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CP1 revision > Deck 4 > Flashcards

Deck 4 Flashcards

1
Q

Aneurysm definition

A

Arterial dilatation 1.5x normal. True has arterial wall, false has another tissue.
Can be fusiform, saccular/berry

Caused by weakening against BP

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2
Q

Common aneurysm sites

A

Aorta is most common, 60% of these are abdominal - 95% below renal artery braches. 40% thoracic.

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3
Q

Aneurysm RF

A

Atherosclerosis, male, 60+, DM, HTN, high LDL, CT disorders, coarctation of aorta, pregnancy, syphilis, infective endocarditis (mycotic aneurysm), syphilis

Aortic and popliteal are atherosclerotic
Berry aneurysms are developmental

Rupture rists are HTN, FHx of rupture, smokers and females

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4
Q

Aneurysm S+S

A

If intact, symptomless unless compressing nearby structures (e.g thoracic can compress aortic valve to give aortic regurgitation)
Ruptured causes Grey Turner (but also pancreatitis), hypotension, tachycardia, syncope, aenaemia, expansile abdomen mass, shock, severe left flank pain, vomiting, collapse

May also present with embolic events (mural thrombi)

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5
Q

AAA surveillance

A

all men >65, consider in younger if COPD, Vardio/cerebrovascular disease, european origin, FHx of AAA, hyperlipidaemia, smoking, HTN

  1. 0-4.5 is 2 yearly monitoring
  2. 5-5.4 is 3 monthly monitoring
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6
Q

Management

A

Acute: A->E, vascular team and haemorrhage protocol
USS to check for evidence of rupture
For ruptured, EVAR (balloon inflates graft, femoral access, can cause CKD through nephrotoxic contrast). Open surgery if complex.
Surgery if symptomatic, asymptomatic and >5.5cm or growing by >1cm/year

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7
Q

popliteal aneurysm S+S

A

85% of peripheral aneurysm
Normally asymptomatic, . Can be pulsatile mass behind knee, may compress tibial nerve, veins, give swelling. If ruptured, can cause acute limb ischaemia.
Could also thrombose and cause chronic limb ischaemia

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8
Q

Popliteal anuerysm investigation and management

A 
Duplex USS (screen, diagnostic for patency and thrombus), CT/MRI gives true lumen. 
Duplex surveillance if <2cm, or EVAR/open if larger
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9
Q

Aortic dissection types

A

De bakey 1 is ascending but carries on to descending
2 is ascending only, 3 is descending only.
stanford A is 1 and 2, B is 3.
First 10cm of aorta is most common.

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10
Q

Aortic dissection RF

A

HTN (main risk), smoking, hyperlipidaemia, thoracic AA, aortic valve abnormality, FHx dissection, previous cardiac surgery, trauma, cocaine, amphetamine, CT disease, pregnancy, syphillis

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11
Q

dissection S+S

A

Sharp chest pain, radiates to back, weak downstream pulse, difference in BP between arms, hypotension/shock if ruptured

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12
Q

Dissection complications

A

Pericardial tamponade, rupture into/out of artery, false lumen compressing nearby vasculature

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13
Q

Dissection management

A

HTN control, beta blockers, resection and replacement

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14
Q

HTN stage 1

A

Clinic>140/90, abm av >135/85

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15
Q

HTN stage 2

A

Clinic >160/100, amb >150/95

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16
Q

Severe HTN

A

> 180/100

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17
Q

Primary HTN

A

Essential HTN. Most common. RF are obesity, excess salt, inactivity, excess alcohol, stress, smoking, diabetes, older age, Fhx, ethnicity, males <65, females >65

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18
Q

Secondary HTN causes

A

5-15% of HTN cases.
Can be due to pregnancy, renal disease (renal stenosis is most common, intrinsic renal disease), endocrine (thyroid, phaeochromocytima, Conns, acromegaly, Cushings), pharma (alcohol, cocaine, COC, herbal remidies, anti-depressants), aortic coarctation, sleep apnoea, CKD, neurogenic cause (raised ICP)

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19
Q

Malignant HTN

A

aka accerlerated HTN
>180/120 developed over short time with signs of end organ damage (cerebral haemorrhage, AKI, aortic dissection, HF). Must have papiloedema

