CLI Week 3 Flashcards
Overview of disorders of blood vessels:
Arteries:
Artherosclerosis normally effect elastic and muscular arteries. Hypertension normally affect resistant (small) arteries. Tunica intima. Tunica media (smooth muscle). Tunica adventitia (nerves and vasa vasorum). Elastic arteries, elastic fibers in media (aorta and major branches – subclavian, carotids, iliac). Muscular, smooth muscle in media. Most inflammation cause WBC exudation at the post-capillary venule because it doesn’t have loose CT.
Vascular anomalies
Arteriovenous fistula – direct connection between arteries and veins, bypassing the capillaries. Put extra strain on the heart because larger volume needs to be pumped.
Fibromuscular dysplasia – focal irregular thickening of medium and large arteries, can occur at any age. Angioplasty show string of beads appearance.
Endothelium
Activation by cytokines, bacteria toxins, advanced glycation end-products, hypoxia, results in vasoconstriction and vasodilation. Relaxing factor NO and contraction factor endothelin. Endothelium dysfunction – change in endothelial phenotype.
All injuries result in tunica intimal thickening by proliferation of smooth muscle, which are special muscle cells that are mobile and have biosynthetic capability.
Hypertension
Essential hypertension 95% idiopathic. Reduced sodium excretion – however at higher pressure, a new steady state is achieved by pressure natriuresis.
Secondary hypertension from renal or adrenal disease. Most common hyperaldosteronism. Renovascular hypertension pathogenesis – renal artery stenosis reduce the volume and pressure of afferent arteriole. This activate renin angiotensin system causing rise in angiotensin II (systemic vasoconstriction) and aldosterone (increase H2O and Na+ retention). Gene mutation of enzyme that break down aldosterone, and Liddle syndrome where there is gain of function of Na+ channel.
Malignant hypertension 200/120 mmHg.
Two vascular pathology of muscular artery. Hyaline arteriolosclerosis – caused by protein exudation (hyalinized) and smooth muscle cells proliferation. Nephrosclerosis impair renal supply. Hyperplastic arteriolosclerosis – concentric laminated thickening of the walls (like onion skin) with luminal narrowing, due to multiplication of basement membrane.
Veins:
Varicose Vein – dilation and tortuous vessels. Stasis dermatitis occur because of extravasated red cells. Esophageal varices – due to embolism of portal vein and dilatation of the portosystemic shunts. Hemorrhoids occur in pregnancy due to dilatation of anorectal junction.
Thrombophlebitis – can occur in varies organs – the dural sinuses, portal vein and pelvic venous plexus. Tumors produce procoagulant factors which cause migratory thrombophlebitis, where it appear in one sit then disappear to another. Deep vein thrombosis – pain, swelling, redness and engorged veins. Immobilization => stasis and thrombus formation. Often associate with PE so any clot above knee needs to be put on anticoagulation medication.
Superior vena cava and inferior vena cava syndrome are due to obstruction. Often by neoplasm that grow in within veins such as hepatocellular and renal cell carcinoma.
Lymph:
Lymphangitis acute inflammation most commonly by bacteria. Red painful subcutaneous streak and enlargement of draining lymph node (lymphadenitis). Primary congenital blockage. Secondary – tumor, radiation. Chronic lead to persistent edema and deposition of interstitial CT that lead to orange peel appearance of skin. Rupture cause accumulations of lymphs leading to chylous ascities, chylothorax and chylopericardium.
Overview of Ulcers:
Venous ulcers – due to increase venous pressure and exudation of fibrinogen. Perivascular fibrin deposition and reduce O2 supply. Commonly found above ankles. Lipodermatosclerosis – induration, redbrown pigmentation (hemosiderin) and inflammation. Can be painful. Manage: high compression bandaging and leg elevation. Doppler to exclude arterial diseases. Skin graft prevent recurrence. Most heal within 6 months.
Arterial – higher up the legs, associated with claudication and PVD. Keep the ulcer clean and vascular reconstruction.
Neuropathic – Pressure area such as metatarsal head due to repeated trauma.
Pressure – immobile patients.
Skin:
BCC – pearly, telangiectasia. Nodular, superficial, ulcerated, basosquamous, sclerosing and pigmented.
SCC – ulcerated with indurated and keratotic skin due to squamous cells hyperplasia.
Melanoma – ABCDE, asymmetry, boarder, colour, diameter above 5cm, elevation.
Raynaud phenomenon:
Red (reactive capillary dilation), white (ischemia) and blue (cyanosis) appearance. Benign uncommon to cause gangrene. Primary – hyper reaction to cold or emotion. Secondary – autoimmune diseases, asymmetrical and progressively worsen, it maybe the first manifestation for underlying immune-mediated vasculitis.
Pulmonary Embolism – etiology, pathophysiology, clinical features and complications
- etiology ® risk factors include; certain medications, immobilization for a long period of time, fractures, severe trauma, surgery, congestive heart failure, oral contraceptive pill with high estrogen content, primary disorders of hypercoagulability.
