Vascular System - Acute & Chronic Ischaemia Flashcards
(290 cards)
1
Q
What is the Circulatory system transport for
A
Oxygen
Nutrients
Waste products
2
Q
What does the circulatory system consist of
A
Heart
Vessels (arteries, capillaries, veins)
Lymphatics (to a lesser extent)
3
Q
General structure of arteries and veins
A
Composed of 3 layers - tunics
Tunica intern, tunica media, tunica externa
Lumen
4
Q
Lumen
A
Central blood-containing space surrounded by tunics
5
Q
What are capillaries composed of
A
Endothelium with sparse basal lamina
6
Q
Structure of elastic (conducting) arteries
A
Large lumen allows low-resistance conduction of blood
Contains elastin all 3 tunics
7
Q
Where are elastic (conducting) arteries found
A
Thick-walled arteries near the heart; the aorta and its major branches
8
Q
Function of elastic (conducting) arteries
A
Withstand and smooth out large blood pressure fluctuations
Allows blood to flow fairly continuously through the body
9
Q
Structure of muscular (distributing) arteries and arterioles
A
Have thick tunica media with more smooth muscle and less elastic tissue
Active in vasoconstriction
10
Q
Arterioles
A
Smallest arteries; lead to capillary beds
Control flow into capillary bed via vasodilation and constriction
11
Q
When are veins formed
A
When venules converges
12
Q
What are veins composed of
A
3 tunics, with a thin tunica media and thick tunica externa consisting of collage fibres and elastic networks
13
Q
Veins as capacitance vessels
A
Blood reservoirs
Contains 65% of the blood supply
14
Q
Special adaptations of veins
A
Large diameter BP, which offer little resistance to flow
Valves, which prevent back flow of blood
15
Q
Venous sinuses
A
Specialised, flattened veins with extremely thin walls (e.g. coronary sinus of the heart and dural sinuses of the brain)
16
Q
Anastomosis
A
Connection between two structures that are normally diverging e.g. arteriovenous
17
Q
What is blood flow equivalent to
A
Cardiac output (CO), considering the entire vascular system
18
Q
What is blood flow, or tissue perfusion, involved in
A
Delivery of oxygen and nutrients to, and removal of waste from tissue cells
Gas exchange in the lungs
Absorption of nutrients from the digestive system
19
Q
What is blood pressure
A
Force per unit area exerted on the wall of a blood vessel by its contained blood
20
Q
Main factors influencing BP
A
Cardiac output (CO) Peripheral resistance (PR) Blood volume
21
Q
Blood pressure eqn
A
CO x PR
22
Q
What is blood flow directly proportional to
A
The difference in bp between two points in the circulation
23
Q
What is blood flow inversely proportional to
A
Resistance
R is more important than difference in bp between 2 points in the circulation
24
Q
Systolic pressure
A
Pressure exerted on arterial walls during ventricular contraction
25
Diastolic pressure
Lowest level of arterial pressure during a ventricular cycle
26
Pulse pressure
The difference between systolic and diastolic pressure
27
Calculating MAP
Diastolic pressure + 1/3 pulse pressure
28
Venous BP throughout cardiac cycle
Steady and changes little during the cardiac cycle
29
Factors aiding venous return
Respiratory pump
Muscular pump
Valves prevent back flow during venous return
30
APBI
Ankle: Brachial Pressure Index
| An objective vascular measurement of the vascular supply to the lower limbs
31
Body sites to palpate pulse
```
Temporal artery
Facial artery
Common carotid artery
Brachial artery
Radial artery
Femoral artery
Popliteal artery
Posterior tibial artery
Dorsalis pedis artery
```
32
Autoregulation
Automatic adjustment of blood flow to each tissue in proportion to the requirements at any given point in time
33
What does atherosclerotic disease have a predilection for
```
Carotid bifurcation
LAD
Aortic bifurcation
Common bifurcation
Superficial femoral
Aorta just distal to left (subclavian)
```
34
Vascular disease - arterial
Narrow and block
Expand and pop
Embolus
35
What points does an aneurysm have a predilection for
Abdominal aorta
Popliteal Arteries
All the vessels
36
Embolus
A mass of clotted blood or other material
| Brought by the blood from one vessel and forced into a smaller one, obstructing the circulation
37
What does a decrease in tissue perfusion promote