May present with headache, confusion (HT encephalopathy), epistaxis, fits, LoC
Urgent Tx, but slow reduction to avoid stroke

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20
Q

HTN end organ damage

A 
cardiovascular events (e.g. left ventricular hypertrophy - >CHF)
Renal events (glomerular ischaemic change. Can get hyperperfusion injury once controlled (glomerulosclerosis and necrosis)
Retinopathy
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21
Q

Retinopathy stages

A

1) tortuous with shiny walls (copper/silver wiring)
Stage 2: AV nipping
Stage 3)Flame haemorrhage and cotton wool spots
Stage 4)papilloedema

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22
Q

HTN Tx

A

If under 55 then ACEi/ARB
Over 55/T2DM/Afrocarribean then CCB/thiazide
Switch if not working
Then combine (ACEi+CCB+thiazide)
Can add K sparing diuretic, or alpha/beta blocker

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23
Q

QRISK2

A

Risk of CVD in 10 years, healthy person is 7%
Intervene if 10%+
Looks at age, sex, ethnicity, postcode, smoking, cholesterol, BMI, systolic, BP, diabetes, previous CVD, Fhx, HTN

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24
Q

HDL role

A

Supports transfer of non HDL cholesterol to liver for clearance. NHDL cholesterol implicated in atherosclerosis and CVD.

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25
Q

Primary dyslipidaemia

A

Familial. Classed by Frederickson I-V. Combined hyperlipidaemia dn TGs are more common types

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26
Q

Secondary hypercholesterolaemia

A

Obesity, hypothyroidism, anorexia nervosa, obstructive jaundice, nephrotic syndrome, ciclosporin use

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27
Q

Secondary hypertriglycerideaemia

A

Obesity, diabetes, alcohol abuse, pregnancy, renal failure, hepatitis, oral contraceptives, beta blockers, isotretinoin, protease inhibitors

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28
Q

Mixed secondary hypertriglycerideaemia and hypercholesterolaemia

A

obesity, thiazides and steroids

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29
Q

When should you consider familial cause?

A

FHx of premature CVD and total cholesterol >7.5mmol

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30
Q

Popliteal vein is formed from

A

Dorsal arch giving off anterior tibial, posterior tibial (medial) and fibular vein.

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31
Q

Femoral vein

A

From popliteal vein as it enters the thigh

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32
Q

Great saphenous vein

A

Dorsal venous arch and dorsal vein of great toe give great saphenous vein.
Medial
Empties into femoral vein inferior to inguinal ligament

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33
Q

Small saphenous vein

A

Dorsal venous arch and dorsal vein of great toe give small saphenous vein.
Lateral
Passes between two heads of gastrocnemius, emptying into popliteal vein in popliteal fossa.

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34
Q

Veins running medial

A

Great saphenous vein, posterior tibial

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35
Q

Veins running lateral

A

Anterior tibial, fibular and small saphenous

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36
Q

Varicose veins

A

Superficial veins drain into deep.

Incompetent valves mean backflow into superficial - > tortuous

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37
Q

Varicose veins RF

A
  • Age
    • Female
    • Obesity
    • Sedentary lifestyle
    • Pregnancy
    • Smoking
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38
Q

Varicose veins clinical features

A

Tortuous veins
Pruritus
Oedema
Haemosiderin stain (red/brown/yellow - > RBC breakdown)
Generalised or local leg pain, worse standing and better with walking

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39
Q

Primary varicose veins

A

More common, esp in women and pregnancy. More likely due to primary superficial valve defect than depe venous incompetence. Often have FHx

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40
Q

Secondary varicose veins

A

Deep venous incompetence. Hx of DVT or raised systemic venous pressure (e.g. pelvic tumour, pregnancy, AV fistula, severe tricuspid incompetence)

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41
Q

Lipodermatosclerosis

A

localised chronic inflammation of skin and subcut - painful and hardened skin. Occurs due to venous insuffficiency (pooling and oedema)
“Champagne legs”

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42
Q

Varicose vein complications

A
  • Venous ulcers
    • Thrombophlebitis (inflammation and thrombosis of superficial vein - red and painful)
    • Excessive bleeding from minor trauma
    • Venous eczema (dry and scaly legs)*
      Lipodermatosclerosis
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43
Q

