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Snippets From Pqs Flashcards

1
Q

Appropriate follow up investigations for someone started on Statins?

A

LFTs..

Before starting.

Every 3 months.

And at 12 months

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2
Q

Baseline tests and follow-up checks for Amiodarone Rx?

A
  1. TFT - every 6months.
  2. LFTs - every 6 months.
  3. E/U/Cr - every 6 months.
  4. ECG - every 12 months.
  5. Chest Xray
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3
Q

Lithium monitoring?

A
  1. Serum lithium should be checked weekly following initiation/dose change until levels/concentrations are stable.
  2. Then every 3 months for the first year.
  3. And every 6 months there after.
  4. Weight and BMI every 6 months.
  5. E/U/Cr and TFTs every 6 months.

*lithium samples should be taken 12 hours after dose.

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4
Q

Diarrhea >14 days?

A
  1. Giardia.
  2. Cryptosporidium.
  3. Cyclospora.
  4. Entamoeba h.
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5
Q

Bloody diarrhoea causes?

A
  1. Salmonella
  2. Shigella
  3. Campylobacter
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6
Q

Cause of non bloody diarrhoea <14 days in traveler until proven otherwise?

A

E coli..

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7
Q

Features that might suggest scleroderma?

A
  1. Joint pain in hands and feet
  2. Dysphagia
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8
Q

Investigations and mgt of scleroderma?

A
  1. Anti-ANA positive in 90%
  2. Anti centromere antibodies
  • Immunosuppressants such as cyclophosphamide
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9
Q

Red flags for lower back pain?

A
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10
Q

First line treatment for paediatric migraine?

A
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11
Q

Clergy man’s knee?

A

Infrapatellar bursitis

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12
Q

Features of Organophosphate poisoning?

A

Mnemonic: ‘DUMBELS’:

D: defaecation & diaphoresis.
U: urinary incontinence.
M: miosis (pupil constriction).
B: bradycardia
E: emesis.
L: lacrimation.
S: salivation.

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13
Q

_______ increases risk of Azathioprine ine toxicity?

A

Allopurinol

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14
Q

Contraindication to gentamicin?

A

Neuromuscular disorder: Myasthenia gravis.

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15
Q

Risk factors for SIDS?

A

The major risk factors for SIDS are:

prone sleeping

parental smoking

bed sharing

hyperthermia and head covering

prematurity

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16
Q

Autosomal Dominant conditions+

A

Autosomal recessive conditions are ‘metabolic’ - exceptions: inherited ataxias

Autosomal dominant conditions are ‘structural’ - exceptions: Gilbert’s, hyperlipidaemia type II.

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17
Q

Causes of haemolytic anaemia

A
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18
Q

About Hereditary Haemorrhagic Telangietasia

A
  1. Also know as Osler-Weber-Rendu Syndrome.
  2. Autosomal Dominant
  3. Vascular dysplasia leading to telangiectasia

Presentation:
1. Recurrent nose/GI bleeds, usually in the teenage years..
2. Affected vessels commonly on the tongue, lips, face, ears and fingers..
3. Sharply demarcated red-purple macules on examination..

Investigation:
1. CT scanning & angiography to identify lesions
2. Capillary microscopy

Treatment:
1. Surgical (laser)
2. Symptomatic Rx

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19
Q

About Topic ezcema

A
  1. Chronic relapsing inflammatory skin condition xtized by an itchy red rash that is commonly seen in skin areas such as elbow folds and behind the knee..
  2. Commonly seen in children. Dry skin and itchiness in flexural areas of the elbow and knees..
  3. Typical hx of asthma or hay fever
  4. Mgt by emollient and topical steroids..
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20
Q

About Discoid (nummular eczema)

A
  1. Occurs in circular or Oval patches on the skin
  2. Nummular means ‘coin shaped’
  3. Peak ages of affectation: ‘15-25’ and ‘50-65’..
  4. Hx of atopic eczema
  5. Worse in the winter months (cold, dry climates)
  6. Common in the extremities, particularly legs.
  7. Rx: Emollient, Skin rehydration, topical steroids..
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21
Q

About Dyshidrotic eczema (pompholyx)

