Test three c Flashcards
Risk factors for AA
age
male
tobacco
high cholesterol
obesity
htn
CAD
lower extremity artery disease
fam history
Causes of AA
degenerative
congenital
mechanical
inflammatory
Infectious
True vs False aneurysms
True
-at least one vessel layer is in tact
-fusiform = circular; saccular = pouch-like
False/pseudo
-bleeding into surrounding structures
-usually from trauma, infection, bypass graft surgeries
Manifestaton of thoracic, abdominal, and arch aneurysms
Thoracic= usually asymptomatic, but might have deep chest pain
Abdominal = back pain, epigastric stuff, bowel issues, claudication, mass, bruits, blue toe syndrome
Arch =
- coronary artery issues = angina and TIA
-laryngeal nerve issues = cough, dyspnea, hoarse, dysphagia
-venous return issues = JVD, edema
Complication of aneurysms
rupture with severe pain and maybe ecchymosis
-patient can die if rupture happens into thoracic or abdominal cavity
hypovolemic shock
Aortic dissection: type A vs Type B
A = ascending aorta and arch
B = descending aorta
Predisposing factors for Aortic dissection
male
age
vascular disease
trauma
tobacco
coke/meth
fam history
pregnancy
htn
marfan
Etiology of aortic dissection
degenerated elastic fibers in arterial wall
tear in inner layer of aorta
blood goes thru tear –> rupture is fatal
Manifestation of Aortic dissection
-Worst pain ever, tearing, ripping, stabbing
- Type A = LOC change, weak carotid/temporal pulse, dizziness/syncope
Old ppl have vague symptoms like hypotension
Complications of aortic dissection
Cardiac tamponade (into pericardial sac)
Hemorrage into body cavities
Spinal cord ischemia
renal ischemia
mesenteric ischemia
rupture leading to death
How often should aneurysms be monitored
every 6-12 months
2-3 yrs for smaller ones
Surgeries for aneurysms
Endovascular Aneurysm Repair –> uses femoral artery
post surgical complications for aorta stuff
Intraabdominal htn w/ associated abdominal compartment syndrome
Endoleak –> from inadequate seal in graft
Ischemia below graft site
Aneurysm growth above or below graft
Aneurysm rupture
Aortic dissection and bleeding
Renal artery occlusion
Preop aneurysm surgery
Monitor for rupture, intraabdominal htn, compartment syndrome –> signs are diaphoresis, pallor, weakness, tachycardia, hypotension, pain, LOC change, pulsating ab mass
Get baseline data
NPO, antibiotics, BBs, bowel prep, skin cleaned
Virchow’s triad
venous stasis
damage of endothelium (direct or indirect)
hypercoagulability
Pathophysiology of VTE
thrombus forms and gets bigger and forms a tail that occludes vein
if only partial blockage, is covered by endothelial cells
If doesn’t detach, undergoes lysis or becomes adherent within 5-7 days
May become PE
weird venous stasis risks
old age
afib
stroke
weird endothelial damage risks
hypertonic IV drugs
IV drug abuse
indwelling catheters
weird hypercoagulability risks
high altitudes
HRT
Pregnancy and post partum
anemia
protein C and S deficiency
tobacco
Superficial vein thrombosis manifestation
cordlike vein
surrounding area is itchy, tender, red, and warm
mild temp elevation
leukocytosis
edema of extremeties
lower extremity venous thromboembolism
unilateral leg edema, pain, tenderness, dilated superficial veins
paresthesia
systemic temp over 100.4
if IVC i involved, both legs could be edema and blue
if SVC is involved - similar stuff in arms and face
Pulmonary embolism manifestation
dyspnea
hypoxia
tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope
Big ones = mental changes, hypotension, impending doom
Diagnostic studies for TE
ACT, aPTT, INR, bleeding time, platelet count
D-dimer –> elevation suggests VTE
venous compression ultrasound –> bad if veins don’t collapse with pressure
Duplex ultrasound: determines location and extent of thrombus
CT venography (contrast)
MR venography
preventing VTE (positioning)
reposition every 2 hrs
flex/extend feet, knees, and hips every 2 hrs while awake
sit in chair for meals and walk around 4-6 times a day
wear compression stockings
Intermittent pneumatic compression devices`
VTE drugs: vit K antagonists
warfarin PO
use INR to monitor
VTE drugs: thrombin inhibitors (indirect)
UH (IV or subq) and
LMWH (subq) –> don’t rub site after injection
use aPTT or ACT to monitor
watch for heparin-induced thrombocytopenia (HIT)
VTE drugs: synthetic thrombin (direct)
administered all the ways
aPTT or ACT to monitor
used for those at high risk for HIT
VTE drugs: Factor Xa inhibitors
PO or subq
dont need routine coagulation tests
monitor CBC and creatinine
can cause thrombocytopenia
interventional radiology for occluded vein
mechnical thrombectomy
insertion of pharmacomechanical device
postthrombus extraction
angioplasty
stenting
vena cava interruption devices inserted percutaneously thru right femoral or right internal jugular vein
what substances are bad for VTE?
nicotine and caffeine
special considerations for warfatin
eat lots of vit K, but don’t take vit K supplements
hydration is important
blood monitoring
varicose veins
vein walls weaken and then the leaflets don’t fit together and blood pools backwards
-achy and heavy
-seen with duplex ultrasound
CVI
chronic venous insufficiency
-functional abnormalities of venous system which can lead to venous ulcers
-can be caused by varicose veins or PTCs
-serous fluid and RBCs leak from capillaries into the tissue
-enzymes break down the RBCs and release hemosiderin, causing brown skin
-skin and tissue replaced with fibrous tissue
CVI ulcers
usually above medial malleolus
irregular shape
yellow or ruddy with granulation
drainage
Varicose vein treatment
sclerotherapy
compression stockings
transcutaneous lasers
surgery if recurrent superficial vein thrombosis
CVI treatment
compression of all sorts
healthy food (including good glucose for DM)
CVI ulcer treatment
Pentoxifylline ointment- minimizes WBC activation
micronized purified flavonoid - acts on WBC to decrease inflammation and edema
antibacterials
surgery for CVI
for ulcers that don’t get better in 4-6 weeks
-need skin grafts
-will need lifelong compression therapy
