week 3 term 1 Flashcards
what is the lower limb anatomy of arteries? and veins? explain from pelvis
➢ Arterial Supply
- The femoral artery is the main artery in the lower limb. Is a continuation of the external iliac artery & enters thigh behind the inguinal ligament
- The femoral artery becomes the popliteal artery at the popliteal space (behind knee) & contributes to arterial anastomosis that supplies knee region during flexion
- The popliteal artery then splits to become anterior & posterior tibial arteries
o The anterior tibial artery supplies extensor muscles in anterior leg
o The posterior tibial artery supplies flexor muscles of leg. One branch, the fibular artery, supplies the lateral muscles of the leg
- The lateral & medial plantar arteries supply plantar foot surface with dorsalis pedis supplying the dorsal foot
- SNS innervations from lower 3 thoracic & upper 2 lumbar segments of spinal cord
venous supply:
Venous Supply
- Can be divided into two groups:
1) Superficial veins
o Lie in superficial fascia and have relatively thick muscle walls
o Great and small saphenous veins originate from dorsal venous arch of foot
2) Deep veins
o Accompany the main arteries and have thin walls
o Include: popliteal, femoral, dorsalis pedis, fibular, posterior tibial, anterior tibial, etc.
- Blood drains from the superficial veins to deep veins to inferior vena cava to heart
- Utilise the ‘muscle pump’ of leg muscles to ‘pump blood upwards’
- Have a system of valves to prevent backflow of blood
Varicosities—Why do they form and where?—Pathophysiology of varicose vein
formation?
Varicose Veins - Pathogenesis
The superficial and deep veins of the lower extremity communicate via communication and perforating veins
the direct flow is normally from the superficial to the deep system aided by the presence of valves and the function of the calf muscle pump
The congenital absence of valves, deep venous obstruction or ineffective function of the calf muscle pump impair venous return resulting in venous hypertension
the gravitational weight of the column of blood and the insufficiency of the pump and valves creates hydrostatic pressure that causes backflow of the blood → dilation of the veins
In contrast to the superficial veins the deep veins do not become excessively distended due to the fascia and muscle in which support them.
Varicosities
an abnormal condition usually of a vein characterised by swelling and tortuosity, when the valves get distended from increased flow or failure of the pump
venous dilations in two other sites merit special attention
Esophageal varices: liver cirrhosis causes portal vein hypertension. In turn this leads to the opening of the porto-systemic shunts and increase blood flow into veins at the gastroesophageal junction forming varices, rectum forming haemorrhoids and periumbilical veins of the abdominal wall forming a caput medusae. The esophageal varices are prone to rupture and can lead to massive upper GIT bleed
Hemorrhoids are varicose dilations of the venous plexus at the anorectal junction that result from prolonged pelvic vascular congestion associated with pregnancy or straining to defecate
what are the Clotting Cascade‐Intrinsic and Extrinsic Systems?
Intrinsic pathway
A cascade of protease reactions initiated by factors that are all present within blood.
Activated when plasma comes into contact with constituents of subendothelial tissues. This results in the exposure of collagen (activates contact factors) and damaged platelets (release of phospholipids).
The initial triggering event - activation of factor XII, factor XI, Prekallikrein (PK) and HMWK are also involved (all apart of the contact group). Autoactivation of factor XII and PK occurs whenever blood contacts an artificial surface. Deficiency of factors may or may not cause bleeding (not as essential as tissue factor à extrinsic pathway).
Factor XIIa (together with HMWK) proteolytically cleaves factor XI to factor XIa.
Factor XIa proteolytically cleaves factor IX.
Factors IXa (and factors Xa and thrombin) proteolytically cleave factor VII to VIIIa.
Factor IXa and VIIIa together with Ca2+ and negatively charged phospholipids form a trimolecular complex à tenase. Tenase converts X to Xa
Extrinsic pathway
Begins with activation of tissue factor. Tissue factor (tissue thromboplastin or factor III) - integral membrane protein expressed in the non-vascular cells. Pathway is initiated at the site of injury in response to the release of TF.
Tissue factor is a receptor for factor VII. When an injury in the endothelium allows factor VII to come into contact with tissue factor - the tissues activates factor VII to VIIa.
Tissue factor, factor VIIa and Ca2+ form a trimolecular complex which proteolytically cleaves factor X to Xa. Activated factor Xa is the site at which the intrinsic and extrinsic coagulation pathways converge à common pathway.
Outline the clinical features of peripheral vascular disease—Arterial and Venous
disease?
Clinical features of arterial disease (5’ P’s)
Pain: intermittent claudication
Worse upon walking, subsidies on stopping walking
Usually felt in calf because superficial femoral artery is most commonly affected.
Pain
Pulselessness
Paresthesia
Perishing cold
Paralysis
Critical limb ishcaemia
Rest/night pain and/or tissue ulceration/gangrene
Can lead to arterial ulcers:
Dry, dark, painful, irregular, demarcated, and do not bleed on touch.