Compensatory mechanisms e..g vasodilation, development of collateral vessels and anaerobic metabolism
38
True aneurysm
When an aneurysm involves an intact attenuated arterial wall or thinned ventricular wall of the heart
Involves all 3 layers
39
When does an arterial dissection arise
Tear in the intima
| When blood enters the arterial wall itself, a haematoma dissecting between its layers
40
False aneurysm (pseudo-aneurysm)
Defect in the vascular wall leading to an extravascular haematoma
Does not consist of the true layers of the arterial wall
41
Saccular aneurysms
Spherical out pouching
Vary from 5-20 cm in diameter
Often contain thrombus
42
Fusiform aneurysms
Involve diffuse, circumferential dilation of a long vascular segment
Vary in diameter (up to 20cm)
43
Factors of pathogenesis of aneurysms
The intrinsic quality of the vascular wall connective tissue is poor
The balance of collagen degradation and synthesis is altered
The vascular wall is weakened through loss of smooth muscle cells
44
Examples of poor intrinsic quality of the vascular wall
1. Marfan syndrome – defective synthesis of fibrillin
2. EDS – defective type III collagen causing weak vessel wall
3. Vit C deficiency – altered collagen cross-linking
45
When does ischaemia of the inner media occur
When there is atherosclerotic thickening of the intima “increases the distance that oxygen and nutrients must diffuse”
46
Factors predisposing weakening of arterial wall
```
Atherosclerosis
HTN
Trauma
Vasculitis
Congenital defects
Infections
```
47
How can mycotic aneurysms originate
From embolisation of a septic thrombus, usually as a complication of infective endocarditis
By circulating organisms directly infecting the arterial wall
48
Syphilitic aneurysms
3' syphilis is now a rare cause of aortic aneurysms
| Ischaemic injury can be caused by obliterative endarteritis
49
What are AAA's associated with
Atherosclerotic plaque in the intima compresses the underlying media
50
Risk factors for AAA
Men
Smokers
Age 50+
Atherosclerosis
51
Where are AAA's usually found
Usually positioned below the renal arteries and above the bifurcation of the aorta
Can be saccular or fusiform
52
Consequences of AAA
Rupture into the peritoneal cavity or retroperitoneal tissues with potentially fatal haemorrhage
Obstruction of a branch vessel resulting in ischaemic injury of downstream tissue
Embolism forms atheroma or mural thrombus
53
Px of AAA
Abdominal mass (pulsating) that simulates a tumour
54
When can aortic dissection be catastrophic
If the dissection then ruptures through the adventitia and haemorrhages into adjacent spaces
55
Aortic dissection classification
Type A dissection
| Type B dissection
56
Type A dissection - aortic dissection
```
More common (dangerous) proximal lesions
Involving either both ascending & descending aorta or just the ascending aorta
```
57
Type B dissection - aortic dissection
Distal lesions usually beginning distal to the L subclavian artery
58
Classical clinical symptoms of aortic dissection
Sudden onset of excruciating pain:
Beginning in the anterior chest
Radiating to the back between the scapulae
Moving downward as the dissection progresses
Confused with that of MI
59
Pathogenic mechanisms of vasculitis
Immune-mediated infl
Direct invasion of vascular walls by infectious pathogens
Infections can indirectly induce non-infectious vasculitis - by generating immune complexes or triggering cross-reactivity
60
Types of vasculitis
Large vessel
Medium vessel
Small vessel
61
Thromboangitis Obliterans (Buerger disease)
Distinctive disease that often leads to vascular insufficiency
Segmental, thrombosing, acute and chronic infl of medium-sized and small arteries
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Epidemiology of Buerger disease
Occurs almost exclusively in heavy cigarette smokers, usually before the age of 35
63
Pathogenesis of Buerger disease
Strong rship to cigarette smoking
| Genetic influences - certain HLA halotypes
64
Clinical features of Buerger's disease
Cold sensitivity of the Raynaud type in the hands
Pain in the instep of the foot
Severe pain, related to the neural involvement
Chronic ulcerations of the toes, feet or fingers
65
What can bring drastic relief from further attacks of Buerger's diesase
