disorders of circulation Flashcards
Describe the pathophysiology and manifestations of disorders of arterial circulation, including dyslipidemia, atherosclerosis, aneurysms, vasculitis and arterial disease of the extremities. Explain the mechanisms of blood pressure regulation. Summarize the pathophysiology, etiology and manifestations of hypertension. Differentiate between varicose veins, venous insufficiency, and venous thrombosis. (97 cards)
1
Q
what makes up the tunica externa?
A
collagen and elastic fibers
2
Q
what makes up the tunica media?
A
smooth muscle cells
3
Q
what makes up the tunica intima?
A
internal elastic membrane
connective tissue
endothelial cells
4
Q
what is the lumen?
A
inside of the BV where the blood travels
5
Q
blood flow:
heart to artery to _______ to capillaries to __________ to veins to heart
A
arteriole
venules
6
Q
How is the structure of arteries different than veins?
A
arteries have elastic fiber and smooth m
veins have valves
7
Q
what are the 2 layers that make up capillaries?
A
endothelium
basement membrane
8
Q
what are the 2 layers that make up arterioles?
A
tunica interna
tunica media
9
Q
what are the 3 layers that make up the venule?
A
tunica intima
tunica media
tunica externa
10
Q
what makes up the tunica interna?
A
endothelium
basement membrane
11
Q
STRUCTURE OF ARTERY:
____-layered wall with thick tunica ______, helps with contractility and _________
A
three
media
elasticity
12
Q
FUNCTION OF ARTERY:
transport of blood _______ from heart, maintain _______ _______
A
away
blood pressure
13
Q
STRUCTURE OF ARTERIOLE
_____-layered wall, with much _________ layers and ________ lumen than arteries
A
three
thinner
smaller
14
Q
FUNCTION OF ARTERIOLE:
Transport blood _____ from heart, helps control BP by regulating peripheral resistance with _________/_________
A
away
vasoconstriction/vasodilation
15
Q
STRUCTURE OF CAPILLARY
microscopic size with ______-layered wall of _________
A
single
endothelium
16
Q
FUNCTION OF CAPILLARY
thin walls permit the exchange of materials between blood and ________ fluid
A
interstitial
17
Q
STRUCTURE OF VENULE:
three-layered wall with very ___ layers, that gradually enlarge as they near the ______
A
thin
heart
18
Q
FUNCTION OF VENULE:
transport of blood from ______ beds toward the heart
A
capillary
19
Q
STRUCTURE OF VEIN
three-layered wall, with _______ tunica media and _______ lumen than arteries with ______ that aid with __________ flow of blood to heart
A
thinner
larger
valves
unidirectional
20
Q
FUNCTION OF VEINS:
transport of blood from _____ to heart
A
venules
21
Q
what is dyslipidemia?
A
abnormal amounts of lipids (triglycerides, phospholipids, cholesterol)
22
Q
Cholesterol and TGs combine to form _________
A
lipoproteins
23
Q
what are the 3 kinds of lipoproteins?
A
very-low density (VDL)
low density (LDL)
high density (HDL)
24
Q
what causes an increase in serum cholesterol levels?
A
increase in any lipoprotein (VDL, HDL, LDL)
25
what is primary dyslipidemia?
dyslipidemia that is not associated with another disease, genetics
26
what is secondary dyslipidemia?
increase in lipids due to a disease in the body
ex) obesity, diet, DM type 2
27
what are manifestations of dylipidemia? (3)
increase in fasting glucose
increase in BP (viscosity/calcific.)
inc in waist circumfrence
28
what is artherosclerosis?
Thickening and hardening of vessel walls - can lead to occlusions of the vessel lumen
formation of fibrous plaques in the lining of large and medium arteries
29
What are the non-modifiable risk factors of atherosclerosis? (3)
age
gender (M>F, until menopause)
family history
30
What are the modifiable risk factors of atherosclerosis? (5)
obesity (chronic inflammatory state)
smoking
type 2 DM
hptn (constant stretch = weak)
Hypercholesterolemia (high chol, diet and exercise,
31
What are the non-traditional risk factors of atherosclerosis? (3)
increase in CRP (c-reactive protein)
increase in lipoproteins
broad and generalized
32
what are the 4 things that lead to the development of atherosclerosis?
endothelial cell injury
migration of inflammatory cells
lipid accumulation and smooth m cell proliferation
plaque structure
33
What is the first step in the development of atherosclerosis?
