Textbook Reference-

Unit VI (p449)

Part 1 of 3
 Disorders of Blood Flow
 Disorders of the Arterial circulation:
 Atherosclerosis (previously covered Path 1)
 Hyperlipidaemia
 Raynaud’s disease
 Aneurysms

 Disorders of the Venous circulation:

 Varicose veins
 Venous thrombosis

 Disorders of Blood flow due to extra-vascular

forces:
 Pressure ulcers
 1. Hyperlipidaemia - Lipids
Hyperlipidaemia is the presence of abnormally high
levels of lipids in the blood.
 The lipids
include:
– Triglycerides
– Phospholipids
– Cholesterol
 Hyperlipidaemia
Lipoproteins
 Lipoproteins transport cholesterol and
triglycerides in the blood as they are insoluble
in plasma.
 There are five types of lipoprotein:
 Chylomicrons
 Very low density lipoproteins (VLDL)
 Intermediate density lipoproteins (IDL)
 Low density lipoproteins (LDL)
 High density lipoproteins (HDL)
 Lipoproteins movement
throughout the body
Chylomicrons:
 Are mostly TGs from diet travelling through lymph and then
blood
 Deposit lipids as needed by cells
 Remnants return to liver

VLDL’s:
 Transport TGs + other lipids from liver to tissues, but mostly to
adipose
 VLDLs converted to LDLs after delivery of TGs

LDL’s:
 Transport cholesterol to peripheral tissues

HDL’s:
 Synthesised by the liver as an “empty” envelope
 Picks up excess cholesterol found in peripheral tissues back to the
liver to become bile
 Delivers cholesterol to steroid-producing organs
 Hyperlipidaemia-Apoproteins
Apoproteins are cell markers. They control the interactions
and ultimate metabolic fate of the lipoproteins. They
facilitate the removal of lipids from lipoproteins.
 There are four classes of apoproteins: A, B, C, and
E.
 Uptake of lipids by cells:
 Relies on interaction between apoproteins and receptors
on target tissue.

 Causes of hyperlipidaemia:
 Nutrition
 Genetics
 Metabolic diseases
 Hyperlipidaemia -
Hypercholesterolaemia
 Serum cholesterol may be elevated as a result of
any of the lipoproteins.
 Testing: profiles must be conducted
 Total cholesterol: < 5.5 mmol/L
 LDL
 HDL: > 1.0 mmol/L
 Triglycerides: < 1.7 mmol/L
 HDLs rise with:
 Exercise and high unsaturated fat intake
 LDLs rise with:
 High kilojoule intake
 High saturated fat levels
 High cholesterol intake
You could:
 reduce cheese intake and/or substitute low fat varieties
 choose reduced fat milks
 substitute polyunsaturated margarine for butter
 choose lean cuts of meat and remove all visible fat
 eat skinless chicken, fish or beans
 beware of pies, pasties, fish and chips and commercial cakes
(hidden fat)
 make cakes at home with polyunsaturated fat, cook chips with
polyunsaturated or monounsaturated oil
 lose weight if overweight.
 Covered in Path 1.
 See pages 481-485 Porth
 Please revise.
 Clinical manifestations:
 Depend on the artery involved and the extent of
vessel obstruction.
 End result is ischaemia, plaque haemorrhage or
rupture, thrombosis, formation of emboli, or
aneurysm.
 Ischaemia and infarction in the heart and brain
(TIA) are more common.
 Kidneys, lower extremities and small intestine
are also frequently involved.
 Named for French
physician Maurice
Raynaud (1834–1881).
 Some refer to
Raynaud's disease as
"being allergic to
coldness".
 Functional disorder caused by intense vasospasm of the
arteries and arterioles in the fingers and less often in
the toes.
 Vasospasm: excessive vasoconstriction
 Limited to fingers
 2 types:
 Raynaud’s disease occurs without demonstrable cause
(idiopathic form).
 Raynaud’s phenomenon/syndrome associated with
other disorders.

