Brainscape's Knowledge GenomeTM

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


See full index

CP1 > Vascular and Haematology > Flashcards

Vascular and Haematology Flashcards

1
Q

What is an aneurysm?

A

a localised dilatation of an artery with a permanent diameter that is >1.5x its usual size

can be true or false

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

True aneurysms

A

where the wall of the artery forms the aneurysm

Can be fusiform or saccular

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

False aneurysms

A

aka pseudoaneurysm

where other surrounding tissues form the wall of the aneurysm

A small hole in the blood vessel wall allows blood to leak out and pool around the vessel.

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

Fusiform aneurysm

A

where artery wall balloons out symmetrically

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

Saccular aneurysm

A

where artery wall only balloons out on one side of the artery

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

The pathophysiology of aneurysms

A
  1. weakening of the blood vessel wall => vessel struggles to contain the pressure of the blood pushing against its walls causing it to dilate.
  2. This leads to dilatation of blood vessel wall= ANEURYSM.
  3. When the diameter of the vessel lumen increases, the pressure flowing through it increases
  4. This leads to a positive feedback loop, of continuous bulging of arterial wall (which means aneurysm gets bigger)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where do aneurysms most commonly occur?

A

Most commonly in the aorta

~60% occur in abdominal aorta (AAA).
~40% occur in thoracic aorta.

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

Where do AAAs most commonly occur?

A

95% of AAA occur below the point where the renal arteries branch out of the abdominal aorta

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

What is the most common peripheral aneurysm?

A

popliteal artery aneurysm

~50% of people with these also have AAAs.

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

Risk factors for aortic aneurysm

A

Similar to those for atherosclerosis:

  • Hypertension
  • History of smoking (ex- and current)
  • Male and >60 years
  • Diabetes
  • High LDL levels

Other risk factors include:

  • Genetic disorders (anything affecting connective tissue)
  • Coarctation of aorta
  • Pregnancy
  • Coronary, cerebrovascular or peripheral arterial disease.
  • COPD
  • European family origin
  • FH of AAA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does Marfan’s Syndrome impact blood vessels?

A

fibrillin and other elastic properties are impaired therefore causing weak blood vessel walls

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

How does Ehler’s Danlos syndrome impact blood vessels?

A

ability to form collagen properties are disrupted

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

Complications of an aneurysm

A

If intact - may have effects from an aneurysm compressing nearby structures (such as IVC).

Main concern is rupture
=> subarachnoid haemorrhage
=> aortic insufficiency
=> Blood flow into retroperitoneal space

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

How can a thoracic aortic aneurysm cause aortic insufficiency?

A

if near the aortic valve, prevents the valve from shutting properly => backflow of blood into the left ventricle during diastole

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

Clinical presentation of stable aneurysm

A

usually no S+S, found incidentally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical presentation of unstable/ruptured aneurysm

A 
Severe pain (usually epigastric, radiating to back/groin)
Hypotension
Collapse, syncope
Tachycardia
Anaemia
Shock
Vomiting
Expansile mass in abdomen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aneurysm - investigations

A

Abdominal Ultrasound scan – location and staging

CT Angiography – to create highly detailed image of aneurysm and surrounding structures

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

Management of ruptured aneurysm

A

A-E assessment

Bloods - FBC, U&E, coagulation, G&S, XM

Fluids

Activate major haemorrhage protocol

Vascular Team

Imaging

Surgery as soon as stabilised

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

Management of AAA

When is surgery indicated?

A

AAAs <5.5cm
=> regular imaging
=> modification of risk factors
=> Will probably eventually require surgery

Surgery if:
=> AAA >6cm (risk of rupture greatly increases at 6cm)
=> AAA expanding at <1cm/year
=> Symptomatic aneurysm

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

Aneurysm surveillance

A

All men >66 years are screened for AAA.
=> involves having an abdominal USS done to measure size of the artery and check if there is any aneurysm

Anyone with increased risk also requires surveillance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Aortic dissection

A

The inner layer (intima) of the aorta tears due to a weakening of the wall.

This causes blood to surge through, causing the intima and media layers to separate.

This separation creates a new ‘false’ lumen, which can lead to rupture.

MEDICAL EMERGENCY

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

What can a weakening in the aortic wall cause?

A
  1. aneurysm

2. dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DeBakey Classification of aortic dissection

A

I. Intimal tear in the ascending aorta and descending aorta is also involved.

II. Only ascending aorta is involved.

III. Only descending aorta is involved.

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

Standford Classification of aortic dissection

Which type is more common?

A

A. Ascending aorta is involved (same as DeBakey I & II)

B. Descending aorta is involved (same as DeBakey III)

Type A is more common than type B.

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

Complications of aortic dissection

A
  1. Pericardial tamponade = FATAL.
  2. External rupture and massive haemorrhage = FATAL.
  3. compression of nearby vasculature such as subclavian or renal artery leading to hypoxia of upper limbs or kidneys respectively.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Risk factors for aortic dissection

A 
Hypertension – main risk factor
Smoking 
Hyperlipidaemia
Thoracic Aortic Aneurysm
Aortic Valve abnormalities 
Family History of aortic dissection
Previous cardiac surgery 
Trauma  
Cocaine/Amphetamine Use

Connective Tissue Disease – e.g. Ehlers-Danlos or Marfan’s

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

Aortic Dissection - clinical features

A

Severe, very sudden onset chest pains.
=> Radiation to back/arm (can mimic MI)
=> Described as “tearing”

Weak pulses in downstream arteries

Difference in BP between right and left arm.

Hypotension

Shock – significant blood loss if rupture.

