Cardiac 1 Flashcards
1
Q
Diseases of the veins
A
Varicose veins
Chronic venous insufficiency (CVI)
Superior vena cava syndrome (SVCS)
2
Q
Diseases of the arteries
A
Hypertension
Orthostatic hypotension
Aneurysm
Peripheral vascular disease
Buerger, Raynauds
Atherosclerosis
Peripheral artery
disease
Coronary artery disease
MI
Acute coronary syndrome
3
Q
Varicose veins causes predisposing factors risk factors clinical features
A
A vein in which blood has pooled
Damage to valve, causing malfunction
Trauma, gravity
Female, age, family hx, obesity, pregnancy, DVT, previous injury
Distended, tortuous, palpable vessels, edema
4
Q
Varicose veins tend to happen in what veins?
A
Superficial veins
Saphenous vein
5
Q
Chronic vein insufficiency leads to? causes risk factors clinical features
A
Inadequate venous return over a long period of time
Leads to venous hypertension, blood stasis, and tissue hypoxia in lower extremities
Varicose veins and valvular incompetence
Obesity
Edema up to knee, hyperpigmentation
6
Q
Chronic venous insufficiency complications
A
Inflammation, fibrosclerotic remodeling, any trauma/pressure can lead to ulceration
Venous Stasis Ulcer
Leads to high risk of infection
7
Q
Venous/Arterial disease examples
A
Thrombus
Thromboembolus or Embolus
Embolism
DVT
8
Q
Thrombus
A
Blood clot attached to vessel wall
More common in venous system
9
Q
Thromboembolus or Embolus
A
A detached/moving thrombus
Moves freely
10
Q
Embolism
A
The obstruction of a vessel by an embolus
11
Q
DVT
A
occurs in lower extremity
12
Q
Venous vs. Arterial emboli
A
Venous
Origin: DVT, right
heart
Destination:
pulmonary (PE)
Arterial
Origin: left heart (post
MI, valve disease,
endocarditis,
dysrhythmias)
Destination: lower
extremities, coronary
arteries (MI), cerebral
vasculature (stroke)
13
Q
Virchow’s Triad
Etiology
A
Factors that promote thrombus formation
Stasis of blood flow
Endothelial injury
Blood hypercoagulability
14
Q
Virchow’s Triad
Stasis of blood
A
prolonged bedrest
dependent extremities
immobilization
15
Q
Virchow’s Triad
Endothelial injury
A
trauma (fractures)
caustic intravenous medications
previous thrombus
16
Q
Virchow’s Triad
Blood hypercoagulability
A
inherited coagulopathy medications malignancies pregnancy oral contraceptive/HRT
17
Q
DVT locations
A
popliteal site most common
18
Q
DVT clinical features
A
Insidious - asymptomatic Swelling from venous pooling Edema with obstruction Pain (most common) walking increases Homan's sign
19
Q
Homan’s sign
A
dorsiflexion of the foot
not a reliable test and is contraindicated
increases chance of thrombus being thrown into blood system
20
Q
DVT complications
A
Most dissolve High risk of PE where it lodges is an important factor in seriousness size as well
21
Q
DVT prevention
A
Early ambulation (any possible movements) Pneumatic devices (SCDs) Prophylactic anticoagulation
22
Q
DVT diagnosis
A
D-Dimer (typically high in those that have a DVT)
Doppler
23
Q
DVT treatment
A
Anticoagulants
Thrombolytic therapy
Inferior vena cava filter
24
Q
Superior vena cava syndrome
A
progressive occlusion of the superior vena cava that leads to venous distension in the upper extremities and head
25
Superior vena cava syndrome
| causes
Bronchogenic cancer (tumors)
Invasive therapies (pacemakers, catheters (central venous and pulmonary artery))
Lymphomas
CA mets
26
Superior vena cava syndrome
| symptoms
```
Edema
Venous distension in UE/face