These subtypes can be referred to as primary and

secondary Raynaud’s respectively.
 Aetiology: Unknown
 Hyper-reactivity of the sympathetic nervous system has
been suggested as a contributing cause.
 Genetic predisposition but genes haven’t been
identified yet.
 Precipitated by cold and strong emotions in
young women.
 Limited to the fingers:
 Rarely causes necrosis of the fingers
 Symptoms:
 Changes in skin colour from pallor to cyanosis only
in fingers and toes (1 or more)
 Cold sensation
 Numbness and tingling
 The disease does not generally follow a severe path,
and there are minimal complications.

 Treatment:
– Abstinence from smoking/caffeine, Protection of
body from low temperatures, Avoidance of
emotional stress
– Medications and surgery may be used.
 When exposed to cold temperatures, the blood supply
to the fingers or toes, and in some cases the nose or
earlobes, is markedly reduced; the skin turns pale or
white (called pallor), and becomes cold and numb.
 When the oxygen supply is depleted, the skin colour
turns blue (called cyanosis).
 These events are episodic, and when the episode
subsides or the area is warmed, the blood flow returns
and the skin colour first turns red (rubor), and then
back to normal, often accompanied by swelling and
tingling.
 Can be associated with previous vessel injury
 E.g. frost-bite, occupational trauma (vibrating tools), collagen
diseases and neurological disorders & chronic arterial occlusive
disorders.
 Connective tissue disorders:
 scleroderma
 systemic lupus erythematosus
 rheumatoid arthritis
 Sjögren's syndrome
 dermatomyositis
 polymyositis
 mixed connective tissue disease

Raynaud's phenomenon is the initial symptom that presents for

70% of patients with scleroderma, a skin and joint disease.
 The disease does not generally follow a severe
path, and there are minimal complications.
 In some severe & chronic cases there may be
atrophy of the skin, subcutaneous tissues and
muscle, with in very severe cases, ulceration
and gangrene.

An aneurysm is
a localised,
abnormal
dilation of any
blood vessel.

Occur in arteries
and veins.

Most common
in the aorta
before iliac
arteries.
 A swelling that can occur in any region of the aorta-
ascending/descending/thoracoabdominal, thoracic and abdominal
arteries.


Common risk factors: atherosclerosis and degeneration of the
vessel media.

50% with aortic aneurysms have hypertension.

More common in men and after the age of 50.

Symptoms depends on size and location, though most are
asymptomatic. While enlarging they may cause abdominal
pain or back pain. Nerve compression and leg pain may also
occur.

Diagnosed with CT scans, MRI, and ultrasounds.
 Sudden, intense pain in the back or abdomen, possibly spreading to
the groin, buttocks and legs
 Throbbing lump-like mass or sensation in the abdomen
 Abdominal rigidity
 Symptoms of shock, including trembling, dizziness, sweating,
fainting and elevated heart rate
 Nausea and vomiting
 Anxiety
 Pale skin
 Dry mouth and great thirst

Survival rate is ~30% if patient is hospitalised- if not the rate is only about
10%. Ruptured aneurysms cause approx. 15,000 deaths per year in the
USA.

Treatment: surgical repair with a graft of
woven Dacron.
 It involves haemorrage into the vessel wall with
longitudinal tearing of the vessel wall to from a blood-
filled channel.
 Unlike atherosclerosis aneurysms, aortic dissection often
occurs without evidence of previous vessel dilation.
 Dissections can originate anywhere within the length of
the aorta with over 60% occurring in the ascending aorta.
 Most common in the 40-60yr group with more men than
women (2:1) afflicted.
 Risk factors include hypertension and degeneration of the
vessel wall.
 Aortic dissections resulting in rupture have an 80% mortality
rate, and 50% of patients die before they even reach the
hospital.
 About 96% of individuals with aortic dissection present
with severe pain that had a sudden onset. It may be
described as tearing in nature, or stabbing or sharp in
character.
 17% of individuals will feel the pain migrate as the
dissection extends down the aorta. The location of pain is
associated with the location of the dissection.
 Anterior chest pain is associated with dissections involving the
ascending aorta, while interscapular (posterior chest pain) is
associated with descending aortic dissections.
 A bicuspid aortic valve (a type of congenital heart
disease involving the aortic valve) is found in 7–14% of
individuals who have an aortic dissection.
 Marfan’s syndrome is noted in 5–9% of individuals
who suffer from aortic dissection.
 Turner syndrome also increases the risk of aortic
dissection.
 Chest trauma leading to aortic dissection can be
divided into two groups based on etiology: blunt chest
trauma (commonly seen in car accidents).
It has a sensitivity of 96 to 100% and a specificity of 96 to 100%.
Disorders of the venous system produce congestion of
the affected tissue and predispose to clot formation
because of stagnation of flow and activation of the
clotting system.