A
  1. Causes blisters to erupt in the palms of the hand following intense itching and burning of the skin on hand and fingers.
  2. Usually symmetrical; palms and soles may be red and wet with perspiration.
  3. Common in the spring and summer (countries with warm climates)
  4. Rx: Emollient and topical steroids
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22
Q

About serborrheic eczema

A
  1. Develops on the sides of the nose, eyebrows, ears and scalp.
  2. Affects areas rich in serborrheic glands (face and scalp)
  3. Inflamed greasy areas with fine scaling on the face affecting nasolabial folds or the bridge of the nose, eyebrows or behind the ears..
  4. Rx: ketoconazole cream
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23
Q

Features that might make RA more likely

A
  1. Female sex
  2. Bilateral, symmetrical involvement of the wrists and metacarpophalangeal joints.
  3. Small joint involvement.

Referral considerations:

  • Any adult suspected with persistent synovitis of undetermined cause

Refer urgently if:
1. Small joints of the hands and feet are affected..

  1. More than one joint is affected..
  2. Delay of 3 months or longer between onset of symptoms..
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24
Q

Extraarticular features of RA

A
  1. Eyes: Sjogren’s syndrome
  2. Skin: Leg ulcers in felty’s syndrome
  3. Neurological: Polyneuropathy
  4. RS: pleural involvement, pulmonary nodules, pulmonary fibrosis
  5. CVS: CVS d6, Pericardial involvement.
  6. Rheumatoid nodules in the eyes, lungs and heart..
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25
Q

Acetylcholine receptor Autoantibodies?

A

Myasthenia gravis

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26
Q

ANA Autoantibodies?

A
  1. SLE (95%)
  2. JIA (76%)
  3. Chronic active hepatitis (75%)
  4. Sjogren’s syndrome (70%)
  5. Systemic sclerosis (64%)
  6. RA (32%)
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27
Q

Anticardiolipin Autoantibodies?

A

Primary antiphospholipid syndrome

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28
Q

Anti-centromere Autoantibodies?

A

Limited systemic sclerosis (70%)

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29
Q

Anti-Ro Autoantibodies?

A
  1. Sjogren’s syndrome
  2. Subacute cutaneous Lupus SLE (30%)
  3. Systemic sclerosis (60%)
  4. Intestinal pneumonitis
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30
Q

Anti-La Autoantibodies?

A
  1. Sjogren’s syndrome (65%)
  2. SLE (15%)
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31
Q

c-ANCA/Anti-MPO Autoantibodies?

A
  1. Wegener’s granulomatosis (90%)
  2. Microscopic polyangiitis (MPA) :(11%)
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32
Q

p-ANCA/ Anti-PR3 Autoantibodies?

A

Churg-Strauss syndrome (60%)

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33
Q

dsDNA Autoantibodies?

A

SLE (60%)

34
Q

ssDNA Autoantibodies?

A
  1. SLE (70%)
  2. Autoimmune Rheumatic disease
  3. Inflammation
35
Q

Anti-cyclic citrullinated peptide Autoantibodies?

A

Rheumatoid Arthritis

36
Q

Glomerular basement membrane Autoantibodies?

A

Good pasture’s syndrome

37
Q

IgA-endomysial Autoantibodies?

A

Coeliac d6

38
Q

Anti-Jo-1 Autoantibodies?

A

Myositis

39
Q

Mitochondrial Autoantibodies?

A

Primary biliary cirrhosis (>95%)

40
Q

Rheumatoid factor?

A
  1. RA (50-90%)
  2. SLE (15-35%)
  3. Systemic sclerosis (20-30%)
  4. Juvenile RA (7-10%)
  5. Polymyositis (5-10%)
  6. Infection (0-50%)
41
Q

Anti smith Autoantibodies?

A

SLE (30-40%)

42
Q

Anti-Scl-70 Autoantibodies?

A

Diffuse Systemic sclerosis

43
Q

Smooth muscle Autoantibodies?

A
  1. Primary biliary cirrhosis (30-80)
  2. Idiopathic cirrhosis (25-30%)
  3. Viral infections (80%)
  4. Autoimmune sclerosing cholangitis
44
Q

Thyroid peroxidase Autoantibodies?

