General Practice/ Primary Care (Ben) Flashcards

1
Q

What is the definition of Influenza?

A

Influenza or ‘flu’ is a single-stranded RNA virus and is the most common cause of viral pneumonia in immunocompetent adults.

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2
Q

What are the different pathogenic serotypes of Influenza?

A
  • Influenza A – capable of causing pandemics and epidemics; no animal reservoir
  • Influenza B –capable of epidemics only, animal hosts include pigs and birds
  • Influenza C – only found in cattle

The influenza serotype is determined by surface antigens haemagglutinin and neuraminidase, which are rearranged in host organisms such as birds and animals to produce different strains.

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3
Q

How is Influenza transmitted?

A

The influenza virus is highly contagious and transmitted via respiratory secretions.

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4
Q

What is the incubation period for the influenza virus?

A

The incubation period is typically 1–4 days

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5
Q

How long do patients with Influenza remain infectious for?

A

Patients can remain infectious for 7–21 days

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6
Q

What is the clinical presentation of Influenza?

A
  • Fever ≥ 37.8°C
  • Nonproductive (dry) cough
  • Myalgia
  • Lethargy and Fatigue
  • Headache
  • Malaise
  • Sore throat
  • Rhinitis
  • Anorexia
  • Muscle and joint aches
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7
Q

How can you differentiate between Flu and the common cold?

A
  • Flu tends to have an abrupt onset,
  • Whereas a common cold has a more gradual onset.
  • Fever is a typical feature of the flu but is rare with a common cold.
  • Finally, people with the flu are “wiped out” with muscle aches and lethargy.
  • Whereas people with a cold can usually continue many activities.
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8
Q

What investigations can be done for Influenza?

A
  • Rapid Polymerase Chain Reaction (PCR) Test - Is now first line and can confirm the diagnosis. Nasal or Throat swabs are used to get a sample.
  • Point of Care Tests - Using swabs, detects viral antigens and can give a rapid result. However, they are not as sensitive as formal lab tests and do not give information about the subtypes.
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9
Q

What is the management of Influenza?

A
  • Healthy patients (who aren’t at risk of complications) don’t need treatment. The infection will resolve with self-care measures (such as adequate fluid intake and rest).

Treatment for patients at risk of complications:
* Oral oseltamivir (twice daily for 5 days)
* Inhaled zanamivir (twice daily for 5 days)

Post-Exposure Prophylaxis
* Can be given to patients who meet specific criteria after exposure to someone with the flu.
* Oral oseltamivir 75mg once daily for 10 days
* Inhaled zanamivir 10mg once daily for 10 days

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10
Q

What is the criteria for people to recieve Post-Exposure Prophylaxis for Influenza?

A
  • It is started within 48 hours of close contact with influenza
  • Increased risk (e.g., chronic disease or immunosuppression)
  • Not protected by vaccination (e.g., it has been less than 14 days since they were vaccinated)
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11
Q

What are the possible complications of Influenza?

A
  • Pulmonary
    Viral pneumonia, secondary bacterial pneumonia (particularly S. aureus) , worsening of chronic conditions (eg. COPD and asthma)
  • Cardiovascular
    Myocarditis, heart failure
  • Neurological
    encephalopathy
  • Gastrointestinal
    Anorexia and vomiting are common
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12
Q

Who is entitled to a free Influenza vaccine on the NHS?

A

Those at higher risk of developing flu or flu-related complications:

  • Aged 65 and over
  • Young children
  • Pregnant women
  • Chronic health conditions, such as asthma, COPD, heart failure and diabetes
  • Healthcare workers and carers
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13
Q

What is the definition of Irritable Bowel Syndrome (IBS)?

A

Irritable Bowel Syndrome (IBS) is a common, chronic gastrointestinal disorder characterized by abdominal pain or discomfort associated with altered bowel habits, without any identifiable structural or biochemical abnormalities.

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14
Q

What is the epidemiology of IBS?

A
  • It occurs in up to 20% of the population.
  • Affects women more than men
  • More common in younger adults.
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15
Q

What causes IBS?

A

The precise cause of IBS remains unknown. It is considered a multifactorial condition, potentially involving:
* Genetic predisposition
* Altered gut microbiota
* Low-grade inflammation
* Abnormalities in the gut-brain axis.

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16
Q

What is the clinical presentation of IBS?

A

The Manning criteria for diagnosis of IBS includes:

Abdominal discomfort or pain relieved by defecation OR Associated with altered bowel frequency or stool form. And two or more of the following:
* Altered stool passage (e.g., straining or urgency)
* Abdominal bloating
* Symptoms worsened by eating
* Passage of mucus

Additional symptoms such as lethargy, nausea, backache, and bladder symptoms may also be present.
Physical examination typically reveals no abnormalities.

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17
Q

What can the symptoms of IBS be worsened by?

A
  • Anxiety
  • Depression
  • Stress
  • Sleep disturbance
  • Illness
  • Medications
  • Certain foods
  • Caffeine
  • Alcohol
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18
Q

What are some differentials for IBS?

A
  • Inflammatory Bowel Disease (IBD)
    Symptoms may include bloody diarrhea, weight loss, and fever.
  • Coeliac Disease
    Symptoms may include diarrohea, weight loss, and anemia.
  • Colorectal Cancer
    Symptoms may include rectal bleeding, weight loss, and changes in bowel habits.
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19
Q

What investigations are done for IBS?

A

The following investigations are often performed to rule out other organic diseases:

  • Full blood count for anaemia
  • Inflammatory markers (e.g., ESR and CRP)
  • Coeliac serology (e.g., anti-TTG antibodies)
  • Faecal calprotectin for inflammatory bowel disease
  • CA125 for ovarian cancer
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20
Q

What does the management of IBS involve?

A

1st Line is Lifestyle Advice including:
* Drinking enough fluids
* Regular small meals
* Adjusting fibre intake according to symptoms (more fibre if predominantly constipated, less with diarrhoea/bloating)
* Limit caffeine, alcohol and fatty foods
* Low FODMAP diet, guided by a dietician
* Probiotic supplements may be considered over-the-counter (discontinuing after 12 weeks if there is no benefit)
* Reduce stress where possible
* Regular exercise

1st Line Pharmocological options (depends on symptoms)
* Loperamide for diarrhoea
* Bulk-forming laxatives (e.g., ispaghula husk) for constipation (lactulose can cause bloating and is avoided)
* Antispasmodics for cramps (e.g., mebeverine, alverine, hyoscine butylbromide or peppermint oil)

Other Options when symptoms remain uncontrolled:
* Linaclotide when 1st line laxatives are insufficient
* Low-dose tricyclic antidepressants (e.g., amitriptyline)
* SSRI antidepressants
* Cognitive behavioural therapy (CBT)

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21
Q

What is the definition of Lyme Disease?

A
  • Lyme disease is an infectious condition caused by the spirochaete Borrelia burgdorferi
  • Its transmitted via the bite of Ixodes ticks predominantly found in wooded areas.
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22
Q

What is the epidemiology of Lyme Disease?

A

Most cases originate from northeastern regions of the USA and northern-eastern Europe.

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23
Q

What causes Lyme Disease?

A
  • Lyme disease is caused by transmission of Borrelia burgdorferi via the bite of an infected Ixodes tick.
  • The diverse clinical manifestations of the disease are attributed to the variety of Borrelia species and the host immune response to the infection.
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24
Q

What is the clinical presentation of Lyme Disease?

A

There are 3 clinical stages of Lyme Disease:

Stage 1 - Localised disease, lasting several weeks.
* Tick bite (recalled in approximately 75% of cases)
* Flu-like symptoms
* Regional lymphadenopathy
* Erythema chronicum migrans (circular, target-shaped lesion observed in 80% of cases within 30 days)
* Borrelia lymphocytoma - blue patch on the earlobe, nipple or scrotum (predominantly seen in children)

Stage 2 - Early disseminated disease, lasting from days to months.
* Continued flu-like symptoms
* Neuroborreliosis: facial nerve (single or bilateral) and other cranial nerve palsies, aseptic meningitis, encephalitis, polyradiculitis, and Bannwarth’s Syndrome, peripheral mononeuritis
* Cardiovascular involvement: myocarditis, heart block and other arrhythmias, pericarditis
* Early painful arthritis

Stage 3 - Late disseminated disease, lasting from months to years
* Arthritis: recurrent attacks, usually affecting large joints such as the knee, typically non-destructive
* Late neurological disorders: polyneuropathy, chronic encephalomyelitis, dementia, psychosis
* Acrodermatitis chronica atrophicans: blue-red discoloration and swelling at extensor surfaces, may be associated with peripheral neuropathy
* Controversial association with fibromyalgia and chronic fatigue syndromes

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25
Q

What are the differentials for Lyme Disease?

A

Other spirochaetal infections:

  • Borrelia recurrentis
    Typically presents with recurring fever episodes
  • Leptospirosis (Weil’s disease)
    Presents with jaundice, renal failure, and hemorrhage
  • Treponema infections (syphilis, yaws, and pinta)
    Present with distinct skin lesions and systemic symptoms

Other tick-borne diseases:

  • Rickettsia (Rocky Mountain spotted fever or tick typhus)
    Presents with fever, headache, and a characteristic rash
  • Babesiosis
    Presents with fever, fatigue, and hemolytic anemia
  • Tularaemia
    Presents with ulcerative skin lesions and lymphadenopathy
  • Tick-borne relapsing fever
    (Caused by other Borrelia species) presents with recurring fever episodes
  • Human monocytic ehrlichiosis and human granulocytic anaplasmosis
    Present with non-specific flu-like symptoms
  • Q fever
    Presents with high fever, severe headache, and pneumonia
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26
Q

What investigations are done to diagnose Lyme Disease?

A
  • Borella species cannot be cultured, so diagnosis of Lyme disease relies heavily on serology.
  • However if the typical Erythema Migrans (target rash) is present, antibody testing is not nescesary for diagnosis.
  • ELISA testing if suspected Lyme disease but no evidence of erythema migrans
  • If initial tests are negative but symptoms persist, retesting 3-4 weeks later is recommended
  • In cases presenting with arthritis, a synovial fluid sample may be obtained for PCR Borrelia DNA testing.
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27
Q

What is the management of Lyme Disease?

A
  • Ensure complete removal of tick and monitor bite area for signs of infection (if asymptomatic, no antibiotics are required)

Antibiotic Management:
* Oral Doxycycline for 3 weeks (1st line)
* Oral Amoxicillin (if patient is pregnant)
* IV Ceftriaxone (is first line in complicated Lyme Disease, with CNS involvement or Lyme carditis with haemodynamic instability)

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28
Q

What is a Jarisch-Herxheimer reaction?

A
  • It is reaction that can develop within the first 24 hours of treatment with any antibiotic for Lyme disease.
  • It is a systemic reaction thought to be caused by the release of cytokines when antibiotics kill large numbers of bacteria, resulting in worsening of fever, chills, muscle pains and headache.
  • Its often mistaken for an allergic reaction, however if there are no features of anaphylaxis/allergy then the antibiotics can be continued.
  • There is usually complete resolution within 48 hours.
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29
Q

What is the definition of Measles?

A
  • Measles is a highly contagious disease caused by the Measles morbillivirus.
  • It is transmitted via droplets from the nose, mouth, or throat of infected persons.
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30
Q

What is the epidemiology of Measles?

A
  • It is most common in unvaccinated children
  • It is still prevalent in areas with low vaccination rates and can cause large outbreaks.
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31
Q

What causes Measles?

A
  • Measles is caused by the Measles morbillivirus, which is a single-stranded, enveloped RNA virus.
  • The virus is transmitted by respiratory droplets or by direct contact with nasal or throat secretions of infected individuals.
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32
Q

What is the clinical presentation of Measles?

A
  • High fever above 40 degrees Celsius
  • Coryzal symptoms
  • Conjunctivitis
  • A rash appearing 2-5 days after onset of symptoms
  • Koplik spots: small grey discolourations of the mucosal membranes in the mouth, appearing 1-3 days after symptoms begin during the prodrome phase of infection. These are pathognomonic for measles.

Symptoms usually develop 10-14 days post-exposure and last for 7-10 days.

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33
Q

What are some differentials for Measles?

A
  • Rubella
    Similar to measles but often milder. The rash typically begins on the face and spreads to the rest of the body. Enlarged lymph nodes, particularly behind the ears and at the back of the skull, are common.
  • Roseola
    Characterized by a sudden high fever followed by a rash once the fever subsides. The rash usually starts on the chest, back, and abdomen, spreading to the neck and arms.
  • Scarlet Fever
    Presents with a characteristic sandpaper-like rash, a high fever, and a sore throat. The tongue may also become red and bumpy, giving it a ‘strawberry’ appearance.
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34
Q

What investigations are done for Measles?

A
  • 1st: Measles-specific IgM and IgG serology (ELISA), most sensitive 3-14 days after onset of the rash.
  • 2nd: Measles RNA detection by PCR, best for swabs taken 1-3 days after rash onset.
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35
Q

What does the management of Measles involve?

A

Management of measles involves:

  • Supportive care, usually involving antipyretics.
  • Vitamin A administration for all children under 2 years.
  • Ribavirin may reduce the duration of symptoms but is not routinely recommended due to the potential side effects.
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36
Q

What are some complications that may arise as a result of measles?

