Core conditions Flashcards

1
Q

DVT

A

A thrombus within the deep venous system, normally in the legs. Can become dislodged becoming an embolus and causing a PE in the lungs. PE and DVT’s are both types of venous thromboembolism (VTE).

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2
Q

Risk factors for DVT

A

Virchows triad: hypercoagulability, endothelial injury and stasis

  • Inherited thrombophilia (factor V leiden)
  • Pregnancy and oestrogen
  • Malignancy, infection and inflammation
  • Dehydration
  • Immobility
  • Varicose veins
  • Obesity
  • Physical trauma (including surgery)
  • Foreign devices i.e. stents
  • Hypertension
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3
Q

Clinical features of a DVT

A
  • Oedema
  • Pain (often cramping, may progress over several days)
  • Erythema and warmth
  • Peripheral venous distention
  • Often unilateral unless DVT is on both sides
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4
Q

Red flags for PE

A
  • Sudden onset shortness of breath
  • Tachycardia
  • Haemoptysis
  • Chest pain (usually pleuritic)
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5
Q

Questions asked in the Wells score

A
  • Active cancer (currently receiving treatment or treatment within 6 months or palliative)
  • Paralysis, paresis or recent plaster immobilisation
  • Recently bedridden (3 days or more), or major surgery within the last 3 months
  • Localised tenderness along the distribution of the deep venous system
  • Entire leg swollen
  • Calf swelling at least 3cm larger than the asymptomatic side
  • Pitting oedema in the symptomatic leg
  • Collateral superficial veins (non-varicose)
  • Previously documented DVT
  • An alternative diagnosis is at least as likely as DVT
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6
Q

Interpretation of the Wells score

A
  • DVT likely: ≥2 points
  • DVT unlikely: <2 points
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7
Q

DVT likely (>2 points)

A
  • If a DVT is likely, a proximal leg vein doppler ultrasound should be requested with the results available within four hours:
  • If the ultrasound is positive: treat the DVT with an anticoagulant.
  • If the ultrasound can’t be done within 4 hours: D-dimer and offer an interim anticoagulant until results are available.
  • If the ultrasound is negative: check the D-dimer. If it is positive, repeat the scan in 6-8 days (stop interim coagulation if started). If it is negative, another diagnosis should be considered and no anticoagulation given.
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8
Q

DVT unlikely (<2 points)

A
  • If DVT is unlikely, offer a D-dimer test with the results available within four hours:
  • If the D-dimer is positive: offer a proximal leg vein doppler ultrasound or provide interim coagulation if ultrasound results cannot be obtained within four hours. If the ultrasound is positive treat the DVT with an anticoagulant.
  • If the D-dimer results can’t be obtained within four hours: offer interim anticoagulation until results are available.
  • If the D-Dimer is negative: another diagnosis should be considered and no anticoagulation given.
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9
Q

VTE prophylaxis

A
  • If at increased risk of VTE, a low molecular weight heparin such as enoxaparin.
  • Contraindicated in active bleeding or existing anticoagulation with warfarin or a DOAC.
  • Anti-embolic compression such can be used, contraindicated in peripheral arterial disease.
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10
Q

Diagnosis of VTE

A
  • D dimer
  • Doppler ultrasound, repeat negative ultrasound after 6-8 days if positive D-dimer and the wells score suggests DVT is likely
  • PE can be diagnosed with CT pulmonary angiogram (CTPA) and ventilation-perfusion (VQ) sscan
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11
Q

Management of VTE

A
  • Immediately start apixaban or rivaroxaban even if there is a delay in getting the scan (direct oral anticoagulant)
  • Catheter directed thrombolysis in patients with symptomatic iliofemoral DVT and symptoms last less than 14 days
  • Long term anticoagulation is DOAC, warfarin or LMWR
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12
Q

VTE- long term anticoagulation

A
  • DOAC’s: apixaban, rivaroxaban, edoxaban and dabigatran. Suitable for all patients
  • Warfarin: vitamin K antagonist, target INR is between 2 and 3. First line treatment for patients with antiphospholipid syndrome
  • Low molecular weight heparin is first line in pregnancy
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13
Q

