Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

JazCardio > Atheroma and Vessel Pathologies > Flashcards

Atheroma and Vessel Pathologies Flashcards

1
Q

ulcer definition

A

non-healing break in skin/mucous membrane - internal/external

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The majority of ulcers are ____

A

Venous 80%
Arterial 15%
Neuropathic (pressure) 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

___ ulcers are associated with oedema and varicose veins and atrophie blanche

A

venous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

___ ulcers are associated with shiny, hairless, cold pale skin, nail dystrophy and atrophy of calf muscles

A

arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

___ ulcers are worse at night and relieved by dangling legs

A

arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

____ ulcers are better when elevated

A

venous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

atrophie blanche =

A

smooth ivory-white plaques stippled with telangiectasis and surrounding hyperpigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

neuropathic ulcers tend to occur in sufferers of

A

diabetes + rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ABPI =

A

systolic P in ankle/systolic P in brachial artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lipid storage disorder that causes tendon xanthomas

A

cerebrotendinous xanthomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

tuberous xanthomas=

caused by ___

A

lipid deposits in dermis + S/C tissue on extensor surfaces

hypertri./biliary cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

eruptive xanthomas =

caused by ___

A

small reddish-yellow papules

rapid increase in serum tri.s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

fatty streak is a ___ fatty deposit

It is ir/reversible

A

subendothelial reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

aneurysm =

A

abnormal dilation of an artery >50% normal diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If an AA is ___ operate

A

greater than 6cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

arterial dissection =

A

blood splits media between (SM and elastic) and plaque => false lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Causes of aortic dissection =

A 
connective tissue disorders - Marfan's
hbp
atheroma
trauma
coarctation
pregnancy (due to vol. expansion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Haemostasis =

A

mechanism to arrest blood loss from a damaged vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When the endothelium is damaged ___ and ___ are exposed to circulating ____
____ binds to ____

A

collagen + tissue factor (thromboplasmin)
vWF
vWF+collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Activated platelets

1) extend ____ to interact with other platelets
2) synthesis ___ from ___ via ___.

A

pseuodopodia

TXA2 from arachidonic acid via COX-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

TXA2 binds to ____ on platelets => mediator release

1) ____ from dense granules
2) _____ from α granules

A

GPCR TXA2 receptors
5-HT + ADP
vWF + factor V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

TXA2 binding to platelets and release of 5-HT both cause ____

A

vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ADP binds to ____ =>

1) further _______
2) increased expression of ____ that bind ___
3) exposes ____ on platelet surface, facilitates formation of ___

A

platelet GPCR P2Y12 receptors
platelet activation
GPIIa+IIIa receptors bind fibrinogen => soft plug
acidic phospholipids => clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Key events in Primary haemostasis:

A

local vasoconstriction

platelets adhere, activate and aggregate (by fibrinogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Basis of coagulation:

A

fibrinogen—thrombin—>fibrin (solid clot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

`Initial phase of coagulation = TF on _____ cells binds to ___ = ___ activates ___ > activates ___
__ + ___ activate ___ to form thrombin

A 
subendothelial
factor 7 =>TF:VIIa
X->Xa
V->Va
Va+Xa activate II(prothrombin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Amplification phase of coagulation = ___ activates further platelets

1) causes α granules to release ___
2) frees ___ from vWF and activates it at the platelet membrane

A

thrombin IIa
V
VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

XIa (activated by IIa) / TF:VIIIa activate __. It forms a complex with __ = ___ which powerfully activates ___

A

IX->IXa
IXa+VIIIa = tenase
X->Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Xa:Va bind to ___ at platelet membrane to ___

which cleaves ____ and the fragments ___ to form ___

A

II -> form thrombin -> cleaves fibrinogen = fragments polymerise to form fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

____ crosslinks with ____ to form a solid clot

A

VIIIa:fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3 stages in coagulation cascade =

A

Initial phase
Amplification
Propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Thrombosis =

A

pathological haemostasis ie. inappropriate clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Arterial thrombi are __ thrombi
many ___ in a fibrin mesh around few ___
normally lodge in ___
treated with ____

A

white
many platelets ; few RBCs
brain or other organ
antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Venous thrombi are ___ thrombi
___ head, jelly-like __ tail of many ___ and ___-rich
normally lodge in ___
treated with ____

A

red
white head ; red tail of many RBCs and fibrin rich
lungs
anti-coagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Clotting factors _____ require Vitamin K to reduce O2,CO2 and glutamic acid residues in them to form ______

A

2 7 9 10

γ-carboxyglutamic acid residues in their precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

The ____ from of vitamin K =

It is used to form Factors 2 7 9 10’s precursors

A

reduced = hydroquinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

oxidised vitamin K (___) is reduced to reduced vit K (___) by ___

A

epoxide->hydroquinone

by Vitamin K reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Infarction =

A

ischaemic necrosis 2ndry to occlusion/reduction of artial flow or venous drainage (back P)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Thrombus/clot = in vasculature and when alive

A

Thrombus

Clot = when dead/ outwith vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Platelet α granules release ___ components eg.