A
  • Acute otitis media
  • Bronchopneumonia
  • Encephalitis
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37
Q

What is the definition of Mumps?

A
  • Mumps is a viral infection caused by a paramyxovirus and spread by respiratory droplets.
  • Mumps is usually a self limiting condition that lasts around 1 week.
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38
Q

What is the incubation period of Mumps?

A

14 – 25 days

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39
Q

What is the epidemiology of Mumps?

A

Its prevalence has decreased considerably due to the introduction of the MMR vaccine in the 1980s, but there have been a number of outbreaks in unvaccinated/partially vaccinated groups (mostly men over 19 years at University)

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40
Q

What are some risk factors for Mumps?

A
  • Vaccination status (unvaccinated)
  • International travel
  • Exposure to a known case or outbreak.
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41
Q

What is the clinical presentation of Mumps?

A

Patients experience generalised symptoms like:
* Fever
* Muscle aches
* Lethargy
* Reduced appetite
* Headache
* Dry mouth

Alongside the following organ involvement:
* Parotitis
The parotid glands are almost always affected, usually bilaterally (though can be unilateral). Swelling can be severe enough to prevent the mouth from being opened and usually lasts 3-4 days.

  • Epididymo-orchitis
    Presents as severely painful swelling of one or both testicles and/or backache. It usually develops 4-5 days after onset of parotitis.
  • Aseptic meningitis
    Is relatively common, but tends to be mild and self limiting
  • Encephalitis
    Rare complication presenting as headache, vomiting, seizures, unconsciousness.
  • Deafness
    Mumps can be a cause of acute or insidious sensorineural hearing loss (usually unilateral) in children.
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42
Q

How is Mumps investigated?

A
  • Need laboratory confirmation using oral fluid sample (salivary IgM) to confirm a diagnosis
  • Can use serum serology (IgM or IgG)
  • High-resolution ultrasound can differentiate orchitis from torsion.
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43
Q

What does the management of Mumps involve?

A
  • Supportive, symptomatic treatment only: fluids, analgesia, antipyretics
  • The disease is usually benign and self-limiting. Although Mumps encephalitis has a fatality of 1.5%.
  • Patients should be isolated to prevent transmission (usually until 5 days after onset of parotitis)
  • Mumps is a notifiable disease, meaning you need to notify public health of any suspected and confirmed cases.
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44
Q

What are some differentials for Mumps?

A
  • Infection
    STI, Mumps, TB, brucellosis
  • Trauma
  • Torsion
  • Malignancy
    Usually painless, or gradual onset of pain.
  • Vasculitis
    PAN, Henoch-Schonlein Purpura
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45
Q

How is Obesity classified?

A

Underweight < 18.49

Normal 18.5 - 25

Overweight 25 - 30

Obese class 1 30 - 35

Obese class 2 35 - 40

Obese class 3 > 40

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46
Q

What does the management of Obesity involve?

A

The management of obesity consists of a step-wise approach:
* 1st Line - conservative Management including a healthy diet and more exercise

Pharmacological management:
* Orlistat - is a pancreatic lipase inhibitor.
* Liraglutide - is a glucagon-like peptide-1 (GLP-1) mimetic that is used in the management of type 2 diabetes mellitus (T2DM)

Surgical Management
* Bariatric Surgery

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47
Q

What are the side effects of Orlistat?

A
  • Faecal urgency/incontinence
  • Flatulence
  • fatty or oily poo
  • Oily discharge from the rectum
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48
Q

When is Orlistat indicated for use in the management of Obesity?

A

It should only be prescribed as part of an overall plan for managing obesity in adults who have:

  • BMI of 28 kg/m2 or more with associated risk factors (e.g. hypertension or T2DM), or
  • BMI of 30 kg/m2 or more
  • Continued weight loss e.g. 5% at 3 months

Orlistat is usually only used for less than a year

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49
Q

When is Liralutide used in the management of Obesity?

A
  • BMI of 35 or more
  • BMI of 32.5 or more (if patient is of south Asian, Chinese, Black African or African-Caribbean origin)
  • Non-diabetic hyperglycaemia
  • At high risk of heart problems such as heart attacks and strokes, for example because you have high blood pressure (hypertension) or high cholesterol
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50
Q

When is Bariatric surgery used in the management of obesity?

A
  • BMI of 40 or more, or
  • BMI of between 35 and 40 and another health condition that could be improved with weight loss, such as type 2 diabetes or high blood pressure.
  • When all appropriate non-surgical measures have been tried, but the person hasn’t achieved or maintained adequate, clinically beneficial weight loss
  • The person is fit enough to have anaesthesia and surgery
  • The person has been receiving, or will receive, intensive management as part of their treatment.
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51
Q

What is the definition of Osteoarthritis?

A

Osteoarthritis is a chronic, degenerative joint disease involving the breakdown and eventual loss of the articular cartilage in synovial joints.

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52
Q

What is the epidemiology of Osteoarthritis?

A
  • It is the most common form of arthritis
  • Its associated with ageing
  • More common in Females
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53
Q

What are the risk factors for osteoarthritis?

A
  • Increased Age
  • Female
  • Obesity
  • Previous joint injury (history of trauma)
  • Overuse of the joint
  • Genetics (family history)
  • Bone deformities
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54
Q

What is the pathophysiology of Osteoarthritis?

A
  • Synovial joints are composed of articular cartilage (coats the bones and Synovium (fills the space between the bones)
  • In osteoarthritis, there is a progressive loss of the articular cartilage, allowing the bones to rub against each other, causing friction and pain.
  • This results when a stimulus damages the articular cartilage (be it from obesity, sport, etc…); which cause the chondrocytes to try and repair the cartilage. In doing this they produce less proteoglycans than usual and an increased level of type 1 Collagen (compared to the usual type 2 collagen). This results in a decreased elasticity of the articular cartilage.
  • Over time, the cartilage continues to lose elasticity; and as a result it begins to flake off into the synovium as ‘joint mice’. This results in an inflammatory responce within the synovium.
  • As time progresses, the cartilage continues to erode until its almost completely gone. This means the bones of the joint are able to rub against each other (leading to friction between the 2 bones); resulting in inflammation and pain.
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55
Q

What joints are commonly affected by Osteoarthritis?

A
  • Hips
  • Knees
  • Distal interphalangeal (DIP) joints in the hands
  • Carpometacarpal (CMC) joint at the base of the thumb
  • Lumbar spine
  • Cervical spine (cervical spondylosis)
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56
Q

What is the presentation of Osteoarthritis?

A
  • Joint pain and stiffness that is worsened by activity and tends to be worse at the end of the day.
  • No morning stiffness or morning stiffness that lasts less than 30 mins
  • Bulky, bony enlargement of the joint
  • Restricted range of motion
  • Crepitus on movement
  • Effusions (fluid) around the joint
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57
Q

What are some signs of osteoarthritis in the hands?

A
  • Heberden’s nodes (in the DIP joints)
  • Bouchard’s nodes (in the PIP joints)
  • Squaring at the base of the thumb (CMC joint)
  • Weak grip
  • Reduced range of motion
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58
Q

What are some differentials for Osteoarthritis?

A
  • Rheumatoid arthritis
    Involves pain, swelling, and stiffness in multiple joints, often symmetrically. It is often accompanied by systemic symptoms like fever and fatigue.
  • Gout
    Known for sudden, severe attacks of pain, swelling, redness, and warmth in a joint, usually the big toe.
  • Lyme disease
    May present with joint pain and stiffness along with other symptoms like fever, fatigue, and skin rash.
  • Psoriatic arthritis
    Presents with joint pain, stiffness, and swelling, and is usually accompanied by psoriasis skin lesions.
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59
Q

How is Osteoartrhitis diagnosed?

A

A diagnosis can be made without investigations if the patient is:
* Over 45
* Has typical pain associated with activity and
* Has no morning stiffness (or stiffness lasting under 30 minutes).

Although imaging is used to confirm the diagnosis:
* X-Ray (1st Line imaging)
* MRI (shows more detailed view of the joint and reveal changes in the early stages of the disease)

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60
Q

What are the X-Ray changes seen in Osteoarthritis?

A

LOSS:

  • L – Loss of joint space
  • O – Osteophytes (bone spurs)
  • S – Subarticular sclerosis (increased density of the bone along the joint line)
  • S – Subchondral cysts (fluid-filled holes in the bone)
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61
Q

What is the management of osteoarthritis?

A

Non-Pharmacological
* Therapeutic exercise to improve strength and function and reduce pain
* Weight loss if overweight, to reduce the load on the joint
* Occupational therapy to support activities and function (e.g., walking aids and adaptations to the home)

Pharmacological
* Topical NSAIDs (first-line for knee osteoarthritis)
* Oral NSAIDs (co-prescribed with a proton pump inhibitor for gastroprotection)
* Weak opiates and paracetamol are only recommended for short-term, infrequent use. NICE recommend against using any strong opiates for osteoarthritis.
* Intra-articular steroid injections may temporarily improve symptoms (usually up to 10 weeks)

Surgical
* Joint replacement may be used in severe cases. The hips and knees are the most commonly replaced joints.

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62
Q

What are the side effects of NSAIDs?

A

NSAIDs (like ibuprofen and naproxen) are very effective for musculoskeletal pain. However, they must be used cautiously, particularly in older patients and those on anticoagulants. Side effects include:

  • Gastrointestinal side effects
    Such as gastritis and peptic ulcers (leading to upper gastrointestinal bleeding)
  • Renal side effects
    Such as acute kidney injury (e.g., acute tubular necrosis) and chronic kidney disease
  • Cardiovascular side effects
    Such as hypertension, heart failure, myocardial infarction and stroke
  • Exacerbating asthma
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63
Q

What is the definition of Osteoporosis?

A
  • Osteoporosis is a systemic skeletal disease characterized by reduced bone mass and altered microarchitecture of the bone tissue.
  • It leads to increased bone fragility and a consequent increase in fracture risk.
  • It is typically defined by a DEXA scan T-score of -2.5 or lower (Bone mineral density).
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64
Q

What is the definition of Osteopenia?

A
  • Osteopenia is a precursor to Osteoporosis.
  • Its defined as a Bone mineral density (T-Score) of -1 to -2.5.
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65
Q

What is the definition of Osteomalacia?

A

Osteomalacia is defined as poor bone mineralisation; leading to soft bones due to a lack of calcium.

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66
Q

What is a T-Score?

A
  • The T-Score is T-score is the number of standard deviations the patient’s bone mineral density is from an average healthy young adult.
  • Its measured by a DEXA Scan at the Femoral Neck
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67
Q

What are the risk factors for Osteoporosis?

A

SHATTERED:
* S – Steroid use and Smoking
* H – Hyperthyroidism, hyperparathyroidism
* A – Alcohol
* T – Thin (BMI < 22)
* T – Testosterone deficiency
* E – Early menopause
* R – Renal/liver failure
* E – Erosive/inflammatory bone disease
* D – Diabetes
* FAMILY HISTORY

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68
Q

What is the epidemiology of Osteoporosis?

A
  • Osteoporosis primarily affects postmenopausal women and elderly men.
  • But it is more common in postmenopausal women compared to elderly men.
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69
Q

What is the pathophysiology of Osteoporosis?

A
  • Osteoporosis is the result of an imbalance between Osteoblasts (which form bone) and Osteoclasts (which resorb bone). Therefore there’s more bone breakdown compared to formation resulting in decreased bone mass.
  • There are various factors that cause this; e.g. decreased oestrogen levels after the menopause (leads to increased bone resorption). As we age, the activity of osteoblasts naturally decreases (while osteoclast action remains the same).
  • This imbalance results in changes to the bone architecture including; thinning of the cortical bone as well as a decrease in trabecular thickness.
  • This results in a lower bone mass and strength; drastically increasing frailty and the risk of pathological fracture.
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70
Q

What is the presentation of Osteoporosis?

A

It is usually asymptomatic until a fracture occurs

But some clinical features include:
* Back pain, caused by a fractured or collapsed vertebra
* Loss of height over time
* A stooped posture
* A bone fracture that occurs much more easily than expected

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71
Q

What are some of the common places for an Osteoporotic fracture to occur?

A
  • Hip - Femoral Neck Fracture (when someone falls on their side or back)
  • Wrist - Fracture of the distal radius (Collins/Smith fracture) after falling on an outstretched arm.
  • Vertebrae - Causes sudden onset severe back pain, often radiating to the front.
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72
Q

What are the differentials for Osteoporosis?

A
  • Metabolic bone diseases
    Such as osteomalacia and hyperparathyroidism, which can present similarly with low bone mass and increased fracture risk.
  • Malignancies
    Like multiple myeloma or metastatic disease, which can lead to pathologic fractures similar to those seen in osteoporosis.
  • Secondary causes of osteoporosis
    Such as Cushing’s syndrome, hyperthyroidism, and certain medications (e.g., glucocorticoids, anticonvulsants).
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73
Q

How is Osteoporosis diagnosed?

A

DEXA Scan:
* with a T-Score of -2.5 is diagnostic for osteoporosis
* Stands for Dual Energy X-Ray Absorbtiometry
* It measures a patient’s Bone mineral density at the femoral neck.

Other investigations include:
* X-rays for suspected fractures
* MRI of the spine to assess vertebral fractures
* Blood tests to exclude metabolic bone diseases and assess vitamin D, calcium, and hormone levels.

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74
Q

What is FRAX Score?

A

The FRAX (Fracture Risk Assessment Tool) score is used to estimate the 10-year probability of a major osteoporotic fracture.

Interpretation of FRAX scores:
* Normal: 10-year probability < 10%
* Osteopenia: 10-year probability 10-20%
* Osteoporosis: 10-year probability >20%

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75
Q

What is the management of Osteoporosis?

A

Non-Pharmacological:
* Reducing risk factors, such as quitting smoking and improving diabetic control, maintain healthy weight.
* Ensuring adequate intake of vitamin D, calcium, and protein
* Regular weight-bearing exercise
* Use of hip protectors in nursing home patients

Pharmacological:
Bisphosphonates are the 1st line treatment for osteoporosis. Example regimes include:
* Alendronate 70 mg once weekly (oral)
* Risedronate 35 mg once weekly (oral)
* Zoledronic acid 5 mg once yearly (intravenous)

Other options (for when bisphosphonates aren’t suitable):
* Denosumab (a monoclonal antibody that targets osteoclasts)
* Romosozumab (a monoclonal antibody that targets sclerostin – a protein in osteocytes that inhibits bone formation)
* Teriparatide (acts as parathyroid hormone)
* Hormone replacement therapy (particularly in women with early menopause)
* Raloxifene (a selective oestrogen receptor modulator)
* Strontium ranelate (a similar element to calcium that stimulates osteoblasts and blocks osteoclasts)

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76
Q

How do Bisphosphonates need to be taken?

A

Oral bisphosphonates should be:
* Taken on an empty stomach with a full glass of water.
* Afterwards, the patient should sit upright for 30 minutes before moving or eating to reduce the risk of reflux and oesophageal erosions.

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77
Q

What are the side effects of bisphosphonates?

A
  • Reflux and oesophageal erosions
  • Atypical fractures (e.g., atypical femoral fractures)
  • Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)
  • Osteonecrosis of the external auditory canal
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78
Q

What are the possible side effects of Strontium Ranelate?

A

Increased risk of:
* Venous thromboembolism
* Myocardial infarction

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79
Q

What is the definition of Otitis Externa?

A
  • Otitis externa is inflammation of the skin in the external ear canal (external auditory meatus).
  • It’s sometimes called “swimmers ear”, as exposure to water whilst swimming can lead to inflammation in the ear canal.
  • Its a common cause of otalgia (ear pain)
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80
Q

What can cause Otitis Externa?

A
  • Bacterial Infection
  • Fungal infection (e.g. aspergillus or candida)
  • Trauma (e.g. from cotton buds or ear plugs)
  • Exposure to water (swimmer’s ear)
  • Eczema
  • Seborrhoeic dermatitis
  • Contact dermatitis
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81
Q

What are the most common causative organisms of Otitis Externa?

A
  • Pseudomonas aeruginosa
  • Staphylococcus aureus
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82
Q

What is the clinical presentation of Otitis Externa?

A
  • Otalgia (ear pain)
  • Minimal discharge (or pus)
  • Itchiness
  • Inflammation (erythema and swelling in the ear canal)
  • Conductive hearing loss (if the meatus becomes blocked by swelling or discharge)
  • Tenderness in the ear canal
  • Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
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83
Q

What are the differentials for Otitis Externa?

A
  • Otitis media:
    Characterised by middle ear pain, fever, hearing loss and sometimes discharge.
  • Furunculosis:
    Presents with localised pain, swelling and redness, and occasionally fever.
  • Eczema:
    Features include itching, redness, and scaling of the skin.
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84
Q

How is Otitis Externa diagnosed?

A
  • The diagnosis can be made clinically with an examination of the ear canal (otoscopy).
  • An ear swab can be used to identify the causative organism but is not usually required.
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85
Q

What is the management of Otitis Externa?

A

Mild Otitis Externa
* Acetic acid 2% (drops in the ear) - Has both antifungal and antibacterial effect
* Patients should keep their ear dry for 7-10 days

Moderate Otitis Externa
Is treated with topical antibiotics and steroids. E.g.
* Neomycin, dexamethasone and acetic acid (e.g., Otomize spray) - is most common
* Neomycin and betamethasone
* Gentamicin and hydrocortisone
* Ciprofloxacin and dexamethasone
* Fungal infections can be treated with clotrimazole ear drops.

Severe Otitis Externa
* Oral antibiotics (flucloxacillin or clarithromycin)
* IV antibiotics in very severe cases
* An Ear Wick can be used if the if the canal is very swollen, and treatment with ear drops or sprays will be difficult. They contain antibiotics and steroids and are left in place for a prolonged period (e.g. 48 hours).

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86
Q

What do we need to make sure of when perscribing Aminoglycosides (gentamicin and neomycin) for Otitis Externa?

A
  • It is essential to exclude a perforated tympanic membrane before using topical aminoglycosides in the ear.
  • This is because aminoglycosides are potentially Ototoxic (causing hearing loss) if they get past the tympanic membrane.
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87
Q

What is Malignant Otitis Externa?

A
  • It is a severe and potentially life-threatening form of otitis externa.
  • It is when the infection spreads to the bones surrounding the ear canal and skull.
  • It progresses to osteomyelitis of the temporal bone of the skull.
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88
Q

How can Malignant Otitis Externa Occur?

A

It is usually related to underlying risk factors for severe infection, such as:
* Diabetes
* Immunosuppressant medications (e.g., chemotherapy)
* HIV

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89
Q

What is the clinical presentation of Malignant Otitis Externa?

A

Symptoms are generally more severe than otitis externa with:
* Persistent headache
* Severe pain
* Fever.

Granulation tissue at the junction between the bone and cartilage in the ear canal (about halfway along) is a key finding of malignant otitis externa.

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90
Q

What does the management of Malignant Otitis Externa involve?

A

Malignant otitis externa requires emergency management, with:

  • Admission to hospital under the ENT team
  • IV antibiotics
  • Imaging (e.g., CT or MRI head) to assess the extent of the infection
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91
Q

What are the possible complications Malignant Otitis Externa?

A
  • Facial nerve damage and palsy
  • Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves)
  • Meningitis
  • Intracranial thrombosis
  • Death
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92
Q

What is the definition of Otitis Media?

A
  • Otitis media is an infection-induced inflammation of the middle ear.
  • Frequently occurring after a viral upper respiratory tract infection.
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93
Q

What is the epidemiology of Otitis Media?

A

Predominantly affects young children

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94
Q

What causes Otitis Media?

A
  • It is primarily caused by a bacterial infection
  • The bacteria are able to enter the middle ear through the eustachian tube from the back of the throat. This is why otitis media is usually preceeded by an Upper Respiratory Tract infection.
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95
Q

What is the most common bacterial cause of Otitis Media?

A

Streptococcus pneumoniae

Other causes include:
* Haemophilus influenzae
* Moraxella catarrhalis
* Staphylococcus aureus

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96
Q

What is the clinical presentation of Otitis Media?

A
  • Rapid onset of deep-seated ear pain
  • Reduced hearing in the affected ear
  • Systemic symptoms, e.g. fever, irritability, anorexia, vomiting
  • Symptoms of an upper airway infection such as cough, coryzal symptoms and sore throat
  • When the infection affects the vestibular system, it can cause balance issues and vertigo.
  • When the tympanic membrane has perforated, there may be discharge from the ear. (After this, there will be a reduction of pain)
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97
Q

What is the presentation of Benign chronic otitis media?

A

A dry tympanic membrane perforation without chronic infection

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98
Q

What is the presentation of Chronic secretory otitis media?

A

Also known as “Glue Ear”. It presents with persistent pain lasting weeks after the initial episode with an abnormal-looking drum and reduced membrane mobility.

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99
Q

What is the clinical presentation of Chronic suppurative otitis media?

A

Persistent purulent drainage through the perforated tympanic membrane

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100
Q

What does a normal looking tympanic membrane look like under otoscope?

A
  • “pearly-grey”, translucent and slightly shiny.
  • You should be able to visualise the malleus through the membrane.
  • Look for a cone of light reflecting the light of the otoscope.
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101
Q

What does the tympanic membrane look like in otitis media?

A
  • Otitis media will give a bulging, red, inflamed looking membrane.
  • When there is a perforation, you may see discharge in the ear canal and a hole in the tympanic membrane.
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102
Q

What are the differentials for otitis media?

A
  • Otitis externa
    Characterized by pain exacerbated by tugging of the auricle, accompanied by otorrhea and possible hearing loss
  • Mastoiditis
    Presenting with postauricular pain, erythema, and swelling, as well as protrusion of the ear
  • Temporomandibular joint disorder
    Characterized by jaw pain, difficulty in opening the mouth, and clicking or popping sounds during jaw movement
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103
Q

How is otitis media diagnosed?

A

Diagnosis of otitis media is primarily clinical, based on history and physical examination, notably the appearance of the tympanic membrane (with an Otoscope).

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104
Q

What does the management of Otitis media involve?

A
  • Most cases will resolve without antibiotics within around three days, sometimes up to a week.
  • Simple analgesia (e.g., paracetamol or ibuprofen) can be used for pain and fever.
  • A delayed prescription of antibiotics can be given after three days if symptoms have not improved or have worsened at any time
  • Consider Immediate antibiotics in patients who have significant co-morbidities, are systemically unwell or are immunocompromised.

Antibiotic options include:
* Amoxicillin for 5-7 days first-line
* Clarithromycin (in pencillin allergy)
* Erythromycin (in pregnant women allergic to penicillin)

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105
Q

What are the possible complications of otitis media?

A
  • Otitis media with effusion
  • Hearing loss (usually temporary)
  • Perforated tympanic membrane (with pain, reduced hearing and discharge)
  • Labyrinthitis (causing dizziness or vertigo)
  • Mastoiditis (rare)
  • Abscess (rare)
  • Facial nerve palsy (rare)
  • Meningitis (rare)
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106
Q

What is the definition of Pelvic Inflammatory Disease (PID)?

A

Pelvic inflammatory disease is inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix.

The terms for the individual affected organs include:
* Endometritis - inflammation of the endometrium
* Salpingitis - inflammation of the fallopian tubes
* Oophoritis - inflammation of the ovaries
* Parametritis - inflammation of the parametrium, which is the connective tissue around the uterus
* Peritonitis - inflammation of the peritoneal membrane

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107
Q

What causes Pelvic Inflammatory disease?

A

Most cases of pelvic inflammatory disease are caused by one of the sexually transmitted pelvic infections:
* Neisseria gonorrhoeae (tends to produce more severe PID)
* Chlamydia trachomatis
* Mycoplasma genitalium

However less commonly, PID be caused by non-sexually transmitted infections, such as:
* Gardnerella vaginalis (associated with bacterial vaginosis)
* Haemophilus influenzae (associated with respiratory infections)
* Escherichia coli (associated with urinary tract infections)

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108
Q

What are the risk factors for PID?

A

(The same as any other sexually transmitted infection):

  • Not using barrier contraception
  • Multiple sexual partners
  • Younger age
  • Existing sexually transmitted infections
  • Previous pelvic inflammatory disease
  • Intrauterine device (e.g. copper coil)
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109
Q

What is the presentation of PID?

A
  • Bilateral abdominal pain
  • Vaginal discharge
  • Post-coital bleeding
  • Adnexal tenderness
  • Cervical motion tenderness upon bi-manual examination
  • Fever
  • Right upper quadrant pain (Fitz-Hugh-Curtis Syndrome)
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110
Q

What are some differentials for PID?

A
  • Appendicitis
    Presents with right lower quadrant abdominal pain, fever, nausea, and vomiting.
  • Ectopic Pregnancy
    Symptoms may include unilateral lower abdominal pain and vaginal bleeding. A positive pregnancy test is a key distinguishing factor.
  • Endometriosis
    Chronic pelvic pain, dysmenorrhea, and dyspareunia are common. Pain typically worsens during menstruation.
  • Ovarian Cyst
    Symptoms can include unilateral lower abdominal pain, bloating, and a palpable mass on examination.
  • Urinary Tract Infection
    Symptoms usually include dysuria, frequency, urgency, suprapubic pain, and possible fever.
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111
Q

What investigations are done for a PID?

A
  • Pelvic Examination
  • Pregnancy test - to exclude ectopic pregnancy
  • Blood tests (inflammatory markers)
  • Transvaginal ultrasound

Testing for causative organisms:
* NAAT swabs for gonorrhoea and chlamydia
* NAAT swabs for Mycoplasma genitalium if available
* HIV test
* Syphilis test
* High vaginal swab can be used to look for bacterial vaginosis, candidiasis and trichomoniasis

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112
Q

What is the management of PID?

A

Management involves a combination of antibiotics managed in an outpatient setting. A common regime includes:
* A single dose of intramuscular ceftriaxone 1g (to cover gonorrhoea)
* Doxycycline 100mg twice daily for 14 days (to cover chlamydia and Mycoplasma genitalium)
* Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)

Empirical treatment for PID is often initiated in sexually active young women presenting with bilateral lower abdominal pain and adnexal tenderness due to the substantial number of women with PID that remain undiagnosed.

Analgesia may also be required

In severe cases of PID, admission to hospital may be required for IV antibiotics.

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113
Q

What are the possible complications of PID?

A
  • Chronic pelvic pain (in around 40% of cases)
  • Infertility (approximately 15%)
  • Ectopic pregnancy (about 1%)
  • Sepsis
  • Abscess
  • Fitz-Hugh-Curtis syndrome
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114
Q

What is Fitz-Hugh-Curtis syndrome?

A
  • It’s a complication of pelvic inflammatory disease where there is inflammation and infection of the liver capsule (Glisson’s capsule), leading to adhesions between the liver and peritoneum.
  • It presents with right upper quadrant pain that can be referred to the right shoulder tip if there is diaphragmatic irritation.
  • Laparoscopy can be used to visualise and also treat the adhesions by adhesiolysis.
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115
Q

What is the definition of Peripheral Arterial Disease (PAD)?

A
  • (Also known as peripheral vascular disease)
  • It refers to the narrowing of the arteries (distal to the aortic arch (supplying the limbs and periphery), reducing the blood supply to these areas.
  • It usually affects the lower limbs.
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116
Q

What is the epidemiology of PAD?

A

Prevalence increases with age

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117
Q

What are the risk factors for developing PAD?

A
  • Smoking
  • Diabetes mellitus
  • Hypertension
  • Hyperlipidaemia, (characterised by high total cholesterol and low high-density lipoprotein (HDL) cholesterol levels)
  • Physical inactivity
  • Obesity
  • Increased age
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118
Q

What causes PAD?

A
  • The most common cause is Atherosclerosis
  • Atherosclerosis involves both the formation of fatty deposits in the artery wall (Atheroma) as well as the hardening/stiffening of the artery wall (Sclerosis).
  • Atherosclerosis results in the narrowing of the arteries. As a result, this resricts blood flow through these ateries (usually in the leg. As a result of this reduced blood flow, the tissues that arteries supply don’t recieve enough oxygen.
  • A reduction in oxygen, results initially in muscle ischaemia (presents as claudication); followed by wide spread cell death, necrosis and gangrene if it occurs for long enough.
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119
Q

What are the 4 stages of Peripheral Arterial Disease?

A
  • Stage 1 - Asymptomatic
  • Stage 2 - Intermittant Claudication
    This is like angina of the leg
  • Stage 3 - Critical Limb Ischaemia
    Is the end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. There is a significant risk of losing the limb.
  • Stage 4 - Acute Limb Ischaemia
    Refers to a rapid onset of ischaemia in a limb. Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb
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120
Q

What is the clinical presentation of Peripheral Arterial Disease?

A

Intermittant Claudication
* Crampy leg pain that predictably occurs after walking a certain distance; that resolves with rest.
* The most common location is the calf muscles, but it can also affect the thighs and buttocks.

Critical Limb Ischaemia
* Pain at rest
* The pain is also worse at night when the leg is raised.
* Non-healing ulcers
* Gangrene

Acute Limb Ischaemia (6 P’s)
* Pain
* Pallor
* Pulseless
* Paralysis
* Paraesthesia (abnormal sensation or “pins and needles”)
* Perishing cold

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121
Q

What are the differences between Arterial and Venous Ulcers?

A

Arterial Ulcers - Are caused by ischaemia secondary to an inadequate blood supply.
* Are smaller than venous ulcers
* Are deeper than venous ulcers
* Have well defined borders
* Have a “punched-out” appearance
* Occur peripherally (e.g., on the toes)
* Have reduced bleeding
* Are painful

Venous Ulcers - Are caused by impaired drainage and pooling of blood in the legs.
* Occur after a minor injury to the leg
* Are larger than arterial ulcers
* Are more superficial than arterial ulcers
* Have irregular, gently sloping borders
* Affect the gaiter area of the leg (from the mid-calf down to the ankle)
* Are less painful than arterial ulcers
* Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)

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122
Q

What is Leriche Syndrome?

A

It is when there is occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of:

  • Thigh/buttock claudication
  • Absent femoral pulses
  • Male impotence
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123
Q

What are some differentials for Peripheral Arterial Disease?

A
  • Lumbar spinal stenosis
    Presents with neurogenic claudication, numbness, tingling, or weakness in the legs, and lower back pain.
  • Deep vein thrombosis
    Swelling, pain, warmth, and redness are commonly observed in the affected leg.
  • Diabetic neuropathy
    Presents with burning or shooting pain, increased sensitivity to touch, and numbness or reduced ability to feel pain or temperature changes.
124
Q

What investigations are done for Peripheral Arterial Disease?

A
  • Buerger’s Test - Used to assess for used to assess for PAD clinically
  • Ankle-brachial pressure index (ABPI) - 1st Line

A normal ABPI doesnt exclude PAD, so more investigations may be nescesary:
* Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
* Angiography (CT or MRI) – using contrast to highlight the arterial circulation

125
Q

What does the Ankle-brachial pressure index measure?

A
  • It is the ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm.
  • The readings are taken using a doppler probe
126
Q

What do the different results of the Ankle-brachial pressure index indicate?

A
  • Normal:
    0.9 – 1.3
  • Mild peripheral arterial disease:
    0.6 – 0.9
  • Moderate to severe peripheral arterial disease:
    0.3 – 0.6
  • Severe disease to critical ischaemic:
    Less than 0.3

Above 1.3 can indicate calcification of the arteries, making them difficult to compress (more common in diabetics)

127
Q

What is Buerger’s Test?

A

Buerger’s test is a clinical test used to assess for peripheral arterial disease. There are 2 parts to the test:

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:
* Blue initially, as the ischaemic tissue deoxygenates the blood
* Dark red (Rubor) after a short time, due to vasodilation in response to the waste products of anaerobic respiration

128
Q

What is Buerger’s Angle?

A

Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply

129
Q

What is the management of Intermittant Claudication?

A

Conservative Management (1st Line)
* Lifestyle changes - to manage modifiable risk factors (e.g., stop smoking).
* Optimise medical treatment of co-morbidities (such as hypertension and diabetes).
* Exercise training, involving a structured and supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating.

Medical Management
* Atorvastatin 80mg
* Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
* Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)

Surgical Management
* Endovascular angioplasty and stenting
* Endarterectomy – cutting the vessel open and removing the atheromatous plaque
* Bypass surgery – using a graft to bypass the blockage

130
Q

What is the management of critical limb ischaemia?

A

Patients require urgent revascularisation. This can be achieved by:
* Endovascular angioplasty and stenting
* Endarterectomy
* Bypass surgery
* Amputation of the limb if it is not possible to restore the blood supply

131
Q

What is the management of Acute Limb Ischaemia?

A

Patients need need an urgent referral to the on-call vascular team. Management options involve:
* Endovascular thrombolysis – inserting a catheter through the arterial system to apply thrombolysis directly into the clot
* Endovascular thrombectomy – inserting a catheter through the arterial system and removing the thrombus by aspiration or mechanical devices
* Surgical thrombectomy – cutting open the vessel and removing the thrombus
* Endarterectomy
* Bypass surgery
* Amputation of the limb - if it is not possible to restore the blood supply

132
Q

What is the definition of Polymyalgia Rheumatica?

A
  • Polymyalgia rheumatica (PMR) is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck.
  • There is a strong association with giant cell arteritis, and the two conditions often occur together.
133
Q

What is the epidemiology of Polymyalgia Rheumatica?

A
  • It occurs exclusively in patients aged over 50.
  • It’s most common in patients with Northern European ancestry.
134
Q

What is the clinical presentation of Polymyalgia Rheumatica?

A

The core symptoms are pain and stiffness of the:
* Shoulders, potentially radiating to the upper arm and elbow
* Pelvic girdle (around the hips), potentially radiating to the thighs
* Neck

Features of the pain and stiffness:
* Worse in the morning
* Worse after rest or inactivity
* Interfere with sleep
* Take at least 45 minutes to ease in the morning
* Somewhat improve with activity

Other associated features:
* Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
* Muscle tenderness
* Carpel tunnel syndrome
* Peripheral oedema

There’s a relatively rapid onset of symptoms over days to weeks. And the symptoms should be present for at least two weeks before its considered

135
Q

What are some differentials for Polymyalgia Rheumatica?

A

Autoimmune rheumatic disease:
* Polymyositis
Myositis causes bilateral proximal muscle weakness, while pain is either absent or mild . Whereas in polymyalgia rheumatica, pain and stiffness are prominent, but there should not be muscle weakness on examination
* rheumatoid arthritis
* SLE

Infection, such as tuberculosis or subacute bacterial e
Endocarditis
Malignancy
Chronic fatigue syndrome
Hypothyroidism

136
Q

How is Polymyalgia Rheumatica diagnosed?

A

Diagnosis is based on:
* clinical presentation
* Response to steroids - Improvement of symptoms
* Excluding differentials

Investigations that should be done before starting steroids:
* Full blood count
* Renal profile (U&E)
* Liver function tests
* Calcium (abnormal in hyperparathyroidism, cancer and osteomalacia)
* Serum protein electrophoresis for myeloma
* Thyroid-stimulating hormone for thyroid function
* Creatine kinase for myositis
* Rheumatoid factor for rheumatoid arthritis
* Urine dipstick

Other investigations to consider:
Anti-nuclear antibodies (ANA) for systemic lupus erythematosus
Anti-cyclic citrullinated peptide (anti-CCP) for rheumatoid arthritis
Urine Bence Jones protein for myeloma
Chest x-ray for lung and mediastinal abnormalities (e.g., lung cancer or lymphoma)

137
Q

What is the management of Polymyalgia Rheumatica?

A
  • 15mg prednisolone daily initially
  • Follow up after 1 week
  • Patients will show a dramatic improvement in symptoms within one week.
  • A poor response to steroids suggests an alternative diagnosis.

Treatment with steroids typically lasts 1-2 years. The following Reducing regime of prednisolone is recommeded:

  • 15mg until the symptoms are fully controlled, then
  • 12.5mg for 3 weeks, then
  • 10mg for 4-6 weeks, then
  • Reducing by 1mg every 4-8 weeks
138
Q

What additional management do people on long term steroids require?

A

DON’T STOP mnemonic:
* Don’t - steroid dependence occurs after 3 weeks of treatment, and abruptly stopping risks adrenal crisis
* SSick day rules (steroid doses may need to be increased if the patient becomes unwell)
* TTreatment card – patients should carry a steroid treatment card to alert others that they are steroid-dependent
* OOsteoporosis prevention may be required (e.g., bisphosphonates and calcium and vitamin D)
* PProton pump inhibitors are considered for gastro-protection (e.g., omeprazole)

139
Q

What is the definition of Prostate Cancer?

A
  • Prostate cancer is a malignant tumour that arises from the cells of the prostate.
140
Q

What is the epidemiology of prostate cancer?

A
  • It is the most common cancer in men
  • Prevalence increases with age
141
Q

What are the risk factors for prostate cancer?

A

Non-Modifiable
* African ethnicity
* BRCA gene mutations
* Family history of prostate cancer
* Age (risk increases with advancing age)
* Tall stature

Modifiable
* Obesity
* Smoking
* Diet rich in animal fats and dairy products
* Anabolic steroids

142
Q

What is the pathophysiology of prostate cancer?

A
  • Prostate cancers are almost always androgen-dependent, (meaning they rely on androgen hormones (e.g., testosterone) to grow).
  • The majority are adenocarcinomas and grow in the peripheral zone of the prostate.
  • They vary in how aggressive they can be; but most prostate cancers are very slow-growing and do not cause death.
143
Q

Where do advanced prostate cancers most commonly spread to?

A

Lymph nodes and Bones

144
Q

What is the clinical presentation of prostate cancer?

A

Early prostate cancer is often asymptomatic. While later in the course of the disease it can present with LUTs (similar to BPH) including:
* Hesitancy
* Frequency
* Weak flow
* Terminal dribbling
* Nocturia

Other symptoms include:
* Haematuria
* Erectile dysfunction
* Haematospermia (blood in semen)
* Pelvic discomfort

Symptoms of advanced disease (or metastasis):
* Weight loss
* Bone pain
* Cauda equina syndrome

145
Q

What are some differentials for prostate cancer?

A
  • Benign Prostatic Hyperplasia (BPH):
    Characterised by difficulty in urination, increased frequency of urination, nocturia, and potentially, haematuria.
  • Prostatitis:
    Acute or chronic inflammation of the prostate that can cause pelvic pain, urinary symptoms, and potentially, systemic symptoms such as fever and malaise.
  • Urinary Tract Infection (UTI):
    Can cause dysuria, urinary frequency, urgency, and potentially, systemic signs of infection.
  • Bladder cancer:
    May present with haematuria, dysuria, and urinary frequency.
146
Q

What investigations are done for prostate cancer?

A

Digital Rectal Examination
* A cancerous prostate may feel firm or hard, asymmetrical, craggy or irregular, with loss of the central sulcus. There may be a hard nodule.
* Any of these findings require a 2 week urgent cancer referral

Multiparametric MRI
* Is the 1st line investigation
* The results are scored on the Likert scale (from 1 - very low suspicion to 5 - definite cancer)

Prostate Biopsy
* Establishes a definitive diagnosis
* Performed when the Likert scale of an MRI is 3 or above
* There are 2 types (Transrectal ultrasound-guided biopsy (TRUS) and Transperineal biopsy)
* Due to the risk of a false negative result, (if the biopsy misses the cancerous area); multiple needles are used to take samples from different areas of the prostate.

Isotope Bone Scan
* Is also called a radionuclide scan or bone scintigraphy.
* It is used to look for bony metastasis.

147
Q

What are the main risks of a prostate biopsy?

A
  • Pain (particularly lower abdominal, rectal or perineal pain)
  • Bleeding (blood in the stools, urine or semen)
  • Infection
  • Urinary retention due to short term swelling of the prostate
  • Erectile dysfunction (rare)
148
Q

What is the Gleeson Grading System?

A
  • Gleason grading system is based on the histology from the prostate biopsies.
  • The greater the Gleason score, the more poorly differentiated the tumour is (the cells have mutated further from normal prostate tissue) and the worse the prognosis is.
  • The tissue samples are graded 1 (closest to normal) to 5 (most abnormal).

Its made up of two numbers added together:
* The first number is the grade of the most prevalent pattern in the biopsy
* The second number is the grade of the second most prevalent pattern in the biopsy

A score of:
* 6 is considered low risk
* 7 is intermediate risk (3 + 4 is lower risk than 4 + 3)
* 8 or above is deemed to be high risk

149
Q

What is the staging system for prostate cancer?

A

TNM staging system - This rates the T (tumour), N (lymph nodes) and M (metastasis) of the cancer.

T for Tumour:
* TX – unable to assess size
* T1 – too small to be felt on examination or seen on scans
* T2 – contained within the prostate
* T3 – extends out of the prostate
* T4 – spread to nearby organs

N for Nodes:
* NX – unable to assess nodes
* N0 – no nodal spread
* N1 – spread to lymph nodes

M for Metastasis:
* M0 – no metastasis
* M1 – metastasis

150
Q

What is Prostate Specific Antigen (PSA)?

A
  • PSA is a glycoprotein thats produced from epithelial cells of the prostate and is secreted in the semen (with a small amount entering the blood).
  • It helps to thin the semen after ejaculation
  • Its specific to the prostate and a raised PSA is an indicator of prostate cancer.
151
Q

What are the advantages and disadvantages of testing for PSA?

A

Advantages
* PSA testing can lead to the early detection of prostate cancer, potentially resulting in effective treatment and preventing significant problems.

Disadvantages
* PSA testing is unreliable, with a high rate of false positives (75%) and false negatives (15%
* There are various other causes of a raised PSA (other than prostate cancer)
* False positives may lead to further investigations, including invasive prostate biopsies, which have complications and may be unnecessary. It may also lead to the unnecessary diagnosis and treatment of prostate cancer that would never have caused problems
* False negatives may lead to false reassurance.

152
Q

What are the most common causes of a raised PSA?

A
  • Prostate cancer
  • Benign prostatic hyperplasia
  • Prostatitis
  • Urinary tract infections
  • Vigorous exercise (notably cycling)
  • Recent ejaculation or prostate stimulation
153
Q

What does the management of prostate cancer involve?

A

Depending on the grade and stage of prostate cancer, treatment can involve:

Surveillance or watchful waiting
* Is suitable for patients with early or low-grade prostate cancer and involves repeating investigations periodically to monitor disease progression.

External beam radiotherapy directed at the prostate
* Can be used either as a curative measure or for palliation pain relief without removing the cause) to reduce tumour bulk and associated pain.

Brachytherapy
* Involves implanting radioactive metal “seeds” into the prostate. This delivers continuous, targeted radiotherapy to the prostate.

Hormone therapy
* Aims to reduce testosterone levels, slowing the progression of metastatic prostate cancer.
* This can be achieved with GnRH analogues, androgen antagonists, or GnRH antagonists.

Surgery
* Radical prostatectomy involves a surgical operation to remove the entire prostate. The aim is to cure prostate cancer confined to the prostate.
* Minimally invasive techniques such as robotically assisted laparoscopic prostatectomy (RALP) are becoming more common.

154
Q

What is the key complication of External Beam Radiotherapy?

A

Proctitis - inflammation of the rectum

  • Proctitis can cause pain, altered bowel habit, rectal bleeding and discharge.
  • Prednisolone suppositories can help reduce inflammation.
155
Q

What are the side effects of Brachytherapy?

A
  • Inflammation in nearby organs, such as the bladder (cystitis) or rectum (proctitis).
  • Erectile dysfunction
  • Incontinence
  • Increased risk of bladder or rectal cancer
156
Q

What are the options for hormone therapy to treat prostate cancer?

A
  • Androgen-receptor blockers such as bicalutamide
  • GnRH agonists such as goserelin (Zoladex) or leuprorelin (Prostap)
  • Bilateral orchidectomy to remove the testicles (rarely used)
157
Q

What are the side effects of hormone therapy (to treat prostate cancer)?

A
  • Hot flushes
  • Sexual dysfunction
  • Gynaecomastia
  • Fatigue
  • Osteoporosis
158
Q

What are the possible complications of a radical prostatectomy?

A

Erectile dysfunction and Urinary incontinence

159
Q

What is the definition of Psoriasis?

A

Psoriasis is a chronic autoimmune disease characterised by well-demarcated, erythematous, scaly plaques.

160
Q

What are the different types of Psoriasis?

A

Plaque psoriasis
* Features the thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp.
* The plaques are 1cm – 10cm in diameter.
* This is the most common form of psoriasis in adults.

Guttate psoriasis
* Is the second most common form of psoriasis and commonly occurs in children.
* It presents with many small raised papules across the trunk and limbs. The papules are mildly erythematous and can be slightly scaly.
* Over time the papules in guttate psoriasis can turn into plaques.
* Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications. It often resolves spontaneously within 3 – 4 months.

Flexural (inverse) psoriasis
* Smooth, erythematous plaques without scale in flexures and skin folds.

Pustular psoriasis
* Is a rare severe form of psoriasis where pustules form under areas of erythematous skin. The pus in these areas is not infectious.
* Patients can be systemically unwell.
* It should be treated as a medical emergency and patients with pustular psoriasis initially require admission to hospital.

Erythrodermic psoriasis
* Is a rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin.
* The skin comes away in large patches (exfoliation) resulting in raw exposed areas.
* It should be treated as a medical emergency and patients require admission.

161
Q

What different factors can trigger psoriasis?

A
  • Skin trauma (Koebner phenomenon)
  • Infection: Streptococcus, HIV
  • Drugs: B-blockers, Anti-malarials, Lithium, Indomethacin/NSAIDs (BALI)
  • Withdrawal of steroids
  • Stress
  • Alcohol + smoking
  • Cold/dry weather

Other risk factors include:
Family history, HIV infection and obesity

162
Q

What is the presentation of psoriasis?

A

Key Presentation:
Itchy, well-demarcated circular-to-oval bright red/pink elevated lesions (plaques) with overlying white or silvery scale, distributed symmetrically over extensor body surfaces and the scalp.

Other psoriatic specific signs:
* Auspitz sign - refers to small points of bleeding when plaques are scraped off
* Koebner phenomenon - refers to the development of psoriatic lesions to areas of skin affected by trauma
* Residual pigmentation of the skin after the lesions resolve

Nail Changes in psoriasis:
* Nailbed pitting - superficial depressions in the nailbed
* Onycholysis - separation of nail plate from nailbed
* Subungual hyperkeratosis - thickening of the nailbed

163
Q

What are some differentials for Psoriasis?

A

There are various differentials for a scaly rash:
* Pityriasis rosea
* Tinea
* Seborrhoeic dermatitis
* Bowen’s disease
* Discoid eczema
* Mycosis fungoides
* Discoid lupus
* Scabies

164
Q

What does the management of Psoriasis involve?

A

The treatment of plaque psoriasis targets this pathology:
* Corticosteroids to reduce inflammation and
* Vitamin D to reduce keratinocyte proliferation.

Topical Treatment - is first line
* All patients should use an emollient to reduce scale and itch
* 1st - potent topical corticosteroid OD (eg Betnovate) + topical vitamin D OD (eg Dovonex) applied at different times
* 2nd: stop the topical corticosteroid, apply topical vitamin D twice daily
* 3rd: stop the topical vitamin D, apply potent topical corticosteroid twice daily

Phototherpy
* With narrow band ultraviolet B light
* Is useful in extensive guttate psoriasis

Systemic treatment - when topical treatment fails
* 1st line: Methotrexate
* 2nd line: Ciclosporin (1st line if rapid disease control needed/palmoplantar pustulosis/are considering conception)
* 3rd line: Acitretin
* 4th line: Biologic therapy (e.g. Infliximab, Etanercept or Adalimumab)

165
Q

What are the complications of systemic therapy in the treatment of psoriasis?

A

Methotrexate
* Can cause pneumonitis and hepatotoxicity (monitor LFTs).
* It can also cause myelosuppression leading to pancytopenia.

Acitretin
* Is teratogenic
* It can cause hepatotoxicity and elevated lipids

Anti-TNF biological drugs
* (such as adalimumab)
* Associated with reactivation of latent tuberculosis (always do CXR before initiation of treatment)

Ciclosporin
* Side effects can can be remembered by the 5 H’s:
* Hypertrophy of the gums, Hypertrichosis, Hypertension, Hyperkalaemia and Hyperglycaemia (diabetes)

166
Q

What is the definition of Spinal Stenosis?

A
  • Spinal stenosis refers to the narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots.
  • This usually affects the cervical or lumbar spine.
167
Q

What is the epidemiology of spinal stenosis?

A
  • Lumbar spinal stenosis is the most common type of spinal stenosis
  • More common in patients older than 60 years (relating to degenerative changes in the spine)
168
Q

What are the different types of spinal stenosis?

A
  • Central stenosis – narrowing of the central spinal canal
  • Lateral stenosis – narrowing of the nerve root canals
  • Foramina stenosis – narrowing of the intervertebral foramina
169
Q

What can cause spinal stenosis?

A
  • Congenital spinal stenosis
  • Degenerative changes, including facet joint changes, disc disease and bone spurs
  • Herniated discs
  • Thickening of the ligamenta flava or posterior longitudinal ligament
  • Spinal fractures
  • Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
  • Tumours
170
Q

What is the presentation of spinal stenosis?

A
  • Gradual symptom onset (as opposed to cauda equina syndrome or sudden disc herniation with cord compression)

Central stenosis
* Intermittent neurogenic claudication is the key presentation. It involves typical symptoms involve: Lower back pain, Buttock and leg pain, Leg weakness.
* Symptoms are absent at rest and when seated but occur with standing and walking.
* Bending forward (flexing the spine) expands the spinal canal and improves symptoms.
* Standing straight (extending the spine) narrows the canal and worsens the symptoms.

Lateral stenosis and Foramina stenosis
* Cause symptoms of Sciatica

Severe spinal stenosis
* Can present with features of cauda equina syndrome (saddle anaesthesia, sexual dysfunction and incontinence of the bladder and bowel).

171
Q

What does the term Radiculopathy mean?

A
  • It refers to compression of the nerve roots as they exit the spinal cord and spinal column.
  • This leads to motor and sensory symptoms.
  • Caused by things like spinal stenosis
172
Q

What are some differentials for Spinal Stenosis?

A
  • Peripheral Vascular Disease (PVD):
    Characterized by intermittent claudication, but with associated vascular risk factors, diminished or absent pulses, and skin changes
  • Herniated Lumbar Disc:
    Presents with radicular pain, but the pain is often exacerbated by flexion and relieved by extension, the opposite of the presentation in LSS
  • Spinal Tumors:
    Can cause similar neurological symptoms, but often associated with weight loss, night sweats, or other systemic symptoms
  • Arthritis:
    Although it can cause back pain, it’s typically associated with morning stiffness and may involve other joints
173
Q

What investigations are done for spinal stenosis?

A
  • Diagnostic - MRI Scan
  • Physical examination is usually the first step; to examine the patient for neurological signs and vascular risk factors
  • Electromyography (EMG) - Can be used to evaluate nerve function in patients with LSS
174
Q

What is the management of Spinal Stenosis?

A

Conservative Management - is first line
* Exercise and weight loss (if appropriate)
* Analgesia (NSAIDs, opioids, or nerve block injections)
* Physiotherapy

Surgical Management - when conservative measures fail or for patients with severe, disabling pain.
* Common procedures involve laminectomy, laminoplasty, or spinal fusion.

175
Q

What is the definition of Reactive Arthritis?

A
  • Reactive arthritis is a sterile inflammatory arthritis occurring within 4 weeks of an infection.
176
Q

What are the risk factors for Reactive Arthritis?

A
  • Male
  • Early adulthood, commonly presents between the age of 20 and 40
  • HLA-B27 positive (it is a seronegative spondyloarthropathy)
177
Q

What are the common triggers for Reactive Arthritis?

A

A previous Sexually transmitted or Gastrointestinal infection occuring within a month of the reactive arthritis.
* Most common infections include Chlamydia, Shigella, Yersinia or Salmonella (Gonorrhoea more commonly causes Septic arthritis instead)
* Sometimes this infection is asymptomatic, and is only identified half of the time

178
Q

What is the clinical presentation of Reactive Arthritis?

A

Reiter’s Triad:
* Conjunctivitis
* Urethritis and Circinate balanitis (dermatitis at the head of the penis)
* Oligoarthritis
* Can’t see, Can’t pee, Can’t climb a tree

It typically presents as a warm and painful swollen joint (commonly affecting the large joints of the lower limb). It is typically an Asymmetrical Oligoarthritis.

179
Q

What is the main differential for reactive arthritis that needs to be excluded?

A

Septic Arthritis

180
Q

What is the management of Reactive arthritis?

A

Septic arthritis needs to be excluded; and antibiotics are given until it is. To do this:
* Joint aspiration is done
* The synovial fluid obtained is sent off for microscopy, culture and sensitivity testing for infection, and crystal examination for gout and pseudogout.

When Septic Arthirtis has been excluded:
* Treatment of the triggering infection (e.g., chlamydia)
* NSAIDs
* Steroid injection into the affected joints
* Systemic steroids may be required, particularly where multiple joints are affected

Most cases resolve within 6 months and do not recur. However, recurrent cases may require DMARDs or anti-TNF medications.

181
Q

What is the definition of Rhinosinusitis?

A
  • Rhinosinusitis is defined as inflammation of the nose and paranasal sinuses.
  • The diagnosis requires the presence of at least two symptoms, one of which must be either nasal blockage/obstruction/congestion or nasal discharge (anterior/posterior nasal drip).
182
Q

What is the epidemiology of Rhinosinusitis?

A

It is a very common disorder affecting around 10% to 15% of the adult population globally.

183
Q

What can cause Rhinosinusitis?

A

Inflammation of the sinuses can be caused by:

  • Infection - particularly following viral upper respiratory tract infections
  • Allergies - such as hayfever (with allergic rhinitis)
  • Obstruction of drainage - for example, due to a foreign body, trauma or polyps
  • Smoking

Patients with asthma are more likely to suffer from sinusitis.

184
Q

What is the difference between Acute and Chronic Rhinosinusitis?

A
  • Acute lasts less than 12 weeks
  • Chronic lasts more than 12 weeks
185
Q

What is the presentation of Rhinosinusitis?

A
  • Nasal blockage/obstruction/congestion
  • Nasal discharge
  • Facial pain or heaviness
  • Reduced olfaction
  • Other symptoms may include headache, ear pain, sore throat, and cough.
186
Q

What are some differentials for Rhinosinusitis?

A
  • Common cold:
    Symptoms typically include runny or stuffy nose, sore throat, cough, and fatigue. Cold symptoms usually peak within 2-3 days and resolve within 7-10 days.
  • Allergic rhinitis:
    Presents with nasal itching, sneezing, rhinorrhea, and nasal congestion. Ocular symptoms such as tearing and itching of the eyes can also be present.
  • Nasal polyps:
    Commonly associated with a history of chronic sinusitis, asthma, or aspirin allergy. Symptoms include nasal obstruction, anosmia, and often a runny nose.
187
Q

What investigations are done for Rhinosinusitis?

A
  • Nasal endoscopy - Allows for the visual examination of the internal nasal passages and the sinus openings.
  • Computed tomography (CT) - Provides detailed images of the sinuses and can reveal evidence of sinus inflammation or obstruction.
  • Cultures - Can be useful when bacterial sinusitis is suspected and previous treatments have failed.
188
Q

What does the management of Rhinosinusitis involve?

A

Where symptoms persist for longer than 10 days:
* High dose corticosteroid nasal spray for 14 days (e.g., mometasone 200 mcg twice daily)
* A delayed antibiotic prescription, used if worsening or not improving within 7 days (after corticosteroid spray)(phenoxymethylpenicillin first-line) - Antibiotics are not used first line as most cases are viral and resolve within 2-3 weeks.

Other options
* Saline nasal irrigation
* Functional endoscopic sinus surgery (FESS) - Can be used to remove or correct any obstructions to the sinuses. And balloons may be used to inflate the opening of the sinus. A CT scan is done before this to confirm there is a blockage.

189
Q

What is the definition of a tension headache?

A
  • A tension headache is a cause of chronic recurring head pain.
  • It typically cause a mild ache or pressure in a band-like pattern around the head
190
Q

What is the epidemiology of a tension headache?

A
  • They are the most common cause of chronic recurring head pain
  • More likely to affect women
191
Q

What is the presentation of a tension headache?

A
  • Bilateral, non-pulsatile headaches
  • Tightness sensation, like a band around the head
  • Scalp muscle tenderness

They develop and resolve gradually and do not produce visual changes.

192
Q

What can cause a tension headache?

A

Triggers include:
* Missed Meals
* Conflict
* Stress
* Clenched Jaw
* Overexertion
* Lack of Sleep
* Depression

193
Q

What is the management of a tension headache?

A

First Line:
* Reassurance
* Lifestyle Advice
* Simple Analgaesia (Ibuprofen and paracetamol)

Medication - Used for chronic or frequent tension headaches
* Amitriptyline is first line

194
Q

What is the definition of Tonsilitis?

A
  • Tonsilitis refers to inflammation of the tonsils.
  • Its primarily caused by infection (either viral or bacterial)
195
Q

What is the epidemiology of Tonsilitis?

A

It is a very common condition that predominantly affects children and adolescents

196
Q

What causes Tonsilitis?

A

The most common cause is a viral infection. Common viruses include:
* Epstein-Barr virus
* Influenza virus
* Adenovirus
* Rhinovirus.

It can also be caused by a bacterial infection:
* Most common - Group A streptococcus (Streptococcus pyogenes).
* 2nd most common - Streptococcus pneumoniae

197
Q

What is the presentation of Tonsilitis?

A
  • Sore throat
  • Fever (above 38°C)
  • Pain on swallowing

Examination will show:
Red, inflamed and enlarged tonsils, with or without exudates (small white patches of pus on the tonsils)

There may be anterior cervical lymphadenopathy

198
Q

Where are the Tonsillar Lymph Nodes?

A

The tonsillar lymph nodes are just behind the angle of the mandible (jawbone).

199
Q

What are the 2 scoring systems for estimating whether the tonsilitis is viral or bacterial called?

A
  • The Centor criteria - estimates the probability that tonsillitis is due to bacterial infection and will benefit from antibiotics.
  • The FeverPAIN score is an alternative to the Centor criteria.
200
Q

Describe the scoring of the Censor Criteria

A

A score of 3 or more gives a 40 – 60 % probability of bacterial tonsillitis, and it is appropriate to offer antibiotics.

A point is given if each of the following features are present:
* Fever over 38ºC
* Tonsillar exudates
* Absence of cough
* Tender anterior cervical lymph nodes (lymphadenopathy)

201
Q

Describe the scoring of the FeverPAIN Score

A

A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis:

  • Fever during previous 24 hours
  • P – Purulence (pus on tonsils)
  • A – Attended within 3 days of the onset of symptoms
  • I – Inflamed tonsils (severely inflamed)
  • N – No cough or coryza
202
Q

What are the differentials for Tonsilitis?

A
  • Pharyngitis
    Symptoms include sore throat, fever, and headache. Unlike tonsillitis, patients do not usually present with lymphadenopathy.
  • Mononucleosis
    Characterized by fatigue, sore throat, fever, and swollen lymph nodes. A key difference is the presence of severe fatigue and splenomegaly.
203
Q

What investigations are done for tonsilitis?

A
  • Investigation for Tonsilitis typically involves clinical examination and patient history.
  • Throat swabs and rapid antigen tests are can be done if bacterial infection is suspected.
  • Blood tests are reserved for those with suspected immunodeficiency.
204
Q

What is the management of Tonsilitis?

A
  • Calculate the Centor Criteria or FeverPAIN Score

If Centor score is less than 3:
* Simple analgesia with paracetamol and ibuprofen to control pain and fever.
* Advise to return if the pain has not settled after 3 days or the fever rises above 38.3ºC.
* Delayed perscriptions (for antibiotics) are an option for if the symptoms get worse.

If Centor score is 3 or more:
* Consider Antibiotics
* Penicillin V (phenoxymethylpenicillin) for a 10-day course is 1st line
* Clarithromycin is first line in a patient with a penicillin allergy

205
Q

What are some possible complications of Tonsilitis?

A
  • Recurrent Tonsillitis (most common)
  • Peritonsillar abscess, also known as quinsy
  • Otitis media, if the infection spreads to the inner ear
  • Scarlet fever
  • Rheumatic fever
  • Post-streptococcal glomerulonephritis
  • Post-streptococcal reactive arthritis
206
Q

What are the different types of incontinence?

A
  • Stress incontinence
  • Urge incontinence
  • Overflow incontinence
  • Functional incontinence
  • Mixed incontinence
207
Q

What are the reversible causes of incontinence?

A

DIAPPERS

  • D - Delirium
  • I - Infection
  • A - Atrophic vaginitis or urethritis
  • P - Pharmaceutical (medications)
  • P - Psychiatric disorders
  • E - Endocrine disorders (e.g. diabetes)
  • R - Restricted mobility
  • S - Stool impaction
208
Q

What is the definition of Stress Incontinence?

A
  • Stress incontinence involves the leaking of urine when intra-abdominal pressure is raised (e.g. when coughing, laughing or straining).
  • Its due to due to weakness of the pelvic floor and sphincter muscles.
209
Q

What are the risk factors for stress incontinence?

A
  • Childbirth (especially vaginal) - This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.
  • Hysterectomy
210
Q

What are some possible triggers for stress incontinence?

A

Anything that can increase abdominal pressure sufficiently:
* Coughing
* Laughing
* Sneezing
* Exercising

211
Q

What is management of Stress Incontinence?

A

Conservative Management
* Avoiding caffeine, fizzy and sugary drinks
* Avoiding excessive fluid intake
* Supervised pelvic floor exercises (for at least three months before considering surgery)

Surgical Management
* Tension-free vaginal tape (TVT) - involves a mesh sling looped under the urethra and up behind the pubic symphysis to the abdominal wall. This supports the urethra, reducing stress incontinence.
* Autologous sling procedures - work similarly to TVT procedures but a strip of fascia from the patient’s abdominal wall is used rather than tape
* Colposuspension - involves stitches connecting the anterior vaginal wall and the pubic symphysis, around the urethra, pulling the vaginal wall forwards and adding support to the urethra
* Intramural urethral bulking - involves injections around the urethra to reduce the diameter and add support

Medical Management
* Duloxetine is an SNRI antidepressant and is used second line where surgery is less preferred

212
Q

What is the definition of Urge Incontinence?

A
  • Urge incontinence involves the sudden and involuntary loss of urine associated with urgency.
  • It is caused by overactivity of the detrusor muscle and is often called an Overactive Bladder
213
Q

What are the risk factors for urge incontinence?

A
  • Recurrent urinary tract infections
  • High BMI
  • Advancing age
  • Smoking
  • Caffeine
214
Q

What is the management of Urge incontinence?

A

Conservative Management
* Bladder retraining (gradually increasing the time between voiding) for at least six weeks - is first-line
* Avoiding caffeine, fizzy and sugary drinks; as well as avoiding excessive fluid intake.
* Pelvic floor exercises (can also help)

Medical Management - 2nd line when conservative management fails
* Anticholinergic medication (e.g. oxybutynin, tolterodine and solifenacin) - work by inhibiting the parasympathetic action on the detrusor muscle.
* Mirabegron (a beta-3 receptor agonist) is an alternative often used in older patients as it has less of an anticholinergic burden.

Surgical Management
* Botulinum toxin type A injection into the bladder wall
* Percutaneous sacral nerve stimulation involves implanting a device in the back that stimulates the sacral nerves
* Augmentation cystoplasty involves using bowel tissue to enlarge the bladder
* Urinary diversion involves redirecting urinary flow to a urostomy on the abdomen

215
Q

What are some anticholinergic side effects?

A
  • Dry mouth
  • Dry eyes
  • Urinary retention
  • Constipation
  • Postural hypotension

It can also lead to a cognitive decline, memory problems and worsening of dementia, which can be very problematic in older, more frail patients.

216
Q

What condition is Mirabegron contraindicated in?

A

Uncontrolled hypertension

As it works as a beta-3 agonist, stimulating the sympathetic nervous system, leading to raised blood pressure. This can lead to a hypertensive crisis and an increased risk of TIA and stroke.

217
Q

What is the definition of Functional Incontinence?

A

Functional incontinence involves an individual having the urge to pass urine, but for whatever reason they’re unable to access the necessary facilities and as a result are incontinent.

218
Q

What are some possible causes of functional incontinence?

A

Functional incontinence is associated with:

  • Sedating medications
  • Alcohol
  • Dementias
219
Q

What is the definition of Overflow incontinence?

A
  • Overflow incontinence occurs when small amounts of urine leak without warning.
  • It can occur when there is chronic urinary retention due to an obstruction to the outflow of urine.
  • The chronic urinary retention results in an overflow of urine, and the incontinence occurs without the urge to pass urine.
220
Q

What are some causes of overflow incontinence?

A
  • Anticholinergic medications
  • Fibroids
  • Pelvic tumours

Neurological conditions such as:
* Multiple sclerosis
* Diabetic neuropathy
* Spinal cord injuries.

221
Q

What should an assesment of Urinary Incontinence involve?

A

Medical History - Should be able to distinguish between the different types of incontinence

Assess the modifiable lifestyle factors that can contribute to symptoms:
* Caffeine consumption
* Alcohol consumption
* Medications
* Body mass index (BMI)

Assess severity by asking:
* Frequency of urination
* Frequency of incontinence
* Nighttime urination
* Use of pads and changes of clothing

An Examination to assess for pelvic tone, and should look for:
* Pelvic organ prolapse
* Atrophic vaginitis
* Urethral diverticulum
* Pelvic masses

The strength of pelvic muscle contraction should be assesed and graded using the modified Oxford grading system

222
Q

Describe the modified Oxford grading system for Pelvic muscle contraction?

A
  • 0 - No contraction
  • 1 - Faint contraction
  • 2 - Weak contraction
  • 3 - Moderate contraction with some resistance
  • 4 - Good contraction with resistance
  • 5 - Strong contraction, a firm squeeze and drawing inwards
223
Q

What investigations can be done for urinary incontinence?

A
  • A bladder diary should be completed, tracking fluid intake and episodes of urination and incontinence over at least three days. There should be a mix of work and leisure days.
  • Urine dipstick testing should be performed to assess for infection, microscopic haematuria and other pathology.
  • Post-void residual bladder volume should be measured using a bladder scan to assess for incomplete emptying.
  • Urodynamic testing can be used to investigate patients with urge incontinence not responding to first-line medical treatments, difficulties urinating, urinary retention, previous surgery or an unclear diagnosis. It is not always required where the diagnosis is possible based on the history and examination.
224
Q

What tests can be involved in Urodynamic Testing?

A
  • Cystometry measures the detrusor muscle contraction and pressure
  • Uroflowmetry measures the flow rate
  • Leak point pressure is the point at which the bladder pressure results in leakage of urine. The patient is asked to cough, move or jump when the bladder is filled to various capacities. This assesses for stress incontinence.
  • Post-void residual bladder volume tests for incomplete emptying of the bladder
  • Video urodynamic testing involves filling the bladder with contrast and taking xray images as the bladder is emptied. Theses are only performed where necessary and not a routine part of urodynamic testing.
225
Q

What is the definition of a Lower Urinary Tract Infection?

A

A Lower Urinary Tract infection is generally defined as an infection of the bladder, often manifesting as cystitis (inflammation of the bladder).

226
Q

What is the definition of an Upper Urinary Tract Infection (Pylonephritis)?

A
  • Upper urinary tract infections or Pyelonephritis refers to inflammation of the kidney resulting from bacterial infection.
  • The inflammation affects the kidney tissue (parenchyma) and the renal pelvis (where the ureter joins the kidney).
227
Q

What is the epidemiology of Urinary Tract infections?

A

Much more common in women (as urethra is alot shorter, making it easier for bacteria to get into the bladde)r.

228
Q

What are the most common causes of UTIs?

A

Escherichia coli (gram-negative, anaerobic, rod-shaped bacteria) - is most common

Other causes:
* Klebsiella pneumoniae (gram-negative, anaerobic, rod-shaped bacteria)
* Enterococcus
* Pseudomonas aeruginosa
* Staphylococcus saprophyticus
* Candida albicans (fungal)

Bacteria can spread from faeces to the urinary tract through:
* Sexual Activity
* Faecal Incontinence
* Poor Hygeine

Urinary catheters are another possible source of infection

229
Q

What is the presentation of a Lower Urinary Tract Infection?

A
  • Dysuria (pain, stinging or burning when passing urine)
  • Suprapubic pain or discomfort
  • Frequency
  • Urgency
  • Incontinence
  • Haematuria
  • Cloudy or foul-smelling urine
  • Confusion is commonly the only symptom in older and frail patients
230
Q

What is the presentation of Pylonephritis?

A

Can present with the same symptoms as a lower UTI Plus:

  • Fever
  • Loin or back pain (bilateral or unilateral)
  • Nausea or vomiting
  • Renal angle tenderness

If there is evidence of Systemic Illness, its much more likely to be Pylonephritis

231
Q

What investigations are done for a Urinary Tract Infection?

A

Urine Dipstick - Nitrites or leukocytes plus red blood cells indicate that the patient will likely have a UTI.

Midstream urine (MSU) sample sent for microscopy, culture and sensitivity testing. This will determine the infective organism and the antibiotics that will be effective in treatment. It is important in:
* Pregnant patients
* Patients with recurrent UTIs
* Atypical symptoms
* When symptoms do not improve with antibiotics

232
Q

What is the management of a Lower Urinary Tract Infection?

A

First Line Oral Antibiotics:
* Nitrofurantoin (avoided in patients with an eGFR < 45)
* Trimethoprim (often associated with high rates of bacterial resistance)

Duration of Antibiotic Course:
* 3 days of antibiotics - for simple lower urinary tract infections in women
* 5-10 days of antibiotics - for immunosuppressed women, abnormal anatomy or impaired kidney function
* 7 days of antibiotics - for men, pregnant women or catheter-related UTIs

Possible Alternatives:
* Pivmecillinam
* Amoxicillin
* Cefalexin

233
Q

What extra steps should you take with a catheter related UTI?

A

Changing the catheter

234
Q

What is the management of Pylonephritis?

A

First-line antibiotics for 7-10 days:
* Cefalexin
* Co-amoxiclav (if culture results are available)
* Trimethoprim (if culture results are available)
* Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)

Patients require referral to hospital if there are features of Spesis. They then need the sepsis six.

235
Q

How does the management of UTIs differ in pregnancy?

A
  • Management requires 7 days of antibiotics.
  • All women should have an MSU for microscopy, culture and sensitivity testing.

The antibiotic options are:
* Nitrofurantoin (avoided in the third trimester)
* Amoxicillin (only after sensitivities are known)
* Cefalexin (the typical choice)

236
Q

Why is Trimethoprim generally avoided entirely in pregnancy?

A
  • Trimethoprim works as a folate antagonist
  • Folate is essential in early pregnancy for the normal development of the fetus
  • This means that trimethoprim can cause congenital malformations, particularly neural tube defects (e.g., spina bifida).
237
Q

What is the definition of Urticaria?

A
  • Urticaria are also known as hives.
  • They are small itchy lumps that appear on the skin.
  • Urticaria can be classified as acute urticaria or chronic urticaria.
238
Q

What is the pathophysiology of Urticaria?

A
  • Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.
  • This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.
239
Q

What are the causes of acute urticaria?

A

Acute urticaria is typically triggered by something that stimulates the mast cells to release histamine. This may be:
* Allergies to food, medications or animals
* Contact with chemicals, latex or stinging nettles
* Medications
* Viral infections
* Insect bites
* Dermatographism (rubbing of the skin)

240
Q

What causes chronic Urticaria?

A

Chronic urticaria is an autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals.

It can be sub-classified depending on the cause:
* Chronic idiopathic urticaria - describes recurrent episodes of chronic urticaria without a clear underlying cause or trigger.
* Chronic inducible urticaria - Describes episodes of chronic urticaria that can be induced by certain triggers
* Autoimmune urticaria - describes chronic urticaria associated with an underlying autoimmune condition, such as SLE.

241
Q

What are some possible triggers for Chronic inducible urticaria?

A
  • Sunlight
  • Temperature change
  • Exercise
  • Strong emotions
  • Hot or cold weather
  • Pressure (dermatographism)
242
Q

What does the management of Urticaria involve?

A
  • Antihistamines are first line for urticaria.
  • Fexofenadine is usually the antihistamine of choice for chronic urticaria.
  • Oral steroids may be considered as a short course for severe flares.

In very problematic cases, the following may be considerred:
* Anti-leukotrienes such as montelukast
* Omalizumab, which targets IgE
* Cyclosporin

243
Q

What is the other name for the Varicella zoster virus (VZV)?

A
  • Human alpha-herpesvirus 3 (HHV-3)
  • It is a member of the human herpes virus family
244
Q

What is the definition of chickenpox?

A
  • Chickenpox is an acute infectious disease caused by the varicella-zoster virus (VZV), a member of the human herpes virus family.
  • This highly contagious illness, predominantly seen in children, is characterised by a vesicular rash, mild fever, and malaise.
245
Q

What is the epidemiology of chickenpox

A
  • It is a common global disease
  • The majority of cases occur in children aged 1-9 years.
  • The illness is typically mild in children but can be severe in adults or immunocompromised individuals.
  • Its highly contagious, with a 90% secondary infection rate in susceptible household contacts.
246
Q

What is the pathophysiology of chickenpox?

A
  • Its caused by the VZV
  • The virus is airborne and spreads through direct contact with the rash or by breathing in particles from an infected person’s sneezes or coughs.
247
Q

What is the presentation of chickenpox?

A

The cardinal sign of chickenpox is a distinctive rash that:

  • Starts as raised red, itchy spots, primarily on the face or chest, before spreading to the rest of the body.
  • Progresses into small, fluid-filled blisters over a span of a few days.
  • Eventually crusts over and heals, typically leaving no scars unless the blisters have been scratched and infected.

Other accompanying symptoms include:
* Mild fever
* Fatigue
* Loss of appetite
* General discomfort.

248
Q

What are some differentials for Chickenpox?

A
  • Herpes simplex: Characterised by painful, grouped vesicles on an erythematous base, usually around the mouth or genital area.
  • Hand, foot, and mouth disease: Presents with a rash on the hands, feet, and inside the mouth, often alongside fever and malaise.
  • Scabies: Manifests as intense itching, especially at night, and a pimple-like rash.
249
Q

How is Chickenpox diagnosed?

A
  • Diagnosis of chickenpox is usually made clinically due to the characteristic nature of the rash and a history of exposure.
  • Laboratory testing is reserved for severe cases, immunocompromised patients, or when the diagnosis is uncertain.
250
Q

What does the management of Chickenpox involve?

A

Management is primarily conservative as the condition is self limiting:
* Keeping the patient’s fingernails short to prevent scratching and subsequent infection
* Encouraging the use of loose, long-sleeved clothing to limit skin exposure and scratching
* Cooling measures like oatmeal baths or calamine lotion to reduce itching
* Analgesics and antipyretics for symptom relief

Management of Immunocompromised patients or previously unexposed pregnant women/neonate with peripartum exposure:
* IV Aciclovir
* Human varicella-zoster immunoglobulin (VZIG)

It is recommended to isolate the patient to prevent the spread of the virus to others. NICE recommends school exclusion during the most infectious period.

251
Q

When is the most infectious period of Chickenpox?

A

1-2 days before the rash appears, until all of the lesions are dry and have crusted over (usually 5 days after the rash appears)

252
Q

What are the complications of Chickenpox?

A
  • Secondary bacterial skin infections due to scratching
  • Pneumonia (more common in adults)
  • Encephalitis (rare)
  • Reye’s syndrome (a severe complication, primarily in children)
  • Congenital varicella syndrome (if infection occurs during early pregnancy)
  • Reactivation of the virus as herpes zoster (shingles) later in life
253
Q

What is the definition of Shingles?

A

Shingles is a reactivation of the varicella zoster virus which can lie dormant in nerve ganglia following primary infection (chickenpox).

254
Q

What is the epidemiology of Shingles?

A

More common in the elderly

255
Q

What is the presentation of Shingles?

A
  • It manifests first as a tingling feeling in a dermatomal distribution.
  • It then progresses to erythematous papules occurring along one or more dermatomes within a few days.
  • The erythematous papules then develop into fluid-filled vesicles which then crust over and heal.
  • There may also be systemic symptoms like fever, headache and malaise.
256
Q
A
257
Q

What are some differentials for Shingles?

A
  • Herpes zoster ophthalmicus (HZO)
    Presents with symptoms including a painful red eye, fever, malaise, and headache, followed by an erythematous vesicular rash over the trigeminal division of the ophthalmic nerve. A lesion on the nose, known as Hutchinson’s sign, may suggest ocular involvement.
258
Q

What is the management of Shingles?

A
  • Oral antivirals (e.g. valaciclovir 1g three times per day for 7 days) within 72h of rash onset.
  • Pain management with NSAIDs (e.g. ibuprofen)
  • If the pain isn’t controlled with NSAIDs, consider amitriptyline , duloxetine, gabapentin, or pregabalin.
  • Admit to hospital for IV antivirals in severe disease or immunocompromise, ophthalmic symptoms or suspicion of meningitis/encaphalitis/myelitis.
259
Q

What age is the one-off Shingles vaccine adviced for?

A

Over 70s

260
Q

What are the possible complications of Shingles?

A
  • Secondary bacterial infection of skin lesions
  • Corneal ulcers, scarring and blindness if eye involved

Post-herpetic neuralgia:
* Pain occurring at site of healed shingles infection
* Can cause neuropathic type pain (burning, pins and needles)
* Can cause allodynia (perception of pain from a normally non-painful stimulus e.g. light touch)

261
Q

What is the definition of Varicose Veins?

A

Varicose veins are dilated and tortuous superficial veins measuring more than 3mm in diameter, usually affecting the legs.

262
Q

What is the definition of Reticular veins?

A

Reticular veins are dilated blood vessels in the skin measuring less than 1-3mm in diameter

263
Q

What is the epidemiology of Varicose Veins?

A
  • They are very common affecting 1/3 of adults
  • More common with increased age
  • More common in Women (due to hormonal influences)
264
Q

What are the risk factors for Varicose Veins?

A
  • Increasing age
  • Family history
  • Female
  • Pregnancy
  • Obesity
  • Prolonged standing (e.g., occupations involving standing for long periods)
  • Deep vein thrombosis (causing damage to the valves)
265
Q

How do Varicose Veins develop?

A
  • Varicose veins develop when the valves within perforating veins (veins that connect the superficial and deep veins) become incompetant.
  • This allows blood to flow backwards from the deep veins into the superficial veins, and overloads them.
  • This leads to dilatation and engorgement of the superficial veins, forming varicose veins.
266
Q

What is the presentation of Varicose Veins?

A

Varicose Veins present with engorged and dilated superficial leg veins. There may also be:
* Heavy or dragging sensation in the legs
* Aching
* Itching
* Burning
* Oedema
* Muscle cramps
* Restless legs

There can also be symptoms of chronic venous insufficiency

267
Q

What are some differentials for Varicose Veins?

A
  • Deep vein thrombosis:
    Presents with pain, swelling, redness or discoloration, and warmth in the affected limb.
  • Chronic venous insufficiency:
    Characterized by chronic oedema, skin changes such as pigmentation or eczema, and venous ulcers.
  • Superficial thrombophlebitis:
    Presents with a firm, red, tender vein and may have associated systemic symptoms such as fever.
  • Peripheral artery disease:
    Presents with intermittent claudication, non-healing ulcers, and in severe cases, rest pain.
268
Q

What investigations are done for Varicose Veins?

A

Investigation starts with a thorough history and physical examination (including special tests). Folowed by:

  • Doppler ultrasound - The key diagnostic method for varicose veins. It provides information on the anatomy of the veins and the competence of the valves.
  • Duplex ultrasound - Used to measure blood flow and detect blockages or abnormalities of the veins.
  • Venography - May be considered in complex cases where other investigations are inconclusive.
  • MR venography - May be used when non-invasive tests are inconclusive and surgery is being considered.
269
Q

What special tests can be done for Varicose Veins?

A
  • Tap test – apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.
  • Cough test – apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).
  • Trendelenburg’s test – with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.
  • Perthes test – apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.
270
Q

What is the management of Varicose Veins?

A

Treatment is typically not required unless symptoms like bleeding, pain, ulceration, thrombophlebitis arise or significant psychological morbidity is noted. Management can involve:

Conservative Management
* Weight loss if appropriate
* Staying physically active (to promote venous return)
* Keeping the leg elevated when possible to help drainage
* Compression stockings
* Reduction of long periods of standing

Surgical Management
* Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation
* Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein
* Stripping – the veins are ligated and pulled out of the leg

271
Q

What are the possible complications of Varicose Veins?

A
  • Prolonged and heavy bleeding after trauma
  • Superficial thrombophlebitis (thrombosis and inflammation in the superficial veins)
  • Deep vein thrombosis
  • All the issues of chronic venous insufficiency (e.g., skin changes and ulcers)
272
Q

What is the definition of Syncope?

A
  • Syncope refers to a sudden and transient loss of consciousness that is associated with a loss of postural tone; and resolves spontaneously and completely without intervention.
  • Syncopal episodes are also known as vasovagal episodes, or simply fainting.
273
Q

What is the pathophysiology of a vasovagal episode?

A
  • A vasovagal episode (or attack) is caused by a problem with the autonomic nervous system regulating blood flow to the brain.
  • When the vagus nerve receives a strong stimulus, such as an emotional event, painful sensation or change in temperature it can stimulate the parasympathetic nervous system.
  • Parasympathetic activation counteracts the sympathetic nervous system, (which keeps the smooth muscles in blood vessels constricted).
  • As the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”.
274
Q

What is the period immediately prior to a vasovagal episode called?

A

Prodrome

275
Q

What is the presentation of a vasovagal episode?

A

Prodrome:
* Hot or clammy
* Sweaty
* Heavy
* Dizzy or lightheaded
* Vision going blurry or dark
* Headache

The Vasovagal Episode itself:
* Suddenly losing consciousness and falling to the ground
* Unconscious on the ground for a few seconds to a minute as blood returns to their brain
* There may be some twitching, shaking or convulsion activity, which can be confused with a seizure
* There can also be incontinence
* The patient may be a bit groggy following a faint, however, this is different to the postictal period following a faint.

276
Q

What is the difference between a vasovagal episode and a seizure?

A
277
Q

What are the possible causes of syncope (both primary and secondary)?

A

Primary syncope (simple fainting):
* Dehydration
* Missed meals
* Extended standing in a warm environment, such as a school assembly
* A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

Secondary Syncope:
* Hypoglycaemia
* Dehydration
* Anaemia
* Infection
* Anaphylaxis
* Arrhythmias
* Valvular heart disease
* Hypertrophic obstructive cardiomyopathy

278
Q

What investigations are done for Vasovagal Syncope?

A
  • ECG - particularly assessing for arrhythmia and the QT interval for long QT syndrome
  • 24 hour ECG - if paroxysmal arrhythmias are suspected
  • Echocardiogram - if structural heart disease is suspected
  • Bloods - including a full blood count (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)
279
Q

What is the epidemiology of Vasovagal Syncope?

A

More common in children (particularly teenage girls)

280
Q

What is the management of Vasovagal Syncope?

A

Seizures or underlying pathology need to be managed by an appropriate specialist.

Once a simple vasovagal episode is diagnosed, reassurance and simple advice can be given to:
* Avoid dehydration
* Avoid missing meals
* Avoid standing still for long periods
* When experiencing prodromal symptoms such as sweating and dizziness, sit or lie down, have some water or something to eat and wait until feeling better.

281
Q

What is the definition of venous ulcers?

A

Venous ulcers, are a form of skin ulcers predominantly caused by sustained venous hypertension, resulting in venous valve incompetence.

282
Q

What are some risk factors for developing venous ulcers?

A
  • Obesity
  • Immobility
  • Presence of varicose veins
  • History of deep vein thrombosis (DVTs)
  • Advanced age
  • Prior trauma to the leg
283
Q

What is the presentation of venous ulcer disease?

A
  • Predominantly found over the medial malleolus
  • Shallow and sloughy in nature
  • Presence of haemosiderin deposition in the lower leg
  • Oedema
  • Skin thickening
  • Eczema
284
Q

What investigations are done for venous ulcer disease?

A

Ankle-Brachial Pressure Index (ABPI) - Is the first line investigation in order to rule out any co-existing arterial disease that might be exacerbated if compression bandaging is applied. (As this would worsen arterial supply to the leg).

285
Q

What is the management of venous ulcers?

A

Conservative Management
* Maintain cleanliness of the ulcer
* Promote mobility
* Suggest weight reduction
* Recommend leg elevation at rest
* Emollient treatment for the leg
* Compression bandaging - This technique aims to improve venous return from the leg.

Medical Management
* Pentoxifylline may be considered if the ulcer fails to respond to initial treatment.

Surgical Management
* Though rarely necessary, options include debridement and skin grafting.

286
Q

What are some potential complications of venous ulcer disease?

A
  • Decreased mobility due to pain
  • Risk of infection, which can progress to sepsis
  • Possibility of osteomyelitis
  • Decreased quality of life due to persistent pain and disability
287
Q

What is the definition of Chronic Venous Insufficiency?

A
  • Chronic venous insufficiency occurs when blood does not efficiently drain from the legs back to the heart.
  • This results in blood pooling in the legs, causing venous hypertension and the skin changes associated with chronic venous insufficiency.
  • Its often associated with Varicose Veins
288
Q

What is the pathophysiology of chronic venous insufficiency?

A
  • Chronic venous insufficiency usually occurs as a result of damage to the valves inside the veins.
  • These valves are usually responsible for ensuring blood flows in one direction as the leg muscles contract and squeeze the veins.
  • When they are damaged however, the pumping effect of the leg muscles becomes less effective in draining blood towards the heart; and blood pools in the veins of the legs, causing venous hypertension.
  • Chronic pooling of blood in the legs leads to skin changes. The area between the top of the foot and the bottom of the calf muscle is the area most affected by these changes. This is known as the gaiter area.
289
Q

What is the presentation of Chronic Venous Insufficiency?

A
  • Brown discolouration of the lower legs - This occurs as when blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs (giving the brown colour).
  • Venous Eczema - The pooling of blood in the distal tissues results in inflammation; resulting in dry and inflamed skin.
  • lipodermatosclerosis - The skin and soft tissues also become fibrotic and tight, causing the lower legs to become narrow and hard.
290
Q

What is the clinical presentation of Chronic Venous Insufficiency?

A

Skin Changes:
* Haemosiderin staining (is a red/brown discolouration to the legs) - This occurs as small ammounts of blood leaks out of the veins into the nearby tissues (due to the venous hypertension). haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs (giving the brown colour).
* Venous eczema (or varicose eczema) - Is dry, itchy, flaky, scaly, red and cracked skin. These eczema-like changes are caused by a chronic inflammatory response in the skin in response to the pooled blood.
* Lipodermatosclerosis - is hardening and tightening of the skin as well as the tissue beneath. This occurs as, chronic inflammation causes the subcutaneous tissue to become fibrotic.
* Atrophie blanche - refers to patches of smooth, porcelain-white scar tissue on the skin, often surrounded by hyperpigmentation.

Other symptoms:
* Cellulitis
* Poor healing after injury
* Skin ulcers
* Pain

291
Q

What is the management of chronic venous insufficiency?

A

Management involves:
* Keeping the skin healthy
* Improving venous drainage to the legs
* Managing complications

The skin is kept healthy by:
* Monitoring skin health and avoiding skin damage
* Regular use of emollients (e.g., diprobase, oilatum, cetraben and doublebase)
* Topical steroids to treat flares of venous eczema
* Very potent topical steroids to treat flares of lipodermatosclerosis

Improving venous drainage to the legs involves:
* Weight loss if obese
* Keeping active
* Keeping the legs elevated when resting
* Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)

Management of complications involves:
* Antibiotics for infection
* Analgesia for pain
* Wound care for ulceration

292
Q

What is the definition of an exanthem?

A
  • An “exanthem” is an eruptive widespread rash.
  • Originally there were six “viral exanthemas” known as first, second, third, fourth, fifth and sixth disease.
293
Q

What are the six “viral exanthemas” now known as?

A
  • First disease: Measles
  • Second disease: Scarlet Fever
  • Third disease: Rubella (AKA German Measles)
  • Fourth disease: Dukes’ Disease
  • Fifth disease: Parvovirus B19
  • Sixth disease: Roseola Infantum
294
Q

What is Duke’s Disease?

A
  • (Also known as fourth disease), it has been mostly forgotten and is never now used in clinical practice.
  • No organism has been found that could explain a specific “fourth disease”.
  • Its likely the term fourth disease, was used to decribe the various non-specific viral rashes with no one specific viral cause.
295
Q

What causes Roseola Infantum?

A

It’s caused by human herpesvirus 6 (HHV-6) and less frequently by human herpesvirus 7 (HHV-7).

296
Q

What is the presentation of Roseola Infantum?

A
  • It presents 1 – 2 weeks after infection with a high fever (up to 40ºC) that comes on rapidly, lasts for 3 – 5 days and then disappears suddenly.
  • During this period, there may also be coryzal symptoms, sore throat and swollen lymph nodes.
  • When the fever settles, a mild erythematous macular rash across the arms, legs, trunk and face appears for 1 – 2 days. The rash is not itchy.
  • Children make a full recovery within a week
297
Q

What is the main complication of Roseola Infantum?

A

Febrile convulsions due to the high temperature

298
Q

What is the definition of Acute Gastritis?

A

Acute gastritis is inflammation of the stomach and presents with nausea and vomiting.

299
Q

What is the definition of Enteritis?

A

Enteritis is inflammation of the intestines and presents with diarrhoea.

300
Q

What is the definition of Gastroenteritis?

A

Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

301
Q

What is the most common cause of gastroenteritis?

A

The most common cause of gastroenteritis is viral infection:
* Norovirus - most common cause of viral gastroenteritis overall
* Rotavirus - most common cause of infantile gastroenteritis
* Adenovirus - more commonly causes respiratory infection. But it can also cause gastroenteritis, especially in children.

302
Q

What are the bacterial causes of gastroenteritis?

A
  • Escherichia coli (including E.coli 0157 which can cause haemolytic uraemic syndrome)
  • Campylobacter Jejuni - The most common cauase of bacterial gastroenteritis worldwide (is a common cause of travellers diahorrea)
  • Staph. aureus
  • Shigella
  • Salmonella
  • Bacillus Cereus
303
Q

What are the possible differentials for Diarrhoea?

A
  • Infection (gastroenteritis)
  • Inflammatory bowel disease
  • Lactose intolerance
  • Coeliac disease
  • Cystic fibrosis
  • Toddler’s diarrhoea
  • Irritable bowel syndrome
  • Medications (e.g. antibiotics)
304
Q

What are the principles of Gastroenteritis management?

A

Prevent the spread:
* When patients develop symptoms they should immediately be isolated to prevent spread.
* Barrier nursing and rigorous infection control is important for patients in hospital to prevent spread to other patients.
* Children need to stay off school until 48 hours after the symptoms have completely resolved.

Faeces sample with microscopy, culture and sensitivities to establish the causative organism

Rehydration:
* The key to managing gastroenteritis is to ensure they remain hydrated whilst waiting for the diarrhoea and vomiting to settle.
* Fluid challenge - This involves recording a small volume of fluid given orally every 5-10 minutes to ensure they can tolerate it.
* Oral Rehydration solutions (e.g. dioralyte) can be used if tolerated
* If oral fluid isn’t tolerated, then IV fluid rehydration may be nescesary

Antibiotics
* Antibiotics should only be given in patients that are at risk of complications once the causative organism is confirmed.

305
Q

What are some possible post gastroenteritis complications?

A
  • Lactose intolerance
  • Irritable bowel syndrome
  • Reactive arthritis
  • Guillain–Barré syndrome
306
Q
A