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

Aortic Dissection - Imaging

A
  1. CXR – would show a widened mediastinum due to widened aorta
  2. Transoesophageal Echo (TOE) – more sensitive for detecting false lumen.
  3. CT Angio – will give a more detailed picture of the blood vessels and tear in the vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Stage 1 HTN

A

Clinic > 140/90 + Ambulatory BP average > 135/85

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

Stage 2 HTN

A

Clinic > 160/100 + Ambulatory BP average > 150/95

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Severe HTN

A

> 180/110

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

Primary vs secondary HTN

A
  1. Primary (essential)
    => no known cause, multifactorial
    => accounts for 85-95% of HTN cases in adults
  2. Secondary hypertension
    => caused by an identifiable underlying condition
    => accounts for 5-15% of HTN cases in adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Modifiable risk factors for essential HTN

A 
Obesity
?excess salt
Lack of exercise
Stress
Smoking
Excess of Alcohol
Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Non-modifiable risk factors for essential HTN

A 
Older age
FHx
Ethnicity
Male (if <65)
Female (if >65)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are some causes of secondary HTN?

A 
Pregnancy
Renal disease
Endocrine 
Pharmacology
Coarctation of aorta
Obstructive sleep apnoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What endocrine conditions can cause HTN?

A 
Phaeochromocytoma
Conn's
Cushing's
Thyroid dysfunction
Acromegaly
Hyperparathyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What drugs can cause HTN?

A

Alcohol, cocaine
COCP
anti-depressants
herbal remedies

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

Benign hypertension

A

= gradual elevation of blood pressure over years.

Leads to gradual hypertrophy of the muscular media in artery walls, reducing their capacity to expand and increasing their fragility

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

Malignant hypertension

A

= severe HTN, which develops over a short period of time

Leads to intimal proliferation, reducing luminal size and leading to cessation of blood flow through small vessels
=> signs of end organ damage

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

How can malignant HTN present?

A

May present with headache, confusion, visual disturbances, seizures (hypertensive encephalopathy)

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

Hypertensive Encephalopathy

A

= general brain dysfunction due to significantly high blood pressure

Sudden onset

Symptoms may include headache, vomiting, trouble with balance, and confusion

When it occurs in pregnancy it is known as eclampsia.

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

Management of malignant HTN

A

Need to reduce the BP

This needs to be done gradually to reduce the chance of stroke occuring

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

End organ damage due to HTN - cardiovascular

A 
Left ventricular hypertrophy 
=>
 diastolic dysfunction 
=>
congestive heart failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

End organ damage due to HTN - renal

A

CKD, Renal failure and other renal problems.

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

End organ damage due to HTN - retinal

A

Hypertensive retinopathy (4 grades)

I Tortuous arteries with shiny walls (copper/silver wiring)
II A-V nipping – narrowing as arterioles cross veins
III Flame haemorrhages and cotton wool spots
IV Papilloedema

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

End organ damage due to HTN - cerebrovascular

A

Higher risk of infarction and haemorrhage.

Can lead to vascular dementia, stroke, encephalopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How can you assess for a secondary cause of HTN?

A
  • 24-hour urinary metanephrines
  • Cortisol
  • Renin:aldosterone ratio
  • Calcium
  • Imaging of renal arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How can you assess for end organ damage in HTN?

A
  • Urine dipstick (protein and blood)
  • Renal function
  • Renal ultrasound
  • 12 lead ECG (LVH)
  • Echo
  • Fundoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the two main superficial veins in the lower limb?

What is their course?

A

Great saphenous vein – ascends up medial side of leg and eventually drains into Femoral vein.

Small Saphenous vein – ascends at posterior aspect of leg and drains into Popliteal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the deep veins in the lower limb?

A

Anterior Tibial vein – formed from the dorsal venous arch (which drains the foot).

Posterior Tibial

Fibular vein

Popliteal vein – Anterior & posterior tibial and fibular vein unite to form this.

Femoral vein – when the popliteal vein enters the thigh.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are varicose veins?

A

tortuous, dilated veins which occur due to incompetent venous valves causing further reflux of blood into superficial veins, causing them to become tortuous.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Risk factors for varicose veins?

A
  • Increased age
  • F>M
  • Obesity
  • Sedentary lifestyle
  • Pregnancy
  • Smoking

can also occur secondary to deep venous incompetence, due to:

  • Previous DVT
  • Raised systemic venous pressure – compression, arterio-venous fistula or severe tricuspid incompetence.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Varicose veins - clinical features

A

Enlarged, tortuous veins in leg

Pruritis of leg

Oedema – starts at ankle and may move up to calf.

Tiredness and aching/throbbing of the legs.

Yellow or red-brown skin pigmentation – RBC breakdown causing haemosiderin release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Characteristics of venous ulcers

A
  • Shallow
  • Sloping, gradual outline.
  • Generally minimal pain
  • Often fairly large.
  • Very wet, lots of exudate.
  • Usually present at medial malleolus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Complications of varicose veins

A 
Venous ulcers
Thrombophlebitis
Excessive bleeding from minor trauma
Venous eczema
Lipodermatosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Lipodermatosclerosis

A

Localised, chronic inflammation and fibrosis of skin and subcutaneous tissues of the lower leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Thombophlebitis

A

Inflammation and thrombosis of a superficial vein.

Painful and red veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Varicose veins - investigations

A

Usually diagnosis is made on clinical history and examination.

Can do Duplex USS:
=> Look at structure of vein and valves
=> Look at blood flow through veins to check for retrograde flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Varicose veins - management

A

Conservative - compression stockings

Surgical - Vein ablation or Complete removal of the vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Use of compression stockings

A

may improve venous return

MUST rule out arterial disease first, otherwise these can block blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Lymphoedema

A

a chronic swelling resulting from failure of lymphatic drainage.

i.e. when capillary filtration exceeds lymphatic drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the two types of lymphoedema?

A
  1. Primary – occurs due to intrinsic genetic abnormality of lymphatic system.
  2. Secondary – occurs when there is damage to otherwise normally functioning lymphatic system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Causes of secondary lymphoedema

A
  • Cancer treatment, infection, trauma
  • Venous oedema
  • Oedema associated with immobility
  • Obesity
  • Heart Failure
  • Oedema of advanced cancer or other advanced condition (e.g. liver disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Pathophysiology of VTE

A

Thrombi do not form through atheroma (as in arteries) but usually at the site of valves

Valves within veins protrude into the lumen and often become a site of turbulent flow leading to thrombus formation.

