W2 Abdominal And Chest Pain Flashcards
What are the three categories of peripheral vascular disease?
—structural changes in the vessels, secondary to degenerative conditions, infections or inflammation
—narrowing of the lumen
—spasm of vascular smooth muscle
Describe the sections and branches of the aorta
What are the layers of the aorta
How is it exposed to injury?
What are the two diseases?
Vasa vasorum supplies nutrients to the arterial wall
—ascending aorta which includes the root
—aortic arch gives way to great vessels : brachiocephalic (which has right subclavian and right common carotid artery), left common carotid, left subclavian
—descending aorta that provides intercostal vessels
—abdominal aorta which begins after the diaphragm and contains the branch renal and common iliac arteries
Layers
—intima
—media
—adventitia
Exposed to high pulsation pressure and shear stress
Diseases: aneurysms and dissection
What is an aortic aneurysm, it terms of measurement
What does it involve, layer wise, called what?
What is pseudoaneurysm or false aneurysm?
—diameter exceeds 1.5 its normal size
—involves all three layers of the aorta = TRUE
—pseudoaneurysm or FALSE aneurysm is a contained rupture, by the adventitia
Aortic aneurysm
How are they defined? 2 categories, 1 is further subdivided
Defined by:
—location (abdominal/thoracic)
—vessel circumference
Fusiform: more common/symmetrical dilation of entire circumference
Saccular/Berry: localised outpouching involving only a portion of the circumference
What are the 4 main causes of an aneurysm?
-
Genetic
—inherited connective tissue disorders
—affects mostly the ascending thoracic aorta
—Marfan Syndrome : elastin affected by mutation of fibrillin gene
—Ehler’s Danlos Syndrome: loss of collagen from mutation
2 Atherosclerosis
—usually a cause of descending thoracic and abdominal aorta aneurysms
—prevents O2 from entering media > hypoxia and muscle atrophy/weakening
—risk factors: HTN > hyaline atherosclerosis > lumen fibrosis > dec diameter > Ischemia
-
Infection
—tertiary syphilis > inflammation of vaso vasorum leading to fibrosis, ischemia and media degeneration
—mycotic aneurysm from bacteria embolising, adhering to the endothelium, entering media and eventually weakening the wall -
Vasculitis
—cell mediated AI response against vessel wall
—activated complement cascade
—neutrophils cause lysosomal degradation
—t-lymphocytes recruit macrophages > vascular necrosis and local thrombosis
What is an AAA?
What is the rupture rate?
Growth rate per year?
See disease table
Rupture rate
>6m = 20%
5-6cm = 6%
It grows at a 0.2-0.3cm per year rate
AAA: what is the clinical presentation, what is found on PE? 3
What about if it ruptures?
See disease table
Discovered accidentally on PE/Rad
Asymptomatic
+/- flank/back pain
Palpable pulsatile mass felt in abdomen
+/- abdom/fem bruit on ausc.
Rupture → shock + hypotension
How do you diagnose AAA?
Where do they commonly occur?
See disease table
Abdominal U/S
CT aortography and MRA which includes branch vessels + can see extravasation of blood
Usually after renal arteries but before the common iliac bifurcation
What are the treatment options for AAA?
Treatment according to size
See disease table
Annual imaging U/S or CT once aneurysm reaches 2.5cm
Every 6mo when 4-5cm
3-6mo when 5-5.5cm
One time screen for M >65y/o
>5.5cm → repair:
1. Endovascular aortic repair (EVAR): place a stent graft over the aneurysm
-
Surgery: >5.5 or growing resection of the aneurysm and replacement with a dacron tube graft.
Controversial to repair AAAs <5cm
TAA
Where does it occur?
What are the clinical presentations? Think about what it can compress…
See disease table
Mostly asymptomatic, however:
+/- cough/dyspnea if compressed trachea
+/- dysphagia if compressed esophagus
+/- hoareseness if presses against recurrent laryngeal nerve
+/- aortic valve regurg murmur
TAA:
How do you diagnose it?
How do you treat it?
See disease table
Diagnosis
CXR: widened mediastinum
CTA and MRA excellent visual
Aortography
TEE
Coronary angiogram should be performed before any surgery to ensure pt doesn’t need bypass
Treatment
—Repair >5.5cm
—Earlier repair if pt has symptoms or underlying emdial necrosis
—TEVAR : reserved for TAA pts and high risk of open repair.
—Dacron tube graft. If aneurysm extends in aortic valve, prosthetic valve will need to be performed.
—Tight blood pressure control +/- beta blockers “
TAA
What are the management options?
See disease table
Repair >5.5cm
Earlier repair if pt has symptoms or underlying emdial necrosis
TEVAR: reserved for TAA pts and high risk of open repair. a stent graft is used to reinforce the aneurysm. A stent graft is a metal tube covered in fabric. It helps prevent the aneurysm from bursting.
thoracic endovascular aortic repair
Surgery: Dacron tube graft. If aneurysm extends in aortic valve, prosthetic valvue will need to be performed.
Tight blood pressure control +/- beta blockers
Aortic dissection
What is the Pathophysiology?