A
  1. Hashimoto’s thyroiditis
  2. Grave’s disease (50%)
45
Q

Thyrotropin receptor Autoantibodies (TSH receptor antibodies) ?

A

Grave’s disease (50-60%)

46
Q

Webers tests?

A

Lateralises towards the ear with conductive deafness and away from the ear with Sensorineural deafness.

So, if webers test is conducted on an individual, and it Lateralises to the left, the person either has Left sided CD or Right sided SND.

You may confirm which with the Rinnes test..

47
Q

Normal in Rinnes test

A

AC>BC

48
Q

About Immediate (within 24hrs) Hearing loss referrals

A
  1. Sudden onset (over 3days or less) unilateral or bilateral hearing loss which has occurred within the past 30 days and cannot be explained by external or middle ear causes.
  2. Uniteral hearing loss associated with focal neurological deficit (altered sensation or facial droop)
  3. Hearing loss associated with head/neck injury
  4. Hearing loss associated with severe infection such as necrotising otitis externa or ramsay Hunt syndrome
49
Q

About Urgent Hearing loss referrals

A
  1. Sudden onset (over 3days or less) unilateral or bilateral hearing loss which developed more than 30 days ago and cannot be explained by external or middle ear causes..
  2. Rapidly progressive hearing loss (over a period of 4-90 days) which cannot be explained by external or middle ear causes
  3. Suspected head or neck malignancy..
50
Q

About Routine Hearing loss referrals

A
  1. Unilateral or asymmetrical gradual hearing loss
  2. Fluctuating hearing loss that is not associated with URTI
  3. Hearing loss associated with hyperacusis
  4. Hearing loss associated with persistent tinnitus
  5. Hearing loss associated with persistent or recurrent vertigo
  6. Hearing loss that is not age related
51
Q

About Breast cyst?

A
  1. Common in women approaching menopause (>35yrs)
  2. Oval round, firm, smooth
  3. May appear before period and disappear right after period.
  4. Recurrence
52
Q

About Fibrocystic Disease of the Breast-Fibroadenosis:

A

Nature: Non-cancerous changes in the breast tissue characterized by lumps or nodules.

Age Group: Commonly seen in women aged 30–50 years.

Hormonal Influence: Symptoms often fluctuate with the menstrual cycle and may worsen premenstrually.

Presentation:

Diffuse nodularity or “lumpy breasts.”

May be associated with pain or tenderness.

Usually bilateral.

Consistency: Lumps are irregular, soft to firm, and can feel rope-like.

Mobility: Not discrete; changes in texture rather than a solitary lump.

Risk of Malignancy: Slightly increased if associated with atypical hyperplasia.

Investigations:

Ultrasound may show cysts.

Fine-needle aspiration (FNA) may yield fluid.

53
Q

About Fibroadenoma?

A

Nature: Benign tumor of glandular and stromal breast tissue.

Age Group: Commonly seen in women aged 15–35 years.

Hormonal Influence: Growth may occur during pregnancy or with estrogen therapy but is usually stable.

Presentation:

Single, well-circumscribed lump.

Typically painless, but larger fibroadenomas may cause discomfort.

Often unilateral.

Consistency: Smooth, rubbery, and firm.

Mobility: Highly mobile; often described as a “breast mouse.”

Risk of Malignancy: Minimal; complex fibroadenomas may have a slightly increased risk.

Investigations:

Ultrasound shows a well-defined, solid mass.

Core needle biopsy for definitive diagnosis if uncertain.

54
Q

Key differences between Fibroadenosis and Fibroadenoma?