Once formed, a thrombus in a vein grows by successive adherence of platelets and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How can valves in veins be damaged?

A

trauma, stasis and occlusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the potential outcomes of thrombus formation in a vein

A
  1. Lysis and resolution – if small, the thrombus resolves (fibrinolytic action e.g. plasmin)
  2. Organisation – scar tissue obliterates lumen and blood flows through collateral vessels
  3. Recanalisation – leads to scar formation and residual thrombus in lumen
  4. Embolism – fragmentation of thrombus leads causes embolus to travel through the vessel.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is the main cause of PE?

How does this occur?

A

thrombosis in leg veins

thromboemboli travel up the IVC through the right atrium through the right ventricle and into the pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Virchow’s triad for risk of thrombosis

A
  1. Hypercoagulable state
  2. Vessel wall injury
  3. Stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What can contribute to a hypercoagulable state?

A 
Oestrogen therapy (HRT, COCP)
Pregnancy and puerperium 
Sepsis (and severe infections)
Malignancy
Nephrotic syndrome
Myeloproliferative disorders
Congestive heart disease
Inherited thrombophilia
Acquired thrombophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What can contribute to Vessel Wall Injury?

A

Trauma or surgery (particularly to lower limbs)
Indwelling venous catheters
Chemical irritation (e.g. chemotherapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What can contribute to stasis in vessels?

A 
Age 
Venous insufficiency
Varicose veins
Obesity (BMI >30)
Immobility (>3 days bed rest)
Long travel (>3-4h)
Hospitalisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Risk factors for VTE:

A

Virchow’s Triad
Previous history of VTE
Family history of VTE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the MOST SIGNIFICANT risk factors for VTE?

A 
Trauma to lower legs or pelvis
Major trauma 
Hip or knee arthroplasty
Major general surgery
Spinal cord injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

VTE prophylaxis

A

VTE = recognised preventable complication of hospital treatment

A low-dose anticoagulant may be given to the patient during their hospital stay (commonly enoxaparin)

Compression stockings can be worn and early mobilisation of the patient encouraged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Diagnosing VTE - Hx

A

PC, HPC

PMHx - any prior VTE? Inflammatory disease/malignancy/thrombophilia?

PSHx - any recent surgeries? recent hospital admissions?

DHx - anything with oestrogen, any prior need for anticoagulation

Obstetric Hx - Pregnancy, Termination, Birth in past 6 weeks

FHx and SHx

Travel Hx - recent travel >3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does a DVT typically present?

A

Unilateral localised pain (usually throbbing) in one leg.
=> Uncommonly occurs in arm or bilateral legs.

Oedema of leg.
Calf swelling/tenderness
Redness and warmth of calf.
Distension of superficial veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Well’s score for ?DVT

A

= a diagnostic aid for determining the probability of a patient having DVT, which can then influence clinical decision making.

it is NOT a replacement for clinical reasoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

D-dimer test - sensitivity and speciticity

A

D-dimer assay measures a degradation product released by the lysis of a cross-linked fibrin clot.

=> elevated levels have a 99.5% sensitivity for the diagnosis.

=> there is VERY POOR SPECIFICITY and can be elevated in many clinical scenarios: older patients, sepsis, recent surgery, pregnancy, chronic inflammatory disease, malignancy, Covid-19.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When should a D-dimer test be done in ?VTE ?

A

D-Dimer is typically elevated in VTE

A negative D-dimer can exclude patients with a LOW probability of PE, but it is not useful in confirming diagnosis in high-risk patients.

D-dimer SHOULD NOT be done I those with a high clinical probability of VTE (as it will not change management).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is an unprovoked DVT?

A

DVT when there are no major risk factors in the patient’s history.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

May-Thurner Syndrome

A

also “Iliac vein compression Syndrome”

Compression of the left common iliac vein by the right common iliac artery.

This causes stasis in the vein and a DVT can form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

When would a doppler USS be requested in ?VTE

A

Request to Radiology in patients with:

  • Wells score ≥2,
  • High clinical suspicion
  • A low Wells score but positive D-dimer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Saddle embolism

A

= a large embolus that straddles the bifurcation of the pulmonary trunk, extending into both the right and left pulmonary arteries

This commonly causes near-immediate death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Minor PE

A

small peripheral vessels are blocked, and patients may be asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Major PE

A

middle-sized pulmonary arteries are blocked, leading to breathlessness, pleuritic chest pain and haemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Massive PE

A

> 60% of the pulmonary circulation is blocked (large or extensive thrombus; saddle PE; bilateral PE), leading to rapid cardiovascular collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Premonitory Embolus

A

= a massive PE following a minor PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Clinical features of PE

A 
Dyspnoea (may present as tachypnoea) 
Pleuritic chest pain 
Signs of DVT
Cough
Substernal chest pain
Fever 
Haemoptysis
Syncope
Unilateral leg pain
Tachypnoea
Tachycardia
Reduced consciousness (GCS or AVPU)
Hypoxia
Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What 3 symptoms are patients with PE most likely to present with >1 of?

A

Dyspnoea (may present as tachypnoea)

Pleuritic chest pain

Signs of DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What day post-surgery is PE most likely?

A

~10 days post surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Diagnosis of PE

A

Well’s score of PE

=> If score is low (0-4) and D-dimer is negative, then PE is unlikely.
=> If score is low (0-4), and D-dimer is positive, then CTPA.

=> If Score >4, PE is likely and CTPA is needed

92
Q

Investigations for PE

A 
FBC, U&E, clotting, D-dimer
ABG – type 1 RF
CXR – can be normal, or show dilated pulmonary arteries.
ECG – tachycardia, RBBB, RV strain
Echo – can confirm right heart strain.

CTPA – gold-standard
=> V/Q scan if unavailable to do CTPA, but less accurate if there is pre-existing lung disease

93
Q

When would a patient not be able to have a CTPA?

A

if they cannot receive contrast - e.g. in (renal failure or anaphylactic contrast allergy

94
Q

V/Q scan

A

Ventilation (V): shows how well air reaches the lung parenchyma.

Perfusion (Q): shows how well blood circulates in the lung parenchyma

V/Q mismatch = pulmonary emboli

95
Q

ECG changes in PE

A

ECG changes are not specific or sensitive enough to diagnose PE - The ECG may be completely normal.

  • Sinus tachycardia is the most common finding in PE.

Other changes:

  • Dominant R wave in lead V1.
  • T wave inversion in leads V1-V4 (right heart strain) or RBBB
  • “Classical” ECG findings of SI QIII TIII indicates cor pumonale (rare finding).
96
Q

What is the SI QIII TIII ECG sign?

What does it indicate?

A

slurred S wave in lead I, with a Q wave and T wave inversion in III

indicates cor pumonale

97
Q

Management of PE

A
  1. Anticoagulation (oral or parenteral) in low-risk cases.
  2. Thrombolysis (in patients with haemodynamic compromise) by IV infusion => high risk of bleeding.
  3. Interventional radiology or endovascular techniques (often where thrombolysis fails or is contraindicated) – e.g. catheter assisted thrombolysis or thrombectomy.
98
Q

What is important to remember in the management of PE?

A

patients with a PE can deteriorate – low risk can become sub-massive or massive.

Deterioration to massive could lead to heart failure and pulmonary hypertension

99
Q

Peripheral Arterial Disease

A

narrowing or occlusion of peripheral arteries, affecting the blood supply to lower limbs.

100
Q

How can chronic limb ischaemia present?

A
  1. Intermittent claudication
  2. Critical limb ischaemia
  3. Chronic limb-threatening ischaemia
101
Q

Intermittent claudication

A

= diminished circulation leads to pain in the lower limb on walking or exercise that is relieved by rest

(can also be caused by Cauda equine syndrome)

102
Q

Critical limb ischaemia

A

= where circulation is so severely impaired that there is an imminent risk of limb loss

103
Q

Chronic limb-threatening ischaemia

A

= represents end stage peripheral arterial disease where there is threatened limb viability relayed to several factors.

104
Q

Acute Limb Ischaemia

A

a SUDDEN decrease in arterial limb perfusion, due to thrombotic or embolic causes

105
Q

Where does atherosclerosis tend to occur?

A

where the vessels branch, curve or are irregular and where blood undergoes sudden changes in velocity and in direction of flow

Most commonly:

  1. Circle of Willis
  2. Carotid arteries
  3. Popliteal arteries
  4. Coronary arteries
  5. Abdominal aorta
106
Q

What is the resulting pathology of atherosclerosis?

A

Weakening of vessel wall – arterial aneurysm or dissection

Demand-supply mismatch – coronary heart disease, peripheral arterial disease, vascular dementia

Thrombosis – acute coronary syndromes, acute ischaemic stroke, acute limb ischaemia

Renovascular hypertension

107
Q

Risk factors for atherosclerosis

A 
Obesity
Physical inactivity
Hypertension
Smoking
Hypercholesterolaemia
Diabetes mellitus
Older age
108
Q

Clinical features of atherosclerosis

A

Mostly asymptomatic until complications occur.

Signs may include:
•	Xanthelasma 
•	Bruits (carotid or abdominal)
•	Aortic aneurysm on palpation
•	Poor peripheral pulses
109
Q

Risk factors for chronic peripheral arterial disease

A

The same as for atherosclerosis:

  • Obesity
  • Physical inactivity
  • HTN
  • Smoking (one of the strongest risk factors for PAD)
  • Hypercholesterolaemia
  • Diabetes mellitus
  • Particularly if poorly controlled.
  • Older age

The more risk factors you have, the increased chance of getting peripheral vascular disease.

110
Q

Causes of chronic PAD?

A

Atherosclerosis = most common cause
=> Narrowing of affected arteries limits blood flow to affected limb.

Vasculitis
=> Inflammation of artery causes stenosis and limits blood supply.

Fibromuscular dysplasia
=> Non-inflammatory artery wall thickening.

111
Q

Why is intermittent Claudication only pain on exercise?

A

At rest, perfusion is adequate to meet O2 demands of the tissue.

During exercise, perfusion is not adequate enough to meet increased O2 demands of the tissue.

112
Q

Classical features of intermittent Claudication

A
  • Gripping, cramp-like pain (typically, in the calves)
  • Induced by exercise
  • Typically relieved by rest
  • Usually predominates in one leg
  • Reproducible
113
Q

Where is the lesion causing calf claudication

A

typically a lesion causing narrowing of arteries in the thighs

114
Q

Where is the lesion causing buttock claudication

A

a narrowing in the internal iliac arteries (or higher up)

If bilateral, both iliac arteries are compromised.

115
Q

Leriche’s Syndrome

A

absent femoral pulses;
intermittent claudication of the buttocks;
pale, cold legs;
impotence.

116
Q

Cauda Equina Syndrome

A

= compression of the cauda equina in the spinal canal by central disc protrusion or canal stenosis.

117
Q

How to differentiate Cauda Equina syndrome from arterial insufficiency

A

CAUDA EQUINA
Variable claudication distance
Pain often better when walking uphill, but worse downhill.
Pain disappears after 15-30 mins typically
LMN findings such as reduced reflexes but pulses present as normal

ARTERIAL INSUFFICIENCY
Fixed claudication distance
Pain exacerbated by walking uphill, but better downhill.
Pain disappears after 1-2 mins of rest typically
Absent peripheral pulses and reduced ABPI but no evidence of neurological findings.

118
Q

Progression of Symptoms of PAD

A
  1. At first, generally symptoms of exercise-induced claudication.
  2. Claudication distance reduces (e.g. from 10 metres to 2 metres).
  3. Ischaemic rest pain
  4. Limb ischaemia – gangrene
119
Q

What are the clinical features of ischaemic rest pain?

A

Generally worse at night due to reduced cardiac output and loss of gravity.

Improvement of symptoms if hang legs out of bed or sleep in a chair.

