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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

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.

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

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.
Perishing cold

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

Distal oedema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling and pain


Describe the risk factors for DVT –especially travel?

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)
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.
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‐ 

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
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


what are the clinical features of venous, arterial, diabetic/neuropathic ulcers?

They are larger but shallower than other ulcers. Stasis ulcers have a moist granulating base and an irregular border. This base oozes venous blood when handled. There may be varicose veins and varicose eczema. There may be signs of stasis dermatitis around the ulcer. Hyperpigmentation is due to haemosiderin deposition or iron pigments in the skin. Lipodermatosclerosis is dermatitis followed by induration and dermal fibrosis.

Initially they have irregular edges but this may become more clearly defined. The ulcer base contains greyish, granulation tissue. Handling, such as debriding these ulcers, produces little or no blood. There are often features of chronic ischaemia, such as hairlessness, pale skin, absent pulses, nail dystrophy and wasting of calf muscles.

They have a punched-out appearance with a deep sinus. These are often under calluses or over pressure points such as the plantar aspect of the first or fifth metatarsophalangeal joint. They are often surrounded by chronic inflammatory tissue. Probing or debriding may lead to brisk bleeding. They are usually painless and the surrounding area will show diminished or absent sensation


How is there spread of MRSA; Vancomycin resistance organism? what is the infection control needed?

MRSA (methicillin resistant staph aureus)
- Strains of staphylococcus aureus which are resistant to penicillin antibiotics through the developed ability to produce betalactamase.
- Are endemic in hospitals and are increasing in communities. There are two main types:
o Non-multiresistant MRSA – usually community acquired & only resistant to beta lactams
o Multiresistant MRSA – endemic in large hospitals & resistant to multiple antibiotics

Closer look at Staph Aureus/MRSA...
- Staph aureus is a gram positive cocci bacteria which exists in clusters
- Diseases caused: Boils, skin sepsis, postoperative wound infection, scalded skin syndrome, food-borne infection, septicaemia, endocarditis, toxic shock syndrome, osteomyelitis, pneumonia
- Virulence factors: Coagulase, lipase, staphlokinase, capsule, enerotoxins
- Treatment: Antibiotics of choice are beta-lactamase penicillins. However, resistance  problems with treatment
- Prevention: Isolation and/or treatment of carriers in high risk areas of hospital *infection control*

Spread of MRSA: Vancomycin resistance, infection control
- Factors contributing to the emergence of anti-microbial resistant include:
o Inappropriate use of antibiotics when not indicated
o Inadequate dosage or treatment duration
o Incomplete treatment courses
o Extensive use of broad-spectrum agents
o Use of antibiotics as growth-promoters in animal feeds
o Increased use of ‘mega hospitals’

Measures to decrease spread of nocosomal infections / resistant organisms:

o Early identification & isolation of patients colonised with multiresitant organisms
o Education about effective use of antibiotics
 Rational anti-microbial prescribing
 Patients aware about importance of taking the full course
o Minimise use of indwelling devices such as IV lines and urinary catheters
o Sterilisation / cleaning of equipment
o Basic hygiene  WASH HANDS 


. How do you stop her bleeding? (warfarin)

1) vitamin K (1-2mg orally)
2) Prothrombin X
3) Fresh frozen plasma


Why do patients get confused with Warfarin prescribing?

This is because of the need to constantly correct there dosage according to their INR, when this changes so does there dosage of warfarin to compensate


What does ‘numbers needed to treat mean’? how do we make sense of how to treat patients with DVTs?

The number needed to treat (NNT) can be thought of as the number of patients that need to be treated in order for one to benefit. It provides an attractive means of summarising the results of a clinical trial in a single figure, because the meaning of a sentence such as ‘20 patients need to be treated to avoid one additional death over a five year period’ is easily understood by both doctors and patients.1

The NNT is the inverse of the absolute risk reduction – the difference between the proportion or rate of events in the active treatment intervention group (Pa) and the proportion of events in the control group (Pc):
Number needed to treat =1/(Pa-Pc)

The ideal NNT would be 1, where all the patients in the treatment group have improved, but no-one has in the control arm. In theory, the higher the NNT, the less effective is treatment, because more people need to receive the treatment to see a benefit in one. However, the value of an NNT should be interpreted in light of the clinical contact. For example, an NNT of between 2-5 would normally indicate an effective therapy, such as a pain killer for acute pain. On the other hand, an NNT of 1 might be seen when treating a sensitive bacterial infection with antibiotics, whilst an NNT of 40+ might be useful in other situations, such as using aspirin after a heart attack.

NNT can be used to help us choose between two treatment options. If, for example, the NNT for drug A is lower than that for drug B, it suggests that it may be more effective and – all other things being equal – choosing A rather than B would make sense.
If the drug or intervention is harmful (Pa – Pc), and thus the NNT, will be negative. This is sometimes referred to as the ‘Number Needed to Harm’ (NNTH). This can also be used to describe adverse effects, for example as a result of the treatment under study.


How do we screen for risk factors of peripheral vascular disease?

Risk Factors
Non modifiable
History of Heart Disease
Male gender
Diabetes mellitus Type 1
Post menopausal women
Family history of dyslipidemia, HTN or PVD
Family History of atherosclerosis

Coronary artery disease
Impaired glucose tolerance
Physical inactivity
Smoking and use of tobacco products


what is the Prevalence and Incidence of Skin Cancers?

Approx. 2 in 3 Australians will be diagnosed with skin cancer by the time they are 70, with more than 750,000 people treated for one or more non-melanoma skin cancers in Australia each year.
Non-melanoma skin cancer is more common in men - almost double the incidence compared to women.
Excluding non-melanoma skin cancer (not notified to cancer registries), melanoma is the third most common cancer in Australian women and the fourth most common cancer in men and the most common cancer in Australians aged 15-44 years.
12, 744 Australians diagnosed with melanoma in 2013.
Every year in Australia,
Skin cancers account for around 80% of all newly diagnosed cancers.
The incidence of skin cancer is one of the highest in the world, 2-3x the rates in Canada, the US and UK.
1 million GP consultations.


how do we manage patient with comorbidities?

Consider patient’s goals and priorities as it is long term management
Co-ordination of care
Communication between multidisciplinary team
Continuity of care
Managment plan
Polypharmacy management
Reviewing medications regularly
Adherence to the multiple clinical guidelines
Transportation, and financial issues