VTE- continue anticoagulation for

A
  • 3 months if there is a reversible cause (then review)
  • Beyond 3 months if the cause is unclear, there is recurrent VTE, or there is an irreversible underlying cause such as thrombophilia (often 6 months in practice)
  • 3-6 months in active cancer (then review)
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14
Q

Inferior vena cava filter

A

Inserted into the inferior vena, designed to filter the blood and capture any blood clots going towards the heart and lungs. They are used in patients with recurrent PE’s or those that are unsuitable for anticoagulation

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15
Q

Investigating unprovoked VTE: test for

A
  • Antiphospholipid syndrome: check antiphospholipid antibodies
  • Hereditary thrombophilia’s: only if they have a first degree relative also affected by DVT or PE
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16
Q

Types of bleeding

A
  • Primary bleeding: during the surgical procedure
  • Reactive bleeding: within 24 hours of the operation, during surgery patients become relatively hypotensive and vasoconstricted. Post-op as blood pressure rises and vasodilation occurs a damaged blood vessel may begin to bleed
  • Secondary bleeding: 7-10 days after the operation, often associated with wound infection
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17
Q

Signs of post op bleeding

A
  • Tachycardia
  • Hypotension (typically develops late, only after a significant volume of blood has been lost)
  • Tachypnoea
  • Cool peripheries
  • Pre-syncope/syncope
  • Confusion/agitation
  • Swelling and/or bruising at the wound site (secondary to haematoma formation)
  • Bleeding from the wound site
  • Increasing tenderness at the wound site
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18
Q

class 1 of blood loss

A

Blood loss: <750ml, 15%
Heart rate: <100
Blood pressure: normal
Respiratory rate: 14-20
Urine output: >30ml/hr

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19
Q

Class II of blood loss

A

Blood loss: 750-1500ml, 15-30%
Heart rate: 100-120
Blood pressure: normal
Respiratory rate: 20-30
Urine output: 20-30ml/hr

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20
Q

Class III of blood loss

A

Blood loss: 1500-2000ml, 30-40%
Heart rate: 120-140
Blood pressure: decreased
Respiratory rate: 30-40
Urine output: 5-20ml/hr

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21
Q

Class IV blood loss

A

Blood loss:>2000ml, >40%
Heart rate: >140
Blood pressure: Decreased
Respiratory rate: >40
Urine output: <5ml/hr

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22
Q

Pressure ulcers

A

Occurs in patients with reduced mobility, where there is prolonged pressure over particular areas causing the skin to break down.

23
Q

Pathology of pressure ulcers

A

Due to reduced blood supply and localised ischaemia, reduced lymph drainage and an abnormal change in shape (deformation) of the tissues under pressure

24
Q

Waterlow score: covers these risk factors

A
  • Age and gender
  • BMI
  • Level of continence
  • Skin condition (healthy or broken)
  • Appetite
  • Level of mobility (fully mobile to bed bound)
  • Individual risk factors i.e. medication, surgery and trauma
    The waterlow score judges how at risk the patient is of getting a pressure sore
25
Q

Grading pressure ulcers

A
  • Stage 1 ulcers have not yet broken through the skin
  • Stage 2 ulcers have a break in the top two layers of the skin
  • Stage 3 ulcers affects the top two layers of the skin as well as fatty tissue
  • Stage 4 ulcers are deep wounds that may impact muscle, tendons, ligaments and bone
26
Q

Common sites for pressure ulcers

A
  • On any skin that covers bony areas of the body
  • Butt, tailbone, heels, ankles, hips, back, elbows, shoulder blades, back of head
27
Q

Stage 1 pressure ulcer

A
  • Appear red in people with lighter skin and blue or purple in people with darker skin
  • Remain red or darker for more than 30 minutes after pressure is removed
  • Not turn pale if pressed firmly
  • Be sore to touch
  • Have a warmer temperature from the surrounding normal tissues
  • Feel firmer than surrounding tissues
  • Cause mild burning or itching
  • Treatment: reduce pressure, use pillows or blankets. Keep area clean and dry. Stay well hydrated and have a healthy diet
28
Q