120
Q

Clinical Signs of PAD

A 
Pale, cold and hairless legs
Reduced Capillary refill
Arterial ulceration
Arterial bruits
Weak/absent pulses
121
Q

Arterial Ulcers

A
  • Deep
  • Punched out
  • Painful
  • Small
  • Present over toe joints, heel and lateral aspect of leg (malleolus commonly)
122
Q

What are the two main symptoms of critical Limb Ischaemia?

A
  1. Rest pain due to insufficient blood supply to the limbs.

2. Tissue loss – development of necrotic tissue which if infected becomes gangrene

123
Q

PAD - Investigations

A

BEDSIDE TESTS:
Observations
ECG

BLOODS:
FBC, ESR, lipid levels, blood glucose.
Thrombophilia screen

IMAGING:
ABPI
Duplex USS
MRI/CT angiography (gold-standard)

124
Q

What two things seen on an FBC can aggravate PAD?

A

anaemia

polycythaemia

125
Q

Ankle Brachial Pressure Index (ABPI)

A

= a method of quantifying severity of arterial disease in the legs

  • Uses a doppler to measure the blood pressure in the brachial artery and the two arteries in the foot
  • As arterial disease progresses in the legs, we get reduced flow through the arteries and hence the blood pressure falls
  • This is commonly measured in patients with ulcers to help differentiate the type of ulcer.
126
Q

Management of PAD

A

ABPI >0.6 - conservative management

ABPI <0.6 or highly symptomatic - invasive measures

127
Q

What are the causes of acute limb ischaemia?

A

Thrombotic – Blood clot forms around a ruptured atherosclerotic plaque (most common)

Embolic – Dislodged blood clot, usually cardiac in origin.

Trauma

128
Q

Embolic vs thrombotic acute limb ischaemia

A

Embolic is more sudden

Embolic often more severe due to lack of collateral circulation

129
Q

What is the prognosis for acute limb ischaemia?

A

Mortality rate = 15-20%

Limb prognosis is linked to severity of arterial disease, acute onset and how rapidly reperfusion is achieved

130
Q

6P’s of acute limb ischaemia

A

Pain — constantly present and persistent.

Pulseless — ankle pulses are always absent.

Pallor (or cyanosis or mottling).

Power loss/paralysis due to nerve ischaemia

Paraesthesia or reduced sensation or numbness.

Perishingly cold.

131
Q

Which symptoms suggest a threatened acute ischaemic limb?

A

Paralysis and paraesthesia

also pain on passive movement or squeezing the calf.

132
Q

Irreversible limb ischaemia

A

appears as mottled, non-blanching appearance with hard woody muscles and skin blistering

requires urgent amputation or taking a palliative approach.

133
Q

DDx for acute limb ischaemia

A

Chronic peripheral neuropathy
=> pulses should be present and Temp normal

Compartment syndrome
=> muscles will be tense

DVT
=> red, hot, swollen calf

134
Q

Acute limb ischaemia - management

A

SURGICAL EMERGENCY

Urgent admission
Heparinisation
Surgical management depends on cause

135
Q

Reperfusion injury

A

Inflammation and oxidative damage when blood flow is restored to a tissue after long period of anoxia.

Products of cell death are released can result in rhabdomyolysis, cardiac dysrhythmia, AKI, multiorgan failure and DIC.

Can lead to oedema and compartment syndrome due to increased compartmental pressure.

136
Q

What are the main vasospastic disorders?

A

Raynaud’s syndrome
Acrocyanosis
Livedo reticularis.

137
Q

What is the colour change involved in Raynaud’s disease/phenomenon?

A
  1. Pale (ischaemia)
  2. Blue (cyanosis)
  3. Red (reactive hyperaemia)

As the fingers return to normal there may be numbness, burning sensation or severe pain

138
Q

What is Raynaud’s disease/phenomenon?

A

paroxysmal vasospastic and subsequent vasodilatory chain of events affecting small peripheral arterioles

attacks usually <45mins but can last for hours

139
Q

What can cause Raynaud’s?

A

More common in women

Precipitated by the cold and emotion/stress

Sometimes other triggers – beta-blockers, injuries/trauma, extended use of digits, smoking.

Usually affects hands (but usually the thumb is spared) and feet.

140
Q

Primary vs secondary Raynaud’s

A

Primary is more likely to present as a younger patient, female with a genetic component with no features of underlying disease.

Secondary is more likely to present as an older patient, with more severe symptoms (digital scars, ulceration or gangrene and nail changes)

141
Q

What is anaemia?

A

Anaemia = decreased haemoglobin in the blood, such that there is inadequate oxygen delivery to tissues

Typically Hb <135 g/L in men; Hb <115 g/L in women.

142
Q

Symptoms of Anaemia

A
  • Tired
  • Short of breath – (normal oxygen saturations)
  • Lightheaded/feeling faint
  • Pounding heart/palpitations
  • Pounding in ears
  • Pale
143
Q

RBC lifecycle

A

Erythropoiesis (production of red blood cells) occurs in the bone marrow.
=> Stimulated by erythropoietin (EPO) produced by the kidneys

Average RBC lifespan is 120 days.
=> The ageing RBC are removed from the circulation.

This process normally occurs at the same rate of production by erythropoiesis, balancing the total circulating red blood cell count hence patients have a stable Hb

144
Q

When can patients become anaemic?

A
  1. Not making enough RBCs
    => Reduced erythropoiesis (or haematopoiesis)
  2. Losing or breaking down RBCs too quickly.
    => Bleeding
    => Haemolysis
145
Q

What are some causes of reduced erythropoeisis?

A 
Haematinic deficiency
Bone marrow disorders
Myelosuppressive drugs
CKD
Chronic disease/inflammation
Endocrine dysfunction
146
Q

What does the MCV and MCH represent?

A

MCV - the size of each RBC

MCH - the amount of haemoglobin in each RBC

147
Q

what is microcytic anaemia and what are some causes?

A

= low Hb and MCV

Iron Deficiency
Thalassaemia
Anaemia of chronic disease
Lead poisoning

148
Q

what is normocytic anaemia and what are some causes?

A

= low Hb and normal MCV

Acute blood loss
Anaemia of chronic disease
Haemolysis
Combined deficiency (e.g. iron and B12 deficient)
Bone marrow disorders
149
Q

what is macrocytic anaemia and what are some causes?

A

= low Hb and high MCV

B12 deficiency
Folate deficiency
Myelodysplasia
Alcohol excess
Haemolysis
Other defects of DNA synthesis (e.g. chemotherapy)
Severe hypothyroidism
150
Q

Investigations for anaemia

A
  • B12, folate, ferritin, transferrin saturation
  • Blood film
  • Reticulocyte count
  • LDH (raised in haemolysis), haptoglobin (low), bilirubin (high)
  • Immunoglobulins, serum free light chains
  • Review medication chart
151
Q

Iron storage

A

Iron is absorbed in the duodenum - promoted by gastric HCl.

Ionized iron is toxic so nearly all iron in the body is bound to protein - E.g. Hb, myoglobin, transferrin, ferritin, haemosiderin

Iron is stored in 2 forms – ferritin and haemosiderin

=> Ferritin is soluble, haemosiderin insoluble.

Iron continuously circulates in plasma bound to transferrin

152
Q

Causes of iron deficiency

A

Inadequate intake.

Increased requirements – e.g. pregnancy.

Malabsorption – e.g. coeliac, gastrectomy.

Chronic haemorrhage – e.g. hookworm, menorrhagia, GI tract bleed.

153
Q

Diagnosing IDA

A
  1. MCV low
  2. Blood film - hypochromic, microcytic, pencil cells
  3. A gold-standard would be iron stain on bone marrow
  4. Serum ferritin – roughly correlates with the amount of iron stored in the tissues.

=> Ferritin levels increase in inflammatory conditions (e.g. acute/chronic infection, malignancy) Therefore, can be iron deficient with normal or high ferritin levels.

  1. Transferrin saturation (%)
    => If iron levels are low, less transferrin has iron bound to it.
    => Transferrin saturation is a marker of iron status.
154
Q

Hx to identify cause of iron deficiency anaemia

A

diet
recent blood loss - e.g. menorrhagia

Systems review – any PV/PR bleeding, weight loss, bowels.

155
Q

Management of IDA

A

Address the underlying cause as appropriate.

Oral ferrous sulphate 200mg

Advise dietary increase in dark green vegetables, fortified bread/cereals, lean red meat and prunes/raisins.

If ferrous sulphate not tolerated, consider switch to ferrous gluconate.

Monitor for improvement in symptoms and blood parameters after one month.
=> Should be a 20 g/L increase in Hb (if bleeding has stopped)

Treatment should be continued for 3 months after blood parameters return to normal, to replenish stores.

156
Q

Side effects of iron supplementation

A

GI-related – cramping, bloating, nausea, vomiting, constipation, black stools

157
Q

B12 Absorption

A
  • B12 in food is mainly bound to protein – pepsin in the stomach releases B12 from protein.
  • B12 binds to intrinsic factor, produced by gastric parietal cells in the stomach.

• Intrinsic factor transports B12 into the epithelial cells of the distal half of small intestine.
=> B12 absorbed in the ileum.

• The body generally has stores of B12 for 2+ years

158
Q

what foods generally contain vitamin B12?

A

Generally animal sources – meat, fish, eggs, milk

159
Q

What neurological symptoms can B12 deficiency cause?

A

peripheral neuropathy,

subacute combined degeneration of the cord

160
Q

Causes of B12 deficiency

A

• Inadequate intake

• Inadequate secretion of intrinsic factor
=> Pernicious anaemia
=> Gastrectomy

  • Malabsorption - Crohns, ileal resection
  • B12 levels will measure low if patient is taking OCP or HRT, even if there are normal levels.
161
Q

What is pernicious anaemia?

A

Antibodies against intrinsic factor and/or gastric parietal cells

162
Q

How does B12/folate deficiency cause macrocytic anaemia?

A

B12 deficiency causes macrocytic anaemia, as B12 acts as a co-enzyme for the conversion of folate (B9) to activated folate.

Activated folate is required for DNA synthesis – so B12/folate deficiencies lead to DNA synthesis malfunctions.

DNA fails to “stop” erythrocyte development, leading to very large cells.

Large cells are eventually trapped and destroyed in the reticulo-endothelial system.

163
Q

diagnosis - B12 deficiency anaemia

A
  • Raised MCV
  • Blood film – oval macrocytes, hypersegmented neutrophils, tear drop cells
  • Low B12
  • Test for anti-parietal cell or anti-IF antibodies.
  • Schilling Test – distinguishes between pernicious anaemia and small bowel disease
164
Q

Folate deficiency

A

Folate is absorbed in the duodenum and jejunum. The body generally has folate stores for ~5-6 months

  • Inadequate intake
    => Poor diet, alcohol excess (impairs utilisation), anorexia.
  • Increased requirements
    => Pregnancy, haemolytic anaemia, lactation, prematurity, malignancy.
  • Malabsorption
    => Coeliac disease, jejunal resection
  • Anti-folate drugs
    => Trimethoprim, methotrexate, anti-convulsants.
165
Q

diagnosis - folate deficiency anaemia

A
  • Raised MCV
  • Blood film – macrocytes, hypersegmented neutrophils (i.e. same picture as B12 deficiency).

• Reduced folate – can measure serum or red cell
=> Serum folate levels are readily affected by a short period of negative folate balance
=> Red cell folate often a more reliable assessment of folate stores

166
Q

Management of folate deficiency

A

Folic acid 5mg daily – at least 3 months

Treat underlying cause

Borderline/slightly low B12 and/or folate doesn’t cause significant anaemia

167
Q

What type of antibody do people have against ABO antigens?

A

IgM antibodies against whichever antigen they do not express on their RBCs.

168
Q

What type of antibody do people have against rhesus D antigens?

A

If a rhesus negative individual is exposed to rhesus positive blood, they can develop IgG antibodies directed against the rhesus D antigen

If exposed to rhesus positive blood products again, there will be haemolysis

169
Q

What is a mismatched transfusion?

A

= when a patient receives a transfusion from an incompatible blood group

170
Q

What occurs in cross-matching for transfusion?