See disease table
Small tear in the intima → separation of intima from media
creates two passages for blood: true lumen and false lumen
Blood flows through the false lumen and enlarges/tears further.
Diverts blood, oxygen and nutrients
Aortic dissection
What are the driving factors/risks? 2 main ones
Where is it most commonly found along the aorta?
See disease table
most common in ascending aorta
Any condition that affects integrity of elastic/muscular component of the medial layer
Age and “career HTN”
Other: tobacco, hyperlipidemis, cocaine, vasculitis diseases, infection, aotic trauma, genetic connective tissue syndromes
Pregnancy
Location:
Ascending (65%)
Descending (20%)
Aortic arch (10% and
Abdominal aorta (5%”
Aortic dissection
How are they classified?
See disease table
Type II is ascending only. See my table
Aortic dissection
How do patients present? Mention 2 main things
—Severe, tearing chest pain that radiates to the intrascapular area
—Unequal BP in UE
[SKILLS OSCE]
Aortic dissection
How do you diagnose ?
—most specific/sensitive
—other tests
Location categories: Stanford & DeBakey
Recognise this CT image
See disease table
CTA and MRA have the highest specificity and sensitivity
—CXR: widened mediastinum back lacks sensitivity
—Aortography: excellent to visualise but invasive
—ECG to r/o ACS
LOCATION
Stanford:
Type A involves the ascending aorta
Type B does not, just descending
DeBakey
Type 1: aortic arch and beyond (combo)
Type 2: ascending ONLY
Type 3: descending aorta
Acute: <2w from onset
Chronic: >2w from onset”
Aortic dissection
How do you manage/treat for type A and type B?
Medical management?
1st line and 2nd line pharmacotherapy?
Follow up?
Surgery:
Type A (must do surgery other could extend to carotids & brain)
Type B with evidence of end organ damage or progression of the dissection
Medical mngt:
Type B, uncomplicated distal
Reduce aortic wall stress by reducing HR <60bpm and BP to <120 systolic
Pharmacotherapy:
1st line: beta blockers
Labetalol
Esmolol (IV BB for descending dissection)
2nd line: non-DHP CCBs
IV nondihydrophyridine calcium channel blockers:
Verpamil, diltiazem
If BP is not at goal, can add IV ACE inhibitors or vasodilators
Follow up: CTA/MRA at 1,3,6 and 12 months”
Aortic dissection
What are the first line agents?
Second line agents?
What about post-op?
Pharmacotherapy:
1st line:
Labetalol
Esmolol (IV BB for descending dissection)
2nd line:
IV nondihydrophyridine calcium channel blockers:
Verpamil, diltiazem
If BP is not at goal, can add IV ACE inhibitors or vasodilators
What is peripheral artery disease?
How is it defined?
Flow-limiting lesion in a non-coronary artery that provides blood supply to the limbs or an organ
Normal: Skeletal muscle exercise → adenosine released into arterioles & NO → dilate and inc blood flow
Stenotic vessel lumen → supply-demand mismatch of O2 to tissues →ischemia of muscle →denervation of muscle fibres →dec strength & atrophy
In PAD, dysfunctional atherosclerotic endothelium does not release vasodilators and the obstructed arteries do not respond to stimuli
PAD
What are the risk factors?
Arterial occlusion from atherosclerosis/stenosis (most common) or thromboembolism
Occurs in 15-20% population over the age of 70
Risk factors:
–smoking
–DM
–HTN
–hyperlipidemia (HPL)
–40% of PAD pts have underlying CAD
–Majority of deaths in patients with PAD occur from CAD”
PAD
What is happening to the peripheral arteries?
What impact does this have?
What can the endothelium not do?
Flow-limiting lesion in a non-coronary artery that provides blood supply to the limbs or an organ
Normal: Skeletal muscle exercise → adenosine released into arterioles & NO → dilate and inc blood flow
Stenotic vessel lumen → supply-demand mismatch of O2 to tissues →ischemia of muscle →denervation of muscle fibres →dec strength & atrophy
In PAD, dysfunctional atherosclerotic endothelium does not release vasodilators and the obstructed arteries do not respond to stimuli
PAD
What are the clinical manifestations?
Where is pain located?
Clinical manifestation:
Claudication - limb fatigue that relieves w/ rest
Pain located in small area below the stenotic artery:
—Distal aorta or iliac arteries»_space;> pain in buttocks, hips, thighs, calves
—Femoral or popliteal arteries»_space;> pain in calves
—Subclavian or axillary arteries»_space;> pain arms
PAD
What should you check during a PE? 5
All peripheral pulses
Abdominal bruits
Wounds/ulcers
Complete CV exam, assess carotids
Take BP in both arms
PAD
How do you diagnose? List 3 tests, one of which is the gold standard
—ankle/brachial index
—U/S
—angiography
PAD
What are the treatment options? 4
What is the pharmacotherapy?
Acetylsalicylic acid (ASA) belongs to the groups of medications called analgesics (pain relievers), antipyretics (fever reducers), anti-inflammatories (inflammation reducers), and platelet aggregation inhibitors (anticlotting agents).