Venous ulcer

A

Formed due to hypoxia and hypoperfusion. Shallow, sloping, minimal pain, large exudate.
Often medial malleolus. Often gauter area.
Oedema gives venous eczema lipodermatosis sclerosis -> skin breakdown

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44
Q

Most common ulcer out of venous and arterial

A

Venous

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45
Q

Investigations for venous disease

A

Clinical Hx and exam. Use Trendelenburg tourniquet to assess location.
USS for structure, valves and blood flow
Venography can be used to visualise veins

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46
Q

Management of venous disease

A

Compression stocking IF ruled out arterial disease
Surgical Tx can be ablation (First choice) - seals vein and diverts to better vessel. Can also use chemical ablation (sclerotherapy) or surgical stripping

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47
Q

Indications for surgical intervention in varicose veins

A

Grossly dilated/symptomatic, haemorrhage, concomitant deep venous insufficiency. Could also be done if just incompetent perforator veins (minimal invasion)

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48
Q

Trendelenburg tourniquet

A

Striaght leg raise and empty vein. Tie tourniquet to upper thigh and get patient to stand.
If non on standing but rapid filling on release then isolated sepheno-femoral junction defect. If filling with tourniquet then perforator valves involved too

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49
Q

Deep venous insuffiency

A

AKA postphlebetic limb
Incompetent deep venous valves and stasis gives superficial varicose veins, oedema, haemosiderin deposition, eczema, pruritus, atrophie blanche, lipodermosclerosis, ulcers

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50
Q

Primary lymphoedema

A

Intrinsic abnormality (e.g. milroy disease with deficiency in lymphatic vessels),

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51
Q

Secondary lymphoedema

A

Damage to lymphatic system. Can be cancer Tx, infection, trauma, venous oedema, immobility, obesity, HF, advanced cancer, liver disease

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52
Q

Investigation for lymphatic disease and management

A

Lymphoscintography.

Management involves elevation, compression stockings and physical massage. May need Abx due to cellulitis risk

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53
Q

PAD definition

A

Narrowing/occlusion of peripheral arteries, affecting blood supply to the lower limbs

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54
Q

Chronic limb ischaemia types

A
  • Intermittent claudication (ischaemic walking pain, rest relief)
    • Critical limb ischaemia (imminent limb loss risk)
      Chronic limb threatening ischaemia (end stage PAD, threatened limb viability relayed to several factors)
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55
Q

Acute limb ischaemia

A

Sudden perfusion decrease due to thrombus/embolus

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56
Q

Classification of PAD chronic limb ischaemia

A 
Fontaine classification has 4 stages:
	1) Asymptomatic
	2) Intermittent claudication
	3) Ischaemic rest pain
Ulceration/gangrene
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57
Q

Atheroma sequalae

A
  • Weakened vessel wall (aneurysm/dissection)
    • Demand/supply mismatch (angina, PAD, vascular dementia)
    • Thrombosis (ACS, stroke, acute limb ischaemia)
      Renovascular HTN
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58
Q

Common atheroma sites mnemonic

A

Wills catches perceptive criminal hAns

Circle of willis, carotid arteries, popliteal arteries, coronary arteries, abdominal aorta

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59
Q

Chronic PAD RF

A
  • Weakened vessel wall (aneurysm/dissection)
    • Demand/supply mismatch (angina, PAD, vascular dementia)
    • Thrombosis (ACS, stroke, acute limb ischaemia)
      Renovascular HTN
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60
Q

Causes of chronic PAD

A

Mainly atherosclerosis, but can be vasculitis (inflammatory) and fibromuscular dysplasia (non-inflammatory)
Can also be Buerger’s disease (thromboangiitis obliterans)- > acute inflammation and thrombosis of lower limb arteries/veins - more common in young, heavy smokers

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61
Q

Intermittent claudication

A

Angina of the limb. Pain on exercise, relieved by rest. Generally femoral artery atheroma, with collateral from produnda femoris.
Usually predominates in one leg.
Reproduced on walking same distance.