A
  • The patient’s pre-transfusion blood sample is tested to determine the ABO and RhD groups
  • The patient’s plasma is screened for the presence of antibodies against other non-ABO red cell antigens which could still be capable of causing a haemolytic transfusion reaction.
  • Antibody screening is performed using a panel of red cells that contains examples of the clinically important blood group antigens.
  • Once the blood group and screen has been performed, compatible blood units can be selected
171
Q

Transfusion Reactions

A

Anti-A and/or anti-B in the recipient’s plasma binds to the transfused cells and activates the complement pathway.

This leads to destruction of the transfused red cells (intravascular haemolysis) and the release of inflammatory cytokines that can cause:

  • Shock
  • Renal failure
  • Disseminated intravascular coagulation (DIC).
  • Death
172
Q

what is the role of WBCs?

A

protection against invading microorganisms/immune attack

173
Q

differentiation of blood cells

A

Blood cells are all derived from a self-renewing pluripotent stem cell.

Differentiation into committed MYELOID or LYMPHOID progenitors which then mature into all the mature blood cells

174
Q

What is the purpose of neutrophils?

A

Respond chemotactically to various stimuli
=> complement, lymphokines and bacterial membrane components

Perform phagocytosis of foreign particles and microbes

175
Q

What can cause neutrophilia?

A 
Infection/inflammation (bacterial or fungal)
Neoplasia
Bleeding
Infarction (including MI)
Smoking
Burns
Drugs (glucocorticoids)
176
Q

What can cause neutropenia?

A 
Viral or malaria infection
Drugs (e.g. carbimazole, chemotherapy)
B12/folate deficiency
Autoimmune
Cyclical neutropenia
Haematological malignancy 
Hereditary
177
Q

What is important to know in neutropenia?

A 
Is the patient unwell?
Any previous normal counts?
Ethnicity?
Any other cytopenia?
Is the patient on chemotherapy?
Other DHx?
178
Q

Severity of neutropenia?

A

Normal = 2.0 - 8.0

  • Mild (1.0-1.7), functionally normal
  • Moderate (0.5-1.0)
  • Severe (<0.5) – RISK OF INFECTION
179
Q

Neutropenic sepsis

A

fever >38*C and neutrophils <1.0

a medical emergency requiring urgent hospital admission and IV broad spectrum antibiotics within 1 hour.

180
Q

What are the major cell types of lymphocyte?

A
  1. T lymphocytes – 80% (derived from thymus, circulate in blood)
  2. B lymphocytes – 20% (mainly in the lymph nodes, few in blood)
  3. Natural Killer cells (large, granular lymphocytes)
181
Q

T-lymphocytes

A

Involved in cell-mediated immunity and regulating go B-lymphocytes

182
Q

B-lymphocytes

A

Production and secretion of antibodies

Participation in “immunological memory”

183
Q

Primary causes of lymphocytosis

A

Lymphoid malignancies

  • Chronic lymphocytic leukaemia
  • Lymphomas
  • Monoclinal B lymphocytosis
184
Q

Reactive causes of lymphocytosis

A

Viral (EBV, CMV, HSV, VZV)
Whooping cough
TB
Stress – septic shock, trauma, MI, drug-induced

185
Q

Chronic causes of lymphocytosis

A 
Cigarette smoking
Autoimmune disorder
Chronic inflammation
Sarcoid
Raised BMI/metabolic syndrome.
186
Q

What do monocytes do?

A

Phagocytosis – ingest and destroy fungi, bacteria and damaged or degenerated cell

Stimulate the immune response by presenting the products of phagocytosis to lymphocytes

Attract neutrophils to the damaged site by secreting chemical attractants.

Aid in maintenance of blood vessels

187
Q

Causes of monocytosis

A

Atypical Infections – e.g. TB
Inflammation
Autoimmune diseases

Haematological malignancies – e.g. chronic myelomonocytic leukaemia (CMML)

188
Q

Causes of eosinophilia

A
  • Parasitic infections
  • Allergy
  • Asthma
  • Drugs
  • Skin disorders – e.g. eczema
  • Haematological malignancies – e.g. Hodgkin’s disease, CML
189
Q

Causes of basophilia

A

very rare - usually only seen in chronic myeloid leukaemia

190
Q

What do basophils do?

A

Secretes substances during an allergic reaction

Secretes large amounts of heparin (anticoagulant)

Secretes histamine, which participates in constriction of the blood vessels, bronchioles and intestines

191
Q

What is leukaemia and what is its incidence?

A

= Cancer of the WBCs

Most common of childhood cancers but seen most commonly in age >50

Increasing incidence (aging population)

192
Q

what is the most common leukaemia in children?

A

Acute lymphoblastic leukaemia (ALL)

193
Q

Acute leukaemias

A

= no differentiation, primitive “blast” cells

Acute myeloid leukaemia (AML)
Acute lymphoblastic leukaemia (ALL)
Acute bi-phenotypic leukaemia

194
Q

Chronic leukaemias

A

= normal differentiation into mature white cells

Chronic myeloid leukaemia (CML)
Chronic lymphoblastic leukaemia (CLL)

195
Q

Symptoms of leukaemia

A

symptoms resulting from:

  1. bone marrow failure
  2. organ infiltration with leukaemic cells
  3. both.

The time course is variable
=> Some patients, particularly younger ones, present with acute symptoms over a few days to 1-2 weeks.
=> Others have a longer course, with fatigue or other symptoms lasting from weeks to months.

196
Q

What symptoms indicate bone marrow failure?

A

anaemia (tiredness / lethargy/ SOB),
neutropenia (infection),
thrombocytopenia (bruising and petechiae).

197
Q

Signs of leukaemia

A
  • Anaemia
  • Low OR High white cell count
  • Thrombocytopenia
  • Pancytopenia
  • May be circulating ‘blast’ cells seen on blood film
198
Q

What is Westermark sign?

A

on CXR
=> enlarged pulmonary artery
=> distally to this there are fewer lung markings

199
Q

“Tennis ball sign” in aorta

A

indicates tear in the intima

= aortic dissection

200
Q

What is haemostasis?

