Atheroma and Vessel Pathologies Flashcards
1
Q
ulcer definition
A
non-healing break in skin/mucous membrane - internal/external
2
Q
The majority of ulcers are ____
A
Venous 80%
Arterial 15%
Neuropathic (pressure) 5%
3
Q
Arterial ulcers tend to be prox/distal
More/less painful
more superficial/deep
Appear:
A
distal -ankle/foot
more painful
deeper
circular and tend not to bleed
4
Q
Venous ulcers tend to be prox/distal
More/less painful
more superficial/deep
Appear:
A
Proximal to medial malleolus
Less painful
More superficial but larger
purplish/blue and weep blood
5
Q
___ ulcers are associated with oedema and varicose veins and atrophie blanche
A
venous
6
Q
___ ulcers are associated with shiny, hairless, cold pale skin, nail dystrophy and atrophy of calf muscles
A
arterial
7
Q
___ ulcers are worse at night and relieved by dangling legs
A
arterial
8
Q
____ ulcers are better when elevated
A
venous
9
Q
atrophie blanche =
A
smooth ivory-white plaques stippled with telangiectasis and surrounding hyperpigmentation
10
Q
neuropathic ulcers tend to occur in sufferers of
A
diabetes + rheumatoid arthritis
11
Q
ABPI =
A
systolic P in ankle/systolic P in brachial artery
12
Q
Lipid storage disorder that causes tendon xanthomas
A
cerebrotendinous xanthomatosis
13
Q
tuberous xanthomas=
caused by ___
A
lipid deposits in dermis + S/C tissue on extensor surfaces
hypertri./biliary cirrhosis
14
Q
eruptive xanthomas =
caused by ___
A
small reddish-yellow papules
rapid increase in serum tri.s
15
Q
fatty streak is a ___ fatty deposit
It is ir/reversible
A
subendothelial reversible
16
Q
cardiac ischaemia as a result of atheroma causes cardiac myocyte ___+___ => replaced by ___ => ___
A
shrinkage+apoptosis
fibroblasts
deceased elasticity and filling => infarct and HF
17
Q
aneurysm =
A
abnormal dilation of an artery >50% normal diameter
18
Q
If an AA is ___ operate
A
greater than 6cm
19
Q
arterial dissection =
A
blood splits media between (SM and elastic) and plaque => false lumen
20
Q
Causes of aortic dissection =
A
connective tissue disorders - Marfan's hbp atheroma trauma coarctation pregnancy (due to vol. expansion)
21
Q
Haemostasis =
A
mechanism to arrest blood loss from a damaged vessel
22
Q
When the endothelium is damaged ___ and ___ are exposed to circulating ____
____ binds to ____
A
collagen + tissue factor (thromboplasmin)
vWF
vWF+collagen
23
Q
vWF(bound to collagen) on the damaged endothelium binds to ____ on platelets
Platelets then bind to collagen via ____ and become ___
A
GPIb receptors
integrin α2β1 + GPVI receptors
activated
24
Q
Activated platelets
1) extend ____ to interact with other platelets
2) synthesis ___ from ___ via ___.
A
pseuodopodia
TXA2 from arachidonic acid via COX-1
25
TXA2 binds to ____ on platelets => mediator release
1) ____ from dense granules
2) _____ from α granules
GPCR TXA2 receptors
5-HT + ADP
vWF + factor V
26
TXA2 binding to platelets and release of 5-HT both cause ____
vasoconstriction
27
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
28
Key events in Primary haemostasis:
local vasoconstriction
| platelets adhere, activate and aggregate (by fibrinogen)
29
Basis of coagulation:
fibrinogen---thrombin--->fibrin (solid clot)
30
`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)
```
31
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
32
XIa (activated by IIa) / TF:VIIIa activate __. It forms a complex with __ = ___ which powerfully activates ___
IX->IXa
IXa+VIIIa = tenase
X->Xa
33
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
34
____ crosslinks with ____ to form a solid clot
VIIIa:fibrin
35
3 stages in coagulation cascade =
Initial phase
Amplification
Propagation
36
Thrombosis =
pathological haemostasis ie. inappropriate clotting
37
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
38
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
39
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
40
The ____ from of vitamin K =
| It is used to form Factors 2 7 9 10's precursors
reduced = hydroquinone
41
oxidised vitamin K (___) is reduced to reduced vit K (___) by ___
epoxide->hydroquinone
| by Vitamin K reductase
42
Infarction =
ischaemic necrosis 2ndry to occlusion/reduction of artial flow or venous drainage (back P)
43
Thrombus/clot = in vasculature and when alive
Thrombus
| Clot = when dead/ outwith vasculature
44
Platelet α granules release ___ components eg.