Pain in calf implies occlusion in thigh.
Can get bilateral in internal iliacs (ED)

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62
Q

Leriche syndrome

A

Bilateral occlusion in internal iliacs, associated with ED

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63
Q

Distinguishing Intermittent claudication from cauda equina

A

CE worse downhill, IC worse uphill
CE variable distance, IC fixed distance
CE pain stays 15-30 mins, IC pain relief after 1-2 mins
CE pulses present, but LMN findings. IC pulses absent, reduced ABPI, no neuro

64
Q

DDx for intermittent claudication

A

spinal stenosis (due to spinal osteophyte formation), cauda equina, venous cladication (obstruction of venous outflow leads to pain on initiating walking (typically whole leg and “bursting” in nature - may have DVT Hx and venous disease Hx)

65
Q

Critical limb ischaemia

A

Circulation so impaired that imminent risk of limb loss. Requires rest pain or tissue loss

66
Q

Critical limb ischaemia S+S

A

Pale, cold, hairless leg, reduced capillary refil, weak/absent pulse, arterial bruit, arterial ulceration (deep, punched out, painful, small over pressure points or lateral leg)

67
Q

Investigation of Critical limb ischaemia

A

Obs, ECG, FBC, ESR, thrombophilia screen, lipid profile, BM, scans (ABPI, duplex, MRI/CT angiography)

68
Q

ABPI

A

Take highest in foot and arm.
>1.2 is abnormal (calcified vessel)
1.0-1.2 is normal
0.8-0.9 is mild disease (manage risk)
0.5-0.79 is moderate disease/severe claudication (routine referral)
<0.5 is severe disease and critical limb ischaemia (urgent referral)

69
Q

ABPI of 0.8-0.9

A

Mild disease/claudication - just manage RF

70
Q

ABPI 0.5-0.79

A

Moderate disease/severe claudication - routine referral

71
Q

ABPI <0.5

A

Severe disease with critical limb ischaemia

72
Q

Management of PAD

A

Conservative: smoking cessation, diet/exercise, lipid modifications, manage comorbidities, antiplatelets, peripheral vasodilators
Surgery (angioplasty, surfgcal reconstruction, sympathectomy, amputation)

73
Q

Acute limb ischaemia types

A

85% are thrombotic (clot forms around ruptured atherosclerotic plaque)
15% are embolic

74
Q

Embolic acute limb ischaemia

A

Sudden and severe (lack of collaterals). RF are endocarditis, mitral stenosis, aneurysm, atherosclerotic disease, graft presence

75
Q

Thrombotic acute limb ischaemia

A

Acute on chronic. Generally less severe. RF are PAD, IHD, CVD, graft presence, blood disorders.

76
Q

S+S of acute limb ischaemia

A

Pain (not relieved by analgesia), paralysis (nerve damage), pulseless, pallor (cyanosed, +/- mottled skin), paraesthesia, perishingly cold.
If irreversible, see fixed mottling, blisters and hard, woody muscles

77
Q

DDx for acute limb ischaemia

A
  • Chronic peripheral neuropathy (e.g. diabetic, but see normal temp and pulse)
    • Compartment syndrome (hard muscles)
    • DVT (red, hot swollen calf, pulses present)
78
Q

Management of acute limb ischaemia

A 
Surgical emergency (6h to save limb). 
Tx with heparin.

If embolus, surgical embolectomy with balloon catheter in femoral artery
If thrombus, angioplasty, bypass surgery or intra-arterial thrombolysis

79
Q

Acute limb ischaemia complications

A

Reperfusion can cause oedema, might lead to compartment syndrome
Products of cell dealth (myoglobin, potassium phyosphate) can give rhabdomyolysis and AKI
Risk of amputation after 6h due to necrosis

80
Q

Marjolin’s ulcer

A

SCC progression from arterial ulcer.

81
Q

Vasospastic disorder

A

Arterial spasms cause vasoconstriction, tissue ischaemia and necrosis

  • Raynaud’s
  • Acrocyanosis
  • Livedo Reticularis
82
Q

Raynaud’s

A

Toes and fingers, thumb normally spared. Clear demarcation. Precipitated by cold/emotion/trauma/smoking/overuse.
Ischaemia - >cyanosis - > reactive hyperaemia.
Can manage with CCB and peripheral dilators.