A

= the process by which the body stops bleeding if there is injury to a blood vessel

201
Q

What is the role of primary haemostasis?

A

Begins immediately after endothelial disruption

vascular contraction, platelet adhesion and aggregation, and formation of a soft haemostatic plug

202
Q

What is the role of secondary haemostasis?

A

the process of stabilisation of the soft haemostatic plug through a complex interaction between platelet membrane, enzymes and coagulation factors

203
Q

Process of primary haemostasis

A
  • Injury causes vasoconstriction (slows blood flow, enhancing platelet adhesion and activation) and exposure of collagen (trigger for platelet activation)
  • Von Willebrand factor attaches to the sub-endothelium. Glycoproteins on the platelet surface adhere to vWF.
  • Platelets collect across injured surface. Platelets are activated by contact with collagen.
  • Collagen-activated platelet membranes expose receptors which bind circulating fibrinogen.
  • Aggregation of platelets and fibrinogen build up to form a soft haemostatic plug
204
Q

What are some important molecules involved in primary haemostasis?

A 
Thromboxane A2
Arachidonic acid
ADP
vWF
GPIb, GPIIb/IIIa
205
Q

What are the clinical features of impaired primary haemostasis?

A 
1. Mucocutaneous bleeding
•	 Bruising
•	 Epistaxis
•	 Gum bleeding
•	 Menorrhagia
  1. Intra-op or immediate post-op bleeding
206
Q

What are the causes of impaired primary haemostasis?

A

Reduced platelet number (i.e. thrombocytopenia)

Impaired platelet function - congenital or acquired

Reduced amount/impaired function of vWF (i.e. von Willebrand disease)

207
Q

What is coagulation factor I?

A

Fibrinogen

208
Q

What is coagulation factor II?

A

Prothrombin

209
Q

What is coagulation factor IIa?

A

thrombin

210
Q

Vitamin K deficiency - causes and consequence

A

can be caused by:

  • Malabsorptive conditions (K = fat soluble vitamin)
  • Cholestatic jaundice (no bile salts)
  • Antibiotics (gut flora disturbances)

leads to a reduction in activated factors, which will lead to an increased PT and haemorrhage

211
Q

Which factors are dependent on vitamin K?

A

II, VII, IX, X

212
Q

What are the causes of thrombocytopenia?

A 
INCREASED PLATELET DESTRUCTION
Sepsis/inflammation
DIC
Thrombotic thrombocytopenic purpura
Autoimmune, Alloimmune
Drug-induced
DECREASED PLATELET PRODUCTION
Alcohol 
Cytotoxic drugs
Bone marrow failure
Infections

OTHER
Hypersplenism
Haemodilution

213
Q

Which drugs can cause increased platelet destruction?

A

heparin, antibiotics, antimalarials, NSAIDs

214
Q

What are anti platelet drugs?

A

Aspirin
Clopidogrel
Ticagrelor
Abciximab or Eptifibatide

215
Q

Coagulation factors

A

Mostly produced in the liver.

Factors circulate in an inactive form until the coagulation cascade is initiated

When active, these factors mainly act as serine proteases to activate other factors

216
Q

What are the pathways to activate the coagulation cascade?

A
  1. intrinsic pathway (damaged endothelial surface)

2. extrinsic pathway (trauma)

217
Q

What does the coagulation cascade ultimately result in?

A

The conversion of fibrinogen to fibrin

218
Q

What are the physiological inhibitors of the coagulation cascade?

A

Anti-thrombin III – serine protease inhibitor

Activated protein C – activated by thrombin and acts with the co-factor protein S
=> destroys factor V and VIII, reducing further thrombin generation and inhibits stabilisation of the fibrin clot

219
Q

What are the clinical features of impaired secondary haemostasis?

A

Haemarthrosis

Muscular/soft tissue bleeding

Extensive bruising

Delayed post-op bleeding and poor wound healing (rather than immediate effects)

220
Q

Causes of impaired secondary haemostasis

A

Reduced coagulation factors

=> congenital (haemophilia A or B)
=> acquired - anticoagulation, liver dysfunction, DIC, acquired haemophilia

221
Q

Coagulation tests - primary haemostasis

A

FBC and Blood Film – platelet number and morphology

Platelet function tests and complex platelet test by specialist

Von Willebrand factor assays

222
Q

Coagulation tests - secondary haemostasis

A

Clotting Screen

  • Prothrombin time (PT) = “extrinsic”
  • Activated partial thromboplastin time (APTT) = “intrinsic”

Mixing studies – patient plasma mixed with normal fresh frozen plasma.
=> If this fully corrects then factor deficiency
=> If not then there is presence of inhibitor

Clauss fibrinogen test

Clotting factor assays – measure individual factor level

223
Q

Process of PT/APTT

A
  1. Citrated blood sample (i.e. blue bottle) Citrate removes Calcium.
  2. Samples is centrifuged to remove platelets (creating Platelet Poor Plasma)
  3. Platelet poor plasma is mixed with an activator and calcium
    => PT (extrinsic) = add Tissue Factor and Calcium
    => APTT (intrinsic) = add Kaolin, Phospholipids and Calcium
  4. The time to clot formation is calculated.
224
Q

What is DIC?

A

= systemic activation of coagulation pathways leading to extensive intravascular coagulation and fibrin clot development

Thrombotic occlusion of the arterial microvasculature

Simultaneous depletion of clotting factors and consumption of platelets leads to haemorrhage.

Eventually organ failure develops.

225
Q

Haemophilia A vs. B

A 
A = factor VIII
B = factor IX

A is more common than B, as the factor VIII gene is larger

226
Q

How does haemophilia affect more severely?

A

Both X-linked recessive disorders

Affects males more severely, women can be affected severely but tend to be carriers and only mildly affected.

227
Q

Severity of haemophilia

A

Based on the amount of the factor present, compared to normal

– Severe <1%
– Moderate 1-5%
– Mild >5%

Severe => spontaneous bleeding
Mild => just excessive bleeding if injured

CP1 (12 decks)

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