adhesion components - fibrinogen, fibronection, PDGF, anti-heparin etc.
45
Platelet dense granules release___ components eg.
aggregation components eg. ADP
46
Endothelial-released regulators of cell growth
```
stim = PDGF, CSF, FGF
inhibitors = heparin, TGF-β
```
47
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
48
Genetic hypercoagulability states
Factor V mutations
defects in anti-coag pathway: ATIII/ ProteinC/S deficiency
defects in fibrinolysis
49
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)
50
Wedge-shaped infarct =
PE
51
Venous emboli only cause peripheral arterial circulation if ___ = a ____ emboli
septal defect => paradoxical emboli
52
Fat embolism occur after ___
soft tissue/ bone trauma
53
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
54
Systemic emboli start in the ___ > ___ circulation > ____ (80%), ___ and ___
heart>arterial>gangrene in legs (80%), visceral and brain
55
Monckeberg medial calcific stenosis =
calcification of medium arteries in over 50yos
56
arteriolosclerosis = ___ / ___ type
| ass. w. ___ and ___
hyaline/hyperplastic
diabetes mellitus
hbp
57
common sites of atherosclerosis:
branchpoints in thoracic aorta
carotid bifurcations esp. internal carotid
circle of Willis
ostia and LAD
58
Can't measure ABPI in ____ vessels
calcified
59
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
60
If see mixed blood flow on duplex US of legs =
turbulence
61
Investigations for claudication:
```
ABPI
Duplex US
MRA
CT angiography
Catheter angiogram
```
62
Endartectomy =
clean artery
| remove inner lining and plaque
63
Treatment for intermittent claudication
lifestyle - exercise to increase collaterals
angioplasty+/stent
endartectomy
bypass - not great
64
critical limb ischaemia =
resting pain in toe/foot when lying or sleeping
65
Symptoms of critical limb ischaemia:
worse at night, strong analgesic need, helped by dangling legs/walking
due to collateral and main artery occlusion
66
treatment for critical limb ischaemia=
amputation most likely
67
True aneurysm =
all 3 layers of vessel wall still intact
68
pseudo aneurysm =
breach in wall + surrounding structures act as vessel wall
69
Who gets AAA?
