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114 Cards in this Set

  • Front
  • Back
What are the 3 type of arteries?
Elastic, muscular, & arterioles
What type of arteries are the largest & what are they prone to?
Elastic arteries are the largest & are prone to aneurysms.
What are the intermediate sized arteries and what are they prone to?
Muscular arteries are intermediate in size & are prone to atherosclerosis.
What are the smallest arteries & what are they prone to?
Arterioles are the smallest arteries and are prone to hypertensive changes.
How is the resistance to flow related to the diameter of blood vessels?
Resistance to flow is inversely proportional to the 4th power of the diameter.
From aorta to capillaries, how does the cross-sectional cumulative luminal area change? How does the flow rate change?
From aorta to capillaries, cross-sectional area increases but flow rate decreases.
What are the 3 layers of blood vessels?
endothelium, tunica media, tunica adventitia
What is the blood supply to blood vessels?
vaso vasorum
what are 3 components of tunica media?
internal elastic membrane (lamina), muscular & elastic tissue, & external elastic membrane (lamina)
What does a histo slide of the largest arteris (aorta) look like?
Elastic arteries are thickened, with parallel estastic fibers that give it elasticity & strength
What sized arteries are muscular arteries & what are they prone to?
intermediate sized arteries - prone to atherosclerosis
Is the vascular system static?
No, vascular system is NOT static, there is new growth = plasticity
What are the 3 main functions of endothelium?
1)barrier function
2)transport function
3)metabolic function
What type of cholesterol is proatheroscleotic & what do endothelial cells to to this cholesterol?
LDL is found in plaques & thought to be proatherosclerotic. Endothelial cells oxidize LDL so macrophages & SMC can injest it.
How do endothelial cells prevent thrombosis?
Maintain vascular integrity
What are 3 components involved in forming clots?
coagulation factors, platelets, & endothelial cells
What happens if there when there is endothelial injury?
There is a loss of antithrombic function of endothelial cells.
What is exposed in endothelial injury?
there is exposure of underlying collagen & von Wilebrand factor so platelets can bind and form an initial hemostatic plug.
How do platelets recruit other platelets to the site?
ADP & TxA2 (thromboxane A2)
What is the end result of clotting cascade?
thrombin cleaves fibrinogen to fibrin, which help create a more stable fibrin clot.
What antithrombotic prostaglandin do endothelial cells release?
Prostaglandin I2
What is the most common form of arteriosclerosis?
How many deaths is the US are related to atherosclerosis?
50% of deaths in US
What is progression of atherosclerosis like?
chronic, slowly progressive disease
What type of arteries does atherosclerosis affect?
large & medium sized arteries
What are the common sites of atherosclerosis?
commonly at sites of hemodynamic turbulance (ex. bifrications)
What layer of the blood vessels does atherosclerosis affect?
INTIMAL disease
What are 4 componets involved in atherosclerosis?
1) smooth muscle
2) lipid
3) connective tissue
4) macrophages
What are 5 steps in the evolution of atherosclerosis?
1) endothelial dysfunction
2) lipid accumulation, smooth muscle cell proliferation in intima
3) lipids cause cell injury so macrophages enter
4) macrophages scavenge extracellular lipid & release growth factors (FGF, TNF, IL-1, interferon, TGF-B)
5) eventual damage to endothelium causeing platelet adherence
What happens to the intima?
it thickens
What are lipid-laden macrophages?
Foam cells
What are 2 possible precursors of atherosclerosis?
1) fatty streak
2) intimal cell mass
What are pros & cons of fatty streaks as atherosclerotic precursor?
Pros: composed of foamy macrophages (lipid) & they're seen in children & adults

Cons: Thoracic > abdominal aorta, seen in regions of low prevalence of atherosclerosis
What are pros & cons of intimal cell mass as atherosclerotic precursor?
Pro: Nodules of intimal smooth muscle at arterial branch points

Cons: May only be age-related change; no lipid depostion
What are the 6 pathogenesis hypotheses of atherosclerosis?