Abstinence of cigarette smoking
66
Varicose veins
Abnormally dilated, tortuous veins
| The superficial veins of the upper and lower leg are typically involved
67
What are varicose veins produced by
Prolonged, increased intraluminal pressure
| Loss of vessel wall support
68
What can happen when legs are dependent for prolonged periods
Venous pressure in these sites can be markedly elevated (up to 10x) and can lead to venous stasis and pedal oedema
69
Why is there a higher incidence of varicose veins in females
A reflection of the elevated venous pressure in lower legs caused by pregnancy
70
Most disabling sequelae of varicose veins
Incl persistent oedema in the extremity and ischaemic skin changes manifesting as stasis dermatitis and ulcerations
71
Where do venous ulcers usually occur
Gaiter areas
72
Thrombosed deep veins vs superficial
Embolism from the superficial veins is rare but thromboembolism is relatively frequent in thrombosed deep veins
73
Venous leg ulcers pathophysiology
80-85% of all cases develop when persistently high bp in the veins of the legs (venous htn) causes damage to the skin, which eventually breaks down and forms an ulcer
74
Interchangable names for venous thrombosis and infl
Thrombophlebitis
| Phlebothrombosis
75
Portal vein thrombosis
```
Peritoneal infections (peritonitis, appendicitis, salpingitis and pelvic abscesses)
Thrombophilic condn associated with platelet hyperactivity (e.g., polycythaemia vera)
```
76
Mechanical factors that slow venous return and promote DVT
Congestive heart failure
Pregnancy
Obesity
77
Trousseau sign
Venous thromboses classically appear at one site, disappear and then reoccur in other veins – migratory thrombophlebitis
78
Local manifestations of thrombi in legs incl
```
Distal oedema
Cyanosis
Superficial vein dilation
Heat
Tenderness
Redness
Pain
```
79
PE as a serious complication of DVT
Fragmentation/ detachment of the whole venous thrombus
Can be 1st manifestation of thrombophlebitis
Outcome ranges from no symptoms to death
80
What does Raynaud's phenomenon result from
Exaggerated vasoconstriction of digital arteries and arterioles
81
What does secondary Raynaud's refers to
Vascular insufficiency of the extremities 2’ to arterial disease caused by SLE, scleroderma, Buerger disease or even atherosclerosis
82
Peripheral Arterial Disease
Term used to describe a narrowing or occlusion of the peripheral arteries, affecting the blood supply to the lower limbs
83
What is PAD most caused by
Atherosclerosis which narrows the affected arteries. This limits blood flow to the affected limb
84
Epidemiology of PAD
More common in males
| Prevalence rises with age
85
What diseases are PAD associated with
Coronary artery disease
| Cerebrovascular disease
86
Fontaine classification of PAD
```
Stage I - Asymptomatic
Stage IIa - mild claudication
Stage IIb - moderate to severe (short distance) claudication
Stage III - ischaemic rest pain
Stage IV - ulceration or gangrene
```
87
Most common symptom of PAD
IC
88
Intermittent claudication
Exercise–induced muscle pain
Most commonly in the calf, thighs, buttocks
Worse walking uphill or hurrying
Relieved by rest <10 mins
89
Possible Intermittent Claudication sites
Buttock and hip
Thigh
Calf
Foot claudication
90
IC site - buttock and hip
Aortoiliac disease (Leriche syndrome triad)
91
IC site - thigh
Aortoiliac or common femoral artery
92
IC site - upper 2/3 of the calf
Superficial femoral artery
93
IC site - lower 1/3 of the calf
Popliteal artery
94
IC site - foot claudication
Tibial or peroneal artery
95
Types of ddx of PAD
Vascular
Neurological pain
MSK
96
Vascular ddx for PAD
```
Aneurysm
Limb trauma
Radiation exposure
Vasculitis or ergot use for migraines
Popliteal entrapment syndrome
Chronic venous disease
```
97
Neurological ddx for PAD
```
Neurospinal (e.g. disc disease, spinal stenosis, tumour)
Neuropathic causes (e.g. DM, alcohol abuse)
```
98
Prevalence of Chronic Limb Threatening Ischaemia
1 - 2%
99
When is Chronic Limb Threatening Ischaemia seen
When two or more levels of arterial tree are diseased
100
Ischaemic rest pain
Severe pain at rest due to inadequate oxygen perfusion
101
Chronic limb threatening ischaemia and Critical limb threatening ischaemia
Chronic limb threatening limb ischaemia can develop into Critical Limb ischaemia
102
Where do ischaemic ulcers form
At sites of increased focal pressure
Malleoli, tips of toes, metatarsal heads, heels
Usually dry and punctuate
103
What condn is dry gangrene most likely seen in
DM
103
When does dry gangrene develop
When blood flow to the affected area is impaired
The tissue dries up and may be brown to purplish-blue to black in colour
Can be left to auto-amputate or can be amputated after revascularisation
104
Wet gangrene
Liquefactive necrosis due to infection
| The tissue swells and blisters and is called ‘wet’ because of pus
105
Why is wet gangrene v serious
Infection from wet gangrene can spread quickly throughout the body
106
Treatment of wet gangrene
Needs IV high dose Abx
| Revascularisation, debridement +-/- amputation
107
Clinical exam for PAD
```
Inspection (scars, ulcers, gangrene, venous guttering)
Buerger's test
Palpation of pulses
Auscultation for bruits
APBI measurement
```
108
Vascular ix for PAD
Duplex ultrasound
CT angiography
Magnetic resonance angiography
109
Lifestyle modifications for asymptomatic PAD pts or mild claudication
Smoking cessation
Exercise
Diet control
110
Pharmacological therapy for asymptomatic PAD pts and mild claudication
Risk factor modification (control BP, diabetes, dyslipidaemias)
Antiplatelet therapy (clopidogrel 75mg OD)
Cholesterol lowering medication (atorvastatin 80mg OD)
111
Mx for short distance claudication - Lifestyle modification
Supervised exercise classes
112
Mx for short distance claudication - Pharmacological
BP/ DM/ Cholesterol control
Antiplatelet and statins
Naftidofuryl/ cilostazol
113
Mx of short distance claudication - endovascular
Angioplasty +/- stent placement
114
Mx of short distance claudication - Surgical
Endarterectomy
| Peripheral bypass graft: autologous vein, prosthetic (long blockages of vessels)
115
Angioplasty
Pressure controlled balloon inflation to fracture arterial plaque and remodel the artery
116
What's angioplasty most effective for
Short focal stenoses without heavy calcification
| Excessive calcification is resistant to angioplasty
117
Complications of angioplasty
```
Arterial puncture site haemorrhage
Arterial rupture
Dissection
Distal embolism
Contrast induced nephropathy
```
118
Stents
Supportive framework that apply radial force to diseased arteries and promotes vessel remodelling
119
What are stents made from
Stainless steel or Nitinol
120
2 types of stents
Balloon expandable
| Self-expanding stents
121
Surgical revascularisation
Endarterectomy
| Surgical bypass
122
When is endarterectomy used in surgical revascularisation
For lesions in readily accessible sites, such as common femoral artery
123
Which surgical bypasses require a prosthetic graft
Infra-inguinals bypasses
Aorta-iliac
Femoral-femoral crossover
Axillo-bifemoral
124
Complications of surgical revascularisation
```
Bleeding
Infection
Distal embolism
Limb loss
Heart/ lung/ kidney complications
DVT
Death
```
125
Mx of CLTI
```
Lifestyle modification
Pharmacological therapy
Wound care - conservative mx
Revascularisation
Amputation
```
126
Leading cause of amputation in western world
PAD
127
How many more times likely are diabetics to suffer amputation
8-12x
128
What must be considered before amputation
Rehabilitative potential of the pt
Level and pattern of vascular disease
Likely healing
129
Common amputation sites
```
Toe amputation
Ray amputation
Tran-metatarsal amputation
Below knee amputation
Above knee amputation
```
130
Toe amputation
Removal of toe through proximal phalanx
131
Ray amputation
Removal of toe through metatarsal bone
132
Trans-metatarsal amputation
Amputation of all the toes through mid-metatarsal bones
133
Below knee amputation
Through tibia 10-12 cm distal to tibial tuberosity
| Through fibula 2cm proximal to tibia
134
Above knee amputation
At mid-femoral level >15 cm from tibial plateau
135
Amputation complications
```
Failure of wound to heal
Flap necrosis
Wound infection
Post amputation pain
Stump haematoma
Flexion contractures
Psychological problems
```
136
Why should rehab be started ASAP after amputationn
Prevents flexion contractures
137
What happens after stump heals - amputation
Elasticated compression, stump socks fitted to shrink stump to an acceptable size for fitting for prosthesis
138
When is limb fitting usually delayed until
>6/52 post-op to allow stump oedema to subside
139
Prognosis for IC
Variable, over 5-years most people continue to have stable claudication
10-20% develop worsening symptoms
5-10% develop critical limb ischaemia
Amputation in required in 1-2%
140
Prognosis of CLTI
High risk of amputation and premature death
50 - 90% will have a revascularisation procedure
1/3 require LL amputation if no revascularisation
5-yrs all cause mortality of 50%
141
ALI
A sudden decrease in limb perfusion that causes a potential threat to limb viability in pts who present within 2 weeks of the acute event
Surgical emergency
142
Incidence of ALI
1.5 cases per 10,000 people per yr but is a frequent missed or delayed dx
143
Aetiology of ALI
Embolus
Thrombosis
Trauma
144
Aetiology of ALI - Embolus
Cardiac source - AF, MI, endocarditis, valvular disease, atrial myxoma, prosthetic valves
Arterial source - aneurysms, atherosclerotic plaque
145
Aetiology of ALI - thrombosis
```
Vascular grafts
Atherosclerosis
Thrombosis of aneurysm
Entrapment syndrome
Hypercoaguable state
Low flow state
```
146
Aetiology of ALI - Trauma
Blunt
Penetrating
Iatrogenic
147
6P's of acute ischaemia
```
Pain
Pulselessness
Pallor
Paresthesia
Paralysis
Poikilothermic (perishingly cold)
```
148
Imaging for ALI
CT angiography - distinguishes between thrombosis and embolism
Bedside Doppler ultrasound scan
149
Initial mx for ALI
```
ABC
Analgesia
FBC
U&Es
Baseline clotting profile
Heparin
IV access and IV resus
ECG
Catheterise and hourly UO
```
150
Giving heparin for ALI
Once the dx of acute arterial occlusion has been made the pt should immediately receive an IV-heparin bolus of 5,000 units followed by continuous infusion
151
What does mx of ALI depend on
Type of occlusion (thrombosis or embolus)
Location
Duration of ischaemia
Neurological deficit
Co-morbidities
Type of conduit (artery or graft, the risks of treatment and the viability of the limb)
152
Endovascular therapies for ALI
Percutaneous catheter-directed thrombolytic therapy
| Percutaneous mechanical thrombus extraction
153
Surgical mx for ALI - emboli cause
Surgical embolectomy
Bypass surgery (if there is insufficient flow back)
Local intra-arterial thrombolysis
Amputation if limb is unsalvageable
154
Thromboembolectomy
Balloon connected to Fogarty catheter inflated removing thrombi
155
Complications of ALI
Compartment syndrome
| Reperfusion injury
156
Compartment syndrome - complication of ALI
Reperfusion of ischaemic muscles can cause oedema and increased compartmental pressure
157
Reperfusion injury - complication of ALI
Products of cell death (e.g K, CO2 and myoglobin) are released when blood flow to ischaemic limb is restored
158
What can reperfusion injury result in
```
Rhabdomyolysis
Cardiac dysrhythmia
AKI
Multi-organ failure
Disseminated IV coagulation
```
159
Mortality of ALI
15 - 20% with about a 1/3 of deaths resulting from metabolic complications associated with revascularisation e.g. acidosis and hyperkalemia
160
Limb prognosis of ALI
Related to the severity of arterial disease, the acuteness of ischaemia onset, and how rapidly perfusion is restored
161
Causes of lower limb loss in less developed countries
Industrial, railway, farming accidents where safety measures are poor
162
Causes of lower limb loss in western world
90% vascular (60% PVD/ 30% DM)
Trauma - 5%
Neoplasm - 1%
Other (infection/ psychiatric ) - 4%
163
Levels of lower limb amputation
```
Hemi- pelvictomy
Hip disartictlatrion
Transfemoral
Through knee
Transtibial
Symes (Ankle disarticulation)
Chopart (mid-tarsal)
Lisfrank (traso-metatrsal)
```
164
What does the energy required after amputation depend on
Level of amputation
Length of stump
Pt's health/ commodity
Reason for amputation
165
Which level of amputation has the biggest increase in energy needed for gait above normal
Bilateral transfemoral - 200%
166
ICF
International Classification of Functioning, Disability and Health Framework
Forms basis of rehab med
167
What does ICF demonstrate the rship between
Health (disorder/ disease)
Function - body functions & structure, activity, participation
Disability - impairment, activity limitation, participation restriction
168
Role of rehab - pre-amp
Pt education
Defining expectations (ICE)
Determining suitability for artificial limb
Phantom limb prophylaxis
169
Determining suitability for artificial limb
Energy needed
Contratures
Allodynia
Cognition
170
PLP prophylaxis
PLP is associated with pre-operative pain and can be reduced with analgesia at least 72 hrs before surgery and 48 hrs after
171
Role of rehab immediately post-amp
Reduce complications
Maximise independence
Minimise pain and discomfort
Co-ordination and better use of resources
172
Role of amp rehab on the ward
Post-op care
Artificial limb fitting and training
Long term follow up
173
What does artificial limb fitting and training involve
Goal establishment
Stump casting and measurement and limb prescription from week 3 post-op
Gait retraining
Education on skincare, and artificial limb maintenance
174
Long-term follow up - rehab
Checking if new limb is required
Checking for changes in stump size and condn
Checking for changes in residual
Pain management and medical complications
175
Early walking aids (EWAs)
Used as early 5-7 days post amp
Temporary devices
Useful as part of the assessment process for suitability of artificial limb
176
Examples of EWA
Post-amputation mobility aid for TT
| Femurett for TF
177
Gait retraining sequence
Full wt-bearing and transfer
Walking with 2 parallel bars
Walking with 2 stick between parallel bars
Walking with 1 stick outside bars
178
Gait challenges for an amputee
Ground clearance
Times initial (Heel) contact without proprioception
Loss of ability to aboard energy
Maintaining mid-stance on the prosthetic limb
Loss of foot eversion/ inversion AKA stopping knee from buckling
Transmit centre of gravity
Loss of push off in terminal stance
179
Phantom sensation
Feeling the missing part
180
Phantom pain
Pain in missing part
181
Superadded Phantom
Tight band, tight shoes, tight wristwatch over the missing part
182
Incidence of PLP
54% of all amputees
| 100% of all LL amputees
183
Mechanism of PLP
Unknown
Lacking peripheral input
Central cortical reorganisation
Psycho factors - grieving, depression
184
Why is PLP not a peripheral nervous phenomenon
Changes with time (telescoping)
| Changes with interceptive stimuli e.g. micturition
185
Pharmacological mx of PLP
Analgesic ladder - paracetamol, NSAIDs, opioids
Anticovulsants
Low dose amitriptyline - 10mg then increase gradually up to 50mg
Treatment of clinical depression (if applicable)
Misc - baclofen, botulinum, beta-blockers
186
Examples of anticonvulsants
Gabapentin
Pregabalin
Carbamazepine
187
Physical mx of PLP
```
Massage
Heat
Accupuncture
Electromagnetic
TENS
Electro-accupunture
```
188
Psychotherapy as mx for PLP
Distrcation
Relaxation
Autogenic hypnosis (controlling the phantom hypnosis)
Biofeedback (Ramachandran's Mirror Box)
189
Local stump complications after amp
Skin breakdown/ ulcers
| Pressure areas
190
What causes local stump complications
```
Poor donning technique
Poor socket
Associated neuropathy
Change in stump volume
Change in gait pattern
Infection with or without ischaemia
```
191
Mx for local stump complications
Establish cause
Minimise prothetic use
Dynamic socket fitting/ repeat casting
Abx, regular dressing and reviews
192
Components of TT artificial limb
```
Socket
Suspension mechanism
Adaptor
Shin tube
Shock/ torque absorber
Foot
```
193
Factors that would influence unemployment after amputation
Occupational ability
| Work environment
194
What affects occupational ability after amputation
Individual - psychology, physical
| Social factors - family support, organisational support
195
Work environment affecting employment after amputation
```
Legislations
Social security system
Welfare rights
Labour market
Employer - size of firm, work force flexibility
```
196
How does ionised state of drug affect passive diffusion
```
Unionised = lipid soluble = easy passage
Ionised = water soluble = difficult passage
```
197
What does level of ionisation depend on
Dissociation constant Ka acid or base
| pH of bodily fluid
198
Recommended treatment for aspirin overdose
NaHCO3
199
Examples of unionised drugs
Digoxin (for AF)
| Prednisolone
200
Major rate-limiting factor for drugs
BBB - blood brain barrier
201
First order kinetics - exponential
As conc of drugs increases, rate of reaction (or breakdown of drugs) goes up
Has predictable half life
202
Zero order kinetics
Saturation = rate limited
Limited capacity of body to process drug
Dose increase - sudden toxicity
203
Bioavailability
Proportion of parenteral drug that passes into systemic circulation after administration
204
Improving bioavailability
Change in formulation
Route
Concurrent use of inhibitor
205
Apparent volume of distribution
Reflects amount of drug in plasma after being taken up
| Total amount of drug in body/ plasma conc
206
Clearance of drugs
Amount of plasma totally cleared of drug
| Elimination of drug from plasma
207
Main parameters of half-life
Clearance
| Volume of distribution
208
How does clearance affect half life
High clearance = shorter half life
209
How does volume of distribution affect half life
High volume volume of distribution - longer half life
210
When will a drug reach a steady state
When drugs are given at a constant rate and after 5 half-lives
Either continuous infusion or intermittent chronic dosing
211
When do you use a large priming or loading dose
Quicker effect
| Useful in urgent situation e.g Abx for sepsis
212
What if drug t 1/2 is short
Give larger dose frequently
Inhibit clearance
Reduce movement of drug to plasma
Modify formulation
213
Examples of modified release formulations
Sustained release tablets
| Depot injectables
214
Atheroma
Cholesterol plaque
215
Risk factors of ALI
```
DM
HTN
Increased cholesterol & triglycerides
AF (a/c blood clots)
Obesity
Fhx of PVD
Trauma (immobilised --> DVT can embolise)
Male sex
```
216
Spinal stenosis as ddx of IC
Pain gets better when walking uphill due to simian posture (extension) but worse in IC
217
Why are IC pts advised to exercise to point of pain and past
Hypoxia promotes angiogenesis
218
Sex difference of venous ulcers
F > M
219
Sex difference of arterial ulcers
M < F
220
Sex difference of neuropathic ulcers
F = M
221
Risk factors of venous ulcers
Previous DVT
Varicose veins
Incompetent valve
222
Risk factors of arterial ulcers
Smoking
HTN
DM
223
Risk factor of neuropathic ulcers
DM
224
Pain levels of different ulcers
Venous - not painful
Arterial - pressure areas
Neuropathic - usually painless, nerves are dead
225
Site of venous ulcers
Gaitar areas
226
Site of arterial ulcers
Pressure areas e.g. in between toes, heel
227
Vein in venous ulcers
Full, dilated
228
Veins in arterial ulcers
Not visible
| Guttering
229
Veins in neuropathic ulcers
Veins are normal
230
Temperature of venous ulcers
Normal to warm
231
Temp of arterial ulcers
Cool
232
Temp of neuropathic ulcers
Warm or cold
233
Appearance of venous ulcers
Shallow and flat
Irregular margin
Slough at base
Moderate to heavy exudate
234
Appearance of arterial ulcers
Punched out
Regular shape
Presence of necrotic tissue
235
Apperance of neuropathic ulcers
Callous
Trophic
Insensate
Macerated
236
Site of neuropathic ulcers
Plantar aspect of foot
Tip of toe
Lateral to 5th metatarsal
237
Condn of leg when venous ulcer is present
Hemosiderin staining
Thickening and fibrosis
Eczematous and itchy skin
Normal CRT
238
Condn of leg when arterial ulcer is present
Thin, shiny skin
Pallor on leg elevation
Absent/ weak pulses
Delayed CRT
239
Treatment of venous ulcers
Compression stockings - check ABPI
Leg elevation
Surgical mx
240
Treatment of arterial ulcers
Revascularisation
Anti-platelet med
Mx of risk factors
241
Treatment of neuropathic ulcers
Off-loading of pressure
| Topical growth factors
242
Features of asymptomatic PAD
Abnormal/absent pedal pulses
Age 70+
Age 50-69 and hx of smoking and DM
243
Tunica interna composition
Thin single layer of endothelium
244
Tunica media composition
Thicker contractile tissue made from circularly arranged elastic fibres, connective tissue and smooth muscle cells
245
Tunica externa composition
Connective tissue
246
Bifurcation
Where an artery splits into 2, common site for cholesterol build up and thrombus formation
247
Mural thrombus
Thrombus attaching two chamber walls
248
Where is mitral valve found
Between left atrium and left ventricle
249
Claudication hx
Exercise tolerance - how far can they work
How long to rest for
Rest pain?