Stage 2 bedsores

A
  • Wounds may appear as: a shallow, crater like wound or a serum filled (clear to yellowish fluid) blister that may or may not have burst
  • Some drainage or pus at the ulcer
  • Pain
  • Swollen, sore or red tissue around the sore which indicates tissue death or damage
  • Treatment: remove pressure, use specialised wound dressings to keep the area dry and clean, preventing the wound from becoming more severe or infected. Clean the ulcer and monitor for infection
29
Q

Stage 3 bedsores

A
  • An ulcer which may resemble a hole or crater
  • Includes signs of infection: foul odor, pus, redness, discolored drainage
  • Treatment: antibiotic therapy and remove any dead tissue. Ulcers may need 1 to 4 months to heal
30
Q

Stage 4 bedsores

A
  • Extreme pain, drainage, dead tissue which may appear black, visible muscles and sometimes bone.
  • Common signs of infection like a foul smell and pus
  • A dark hard substance known as eschar (hardened dead wound tissue)
  • Treatment: hospitalisation
31
Q

Treatment of pressure ulcers

A
  • Treatment of any infection that is present, which may include: antibiotic cream, oral antibiotics
  • Intravenous (IV) antibiotics
  • Local wound care, including specific cleaning and dressing recommendations
  • Using special bandages that help remove dead tissue
  • Medication to relieve or reduce any discomfort
  • Debridement, which removes dead or infected tissue
  • Repositioning frequently
  • Reducing friction and moisture in the location
  • Using special off-loading cushions to reduce pressure on the sore
  • Surgery
32
Q

Risk factors for a PE

A
  • Recent surgery
  • Recent fractures
  • Recent immobility
  • Personal or family history of a clotting disorder or PE/DVT
  • Obesity
  • Malignancy
  • Infection
  • Pregnancy
  • Medications such as the combined oral contraceptive pill or hormone replacement therapy
33
Q

Clinical features of a PE

A
  • Shortness of breath
  • Pleuritic chest pain: with each breath, the pleura comes into contact with an ischaemic area of the lung.
  • Cough
  • Haemoptysis: secondary to infarcted lung tissue.
  • Dizziness or syncope: due to haemodynamic instability (i.e. right ventricular strain).
34
Q

Signs of PE

A
  • Tachypnoea: a respiratory rate of more than 20 breaths per minute.
  • Tachycardia: a heart rate of more than 100 beats per minute.
  • Hypotension: suggestive of right ventricular strain.
  • Evidence of deep vein thrombosis (DVT) such as a red, swollen calf.
  • Pleural rub: a squeaking or grating sound caused by ischaemic lung tissue coming in contact with the pleura.
  • Cyanosis: a late sign that indicates a significant drop in blood oxygen levels (SpO2).
35
Q

Wells score- PE

A
  • PE likely: more than 4 points. CTPA is indicated
  • PE unlikely: 4 points or less. D dimer is indicated
36
Q

PE treatment

A
  • Anticoagulant treatment: apixaban or rivaroxaban
  • For at least 3 months, longer if PE was unprovoked
  • In confirmed PE and haemodynamic instability: off continuous unfractionated heparin infusion and consider systemic thrombolytic treatment
37
Q

Signs of a massive PE occuring secondary to right ventricular strain

A

hypotension, raised JVP, heart failure, cardiac arrest

38
Q

Urinary retention

A

An inability to pass urine which leads to pain and discomfort with significant residual volume. Most common in older male patients, normally due to an enlarged prostate causing bladder outflow obstruction.