Damage to the endothelium (inner lining of blood vessels) occurs due to factors like hypertension, smoking, high LDL cholesterol, and toxins. This makes the vessel wall more susceptible to plaque formation
34
What causes endothelial cell injury in atherosclerosis?
Common causes include hypertension, smoking, high LDL cholesterol, diabetes, and oxidative stress. These factors damage the endothelium, making it more permeable and prone to inflammation.
35
What happens after endothelial cell injury?
Migration of inflammatory cells
White blood cells (mainly monocytes) are attracted to the injured area and migrate into the vessel wall. Monocytes turn into macrophages and begin engulfing lipids.
36
How do macrophages contribute to atherosclerosis?
Macrophages engulf oxidized LDL, forming foam cells. These cells accumulate and create fatty streaks, which are early signs of plaque formation.
37
What happens after inflammatory cells migrate into the vessel wall?
Lipid accumulation and smooth muscle proliferation – Lipids (especially LDL) build up in the artery wall, and smooth muscle cells migrate from the deeper layers of the vessel. This thickens the arterial wall and narrows the lumen.
38
Why does smooth muscle proliferation occur in atherosclerosis?
The body tries to "repair" the damaged artery by activating smooth muscle cells. However, these cells secrete extracellular matrix proteins, which contribute to plaque formation.
39
What is the final structure of an atherosclerotic plaque?
The plaque consists of a lipid core (foam cells, cholesterol, and cellular debris) and a fibrous cap made of smooth muscle cells and connective tissue. Over time, plaques can rupture, leading to thrombosis and cardiovascular events.
40
What happens when an atherosclerotic plaque ruptures?
Rupture exposes the inner lipid core, triggering platelet aggregation and clot formation (thrombosis). This can lead to heart attacks (if in coronary arteries) or strokes (if in cerebral arteries).
41
what are aneurysms?
abnroal localized dilation of a BV
Arteries or veins
42
What are factors that contribute to aneurysms (weak vessel wall)? (4)
atherosclerosis, hypertension, congenital defects, infection (Inflammatory process)
43
what is a true aneurysm?
bounded by complete vessel wall, no tear just an outpouch
ex) balloon popped
44
what is a false aneurysm?
localized dissection/tear in inner wall, painful and life-threatening
ex) water ballon popped inside a blown up balloon
45
what is vasculitis?
group of vascular disorders that cuase inflammatory injury and necrosis of the BV wall
46
manifestations of vasculitis? (4)
fever
myalgia (muscle pain)
Arthralgia (joint pain)
malaise (weakness)
47
what causes vasculitis?
direct injury to vessel (trauma/poke)
infectious agents
immune processes
secondary to disease (obesity, DM)
48
SMALL VESSEL VASCULITIS:
Characteristics:
examples:
C: necrotizing vasculitis affecting small and medium BVs (capillaries, venules, arterioles) // common in pulmonary capillaries
E: Microscopic polyangitis
49
MEDIUM-SIZE VESSEL VASCULITIS:
Characteristics:
examples:
C: incolves large, medium-sized and small arteries (freq. coronaries) // associated with mucocutaneous lymph node syndrome
E: Kawasaki disease
50
LARGE VESSEL VASCULITIS:
characteristics:
examples:
C: granulomatous inflammation of the aorta and its branches
E: takayasu arteritis
51
ARTERIAL DISEASE OF EXTREMITIES: Peripheral artery disease (PAD)
?: (1)
RF: (3)
P: (4 aspects)
M: (6)
?: obstruction to large arteries in the extremities
RF: males 60+ years, smoking, DM
Patho: Interrupted arterial blood flow --> gradual/chronic occlusion --> collateral circulation --> ischemia/necrosis
M: cool extremity, pain w mvmnt, atrophic changes, pale and tingling, weak/absent pulses, ischemia/necrosis
52
ARTERIAL DISEASE OF EXTREMITIES:
acute vs chronic PAD
chronic: more frequent, gradual
acute: less frequent, quicker and more severe (pink to white, fast)
53
ARTERIAL DISEASE OF EXTREMITIES:
what causes interrupted arterial blood flow in PAD (4)
atherosclerosis
inflammatory stenosis
thrombus
embolus
54
ARTERIAL DISEASE OF EXTREMITIES:
thromboangitis obliterans (Buerger disease)
?:
characterized by: (2)
Etiology: (3)
Manifestations: (4)
?: Inflammatory arterial disorder that causes thrombus formation // affects medium-sized arteries (planter/digital vessels in foot/lower leg)
C: segmental, thrombosing, acute/chronic inflammation
E: genetics, smoking, tobacco
M: pain d/t intermittent claudication (w activity), increased sensitivity to cold, diminished or absent peripheral pulses, changes in extremely color (blue/black)
55
ARTERIAL DISEASE OF EXTREMITIES: Raynaud disease
?:
E:
M:
?: functional disorder caused by intense vasospasm of the arteries and arterioles in the fingers (toes)
E: precipitated by exposure to cold or strong emotions: cause of vasospasm
M: pallor/cyanosis, sensation to cold, changes in sensory perception, severe: brittle nails and thick skin over affected fingers
56
ARTERIAL DISEASE OF EXTREMITIES:
Raynaud phenomenon cause
d/t previous vessel injury (frostbite, trauma, neuro disorders, chronic arterial occlusive disorders)
aka secondary cause
57
what is systolic BP
measures the force of blood pushing against artery walls during the heart's contraction phase
58
what is diastolic BP
measures the pressure when the heart rests between beats.