Fullness in head
Headache
Visual disturbance
Changes in LOC
Skin head/neck: purple, tight, respiratory distress
```
27
Superior vena cava syndrome
| diagnosis
X-ray
CT
MRI
US
28
Superior vena cava syndrome
| treatment
Malignancy - treatment of cancer
| Nonmalignancy - bypass, thrombolysis, balloon angioplasty, stents
29
Hypertension
definition
incidence
Consistent elevation of systemic arterial blood pressure
1 in 3 U.S. adults;
>2/3 over 60
in children
30
Hypertension
| risk factors
```
Family hx
Advancing age
Black race
Gender:
M>W before 55
W>M after 55
Smoking
Obesity, DM, sedentary
Diet - heavy alcohol
Metabolic syndrome
```
31
Metabolic syndromes
Obesity
HTN
Dyslipidemia
Glucose intolerance condition that increases risk of HD, stroke, and DM
32
Types of HTN
Primary
Secondary
Complicated
Hypertensive Crisis
33
Primary HTN
```
Idiopathic - multiple pathologic mechanisms
92-95% of cases
SNS hyperactivity
Overactive RAAS
Defect in natriuresis
Insulin resistance (obesity hormones)
Inflammation and endothelial dysfunction
```
34
Clinical manifestations of HTN
```
Often no signs or symptoms (early) - silent disease
Headaches
Dizziness
Blurred vision
Tinnitus
Anxiety
Chest pain
SOB
Nausea
```
35
HTN evaluation
Diagnosis: requires measurement on 2 separate occasions
Conditions: at rest for 5 min, seated, arm at heart level, no caffeine or smoke within 30 min
May do 24 hr BP monitoring
Can keep a log and self check
36
Complicated HTN
Prolonged high pressure on vessel walls causes thickening and stiffening
Causes arterial smooth muscle hypertrophy and hyperplasia
Vessel lumen narrows
Vessel thickening - increases smooth muscle contraction
Vasoconstriction - increased pressure
37
HTN Heart complications
```
Increased workload
Increased afterload
LV hypertrophy
Accelerated CAD/HF
Decreased myocardial O2
Aorta - aneurysms
```
38
HTN Vessel complications
Extremities: arterial vessels of lower extremities
Accelerated atherosclerosis results in PVD/PAD
May have no symptoms then develop pain, loss of circ - amputation
Results in intermittent claudication
39
HTN Renal complications
Decreased renal blood flow
| Increased RAA
40
HTN Brain complications
Reduced blood flow
Ischemia
Vessel damage/rupture
41
HTN Eye complications
Retinal damage
42
Hypertensive Crisis
| Malignant HTN
Rapidly progressing HTN with DBP >140
| A medical emergency
43
Hypertensive Crisis
| causes
complication in pregnancy
cocaine/amphetamines
adrenal tumors (pheochromocytoma)
drug/alcohol withdrawal
44
Hypertensive Crisis
| symptoms
chest pain
blurred vision
SOB
45
Hypertensive Crisis
| consequences
HTN -> cerebral arterioles/capillaries unable to regulate blood flow -> fluid shifts = cerebral edema, dysfunction, cerebrovascular accident
Also cardiac failure, kidney failure, retinopathy
46
Hypotension
Decrease in SBP of at least 20 mmHg or DBP of at least 10 mmHg within 3 min of moving to standing
Neurogenic - often seen in older adults (risk for falls)
Normal compensation - arteriolar/venous constriction and increased HR
Abnormal: blood pools, BP drops
Symptoms: dizziness, blurred vision, fainting, nausea, weakness
47
Aneurysm
| definition
Localized dilation or outpouching of a vessel wall or cardiac chamber
48
Aneurysm
| weakened medial layer
Atherosclerosis (most common)
Genetic/congenital
HTN, smoking, diet
Collagen-Vascular disorders (Marfan)
49
Types of Aneurysms
```
True
Involve all 3 layers