A

adhesion components - fibrinogen, fibronection, PDGF, anti-heparin etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Platelet dense granules release___ components eg.

A

aggregation components eg. ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Endothelial-released regulators of cell growth

A 
stim = PDGF, CSF, FGF
inhibitors = heparin, TGF-β
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Results in more contact between platelets and endothelium, activated clotting factors not being diluted, inflow of anti-coag factors slowed, endothelial activation promoted =

A

Blood flow stasis

48
Q

Genetic hypercoagulability states

A

Factor V mutations
defects in anti-coag pathway: ATIII/ ProteinC/S deficiency
defects in fibrinolysis

49
Q

Lines of Zahn are found in ___ thrombi

due to alternating bands of ___ + ___

A

arterial - ass. w atheroma and firmly attached to mural
pale (platelet and fibrin)
dark (RBC+WBC)

50
Q

Wedge-shaped infarct =

A

PE

51
Q

Venous emboli only cause peripheral arterial circulation if ___ = a ____ emboli

A

septal defect => paradoxical emboli

52
Q

Fat embolism occur after ___

A

soft tissue/ bone trauma

53
Q

More than ___ of air is needed to form a pathogenic emboli as any less ____

A

more than 100ml

less than that is filtered out by lungs

54
Q

Systemic emboli start in the ___ > ___ circulation > ____ (80%), ___ and ___

A

heart>arterial>gangrene in legs (80%), visceral and brain

55
Q

Monckeberg medial calcific stenosis =

A

calcification of medium arteries in over 50yos

56
Q

arteriolosclerosis = ___ / ___ type

ass. w. ___ and ___

A

hyaline/hyperplastic
diabetes mellitus
hbp

57
Q

common sites of atherosclerosis:

A

branchpoints in thoracic aorta
carotid bifurcations esp. internal carotid
circle of Willis
ostia and LAD

58
Q

Can’t measure ABPI in ____ vessels

A

calcified

59
Q

In normal ABPI ____ with exercise and then ____ after

In claudication ABPI ___ with exercise and then ___ after

A

normal increases with and decreases after

claudication decreases with and increases after

60
Q

If see mixed blood flow on duplex US of legs =

A

turbulence

61
Q

Investigations for claudication:

A 
ABPI
Duplex US
MRA
CT angiography
Catheter angiogram
62
Q

Endartectomy =

A

clean artery

remove inner lining and plaque

63
Q

Treatment for intermittent claudication

A

lifestyle - exercise to increase collaterals
angioplasty+/stent
endartectomy
bypass - not great

64
Q

critical limb ischaemia =

A

resting pain in toe/foot when lying or sleeping

65
Q

Symptoms of critical limb ischaemia:

A

worse at night, strong analgesic need, helped by dangling legs/walking
due to collateral and main artery occlusion

66
Q

treatment for critical limb ischaemia=

A

amputation most likely

67
Q

True aneurysm =

A

all 3 layers of vessel wall still intact

68
Q

pseudo aneurysm =

A

breach in wall + surrounding structures act as vessel wall

69
Q

Who gets AAA?

A

older, M9:1F, smoking, hbp

70
Q

trashing =

seen in AAA

A

clot sits in it and breaks off

71
Q

Signs of ruptured AAA

A 
tachycardic (or not)
hypotensive (or not)
pulsatile and expansile mass +/- tender
transmitted pulse 
loss of peripheral pulses
sudden epigastric pain
72
Q

____ AAA rupture is contained

_____ rupture is rapidly fatal

A

retroperitoneal contained

intraperitoneal rapidly fatal

73
Q

To monitor AAA ___

Shows ___

A

US

AP diameter and if iliac arteries involved

74
Q

Imaging used to see if AAA has ruptured ___

Shows ___

A

CT

shape, size, iliac involvement

75
Q

Elective surgery for AAA is when greater than ___

or expansion of ___

A

greater than 6/5.5cm

more than 0.5cm/6month

76
Q

To determine if fit for elective AAA surgery:

A

ECG, PFT, CPX (cardiopulmonary exercise testing), renal test, ABPI, anaesthetic assessment, end of bed

