Vascular & Ihd

Front 1

4 big risk factors for PERIPHERAL VASCULAR DISEASE (PVD/ PAD/ POAD)

Back 1

DM
smoking
HTN
hyper-cholesterolaemia/ lipidaemia

Front 2

6 P's for acute limb ischaemia

Back 2

Pulseless
Perishingly cold
Pale
Paralysis
Pain on squeezing
Paresthesia

Front 3

Signs of acute limb ischaemia
(POAD inspection: PHU-PAV)

Back 3

Pale
Hair loss
Ulcers
Pigmentation/ gangrene
Amputations
Varicosities

Front 4

S&Ss of DVT
(remember: may be aysymp)

Back 4

unilateral swelling (oedema)
discomfort/ cramp
tender (weight-bearing)
warmth (rubor), fever
discolouration
PE
pyrexia
superficial vein distension

Front 5

Predisposing risk factors for DVT

Back 5

long haul flight
recent trauma / surgery
immobility
FH
cancer
obese
preg/ the pill
smoking

Front 6

how does heart increase O2 supply/ extraction

Back 6

increasing coronary blood flow

Front 7

3 special coronary adaptations

Back 7

↑capillary density
↑basal blood flow
↑O2 extraction

Front 8

which coronary artery is likely affected in an;
- anterior MI
- anterolateral MI
- lateral MI

Back 8

ant: LAD
ant-lat: LAD & circumflex
let: circumflex

Front 9

which coronary arteries likely affected in a;
- posterior MI
- inferior MI

Back 9

post: post interventricular (of RCA)
inferior: R marginal (other)

Front 10

3 INTRINSIC regulations of coronary blood flow

Back 10

- ↓PCO2 = coronary vasodilatation
- metabolic hyperaemia = ↑O2 extraction
- adenosine (from ATP metabolism) = vasodilatation

Front 11

2 EXTRINSIC regulations of coronary blood flow

Back 11

- symp control to heart B2 = vasoDILATATION
- adrenaline (adrenal medulla)--> B2 = coronary vasoDILATATION

(a1 = vasoCONSTRICTION to non-vital organs)

Front 12

which sympathetic GPC receptor signals via IP3 to cause smooth muscle vasoconstriction

which GPCR & 2nd messenger does it use

Back 12

a1 - Gq - phospholipase C - IP3 - Ca+

Front 13

which phase in cardiac cycle is coronary blood flow greatest?

what importance does this have in ↑HR

Back 13

diastole

↑HR= shorter diastole = ↓perfusion

Front 14

cerebral arteries: which 2 important blood vessels anastemose to form what

Back 14

Front 15

What protective regulation guards the brain against changes in MAP

Back 15

AUTOREGULATION from MYOGENIC resposne
when MAP ~70-105

Front 16

what danger does hypercapnia ↑PCO2 pose to the cerebral blood flow

Back 16

↑PCO2 = cerebral vasoDILATATION (overrides autoregulation)
ceretral hyperaemia

Front 17

calc cerebral perfusion pressure (CPP)
what effect does raised ICP have on cerebral blood flow

Back 17

CPP= MAP - ICP
↑ICP = ↓CPP

Front 18

concept of BBB
what is the BBB permeable/ impermeable to

Back 18

capillaries have highly sensitive, very TIGHT intracellular junction
Permeable: O2 & CO2, glucose (facilitated dif)
Impermeable: hydroPHILIC molecules (ions, proteins...)

Front 19

what the resistance in the po circulation like (compared to systemic)

what benefit does this have

Back 19

LOW resistance! = ↑flow

ABSORPTIVE forces > filtration (ie protects against po oedema)

Front 20

what the po vascular response to hypoxia and why

Back 20

vasoCONSTRICTION
diverts blood away from poorly ventilated areas

Front 21

difference between ischaemia & infarct

Back 21

ischaemia: impaired vascular perfusion, reversible

infarct: ischaemic NECROSIS (secondary to ischaemia) reversibility depends on regenerative ability of tissue.

Front 22

compare haemostasis & thrombosis

Back 22

haemostasis is physiological: maintain fluidity of blood & clot where appropriate

thrombosis: PATHOLOGICLA corruption of haemostasis

Front 23

causes of acquired hypercoaguability
(can also be genetic)

Back 23

MI, prosethetic heart valves, DIC
Ca
immobilisation
tissue damage
heparin-induced
(AF, cardiomyopathy, the pill, preg, smoking, sickle cell anaemia)

Front 24

changes in blood flow (stasis or turbulence) is part of Virchow's triad. How does this pathologically contribute to thrombosis

Back 24

platelets contact endothelium
activated clotting factors
activated endothelial cells

Front 25

4 examples of conditions predisposing to changes in blood flow

Back 25

DVT (impaired venous drainage)
AF
aneurysm
MS (left atrial dilatation)

Front 26

name 3 prothrombotic molecules elaborated by endothelial cells

Back 26

tissue factor
VWF
plasminogen activator

Front 27

risk factors causing injury to endothelial cells

Back 27

smoking
hyperlipidaemia
toxins
HTN
vasculitis
viruses
immune reactions

Front 28

3 types of thrombi

Back 28

arterial
mural (wall of endocardium)
venous

Front 29

morphology of an arterial thrombus (appearance)
what are they associated with
where are they commonly found

Back 29

lines of ZHAN, WHITE thrombus, mainly PLATELETS in a fibrin mesh.
- atherosclerosis
- carotid, femoral, cerebral

Front 30

morphology (appearance) of a venous thrombus

Back 30

RED - fibrin-rich, white head

Front 31

4 fates of a thrombus

Back 31

1) resolution (fibrinolysis)
2) organisation (granulation, recanalisation)
3) propagation/ embolism
4) DIC (clot)

Front 32

6 types of embolism

Back 32

thromboembolism
fat
air (can cause PE)
tumour
amniotic fluid
septic

Front 33

80% systemic emboli originate from where

what 3 common reasons

Back 33

heart! ♥
- AF, post-MI, aneurysm

Front 34

what's Monvkeberg Medial Calcific Sclerosis

Back 34

calcification of medium sized arteries in >50yrs

Front 35

differentiate artherosclerosis and arteriosclerosis

Back 35

arthero: INTIMAL
arterio: small arteries/ arterioles, hyaline & hyperplastic (DM & HTN)

Front 36

3 main targets for atherosclerosis

Back 36

cerebral arteries
coronary arteries
aorta

Front 37

what happens to the walls and linings of arteries in atherosclerosis

Back 37

raised focal lesion of intima
media degraded / weakened (aneurysm)
lipid core
fibrous cap

Front 38

in atherosclerosis, what effecst does lipoprotein oxidation have

Back 38

cytokine & GF release
direct damage endothelial & SM cells
ab response
trap MACs
engulfed by MACs
chemotactic

Front 39

what migrates and proliferates within an atheromatous plaque

Back 39

smooth muscle cells

Front 40

after smooth muscle proliferation and collagen deposition, what does a fatty streak become

Back 40

fibrofatty atheroma (plaque)

Front 41

what 2 syndromes come under acute coronary syndrome (ACS)

Back 41

unstable angina
AMI

Front 42

characteristic pain of angina pectoris

Back 42

visceral (myocardial hypoxia): dull, heavy, tight.
predictable
retrosternal
exertion, cold, heavy meals
may radiate
<30mins
ease at rest / GTN
(may be associated with: sweating, nausea, dyspnoea, faint)

Front 43

Ddx's chest pain

Back 43

Gi (reflux, ulcer, biliary colic)
musculoskeletal
pericarditis (posture related)
Resp- PE, pneumothorax (pleuritic)
tumour
MI!!
dissection

Front 44

3 Ix's for angina (type of CHD/ IHD)

NOT ACS

Back 44

☆ exercise testing☆ (& baseline ECG)
perfusion scanning (thallium)
CT coronary ANGIOGRAPHY (high risk)

Front 45

What's the difference betwees CCBs:
- dihydropyradines
- rate-liminting
eg for each
(clinical use)

Back 45

Dihydro: amlodipine - act on systemic vascular smooth muscle (HTN)

Rate-limiting: verapamil - myocyte specific (angina)

NB: diltiazem is an intermediate

Front 46

first line therapy for stable angina (e.g)
alternative if intolerant

Back 46

cardio-selective BBs (e.g. bisiprolol, atenolol)
GTN

intolerant: rate-limiting CCB (verapamil), isosorbide mononitrate (long-acting), K-channel opener (nicorandil)

Front 47

2nd line addition to 1st line management (BBs / GTN) of stable angina

Back 47

CCB (dihydropyradine- amlodipine)

NB: rate-limiting CCBs + BBs used with CAUTION!

Front 48

side effects of GTN

Back 48

flushing
light headed
headache

Front 49

If angina is due to atherosclerotic (CHD) disease, what 2/3 secondary preventative drugs do you add to:
1st line BB/ GTN
2nd line CCB (dihyd)

Back 49

★aspirin★
★statins★
?ACEI (consider)

Front 50

which 2 revascularisation procedures are appropriate for alleviating anginal symptoms

Back 50

CABG
PCI (percutaneous coronary intervention)

Front 51

which 3 vessels can be used in CABG

Back 51

internal thoracic artery (mammary artery)
radial artery
long saphenous vein

Front 52

Indications for CTCA
why (with a veiw to what)

Back 52

severe stable angina
unstable angina
ACS non-ST elevation
ASC ST-elevation treated with throbolytic therapy
view to REVASCULARISATION

Front 53

name some medical and haematological conditions that predispose to DVT/PE

Back 53

medical: vasculitis, ca, AMI, CHF, sepsis, nephritis, IBS, ==.

haem: polycythaemia, thrombosytosis, coagulation, antithrombin def, protein C/S def, prothrombin mutation, factor V leiden

Front 54

some medications predisposing to DVT

Back 54

oestrogen
oral contraceptives
IVDUs
chemo
heparin-induces

Front 55

S&Ss of DVT

Back 55

unilateral
calf: pain, red, inflamed, warm, pitting oedema, prominent superficial veins
fever

Front 56

Ix's for DVT

Back 56

FBC & U&Es (clotting)
★D dimer
★doppler USS

Front 57

management of DVT

Back 57

anticoagulation: ★LMWH & warfarin★
mobilisation
compression stockings

Front 58

management of phlegmasia dolens (severe DVT obstructing arterial flow in POAD) --> venous gangrene

Back 58

EMERGENCY
★IVC filter ★

Front 59

S&S's of PE

Back 59

tachypnoea, breathless, hypoxia, cyanosis
chest pain
haemoptysis
collapse
tachycardia
hypotension
↑JVP, pleural rub

Front 60

Ix's for PE

Back 60

FBC & U&Es (clotting)
ABG, CXR (effusion, collapse, consolidation, oedema, WEDGE-shaped infarcts)
★CTPA★
ECG/ echo (R heart strain)

?V/Q scan

Front 61

management of PE

Back 61

anti-coagulant: LMWH & warfain
thrombolysis: for major PE (RV dysfunction)
IVC filter

suspect DVT?- assess

Front 62

anticoagulant, warfarin, is an anti-thrombotic. How does it work?

how is it monitored

Back 62

vit K antagonist- blocks ability to activate ALL serine coagulation factors

INR

Front 63

anticoagulant, LMWH, is an anti-thrombotic. How does it work?