1) Insudation hypothesis
2) Encrustation hypothesis
3) Rxn to injury hypothesis
4) Monoclonal hypothesis
5) Intimal cell mass hypothesis
5) Hemodynamic hypothesis
(1) What is the Insudation hypotheis?
lipid in atherosclerotic lesions is derived from plasma lipoproteins, esp LDL (doesn't explain SMC proliferation, ect)
(2) What is the encrustation hypothesis?
(involves platelets) - small mural thrombi represent initial event of atherosclerosis [not true but thrombi involved LATE in progression, such as occlusion)
(3) What is Rxn to injury hypothesis?
injury of endothelial cells is primary event - macrophages & endothelial cells release growth factors that are chemotactic for SMC & tell SMC to proliferate
(4) What is monoclonal hypothesis?
SMC (1 or a few) are stimulated to proliferate (possibly due to virus); increased SMC that come from same cell
(5) What is the intimal cell mass hypothesis?
Intimal cell mass (SMCs) as precursors to atherosclerosis
(6) What is hemodynamic hypothesis?
low shear areas when blood fluctuates rapidly more prone to atherosclerosis - increased BP role in atherosclerosis - physical damage from hypertension
What are slit-like features seen in an atherosclerotic vessel?
cholesterol clefts
What are 5 sites of atherosclerotic disease of lg & med sized arteries in order of frequency?
1) abdominal aorta & iliac arteries
2) proximal coronary arteries
3) throacic aorta, femoral & popliteal artieris
4) Internal carotid arteries
5) vertebral, baisilar, & middle cerebral artery
At what sites is atherosclerosis common?
Sites of hemodynamic turbulence
What are 6 complications of atherosclerosis?
1) Thrombosis (acute occlustion) (ex. MI or CVA)
2) Chronic stenosis (ischemia) (ex. angina)
3) Hemorrhage (into plaque)
4) Aneurysm formation
5) Ulceration (w/ atheroemboli) (ex. leads to losing a toe)
6) Calcification
What are 6 common places/organs of extreme complication with atherosclerosis & what are the complications?
1) brain - stroke
2) kidney - infarct
3) Abnominal Aortic Aneurismal rupture leading to death
4) occlusion of peripheral vessel in foot causing ulceration
5) occlusion of colonic vessel leading to ischemia of bowels
6) occlusion of coronaries leading to MI
What can arterial stenosis of a peripheral vessel lead to?
chronic ischemia (ulceration on skin)
Where is a common place for an aortic aneurysm?
AAA - infrarenal
What gross appearance might a kidney have that is affected ischemically due to atherosclerosis?
cortex of kidney might have a granular appearance
What are 3 non-modifiable risk factors for atherosclerosis?
1) Age
2) sex (M>F)
3) genetics
What are 6 modifiable risk factors?
1) diet
2) lifestyle (personality type, exercise habits)
3) hyperlipidemia (cholesterol>triglicerides)
4) hypertension (esp after age 40)
5) cigarette smoking
6) diabetes mellitus
Which 4 modifiable risk factors are physican's most importantly involved with?
1) hyperlipidemia (cholesterol>triglicerides)
2) hypertension (esp after age 40)
3) cigarette smoking
4) diabetes mellitus
What are the names of essential lipids?
cholesterol & triglycerides are essential
Are cholesterol & triglycerides soluble?
No, Cholesterol & triglycerides are insoluble, need transport system
How much of total body cholesterol is contained in the plasma?
Plasma contains 7% of total body cholesterol
How does LDL & HDL correlate with atheroslerosis?
LDL level correlates directly w/ atheroslerosis (exp oxidized LDL)
HDL level correlates inversely with atherosclerosis
What are the 5 ways in which lipids are carried in the body from largest to smallest size?
1) chylomicron
3) IDL
4) LDL
5) HDL
What are the lipids & apoproteins of chylomicrons?
80 - 90% TG (dietary)
C proteins, AI, AII, B48
What are the lipids & apoproteins of VLDL?
45 - 65 % TG (endogenous)
25% cholesterol
C proteins, (B48/B100?), E
What are the lipids & apoproteins of IDL?
45% cholesterol
B100, E
What are the lipids & apoproteins of LDL?
70% cholesterol
What are the lipids & apoproteins of HDL?
<25% cholesterol
What is involved in the exogenous pathway of lipid metabolism?
cholesterol absorbed from intestine is carried by chylomicrons (B48) to capillaries, where lipoprotein lipase breaks up chylomicrons in to remnants which are taken into the liver
How does cholesterol leave the liver & where does LDL made?
Cholesterol leaves liver as VLDL, is broken up in capillaries by LPL into IDL, and then further to LDL (B100).
What are 2 possible fates of LDL in the blood?
LDL can be taken up by the liver or stored in extraheptaic tissues.
Where does HDL come from?
Extrahepatic tissues release cholesterol by HDL, which is then transformed in plasma by LCAT to IDL, then to LDL, which can be taken up by liver or extrahepatic tissues.
Will an increase in chylomicrons increase atherogenicity?
Will an increase in LDL increase atherogenicity? Increased VLDL increase atherogenicity?
Yes! When mutations occur in LDL receptors, ect. increased LDL increases atherogenicity;
Increased VLDL has a slight increase in atherogenicity
What is a cholesterol genetic disease in which LDL receptors are malfunctioning due to a mutation?
Familial Hypercholesterolemia (Type II)
What are the genetics of Family Hypercholesterolemia Type 2? [how is it passed? what chrom?]
Autosomal dominant, many different mutations, genes on short arm of chromosome 19
How many heterozygotes for FH2 are there? How high is their cholesterol? When do they get CVD?
Heterozygotes 1:500
Cholesterol is 2 x normal
Cardiovascular disease in 30s & 40s
How many homozygotes for FH2 are there? How high is their cholesterol? When do they get CVD?
have cholesterol 4-6 x normal
Cardiovascular disease in childhood
How are LDLs processed in FH2?
Elevated LDLs are processed via receptor-independent pathway
What might occur on someone's face or knees, ect that has familial hyperlipidemia?
What are secondary causes of hyperlipoproteinemia?
HYPOTHYROIDISM, diabetes mellitus, nephrotic syndrome, renal failure (uremia), alcoholism, obstructive liver disease, pancreatitis, dysglobulinemia, glycogen storage disease, porphyria
What are 3 current areas of focus on theories of atherosclerosis?
1) Inflammatory/Immune Factors
2) Chronic Infection
3) Homocysteine
What are 3 Inflammatory/Immune factors that are increased in atherosclerosis?
1) IL-1, IL-6 increased
2) C-reactive protein increased
3) Macrophage colony stimulating factor increased
What are 3 infectious ageants that may be involved in chronic infections leading to atherosclerosis?
1) chlamydia pneumoniae
2) Helicobacter pylori
3) CMV
What is the theory of how homocysteine might be involved in atherosclerosis?
Increased levels of homocycteine are associated w/ atherosclerosis, possibly via increasing oxidized LDLs
What 6 complications have been associated with hypertension?
1) Atherosclerosis
2) Angina pectoris
3) Sudden cardiac death (arrhythmia due to hypertension)
4) Aortic dissection
5) Cerebral infarction
6) Intracerebral hemorrhage
What is the pathogenesis of hypertension?
95% idiopathic (don't know cause)
5% renal disease, renovascular, endocrine-related, other
How is BP related to CO & TPR?

CO = HR x SV
What are cardiac & blood volume factors that affect cardiac output?
Cardiac factors: HR & contractility

Blood Volume: sodium, mineralocorticoids, atriopeptin
What are local factors that affect peripheral resistance (TPR)?
Ionic (pH, hypoxia)
What are humoral factors (5 constrictors & 3 dilators) that affect peripheral resistance?
Constrictors: angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin
Dilators: prostaglandins, kinins, NO/EDRF
What are neural factors (1 constrictor, 1 dilator) that affect peripheral resistance?
Constrictor: alpha-adrenergic
Dilator: beta-adrenergic
What are JNC 7 standards for normal BP?
<120 & <80
What is prehypertension? Should you give meds?
120-139 or 80-89
Drugs only for compelling indications. Most people - no drugs.
What is stage 1 hypertension? Should you give meds?