Clopidigrel (Plavix) — anti-platelet
Cilostazol — platelet aggregation inhibitor
Acute Arterial Occulsion
What is it?
How is it caused?
Types? 2
Caused by either
—embolisation from the heart or
—thrombus formation in situ
Paradoxical embolism:
—embolization from the venous circulation that arrives at the arterial circulation through a defect in the atrial septal wall (PFO or ASD)
Critical limb:
—chronic resting limb pain that results from:
—severe athersclerotic disease and compromised blood flow → ischemic ulcers → gangrene
Acute limb:
—an emergency due to abrupt occlusion of periph artery flow.
—Usually due to embolic event or arterial thrombosis
Acute Arterial Occulsion
How is it managed ? 3
Reduce risk of add’l embolic events
—Prevent propagation of clot with anti-thrombin agents (HEPARIN) and anti-platelet drugs
—Revascularisation w/ either percutaneous intervention or surgery
—If limb is necrotic and not viable → amputation
Heparin is an anticoagulant. It is used to decrease the clotting ability of the blood and help prevent harmful clots from forming in blood vessels
This condition has the 6Ps
What is this?
Peripheral artery disease
— acute limb ischemia
Renal Artery Stenosis
What is it?
Commonly associated with?
What would you see? 4
Etiology? 2
Commonly associated with HTN & ischemic nephropathy
—abrupt onset HTN
—previously controlled HTN that is now resistant (so this would be secondary HTN)
—azotemia (Elevated levels of urea and other nitrogen compounds in the blood)
—flash pulmonary edema
Caused by renin-angiotensin mediated peripheral constriction and volume retention
Etiology of RAS
—atherosclerosis (90%)
—fibromuscular dysplasia FMD (non-atherosclerosis) string of beads on angiography (uncommon medical condition involving abnormal cell growth in artery walls. )
Renal Artery Stenosis
Etiology? 2
Who does it affect?
PE findings 2
Etiology of RAS
–atherosclerosis (90%)
–fibromuscular dysplasia FMD (non-atherosclerosis) string of beads on angiography
Affects young women and should be suspected in patients with low likelihood of atherosclerosis
Epigastric bruits
Evidence of atherosclerosis: carotid bruits, diminished pulses
Renal Artery Stenosis
What would you find on exam?
What tests would you order? 4 — which is gold standard?
Epigastric bruits
Evidence of atherosclerosis: carotid bruits, diminished pulses
—Renal U/S
—MRA
—CTA
—Renal angiography (gold standard)
Renal Artery Stenosis
Treatment 3
Prevent renal ischemia and loss of renal function
-
Medical therapy = mainstay
ACE-I or ARB (unilateral RAS only), BB, CCB - Percutaneous revascularisation
Poor data to support stents to prevent HTN and renal insufficiency.
Reserved for uncontrolled RAS with pulm edema & HR - Surgical revascularisation
Rarely performed.
High peri-op mortality
Carotid Artery Stenosis
What is it?
(Will be covered more in neuro)
See disease table
Vasculitis
What is it?
Cause?
See disease table
Vasculitis [know]
Large vessel — Takayasu arteritis
Who is affected?
S/S
TX 2
Large vessel – takayasu arteritis
–Women 10-40y/o
–aorta and main branches
–causes: aneurysms, ischemia, dissection
S/S
–claudication and pulselessness due to abscence of carotid and limb pulses
DX:
Angiogram
TX
–steroids and cytotoxic drugs → reduce inflammation
–surgical bypass of obstructed vessels “
Vasculitis [know]
Large vessel — giant cell arteritis (temporal arteritis)
Who is affected?
S/S 4
DX 1 + what would you see on lab?
TX 1
“Large vessel – giant cell arteritis (temporal)
– women >50 y/o
–med-large vessels of the aortic aarch or cranial vessels (temporal, occiptal, ophthalmic)
S/S
–diminished temporal pulses
–headache and pain on side of head
–jaw claudication when chewing/talking
–facial pain
–impaired vision
DX:
—temporal artery biopsy (showing mononuclear cell infiltration or granulomatous inflammation, or MN giant cells)
—↑ CRP, ESR
TX: high dose steroids
Vasculitis [know]
Small - medium sized vessels
Thromboangitis obliterates (Buerger disease)
Who does it affect? 2
What are the S/S? (Triad)
Dx
Tx
Which Tx is contraindicated?
—distal vessels of UE/LE
—men >45y/o
—smoking
- Distal artery occlusion
- Raynauds
- Superficial vein trhombophlebitis
Dx: tissue biopsy
Tx: stop smoking
no revascularisation due to distal location of the disease
Vasospasm
What is it?
What colours do you see and what do they mean?
Primary vs secondary?
—vasospastic disease of digital arteries — exaggerated sympathetic discharge to stress/cold
—cool temp, emotional stress
—white: toes/fingers
—cyanosis: accumulation of desaturated hemoglobin
—ruddy colour: blood resumes
primary
—women 20-40
—primary fingers
—benign
secondary
—distal vascular lumen obliterated by sclerosis
—part of another condition, such as connective tissue disease
