Atheroma and Vessel Pathologies Flashcards
ulcer definition
non-healing break in skin/mucous membrane - internal/external
The majority of ulcers are ____
Venous 80%
Arterial 15%
Neuropathic (pressure) 5%
Arterial ulcers tend to be prox/distal
More/less painful
more superficial/deep
Appear:
distal -ankle/foot
more painful
deeper
circular and tend not to bleed
Venous ulcers tend to be prox/distal
More/less painful
more superficial/deep
Appear:
Proximal to medial malleolus
Less painful
More superficial but larger
purplish/blue and weep blood
___ ulcers are associated with oedema and varicose veins and atrophie blanche
venous
___ ulcers are associated with shiny, hairless, cold pale skin, nail dystrophy and atrophy of calf muscles
arterial
___ ulcers are worse at night and relieved by dangling legs
arterial
____ ulcers are better when elevated
venous
atrophie blanche =
smooth ivory-white plaques stippled with telangiectasis and surrounding hyperpigmentation
neuropathic ulcers tend to occur in sufferers of
diabetes + rheumatoid arthritis
ABPI =
systolic P in ankle/systolic P in brachial artery
Lipid storage disorder that causes tendon xanthomas
cerebrotendinous xanthomatosis
tuberous xanthomas=
caused by ___
lipid deposits in dermis + S/C tissue on extensor surfaces
hypertri./biliary cirrhosis
eruptive xanthomas =
caused by ___
small reddish-yellow papules
rapid increase in serum tri.s
fatty streak is a ___ fatty deposit
It is ir/reversible
subendothelial reversible
cardiac ischaemia as a result of atheroma causes cardiac myocyte ___+___ => replaced by ___ => ___
shrinkage+apoptosis
fibroblasts
deceased elasticity and filling => infarct and HF
aneurysm =
abnormal dilation of an artery >50% normal diameter
If an AA is ___ operate
greater than 6cm
arterial dissection =
blood splits media between (SM and elastic) and plaque => false lumen
Causes of aortic dissection =
connective tissue disorders - Marfan's hbp atheroma trauma coarctation pregnancy (due to vol. expansion)
Haemostasis =
mechanism to arrest blood loss from a damaged vessel
When the endothelium is damaged ___ and ___ are exposed to circulating ____
____ binds to ____
collagen + tissue factor (thromboplasmin)
vWF
vWF+collagen
vWF(bound to collagen) on the damaged endothelium binds to ____ on platelets
Platelets then bind to collagen via ____ and become ___
GPIb receptors
integrin α2β1 + GPVI receptors
activated
Activated platelets
1) extend ____ to interact with other platelets
2) synthesis ___ from ___ via ___.
pseuodopodia
TXA2 from arachidonic acid via COX-1
TXA2 binds to ____ on platelets => mediator release
1) ____ from dense granules
2) _____ from α granules
GPCR TXA2 receptors
5-HT + ADP
vWF + factor V
TXA2 binding to platelets and release of 5-HT both cause ____
vasoconstriction
ADP binds to ____ =>
1) further _______
2) increased expression of ____ that bind ___
3) exposes ____ on platelet surface, facilitates formation of ___
platelet GPCR P2Y12 receptors
platelet activation
GPIIa+IIIa receptors bind fibrinogen => soft plug
acidic phospholipids => clot
Key events in Primary haemostasis:
local vasoconstriction
platelets adhere, activate and aggregate (by fibrinogen)
Basis of coagulation:
fibrinogen—thrombin—>fibrin (solid clot)
`Initial phase of coagulation = TF on _____ cells binds to ___ = ___ activates ___ > activates ___
__ + ___ activate ___ to form thrombin
subendothelial factor 7 =>TF:VIIa X->Xa V->Va Va+Xa activate II(prothrombin)
Amplification phase of coagulation = ___ activates further platelets
1) causes α granules to release ___
2) frees ___ from vWF and activates it at the platelet membrane
thrombin IIa
V
VIII
XIa (activated by IIa) / TF:VIIIa activate __. It forms a complex with __ = ___ which powerfully activates ___
IX->IXa
IXa+VIIIa = tenase
X->Xa
Xa:Va bind to ___ at platelet membrane to ___
which cleaves ____ and the fragments ___ to form ___
II -> form thrombin -> cleaves fibrinogen = fragments polymerise to form fibrin
____ crosslinks with ____ to form a solid clot
VIIIa:fibrin
3 stages in coagulation cascade =
Initial phase
Amplification
Propagation
Thrombosis =
pathological haemostasis ie. inappropriate clotting
Arterial thrombi are __ thrombi
many ___ in a fibrin mesh around few ___
normally lodge in ___
treated with ____
white
many platelets ; few RBCs
brain or other organ
antiplatelets
Venous thrombi are ___ thrombi
___ head, jelly-like __ tail of many ___ and ___-rich
normally lodge in ___
treated with ____
red
white head ; red tail of many RBCs and fibrin rich
lungs
anti-coagulants
Clotting factors _____ require Vitamin K to reduce O2,CO2 and glutamic acid residues in them to form ______
2 7 9 10
γ-carboxyglutamic acid residues in their precursors
The ____ from of vitamin K =
It is used to form Factors 2 7 9 10’s precursors
reduced = hydroquinone
oxidised vitamin K (___) is reduced to reduced vit K (___) by ___
epoxide->hydroquinone
by Vitamin K reductase
Infarction =
ischaemic necrosis 2ndry to occlusion/reduction of artial flow or venous drainage (back P)
Thrombus/clot = in vasculature and when alive
Thrombus
Clot = when dead/ outwith vasculature
Platelet α granules release ___ components eg.