 Problems include:
– Varicose veins
 Primary
 Secondary
– Venous thrombosis
– Venous ulcers
 Veins return
blood to the
heart and are
helped by the
pumping
action of the
muscles and
venous valves
to prevent
backflow.
 Common in the lower extremities and often lead
to secondary problems of venous insufficiency.
 Become enlarged, dilated, and very tortuous.
 Primary
varicose veins
originate in the
superficial
saphenous
veins.
 Secondary
varicose veins
occur in the
deep venous
channels.
 Most common
cause of is deep
vein thrombosis
(DVT).
 Prolonged standing (increased hydrostatic
pressure)
 Increases in intra-abdominal pressure:
 Constipation
 Pregnancy
 Lifting
 Obesity
 Increased pressure on valves causes them to
become incompetent so they no longer close
properly.
Symptoms:
 Tortuous looking veins
 Ache in the lower extremities
 Oedema may occur

Diagnosis:
 Physical inspection

Treatment:
 Prevention is better than cure
 Elastic support stockings
 Sclerotherapy
 Surgical removal only for unobstructed deep venous
channels
DVT
 A.k.a. Thrombophlebitis

 Presence of thrombus (clot) in a vein which is

accompanied with inflammatory response in vessel
wall.
 Develops in superficial or deep veins
 Most common in lower extremities
 Risk factors - Triad
 Stasis of blood
 Hypercoagulability
 Vessel wall injury

 - Please refer to Chart 22-2 p501 in your textbook for expression

of risk factors-
 Symptoms:
 Condition can be asymptomatic due to partial occlusion
of the vein or collateral circulation.
 Symptoms are related to an inflammatory response:
 Pain in the effected body part
 Swelling (oedema)
 Muscle tenderness.
 Additional signs such as fever, malaise, elevate WBC
count and ESR also are supportive.
 Importantly, many patients are asymptomatic
 Development of pulmonary embolism is a major
complication.
 Homan’s sign can be
used to help diagnose
DVT.
 Ultrasound has much
better sensitivity and
specificity to detect
this condition.
 Treatment:
 Medications analgesics (pain medications)
 Anticoagulants e.g warfarin or heparin to prevent new clot
formation
 Thrombolytics to dissolve an existing clot such as
intravenous streptokinase.
 Nonsteroidal anti-inflammatory medications (NSAIDS)
such as ibuprofen to reduce pain and inflammation
 Antibiotics (if infection is present) selection will usually
depend with the causative agent.
 Support stockings and wraps to reduce discomfort
 Drugs to prevent and dissolve clot formation.

 Surgical removal, stripping, or bypass of the vein is rarely

needed but may be recommended in some situations.
 Some malignancies, especially adenocarcinomas of the pancreas
and lung, are associated with hypercoagulability (the tendency to
form blood clots) for reasons that are incompletely understood,
but may be related to factors secreted by the tumors, in particular
a circulating pool of cell-derived tissue factor-containing
microvesicles.
 In patients with malignancy-associated hypercoagulable states,
the blood may spontaneously form clots in the portal vessels, the
deep veins of the extremities (such as the leg), or the superficial
veins anywhere on the body.
 A.k.a. “bed sores” or pressure ulcers.

Ischaemic lesions of the skin and underlying

tissues caused by compression of blood vessels
due to external pressure.
 Most likely develop over a bony
prominence.
 Lower parts of body is more likely to be
affected (sacrum and heel).
 Frequently painful; they can take a long
time to heal and frequently reoccur.
Pathophysiology:
 Venous stasis results from damage to the vein

valvular system in the lower extremity and in

extreme cases allows the pressure in the veins
to be higher than the pressure in the arteries.
This pressure results in transudation of
inflammatory mediators into the subcutaneous
tissues of the lower extremity and subsequent
breakdown of the tissue including the skin.
Venous Ulcers