A
55
Q

About Anaemia

A
  1. In children 12-14yrs: Hb conc <120g/l
  2. In men (>15yrs): Hb conc <130g/l
  3. In women (>15yrs): Hb conc <120g/l
  4. In pregnant women: Hb conc <110g/l
  5. Postpartum women: Hb conc <100g/l
56
Q

Causes of normocytic Anaemia (MCV: 76-96)

A
  1. Anaemia of chronic d6
  2. Bone marrow failure
  3. Renal failure
  4. Pregnancy
  5. Haemolysis
  6. Acute blood loss
57
Q

Causes of microcytic Anaemia (MCV: <76fl)

A
  1. Iron deficiency
  2. Thalassemia
  3. Congenital sideroblastosis
58
Q

Causes of macrocytic Anaemia (MCV: >96)

A
  1. B12 and folate def.
  2. Alcohol
  3. Liver d6
  4. Hypothyroidism
  5. Anti folate therapy (phenytoin or trimethoprim)
59
Q

Signs of iron deficiency

A
  1. Atrophic glossitis
  2. Koilonychia: spoon shaped nails with longitudinal ridges
  3. Angular cheilitis
  4. Pallor
  5. Flow murmur, tachycardia, cardiac enlargement and failure.
60
Q

Features that may suggest coeliac d6 in a child

A
  1. Weighloss/ faltering growth
  2. Chronic diarrhoea
  3. Anaemia from unexplained iron, folate or B12 deficiency

Associated conditions:
1. Irritable Bowel d6

  1. Autoimmune thyroid d6
  2. Dermatitis herpetiformis
  3. T-1 DM
61
Q

A child with chronic constipation and palpable mass in the left Lower quadrant?

A
  1. Hirschsprung d6
    2.? Faecal impaction

Inv:
1. Rectal biopsy will confirm absence of ganglion cells

  1. Barium enema will show a transition zone..

Rx:

  1. IO: Rehydration, gastric and intestinal decompression, NPO
  2. Enterocolitis: BS-antibiotics
  3. Swenson’s procedure to release defective distal colon
62
Q

About Acoustic Neuroma?

A
  1. Caused by compression of the cochlear nerve leading to Sensorineural deafness
  2. Signs of RICP
  3. DVT + aural fullness + neurological signs
  4. Cranial nerves 5,6,7,9,10 affectation with facial pain numbness, ataxias..
  5. Family hx, probably
  6. MRI is the Inv of choice. CT if not available
  7. Microsurgery is the Rx of choice..
63
Q

About Presbycusis?

A
  1. Gradual onset: >40yrs
  2. Bilateral progressive and symmetrical SNHL; nil noise exposure
  3. Affectation of high pitched sounds
  4. Inv: otoscopy, pure tone audiogram
  5. Rx: Hearing aids, Cochlear implants
64
Q

Most common hepatic disorder related to pregnancy in women

A

Intra hepatic cholestasis of pregnancy (ICP)

Develops in the third trimester, typically..

Risk factors may include a past hx of obstetric cholestasis, family hx of obstetric cholestasis and multiple pregnancies..

LFT may show elevated ALT, AST, ALP, and Bilirubin..

Rx: topical emollients, Ursodeoxycholic Acid (UDCA) - mainstay.
Elective delivery from 37 week gestation - considered on an individual basis..

*Settles spontaneously following delivery

65
Q

key points to know about plantar fasciitis for an exam

A
  1. Definition:

Chronic inflammation or degeneration of the plantar fascia, a thick band of tissue supporting the arch of the foot.

  1. Etiology/Risk Factors:

Aged btwn 40-60yrs

Overuse (common in runners, dancers).

Obesity.

Prolonged standing or walking on hard surfaces.

Pes planus (flat feet) or pes cavus (high arches).

Tight Achilles tendon.

  1. Clinical Features:

Heel pain, especially:

On the medial aspect of the heel.

Worse with the first steps in the morning or after prolonged sitting.

Improves with activity but worsens again with prolonged use.

Tenderness over the medial calcaneal tubercle.

Antalgic gait

  1. Diagnosis:

Clinical diagnosis based on history and examination. Positive Wind glass test.

Imaging (if needed for atypical cases):

X-ray: May show calcaneal heel spur (not diagnostic).

Ultrasound: Thickened plantar fascia (>4 mm). Preferred imaging modality, if needed..

MRI: For chronic or refractory cases.

  1. Management:

Conservative (first-line):

Rest and activity modification.

Stretching exercises (plantar fascia and Achilles tendon).

Ice application.

Arch supports or orthotic insoles.

Non-steroidal anti-inflammatory drugs (NSAIDs).