- Pathophysiology ® PE occurs when a blood clot gets wedged into an artery in your lungs. These blood clots most commonly come from the deep veins in your legs (deep vein thrombosis). In the lungs it decreases blood flow, causing a decrease in oxygenated blood thus you get symptoms of shortness of breath.
- Clinical features ® pulmonary hypertension, chest pain, SOB, acute right-sided heart failure
- Complications ® cardiac arrest and sudden death, shock, abnormal heart rhythms, death of part of the lung (pulmonary infarction), pleural effusion, paradoxical embolism, pulmonary hypertension.
- Varicose veins – pathology and clinical features
- Varicose veins are the most common cause of venous ulcers (wet, oozing, dermatitis, gaiter region)
- Dilated, tortuous superficial veins due to reversal of venous flow
- Can be congenital or acquired (more common)
- Veins become dilated due to increased pressure (venous HTN) and weak walls (note: superficial veins have no muscle/fascia to support them and therefore dilate when overloaded)
- Normally: skeletal muscle pump helps guide venous blood back to the heart and the valves stop backflow of blood
- therefore if the skeletal muscle pump is not being engaged (long periods of immobility – travel/depression/hospitalization) the venous blood can pool increasing pressure in the superficial veins of the lower limbs
- also: congenital valve defects can lead to inadequate forward venous flow to the heart à blood falls back into the superficial vessels
- complications: dermatitis, skin ulcers, superficial thrombophlebitis (painful!)
- Important: rare for varicose veins to cause DVT because of flow reversal (unlikely for thrombus to go backwards from superficial veins to deep veins)
- Risk factors: obesity (increased intra-abdo pressure = decreased venous return) , job that requires long periods of standing (gravity – venous pooling)
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Clinical features:
- Large tortuous veins
- Mild swelling of ankles/feet
- Painful/achy or heavy legs
- Pain worse after standing/sitting for a long time
- If complications: may see ulcers, venous stasis dermatitis (itching) and patient may have sore/red/swollen/hot area of skin over veins affected by superficial thrombophlebitis
- Revision: skin malignancies – SCC, BCC and melanoma à gross and microscopic features
Gross features
Microscopy
SCC
arise from pre-existing solar keratoses
indurated nodules with keratotic surface
highly variable appearance
no telangiectasia, no peary edge
often a crusted surface, rolled edge and ulceration
note: squamous cell carcinoma in any tissue looks similar
keratin pearl aggregate formations – concentric layers of abnormal squamous cells
appear pink
BCC
arise in normal skin
telangiectasia
pearly appearance
different types:
- Nodular
- Superficial
- Ulcerative
- Morphoeic
- Pigmented
- recurrent
abnormal proliferation of basal skin cells
Melanoma
ABCDE -
asymmetric – in pigment, shape
border is irregular
colour usually pigmented (note: amelanotic can occur)
diameter greater than 6mm
can occur in areas not exposed to sun
evolve over time (depends on type)
EFG – nodular melanoma
E – elevated above the skin surface
F – firm to touch
G – growing
different types:
- Superficial spreading
- Lentigo maligna melanoma
- Acral lentiginous/sub-ungual melanoma
- Amelanotic
- Desmoplastic melanoma
- Nodular melanoma (most dangerous)
excess proliferation of large bluish cells producing pigment = melanocyte cells
Vasculitis – Overview of Different Types:
Vasculitis – Overview of Different Types:
Buerger’s:
- Characterised by segmental, thrombosing, acute and chronic inflammation of the medium-sized and small arteries
- Principally the tibial and radial arteries with occasional secondary extension into the veins and nerves of the extremities.
- Often leads to vascular insufficiency, especially of extremities
- Almost exclusively occurs in smokers, before age 35
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Pathogenesis
- Tobacco à idiosyncratic endothelial cell toxicity OR immune response to components of tobacco smoke that modify host vascular wall proteins
- Smoking abstinence in early stages can often ameliorate further attacks but once established vascular lesions typically do not respond to smoking abstience
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Clinical features
- Raynaud phenomenon
- Intermittent claudication
- Instep claudication
- Venous inflammation
- Severe pain
- Ulcerations à gangrene
Giant Cell:
- Chronic inflammatory disorder of large to small-sized arteries that principally affects arteries in the head
- Especially temporal arteries but also vertebral and ophthalmic
- Medical emergency
-
Pathogenesis
- T cell mediated immune response against one of handful of vessel wall antigens à proinflammatory cytokine production (TNF in particular) à granulomatous response (Responds to steroids)
- Predilection for a single vascular site unknown
- Microbiology – Anti-endothelial cell and anti-smooth muscle cell antibodies can also be demonstrated in roughly 2/3 of patients
Polyarteritis:
- Systemic vasculitis of small or medium sized muscular arteries, typically involving renal and visceral vessels but sparing the pulmonary circulation
- 30% have chronic Hep B and deposits containing HBsAg-HBsAb complexes in affected vessels, indicate an immune complex- mediated etiology
- Unknown cause
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Clinical features
- Typically young adults, but can occur in older and pediatric
- Ischemia à clinical manifestations
- Remitting and episodic – long term symptom free intervals
- Classic – rapidly accelerating hypertension due to renal artery involvement, abdominal pain and bloody stools caused by vascular GIT lesions; diffuse myalgia’s, peripheral neuritis (predominantly motor nerves)
- Treated with immunosuppression
- Typically fatal untreated
Arteriosclerosis vs Arteroelosclerosis:
- Atherosclerosis → a hardening of an artery specifically due to an atheromatous plaque
- Arteriosclerosis → a general term describing a hardening of medium or large arteries
- Arteriolosclerosis → a hardening of arterioles
Varicosities—Why do they form and where? —Pathophysiology of varicose vein formation.