250
When should duplex ultrasound not be done when investigating ischaemia
Absent limb pulses
251
Pre op work for vascular surgery
NTProBNP
LFT
Fibroscan
Consultant anaesthetic review
252
How is chronic limb ischaemia clinically defined
Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
Presence of ischaemic lesions or gangrene
ABPI less than 0.5
253
Acute-on-chronic ischaemia
There is an acute often embolic event in a pt w/ previous PAD
254
What can cause a falsely high ABPI
Calcification and hardening of the arteries so any ABPI value >1.2 should be interpreted with caution
255
What can chronic limb ischaemia result in
Sepsis (2’ to infected gangrene)
Acute-on-chronic ischaemia
Amputation
Reduced mobility and QoL
256
Signs of Chronic Limb Ischaemia
```
Pale and cold limbs
Weak/ absent pulses
Limb hair loss
Skin changes (atrophic skin, ulceration or gangrene)
Thickened nails
```
257
Sensitive sign of ALI caused by emboli occlusion
A normal, pulsatile contralateral limb
258
What can cause a mural thrombus
Recent MI
259
Surgical mx for ALI - thrombotic cause
Local intra-arterial thrombolysis
Angioplasty
Bypass surgery
Thrombolectomy
260
Irreversible limb ischaemia
Mottled, non-blanching appearance
| Requires urgent amputation or taking a palliative approach
261
What can release of substances in reperfusion injury cause
K+ - hyperkalemia
H+ - acidosis
Myoglobin - significant AKI
262
Leriche syndrome triad
Claudication
Absent femoral pulses
Erectile dysfunction
263
Conditions for use of compression stockings (venous)
Patent arteries and ABPI above 0.8
264
What does an ABPI of 1.3+ indicate
Abnormally hard vessel e.g. calcification
| Common in diabetics
265
When would we hear biphasic signals on the Doppler
Beginning of arterial disease
| Old age - vessels losing elasticity
266
Lipodermatosclerosis
Induration, pigmentation and infl of skin
267
When does an ulcer become chronic
4 weeks
268
Ulcers in which areas suggest pressure sores
Sacrum
Greater trochanter
Heel
269
Slough
Mixture of fibrin, cell breakdown products, serous exudate, leukocytes and bacteria
Does not always imply infection
270
Granulation tissue
Deep, pink, gel-like matrix contained within a fibrous collagen network
Evidence of a healing wound
271
What does associated lymphadenopathy w/ ulcers suggest
Infection or malignancy
272
Signs of high cholesterol in eyes
Corneal arcus
| Xanthelasma
273
Signs of central cyanosis
Blue tongue and mouth
274
What can radio-radial delay be caused by
```
Aortic dissection (Type A)
Difference in bp (>20 mmHg)
```
275
What can radio-femoral delay be caused by
Type B aortic dissection
| Coarctation of the aorta
276
Differentiating between thrombotic and embolic cause of ALI
Pts with cardiac sources will have no hx of IC or PAD, and ABPI will not be low in both limbs
277
ABCDE approach - A
Voice, breath sounds
278
ABCDE approach - treatment of A
Head tilt, chin lift
Oxygen (15 litres)
Suction
279
ABCDE approach - B
```
Resp rate
Chest wall movements
Chest percussion
Lung auscultation
Pulse oximetry
```
280
ABCDE approach - treatment of B
Rescue breaths
| Bag-mask ventilation
281
ABCDE approach - C
```
Skin colour, sweating
CRT
Pulse rate
Heart auscultation
BP
ECG
```
282
ABCDE approach - treatment of C
Cannulate:
Give 500ml IV bolus for hypotension (saline or Hartmann's)
Take bloods - FBC, cross-match, LFTs, U&E's, ESR/CRP, ABG/VBG
283
ABCDE approach - D
Level of consiousncess - GCS
AVPU
Limb movements
Blood glucose
284
ABCDE approach - E
Expose skin - looking for lesions, erythema, wounds, fractures, rashes etc
Temp
285
What is key in ABCDE approach
Checking to see if interventions have helped
286
Leriche syndrome triad
IC
Erectile dysfunction
Absence of femoral pulse
287
Types of thrombotic ischaemia
Incomplete
| Complete
288
Mx of incomplete ischaemia - thrombotic
Angiography to map out occlusion and plan intervention
289
Mx of complete ischaemia - thrombotic
Surgical bypass
| Angio and thrombolysis delays mx - takes too long