83
Q

Raynaud’s phenomenon

A

primary disease. More common in young females. Genetic cause? No underlying vascular disease

84
Q

Raynaud’s syndrome

A

Secondary. Generally older patient and has presence of severe symptoms (scaring, ulceration, gangrene, nail changes).
Seen in SLE, scleroderma, RA, smoking, trauma, vibration, chemical, DM, hypothyroidism, Beurger’s disease, lymphoma, polycythaemia, beta blockers, CoC and cytotoxic drugs

85
Q

Buerger’s disease

A

Thromboangiitis obliterans

Acute inflammation and thrombosis of lower limb arteries and veins. More common in young, heavy smokers

86
Q

Acrocyanosis

A

Peristent mottled/reticular pattern on extremities and face

87
Q

Livedo reticularis

A

Persistent mottled/reticular pattern on extremities and trunk - may have pain.

88
Q

Anaemia symptoms

A

SOB,fatigue, dizziness, palpitations, pounding in ears, pale

89
Q

Erythropoesis reduced in

A

reduced haematinics, bone marrow disorders, myelosuppressive drugs, CKD, anaemia of chronic disease, endocrine (hypothyroid, reduced testosterone)

90
Q

Pancytopoenia

A

Bone marrow disorder

91
Q

Microcytic anaemia

A

Thalassaemia, IDA and anaemia of chronic disease

92
Q

Normocytic anaemia

A

Anaemia of chronic disease, haemolysis, combined iron/B12 deficiency, acute blood losss

93
Q

Macrocytic anaemia

A

B12/folate deficiency, myelodysplasia, alcohol, haemolysis, DNA synthesis defect (chemo), hypothyroid

94
Q

Anaemia of chronic disease

A

Can be microcytic or normocytic
Serum iron decreased, TIBC decreased, STR normal, ferritin raised
Seen in RA, lupus, CKD, malignancy, IBD

95
Q

Distinguishing IDA from anaemia of chronic disease in microcytic anaemia

A

IDA has low iron, raised TIBC, ferritin decreased

ACD has low iron, high ferritin and low TIBC

96
Q

Haemolysis markers

A

High LDH, low haptoglobin, high bilirubin and positive DAT

97
Q

IDA

A

Iron absorbed in duodenum, needs acidification. Protein bound as free is toxic (Hb, myoglobin, transferrin, ferritin, haemosiderin).
Deficiency can be reduced intake, pregnancy, malabsorption (coeliac, gastrectomy), chronic haemorrhage,
Get pallor, tachycardia koilonychia

98
Q

Ferritin and haemosiderin solubility

A

Ferritin is soluble, haemosiderin is insoluble

99
Q

IDA diagnosis

A

Microcytic, hypochromic, pencil cells. GSTD is Fe stain on bone marrow but not needed.
Ferritin should be low, but can increase in inflammation/malignancy so may be normal. Transferrin saturation is better measure as not impacted by inflammation

100
Q

IDA management and Tx

A

Hx of blood loss, weight loss and bowel change
Refer for upper/lower GI endoscopy if no cause found
\
Tx with oral iron if ferritin <25 or TF sat <20.
Get 10hb rise 1-2 weeks.
Can also give IV

101
Q

Hb rule of 10

A

Max rise in Hb/week is 10g/L
If >10g/L lost/week then blood lost
If transfusing, 1 bag raises Hb by 10g/L

102
Q

Thalassaemia

A

Hb synthesis defect - more common in middle east.

103
Q

Beta thalassaemia minor

A

Mild/asymptomatic carrier

104
Q

Beta thalassaemia major

A

Cooley’s. Presents in first year with severe anaemia and splenomegaly and FTL. Can have facial abnormality. Needs transfusions

105
Q

Alpha thalassaemia

A

Range from 1 (normal) 2 genes (carrier state, reduced MCV), 3 genes (mod microcytic anaemia and haemolysis) and 4 genes (death in utero)

106
Q

Sideroblastic anaemia

A

Bone marrow makes sideroblasts rather than erythrocytes

107
Q

B12 defieicny
Causes
S+S

A

Needs IF for absorption in terminal ileum. 2 year store in body.
Causes are reduced intake, gastrectomy, PA, Crohns, ileal resection. May appear low in Coc, HRT

Causes peripheral neuropathy, extensor plantars, brisk knee jerl but ankle jerk absent

108
Q

Diagnosis of B12 deficiency

Management

A

Oval macrocytes, tear drop cells, hypersegmented nuclei, low B12, IF antibodies, gastric parietal cell antibodies (but not specific), raised bilirubin

Oral B12 or IM hydroxocobalamin

109
Q

Folate deficiency

A

Converted to folate in upper GI, absorbed in jejunum. Stores for 6 months.
Destroyed by cooking

110
Q

no

A

n

111
Q

Rhesus

A

IgG antibodies, only present in RhD negative people via exposure

112
Q

Group and save

A

Test ABO/RhD but also antibodies against other antigens.