of the arterial wall
Weakening of the
vessel wall
Fusiform/saccular
Can happen on 1 or
both sides of the wall
False
Extravascular
hematoma that
communicates with
the intravascular
space
```
50
Aneurysms
| affected sites
Abdominal aorta - 75%
Thoracic aorta
Large peripheral arteries
Cerebral
51
Aneurysms
| clinical features
Often asymptomatic
Detected by US, CT, MRI
Sx indicate large aneurysms or rupture and depend on site
Rupture: severe pain and hypotension
52
Aneurysms
| treatment
Meds: BP reduction
| Surgery (graft)
53
Drugs for Hypertension (Angina)
FIRST LINE: Diuretics, ACE Inhibitors, ARBs, Calcium Channel Blockers
SECOND LINE: Beta Blockers, Adrenergic Agonists/Antagonists, Vasodilators/Nitrates
54
Monitoring for any drugs that affect BP
```
BP (both arms / lying, sitting)
HR (at home too)
Intake/Output
Electrolytes
ECG
Weight - BMI
Report: sx of liver dysfunction - weight gain, edema, SOB
```
55
Review lifestyle modifications for HTN
```
Sodium restrictions
DASH diet
Alcohol restrictions
Smoking cessation
Aerobic activity
Weight loss
```
56
Volume x Vasoconstriction =
Hypertension
57
Cardiac output x Peripheral resistance =
Arterial pressure
58
First line HTN drug classes
```
Angiotensin converting enzyme (ACE) inhibitors - prils
Angiotensin receptor blockers (ARBs)
- sartans
Calcium channel blockers (CCBs)
- pines
Thiazide diuretics (used in combo)
```
59
ACE inhibitors
reduce blood volume and is a vasodilator
60
ARBs
reduce blood volume and is a vasodilator
61
CCBs
vasodilator
62
Thiazide diuretics
reduce blood volume
| best at reducing BP, improving HTN related mortality, least risky, cheapest
63
ACE inhibitors
| MOA
Inhibit conversion of angiotensin I to angiotensin II:
- Arteriole vasodilation, less effect on veins
- Reduction of blood volume - reduction in aldosterone
- Reduction of remodeling: cardiac and vascular hypertrophy (redistribution of mass)
64
ACE inhibitor
| Drugs
PRIL
- Older (first drugs): captopril (Capoten), enalapril (Vasotec)
- Newer drugs: enalapril (Vasotec),benazepril (Lotensin), fosinopril (Monopril), lisinopril (Prinivil),, moexipril, quinapril, ramipril, trandolapril
65
ACE inhibitors
| HTN use
-Vasodilation
-Reduced blood volume
-Better than adrenergic agents
-no effect on cardiac
contractility or
exercise ability
-no orthostasis, no
bronchial effects,
CNS
-reduce the risk of CV
mortality due to HTN
-Better than diuretics – no fluid and electrolyte effects
66
ACE inhibitors
| HF use
-lowers arterial resistance
-reduces afterload
-increases CO
-reduces pulmonary
congestion
-renal vessel dilation
-increased renal
blood flow
-Na/water excretion
-reduced edema and
blood volume
-Reduce pathologic wall thickening
67
ACE inhibitors
| MI use
- Reduced mortality and heart failure after MI
| - Start right after MI – low dose – remodel heart muscle
68
ACE inhibitors
| Diabetic and non-DM nephropathy use
- Increases renal blood flow
- Decreases glomerular filtration pressure
- Slows progression of renal disease
69
ACE inhibitors
| High CV risk use
- Those with stroke, CAD, DM, PVD, and a CV risk factor
| - To reduce the CV event
70
ACE inhibitors
| Pharmacokinetics
-good oral absorption – most all PO but also IV
-most have long half-life
-(except captopril –
older drug)
-significant drug accumulation in renal disease
-DO NOT TAKE IF PREGNANT
71
ACE inhibitors
| Drug reactions
- Hypotension – syncope - most often with first dose, high BP and dehydrated