Clinical features of venous disease
Varicose veins Peripheral oedema, stasis, congestion, pain and thrombosis Stasis dermatitis Ulcerations (venous) haemosidirin deposition
DVT
Distal oedema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling and pain
Describe the risk factors for DVT –especially travel?
Immobility:
Hospitalization
Being paralyzed
Prolonged sitting
Surgery and Trauma:
Major surgery (especially of the pelvis, abdomen, hip, knee)
Bone fracture or cast
Catheter in a big vein (PICC line, central venous catheter, or port)
Increased estrogens:
Birth control pills, patches, rings
Pregnancy, including up to 6 weeks after giving birth
Estrogen and progestin hormone therapy
Medical conditions:
Cancer and chemotherapy
Heart failure
Inflammatory disorders (lupus, rheumatoid arthritis, inflammatory bowel disease)
The kidney disorder called nephrotic syndrome
Other risk factors: Previous blood clot Family history of clots Clotting disorder (inherited or acquired) Obesity Older age Cigarette smoking Varicose veins
Outline the symptoms and signs of DVT?
Clinical examination cannot accurately diagnose a DVT.
DVT in Calf
Acute signs of DVT include: swelling, pain, pitting edema
1) Swelling of the affected leg relative to the other leg (>3 cm in circumference)
2) Pain on dorsiflexion of the foot (Homans sign) and compression of the calf
3) Pitting edema distal to the thrombosis due to increased hydrostatic pressure
Chronic signs of DVT in lower leg
Stasis dermatitis
Secondary varicosities may develop in the superficial system
what is Wells criteria for PE?
The Wells score:
clinically suspected DVT — 3.0 points
alternative diagnosis is less likely than PE — 3.0 points
tachycardia (heart rate > 100) — 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
history of DVT or PE — 1.5 points
hemoptysis — 1.0 points
malignancy (with treatment within six months) or palliative — 1.0 points
Traditional interpretation
Score >6.0 — High (probability 59% based on pooled data)[35]
Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data)[35]
Score <2.0 — Low (probability 15% based on pooled data)
Alternative interpretation[]
Score > 4 — PE likely. Consider diagnostic imaging.
Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.
Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.
Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has a 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.
High clinical probability. Proceed to MDCT. If positive, treat, if negative, more tests are needed to exclude PE. A D-dimer of less than 750 ug/L does not rule out PE in those who are at high risk
What are the risk factors for leg ischaemia?
Increasing age, hypertension, diabetes, smoking, hypercholesterolaemia, increased CRP, Hx of cardiovascular disease, female
history of cardiovascular disease, sedentary lifestyle, and obesity.
Symptoms and signs of ischemic lower limb, including critical ischaemia?
Acute lower limb ischemia is caused by sudden obstruction of an artery due to an embolus or thrombosis.
Chronic and critical lower limb ischemia is a slowly progressing disease process that is usually caused by an obliterating arterial disease.
In all stages of ischemia, the patient will complain of cold feet and the skin is cold to touch.
Intermittent claudication: repeated pain in the lower limbs, usually in the calves, which develop during walking. Pain is relieved by a rest of 5–15 minutes, after which the patient is again able to walk the same distance.
The severity of intermittent claudication does not correlate with the stage of the disease. Of the patients with critical ischemia, 50% present with no previous history of intermittent claudication; the mobilisation of many elderly patients is very limited.
In Leriche’s syndrome the occlusion is situated in the distal aorta, and the patient will have claudication pain in both limbs up to the buttocks. Men may also have erectile dysfunction.
Occlusion at the iliac artery results in thigh and calf claudication. Occlusion at the superficial femoral artery leads to claudication in the calf, and popliteal occlusion to foot numbness during exercise.
Leg pain at rest, which is relieved by standing upright or hanging the limb over the edge of the bed, is suggestive of severe ischaemia; pain in the foot, ankle brachial index (ABI) often < 0.5.
Ischaemic tissue damage: necrosis areas or ulcers which may be dry and localised or become infected and may, at the worst, lead to a septic infection.
Palpation for foot pulses
First-line examination. The arteries to palpate are the dorsalis pedis artery and the posterior tibial artery.
There is inter-individual variation as regards the anatomic position of the dorsalis pedis artery
Critical Limb ischemia (severest form of lower leg ischemia is a manifestation of ongoing ischemia)
Critical limb ischemia (CLI), also referred to as limb threat, is an advanced stage of peripheral artery disease (PAD). It is defined as a triad of ischemic rest pain, arterial insufficiency ulcers, and gangrene. The latter two conditions are jointly referred to as tissue loss, reflecting the development of surface damage to the limb tissue due to the most severe stage of ischemia. OVERALL: (TALLY) Clinical signs of acute arterial occlusion of major or peripheral limbs results in the (6 p’s) 1) Painful 2) Paralysed 3) Pulseless 4) Pale 5) Perishingly cold 6) paraesthesia’s
Value of d Dimer and First line investigations for suspected DVT and thrombo‐
embolism?
D Dimers: These are used to rule out the probability that a thrombus has formed. It can also be used to determine if more investigations are necessary to investigate the chance of a hyper-coagulable disease. D Dimers are useful in assisting to rule out DVTs, PE and strokes.
First line Investigations for a DVT:
● D Dimer: Sensitive but not specific thus (–ve D-Dimer is more useful than +ve). As it is raised in many conditions like pregnancy, infection and malignancy
● Ultrasound scan: Thrombus presence can be identified because the vein is not compressed by the ultrasound probe.
● One can also do FBC, LFT, Urine dipstick and other tests to search for an underlying abnormality or malignancy.
- The therapeutic range for INR is very narrow. A number of different factors can affect the INR. This is more notable when the person is doing a lot of different sporadic activities that is affecting their INR.
Why is she bleeding on second presentation??
The patient is bleeding on her second presentation due to the warfarin that was started.
She is no longer in the therapeutic range of 2-4 (INR) for her condition, her reading was 7
At this high reading it will be taking substantially longer to clot her blood, leading to the bleeding incident
WellS criteria for DVT
In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform. The most studied clinical prediction rule is the Wells score.
Wells score or criteria: (possible score −2 to 9) Active cancer (treatment within last 6 months or palliative): +1 point Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm below tibial tuberosity): +1 point Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point Unilateral pitting edema (in symptomatic leg): +1 point Previous documented DVT: +1 point Swelling of entire leg: +1 point Localized tenderness along the deep venous system: +1 point Paralysis, paresis, or recent cast immobilization of lower extremities: +1 point Recently bedridden ≥ 3 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point
Alternative diagnosis at least as likely: −2 points[4]
Those with Wells scores of two or more have a 28% chance of having DVT, those with a lower score have 6% odds. Alternatively, Wells scores can be categorized as high if greater than two, moderate if one or two, and low if less than one, with likelihoods of 53%, 17%, and 5%, respectively
What is the first line investigation and management for DVT?
First-line Investigations
- Ultrasound Doppler studies – Test uses reflected sound waves to show how blood is flowing through veins and arteries. It is very effective in detecting thrombi.
- Venography – radiographic demonstration of a vein after injection of contrast medium to look for blockages
- Exclude possibility of a pulmonary embolism (if associated symptoms, arrange for a V/Q scan, pulmonary angiogram, etc.)
- Management: Anticoagulation therapy
o Heparin should be given in hospital (short-term measure)
o Warfarin should be taken by patient as a long term control method - If large clots present, thrombolytic therapy can also be used
Colonisers and pathogens and interpretation of ulcer swab?
Ulcers can occur as result of primary infections disease (not common). Alternatively, ulcers of noninfectious etiology can have a secondary infection.
Ulcers can be colonized by many species of microorganisms and only a small number are detected with routine methods, thus standard bacterial swabs have little clinical value. If there are clinical signs of infection, wound swabs together with blood cultures are helpful to guide therapy if a recognized pathogen is isolated, e.g. S. aureus.
Clinical signs of infection:
systemic features of sepsis, with no apparent focus other than the ulcer
Local signs of infection:
spreading cellulitis
lymphangitis
increasing purulence and quantity of exudate
increased pain
increased local temperature
rapid increase in ulcer size
Signs of infection of underlying structures (eg osteomyelitis).
Systemic antimicrobials: only when clinical signs of infection beyond that of local wound colonisation are present.
Topical antimicrobial therapy: not recommended as may act as sensitizing agents and have no demonstrated effect of healing, may also promote resistance.
what are the principles of antimicrobial therapy and major classes of antibiotics?
Principles of antimicrobial therapy
- Selective toxicity (exploit differences between host and microbes)
- Microbe specific (eg. anti-bacterial, anti-fungal, etc.)
- Broad spectrum works against wide range of activities while narrow spectrum = limited range
- …cidal (compounds kill microbe [eg. penicillin]) vs …static (stop growth [eg. tetracycline])
The antibiotic creed
restraint in use of antimicrobials is best way to ensure their efficacy
- M – Microbiology guides therapy wherever possible
- I – Indications should be evidence based
- N – Narrowest spectrum
- D – Dosage appropriate to site & type of infection
- M – Minimise duration of therapy
- E – Ensure monotherapy in most situations
Types of antimicrobials The most common antibacterial classes are:
1) Betalactams (eg. penicillins, cephalosporins) Inhibit cell wall synthesis
2) Aminoglycosides (eg. gentamycin, tobramycin) Inhibit protein synthesis by interfering with binding of tRNA to ribosomes
3) Glycopeptides (eg. vavncomycin, teicoplantin) Inhibit peptidoglycan biosynthesis at different site to betalactams
4) Macrolides (eg. erythromycin, azithromycin) Inhibit protein synthesis by binding to 50S of bacterial ribosome
5) Tetracyclins (eg. tetracycline, doxycyclin) Inhibit protein synthesis by inhibiting binding of 30S and subsequent protein translocation