adhesion components - fibrinogen, fibronection, PDGF, anti-heparin etc.
Platelet dense granules release___ components eg.
aggregation components eg. ADP
Endothelial-released regulators of cell growth
stim = PDGF, CSF, FGF inhibitors = heparin, TGF-β
Results in more contact between platelets and endothelium, activated clotting factors not being diluted, inflow of anti-coag factors slowed, endothelial activation promoted =
Blood flow stasis
Genetic hypercoagulability states
Factor V mutations
defects in anti-coag pathway: ATIII/ ProteinC/S deficiency
defects in fibrinolysis
Lines of Zahn are found in ___ thrombi
due to alternating bands of ___ + ___
arterial - ass. w atheroma and firmly attached to mural
pale (platelet and fibrin)
dark (RBC+WBC)
Wedge-shaped infarct =
PE
Venous emboli only cause peripheral arterial circulation if ___ = a ____ emboli
septal defect => paradoxical emboli
Fat embolism occur after ___
soft tissue/ bone trauma
More than ___ of air is needed to form a pathogenic emboli as any less ____
more than 100ml
less than that is filtered out by lungs
Systemic emboli start in the ___ > ___ circulation > ____ (80%), ___ and ___
heart>arterial>gangrene in legs (80%), visceral and brain
Monckeberg medial calcific stenosis =
calcification of medium arteries in over 50yos
arteriolosclerosis = ___ / ___ type
ass. w. ___ and ___
hyaline/hyperplastic
diabetes mellitus
hbp
common sites of atherosclerosis:
branchpoints in thoracic aorta
carotid bifurcations esp. internal carotid
circle of Willis
ostia and LAD
Can’t measure ABPI in ____ vessels
calcified
In normal ABPI ____ with exercise and then ____ after
In claudication ABPI ___ with exercise and then ___ after
normal increases with and decreases after
claudication decreases with and increases after
If see mixed blood flow on duplex US of legs =
turbulence
Investigations for claudication:
ABPI Duplex US MRA CT angiography Catheter angiogram
Endartectomy =
clean artery
remove inner lining and plaque
Treatment for intermittent claudication
lifestyle - exercise to increase collaterals
angioplasty+/stent
endartectomy
bypass - not great
critical limb ischaemia =
resting pain in toe/foot when lying or sleeping
Symptoms of critical limb ischaemia:
worse at night, strong analgesic need, helped by dangling legs/walking
due to collateral and main artery occlusion
treatment for critical limb ischaemia=
amputation most likely
True aneurysm =
all 3 layers of vessel wall still intact
pseudo aneurysm =
breach in wall + surrounding structures act as vessel wall
Who gets AAA?