- Orthostatic hypotension
- Nagging, dry cough; 5-10% (bradykinin)
- Hyperkalemia – aldosterone effects, esp combined with K sparing drugs or K supplements
- Angioedema – rare 1%, life-threatening
72
ARBS
| MOA
```
Block angiotensin II action (not production)
-Receptor antagonists
-On blood vessels –
causing vasodilation
(arterioles and veins)
-In the heart – reduce
cardiac remodeling
-In adrenal glands –
decrease release of
aldosterone –
promotes excretion
of Na and water
-Does not increase
bradykinin which
causes the ACEI
cough
```
73
ARBs
| Drugs
-Losartan (Cozar) – prototype
-Losartan and
Hydrochlorothiazide =
Hyzaar
-Valsartan (Diovan)
-Irbesartan (Avapro)
74
ARBs
| Uses
-HTN
-HF
-small amount of data
-increases function
(ejection fraction)
-Diabetic nephropathy
-in pts with HTN and
DM
-slowed disease
75
ARBs
| Pharmacokinetics
- First pass limits bioavailability to 30%
- Active metabolite is more powerful than the drug
- Highly bound to protein (99%)
76
ARBs
| Adverse effects
- Very few cases of hyperkalemia, cough
| - Angioedema
77
ACE inhibitors vs ARBs
- ACE inhibitors reduce overall mortality when compared to ARBs
- ACE inhibitors are first line treatment
- If ACE inhibitors are not tolerable due to SE, ARBs are introduced
78
CCBs
| original treatment
Treated angina, but SE was reduced BP
| -Typically not used as HTN monotherapy, but good if not responsive to other anti-HTN therapies
79
CCBs
| MOA
-Cardiac and smooth muscle cells depend on influx of calcium for maintenance of contraction or tone
-inhibit Ca from
entering cell, limits
muscular contraction
and thus relaxation of
muscle
80
CCBs
| Classes
```
Selective and Non-selective
-vascular selective: dihydropyridines
-relax arterial smooth
muscle = lower
peripheral resistance
-overall primary effect:
arterial vasodilation
-nonselective: non-dihydropyridines
-relax cardiac muscle
and arterial smooth
muscle
-overall primary effect:
cardiac muscle
relaxation
```
81
Vascular selective CCBs
| pines
Nifedipine (procardia)
-Vasodilation in vascular smooth muscles PRIMARILY - in peripheral arterioles and in coronary arteries
-Arteriole vasodilation PRIMARILY
-Uses – HTN and angina
-ADRs
-Reflex (baro)
tachycardia – as BP
falls, HR increases
Amlodipine (Norvasc)
-effective in cerebral vessel spasm; and for effort induced spasm of coronary vasospam
Nimodipine
-effective in cerebral vessel spasm -cerebral aneurysm
Other drugs = felodipine, amlodipine, nicardipine, isradipine
82
Non-selective CCBs
```
Uses: angina and dysrhythmias
More cardiac, less vascular
-Diltiazem (Cardiazem) - anti-anginal
-Blocks calcium
channels in the
myocardium
-Decreased cardiac
contractility,
-Conduction effects
-Used for
tachydysrhythmias,
angina, HTN
-ADRs – bradycardia,
conduction blocks,
depression of
myocardial
contractility, HA,
flushing, peripheral
edema, hypotension
-Verapamil – anti-dysrhythmic
-Blocks calcium
channels in blood
vessels AND the heart
-Arteriole vasodilation
(decreased BP,
increase flow in
coronary arteries)
-Decreased cardiac
contractility
```
83
Second Line
| HTN drugs
```
Alpha 2-adrenergic agonists
Alpha 1-adrenergic blockers (zosins)
Beta-adrenergic blockers (olos)
Centrally acting alpha and beta blockers
Direct acting vasodilators
Direct renin inhibitors
Peripherally acting adrenergic neuron blockers
```
84
Parasympathetic Division
```
Rest and Digest
constricts pupil