Indirect antibody test uses Coombs reagent (antiglobulin) used to screen patient serum against donor RBCs

113
Q

Transfusion reactions

A

Shock, renal failure, DIC, death

114
Q

Acute neutrophilia

A

Infection, inflammation, neoplasia, bleeding, smoking, steroid

115
Q

Chronic neutrophilia

A

Reactive, drugs, metabolic syndrome, CML/myeloproliferative disorder

116
Q

Neutropoenia

A

Viral infection, carbimazole, chemotherapy, Felty syndrome, cyclical (?young women), acute leukaemia, myelodysplasia, hereditary, Kostmann’s syndrome, neutropoenic sepsis

117
Q

Felty syndrome

A

RA, neutropoenia and splenomegaly

118
Q

Kostmann’s syndromeq

A

Congenital neutrophil defect

119
Q

Lymphocytosis

A 
Lymphoid malignancy (CLL, lymphoma), reactive (viral, whooping cough, TB, brucellosis, stress), drug induced (phenytoin), septic shock, MI, trauma,
Chronic raise in smoking, autoimmune, chronic inflammation, sarcoid, metabolic syndrome. if Clonal then ?malignancy
120
Q

Lymphocyte make up

A

80% T cells, circulate.few ER

20% B cells, mainly in lymph nodes. Also get NKs

121
Q

Lymphocytopoenia

A

bone marrow failure, steroids, SLE, uraemia, HIV, cytotoxic drugs

122
Q

monocytosis

A

atypical infections (TB, inflammation, autoimmune disease, haemoatoligical malignancy,

123
Q

Eosinophilcytosis

A

Parasitic infections, asthma, drugs, eczema, Hodhkings, CML

124
Q

Basophilcytosis

A

Very rare, usually only in CML

125
Q

Haematological Urgent referral

A

WCC>50
Blood film suggest CML/CMML
Mention of blasts
Neutrophils <0.5

Consider referral if Chronic neutrophilia, lymphocytosis, persistent basophilia (?CML) or neutrophils <1.0 with no clear cause

126
Q

Leukostasis

A

High WCC, medical emergency. Needs urgent chemo

Papilledema and retinal venous distension

127
Q

CML

A

raised myeloid cells, see immature myelocytes and metamyelocytes in blood (instead of marrow.). Philadelphia chromosome (9-21_. Insiduous. splenomegaly

128
Q

Aplastic anaemia

A

pancytopoenia but no blasts. Can be idiopathic or drug induced

129
Q

Glandular fever

A

EBV infects B cells, allowing them to circulate. Confirm with monospot test (heterophile antibodies).
Can reactive during immunosuppression

130
Q

Leukaemia Acute vs chronic

A

Acute has no differentiation (blast cells).
Bone marrow failure over 1-2 weeks. Anaemia, neutropoenia, infection, thrombocytopoenia, bruising.
Chronic has normal maturation

Children -acute is more common (esp ALL), AML is most common adult acute. CLL most common chronic

131
Q

Platelet homeostasis

A

Endothelium secretes PGI2 (prostacyclin) and NO to prevent adhesion. Damage exposes collagen and vWF. platelets adhere and degranulate, release ADP and aggregate more

Platelets also synthesis TXA2 (vasoconstriction and aggregation)

132
Q

Thrombocytoponeia

A

Can be increased destruction (ITP, SLE, CLL, viruses, TTP, HUS), reduced production (aplastic anaemia, marrow infiltration, marrow suppression) - epistaxis, menorrhagia, bruising

133
Q

ITA

A

immune thrombocytic anaemia. Can be acute in children following virus or vaccine. In adults, less acute and generaly women with autoimmune disorder

134
Q

TTP

A

Thrombotic thrombocytopoenic purpura. Widespread clotting and petichial rash. Can be congenital or acquired

135
Q

HUS

A

Haemolytic uraemic syndrome. Can occur post E coli. Causes haemolysis, clots and AKI

