T1W3 Flashcards
(33 cards)
branches of common iliac artery and their next branches
common iliac artery –> internal and external iliac
external –> femoral and lower limb supply
internal –> gluteal arteries
branches of external iliac artery
external iliac artery –> common femoral artery (after passing inguinal ligament) –> superficial and deep femoral artery
branches of superficial femoral artery
superficial femoral artery –> popliteal artery –> genicular branches (supplying the knee)
popliteal artery –> anterior and posterior tibial arteries
branches of anterior tibial artery
dorsalis pedis artery
branches of posterior tibial artery
fibular artery
what is primary hemostasis
endothelial damage –> underlying collagen exposure –> binding of platelets via specific glycoprotein receptors (this adhesion is accelerated by vWF) –> platelet adherence and activation –> degranulation (5HT, vWF, PAF, TXA2 –> further platelet adhesion and activation –> +ve feedback loop –> platelet plug formation
components of secondary hemostasis (coagulation cascade)
intrinsic pathway (XII) extrinsic pathway (TF, VII) common pathway (Xa, thrombin, fibrin)
what are the anticoagulant systems
- protein C –> aPC –> activated protein S –> prothrombinase complex (Xa) inhibition
- antithrombin system - inhibit thrombin (II–> IIa) AND also Xa
- plasminogen/plamin - lyses clot to FDPs
components of Well’s PE score
Don’t, Die, Tell, The Team, To, Calculate, Criteria
DVT/PE symptoms/signs present
DVT/PE is #1 diagnosis or equally likely
3 days immobilisation or thirty days surgery
Thromboembolism in the past
Coughing up blood - hemoptysis
Cancer - ongoing malignancy and treatment
well’s scoring for PE
two tier model
PE unlikely: 0-4 points - consider D Dimer testing/PERC score
PE likely: >4 points - consider CTA testing
causes of raised D dimer
physiological: pregnancy, older age, smoking, post operative, race (blacks)
pathological: ACS, acute upper GI hemorrhage, aortic dissection, malignancy, infection, AF or tachyarrhythmias, consumptive coagulopathy
causes of arterial ulcers
PVD - atherosclerosis, T2DM, smoking
vasculitis - rheumatoid arthritis, SLE, polyarteritis nodosa
causes of venous ulcers
DVT, varicose veins
chronic venous insufficiency
causes of neuropathic ulcers
T2DM, renal failure, trauma, surgery
causes of malignant ulcers
BCC, SCC, melanoma
when is bacteriological swabbing indicated
only if evidence of clinical infection - inflammation, redness, cellulitis, hyperalgesia, purulent exudate, rapid progression, pyrexia, foul odour - i.e. looks infected
why still swab chronic ulcers?
no evidence, however need to determine if any resistant organisms - Abx planning
features of a venous ulcer
painful, wet, oozing
bleeds on touch - moist granulating base
large, irregular, shallow
gaiter region and surrounding stasis dermatitis/hemosiderin staining
features of an arterial ulcer
painful, dry, irregular clear border
does not bleed on touch - dry granulating base
surrounding gangrenous tissue (black/grey)
associated with CLI - cold, pale feet and weak or absent pulses
shiny atrophic skin with hair loss
distal sites
features of neuropathic ulcers
punched out, deep and caving, painless
occurs on pressure points in distal areas
surrounded by calluses (hyperkeratosis)
bleeds
associated with pulselesness and poor peripheral sensation
groups who get neuropathic ulcers
diabetics, spinal cord injuries, B12 neuropathy
warfarin reversal
vitamin K stat 10mL IV - takes 24hrs to achieve effect
give prothrombin complex concentrate and FFP
modifiable risk factors for PVD
Same as CV risk factors:
hyperlipidemia, HTN, high TAG, smoking, T2DM, sedentary lifestyle and physical inactivity
non modifiable risk factors for PVD
FMH, male gender, age, genetics - race (more common in blacks)