Varicose veins are abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure leading to vessel dilation and incompetence of the venous valves.
In healthy veins, the flow of blood is generally through the superficial system into the deep system and then towards the right atrium. One way valves are found in both the deep and superficial systems and incompetence in any of the valves can cause bi-directional flow (in the opposite direction) of blood and lead to venous hypertension.
Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious cycle. Pooled blood and venous hypertension leads to dilated veins which then worsen valvular incompetency. This is more likely to occur in the superficial veins rather than the deep veins. Deep veins can withstand higher levels of pressures.
- Outline the clinical features of peripheral vascular disease—Arterial and Venous
Disease.
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Staging of PVD
- Fontaine Stages
- Asymptomatic
- Mild claudication
- Moderate-severe claudication
- Ischaemic rest pain
- Ulceration or gangrene
- Rutherford grades and categories – basically the same thing
- Fontaine Stages
Arterial
Venous
Dry, dark, painful
Wet, oedematous, oozing
Clear border, with no bleeding
Irregular and shallow
Painful
Painless
Dorsum of foot and distal areas e.g. toes
Gaiter region
Shiny skin, loss of hair, atrophy surrounding area
Stasis dermatitis surrounding area
Due to atherosclerosis
Due to varicose veins and lack of venous outflow
Do not use compression bandage
Use compression bandage
2. Describe the risk factors for DVT –especially travel – think Virchow’s Triad.
- Pregnancy and post-partum period Ú hypercoagulability
- Recent sepsis
- Malignancy Ú hypercoagulability
- Prior VTE
- Central venous access
- Hormonal contraceptives or hormonal replacement therapy
- Other drugs such as antipsychotics, tamoxifen
- Prolonged travel – flights 6-8 hours long or any travel longer than 4 hours
- Thrombophilia
- Family history of VTE
- CV risk factors incl. obesity
- Prolonged sitting
- Invasive procedures
- Q Thrombosis risk calculator predicts risk of VTE in primary care patients
- Based on:
- Age
- Gender
- BMI
- Smoking status
- Medical history
- Current medication
- Based on:
3. Outline the symptoms and signs of DVT.
- Unilateral pitting oedema
- Leg swelling, especially if circumference is more than 3cm compared to asymptomatic leg
- Calf tenderness, especially upon compression of calf muscles
- Be careful not to palpate too hard bc risk of dislodging clot into systemic circulation and causing PE
- Prominent superficial veins (superficial vein distension)
- Note: Homans’ sign is not particularly useful (pain during dorsiflexion of foot)
Wells criteria for PE
4. Wells criteria for PE
- Wells Score System is used for DVT probability
- One point each for the below clinical findings
- Negative 2 if alternative diagnosis as likely or more likely than DVT
- Note: not good for:
- Elderly patients
- Patients with comorbidities
- Recurrent DVT
- Pulmonary embolism
- Clinical findings (BPTSOCCCA):
- Bedridden – recently for more than 3 days or major surgery within past 4 weeks
- Paralysis, paresis or recent orthopaedic casting of lower extremity
- Tenderness – localised in deep vein system
- Swelling – entire leg
- Oedema – pitting in the symptomatic leg
- Calf swelling – 3cm greater than asymptomatic leg
- Cancer – active or cancer treated within 6 months
- Collateral non-varicose superficial veins
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Alternative diagnosis – more likely than DVT e.g. Baker’s cyst, cellulitis, muscle damage, superficial vein thrombosis, inguinal lymphadenopathy, external venous compression etc.
- NOTE this is -2 points!
What are the risk factors for ischemia?
- Smoking
- Diabetes
- Overweight or obesity
- Sedentary lifestyle
- High cholesterol
- High blood pressure
- Family history of vascular disease
Symptoms and signs of ischemic lower limb, including critical ischemia?
- rest pain in legs
- non-healing wounds
- tissue necrosis (gangrene)
- burning pain in feet and toes that is worse at night
- pain is exacerbated by the recumbent position
- edema of the feet and ankles
Value of D dimer and first line investigations for suspected DVT and thrombo-embolism
D dimer is used as a biological marker for early DVT after TKA, sensitivity is 68%, specificity is 55%, accuracy is 60%. So it cant be relied on as a sole diagnosis.
First line investigations ® ultrasound, a D-dimer test, venography.