39
Q

Causes of acute urinary retention

A
  • Benign prostatic hyperplasia: most common in men, also urethral strictures of prostate cancer
  • UTI: can cause urethral sphincter to close, constipation can compress the urethra causing acute retention
  • Severe pain
  • Medications: anti-muscarinics, spinal or epidural anaesthesia
  • Neurological causes: peripheral neuropathy, pelvic surgery, upper motor neurone disease (MS, parkinsons) or bladder sphincter dysinergy
40
Q

Clinical features of acute urinary retention

A
  • Acute suprapubic pain and inability to micturate
  • Palpable distended bladder with suprapubic tenderness
  • Fever or rigors: suggest an infective cause
  • PR exam: prostate enlargement or constipation
41
Q

Investigations into urinary retention

A
  • Post void bedside bladder scan: shows volume of retained urine
  • Bloods: FBC, CRP and U&E’s
  • CSU (catheterised specimen of urine): to assess for the presence of infection
  • Ultrasound scan of urinary tract to assess for the presence of associated hydronephrosis
42
Q

High pressure urinary retention

A

Urinary retention causing high intra-vesicular pressure, so the anti-reflux mechanism of the bladder and ureters is overcome. Urine backs up into the upper renal tract.

43
Q

Management of urinary retention

A
  • Immediate urethral catheterisation: measure the volume drained post catheterisation
  • For an enlarged prostate: Tamsulosin (an alpha receptor antagonist)
  • Check the CSU for evidence of infection and treat with antibiotics

For patients with a large retention volume (>1000ml) they need to be monitored post catheterisation for post-obstructive diuresis

44
Q

Definitive management of urinary retention

A
  • High pressure urinary retention: keep their catheter in situ until definitive management can be arranged i.e. TURP
  • If no evidence of renal impairment, a TWOC (trial without catheter) can be attempted, where the catheter is removed 24-48hrs after insertion. If they re-enter retention the patient will require re-catheterisation
  • May need a long term catheter
45
Q

Complications of urinary retention

A
  • An AKI can lead to chronic kidney injury if episodes of retention led to renal scarring
  • Increased risk of UTI and renal stones due to urinary stasis
46
Q

Cystitis and Pyelonephritis

A

Cystitis- inflammation of the bladder
Pyelonephritis- inflammation of the kidneys

47
Q

Risk factors and sources of a UTI

A

Risk factors: unprotected sex, female, catheters, incontinence, poor hygiene
Source: from faeces, E.coli can travel from the anus to the urethral opening

48
Q

What do lower urinary tract infections present with

A
  • Dysuria (pain, stinging or burning when passing urine)
  • Suprapubic pain or discomfort
  • Frequency
  • Urgency
  • Incontinence
  • Confusion is commonly the only symptom in older more frail patients
49
Q

Pyelonephritis presents with

A
  • Fever is a more prominent feature than lower urinary tract infections.
  • Loin, suprapubic or back pain. This may be bilateral or unilateral.
  • Looking and feeling generally unwell
  • Vomiting
  • Loss of appetite
  • Haematuria
  • Renal angle tenderness on examination
50
Q

Urine dipstick

A
  • Presence of Nitrites
  • Leukocytes- significant rise
  • Nitrites are better indicator then leukocytes, if only leukocytes are present you should treat them only if there is clinical evidence they have a UTI
  • Midstream urine (MSU) sample should be cultures
51
Q

Causes of a UTI

A
  • E.coli- most common, found in faeces
  • Klebsiella pneumoniae (gram-negative anaerobic rod)
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
52
Q

Management of a UTI

A
  • 3 days of antibiotics for a simple lower urinary tract infection in women
  • 5-10 days of antibiotics for women that are immunosuppressed, have abnormal anatomy or impaired kidney function
  • 7 days of antibiotics for men, pregnant women or catheter related UTIs
  • Change the catheter in catheter related UTI
  • Antibiotics: Trimethoprim, Nitrofurantoin (pregnancy)
53
Q

What do UTI’s increase the risk of

A

Pyelonephritis, premature rupture of membranes and pre-term labour.

54
Q

Management of UTI in pregnancy

A
  • 7 days of antibiotics (even with asymptomatic bacteruria)
  • Urine for culture and sensitivities
  • First line: nitrofurantoin
  • Second line: cefalexin or amoxicillin
  • Nitrofurantoin is generally avoided in the third trimester as it is linked with haemolytic anaemia in the newborn.
  • Trimethroprin cants be taken with folic acid as it had anti-folate effects