136
Q

DVT

A

Thrombi form at venous valve sites (as they disturb flow). Grow via Virchow’s triad (stasis, vessel wall damage and hypercoagulable state)

137
Q

Thrombus sequalae

A

Lye and resolve (fibrinolytic plasmin)
Organisation (scars and collateral circulation)
Recanalisation (thrombus remains in lumen)
Embolism (can be numerous small, or larger)

138
Q

Hypercoagulable state RF

A

oestrogen therapy, pregnancy, sepsis, malignancy, nephrotic syndrome, myeloproliferative disorders, CHF, thrombophilia (factor V leiden, antithrombin deficiency, protein C/S deficiency), aquired antiphospholipid/lupus anticoagulant

139
Q

Stasis RF

A
  • Older age
    • Venous insufficiency/varicose veins
    • Obesity
    • Immobility (>3 days bed rest)
    • Continuous travel
    • Hospitalisation
140
Q

Vessel wall injury RF

A

Trauma/surgery (esp leg surgery), indwelling venous catheter, chemical irritation (e.g. chemo)

141
Q

DVT S+S

A

To examine leg - use 10cm distal to tibial tuberosity

Generally unilateral leg, but can be bilateral leg or can be arms.
Often throbbing pain, oedema, swelling, tenderness, erythema, warmth and venous distension.
Hofman’s sign (pain on dorsiflexion of the ankle - but unreliable and may dislodge thrombus so should not be used).

142
Q

Wells score for DVT

A 
Clinical features (tenderness, swelling (esp unilateral), collateral veins, pitting oedema), RF (cancer, bed rest, surgery, previous DVT). Each worth 1 point. 
2 points if alterative likely diagnosis
Score 2 is likely, 1 unlikely. D dimer to rule out if not likely
143
Q

Diagnosis of DVT

A

Doppler USS (request if Wells>2 or low wells and positive D dimer)

144
Q

May Thurner

A

Compression of left common iliac vein by right common iliac artery

145
Q

PE S+S

A

dyspnoea, pleuritic chest pain, DVT signs, cough, fever, haemoptysis, syncope

146
Q

Wells score for PE

A

Uses:
- clinical features (dVT signs, tachycardia, haemoptsis)
- RF (immobilisation, previous DVT/PE, malignancy)
Clinical judgement (3 points for no more likely diagnosis)

4 or less is unlikely (D dimer to rule out within 4 hours). If positive then CTPA
Above 4 is likely (CTPA or VQ).

147
Q

CTPA

A

Definitive diagnosis. Can see right heart strain.Ok in pregnancy, not ok in renail impairment

148
Q

V/Q

A

not suitable for pregnancy

149
Q

ECG changes in PE

A

Not specific or sensitive for PE. Most common finding is sinus tachycardia.
Mat get dominant R wave in V1, T wave insersion in V1-V4, or RBBB
Slurred S in lead 1, Q wave and T inversion in III (cor pulmonale - rare)

150
Q

CXR in PE

A

OFten normal. May have exudate, may see Westermark sign (fewer lung markings, enlarged pulmonary trunk)

151
Q

PE classification ; Massive

A

Acute PE, sustained hypotension (<90 sys or 40 below basline or <40bpm for 15 mins)

152
Q

PE classification: submassive

A

Submassive (40%. Right heart strain). Acute PE, no hypotension. RB dysfunction or myocardial necrosis - ECG abnormality/echo changes/elevated troponins. May have tachycardia.

153
Q

PE classification (low risk)

A

Low risk (55%). Acute PE, no clinical markers of massive or submassive. May have tachycardia. Can be asymptomatic, but common to have pleuritic chest pain, SOB and DVT

154
Q

PE management

A

anticoagulation, thrombolysis if haemodynamic compromise. If failed then interventional radiology or endovascular techniques.

155
Q

Distinguishing embolic and thrombosis occlusion

A

Embolic is sudden onset and severe, thrombosis is insidious
Source in embolis is often identifiable (AF/AAA) but not in thrombosis
Pulses previously normal in embolis, now absent, but contralateral normal. Thrombosis has progressive bilateral decline.
In embolus, Hx often absent, but thrombosis often has Hx of stroke, MI

CP1 revision (16 decks)

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