older, M9:1F, smoking, hbp
70
trashing =
| seen in AAA
clot sits in it and breaks off
71
Signs of ruptured AAA
```
tachycardic (or not)
hypotensive (or not)
pulsatile and expansile mass +/- tender
transmitted pulse
loss of peripheral pulses
sudden epigastric pain
```
72
____ AAA rupture is contained
| _____ rupture is rapidly fatal
retroperitoneal contained
| intraperitoneal rapidly fatal
73
To monitor AAA ___
| Shows ___
US
| AP diameter and if iliac arteries involved
74
Imaging used to see if AAA has ruptured ___
| Shows ___
CT
| shape, size, iliac involvement
75
Elective surgery for AAA is when greater than ___
| or expansion of ___
greater than 6/5.5cm
| more than 0.5cm/6month
76
To determine if fit for elective AAA surgery:
ECG, PFT, CPX (cardiopulmonary exercise testing), renal test, ABPI, anaesthetic assessment, end of bed
77
___/___ used to repair AAA
EVAR - endovascular aneurysm repair
| Open repair
78
AAA repair that is possible in everyone, effective for life but with greater mortality risk and slower recovery
open repair
79
AAA repair that is only possible in 25% of pop., may need further intervention, lower mortality risk, faster recovery
EVAR
80
Deep venous system in legs =
tibial, popliteal, femoral
81
Superficial venous system in legs =
saphenous, perforators
82
Tortuous and dilated long and short saphenous veins
Varicose veins
83
Primary varicose veins are due to ___
valves incompetent
84
2ndry varicose veins are due to ___
develop as collaterals to deep obstruction
| eg. DVT/stenosis
85
Sustained ambulatory venous hbp => irreversible skin damage =
chronic venous insufficiency
86
Chronic venous insufficiency can => ___=>___=>___
haemosiderin deposits
lipodermatosclerosis
ulceration (>6wks - between malleolus+tibial tuberosity)
87
in chronic venous insufficiency haemosiderin deposits are due to:
RBCs leak from capillaries, break down and leave iron residue
88
in chronic venous insufficiency lipodermatosclerosis are due to:
WBC leak out of capillaries => inflam from toxins and fibrosis may => champagne bottle legs
89
Investigation for chronic venous insufficiency
Duplex US - shows state of deep veins
90
Management of chronic venous insufficiency =
Compression (not if low ABPI)
foam sclerotherapy
endovenous ablation
surgical - less used
91
Complications of chronic venous insufficiency interventions:
thrombophlebitis, skin staining, local ulceration, infection, nerve damage, recurrence
92
6 signs of acute limb ischaemia
6Ps
| pain, pallor, perishingly cold, paralysis, paraesthesia, pulseless
93
How to distinguish acute from acute on chronic limb ischaemia
no Hx of claudication, know emboli cause, all of contra-lateral pulses
94
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
95
Investigations for acute limb ischaemia
ABC, FBC, CK, Troponin, ECG, CXR
| DON'T do arterial imaging
96
Surgery for acute limb ischaemia:
embelectomy
thrombolysis
possibly amputation
97
Diabetic foot sepsis is due to ___
| results in ___
neuropathy, PVD and infection
| ulceration, necrosis and gangrene
98
Management of diabetic foot sepsis:
broad spectrum antibiotics
surgical debridement
prevent = podiatrist, correct footwear
99
Diabetic foot sepsis is a ___ problem
| ___ builds up in compartments -> blocks __> ____
pressure - pus builds up + blocks capillary flow = necrosis
100
Distal DVT are found in ____
calves
101
Proximal DVT are found in ___
popliteal/femoral - above knee in the thigh
102
Unprovoked DVT = _____
| More/less likely to have recurrency
idiopathic
| more
103
DVT of know cause =
provoked
104
PTS - post-thrombotic syndrome is when ____
| signs =
valves are incompetent after DVT
| pain, oedema, hyperpigmentation, eczema, varicosity, ulcers
105
Tests for DVT =
D-dimer and Wells score
106
If D-dimer is low and Wells score moderate/high for DVT =>
imaging needed
107
If D-dimer high and suspect DVT then
need imaging
108
Gold-standard imaging for diagnosing DVT
Doppler US
109
Gold standard for PE diagnosis
CTPA
110
Better than CTPA for small vessel PE diagnosis
V/Q scan
111
In PE CXR can show:
```
pleural effusion (present in 5%)
wedge-shaped infarct
```
112
Gold standard for treatment of DVT =
anticoagulants
113
treatment for DVT:
```
anticoagulants
thrombolysis (if symptomatic)
analgesia
compression stockings
IVC filter (for proximal DVT temporarily)
```
114
Thrombolysis in PE if:
```
haemodynamically unstable (h/lbp + ^HR)
or haemodynamically stable w risk of deteriorating
```
115
phlegmasis =
extensive DVT impairs arterial flow - life threatening and aggressive treatment
116
Gold-standard treatment for PE:
Anti-coagulation