stimulates salivation
slows heart
constricts bronchioles
stimulates digestion
stimulates gallbladder
contracts bladder
stimulates sex organs
```
85
Sympathetic Division
```
Fight or flight
dilates pupils
inhibits salivation
accelerates heart
dilates bronchioles
inhibits digestion
stimulates glucose release
secretes epi and norepi
relaxes bladder
inhibits sex organs
```
86
Beta blockers
| HTN
decrease HR and myocardial contractility
| reduces CO
87
Alpha2 agonists
| HTN
decreases sympathetic impulses from CNS to heart and arterioles
causes vasodilation
88
Alpha1 blockers
| HTN
inhibits sympathetic activation in arterioles
| causes vasodilation
89
Direct vasodilators
act on smooth muscle of arterioles
| causes vasodilation
90
Drug indications
| Beta 1 agonists
bradycardia
HF
shock
91
Drug indications
| Beta 1 antagonists
acute MI
angina
HTN
dysrhythmias
92
Drug indications
| Beta 2 agonists
severe allergic reactions
asthma
COPD
93
Drug indications
| Alpha 1 agonists
nasal congestion
| opthalmic hyperemia
94
Drug indications
| Alpha 1 antagonists
HTN
| BPH
95
Drug indications
| Alpha 2 agonists
HTN
96
Drug indications
| Alpha 2 antagonists
erectile dysfunction
97
Beta 1
| Normal actions
```
Increased:
AV conduction
Cardiac contraction
HR
Renin release
```
98
Beta 2
| Normal actions
```
Bronchodilation
Glycogenolysis
Relaxation:
bladder
eye muscle
smooth muscle
uterine
```
99
Beta 2
| Normal actions
```
Bronchodilation
Glycogenolysis
Relaxation:
bladder
eye muscle
smooth muscle
uterine
```
100
Alpha 1
| Normal actions
Vasoconstriction
Increased PVR
Constriction - bladder sphincter
Mydriasis (pupil dilation)
101
Alpha 2
| Normal actions
Controls release of NE
102
Alpha 1 Blockers
Drugs
Use
Doxazosin (cardura)
Others: Prazosin (minipress), Terazosin
-Blocks a1 receptors on arterioles and veins
-dilation of arterioles: lower BP
-dilation of veins: decreases venous return, decreases CO, lowers BP
103
Alpha 1 blockers
| adverse effects
orthostatic hypotension
reflex tachycardia
nasal congestion
inhibition of ejaculation
104
Alpha 2 agonists
Drugs
Use
Clonidine (catapress), Methyldopa (aldomet)
- suppresses sympathetic outflow from CNS
- lowers a and b adrenergic receptor peripheral activation
- dilation of arterioles
- slows HR conduction velocity (reducing CO)
105
Alpha 2 agonists
| adverse effects
```
orthostatic hypotension
dry mouth
sedation
Clonidine: rebound HTN
Methyldopa: hemolytic anemia, liver disorder
```
106
Beta 1 blockers
Receptors
Use
```
receptors in heart and kidneys
reduced HR
decreased force of contraction
suppressed conduction through AV node
--reduce CO, lower BP
suppresses renin secretion
blocks receptors at JG app
```
107
Beta 2 blockers
Receptors
Use
receptors in lungs, liver, and skeletal muscle
bronchoconstriction
inhibition of glycogenolysis in skeletal muscle and liver
108
Beta 1 blockers
| Adverse effects
bradycardia
reduced CO
HF
AV heart block
109
Beta 2 blockers
| Adverse effects
bronchoconstriction
inhibition of glycogenolysis
decreased libido and impotence
110
Types of Beta blocking drugs
```
Nonselective: propranolol (inderal)
-block B1 and B2 receptors
Cardio selective: metoprolol (lopressor)
-block B1 receptors
-dose dependent - high doses lose selectivity
```
111
Nonselective Beta blockers
Drugs
Use
```
Propanolol
Others: Timolol (blocadren), Pindolol (visken), Nadolol (corgrard), Penbutolol (levatol), Sotalol (betapace)
Use:
-HTN - reduced CO, RAA
-Angina - decreased workload
-Dysrhythmias
-MI
-Reduces pain, infarct size
-Reduces mortality, risk of infarction
-Migraine, stage fright
```
112
Nonselective Beta blockers
| Pharmacokinetics
highly lipid soluble
well absorbed PO
extensive first pass: 30% available
hepatic metabolism - renal excretion
113
Nonselective Beta blockers
| Adverse effects
```
bradycardia
AV heart block
CNS (depression, insomnia)
HF (decreased contraction force)
rebound cardiac excitation (abrupt drug withdrawal)
bronchoconstriction
glycogenolysis
```
114
Bronchoconstriction
block beta2 receptors in the lung
| block normal bronchodilation when needed - bronchospasm
115
Inhibition of glycogenolysis
decreases breakdown of glycogen to glucose
dangerous for diabetics who need glucose if insulin is too much
suppress early symptoms of hypoglycemia
116
Cardio-selective Beta blockers
Drugs
Use
Metoprolol
Others: Atenolol (Tenormin), Metoprolol slow release (Toprol XL), Acebutolol (Sectral), Betaxolol (Kerlone), Carvedilol (Coreg)
Use
-HTN
-Angina, MI, HF
-helps to balance O2 supply and demand by reducing demand/workload
117
Cardio-selective Beta blockers
| Pharmacokinetics
highly lipid soluble
well absorbed PO
extensive first pass: 30% available
hepatic metabolism - renal excretion
118
Cardio-selective Beta blockers
| Adverse effects
Bradycardia
AV heart block
HF
Rebound cardiac excitation
119
Direct Vasodilators
| Types
Nitrates
| Hydralazine
120
Vasodilators
| Action
```
On arterioles: resistance vessels
-decrease afterload
-increase CO
On veins: capacitance vessels
-reduce force with which blood is returned to heart, reduced volume
-decreased preload
```
121
Vasodilators
| Adverse reactions
postural hypotension due to vasodilation of veins
reflex tachycardia
expansion of blood volume - low kidney perfusion (RAAS)
122
Vasodilators
Nitrates
MOA
Pharmacokinetics
```
Nitroglycerin
Used for angina
MOA:
-dilates veins (reduces pre and afterload)
-dilates coronary arteries
-decreases workload
-reduces angina and BP
Pharmacokinetics:
-highly soluble
-given many diff ways
-PO-most destroyed on first pass
-rapid hepatic inact.
-half life: 5-7 min
```
123
Vasodilators
Nitrates
Admin
Route – acute vs prophylactic therapy
- SL – quick acting, small dose (0.3-0.6), no more than 3 in 15 min
- Transdermal – slow release up to 14hrs
- Spray – acute attack (0.4 mg), same as SL
- Topical – ointment, 1-2”, release same as transdermal
- IV – continuous infusion
- PO – large dose to survive first pass
124
Vasodilators
Nitrates
Adverse Effects
Tolerance
Headache, facial flush
Orthostatic Hypotension
Reflex tachycardia
happens rapidly - with high dose use
use lowest dose: long action formulations
6-12 hr nitrate free interval
125
Vasodilators
Hydralazine
MOA
Hydralazine (apresoline)
MOA:
-acts directly on smooth muscle in arterioles to cause dilation - no effect on veins
HF AA pts: combo with isosorbide dinitrate for selective dilation
126
Vasodilators
Hydralazine
Contraindication
Adverse effects
Lupus: sx worsen
Rheumatic heart disease, MI, angina, tachycardia
Causes reflex tachycardia (used with beta blocker to counteract tachycardia)
Na and H2O retention
127
Treatment of HTN crisis
| adverse effects
```
When RAPID reduction in BP is warranted
Vasodilators: Nitroprusside (arterioles and veins)
-IV admin
-rapid onset: half life is 2 min
-short term use, less than 72 hrs
-metabolized to cyanide: toxic
