Arterial Vascular Disease Flashcards
Four main arterial vascular diseases and one minor
- Giant cell Arteritis
- Polymalgia Rheumatica
- Arterial Insufficiency
- Peripheral Arterial Disease
- Aortic Aneurysm/Dissection
Giant Cell Arteritis
- aka
- who does it affect
- what can it cause
- how treat
- temporal arteritis
- primarily people over 50
- blindness
- high-dose steroids
Polymyalgia rheumatica
- who does it affect
- what other dz is it associated with
- how treat
- where see sx on body
- primarily people over 50
- 50% pts with giant cell arteritis have polymyalgia rheumatica
- low dose steroids
- sx below the neck
Pathophysiology of GCA
- exact etiology unknown
- theories: age, ethnicity, genetic disposition (maladaptive response to endothelial injury= inappropriate activation of cell-mediated immunity)
What is the progression of GCA
- vessel wall damage
- intimal hyperplasia
- stenotic occlusion
What blood cell is seen in GCA
eosinophils
- likely but not always high WBC
GCA
- which vessels are affected
- epidemiology
- medium and large arteries, most often the temporal artery
- older than 50, mean age 72
- Women > men
GCA
classic presentation
- HA (temporal region)
- scalp tenderness
- vision: loss of sight in one eye, diplopia
- jaw claudication
what is the highest positive predictive value sx for GCA
jaw claudication
GCA
Non-classic sx
- dry cough (inflammation of aortic arch)
- mononeuritis multiplex, often in shoulder
- idiopathic fever
- > 65
- normal WBC
GCA
- how does blindness occur
occlusive arteritis of posterior ciliary branch of the ophthalmic artery
Timing of funduscopic findings in GCA
might not appear in first 24-48 hours
**don’t rely heavily on funduscopic exam for dx
GCA
- PE head findings
- scalp tenderness
- temporal artery can be normal, nodular, enlarged
- erythema, warmth, swelling
GCA
- PE eye findings
- iritis, fine vitreous opacities
- optic nerve edema
- swollen, pale disc with blurred margins
- pallor
- hemorrhage
- scattered cotton-wool spots
- vessel engorgement/exudates later in dz
GCA
- lab findings
- ESR (90% >50mm/h, typically see >100mm/h)
- CRP
- CBC (mild normochromic anemia, thrombocytosis, WBC normal or elevated)
- Elevated liver function tests, PT
- NL CPK, renal fn, UA
- Elevated interleukin-6 during flairs
ESR vs CRP - which is more sensitive for GCA
CRP is slightly higher
GCA
- imaging
- doppler US to show vascular occlusion, stenosis, edema
What is GCA gold standard for dx
temporal artery biopsy (min length 2 cm d/t incidence of skip lesions)
- will see giant, multinucleated cells
- do contralateral biopsy if suspicion is high but first biopsy was negative
GCA
- Treatment
- 1st line: HIGH dose steroids
- rheumatology and neuro referral
- consider ASA to avoid clots
- PPI for GI protection
- Ca2+, Vit D, bisphosphonate for bone protection
GCA
- major complications (3)
- irreversible blindness
- aortic aneurysms
- polymyalgia rheumatica
Polymyalgia Rheumatica
- describe
- 3 common sx and pertinent negative
- pts won’t be able to do what
- pain and stiffness below the neck
- fever, malaise, weight loss, NO muscular weakness
- pts will have trouble combing hair, putting on coat, getting out of chair
Polymyalgia Rheumatica
- two common lab findings
- anemia
- elevated ESR
- most, not all cases
Polymyalgia Rheumatica
- treatment
- LOW dose steroids
- no improvement in 72 hours f/u
- flair ups can occur
What sx should cause you to put GCA in differential
- > 50
- HA
- Jaw claudication
- fever
- vision changes
what medical hx might find with GCA
DM
Cardiac dz
HTN
Thrombus/thrombi def
clot (platelets and/or fibrin) that forms and is stationary in vessel
embolus/emboli def
piece of thrombus breaks off and travels through bloodstream until it gets stuck
(can be plaque, fat, air, etc.)
Thromboembolism
clot formed in blood vessel and breaks loose, carried by blood stream until gets stuck in another vessel
Arterial insufficiency
- def
- acute, chronic, or both?
- loss of perfusion
- distal to occlusion of major artery due to embolus
- acute AND chronic
Arterial insufficiency
- secondary to what
- emboli
- thrombosis
- trauma
- infection
- inflammation
Arterial insufficiency
- epidemiology
- > 65
- male
- More common in AA
Arterial insufficiency
- leading cause of what in the elderly
limb loss
Arterial insufficiency
- risk factors
- Tobacco use (vasoconstriction)
- endocarditis (clots from affected valves)
- DM
- drug abuse
- cardiac arrhythmia (most likely a fib)
- atherosclerotic dz
- trauma
Arterial insufficiency
- how is genetics related
can be associated with inheritable hyper coagulable states and premature atherosclerotic syndromes
Arterial insufficiency will cause what in the:
- Heart
chest pain
MI
Arterial insufficiency will cause what in the:
- Brain
weakness
CVA
Arterial insufficiency will cause what in the:
- LE
severe claudication
PAD
Arterial insufficiency will cause what in the:
- Mesenteric arteries
- pain after eating
- pain out of proportion to exam
- MAI (mesenteric artery ischemia)
Arterial insufficiency will cause what in the:
- Renal arteries
CVA tenderness
RAI (renal angina index OR renal artery ischemia)
Arterial insufficiency
- four classifications
- Asymptomatic - ex. DM
- Claudication - inadequate blood flow during exercise
- Critical limb ischemia - compromise of blood flow to extremity, limb pain at rest. Often ulcers or gangrene
- Acute limb ischemia - sudden decrease in perfusion that threatens limb viability
What is associated with acute limb ischemia
5 P’s
- pain
- paralysis
- paresthesia
- pulselessness
- pallor