140-159 or 90-99
Most patients should get thiazide drugs. Give additional meds in compelling indications.
What is stage 2 hypertension? What drugs do you give?
> or = 160 or
> or = 100
2 drug combo for most people thiazide + (ACEI, ARB, BB, or CCB)
What are 4 identifiable causes of hypertension?
1) renal
2) endocrine
3) cardiovascular
4) other
What are 2 renal conditions that may cause hypertension?
1) chronic renal disease (increased renin)
2) renovascular disease
What are 4 endocrine conditions that could cause hypertension?
1) primary aldosteronism
2) chronic steroid therapy, cushing syndrome, congenital adrenal hyperplasia
3) pheochromocytoma (tumor of adrenal medulla,increases epi)
4) thyroid or parathyroid disease
What are 2 cardiovascular conditions that might cause hypertension?
1) coarction of the aorta (legs low BP, arms high BP)
What are 2 other causes of hypertension?
1) sleep apnea
2) drug-induced or drug-related
How & what produces renin?
decreased vascular tone causes sympathetic stim & macular densa feedback to JG cells that secrete renin.
What does renin do?
renin converts angiotensinogen (constantly secreted by liver) to angiotensin I, which is converted by ACE in lungs to angiotensin II.
What is the end result of angiotensin II & what are 2 ways in which it accomplishes this goal?
goal of angiotensin II is to increase BP by
1) vasoconstriction (directly)
2) increase aldosterone, which increases Na retention
What are 2 ways in which hypertension chronically changes blood vessels?
1) hyaline arterisoclerosis (benign arteriosclerosis)
2) hyperplastic arteriosclerosis
(malignant arteriosclerosis)
What often causes hyaline arteriolosclerosis? What physically happens?
Often caused by benign (chronic) hypertension
Hyaline material in vessel walls, basement membrane thickening
Is hyaline arteriolosclerosis specific to hypertension?
What might hyaline arteriolosclerosis do to the kidney?
Nonspecific, can be seen in old age, diabetes mellitus.
May cause chronic renal insufficiency via arteriolar nephrosclerosis (surface of kidney becomes granular).
How can hyaline arteriolosclerosis affect the glomerulus?
decreased blood flow leads to sclerosis of the glomerulus & decreased functin of glomeruls & a scar is formed
Hyperplastic arteriolosclerosis:
What type of necrosis?
What does it look like?
What is it a reaction to?
What might affected vessels do?
Hyperplastic arteriolosclerosis:
fibrinoid necrosis
"onion-skin" arterioles
reaction to pressures
affected vessels may rupture
What type of hypertension might you see hyperplastic arteriolosclerosis?
What sign/symptoms may also occur?
Seen in malignant (accelerated) HTN = rapidly progressive HTN.
Headache, blurred vision, malaise
(30s or 40s)
When do you worry about cerebral hemmorrhage?
systolic >200, diastolic >100
What causes onion skin appearance in hyperplastic arteriolosclerosis?
reduplication of internal elastic membrane
How might hyperplastic arteriolosclerosis affect the kidney? The brain?
kidney: fibrinoid necrosis in afferent arterioles can damage glomeruli
Brain: intra-cerebral hemorrhage
In what arterial disease do elderly individuals get in which there is degenerative calcification of the media?
Monckeberg's Medial Calcific Sclerosis
Does Monckeberg's medial calcific sclerosis affect the intima or lumen?
No effect on intima or lumen, only affects the media (calcified media)
What might an x-ray of a patient with Monckeberg's medial sclerosis look like?
May account for incidental vascular calcification seen on x-rays in medium-sized artieris.
What arterial disease typically affects women of reproductive age?
Fibromuscular dysplasia
In fibromuscular dysplasia, what sized arteries are affected & what do they look like? What specific arteries are usually affected?
segments of irregular wavy thickening of medium-sized arteries
Renal, carotid arteries typically affected
Besides women of reproductive age, what other type of patients might get fibromuscular dysplasia?
Patients with alpha-1-antitrypsin deficiency
What 2 complications might you worry about in a patient who has fibromuscular dysplasia?
1) renovascular hypertension
2) arterial dissection