```
Adverse effects: cerebral ischemia, MI, renal failure
Preeclampisa/eclampsia: delivery, magnesium sulfate, labetolol
128
Arteriosclerosis vs Atherosclerosis
Art: thickening and hardening of the vessel wall
Ath: form of art that is caused by accumulation of lipid-laden macrophages within the arterial wall
-leads to lesions called plaques
-leading cause of:
-CAD
-Cerebrovascular
disease
129
Atherosclerosis
| Pathologic process
1. Injury-damaged endothelium
2. Fatty streak
3. Fibrous plaque
4. Complicated lesion
130
Injury: damaged endothelium
| risk factors
```
Injured endothelium becomes:
-inflamed and can't make normal antithrombic and vasodilating cytokines
-stimulates inflammatory cascade
Risk factors:
-HTN
-Smoking
-Hyperlipidemia
-Hyperhomocysteinemia
-Hemodynamic factors
-Toxins
-Viruses
-Immune reactions
```
131
Injury: damaged endothelium
| progression
1. LDL enters intima (hypercholesterolemia) and is oxidized
2. Oxidized LDL generates proinflammatory lipids that induce adhesion molecules
3. Monocytes are recruited and phagocytize oxidized LDL and transform to foam cells
4. Foam cells present oxidized LDL to T cells, release growth factors that stimulate smooth muscle proliferation, secrete cytokines that are proinflammatory and procoagulant (more injury)
132
Fatty Streak
when there is an accumulation of enough foam cells they become a fatty streak
- seen most in teens & 20s, and kids
- leads to more T cell recruitment, more macrophages, more inflammation, more smooth muscle cells, proliferation, more damage
133
Fibrous Plaque
fatty streaks develop into fibrous plaque
-smooth muscle cells proliferate and produce collagen
-smc and fibroblasts migrate over fatty streak
-fibrous plaques may calcify and protrude into lumen/create fissures
-stable: thick fibrous
cap
-unstable: thin fibrous
cap, thick lipid pool,
prone to rupture
-all equal: narrowing of vessel lumen = obstruction of blood flow which can produce: angina and intermittent
claudication
134
Complicated lesion
```
complicated plaques: unstable and can rupture prior to occlusion
-rupture caused by immune response to endothelial injury/fissure
-exposes underlying
tissue, causes
platelet adhesion,
initiates clotting
cascade, and rapid
thrombus formation
-thrombus formation
can occlude; results
in ischemia or
infarction
```
135
Symptoms of atherosclerosis
```
associated with:
-amount of narrowing/occlusion
-progression
-acute: ischemia, pain,
poor perfusion
-chronic:
asymptomatic, can
develop collateral
circulation
-rupture
-location: may have sx in several tissues/areas at same time
```
136
Atherosclerotic lesion locations
1. large vessels
- coronary: MI
- cerebral: stroke
- renal: kidney disease/HTN
2. at bifurcations
3. localized, focal in distribution
4. PAD
137
Atherosclerosis
| primary risk factor
CAD, MI, and acute coronary syndromes (infarction)
138
PAD
risk factors
progression
```
atherosclerotic disease of the arteries that perfuse the limbs - particularly lower
risk:
-CAD
-advanced age, DM, smoking
progression: gradual or acute
```
139
PAD
symptoms
diagnosis
sx:
-asymptomatic (2/3 case)
-intermittent claudication
-severe pain, pallor, loss of pulse, skin color change
Diagnosis: history, bruits, BP: ankle-brachial index, doppler
140
PAD
| treatment
```
Risk factor reduction
Exercise
Meds:
-vasodilators
-anticoagulants
-cholesterol lowering
-surgical revascularization
```