Advanced options:

Corticosteroid injections (limited use due to risk of rupture).

Platelet-rich plasma (PRP) therapy.

Surgery: Rare, for refractory cases.

  1. Prognosis:

Most cases resolve with conservative treatment in 6–18 months.

66
Q

key points on Morton’s neuroma:

A

Definition:

A benign enlargement of the interdigital nerve, commonly due to chronic irritation or entrapment.

Epidemiology:

Most common in women, aged 40–60 years.

Associated with tight, narrow, or high-heeled shoes.

Location:

Typically affects the 3rd intermetatarsal space (between the 3rd and 4th toes).

Clinical Features:

  1. Pain:

Burning or sharp pain in the forefoot, often radiating to the toes.

Worse with walking or wearing tight shoes.

  1. Numbness or tingling:

May affect the toes adjacent to the affected interspace.

  1. “Pebble in the shoe” sensation:

Described as feeling like a lump underfoot.

  1. Mulder’s Sign:

Pain and/or a palpable “click” when compressing the forefoot and squeezing the interspace.

Diagnosis:

Clinical examination is usually sufficient.

Imaging (if needed):

Ultrasound: Can show nerve enlargement. (preferred)

MRI: For more detailed evaluation in refractory cases.

Differential Diagnoses:

Metatarsalgia.

Stress fractures.

Peripheral neuropathy.

Tarsal tunnel syndrome.

Management:

  1. Conservative:

Modify footwear: Wide, soft-soled shoes with low heels.

Orthotics: Metatarsal pads to offload pressure.

NSAIDs for pain relief.

  1. Interventions:

Corticosteroid or alcohol injections for persistent pain.

  1. Surgery:

Neurectomy (removal of the neuroma) for refractory cases.

Key Exam Points:

Interdigital pain and Mulder’s sign are diagnostic.

Conservative management is first-line.

Surgical neurectomy is reserved for severe or persistent cases.

67
Q

Key Points on March Fracture (Stress Fracture of the Metatarsals)

A

Definition:

A stress fracture of the metatarsal bones, typically caused by repetitive stress or overuse.

Commonly affects the 2nd or 3rd metatarsal (less flexible and more rigid).

Etiology/Risk Factors:

  1. Overuse injury:

Military recruits (hence “march” fracture).

Athletes (e.g., runners, dancers).

  1. Risk Factors:

Sudden increase in physical activity.

Poor footwear.

Osteoporosis or bone insufficiency (e.g., elderly, postmenopausal women).

Pes planus (flat feet).

Clinical Features:

Gradual onset of pain over the dorsum of the foot.

Pain worsens with weight-bearing and activity; relieved by rest.

Localized tenderness and swelling over the affected metatarsal.

May have a history of recent increase in physical activity.

Diagnosis:

  1. Clinical suspicion based on history and examination.
  2. Imaging:

X-ray:

Initially normal; fractures may become visible 2–3 weeks later as callus forms.

Bone scan or MRI:

More sensitive for early detection if X-ray is inconclusive.

Differential Diagnoses:

Metatarsalgia.

Tendinopathy.

Acute metatarsal fracture.

Osteomyelitis.

Management:

  1. Conservative (first-line):

Rest and avoidance of weight-bearing (4–6 weeks).

Supportive footwear or stiff-soled shoes.

Analgesics (e.g., NSAIDs) for pain relief.

  1. Gradual return to activity after healing.
  2. Surgery:

Rare, for fractures that fail to heal or in high-risk locations.

68
Q

Key Points on Metatarsalgia (Adult forefoot pain)

A

Definition:

A condition characterized by pain and inflammation in the ball of the foot (metatarsal heads), often due to increased pressure or overuse.

Etiology/Risk Factors:

  1. Mechanical Causes:

Overuse (e.g., running, jumping).

High heels or poorly fitting shoes.

Foot deformities:

Pes cavus (high arches).

Hammer toes or bunions.

Loss of the fat pad in the elderly.

  1. Medical Conditions:

Rheumatoid arthritis.

Gout.

Diabetes (leading to neuropathy).

Clinical Features:

Pain:

Localized to the ball of the foot (under metatarsal heads).

Worsens with standing, walking, or high-impact activities.