59
what is mean arterial BP (MAP)
average pressure that drives blood throughout the circulatory system during both contraction (systole) and relaxation (diastole) of the heart
shows perfusion to tissue/organs
Goal: 60-65
60
what are the short term controls of BP?
________ mechanisms: (3)
________ mechanisms (1)
neural: ANS, instrinsic and extrinsic refelexes
humoral: RAAS
61
SHORT TERM REG OF BP:
how does the ANS affect BP regulation?
parasymp:
symp:
P: vasodilation to decrease BP and HR via vagus stimulation
S: Vasoconstriction to increase BP and HR
62
SHORT TERM REG OF BP:
Intrinsic reflexes (2)
Baroreceptors: pressure sensors in heart vessels to VC or VD
Chemoreceptors: Detects changes in blood CO2 and stimulates sympathetic (high CO2 = VC = inc BP)
63
SHORT TERM REG OF BP:
extrinsic reflexes (3)
panic, stress, pain
64
LONG TERM REG OF BP:
kidney regulation
hold onto or diuresis to maintain fluid volume via aldosterone/ADH
65
non-modifiable risk factors of hypertension (5)
age
gender
race
family history
genetics
66
modifiable risk factors of hypertension (9)
dietary factors
dyslipidemia
toabacco
ETOH consumtion
fitness level
obesity
insulin resistance
metabolic abnormalites
OSA (obstructive sleep apnea)
67
what is hypertension?
sustained elevation of BP within the arterial circuit
68
what is normal BP?
systolic: <120
diastolic: and < 80
69
what is elevated BP?
systolic: 120 - 129
diastolic: and < 80
70
What is stage 1 hypertension?
systolic: 130 - 139
diastolic: or 80 - 89
71
What is stage 2 hypertension?
systolic: > 140
diastolic: or >/= 90
72
CLINICAL MANIFESTATIONS OF HTN
target organ damage: heart (4)
inc workload (harder to pum against pressure)
LV hypertrophy
Heart failure (fatigue)
aneurysm
73
CLINICAL MANIFESTATIONS OF HTN
target organ damage: kidney (1)
kidney disease/failure CKD
74
CLINICAL MANIFESTATIONS OF HTN
target organ damage: brain (4)
dementia
cognitive impairments
stroke
aneurysm (berry)
75
CLINICAL MANIFESTATIONS OF HTN
target organ damage: eyes (1)
retinal damage --> blindness
76
CLINICAL MANIFESTATIONS OF HTN
lower extremity: (3)
decreased blood flow and high arteriole pressure --> intermittent claudication, ulcers, necorsis/gangrene
77
MALIGNANT HTN (hypertensive crisis)
* medical _________
rapidly progressive HTN (systolic greater than ______ mmHg or diastolic greater than ____ mmHg)
occurs so fast _______ doesn't occur
Manifestations: (6)
emergency
180, 120
hypertophy
cerebral edema and encephalopathy, papilledema, headache, restlessness, confusion
78
SPECIAL CONSIDERATIONS OF HTN:
pregnancy
pre-eclampsia: kidney issues
Eclampsia: kidney issues and seizures
79
SPECIAL CONSIDERATIONS OF HTN:
children and adolescents
Seeing an increase in primary htn d/t obesity
80
SPECIAL CONSIDERATIONS OF HTN: elderly
70% have htn
not normal!
81
ORTHOSTATIC HTN (_____ htn)
systolic BP drop of ____ or greater
diastolic drop of ______ of greater
all within ____ minutes of standing
indicated shift in blood vol to _______ body (500 - 700mL)
postural
20, 10, 3
lower
82
ORTHOSTATIC HTN
etiology: (5)
manifestations: (4)
E: reduced blood vol, drugs, increased age, bedrest or immobility, ANS malfunction
M: lightheaded, dizzy, blurred/loss of vision, syncope/fainting
83
DISORDERS OF VENOUS CIRCL:
varicose veins
Patho: (5 aspects)
manifestations: (3)
RF: (5)
P: incompetent valves/decreased muscle pump --> gradual venous distention --> inc. hydrostatic pressure --> pooled blood causes distended, tortous, palpable veins --> tissue edema @ site
M: Edema, cramping, heaviness in extremity
RF: increased age, female, obesity, increased intra-abdominal pressure, prolonged sitting
84
DISORDERS OF VENOUS CIRCL:
chronic venous insufficiency
?:
P:
E: (3)
?: inadequate venous return over a long period of time
P: venous htn, slow blood flow, tissue hypoxia --> inc hydrostatic pressure --> tissue congestion, edema, impaired tissue perfusion --> metabolic demands not met (lack of O2/nutrients, waste products not excreted) --> necrosis --> breakdown of RBCs --> brown pigmentation --> venous stasis ulcer formation
E: reflux through incompetent venous valves, venous outflow obstruction, impaired skeletal m function
85
DISORDERS OF VENOUS CIRCL:
chronic venous insufficiency PATHO
venous htn, ____ blood flow, tissue ______ --> inc _______ pressure --> tissue congestion, _______, impaired tissue perfusion --> metabolic demands not met (lack of ___/________, waste products not excreted) --> _______ --> breakdown of _____ --> _____ pigmentation --> venous stasis _____ formation
slow, hypoxia
hydrostatic
edema
O2/nutrients
necrosis
RBCs
brown
ulcer
86
DISORDERS OF VENOUS CIRCL:
venous thrombosis
E/P: (3 aspects)
M: (5)
E/P: vessel inflammation w increased platelet aggregation --> promotes venous thrombosis --> obstructs blood flow and embolize
M: Localized pain, redness, warmth, edema, fever
87
what circulation disorder has the virchow triad?
venous thrombosus
88
DISORDERS OF VENOUS CIRCL:
venous thrombosis
what are the three components of Virchow’s Triad?
1. Endothelial injury
2. Hypercoagulability
3. Stasis (abnormal blood flow)
89
DISORDERS OF VENOUS CIRCL:
venous thrombosis
How does endothelial injury contribute to thrombosis?
Damage to the endothelium (e.g., from trauma, surgery, or inflammation) exposes underlying tissue, leading to platelet activation and clot formation.
90
DISORDERS OF VENOUS CIRCL:
venous thrombosis
How does hypercoagulability increase the risk of thrombosis?
It refers to an increased tendency of blood to clot due to genetic (e.g., Factor V Leiden mutation) or acquired conditions (e.g., cancer, pregnancy, or oral contraceptive use).
91
DISORDERS OF VENOUS CIRCL:
venous thrombosis
How does stasis contribute to clot formation?
Slow or stagnant blood flow allows clotting factors to accumulate and promotes platelet aggregation, leading to thrombosis.
92
DISORDERS OF VENOUS CIRCL:
venous thrombosis
Which types of thrombosis are associated with Virchow's Triad?
Deep vein thrombosis (DVT), pulmonary embolism (PE), and arterial thrombosis (e.g., stroke, myocardial infarction).
93
DISORDERS OF VENOUS CIRCL:
venous thrombosis
causes of stasis (3)
inacitivty
age
CHF
94
DISORDERS OF VENOUS CIRCL:
venous thrombosis
causes of hypercoagulable state (3)
cancer
hormone replacement/contraceptives
post-partum (d/t inc in clot factors to prevent hemorrhage)
95
DISORDERS OF VENOUS CIRCL:
venous thrombosis
causes of vessel wall injury (5)
trauma
IV insertion
smoking
htn
surgery
96
pts who undergo ortho or ob surgeres, their risk for venous thrombosis increases to _____
100%
97