older, M9:1F, smoking, hbp
trashing =
seen in AAA
clot sits in it and breaks off
Signs of ruptured AAA
tachycardic (or not) hypotensive (or not) pulsatile and expansile mass +/- tender transmitted pulse loss of peripheral pulses sudden epigastric pain
____ AAA rupture is contained
_____ rupture is rapidly fatal
retroperitoneal contained
intraperitoneal rapidly fatal
To monitor AAA ___
Shows ___
US
AP diameter and if iliac arteries involved
Imaging used to see if AAA has ruptured ___
Shows ___
CT
shape, size, iliac involvement
Elective surgery for AAA is when greater than ___
or expansion of ___
greater than 6/5.5cm
more than 0.5cm/6month
To determine if fit for elective AAA surgery:
ECG, PFT, CPX (cardiopulmonary exercise testing), renal test, ABPI, anaesthetic assessment, end of bed
___/___ used to repair AAA
EVAR - endovascular aneurysm repair
Open repair
AAA repair that is possible in everyone, effective for life but with greater mortality risk and slower recovery
open repair
AAA repair that is only possible in 25% of pop., may need further intervention, lower mortality risk, faster recovery
EVAR
Deep venous system in legs =
tibial, popliteal, femoral
Superficial venous system in legs =
saphenous, perforators
Tortuous and dilated long and short saphenous veins
Varicose veins
Primary varicose veins are due to ___
valves incompetent
2ndry varicose veins are due to ___
develop as collaterals to deep obstruction
eg. DVT/stenosis
Sustained ambulatory venous hbp => irreversible skin damage =
chronic venous insufficiency
Chronic venous insufficiency can => ___=>___=>___
haemosiderin deposits
lipodermatosclerosis
ulceration (>6wks - between malleolus+tibial tuberosity)
in chronic venous insufficiency haemosiderin deposits are due to:
RBCs leak from capillaries, break down and leave iron residue
in chronic venous insufficiency lipodermatosclerosis are due to:
WBC leak out of capillaries => inflam from toxins and fibrosis may => champagne bottle legs
Investigation for chronic venous insufficiency
Duplex US - shows state of deep veins
Management of chronic venous insufficiency =
Compression (not if low ABPI)
foam sclerotherapy
endovenous ablation
surgical - less used
Complications of chronic venous insufficiency interventions:
thrombophlebitis, skin staining, local ulceration, infection, nerve damage, recurrence
6 signs of acute limb ischaemia
6Ps
pain, pallor, perishingly cold, paralysis, paraesthesia, pulseless
How to distinguish acute from acute on chronic limb ischaemia
no Hx of claudication, know emboli cause, all of contra-lateral pulses
Stages of acute limb ischaemia
0-4hrs blanching+mottling - salvageable
4-12: mottling - partially salvageable
more than 12: unsalvageable - toxins released: red, tender, non-blanching
Investigations for acute limb ischaemia
ABC, FBC, CK, Troponin, ECG, CXR
DON’T do arterial imaging
Surgery for acute limb ischaemia:
embelectomy
thrombolysis
possibly amputation
Diabetic foot sepsis is due to ___
results in ___
neuropathy, PVD and infection
ulceration, necrosis and gangrene
Management of diabetic foot sepsis:
broad spectrum antibiotics
surgical debridement
prevent = podiatrist, correct footwear
Diabetic foot sepsis is a ___ problem
___ builds up in compartments -> blocks __> ____
pressure - pus builds up + blocks capillary flow = necrosis
Distal DVT are found in ____
calves
Proximal DVT are found in ___
popliteal/femoral - above knee in the thigh
Unprovoked DVT = _____
More/less likely to have recurrency
idiopathic
more
DVT of know cause =
provoked
PTS - post-thrombotic syndrome is when ____
signs =
valves are incompetent after DVT
pain, oedema, hyperpigmentation, eczema, varicosity, ulcers
Tests for DVT =
D-dimer and Wells score
If D-dimer is low and Wells score moderate/high for DVT =>
imaging needed
If D-dimer high and suspect DVT then
need imaging
Gold-standard imaging for diagnosing DVT
Doppler US
Gold standard for PE diagnosis
CTPA
Better than CTPA for small vessel PE diagnosis
V/Q scan
In PE CXR can show:
pleural effusion (present in 5%) wedge-shaped infarct
Gold standard for treatment of DVT =
anticoagulants
treatment for DVT:
anticoagulants thrombolysis (if symptomatic) analgesia compression stockings IVC filter (for proximal DVT temporarily)
Thrombolysis in PE if:
haemodynamically unstable (h/lbp + ^HR) or haemodynamically stable w risk of deteriorating
phlegmasis =
extensive DVT impairs arterial flow - life threatening and aggressive treatment
Gold-standard treatment for PE:
Anti-coagulation