Back 63

binds to natural antithrobotic- ATIII to increase affinity and rate of coagulation factor Xa inactivation

Front 64

2 new direct oral inhibitors

Back 64

direct thrombin (lla) inhib- dabigatran
Xa inhib- fondaparinux

Front 65

egs of some thrombolytic drugs and how they work

Back 65

fibrinolytics: tPA, streptokinase.
activate plasminogen --> plasmin which degrades fibrin clots

accelerates resolution

Front 66

when are thrombolytics used

Back 66

when PCI for ST-elevation ACS can't be done within 90min

(not often used in VTE)

Front 67

Anticoagulants pose a risk of bleeding- in which pt's in particular

Back 67

DM
renal failure
>65
prev stroke
GI bleed
MI
anaemia

Front 68

how do you reverse overdose of warfarin and LMWH

Back 68

warfarin- Vik K/ fresh frozen plasma
LMWH- protamine sulphate

Front 69

2 types stroke & why

Back 69

Haemorrhagic: ⇧BP, weak walls (structural, inflam)

Ischaemic: thrombosis, embolism, hypoperfusion

Front 70

gender and race risk factor for stroke

Back 70

female♀
african-american

Front 71

what common heart abnormality is associated with ⇧ risk stroke

Back 71

AF

Front 72

Ix's stroke
- general
- caused by cardioembolism

Back 72

CT +/- angiography
MRI

ECG, ECHO

Front 73

medical treatment of stroke

Back 73

ANTIPLATELETS(aspirin, clopidogrel [ADP rec antag], tirofiban [GP rec antag])

THROMBOLYSIS- in emergency

statins- preventative
anticoagulants- AF
antihypertensives- HTN

Front 74

how do you differentiate between peripheral arterial disease and peripheral venous disease

Back 74

arterial: INTERMITTENT CLAUDICATION , ulceration, gangrene

venous: DVT signs, VARICOSE veins

Front 75

2 types of PAD

Back 75

atherosclerotic (obstructive)

aneurysmal

Front 76

major risk factors in PAD

Back 76

male
DM
SMOKING
HTN
age
...

Front 77

S&Ss PAD

Back 77

INTERMITTENT CLAUDICATION, cramping
pain on movement
ulceration, gangrene
distally --> proximally
pale, pulseless, cold, paralysis, paresthesia,
loss hair, loss pigmentation, amputations, nail changes
bruits

Front 78

Ix's for PAD (& critical limb ischaemia)

Back 78

★ANKLE-BRACHIAL PRESSURE INDEX★ (leg BP)
<1 = PAD

DUPLEX USS- artery flow
(MRA or arteriography)

Front 79

management of claudication/ PAD

Back 79

CONSERVATIVE:
- quit smoking
- lose weight
- exercise (collateral circulation)
- treat underlying HTN, DM, hypercholesterolemia

drugs when QOL poor (vasodilators)
surgery (angioplasty)

Front 80

what can PAD develop into if untreated- how would you distinguish this clinically

Back 80

CRITICAL limb ischaemia:
- REST pain (wakes at night)
- Ulcers
- Gangrene

Front 81

what's the GOLD standard treatment for critical limb ischaemia

Back 81

SURGERY / ANGIOPLASTY
treat underlying risks (e.g. DM, HTN, smoking,..)

Front 82

what are varicose veins

Back 82

VENOUS disease- incompetent VALVES
blood deep--> superficial veins (reverse)
venous HTN

Front 83

S&Ss of varicose veins

Back 83

dilated veins from venous HTN
pain, cramps, tingling, heaviness
oedema, ulcers, tenderness
gravitational

Front 84

what's chronic venous insufficiency

if untreated, what can it lead to

Back 84

irreversible skin damage from sustained venous HTN
relief on raising
--> chronic venous ulceration

Front 85

what's chronic venous ulceration

Back 85

break in skin >6/52 between MALLEOLUS & TIBIAL TUBEROSITY
develops from chronic venous insifficiency

Front 86

Ix's for varicose veins (venous disease)

Back 86

★DOPPLER USS★

Front 87

management of venous diseases/ varicose veins

Back 87

★COMPRESSion stockings★ + pt EDUCATION
ulcers- topical
SURGICAL removal
SCLEROSANT therapy

Front 88

ddx for ulceration

Back 88

PAD - distally
CVI- malleolus---> tibial tuberosity
VASCULITIS- proximal