Tenderness: Over one or more metatarsal heads on palpation.

Callus Formation: May occur due to excessive pressure.

Diagnosis:

  1. Clinical Examination:

Localized pain over the metatarsal heads.

Assess footwear and foot biomechanics.

  1. Imaging:

X-ray: Rule out fractures or deformities.

Ultrasound or MRI: For soft tissue pathologies (e.g., Morton’s neuroma).

  1. Blood tests

Differential Diagnoses:

Morton’s neuroma (pain radiates to toes).

Stress fractures.

Plantar plate injuries.

Sesamoiditis.

Management:

  1. Conservative:

Rest and activity modification.

Proper footwear with cushioning and arch support.

Metatarsal pads to redistribute pressure.

Ice and NSAIDs for pain relief.

  1. Physiotherapy:

Stretching and strengthening exercises.

  1. Surgery:

Rarely needed, for severe or refractory cases (e.g., osteotomy for deformities).

Prognosis:

Usually resolves with conservative measures.

Recurrence possible without addressing underlying causes.

Key Exam Tips:

Common in high-impact activities or with inappropriate footwear.

Pain localized to metatarsal heads, worse with weight-bearing.

Managed conservatively with rest, proper footwear, and pressure offloading.

69
Q

Key Points on Achilles Tendinopathy

A

Definition:

A degenerative condition of the Achilles tendon, causing pain, stiffness, and impaired function.

Often due to overuse or repetitive strain.

Types:

  1. Non-insertional:

Affects the mid-portion of the tendon.

Common in younger, active individuals.

  1. Insertional:

Involves the tendon’s insertion into the calcaneus.

More common in older or less active individuals.

Etiology/Risk Factors:

  1. Overuse:

Repetitive activities (e.g., running, jumping).

  1. Intrinsic Factors:

Poor biomechanics (e.g., flat feet, high arches).

Tight calf muscles.

Age-related tendon degeneration.

  1. Extrinsic Factors:

Sudden increase in training intensity.

Inappropriate footwear.

Clinical Features:

Pain:

Localized to the Achilles tendon, worse with activity (especially running or jumping).

Often improves with mild activity (“warming up”).

Morning stiffness: Common, especially in the tendon.

Swelling or thickening of the tendon.

Tenderness: On palpation along the tendon or at its insertion.

Possible crepitus on movement.

Diagnosis:

  1. Clinical Diagnosis: Based on history and examination. Exclude rupture with Simmond’s and Thompson’s test
  2. Imaging:

Ultrasound: Shows thickened tendon, hypoechoic areas, or neovascularization.

MRI: Used for detailed assessment or if rupture is suspected.

Management:

  1. Conservative (first-line):

Rest and activity modification.

Eccentric exercises: Proven effective in tendon rehabilitation.

Ice and NSAIDs for pain relief.

Proper footwear or heel lifts to reduce strain.

  1. Adjunct Therapies:

Shockwave therapy for chronic cases.

Platelet-rich plasma (PRP) injections (controversial).

  1. Surgery:

For refractory cases or tendon rupture.

Prognosis:

Most cases improve with conservative management within 3–6 months.

Chronic cases may require prolonged treatment or advanced interventions.

Key Exam Tips:

Look for pain and stiffness along the Achilles tendon, worsened by activity.

Differentiate insertional vs. non-insertional tendinopathy.

Eccentric exercises are a cornerstone of management.

Imaging is used only for atypical or refractory cases.

70
Q

Key Points on Achilles Tendon Rupture

A

Definition:

Complete or partial rupture of the Achilles tendon, often resulting from a sudden force or excessive load on the tendon.

Etiology/Risk Factors:

  1. Trauma: Sudden eccentric loading (e.g., push-off during running or jumping).
  2. Risk Factors:

Sports (e.g., basketball, tennis).

Age (more common in individuals 30–50 years).

History of Achilles tendinopathy.

Steroid injections, systemic diseases (e.g., diabetes, gout).