77
Q

___/___ used to repair AAA

A

EVAR - endovascular aneurysm repair

Open repair

78
Q

AAA repair that is possible in everyone, effective for life but with greater mortality risk and slower recovery

A

open repair

79
Q

AAA repair that is only possible in 25% of pop., may need further intervention, lower mortality risk, faster recovery

A

EVAR

80
Q

Deep venous system in legs =

A

tibial, popliteal, femoral

81
Q

Superficial venous system in legs =

A

saphenous, perforators

82
Q

Tortuous and dilated long and short saphenous veins

A

Varicose veins

83
Q

Primary varicose veins are due to ___

A

valves incompetent

84
Q

2ndry varicose veins are due to ___

A

develop as collaterals to deep obstruction

eg. DVT/stenosis

85
Q

Sustained ambulatory venous hbp => irreversible skin damage =

A

chronic venous insufficiency

86
Q

Chronic venous insufficiency can => ___=>___=>___

A

haemosiderin deposits
lipodermatosclerosis
ulceration (>6wks - between malleolus+tibial tuberosity)

87
Q

in chronic venous insufficiency haemosiderin deposits are due to:

A

RBCs leak from capillaries, break down and leave iron residue

88
Q

in chronic venous insufficiency lipodermatosclerosis are due to:

A

WBC leak out of capillaries => inflam from toxins and fibrosis may => champagne bottle legs

89
Q

Investigation for chronic venous insufficiency

A

Duplex US - shows state of deep veins

90
Q

Management of chronic venous insufficiency =

A

Compression (not if low ABPI)
foam sclerotherapy
endovenous ablation
surgical - less used

91
Q

Complications of chronic venous insufficiency interventions:

A

thrombophlebitis, skin staining, local ulceration, infection, nerve damage, recurrence

92
Q

6 signs of acute limb ischaemia

A

6Ps

pain, pallor, perishingly cold, paralysis, paraesthesia, pulseless

93
Q

How to distinguish acute from acute on chronic limb ischaemia

A

no Hx of claudication, know emboli cause, all of contra-lateral pulses

94
Q

Stages of acute limb ischaemia

A

0-4hrs blanching+mottling - salvageable
4-12: mottling - partially salvageable
more than 12: unsalvageable - toxins released: red, tender, non-blanching

95
Q

Investigations for acute limb ischaemia

A

ABC, FBC, CK, Troponin, ECG, CXR

DON’T do arterial imaging

96
Q

Surgery for acute limb ischaemia:

A

embelectomy
thrombolysis
possibly amputation

97
Q

Diabetic foot sepsis is due to ___

results in ___

A

neuropathy, PVD and infection

ulceration, necrosis and gangrene

98
Q

Management of diabetic foot sepsis:

A

broad spectrum antibiotics
surgical debridement
prevent = podiatrist, correct footwear

99
Q

Diabetic foot sepsis is a ___ problem

___ builds up in compartments -> blocks __> ____

A

pressure - pus builds up + blocks capillary flow = necrosis

100
Q

Distal DVT are found in ____

A

calves

101
Q

Proximal DVT are found in ___

A

popliteal/femoral - above knee in the thigh

102
Q

Unprovoked DVT = _____

More/less likely to have recurrency

A

idiopathic

more

103
Q

DVT of know cause =

A

provoked

104
Q

PTS - post-thrombotic syndrome is when ____

signs =

A

valves are incompetent after DVT

pain, oedema, hyperpigmentation, eczema, varicosity, ulcers

105
Q

Tests for DVT =

A

D-dimer and Wells score

106
Q

If D-dimer is low and Wells score moderate/high for DVT =>

A

imaging needed

107
Q

If D-dimer high and suspect DVT then

A

need imaging

108
Q

Gold-standard imaging for diagnosing DVT

A

Doppler US

109
Q

Gold standard for PE diagnosis

A

CTPA

110
Q

Better than CTPA for small vessel PE diagnosis

A

V/Q scan

111
Q

In PE CXR can show:

A 
pleural effusion (present in 5%)
wedge-shaped infarct
112
Q

Gold standard for treatment of DVT =

A

anticoagulants

113
Q

treatment for DVT:

A 
anticoagulants
thrombolysis (if symptomatic)
analgesia
compression stockings
IVC filter (for proximal DVT temporarily)
114
Q

Thrombolysis in PE if:

A 
haemodynamically unstable (h/lbp + ^HR)
or haemodynamically stable w risk of deteriorating
115
Q

phlegmasis =

A

extensive DVT impairs arterial flow - life threatening and aggressive treatment

116
Q

Gold-standard treatment for PE:

A

Anti-coagulation

JazCardio (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions