LDL = foam cell
- create a fatty streak in the vessel
- chronic inflammation keeps occuring & the cycle continues and dump more and more
- — smooth muscle cells begin to grow overtop – create a fiberous capsule on the plaque
- dead center can now become necrotic
- VEGF recruits more vessels and the cycel continues
- ** plaque remodeling occurs as it rips apart and remakes itself**
- strucutre of a plaque
- determine stable from unstable plaques
fiberous cap: smooth mucles cells, macrophages & lymphocytes creat the fiberous cap
necrotic core: of dead cell debris, foam cells, etc.
ECM: factors like collage, elastin, proteoglycans line the outer layer
Stable Plaque: less likely to rupture and travel to become a clot
- THICK fiberous cap
- small lipid core
- minimal inflamamtion
Unstable/Vulnerable Plaque: high risk of rupturing
- THIN fiberous cap
- Large lipid core
- lots of inflammation
what is vasculitis?
pathogenesis?
signs and symptoms
vasculitis: inflammation of a vessel wall
patho
- a result of direct injury to the wall (by infectious pathogens)
- an immune-mediated damage to the wall (like antibodies)
histology
- inflammatory infiltrates
- wall thickening
- necrosis
signs and symptoms
- fever, myaligs, arthlargias, malaise
what is Giant Cell Ateritis?
pathology
clinical
what is polyateritis nodosa (PAN?)
pathology
clinical
GCA: most common form of vasculitis in the elderly
- occurs in women > men
- a granulomatous inflammation of the aorta and its main branches
- specifically those which are supplying the head
- think, temporal, vertebral, opthalmic
pathology
- multinucleated giant cells – collection of macrophages to create a granuloma
clinical
- facial pain, headache
- tender temporal artery inflammed skin
- blurred vision
- can result in aortic aneurysum
- treat with corticosteroids
PAN
- a multisystem inflammatory disease of small & medium arteriers
- kideny (MC), liver, heart and GI tract most commonly
- men > women
- due to drug use, hepatitis B or sjorgens syndrome
Pathology
- segmental transmural necrotizing
- so only parts of the vessel is impacted (not continuous like giant cell)
clincial
- presentation will depend on what organ its affecting
- treat with corticosteroids or immunomodulators
aneurysm v dissection
- causes of aortic aneurysums and dissections
aneurysm: congenital or aquired dialtion of the blood vessel of all three layers (like a buldge)
Dissection: a TEAR in the lining (intima) so that there is accumulation of blood within the wall
** both can lead to a thrombus or a rupture**
causes of aortic anuerysum
- atherosclerosis
- hypertension
- trauma
- vasculitis
- congeital defects
- infections!
- majorty of abdomial – see pulsing aorta
- throacic: possible = compression of airway and esophagus and hoarsness
- risk of rupture –> > 5 cm = 5-10% inc. risk /yearly
causes of aortic dissection
- hypertension
- connective tissue disorder (marfans)
- clincal: SUDDEN onset of pain that it tearing
Varicose veins
- abnormally dialted veins due to increased intraluminal pressure, weakened walls or damanged valves in veins
- most commonly seen in lower legs superfiscially
risks
- obestiy
- pregnancy
- long standing
treatment
- compression socks, laser
DVT
a blood clot in a DEEP vein
risk of a PE!!!
Virchows triad
- stasis
- wall injury
- pro-thromboic/hypercoag.
clinical
- can be asymptomatic
- pain or swelling in posterior tibial or peronal veins
- femoral vein possible too
- treat with anti-coags.