Clinical Features:

  1. Sudden, severe pain: At the back of the heel or lower calf.
  2. Audible pop or snap: Often heard at the time of injury.
  3. Inability to plantarflex: Difficulty or inability to push off or stand on tiptoe.
  4. Swelling and bruising: In the lower calf or heel area.
  5. Palpable gap: Defect in the tendon (especially in complete ruptures).

Diagnosis:

  1. Clinical Diagnosis:

Thompson Test (Simmonds test): Absence of plantarflexion when calf is squeezed suggests rupture.

  1. Imaging:

Ultrasound or MRI: Confirm the rupture and assess the degree.

Management:

  1. Non-surgical:

Casting or functional bracing (for less active patients).

Rehabilitation with progressive weight-bearing and exercises.

  1. Surgical:

Preferred for active individuals or in high-risk cases.

Involves tendon repair and immobilization.

Prognosis:

Good in most cases, but prolonged rehabilitation required.

Surgical repair generally results in better functional outcomes.

Key Exam Tips:

Look for sudden pain, audible snap, and weakness in plantarflexion.

Thompson test is key to diagnosis.

Surgical repair may be indicated for active patients.

71
Q

Key Points on Charles Bonnet Syndrome (CBS)

A
  1. Definition:

CBS is a condition characterized by visual hallucinations in individuals who have significant vision loss (e.g., macular degeneration, glaucoma).

  1. Hallucinations:

The hallucinations are typically visual and non-threatening, often involving complex images like people, animals, or patterns.

Patients are aware that these images are not real.

  1. Cause:

It is believed to result from the brain’s response to vision loss, where the lack of visual input leads to spontaneous neural activity in the visual cortex, producing hallucinations.

  1. Risk Factors:

Common in older adults with severe vision impairment (e.g., age-related macular degeneration, diabetic retinopathy).

More frequent in patients with significant central vision loss.

  1. Management:

Reassurance: Most cases resolve with time and do not require treatment.

Vision rehabilitation and management of the underlying visual impairment are important.

In rare cases, medications (e.g., antipsychotics) may be used if hallucinations are distressing.

Key Exam Tips:

Visual hallucinations occur in the context of severe vision loss.

Patients are typically aware that their hallucinations are not real.

Reassurance and management of underlying vision problems are essential in treatment.

72
Q

comparison table summarizing the key points of Perthes disease, Slipped upper femoral epiphysis (SUFE), Congenital hip dysplasia, Septic arthritis, Slipped capital femoral epiphysis (SCFE), and Irritable hip:

A
73
Q

Key Exam Points on Intussusception

A

Definition:
Intussusception is a medical condition where a part of the intestine telescopes into an adjacent segment, causing obstruction and ischemia.

Epidemiology:

Most common in infants and young children (ages 6 months to 3 years).

More common in males than females.

Etiology:
Often idiopathic, but can be associated with:

Viral infections (e.g., rotavirus).

Anatomical abnormalities (e.g., Meckel’s diverticulum, polyps).

Hirschsprung disease or intestinal lymphoma (in older children or adults).

Clinical Features:

  1. Classic Triad (though not always present):

Colicky abdominal pain: Sudden onset, intermittent.

Abdominal mass: Often palpable (sausage-shaped mass).

Currant jelly stool: Blood and mucus in stool, sign of bowel ischemia.

  1. Other symptoms:

Vomiting (often bilious).

Lethargy.

Fever (in severe cases).

Abdominal distension.

Diminished or absent bowel sounds.

Dance sign (absence of bowel in the RLQ

Diagnosis:
1. Clinical Diagnosis: Often based on history and physical examination.

  1. Imaging:

Abdominal ultrasound: “Target sign” or “Doughnut sign” (shows concentric rings or bowel within bowel). Also pseudokidney/sandwich appearance.

X-ray: May show signs of bowel obstruction.

Air or contrast enema: Crescent sign, filling defect; Can be both diagnostic and therapeutic (reduction of the intussusception).

Management:
1. Non-surgical:

Air or contrast enema: First-line treatment for reduction, performed under radiological guidance. 3 times for three minutes each.

Hydration and stabilization (IV fluids, monitoring).

  1. Surgical:
    If enema reduction is unsuccessful or if signs of bowel perforation, peritonitis or ischemia are present, surgical reduction or resection may be required.

Exploratory laparotomy is performed if there’s suspicion of other underlying pathology (e.g., tumors, anatomical issues).

Prognosis:
Good: Most cases of intussusception can be treated successfully with enema reduction.

Complications: If untreated or delayed treatment, can lead to bowel necrosis, perforation, or sepsis.

Key Exam Tips:
Look for abdominal pain, abdominal mass, and currant jelly stool.

Diagnosis is often confirmed with ultrasound (target or doughnut sign).

Air enema is both diagnostic and therapeutic.

Surgical intervention is needed if non-surgical reduction fails or if there are complications.

74
Q

Key Exam Points on Intussusception

A

Definition:
Intussusception is a medical condition where a part of the intestine telescopes into an adjacent segment, causing obstruction and ischemia.

Epidemiology:

Most common in infants and young children (ages 6 months to 3 years).

More common in males than females.

Etiology:
Often idiopathic, but can be associated with:

Viral infections (e.g., rotavirus).

Anatomical abnormalities (e.g., Meckel’s diverticulum, polyps).

Hirschsprung disease or intestinal lymphoma (in older children or adults).

Clinical Features:

  1. Classic Triad (though not always present):

Colicky abdominal pain: Sudden onset, intermittent.

Abdominal mass: Often palpable (sausage-shaped mass).

Currant jelly stool: Blood and mucus in stool, sign of bowel ischemia.

  1. Other symptoms:

Vomiting (often bilious).

Lethargy.

Fever (in severe cases).

Abdominal distension.

Diminished or absent bowel sounds.

Dance sign (absence of bowel in the RLQ

Diagnosis:
1. Clinical Diagnosis: Often based on history and physical examination.

  1. Imaging:

Abdominal ultrasound: “Target sign” or “Doughnut sign” (shows concentric rings or bowel within bowel). Also pseudokidney/sandwich appearance.

X-ray: May show signs of bowel obstruction.

Air or contrast enema: Crescent sign, filling defect; Can be both diagnostic and therapeutic (reduction of the intussusception).

Management:
1. Non-surgical:

Air or contrast enema: First-line treatment for reduction, performed under radiological guidance. 3 times for three minutes each.

Hydration and stabilization (IV fluids, monitoring).

  1. Surgical:
    If enema reduction is unsuccessful or if signs of bowel perforation, peritonitis or ischemia are present, surgical reduction or resection may be required.

Exploratory laparotomy is performed if there’s suspicion of other underlying pathology (e.g., tumors, anatomical issues).

Prognosis:
Good: Most cases of intussusception can be treated successfully with enema reduction.

Complications: If untreated or delayed treatment, can lead to bowel necrosis, perforation, or sepsis.

Key Exam Tips:
Look for abdominal pain, abdominal mass, and currant jelly stool.

Diagnosis is often confirmed with ultrasound (target or doughnut sign).

Air enema is both diagnostic and therapeutic.

Surgical intervention is needed if non-surgical reduction fails or if there are complications.

75
Q

About BPH

A
  1. Recommended first line is alpha adrenoceptor blocker eg tamsulosin
  2. 5 alpha reductase inhibitors may be offered to men with LUTS and a Prostate gland >30g or PSA > 1.4ng/ml, and a high risk of progression.
76
Q

Side effects of alpha blockers?

A
  1. Sexual dysfunction
  2. Postural hypotension
  3. Micturiction syncope
  4. Dizziness
77
Q

Side effect of 5-alpha reductase inhibitors e.g. Finasteride

A

Erectile dysfunction

78
Q

Monitoring of treatment with terbinafine

A

LFT: within 4-6 weeks of Rx..

79
Q

About Acne vulgaris?

A
  1. Age: between 16-18 years
  2. Typical lesions are papules and pustules
  3. Typical location of lesions: Face, chest, and back..
80
Q

Triggers of Acne rosasea

A
  1. Spicy foods
  2. Calcium channel blockers and topical steroids
  3. Alcohol
  4. Hot or cold temperatures
81
Q

Red pustules on the face which worsens with shaving beard?

A

Folliculitis

*Caused by Staff aureus

*Heals without scarring..

DrFeelGood (3 decks)

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